text
stringlengths 11
320k
| source
stringlengths 26
161
|
|---|---|
Acta Oncologica is a peer-reviewed medical journal of oncology and the official journal of the five Nordic oncological societies. It is published by Taylor and Francis Group and was established in 1963. The editor-in-chief is Mef Nilbert ( Lunds University ). According to the Journal Citation Reports , the journal has a 2021 impact factor of 4.311. [ 1 ]
This article about an oncology journal is a stub . You can help Wikipedia by expanding it .
See tips for writing articles about academic journals . Further suggestions might be found on the article's talk page .
|
https://en.wikipedia.org/wiki/Acta_Oncologica
|
Acta Orthopaedica et Traumatologica Turcica is a peer-reviewed medical journal published bi-monthly by the Turkish Association of Orthopaedics and Traumatology . It is also the official journal of the Turkish Society of Orthopaedics and Traumatology . The journal is included in the Science Citation Index Expanded , Index Medicus , and TUBITAK-ULAKBIM .
Acta Orthopaedica et Traumatologica Turcica was established in 1962 and published semi-annually until 1974 after which publication was quarterly. The journal has been published 6 times a year since 1988. Articles have been peer-reviewed since 1991.
The journal publishes articles pertaining to diagnostic , treatment, and prevention methods as well as studies in basic sciences related to orthopedics and traumatology . Article types published are:
This article about a surgery journal is a stub . You can help Wikipedia by expanding it .
See tips for writing articles about academic journals . Further suggestions might be found on the article's talk page .
|
https://en.wikipedia.org/wiki/Acta_Orthopaedica_et_Traumatologica_Turcica
|
Activated charcoal cleanses , also known as charcoal detoxes , are a pseudoscientific use of a proven medical intervention for poisoning, activated charcoal . Activated charcoal is available in powder, tablet, and liquid form. Its proponents claim the use of activated charcoal regularly will detoxify and cleanse the body as well as boost one's energy and brighten the skin . Such claims violate basic principles of chemistry and physiology . There is no medical evidence for any health benefits of cleanses or detoxes via activated charcoal or any other method. Charcoal, when ingested , will absorb vitamins and nutrients as well as prescription medications present in the gastrointestinal tract which can make it dangerous to use unless directed by a medical doctor .
Activated charcoal, also known as activated carbon, is commonly produced from high-carbon source materials such as wood or coconut husk . [ 1 ] It is made by treating the source material with either a combination of heat and pressure, or with a strong acid or base followed by carbonization to make it highly porous . [ 2 ] This gives it a very large surface area for its volume , up to 3000 square metres per gram . [ 3 ] It has a large number of industrial uses including methane and hydrogen storage, air purification , decaffeination , gold purification , metal extraction , water purification , medicine , sewage treatment and air filters in gas masks and respirators . [ 4 ]
Activated charcoal is used to detoxify people, but only in life-threatening medical emergencies such as overdoses or poisonings . [ 5 ] [ 6 ] As it is indigestible it will only work on poisons or medications still present in the stomach and intestines . [ 6 ] Once these have been absorbed by the body the charcoal will no longer be able to adsorb them so early intervention is desirable. [ 2 ] Charcoal is not an effective treatment for alcohol , metals or elemental poisons such as lithium or arsenic as it will only adsorb certain chemicals and molecules . [ 2 ] It is usually administered by a nasogastric tube into the stomach as the thick slurry required for maximum adsorption is very difficult to swallow. [ 7 ]
Activated charcoal, as used in cleanses or detoxes, became popular around 2014 after it was brought to mainstream attention by Gwyneth Paltrow's Goop company where it was described as "one of the best juice cleanses". [ 8 ] In the following years, it became a popular additive to many different types of foods and drinks including juices, lemonades , coffee , pastries , ice cream , burgers , pizzas and pet food . [ 9 ] [ 10 ] The City of New York has banned activated charcoal in food products unless approval for their use is granted from the FDA . [ 11 ] Activated charcoal, excluding products designed for emergency medical interventions, is available in many pharmacies , wellness and health food stores in tablet , capsule and powder forms. [ 1 ]
Proponents of charcoal detoxes claim that it will cleanse the body by aiding in the removal of excess toxins that the body is unable to get rid of by itself. [ 12 ] Other claims made include that the use of activated charcoal provides anti-ageing benefits, will increase energy , brighten skin, decrease flatulence and bloating , and aid weight loss. [ 5 ] [ 8 ] [ 11 ] It is also said to be an ideal product in skincare products for improving acne and scarring. [ 13 ]
Scott Gavura of Science Based Medicine was highly critical of the use of activated charcoal in the wellness industry. In his 2015 article "Activated charcoal: The latest detox fad in an obsessive food culture", he said: [ 1 ]
Fake detox, the kind you find in magazines, and sold in pharmacies, juice bars, and health food stores, is make-believe medicine. The use of the term 'toxin' in this context is meaningless. There are no toxins named, because there's no evidence that these treatments do anything at all, but it sounds just scientific enough to be plausible.
Sophie Medlin, a lecturer in nutrition and dietetics at King's College in London suggests avoiding the use of activated charcoal cleanses for several reasons:
Jay Rayner of The Guardian contacted a manufacturer of activated charcoal lemonade to ask about its detoxifying properties. He was told that they make no claims at all about the product. When he then asked how the product detoxes the body, he was told that he was confusing the term " detox " with the medical term " detoxification ". [ 14 ]
Carrie Dennett of The Seattle Times said of activated charcoal: [ 12 ]
unless you have a rare health condition that renders your liver —or its supporting players: your kidneys , digestive system , lungs and lymphatic system —unable to perform as designed, then your body doesn't need help. Unless you have overdosed or been poisoned, there's no substantial evidence that activated charcoal will benefit you.
Charcoal is also used as an alternative to whitening products in toothpastes , but was found to not be as effective in whitening the teeth as regular products such as hydrogen peroxide . [ 11 ] [ 15 ]
|
https://en.wikipedia.org/wiki/Activated_charcoal_cleanse
|
An active placebo is a placebo that produces noticeable side effects that may convince the person being treated that they are receiving a legitimate treatment, rather than an inert placebo.
According to a 1965 paper, [ 1 ] the term "concealed placebo" (German: Kaschiertes Placebo) was suggested in a 1959 paper published in German. [ 2 ]
An example of an active placebo is the 1964 work of Shader and colleagues who used a combination of low-dose phenobarbital plus atropine to mimic the sedation and dry mouth produced by phenothiazines.
Morphine and gabapentin are painkillers with the common side effects of sleepiness and dizziness. In a 2005 study assessing the effects of these painkillers on neuropathic pain , lorazepam was chosen as an active placebo because it is not a painkiller but it does cause sleepiness and can cause dizziness. [ 3 ]
Testing from the late 1950s onwards on narcotic analgesics like morphine also has used dicyclomine as an active placebo, and on some occasions it was reported to cause the Straub mouse tail reaction, as do most narcotics. Clonidine is now finding more use as an active placebo for narcotics.
|
https://en.wikipedia.org/wiki/Active_placebo
|
In medicine , describing a disease as acute denotes that it is of recent onset ; it occasionally denotes a short duration . The quantification of how much time constitutes "short" and "recent" varies by disease and by context, but the core denotation of "acute" is always qualitatively in contrast with " chronic ", which denotes long-lasting disease (for example, in acute leukaemia and chronic leukaemia ).
In the context of the mass noun "acute disease", it refers to the acute phase (that is, a short course) of any disease entity. [ 1 ] [ 2 ] For example, in an article on ulcerative enteritis in poultry , the author says, "in acute disease there may be increased mortality without any obvious signs ", [ 3 ] referring to the acute form or phase of ulcerative enteritis.
A mild stubbed toe is an acute injury. Similarly, many acute upper respiratory infections and acute gastroenteritis cases in adults are mild and usually resolve within a few days or weeks. [ citation needed ]
The term "acute" is also included in the definition of several diseases, such as severe acute respiratory syndrome , acute leukaemia , acute myocardial infarction , and acute hepatitis . This is often to distinguish diseases from their chronic forms, such as chronic leukaemia , or to highlight the sudden onset of the disease, such as acute myocardial infarct. [ 2 ]
Related terms include:
P er acute ("very") is not to be confused with p re acute ("before", the opposite of postacute ).
Acute care is the early and specialist management of adult patients who have a wide range of medical conditions requiring urgent or emergency care usually within 48 hours of admission or referral from other specialties. [ 2 ]
Acute hospitals are those intended for short-term medical and/or surgical treatment and care which is a medical speciality of acute medicine , as often primary care is not positioned to assume this role. [ 12 ]
Signs and symptoms Syndrome Disease
Medical diagnosis Differential diagnosis Prognosis
Acute Chronic Cure
Eponymous disease Acronym or abbreviation Remission
|
https://en.wikipedia.org/wiki/Acute_(medicine)
|
An acute abdomen refers to a sudden, severe abdominal pain . [ 1 ] It is in many cases a medical emergency, requiring urgent and specific diagnosis. [ 2 ] Several causes need immediate surgical treatment .
Common causes of an acute abdomen include a gastrointestinal perforation , peptic ulcer disease , mesenteric ischemia , acute cholecystitis , appendicitis , diverticulitis , pancreatitis , and an abdominal hemorrhage. However, this is a non-exhaustive list and other less common causes may also lead to an acute abdomen. [ 3 ] In pregnant patient, a tubo-ovarian abscess , ruptured ovarian cyst or a ruptured ectopic pregnancy are common causes of an acute abdomen. [ 3 ]
Vascular disorders are more likely to affect the small bowel than the large bowel. Arterial supply to the intestines is provided by the superior and inferior mesenteric arteries (SMA and IMA respectively), both of which are direct branches of the aorta. [ 4 ]
Clinically, patients present with diffuse abdominal pain, bowel distention, and bloody diarrhea. On physical exam, bowel sounds will be absent. Laboratory tests reveal a neutrophilic leukocytosis, sometimes with a left shift, and increased serum amylase. Abdominal radiography will show many air-fluid levels, as well as widespread edema. Acute ischemic abdomen is a surgical emergency. Typically, treatment involves removal of the region of the bowel that has undergone infarction , and subsequent anastomosis of the remaining healthy tissue. [ 5 ]
Traditionally, the use of opiates or other pain medications in patients with an acute abdomen has been discouraged before the clinical examination because of the concern that pain medications may mask the signs and symptoms of the condition and therefore may lead to a delay in diagnosis. However, the scientific literature has shown that early administration of pain medications, including opiates, in those with acute abdomen does not lead to delayed diagnosis, delayed treatment or errors in management (the incorrect surgical treatment administered or performing un-necessary surgery). [ 6 ] [ 7 ] [ 3 ] In a meta-analysis of those with acute appendicitis, early administration of opiates was found to alter treatment approach (with a slightly higher rate of appendectomy in those who received opiates) but diagnostic accuracy and surgical outcomes were unaffected by pain medication use. [ 8 ] Clinical guidelines also recommend early analgesic use before a cause is established. [ 9 ]
Medical imaging aids in the diagnosis of potential causes of an acute abdomen. A CT scan or ultrasound of the abdomen and pelvis are the preferred imaging modalities in the evaluate of an acute abdomen. [ 9 ] The use of radiocontrast agents with CT scans improve diagnostic accuracy. [ 3 ] Some authors advocate for the use of CT angiography with contrast of the abdomen and pelvis as the preferred imaging modality. [ 3 ] An ultrasound is the preferred imaging modality in pregnant patients as CT scans expose the fetus to ionizing radiation which may lead to adverse pregnancy outcomes. [ 3 ] An abdominal x-ray may show free air in the abdominal cavity due to a perforation in the gastrointestinal tract. However, abdominal x-ray is not recommended as part of the diagnostic evaluation in acute abdomen due to its low sensitivity and specificity. [ 9 ] [ 3 ] Delays in medical imaging acquisition and interpretation greater than 2 hours are associated with an increased risk of complications and death. [ 3 ] [ 10 ]
In a population based study of Medicare patients in the United States, Black patients who were admitted to the hospital for an acute abdomen requiring general surgery consultation were 14% less likely to receive surgical consultation as compared to White patients. These racial disparities in care persisted (with an 11% difference) when socioeconomic factors were standardized. [ 11 ] In another population based study in the United States, Black patients and patients from other racial minority groups were 22-30% less likely to receive pain medication for an acute abdomen as compared to White patients. [ 12 ]
|
https://en.wikipedia.org/wiki/Acute_abdomen
|
Acute basophilic leukemia (ABL) is a very rare & clinically aggressive subtype of acute myeloid leukemia (AML) designated by the WHO as a distinct entity within the subcategory of AML, Not Otherwise Specified (NOS), [ 1 ] which accounts for roughly 4-5% of all "acute non-lymphocytic" cases of leukemia. [ 2 ] ABL can be either primary (sporadic) or secondary to an existing bone marrow neoplasm (commonly CML or AML with BCR - ABL1 ). [ 3 ] In either case, the disease is characterized by rapid proliferation of abnormal basophils & immature blasts in the bone marrow and peripheral blood. [ 1 ] This process interferes with normal blood cell production, giving rise to classic symptoms of AML & ultimately bone marrow failure. [ 4 ] Given the role of basophils in coordinating histamine release during inflammatory reactions, those with ABL also typically experience symptoms of hyper-histaminemia which can manifest cutaneously & within the gastrointestinal tract . [ 4 ]
Common clinical manifestations can include: [ 4 ]
Similar to other subtypes of AML, sporadic cases of ABL typically arise from genetic mutations disrupting normal hematopoiesis in the bone marrow. [ 4 ] However, ABL to this point, lacks a defining genetic abnormality. [ 1 ] Thus far, it has been found to be cytogenetically heterogeneous but frequently associated with Philadelphia chromosome in CML & AML with t(9;22) BCR-ABL1. [ 5 ]
Recently, a particular translocation of interest has come into focus due to its recurrence in sporadic cases of ABL observed in male infants. [ 4 ] The t(X;6)(p11;q23) translocation results in the formation of MYB-GATA1 fusion gene, which enhances the expression of cellular markers of immaturity, such as CD34 and limit further differentiation. [ 4 ] Expression of this fusion gene also directly activates the transcription of two important cell membrane receptors. When active, NTRK1 (neurotrophic receptor tyrosine kinase 1) and IL-1RL1 (ligands of IL-1 receptor-like 1) induce myeloblasts to differentiate into basophils, which likely contributes to the profound basophilia observed in cases of ABL. [ 6 ]
Comprehensive clinical workup for ABL can include any of the following: complete blood count (CBC), serum chemistries, inflammatory markers (ESR/CRP), bone marrow aspiration + biopsy, immunohistochemical stains , electron microscopy, immunophenotyping, peripheral blood smear , chromosomal analysis + FISH panel to rule out MDS/MPD, molecular studies & cytogenic analysis, reverse transcription(RT)-PCR to evaluate for presence of BCR-ABL1, JAK2 & other oncogenic mutations, and CT scan to evaluate for organomegaly/LN involvement. [ 2 ] [ 3 ]
Consensus diagnostic criteria of ABL, as specified according to the AML subtypes, defined by differentiation markers according to the WHO: [ 1 ]
Another proposed diagnostic criteria of basophilic leukemia that subcategorizes the disease as either acute (ABL) vs chronic (CBL), based on the percentage of blasts (myeloblasts and metachromatic blasts) in the BM & PB. [ 3 ]
Acute Basophilic Leukemia:
Chronic Basophilic Leukemia:
Given the aggressive nature of ABL, patients will likely need stem cell transplant . Those patients who are not candidates for transplant require chemotherapy or targeted immunotherapy in combination with prophylactic antihistamines agents for symptomatic support. [ 3 ]
Given the rarity of this disease, little information is available to provide a definitive prognosis. However, the few studies done to this point indicate the overall prognostic outlook for ABL to be very poor. Survival time ranges from 2-16 months. [ 3 ]
This oncology article is a stub . You can help Wikipedia by expanding it .
|
https://en.wikipedia.org/wiki/Acute_basophilic_leukemia
|
Acute cardiac unloading is any maneuver, therapy, or intervention that decreases the power expenditure of the ventricle and limits the hemodynamic forces that lead to ventricular remodeling after insult or injury to the heart . This technique is being investigated as a therapeutic to aid after damage has occurred to the heart, such as after a heart attack . The theory behind this approach is that by simultaneously limiting the oxygen demand and maximizing oxygen delivery to the heart after damage has occurred, the heart is more fully able to recover. This is primarily achieved by using temporary minimally invasive mechanical circulatory support to supplant the pumping of blood by the heart. Using mechanical support decreases the workload of the heart, or unloads it.
Cardiac traumas such as myocardial infarction (commonly called a heart attack), myocarditis , peripartum cardiomyopathy , cardiogenic shock , and takotsubo cardiomyopathy result in an impaired ability of the heart to pump blood. Without proper blood flow the person will ultimately die. Maintaining sufficient cardiac output is the primary objective of therapeutic approaches treating these cardiac conditions. However, many therapies aimed at increasing cardiac output place further stress on the heart. In this way a well-document vicious cycle begins in which increased cardiac output is required, but in order to achieve this the heart must work harder. This exacerbated stress leads to poorer outcomes. [ 1 ] With the exception of cardiopulmonary bypass , current therapeutic approaches do not allow the heart to rest and recover. The workload of the heart (pumping blood) is never uncoupled from heart function. Acute cardiac unloading is able to functionally uncouple [ 2 ] the heart from cardiac output, allowing the heart to rest and recover from damage.
The pumping of blood is considered the workload of the heart and requires power expenditure. Acute cardiac unloading is any maneuver, therapy, or intervention that decreases the power expenditure of the ventricle while maintaining cardiac output. Oxygen consumption (MVO2) is a direct measure of the total energy requirements of the heart, including the energy needed to pump blood. [ 3 ]
Pressure-volume (PV) loop analysis provides a framework for understanding how acute cardiac unloading reduces MVO2 in the heart. [ 4 ] [ 5 ] The PV loop characterizes the events occurring during a single cardiac cycle (a single heartbeat). The total area bound by the PV loop is the mechanical energy ( pressure-volume work ) used to actively pump blood every beat, measured in mmHg·mL (aka, a joule ). This is known as the stroke work (SW). The remaining area bound by the ESPVR and EDPVR that is outside of the loop is the potential energy (PE) that resides in the myofilaments that was not transduced into the work of pumping blood. The sum of these two areas (PE + SW) is known as the pressure-volume area (PVA). PVA is a first order approximation of MVO2. [ 3 ]
Acute cardiac unloading decreases the workload of and the oxygen demand of the heart. This can be visualized as an overall decrease in the PVA of the PV loop. [ 3 ] [ 2 ] Mechanical unloading of the heart by a percutaneous ventricular support device such as the Impella device can achieve this in two ways. First, the device is a continuous flow device. It directly aspirates blood from the ventricle into the aorta . This decreases the preload and results in a left-shift and loss of the normal isovolumic contraction line. [ 2 ]
Under conditions of mechanical support, mean aortic pressure (MAP) is maintained independent of native ventricular function, and ventricular and aortic pressures become uncoupled. [ 2 ]
When the heart is damaged by a myocardial infarction a portion of muscle is permanently lost. The heart has a limited innate ability to replace dead muscle with new, functional muscle . [ 6 ] The dead heart muscle is replaced by non-contractile fibrotic tissue, forming the myocardial scar . Scar tissue does not contract, and it does not help the heart pump blood. This persistently stresses the heart and increases the workload of the lasting myocardium as measured by MVO2. Clinical research indicates that as the size of the myocardial scar increases, so does the likelihood of the patient to develop heart failure. [ 7 ] Acute cardiac unloading decreases cardiac MVO2 and has been demonstrated to limit the amount of scar tissue that forms, thus preserving heart function after a heart attack. [ 8 ] [ 9 ]
|
https://en.wikipedia.org/wiki/Acute_cardiac_unloading
|
Acute decompensated heart failure ( ADHF ) is a sudden worsening of the signs and symptoms of heart failure , which typically includes difficulty breathing ( dyspnea ), leg or feet swelling , and fatigue . [ 1 ] ADHF is a common and potentially serious cause of acute respiratory distress . The condition is caused by severe congestion of multiple organs by fluid that is inadequately circulated by the failing heart. An attack of decompensation can be caused by underlying medical illness, such as myocardial infarction , an abnormal heart rhythm , infection , or thyroid disease .
Heart failure or cardiovascular insufficiency can be acute without being decompensated from a chronic condition. In this case, the signs of congestion such as weight gain and edema will not yet have developed. This is commonly due to pump failure or cardiovascular insufficiency after myocardial infarction when a significant loss of cardiac function occurs. Such patients will, have shortness of breath due to poor tissue perfusion, tissue hypoxia and metabolic acidosis . [ 2 ]
Cardiac symptoms of heart failure include chest pain/pressure and palpitations . Common noncardiac signs and symptoms of heart failure include loss of appetite , nausea, weight loss, bloating, fatigue, weakness, low urine output , waking up at night to urinate , and cerebral symptoms of varying severity, ranging from anxiety to memory impairment and confusion. [ 3 ]
Flash Pulmonary Edema or Crash Pulmonary Edema is a clinical characterization of acute heart failure with a dramatic presentation. [ 4 ] It is an acute cardiac disease precipitated by cardiac events and usually associated with severe hypertension.
Chronic stable heart failure may easily decompensate . This most commonly results from an intercurrent illness (such as pneumonia ), myocardial infarction (a heart attack), abnormal heart rhythms (such as atrial fibrillation ), uncontrolled high blood pressure , or the person's failure to maintain a fluid restriction, diet, or medication. [ 5 ] Other well recognized precipitating factors include anemia and hyperthyroidism which place additional strain on the heart muscle. Excessive fluid or salt intake, and medication that causes fluid retention such as NSAIDs and thiazolidinediones , may also precipitate decompensation. [ 6 ]
A jugular venous distension is the most sensitive clinical sign for acute decompensation. [ 7 ]
In acute decompensated heart failure, the immediate goal is to re-establish adequate perfusion and oxygen delivery to end organs. This entails ensuring that airway, breathing, and circulation are adequate. Management consists of propping up the head of the patient, giving oxygen to correct hypoxemia, administering morphine, diuretics like furosemide , addition of an ACE inhibitor, use of nitrates and use of digoxin if indicated for the heart failure and if arrhythmic. [ 8 ]
Supplemental oxygen may be administered if blood levels of oxygen are low ; the Heart Failure Society of America, however, has recommended that it not be used routinely. [ 8 ]
Initial therapy of acute decompensated heart failure usually includes some combination of a vasodilator such as nitroglycerin, a loop diuretic such as furosemide , and non-invasive positive pressure ventilation (NIPPV). [ 9 ]
A number of different medications are required for people who are experiencing heart failure. Common types of medications that are prescribed for heart failure patients include ACE inhibitors , vasodilators , beta blockers , aspirin , calcium channel blockers , and cholesterol lowering medications such as statins . Depending on the type of damage a patient has suffered and the underlying cause of the heart failure, any of these drug classes or a combination of them can be prescribed. Patients with heart pumping problems will use a different medication combination than those who are experiencing problems with the heart's ability to fill properly during diastole . Potentially dangerous drug interactions can occur when different drugs mix together and work against each other. [ 10 ]
Nitrates such as nitroglycerin ( glyceryl trinitrate ) and isosorbide dinitrate are often used as part of the initial therapy for ADHF. [ 9 ]
Another option is nesiritide , although it should only be considered if conventional therapy has been ineffective or contraindicated as it is much more expensive than nitroglycerin and has not been shown to be of any greater benefit. [ 11 ]
A 2013 Cochrane review, compared nitrates and other pharmacological, non-pharmacological, and placebo interventions. [ 9 ] The review found no significant difference between the interventions in terms of symptom control or haemodynamic stability. [ 9 ]
The National Institutes for Health and Care Excellence (NICE) guidelines do not recommend routinely offering nitrates in acute heart failure. [ 12 ]
Heart failure is usually associated with a volume overloaded state. Therefore, those with evidence of fluid overload should be treated initially with intravenous loop diuretics. In the absence of symptomatic low blood pressure intravenous nitroglycerin is often used in addition to diuretic therapy to improve congestive symptoms. [ 8 ]
Volume status should still be adequately evaluated. Some heart failure patients on chronic diuretics can undergo excessive diuresis. In the case of diastolic dysfunction without systolic dysfunction, fluid resuscitation may, in fact, improve circulation by decreasing heart rate, which will allow the ventricles more time to fill. Even if the patient is edematous, fluid resuscitation may be the first line of treatment if the person's blood pressure is low. The person may, in fact, have too little fluid in their blood vessels, but if the low blood pressure is due to cardiogenic shock , the administration of additional fluid may worsen the heart failure and associated low blood pressure. If the person's circulatory volume is adequate but there is persistent evidence of inadequate end-organ perfusion, inotropes may be administered. In certain circumstances, a left ventricular assist device (LVAD) may be necessary.
Once the person is stabilized, attention can be turned to treating pulmonary edema to improve oxygenation. Intravenous furosemide is generally the first line. However, people on long-standing diuretic regimens can become tolerant, and dosages must be progressively increased. If high doses of furosemide are inadequate, boluses or continuous infusions of bumetanide may be preferred. These loop diuretics may be combined with thiazide diuretics such as oral metolazone or intravenous chlorothiazide for a synergistic effect. Intravenous preparations are physiologically preferred because of more predictable absorption due to intestinal edema, however, oral preparations can be significantly more cost effective. [ 13 ]
The effectiveness and safety of ACE inhibitors and angiotensin receptor blockers (ARBs) acutely in ADHF have not been well studied, but are potentially harmful. A person should be stabilized before therapy with either of these medication classes is initiated. [ 14 ] Individuals with poor kidney perfusion are especially at risk for kidney impairment inherent with these medications. [ 15 ]
Beta-blockers are stopped or decreased in people with acutely decompensated heart failure and a low blood pressure. However, continuation of beta-blockers may be appropriate if the blood pressure is adequate. [ 16 ]
Inotropes are indicated if low blood pressure ( SBP < 90 mmHg ) is present.
The National Institutes for Health and Care Excellence (NICE) guidelines do not recommend routinely offering inotropes in acute heart failure. [ 12 ] However, they recommend it be considered in patients with ADHF and potentially reversible caradiogenic shock. [ 12 ]
Opioids have traditionally been used in the treatment of the acute pulmonary edema that results from acute decompensated heart failure. A 2006 review, however, found little evidence to support this practice. [ 17 ]
The National Institutes for Health and Care Excellence (NICE) guidelines do not recommend routinely offering opioids in acute heart failure. [ 12 ]
Continuous positive airway pressure may be applied using a face mask; this has been shown to improve symptoms more quickly than oxygen therapy alone, [ 18 ] and has been shown to reduce the risk of death. [ 19 ] [ 20 ] Severe respiratory failure requires treatment with endotracheal intubation and mechanical ventilation .
Ultrafiltration can be used to remove fluids in people with ADHF associated with kidney failure . Studies have found that it decreases health care utilization at 90 days. [ 21 ] One such method is aquapheresis ultra-filtration
A 2022 Cochrane review on the benefits, efficacy, and safety of ultrafiltration compared to diuretic therapy found that ultrafiltration probably reduces the incidence of heart-failure related hospitalisation in the long term. [ 22 ]
The National Institutes for Health and Care Excellence (NICE) guidelines do not recommend routinely offering ultrafiltration in acute heart failure. [ 12 ]
In some cases, doctors recommend surgery to treat the underlying problem that led to heart failure. [ 23 ] Different procedures are available depending on the level of necessity and include coronary artery bypass surgery , heart valve repair or replacement, or heart transplantation . During these procedures, devices such as heart pumps, pacemakers , or defibrillators might be implanted. The treatment of heart disease is rapidly changing and thus new therapies for acute heart failure treatment are being introduced to save more lives from these massive attacks. [ 24 ]
Bypass surgery is performed by removing a vein from the arm or leg, or an artery from the chest and replacing the blocked artery in the heart. This allows the blood to flow more freely through the heart. Valve repair is where the valve that is causing heart failure is modified by removing excess valve tissues that cause them to close too tightly. In some cases, annuloplasty is required to replace the ring around the valves. If the repair of the valve is not possible, it is replaced by an artificial heart valve . The final step is heart replacement. When severe heart failure is present and medicines or other heart procedures are not effective, the diseased heart needs to be replaced.
Another common procedure used to treat heart failure patients is an angioplasty . Is a procedure used to improve the symptoms of coronary artery disease (CAD), reduce the damage to the heart muscle after a heart attack , and reduce the risk of death in some patients. [ 25 ]
A pacemaker is a small device that's placed in the chest or abdomen to help control abnormal heart rhythms. [ 26 ] They work by sending electric pulses to the heart to prompt it to beat at a rate that is considered to be normal and are used to treat patients with arrhythmias. They can be used to treat hearts that are classified as either a tachycardia that beats too fast, or a bradycardia that beats too slow.
|
https://en.wikipedia.org/wiki/Acute_decompensated_heart_failure
|
Acute eosinophilic leukemia (AEL) is a rare subtype of acute myeloid leukemia with 50 to 80 percent of eosinophilic cells in the blood and marrow. It can arise de novo or may develop in patients having the chronic form of a hypereosinophilic syndrome . Patients with acute eosinophilic leukemia have a propensity for developing bronchospasm as well as symptoms of the acute coronary syndrome and/or heart failure due to eosinophilic myocarditis and eosinophil-based endomyocardial fibrosis . [ 1 ] [ 2 ] Hepatomegaly and splenomegaly are more common than in other variants of AML.
A specific histochemical reaction, cyanide-resistant peroxidase, permits identification of leukemic blast cells with eosinophilic differentiation and diagnosis of acute eosinoblastic leukemia in some cases of AML with few identifiable eosinophils in blood or marrow.
When there is eosinophilia with increased immature precursors along with blasts; one need to identify lineage of blasts. As per old FAB classification most of the time blast lineage will be myeloid and may fall in M4EO of FAB classification. [ 3 ] This entity need treatment like acute myeloid leukemia. However more rarely Eosinophilic leukemia may have underlying lymphoid blasts with t(5;14) (IL3;IGH). [ 4 ] with this gene fusion and eosinophilic cytokine comes under control of immunoglobulin heavy chain (IgH) locus. This entity need treatment as ALL. Overall prognosis is not dependent on eosinophilia but underlying lineage and genetic abnormalities.
This oncology article is a stub . You can help Wikipedia by expanding it .
|
https://en.wikipedia.org/wiki/Acute_eosinophilic_leukemia
|
An acute hemolytic transfusion reaction ( AHTR ), also called immediate hemolytic transfusion reaction , is a life-threatening reaction to receiving a blood transfusion . AHTRs occur within 24 hours of the transfusion and can be triggered by a few milliliters of blood. The reaction is triggered by host antibodies destroying donor red blood cells. AHTR typically occurs when there is an ABO blood group incompatibility, and is most severe when type A donor blood is given to a type O recipient. [ 1 ] [ 2 ] [ 3 ]
Early acute hemolytic transfusion reactions are typically characterized by fever, which may be accompanied by rigors (chills). Mild cases are also typically characterized by abdominal, back, flank, or chest pain. More severe cases may be characterized by shortness of breath , low blood pressure , hemoglobinuria , and may progress to shock and disseminated intravascular coagulation . In anesthetized or unconscious patients, hematuria (blood in the urine) may be the first sign of AHTR. Other symptoms include nausea, vomiting, and wheezing . [ 4 ]
The most common cause of acute hemolytic transfusion reaction is ABO incompatibility , which is typically due to human error that results in a recipient receiving the incorrect blood product. Rarely, other blood type incompatibilities can cause AHTR, the most common of which is Kidd antigen incompatibility. [ 4 ] Rh , Kell , and Duffy antigen incompatibility have also been implicated in AHTR. [ 5 ]
Acute hemolytic transfusion reactions result when antibodies against A and/or B antigens (isohemagglutinins) present in the recipient's blood destroy the respective donor red blood cells . [ 4 ] [ 5 ] This is mediated through the antibodies IgM (and to a lesser extent IgG ) which cause activation of the complement cascade , with complement C5-C9 forming the membrane attack complex which leads to pore formation and red blood cell lysis. [ 6 ] The lysed red blood cells release free hemoglobin into the bloodstream, overwhelming hemoglobin binding proteins such as albumin , haptoglobin , and hemopexin , with the excess free hemoglobin leading to renal vasoconstriction (via nitric oxide scavenging), which then leads to acute tubular necrosis and acute kidney injury . [ 6 ]
The antibodies also activate the coagulation cascade (blood clotting system) via factor XII , which can lead to disseminated intravascular coagulation and kidney damage. Isohemagglutinins also activate the complement cascade via C3a and C5a , which then promote inflammatory cytokine release from white blood cells . C3a and C5a also activate mast cells which release serotonin and histamine , which along with fragments of red blood cells that were destroyed, further stimulate the release of inflammatory cytokines. [ 6 ] These inflammatory cytokines include IL-1 , IL-6 , IL-8 , and TNF-alpha , which cause increased capillary permeability and vasodilation leading to symptoms of low blood pressure, fever, chest pain, nausea, vomiting, and wheezing. [ 4 ] [ 6 ]
The diagnosis of AHTR is made with microscopic examination of the recipient's blood and a direct antiglobulin test (direct Coombs test) which detects IgG antibodies or complement bound to red blood cells and is usually diagnostic of acute hemolytic transfusion reactions. [ 6 ] The donor and recipient blood can be re-tested with a type, crossmatch, and antibody screen to determine the cause of the reaction. [ 4 ] The donor blood should be examined for any labelling error or other possible errors from the blood bank, which may help prevent other mislabeled blood products from being distributed. [ 6 ] Testing the donor blood using a gram stain and blood culture can also help to rule out an infectious cause of the symptoms (such as the donor receiving infected blood). [ 6 ] Testing for urine or plasma free hemoglobin may also assist in the diagnosis. [ 6 ]
Initial treatment for any type of transfusion reaction, including AHTR, is discontinuation of the transfusion. Fluid replacement and close monitoring of vital signs are important. People with AHTR are managed with supportive care , which may include diuretics , blood pressure support, and treatment of disseminated intravascular coagulation (with fresh frozen plasma , cryoprecipitate , and platelet transfusion ). [ 6 ] The use of steroids, intravenous immune-globulins ( IVIG ) or plasma exchange is not supported by evidence. [ 6 ] Furosemide is the diuretic of choice in treatment of AHTR with decreased urine output, because it increases the amount of blood that reaches the renal cortex . [ 4 ] Mannitol may also be used. [ 5 ] Dopamine is used for blood pressure support because it causes vasodilation (dilation of blood vessels) in the kidneys as well as increasing the cardiac output (amount of blood pumped by the heart each minute). [ 4 ]
The severity and prognosis of acute hemolytic transfusion depends on the rate of blood administration and the total volume of the transfusion. The levels of anti-A and anti-B antibodies in the recipients blood may also predict the prognosis, with higher levels of antibodies thought to portend a more severe course. [ 6 ] Approximately 2% of cases are fatal. Reactions that begin sooner are typically more severe. [ 4 ]
Acute hemolytic transfusion reaction is estimated to occur in 1 in 38,000 to 1 in 70,000 transfusions. An estimated 41% of ABO-incompatible transfusions result in AHTR. [ 4 ]
|
https://en.wikipedia.org/wiki/Acute_hemolytic_transfusion_reaction
|
Acute myeloblastic leukemia without maturation is a quickly progressing disease in which too many immature white blood cells (not lymphocytes ) are found in the blood and bone marrow . [ 1 ]
It is classified as "M1" in the FAB classification.
This article incorporates public domain material from Dictionary of Cancer Terms . U.S. National Cancer Institute .
This oncology article is a stub . You can help Wikipedia by expanding it .
|
https://en.wikipedia.org/wiki/Acute_myeloblastic_leukemia_without_maturation
|
Acute pericarditis is a type of pericarditis ( inflammation of the sac surrounding the heart, the pericardium ) usually lasting less than 4 to 6 weeks. [ 1 ] It is the most common condition affecting the pericardium.
Chest pain is one of the common symptoms of acute pericarditis. It is usually of sudden onset, occurring in the anterior chest and often has a sharp quality that worsens with breathing in or coughing, due to inflammation of the pleural surface at the same time. The pain may be reduced with sitting up and leaning forward while worsened with lying down, and also may radiate to the back, to one or both trapezius ridges. However, the pain can also be dull and steady, resembling the chest pain in an acute myocardial infarction . As with any chest pain, other causes must also be ruled out, such as GERD , pulmonary embolism , muscular pain, etc.
A pericardial friction rub is a very specific sign of acute pericarditis, meaning the presence of this sign invariably indicates presence of disease. However, absence of this sign does not rule out disease. This rub can be best heard by the diaphragm of the stethoscope at the left sternal border arising as a squeaky or scratching sound, resembling the sound of leather rubbing against each other. This sound should be distinguished from the sound of a murmur , which is similar but sounds more like a "swish" sound than a scratching sound. The pericardial rub is said to be generated from the friction generated by the two inflamed layers of the pericardium ; however, even a large pericardial effusion does not necessarily present a rub. The rub is best heard during the maximal movement of the heart within the pericardial sac, namely, during atrial systole , ventricular systole, and the filling phase of early ventricular diastole .
Fever may be present since this is an inflammatory process.
There are several causes of acute pericarditis. [ 2 ] In developed nations, the cause of most (80–90%) cases of acute pericarditis is unknown but a viral cause is suspected in the majority of such cases. [ 2 ] The other 10–20% of acute pericarditis cases have various causes including connective tissue diseases (e.g., systemic lupus erythematosus ), cancer , or involve an inflammatory reaction of the pericardium following trauma to the heart such as after a heart attack such as Dressler's syndrome . [ 2 ] Familial mediterranean fever and TNF receptor associated periodic syndrome are rare inherited autoimmune diseases capable of causing recurring episodes of acute pericarditis. [ 2 ]
Clinical presentation of diseases of pericardium may vary between: [ 3 ] [ 4 ]
For acute pericarditis to formally be diagnosed, two or more of the following criteria must be present: chest pain consistent with a diagnosis of acute pericarditis (sharp chest pain worsened by breathing in or a cough), a pericardial friction rub , a pericardial effusion , and changes on electrocardiogram (ECG) consistent with acute pericarditis. [ 2 ]
A complete blood count may show an elevated white count and a serum C-reactive protein may be elevated. Acute pericarditis is associated with a modest increase in serum creatine kinase MB (CK-MB). [ 5 ] and cardiac troponin I (cTnI), [ 6 ] [ 7 ] both of which are also markers for injury to the muscular layer of the heart. Therefore, it is imperative to also rule out acute myocardial infarction in the face of these biomarkers. The elevation of these substances may occur when inflammation of the heart's muscular layer in addition to acute pericarditis. [ 2 ] Also, ST elevation on EKG (see below) is more common in those patients with a cTnI > 1.5 μg/L. [ 7 ] Coronary angiography in those patients should indicate normal vascular perfusion. Troponin levels increase in 35-50% of people with pericarditis. [ 8 ]
Electrocardiogram (ECG) changes in acute pericarditis mainly indicates inflammation of the epicardium (the layer directly surrounding the heart), since the fibrous pericardium is electrically inert. For example, in uremia, there is no inflammation in the epicardium, only fibrin deposition, and therefore the EKG in uremic pericarditis will be normal. Typical EKG changes in acute pericarditis includes [ 5 ] [ 9 ]
The two most common clinical conditions where ECG findings may mimic pericarditis are acute myocardial infarction (AMI) and generalized early repolarization. [ 10 ] As opposed to pericarditis, AMI usually causes localized convex ST-elevation usually associated with reciprocal ST-depression which may also be frequently accompanied by Q-waves, T-wave inversions (while ST is still elevated unlike pericarditis), arrhythmias and conduction abnormalities. [ 11 ] In AMI, PR-depressions are rarely present. Early repolarization usually occurs in young males (age <40 years) and ECG changes are characterized by terminal R-S slurring, temporal stability of ST-deviations and J-height/ T-amplitude ratio in V5 and V6 of <25% as opposed to pericarditis where terminal R-S slurring is very uncommon and J-height/ T-amplitude ratio is ≥ 25%. Very rarely, ECG changes in hypothermia may mimic pericarditis, however differentiation can be helpful by a detailed history and presence of an Osborne wave in hypothermia. [ 12 ]
Another important diagnostic electrocardiographic sign in acute pericarditis is the Spodick sign. [ 13 ] It signifies to the PR-depressions in a usual (but not always) association with downsloping TP segment in patients with acute pericarditis and is present in up to 80% of the patients affected with acute pericarditis. The sign is often best visualized in lead II and lateral precordial leads. In addition, Spodick's sign may also serve as an important distinguishing electrocardiographic tool between the acute pericarditis and acute coronary syndrome. The presence of a classical Spodick's sign is often a giveaway to the diagnosis. [ citation needed ]
Rarely, electrical alternans may be seen, depending on the size of the effusion. [ citation needed ]
A chest x-ray is usually normal in acute pericarditis but can reveal the presence of an enlarged heart if a pericardial effusion is present and is greater than 200 mL in volume. Conversely, patients with unexplained new onset cardiomegaly should always be worked up for acute pericarditis. [ citation needed ]
An echocardiogram is typically normal in acute pericarditis but can reveal pericardial effusion, the presence of which supports the diagnosis, although its absence does not exclude the diagnosis. [ citation needed ]
Patients with uncomplicated acute pericarditis can generally be treated and followed up in an outpatient clinic. However, those with high risk factors for developing complications (see above) will need to be admitted to an inpatient service, most likely an ICU setting. High risk patients include the following: [ 14 ]
Pericardiocentesis is a procedure whereby the fluid in a pericardial effusion is removed through a needle. It is performed under the following conditions: [ 15 ]
NSAIDs in viral or idiopathic pericarditis. In patients with underlying causes other than viral, the specific etiology should be treated. With idiopathic or viral pericarditis, NSAID is the mainstay treatment. Goal of therapy is to reduce pain and inflammation. The course of the disease may not be affected. The preferred NSAID is ibuprofen because of rare side effects, better effect on coronary flow, and larger dose range. [ 15 ] Depending on severity, dosing is between 300 and 800 mg every 6–8 hours for days or weeks as needed. An alternative protocol is aspirin 800 mg every 6–8 hours. [ 14 ] Dose tapering of NSAIDs may be needed. In pericarditis following acute myocardial infarction, NSAIDs other than aspirin should be avoided since they can impair scar formation. As with all NSAID use, GI protection should be engaged. Failure to respond to NSAIDs within one week (indicated by persistence of fever, worsening of condition, new pericardial effusion, or continuing chest pain) likely indicates that a cause other than viral or idiopathic is in process. [ citation needed ]
Colchicine , which has been essential to treat recurrent pericarditis, has been supported for routine use in acute pericarditis by recent prospective studies. [ 16 ] Colchicine can be given 0.6 mg twice a day (0.6 mg daily for patients <70 kg) for 3 months following an acute attack. It should be considered in all patients with acute pericarditis, preferably in combination with a short-course of NSAIDs. [ 10 ] For patients with a first episode of acute idiopathic or viral pericarditis, they should be treated with an NSAID plus colchicine 1–2 mg on first day followed by 0.5 daily or twice daily for three months. [ 17 ] [ 18 ] [ 19 ] [ 20 ] [ 21 ] It should be avoided or used with caution in patients with severe chronic kidney disease , hepatobiliary dysfunction, blood dyscrasias, and gastrointestinal motility disorders. [ 10 ]
Corticosteroids are usually used in those cases that are clearly refractory to NSAIDs and colchicine and a specific cause has not been found. Systemic corticosteroids are usually reserved for those with autoimmune disease. [ 17 ]
One of the most feared complications of acute pericarditis is cardiac tamponade . Cardiac tamponade is accumulation of enough fluid in the pericardial space --- pericardial effusion --- to cause serious obstruction to the inflow of blood to the heart. Signs of cardiac tamponade include distended neck veins, muffled heart sounds when listening with a stethoscope , and low blood pressure (together known as Beck's triad ). [ 2 ] This condition can be fatal if not immediately treated.
Another longer term complication of pericarditis, if it recurs over a longer period of time (normally more than 3 months), is progression to constrictive pericarditis . Recent studies have shown this to be an uncommon complication. [ 22 ] The definitive treatment for constrictive pericarditis is pericardial stripping, which is a surgical procedure where the entire pericardium is peeled away from the heart. [ citation needed ]
|
https://en.wikipedia.org/wiki/Acute_pericarditis
|
Adam Castillejo (born 1979 or 1980), also known as "The London Patient", [ 1 ] is the second person known to have been cured of HIV infection. [ 3 ] [ 4 ] [ 5 ] Castillejo, who is British-Venezuelan [ 6 ] and has mixed European ancestry, lives in London. He has previously worked as a chef [ 7 ] and is now a motivational speaker.
Diagnosed in 2003, his body became resistant to HIV infection after receiving a bone marrow transplant in 2016 [ 8 ] to treat Hodgkin's lymphoma . The German donor carried the CCR5-Δ32 mutation which gives resistance from HIV infection. [ 9 ] It is likely because of his half-Dutch father that Adam’s donor was compatible with him. He was treated by Professor Ravindra Gupta . [ 5 ]
This medical article is a stub . You can help Wikipedia by expanding it .
This British biographical article is a stub . You can help Wikipedia by expanding it .
|
https://en.wikipedia.org/wiki/Adam_Castillejo
|
Adamos Adamou (born 30 October 1950) is a Cypriot politician and former Member of the European Parliament (MEP) for the Progressive Party of Working People , sitting with the European United Left–Nordic Green Left group from 2004 to 2009. [ 1 ] He sat on the European Parliament 's Committee on the Environment, Public Health and Food Safety . He did not stand for reelection in the 2009 European elections .
Adamou was deputy director of Pathological Oncology Clinic.
He is the Chairman of the Delegations for relations between EU with the Palestinian Legislative Council . As a chairman, he is a member of the Conference of Delegation Chairmen.
Became (Dec 2009) Patron of The Friends' Hospice Paphos, a charitable organisation established in 2006, attached to the Evangelismos hospital in Paphos, Cyprus.
He is also a substitute of the Committee on Culture and Education and of the Delegation to the EU-Chile Joint Parliamentary Committee.
|
https://en.wikipedia.org/wiki/Adamos_Adamou
|
Adaptive deep brain stimulation ( aDBS ), also known as closed-loop deep brain stimulation ( clDBS ), is a neuro-modulatory technique currently under investigation for the treatment of neurodegenerative diseases . [ 1 ]
Conventional DBS delivers constant electrical stimulation to regions of the brain that control movement through a surgically implanted wire, or lead, that is connected to an implantable pulse generator (IPG). Programming adjustments to the pulse generator are frequently made by the treating neurologist based on what the patient is doing and the medication they take over time to optimize the patient's symptoms. [ 2 ] However, it can lead to side effects. [ 3 ] aDBS and differs from conventional DBS systems (that provide constant stimulation) in that it can both sense the brain activity and deliver the appropriate stimulation in real time. Of note, in the early days of deep brain stimulation , closed loop applications were carried out by multiple pioneers, such as José Delgado , [ 4 ] Robert Heath , [ 5 ] Natalia Bechtereva [ 6 ] and Carl Wilhelm Sem-Jacobsen long before the advent of 'modern' DBS. Perhaps the earliest closed-loop experiment in an animal model was performed by Delgado and colleagues in 1969. [ 4 ] [ 7 ] In the modern era of DBS following the introduction of the method by Alim Louis Benabid , after a demonstration of efficacy of aDBS in the macaque by the team of Hagai Bergman in 2011, [ 8 ] the first in-human application of aDBS was carried out by the team of Peter Brown in 2013, [ 9 ] followed by the team of Alberto Priori in the same year. [ 10 ]
After being developed in the 1950s, and modern versions introduced by the team of Alim Louis Benabid in the 1980s, DBS received recognition as a treatment method for tremor and later Parkinson's disease , dystonia , obsessive–compulsive disorder and epilepsy . [ 11 ] However, the working mechanism of conventional DBS involved the continuous stimulation of the target structure, which is an approach that cannot adapt to patients' changing symptoms or functional status in real-time. [ 12 ]
Keeping in view this unwanted side effect of DBS, concepts that have the capability to sense brain activity and automatically adjust the stimulation in response to fluctuating biomarkers, were re-introduced by multiple teams, with a first peer-reviewed publication in modern times by the teams of Hagai Bergman (in primates) [ 8 ] and Peter Brown (in humans), [ 9 ] followed by the team of Alberto Priori in the same year. [ 10 ] The study, followed by others testing more patients in longer time windows (up to 24 hours) supported the hypothesis that aDBS is effective in controlling PD symptoms while reducing side effects of constant stimulation. [ 13 ] [ 14 ]
The device used in these studies was the external component of the AlphaDBS system developed by Newronika. [ 15 ] While these advancements were ongoing, Medtronic published the architecture of an implantable aDBS device for application in humans. [ 16 ] [ 17 ] This design was embedded in Medtronic's Activa PC + S research device, allowing LFP sensing and recording while delivering targeted DBS therapy. This device was used in 2018 by a research team led by Philip A. Starr at the University of California, San Francisco , in a public-private partnership with Medtronic. The researchers inserted the device into two patients with Parkinson's disease who had traditional DBS but continued to experience dyskinesia after adjustment by a neurologist. Later on, they compared the results of the adaptive stimulation system with traditional stimulation set manually on two patients, and found that the adaptive approach was as effective at controlling symptoms as constant stimulation. [ 18 ] [ 19 ] The AlphaDBS implantable system by Newronika was developed and CE-marked in 2021. A systematic study was also conducted to highlight safety and efficacy of aDBS vs cDBS using this new generation of DBS IPG in PD. [ 20 ]
The AlphaDBS represents a new generation commercially available DBS implantable pulse generator (IPG) for DBS and sensing, with aDBS capabilities. A double-blind systematic multicentre international study consisted of six investigational sites (in Italy, Poland and the Netherlands) was also conducted to highlight safety and efficacy of aDBS vs cDBS using this a new generation of DBS IPG in PD (AlphaDBS system by Newronika SpA, Milan, Italy). [ 21 ] The Medtronic PC+S device was also developed in a commercial IPG allowing stimulation and sensing, the Percept PC, which is approved for aDBS delivery in Japan. Nobutaka Hattori and the group performed a research study, focused on exploring the case of a 51-year-old man with Parkinson's disease (PD) presenting with motor fluctuations, who received bilateral subthalamic deep brain stimulation (DBS) the Percept PC device, showing the feasibility of the approach. While these new devices seem to have various applications in terms of facilitating condition-dependent stimulation, and providing new insights into the pathophysiological mechanisms of PD, they are currently under investigation in larger clinical studies, to definitely allow their use in clinical practice
To adapt to the stimulation parameters, adaptive DBS (aDBS) employs the local field potential (LFP) of the target structure recorded through the implanted electrodes that deliver stimulation. [ 22 ] The present application of adaptive DBS (aDBS) technique is primarily based on the detection of increased beta oscillations in the subthalamic nucleus (STN), [ 23 ] on account of which it has the capability to change the current depending on the strength of the beta band oscillation, and can, therefore, overcome conventional DBS (cDBS) therapy limitations, including stimulation-induced long term side effects, such as dyskinesia [ 13 ] or speech deterioration. [ 24 ]
Adaptive deep brain stimulation (aDBS) is a treatment modality that is being studied for the treatment of multiple neuropsychiatric and movement disorders.
Since 2015, several experiments were carried out to assess the efficacy of aDBS, that uses beta-band power of the subthalamic local field potentials (LFPs) as target to adapt DBS parameters to motor fluctuations. Results of the experiments proved that aDBS is highly effective in controlling the patients PD symptoms in addition to the normal Levodopa therapy , reducing dyskinesias. [ 25 ]
Adaptive deep brain stimulation (aDBS) is currently being studied to be used as a potential treatment for TS . A 2017 research study presented a review on the available literature supporting the feasibility of an LFP-based aDBS approach in patients with TS. In addition to that, researchers have put forward several explorative findings regarding LFP data recently acquired and analysed in patients with TS after DBS electrode implantation at rest, during voluntary and involuntary movements (tics), and during ongoing DBS. It was found out that LFPs recorded from DBS targets can be used to control new aDBS devices capable of adaptive stimulation responsive to the symptoms of TS. [ 26 ] [ 27 ]
The applications of aDBS in the treatment of dystonia have significantly evolved over the past few years. Low-frequency oscillations (LFO) detected in the internal globus pallidus of dystonia patients have been identified as a physiomarker for adaptive Deep Brain Stimulation (aDBS). [ 28 ] Moreover, the characteristics of pallidal low-frequency -namely, average low-frequency (LF) oscillatory power (4-12 Hz ) [ 29 ] - and beta bursts can be helpful in implementing adaptive brain stimulation in the context of parkinsonian and dystonic internal globus pallidus.[23] A significant amount of scientific research to date on pathological oscillations in dystonia has been focused to address potential biomarkers that might be used as a feedback signal for controlling aDBS in patients with dystonia. [ 30 ]
Adaptive deep brain stimulation (aDBS) may be an effective tool in the treatment of essential tremor (ET), which is one of the most common neurological movement disorders. aDBS for ET is however more focused on a closed-loop technology based on external sensors. [ 31 ] [ 32 ] In a recent study, H J Chizeck presented the first translation-ready training procedure for a fully embedded aDBS control system for MDs and one of the first examples of such a system in ET. [ 33 ]
In a 2021 research study conducted by Alberto Priori, a comparative analysis was presented between the impacts on motor symptoms between conventional deep brain stimulation (cDBS) and closed-loop adaptive deep brain stimulation (aDBS) in patients with Parkinson's disease. This work highlighted the safety and effectiveness of aDBS stimulation compared to cDBS in a daily session, both in terms of motor performance and TEED to the patient. [ 2 ] Simon Little has regarded aDBS approach to be superior to conventional DBS in PD in primates using cortical neuronal spike triggering and in humans employing local field potential biomarkers. [ 3 ] While presenting a protocol for a pseudo-randomised clinical study for adaptive deep brain stimulation as advanced Parkinson's disease treatment, it was shown that aDBS do not induce dysarthria, in contrast to cDBS. [ 23 ] Also it has been suggested that aDBS and cDBS can improve patient's axial symptoms to a similar extent, but compared with cDBS, aDBS significantly improves its main symptom, bradykinesia. [ 34 ]
|
https://en.wikipedia.org/wiki/Adaptive_deep_brain_stimulation
|
Adcon-L is a pharmaceutical gel designed to reduce the incidence and severity of scarring in back operations . It consists of a combination of marginally water-soluble artificial sugars , and is re-absorbed into the body within several months of application. This gel was marketed in the United States by Gliatech, approved by the FDA in 1997, and eventually sold to Wright Medical Technologies in result of Gliatech going bankrupt. [ 1 ]
Four randomized controlled trials of particular interest were done regarding Adcon-L's effect on scarring and clinical outcomes. Three of these tests were done in Europe and one in the United States. Together, the trials consisted 468 patients treated with the gel and 473 patients acting as a control group. The first trial done determined that the adhesion reduced the severity of the scarring post-operation as well as have minor improvements in clinical outcomes. The second trial (occurring in the United States) at first agreed with the first trial but the results were then given to independent investigators. These investigators declared there was no effect on the scarring using Adcon-L or any effect on the clinical outcome after 6 months. [ 2 ]
These two trials led to different conclusions. Based on the first trial and the original study from the second, the gel reduces scars but no certain benefit in clinical outcome. The other conclusion is based on the first trial and the reworked second trial, claiming that the results suggest that the practical use of Adcon-L can not recommended due to the conflicting results. Two other randomized controlled trials were then done, both concluding that there are no effects on the scaring or clinical outcome regarding Adcon-L. Based on these four trial, no strong conclusions are made. [ 2 ]
This dermatologic drug article is a stub . You can help Wikipedia by expanding it .
|
https://en.wikipedia.org/wiki/Adcon-L
|
At its simplest, the adductome is the totality of chemical adducts that are present in particular cellular macromolecules such as DNA , and RNA , or proteins found within the organism. [ 1 ] These adducts can detrimentally alter the chemical properties of these macromolecules and are therefore also referred to as damage. Adducts may arise as a consequence of the chemical reaction between a given "physicochemical agent to which an organism is exposed across the lifespan" (sometimes referred to as the exposome ). These physicochemical agents can be exogenous in origin, and include ionizing and non-ionizing radiation, the diet, lifestyle factors, pollution, and xenobiotics . They may damage the macromolecules directly, or indirectly e.g., some xenobiotic substances require metabolism of the xenobiotic to produce a chemically reactive metabolite which can then form a covalent bond with the endogenous macromolecule. Agents that damage macromolecules can also arise from endogenous sources, such as reactive oxygen species that are a side product of normal respiration, leading to the formation of oxidatively damaged DNA [ 2 ] etc., or other reactive species e.g., reactive nitrogen, sulphur, carbon, selenium and halogen species. [ 3 ]
The term "adductome" first appeared in a journal article in 2005. [ 4 ] Although originally the term related to adducts of DNA, the adductomic approach has now been adopted by protein chemists in their attempts to identify protein adducts. More recently, this has been extended by Kanaly's group to include RNA adducts. [ 5 ] Most recently, nucleic acid adductomics has been reported, which has to potential to study a range of DNA and RNA adducts. [ 6 ]
DNA adducts arise from compounds that bind to DNA , that covalently modify the DNA, resulting in damage. This damage can result in mutations . These mutations can result in a variety of adverse health effects, including cancer and birth defects in multicellular organisms . The science of adductomics seeks to identify and measure all DNA, RNA or protein adducts, identify their origins, and determine their role in health and disease.
Cellular DNA and/or RNA adductomics is performed after the target nucleic acid has been extracted from the cells [ 7 ] (e.g., from cultured cells, or tissues). Urinary DNA adductomics non-invasively evaluates DNA adducts that are present in urine, [ 8 ] following their DNA repair . [ 9 ]
Nucleic acid (NA) adductomics brings together DNA-, RNA- and, to some extent, protein adductomics to provide a more comprehensive view of the adduct burden to these molecules. NA adductomics builds upon previous DNA adductomics and DNA crosslinkomics [ 10 ] (which aims to analyze the totality of DNA-DNA crosslinks [ 11 ] ) assays [ 12 ] and encompasses the analysis of modified (2′-deoxy)ribonucleosides (2′-dN/rN), modified nucleobases (nB), plus: DNA-DNA, RNA-RNA, DNA-RNA, DNA-protein, and RNA-protein crosslinks. [ 6 ] Interestingly, many of these types of adducts are seen in urine from healthy humans, using urinary NA adductomics . [ 6 ] Confirmation of the presence of DNA-RNA crosslinks in urine came from a recent study that demonstrated the presence of cellular DNA-RNA crosslinks, arising from formaldehyde exposure. [ 13 ]
|
https://en.wikipedia.org/wiki/Adductome
|
Adenectomy (from Greek aden ' gland ' and ektomē ' to remove ' ) is a surgical removal of all or part of a gland . [ 1 ] [ 2 ] [ 3 ] [ page needed ]
This surgery article is a stub . You can help Wikipedia by expanding it .
|
https://en.wikipedia.org/wiki/Adenectomy
|
Adenoacanthoma is malignancy of squamous cells that have differentiated from epithelial cells . [ 1 ] [ 2 ] [ 3 ] It can be present in the endothelium of the uterus , mouth and large intestine.
If the tumor is well-defined, the treatment is often includes a hysterectomy and radiation treatment. Treatment may vary according to how far the tumor has spread.
Prognosis is dependent upon the presence and abundance of glandular cells. [ citation needed ] Outcomes improve if the tumor is well-defined.
It is associated with hormone replacement therapy (estrogen). The risk is higher in white women than other ethnicities, incidence, prevalence, age distribution, and sex ratio
This oncology article is a stub . You can help Wikipedia by expanding it .
|
https://en.wikipedia.org/wiki/Adenoacanthoma
|
An adenoma is a benign tumor of epithelial tissue with glandular origin, glandular characteristics, or both. Adenomas can grow from many glandular organs , including the adrenal glands , pituitary gland , thyroid , prostate , and others. Some adenomas grow from epithelial tissue in nonglandular areas but express glandular tissue structure (as can happen in familial polyposis coli ). Although adenomas are benign , they should be treated as pre-cancerous. Over time adenomas may transform to become malignant , at which point they are called adenocarcinomas . Most adenomas do not transform. However, even though benign, they have the potential to cause serious health complications by compressing other structures ( mass effect ) and by producing large amounts of hormones in an unregulated, non-feedback-dependent manner (causing paraneoplastic syndromes ). Some adenomas are too small to be seen macroscopically but can still cause clinical symptoms. [ citation needed ]
Adenoma is a benign tumor of glandular tissue, such as the mucosa of stomach, small intestine, and colon, in which tumor cells form glands or gland-like structures.
In hollow organs (digestive tract), the adenoma grows into the lumen - adenomatous polyp or polypoid adenoma. Adenomatous polyps may be classified based on morphology in order to identify lesions at increased risk of malignant transformation. For example, adenomatous polyps in the colon may be pedunculated (lobular head with a long slender stalk) or sessile (broad base).
The adenomatous proliferation is characterized by different degrees of cell dysplasia ( atypia or loss of normal differentiation of epithelium) irregular cells with hyperchromatic nuclei, stratified or pseudostratified nuclei, nucleolus, decreased mucosecretion, and mitosis. The architecture may be tubular, villous, or tubulo-villous. Basement membrane and muscularis mucosae are intact.
Adenomas of the colon, also called adenomatous polyps , are quite prevalent. They are found commonly at colonoscopy . They are removed because of their tendency to become malignant and to lead to colon cancer.
Ashkenazi Jews have a 6% higher risk rate of getting adenomas, and then colon cancer, than do the general population, so it is important that they have regular actual colonoscopies, and specifically none of the less invasive diagnostic methods. [ 1 ]
This is a tumor that is most often small and asymptomatic, and is derived from renal tubules. It may be a precursor lesion to renal carcinoma .
Adrenal adenomas are common, and are often found on the abdomen, usually not as the focus of investigation; they are usually incidental findings. About one in 10,000 is malignant. Thus, a biopsy is rarely called for, especially if the lesion is homogeneous and smaller than 3 centimeters. Follow-up images in three to six months can confirm the stability of the growth.
While some adrenal adenomas do not secrete hormones at all, often some secrete cortisol , causing Cushing's syndrome , aldosterone causing Conn's syndrome , or androgens causing hyperandrogenism .
About one in 10 people is found to have solitary thyroid nodules. Investigation is required because a small percentage of these is malignant. Biopsy usually confirms the growth to be an adenoma, but, sometimes, excision at surgery is required, especially when the cells found at biopsy are of the follicular type.
Pituitary adenomas are seen in 10% of neurological patients. A lot of them remain undiagnosed. Treatment is usually surgical, to which patients generally respond well. The most common subtype, prolactinoma , is seen more often in women, and is frequently diagnosed during pregnancy as the hormone progesterone increases its growth. Medical therapy with cabergoline or bromocriptine generally suppresses prolactinomas; progesterone antagonist therapy has not proven to be successful.
An adenoma of a parathyroid gland may secrete inappropriately high amounts of parathyroid hormone and thereby cause primary hyperparathyroidism .
Hepatic adenomas are a rare benign tumour of the liver, which may present with hepatomegaly or other symptoms.
Breast adenomas are called fibroadenomas . They are often very small and difficult to detect. Often there are no symptoms. Treatments can include a needle biopsy, and/or removal.
Adenomas can also appear in the appendix. The condition is extremely rare. The most common version is called cystadenoma. They are usually discovered in the course of examination of the tissue following an appendectomy. If the appendix has ruptured and a tumor is present, this presents challenges, especially if malignant cells have formed and thus spread to the abdomen.
Bronchial adenomas are adenomas in the bronchi . They may cause carcinoid syndrome , a type of paraneoplastic syndrome . [ 2 ]
A sebaceous adenoma is a cutaneous condition characterized by a slow-growing tumour usually presenting as a pink, flesh-coloured, or yellow papule or nodule.
Most salivary gland tumors are benign – that is, they are not cancer and will not spread to other parts of the body. These tumors are almost never life-threatening.
There are many types of benign salivary gland tumors, with names such as adenomas, oncocytomas, Warthin tumors, and benign mixed tumors (also known as pleomorphic adenomas).
Benign tumors are almost always cured by surgery. Very rarely, they may become cancer if left untreated for a long time or if they are not completely removed and grow back. It's not clear exactly how benign tumors become cancers. There are many types of salivary gland cancers. Normal salivary glands are made up of several different types of cells, and tumors can start in any of these cell types. Salivary gland cancers are named according to which of these cell types they most look like when seen under a microscope. The main types of cancers are described below.
Doctors usually give salivary cancers a grade (from 1 to 3, or from low to high), based on how abnormal the cancers look under a microscope. The grade gives a rough idea of how quickly it is likely to grow and spread.
Prostate adenoma develops from the periurethral glands at the site of the median or lateral lobes.
A physician's response to detecting an adenoma in a patient will vary according to the type and location of the adenoma among other factors. [ citation needed ] Different adenomas will grow at different rates, but typically physicians can anticipate the rates of growth because some types of common adenomas progress similarly in most patients. [ citation needed ] Two common responses are removing the adenoma with surgery and then monitoring the patient according to established guidelines. [ citation needed ]
One common example of treatment is the response recommended by specialty professional organizations upon removing adenomatous polyps from a patient. In the common case of removing one or two of these polyps from the colon from a patient with no particular risk factors for cancer, thereafter the best practice is to resume surveillance colonoscopy after 5–10 years rather than repeating it more frequently than the standard recommendation. [ 4 ] [ 5 ] [ 6 ]
|
https://en.wikipedia.org/wiki/Adenoma
|
An adenomyoepithelioma of the breast is a rare tumour in the breast composed of glandular elements (adeno-) and myoepithelial cells. It is usually benign; [ 1 ] however, there are reports of malignant behaviour. [ 2 ]
The histomorphologic appearance can mimic invasive ductal carcinoma, the most common type of invasive breast cancer .
This oncology article is a stub . You can help Wikipedia by expanding it .
|
https://en.wikipedia.org/wiki/Adenomyoepithelioma_of_the_breast
|
(adenosine may be safe to the fetus in pregnant women)
Adenosine ( symbol A ) is an organic compound that occurs widely in nature in the form of diverse derivatives. The molecule consists of an adenine attached to a ribose via a β-N 9 - glycosidic bond . Adenosine is one of the four nucleoside building blocks of RNA (and its derivative deoxyadenosine is a building block of DNA ), which are essential for all life on Earth. Its derivatives include the energy carriers adenosine mono-, di-, and triphosphate , also known as AMP/ADP/ATP. Cyclic adenosine monophosphate (cAMP) is pervasive in signal transduction . Adenosine is used as an intravenous medication for some cardiac arrhythmias .
Adenosyl (abbreviated Ado or 5'-dAdo ) is the chemical group formed by removal of the 5′-hydroxy (OH) group. It is found in adenosylcobalamin (an active form of vitamin B12 [ 1 ] ) and as a radical in the radical SAM enzymes. [ 2 ]
In individuals with supraventricular tachycardia (SVT), adenosine is a first line treatment used to help identify and convert the rhythm. [ 3 ] [ 4 ] [ 5 ] [ 6 ]
Certain SVTs can be successfully terminated with adenosine. [ 7 ] This includes any re-entrant arrhythmias that require the AV node for the re-entry, e.g., AV reentrant tachycardia (AVRT) and AV nodal reentrant tachycardia (AVNRT). In addition, atrial tachycardia can sometimes be terminated with adenosine. [ 8 ]
Fast rhythms of the heart that are confined to the atria (e.g., atrial fibrillation and atrial flutter ) or ventricles (e.g., monomorphic ventricular tachycardia ), and do not involve the AV node as part of the re-entrant circuit, are not typically converted by adenosine. However, the ventricular response rate is temporarily slowed with adenosine in such cases. [ 8 ]
Because of the effects of adenosine on AV node-dependent SVTs, adenosine is considered a class V antiarrhythmic agent . When adenosine is used to cardiovert an abnormal rhythm, it is normal for the heart to enter ventricular asystole for a few seconds. This can be disconcerting to a normally conscious patient, and is associated with angina-like sensations in the chest. [ 9 ]
Adenosine is used as an adjunct to thallium (TI 201) or technetium (Tc99m) myocardial perfusion scintigraphy (nuclear stress test) in patients unable to undergo adequate stress testing with exercise. [ 10 ]
When used to treat SVT, adenosine is administered intravenously as a rapid bolus (typically 0.10–0.15 mg/kg initially) over 1-2 seconds, followed by a rapid saline flush (often using a 2-way or 3-way stopcock). If the initial dose is ineffective, it may be repeated every 2 minutes with a slightly increased dose (0.05–0.1 mg/kg increments) every 2 minutes up to a maximum total dose of 0.3 mg/kg (not exceeding 12 mg). Due to adenosine's extremely short half-life (less than 10 seconds), it is often injected through a central venous line or a large proximal peripheral vein; administration into lower extremities, PICC lines , or smaller veins may lead to therapeutic failure due to rapid metabolism before reaching the heart. [ 3 ] When given to dilate the arteries, such as in a "stress test", the dosage is typically 0.14 mg/kg/min, administered for 4 or 6 minutes, depending on the protocol.
The recommended dose may be increased in patients on theophylline since methylxanthines prevent binding of adenosine at receptor sites. The dose is often decreased in patients on dipyridamole (Persantine) and diazepam (Valium) because adenosine potentiates the effects of these drugs. The recommended dose is also reduced by half in patients presenting congestive heart failure , myocardial infarction , shock , hypoxia , and/or chronic liver disease or chronic kidney disease , and in elderly patients.
Adverse effects associated with adenosine administration are primarily due to its activation of adenosine receptors on vascular tissue, resulting in vasodilation. Side effects of adenosine include skin flushing, lightheadedness, nausea, sweating, nervousness, numbness, and a sense of impending doom . These effects are typically very short-lived due to adenosine's rapid metabolism and short half-life. Less common, but more serious, cardiovascular effects can occur, such as cardiac arrhythmias (including premature atrial and ventricular contractions and atrioventricular (AV) block), hypotension, cardiac ischemia, and prolonged asystole. [ 11 ]
Dipyridamole potentiates the action of adenosine, requiring the use of lower doses.
Methylxanthines (e.g. caffeine found in coffee, theophylline found in tea, or theobromine found in chocolate) have a purine structure and bind to some of the same receptors as adenosine. [ 13 ] Methylxanthines act as competitive antagonists of adenosine and can blunt its pharmacological effects. [ 14 ] Individuals taking large quantities of methylxanthines may require increased doses of adenosine.
Caffeine acts by blocking binding of adenosine to the adenosine A 1 receptor , which enhances release of the neurotransmitter acetylcholine . [ 15 ] Caffeine also increases cyclic AMP levels through nonselective inhibition of phosphodiesterase. [ 16 ] "Caffeine has a three-dimensional structure similar to that of adenosine," which allows it to bind and block its receptors. [ 17 ]
Common contraindications for adenosine include
Adenosine is an endogenous purine nucleoside that modulates many physiological processes. Cellular signaling by adenosine occurs through four known adenosine receptor subtypes ( A 1 , A 2A , A 2B , and A 3 ). [ 19 ]
Extracellular adenosine concentrations from normal cells are approximately 300 nM; however, in response to cellular damage (e.g., in inflammatory or ischemic tissue), these concentrations are quickly elevated (600–1,200 nM). Thus, in regard to stress or injury, the function of adenosine is primarily that of cytoprotection preventing tissue damage during instances of hypoxia , ischemia , and seizure activity. Activation of A 2A receptors produces a constellation of responses that in general can be classified as anti-inflammatory. [ 20 ] Enzymatic production of adenosine can be anti- inflammatory or immunosuppressive . [ 21 ] [ 22 ] [ 23 ]
All adenosine receptor subtypes (A 1 , A 2A , A 2B , and A 3 ) are G-protein-coupled receptors . The four receptor subtypes are further classified based on their ability to either stimulate or inhibit adenylate cyclase activity. The A 1 receptors couple to G i/o and decrease cAMP levels, while the A 2 adenosine receptors couple to G s , which stimulates adenylate cyclase activity. In addition, A 1 receptors couple to G o , which has been reported to mediate adenosine inhibition of Ca 2+ conductance, whereas A 2B and A 3 receptors also couple to G q and stimulate phospholipase activity.
Researchers at Cornell University have recently shown adenosine receptors to be key in opening the blood-brain barrier (BBB).
Mice dosed with adenosine have shown increased transport across the BBB of amyloid plaque antibodies and prodrugs associated with Parkinson's disease, Alzheimer's, multiple sclerosis, and cancers of the central nervous system. [ 24 ]
Adenosine is an endogenous agonist of the ghrelin/growth hormone secretagogue receptor . [ 25 ] However, while it is able to increase appetite , unlike other agonists of this receptor, adenosine is unable to induce the secretion of growth hormone and increase its plasma levels. [ 25 ]
When it is administered intravenously, adenosine causes transient heart block in the atrioventricular (AV) node . This is mediated via the A 1 receptor , inhibiting adenylyl cyclase, reducing cAMP and so causing cell hyperpolarization by increasing K + efflux via inward rectifier K + channels , subsequently inhibiting Ca 2+ current. [ 26 ] [ 27 ] It also causes endothelial-dependent relaxation of smooth muscle as is found inside the artery walls. This causes dilation of the "normal" segments of arteries, i.e. where the endothelium is not separated from the tunica media by atherosclerotic plaque . This feature allows physicians to use adenosine to test for blockages in the coronary arteries, by exaggerating the difference between the normal and abnormal segments.
The administration of adenosine also reduces blood flow to coronary arteries past the occlusion. Other coronary arteries dilate when adenosine is administered while the segment past the occlusion is already maximally dilated, which is a process called coronary steal . This leads to less blood reaching the ischemic tissue, which in turn produces the characteristic chest pain.
Adenosine used as a second messenger can be the result of de novo purine biosynthesis via adenosine monophosphate (AMP), though it is possible other pathways exist. [ 28 ]
When adenosine enters the circulation, it is broken down by adenosine deaminase , which is present in red blood cells and the vessel wall.
Dipyridamole , an inhibitor of adenosine nucleoside transporter , allows adenosine to accumulate in the blood stream. This causes an increase in coronary vasodilatation .
Adenosine deaminase deficiency is a known cause of immunodeficiency.
The adenosine analog NITD008 has been reported to directly inhibit the recombinant RNA-dependent RNA polymerase of the dengue virus by terminating its RNA chain synthesis. This interaction suppresses peak viremia and rise in cytokines and prevents lethality in infected animals, raising the possibility of a new treatment for this flavivirus . [ 29 ] The 7-deaza-adenosine analog has been shown to inhibit the replication of the hepatitis C virus . [ 30 ] BCX4430 is protective against Ebola and Marburg viruses. [ 31 ] Such adenosine analogs are potentially clinically useful since they can be taken orally.
Adenosine is believed to be an anti-inflammatory agent at the A 2A receptor. [ 32 ] [ 33 ] Topical treatment of adenosine to foot wounds in diabetes mellitus has been shown in lab animals to drastically increase tissue repair and reconstruction. Topical administration of adenosine for use in wound-healing deficiencies and diabetes mellitus in humans is currently under clinical investigation.
Methotrexate 's anti-inflammatory effect may be due to its stimulation of adenosine release. [ 34 ]
In general, adenosine has an inhibitory effect in the central nervous system (CNS). Caffeine 's stimulatory effects are credited primarily (although not entirely) to its capacity to block adenosine receptors, thereby reducing the inhibitory tonus of adenosine in the CNS. This reduction in adenosine activity leads to increased activity of the neurotransmitters dopamine and glutamate . [ 35 ] Experimental evidence suggests that adenosine and adenosine agonists can activate Trk receptor phosphorylation through a mechanism that requires the adenosine A 2A receptor. [ 36 ]
Adenosine has been shown to promote thickening of hair on people with thinning hair. [ 37 ] [ 38 ] A 2013 study compared topical adenosine with minoxidil in male androgenetic alopecia , finding it was as potent as minoxidil (in overall treatment outcomes) but with higher satisfaction rate with patients due to “faster prevention of hair loss and appearance of the newly grown hairs” (further trials were called for to clarify the findings). [ 39 ]
Adenosine is a key factor in regulating the body's sleep-wake cycle . [ 40 ] Adenosine levels build up in the brain during periods of wakefulness, causing a need to sleep when level become too high and lowers during periods of sleep, giving a sensation of restedness when waking. Higher adenosine levels correlate with a stronger feeling of sleepiness , also known as sleep drive or sleep pressure. [ 41 ] Cognitive behavioral therapy for insomnia (CBT-I), which is considered one of the most effective treatments for insomnia , utilizes short-term sleep deprivation to raise and regulate adenosine levels in the body, for the intended promotion of consistent and sustained sleep in the long term. [ 42 ]
A principal component of cannabis delta-9-tetrahydrocannabinol (THC) and the endocannabinoid anandamide (AEA) induces sleep in rats by increasing adenosine levels in the basal forebrain . These components also significantly increase slow-wave sleep during the sleep cycle , mediated by CB1 receptor activation . These findings identify a potential therapeutic use of cannabinoids to induce sleep in conditions where sleep may be severely attenuated. [ 43 ]
It also plays a role in regulation of blood flow to various organs through vasodilation . [ 44 ] [ 45 ] [ 46 ]
|
https://en.wikipedia.org/wiki/Adenosine
|
Adenosquamous carcinoma is a type of cancer that contains two types of cells: squamous cells (thin, flat cells that line certain organs) and gland-like cells. It has been associated with more aggressive characteristics when compared to adenocarcinoma in certain cancers. [ 1 ] [ 2 ] It is responsible for 1% to 4% of exocrine forms of pancreas cancer . [ 3 ]
Light microscopy shows a combination of gland-like cells and squamous epithelial cells. [ 4 ] On immunohistochemistry , it is typically positive for CK5/6 , CK7 and p63 , and negative for CK20 , p16 and p53 . On genetic testing , KRAS and p53 are typically altered. [ 4 ]
This article incorporates public domain material from Dictionary of Cancer Terms . U.S. National Cancer Institute .
This oncology article is a stub . You can help Wikipedia by expanding it .
|
https://en.wikipedia.org/wiki/Adenosquamous_carcinoma
|
Adenylate cyclase toxin is a virulence factor produced by some members of the genus Bordetella . Together with the pertussis toxin it is the most important virulence factor of the causative agent of whooping cough , Bordetella pertussis . Bordetella bronchiseptica and Bordetella parapertussis , also able to cause pertussis-like symptoms, also produce adenylate cyclase toxin. [ 1 ] It is a toxin secreted by the bacteria to influence the host immune system .
Adenylate cyclase toxin from Bordetella pertussis is a 1706 amino acid residue long protein . The protein consists of three domains: from the N-terminus up to roughly residue 400, there is an adenylate-cyclase domain; between residues 500 and 700, there is a hydrophobic domain; and from residue 1000 to the C-terminus , there are calcium binding repeats. Two acylation sites are located at lysine residues K860 and K983. [ 2 ] [ 3 ] The part of the toxin from residue 400 to the C-terminus, called hemolysin , is structurally related to a large family of bacterial toxins - RTX toxins . [ 3 ] Differences between the toxins of different Bordetella species are mainly in the calcium-binding domain. [ 4 ]
The toxin is secreted by the Type I secretion system , which spans both membranes and periplasm space, allowing the toxin to be secreted from the cytoplasm straight outside the cell. [ 1 ] [ 2 ] A large proportion of the toxin remains associated with the bacterium exterior proteins, mainly filamentous haemagglutinin , but these toxin molecules are not active. [ 5 ] [ 1 ] Besides attachment to bacterial proteins, aggregation also inactivates the toxin. [ 5 ] This quick inactivation highlights the necessity of close contact between secreting bacterium and target cell. [ 1 ]
RTX stands for 'repeats in toxins,' but not all members of the family are toxins. Repeating aspartate and glycine rich nonapeptides (repeats 9 amino acids long) are a characteristic feature of this family of proteins, and are able to bind calcium ions . [ 3 ] A feature of the RTX proteins is their ability to form pores in cell membranes, allowing ions to leak. This may manifest as a hemolytic activity on erythrocytes , leading to this group of toxins being called 'hemolysins'. The cell types which are vulnerable to this pore-forming activity varies among the toxins. The acylation of lysines is required for the pore-forming cytotoxic effects of all the RTX proteins. [ 6 ]
Toxins from many known gram-negative pathogenic bacteria are in the RTX family. An example is α-hemolysin from Escherichia coli or RtxA from Vibrio cholerae . [ 6 ]
Adenylate cyclase toxin binds to target cells by the complement receptor 3 (CD11b/CD18, or Mac-1). [ 7 ] Target cell are therefore myeloid lineage cells, mainly phagocytes , such as neutrophils . [ 1 ] Binding to cells without the CR3 also happens, but at a much lower rate. [ 5 ] The portion responsible for binding to the receptor is inside the calcium binding repeats, from residues 1166 to 1287. [ 3 ] The hemolysin portion of the protein then binds to the target membrane and inserts itself into the bilayer . [ 3 ] [ 5 ] The adenylate cyclase (AC) domain is then translocated across the cytoplasmic membrane into the cytoplasm. Translocation of the AC domain is independent of cytotoxic pore-forming activity, as these two activities require to toxin to adopt different conformations. [ 5 ] [ 2 ] The transiently opened pores do, however, contribute to AC domain function by potassium leakage and calcium influx into the target cell, which slows endocytosis of CR3/adenylate cyclase toxin clusters, [ 2 ] also, the CR3/toxin complex is mobilized by detachment from the cytoskeleton . The complex is then recruited into cholesterol -rich lipid rafts . [ 3 ] Calcium influx by itself has many negative effects on target cells, such as deregulation of cellular signalling . [ 5 ]
The adenylate cyclase domain has intrinsic enzymatic activity. Translocation of the AC domain into the cell starts the main process by which this toxin influences target cells: the AC domain binds calmodulin , and catalyzes unregulated production of cAMP from ATP . [ 7 ] cAMP is an important second messenger molecule and its massive overproduction affects many cellular processes. In phagocytes, most of the bactericidal functions are stopped by cAMP-mediated activation of PKA and Epac . [ 7 ]
The above described effects of the adenylate cyclase toxin, mainly the cAMP overproduction, have a profound effect on target cells. Although phagocytic immune cells migrate to the site of infection in the lungs , they are not able to mount an effective response. Not only the phagocytic uptake of bacteria is blocked, but subsequent production of ROS by neutrophils and monocytes , NETs by neutrophils, and NO by macrophages , is also inhibited. [ 5 ] [ 7 ] [ 3 ] The effect on neutrophils is most important in early infection with Bordetella , impairing most of their antimicrobial functions. [ 3 ] Intoxication with the adenylate cyclase toxin leads to shift in polarization of macrophages from M1 ( proinflammatory ) phenotype to M2 (immunoregulatory) phenotype and may lead to macrophage apoptosis . [ 7 ] [ 3 ] cAMP accumulation after adenylate cyclase intoxication also interferes with IRF signalling in dendritic cells , which leads to lower IL-12 production. IL-12 is important for T-cell response polarization. [ 7 ] Other effects of cAMP on dendritic cell interaction with T-cells are also detrimental to the immune response. Although cAMP induces dendritic cell migration into lymph nodes , it lowers their capacity to interact with T-cells and present antigen . This has a tolerogenic effect on the T-cell population. [ 7 ]
Vaccination against Bordetella pertussis is used in infancy to prevent whooping cough. The recent switch from whole-cell pertussis vaccine to acellular component vaccine in many countries has led to the fact that adenylate cyclase toxin is not present in most vaccines. [ 4 ] Although not included in current vaccines, research shows that immunization with adenylate cyclase toxin elicits neutralizing antibodies . Neutralizing antibodies can block binding of the toxin to CR3. [ 3 ] Antibodies against adenylate cyclase toxin are also present in the serum of humans infected with B. pertussis. [ 4 ]
Adenylate cyclase toxin based constructs have been proven to elicit the production of neutralizing antibodies, but lack the cytotoxicity associated with the complete toxin. Genetically detoxified adenylate cyclase toxin also serves in promoting the Th1/Th17 response , acting as an adjuvant . [ 4 ]
Adenylate cyclase toxin, or its parts, also serve as a tool for cell biologists. The AC domain finds use as a reporter protein . This reporter activity is based on activating cAMP production if translocated into a cell, conjugated to a studied protein. The AC domain consists of two subdomains, both are required for cAMP production. Conjugating each subdomain to a different protein allows protein-protein interactions to be studied, because cAMP production indicates close interaction of the proteins. Similarly, the two subdomains can be linked by a studied protein, which is then digested by proteases . Loss of cAMP production indicates cleavage by protease. [ 8 ]
|
https://en.wikipedia.org/wiki/Adenylate_cyclase_toxin
|
In medicine, patient compliance (also adherence , capacitance ) describes the degree to which a person correctly follows medical advice. Most commonly, it refers to medication or drug compliance, but it can also apply to other situations such as medical device use, self care , self-directed exercises, therapy sessions, or medical follow-up visits. Both patient and health-care provider affect compliance, and a positive physician-patient relationship is the most important factor in improving compliance. [ 1 ] Access to care plays a role in patient adherence, whereby greater wait times to access care contributing to greater absenteeism. [ 2 ] The cost of prescription medication and potential side effects also play a role. [ 3 ] [ 4 ]
Compliance can be confused with concordance , which is the process by which a patient and clinician make decisions together about treatment. [ 5 ]
Worldwide, non-compliance is a major obstacle to the effective delivery of health care. 2003 estimates from the World Health Organization indicated that only about 50% of patients with chronic diseases living in developed countries follow treatment recommendations with particularly low rates of adherence to therapies for asthma , diabetes , and hypertension . [ 1 ] Major barriers to compliance are thought to include the complexity of modern medication regimens, poor health literacy and not understanding treatment benefits, the occurrence of undiscussed side effects, poor treatment satisfaction, cost of prescription medicine, and poor communication or lack of trust between a patient and his or her health-care provider. [ 6 ] [ 7 ] [ 8 ] Efforts to improve compliance have been aimed at simplifying medication packaging, providing effective medication reminders, improving patient education, and limiting the number of medications prescribed simultaneously. Studies show a great variation in terms of characteristics and effects of interventions to improve medicine adherence. [ 9 ] It is still unclear how adherence can consistently be improved in order to promote clinically important effects. [ 9 ]
In medicine, compliance (synonymous with adherence, capacitance) describes the degree to which a patient correctly follows medical advice. Most commonly, it refers to medication or drug compliance, but it can also apply to medical device use, self care , self-directed exercises, or therapy sessions. Both patient and health-care provider affect compliance, and a positive physician-patient relationship is the most important factor in improving compliance. [ 1 ]
As of 2003, US health care professionals more commonly used the term "adherence" to a regimen rather than "compliance", because it has been thought to reflect better the diverse reasons for patients not following treatment directions in part or in full. [ 7 ] [ 10 ] Additionally, the term adherence includes the ability of the patient to take medications as prescribed by their physician with regards to the correct drug, dose, route, timing, and frequency. [ 11 ] It has been noted that compliance may only refer to passively following orders. [ 12 ] The term adherence is often used to imply a collaborative approach to decision-making and treatment between a patient and clinician. [ 13 ]
The term concordance has been used in the United Kingdom to involve a patient in the treatment process to improve compliance, and refers to a 2003 NHS initiative. In this context, the patient is informed about their condition and treatment options, involved in the decision as to which course of action to take, and partially responsible for monitoring and reporting back to the team. [ 14 ] Informed intentional non-adherence is when the patient, after understanding the risks and benefits, chooses not to take the treatment. [ 15 ]
As of 2005, the preferred terminology remained a matter of debate. [ 16 ] As of 2007, concordance has been used to refer specifically to patient adherence to a treatment regimen which the physician sets up collaboratively with the patient, to differentiate it from adherence to a physician-only prescribed treatment regimen. [ 17 ] [ 18 ] [ 19 ] Despite the ongoing debate, adherence has been the preferred term for the World Health Organization , [ 1 ] The American Pharmacists Association , [ 6 ] and the U.S. National Institutes of Health Adherence Research Network. [ 20 ] The Medical Subject Headings of the United States National Library of Medicine defines various terms with the words adherence and compliance . Patient Compliance and Medication Adherence are distinguished under the MeSH tree of Treatment Adherence and Compliance .
In 2003 WHO estimated that half of those for whom long term treatment regimens are prescribed do not follow them as directed. [ 1 ] In general, adherence is higher in diseases where people see a greater health threat, such as HIV/AIDS and cancer, and it is lower for chronic conditions such as hypertension, asthma or diabetes. [ 21 ]
Factors can be categorized on 3 levels: individual, cultural and healthcare system level. [ 21 ]
Depressive symptoms and perceived discrimination have been correlated with poor adherence. [ 21 ]
Negative side effects of a medicine can influence adherence. [ 22 ] : 280
Medication adherence rates are typically lower with lower socioeconomic status , increased stress related to difficult life circumstances. [ 21 ]
Poverty is associated with Low levels of literacy and numeracy . [ 23 ] Adults in more deprived areas, such as the North East of England, performed at a lower level than those in less deprived areas such as the South East. Local authority tenants and those in poor health were particularly likely to lack basic skills. [ 23 ]
In 1999 one fifth of UK adults, nearly seven million people, had problems with basic skills, especially functional literacy and functional numeracy, described as: "The ability to read, write and speak in English, and to use mathematics at a level necessary to function at work and in society in general." This made it impossible for them to effectively take medication, read labels, follow drug regimes, and find out more. [ 24 ]
In 2003, 20% of adults in the UK had a long-standing illness or disability and a national study for the UK Department of Health , found more than one-third of people with poor or very poor health had literary skills of Entry Level 3 or below. [ 23 ]
A study of the relationship of literacy to asthma knowledge revealed that only 31% of asthma patients with a reading level of a ten-year-old knew they needed to see the doctors, even when they were not having an asthma attack, compared to 90% with a high school graduate reading level. [ 25 ]
In 2013 the US National Community Pharmacists Association sampled for one month 1,020 Americans above age 40 for with an ongoing prescription to take medication for a chronic condition and gave a grade C+ on adherence. [ 26 ] [ better source needed ] In 2009, this contributed to an estimated cost of $290 billion annually. [ 27 ] In 2012, increase in patient medication cost share was found to be associated with low adherence to medication. [ 28 ]
The United States is among the countries with the highest prices of prescription drugs mainly attributed to the government's lack of negotiating lower prices with monopolies in the pharmaceutical industry especially with brand name drugs. [ 29 ] In order to manage medication costs, many US patients on long term therapies fail to fill their prescription, skip or reduce doses. According to a Kaiser Family Foundation survey in 2015, about three quarters (73%) of the public think drug prices are unreasonable and blame pharmaceutical companies for setting prices so high. [ 30 ] In the same report, half of the public reported that they are taking prescription drugs and a "quarter (25%) of those currently taking prescription medicine report they or a family member have not filled a prescription in the past 12 months due to cost, and 18 percent report cutting pills in half or skipping doses". [ 30 ] In a 2009 comparison to Canada, only 8% of adults reported to have skipped their doses or not filling their prescriptions due to the cost of their prescribed medications. [ 31 ]
Cost and poor understanding of the directions for the treatment, referred to as ' health literacy ' have been known to be major barriers to treatment adherence. [ 32 ] [ 7 ] [ 33 ] Misinformation from the internet and social media can also lead to a delay or lack of compliance in following medical advice. [ 34 ]
The recent National Service Framework on the care of older people highlighted the importance of taking and effectively managing medicines in the elderly. Elderly individuals may face challenges, including multiple medications with frequent dosing, and potentially decreased dexterity or cognitive functioning. Patient knowledge is also a factor. [ 35 ]
In 1999 Cline et al. identified several gaps in knowledge about medication in elderly patients discharged from hospital. [ 36 ] Despite receiving written and verbal information, 27% of older people discharged after heart failure were classed as non-adherent within 30 days. Half the patients surveyed could not recall the dose of the medication that they were prescribed and nearly two-thirds did not know what time of day to take them. A 2001 study by Barat et al. evaluated the medical knowledge and factors of adherence in a population of 75-year-olds living at home. They found that 40% of elderly patients do not know the purpose of their regimen and only 20% knew the consequences of non-adherence. [ 37 ] Comprehension, polypharmacy , living arrangement, multiple doctors, and use of compliance aids was correlated with adherence.
In children with asthma, self-management compliance is critical and co-morbidities have been noted to affect outcomes; in 2013 it has been suggested that electronic monitoring may help adherence. [ 38 ]
People of different ethnic backgrounds have unique adherence issues through, for example, limited English language proficiency , their cultural belief system rooted in historical experience ( Tuskegee experiment ), resulting in medical mistrust. [ 21 ] There are few published studies on adherence in medicine taking in ethnic minority communities. Ethnicity and culture influence some health-determining behaviour, such as participation in health screening programmes and attendance at follow-up appointments. [ 39 ] [ 40 ]
Ethnic groups differ in their attitudes, values, culture and beliefs about health and illness, particularly with preventive treatments and medication for asymptomatic conditions. Additionally, some cultures fatalistically attribute their good or poor health to their god(s), and attach less importance to self-care than others. [ 41 ] Complementary and alternative medicine may be taken with or instead of the prescribed medications especially in Mexican American and Vietnamese people. [ 21 ]
Studies have shown that black patients and those with non-private insurance are more likely to be labeled as non-adherent. [ 42 ] An increased risk for non adherence was observed even after controlling for A1c, and socioeconomic factors. [ 43 ]
Not all patients will fill the prescription at a pharmacy. In a 2010 U.S. study, 20–30% of prescriptions were never filled at the pharmacy. [ 44 ] [ 45 ] Reasons people do not fill prescriptions include the cost of the medication, [ 3 ] [ 6 ] A US nationwide survey of 1,010 adults in 2001 found that 22% chose not to fill prescriptions because of the price, which is similar to the 20–30% overall rate of unfilled prescriptions. [ 3 ] Other factors are doubting the need for medication, or preference for self-care measures other than medication. [ 46 ] [ 47 ] Convenience, side effects and lack of demonstrated benefit are also factors. [ citation needed ]
Prescription medical claims records can be used to estimate medication adherence based on fill rate. Patients can be routinely defined as being 'Adherent Patients' if the amount of medication furnished is at least 80% based on days' supply of medication divided by the number of days patient should be consuming the medication. This percentage is called the medication possession ratio (MPR). 2013 work has suggested that a medication possession ratio of 90% or above may be a better threshold for deeming consumption as 'Adherent'. [ 48 ]
Two forms of MPR can be calculated, fixed and variable. [ 49 ] Calculating either is relatively straightforward, for Variable MPR (VMPR) it is calculated as the number of days' supply divided by the number of elapsed days including the last prescription.
V M P R = All days' supply Elapsed days (inclusive of last prescription) {\displaystyle VMPR={\dfrac {\text{All days' supply}}{\text{Elapsed days (inclusive of last prescription)}}}}
For the Fixed MPR (FMPR) the calculation is similar but the denominator is the number of days in a year whilst the numerator is constrained to be the number of days' supply within the year that the patient has been prescribed.
F M P R = All days' supply ≤ 365 365 {\displaystyle FMPR={\dfrac {{\text{All days' supply}}\leq 365}{365}}}
For medication in tablet form it is relatively straightforward to calculate the number of days' supply based on a prescription. Some medications are less straightforward though because a prescription of a given number of doses may have a variable number of days' supply because the number of doses to be taken per day varies, for example with preventative corticosteroid inhalers prescribed for asthma where the number of inhalations to be taken daily may vary between individuals based on the severity of the disease. [ citation needed ]
Contextual factors along with intrapersonal circumstances such as mental states affect decisions. They can accurately predict decisions where most contextual information is identified. [ 50 ] General compliance with recommendations to follow isolation is influenced beliefs such as taking health precaution to be protected against infection, perceived vulnerability, getting COVID-19 and trust in the government. [ 51 ] Mobility reduction, compliance with quarantine regulations in European regions where level of trust in policymakers is high can influence whether one complies with isolation rules. [ 52 ] In addition, perceived infectiousness of COVID-19 is a strong predictor of rule compliance such that the more contagious people think COVID-19 is, the less willing social distancing measures are taken, while the sense of duty and fear of the virus contribute to staying at home. [ 53 ] [ 54 ] [ 55 ] People might not leave their homes due to trusting regulations to be effective or placing it in a higher power such that individuals who trust others demonstrate more compliance than those who do not. [ 56 ] [ 57 ] Compliant individuals see protective measures as effective, while non-compliant people see them as problematic. [ 58 ]
Once started, patients seldom follow treatment regimens as directed, and seldom complete the course of treatment. [ 6 ] [ 7 ] In respect of hypertension, 50% of patients completely drop out of care within a year of diagnosis. [ 59 ] Persistence with first-line single antihypertensive drugs is extremely low during the first year of treatment. [ 60 ] As far as lipid-lowering treatment is concerned, only one third of patients are compliant with at least 90% of their treatment. [ 61 ] Intensification of patient care interventions (e.g. electronic reminders, pharmacist-led interventions, healthcare professional education of patients) improves patient adherence rates to lipid-lowering medicines, as well as total cholesterol and LDL-cholesterol levels. [ 62 ]
The World Health Organization (WHO) estimated in 2003 that only 50% of people complete long-term therapy for chronic illnesses as they were prescribed, which puts patient health at risk. [ 63 ] For example, in 2002 statin compliance dropped to between 25 and 40% after two years of treatment, with patients taking statins for what they perceive to be preventative reasons being unusually poor compliers. [ 64 ]
A wide variety of packaging approaches have been proposed to help patients complete prescribed treatments. These approaches include formats that increase the ease of remembering the dosage regimen as well as different labels for increasing patient understanding of directions. [ 65 ] [ 66 ] For example, medications are sometimes packed with reminder systems for the day and/or time of the week to take the medicine. [ 66 ] Some evidence shows that reminder packaging may improve clinical outcomes such as blood pressure. [ 66 ]
A not-for-profit organisation called the Healthcare Compliance Packaging Council of Europe] (HCPC-Europe) was set up [ when? ] between the pharmaceutical industry, the packaging industry with representatives of European patients organisations. The mission of HCPC-Europe is to assist and to educate the healthcare sector in the improvement of patient compliance through the use of packaging solutions. A variety of packaging solutions have been developed by this collaboration. [ 67 ]
The World Health Organization (WHO) groups barriers to medication adherence into five categories; health care team and system-related factors, social and economic factors, condition-related factors, therapy-related factors, and patient-related factors. Common barriers include: [ 68 ]
Health care providers play a great role in improving adherence issues. Providers can improve patient interactions through motivational interviewing and active listening. [ 69 ] Health care providers should work with patients to devise a plan that is meaningful for the patient's needs. A relationship that offers trust, cooperation, and mutual responsibility can greatly improve the connection between provider and patient for a positive impact. [ 12 ] The wording that health care professionals take when sharing health advice may have an impact on adherence and health behaviours, however, further research is needed to understand if positive framing (e.g., the chance of surviving is improved if you go for screening) versus negative framing (e.g., the chance of dying is higher if you do not go for screening) is more effective for specific conditions. [ 70 ]
In 2012 it was predicted that as telemedicine technology improves, physicians will have better capabilities to remotely monitor patients in real-time and to communicate recommendations and medication adjustments using personal mobile devices, such as smartphones, rather than waiting until the next office visit. [ 71 ]
Medication Event Monitoring Systems (MEMS), as in the form of smart medicine bottle tops, smart pharmacy vials or smart blister packages as used in clinical trials and other applications where exact compliance data are required, work without any patient input, and record the time and date the bottle or vial was accessed, or the medication removed from a blister package. The data can be read via proprietary readers, or NFC enabled devices, such as smartphones or tablets. A 2009 study stated that such devices can help improve adherence. [ 72 ] More recently a 2016 scoping review suggested that in comparison to MEMS, median mediction adherence was grossly overestimated by 17% using self-report, by 8% using pill count and by 6% using rating as alternative methods for measuring medication adherence. [ 73 ]
The effectiveness of two-way email communication between health care professionals and their patients has not been adequately assessed. [ 74 ]
As of 2019 [update] , 5.15 billion people, which equates to 67% of the global population, have a mobile device and this number is growing. [ 75 ] Mobile phones have been used in healthcare and has fostered its own term, mHealth . They have also played a role in improving adherence to medication. [ 76 ] For example, text messaging has been used to remind patients to take medication in patients with chronic conditions such as asthma and hypertension . [ 77 ] Other examples include the use of smartphones for synchronous and asynchronous Video Observed Therapy (VOT) as a replacement for the currently resource intensive [ 78 ] standard of Directly Observed Therapy (DOT) (recommended by the WHO [ 79 ] ) for Tuberculosis management. [ 80 ] Other mHealth interventions for improving adherence to medication include smartphone applications, [ 81 ] voice recognition in interactive phone calls [ 82 ] and Telepharmacy . [ 83 ] Some results show that the use of mHealth improves adherence to medication and is cost-effective, [ 83 ] though some reviews report mixed results. [ 84 ] Studies show that using mHealth to improve adherence to medication is feasible and accepted by patients. [ 84 ] [ 83 ] Specific mobile applications might also support adherence. [ 85 ] [ 86 ] mHealth interventions have also been used alongside other telehealth interventions such as wearable wireless pill sensors, [ 87 ] smart pillboxes [ 87 ] and smart inhalers [ 88 ]
Depot injections need to be taken less regularly than other forms of medication and a medical professional is involved in the administration of drugs so can increase compliance. Depot's are used for oral contraceptive pill [ 89 ] and antipsychotic medication used to treat schizophrenia [ 90 ] and bipolar disorder . [ 91 ]
Sometimes drugs are given involuntarily to ensure compliance. This can occur if an individual has been involuntarily committed [ 92 ] or are subjected to an outpatient commitment order, where failure to take medication will result in detention and involuntary administration of treatment. [ 93 ] : 16 This can also occur if a patient is not deemed to have mental capacity to consent to treatment in an informed way. [ 94 ]
A WHO study estimates that only 50% of patients with chronic diseases in developed countries follow treatment recommendations. [ 1 ]
Asthma non-compliance (28–70% worldwide) increases the risk of severe asthma attacks requiring preventable ER visits and hospitalisations; compliance issues with asthma can be caused by a variety of reasons including: difficult inhaler use, side effects of medications, and cost of the treatment. [ 95 ]
200,000 new cases of cancer are diagnosed each year in the UK. One in three adults in the UK will develop cancer that can be life-threatening, and 120,000 people will be killed by their cancer each year. This accounts for 25% of all deaths in the UK. However while 90% of cancer pain can be effectively treated, only 40% of patients adhere to their medicines due to poor understanding. [ citation needed ]
Results of a recent (2016) systematic review found a large proportion of patients struggle to take their oral antineoplastic medications as prescribed. This presents opportunities and challenges for patient education, reviewing and documenting treatment plans, and patient monitoring, especially with the increase in patient cancer treatments at home. [ 13 ]
The reasons for non-adherence have been given by patients as follows:
Partridge et al (2002) identified evidence to show that adherence rates in cancer treatment are variable, and sometimes surprisingly poor. The following table is a summary of their findings: [ 96 ]
In 1998, trials evaluating Tamoxifen as a preventative agent have shown dropout rates of around one-third:
In March 1999, the "Adherence in the International Breast Cancer Intervention Study" evaluating the effect of a daily dose of Tamoxifen for five years in at-risk women aged 35–70 years was [ 99 ]
Patients with diabetes are at high risk of developing coronary heart disease and usually have related conditions that make their treatment regimens even more complex, such as hypertension, obesity and depression [ 100 ] which are also characterised by poor rates of adherence. [ 101 ]
Other aspects that drive medicine adherence rates is the idea of perceived self-efficacy and risk assessment in managing diabetes symptoms and decision making surrounding rigorous medication regiments. Perceived control and self-efficacy not only significantly correlate with each other, but also with diabetes distress psychological symptoms and have been directly related to better medication adherence outcomes. [ 103 ] Various external factors also impact diabetic patients' self-management behaviors including health-related knowledge/beliefs, problem-solving skills, and self-regulatory skills, which all impact perceived control over diabetic symptoms. [ 104 ]
Additionally, it is crucial to understand the decision-making processes that drive diabetics in their choices surrounding risks of not adhering to their medication. While patient decision aids (PtDAs), sets of tools used to help individuals engage with their clinicians in making decisions about their healthcare options, have been useful in decreasing decisional conflict, improving transfer of diabetes treatment knowledge, and achieving greater risk perception for disease complications, their efficacy in medication adherence has been less substantial. [ 105 ] Therefore, the risk perception and decision-making processes surrounding diabetes medication adherence are multi-faceted and complex with socioeconomic implications as well. For example, immigrant health disparities in diabetic outcomes have been associated with a lower risk perception amongst foreign-born adults in the United States compared to their native-born counterparts, which leads to fewer protective lifestyle and treatment changes crucial for combatting diabetes. [ 106 ] Additionally, variations in patients' perceptions of time (i.e. taking rigorous, costly medication in the present for abstract beneficial future outcomes can conflict with patients' preferences for immediate versus delayed gratification) may also present severe consequences for adherence as diabetes medication often requires systematic, routine administration. [ 107 ]
As a result of poor compliance, [ citation needed ] 75% of patients with a diagnosis of hypertension do not achieve optimum blood-pressure control. [ citation needed ]
A 2003 review found that 41–59% of patients prescribed antipsychotics took the medication prescribed to them infrequently or not at all. [ 109 ] Sometimes non-adherence is due to lack of insight , [ 110 ] but psychotic disorders can be episodic and antipsychotics are then use prophylactically to reduce the likelihood of relapse rather than treat symptoms and in some cases individuals will have no further episodes despite not using antipsychotics. [ 111 ] A 2006 review investigated the effects of compliance therapy for schizophrenia: and found no clear evidence to suggest that compliance therapy was beneficial for people with schizophrenia and related syndromes. [ 112 ]
A longitudinal study has shown that adherence with treatment about 60%. [ 113 ] The predictors of adherence were found to be more of psychological, communication and logistic nature rather than sociodemographic or clinical factors. The following factors were identified as independent predictors of adherence:
|
https://en.wikipedia.org/wiki/Adherence_(medicine)
|
Adhesions are fibrous bands that form between tissues and organs , [ 1 ] often as a result of injury during surgery. They may be thought of as internal scar tissue that connects tissues not normally connected.
Adhesions form as a natural part of the body's healing process after surgery in a similar way that a scar forms. The term "adhesion" is applied when the scar extends from within one tissue across to another, usually across a virtual space such as the peritoneal cavity . Adhesion formation post-surgery typically occurs when two injured surfaces are close to one another. According to the "classical paradigm" of adhesion formation, the pathogenesis starts with inflammation and activation of the coagulation system which causes fibrin deposits onto the damaged tissues. [ 2 ] The fibrin then connects the two adjacent structures where damage of the tissues occurred. The fibrin acts like a glue to seal the injury and builds the fledgling adhesion, said at this point to be "fibrinous." In body cavities such as the peritoneal, pericardial , and synovial cavities , a family of fibrinolytic enzymes may act to limit the extent of the initial fibrinous adhesion, and may even dissolve it. In many cases, the production or activity of these enzymes are compromised because of inflammation following injury or infection, however, and the fibrinous adhesion persists. A more recent study suggested that the formation of "fibrinous" adhesions is preceded by the aggregation of cavity macrophages that may act like extravascular platelets in the abdominal cavity. [ 3 ]
If this is allowed to happen, tissue repair cells such as macrophages , fibroblasts , and blood vessel cells penetrate into the fibrinous adhesion and lay down collagen and other matrix substances to form a permanent fibrous adhesion. In 2002, Giuseppe Martucciello's research group showed a possible role could be played by microscopic foreign bodies (FB) inadvertently contaminating the operative field during surgery. [ 4 ] These data suggested that two different stimuli are necessary for adhesion formation: a direct lesion of the mesothelial layers and a solid substrate foreign body (FB).
While some adhesions do not cause problems, others may prevent muscle , nerve and other tissues and organs from moving freely, sometimes causing organs to become twisted or pulled from their normal positions.
In the case of adhesive capsulitis of the shoulder (also known as frozen shoulder), adhesions grow between the shoulder joint surfaces, restricting motion .
Abdominal adhesions (or intra-abdominal adhesions) are most commonly caused by abdominal surgical procedures. The adhesions start to form within hours of surgery and may cause internal organs to attach to the surgical site or to other organs in the abdominal cavity. Adhesion-related twisting and pulling of internal organs may result in complications such as abdominal pain or intestinal obstruction.
Small bowel obstruction (SBO) is a significant consequence of post-surgical adhesions. A SBO may be caused when an adhesion pulls or kinks the small intestine and prevents the flow of content through the digestive tract. Obstruction may occur 20 years or more after the initial surgical procedure, if a previously benign adhesion allows the small bowel to twist spontaneously around itself and obstruct. Without immediate medical attention, SBO is an emergent, possibly fatal, condition.
According to statistics provided by the National Hospital Discharge Survey approximately 2,000 people die every year in the US from obstruction due to adhesions. [ 5 ] Depending on the severity of the obstruction, a partial obstruction may relieve itself with conservative medical intervention. Many obstructive events require surgery, however, to loosen or dissolve the offending adhesion(s) or to resect the affected small intestine .
Pelvic adhesions are a form of abdominal adhesions in the pelvis . In women they typically affect reproductive organs and thus are of concern in reproduction or as a cause of chronic pelvic pain . Other than surgery, endometriosis and pelvic inflammatory disease are typical causes.
Surgery inside the uterine cavity (e.g., suction dilation and curettage , myomectomy , endometrial ablation ) may result in Asherman's syndrome (also known as intrauterine adhesions, intra uterine synechiae), a cause of infertility.
The impairment of reproductive performance from adhesions may happen through many mechanisms, all of which usually stem from the distortion of the normal tubo-ovarian relationship. This distortion may prevent an ovum from traveling to the fimbriated end of the fallopian tube . [ 6 ]
A meta-analysis in 2012 came to the conclusion that there is only little evidence for the surgical principle that using less invasive techniques, introducing fewer foreign bodies, or causing less ischemia reduces the extent and severity of adhesions in pelvic surgery. [ 7 ]
Adhesions forming between the heart and the sternum after cardiac surgery place the heart at risk of catastrophic injury during re-entry for a subsequent procedure.
Adhesions and scarring as epidural fibrosis may occur after spinal surgery that restricts the free movement of nerve roots, causing tethering and leading to pain.
Adhesions and scarring occurring around tendons after hand surgery restrict the gliding of tendons in their sheaths and compromise digital mobility.
Applying adhesion barriers during surgery may help to prevent the formation of adhesions. [ 8 ] There are two methods that are approved by the U.S. Food and Drug Administration (FDA) for adhesion prevention: Intercede and Seprafilm. [ 9 ] One study found that Seprafilm is twice as effective at preventing adhesion formation when compared to just surgical technique alone. [ 9 ] Surgical humidification therapy may also minimise the incidence of adhesion formation. [ 10 ] Laparoscopic surgery has a reduced risk for creating adhesions. [ 11 ] Steps may be taken during surgery to help prevent adhesions such as handling tissues and organs gently, using starch-free and latex-free gloves, not allowing tissues to dry out, and shortening surgery time. [ 12 ]
An unfortunate fact is, that adhesions are unavoidable in surgery and the main treatment for adhesions is more surgery. Besides intestinal obstructions caused by adhesions that may be seen in an X-ray, there are no diagnostic tests available to accurately diagnose an adhesion. [ dubious – discuss ]
A study showed that more than 90% of people develop adhesions following open abdominal surgery and that 55–100% of women develop adhesions following pelvic surgery. [ 13 ] Adhesions from prior abdominal or pelvic surgery may obscure visibility and access at subsequent abdominal or pelvic surgery. In a very large study (29,790 participants) published in British medical journal The Lancet , 35% of patients who underwent open abdominal or pelvic surgery were readmitted to the hospital an average of two times after their surgery, due to adhesion-related or adhesion-suspected complications. [ 14 ] Over 22% of all readmissions occurred in the first year after the initial surgery. [ 14 ] Adhesion-related complexity at reoperation adds significant risk to subsequent surgical procedures. [ 15 ]
Certain organs and structures in the body are more prone to adhesion formation than others. The omentum is particularly susceptible to adhesion formation; one study found that 92% of post-operative adhesions were found in the omentum. [ 16 ] It appears that the omentum is the chief organ responsible for "spontaneous" adhesion formation (i.e. no prior history of surgery). In another study, 100% of spontaneous adhesion formations were associated with the omentum. [ 2 ]
One method to reduce the formation of adhesions following abdominal surgery is hydroflotation , in which the organs are separated from one another by being floated in a solution. [ 17 ]
The long-term use of a wrist splint during recovery from carpal tunnel surgery may cause adhesion formation. [ 18 ] For that reason, it is advised that wrist splints be used only for short-term protection in work environments, but otherwise, splints do not improve grip strength , lateral pinch strength, or bowstringing. [ 18 ] Beyond adhesion they also may cause stiffness or flexibility problems. [ 18 ]
There are three general types of adhesions: filmy, vascular, and cohesive, [ 19 ] however, their pathophysiology is similar. [ 19 ] [ unreliable medical source? ] Filmy adhesions usually do not pose problems. Vascular adhesions are problematic.
|
https://en.wikipedia.org/wiki/Adhesion_(medicine)
|
An adhesion barrier is a medical implant that can be used to reduce abnormal internal scarring ( adhesions ) following surgery by separating the internal tissues and organs while they heal.
Surgeons have realized that proper surgical technique is crucial to reduce adhesion formation. In addition, for more than a century, adjuvants including drugs and materials such as animal membranes, gold foil , mineral oil , sheets made of rubber and Teflon , have been used to reduce the risk of adhesion formation. [ 1 ] Nevertheless, adhesions do occur and appear to be, to some degree, an almost unavoidable consequence of abdominal and pelvic surgery. Adhesions can lead to significant post-surgical morbidity , bowel obstruction , infertility , and chronic pelvic pain or chronic abdominal pain .
Surgeons and healthcare professionals developed several methods for minimizing tissue injury in order to minimize the formation of adhesions. However, even an experienced surgeon despite using advanced techniques may not be able to fully prevent the formation of adhesions following surgery, without the aid of an adhesion barrier. Consequently, many surgeons apply adhesion barriers while performing abdominal and pelvic surgery.
However, one study found the frequency of adhesion barrier use to be very low. The study examined hospital data and found that adhesion barriers were only used in a maximum of 5% of procedures in which the use of a barrier would be appropriate. [ 2 ]
Adhesion barriers are physical films, fabrics , gels or other materials that are applied between layers of tissues at the end of a surgery before the incision site is closed. While in place, the adhesion barrier acts as a physical barrier to separate traumatized tissue surfaces so that they do not adhere to one another while the tissue surfaces heal. Once the tissue surfaces heal, which is usually between 3 and 7 days, the barrier dissolves and is absorbed by the body.
Global Adhesion Barrier Market Size is expected to reach US $ 15Mn by 2025 during the forecast period 2020 to 2025.The first commercially available adhesion barrier was probably Cargile Membrane, a preserved peritoneal membrane of the Danish Ox . [ 3 ] Marketed by Johnson & Johnson around 1904, it was still available in the early 1990s. In the United States, Interceed, [ 4 ] Seprafilm [ 5 ] and Adept [ 6 ] are the three products approved by the U.S. Food and Drug Administration (FDA) for use as an adhesion barrier after abdominal or pelvic surgery.
Seprafilm (made by Genzyme ) is a clear, sticky film composed of chemically modified sugars , some of which occur naturally in the human body. It sticks to the tissues to which it is applied and is slowly absorbed into the body over a period of seven days. It is approved for use in certain types of pelvic or abdominal surgery.
Interceed (made by Johnson & Johnson ) is a knitted fabric composed of a modified cellulose that swells and eventually gels after being placed on the injured site, and, like Seprafilm, forms a barrier and then is slowly absorbed over a period of days. It is approved for use in pelvic surgery. Although it is technically possible to apply either Seprafilm or Interceed laparoscopically , neither product is approved for this use in the U.S.
Adept ( Baxter ) is a solution of Icodextrin that when instilled in a large volume causes organs to float apart, reducing the possibility of attachment.
A number of adhesion barriers are available outside of the United States including Hyalobarrier, [ 7 ] SprayShield, [ 8 ] PrevAdh [ 9 ] and INTERCOAT. [ 10 ] Several products licensed for other uses are used off-label in the USA for adhesion prevention including Evicel, Surgiwrap, CoSeal and Preclude, the latter being a product of Gore-Tex , not being absorbed and requiring a second intervention/operation for removal.
Products available for adhesion prevention outside the abdominal and pelvic cavities inside or outside the U.S. include ADCON Gel [ 11 ] (spine and tendon surgery), Sepragel ENT, INCERT [ 12 ] (spine), Tenoglide (tendon), Oxiplex [ 13 ] (Medishield) (spine) and REPEL CV (Cardiac).
Genzyme also tested a spray-on barrier called Sepraspray. [ 14 ] The company settled a federal Department of Justice lawsuit over claims its sales representatives illegally showed hospital staff how to dissolve Seprafilm with saline into "slurry" and use it in laproscopic surgeries, for which it was not FDA-approved. [ 15 ]
According to Cochrane Summaries , Gore-Tex is more effective than Interceed, but requires a second surgery for removal as it is not absorbable. Seprafilm or Fibrin sheets were not found to be effective. [ 16 ] Vigorous follow-up is crucial, thus more studies are needed in gynecologic surgery as a major drawback of studies is that they do not incorporate the gold standard of success, namely pregnancy rates .
|
https://en.wikipedia.org/wiki/Adhesion_barrier
|
Adie syndrome , also known as Holmes–Adie syndrome , is a neurological disorder characterized by a tonically dilated pupil that reacts slowly to light but shows a more definite response to accommodation (i.e., light-near dissociation). [ 1 ] It is frequently seen in females with absent knee or ankle jerks and impaired sweating.
The syndrome is caused by damage to the postganglionic fibers of the parasympathetic innervation of the eye, usually by a viral or bacterial infection that causes inflammation , and affects the pupil of the eye and the autonomic nervous system . [ 1 ] It is named after the British neurologists William John Adie and Gordon Morgan Holmes , who independently described the same disease in 1931. [ 2 ]
Adie syndrome presents with three hallmark symptoms, namely at least one abnormally dilated pupil ( mydriasis ) which does not constrict in response to light, loss of deep tendon reflexes, and abnormalities of sweating. [ 1 ] Other signs may include hyperopia due to accommodative paresis , photophobia and difficulty reading. [ 3 ] Some individuals with Adie syndrome may also have cardiovascular abnormalities . [ 4 ]
Pupillary symptoms of Holmes–Adie syndrome are thought to be the result of a viral or bacterial infection that causes inflammation and damage to neurons in the ciliary ganglion , located in the posterior orbit, that provides parasympathetic control of eye constriction. Additionally, patients with Holmes-Adie Syndrome can also experience problems with autonomic control of the body. This second set of symptoms is caused by damage to the dorsal root ganglia of the spinal cord . Adie's pupil is supersensitive to ACh so a muscarinic agonist (e.g. pilocarpine ) whose dose would not be able to cause pupillary constriction in a normal patient, would cause it in a patient with Adie's Syndrome. The circuitry for the pupillary constriction does not descend below the upper midbrain, henceforth impaired pupillary constriction is extremely important to detect as it can be an early sign of brainstem herniation. [ 1 ]
Clinical exam may reveal sectoral paresis of the iris sphincter or vermiform iris movements. The tonic pupil may become smaller (miotic) over time which is referred to as "little old Adie's". [ 5 ] Testing with low dose (1/8%) pilocarpine may constrict the tonic pupil due to cholinergic denervation supersensitivity . [ 1 ] A normal pupil will not constrict with the dilute dose of pilocarpine. [ 5 ] CT scans and MRI scans may be useful in the diagnostic testing of focal hypoactive reflexes. [ 6 ]
The usual treatment of a standardised Adie syndrome is to prescribe reading glasses to correct for impairment of the eye(s). [ 1 ] Pilocarpine drops may be administered as a treatment as well as a diagnostic measure. [ 1 ] Thoracic sympathectomy is the definitive treatment of diaphoresis , if the condition is not treatable by drug therapy . [ 1 ]
Adie's syndrome is not life-threatening or disabling. [ 1 ] As such, there is no mortality rate relating to the condition; however, loss of deep tendon reflexes is permanent and may progress over time. [ 1 ]
It most commonly affects younger women (2.6:1 female preponderance) and is unilateral in 80% of cases. [ 5 ] Average age of onset is 32 years. [ 7 ]
|
https://en.wikipedia.org/wiki/Adie_syndrome
|
An adipose tissue neoplasm is a neoplasm derived from adipose tissue .
An example is lipoma .
This oncology article is a stub . You can help Wikipedia by expanding it .
|
https://en.wikipedia.org/wiki/Adipose_tissue_neoplasm
|
Adiposis dolorosa is an outdated term for many years used synonymously as Dercum's disease , lipedema or Anders disease. [ 1 ] While there are numerous references to adiposis dolorosa, it is recommended that the term no longer be used. Dercum's is now recognized as a separate condition, as is lipedema. [ 2 ] [ 3 ]
|
https://en.wikipedia.org/wiki/Adiposis_dolorosa
|
Adipsia , also known as hypodipsia , is a symptom of inappropriately decreased or absent feelings of thirst. [ 1 ] [ 2 ] It involves an increased osmolality or concentration of solute in the urine, which stimulates secretion of antidiuretic hormone (ADH) from the hypothalamus to the kidneys. This causes the person to retain water and ultimately become unable to feel thirst. Due to its rarity, the disorder has not been the subject of many research studies.
Adipsia may be seen in conditions such as diabetes insipidus [ 3 ] and may result in hypernatremia . [ 4 ] It can occur as the result of abnormalities in the hypothalamus , pituitary and corpus callosum , [ 5 ] as well as following pituitary/hypothalamic surgery. [ 6 ]
It is possible for hypothalamic dysfunction, which may result in adipsia, to be present without physical lesions in the hypothalamus, although there are only four reported cases of this. [ 7 ] There are also some cases of patients experiencing adipsia due to a psychiatric disease. In these rare psychogenic cases, the patients have normal levels of urine osmolality as well as typical ADH activity. [ 8 ]
Dopamine , a neurotransmitter , has been linked with feeding behaviors. In an experiment, scientists measured how much food and water mice consumed when they were born without dopamine in their systems. They found that without dopamine, the mice would starve and be dehydrated to the point of death. The scientists then injected the mice without dopamine with its precursor, L-DOPA , and the mice started eating again. But, even though the mice were born without dopamine in their systems, they still had the capacity to control their feeding and drinking behaviors, suggesting that dopamine does not play a role in developing those neural circuits. Instead, dopamine is more closely related to the drive for hunger and thirst. Although the lack of dopamine resulted in adipsia in these rats, low levels of dopamine do not necessarily cause adipsia. [ 9 ]
Other findings in support of the role of dopamine in thirst regulation involved the nigrostriatal pathway . After completely degenerating the pathway, the animal becomes adipsic, aphagic , and loses its interest in exploring. Although dopamine plays a role in adipsia, there is no research involving exclusively the relationship between adipsia and dopamine, as changes in dopamine simultaneously mediate changes in eating and curiosity, in addition to thirst. [ 10 ]
Adipsia can tend to result from lesions to hypothalamic regions involved in thirst regulation. These lesions can be congenital, acquired, trauma, or even surgery. Lesions or injuries to those hypothalamic regions cause adipsia because the lesions cause defects in the thirst regulating center which can lead to adipsia. Lesions in that region can also cause adipsia because of the extremely close anatomical proximity of the hypothalamus to ADH-related osmoreceptors. [ 8 ]
Diagnosing adipsia can be difficult as there is no set of concrete physical signs that are adipsia specific. Changes in the brain that are indicative of adipsia include those of hyperpnea , muscle weakness, insomnia, lethargy, and convulsions (although uncommon except in extreme cases of incredibly rapid rehydration). Patients with a history of brain tumors, or congenital malformations , may have hypothalamic lesions, which could be indicative of adipsia. [ 4 ] Some adults with Type A adipsia are anorexic in addition to the other symptoms. [ 11 ]
Initial testing for adipsia involves electrolyte , blood urea nitrogen (BUN) and creatinine levels, serum and urine osmolality , blood hormone levels, like vasopressin (AVP). In patients who have defects in thirst regulation and vasopressin secretion, serum vasopressin levels are low or absent. [ 12 ] Measurements of urine electrolytes and osmolality are critical in determining the central, rather than renal, nature of the defect in water homeostasis. In adipsia, the fractional excretion of sodium is less than 1%, unless a coexisting defect in AVP secretion is present. In salt intoxication, the urine sodium concentrations are very high and fractional excretion of sodium is greater than 1%. Initial test results may be suggestive of diabetes insipidus. The circulating AVP levels tend to be high, which indicate an appropriate response of the pituitary to hyperosmolality . Patients may have mild stable elevations of serum sodium concentrations, along with elevations in both BUN and creatinine levels and in the BUN/creatinine ratio. [ 4 ]
Type A (essential hypernatremia syndrome) involves an increase of the level in which solvent molecules can pass through cell membranes (osmotic threshold) for vasopressin release and the activation of the feeling of thirst. This is the most characterized sub-type of adipsia, however there is no known cause for Type A adipsia. There is debate over whether osmoreceptor resetting could lead to the increase in threshold. Other studies have shown that it is the loss of osmoreceptors , not resetting, that cause the change in threshold. [ 13 ] Patients with Type A adipsia can be at risk of seizures if they rapidly re-hydrate or quickly add a significant amount of sodium into their bodies. If not treated, Type A adipsia could result in both a decrease in the size of the brain and bleeding in the brain. [ 11 ]
Type B adipsia occurs when vasopressin responses are at decreased levels in the presence of osmotic stimuli. Although minimal, there is still some secretion of AVP. This type may be due to some elimination of osmoreceptors. [ 13 ]
Type C adipsia (type C osmoreceptor dysfunction) involves complete elimination of osmoreceptors, and as a result have no vasopressin release when there normally would be. Type C is generally the adipsia type found in patients with adipsic diabetes insipidus . [ 13 ]
Type D is the least commonly diagnosed and researched type of adipsia. The AVP release in this subtype occurs with normally functioning levels of osmoregulation. [ 13 ]
People affected by adipsia lack the ability to feel thirst; thus, they often must be directed to drink. Adipsic persons may undergo training to learn when it is necessary that they drink water. Currently, there is no medicine available to treat adipsia. For people with adipsia because of hypothalamic damage, there is no surgical or medicinal option to fix the damage. In some cases where adipsia was caused by growths on thirst centers in the brain, surgical removal of the growths was successful in treating adipsia. Although adipsic persons must maintain a strict water intake schedule, their diets and participation in physical activities are not limited.
People affected by diabetes insipidus have the option of using the intranasal or oral hormone desmopressin acetate (DDAVP), which is molecularly similar enough to vasopressin to perform its function. In this case, desmopressin helps the kidneys to promote reabsorption of water. [ 4 ] Some doctors have reported success in treating psychogenic adipsic patients with electroconvulsive therapy , although the results are mixed and the reason for its success is still unknown. [ 8 ] Additionally, some patients who do not successfully complete behavioral therapy may require a nasogastric tube in order to maintain healthy levels of fluids. [ 8 ]
|
https://en.wikipedia.org/wiki/Adipsia
|
A laparoscopic adjustable gastric band , commonly called a lap-band , A band , or LAGB , is an inflatable silicone device placed around the top portion of the stomach to treat obesity , intended to decrease food consumption.
Adjustable gastric band surgery is an example of bariatric surgery designed for obese patients with a body mass index (BMI) of 40 or greater—or between 35 and 40 in cases of patients with certain comorbidities that are known to improve with weight loss , such as sleep apnea , diabetes , osteoarthritis , GERD , hypertension (high blood pressure) , or metabolic syndrome , among others.
In February 2011, the United States Food and Drug Administration (FDA) expanded approval of adjustable gastric bands to patients with a BMI between 30 and 40 and one weight-related medical condition, such as diabetes or high blood pressure. However, an adjustable gastric band may be used only after other methods such as diet and exercise have been tried. [ 2 ]
The inflatable band is placed around the upper part of the stomach to create a smaller stomach pouch. This slows and limits the amount of food that can be consumed at one time, thus giving the opportunity for the sense of satiety to be met with the release of peptide YY (PYY). It does not decrease gastric emptying time. The individual achieves sustained weight loss by choosing healthy food options, limiting food intake and volume, reducing appetite, and progress of food from the top portion of the stomach to the lower portion digestion . [ 3 ]
According to the American Society for Metabolic Bariatric Surgery, bariatric surgery is not an easy option for obesity sufferers. It is a drastic step, and carries the usual pain and risks of any major gastrointestinal surgical operation. However, gastric banding is the least invasive surgery of its kind and is completely reversible, with another "keyhole" operation . Gastric banding is performed using laparoscopic surgery and usually results in a shorter hospital stay, faster recovery, smaller scars, and less pain than open surgical procedures. Because no part of the stomach is stapled or removed, and the patient's intestines are not re-routed, they can continue to absorb nutrients from food normally. Gastric bands are made entirely of biocompatible materials, so they are able to stay in the patient's body without causing harm.
However, not all patients are suitable for laparoscopy. Patients who are extremely obese, who have had previous abdominal surgery, or have complicating medical problems may require the open approach. [ 4 ]
The surgical insertion of an adjustable gastric band is often referred to as a lap band procedure or band placement. First, a small incision (typically less than 1.25 cm or 0.5 in.) is made near the belly button . Carbon dioxide (a gas that occurs naturally in the body) is introduced into the abdomen to create a work space for the surgeon. Then a small laparoscopic camera is placed through the incision into the abdomen. The camera sends a picture of the stomach and abdominal cavity to a video monitor . It gives the surgeon a good view of the key structures in the abdominal cavity. A few additional small incisions are made in the abdomen. The surgeon watches the video monitor and works through these small incisions using instruments with long handles to complete the procedure. The surgeon creates a small, circular tunnel behind the stomach, inserts the gastric band through the tunnel, and locks the band around the stomach.
Clinical studies of laparoscopic (minimally invasive) bariatric surgery patients found that they felt better, spent more time doing recreational and physical activities, benefited from enhanced productivity and economic opportunities, and had more self-confidence than they did prior to surgery. [ 5 ]
The placement of the band creates a small pouch at the top of the stomach. This pouch holds approximately 1/2 cup (~120 mL) of food, whereas the typical stomach holds about 6 cups (~1,440 mL) of food. The pouch fills with food quickly, and the band slows the passage of food from the pouch to the lower part of the stomach. [ 6 ] As the upper part of the stomach registers as full, the message to the brain is that the entire stomach is full, and this sensation helps the person to be hungry less often, feel full more quickly and for a longer period of time, eat smaller portions, and lose weight over time. [ 3 ]
As patients lose weight, their bands will need adjustments, or "fills", to ensure comfort and effectiveness. The gastric band is adjusted by introducing a saline solution into a small access port placed just under the skin. A specialized non-coring needle is used to avoid damage to the port membrane and prevent leakage. [ 7 ] There are many port designs (such as high profile and low profile), and they may be placed in varying positions based on the surgeon's preference, but are always attached (through sutures, staples, or another method) to the muscle wall in and around the diaphragm.
Adjustable gastric bands hold between 4 and 12 cc of saline solution , depending on their design. [ citation needed ] When the band is inflated with saline solution, it places pressure around the outside of the stomach. This decreases the size of the passage between the pouch created from the upper part of the stomach and the lower stomach and further restricts the movement of food. Over the course of several visits to the doctor, the band is filled until the optimal restriction has been achieved – neither so loose that hunger is not controlled, nor so tight that food cannot move through the digestive system. The number of adjustments required is an individual experience and cannot be accurately predicted.
In the U.S. market, one adjustable gastric band is currently approved by the FDA: Lap-Band. The Lap-Band System obtained FDA approval in 2001. [ 8 ] The Realize Band lost FDA approval in 2016. [ 9 ] The device comes in five different sizes and has undergone modification over the years. The latest models, the Lap-Band AP-L and Lap-Band AP-S, feature a standardized injection port sutured into the skin and fill volumes of 14 mL and 10 mL respectively. [ 10 ]
Two other adjustable gastric bands are in use outside of the United States— Heliogast and Midband . Neither band has been approved by the FDA. The Midband was the first to market in 2000. [ 11 ] In order to preserve the gastric wall in event of rubbing, the device contains no sharp edges or irregularities. It is also opaque to x-rays, making it easy to locate and adjust. [ 12 ] The Heliogast band entered the market in 2003. The device features a streamlined band to ease insertion during the operation. [ 13 ]
In general, gastric banding is indicated for people for whom all of the following apply:
Gastric banding is usually not recommended for people with any of the following:
If considering pregnancy, ideally the patient should be in optimum nutritional condition prior to, or immediately following, conception; deflation of the band may be required prior to a planned conception. Deflation should also be considered should the patient experience morning sickness. The band may remain deflated during pregnancy and once breast feeding is completed, or if bottle feeding, the band may be gradually re-inflated to aid postpartum weight loss as needed. [ 17 ]
It is highly advised to take extra precautions during intercourse after surgery, as rapid weight loss increases fertility. Effective birth control methods must be used at all times to avoid unwanted pregnancies. Two factors have been pointed out by experts that may help explain this increase in fertility: reversal of PCOS ( polycystic ovary syndrome ) and reduction in the excess of estrogen , which is produced by fat cells. [ 18 ]
Unlike more open forms of weight loss surgery (e.g. Roux-en-Y gastric bypass surgery (RNY), Biliopancreatic diversion (BPD) and Duodenal Switch (DS)), gastric banding does not require cutting or removing any part of the digestive system. It is removable, requiring only a laparoscopic procedure to remove the band, after which the stomach usually returns to its normal pre-banded size so it is not unusual for a person to gain weight after having a band removed. However, it is not entirely reversible as adhesions and tissue scarring are inevitable. Unlike those who have procedures such as RNY, DS, or BPD, it is unusual for gastric band patients to experience any nutritional deficiencies or malabsorption of micro-nutrients. Calcium supplements and Vitamin B12 injections are not routinely required following gastric banding (as is often the case with RNY, for example). [ 4 ] Gastric dumping syndrome issues also do not occur since intestines are not removed or re-routed.
Typically, patients who undergo adjustable gastric banding procedures lose less weight over the first 3.5 years than those who have RNY gastric bypass, BPD, or DS surgeries. Although other procedures appear to result in greater weight loss than adjustable gastric banding in the short term, results from the study by Maggard suggest that this difference decreases significantly over time. [ 19 ] Gastric banding patients lose an average of 47.5% of their excess weight, according to a meta analysis by Buchwald. [ 5 ]
It is important to note that, in order to maintain their weight reduction, patients must carefully follow post-operative guidelines relating to diet, exercise, and band maintenance. Weight regain is possible with any weight loss procedure, including the more radical procedures that initially result in rapid weight loss. The National Institutes of Health recommendation for weight loss is 1 to 2 pounds (½ to 1 kilogram) per week, and an average banded patient may lose this amount. [ 20 ] This is variable based on the individual and their personal circumstances, motivation, and mobility.
Some studies reveal there is a decrease in adjustable gastric banding surgeries due to the increased risk of reoperation, compared to Roux-en-Y gastric bypass (RYGB) or sleeve gastrectomy (SG) bariatric procedures. [ 21 ]
One commonly reported occurrence for banded patients is regurgitation of non-acidic swallowed food from the upper pouch, commonly known as Productive Burping (PBing). [ 22 ] Productive Burping is not to be considered normal. The patient should consider eating less, eating more slowly and chewing food more thoroughly. Occasionally, the narrow passage into the larger, lower part of the stomach might also become blocked by a large portion of unchewed or unsuitable food. [ 23 ]
Other complications include:
The following are the adverse effects of gastric banding as documented by the FDA. [ 8 ]
The average gastric banding patient loses 500 grams to a kilogram (1–2 pounds) per week consistently, but heavier patients often lose faster in the beginning. [ 28 ] This comes to roughly 22 to 45 kilograms (49 to 99 pounds) the first year for most band patients. It is important to keep in mind that while most of the RNY patients drop the weight faster in the beginning, some studies have found that LAGB patients will have the same percentage of excess weight loss and comparable ability to keep it off after only a couple of years. The procedure tends to encourage better eating habits which, in turn, helps in producing long term weight stability. However, with greater experience and longer patient follow up, several studies have found suboptimal weight loss and high complication rates for the gastric band. [ 25 ]
A systematic review concluded "LAGB has been shown to produce a significant loss of excess weight while maintaining low rates of short-term complications and reducing obesity-related comorbidities. LAGB may not result in the most weight loss but it may be an option for bariatric patients who prefer or who are better suited to undergo less invasive and reversible surgery with lower perioperative complication rates. One caution with LAGB is the uncertainty about whether the low complication rate extends past three years, given a possibility of increased band-related complications (e.g., erosion, slippage) requiring re-operation". [ 29 ]
Researcher Paul O’Brien, MD, of Melbourne, Australia's Monash University says the procedure offers an effective, reversible, long-term solution for weight loss as long as patients get good follow-up care and are willing to carefully control the way they eat. This study was supported by Allergan Inc., which markets a gastric band system. [ 30 ]
A meta-analysis of 174,772 participants published in The Lancet in 2021 found that bariatric surgery was associated with 59% and 30% reduction in all-cause mortality among obese adults with or without type 2 diabetes respectively. [ 31 ] This meta-analysis also found that median life-expectancy was 9.3 years longer for obese adults with diabetes who received bariatric surgery as compared to routine (non-surgical) care, whereas the life expectancy gain was 5.1 years longer for obese adults without diabetes. [ 31 ]
Correct and sensitive adjustment of the band is imperative for weight loss and the long-term success of the procedure. Adjustments (also called "fills") may be performed using an X-ray fluoroscope so that the radiologist can assess the placement of the band, the port, and the tubing that runs between the port and the band. The patient is given a small cup of liquid containing a clear or white radio-opaque fluid similar to barium . When swallowed, the fluid is clearly shown on X–ray and is observed as it travels down the esophagus and through the restriction caused by the band. The radiologist is then able to see the level of restriction in the band and to assess if there are potential or developing issues of concern. [ 32 ] These may include dilation of the esophagus, an enlarged pouch, prolapsed stomach (when part of the stomach moves into the band where it does not belong), erosion or migration. Reflux -type symptoms may indicate too great a restriction, and further assessment may be required.
Under some circumstances, fluid is removed from the band prior to further investigation and reevaluation. In other cases, further surgery may be required, such as removal of the band, should gastric erosion or a similar complication be detected. Some health practitioners adjust the band without the use of X-ray control (fluoroscopy). In these cases, the doctor assesses the patient's weight loss and potential reflex symptoms described by the patient, such as heartburn, regurgitation, or chest pain. From this information, the doctor decides whether a band adjustment is necessary. Adjustments are often indicated if a patient has regained weight, if weight loss has leveled off, or if the patient has a distinct feeling that food is difficult to move through the stomach. [ 32 ]
Clinical visits for regular fill adjustments generally take only about one to two minutes. However, for some patients, this type of fill is not possible because of issues such as partial rotation of the port or excess tissue above the port presenting difficulty in determining its precise location. In these cases, a fluoroscope will generally be used. It is more common practice for the band not to be filled at surgery, although some surgeons choose to place a small amount in the band at the time of surgery. The stomach tends to swell following surgery and it is possible that too great a restriction would be achieved if filled at that time.
Many health practitioners make the first adjustment between four and six weeks post-operatively to allow the stomach time to heal. After that, fills are performed as needed.
No accurate number of adjustments required can be given. The amount of saline/isotonic solution needed in the band varies from patient to patient. There are a small number of people who find that they do not need a fill at all and have sufficient restriction immediately following surgery. Others may need significant adjustments to the maximum that the band is able to hold.
The patient may be prescribed a liquid-only diet, followed by mushy foods and then solids. This is prescribed for a varied length of time and each surgeon and manufacturer varies. Some may find that before their first fill, they are still able to eat fairly large portions, because before the fill, there is little or no restriction in the band. Thus a proper post-op diet and a good after-care plan are essential to success. A recent study found that patients who did not change their eating habits were 2.2 times more likely to be unsuccessful than those who did, and that patients who had not increased their physical activity were 2.3 times more likely to be unsuccessful than those who did. [ 33 ]
A long-term, post-gastric-band surgery diet should consist of normal healthy food that is solid in nature and requires ample chewing to achieve a paste consistency prior to swallowing. This texture will maximise the effect of the band, in contrast to easier wet foods, such as soups, casseroles and smoothies, which pass through the band quickly and easily resulting in greater caloric intake.
Support groups exist for gastric-banding patients. Some mix RNY and gastric-bypass patients with gastric-banding patients. Some gastric-band patients have criticized this approach because, while many of the underlying issues related to obesity are the same, the needs and challenges of the two groups are very different, as are their early rates of weight loss. Some gastric-band recipients feel that the procedure is a failure when they see that RNY patients generally lose weight faster. [ 34 ]
Adjustable gastric-band surgery costs about $15,000 in the United States, although state-specific averages range from about $10,500 (Colorado and Texas) to over $33,000 (Alaska). Services included in these costs vary by surgical clinic and hospital, but most practices include all services necessary to perform the procedure (surgeon's fee, surgical assistant fee, hospital/operating room fee, anesthesiologist fee and the device fee for the gastric band itself). Some practices also bundle a set duration of post-operative follow-up visits for filling and unfilling the gastric band as necessary (e.g., as many fills/unfills as necessary for anywhere from three to 13 months following surgery, depending on the practice), which as a standalone service costs between $15 and $300 per office visit. Most practices do not include within their quoted fees the cost of preoperative care and testing or any potential complications that may arise. [ 35 ]
At the end of the 1970s, Wilkinson developed several surgical approaches with a common aim to limit food intake without disrupting the continuity of the gastrointestinal tract. [ 36 ]
In 1978 Wilkinson and Peloso were the first to place, by open procedure, a non-adjustable band (2 cm Marlex mesh) around the upper part of the stomach. [ 37 ]
The early 1980s saw further developments, with Kolle (Norway), Molina & Oria (U.S.), Naslund (Sweden), Frydenberg (Australia) and Kuzmack (U.S.) implanting non-adjustable gastric bands made from a variety of materials, including marlex mesh, dacron vascular prosthesis, silicone covered mesh and Gore-Tex , among others. [ 38 ] [ 39 ] [ 40 ] [ 41 ] [ 42 ] [ 43 ] In addition, Bashour developed the "gastro-clip", a 10.5 cm polypropylene clip with a 50cc pouch and a fixed 1.25 cm stoma, which was later abandoned because of its high rates of gastric erosion. [ 44 ]
All of these early attempts at restriction using meshes, bands and clips showed a high failure rate because of difficulty achieving correct stomal diameter, stomach slippage, erosion, food intolerance, intractable vomiting and pouch dilatation. Despite these difficulties, silicone was identified as the best-tolerated material, with far fewer adhesions and tissue reactions occurring than with other materials. Nevertheless, adjustability became a primary goal of these early pioneers. [ citation needed ]
The development of the modern adjustable gastric band is a tribute both to the vision and persistence of the early pioneers, particularly Lubomyr Kuzmak and a sustained collaborative effort on the part of bio-engineers, surgeons and scientists. [ 45 ]
Early research on the concept of band “adjustability” can be traced back to the early work of G. Szinicz (Austria) who experimented with an adjustable band, connected to a subcutaneous port, in animals. [ 46 ]
In 1986, Lubomyr Kuzmak , a Ukrainian surgeon who had emigrated to the United States in 1965, reported on the clinical use of the "adjustable silicone gastric band" (ASGB) via open surgery. [ 43 ] Kuzmak, who from the early 1980s had been searching for a simple and safe restrictive procedure for severe obesity, modified his original silicone non-adjustable band, which he had been using since 1983, by adding an adjustable portion. His clinical results showed improved weight loss and reduced complication rates compared with his original non-adjustable band. Kuzmak's major contributions were the application of Mason's teachings about VBG to the development of the gastric band, the volume of the pouch, the need to overcome staple line disruption, the ratification of the use of silicone and the essential element of adjustability.
Separately, but in parallel with Kuzmak, Hallberg and Forsell in Stockholm, Sweden also developed an adjustable gastric band. After further work and modifications this eventually became known as the Swedish Adjustable Gastric Band (SAGB).
In early 1985, Dr. Dag Hallberg applied for a patent for the SAGB within Scandinavian countries. In late March, Dr. Hallberg presented his idea of the "balloon band" at the Swedish Surgical Society and started to use the SAGB in a controlled series of 50 procedures. At the time, laparoscopic surgery was uncommon and Dr. Hallberg and his assistant, Dr. Peter Forsell , started performing the open technique to implant the SAGB.
In 1992, Forsell, who fully owned the patent, was in contact with surgeons in Switzerland, Italy and Germany who began to implant the SAGB with the laparoscopic technique. In 1994, Dr. Forsell presented the SAGB at an international workshop for bariatric surgery in Sweden, and from then on, the SAGB would be implanted laparoscopically. During this time, the SAGB was manufactured by Swedish company ATOS Medical .
The advent of surgical laparoscopy has transformed the field of bariatric surgery and made the gastric band a more appealing option for the surgical management of obesity. In 1992, Prof. Guy-Bernard Cadière was the first to apply an adjustable band (the Kuzmak ASGB device) by the laparoscopic approach. [ 47 ] Over the next few years, the Kuzmak ASGB was modified to make it suitable for laparoscopic implantation, eventually emerging as the modern lap band. This landmark innovation was driven by Belachew , Cadière, Favretti and O’Brien, and the Inamed Development Company engineered the device. The first human laparoscopic implantation of the newly developed lap band was performed by Belachew and le Grand on 1 September 1993 in Huy , Belgium , followed on 8 September by Cadière and Favretti in Padua , Italy . [ 48 ] [ 49 ] In 1993, Broadbent in Australia and Catona in Italy implanted non-adjustable (Molina-type) gastric bands by laparoscopy. [ 50 ] [ 51 ] In 1994, the first international laparoscopic-band workshop was held in Belgium and the first involving the SAGB was held in Sweden .
Single-port laparoscopy (SPL) is an advanced, minimally invasive procedure in which the surgeon operates almost exclusively through a single entry point, typically the navel . Special articulating instruments and access ports make it unnecessary to place trocars externally for triangulation, thus allowing the creation of a small, solitary portal of entry into the abdomen. The SPL technique has been used to perform many types of surgery, including adjustable gastric banding [ 52 ] and sleeve gastrectomy . [ 53 ]
In 2003, the American Institute of Gastric Banding (AIGB) True Results opened the first outpatient surgery center using advanced laparoscopic technology to be recognized by the American College of Surgeons as an accredited outpatient bariatric center in the U.S. The first outpatient lap-band procedure in the U.S. was performed at the AIGB True Results Surgery Center of Richardson, Texas in 2003, and since that time, AIGB True Results has performed more than 30,000 outpatient lap-band procedures. [ citation needed ]
In 2012 there was a request for a congressional investigation by members of the U.S. Congress into lapband safety, prompted by recent patient deaths after lapband surgeries at clinics affiliated with the 1-800-GET-THIN advertising campaign in Southern California . [ 54 ] [ 55 ]
As with many developments in approaches to weight loss, [ citation needed ] some public figures have affected public opinion and increased awareness of gastric banding:
|
https://en.wikipedia.org/wiki/Adjustable_gastric_band
|
An admission note is part of a medical record that documents the patient 's status (including history and physical examination findings ), reasons why the patient is being admitted for inpatient care to a hospital or other facility, and the initial instructions for that patient's care. [ 1 ]
Admission notes document the reasons why a patient is being admitted for inpatient care to a hospital or other facility, the patient's baseline status, and the initial instructions for that patient's care. Health care professionals use them to record a patient's baseline status and may write additional on-service notes , progress notes ( SOAP notes ), preoperative notes , operative notes , postoperative notes , procedure notes , delivery notes , postpartum notes , and discharge notes . These notes constitute a large part of the medical record . Medical students often develop their clinical reasoning skills by writing admission notes. The traditional, rational definition of being admitted usually involves spending an overnight in the hospital. This definition is sometimes stretched in the U.S. medical billing industry , where hospital corporations may blur the definitions of "admission" and "observation" because of reimbursement rules under which healthcare payors pay less for the care if an "admission" was involved. [ 2 ]
An admission note may sometimes be incorrectly referred to as an HPI ( history of present illness ) or H and P (history and physical), which include only portions of an admission note.
An admission note can include the following sections:
Not every admission note explicitly discusses every item listed below, however, the ideal admission note would include:
Typically one sentence including
List of the patient's on-going medical problems. Chronic problems should be addressed as to whether or not they are well controlled or uncontrolled. Include dates of pertinent items.
List of surgeries in the past with dates of pertinent items.
Health or cause of death for:
In medicine, a social history is a portion of the admission note addressing familial, occupational, and recreational aspects of the patient's personal life that have the potential to be clinically significant.
Physical examination or clinical examination is the process by which a health care provider investigates the body of a patient for signs of disease .
e.g.: electrolytes , arterial blood gases , liver function tests , etc.
e.g.: EKG , CXR , CT , MRI
Assessment includes a discussion of the differential diagnosis and supporting history and exam findings.
|
https://en.wikipedia.org/wiki/Admission_note
|
There is an established practice of using the electrical conductance of blood ( PV loops ) in heart ventricles to determine the instantaneous volume of the ventricle. This technique involves inserting a tetra-polar catheter into the ventricle and measuring conductance. This measured conductance is a combination of blood and muscle and various techniques are used to identify the blood conductance from the total measured conductance. Blood conductance can then be converted to volume using a linear (Baan) or a non-linear (Wei) relationship that relates conductance to volume.
This approach is based on the idea that the total conductance, G, of a fluid between two electrodes is a function of the fluid's conductivity (reciprocal of resistivity) and volume. [ citation needed ]
In cardiology , a tetra-polar catheter is inserted into the ventricle and a constant current (I) is applied across the two outer electrodes . This generates an electrical field within the ventricle and the two inner electrodes measure a voltage generated due to the electric field. This measured voltage (V) is used to determine conductance through a modified version of Ohm's Law . Conductance (G) is the reciprocal of resistance (R) which changes the standard Ohm's equation from V=IR to V=I/G. [ citation needed ]
Conductance is then related to blood volume though Baan's equation. [ 1 ] When used in cardiology, the electric field generated is not limited to the blood (the fluid of interest) but also penetrates the heart wall, giving rise to additional conductance often called "parallel conductance" or "muscle conductance", G m which must be removed. [ citation needed ]
Various techniques have been attempted to remove the G m contribution with varying degrees of success. The most common method is the hypertonic saline technique which involves injecting a bolus of hypertonic saline into the ventricle to alter blood conductivity without affecting the surrounding muscle. Another less commonly used technique involves evacuating the ventricle of blood and measuring muscle conductance alone with a conductance catheter. Clearly both techniques are unreliable, somewhat invasive and fail to account for the continuous variation in G m over the cardiac cycle . [ 2 ]
The Admittance technique is an improvement over the Conductance technique for the real-time removal of muscle conductance G m . Blood and muscle respond to alternating (AC) electrical currents very differently. Blood is purely resistive while muscle has both resistive and capacitive properties. The fixed charges in muscle cells create a significant reactance that causes a phase shift (time delay) in the measured signal, relative to the excitation signal. Admittance technology uses this phase shift to determine the instantaneous muscle conductance and remove it from the total measured conductance. [ citation needed ]
The total Admittance (Y), of the blood filled ventricle is given by Y = G b + G m + iωC m where: [ citation needed ]
The signals G m and C m are both properties of cardiac muscle and vary in a fixed ratio. Thus the ratio of G m to C m is equal to the ratio of muscle conductivity (σ) to muscle permittivity (ε). The ratio σ/ε is the constant of proportionality. Although both σ and ε are functions of the health of the heart tissue, they are relatively constant for short periods of time. [ citation needed ]
Using this proportionality, one can rewrite the equation for G m as G m = (σ/ε)C m
Note that the imaginary component of Y depends only on the amount of muscle in the field of the catheter. This makes it easy to isolate by measuring the phase shift, φ, of the measured signal: [ citation needed ] cos(φ) = (G b + G m )/Y sin(φ) = ωC m /Y Hence, C m = Y.sin(φ)/ω also, G m = (σ/ε)C m
Thus, blood conductance is determined as G b = Y.cos(φ) - G m
Wei's equations can be applied to this calculated blood conductance G b to obtain blood volume. [ 3 ] Unlike Baan's equation, Wei's equation takes into account the non-linear nature of the electrical field and the dynamic nature of the cardiac cycle to give a more accurate representation of the blood volume. [ 4 ]
Admittance technique involves the measurement of both phase angle and total conductance in the ventricle. Thus, it is possible to observe how the parallel conductance (muscle conductance) varies throughout the cardiac cycle. A plot showing both the blood and muscle contribution are shown in the figure. [ citation needed ]
|
https://en.wikipedia.org/wiki/Admittance_and_conductance_in_cardiac_performance
|
An admitting privilege is the right of a doctor to admit patients to a hospital for medical treatment without first having to go through an emergency department . This is generally restricted to doctors on the hospital staff, although in some countries such as Canada and the United States , both general practitioners and specialists can have admitting privileges. The practice of credentialing physicians who do not work at a particular hospital to admit has been steadily declining, and as of 2022, is essentially non-existent in many areas. [ 1 ]
Admitting privileges have been used as precedent to impede abortion providers in several U.S. states, including Louisiana , Mississippi , Wisconsin , and Texas . [ 2 ] This means the doctor is unable to provide an abortion to a patient unless that doctor has admitting privileges, regardless of where the procedure occurs. [ 3 ] Supporters of these laws claim that patients should have access to a hospital in case of complications. [ 2 ] The American College of Obstetricians and Gynecologists considers requiring admitting privileges for abortions to be unnecessary given that "[i]n 2019, the Centers for Medicare & Medicaid Services removed its requirement that ambulatory surgical centers participating in Medicaid and Medicare have hospital admitting privileges, asserting they were unnecessary in the promotion of patient health, an inefficient use of health care dollars, and an administrative barrier to efficient operations". [ 4 ] The U.S. Supreme Court ruled in June Medical Services, LLC v. Russo , that some restrictions based on admitting privileges were unconstitutional. [ 5 ]
|
https://en.wikipedia.org/wiki/Admitting_privileges
|
Adolescent and young adult oncology is a branch of medicine that deals with the prevention, diagnosis, and treatment of cancer in adolescent and young adult (AYA) patients aged 16–40. Studies have continuously shown that while pediatric cancer survival rates have gone up, the survival rate for adolescents and young adults has remained stagnant. While many clinical trials exist for adults with cancer and children with cancer, AYAs underutilize clinical trials . [ 1 ] [ 2 ] Most pediatric clinical trials serve patients up to age 21. [ 3 ] Additionally, AYAs face problems that adults and children rarely see including college concerns, fertility , and sense of aloneness. [ 4 ] Studies have often shown that treating young adults with the same protocols used in pediatrics is more effective than adult oriented treatments. [ 5 ]
In countries like the US and the UK, specialized AYA units have started to be built in children's and adult hospitals to cater to the need of these age groups. AYA wards are designed to be bright and welcoming with many games and televisions to keep patients busy. [ 6 ] The need for these spaces come from the findings that AYAs tend to prefer pediatric wards over adult wards, but do not like to be treated like children. [ 7 ]
AYA teams are usually made up of specialists that specialize in both pediatric and adult medicine because people under 21 tend to do better under pediatric care. [ 8 ]
Internationally, different countries tend to treat the AYA age group in different environments. Most AYA treatment centers in the US are within larger children's hospitals . The organization, Teen Cancer America was created to establish more AYA wards in hospitals across the US, and currently there are about 21 hospitals affiliated with Teen Cancer America, [ 9 ] and many more with AYA programs. The American Academy of Pediatrics' opinion is that children should be under the care of a pediatrician until they deem not necessary, and children's hospitals in the US are increasingly treating older patients well into their twenties as a part of AYA and other adult programs. [ 10 ]
The UK is seen to be one of the pioneers of AYA cancer care at its hospitals. Teenage Cancer Trust is a cancer care and support charity in the UK that exists to improve the cancer experience of young people aged 13–24. [ 11 ] Founded in 1990, the charity's key service is providing specialist teenage units in NHS hospitals . It also trains and funds staff who are teenage cancer specialists. [ 12 ] The units are dedicated areas for teenage and young adult patients, who are involved in their concept and creation. Medical facilities on the units are equipped with computers, TVs, game consoles, and bright colored design. The UK has over 28 units in children's hospitals and adult hospitals dedicated to AYAs aged 13–24. [ 13 ] [ 14 ]
|
https://en.wikipedia.org/wiki/Adolescent_and_young_adult_oncology
|
Adolf Meyer (September 13, 1866 – March 17, 1950) was a Swiss-born psychiatrist who rose to prominence as the first psychiatrist-in-chief of the Johns Hopkins Hospital (1910–1941). He was president of the American Psychiatric Association in 1927–28 and was one of the most influential figures in psychiatry in the first half of the twentieth century. [ 1 ] His focus on collecting detailed case histories on patients was one of the most prominent of his contributions. He oversaw the building and development of the Henry Phipps Psychiatric Clinic at Johns Hopkins Hospital, opened in April 1913, making sure it was suitable for scientific research, training and treatment. [ 2 ] Meyer's work at the Phipps Clinic is possibly the most significant aspect of his career. [ who? ]
Meyer's main theoretical contribution was his idea of ergasiology (a term he derived from the Greek for "working" and "doing") to describe a psychobiology . This brought together all the biological, social and psychological factors and symptoms pertaining to a patient. It considered mental illnesses to be a product of dysfunctional personality not a pathology of the brain. Believing that whole-life social and biological factors should be central to both diagnosis and treatment Meyer was one of the earliest psychiatrists to support occupational therapy as an important connection between the activities of an individual and their mental health, and incorporated community based activities and services to develop people's everyday living skills. [ 3 ] [ 4 ]
Adolf Meyer was born in Niederweningen , Switzerland , in 1866. He was the son of a Zwinglian pastor. [ 5 ] Meyer received his MD from the University of Zurich in 1892, where he studied neurology under Auguste Forel . During his time at the university, he studied abroad in Paris, London and Edinburgh, working under John Hughlings Jackson and Jean-Martin Charcot . [ 6 ] His doctorate thesis was published in 1892 and had to do with the reptilian forebrain. [ 7 ] Unable to secure an appointment with the university, he emigrated to the United States in 1892. Meyer married Mary Potter Brooks, of Newburgh, New York , on September 15, 1902. [ 5 ] [ 7 ] They had one daughter, Julia Lathrup Meyer, on February 14, 1916. [ 8 ] Meyer died on March 17, 1950, at his home at 4305 Rugby Road in Baltimore, Maryland, of a heart attack. [ 9 ] He was buried in Druid Ridge Cemetery in Pikesville, Maryland . [ 10 ]
After moving to the United States, Meyer first practiced neurology and taught at the University of Chicago , where he was exposed to the ideas of the Chicago functionalists. He was unable to find a paid full-time post at the University of Chicago, so his time at the university was short-lived; serving from 1892 to 1895. [ 7 ] [ 6 ] From 1893 to 1895, he served as pathologist at the new mental hospital at Kankakee , Illinois, [ 2 ] after which he worked at the state hospital at Worcester, Massachusetts from 1895 to 1902, [ 11 ] all the while publishing papers prolifically in neurology, neuropathology , and psychiatry. [ 12 ] He also served as docent at Clark University . [ 7 ]
In 1902, he became director of the Pathological Institute of the New York State Hospital system (shortly afterwards given its present name, The Psychiatric Institute ), where in the next few years he shaped much of American psychiatry by emphasizing the importance of keeping detailed patient records and by introducing both Emil Kraepelin 's classificatory system and Sigmund Freud 's ideas. While in the New York State Hospital system, Meyer was one of the first importers of Freud's ideas about the importance both of sexuality and of the formative influence of early rearing on the adult personality. Meyer found many of Freud's ideas and therapeutic methods insightful and useful, but he rejected psychoanalysis as a wholesale etiological explanation of mental disorders in favor of his own theory of psychobiology. He never practiced psychoanalysis and always kept it at arm's length from Johns Hopkins because of Freud's increasingly dogmatic insistence on the psychical causation of mental illnesses. [ 13 ] As he wrote in his presidential address to the 84th Annual Meeting of the American Psychiatric Association : "Those who imagine that all psychiatry and psychopathology and therapy have to resolve themselves into a smattering of claims and hypotheses of psychoanalysis and that they stand or fall with one's feelings about psychoanalysis, are equally misguided". [ 14 ] Meyer was Professor of Psychiatry at Cornell University from 1904 to 1909. [ 15 ]
In 1908, Meyer was asked to become the director of a new psychiatric clinic at the Johns Hopkins Hospital after Henry Phipps Jr. donated 1.5 million dollars to open the clinic. [ 16 ] Meyer accepted the offer, which he described as "the most important professorship [in psychiatry] in the English-speaking domain." [ 17 ] He oversaw the building and development of the clinic and made sure the building was suitable for scientific research, training and treatment. [ 18 ] The Henry Phipps Psychiatric Clinic opened in April 1913.
Meyer's work at the Phipps Clinic is arguably the most significant aspect of his career. His model for the Phipps Clinic combined clinical and laboratory work, which was the first time these elements were combined in a mental institute in the United States. [ 19 ] Though the Phipps Clinic did not use the clinical model of Emil Kraepelin, Meyer did incorporate some of Kraepelin's practices into the clinic. [ 19 ] These practices include extensive observations of the patients and studying both the presymptomatic and remissive phases of mental illness, along with periods of acute illness.
Meyer also served as a Professor of Psychiatry at Johns Hopkins School of Medicine from 1910 to 1941. In his beginning years at Johns Hopkins, Meyer helped oversee the work of a few of his aspiring students. Phyllis Greenacre , from the University of Chicago, and Curt Richter , a Harvard graduate, both had the opportunity to study under Meyer. Most notably, Richter studied the behavior of rats with Meyer and John Watson , a behavioral psychologist. [ 20 ] Adolf Meyer worked at Johns Hopkins until his retirement in 1941. [ 2 ] Meyer also conducted a nine-month study of the brain of Giuseppe Zangara , assassin who shot at President Franklin Roosevelt and killed Mayor Anton Cermak . [ 7 ]
Meyer received honorary degrees from Glasgow University in 1901, Clark University in 1909, Yale University in 1934 and Harvard University in 1942. In 1942, Meyer was awarded the Thomas Salmon Medal for distinguished service in psychiatry. [ 9 ] [ 7 ]
In 1938, the neuropsychiatric clinic at Rhode Island State Hospital for Mental Diseases was named after Meyer. [ 9 ] [ 7 ]
Many of Meyer's students went on to make significant contributions to American psychiatry or psychoanalysis , though not necessarily as Meyerians. Most of the founders of the New York Psychoanalytic Society had worked under Meyer at Manhattan State Hospital , including its chief architect Abraham Arden Brill , and Charles Macfie Campbell . [ citation needed ]
Meyer and William Henry Welch played an instrumental role in Clifford Beers ' founding of the Connecticut Society for Mental Hygiene in 1908. [ 21 ] Under Meyer's direction, Leo Kanner founded the first child psychiatry clinic in the United States at the Johns Hopkins Hospital in 1930. [ 22 ]
Meyer's main contribution was in his ideas of psychobiology , where he focused on addressing all biological, social and psychological factors and symptoms pertaining to a patient. Meyer coined the term "ergasiology", which has Greek roots for "working" and "doing", as another way to classify psychobiology. One of his ideas was that mental illnesses were a product of a dysfunctional personality and not from the pathology of the brain. He also stressed the idea that social and biological factors that affect someone throughout their entire life should be heavily considered when diagnosing and treating a patient. Another contribution of Meyer was that he was one of the earlier psychologists that supported occupational therapy. [ 23 ] He thought there was an important connection between the activities of an individual and their mental health. Taking this into consideration he looked for community based activities and services to aid people with everyday living skills. [ 24 ]
Meyer was a strong believer in the importance of empiricism , and advocated repeatedly for a scientific, and, particularly, a biological approach to understanding mental illness. He hoped that the Phipps Clinic would help put mental illness on the same ground as every other human illness. [ 19 ] He insisted that patients could best be understood through consideration of their "psychobiological" life situations. He reframed mental disease as biopsychosocial "reaction types" rather than as biologically specifiable natural disease entities. In 1906, he reframed dementia praecox as a "reaction type", a discordant bundle of maladaptive habits that arose as a response to biopsychosocial stressors . [ 25 ]
Meyer was also involved with the Eugenics Records Office , which he viewed as a natural extension of the mental hygiene movement which he helped to create. He served on the advisory council of the American Eugenics Society for 12 years, from 1923 to 1935. [ 26 ] Meyer's views on eugenics have not yet been studied closely and his association with the Eugenics Record Office cannot be equated straightforwardly with the extremism of some eugenicists, especially in light of the fact that the fundamental premise of Meyerian psychobiology contradicted the genetic determinism that underpinned scientific racism in the first half of the twentieth century. [ 27 ]
Meyer had oversight over Henry Cotton , who ran a psychiatric hospital which regularly extracted the teeth and organs from patients, resulting in about a 45% death rate. Cotton believed that nearly all psychiatric problems could be resolved through the complete removal of teeth and subjected hundreds of patients to this treatment, over their objections and resistance. Although Meyer knew that Cotton's psychiatric hospital was a torture chamber, he actively prevented news of this from reaching the general public and praised Cotton publicly while burying investigations by other doctors. In Madhouse: A Tragic Tale of Megalomania and Modern Medicine , Andrew Scull faults Meyer for this decision. [ 28 ]
Meyer never published a textbook. Between 1890 and 1943, he published roughly 400 articles in scientific and academic journals, mostly in English, but also in his native German and in French. Most were published together after his death in 1950 in four bound volumes called The Collected Papers of Adolf Meyer .
T he Collected Papers of Adolf Meyer , edited by Eunice E. Winters. Baltimore: The Johns Hopkins University Press, 1950–1952. 4 vols.
T he Commonsense Psychiatry of Dr. Adolf Meyer: Fifty-two Selected Papers , edited by Alfred A. Lief. New York: McGraw-Hill, 1948.
Psychobiology: a Science of Man , compiled and edited by Eunice E. Winters and Anna Mae Bowers. Springfield, IL: Charles C Thomas, (1957). This posthumous book was based on the first Thomas W. Salmon Lectures, which Meyer gave in 1931.
George Kirby's Guides for History Taking and Clinical Examination of Psychiatric Cases (Utica: State Hospitals Press 1921) is essentially the form Meyer created and used at Manhattan State Hospital in 1905–1906. It provides an excellent view of Meyer's early approach to taking case histories.
Richard Noll, American Madness: The Rise and Fall of Dementia Praecox (Cambridge, MA: Harvard University Press, 2011).
S. D. Lamb, Pathologist of the Mind: Adolf Meyer and the Origins of American Psychiatry (Baltimore: Johns Hopkins University Press, 2014) Reissued in paperback in 2018.
Susan Lamb, "'My Resisting Getting Well': Neurasthenia and Subconscious Conflict in Patient-Psychiatrist Interactions in Prewar America," Journal of the History of the Behavioral Sciences 52/2 (2016): pages 124–45.
Susan Lamb, "Social Skills: Adolf Meyer's Revision of Clinical Skill for the New Psychiatry of the Twentieth Century. Medical History Vol. 59 No. 3 (2015): pages 443-64.
Susan Lamb, "Social, Motivational, and Symptomatic Diversity: An Analysis of the Patient Population of the Phipps Psychiatric Clinic at Johns Hopkins Hospital, 1913 – 1917," Canadian Bulletin of Medical History Vol. 29 No. 2: pages 243–63.
Adolf Meyer, " What Do Histories of Cases of Insanity Teach Us Concerning Preventive Mental Hygiene during the Years of School Life? ", Psychological Clinic 2, no. 4 (1908): 89–101. PMC 5138873 PMID 28909394
Meyer's influence on American psychology can be explored in Defining American Psychology: The Correspondence Between Adolf Meyer and Edward Bradford Titchener , edited by Ruth Leys and Rand B. Evans. Baltimore/London: The Johns Hopkins University Press, (1990).
Meyer's importance to the introduction and development of American psychoanalysis is discussed and interpreted in: John C. Burnham , Psychoanalysis and American Medicine, 1894–1917: Medicine, Science, and Culture ( New York: International Universities Press, 1967); John Gach, "Culture & Complex: On the Early History of Psychoanalysis in America" (pages 135–160) in Essays in the History of Psychiatry , edited by Edwin R. Wallace IV and Lucius Pressley (Columbia, SC: William S. Hall Psychiatric Institute, 1980); Nathan Hale, Freud and the Americans: The Beginnings of Psychoanalysis in the United States (Oxford: Oxford University Press, 1995); and Chapter Six of S. D. Lamb, Pathologist of the Mind: Adolf Meyer and the Origins of American Psychiatry (Baltimore: Johns Hopkins University Press, 2014); Ruth Leys, "Meyer's Dealings With Jones: A Chapter in the History of the American Response to Psychoanalysis," Journal of the History of the Behavioral Sciences 17 (1981): pages 445–465; Ruth Leys, "Meyer, Jung, and the Limits of Association," Bulletin of the History of Medicine 59 (1985): pages 345–360; Scull, Andrew, and Jay Schulkin, "Psychobiology, Psychiatry, and Psychoanalysis: The Intersecting Careers of Adolf Meyer, Phyllis Greenacre, and Curt Richter." Medical History (National Institute of Health, Jan. 2009). Web. 22 Feb. 2015.
See also Theodore Lidz , "Adolf Meyer and the Development of American Psychiatry." The American Journal of Psychiatry , 123(3), pp 320–332 (1966) and C.H. Christiansen "Adolf Meyer Revisited:Connections between Lifestyle, Resilience and Illness". Journal of Occupational Science 14(2),63-76. (2007).
"Adolf Meyer: His Achievements and Legacy" (2016) Paul R. McHugh
|
https://en.wikipedia.org/wiki/Adolf_Meyer_(psychiatrist)
|
An adrenergic storm is a sudden and dramatic increase in serum levels of the catecholamines adrenaline and noradrenaline (also known as epinephrine and norepinephrine respectively), with a less significant increase in dopamine transmission. It is a life-threatening condition because of extreme tachycardia and hypertension , and is especially dire for those with prior heart problems. If treatment is prompt, prognosis is good; typically large amounts of diazepam or other benzodiazepines are administered alongside beta blockers . Beta blockers are contraindicated in some patients, so other antihypertensive medication such as clonidine may be used. [ 1 ] Antipsychotics are also used to treat the most severe psychiatric reactions such as psychosis, paranoia or terror, after their use was formerly discouraged because of their potential to prolong the QT interval ; however, more recent research performed since 2019 has revealed that this and other severe side effects are rare and their occurrence does not warrant banning antipsychotics from the treatment of adrenergic crises for which they can be extremely useful. [ 2 ] [ 3 ] [ 4 ] [ 5 ] [ 6 ] [ 7 ] [ 8 ]
Adrenergic storms are usually caused by overdoses of stimulants , especially cocaine or methamphetamine , or eating foods high in tyramine while taking monoamine oxidase inhibitors . [ 9 ] A subarachnoid hemorrhage can also cause an adrenergic storm. [ 9 ] A catecholamine storm is part of the normal course of rabies infection, and is responsible for the severe feelings of agitation, terror, and dysautonomia present in the pre-coma stage of the disease. [ 10 ]
The behavioral symptoms are similar to those of an amphetamine , cocaine , or caffeine overdose. Overstimulation of the central nervous system results in a state of hyperkinetic movement and unpredictable mental status including mania, rage and suicidal behavior; hyperthermia is also prominently present. [ 11 ] Delirium can also be present but rarely. [ 12 ]
Physical symptoms are more serious and include heart arrhythmias as well as outright heart attack or stroke in people who are at risk of coronary disease . Breathing is rapid and shallow while both pulse and blood pressure are dangerously elevated. [ 13 ]
Other complications would include rhabdomyolysis , a breakdown of the voluntary muscles because of the excessive physical movement, causing the components of the muscle, most notably myoglobin , to be released into the bloodstream and then clog the kidneys , causing renal failure . [ 14 ] In all, rhabdomyolysis is especially common in adrenergic storms caused by the use of stimulant drugs, most notably those of the phenethylamines such as cathinones or amphetamines. [ 15 ]
There are several known causes of adrenergic storms; in the United States, cocaine overdose is the leading cause. [ 16 ] Any stimulant drug has the capacity to cause this syndrome if taken in sufficient doses, but even non-psychotropic drugs can very rarely provoke a reaction. [ 17 ]
Monoamine oxidase inhibitors (MAOIs) are a class of drugs that inhibit the enzyme monoamine oxidase . This enzyme is responsible for breaking down many compounds; basically, anything with a primary amine moiety is likely to be oxidized by monoamine oxidase. An important substrate of the enzyme MAO is tyramine. MAOIs inhibit the enzyme either reversibly, in which MAO is inhibited only until the drug is cleared from the system, or irreversibly, in which the substrate binds permanently to the enzyme , rendering it inactive and effectively destroying it. Irreversible MAOIs are potentially more dangerous, because the body takes about two weeks to regenerate MAO enzymes to functional levels. [ 18 ] Two subtypes of MAO exist: MAO-A and MAO-B; this is relevant to adrenergic storms, as there are significant differences between the two types, such as their differential expression throughout the body, and range of substrates. While both MAO-A and MAO-B metabolize tyramine, only MAO-A is present in the gastrointestinal tract and singularly metabolizes the majority of consumed tyramine. [ 9 ] (The small portion normally passing into circulation is mostly degraded in the liver where both MAO types act. [ 9 ] )
Subarachnoid hemorrhage is an extremely serious condition in which a neural membrane is breached and the brain itself is compromised. The onset is sudden, described as "the worst headache of one's life," and many grave symptoms follow. Adrenergic storm is often present among these symptoms, and is responsible for some of the dangers, both long-term and short, of subarachnoid hemorrhage adrenergic storm, through a complex cascade of processes starting with the movement of subarachnoid blood into the brain. Apparently, as the intracranial pressure increases, the brain is squeezed and catecholamines are forced out of their vesicles into the synapses and extracellular space. [ 19 ]
Rarely, a pheochromocytoma (tumor of the medullar tissue of the adrenal glands , which are located anterior to the kidney ), may result in an adrenergic storm. [ 20 ] This type of tumor is not common to begin with, and furthermore, the subtype that can cause massive adrenaline release is rarer still. Patients with pheochromocytoma can unexpectedly fly into a rage or sink into trembling fear, possibly dangerous to themselves and others as their judgment is impaired, their senses and pain threshold are heightened, and the level of the adrenaline in their bloodstream is more than most people ever experience; pheochromocytoma can, very rarely, kill by internal adrenaline overdose. [ 21 ] But overall, adrenergic storm is an uncommon but certainly not rare phenomenon associated with the also uncommon condition of pheochromocytoma. [ 22 ]
Because the adrenergic storm overlaps with so many other similar conditions, such as hypertensive crises, stimulant intoxication or overdose, or even panic attack , and because the treatments for these overlapping conditions are largely alike, it is not necessary to obtain a differential and definitive diagnosis before initiating treatment. However, analysis of the patient's medical history , checked against the possible causes of the adrenergic storm such as those above, should be done, because some adrenergic storms can be caused by serious underlying conditions. [ 10 ] If a patient has an adrenergic storm and all or most of the other factors are ruled out, the adrenergic storm could lead to the discovery of a pheochromocytoma , which can become malignant . However, not all cases of adrenergic storm have an identifiable cause. [ 23 ]
Serotonin syndrome , in which an excess of serotonin in the synapses causes a similar crisis of hypertension and mental confusion, could be confused with an adrenergic storm. Serotonin, being a tryptamine (non-catecholamine) involved in higher brain functions, can cause dangerous hypertension and tachycardia from its effects on the sympathetic nervous system . [ 23 ] Symptoms caused by excessive adrenergic signalling can occur alongside those of serotonergic signalling. Abnormal echocardiograms or chest pain are indicative of adrenergic storm. [ 23 ] On the other hand, uncontrollable slow, rhythmic, or jerky movements, contractions and tension—often in every part of the body, dangerously high fever , eye rolling, and bruxism are more indicative of serotonin syndrome. [ 10 ] [ 24 ]
If there is evidence of overdose or it is suspected, the patient should be given gastric lavage , activated charcoal , or both; this could make the difference between life and death in a close situation. [ 25 ] It can however aggravate the patient which should be taken into account. [ 10 ]
The first-line treatments are diazepam and a non-selective beta blocker ; other antihypertensive drugs may also be used. It is important to note that not all benzodiazepines and beta blockers are safe to use in an adrenergic storm; for instance, alprazolam and propranolol ; [ 10 ] alprazolam weakly agonizes dopamine receptors and causes catecholamine release while propranolol mildly promotes some catecholamine release – each worsening the condition. [ 23 ]
Antipsychotics are also used to treat the psychiatric symptoms such as aggression, agitation, psychosis , paranoia , or anxiety . Originally, the use of antipsychotics was discouraged because of their potential to prolong the QT interval ; [ 3 ] however, newer research has revealed that their careful use does not carry the potential for any significant side effects and today their judicious use is encouraged. [ 3 ] [ 2 ] [ 4 ] [ 26 ]
Adrenergic storms are often idiopathic in nature; however if there is an underlying condition, then that must be addressed after bringing the heart rate and blood pressure down. [ 1 ]
|
https://en.wikipedia.org/wiki/Adrenergic_storm
|
2FLY , 2L7S , 4RWF
133
11535
ENSG00000148926
ENSMUSG00000030790
P35318
P97297
NM_001124
NM_009627
NP_001115
NP_033757
Adrenomedullin ( ADM ) is a peptide hormone that plays an important role in various physiological processes throughout the human body. Initially discovered in 1993 from a pheochromocytoma , a tumor of the adrenal medulla , [ 5 ] this 52-amino acid peptide is now recognized for its diverse effects, including vasodilation , regulation of blood pressure, and maintenance of the vascular system . [ 6 ] ADM is widely expressed in tissues and also found in the circulation, exerting its influence on the cardiovascular, lymphatic , and endocrine systems, as well as demonstrating anti-inflammatory and tissue-protective properties. [ 7 ] [ 8 ]
In humans ADM is encoded by the ADM gene . A similar peptide named adreomedullin2 was reported in rats in 2004 which exhibits a similar function. [ 9 ]
The human ADM gene is localized to a single locus on Chromosome 11 with 4 exons and 3 introns. The ADM gene initially codes for a 185-amino acid precursor peptide, that can be differentially excised to form a number of peptides, including an inactive 53-amino acid AM, e PAMP, adrenotensin and ADM95-146. Mature human ADM is activated to form a 52 amino acid, 6-amino acid ring, that shares moderate structural similarity to the calcitonin family of regulatory peptides (calcitonin, CGRP and amylin). Circulating ADM consists of both amidated active form (15%) and the glycated inactive form (85%). It has a plasma half-life of 22min, mean clearance rate of 27.4 mL/kg/min, and apparent volume of distribution of 880 ± 150 mL/kg. [ 10 ]
Adrenomedullin consists of 52 amino acids, has 1 intramolecular disulfide bond, and shows a slight homology with the calcitonin gene-related peptide (CGRP). The precursor, called preproadrenomedullin, consists of 185 amino acids and can be cleaved by plasma kallikrein at the Lys-Arg and Arg-Arg sites. [ 11 ] By RNA-blot analysis, human adrenomedullin mRNA was found to be expressed in all tissues, and most highly expressed in the placenta, fat cells, lung, pancreatic islets, smooth muscle, and skin. [ 12 ]
Adrenomedullin (ADM) is a multifunctional peptide hormone that plays an important role in the homeostasis of the cardiovascular system and in inflammatory response . It acts as a potent vasodilator , regulating vascular tone and blood pressure through both endothelium -dependent and independent mechanisms. [ 7 ] ADM exerts protective effects on the cardiovascular system by inhibiting apoptosis in endothelial cells , reducing oxidative stress , and regulating vascular smooth muscle cell proliferation. [ 13 ] In the heart, it increases cardiac output and augments myocardial contractility . [ 14 ] Beyond its cardiovascular functions, ADM demonstrates significant anti-inflammatory properties, modulating cytokine production and secretion in macrophages . [ 15 ] It also contributes to the maintenance of vascular integrity, potentially reducing vascular permeability during inflammatory conditions. [ 16 ] In addition, ADM has been implicated in angiogenesis , protection of organs, and tissue repair. [ 17 ] Hence because of it;s wide ranging effects, it has potential therapeutic applications in a variety of diseases, including inflammatory bowel disease, sepsis, and cardiovascular disorders. [ 17 ] [ 18 ]
Adrenomedullin (AM) exerts its actions through combinations of the calcitonin receptor like receptor ( CALCRL ) or CLR; and either ( Receptor activity-modifying protein ) 2 ( RAMP2 ) or RAMP3, (known as AM1 and AM2 receptors respectively). Both transduce the hormone binding to intracellular signaling via second messenger cascades. The AM2 receptor has a low affinity for CGRP, but this is of no physiological relevance. Unlike the classical one ligand-one receptor notion of receptor signalling, the interaction of both CALCRL and RAMP at the membrane is required for AM to mediate its action: neither can bind the hormone (and therefore transduce a signal) alone. Stimulation by AM of its receptor increases production of both cyclic AMP (cAMP) and nitric oxide. [ 19 ] [ 20 ]
Before the discovery of the RAMPs and the identification of heteromeric receptors for the calcitonin family of peptides, a single G Protein coupled Adrenomedullin receptor was identified, [ 21 ] but more recent reports have cast doubts as to its importance in the major effects of adrenomedullin.
In more recent research, the roles of the AM1 and AM2 receptors have been clarified through studies in genetically manipulated mice. The adrenomedullin knockout is an embryonic lethal phenotype and dies mid gestation from a condition known as hydrops fetalis. The CALCRL or CLR KO mouse recapitulates the same phenotype, as it lacks both the AM1 and AM2 receptors (incidentally confirming the lack of physiological significance for the earlier single protein AM receptor discovered by Kapas). RAMP2 KO mice also recapitulates the same phenotype showing that major physiological effects of AM are transduced by the AM1 receptor. Even the heterozygote RAMP 2 mice have disturbed physiology with unusual bone and mammary gland defects, and very aberrant endocrinology, leading to poor fertility and lactation problems. [ 22 ] What is very surprising is that the effect of deletion of RAMP3 has no deleterious effects and seems to confer advantages due to higher than normal bone mass, and reduced weight gain in older age. [ 23 ]
While AM could be an important biomarker for bacterial infections like sepsis, AM has diminished value in its utility for cardiovascular diseases (CVD) attributable to its minimal increase in these conditions and reduced half-life. [ 7 ] AM is associated with controlling vascular integrity, blood pressure, and general cardiovascular function. Since AM has been noted for its exacerbated levels in intense diseases with an elevated concern for mortality, AM could still have some value as a predictive biomarker of harmful clinical consequences for an array of cardiovascular illnesses. [ 6 ] AM has conservatory effects against arteriosclerosis and vascular harm. Extended AM administration or hyper-expression of its target gene in rodent model organisms diminishes vascular hyperplasia, fatty streak construction, and intimal expansion. AM also has angiogenic characteristics, leading to organ and tissue maintenance by reducing the risk for ischemic diseases. [ 13 ] AM binds to particular receptors like calcitonin gene-related peptide (CGRP) receptors, which affects the cardiovascular system by contributing to vasodilation as well as elevated heart rate and blood pressure. [ 24 ]
AM function can be compared to another peptide called pro-adrenomedullin N-terminal 20 peptide (PAMP), which both originate from a common precursor leading to angiogenesis, vasodilation, and anti-inflammatory processes These two peptides are expressed in the gastrointestinal (GI) tract at a mass level, serving as GI hormones controlling processes like insulin secretion and gastric emptying. Past studies reveal that AM and PAMP also impact gut microbiome composition by fostering the development of beneficial bacteria (i.e., Bifidobacterium and Lactobacillus) and diminishing detrimental microbes. [ 25 ]
AM concentrations are substantially elevated during intense inflammation from disorders like sepsis, rendering AM a potentially viable therapeutic agent and clinical mode of monitoring such inflammation. [ 7 ] AM contributes to vasodilation, which could be detrimental in leading to septic shock. Researchers seek to mitigate this effect while maintaining ADM's antimicrobial, anti-inflammatory, and endothelial-protective characteristics by employing antibodies that bind to ADM's N-terminus or co-administering ADM with ADM-binding protein-1, which collectively extend ADM's half-life and increase its maintenance role while minimizing this detrimental vasodilation. [ 18 ] While AM has been discussed in regard to its implications for bacterial infections, such as sepsis, prior research explores its potential connection to viral infections too. This annunciates the importance of continual investigation into AM's mechanisms with viral illnesses through exploring its roles in inflammation and immune regulation. [ 26 ]
AM contributes to tumor angiogenesis given its capability to enhance smooth muscle and vascular endothelial cell development in addition to its role in ischemic revascularization. Similarly to other solid tumors, AM expression is increased by hypoxia, which has been regarded as an important regulator of tumor development with respect to the findings from animal and in vitro studies, although the translation application to human tumor development is constrained. [ 27 ] AM is affiliated with endothelium-derived CC chemokine ligand 2 (CCL2) in the tumor microenvironment, employing genetic deletions and in vivo models to display functional associations. Tumor-derived AM stimulates angiogenesis and promotes tumor growth. Also, endothelial-derived CCL2 decreased AM-induced tumor growth. Deprivation of the AM receptor CALCRL or the G-protein Gs in endothelial cells diminishes both tumor and endothelial cell growth. Removing tumor cell CCR2 or endothelial CCL2 would undo this tumor growth decrease demonstrated in mice without endothelial CALCRL or Gs, displaying a reciprocal regulatory loop between AM and CCL2. [ 28 ] AM contributes to cancer pathogenesis through heightened vascularization to equip tumors with nutrients and oxygen, more intense cell phenotypes, and increased cell proliferation. AM receptors (AM1 and AM2) have disparate effects in an array of cancers, with separate regulatory mechanisms and expression patterns. Preclinical studies have displayed the potential of AM receptor antagonists and AM-neutralizing antibodies to diminish tumor growth, angiogenesis, and metastasis. [ 29 ]
This article incorporates text from the United States National Library of Medicine , which is in the public domain .
|
https://en.wikipedia.org/wiki/Adrenomedullin
|
Advanced cardiac life support , advanced cardiovascular life support ( ACLS ) refers to a set of clinical guidelines established by the American Heart Association (AHA) for the urgent and emergent treatment of life-threatening cardiovascular conditions that will cause or have caused cardiac arrest , using advanced medical procedures, medications, and techniques. ACLS expands on Basic Life Support (BLS) by adding recommendations on additional medication and advanced procedure use to the CPR guidelines that are fundamental and efficacious in BLS. ACLS is practiced by advanced medical providers including physicians, some nurses and paramedics; [ 1 ] these providers are usually required to hold certifications in ACLS care.
While "ACLS" is almost always semantically interchangeable with the term " Advanced Life Support " (ALS), when used distinctly, ACLS tends to refer to the immediate cardiac care, while ALS tends to refer to more specialized resuscitation care such as ECMO and PCI . In the EMS community, "ALS" may refer to the advanced care provided by paramedics while "BLS" may refer to the fundamental care provided by EMTs and EMRs ; without these terms referring to cardiovascular-specific care.
Advanced cardiac life support refers to a set of guidelines used by medical providers to treat life-threatening cardiovascular conditions. These life-threatening conditions range from dangerous arrhythmias to cardiac arrest. ACLS algorithms frequently address at least five different aspects of peri-cardiac arrest care: Airway management, ventilation, CPR compressions (continued from BLS), defibrillation, and medications. Due to the seriousness of the diseases treated, the paucity of data known about most ACLS patients, and the need for multiple, rapid, simultaneous treatments, ACLS is executed as a standardized, algorithmic set of treatments. Successful ACLS treatment starts with diagnosis of the correct EKG rhythm causing the arrest. Common cardiac arrest rhythms covered by ACLS guidelines include: ventricular tachycardia , ventricular fibrillation , Pulseless Electrical Activity , and asystole . Dangerous, non-arrest rhythms typically covered includes: narrow - and wide-complex tachycardias , torsades de pointe , atrial fibrillation / flutter with rapid ventricular response, and bradycardia . [ 2 ]
Successful ACLS treatment generally requires a team of trained individuals. Common team roles include: Leader, back-up leader, 2 CPR performers, an airway/respiratory specialist, an IV access and medication administration specialist, a monitor/ defibrillator attendant, a pharmacist, a lab member to send samples, and a recorder to document the treatment. [ 3 ] For in-hospital events, these members are frequently physicians, mid-level providers, nurses and allied health providers; while for out-of-hospital events, these teams are usually composed of a small number of EMTs and paramedics.
ACLS algorithms include multiple, simultaneous treatment recommendations. Some ACLS providers may be required to strictly adhere to these guidelines, however physicians may generally deviate to pursue different evidence-based treatment, especially if they are addressing an underlying cause of the arrest and/or unique aspects of a patient's care. ACLS algorithms are complex but the table, below, demonstrates common aspects of ACLS care. [ 2 ]
Due to the rapidity and complexity of ACLS care, as well as the recommendation that it be performed in a standardized fashion, providers must usually hold certifications in ACLS care. Certifications may be provided by a few different, generally national, organizations but their legitimacy is ultimately determined by hospital hiring and privileging boards; that is, ACLS certification is frequently a requirement for employment as a health care provider at most hospitals. [ 4 ] ACLS certifications usually provide education on the aforementioned aspects of ACLS care except for specialized resuscitation techniques. Specialized resuscitation techniques are not covered by ACLS certifications and their use is restricted to further specialized providers. ACLS education is based on ILCOR recommendations which are then adapted to local practices by authoritative medical organizations such as the American Red Cross, the European Resuscitation Council, or the Resuscitation Council of Asia .
BLS proficiency is usually a prerequisite to ACLS training; however the initial portions of an ACLS class may cover CPR. [ 5 ] The ACLS course covers BLS, airway management, advanced cardiovascular interventions (bradycardia, tachycardia, cardiac arrest), a Mega Code skills test, and a written multiple-choice exam. [ 6 ] Initial training usually takes around 15 hours and includes both classroom instruction and hands-on simulation experience; passing a test, with a practical component, at the end of the course is usually the final requirement to receive certification. [ 7 ] After receiving initial certification, providers must usually recertify every two years in a class with similar content that lasts about seven hours. Widely accepted providers of ACLS certification include, non-exclusively: American Heart Association, American Red cross, European Resuscitation Council or the Australian Resuscitation Council.
Holding ACLS certification simply attests a provider was tested on knowledge and application of ACLS guidelines. The certification does not supersede a provider's scope of practice as determined by state law or employer protocols; and does not, itself, provide any license to practice.
Like a medical intervention, researchers have had to ask whether ACLS is effective. Data generally demonstrates that patients have better survival outcomes (increased ROSC, increased survival to hospital discharge and/or superior neurological outcomes) when they receive ACLS; [ 8 ] however a large study of ROC patients showed that this effect may only be if ACLS is delivered in the first six minutes of arrest. [ 9 ] This study also found that ACLS increases survival but does not produce superior neurological outcomes.
Some studies have raised concerns that ACLS education can be inconstantly or inadequately taught which can result in poor retention, leading to poor ACLS performance. [ 10 ] One study from 1998 looked at the ACLS use of epinephrine, atropine, bicarbonate, calcium, lidocaine, and bretylium in cardiac arrests and found that these medications were not associated with higher resuscitation rates. [ 11 ]
Research on ACLS can be challenging because ACLS is a bundle of care recommendations; with each individual treatment component being profoundly consequential. There is active debate within the resuscitation research community about the value of certain interventions. Active areas of research include determining the value of vasopressors in arrests, [ 12 ] ideal airway use [ 13 ] and different waveforms for defibrillation. [ 14 ]
Stemming from the need for standardized, evidence based ACLS guidelines, an international network of academic resuscitation organizations was created. The International Liaison Committee on Resuscitation (ILCOR) is the central, international institution that regional resuscitation committees strive to contribute to and disseminate information from. The centralization of resuscitation research around ILCOR reduces redundant work internationally, allows for collaboration between experts from many regional organizations, and produces higher quality, higher powered research.
ILCOR serves as a way for international resuscitation organizations to communicate and collaborate. [ 15 ] ILCOR publishes scientific evidence reviews on resuscitation known as "Continuous Evidence Evaluation (CEE) and Consensus on Science with Treatment Recommendations (CoSTRs)". [ 16 ] ILCOR uses 6 international task forces to review over 180 topics through a structured systematic-review process. ILCOR traditionally published updates and recommendations every five years but now conducts continuous review work. [ 17 ] ILCOR produces international recommendations which are then adopted by regional resuscitation committees which publish guidelines. [ 18 ] Regional guidelines can have more medicolegal bearing than ILCOR recommendations. [ 19 ] ILCOR is composed of the following regional organizations:
The International Liaison Committee on Resuscitation (ILCOR) was established 1992 to serve as a way for international resuscitation organizations to communicate and collaborate. [ 15 ]
The ACLS guidelines were first published in 1974 by the American Heart Association and were updated in 1980, 1986, 1992, 2000, 2005, 2010, 2015. [ 23 ] In the 2020 update the guidelines were restructured to align with ILCOR recommendations. These changes include the transition since 2015 away from the previous 5-year update cycle to an online format that can be updated as indicated by continuous evidence review. [ 24 ]
The first version of the European Resuscitation Council (ERC) guidelines were developed in 1992. The 2000 ERC guidelines were developed in collaboration with ILCOR. 5-year updates were published from 2000 to 2015 and annual updates have been published since 2017. [ 25 ]
|
https://en.wikipedia.org/wiki/Advanced_cardiac_life_support
|
Aequanimitas was one of Sir William Osler's most famous essays, delivered to new doctors in 1889 as his farewell address at the Pennsylvania School of Medicine , prior to his transfer to Johns Hopkins . It was published in the same year and in 1904 appeared in his collection of essays titled Aequanimitas with Other Addresses to Medical Students, Nurses and Practitioners of Medicine . A second edition was produced in 1906, and a third in 1932. In the essay, Osler advocates two qualities "imperturbability" and "equanimity", which he defined as "coolness and presence of mind under all circumstances". [ 1 ]
Between 1932 and 1953, Eli Lilly & Company distributed more than 150,000 copies of the third edition to medical graduates.
Through the years Osler's ideal of "Aequanimitas" has been analysed by various academics. Daniel Sokol , medical ethics and law expert, reasons in the British Medical Journal in 2007, that whatever interpretation is made of Aequanimitas , it "tackles head-on a timeless question: what makes a good doctor?". [ 2 ] [ 3 ]
Aequanimitas was an essay by Sir William Osler , delivered to new doctors on 1 May 1889 as his farewell address at the Pennsylvania School of Medicine . [ 2 ] [ 4 ] It was published in the same year. [ 1 ]
Aequanimitas refers to staying calm and composed. [ 3 ] [ 5 ] In the essay, Osler advocates two qualities "imperturbability" and "equanimity", which he defined as "coolness and presence of mind under all circumstances". [ 1 ]
In 1904, Aequanimitas was published by H. K. Lewis in Aequanimitas with Other Addresses to Medical Students, Nurses and Practitioners of Medicine , a collection of his essays. [ 1 ] A second edition was produced in 1906 by P. Blakiston's Son & Co. in Philadelphia, [ 6 ] and H.K. Lewis in London. [ 7 ]
Following Osler's death, an expanded version of the book appeared as a third edition in 1932. [ 8 ] [ 9 ] It omits the essays "A Way of life", "A man's redemption of man" and "The old humanities and new science", and became more widely available than the previous editions. [ 2 ]
Between 1932 and 1953, Eli Lilly & Company distributed more than 150,000 copies of the third edition to medical graduates. [ 8 ] [ 10 ] These volumes were not all the same. [ 8 ] There were at least seven different publications in English and one in each of Spanish and Portuguese. [ 8 ] There were variations in the type of paper, book size, title page, information on the spine , and printing information. [ 8 ] There were also differences in the congratulatory letters from Eli Lilly, placed in each book. [ 8 ]
Through the years Osler's ideal of "Aequanimitas" has been criticised on the grounds that it excludes empathy, sympathy, or emotional resonance with patients. [ 2 ] One of the strongest critiques was presented by Gerald Weissmann in his book The Woods Hole Cantata (1985). [ 11 ] It had been published the previous year in Hospital Practice , as an essay entitled "Against Aequanimitas". [ 12 ] Weissmann's assessment of Osler led him to conclude that Osler's advice held "the public tone of the academic snob". [ 12 ] After reciting Osler's description of "imperturbability", Weissmann held the opinion that "the Oslerian view is not only devoid of passion, but [also] of joy". [ 12 ]
Osler however, did not that day in 1889 intend to give the graduating medical students comprehensive advice about how to practice medicine. [ 13 ] His involvement was a relatively small part of a busy commencement programme, in which the principal honoree was the retiring professor of surgery, David Hayes Agnew ("Agnew day"). [ 2 ] [ 13 ] Charles S. Bryan later explains that Osler deliberately confined his remarks to two of the qualities the students would need in practice. Osler emphasized the need to balance "head" and "heart". [ 14 ] In his interpretation the balance varies according to the nature of the task at hand and Aequanimitas is best understood as emotions appropriate to the circumstances rather than as indifference as suggested by the critiques. [ 14 ]
Daniel Sokol , medical ethics and law expert, reasons in the British Medical Journal in 2007, that whatever interpretation is made of Aequanimitas , it "tackles head-on a timeless question: what makes a good doctor?". [ 2 ] [ 3 ]
Japan's prime minister's physician, Shigeaki Hinohara , was given a copy of Aequanimitas in the early days of the United States Military Occupation of Japan after the Second World War . Hinohara subsequently translated the title address and paraphrased the rest. In 1948, he published a book entitled The Life of Dr. Osler—Pioneer of American Medicine . [ 15 ]
The term aequanimitas has become a motto. [ 16 ] At Johns Hopkins, it appears on ties and scarves worn by the housestaff, [ 16 ] and was mentioned in the television programme House . [ 16 ]
A similar concept to aequanimitas was addressed by Steve Jobs at Stanford University in 2005. [ 17 ] Daniel Goleman 's notion of emotional intelligence has been described as a modern variation of aequanimitas. [ 17 ]
|
https://en.wikipedia.org/wiki/Aequanimitas
|
Aesthetic Plastic Surgery is a bimonthly peer-reviewed medical journal covering all aspects of aesthetic plastic surgery . It was established in 1976 and is published by Springer Science+Business Media on behalf of the International Society of Aesthetic Plastic Surgery . [ 1 ] It is the official journal of the European Association of Societies of Aesthetic Plastic Surgery and the Sociedade Brasileira de Cirurgia Plastica . The editor-in-chief is Bahman Guyuron
The journal is abstracted and indexed in Science Citation Index Expanded , PubMed / MEDLINE , Scopus , EMBASE , Academic OneFile , Current Contents /Clinical Medicine, and INIS Atomindex . According to the Journal Citation Reports , the journal has a 2020 impact factor of 2.326. [ 2 ]
This article about a surgery journal is a stub . You can help Wikipedia by expanding it .
See tips for writing articles about academic journals . Further suggestions might be found on the article's talk page .
|
https://en.wikipedia.org/wiki/Aesthetic_Plastic_Surgery
|
Aesthetic Surgery Journal is a peer-reviewed medical journal that covers the field of plastic surgery . The journal's editor-in-chief is Jeffrey Kenkel ( University of Texas Southwestern Medical Center ). It was established in 1996 as Aesthetic Surgery Quarterly and is currently published by Oxford University Press on behalf of the American Society for Aesthetic Plastic Surgery (ASAPS).
Aesthetic Surgery Journal evolved from an earlier publication that focused primarily on association news for the plastic surgeon membership of ASAPS and gradually grew to incorporate articles of clinical interest in aesthetic surgery . From 1988 through 1994, this newsletter was published three times per year and called Aesthetic Surgery . Beginning in 1995, with an additional issue per year, the name was changed to Aesthetic Surgery Quarterly . It was not until 1996, when ASAPS entered into a publishing agreement with Mosby , that a significant portion of this periodical was designated as the "Clinical Journal" devoted to peer-reviewed original articles. Beginning in January 1997, publication was increased to six issues per year, and the name was changed to Aesthetic Surgery Journal .
The following persons have been editors-in-chief (since 1997, when the publication became Aesthetic Surgery Journal ):
Aesthetic Surgery Journal was indexed with MEDLINE / PubMed in 2008 and with the Thomson Reuters ' Journal Citation Reports (JCR; formerly ISI) in 2011.
Aesthetic Surgery Journal is abstracted and indexed, for example, in: [ 1 ]
Aesthetic Surgery Journal is the offered at a discount to members of ASAPS-affiliated plastic and aesthetic surgery organizations in other languages:
In addition to ASAPS, Aesthetic Surgery Journal is discounted to members of the English-language organizations listed below.
|
https://en.wikipedia.org/wiki/Aesthetic_Surgery_Journal
|
Anterior teeth are some of the most scrutinized teeth, as the size, shape and color of the anterior upper teeth plays an important role in dental aesthetics and smile aesthetics. [ 1 ] A few aesthetic anterior problems, such as dental caries , tooth fracture , [ 2 ] enamel defects [ 3 ] and diastemas , can be solved with composite restorations. Composite restorations can also improve dental aesthetics by changing the shape, color, length and alignment of teeth.
Some uses of direct composite to restore anterior teeth are in: [ 4 ]
The advantages of these procedures are: [ 4 ] [ 8 ] [ 9 ] [ 10 ]
The average survival statistics for direct restoration are not encouraging. [ 4 ] While there is a lack of conclusive data regarding the longevity of anterior composite restoration, it has been well established that the more complex the restoration, the shorter its lifespan. Clinical studies have found that 60 to 80% of all Class III and V composite resin restorations remain acceptable after 5 years of clinical service. [ 11 ] [ 12 ] [ 13 ] [ 14 ] [ 15 ] [ 16 ] The main reason for replacement of anterior composite are typically surface discoloration, secondary caries and fracture of restoration. It is generally accepted that Class IV restorations do not last as long as Class III and Class V. One study compared four different anterior composite restoration types over 5 years. [ 17 ] Variables assessed included handling characteristics, gingival condition, surface staining, marginal staining, color deterioration, and overall longevity. The Class IV restorations had higher failure rates than Class III or V restorations.
Operators should have detailed anatomical knowledge and artistic skill, for example, optimal properties of natural teeth, tooth proportions and their relationships to each other and to the surrounding soft tissues. Operator also must select appropriate restorative materials that match adjacent residual tooth tissue. [ 4 ]
Possible complications include: [ 4 ]
Steps to restore anterior fractured tooth: [ 2 ]
Dental veneers covers the front surface of teeth. Veneers with direct resins are one of the common treatment options for clinical applications following the developments in adhesive and restorative dentistry in recent years. These restorations are applied on prepared tooth surfaces or even without any preparation, with an adhesive agent and a composite resin material directly in a single visit in the dental clinic. [ 21 ] If done properly, the aesthetic outcomes of direct composite veneers are very satisfactory in addition to superior optical and physical properties. [ 21 ] In recent history these restorations were thought to be temporary alternatives to indirect ceramic veneers; however, they are no longer named 'day savior fillings' today. These restorations are called minimally invasive, functional and long-lasting 'direct aesthetic restorations' that perfectly emulate natural dental tissues even in anterior area. [ 22 ] [ 23 ] 3,4 Discolorations of teeth or restorations, dental malformations or mal-positions, diastemas, crown fractures and abrasive or erosive defects are some examples of up-to-date indications of direct composite veneers. [ 21 ] 1 Enamel hypoplasia is a developmental malformation generally resulting in poor aesthetics, tooth sensitivity , malocclusion and predisposition to dental caries . [ 24 ] 5 Direct composite veneer restorations where the whole labial surface is covered with resin, are good treatment options in such cases.,6 [ 25 ] The conventional workflow sequence of a direct composite veneer is:
New method for Aesthetic Anterior direct composite veneers
In the past two and a half years the use of 3D designed and then printed plastic models has become very popular worldwide.
The dentist uses a clear, Vinyl Polysiloxane material to make an index of the 3D printed model and this is placed over the patient's two and a flowable highly filled resin is injected into the mould and light cured.
Midline diastema (spacing in upper teeth) is a common occurrence in the population. [ 26 ] An arbitrary number for the spacing between the teeth to consider as midline diastema is a width of 0.5 from a proximal surface of a teeth to the proximal surface of adjacent teeth. [ 27 ] Midline diastema usually occur in the upper teeth compared to lower. The cause of this spacing includes but not limited to microdontia , labial frenulum, peg-shaped lateral incisors, mesiodens , cysts in midlene region, tongue trusting , finger sucking , dental malformations, maxillary incisor proclination, genetics, imperfect joining of interdental septum, dental skeletal discrepancies. [ 28 ] [ 29 ] The technical factors affecting the course of treatment of the closing of midline diastema includes the size of the existing central incisors, the amount of reduction necessary, the morphology of existing tooth, and the subsequent possibility of a veneer or crown treatment needs to be taken into account, the patient factors affecting the course of treatment includes economic, psychological and time factors of the patient. [ 30 ] [ 31 ] With a successful diastema closure, the normal arrangement of teeth can be established [ 32 ] Continuous improvement in material science and methodology enables the aesthetics of composite restoration to be of a high standard [ 33 ] and realistic in terms of aesthetic, physical and mechanical properties. Composites provides an array of hues, colour and opacities for composite layering techniques which mimics the opalescence of natural teeth. [ 34 ] [ 35 ] The conventional workflow sequence for a diastema closure is 1)Shade selection was done for dentin shade and enamel shade. Composite button samples of different shades are placed on teeth and a dental photography taken to verify 2 )Rubber dam isolation 3)Placing a retraction cord. 3)Etching enamel surface, 4)Application of bonding agent. Agitate the bonding agent against the enamel surface. Use a gentle stream of air to evaporate the solvent. Light polymerize the bonding agent 5)Layer dentin layer, followed by enamel shade 6)finishing with white stone bur, taking care to follow the natural anatomy 7)polishing with interdental strip and polishing disk with grains of increasing fineness, finally with a composite polishing paste. [ 36 ]
|
https://en.wikipedia.org/wiki/Aesthetic_anterior_composite_restoration
|
Aesthetic medicine is a branch of modern medicine that focuses on altering natural or acquired unwanted appearance through the treatment of conditions including scars , skin laxity, wrinkles, moles, liver spots , excess fat, cellulite , unwanted hair, skin discoloration, spider veins [ 1 ] and or any unwanted externally visible appearance. Traditionally, it includes dermatology , oral and maxillofacial surgery , reconstructive surgery and plastic surgery , [ 2 ] surgical procedures ( liposuction , facelifts , breast implants , Radio frequency ablation ), non-surgical procedures ( radio frequency skin tightening , non- surgical liposuction , chemical peel , high-intensity focused electromagnetic field , radio frequency fat removal), and a combination of both. [ 3 ] Aesthetic medicine procedures are usually elective. [ 4 ] There is a long history of aesthetic medicine procedures, dating back to many notable cases in the 19th century, [ 5 ] though techniques have developed much since then.
Physical beauty has been a consistently coveted notion. [ 6 ] Efforts to improve and enhance beauty through aesthetic medical practices can be seen as early as 2000 years ago, in India, where the 'forehead flap' was used to reconstruct the noses and faces of soldiers injured in war and criminal punishments. [ 7 ] This technique, though thoroughly developed and modified, is still used today as a common method to repair nasal defects. [ 5 ] Although Greek and Roman medical practices have been considered the foundation for European and modern-day medicine for a long time, ancient Egyptian texts have revealed that Egyptian medicine produced many key medical discoveries and the basis for many modern practices. [ 8 ] The Egyptians recorded their use of oils, waxes, Cyperus , [ 8 ] and other plant materials to reduce the signs of aging, like wrinkles and spots, and to restore youthful skin. [ 9 ] They studied bodily functions, like inflammatory processes, and were able to make discoveries that allowed them to treat cosmetic wounds and burns using therapies and medicines. This included the initial application of fresh meat to the wound, followed by the use of oil/lipids, honey, and fibers, generally woven linen, until the wound had healed. [ 10 ] As physicians have discovered more about medicine throughout history, these practices have been developed to be more efficient and sanitary and can be seen today in common skin reparation remedies. [ 8 ]
In more recent history, within the past 30 years, the industry of aesthetic medicine has been developing rapidly with the addition of and growing demand for "injectables," [ 11 ] a form of transcutaneous treatment used to rejuvenate and restore the skin of a patient. [ 12 ] These medical injectables have become well established due to their associated low risk, especially compared to other aesthetic surgical practices, as well as the practically non-existent recovery time needed after the procedures are performed. [ 13 ] Within the past ten years, the U.S. Food and Drug Administration has reviewed and approved [ 14 ] over 20 injectable products used for medical aesthetics, in response to the growing demand. [ 11 ] The most commonly used injectables in the industry today are botulinum neurotoxin , commonly referred to as botox, and hyaluronic acid fillers. [ 15 ] According to statistics from an annual survey conducted by the American Society for Aesthetic Plastic Surgery , from 1997 to 2011 the number of nonsurgical procedures performed by aesthetic physicians increased by 356%. [ 11 ]
Aesthetic medicine specializes in altering the cosmetic appearance. It has diverse applications for dermatological and surgical conditions. It includes indications related to minimizing signs of aging, such as skin laxity, wrinkles, and liver spots . Aesthetic medicine also plays a role in the treatment of excess fat, cellulite , and obesity. Laser based therapies can be indicated for the treatment of scars , unwanted hair, skin discoloration, and spider veins . [ 25 ]
Overall health is assessed by a physician to ensure that the symptom being treated (for example, weight gain and excessive hair ) is not a sign of an underlying medical condition (like hypothyroidism) that should be stabilized with medical therapies.
It is also very important for the medical aesthetician to be inclusive in providing a team approach for minimally invasive facial aesthetic procedures.
A career in aesthetic medicine can be approached from a number of professions. A multidisciplinary or team based approach is often necessary to adequately address an aesthetic need. To perform certain procedures, one must be a surgeon , medical doctor (Dermatologist/plastic surgeon/ENT surgeon/Oculoplastic surgeon) or maxillofacial surgeon /Cosmetic Dentist . [ 26 ] Medical Aesthetics requires specialized training and certification beyond a nurse license / aesthetic license. Counselors , psychologists or psychiatrists can help people determine if their reasons for pursuing aesthetic procedures are healthy and help to identify psychiatric disorders such as compulsive eating , anorexia , and body dysmorphic disorder . Reconstructive surgeons can help correct appearance after accidents, burns, surgery for cancer (such as breast reconstruction after mastectomy for cancer), or for congenital deformities like correction of cleft lip . Orthodontists work to improve alignment of teeth, often partially for aesthetic reasons, and oral and maxillofacial surgeons can perform cosmetic facial surgery & correct deformities of the mouth and jaw. Both orthodontists and maxillofacial surgeons can be assisted by dental technicians .
|
https://en.wikipedia.org/wiki/Aesthetic_medicine
|
An Af-nest or Atrial Fibrillation Nest (AFN) is a locus or cluster in the atrial wall with distinct electrical features and properties originated by fibrillar myocardium . It plays as an "electrical multiplier" re-feeding the atrial fibrillation .
One of the currently existing techniques to treat atrial fibrillation (AF) is based on thermo-coagulation of AFN. They are typically numerous at the pulmonary veins antrum. Several evidences have shown that the AFNs represent the true substrate of the AF. Many congenital and acquired conditions may cause this type of myocardium . The higher the number of AFNs the easier the initiation and the longer the AF maintenance. Despite being fundamental in the AF physiopathology the long-lasting AF depends on additional factors. The most important is the "Background Tachycardia " (BKT) which is a focal reentrant tachycardia caused by "Fractal Micro-Reentry". This special tachycardia exists even during AF, keeping the AFNs in a high frequency activation. This tachycardia has a unique mechanism of "protection" that prevents it from being reverted by the large amount of surrounding stimuli generated by the AF itself.
Recent studies have shown that the BKT occurs within a more developed AFN or when there is a confluence of two or more of these elements. By using spectral analysis , it is possible to observe that the "Fractal Micro-Reentry" phenomenon tends to occur depending on a critical amount of fibrillar myocardium . This is a small point in the atrial wall with numerous micro-reentries (in a three-dimensional model) inside the AFN, caused by "cellular electrical disconnection" with progressive dichotomy (biological fractal phenomenon), even without the presence of fibrosis and without the need of major histological changes. By this way, it may be present even in normal hearts that explain the "Lone Atrial Fibrillation". This intense micro-electrical activity stimulates the surrounding atrial myocardium that accepts the activation according to its refractory period. This produces a slightly irregular focal tachycardia, known as "Background Tachycardia " responsible for AF maintenance with or without the contribution of many others AFNs or even of other BKT. The greater the number of these elements is, the longer the AF may last, even becoming permanent.
|
https://en.wikipedia.org/wiki/Af-nest
|
Afferent loop syndrome is an uncommon side effect of gastric surgery. [ 1 ] The afferent loop is made up of a segment of duodenum and/or proximal jejunum located upstream of a double-barrel gastrojejunostomy anastomosis . Abdominal pain and distension are signs of increased intraluminal pressure resulting from the accumulation of enteric secretions in the obstructed afferent loop. [ 2 ]
Afferent loop syndrome may result from volvulus , recurring cancer , stomal stenosis , adhesions, kinking at the anastomotic site, internal herniation , and gastrointestinal stones. [ 1 ]
Laboratory investigations can help diagnose afferent loop syndrome, but imaging scans are required for a confirmation diagnosis. [ 2 ] When diagnosing afferent loop syndrome, abdominal CT is regarded as the preferred radiographic investigation. [ 3 ]
The treatment of afferent loop syndrome is determined by the underlying cause. [ 1 ] Surgical therapy, such as adhesiolysis, bypass , or limb reconstruction, can usually eliminate the source in patients with benign etiologies. [ 4 ] Treatment for patients with afferent loop syndrome due to recurrent tumors shifts to palliation. [ 1 ]
Nonbilious vomiting , nausea , and abrupt onset stomach pain in the right upper quadrant are common symptoms in patients with acute afferent loop syndrome. Abdominal distension and postprandial epigastric discomfort lasting anywhere from a few minutes to an hour are common symptoms experienced by patients with chronic afferent loop syndrome. Bilious projectile vomiting is a typical symptom of chronic afferent loop syndrome that relieves symptoms quickly. In patients with persistent afferent loop syndrome, steatorrhea and diarrhea may exacerbate intestinal stasis. Iron deficiency anemia and/or vitamin B12 deficiency can arise from the deconjugation of bile salts by bacteria. In order to avoid postprandial pain, patients frequently quit eating, which can result in significant weight loss. [ 2 ]
Right upper quadrant abdominal and/or epigastric tenderness is the most common physical finding in afferent loop syndrome patients. There is a palpable abdominal bulge in the right upper quadrant in about one-third of people suffering from acute afferent loop syndrome. Patients may exhibit symptoms of pancreatitis , such as obstructive jaundice or abdominal discomfort radiating to the side or back. Patients may show up with guarding, which is symptomatic of peritonitis , and a stiff abdomen if intestinal perforation has occurred. [ 2 ]
Afferent loop syndrome can have either a benign or malignant etiology, depending on the type of obstructive lesion. Depending on where the lesion is located, there are three primary pathways that lead to benign etiology. [ 5 ]
Anastomotic stricture, foreign body impaction, bezoars , and enteroliths are all potential causes of intraluminal blockage. [ 6 ]
Radiation enteritis and scarring from marginal gastrojejunostomy ulceration are the causes of mechanical blockage of the intramural area. [ 7 ] [ 8 ]
Conditions that cause external compression include internal hernia , volvulus , entrapment, compression, kinking of the afferent loop, postoperative adhesion, and intussusception of the afferent loop. [ 9 ] [ 10 ] [ 11 ]
An antecolic afferent loop's redundancy increases the danger of kinking, volvulus , and adhesion-induced limb entrapment when the bowel length exceeds 30 to 40 cm. Conversely, the risk of an internal herniation developing in a retrocolic afferent loop is increased by incorrectly closed mesocolic abnormalities. [ 12 ]
Locoregional tumor recurrence impeding the afferent loop at the anastomotic site or gastric residual is frequently linked to malignant afferent loop syndrome. [ 13 ] Additional factors contributing to blockage include peritoneal carcinomatosis and regional lymphadenopathy . [ 5 ]
The preferred radiographic study for diagnosing afferent loop syndrome is thought to be abdominal CT . [ 3 ] A blocked intestinal segment can be directly visualized with CT scanning . It is also possible to look at other organs that could be affected by the obstruction, like the biliary tree and pancreas . [ 2 ] When afferent loop syndrome first manifests, the abdominal midline is often crossed by a fluid-filled tubular formation that lies between the super mesenteric artery and the aorta . [ 14 ]
Three parameters determine the treatment plan: the type of obstructive lesion, the blockage site (inframesocolic or supramesocolic), and the patency of the major anastomoses for the hepaticojejunostomy and pancreaticojejunostomy . The standard of care for afferent loop syndrome patients is typically surgery. Adhesiolysis, bypass surgery , and excision with repair of the obstructive malignant lesions are the surgical therapy options available. [ 15 ]
The prognosis is good for patients who receive an early diagnosis and have surgery, with the exception of cases of advanced or recurring cancer . A delay in diagnosis is associated with a mortality rate that varies from 30% to 60%. [ 16 ] Patients who experience afferent limb perforation and subsequent peritonitis and shock have poor prognoses. [ 17 ]
According to reports, 0.2% of patients after distal gastrectomy with Roux-en-Y reconstruction , 1% after laparoscopic distal gastrectomy with Billroth II reconstruction, and 0.3–1.0% of patients following total gastrectomy with Billroth II or Roux-en-Y reconstruction have afferent loop syndrome. [ 15 ]
In 1950, Roux, Pedoussaut, and Marchal initially reported afferent loop syndrome in patients who had undergone gastric surgery and were experiencing bilious vomiting . [ 15 ]
|
https://en.wikipedia.org/wiki/Afferent_loop_syndrome
|
The African Journal of Paediatric Surgery is a peer-reviewed medical journal publishing articles related to clinical or laboratory-based research in paediatric surgery .
The journal is indexed in Abstracts on Hygiene and Communicable Diseases , African Index Medicus , CAB Abstracts , EBSCO Databases , Scopus , MEDLINE , and Index Medicus . [ 1 ]
This article about a surgery journal is a stub . You can help Wikipedia by expanding it .
See tips for writing articles about academic journals . Further suggestions might be found on the article's talk page .
This article about a pediatrics journal is a stub . You can help Wikipedia by expanding it .
See tips for writing articles about academic journals . Further suggestions might be found on the article's talk page .
|
https://en.wikipedia.org/wiki/African_Journal_of_Paediatric_Surgery
|
Afterdepolarizations are abnormal depolarizations of cardiac myocytes that interrupt phase 2, phase 3, or phase 4 of the cardiac action potential in the electrical conduction system of the heart . Afterdepolarizations may lead to cardiac arrhythmias . Afterdepolarization is commonly a consequence of myocardial infarction , cardiac hypertrophy , or heart failure . [ 1 ] It may also result from congenital mutations associated with calcium channels and sequestration. [ 2 ]
Early afterdepolarizations (EADs) occur with abnormal depolarization during phase 2 or phase 3, and are caused by an increase in the frequency of abortive action potentials before normal repolarization is completed. [ 1 ] EADs most commonly originate in mid- myocardial cells and Purkinje fibers , but can develop in other cardiac cells that carry an action potential. Phase 2 may be interrupted due to augmented opening of calcium channels, while phase 3 interruptions are due to the opening of sodium channels . Early afterdepolarizations can result in torsades de pointes , tachycardia , and other arrhythmias . [ 3 ] EADs can be triggered by hypokalemia and drugs that prolong the QT interval , including class Ia and III antiarrhythmic agents , as well as catecholamines . [ 1 ]
Afterhyperpolarizations can also occur in cortical pyramidal neurons. There, they typically follow an action potential and are mediated by voltage gated sodium or chloride channels. This phenomenon requires potassium channels to close quickly to limit repolarization. It is responsible for the difference between regular spiking and intrinsically bursting pyramidal neurons. [ 4 ]
Delayed afterdepolarizations (DADs) begin during phase 4, after repolarization is completed but before another action potential would normally occur via the normal conduction systems of the heart. They are due to elevated cytosolic calcium concentrations, classically seen with digoxin toxicity. [ 5 ] [ 6 ] The overload of the sarcoplasmic reticulum may cause spontaneous Ca 2+ release after repolarization, causing the released Ca 2+ to exit the cell through the 3Na + /Ca 2+ -exchanger. This results in a net depolarizing current. The classical feature is Bidirectional ventricular tachycardia . Also seen in catecholaminergic polymorphic ventricular tachycardia (CPVT). Delayed afterdepolarization is also seen in myocardial infarction. Purkinje fibers which survive myocardial infarction remain partially depolarized due to its high concentration of cations. [ 7 ] Partially depolarized tissue fires rapidly resulting in delayed after depolarization. [ 1 ]
|
https://en.wikipedia.org/wiki/Afterdepolarization
|
This medical article is a stub . You can help Wikipedia by expanding it .
Afterdrop is a continued cooling of core temperature during the initial stages of rewarming from hypothermia .
Afterdrop is attributed to the return of cold blood from extremities to the core due to peripheral vasodilatation , thus causing a further decrease of deep body temperature. [ 1 ] However a second theory explains afterdrop as a side effect of conductive heat transfer . "The hypothermic patient cools from the outside in. Consequently, a heat gradient is established from the relatively warm core to the cool periphery. This heat gradient does not reverse immediately upon initiation of rewarming. Until the gradient is reversed, further heat transfer occurs from the warmer core to cooler peripheral tissues." [ 2 ]
In severe cases, afterdrop can lead to post-rescue collapse, [ 3 ] but has not been shown to be of any clinical importance in rewarming the hypothermic patient. [ 2 ] Afterdrop is not observed in the rewarming of all hypothermic patients. It is more common in patients who were rapidly cooled or rewarmed. Afterdrop was less common in patients for whom rewarming was delayed, or when cooling was slow and prolonged. [ 4 ]
|
https://en.wikipedia.org/wiki/Afterdrop
|
The age of onset is the age at which an individual acquires, develops, or first experiences a condition or symptoms of a disease or disorder. For instance, the general age of onset for the spinal disease scoliosis is "10-15 years old," [ 1 ] meaning that most people develop scoliosis when they are of age between ten and fifteen years.
Diseases are often categorized by their ages of onset as congenital , infantile , juvenile , or adult . Missed or delayed diagnosis often occurs if a disease that is typically diagnosed in juveniles (such as asthma) is present in adults, and vice versa (such as arthritis). [ 2 ] Depending on the disease, ages of onset may impact features such as phenotype, as is the case in Parkinson's and Huntington's diseases. [ 3 ] [ 4 ] For example, the phenotype for juvenile Huntington's disease clearly differs from adult-onset Huntington's disease and late-onset Parkinson's exhibits more severe motor and non-motor phenotypes. [ 3 ] [ 4 ]
Germ-line mutations are often at least in part the cause of disease onset at an earlier age. [ 5 ] [ 6 ] Though many germ-line mutations are deleterious, the genetic lens through which they may be viewed may provide insights to treatment, possibly through genetic counseling . [ 7 ] [ 8 ]
In some cases, the age of onset may be the result of mutation accumulation. [ 9 ] If this is the case, it could be helpful to consider ages of onset as a product of the hypotheses depicted in theories of aging. Even some mental health disorders, whose ages of onset have been found to be harder to define than physical illnesses may have a mutated component. [ 10 ] The symptoms of standard mental disorders often start off non-specific. Pathological changes pertaining to disorders often become more detailed and less fickle before they can be defined in the American Psychiatric Association's DSM. The brain is a dynamic and complex system, it is constantly re-wiring itself and a major concern is what happens to the brain in earlier life that mirrors what occurs later in its psycho-pathological state. [ 11 ] The typical onset of many mental disorders in late adolescence may reflect the critical development that happens at this time. [ 12 ]
The rate-of-living theory of aging states that senescence occurs because individuals accumulate damage to cells and tissues during cell division. This theory is not supported because its postulates that aging rate should be correlated with metabolic rate [ 13 ] and organisms cannot evolve longer lifespans [ 14 ] [ 15 ] were not supported in trials. [ 14 ] [ 15 ] [ 16 ] [ 17 ] [ 18 ] The rate-of-living theory may not be used to draw conclusions about age of onset based on this.
There are two subsets to the evolutionary theory of aging: antagonistic pleiotropy hypothesis and the mutation accumulation hypothesis.
The antagonistic pleiotropy hypothesis was tested by monitoring the age-1 gene in C. elegans . [ 19 ] The age-1 gene plays a role in senescence; nematodes with mutations in this gene live up to 80% longer. [ 19 ] Mutants in the age-1 gene for allele hx546 seem to be otherwise normal until placed under stressful conditions. [ 19 ] Then, the carriers of the mutant gene appear to be at disadvantage—they do not lay eggs while being starved. [ 19 ] This evidence supports antagonistic pleiotropy as a theory of aging, and therefore as an onset cause in some cases.
The mutation accumulation hypothesis was tested by demonstrating how quickly deleterious mutations can accumulate in Musca domestica . [ 20 ] Reed and Bryant demonstrated this by limiting the lifespan of the flies to a few days, which made late-life mutations invisible to selection since they occurred after reproduction. [ 20 ] The lifespan of the flies was monitored by allowing them to carry out their complete lifespan every few generations, which was reported to decline substantially. [ 20 ] Mutation accumulation is supported as a theory of aging, and therefore an onset cause in cases of diseases resulting from mutation accumulation.
|
https://en.wikipedia.org/wiki/Age_of_onset
|
The agene process is a former process for bleaching flour with agene (nitrogen trichloride). The practice was discontinued in 1949 once it became known that agene treated flour caused severe and widespread neurological disorders in humans and dogs. [ 1 ]
This food ingredient article is a stub . You can help Wikipedia by expanding it .
|
https://en.wikipedia.org/wiki/Agene_process
|
In medicine , agenesis ( / eɪ ˈ dʒ ɛ n ə s ə s / [ 1 ] ) refers to the failure of an organ to develop during embryonic growth and development due to the absence of primordial tissue. Many forms of agenesis are referred to by individual names, depending on the organ affected:
Eye agenesis is a medical condition in which people are born with no eyes .
Ear agenesis is a medical condition in which people are born without ears .
Because the middle and inner ears are necessary for hearing, people with complete agenesis of the ears are totally deaf . Minor agenesis that affects only the visible parts of the outer ear, which may be called microtia , typically produces cosmetic concerns and perhaps hearing impairment if the opening to the ear canal is blocked, but not deafness.
|
https://en.wikipedia.org/wiki/Agenesis
|
Aggregatibacter actinomycetemcomitans is a Gram-negative , facultative anaerobe, nonmotile bacterium that is often found in association with localized aggressive periodontitis , a severe infection of the periodontium . It is also suspected to be involved in chronic periodontitis . [ 1 ] Less frequently, A. actinomycetemcomitans is associated with nonoral infections such as endocarditis. Its role in aggressive periodontitis was first discovered by Danish -born periodontist Jørgen Slots , a professor of dentistry and microbiology at the University of Southern California School of Dentistry . [ citation needed ]
'Bacterium actinomycetem comitans' was first described by Klinger (1912) as coccobacillary bacteria isolated with Actinomyces from actinomycotic lesions in humans. It was reclassified as Actinobacillus actinomycetemcomitans by Topley & Wilson (1929) and as Haemophilus actinomycetemcomitans by Potts et al. (1985). The species has attracted attention because of its association with localized aggressive periodontitis. [ 2 ]
Recent studies have shown a phylogenetic similarity of A. actinomycetemcomitans and Haemophilus aphrophilus , H. paraphrophilus , and H. segnis , suggesting the new genus Aggregatibacter for them. [ 2 ]
It is one of the bacteria that might be implicated in destructive periodontal disease . Although it has been found more frequently in localized aggressive periodontitis, [ 3 ] prevalence in any population is rather high. It has also been isolated from actinomycotic lesions (mixed infection with certain Actinomyces species, in particular A. israelii ). It possesses certain virulence factors that enable it to invade tissues, such as the pore-forming toxin leukotoxin A. It has also been isolated from women with bacterial vaginosis and as an etiologic agent in endocarditis. [ 4 ] The pore-forming toxin LtxA of A. actinomycetemcomitans may be a trigger of the autoimmune disease rheumatoid arthritis due to its ability to stimulate protein citrullination , a post-translational protein modification targeted by autoantibodies in this disease. [ 5 ] [ 6 ]
In bacteria, small RNAs are involved in gene regulation. Jorth et al. identified 9 sRNA by Northern blotting from computer-predicted candidates in strain VT1169 and 202 sRNA by RNA seq in strain 624. [ 8 ] [ 9 ] A systematic screen by RNA-seq and RT-PCR in HK1651 strain (a clinical isolate from an aggressive periodontitis patient), quantified 70 sRNAs and further identified 17 differentially expressed sRNAs during growth phases. [ 10 ] Target prediction indicated possibility of sRNA interaction with several virulence genes. [ 10 ] This study confirmed the presence of one of previously identified Fur regulated sRNAs JA04 identified in strain HK1651. [ citation needed ]
|
https://en.wikipedia.org/wiki/Aggregatibacter_actinomycetemcomitans
|
Agitation is a state of heightened motor and cognitive activity characterized by excessive or inappropriate verbal and physical behaviors, emotional excitement , and restlessness , often arising as a symptom of underlying medical, psychiatric, or neurological conditions. [ 1 ] [ 2 ] [ 3 ] It is considered both a medical and psychiatric emergency due to the potential for harm to patients, caregivers, and healthcare providers, and may escalate to aggression or violence if not promptly recognized and managed. [ 1 ] [ 4 ] [ 5 ]
The etiology of agitation is multifactorial, encompassing acute medical illnesses (such as infections, metabolic disturbances, or pain), substance intoxication or withdrawal, delirium, and a spectrum of psychiatric disorders including mood, psychotic, and personality disorders[6]. [ 2 ] [ 4 ] [ 6 ]
Early identification and a systematic evaluation to determine underlying causes are critical, as agitation of unknown origin should be presumed to have a medical cause until proven otherwise, particularly in populations such as the elderly or those without a prior psychiatric history. [ 1 ] [ 3 ]
Effective management relies on a combination of non-pharmacological de-escalation strategies and, when necessary, targeted pharmacological interventions, always prioritizing the safety of all involved. [ 2 ] [ 5 ]
This medical article is a stub . You can help Wikipedia by expanding it .
|
https://en.wikipedia.org/wiki/Agitation_(medical)
|
Agnes B. Fogo is a professor of renal pathology at the Vanderbilt University Medical Center .
Fogo graduated from the University of Oslo , Norway, and the University of Tennessee , USA. She completed her M.D. from Vanderbilt University School of Medicine before going on to do residency and a fellowship in renal pathology. [ 1 ]
Fogo works at the Vanderbilt University Medical Center and is the John L. Shapiro Professor of Pathology, Microbiology and Immunology, Professor of Medicine and Pediatrics, and director of the Renal/Electron Microscopy Laboratory. [ 2 ] [ 3 ]
In 2021 she also became the International Society of Nephrology president for a 2 year term. [ 4 ]
This biographical article related to medicine in the United States is a stub . You can help Wikipedia by expanding it .
This article related to pathology is a stub . You can help Wikipedia by expanding it .
|
https://en.wikipedia.org/wiki/Agnes_Fogo
|
Agnes McLaren (4 July 1837 – 17 April 1913) [ 1 ] FRCPI was a Scottish doctor who was one of the first to give medical assistance to women in India who, because of custom, were unable to access medical help from male doctors. Agnes was active in social justice causes including protests against the white slave trade. [ 2 ] She signed the 1866 women's suffrage petition and was secretary of the Edinburgh National Society for Women's Suffrage alongside her stepmother, Priscilla Bright McLaren. [ 3 ] In 1873 she travelled with Priscilla and Jane Taylour to give suffrage lectures in Orkney and Shetland . [ 4 ] Her father had supported the campaign of first women who sought to study medicine at University of Edinburgh and Agnes became friends with Sophia Jex-Blake , one of the Edinburgh Seven . Her father did not however, support Agnes' own ambitions in this area. And as she could not graduate in medicine in Scotland, she went to study in France and later, in order to be permitted to practice at home, became a member of the Royal College of Dublin. [ 4 ]
She was based with the Franciscan Hospital Sisters when in training, [ 5 ] and later converted to the Catholic faith in order to carry out missionary work even though Roman Catholic law still prevented its sisters-in-vows from being doctors until 1936. [ 6 ]
McLaren was born in Edinburgh, Scotland . [ 1 ] The daughter of Duncan McLaren , a Presbyterian businessman and prominent liberal politician, by his second marriage. Her mother died when she was only three years old. Her father's third wife was Priscilla Bright and in time they would work together.
She entered the school of medicine at the University of Montpellier in 1876, eventually becoming only the tenth woman in Britain to graduate as a doctor. [ 3 ] In 1877 she sat on the governing body of the London School of Medicine for Women . She was a visiting physician at the Cannongate Medical Mission Dispensary in Edinburgh. By 1882, she was also Fellow of the Royal College of Physicians of Ireland , and had a practice in Cannes . [ 3 ] She would spend the summers in Edinburgh and relocate to France in the winter.
In 1898 aged 61, she converted to the Roman Catholic Church , and later went to Rawalpindi , northern India (now Pakistan) with a Catholic mission , she had learned of the tremendous health needs of women in India. [ 3 ] Because of India's custom of seclusion for women ( purdah ), they could not be seen by men other than their immediate family, a custom which meant they also could not receive medical care from male physicians. With so few women doctors in the early 1900s, literally thousands of women died in illness or in childbirth each year and many babies also died in infancy. McLaren responded to this problem by establishing the London Committee, a support group of women which helped finance the opening of a small hospital, St. Catherine's Hospital, in Rawalpindi . [ 7 ]
During her search for women who could help run the hospital, McLaren discovered that Catholic Canon Law prohibited Religious Sisters from giving this level of medical care. She petitioned the Pope and Holy See to lift the restriction and, while waiting for a response, continued looking for women interested in health care abroad. Anna Maria Dengel , an Austrian , responded to McLaren's request, but was never able to meet McLaren, who died shortly after their correspondence began. However, before her death, McLaren encouraged Dengel to study medicine at the Cork University , setting into motion Dengel's becoming a physician and, years later, her starting a new religious congregation , the Medical Mission Sisters . They are a Catholic congregation of Sisters who are trained as doctors and nurses and other forms of healthcare professionals, dedicated to providing healthcare to women and children around the world. In 1915, after reading a biographical pamphlet about McLaren's life, Australian doctor Mary Glowrey experienced her vocation to work as a medical missionary in Guntur , India. Mary Glowrey received special permission from Pope Benedict XV to work as a medical doctor and Religious Sister in 1920.
McLaren died in 1913 and was buried in Antibes , France. [ 8 ] Her obituary in the British Medical Journal describes her as "a woman of strong individuality and character, known to a large circle of philanthropic workers of many nations, many kindreds and many creeds." [ 2 ]
|
https://en.wikipedia.org/wiki/Agnes_McLaren
|
Agnosia is a neurological disorder characterized by an inability to process sensory information . Often there is a loss of ability to recognize objects, persons, sounds , shapes, or smells while the specific sense is neither defective nor is there any significant memory loss . [ 1 ] It is usually associated with brain injury or neurological illness , particularly after damage to the occipitotemporal border , which is part of the ventral stream . [ 2 ] Agnosia affects only a single modality , [ 3 ] such as vision or hearing. [ 4 ] More recently, a top-down interruption is considered to cause the disturbance of handling perceptual information. [ 5 ]
Visual agnosia is a broad category that refers to a deficiency in the ability to recognize visual objects. Visual agnosia can be further subdivided into two different subtypes: apperceptive visual agnosia and associative visual agnosia . [ 22 ]
Individuals with apperceptive visual agnosia display the ability to see contours and outlines when shown an object, but they experience difficulty if asked to categorize objects. Apperceptive visual agnosia is associated with damage to one hemisphere, specifically damage to the posterior sections of the right hemisphere. [ 22 ]
In contrast, individuals with associative visual agnosia experience difficulty when asked to name objects. Associative agnosia is associated with damage to both the right and left hemispheres at the occipitotemporal border. [ 22 ] A specific form of associative visual agnosia is known as prosopagnosia. Prosopagnosia is the inability to recognize faces. For example, these individuals have difficulty recognizing friends, family and coworkers. [ 22 ] However, individuals with prosopagnosia can recognize all other types of visual stimuli. [ 23 ]
Speech agnosia, or auditory verbal agnosia , refers to "an inability to comprehend spoken words despite intact hearing, speech production and reading ability". Patients report that they hear sounds being produced, but that the sounds are fundamentally unrecognizable or untranslatable. [ 24 ]
Despite an inability to process what the speaker is saying, some patients have been reported to recognize certain characteristic information about the speaker's voice (such as being a man or woman). [ 24 ]
Agnosia can result from strokes , dementia , or other neurological disorders . It may also be trauma-induced by a head injury, brain infection, or hereditary. Additionally, some forms of agnosia may be the result of developmental disorders. [ 4 ] Damage causing agnosia usually occurs in either the occipital or parietal lobes of the brain. Although one modality may be affected, cognitive abilities in other areas are preserved. [ 4 ]
Patients who experience dramatic recovery from blindness experience significant to total agnosia. [ 25 ]
The effect of damage to the superior temporal sulcus is consistent with several types of neurolinguistic deficiencies, and some contend that agnosia is one of them. The superior temporal sulcus is vital for speech comprehension because the region is highly involved with the lexical interface. According to the 1985 TRACE II Model, the lexical interface associates sound waves (phonemes) with morphological features to produce meaningful words. This association process is accomplished by lateral inhibition/excitement of certain words within an individual's lexicon (vocabulary). [ 24 ] For instance, if an experimenter were to say DOG aloud, the utterance would activate and inhibit various words within the subjects lexical interface:
The consistency of this model to agnosia is shown by evidence that bilateral lesions to the superior temporal sulcus produces 'pure word deafness' (Kussmaul, 1877), or as it is understood today, speech agnosia. Patients with pure word deafness demonstrate the inability to recognize and process speech sounds with normal auditory processing for non-speech sounds below the level of the cortex. [ 24 ]
In order to assess an individual for agnosia, it must be verified that the individual does not have a loss of sensation, and that both their language abilities and intelligence are intact. In order for an individual to be diagnosed with agnosia, they must only be experiencing a sensory deficit in a single modality. To make a diagnosis, the distinction between apperceptive and associative agnosia must be made. This distinction can be made by having the individual complete copying and matching tasks. If the individual has a form of apperceptive agnosia they will not be able to match two stimuli that are identical in appearance. In contrast, if an individual has a form of associative agnosia, they will not be able to match different examples of a stimulus. For example, an individual who has been diagnosed with associative agnosia in the visual modality would not be able to match pictures of a laptop that is open with a laptop that is closed. [ 3 ]
Individuals with pure alexia usually have difficulty reading words as well as difficulty with identifying letters. In order to assess whether an individual has pure alexia, tests of copying and recognition must be performed. An individual with pure alexia should be able to copy a set of words, and should be able to recognize letters. [ 3 ]
Individuals are usually shown pictures of human faces that may be familiar to them such as famous actors, singers, politicians or family members. The pictures shown to the patient are selected to be age and culture appropriate. The task involves the examiner asking the individual to name each face. If the individual cannot name whose face appears in the picture, the examiner may ask a question that would help to recognize the face in the picture. [ 3 ]
For all practical purposes, there is no direct cure. Patients may improve if information is presented in other modalities than the damaged one. Different types of therapies can help to reverse the effects of agnosia. In some cases, occupational therapy or speech therapy can improve agnosia, depending on its cause. [ citation needed ]
Initially many individuals with a form of agnosia are unaware of the extent to which they have either a perceptual or recognition deficit. This may be caused by anosognosia which is the lack of awareness of a deficit. This lack of awareness usually leads to a form of denial and resistance to any form of help or treatment. There are various methods that can be used which can help the individual recognize the impairment in perception or recognition that they may have. A patient can be presented with a stimulus to the impaired modality only to help increase their awareness of their deficit. Alternatively, a task can be broken down into its component parts so that the individual can see each part of the problem caused by the deficit. Once the individual acknowledges their perceptual or recognition deficit, a form of treatment may be recommended. There are various forms of treatment such as compensatory strategies with alternate modalities, verbal strategies, alternate cues and organizational strategies. [ 3 ]
Using verbal descriptions may be helpful for individuals with certain types of agnosia. Individuals such as prosopagnosics may find it useful to listen to a description of their friend or family member and recognize them based on this description more easily than through visual cues. [ 3 ]
Alternate cues may be particularly useful to an individual with environmental agnosia or prosopagnosia. Alternate cues for an individual with environmental agnosia may include color cues or tactile markers to symbolize a new room or to remember an area by. Prosopagnosics may use alternate visual cues such as a scar on an individual's face or crooked teeth, or cues from other senses, like the sound of an individual's voice, in order to recognize the individual. [ 3 ] Hair color and length can be helpful cues as well. [ 5 ]
Organizational strategies may be extremely helpful for an individual with visual agnosia. For example, organizing clothes according to different hangers provides tactile cues for the individual, making it easier to identify certain forms of clothing as opposed to relying solely on visual cues. [ 3 ]
There are clinical trials being done to further research for treatments. At the National Institute of Neurological Disorders and Stroke (NINDS) they support research for rare diseases like agnosia. [ 4 ] Some organizations that are recruiting for trials are using clincaltrials.gov and give status updates on the trials. [ 26 ]
The term "agnosia" comes from the Ancient Greek ἀγνωσία ( agnosia ), "ignorance", "absence of knowledge". It was introduced by Sigmund Freud in 1891: [ 27 ] "For disturbances in the recognition of objects, which Finkelnburg classes as asymbolia, I should like to propose the term 'agnosia'." Prior to Freud's introduction of the term, some of the first ideas about agnosia came from Carl Wernicke , who created theories about receptive aphasia in 1874. He noted that individuals with receptive aphasia did not possess the ability to understand speech or repeat words. He believed that receptive aphasia was due to lesions of the posterior third of the left superior temporal gyrus . Due to these lesions, Wernicke believed that individuals with receptive aphasia had a limited deafness for certain sounds and frequencies in speech . [ 8 ]
After Wernicke, came Kussmaul in 1877 who attempted to explain why auditory verbal agnosia , also known as word deafness, occurs. Contrary to Wernicke's explanations, Kussmaul believed auditory verbal agnosia was the result of major destruction to the first left temporal gyrus. Kussmaul also posited about the origins of alexia (acquired dyslexia) also known as word blindness. He believed that word blindness was the result of lesions to the left angular and supramarginal gyri . [ 8 ]
Heinrich Lissauer shared his ideas about agnosia after Wernicke and Kussmaul. [ 8 ] In 1890, he theorized that there were two ways in which object recognition impairment could occur. One way in which impairment could occur was if there was damage to early perceptual processing or if there was damage to the actual object representation. If the actual object representation was damaged, this would not allow the object to be stored in visual memory, and therefore the individual would not be able to recognize the object. [ 28 ] During the time of Wernicke, Kussmaul and Lissauer there was little known about the cerebral cortex . Today, with new neuroimaging techniques, we have been able to expand our knowledge on agnosia greatly. [ 3 ]
|
https://en.wikipedia.org/wiki/Agnosia
|
Agrammatism is a characteristic of non-fluent aphasia. Individuals with agrammatism present with speech that is characterized by containing mainly content words, with a lack of function words. For example, when asked to describe a picture of children playing in the park, the affected individual responds with, "trees..children..run." [ 1 ] People with agrammatism may have telegraphic speech , [ 2 ] a unique speech pattern with simplified formation of sentences (in which many or all function words are omitted), akin to that found in telegraph messages. Deficits in agrammaticism are often language-specific, however—in other words, "agrammaticism" in speakers of one language may present differently from in speakers of another. [ 3 ]
Errors made in agrammatism depend on the severity of aphasia. In severe forms language production is severely telegraphic and in more mild to moderate cases necessary elements for sentence construction are missing. Common errors include errors in tense, number, and gender. [ 4 ] Patients also find it very hard to produce sentences involving "movement" of elements, such as passive sentences, wh-questions or complex sentences. [ citation needed ]
Agrammatism is seen in many brain disease syndromes, including expressive aphasia and traumatic brain injury . [ citation needed ]
Agrammatism was first coined by Adolf Kussmaul in 1887 to explain the inability to form words grammatically and to syntactically order them into a sentence. Later on, Harold Goodglass defined the term as the omission of connective words, auxiliaries and inflectional morphemes , all of these generating a speech production with extremely rudimentary grammar. Agrammatism, today seen as a symptom of the Broca's syndrome , [ 5 ] has been also referred as 'motor aphasia ', [ 6 ] 'syntactic aphasia', [ 7 ] 'efferent motor aphasia', [ 8 ] and 'non-fluent aphasia'. [ 9 ]
The early accounts of agrammatism involved cases of German and French participants. The greater sophistication of the German school of aphasiology at the turn of the 20th century and also the fact that both German and French are highly inflected languages , might have been triggers for that situation. [ 10 ] Nowadays, the image has slightly changed: grammatical impairment has been found to be selective rather than complete, and a cross-linguistic perspective under the framework of Universal Grammar (UG) together with a shift from morphosyntax to morphosemantics is à la page. Now the focus of study in agrammatism embraces all natural languages and the idiosyncrasies scholars think a specific language has are put in relation to other languages so as to better understand agrammatism, help its treatment, and review and advance in the field of theoretical linguistics . [ citation needed ]
There is little written about agrammatism in Catalan. The beginnings of the field should be encountered in the work of Peña-Casanova & Bagunyà-Durich (1998), and Junque et al. (1989). These papers do not describe case reports, they are rather dealing with more general topics such as lesion localization or rehabilitation of agrammatic patients. The most updated studies could be found in the work of Martínez-Ferreiro (2009). The work of Martínez-Ferreiro is under the so-called Tree Pruning Hypothesis (TPH) of Friedmann & Grodzinsky (2007). Such a hypothesis is somewhat lagging behind after the findings in Bastiaanse (2008) have been proved by means of a re-analysis of data from Nanousi et al. (2006) and Lee et al. (2008), and the work of Yarbay Duman & Bastiaanse (2009). Other rather updated work for agrammatism in Catalan should be found in Martínez-Ferreiro et Gavarró (2007), in Gavarró (2008, 2003a, 2003b, 2002), Balaguer et al. (2004), in Peña-Casanova et al. (2001), and in Sánchez-Casas (2001).
From a cross-linguistic perspective under the framework of Universal Grammar (UG), grammatical impairment in agrammatism has been found to be selective rather than complete. Under this line of thought, the impairment in tense production for agrammatic speakers is currently being approached in different natural languages by means of the study of verb inflection for tense in contrast to agreement (a morphosyntactic approach) and also, more recently, by means of the study of time reference (which, in a sense, should be seen closer to morphosemantics). The type of studies this paper should be related with are those dealing with tense impairment under the framework of time reference. Prior to explaining that, to help understand the goals of such research, it is good to give a taste of the shift from morphosyntax to morphosemantics the study of agrammatism is undergoing. [ citation needed ]
Verb inflection for tense has been found to be problematic in several languages. Different scholars have come up with different theories to explain it: Friedman & Grodzinsky (1997) introduced the so-called Tree Pruning Hypothesis (TPH) from the study of Hebrew , Arabic , and English ; the same hypothesis has been proved by Gavarró & Martínez-Ferreiro (2007) for what they called Ibero-Romance (that is, Catalan , Galician , and Castilian ); Wenzlaff & Clahsen (2004; 2005) introduced the Tense Underespecification Hypothesis (TUH) for German, and by the same time Bruchert et al. (2005) introduced the Tense and Agreement Underespecification Hypothesis (TAUH) for the same language; and Lee et al. (2008), and Faroqi-Shah & Dickey (2009) introduced a morphosemantic hypothesis, arguing that the diacritic tense features are affected in English agrammatism. [ citation needed ]
Bastiaanse (2008) did not find such dissociation for Dutch but rather that reference to the past is more impaired regardless of verb inflection or agreement. Her research found that finite verbs are more difficult than non-finite verbs , but both within the finite verbs and within the nonfinite verbs, the forms referring to the past (third person singular past tense and participle respectively) are more difficult than their counterparts referring to the present (third person singular present tense and infinitives). None of the hypotheses on verb forms aforementioned (TPH, TUH, and TAUH) can account for these results, ever since participles in Dutch are not inflected for tense and agreement nor do they check their features in the left periphery. Similar findings have been also reported for Greek and for English respectively in a re-analysis of Nanousi et al.'s (2006) and Lee et al.'s (2008) data, and also for Turkish in Yarbay, Duman & Bastiaanse (2009). In any case, the conclusion of Bastiaanse (2008) was that an additional hypothesis expressing that agrammatic speakers have difficulty making reference to the past was needed. In that same paper she unveiled two possible answers: (a) it could be that representations of events in the past are semantically more complex, possibly because there are two time periods of relevance. (b) It might also be the case that it is not so much reference to the past as such that is difficult for agrammatic speakers, but to express this reference by verb inflection. [ citation needed ]
|
https://en.wikipedia.org/wiki/Agrammatism
|
The Agreement on the Application of Sanitary and Phytosanitary Measures , also known as the SPS Agreement or just SPS , is an international treaty of the World Trade Organization (WTO). It was negotiated during the Uruguay Round of the General Agreement on Tariffs and Trade (GATT), and entered into force with the establishment of the WTO at the beginning of 1995. [ 1 ] Broadly, the sanitary and phytosanitary ("SPS") measures covered by the agreement are those aimed at the protection of human, animal or plant life or health from certain risks. [ 2 ]
Under the SPS agreement, the WTO sets constraints on member-states' policies relating to food safety (bacterial contaminants, pesticides , inspection and labelling ) as well as animal and plant health (phytosanitation) with respect to imported pests and diseases. There are 3 standards organizations who set standards that WTO members should base their SPS methodologies on. As provided for in Article 3, they are the Codex Alimentarius Commission (Codex), World Organisation for Animal Health (OIE) and the Secretariat of the International Plant Protection Convention (IPPC).
The SPS agreement is closely linked to the Agreement on Technical Barriers to Trade , which was signed in the same year and has similar goals. The TBT Emerged from the Tokyo Round of WTO negotiations and was negotiated with the aim of ensuring non-discrimination in the adoption and implementation of technical regulations and standards. [ 3 ]
As GATT 's preliminary focus had been lowering tariffs , the framework that preceded the SPS Agreement was not adequately equipped to deal with the problems of non-tariff barriers (NTBs) to trade and the need for an independent agreement addressing this became critical. [ 4 ] The SPS Agreement is an ambitious attempt to deal with NTBs arising from cross-national differences in technical standards without diminishing governments prerogative to implement measures to guard against diseases and pests. [ 5 ]
Some of the most important WTO 'cases' regarding the implementation of SPS measures include:
In 2003, the United States challenged a number of EU laws restricting the importation of Genetically Modified Organisms (GMOs) in a dispute known as EC-Biotech, [ 11 ] arguing they are "unjustifiable" and illegal under SPS agreement. In May 2006, the WTO's dispute resolution panel issued a complex ruling which took issue with some aspects of the EU's regulation of GMOs, but dismissed many of the claims made by the USA. A summary of the decision can be found here .
Another prominent SPS case is the hormone-treated beef case. In 1996, the United States and Canada challenged before the WTO Dispute Settlement Body (DSB) a number of EU directives prohibiting the importation and sale of meat and meat products treated with certain growth hormones . The complainants alleged that the EU directives violated, among other things, several provisions of the SPS Agreement. The EU contended that the presence of the banned hormones in food may present a risk to consumers' health and that, as a consequence, the directives were justified under several WTO provisions authorizing the adoption of trade-restrictive measures that are necessary to protect human health. In 1997 and 1998, the WTO adjudicating bodies admitted USA and Canada claims and invited the EU to bring the directives into conformity with WTO law before the end of May 1999. EU did not comply and the DSB authorized the US and Canada to take countermeasures against the EU. The countermeasures took the form of increased custom duties applied by the US and Canada on certain EU products, including the notorious Roquefort cheese. In 2004, while the ban on hormone-treated meat was still in place, the EU initiated before the DSB new proceedings seeking the lifting of the countermeasures applied by the US and Canada. EU alleged that it had collected new scientific data evidencing that the banned hormones may cause harm to consumers. According to the EU, the new scientific data provides sufficient ground for the ban on hormones, which may no more be sanctioned by the countermeasures imposed by the US and Canada. As of January 2007, the proceedings initiated by the EU were still pending.
While Article 1.5 of the TBT precludes the inclusion of SPS measures from its ambit, in EC-Biotech, the panel recognised that situations could arise where a measure is only partly an SPS measure, and in those cases, the SPS part of the measure will be considered under the SPS Agreement. [ 12 ] If a measure conforms with SPS, under Article 2.4 of the SPS Agreement, it is assumed that the measure falls within the scope of GATT, Article XX(b).
Trade in the products subject to SPS-type measures have the potential to result in significant economic gains for national economies. [ 13 ] Favouring economic concerns over other important public health policy issues, however, is something that requires close scrutiny by governments and the international community. [ 14 ]
The SPS Agreement reflects the precautionary principle – a principle which allows them to act on the side of caution if there is no scientific certainty about potential threats to human health and the environment. Under Article 5.7 Members who enact provisional measures are obligated to seek further information on possible risks and review the measure 'within a reasonable period of time'. The Appellate Body in Japan– Measures Affecting Agricultural Products, stated that the length of a 'reasonable period of time' is to be assessed on a case-by-case basis. [ 15 ] Under SPS rules, the burden of proof is on the complainant country to demonstrate that a measure violates Article 2.2 and Articles 5.1-5.8 before it can be regulated [ 16 ] even though scientific evidence can never be conclusive and it is not possible to test for all health risks that could arise from the importation of a certain product. [ 17 ]
It is important that the views of developing countries are incorporated into the standard-setting process as the effect of exporting countries enacting SPS measures can be damaging to developing economies. This is partly due to these states not possessing the technology and resources needed to readily comply with certain SPS requirements. [ 18 ]
Some commentators pose that the WTO's assumption that trade liberalisation enhances consumer welfare , has resulted in the SPS Agreement being ill-equipped to deal with trade restrictions put in place by governments responding to protectionist pressure from consumers. [ 19 ] This was most noticeable in the Beef Hormones Dispute where, although the science pointed to the relative safety of the growth hormones in question, European consumers pressured governments to ban the import of hormone-treated beef. [ 20 ]
World portal
|
https://en.wikipedia.org/wiki/Agreement_on_the_Application_of_Sanitary_and_Phytosanitary_Measures
|
Aicardi syndrome is a rare genetic malformation syndrome characterized by the partial or complete absence of a key structure in the brain called the corpus callosum , the presence of retinal lacunes, and epileptic seizures in the form of infantile spasms . [ 2 ] Other malformations of the brain and skeleton may also occur. The syndrome includes intellectual disability that is usually severe or moderate. So far, the syndrome has only been diagnosed in girls and in boys with two X chromosomes ( Klinefelter syndrome ). [ 3 ]
Those with Aicardi syndrome are in need of various specialist and habilitation instances. Epilepsy is treated with medication, but additional treatment may also be needed. In order to utilize the individual's eyesight and investigate the need for visual aids, examination by ophthalmologist is indicated early in life. Problems from the gastrointestinal tract are frequent. In adulthood, continued habilitation efforts and support in daily life are needed. [ 3 ]
The syndrome is named after the French child neurologist Jean Dennis Aicardi, who in 1965 described it in eight girls. [ 3 ] A causative gene has not been identified. Symptoms typically appear before a baby reaches about 5 months of age. [ citation needed ]
Those with Aicardi syndrome develop normally during the first months, but later various symptoms appear due to the syndrome's characteristic malformations in the brain. It is common for people with Aicardi syndrome to have a small head ( microcephaly ). [ 3 ]
At three to six months of age, the child begins to have epileptic seizures, often of the infantile spasm type caused by changes in the brain's gray matter, the cerebral cortex. The seizures occur either as so-called flexor spasms, when the child's neck suddenly bends forward while the arms make a clasping movement, or as other types of epileptic seizures. Seizures come in series at short intervals and may increase in number from day to day until they are broken with medication. Epilepsy usually persists for life. [ 3 ]
Most have a severe intellectual disability with a major impact on language, communication and motor skills. A few have a moderate intellectual disability. Mild intellectual disability also occurs but is very rare. [ 3 ]
The eyes are always affected, and most people have impaired vision. During an eye examination , areas with less pigment ( retinal lacunae ) appear as white spots in the fundus, which is due to the absence of retinal pigment cells and other structures in these areas. If the lacunae are located in the macula, they affect acuity. Other types of eye abnormalities are also common, such as one eye being smaller than normal ( microphthalmia ), changes in the optic nerve, and incomplete closure/slitting of the membranes of the eye ( coloboma ). Rapid, involuntary eye movements ( nystagmus ) are common. Since people with Aicardi syndrome have an intellectual disability that makes it difficult to participate in an eye examination, it is difficult to measure vision accurately. [ 3 ]
Problems from the gastrointestinal tract are common, for example constipation, diarrhea and that the normal valve mechanism between the stomach and the esophagus (upper mouth of the stomach) does not work normally and the stomach contents therefore leak up into the esophagus (gastroesophageal reflux). Some may also have difficulty eating. [ 3 ]
Puberty may be entered earlier than normal , but delayed puberty has also been described. [ 3 ] Drooling and bruxism is common. [ 3 ]
Extra ribs or lack of ribs and vertebral deformities often occur. A crooked back ( scoliosis ) may develop while growing up. There are reports of isolated cases of tumors, especially brain tumors. [ 3 ]
Aicardi syndrome is a non-progressive condition and in itself does not lead to any deterioration, but various complications mean that there is an increased mortality associated with the syndrome. Very little is known about the long-term prognosis, but there are occasional reports that the epilepsy may become milder with increasing age. The oldest people with the syndrome described so far are in their 40s. [ 3 ]
A number of tumors have been reported in association with Aicardi syndrome: choroid plexus papilloma (the most common), medulloblastoma , gastric hyperplastic polyps, rectal polyps , soft palate benign teratoma , hepatoblastoma , parapharyngeal embryonal cell cancer, limb angiosarcoma and scalp lipoma . [ 4 ]
The syndrome is probably caused by a change (mutation) in one or more genes on the short arm of the X chromosome (Xp22), but which gene or genes are mutated is not yet (2015) known. [ 3 ]
Male fetuses with this change are unlikely to survive, which is because they only have one X chromosome. The individual boys with the syndrome described have also had the sex chromosome abnormality XXY syndrome (Klinefelter syndrome). Girls, who usually have two X chromosomes, can be born with the syndrome, because their second (normal) X chromosome compensates to some extent for the mutated gene. [ 3 ]
The mutation leads to a characteristic malformation of the brain stem with a complete absence of the corpus callosum . As a rule, there are also signs that groups of brain cells have migrated incorrectly and placed themselves in the wrong place in the brain ( heterotopias ), an incorrect folding of the cerebral cortex ( gyration abnormalities ) or that the brain hemispheres are of different size. [ 3 ]
Aicardi syndrome is an X-linked dominant disease and arises as a new mutation. The mutation has then usually occurred in one of the parents' germ cells (eggs or sperm). The probability that they will again have a child with the disease is then estimated at less than 1 percent. However, the new mutation in the child becomes hereditary and can theoretically be passed on to the next generation. [ 3 ] All cases of Aicardi syndrome are thought to be due to new mutations . No person with Aicardi syndrome is known to have transmitted the X-linked gene responsible for the syndrome to the next generation. [ 5 ]
Aicardi syndrome is typically characterized by the following triad of features - however, one of the "classic" features being missing does not preclude a diagnosis of Aicardi Syndrome, if other supporting features are present. [ 6 ]
Other types of defects of the brain such as microcephaly , polymicrogyria , porencephalic cysts and enlarged cerebral ventricles due to hydrocephalus are also common in Aicardi syndrome. [ citation needed ]
Suspicion of infantile spasms or other epileptic seizures during the first months of life should always be urgently investigated. There can be many different causes besides Aicardi syndrome. The investigation includes EEG (electroencephalogram), which in case of infantile spasms shows a characteristic pattern (hypsarrhythmia), magnetic resonance imaging (MRI) of the brain, blood and urine samples and examination of the spinal fluid (cerebrospinal fluid). [ 3 ]
In Aicardi syndrome, MRI of the brain shows that the cerebral cortex is completely or partially missing. Sometimes it is possible to see that the cerebral cortex is thin and underdeveloped. Other changes can occur at the same time, for example fluid bubbles (cysts) in the brain's fluid-producing structures (plexus choriodeus), different sized brain hemispheres and islands of nerve cells that did not migrate to the right place in the brain during fetal development. It is also possible to see that the fold pattern on the surface of the cerebrum has a different appearance (polygyry, microgyry). Absence of the cerebral cortex and other malformations of the brain also occur in conditions other than Aicardi syndrome. [ 3 ]
On eye examination, the retinal lacunae appear as white spots in the fundus, where the retina is missing. Sometimes there are slits in the eye (coloboma), retinal detachment and abnormally small or differently sized eyes. [ 3 ]
When X-raying the skeleton, it is sometimes possible to see that there are vertebral changes and extra ribs or that ribs are missing. [ 3 ]
Treatment of Aicardi syndrome primarily involves management of seizures and early/continuing intervention programs for developmental delays. [ citation needed ] Additional comorbidities and complications sometimes seen with Aicardi syndrome include porencephalic cysts and hydrocephalus , and gastro-intestinal problems. Treatment for porencephalic cysts and/or hydrocephalus is often via a shunt or endoscopic fenestration of the cysts, though some require no treatment. Placement of a feeding tube , fundoplication, and surgeries to correct hernias or other gastrointestinal structural problems are sometimes used to treat gastro-intestinal issues. [ citation needed ]
Children with Aicardi syndrome come into contact with many different specialists in healthcare early on. It is therefore important that efforts are coordinated. [ 3 ]
The drug treatment given for infantile spasms and other types of epilepsy is also given in cases of Aicardi syndrome. Epilepsy is often difficult to treat. [ 3 ]
If medication does not help, after an examination at a regional hospital, a decision can be made as to whether another treatment may be appropriate. Since the cause of the epileptic seizures is found in many different places in the brain, however, epilepsy surgery is rarely an option in Aicardi syndrome. [ 3 ]
Treatment with a ketogenic diet may be considered. It involves a carefully calculated diet that is rich in fat, contains a minimum of carbohydrates and provides the daily need for protein. The excess of fat forms starvation bodies (ketones) which can be used instead of glucose as a fuel source for the metabolism in the brain. For some children, this leads to fewer seizures. Treatment is started at regional hospitals by special teams with doctors, nurses and dieticians. [ 3 ]
Another treatment option when the drug treatment of the epilepsy does not help is a so-called vagus nerve stimulator (VNS). The vagus nerve is one of twelve nerves that originate directly from the brain (cranial nerves). A small battery-powered box (generator) is operated under the skin under the left collarbone and a thin wire (electrode) from the generator is operated around the left vagus nerve. The generator is then set so that it sends electrical impulses to the brain via the vagus nerve at fixed intervals and fixed strength, which can be gradually increased if necessary. This can lead to a reduction in the number and strength of the seizures but almost never results in the seizures disappearing completely. This treatment is also started and followed up at the regional hospitals. [ 3 ]
It is important that the child's eyesight is used in the best possible way, and should therefore be examined by a pediatric ophthalmologist at an early stage to investigate visual function and the need for visual aids. [ 3 ]
Problems from the gastrointestinal tract need to be investigated and can be treated with medication. If there is difficulty eating, nutrition may need to be received via a nasal tube or a so-called button (PEG, percutaneous endoscopic gastrostomy), an operatively created connection to the stomach via the abdominal wall. It is important to closely monitor the child's growth. [ 3 ]
Preventive dental care and contact with a children's dental care specialist (pedodontist) is needed, as the child may find it difficult to participate in tooth brushing and dental treatments. [ 3 ]
Due to the risk of developing scoliosis, the back should be examined regularly. Scoliosis is primarily treated with a brace but may sometimes require surgery. [ 3 ]
Children with Aicardi syndrome need rehabilitation interventions that also include vision rehabilitation. A habilitation team includes professional categories with special knowledge of disabilities and their effects on everyday life, health and development. The interventions take place in the medical, educational, psychological, social and technical fields. They consist, among other things, of investigation, treatment, testing of assistive devices, information about the disability and conversational support. Information about society's support and advice on adapting the home and other environments in which the child lives is also given. Parents, siblings and other relatives also receive support. The family may need help with the coordination of various efforts. [ 3 ]
The interventions are planned based on the needs of the child and the family, vary over time and always take place in close collaboration with people in the child's network. In order to develop the ability to communicate, it is important to work early on with educational efforts as well as alternative and supplementary communication routes (AKK). [ 3 ]
A close collaboration takes place with the municipality, which can offer various forms of interventions to facilitate the family's everyday life. Personal assistance can be given to those who, due to severe and permanent disabilities, need help with basic needs, but also to expand the possibility of an active life despite extensive disabilities. Respite care, a contact family or short-term accommodation are other examples of support measures. [ 3 ]
Adults with Aicardi syndrome need continued habilitation efforts and support in daily life. This could be, for example, support and care in a home with special services and daily activities. [ 3 ]
The prognosis varies widely from case to case, depending on the severity of the symptoms. However, almost all people reported with Aicardi syndrome to date have experienced developmental delay of a significant degree, typically resulting in mild to moderate to profound intellectual disability . The age range of the individuals reported with Aicardi syndrome is from birth to the mid-40s. [ citation needed ]
There is no cure for this syndrome. [ 7 ]
Worldwide prevalence of Aicardi syndrome is estimated at several thousand, with approximately 900 cases reported in the United States. [ 8 ] There is no definite information on how common Aicardi syndrome is, but the incidence is estimated to be around one in 100,000 newborns. There may be people who do not have the fully developed syndrome and who have not been diagnosed. [ 3 ]
This disorder was first recognized as a distinct syndrome in 1965 by Jean Aicardi , a French pediatric neurologist and epileptologist . [ 9 ] [ 6 ]
This article incorporates text that is in the public domain under the Swedish URL §9 (1960:729) as a constitution, decision or statement by Swedish authorities.
|
https://en.wikipedia.org/wiki/Aicardi_syndrome
|
Ainhum (from Portuguese , pronounced [aj.ˈɲũ] [ 1 ] ), also known as dactylolysis spontanea , [ 2 ] is a painful constriction of the base of the fifth toe frequently followed by bilateral spontaneous autoamputation a few years later.
The groove begins on the lower and internal side of the base of the fifth toe, usually according to the plantar-digital fold. The groove becomes gradually deeper and more circular. The rate of spread is variable, and the disease may progress to a full circle in a few months, or still be incomplete after years. In about 75 percent of cases both feet are affected, though not usually to the same degree. [ 2 ] There is no case reported where it begins in any other toe than the fifth, while there is occasionally a groove on the fourth or third toe. The distal part of the toe swells and appears like a small potato. The swelling is due to lymphatic edema distal to the constriction. After a time crusts can appear in the groove which can be infected with staphylococcus .
While the groove becomes deeper, compression of tendons, vessels and nerves occurs. Bone is absorbed by pressure, without any evidence of infection. After a certain time all structures distal the stricture are reduced to an avascular cord. The toe’s connection to the foot becomes increasingly slender, and if it is not amputated, it spontaneously drops off without any bleeding. Normally it takes about five years for an autoamputation to occur.
Cole describes four stages of ainhum:
Pain is present in about 78% of cases. Slight pain is present in the earliest stage of ainhum, caused by pressure on the underlying nerves. Fracture of the phalanx or chronic sepsis is accompanied with severe pain.
The true cause of ainhum remains unclear. It is not due to infection by parasites , fungi , bacteria or virus , and it is not related to injury. Walking barefoot in childhood had been linked to this disease, but ainhum also occurs in patients who have never gone barefoot. Race seems to be one of the most predisposing factors and it may have a genetic component, since it has been reported to occur within families. Dent et al. discussed a genetically caused abnormality of the blood supply to the foot. It has been related to inadequate posterior tibial artery circulation and absence of plantar arch . [ 2 ]
Histology shows a change in the prickle cell layer, and this is responsible for the laying down of condensed keratin causing the groove. The junctional tissue is reduced to a slender fibrous thread, almost avascular, and all the tissues beyond the constricting band is repressed by a fibro-fatty mass covered by hyperkeratotic integument.
Soft tissue constriction on the medial aspect of the fifth toe is the most frequently presented radiological sign in the early stages. Distal swelling of the toe is considered to be a feature of the disease. In grade III lesions osteolysis is seen in the region of the proximal interphalangeal joint with a characteristic tapering effect. Dispersal of the head of the proximal phalanx is frequently seen. Finally, after autoamputation, the base of the proximal phalanx remains. Radiological examination allows early diagnosis and staging of ainhum. Early diagnosis is crucial to prevent amputation. Doppler shows decreased blood flow in posterior tibial artery.
Ainhum is an acquired and progressive condition, and thus differs from congenital annular constrictions. Ainhum has been much confused with similar constrictions caused by other diseases such as leprosy , diabetic gangrene , syringomyelia , scleroderma or Vohwinkel syndrome . In this case, it is called pseudo-ainhum , treatable with minor surgery or intralesional corticosteroids, as with ainhum. [ 3 ] It has even been seen in psoriasis or it is acquired by the wrapping toes, penis or nipple with hairs, threads or fibers. [ 4 ] Oral retinoids, such as tretinoin, and antifibrotic agents like tranilast have been tested for pseudo-ainhum. [ 2 ] Impending amputation in Vohwinkel syndrome can sometimes be aborted by therapy with oral etretinate. [ 4 ] It is rarely seen in the United States but often discussed in the international medical literature. [ 5 ]
Wearing shoes to protect barefoot trauma has shown decrease in incidence in ainhum. Congenital pseudoainhum cannot be prevented and can lead to serious birth defects. [ 4 ]
Incisions across the groove turned out to be ineffective. Excision of the groove followed by z-plasty could relieve pain and prevent autoamputation in Grade I and Grade II lesions. Grade III lesions are treated with disarticulating the metatarsophalangeal joint. This also relieves pain, and all patients have a useful and stable foot. Intralesional injection of corticosteroids is also helpful. [ 2 ]
Ainhum is an extremely rare disease with prevalence reported between 0.015% and 2.2% of the population. [ 6 ] [ 7 ] Ainhum occurs worldwide, but is most common in people of sub-Saharan African origin. It is more common in men than in women (2:1) between 20 and 50 years of age. [ 2 ] The average age is about thirty-eight. The youngest recorded patient was seven years old. Ainhum is often familial. [ 8 ]
The first description of ainhum in the West appears to have been provided by English surgeon Robert Clarke, who made a passing reference to "dry gangrene of the little toe" as a common occurrence in the Gold Coast in an 1860 report to the Epidemiological Society of London , but did not recognize it as a distinct entity and believed it to be a consequence of "suppressed yaws ". [ 9 ] [ 10 ] [ 11 ] Ainhum was first recognized as a distinct disease and described as such in detail by Brazilian physician José Francisco da Silva Lima (1826–1910), in 1867. [ 9 ] [ 11 ] [ 12 ] The name "ainhum" (from the Yoruba ayùn , meaning "to saw" or "to file") was used to refer to the disease by Yoruba speakers in Bahia , Brazil, where Silva Lima practiced. [ 9 ] [ 11 ] [ 12 ]
The first histological studies of ainhum were conducted by O. E. H. Wucherer and published in 1872, and the first imaging studies were conducted in 1924. [ 9 ]
|
https://en.wikipedia.org/wiki/Ainhum
|
Air abrasion is a dental technique that uses compressed air to propel a thin stream of abrasive particles—often aluminum oxide or silica —through a specialized hand-piece to remove tooth tissue and decay before being suctioned away, similar to sand blasting . It can be used in a variety of dental procedures, including removing tooth decay , stains, and old restorations , as well as to prepare teeth for new restorations, sealants , and bonding . [ 1 ] [ 2 ] [ 3 ] [ 4 ]
Advantages of air abrasion include that it preserves more healthy tooth tissue (which can increase the strength and longevity of restorations), and has less risk of fracturing or chipping a tooth when compared to a traditional pneumatic dental drill . Air abrasion generates minimal noise, vibration, pressure, and heat, all of which can increase patient comfort and reduce or eliminate the need for local anesthesia . [ 1 ] [ 2 ] [ 3 ] [ 4 ]
Disadvantages of air abrasion include not being appropriate for removing decay in all situations (such as deep decay or decay between teeth) and the initial investment costs of an air abrasion system. [ 1 ] [ 2 ] [ 4 ] Additionally, there are some concerns related to the possible health effects of inhaling abrasive particles (including possible aggravation of certain medical conditions such as asthma and chronic obstructive pulmonary disease ) [ 2 ] and clean-up concerns. Risks related to inhaling abrasive particles can be minimized by using a dental dam , appropriate suction, and combining water into the air abrasive steam. [ 2 ] [ 5 ] [ 6 ] [ 7 ]
In the 1940s, dentist Robert Black began researching air abrasion technology and its use in dentistry. In 1951, Black and the S.S. White Dental Manufacturing Co. released the first commercial dental air abrasion system, the Airdent air abrasion unit. [ 6 ] [ 8 ] [ 9 ] The unit failed to gain wide popularity due to several factors, including the inability of air abrasion to prepare the well-defined margins and walls needed for the amalgam restorations used at the time, the lack of high-velocity suction available for powder control, and the introduction of the time-saving air turbine drill. Air abrasion began to resurface in the 1990s with the rise of adhesive dentistry. [ 2 ] [ 6 ]
|
https://en.wikipedia.org/wiki/Air_abrasion
|
An Akers' clasp is the classic direct retainer for removable partial dentures . [ 1 ] Named after its inventor, Polk E. Akers, this suprabulge clasp consists of a rest, a guide plate, a retentive arm and a reciprocal arm. Akers' clasps, as a rule, face away from an edentulous area. Should they face the edentulous area, they are termed reverse Akers' clasps. [ citation needed ]
It is the most simple and versatile clasp (clasp of choice in tooth-borne cases). Clasp assembly has one retentive arm opposed to a reciprocal arm originating from the rest. The retentive arm begins above the height of contour, and curves and tapers to its terminal tip, in the gingival 1/3 of the tooth, well away from the gingiva . The bracing arm is in the middle 1/3 of the tooth, and is broader occluso-gingivally, does not taper and is either entirely above the height of contour or completely on a prepared guiding plane – it should never be designed into an undercut, as it is a rigid element. [ citation needed ]
This dentistry article is a stub . You can help Wikipedia by expanding it .
|
https://en.wikipedia.org/wiki/Akers'_clasp
|
Alacrite (also known as Alloy L-605 , Cobalt L-605 , Haynes 25 , and occasionally F90 [ 1 ] [ 2 ] [ 3 ] ) is a family of cobalt -based alloys . The alloy exhibits useful mechanical properties and is oxidation- and sulfidation -resistant. [ 2 ]
One member of the family, XSH Alacrite, [ 4 ] is described as "a non-magnetic, stainless super-alloy whose high surface hardness enables one to achieve a mirror quality polish." [ 5 ] The Institut National de Métrologie in France has also used the material as a kilogram mass standard. [ 5 ] [ 6 ]
L-605 is composed primarily of cobalt (Co), with a specified mixture of chromium (Cr), tungsten (W), nickel (Ni), iron (Fe) and carbon (C), as well as small amounts of manganese (Mn), silicon (Si), and phosphorus (P). The tungsten and nickel improve the alloy's machinability, [ 3 ] while chromium contributes to its solid-solution strengthening. [ 2 ] The following tolerances must be met to be considered an L-605 alloy: [ 1 ] [ 2 ] [ 4 ] [ 6 ]
The alloy was originally developed for application in aircraft, [ 6 ] including combustion chambers, liners, afterburners and the hot section of gas turbines. It has also been used in aerospace components and turbine engines as well as drug-eluting and other kinds of stents due to its biocompatibility . [ 2 ] When used for implantable medical devices , the ASTM F90-09 and ISO 5832-5:2005 specifications dictate how L-605 is manufactured and tested. [ 2 ] [ 3 ] [ 7 ] [ 8 ]
This alloy-related article is a stub . You can help Wikipedia by expanding it .
|
https://en.wikipedia.org/wiki/Alacrite
|
Alan Bray OAM is an Australian vascular surgeon . [ 1 ]
Born in Newcastle on 10 May 1942, Bray graduated in medicine from Sydney University in 1966. [ 2 ] He was awarded a Doctor of Medicine by the University of Western Australia for his thesis, "Immunity to a murine melanoma" in 1976. [ 3 ]
Bray is known for the introduction and postgraduate teaching of vascular ultrasound in Australia, for which he received the Lifetime Achievement Award from the Australasian College of Phlebology . [ 4 ] He was part of the first group of surgeons to form the International Society of Endovascular Surgery . [ 2 ]
In 2018, he was awarded an Order of Australia Medal for his contribution to medicine, particularly vascular surgery . [ 5 ] [ 6 ]
This biographical article related to medicine in Australia is a stub . You can help Wikipedia by expanding it .
This surgery article is a stub . You can help Wikipedia by expanding it .
|
https://en.wikipedia.org/wiki/Alan_Edward_Bray
|
Alarplasty (or, less commonly, alaplasty ) is a plastic surgery procedure in which a wedge of the wing of the nose is removed in order to alter the shape of the nostrils . [ 1 ] [ 2 ] Alarplasty may be used to increase or decrease the width of the nostrils, for either cosmetic or functional reasons. [ 3 ] [ 4 ] In humans it may also make the nose perceptibly narrower. [ 3 ]
Temporary swelling is a common consequence of alarplasty. [ 3 ]
This surgery article is a stub . You can help Wikipedia by expanding it .
|
https://en.wikipedia.org/wiki/Alarplasty
|
The Albany Medical Center Prize in Medicine and Biomedical Research [ 1 ] is the United States ' second highest value prize in medicine and biomedical research , awarded by the Albany Medical Center . Among prizes for medicine worldwide, the Albany Medical Center Prize is the fourth most lucrative (after the $3 million Breakthrough Prize in Life Sciences , the $1.2 million Nobel Prize in Medicine and the $1 million Shaw Prize in life science and medicine ). [ 2 ]
Awarded annually, the $500,000 prize is bestowed to any physician or scientist, or group, whose work has led to significant advances in the fields of health care and scientific research with demonstrated translational benefits applied to improved patient care.
The prize is a legacy to its founder, the late Morris "Marty" Silverman . At the inaugural awards ceremony in Albany, NY in March 2001, Silverman started a tradition that will be carried on for one hundred years, the duration of the Prize. Silverman's promise was to light one candle each year to honor that year's recipient.
2024: Press Release
2023: Press Release [ 3 ]
2022: Press Release [ 4 ]
2021: Press Release [ 5 ]
2020:
2019: Press Release
2018: Press Release
2017: Press Release
2016: Press Release
2015: Press Release
2014: Press Release
2013: Press Release
2012: Press Release
2011: Press Release
2010: Press Release
2009: Press Release
2008: Press Release
2007: Press Release
2006: Press Release
2005: Press Release
2004:
2003:
2002:
2001:
|
https://en.wikipedia.org/wiki/Albany_Medical_Center_Prize
|
Since 1994, the Albert B. Sabin Gold Medal has been awarded annually by the Sabin Vaccine Institute in recognition of work in the field of vaccinology or a complementary field. It is in commemoration of the pioneering work of Albert B. Sabin . [ 1 ]
|
https://en.wikipedia.org/wiki/Albert_B._Sabin_Gold_Medal
|
Albert Dietrich (4 March 1873 – 1 September 1961) was a German pathologist .
Albert Dietrich was born on 4 March 1873 in Schweidnitz , Province of Silesia . A graduate in medicine , after years as an assistant and subsequent habilitation in pathology in 1906, he received a professorship in pathology at the University of Tübingen . In 1916, he moved to the same professorship at the University of Cologne , until he returned to Tübingen in 1928 to take up the chair of pathology again. Additionally, he served as rector there in the academic years 1933 and 1934. [ 1 ] Dietrich, editor of the Journal for Cancer Research from 1933 to 1944, [ 2 ] chairman of the German Central Committee for Cancer Control and Cancer Research from 1951 to 1955, [ 3 ] was honored in 1952 as one of the first doctors for his contributions to cancer research with the Paracelsus Medal. [ 4 ]
Dietrich focused scientifically on pathological anatomy, experimental pathology, and microbiology . He concentrated his work on the research of malignant tumors , infectious diseases , and thrombosis .
Dietrich was a member of the Burschenschaft Palatia Tübingen in the ADB, [ 5 ] today known as the Old Turnerschaft Palatia Tübingen . [ 6 ] In 1936, he was elected a member of the Leopoldina .
He died on 1 September 1961 in Stuttgart . [ citation needed ]
|
https://en.wikipedia.org/wiki/Albert_Dietrich_(pathologist)
|
Albert H. Ketcham (August 3, 1870 – December 5, 1935) was an American orthodontist and a past president of the American Society of Orthodontists .
He was born in Whiting, Vermont , and attended high school at Vermont Academy , Saxtons River. In 1892, Albert graduate from Boston Dental College and then served as a clinical instructor until 1895. In 1894 he married Mary E. Hickson and had two children, Arthur and May. He later married Flora B. Smith and moved to Colorado after contracting pulmonary tuberculosis. [ 1 ]
Ketcham was a student of Edward Angle at his Angle School of Orthodontia . He graduated from the school in 1902 and practiced in Colorado until his death. [ 2 ] He published more than 40 articles in the Dental and Orthodontic journals between 1902 and 1935. Ketcham served as the first president of the American Society of Orthodontists from 1928 to 1929. He led the pioneering effort to make sure that members also joined local, state, or national dental societies such as the American Dental Association . [ 1 ]
In 1935, he died due to bronchial pneumonia in Denver . [ 2 ] In the year after his death, the American Board of Orthodontics created the Albert H. Ketcham Award to commemorate Ketcham's achievements. [ 3 ] This award is currently known has the highest achievement award given in the field of Orthodontics.
This dentistry article is a stub . You can help Wikipedia by expanding it .
This biographical article related to medicine in the United States is a stub . You can help Wikipedia by expanding it .
|
https://en.wikipedia.org/wiki/Albert_H._Ketcham
|
Albert Wojciech Adamkiewicz ( Polish: [adamˈkʲɛvit͡ʂ] ; 11 August 1850 – 31 October 1921) was a Polish pathologist .
Adamkiewicz was born in Żerków . [ 1 ] He earned his medical doctorate in 1873 from the University of Breslau where he was a student-assistant to physiologist Rudolf Peter Heinrich Heidenhain . From 1879 until 1892, he was chief of general and experimental pathology at the Jagiellonian University in Kraków . [ 2 ]
Adamkiewicz is remembered for his pathological examinations of the central nervous system . His research of the variable vascularity of the spinal cord was an important contribution to the development of modern clinical vascular surgery . He is credited with describing the major anterior segmental medullary artery , which is also known as the Artery of Adamkiewicz . [ 2 ]
In the early 1890s, Adamkiewicz published a series of articles claiming the discovery of a cancer-causing parasite he called Coccidium sarcolytus , as well as the existence of an anti-cancer serum . Further testing proved the serum a failure, and Adamkiewicz was severely criticized by the medical community at Jagiellonian University. Soon afterwards, he relocated to Vienna , where he practiced medicine at Rothschild Hospital . [ 2 ]
He is credited for the creation of the Adamkiewicz test , a test for detecting tryptophan , an α- amino acid that is used in the biosynthesis of proteins .
This article related to pathology is a stub . You can help Wikipedia by expanding it .
This biographical article related to medicine in Poland is a stub . You can help Wikipedia by expanding it .
|
https://en.wikipedia.org/wiki/Albert_Wojciech_Adamkiewicz
|
The Alberta Dental Association and College ( ADA&C ) gives leadership to the dental profession on professional regulations and member services. It provides the public with information and services, to ensure that Albertans receive safe, appropriate, ethical and quality dental care as an integral part of general health.
The ADA&C is a regulatory college which was established in 1906, after the formation of the Province of Alberta . It was called the Alberta Dental Association before 2001. Prior to 1906, the dental profession was regulated by the Northwest Territories Act.
Each dentist practicing in the Province of Alberta is required to follow the Code of Ethics. [ 1 ]
This dentistry article is a stub . You can help Wikipedia by expanding it .
This article about a professional association is a stub . You can help Wikipedia by expanding it .
|
https://en.wikipedia.org/wiki/Alberta_Dental_Association_and_College
|
Albin Oppenheim (January 8, 1875 – November 20, 1945) was an American orthodontist who contributed significantly towards understanding in orthodontics about the biology of tooth movement. [ 1 ]
Oppenheim was born in Brno , Moravia , and received education in that part of Austria-Hungary. He went to Karl Ferdinand's University, Prague in 1899 to earn his Medical Degree. He then went to Berlin Dentalpoliclinic to earn his Dental Degree in 1904. He then practiced with Dr. Weiser in Vienna at his practice until 1914. During World War I, he served as head of Army Hospital and in 1915 was appointed Privatdozent on Head of Orthodontics Department at University of Vienna. In 1938, Oppenheim went to Geneva, Switzerland because of the political tensions of World War II. He moved to the US in 1939 after getting an appointment as a faculty at University of Southern California.
His introduction to Edward Angle happened when he gave lectures at Angle School of Orthodontia when it was in New London, Connecticut. After spending some time in US, Dr. Oppenheim along with Grunberg went back to Europe and brought back teachings of Angle to several institutions.
One of his articles Tissue Changes, Particularly of the Bone, Incident to Tooth Movement was published in Angel Orthodontist in 1911. In this publication, Dr. Oppenheim showed the movement of teeth happens due to complete reorganization of the involved bone tissue. [ 1 ] He also showed that pull that happens from ligatures on a heavy base wire acts like a lever instead of a post in the ground. [ 2 ] In subsequent publications later on, Dr. Oppenheim proposed that using gentle forces with long intervals of rest between had many advantages in Orthodontics. [ 3 ]
Oppenheim died in Hollywood, California, on November 20, 1945.
This dentistry article is a stub . You can help Wikipedia by expanding it .
This biographical article related to medicine in the United States is a stub . You can help Wikipedia by expanding it .
|
https://en.wikipedia.org/wiki/Albin_Oppenheim
|
The Albrecht Kossel Institute for Neuroregeneration is a medical research hospital located in Rostock , Germany . It was formed from the neurobiological laboratory of the hospital for neurology at the University of Rostock , [ 1 ] and it operates under the auspices of The University Clinic of Rostock. [ 2 ]
The institute conducts research into rare congenital metabolic illnesses such as Fabry's disease and Gaucher's disease . It enjoys worldwide recognition as a diagnostic and treatment center for rare illnesses. [ 1 ] Its stated area of research is neuroregeneration , the regrowth or repair of nervous tissues and cells .
The institute is named for Albrecht Kossel , noted German biochemist , 1910 Nobel laureate in Physiology or Medicine , and graduate of the university.
In 2007, the Institute initiated Sifap , a Pan- European study dedicated to investigating the correlation of juvenile stroke and a genetic disorder known as Fabry's disease . [ 3 ] The institute will engage in professional cooperation with international partners in the fields of economics, science and research. The expected results are an improved understanding into the nature of juvenile stroke, and improvement in its therapeutic treatment. [ 1 ]
The institute works in close cooperation with national and international universities in the context of scientific cooperatives . The institute participates in LEUKONET, the German Leukodystrophy network, which is run by the German Federal Ministry of Education and Research . [ 1 ]
The Institute participates in and promotes the EuroStemCell project, an initiative of the Framework Programmes for Research and Technological Development by the European Commission . In 2008, it hosted the 5th International Stem Cell School in Regenerative Medicine, an international academic conference . [ 4 ]
The institute also participates in the Graduiertenkolleg , a means of providing advanced training to medical researchers. [ 1 ]
The institute is one of only a few medical facilities in Germany that is authorized by the government to conduct human embryonic stem cell research. [ 1 ]
|
https://en.wikipedia.org/wiki/Albrecht_Kossel_Institute_for_Neuroregeneration
|
Alcohol withdrawal syndrome ( AWS ) is a set of symptoms that can occur following a reduction in or cessation of alcohol use after a period of excessive use. [ 1 ] Symptoms typically include anxiety , shakiness , sweating, vomiting, fast heart rate , and a mild fever. [ 1 ] More severe symptoms may include seizures , and delirium tremens (DTs); which can be fatal in untreated patients. [ 1 ] Symptoms start at around 6 hours after the last drink. [ 2 ] Peak incidence of seizures occurs at 24 to 36 hours [ 5 ] and peak incidence of delirium tremens is at 48 to 72 hours. [ 6 ]
Alcohol withdrawal may occur in those who are alcohol dependent . [ 1 ] This may occur following a planned or unplanned decrease in alcohol intake. [ 1 ] The underlying mechanism involves a decreased responsiveness of GABA receptors in the brain. [ 3 ] The withdrawal process is typically followed using the Clinical Institute Withdrawal Assessment for Alcohol scale (CIWA-Ar). [ 3 ]
The typical treatment of alcohol withdrawal is with benzodiazepines such as chlordiazepoxide or diazepam . [ 2 ] Often the amounts given are based on a person's symptoms. [ 2 ] Thiamine is recommended routinely. [ 2 ] Electrolyte problems and low blood sugar should also be treated. [ 2 ] Early treatment improves outcomes. [ 2 ]
In the Western world about 15% of people have problems with alcoholism at some point in time. [ 3 ] Alcohol depresses the central nervous system, slowing cerebral messaging and altering the way signals are sent and received. Progressively larger amounts of alcohol are needed to achieve the same physical and emotional results. The drinker eventually must consume alcohol just to avoid the physical cravings and withdrawal symptoms. About half of people with alcoholism will develop withdrawal symptoms upon reducing their use, with four percent developing severe symptoms. [ 3 ] Among those with severe symptoms up to 15% die. [ 2 ] Symptoms of alcohol withdrawal have been described at least as early as 400 BC by Hippocrates . [ 7 ] [ 8 ] It is not believed to have become a widespread problem until the 1700s. [ 8 ]
Signs and symptoms of alcohol withdrawal occur primarily in the central nervous system. The severity of withdrawal can vary from mild symptoms such as insomnia, trembling, and anxiety to severe and life-threatening symptoms such as alcoholic hallucinosis , delirium tremens , and autonomic instability . [ 9 ] [ 10 ]
Withdrawal usually begins 6 to 24 hours after the last drink. [ 11 ] Symptoms are worst at 24 to 72 hours, and improve by seven days. [ 2 ] [ 3 ] To be classified as alcohol withdrawal syndrome, patients must exhibit at least two of the following symptoms: increased hand tremor, insomnia, nausea or vomiting, transient hallucinations (auditory, visual or tactile), psychomotor agitation , anxiety, generalized tonic–clonic seizures , and autonomic instability. [ 12 ]
The severity of symptoms is dictated by a number of factors, the most important of which are degree of alcohol intake, length of time the individual has been using alcohol, and previous history of alcohol withdrawal. [ 12 ] [ 13 ] Symptoms are also grouped together and classified:
Six to 12 hours after the ingestion of the last drink, withdrawal symptoms such as shaking, headache, sweating, anxiety, nausea or vomiting may occur. [ 15 ] Twelve to 24 hours after cessation, the condition may progress to such major symptoms as confusion, hallucinations [ 15 ] (with awareness of reality), while less severe symptoms may persist and develop including tremor, agitation, hyperactivity and insomnia. [ 13 ]
At 12 to 48 hours following the last ethanol ingestion, the possibility of generalized tonic–clonic seizures should be anticipated, occurring in 3–5% of cases. [ 13 ] Meanwhile, none of the earlier withdrawal symptoms will typically have abated. Seizures carry the risk of major complications and death for individuals with an alcohol use disorder. [ 16 ] [ 13 ]
Although the person's condition usually begins to improve after 48 hours, withdrawal symptoms sometimes continue to increase in severity and advance to the most severe stage of withdrawal, delirium tremens . This occurs in 5–20% of patients experiencing detoxification and one third of untreated cases, [ 14 ] [ 13 ] which is characterized by hallucinations that are indistinguishable from reality, severe confusion, seizures, high blood pressure, and fever that can persist anywhere from 4 to 12 days. [ 15 ]
A protracted alcohol withdrawal syndrome occurs in many with Alcohol Use Disorder (AUD) when withdrawal symptoms continue beyond the acute withdrawal stage but usually at a subacute level of intensity and gradually decreasing with severity over time. This syndrome is sometimes referred to as the post-acute-withdrawal syndrome . Some withdrawal symptoms can linger for at least a year after discontinuation of alcohol. Symptoms can include a craving for alcohol, inability to feel pleasure from normally pleasurable things (known as anhedonia ), clouding of sensorium , disorientation, nausea and vomiting or headache. [ 17 ]
Insomnia is a common protracted withdrawal symptom that persists after the acute withdrawal phase of alcohol. Insomnia has also been found to influence relapse rate. Studies have found that magnesium or trazodone can help treat the persisting withdrawal symptom of insomnia in AUD recovery. Insomnia can be difficult to treat in these individuals because many of the traditional sleep aids (e.g., benzodiazepine receptor agonists and barbiturate receptor agonists) work via a GABA A receptor mechanism and are cross-tolerant with alcohol. However, trazodone is not cross-tolerant with alcohol. [ 18 ] [ 19 ] [ 20 ] The acute phase of the alcohol withdrawal syndrome can occasionally be protracted. Protracted delirium tremens has been reported in the medical literature as a possible but unusual feature of alcohol withdrawal. [ 21 ]
Chronic use of alcohol leads to changes in brain chemistry especially in the GABAergic system. Various adaptations occur such as changes in gene expression and down regulation of GABA A receptors . During acute alcohol withdrawal, changes also occur such as upregulation of alpha4 containing GABA A receptors and downregulation of alpha1 and alpha3 containing GABA A receptors. Neurochemical changes occurring during alcohol withdrawal can be minimized with drugs which are used for acute detoxification. With abstinence from alcohol and cross-tolerant drugs these changes in neurochemistry may gradually return towards normal. [ 22 ] [ 23 ] Adaptations to the NMDA system also occur as a result of repeated alcohol intoxication and are involved in the hyper-excitability of the central nervous system during the alcohol withdrawal syndrome. Homocysteine levels, which are elevated during chronic drinking, increase even further during the withdrawal state, and may result in excitotoxicity . [ 24 ] Alterations in ECG (in particular an increase in QT interval ) and EEG abnormalities (including abnormal quantified EEG) may occur during early withdrawal. [ 24 ] Dysfunction of the hypothalamic–pituitary–adrenal axis and increased release of corticotropin-releasing hormone occur during both acute as well as protracted abstinence from alcohol and contribute to both acute and protracted withdrawal symptoms. Anhedonia / dysphoria symptoms, which can persist as part of a protracted withdrawal , may be due to dopamine underactivity. [ 25 ]
Kindling is a phenomenon where repeated alcohol detoxifications leads to an increased severity of the withdrawal syndrome. For example, binge drinkers may initially experience no withdrawal symptoms, but with each period of alcohol use followed by cessation, their withdrawal symptoms intensify in severity and may eventually result in full-blown delirium tremens with convulsive seizures. Alcoholics who experience seizures during detoxification are more likely to have had previous episodes of alcohol detoxification than patients who did not have seizures during withdrawal. In addition, people with previous withdrawal syndromes are more likely to have more medically complicated alcohol withdrawal symptoms. [ 26 ]
Kindling can cause complications and may increase the risk of relapse, alcohol-related brain damage and cognitive deficits. Chronic alcohol misuse and kindling via multiple alcohol withdrawals may lead to permanent alterations in the GABA A receptors. [ 27 ] The mechanism behind kindling is sensitization of some neuronal systems and desensitization of other neuronal systems which leads to increasingly gross neurochemical imbalances. This in turn leads to more profound withdrawal symptoms including anxiety , convulsions and neurotoxicity . [ 26 ]
Binge drinking is associated with increased impulsivity, impairments in spatial working memory and impaired emotional learning. These adverse effects are believed to be due to the neurotoxic effects of repeated withdrawal from alcohol on aberrant neuronal plasticity and cortical damage. Repeated periods of acute intoxication followed by acute detoxification has profound effects on the brain and is associated with an increased risk of seizures as well as cognitive deficits. The effects on the brain are similar to those seen in alcoholics who have detoxified repeatedly but not as severe as in alcoholics who have no history of prior detox. Thus, the acute withdrawal syndrome appears to be the most important factor in causing damage or impairment to brain function. The brain regions most sensitive to harm from binge drinking are the amygdala and prefrontal cortex . [ 28 ]
People in adolescence who experience repeated withdrawals from binge drinking show impairments of long-term nonverbal memory. Alcoholics who have had two or more alcohol withdrawals show more frontal lobe cognitive dysfunction than those who have experienced one or no prior withdrawals. Kindling of neurons is the proposed cause of withdrawal-related cognitive damage. Kindling from repeated withdrawals leads to accumulating neuroadaptive changes. Kindling may also be the reason for cognitive damage seen in binge drinkers. [ 29 ]
Many hospitals use the Clinical Institute Withdrawal Assessment for Alcohol (CIWA) protocol in order to assess the level of withdrawal present and therefore the amount of medication needed. [ 12 ] When overuse of alcohol is suspected but drinking history is unclear, testing for elevated values of carbohydrate-deficient transferrin or gammaglutamyl transferase can help make the diagnosis of alcohol overuse and dependence more clear. The CIWA has also been shortened (now called the CIWA-Ar), while retaining its validity and reliability, to help assess patients more efficiently due to the life-threatening nature of alcohol withdrawal. [ 30 ]
Benzodiazepines are effective for the management of symptoms as well as the prevention of seizures. [ 31 ] Certain vitamins are also an important part of the management of alcohol withdrawal syndrome. In those with severe symptoms inpatient care is often required. [ 11 ] In those with lesser symptoms treatment at home may be possible with daily visits with a health care provider. [ 11 ]
Cohort studies have demonstrated that the combination of anticonvulsants and benzodiazepines is more effective than other treatments in reducing alcohol withdrawal scores and shortening the duration of intensive care unit stays. [ 32 ]
Benzodiazepines are the most commonly used medication for the treatment of alcohol withdrawal and are generally safe and effective in suppressing symptoms of alcohol withdrawal. [ 33 ] This class of medication is generally effective in symptoms control, but needs to be used carefully. Although benzodiazepines have a long history of successfully treating and preventing withdrawal, there is no consensus on the ideal one to use. The most commonly used agents are long-acting benzodiazepines, such as chlordiazepoxide and diazepam . These are believed to be superior to other benzodiazepines for treatment of delirium and allow for longer periods between doses. However, benzodiazepines with intermediate half-lives like lorazepam may be safer in people with liver problems. [ 34 ] Benzodiazepines showed a protective benefit against alcohol withdrawal symptoms, in particular seizure, compared to other common methods of treatment. [ 35 ]
The primary debate between use of long-acting benzodiazepines and short-acting is that of ease of use. Longer-acting drugs, such as diazepam, can be administered less frequently. However, evidence does exist that "symptom-triggered regimens" such as those used when treating with lorazepam, are as safe and effective, but have decreased treatment duration and medication quantity used. [ 34 ]
Although benzodiazepines are very effective at treating alcohol withdrawal, they should be carefully used. Benzodiazepines should only be used for brief periods in alcoholics who are not already dependent on them, as they share cross tolerance with alcohol. There is a risk of replacing an alcohol addiction with benzodiazepine dependence or adding another addiction. Furthermore, disrupted GABA benzodiazepine receptor function is part of alcohol dependence and chronic benzodiazepines may prevent full recovery from alcohol induced mental effects. [ 36 ] [ 37 ] The combination of benzodiazepines and alcohol can amplify the adverse psychological effects of each other causing enhanced depressive effects on mood and increase suicidal actions and are generally contraindicated except for alcohol withdrawal. [ 38 ]
Alcoholics are often deficient in various nutrients, which can cause severe complications during alcohol withdrawal, such as the development of Wernicke syndrome . To help to prevent Wernicke syndrome, these individuals should be administered a multivitamin preparation with sufficient quantities of thiamine and folic acid. During alcohol withdrawal, the prophylactic administration of thiamine , folic acid , and pyridoxine intravenously is recommended before starting any carbohydrate-containing fluids or food. These vitamins are often combined into a banana bag for intravenous administration. [ 39 ]
Very limited evidence indicates that topiramate or pregabalin may be useful in the treatment of alcohol withdrawal syndrome. [ 40 ] Limited evidence supports the use of gabapentin or carbamazepine for the treatment of mild or moderate alcohol withdrawal as the sole treatment or as combination therapy with other medications; however, gabapentin does not appear to be effective for treatment of severe alcohol withdrawal and is therefore not recommended for use in this setting. [ 40 ] [ 41 ] A 2010 Cochrane review similarly reported that the evidence to support the role of anticonvulsants over benzodiazepines in the treatment of alcohol withdrawal is not supported. [ 42 ] Paraldehyde combined with chloral hydrate showed superiority over chlordiazepoxide with regard to life-threatening side effects and carbamazepine may have advantages for certain symptoms. [ 42 ] Long term anticonvulsant medications are not usually recommended in those who have had prior seizures due to withdrawal. [ 43 ]
There are three medications used to help prevent a return to drinking: naltrexone , acamprosate , and disulfiram . They are used after withdrawal has occurred. [ 44 ]
Clonidine may be used in combination with benzodiazepines to help some of the symptoms. [ 12 ] No conclusions can be drawn concerning the efficacy or safety of baclofen for alcohol withdrawal syndrome due to the insufficiency and low quality of the evidence. [ 45 ]
Antipsychotics , such as haloperidol , are sometimes used in addition to benzodiazepines to control agitation or psychosis. [ 12 ] Antipsychotics may potentially worsen alcohol withdrawal as they lower the seizure threshold. Clozapine , olanzapine , or low-potency phenothiazines (such as chlorpromazine ) are particularly risky; if used, extreme caution is required. [ 46 ]
While intravenous ethanol could theoretically be used, evidence to support this use, at least in those who are very sick, is insufficient. [ 47 ]
Hypertension is common, and some doctors also prescribe beta blockers during withdrawal.
Failure to manage the alcohol withdrawal syndrome appropriately can lead to permanent brain damage or death. [ 48 ] It has been proposed that brain damage due to alcohol withdrawal may be prevented by the administration of NMDA antagonists , calcium antagonists , and glucocorticoid antagonists . [ 49 ]
Continued use of benzodiazepines may impair recovery from psychomotor and cognitive impairments from alcohol. [ 50 ] Cigarette smoking may slow down or interfere with recovery of brain pathways in recovering alcoholics. [ 51 ]
|
https://en.wikipedia.org/wiki/Alcohol_withdrawal_syndrome
|
Alcoholic hallucinosis is a complication of alcohol misuse in people with alcohol use disorder . [ 1 ] [ 2 ] It can occur during acute intoxication or withdrawal with the potential of having delirium tremens . Alcohol hallucinosis is a rather uncommon alcohol-induced psychotic disorder almost exclusively seen in chronic alcoholics who have many consecutive years of severe and heavy drinking during their lifetime. [ 3 ] Alcoholic hallucinosis develops about 12 to 24 hours after the heavy drinking stops suddenly, and can last for days. It involves auditory and visual hallucinations , most commonly accusatory or threatening voices. [ 4 ] The risk of developing alcoholic hallucinosis is increased by long-term heavy alcohol abuse and the use of other drugs. [ 5 ] Descriptions of the condition date back to at least 1907. [ 6 ]
There are many symptoms that could possibly occur before the hallucinations begin. Symptoms include headache, dizziness, irritability, insomnia, and indisposition. Typically, alcoholic hallucinosis has a sudden onset. [ 7 ]
The cause of alcoholic hallucinosis is unclear. It seems to be highly related to the presence of dopamine in the limbic system with the possibility of other systems, [ 7 ] particularly noteworthy is the intricate interplay involving cholinergic mechanisms.
Both alcoholic hallucinosis and DTs have been thought of as different manifestations of the same physiological process in the body during alcohol withdrawal. [ 8 ] Alcoholic hallucinosis is a much less serious diagnosis than delirium tremens. Delirium tremens (DTs) do not appear suddenly, unlike alcoholic hallucinosis. DTs also take approximately 48 to 72 hours to appear after the heavy drinking stops. A tremor develops in the hands and can also affect the head and body. A common symptom of delirium tremens is that people become severely uncoordinated. Alcoholic hallucinosis has a much better prognosis than DTs. [ 9 ] Untreated DTs can be fatal. [ 4 ]
In general, alcohol abusers with withdrawal symptoms, such as alcoholic hallucinosis, have a deficiency of several vitamins and minerals and their bodies could cope with the withdrawal more easily by taking nutritional supplements. Long-term alcohol abuse can create a deficiency of thiamine , magnesium , zinc , folate , and phosphate as well as cause low blood sugar . [ 10 ] However, several drugs have been shown to stop the hallucinations. Neuroleptics and benzodiazepines showed normalization. Common benzodiazepines include chlordiazepoxide and lorazepam . Management with a combination of abstinence from alcohol and the use of neuroleptics has been shown to be effective. [ 11 ] It is also possible to treat withdrawal before major symptoms start to happen in the body. Diazepam and chlordiazepoxide have proven to be effective in treating alcohol withdrawal symptoms such as alcoholic hallucinosis. With the help of these specific medications, the process of withdrawal is easier to go through, making alcoholic hallucinosis less likely to occur. [ 12 ]
|
https://en.wikipedia.org/wiki/Alcoholic_hallucinosis
|
Alcoholic liver disease ( ALD ) , also called alcohol-related liver disease ( ARLD ), is a term that encompasses the liver manifestations of alcohol overconsumption, including fatty liver , alcoholic hepatitis , and chronic hepatitis with liver fibrosis or cirrhosis . [ 1 ]
It is the major cause of liver disease in Western countries, and is the leading cause of death from excessive drinking. [ 2 ] [ 3 ] Although steatosis ( fatty liver disease ) will develop in any individual who consumes a large quantity of alcoholic beverages over a long period of time, this process is transient and reversible. [ 1 ] More than 90% of all heavy drinkers develop fatty liver whilst about 25% develop the more severe alcoholic hepatitis , and 15% liver cirrhosis . [ 4 ]
For patients with chronic hepatitis B , a strict adherence to abstinence from alcohol is highly recommended. [ 5 ]
As of 2010, known risk factors of ALD are:
The mechanism of ALD is not completely understood. 80% of alcohol passes through the liver to be detoxified. Chronic consumption of alcohol results in the secretion of pro-inflammatory cytokines ( TNF-alpha , interleukin 6 and interleukin 8 ), oxidative stress , lipid peroxidation , and acetaldehyde toxicity . These factors cause inflammation , apoptosis and eventually fibrosis of liver cells. Why this occurs in only a few individuals is still unclear. Additionally, the liver has tremendous capacity to regenerate and even when 75% of hepatocytes are dead, it continues to function as normal. [ 8 ] [ failed verification ]
Fatty change, or steatosis , is the accumulation of fatty acids in liver cells . This can be seen as fatty globules under the microscope. Alcoholism causes development of large fatty globules ( macro - vesicular steatosis) throughout the liver and can begin to occur after a few days of heavy drinking. [ 9 ] Alcohol is metabolized by alcohol dehydrogenase ( ADH ) into acetaldehyde , then further metabolized by aldehyde dehydrogenase (ALDH) into acetic acid , which is finally oxidized into carbon dioxide (CO 2 ) and water ( H 2 O ). [ 10 ] This process generates NADH , and increases the NADH/ NAD+ ratio. A higher NADH concentration induces fatty acid synthesis while a decreased NAD level results in decreased fatty acid oxidation. Subsequently, the higher levels of fatty acids signal the liver cells to compound it to glycerol to form triglycerides . These triglycerides accumulate, resulting in fatty liver. [ citation needed ]
Alcoholic hepatitis is characterized by the inflammation of hepatocytes. Between 10% and 35% of heavy drinkers develop alcoholic hepatitis (NIAAA, 1993). While development of hepatitis is not directly related to the dose of alcohol, some people seem more prone to this reaction than others. This is called alcoholic steato - necrosis and the inflammation appears to predispose to liver fibrosis . Inflammatory cytokines (TNF-alpha, IL-6 and IL-8) are thought to be essential in the initiation and perpetuation of liver injury and cytotoxic hepatomegaly by inducing apoptosis and severe hepatotoxicity. One possible mechanism for the increased activity of TNF-α is the increased intestinal permeability due to liver disease. This facilitates the absorption of the gut-produced endotoxin into the portal circulation. The Kupffer cells of the liver then phagocytose endotoxin, stimulating the release of TNF-α. TNF-α then triggers apoptotic pathways through the activation of caspases, resulting in cell death. [ 7 ]
Cirrhosis is a late stage of serious liver disease marked by inflammation (swelling), fibrosis (cellular hardening) and damaged membranes preventing detoxification of chemicals in the body, ending in scarring and necrosis (cell death). [ 11 ] Between 10% and 20% of heavy drinkers will develop cirrhosis of the liver (NIAAA, 1993). Acetaldehyde may be responsible for alcohol-induced fibrosis by stimulating collagen deposition by hepatic stellate cells . [ 7 ] The production of oxidants derived from NADPH oxi- dase and/or cytochrome P-450 2E1 and the formation of acetaldehyde-protein adducts damage the cell membrane . [ 7 ] Symptoms include jaundice (yellowing), liver enlargement, and pain and tenderness from the structural changes in damaged liver architecture. Without total abstinence from alcohol use, cirrhosis will eventually lead to liver failure . Late complications of cirrhosis or liver failure include portal hypertension (high blood pressure in the portal vein due to the increased flow resistance through the damaged liver), coagulation disorders (due to impaired production of coagulation factors), ascites (heavy abdominal swelling due to buildup of fluids in the tissues) and other complications, including hepatic encephalopathy and the hepatorenal syndrome .
Cirrhosis can also result from other causes than hazardous alcohol use, such as viral hepatitis and heavy exposure to toxins other than alcohol . The late stages of cirrhosis may look similar medically, regardless of cause. This phenomenon is termed the "final common pathway" for the disease.
Fatty change and alcoholic hepatitis with abstinence can be reversible. The later stages of fibrosis and cirrhosis tend to be irreversible, but can usually be contained with abstinence for long periods of time. [ citation needed ]
In the early stages, patients with ALD exhibit subtle and often no abnormal physical findings. It is usually not until development of advanced liver disease that stigmata of chronic liver disease become apparent. Early ALD is usually discovered during routine health examinations when liver enzyme levels are found to be elevated. These usually reflect alcoholic hepatic steatosis. Microvesicular and macrovesicular steatosis with inflammation are seen in liver biopsy specimens. These histologic features of ALD are indistinguishable from those of nonalcoholic fatty liver disease. Steatosis usually resolves after discontinuation of alcohol use. Continuation of alcohol use will result in a higher risk of progression of liver disease and cirrhosis. In patients with acute alcoholic hepatitis, clinical manifestations include fever, jaundice, hepatomegaly , and possible hepatic decompensation with hepatic encephalopathy, variceal bleeding, and ascites accumulation. Tender hepatomegaly may be present, but abdominal pain is unusual. Occasionally, the patient may be asymptomatic. [ 12 ]
In people with alcoholic hepatitis, the serum aspartate aminotransferase (AST) to alanine aminotransferase (ALT) ratio is greater than 2:1. AST and ALT levels are almost always less than 500. The elevated AST to ALT ratio is due to deficiency of pyridoxal phosphate , which is required in the ALT enzyme synthetic pathway. Furthermore, alcohol metabolite–induced injury of hepatic mitochondria results in AST isoenzyme release. Other laboratory findings include red blood cell macrocytosis ( mean corpuscular volume > 100) and elevations of serum gamma-glutamyl transferase (GGT), alkaline phosphatase , and bilirubin levels. Folate level is reduced in alcoholic patients due to decreased intestinal absorption, increased bone marrow requirement for folate in the presence of alcohol, and increased urinary loss. The magnitude of leukocytopenia ( white blood cell depletion) reflects severity of liver injury. Histologic features include Mallory bodies , giant mitochondria, hepatocyte necrosis , and neutrophil infiltration in the area around the veins. Mallory bodies, which are also present in other liver diseases, are condensations of cytokeratin components in the hepatocyte cytoplasm and do not contribute to liver injury. Up to 70% of patients with moderate to severe alcoholic hepatitis already have cirrhosis identifiable on biopsy examination at the time of diagnosis. [ 13 ]
Not drinking further alcohol is the most important part of treatment. [ 14 ] People with chronic HCV infection should abstain from any alcohol intake, due to the risk for rapid acceleration of liver disease. [ 13 ]
A 2006 Cochrane review did not find evidence sufficient for the use of androgenic anabolic steroids . [ 15 ] Corticosteroids are sometimes used; however, this is recommended only when severe liver inflammation is present. [ 14 ]
Silymarin has been investigated as a possible treatment, with ambiguous results. [ 16 ] [ 17 ] [ 18 ] One review claimed benefit for S-adenosyl methionine in disease models. [ 19 ]
The effects of anti-tumor necrosis factor medications such as infliximab and etanercept are unclear and possibly harmful. [ 20 ] Evidence is unclear for pentoxifylline . [ 14 ] [ 21 ] Propylthiouracil may result in harm. [ 22 ]
Evidence does not support supplemental nutrition in liver disease. [ 23 ]
Although in rare cases liver cirrhosis is reversible, the disease process remains mostly irreversible. Liver transplantation remains the only definitive therapy. Today, survival after liver transplantation is similar for people with ALD and non-ALD. The requirements for transplant listing are the same as those for other types of liver disease, except for a 6-month sobriety prerequisite along with psychiatric evaluation and rehabilitation assistance. [ 24 ] [ clarification needed ] Specific requirements vary among the transplant centers. Relapse to alcohol use after transplant listing results in delisting. Re-listing is possible in many institutions, but only after 3–6 months of sobriety. There are limited data on transplant survival in patients transplanted for acute alcoholic hepatitis, but it is believed to be similar to that in nonacute ALD, non-ALD, and alcoholic hepatitis with MDF less than 32. [ 25 ]
The prognosis for people with ALD depends on the liver histology as well as cofactors, such as concomitant chronic viral hepatitis. Among patients with alcoholic hepatitis , progression to liver cirrhosis occurs at 10–20% per year, and 70% will eventually develop cirrhosis. Despite cessation of alcohol use, only 10% will have normalization of histology and serum liver enzyme levels. [ 26 ] As previously noted, the MDF has been used to predict short-term mortality (i.e., MDF ≥ 32 associated with spontaneous survival of 50–65% without corticosteroid therapy, and MDF < 32 associated with spontaneous survival of 90%). The Model for End-Stage Liver Disease (MELD) score has also been found to have similar predictive accuracy in 30-day (MELD > 11) and 90-day (MELD > 21) mortality. Liver cirrhosis develops in 6–14% of those who consume more than 60–80 g of alcohol daily for men and more than 20 g daily for women. Even in those who drink more than 120 g daily, only 13.5% will experience a serious alcohol-related liver injury. Nevertheless, alcohol-related mortality was the third leading cause of death in 2003 in the United States. Worldwide mortality is estimated to be 150,000 per year. [ 27 ] Alcoholic liver disease can lead to the development of exocrine pancreatic insufficiency . [ 28 ]
|
https://en.wikipedia.org/wiki/Alcoholic_liver_disease
|
Alder–Reilly anomaly , or Alder anomaly , is an inherited abnormality of white blood cells associated with mucopolysaccharidosis . When blood smears and bone marrow preparations from patients with Alder–Reilly anomaly are stained and examined microscopically, large, coarse granules may be seen in their neutrophils , monocytes , and lymphocytes . The condition may be mistaken for toxic granulation , a type of abnormal granulation in neutrophils that occurs transiently in inflammatory conditions. [ 1 ] [ 2 ] : 477 [ 3 ]
In addition to mucopolysaccharidosis, Alder–Reilly anomaly may occur in lipofuscinosis [ 4 ] : 32 and Tay–Sachs disease . [ 5 ] : 124 While the anomaly is generally considered to exhibit autosomal recessive inheritance , [ 1 ] [ 2 ] : 477 it may also occur in carriers who are heterozygous for the Tay–Sachs mutation, although the inclusions are much less frequent than in homozygotes. [ 5 ] : 124 Alder–Reilly anomaly is not diagnostic of any disorder and does not correlate with disease severity. [ 4 ] : 32 Affected white blood cells function normally. [ 2 ] : 477
Alder–Reilly inclusions stain appear violet when treated with Wright–Giemsa stain and, in mucopolysaccharidosis, stain metachromatically with toluidine blue . Metachromatic staining is not seen in Tay–Sachs disease. The granules tend to be round or comma-shaped and may be surrounded by a clearing in the cytoplasm . [ 5 ] : 124
This article related to pathology is a stub . You can help Wikipedia by expanding it .
|
https://en.wikipedia.org/wiki/Alder–Reilly_anomaly
|
Aldosterone-to-renin ratio ( ARR ) is the mass concentration of aldosterone divided by the plasma renin activity or by serum renin concentration in blood. The aldosterone/renin ratio is recommended as screening tool for primary hyperaldosteronism . [ 1 ]
The cutoff normal individuals from those with primary hyperaldosteronism is significantly affected by the conditions of testing, such as posture and time of day. On average, an ARR cutoff of 23.6 ng/dL per ng/(mL·h), expressed in alternative units as 651 pmol/L per μg/(L·h), has been estimated to have a sensitivity of 97% and specificity of 94%. [ 2 ] An ARR value in an individual that is higher than the cutoff indicates primary hyperaldosteronism.
If the inverse ratio (i.e. renin-to-aldosterone) ratio is used, a value lower than the cutoff indicates primary hyperaldosteronism.
|
https://en.wikipedia.org/wiki/Aldosterone-to-renin_ratio
|
Aldrete's scoring system is a commonly used scale for determining when postsurgical patients can be safely discharged from the post-anesthesia care unit (PACU), generally to a second stage (phase II) recovery area, hospital ward, or home. It was devised in 1970 [ 1 ] by Jorge Antonio Aldrete [ de ] , a Mexican anesthesiologist , while working at the Denver Veterans Affairs Hospital.
The original scoring system was developed before the invention of pulse oximetry and used the patient's colouration as a surrogate marker of their oxygenation status. A modified Aldrete scoring system was described in 1995 [ 2 ] which replaces the assessment of skin colouration with the use of pulse oximetry to measure SpO 2 .
Able to move 2 extremities voluntarily or on command (1 Point)
Unable to move extremities voluntarily or on command (0 Points)
Requires Assistance (1 Point)
Unable to ambulate (0 Points)
Dyspnoea or limited breathing (1 Point)
Apnoeic (0 Points)
BP ± {\displaystyle \pm } 20-49% of pre-anaesthetic level (1 Point)
BP ± {\displaystyle \pm } 50% of pre-anaesthetic level (0 Points)
Heart rate ± {\displaystyle \pm } 20bpm pre-anaethetic level (2 points)
Heart rate ± {\displaystyle \pm } 20-35bpm pre-anaesthetic level
Heart rate ± {\displaystyle \pm } 35-50bpm pre-anaesthetic level
Patients ± {\displaystyle \pm } 50bpm or >110bpm or with a change in ECG rhythm must be evaluated by an anaesthesiologist.
These additional points change the overall target score.
BP ± {\displaystyle \pm } 20-40% of pre-anaesthetic level (1 Point)
BP ± {\displaystyle \pm } 40% of pre-anaesthetic level (0 Points)
Arousable on calling (1 Point)
Not responding (0 Points)
Pale, dusky, blotchy, jaundiced, or other (1 Point)
Cyanotic (0 Points)
Needs supplementary O 2 to maintain SpO 2 >90% (1 Point)
SpO 2 <90% despite supplementary O2 (0 Points)
This target not met (1 Point)
Moderate/Up to two dressing changes required (1 Point)
Severe/More than three dressing changes required (0 Points)
Moderate (1 Point)
Severe (0 Points)
The following criteria also exist: [ 4 ]
|
https://en.wikipedia.org/wiki/Aldrete's_scoring_system
|
The Alexander technique , named after its developer Frederick Matthias Alexander (1869–1955), is an alternative therapy based on the idea that poor posture causes a range of health problems. [ 1 ] [ 2 ] : 221 The American National Center for Complementary and Integrative Health classifies it as a "psychological and physical" complementary approach to health when used "together with" mainstream conventional medicine. [ 3 ]
Alexander began developing his technique's principles in the 1890s [ 4 ] to address his own voice loss during public speaking. [ 2 ] : 34–35 He credited his method with allowing him to pursue his passion for performing Shakespearean recitations . [ 5 ]
Proponents and teachers of the Alexander technique believe the technique can address a variety of health conditions, but there is a lack of research to support the claims. [ 6 ] [ 7 ] As of 2021 [update] , the UK National Health Service and the National Institute for Health and Care Excellence (NICE) cite evidence that the Alexander technique may be helpful for long-term back pain and for long-term neck pain , and that it could help people cope with Parkinson's disease . [ 7 ] [ 8 ] Both the American health-insurance company Aetna and the Australian Department of Health have conducted reviews and concluded that there is insufficient evidence for the technique's health claims to warrant insurance coverage. [ 6 ] [ 9 ]
The Alexander technique is most commonly taught in a series of private lessons which may last from 30 minutes to an hour. The number of lessons varies widely, depending on the student's needs and level of interest. Students are often performers, such as actors, dancers, musicians, athletes and public speakers, people who work on computers, or those who are in frequent pain for other reasons. Instructors observe their students, and provide both verbal and gentle manual guidance to help students learn how to move with better poise and less strain. [ 10 ] Sessions include chair work – often in front of a mirror – during which the instructor will guide the student while the student stands, sits and walks, learning to move efficiently while maintaining a comfortable relationship between the head, neck, and spine, and table work or physical manipulation . [ 11 ]
In the United Kingdom, there is no regulation for who can offer Alexander technique services. Professional organisations do exist, however, typically offering three-year courses to people becoming instructors. [ 7 ]
The Alexander technique is based on the personal observations of Frederick Matthias Alexander (1869–1955). Alexander's career as an actor was hampered by recurrent bouts of laryngitis , but he found he could overcome it by focusing on his discomfort and tension, and relaxing. Alexander also thought posture could be improved if a person became more conscious of their bodily movements. [ 12 ]
While on a recital tour in New Zealand (1895), Alexander came to believe in the wider significance of improved carriage for overall physical functioning, although evidence from his own publications appears to indicate it happened less systematically and over a long period of time. [ 2 ] : 36
Alexander did not originally conceive of his technique as therapy, but it has become a form of alternative medicine . [ 1 ]
When considering how to classify the Alexander technique in relation to mainstream medicine, some sources describe it as alternative and/or complementary , depending on whether it is used alone or with mainstream methods. The American National Center for Complementary and Integrative Health classifies it as a "psychological and physical" complementary approach to health when used with mainstream methods. When used "in place of" conventional medicine, it is considered "alternative". [ 3 ]
The American philosopher and educator John Dewey became impressed with the Alexander technique after his headaches, neck pains, blurred vision , and stress symptoms largely improved during the time he used Alexander's advice to change his posture. [ 13 ] In 1923, Dewey wrote the introduction to Alexander's Constructive Conscious Control of the Individual . [ 14 ]
Fritz Perls , who originated Gestalt therapy , credited Alexander as an inspiration for his psychological work. [ 15 ]
The Alexander technique is used as a therapy for stress-related chronic conditions. It does not attempt to cure the underlying cause, but to teach people how to avoid bad habits which might exacerbate their condition. [ 12 ]
The technique is used as an alternative treatment to improve both voice and posture for people in the performing arts . As of 1995 [update] it was on the curriculum of prominent Western performing arts institutions. [ 16 ]
According to Alexander technique instructor Michael J. Gelb , people tend to study the Alexander technique for reasons of personal development . [ 17 ]
The UK National Health Service says that advocates of the Alexander technique made claims for it that were not supported by evidence, but that there was evidence suggesting that it might help with chronic back or neck pain. According to the NHS, Alexander technique may be of benefit for people with Parkinson disease . [ 7 ] The National Institute for Health and Care Excellence (NICE) guidelines state that people with Parkinson disease who are experiencing balance or motor function problems should consider the Alexander technique along with disease-specific physiotherapy. [ 8 ] There is limited evidence for chronic pain, stammering, and balance skills in older people. There was no good evidence of benefit for other conditions including asthma , headaches , osteoarthritis , difficulty sleeping , and stress. [ 7 ]
A 2012 Cochrane systematic review found that there is no good evidence that the Alexander technique is effective for treating asthma, and randomized clinical trials are needed in order to assess the effectiveness of this type of treatment approach. [ 18 ]
A review published in BMC Complementary and Alternative Medicine in 2014 focused on "the evidence for the effectiveness of AT sessions on musicians' performance, anxiety, respiratory function and posture" concluded that "evidence from RCTs and CTs suggests that AT sessions may improve performance anxiety in musicians. Effects on music performance, respiratory function and posture yet remain inconclusive." [ 19 ]
A 2015 review, conducted for the Australian Department of Health in order to determine what services the Australian government should pay for, examined clinical trials published to date and found that "overall, the evidence was limited by the small number of participants in the intervention arms, wide confidence intervals or a lack of replication of results." It concluded that "the Alexander technique may improve short-term pain and disability in people with low back pain, but the longer-term effects remain uncertain. For all other clinical conditions, the effectiveness of the Alexander technique was deemed to be uncertain, due to insufficient evidence." It also noted that "evidence for the safety of Alexander Technique was lacking, with most trials not reporting on this outcome." [ 6 ] Subsequently, in 2017, the Australian government named the Alexander technique as a practice that would not qualify for insurance subsidy, saying this step would "ensure taxpayer funds are expended appropriately and not directed to therapies lacking evidence". [ 20 ]
A review by Aetna last updated in 2021 stated: "Aetna considers the following alternative medicine interventions experimental and investigational because there is inadequate evidence in the peer-reviewed published medical literature of their effectiveness." The Alexander technique is included in that list. [ 9 ]
|
https://en.wikipedia.org/wiki/Alexander_technique
|
Alexandre Petrovic (1925 – November 22, 2003) was a scientist who is known for formulating the Cybernetic Theory of Craniofacial Growth in 1977. [ 1 ]
Alex was born in Belgrade , Serbia. His father was a Serbian physician who at that time was doing his post-graduate training in surgery at University of Strasbourg School of Medicine. After birth, Alex's mother and him joined their father in Strasbourg where they lived for about 10 years before returning to Belgrade. Petrovic obtained his Medical degree in 1954, did his speciality in hematology in 1957 and his Doctorate in 1961. He completed his a postdoctoral fellowship at McGill University in 1962 under Charles Philippe Leblond on autoradiography , later influencing his methodologies on determining skeletal growth.
He was a professor of physiology and physiopathology at Louis Pasteur University . He also served as a visiting professor at Department of Orthodontics at Louisiana State University School of Dentistry where he taught craniofacial biology and research methodology.
He was the founder and long time director of Research Laboratory for Craniofacial Cartilage and Bone Growth Center. He also helmed the directorship for French Institute of Health and Medical Research . Dr. Petrovic is known for developing a cybernetic model of growth to help understand how the facial growth takes places through the different control processes. Dr. Petrovic was first introduced to American Orthodontic community at Moyer's Growth Symposium at University of Michigan School of Dentistry .
Dr. Petrovic's lab was known to introduce orthodontics to the following ideas [ 2 ]
This dentistry article is a stub . You can help Wikipedia by expanding it .
This biographical article related to medicine in the United States is a stub . You can help Wikipedia by expanding it .
|
https://en.wikipedia.org/wiki/Alexandre_Petrovic
|
The Alexandria School of Medicine is one of the oldest empirical educational institutions in the history of medicine initiated during the Hellenistic period in the city of Alexandria (311 BC). At one historical juncture, in Egypt, they united all the different medical doctrines that originated in the East and in Alexandria (increasingly resembling a cosmopolitan city), and merged into one universal "critical mass of knowledge" the Alexandrian empirical school. As the Alexandria School grows more developed Medical Schools in Knossos and in Knidos over time lost their meaning and significance.
The Greek city of Alexandria, at the mouth of the Nile, was planned and founded by Alexander the Great in 331 BC, and concentrated in it cultural streams from various places: the mysticism of the East and Greek rationalism, in a rich library, with about 700,000 written rolls (the treasure trove of all human knowledge to date; the richest in the world). Thus, with its schools, Alexandria was a kind of university where the most prominent writers, physicians, scientists, and philosophers of the historical period gathered and worked.
The ancient Greeks appreciated Egypt and saw in it a mysterious land, fertile with hidden wisdom. At one point, they united all the different medical doctrines originating in the East and in Alexandria (which increasingly resembled a cosmopolitan city) in Egypt, and merged it into one universal critical mass of knowledge. [ citation needed ] In Alexandria, special importance was given to the study of medicine. The medical works of Hippocrates and Aristotle were studied and the first " Hippocratic Corpus " was collected. Anatomy and methodical study of human corpses are introduced for the first time. [ citation needed ]
As the medical science of ancient Greece plunged into political decadence and setbacks - scientific work was renewed in this area, especially in the field of anatomy: numerous sections on corpses and even vivisection on death row inmates were done. [ 1 ] From such work the first meaningful written texts about human anatomy were written, as these were the first instances of human dissection in Greek medical practice. Prior to this period, human dissection was taboo. [ 2 ]
Anatomists and doctors of the Alexandria School were Herophilos and Erasistratus. [ citation needed ]
Although Herophilos ( c. 300 BC ) is considered to be the founder of true anatomy, it is also a versatile advocate for the use of medicines. He studied all the organs in the body anatomically, and considered the brain a nerve center and soul-carrier. [ 3 ]
Herophilos was not only an anatomist but also one of the physicians of that school. He also describes numerous brain structures, which he calls the brain sheaths, choroid plexus and four brain chambers. [ citation needed ]
Erasistratus (304-250 BC), a Greek physician who grew up in Antioch , was an anatomist of that time, who described the numerous anatomical structures of the human body. He was a young contemporary of Herophilos and, with him, the principal representative of the Alexandrian Medical School.
He systematically dissected the corpses, the death row convicts, and probably the bodies of living animals, and thus scientifically advanced the anatomy. He described the heart and its valves , blood vessels and nerves , the brain and its chambers and eddies, brain nerve outputs, lymphatic vessels in the mesentery and liver . [ citation needed ]
However, Erasistratus's greatest merits are in the field of Physiology . He was the first to correctly describe the physiological functions of ventricular heart valves . Under the influence of the Democritus of atomistics and the peripatetic school , he sought to interpret all life phenomena in a strictly mechanical manner. In his view, three organ systems pass through and are connected by the whole organism: arteries, veins and nerves; the first water pneuma , the second blood, and the third the nerve fluid. The melting of the pneuma down it was reduced to the mechanical work of the heart. [ 4 ]
He also tried to explain to the mechanical principles breathing and digestion. The former realized the difference between motor and sensory nerves, and he "threw out" Hippocrates learning, and advocated the use of weak drugs. [ citation needed ] Erasistratus rejected the humoral and pathology of the "four juices", starting from the view that the diseases were the result of accumulation of blood (plethora) or its deficiency in some part of the body, which resulted in humoral dyscrasia. According to him, the plethora is a vein full of blood, which flows into the arteries and mechanically expels the pneuma there. [ citation needed ]
As most of the diseases, Erasistratus considered to be due to over-nutrition, he suggested that not much release be used against the plethora
blood as a post. [ 5 ]
The Alexandria School leads to the development of surgery and pharmacology. Medicines are prepared there, but at the same time poisons are investigated and antidotes are prepared. [ citation needed ]
The flourishing of anatomy in the Alexandrian school led to scientific results that were not always in line with the dogmatic school hypotheses. In response to sterile dogmatism, it originated in the 3 BC in Alexandria the so-called. an empirical school that abandoned assumptions, philosophy and theory, adhering only to experience (empirics) as the only means of acquiring new, positive knowledge. [ citation needed ]
An empiricist school is being developed in Alexandria in parallel. Although the empiricist mode of learning will only gain significance in 17th century when physicians are increasingly seeking success in their work, rather than theoretical knowledge, we find the traces of this teaching in the works of the doctors of the Alexandria School. Its chief representative was the physician Glaucko Tarencio (1 BC), who could be said to have been the forerunner of evidence-based medicine .
For him, only results were the reliable basis; acquired through personal experience, or the experience of other physicians, or similar analogy when he did not have prior data to compare from his or her own or others' experience.
Of the other greats of this school, one should also mention Oribasius a (6th century), who wrote collected works on medicine in 70 books and Paul of Aegina (7th century, the most prominent representative of the Byzantine. [ 6 ] [ 7 ] [ 8 ] [ 9 ] [ 10 ] [ 11 ] [ 12 ]
The empirical school had its downsides. The abandonment of the theory caused a decline in the scientific level of medicine, which increasingly began to focus solely on practical problems. The link between physiology and pathology disappeared, and in the end, only the external signs of the disease, the symptoms, were important to the physician at that time. [ 13 ]
The beginnings of Medical astrology are found in the works of physicians and philosophers from the Greco-Alexandrian period. Philosophers, but above all physicians at the Alexandria Medical School, resorted to astrology and valued it as a skill that significantly helps man.
With all the differences between astrology and medicine, which are actually skills - artes (and medicine is actually until the 19th century, although such determination is still heated today), ^ there are significant connections. Both disciplines are based on observation and experience and involve both theoretical and practical aspects. If we take into account the fact that astrology is first and foremost a branch of divination, then it is clear that at least one part of medicine, i.e. prognostics, can be related to astrology. However, if we look back at the history of medicine and start from Greek medicine, we will see that according to many sources, astrology throughout the history of medicine is already a significant part of it Hippocrates (which respected many astrological rules). [ 14 ]
The role of astrology in medicine is indicated by a large group of texts in the so-called. popular Hermeticism, a scripture attributed to the legendary Egyptians Neheps and Petoziris and Hermes Trismegistos (who was considered the patron saint of astrology and alchemy), dated as early as 3 BC, in which the connection between astrology and medicine was discovered. In their works they are mainly texts that study the field of botany, mineralogy, but also medicine and medical astrology. In these, certain medicinal plants and minerals, as well as parts of the human body, are associated with zodiac signs , with planets and their positions, etc. In all these astrological-alchemical-magical tracts, the basic assumption is the thesis about the interconnectedness of all parts of the cosmos, the thesis about the operation of the laws of sympathy and antipathy.
Astrology plays an important role in medicine, not only in predicting the course of the disease, but also in their treatment. The connection between astrology and medicine is also emphasized in the works of Claudius Ptolemy (2nd century), especially in those in which astrology, such as the "Quadripartitum and Centiloquium", were works widely used by physicians, which also existed under the name Kαρπος , and which were attributed to and reproduced throughout the Middle Ages and the Renaissance (later, however, this attribution proved to be incorrect).
|
https://en.wikipedia.org/wiki/Alexandria_School_of_Medicine
|
Alexios Aspietes ( Greek : Ἀλέξιος Ἀσπιέτης , fl. 1159–1205 ) was a Byzantine governor and military leader who was captured by the Bulgarians , and led an anti-Bulgarian rebellion at Philippopolis in 1205, being acclaimed emperor by the citizens.
A member of the Aspietes family, of noble Armenian origin, [ 1 ] Alexios Aspietes was probably a relative of the generals Michael Aspietes and Constantine Aspietes , who were active in the late 12th century. [ 2 ] Alexios Aspietes first appears in 1195, when he was governor of the town of Serres , and was ordered by Emperor Alexios III Angelos to march against the Bulgarian – Vlach rebellion of the brothers Peter and Ivan Asen . In the event, in the summer or autumn of the same year, Aspietes and his army were defeated by the rebels, who took many prisoners, including Aspietes himself. [ 3 ]
Aspietes disappears from the record for the next decade, but was apparently released from captivity, since in 1205 he is mentioned as being in Philippopolis (modern Plovdiv in Bulgaria). In the aftermath of the crushing victory by the Bulgarian tsar Kaloyan over the forces of the Latin Empire at the Battle of Adrianople on 14 April, the mostly Byzantine Greek citizenry of Philippopolis rose up in opposition to the imminent conquest of their city by Kaloyan, and proclaimed Aspietes as emperor . Kaloyan immediately turned his army on the city, and after a brief resistance, the inhabitants were forced to surrender on terms in June. Kaloyan, however, enraged by the Greeks' collusion with the Latins, did not keep his word and executed the city's leaders, including Aspietes who, according to Niketas Choniates , was first left hanging upside down before being dismembered and thrown into a ravine to be eaten by the vultures. [ 4 ]
|
https://en.wikipedia.org/wiki/Alexios_Aspietes
|
Alfred Blalock (April 5, 1899 – September 15, 1964) was an American surgeon most noted for his work on the medical condition of shock as well as tetralogy of Fallot – commonly known as blue baby syndrome. He created, with assistance from his research and laboratory assistant Vivien Thomas and pediatric cardiologist Helen Taussig , the Blalock–Thomas–Taussig shunt , a surgical procedure to relieve the cyanosis from tetralogy of Fallot. [ 1 ] This operation ushered in the modern era of cardiac surgery. He worked at both Vanderbilt University and Johns Hopkins University , where he studied medicine and later served as chief of surgery. [ 2 ] He is known as a medical pioneer who won various awards, including Albert Lasker Clinical Medical Research Award . Blalock was also nominated several times for the Nobel Prize in Medicine . [ 3 ]
Blalock was born in Culloden, Georgia , the son of Martha "Mattie" (Davis) and George Zadock Blalock, a merchant. [ 4 ] At the age of 14, he entered as a senior at Georgia Military College , a preparatory school for the University of Georgia . [ 5 ]
Shortly after, Blalock attended the University of Georgia as a sophomore undergraduate, skipping his freshman year. While in college, Blalock was heavily involved in the university social life and athletics. He played tennis and golf, was a member of the Delta chapter of the Sigma Chi fraternity, and was secretary and treasurer of his senior class.
After graduating with an A.B. in 1918 at the age of 19, Blalock entered Johns Hopkins School of Medicine , where he roomed with and began a lifelong friendship with Tinsley Harrison , a student who would go on to specialize in cardiovascular medicine. At Johns Hopkins, his record was not considered "outstanding,” given that he graduated near the middle of his class.” [ 6 ] Nevertheless, Blalock excelled in surgical courses while he was a student at Hopkins, and this made him come to the realization that he wanted to be a surgeon. [ 5 ] In medical school, Blalock was known by his friends and classmates as a "ladies man" due to his frequent trips to Goucher College , a women's school located nearby. [ 5 ]
Blalock earned his medical degree at Johns Hopkins in 1922, hoping to gain appointment to a surgical residency at Johns Hopkins due to his admiration of William S. Halsted. Because of this, Blalock decided to remain in Baltimore for the next three years. However, he was denied a surgical residency with Halsted because of his average academic record. Instead, Blalock decided to complete an internship in urology , in which he performed exceptionally well. He also completed one year of an assistant residency on the general surgical service (his contract was not renewed), and an externship in otorhinolaryngology . [ 5 ]
In September 1925, Blalock joined Tinsley Harrison at Vanderbilt University in Nashville to complete his residency under Barney Brooks , Vanderbilt University School of Medicine’s first Professor and Chief of Surgery. [ 6 ] During his Vanderbilt years, Blalock spent much of his time in the surgical research laboratory, which he found both challenging and exciting. [ 6 ] While at Vanderbilt, Blalock became interested and began studying the nature and treatment of hemorrhagic and traumatic shock. At Vanderbilt, in 1938, Blalock conducted an experiment where the left subclavian artery was connected to the left pulmonary artery. The experiment was meant to induce pulmonary hypertension, but it ended up failing. [ 7 ] By conducting his research and mainly experimenting on dogs, Blalock discovered that surgical shock resulted from the loss of blood, which led him to encourage the use of blood plasma or whole blood products to prevent. Blalock's innovative research resulted in the saving of many lives on the battlefield during World War II . Unfortunately, Blalock had frequent bouts of tuberculosis , which developed during his later years at Vanderbilt.
While working in Vanderbilt in 1930, Blalock became increasingly busy and had several obligations that kept him from spending much time in the laboratory. Because of this, Blalock began searching for a new lab assistant that he would be able to count on to carry out all of his experiments. He ended up hiring Vivien Thomas , a young black carpenter, as his lab assistant. Although Blalock hired Thomas as a lab assistant, he was officially titled a janitor. From Blalock's perspective, Thomas quickly learned how to perform surgical procedures, carry out experiments, and record data for Blalock's research. As they got to know each other, Blalock granted Thomas increased independence in the laboratory, something that was very uncommon, especially for someone black at that time. [ 2 ] Blalock and Thomas carried out various experiments relating to shock and cardiac output, as well as developing a technique for adrenal transplantation. Together, they developed innovative, unheard of techniques such as the transplantation of the kidney to the neck in order to remove the kidney's nerve supply and study the effect on “Goldblatt hypertension”. Blalock and Thomas built a strong, though unequal, relationship over the years, somewhat marred toward the end by Blalock's unwillingness to give Thomas full credit for his contribution to their collaboration. [ 2 ]
In 1941 Blalock was asked to return to Johns Hopkins Hospital to work as chief of surgery, professor, and director of the department of surgery of the medical school. [ 8 ] When Blalock was offered this position, he immediately requested that his assistant Vivien Thomas come with him. While working together at Hopkins, Blalock and Thomas developed a shunt technique to bypass coarctation of the aorta . Simultaneously, Helen Taussig , a cardiologist, presented to Blalock the problem of the blue baby syndrome - a congenital heart defect known as Tetralogy of Fallot which results in inadequate oxygenation of the blood. [ 8 ]
In 1944 Blalock, with Thomas by his side, performed the first "blue baby" operation on Eileen Saxon , a 15-month-old baby. The operation was successful, although the baby died a few months later. After the innovative first completion of the surgery, Blalock became comfortable with the procedure and performed it on thousands of children, often with Thomas by his side. The new operation not only directly saved thousands of lives, it marked the start of the modern era of cardiac surgery, as it was the first successful surgery on the human heart of the modern medical era. [ 1 ] [ 9 ]
During his later years at Hopkins, Blalock continued his research on the heart and vascular surgery. With Edwards Park, he developed a bypass operation in 1944, and in 1948, with Rollins Hanlon , a cardiac surgeon, he created a technique for overcoming the transposition of the great blood vessels of the heart. [ 10 ]
By the 1950s, Blalock had performed over 1,000 surgeries to correct congenital heart defects.
In teaching and in research, Blalock paved the way for a new generation of surgeons. Students of Blalock appreciated his unique ability to bring out the best of them. [ 5 ] As chief of surgery at Hopkins, Blalock trained 38 chief residents, as well as 9 chairmen of departments, 10 division chiefs, and many others. Many of Blalock's students went on to become cardiovascular surgeons themselves and rose to high levels of importance in the surgical world. His colleague and lifelong friend Tinsley Harrison spoke about Blalock's ability to teach saying, "A teacher is an individual who has the capacity to influence the horizons of his pupils. Al has had that capacity all of his life." [ 5 ]
In 1955, Blalock became chairman of the medical board of Johns Hopkins Hospital and held that position until his retirement in 1964. Upon retirement, Blalock held the title of professor and surgeon-in-chief emeritus. [ 5 ]
Blalock retired from Hopkins in 1964 due to health problems. His retirement was just two and a half months before his death.
Blalock married Mary Chambers O'Bryan in October 1930. The two had met while Blalock was at Vanderbilt and she worked for the Vanderbilt admissions office. Together they had three children: William Rice Blalock, Mary Elizabeth Blalock and Alfred Dandy Blalock. Together, they lived a happy marriage for 28 years until her death in 1958. A year later, he married Alice Waters, who was a close neighbor that Blalock had known for many years. [ 11 ]
Blalock was known for having an appreciation of sports and the outdoors. He enjoyed playing tennis, golfing, fishing, and boating. [ 5 ]
In Blalock's later years he developed several health problems and eventually died in 1964 from metastatic urothelial carcinoma of the ureter . [ 11 ] [ 12 ]
In 1955, Blalock was elected chairman of the medical board of Johns Hopkins Hospital. When he retired in 1964, he was named a Professor Emeritus of Surgery, as well as a Surgeon-in-Chief Emeritus for Johns Hopkins School of Medicine and Johns Hopkins Hospital. [ 5 ]
Blalock published more than 200 articles along with a book titled Principles of Surgery, Shock and Other Problems. He also delivered more than 40 honorary lectures, and was awarded honorary degrees from nine universities.
Blalock also belonged to 43 medical societies in the United States and other countries. [ 11 ] These included the American Philosophical Society , the National Academy of Sciences and Royal Society of Medicine. [ 5 ]
In 1954 Blalock received (with Robert Gross and Helen Taussig) the Albert Lasker Clinical Medical Research Award "For distinguished contributions to cardiovascular surgery and knowledge." [ 13 ]
Blalock also received the Chevalier de la Légion d'honneur , the Passano Award , the Matas Award, and the Henry Jacob Bigelow medal. [ 5 ]
The Alfred Blalock Clinical Sciences Building at Hopkins Hospital was named after him. [ 1 ]
Blalock was also honored with the Baltimore "Man of the Year" award in 1948.
In 2012 a modified Blalock clamp was described by prof. Francesco Petrella (Milan, Italy) for clamping the pulmonary artery during lung cancer resection. [ 14 ]
In 2003, the PBS series American Experience premiered the Spark Media documentary "Partners of the Heart", which was about the collaboration between Blalock and Vivien Thomas at Vanderbilt and Johns Hopkins University . The documentary was directed by Andrea Kalin and written by Kalin and Lou Potter, with re-creations directed by Bill Duke and narration by Morgan Freeman . [ 15 ] [ 16 ] [ 17 ] The "Partners of the Heart" went on to win the Organization of American Historians' Erik Barnouw Award for Best History Documentary in 2004. [ 18 ]
In the 2004 HBO film Something the Lord Made about the Blalock-Thomas collaboration, based on Katie McCabe's National Magazine Award winning Washingtonian magazine article of the same name, Blalock was portrayed by Alan Rickman and Thomas by Mos Def . Robert Cort produced the film, which went on to win three Emmy Awards for Outstanding Cinematography for a Miniseries or Movie, Outstanding Single-Camera Picture Editing for a Miniseries, Movie or a Special and Outstanding Made for Television Movie . [ 19 ]
Greg Germann portrayed Blalock in the 2019 Netflix variety special Kevin Hart's Guide to Black History a guide to African-American history through re-enactments with a family sitcom set-up and archival footage.
|
https://en.wikipedia.org/wiki/Alfred_Blalock
|
Algaenan is the resistant biopolymer in the cell walls of unrelated groups of green algae , [ 1 ] and facilitates their preservation in the fossil record . [ 2 ]
This alga -related article is a stub . You can help Wikipedia by expanding it .
This article related to medical technology is a stub . You can help Wikipedia by expanding it .
|
https://en.wikipedia.org/wiki/Algaenan
|
Algor mortis (from Latin algor ' coldness ' and mortis ' of death ' ), the third stage of death , is the change in body temperature post mortem, until the ambient temperature is matched. This is generally a steady decline, although if the ambient temperature is above the body temperature (such as in a hot desert ), the change in temperature will be positive, as the (relatively) cooler body equalizes with the warmer environment. External factors can have a significant influence.
The term was first used by Bennet Dowler in 1849. [ 1 ] The first published measurements of the intervals of temperature after death were done by John Davy in 1839. [ 2 ] [ 3 ]
A measured rectal temperature can give some indication of the time of death. Although the heat conduction which leads to body cooling follows an exponential decay curve, it can be approximated as a linear process: 2 °C during the first hour and 1 °C per hour until the body nears ambient temperature.
The Glaister equation [ 4 ] [ 5 ] estimates the hours elapsed since death as a linear function of the rectal temperature :
or
Generally, temperature change is considered an inaccurate means of determining time of death, as the rate of change is affected by several key factors, including: [ 6 ]
|
https://en.wikipedia.org/wiki/Algor_mortis
|
Alice Domurat Dreger ( / ˈ d r ɛ ɡ ər / ) is an American historian, bioethicist, author, and former professor of clinical medical humanities and bioethics at the Feinberg School of Medicine , Northwestern University , in Chicago, Illinois. [ 2 ]
Dreger engages in academic work and activism in support of individuals born with atypical sex characteristics ( intersex or disorders of sex development ) and individuals born as conjoined twins . [ 3 ] She challenges the perception that those with physical differences are somehow "broken" and need to be "fixed". [ 4 ] She has opposed the use of "corrective" surgery on babies whose genitalia are considered "ambiguous". She has criticized the failure to follow such patients in later life and reported longer-term medical and psychological difficulties experienced by some of the people whose sex is arbitrarily assigned. [ 3 ] [ 5 ]
She supported J. Michael Bailey in the face of controversy over his book The Man Who Would Be Queen . [ 6 ] [ 7 ] [ 8 ] In a 2008 article and in her 2015 book, Galileo's Middle Finger , Dreger argued that the controversy had gone far beyond addressing the scientific theories presented in Bailey's book to become an attack upon the author. [ 8 ] [ 3 ]
Dreger has been a featured speaker at TED talks . She has also worked as a journalist, founding East Lansing Info, a website that covers local affairs in East Lansing, Michigan . [ 9 ] [ 10 ]
Dreger received her Ph.D. in history and philosophy of science from Indiana University Bloomington in 1995. [ 11 ]
Dreger has taught at both Michigan State University , where she received a Teacher-Scholar Award in 2000, [ 12 ] and at Northwestern University (2005–2015). [ 13 ]
During her doctoral work, she became interested in "how and why it is that scientists and medical doctors work to mediate the relationships between our bodies and our selves" and "why it is we often look to scientists and medical doctors to read or even alter our bodies". [ 6 ] In 1995, she published a paper in Victorian Studies , examining 19th-century British medical attitudes toward intersex people. In 1998, she published the book Hermaphrodites and the Medical Invention of Sex [ 6 ] and in 1999, Intersex in the age of ethics . Increasingly, she became engaged in intersex activism as well as scholarship, advocating that doctors accept a wide variety of genital structure rather than "correcting" babies' genitalia to conform to artificially gendered standards. [ 3 ] More recently, she has criticized the prenatal use of dexamethasone to normalize female genitalia in cases of congenital adrenal hyperplasia and tried to charge that its safety has not been sufficiently tested by pediatrician Maria New . [ 7 ]
In 2004, Dreger published One of Us: Conjoined Twins and the Future of Normal , an examination of conjoined twinning and of surgical practice. Described as "a book filled with warmth, humour and unexpected insights", it raised similar issues to her earlier work on intersex people: questioning the ways in which the surgical profession defines "acceptable limits of the normal" and enforces conformity to such norms. She criticized the lack of long-range follow-up studies of separated children. She also introduced more than twenty sets of conjoined twins, most of whom have adapted happily to the challenges of their situations. One reviewer stated that Dreger's intent is "to show us the humanity of people whose anatomies differ from ours". [ 14 ] [ 4 ]
In The Man Who Would Be Queen (2003), J. Michael Bailey defended a theory of transsexualism by Ray Blanchard that characterized male-to-female transsexuals in two groups; this characterization provoked outrage among some. [ 15 ] In 2008, Dreger published an article in Archives of Sexual Behavior , describing in detail the opposition to Bailey and his work. A major concern for her was the ways in which attacks targeted him as a person and a scholar, rather than addressing his ideas. [ 3 ] Dreger asserted that a theory, even if found threatening or offensive, should be judged by its supporting evidence. [ 13 ] She also argued against reduction of the controversy to a simple dualism, [ 3 ] seeing the ideas and actions of all those involved as "significantly more complicated". [ 8 ] As result of the paper, Dreger herself was perceived as attacking trans people and drawn into an ongoing controversy. [ 3 ]
In 2009, Dreger received a Guggenheim fellowship to study conflicts between activists and scientists. She has examined a number of conflicts, including the controversial career of Napoleon Chagnon . Dreger accepts that scientists, being human, have biases and ideologies. But, she argues, they must "put the truth first and the quest for social justice second" and try to "adhere to an intellectual agenda that [isn't] first and only political". [ 3 ]
Forms of scholarship that deny evidence, that deny truth, that deny the importance of facts, even when performed in the name of good, are dangerous, not only to science and to ethics but to democracy.
In 2015, Dreger published Galileo's Middle Finger , a book that covered her observations and experiences with controversies in academic medicine, especially those surrounding human sexuality. This included her work with intersex people, the career of Napoleon Chagnon, Dreger's criticisms of Maria New, and her defense of J. Michael Bailey and its consequences. [ 3 ] [ 16 ] The New York Times described Dreger's "smart, delightful book" as "many things: a rant, a manifesto, a treasury of evocative new terms (sissyphobia, autogynephilia, phall-o-meter) and an account of the author's transformation" from activist to anti-activist and back again. [ 7 ] The book also received positive reviews from the Chicago Tribune , [ 17 ] Chronicle of Higher Education , [ 6 ] Salon , [ 18 ] and activist and author Dan Savage . [ 19 ]
However, Galileo's Middle Finger also reignited controversy over her defense of Bailey and her discussion of transgender issues. The book was removed from consideration for a Lambda Literary Award after complaints. One critic accused Dreger of transphobia , saying that her book promoted the idea that trans women are "just self-hating homosexual men who believe they could have guilt-free sex if they were female and heterosexual men with an out-of-control fetish ( autogynephilia )". [ 20 ] Dreger protested the removal in an open letter to the Lambda Literary Foundation . [ 21 ] Dreger herself has since reiterated her articulation of ideas in Galileo's Middle Finger that relate to trans women, stating that she considers both gender and sexuality to be relevant and valid concerns for people and therefore finds value in Blanchard's dual categorization, if not his terminology. [ 22 ]
I want to emphasize that I think both of these developmental paths are perfectly legitimate ways to become women, and regardless of how someone becomes a woman, if she identifies as such, we owe her the respect of recognizing her identity and addressing her appropriately. [ 22 ]
Dreger resigned from Northwestern University in August 2015, citing censorship issues. [ 23 ] The school had ordered her and other editors of Atrium , a bioethics journal, to take down an article written by a paralysis patient, William Peace, about his purported firsthand experiences of consensual oral sex with nurses in the 1970s. [ 24 ] Although the article was eventually reposted, the university established its own editorial committee to approve future issues of the journal. [ 25 ] [ 26 ]
Dreger is the founder of East Lansing Info, a nonprofit local journalism web outlet covering the city of East Lansing, Michigan . She currently works as publisher, president, and reporter for the organization. [ 10 ]
In June 2022, Dreger published her first novel, The Index Case , under the pseudonym Molly Macallen. [ 27 ] She discussed its origins and planned sequels with Iona Italia on Areo Magazine ' s Two for Tea podcast. [ 28 ]
|
https://en.wikipedia.org/wiki/Alice_Dreger
|
Alice in Wonderland Syndrome ( AIWS ), also known as Todd's Syndrome or Dysmetropsia , is a neurological disorder that distorts perception . People with this syndrome may experience distortions in their visual perception of objects, such as appearing smaller ( micropsia ) or larger ( macropsia ), or appearing to be closer ( pelopsia ) or farther ( teleopsia ) than they are. Distortion may also occur for senses other than vision. [ 3 ]
The cause of Alice in Wonderland Syndrome is currently not known, but it has often been associated with migraines , head trauma , or viral encephalitis caused by Epstein–Barr Virus Infection . [ 4 ] It is also theorized that AIWS can be caused by abnormal amounts of electrical activity, resulting in abnormal blood flow in the parts of the brain that process visual perception and texture. [ 5 ]
Alice in Wonderland Syndrome is also possible to be experienced temporarily under the use of certain psychoactive drugs.
Although there are cases of Alice in Wonderland Syndrome in both adolescents and adults, it is most commonly seen in children. [ 2 ]
The classification is not universally agreed upon in literature, however, some authors distinguish true Alice in Wonderland syndrome based solely on symptoms related to alterations in a person's body image. In contrast, they utilize the term "Alice in Wonderland-like syndrome" to encompass symptoms associated with changes in perception of vision, time, hearing, touch, or other external perceptions. [ 2 ] [ 6 ]
Due to the classification of all the clinical features seen in Alice in Wonderland, the table below illustrates theses features and symptoms by type with Type C having a combination of Type A and Type B symptoms. [ 7 ]
Lilliputianism (people appearing smaller)
With over 60 associated symptoms, AIWS affects the sense of vision, sensation, touch, and hearing, as well as the perception of one's body image. [ 8 ] [ 9 ] Migraines , nausea , dizziness , and agitation are also commonly associated symptoms with Alice in Wonderland syndrome. [ 10 ] Less frequent symptoms also include: loss of limb control and coordination, memory loss , lingering touch and sound sensations, and emotional instability. [ 11 ] Alice in Wonderland syndrome is often associated with distortion of sensory perception, which involves visual, somatosensory , and non-visual symptoms. [ 12 ] AIWS is characterized by the individual being able to recognize the distortion in the perception of their own body [ 3 ] and is episodic . AIWS episodes vary in length from person to person. Episodes typically last from a few minutes to an hour, and each episode may vary in experience. [ 13 ]
Individuals with AIWS can experience illusions of expansion, reduction, or distortion of their body image, such as microsomatognosia (feeling that their own body or body parts are shrinking), or macrosomatognosia (feeling that their body or body parts are growing taller or larger). These changes in perception are collectively known as metamorphopsias , or Lilliputian hallucinations , [ 11 ] which refer to objects appearing either smaller or larger than reality. [ 14 ] People with certain neurological diseases may also experience similar visual hallucinations. [ 15 ]
Within the category of Lilliputian hallucinations, people may experience either micropsia or macropsia . Micropsia is an abnormal visual condition, usually occurring in the context of visual hallucination , in which the affected person sees objects as being smaller than they are in reality. [ 16 ] Macropsia is a condition where the individual sees everything larger than it is. [ 17 ] These visual distortions are sometimes classified as "Alice in Wonderland-like syndrome" instead of true Alice in Wonderland syndrome but are often still classified as Alice in Wonderland syndrome by health professionals and researchers since the distinction is not official. [ 2 ] [ 6 ] Other distortions include teleopsia (objects are perceived further than they actually are) and pelopsia (objects are perceived closer than they actually are). [ 18 ]
Along with size, mass, and shape distortions of the body, those with Alice in Wonderland syndrome often experience a feeling of disconnection from one's own body, feelings, thoughts, and environment known as depersonalization-derealization disorder . [ 2 ] Depersonalization is a term specifically used to express a true detachment from their personal self and identity. It is described as being an observer completely outside of their own actions and behaviors. Derealization is seen as "dreamlike, empty, lifeless, or visually distorted."
Individuals experiencing Alice in Wonderland syndrome can also often experience paranoia as a result of disturbances in sound perception. These disturbances can include the amplification of soft sounds or the misinterpretation of common sounds. [ 19 ] [ 11 ] Other auditory changes include distortion in pitch and tone and hearing indistinguishable and strange voices, noises, or music. [ 10 ]
A person affected by AIWS may also lose a sense of time , a problem similar to the lack of spatial perspective brought on by visual distortion. [ 2 ] This condition is known as tachysensia. For those with tachysensia, time may seem to pass very slowly, similar to an LSD experience, and the lack of time and space perspective can also lead to a distorted sense of velocity. For example, an object could be moving extremely slowly in reality, but to a person experiencing time distortions, it could seem that the object was sprinting uncontrollably along a moving walkway, leading to severe, overwhelming disorientation. [ 20 ] Having symptoms of tachysensia is correlated with various underlying conditions, including substance use, migraine, epilepsy, head trauma, and encephalitis . Regardless of an individual's disease diagnosis, tachysensia is often included as a symptom associated with Alice in Wonderland Syndrome since it is classified as a perceptual distortion. Therefore, a person can be described as having Alice in Wonderland syndrome even if that person is experiencing tachysensia due to an underlying condition. [ 21 ]
Because AlWS is not commonly diagnosed and documented, it is difficult to estimate what the main causes are. The cause of over half of the documented cases of Alice in Wonderland syndrome is unknown. [ 22 ] Complete and partial forms of the AIWS exist in a range of other disorders, including epilepsy, intoxicants, infectious states, fevers, and brain lesions . [ 11 ] [ 23 ] Furthermore, the syndrome is commonly associated with migraines , as well as excessive screen use in dark spaces and the use of psychoactive drugs . It can also be the initial symptom of the Epstein–Barr virus (see mononucleosis ), and a relationship between the syndrome and mononucleosis has been suggested. [ 4 ] [ 24 ] [ 25 ] [ 10 ] Within this suggested relationship, Epstein–Barr virus appears to be the most common cause in children, while for adults it is more commonly associated with migraines. [ 7 ]
A 2021 review found that infectious diseases are the most common cause of Alice in Wonderland syndrome, especially in pediatrics . Some of these infectious agents included Epstein–Barr virus , Varicella Zoster virus , Influenza , Zika , [ 26 ] Coxsackievirus , Plasmodium falciparum protozoa, and Mycoplasma pneumonia / Streptococcus pyogenes bacteria. [ 9 ] The association of Alice in Wonderland syndrome is most commonly seen with the Epstein–Barr virus. However, pathogenesis is not well understood beyond these reviews. In some instances, Alice in Wonderland syndrome was reported to be associated with an Influenza A infection. [ 27 ] [ 28 ]
Alice in Wonderland syndrome can be caused by abnormal amounts of electrical activity resulting in abnormal blood flow in the parts of the brain that process visual perception and texture. [ 5 ] Nuclear medical techniques using technetium , performed on individuals during episodes of Alice in Wonderland syndrome, have demonstrated that Alice in Wonderland Syndrome is associated with reduced cerebral perfusion in various cortical regions ( frontal , parietal , temporal and occipital ), both in combination and in isolation. One hypothesis is that any condition resulting in a decrease in perfusion of the visual pathways or visual control centers of the brain may be responsible for the syndrome. For example, one study used single photon emission computed tomography to demonstrate reduced cerebral perfusion in the temporal lobe in people with Alice in Wonderland syndrome. [ 29 ]
Other theories suggest the syndrome is a result of non-specific cortical dysfunction (e.g. from encephalitis, epilepsy , decreased cerebral blood flow), or reduced blood flow to other areas of the brain. [ 11 ] [ 10 ] Other theories suggest that distorted body image perceptions stem from within the parietal lobe. This has been demonstrated by the production of body image disturbances through electrical stimulation of the posterior parietal cortex . Other researchers suggest that metamorphopsias, or visual distortions, may be a result of reduced perfusion of the non-dominant posterior parietal lobe during migraine episodes. [ 11 ]
Throughout all the neuroimaging studies, several cortical regions (including the temporoparietal junction within the parietal lobe , and the visual pathway, specifically the occipital lobe ) are associated with the development of Alice in Wonderland syndrome symptoms. [1]
1 in 10 people who experience migraines have symptoms of Alice in Wonderland syndrome. [ 18 ] The role of migraines in Alice in Wonderland syndrome is still not understood, but both vascular and electrical theories have been suggested. For example, visual distortions may be a result of transient, localized ischemia in areas of the visual pathway during migraine attacks. In addition, a spreading wave of depolarization of cells (particularly glial cells) in the cerebral cortex during migraine attacks can eventually activate the trigeminal nerve 's regulation of the vascular system. The intense cranial pain during migraines is due to the connection of the trigeminal nerve with the thalamus and thalamic projections onto the sensory cortex. Alice in Wonderland syndrome symptoms can precede, accompany, or replace the typical migraine symptoms. [ 11 ] Typical migraines (aura, visual derangements, hemicrania headache, nausea, and vomiting) are both a cause and an associated symptom of Alice in Wonderland Syndrome. [ 3 ] Alice in Wonderland Syndrome is associated with macrosomatognosia which can mostly be experienced during migraine auras. [ 30 ]
While there currently is no identified genetic locus/loci associated with Alice in Wonderland syndrome, observations suggest that a genetic component may exist but the evidence so far is inconclusive. There is also an established genetic component for migraines which may be considered to be a possible cause and influence for hereditary Alice in Wonderland syndrome. Though most frequently described in children and adolescents, observational studies have found that many parents of children experiencing Alice in Wonderland syndrome have also experienced similar symptoms themselves, though often unrecognized. [ 22 ] Family history may then be a potential risk factor for Alice in Wonderland syndrome.
One example of environmental influences on the incidence of Alice in Wonderland syndrome includes the drug use and toxicity of topiramate . [ 31 ] Other reports of tyramine usage and the association with Alice in Wonderland syndrome has been reported but current evidence is inconclusive. Further research is required to establish the genetic and environmental influences on Alice in Wonderland syndrome. [ 10 ]
The neuronal effect of cortical spreading depression (CSD) on TPO-C may demonstrate the link between migraines and Alice in Wonderland Syndrome. As children experience Alice in Wonderland Syndrome more than adults, it is hypothesized that structural differences in the brain between children and adults may play a role in the development of this syndrome. [ 7 ] [ 32 ]
Alice in Wonderland syndrome is not part of any major classifications like the ICD-10 [ 33 ] and the DSM-5. [ 34 ] Since there are no established diagnostic criteria for Alice in Wonderland syndrome, and because Alice in Wonderland syndrome is a disturbance of perception rather than a specific physiological condition, there is likely to be a large degree of variability in the diagnostic process and thus it can be poorly diagnosed. [ 7 ]
Often, the diagnosis can be presumed when other causes have been ruled out . Additionally, Alice in Wonderland syndrome can be presumed if the patient presents symptoms along with migraines and complains of onset during the day (although it can also occur at night). Ideally, a definite diagnosis requires a thorough physical examination, proper history taking from episodes and occurrences, and a concrete understanding of the signs and symptoms of Alice in Wonderland syndrome for differential diagnosis. A person experiencing Alice in Wonderland syndrome may be reluctant to describe their symptoms out of fear of being labeled with a psychiatric disorder, which can contribute to the difficulty in diagnosing Alice in Wonderland syndrome. In addition, younger individuals may struggle to describe their unusual symptoms, and thus, one recommended approach is to encourage children to draw their visual illusions during episodes. [ 11 ]
Cases that are suspected should warrant tests and exams such as blood tests, ECG , brain MRI , and other antibody tests for viral antibody detection. [ 3 ] Differential diagnosis requires three levels of conceptualization. Symptoms need to be distinguished from other disorders that involve hallucinations and illusions. It is usually easy to rule out psychosis as those with Alice in Wonderland syndrome are typically aware that their hallucinations and distorted perceptions are not 'real' . [ 10 ] Once these symptoms are distinguished and identified, the most likely cause needs to be established. Finally, the diagnosed condition needs to be evaluated to see if the condition is responsible for the symptoms that the individual is presenting. [ 12 ] Given the wide variety of metamorphopsias and other distortions, it is not uncommon for Alice in Wonderland syndrome to be misdiagnosed or confused with other etiologies.
An area of the brain that is important to the development of Alice in Wonderland syndrome is the temporal-parietal-occipital carrefour (TPO-C), [ 7 ] [ 35 ] where TPO-C region is the meeting point of temporooccipital, parietooccipital, and temporoparietal junctions in the brain. The TPO-C region is also crucial as it is the location where somatosensory and visual information are interpreted by the brain to generate any internal or external manifestations. Thus, modifications to these regions of the brain may trigger the cause of Alice in Wonderland Syndrome and body schema disorders simultaneously . [ 7 ]
Depending on which portion of the brain is damaged, the symptoms of Alice in Wonderland syndrome may differ. For example, it has been reported that injury to the anterior portion of the brain is more likely to be correlated to more complex and a wider range of symptoms, whereas damage to the occipital region has mainly been associated with only simple visual disturbances. [ 7 ]
The symptoms of Alice in Wonderland syndrome themselves are not physically harmful for the experiencer. Since there is no established treatment for Alice in Wonderland syndrome, prognosis varies between patients and is based on whether an underlying cause has been identified. [ 22 ] In many cases, the intensity of the episodes and symptoms decline. Since it is predominately a benign condition, treatment isn't always required. Limitations of the prognosis of Alice in Wonderland syndrome are due to the disorder's low prevalence. Because of this, symptoms require careful evaluation and observation by healthcare professionals. [ 12 ]
Some cases include recurring symptoms in which other medical conditions have to be ruled out before diagnosing AIWS [ 12 ] If Alice in Wonderland Syndrome is caused by underlying conditions, symptoms typically occur during the underlying disease and can last from few days to months. [ 10 ] In most cases, symptoms may disappear either spontaneously, with the treatment of underlying causes, or after reassurances that symptoms are momentary and harmless. [ 12 ] In some cases, individuals experience only a few episodes of symptoms. In other cases, symptoms may repeat over several episodes before resolution. In rare cases, symptoms continue to manifest years after the initial experience, sometimes with the development of new visual disorders or migraines. [ 22 ] In these cases, medication can be introduced to counteract some of these distortions and manifestations. However, medications may also have inducing effects. [ 12 ]
At present (2025), Alice in Wonderland Syndrome has no standardized treatment plan. [ 10 ] Tests including electroencephalogram (EEG) and magnetic resonance imaging (MRI) are used to view brain activity to examine possible brain injury or deficits. [ 36 ] Since symptoms of Alice in Wonderland syndrome often disappear, either spontaneously on their own, or with the treatment of the underlying disease, most clinical and non-clinical Alice in Wonderland Syndrome cases are considered to be benign. In cases of Alice in Wonderland syndrome caused by underlying chronic disease, however, symptoms tend to reappear during the active phase of the underlying cause (e.g., migraine, epilepsy). If treatment of Alice in Wonderland Syndrome is determined necessary and useful, it should be focused on treating the suspected underlying disease. Treatment of these underlying conditions mostly involves prescription medications such as antiepileptics , migraine prophylaxis , antivirals, or antibiotics. Antipsychotics are rarely used in treating Alice in Wonderland Syndrome symptoms due to their minimal effectiveness. [ 12 ] There are also rare cases in which these prescription medications, specifically antipsychotics, may worsen psychosis and psychotic symptoms due to the severity of distortions. [ 12 ]
In 2011, a patient was examined for having verbal auditory hallucinations (VAHs) and functional MRI (fMRI) was employed to localize cerebral activity during self-reported VAHs. Repetitive transcranial magnetic stimulation (rTSMS) was used on the patient's Brodmann's area 40, in charge of meaning and phonology, at a frequency of 1 Hz at T3P3. After the second week of treatment, all VAHs and sensory distortions have no effected on the patient and went through a full remission. Follow up appointments were conducted with no signs of any symptoms. By month 8, the symptoms returned. A second treatment was done with complete remission. [ 37 ]
Treatment methods revolving around migraine prophylaxis include medications and following a low- tyramine diet. Drugs that may be used to prevent migraines include anticonvulsants , antidepressants , calcium channel blockers , and beta blockers . Other treatments that have been explored for migraines include repetitive transcranial magnetic stimulation (rTMS). However, further research is needed to establish the effectiveness of this treatment regime. [ 10 ]
The lack of established diagnostic criteria or large-scale epidemiological studies, low awareness of the syndrome, and the unstandardized diagnosis criteria and definition for Alice in Wonderland syndrome mean that the exact prevalence of the syndrome is currently unknown. One study on 3,224 adolescents in Japan demonstrated the occurrence of macropsia and micropsia to be 6.5% in boys and 7.3% in girls, suggesting that the symptoms of Alice in Wonderland syndrome may not be particularly rare. [ 38 ] This also seems to suggest a difference in the male-to-female ratio of people with Alice in Wonderland syndrome. However, according to other studies, it appears that the male/female ratio is dependent on the age range being observed. Studies showed that younger males (age range of 5 to 14 years) were 2.69 times more likely to experience Alice in Wonderland syndrome than girls of the same age, while there were no significant differences between students of 13 to 15 years of age. Conversely, female students (16- to 18-year-olds) showed a significantly greater prevalence. [ 7 ]
Alice in Wonderland syndrome is more frequently seen in children and young adults. [ 32 ] The average age of the start of Alice in Wonderland syndrome is six years old, but it is typical for some people to experience the syndrome from childhood up to their late twenties. [ 10 ] Because many parents who have Alice in Wonderland syndrome report their children having it as well, the condition is thought possibly to be hereditary. [ 3 ] Some parents report not realizing they have experienced Alice in Wonderland syndrome symptoms until after their children have been diagnosed, further indicating that many cases of Alice in Wonderland syndrome likely go unrecognized and under-reported. [ 22 ]
Research is still being expanded upon and developed on this syndrome in a multitude of different regions and specialties. [ 39 ] Future studies are encouraged to include global collaborative efforts that may help improve understanding of Alice in Wonderland syndrome and its epidemiology.
The syndrome is sometimes called Todd's syndrome, about a description of the condition in 1955 by Dr. John Todd (1914–1987), a British consultant psychiatrist at High Royds Hospital at Menston in West Yorkshire ('AIWS had been described by American Neurologist Caro Lippman in 1952, but Todd's report was the most influential'). [ 40 ] [ 41 ] Todd discovered that several of his patients experienced severe headaches causing them to see and perceive objects as greatly out of proportion. In addition, they had altered sense of time and touch, as well as distorted perceptions of their own body. Despite having migraine headaches, none of these patients had brain tumors, damaged eyesight, or mental illness that could have accounted for these and similar symptoms. They were all able to think lucidly and could distinguish hallucinations from reality, however, their perceptions were distorted. [ 42 ]
Dr. Todd speculated that author Lewis Carroll had used his own migraine experiences as a source of inspiration for his famous 1865 novel Alice's Adventures in Wonderland . Carroll's diary reveals that, in 1856, he consulted William Bowman, an ophthalmologist , about the visual manifestations of the migraines he regularly experienced. [ 43 ] In Carroll's diaries, he often wrote of a "bilious headache" that came coupled with severe nausea and vomiting. In 1885, he wrote that he had "experienced, for the second time, that odd optical affection of seeing moving fortifications, followed by a headache". [ 44 ] Carroll wrote two books about Alice , the heroine after which the syndrome is named. In the story, Alice experiences several strange feelings that overlap with the characteristics of the syndrome, such as slowing time perception. In chapter two of Alice's Adventures in Wonderland (1865), Alice's body shrinks after drinking from a bottle labeled "DRINK ME", after which she consumed a cake that made her so large that she almost touched the ceiling. [ 45 ] These features of the story describes the macropsia and micropsia that are so characteristic to this disease.
These symptoms have been reported before in scientific literature, including World War I and II soldiers with occipital lesions, so Todd understood that he was not the first person to discover this phenomenon. Additionally, as early as 1933, other researchers such as Coleman and Lippman had compared these symptoms to the story of Alice in Wonderland. Caro Lippman was the first to hypothesize that the bodily changes that Alice encounters mimicked those of Lewis Carroll's migraine symptoms. Others suggest that Carroll may have familiarized himself with these distorted perceptions through his knowledge of hallucinogenic mushrooms. [ 12 ] It has been suggested that Carroll would have been aware of mycologist Mordecai Cubitt Cooke 's description of the intoxicating effects of the fungus Amanita muscaria (commonly known as the fly agaric or fly amanita), in his books The Seven Sisters of Sleep and A Plain and Easy Account of British Fungi. [ 46 ] [ 47 ]
Alice in Wonderland syndrome's symptom of micropsia has also been related to Jonathan Swift's novel Gulliver's Travels . It has been referred to as "Lilliput sight" and " Lilliputian hallucination ", a term coined by British physician Raoul Leroy in 1909. [ 49 ]
Alice in Wonderland syndrome was named after Lewis Carroll 's 19th-century novel Alice's Adventures in Wonderland . In the story, Alice, the titular character, experiences numerous situations similar to those of micropsia and macropsia. The thorough descriptions of metamorphosis clearly described in the novel were the first of their kind to depict the bodily distortions associated with the condition. There is some speculation that Carroll may have written the story using his own direct experience with episodes of micropsia resulting from the numerous migraines he was known to experience. [ 43 ] It has also been suggested that Carroll may have had temporal lobe epilepsy . [ 50 ]
The condition is diagnosed in the season 8 episode " Risky Business ".
In episode ten of the Korean drama Secret Garden , the leading man, Kim Joo Won, suspects that he is suffering from Alice in Wonderland syndrome.
In April 2020, a case of Alice in Wonderland syndrome was covered in an episode of the BBC daytime soap opera Doctors , when patient Hazel Gilmore (Alex Jarrett) experienced it. [ 51 ]
|
https://en.wikipedia.org/wiki/Alice_in_Wonderland_syndrome
|
Alien hand syndrome ( AHS ) or Dr. Strangelove syndrome [ 1 ] is a category of conditions in which a person experiences their limbs acting seemingly on their own, without conscious control over the actions. [ 2 ] There are a variety of clinical conditions that fall under this category, most commonly affecting the left hand. [ 3 ] There are many similar terms for the various forms of the condition, but they are often used inappropriately. [ 4 ] The affected person may sometimes reach for objects and manipulate them without wanting to do so, even to the point of having to use the controllable hand to restrain the alien hand. [ 5 ] The occurrence of alien hand syndrome can be usefully conceptualized as a phenomenon reflecting a functional "disentanglement" between thought and action.
Alien hand syndrome is best documented in cases where a person has had the two hemispheres of their brain surgically separated , [ 6 ] a procedure sometimes used to relieve the symptoms of extreme cases of epilepsy and epileptic psychosis , e.g., temporal lobe epilepsy . It also occurs in some cases after brain surgery , stroke , infection , tumor , aneurysm , migraine and specific degenerative brain conditions such as Alzheimer's disease , corticobasal degeneration [ 7 ] and Creutzfeldt–Jakob disease . [ 8 ] Other areas of the brain that are associated with alien hand syndrome are the frontal , occipital , and parietal lobes . [ 9 ] [ 10 ] [ unreliable medical source? ] [ 8 ]
"Alien behavior" can be distinguished from reflexive behavior in that the former is flexibly purposive while the latter is obligatory. Sometimes the affected person will not be aware of what the alien hand is doing until it is brought to his or her attention, or until the hand does something that draws their attention to its behavior. There is a clear distinction between the behaviors of the two hands in which the affected hand is viewed as "wayward" and sometimes "disobedient" and generally out of the realm of their own voluntary control, while the unaffected hand is under normal volitional control. At times, particularly in individuals who have sustained damage to the corpus callosum that connects the two cerebral hemispheres (see also Split-brain ) , the hands appear to be acting in opposition to each other. [ 11 ]
A related syndrome described by the French neurologist François Lhermitte involves the release through disinhibition of a tendency to compulsively utilize objects that present themselves in the surrounding environment around the patient. [ 12 ] [ 13 ] The behavior of the patient is, in a sense, obligatorily linked to the "affordances" (using terminology introduced by the American ecological psychologist, James J. Gibson ) presented by objects that are located within the immediate peri-personal environment. [ citation needed ]
This condition is known as utilization behavior . It is most often associated with extensive bilateral frontal lobe damage and might actually be thought of as "bilateral" alien hand syndrome in which the patient is compulsively directed by external environmental contingencies (such as the presence of a hairbrush on the table in front of them elicits the act of brushing the hair) and has no capacity to "hold back" and inhibit pre-potent motor programs that are obligatorily linked to the presence of specific external objects in the peri-personal space of the patient. When the frontal lobe damage is bilateral and generally more extensive, the patient completely loses the ability to act in a self-directed manner and becomes totally dependent upon the surrounding environmental indicators to guide their behavior in a general social context, a condition referred to as " environmental dependency syndrome ". [ 14 ]
To deal with the alien hand, some individuals engage in personification of the affected hand. [ 15 ] Usually these names are negative in nature, from mild such as "cheeky" to malicious "monster from the moon". [ 16 ] For example, Rachelle Doody and Jankovic described a patient who named her alien hand "baby Joseph". When the hand engaged in playful, troublesome activities such as pinching her nipples (akin to biting while nursing), she would experience amusement and would instruct baby Joseph to "stop being naughty". [ 16 ] Furthermore, Bogen suggested that certain personality characteristics, such as a flamboyant personality, contribute to frequent personification of the affected hand. [ 17 ]
Neuroimaging and pathological research shows that lesions of the frontal lobe (in the frontal variant) and corpus callosum (in the callosal variant) are the most common anatomical lesions responsible for the alien hand syndrome. [ citation needed ] These areas are closely linked in terms of motor planning and its final pathways. [ 18 ]
The callosal variant includes advanced willed motor acts by the non-dominant hand, where individuals frequently exhibit "intermanual conflict" in which one hand acts at cross-purposes with the other "good hand". [ 17 ] For example, one patient was observed putting a cigarette into her mouth with her intact, "controlled" hand (her right, dominant hand), following which her left hand rose, grasped the cigarette, pulled it out of her mouth, and toss it away before it could be lit by the right hand. The patient then surmised that "I guess 'he' doesn't want me to smoke that cigarette." Another patient was observed to be buttoning up her blouse with her controlled dominant hand while the alien non-dominant hand, at the same time, was unbuttoning her blouse. The frontal variant most often affects the dominant hand, but can affect either hand depending on the lateralization of the damage to medial frontal cortex, and includes grasp reflex, impulsive groping toward objects or/and tonic grasping (in other words, difficulty in releasing grip). [ 18 ]
In most cases, classic alien-hand signs derive from damage to the medial frontal cortex, accompanying damage to the corpus callosum. [ 15 ] In these individuals, the main cause of damage is unilateral or bilateral infarction of cortex in the territory supplied by the anterior cerebral artery or associated arteries. [ 18 ] Oxygenated blood is supplied by the anterior cerebral artery to most medial portions of the frontal lobes and to the anterior two-thirds of the corpus callosum, [ 19 ] and infarction may consequently result in damage to multiple adjacent locations in the brain in the supplied territory. As the medial frontal lobe damage is often linked to lesions of the corpus callosum, frontal variant cases may also present with callosal form signs. Cases of damage restricted to the callosum however, tend not to show frontal alien-hand signs. [ 15 ]
The common emerging factor in alien hand syndrome is that the primary motor cortex controlling hand movement is isolated from premotor cortex influences but remains generally intact in its ability to execute movements of the hand. [ citation needed ]
A 2009 fMRI study looking at the temporal sequence of activation of components of a cortical network associated with voluntary movement in normal individuals demonstrated "an anterior-to-posterior temporal gradient of activity from supplemental motor area through premotor and motor cortices to the posterior parietal cortex". [ 20 ] Therefore, with normal voluntary movement, the emergent sense of agency appears to be associated with an orderly sequence of activation that develops initially in the anteromedial frontal cortex in the vicinity of the supplementary motor complex on the medial surface of the frontal aspect of the hemisphere (including the supplementary motor area ) prior to activation of the primary motor cortex in the pre-central gyrus on the lateral aspect of the hemisphere, when the hand movement is being generated. Activation of the primary motor cortex, presumed to be directly involved in the execution of the action via projections into the corticospinal component of the pyramidal tracts , is then followed by activation of the posterior parietal cortex , possibly related to the receipt of recurrent or re-afferent somatosensory feedback generated from the periphery by the movement which would normally interact with the efference copy transmitted from primary motor cortex to permit the movement to be recognized as self-generated rather than imposed by an external force. That is, the efference copy allows the recurrent afferent somatosensory flow from the periphery associated with the self-generated movement to be recognized as re-afference as distinct from ex-afference . Failure of this mechanism may lead to a failure to distinguish between self-generated and externally generated movement of the limb. This anomalous situation in which re-afference from a self-generated movement is mistakenly registered as ex-afference due to a failure to generate and successfully transmit an efference copy to sensory cortex, could readily lead to the interpretation that what is in actuality a self-generated movement has been produced by an external force as a result of the failure to develop a sense of agency in association with emergence of the self-generated movement (see below for a more detailed discussion). [ citation needed ]
A 2007 fMRI study examining the difference in functional brain activation patterns associated with alien as compared to non-alien "volitional" movement in a patient with alien hand syndrome found that alien movement involved anomalous isolated activation of the primary motor cortex in the damaged hemisphere contralateral to the alien hand, while non-alien movement involved the normal process of activation described in the preceding paragraph in which primary motor cortex in the intact hemisphere activates in concert with frontal premotor cortex and posterior parietal cortex presumably involved in a normal cortical network generating premotor influences on the primary motor cortex along with immediate post-motor re-afferent activation of the posterior parietal cortex. [ 21 ]
Combining these two fMRI studies, one could hypothesize that the alien behavior that is unaccompanied by a sense of agency emerges due to autonomous activity in the primary motor cortex acting independently of premotor cortex pre-activating influences that would normally be associated with the emergence of a sense of agency linked to the execution of the action. [ citation needed ]
As noted above, these ideas can also be linked to the concept of efference copy and re-afference , where efference copy is a signal postulated to be directed from premotor cortex (activated normally in the process associated with emergence of an internally generated movement) over to somatosensory cortex of the parietal region, in advance of the arrival of the "re-afferent" input generated from the moving limb, that is, the afferent return from the moving limb associated with the self-generated movement produced. It is generally thought that a movement is recognized as internally generated when the efference copy signal effectively "cancels out" the re-afference. The afferent return from the limb is effectively correlated with the efference copy signal so that the re-afference can be recognized as such and distinguished from "ex-afference", which would be afferent return from the limb produced by an externally imposed force. When the efference copy is no longer normally generated, then the afferent return from the limb associated with the self-generated movement is mis-perceived as externally produced "ex-afference" since it is no longer correlated with or canceled out by the efference copy. As a result, the development of the sense that a movement is not internally generated even though it actually is (i.e. the failure of the sense of agency to emerge in conjunction with the movement), could indicate a failure of the generation of the efference copy signal associated with the normal premotor process through which the movement is prepared for execution. [ citation needed ]
Since there is no disturbance of the sense of ownership of the limb in this situation, and there is no apparent physical explanation for how the owned limb could be moving in a purposive manner without an associated sense of agency, a cognitive dissonance is created which may be resolved through the assumption that the goal-directed limb movement is being directed by an "alien" unidentifiable external force with the capacity for directing goal-directed actions of one's own limb. [ citation needed ]
It is theorized that alien hand syndrome results when disconnection occurs between different parts of the brain that are engaged in different aspects of the control of bodily movement. [ 22 ] As a result, different regions of the brain are able to command bodily movements, but cannot generate a conscious feeling of self-control over these movements. As a result, the sense of agency that is normally associated with voluntary movement is impaired or lost. There is a dissociation between the process associated with the actual execution of the physical movements of the limb and the process that produces an internal sense of voluntary control over the movements, with this latter process thus normally creating the internal conscious sensation that the movements are being internally initiated, controlled and produced by an active self. [ 23 ]
Recent studies have examined the neural correlates of emergence of the sense of agency under normal circumstances. [ 24 ] This appears to involve consistent congruence between what is being produced through efferent outflow to the musculature of the body, and what is being sensed as the presumed product in the periphery of this efferent command signal. In alien hand syndrome, the neural mechanisms involved in establishing that this congruence has occurred may be impaired. This may involve an abnormality in the brain mechanism that differentiates between "re-afference" (the return of kinesthetic sensation from the self-generated "active" limb movement) and "ex-afference" (kinesthetic sensation generated from an externally produced 'passive' limb movement in which an active self does not participate). This brain mechanism is proposed to involve the production of a parallel "efference copy" signal that is sent directly to the somatic sensory regions and is transformed into a "corollary discharge", an expected afferent signal from the periphery that would result from the performance driven by the issued efferent signal. The correlation of the corollary discharge signal with the actual afferent signal returned from the periphery can then be used to determine if, in fact, the intended action occurred as expected. When the sensed result of the action is congruent with the predicted result, then the action can be labelled as self-generated and associated with an emergent sense of agency. [ citation needed ]
If, however, the neural mechanisms involved in establishing this sensorimotor linkage associated with self-generated action are faulty, it would be expected that the sense of agency with action would not develop as discussed in the previous section. [ citation needed ]
One theory posed to explain these phenomena proposes that the brain has separable neural "premotor" or "agency" systems for managing the process of transforming intentions into overt action. [ 22 ] An anteromedial frontal premotor system is engaged in the process of directing exploratory actions based on "internal" drive by releasing or reducing inhibitory control over such actions. [ citation needed ]
A 2011 paper reporting on neuronal unit recording in the medial frontal cortex in human subjects showed a clear pre-activation of neurons identified in this area up to several hundred milliseconds prior to the onset of an overt self-generated finger movement and the authors were able to develop a computational model whereby volition emerges once a change in internally generated firing rate of neuronal assemblies in this part of the brain crossed a threshold. [ 25 ] Damage to this anteromedial premotor system produces disinhibition and release of such exploratory and object acquisition actions which then occur autonomously. A posterolateral temporo-parieto-occipital premotor system has a similar inhibitory control over actions that withdraw from environmental stimuli as well as the ability to excite actions that are contingent upon and driven by external stimulation, as distinct from internal drive. These two intrahemispheric systems, each of which activates an opposing cortical "tropism", interact through mutual inhibition that maintains a dynamic balance between approaching toward (in other words, with "intent-to-capture" in which contact with and grasping onto the attended object is sought) versus withdrawing from (that is, with "intent-to-escape" in which distancing from the attended object is sought) environmental stimuli in the behavior of the contralateral limbs. [ 26 ] [ 27 ] Together, these two intrahemispheric agency systems form an integrated trans-hemispheric agency system. [ citation needed ]
When the anteromedial frontal "escape" system is damaged, involuntary but purposive movements of an exploratory reach-and-grasp nature – what Denny-Brown referred to as a positive cortical tropism – are released in the contralateral limb. [ 26 ] [ 27 ] This is referred to as a positive cortical tropism because eliciting sensory stimuli, such as would result from tactile contact on the volar aspect of the fingers and palm of the hand, are linked to the activation of movement that increases or enhances the eliciting stimulation through a positive feedback connection (see discussion above in section entitled "Parietal and Occipital Lobes"). [ citation needed ]
When the posterolateral parieto-occipital "approach" system is damaged, involuntary purposive movements of a release-and-retract nature, such as levitation and instinctive avoidance – what Denny-Brown referred to as a negative cortical tropism – are released in the contralateral limb. [ 27 ] This is referred to as a negative cortical tropism because eliciting sensory stimuli, such as would result from tactile contact on the volar aspect of the fingers and palm of the hand, are linked to the activation of movement that reduces or eliminates the eliciting stimulation through a negative feedback connection (see discussion above in section entitled "Parietal and Occipital Lobes"). [ citation needed ]
Each intrahemispheric agency system has the potential capability of acting autonomously in its control over the contralateral limb although unitary integrative control of the two hands is maintained through interhemispheric communication between these systems via the projections traversing the corpus callosum at the cortical level and other interhemispheric commissures linking the two hemispheres at the subcortical level. [ citation needed ]
One major difference between the two hemispheres is the direct connection between the agency system of the dominant hemisphere and the encoding system based primarily in the dominant hemisphere that links action to its production and through to its interpretation with language and language-encoded thought. [ citation needed ] It is proposed that while relational action in the form of embodied inter-subjective behavior [ 28 ] precedes linguistic capacity during infant development, a process ensues through the course of development through which linguistic constructs are linked to action elements in order to produce a language-based encoding of action-oriented knowledge. [ citation needed ]
When there is a major disconnection between the two hemispheres resulting from callosal injury, the language-linked dominant hemisphere agent which maintains its primary control over the dominant limb loses, to some degree, its direct and linked control over the separate "agent" based in the nondominant hemisphere, and the nondominant limb, which had been previously responsive and "obedient" to the dominant conscious agent. The possibility of purposeful action occurring outside of the realm of influence of the conscious dominant agent can occur and the basic assumption that both hands are controlled through and subject to the dominant agent is proven incorrect. The sense of agency that would normally arise from movement of the nondominant limb now no longer develops, or, at least, is no longer accessible to consciousness. A new explanatory narrative for understanding the situation in which the now inaccessible nondominant hemisphere based agent is capable of activating the nondominant limb is necessitated. [ citation needed ]
Under such circumstances, the two separated agents can control simultaneous actions in the two limbs that are directed at opposing purposes although the dominant hand remains linked to the dominant consciously accessible language-linked agent and is viewed as continuing to be under "conscious control" and obedient to conscious will and intent as accessible through thought, while the nondominant hand, directed by an essentially non-verbal agent whose intent can only be inferred by the dominant agent after the fact, is no longer "tied in" and subject to the dominant agent and is thus identified by the conscious language-based dominant agent as having a separate and inaccessible alien agency and associated existence. This theory would explain the emergence of alien behavior in the nondominant limb and intermanual conflict between the two limbs in the presence of damage to the corpus callosum. [ citation needed ]
The distinct anteromedial, frontal, and posterolateral temporo-parieto-occipital variants of the alien hand syndrome would be explained by selective injury to either the frontal or the posterior components of the agency systems within a particular hemisphere, with the relevant and specific form of alien behavior developing in the limb contralateral to the damaged hemisphere. [ citation needed ]
Damage to the corpus callosum can give rise to "purposeful" actions in the person's non-dominant hand (an individual who is left-hemisphere-dominant will experience the left hand becoming alien, and the right hand will turn alien in the person with right-hemisphere dominance). [ citation needed ]
In "the callosal variant", the patient's hand counteracts voluntary actions performed by the other, "good" hand. Two phenomena that are often found in individuals with callosal alien hand are agonistic dyspraxia and diagonistic dyspraxia . [ citation needed ]
Agonistic dyspraxia involves compulsive automatic execution of motor commands by one hand when the patient is asked to perform movements with the other hand. For example, when a patient with callosal damage was instructed to pull a chair forward, the affected hand would decisively and impulsively push the chair backwards. [ 18 ] Agonistic dyspraxia can thus be viewed as an involuntary competitive interaction between the two hands directed toward completion of a desired act in which the affected hand competes with the unaffected hand to complete a purposive act originally intended to be performed by the unaffected hand. [ citation needed ]
Diagonistic dyspraxia, on the other hand, involves a conflict between the desired act in which the unaffected hand has been engaged and the interfering action of the affected hand which works to oppose the purpose of the desired act intended to be performed by the unaffected hand. For instance, when Akelaitis's individuals underwent surgery to the corpus callosum to reduce epileptic seizures, one patient's left alien hand would frequently interfere with the right hand. For instance, while trying to turn over to the next page with the right hand, his left hand would try to close the book. [ 29 ]
In another case of callosal alien hand, the patient did not have intermanual conflict between the hands but rather from a symptom characterized by involuntary mirror movements of the affected hand. [ 30 ] When the patient was asked to perform movements with one hand, the other hand would involuntarily perform a mirror image movement which continued even when the involuntary movement was brought to the attention of the patient, and the patient was asked to restrain the mirrored movement. The patient had a ruptured aneurysm near the anterior cerebral artery , which resulted in the right hand being mirrored by the left hand. The patient described the left hand as frequently interfering and taking over anything the patient tried to do with the right hand. For instance, when trying to grasp a glass of water with the right hand with a right side approach, the left hand would involuntary reach out and grasp hold of the glass through a left side approach. [ citation needed ]
More recently, Geschwind et al. described the case of a woman with severe coronary heart disease . [ 31 ] One week after undergoing coronary artery bypass grafting, she noticed that her left hand started to "live a life of its own". It would unbutton her gown, try to choke her while asleep and would automatically fight with the right hand to answer the phone. She had to physically restrain the affected hand with the right hand to prevent injury, a behavior which has been termed "self-restriction". The left hand also showed signs of severe ideomotor apraxia . It was able to mimic actions but only with the help of mirror movements executed by the right hand (enabling synkinesis). Using magnetic resonance imaging (MRI), Geschwind et al. found damage to the posterior half of the callosal body, sparing the anterior half and the splenium extending slightly into the white matter underlying the right cingulate cortex . [ 31 ]
Park et al. also described two cases of infarction as the origin of alien hand symptoms. Both individuals had had infarction of the anterior cerebral artery (ACA). One individual, a 72-year-old male, had difficulty controlling his hands, as they often moved involuntarily, despite his trying to stabilize them. Furthermore, he often could not let go of objects after grasping them with his palms. The other individual, a 47-year-old female with an ACA in a different location of the artery, complained that her left hand would move on its own and she could not control its movements. Her left hand could also sense when her right hand was holding an object and would involuntarily, forcibly take the object out of her right hand. [ 32 ]
Unilateral injury to the medial aspect of the brain's frontal lobe can trigger reaching, grasping and other purposeful movements in the contralateral hand. With anteromedial frontal lobe injuries, these movements are often exploratory reaching movements in which external objects are frequently grasped and utilized functionally, without the simultaneous perception on the part of the patient that they are "in control" of these movements. [ 33 ] Once an object has been acquired and is maintained in the grasp of this "frontal variant" form of alien hand, the patient often has difficulty with voluntarily releasing the object from grasp and can sometimes be seen to be peeling the fingers of the hand back off the grasped object using the opposite controlled hand to enable the release of the grasped object (also referred to as tonic grasping or the "instinctive grasp reaction" [ 34 ] ). Some (for example, the neurologist Derek Denny-Brown ) have referred to this behavior as "magnetic apraxia" [ 35 ]
Goldberg and Bloom described a woman with a large cerebral infarction of the medial surface of the left frontal lobe in the territory of the left anterior cerebral artery which left her with the frontal variant of the alien hand involving the right hand. [ 22 ] There were no signs of callosal disconnection nor was there evidence of any callosal damage. The patient displayed frequent grasp reflexes; her right hand would reach out and grab objects without releasing them. In regards to tonic grasping, the more the patient tried to let go of the object, the more the grip of the object tightened. With focused effort the patient was able to let go of the object, but if distracted, the behaviour would re-commence. The patient could also forcibly release the grasped object by peeling her fingers away from contact with the object using the intact left hand. Additionally, the hand would scratch at the patient's leg to the extent that an orthotic device was required to prevent injury. [ 22 ] Another patient reported not only tonic grasping towards objects nearby, but the alien hand would take hold of the patient's penis and engage in public masturbation. [ 36 ]
A distinct "posterior variant" form of alien hand syndrome is associated with damage to the posterolateral parietal lobe and/or occipital lobe of the brain. The movements in this situation tend to be more likely to withdraw the palmar surface of the hand away from sustained environmental contact rather than reaching out to grasp onto objects to produce palmar tactile stimulation, as is most often seen in the frontal form of the condition. In the frontal variant, tactile contact on the ventral surface of the palm and fingers facilitates finger flexion and grasp of the object through a positive feedback loop (i.e. the stimulus generates movement that reinforces, strengthens and sustains the triggering stimulation). [ citation needed ]
In contrast, in the posterior variant, tactile contact on the ventral surface of the palm and fingers is actively avoided through facilitation of extension of the fingers and withdrawal of the palm in a negative feedback loop (i.e. the stimulus, and even anticipation of stimulation of the palmar surface of the hand, generates movement of the palm and fingers that reduces and effectively counteracts and eliminates the triggering stimulation, or, in the case of anticipated palmar contact, decreases the likelihood of such contact). Alien movements in the posterior variant of the syndrome also tend to be less coordinated and show a coarse ataxic motion during active movement that is generally not observed in the frontal form of the condition. This is generally thought to be due to an optic form of ataxia since it is facilitated by the visual presence of an object with visual attention directed toward the object. The apparent instability could be due to an unstable interaction between the tactile avoidance tendency biasing toward withdrawal from the object, and the visually based acquisition bias tendency pushing toward an approach to the object. [ citation needed ]
The alien limb in the posterior variant of the syndrome may be seen to "levitate" upward into the air withdrawing away from contact surfaces through the activation of anti-gravity musculature. Alien hand movement in the posterior variant may show a typical posture, sometimes referred to as a "parietal hand" or the "instinctive avoidance reaction" (a term introduced by neurologist Derek Denny-Brown as an inverse form of the "magnetic apraxia" seen in the frontal variant, as noted above), in which the digits move into a highly extended position with active extension of the interphalangeal joints of the digits and hyper-extension of the metacarpophalangeal joints, and the palmar surface of the hand is actively pulled back away from approaching objects or up and away from supporting surfaces. The "alien" movements, however, remain purposeful and goal-directed, a point which clearly differentiates these movements from other disorganized non-purposeful forms of involuntary limb movement (e.g. athetosis , chorea , or myoclonus ). [ citation needed ]
In both the frontal and the posterior variants of the alien hand syndrome, the patient's reactions to the limb's apparent capability to perform goal-directed actions independent of conscious volition is similar. In both of these variants of alien hand syndrome, the alien hand emerges in the hand contralateral to the damaged hemisphere. [ citation needed ]
There is no cure for the alien hand syndrome. [ 30 ] However, the symptoms can be reduced and managed to some degree by keeping the alien hand occupied and involved in a task, for example by giving it an object to hold in its grasp. Specific learned tasks can restore voluntary control of the hand to a significant degree. One patient with the "frontal" form of alien hand who would reach out to grasp onto different objects (e.g., door handles) as he was walking was given a cane to hold in the alien hand while walking, even though he really did not need a cane for its usual purpose. With the cane firmly in the grasp of the alien hand, it would generally not release the grasp and drop the cane in order to reach out to grasp onto a different object. Other techniques proven to be effective include; wedging the hand between the legs or slapping it; warm water application and visual or tactile contact. [ 37 ] Additionally, Wu et al. [ 38 ] found that an irritating alarm activated by biofeedback reduced the time the alien hand held an object.
In the presence of unilateral damage to a single cerebral hemisphere, there is generally a gradual reduction in the frequency of alien behaviors observed over time and a gradual restoration of voluntary control over the affected hand. Actually, when AHS originates from focal injury of acute onset, recovery usually occurs within a year. [ 39 ] One theory is that neuroplasticity in the bihemispheric and subcortical brain systems involved in voluntary movement production can serve to re-establish the connection between the executive production process and the internal self-generation and registration process. Exactly how this may occur is not well understood, but a process of gradual recovery from alien hand syndrome when the damage is confined to a single cerebral hemisphere has been reported. [ 22 ] In some instances, individuals may resort to constraining the wayward, undesirable and sometimes embarrassing actions of the impaired hand by voluntarily grasping onto the forearm of the impaired hand using the intact hand. This observed behavior has been termed "self-restriction" or "self-grasping". [ 22 ]
In another approach, the patient is trained to perform a specific task, such as moving the alien hand to contact a specific object or a highly salient environmental target, which is a movement that the patient can learn to generate voluntarily through focused training in order to effectively override the alien behavior. It is possible that some of this training produces a re-organization of premotor systems within the damaged hemisphere, or, alternatively, that ipsilateral control of the limb from the intact hemisphere may be expanded. [ citation needed ]
Another method involves simultaneously "muffling" the action of the alien hand and limiting the sensory feedback coming back to the hand from environmental contact by placing it in a restrictive "cloak" such as a specialized soft foam hand orthosis or, alternatively, an everyday oven mitt. Other individuals have reported using an orthotic device to restrict perseverative grasping [ 22 ] or restraining the alien hand by securing it to the bed pole. [ 40 ] Of course, this can limit the degree to which the hand can participate in addressing functional goals for the patient and may be considered to be an unjustifiable restraint. [ citation needed ]
Theoretically, this approach could slow down the process through which voluntary control of the hand is restored if the neuroplasticity that underlies recovery involves the recurrent exercise of voluntary will to control the actions of the hand in a functional context and the associated experiential reinforcement through successful willful suppression of the alien behavior. [ citation needed ]
The first known case described in the medical literature appeared in a detailed case report published in German in 1908 by the preeminent German neuro-psychiatrist, Kurt Goldstein . [ 41 ] In this paper, Goldstein described a right-handed woman who had had a stroke affecting her left side from which she had partially recovered by the time she was seen. However, her left arm seemed as though it belonged to another person and performed actions that appeared to occur independent of her will. [ 41 ]
The patient complained of a feeling of "strangeness" in relationship to the goal-directed movements of the left hand and insisted that "someone else" was moving the left hand, and that she was not moving it herself. When the left hand grasped an object, she could not voluntarily release it. The senses of touch and proprioception of the left side were impaired. The left hand would make spontaneous movements, such as wiping the face or rubbing the eyes, but these were relatively infrequent. With significant effort, she was able to move her left arm in response to spoken command, but conscious movements were slower or less precise than similar involuntary motions. [ 41 ]
Goldstein developed a "doctrine of motor apraxia" in which he discussed the generation of voluntary action and proposed a brain structure for temporal and spatial cognition , will and other higher cognitive processes. Goldstein maintained that a structure conceptually organizing both the body and external space was necessary for object perception as well as for voluntary action on external objects. [ 41 ]
In his classic papers reviewing the wide variety of disconnection syndromes associated with focal brain pathology, Norman Geschwind commented that Kurt Goldstein "was perhaps the first to stress the non-unity of the personality in individuals with callosal section, and its possible psychiatric effects". [ 42 ]
|
https://en.wikipedia.org/wiki/Alien_hand_syndrome
|
In ufology , alien implants is a term used to describe physical objects allegedly placed in someone's body after they have been abducted by aliens . Claimed capabilities of the implants range from telepresence to mind control to biotelemetry (the latter akin to humans tagging wild animals for study). As with UFO subjects in general, the idea of "alien implants" has seen very little attention from mainstream scientists.
According to Peter Rogerson writing in Magonia magazine, the concept of alien implants can be traced to a March 1957 Long John Nebel radio show interview with UFOlogist John Robinson where Robinson recounted a neighbor's claim of being kidnapped by aliens in 1938 and kept subdued by "small earphones" placed behind his ears. [ 1 ]
Massachusetts resident Betty Andreasson claimed that aliens had implanted a device in her nose during her supposed alien abduction in 1967, first publicized by Raymond Fowler in his book, The Andreasson Affair . A Canadian woman named Dorothy Wallis claimed a similar experience in 1983. In later years, the claims of authors like Whitley Strieber would popularize alien abduction ideas in general, including reports of unusual "implants" associated with abductions. John E. Mack wrote in his book Abduction: Human Encounters With Aliens that he examined a "1/2- to 3/4-inch thin, wiry object" given to him by a twenty-four-year-old woman client who claimed it came out of her nose following an abduction experience. California podiatrist Roger Leir also claims to have removed alien implants from patients. [ 2 ]
According to skeptical investigator Joe Nickell , supposed alien implants appear to be ordinary materials such as a shard of glass, a jagged piece of metal, and a carbon fiber. The objects are often found lodged in extremities such as toes, hands and shins. Nickell cites Israeli teaching hospital department head Virgil Priscu's opinion that there's "No mystery, no implants", explaining that normal objects picked up during a fall or by walking barefoot often become surrounded by scar tissue. [ 2 ]
Alien implants, pictured as small needles inserted into victim's necks and stomachs, first appeared in the 1953 film Invaders from Mars . [ 3 ]
|
https://en.wikipedia.org/wiki/Alien_implants
|
Alifedrine ( INN Tooltip International Nonproprietary Name ; developmental code name D-13625 ) is a drug described as a sympathomimetic and cardiotonic or positive inotropic agent which was never marketed. [ 3 ] [ 4 ] [ 5 ] [ 6 ] It is a β-adrenergic receptor partial agonist and was studied in the treatment of heart failure . [ 4 ] [ 1 ] [ 2 ] [ 7 ] The drug is taken by mouth or intravenously . [ 1 ] [ 2 ] It is a β- hydroxylated substituted amphetamine derivative . [ 8 ]
This drug article relating to the cardiovascular system is a stub . You can help Wikipedia by expanding it .
|
https://en.wikipedia.org/wiki/Alifedrine
|
Alison Dougall (née Pughe, born 27 May 1964) is Associate Professor and Director of the Special Care Dentistry doctorate programme at Trinity College Dublin , Head of Department of Child and Dental Public Health at Trinity College Dublin and Consultant for medically complex patients at Dublin Dental Hospital. [ 1 ]
Dougall was born and brought up in Coventry . She is the eldest daughter of June Pughe FBBO, the Founder and Principal of the Allesley School of Dance in Coventry. [ 2 ] Dougall was one of the first 30 girls to attend King Henry VIII School . [ 3 ] In 1978, Dougall competed in the inaugural BBC Young Musician of the Year competition.
Dougall was inaugurated as President of the International Association of Disability and Oral Health (iADH) at its general assembly meeting on 3 October 2020. [ 4 ] [ 5 ]
|
https://en.wikipedia.org/wiki/Alison_Dougall
|
The term All-on-4 , also known as All-on-Four [ 1 ] and All-in-Four , [ 2 ] refers to 'all' teeth being supported 'on four' dental implants . The name All-on-4 is a registered trademark of Nobel Biocare, used globally for both dental products and services. The treatment concept is a prosthodontics procedure [ 3 ] [ 4 ] for total rehabilitation of the edentulous (toothless) patient, or for patients with badly broken down teeth, decayed teeth , or compromised teeth due to gum disease . It consists of the rehabilitation of either edentulous or dentate maxilla and / or mandible with fixed prosthesis by placing four implants in the anterior maxilla , where bone density is higher. The four implants support a fixed prosthesis with 10 to 14 teeth, and it is placed immediately, typically within 24 hours of surgery.
The All-On-4 solution, with the latest technology in computer aid design/Mill (cad/cam) has evolved including the All-on-bar concept, which is adding a milled titanium bar structure to the dental implants, which helps them working together to protect the implants from failure, even after the hybrid bridge is broken. This concept helps the clinician provide a better long-lasting solution, instead of a conversion-denture which is a chair side repair and modified denture. The All-On-Bar reduces the appointments, eliminating the Denture Conversion technique, by replacing it with a long lasting hybrid. Some patients keep this option as their final due to a lower budget or because the space is limited for other final solutions.
PMMA (polymethyl methacrylate AKA acrylic) or denture teeth over the titanium bar wears out over time and needs replacement, this is a controversial topic since the PMMA has the advantage of being shock absorbent. This helps the implants receive less stress during mastication forces but keeping a solid structure on the inside. Many professionals think this is a better solution, keeping in mind that the bridge can be switched to a new one a few years after.
In recent years zirconium has become a highly researched material and has shown to be one of the best options for the prosthetic teeth (Manufactured by Zirkonzahn [ 5 ] ) used in the All-on-4 procedure. [ 6 ] Implants created from zirconium have many benefits and are much more durable than your average, run of the mill ceramic or PMMA implants. Unlike dentures which can slip out of place or ceramic and PMMA veneers which are prone to chip, zirconium implants offer longer longevity. Thus, they are often seen as a lifelong investment rather than a temporary solution. Zirconia is also a natural compound, and its translucent material allows light to pass through, creating a more natural and whiter smile compared to more traditional materials that block the light making teeth appear false. [ 7 ]
Implant manufacturer Nobel Biocare AB of Gothenburg , Sweden, was among the first to identify the evolution of the All-on-4 technique as a potential valid and cost-effective alternative to conventional implant techniques, [ 8 ] and funded studies by Portuguese dentist Paulo Maló [ 1 ] to determine the efficacy of this approach. [ 9 ] [ 10 ] During this time, this technique was also used by various other clinicians around the world.
All-on-4 is not an invention, but rather a treatment technique that has evolved over time, and has the following features:
The All-on-4 treatment concept is a prosthodontic procedure (i.e replacement of missing teeth) that provides a permanent, screw-retained, same-day replacement for the entire upper and / or lower set of teeth with a bridge or denture . The procedure is best for patients with significant tooth loss or decay, and for people whose bone loss in the jaw area prevents them from getting conventionally oriented (vertical) dental implants. Often, tooth loss is accompanied by loss of the jaw bone, which poses the problem of reconstruction of the jaw bone requiring bone grafting . The All-on-4 technique takes advantage of the dense bone that remains in the front part of the jaws, and by placing the two posterior implants on an angle to avoid the sinus cavities in the upper jaw and the nerve canal in the lower jaw.
The cost of the All on 4 procedure varies based on the final prosthetic material. Acrylic resin teeth over titanium bar is substantially cheaper resulting in a total cost of around $30K per arch/jaw in the United States. Premium prosthetic materials like Zirconium can result in a total treatment cost between $36K to $40k per arch/jaw in the United States. The cost of all on 4 dental implants are similar in Europea and in the Uk but with the rising popularity of dental tourism the average costs are significantly lower (50%-70%)in countries such as Thailand, Mexico and Turkey. [ 14 ] For the implementation to be successful a careful analysis of the bone structure needs to be made. The most ideal way to evaluate the bone is by a cone beam computed tomography (CBCT) scan. The All-on-4 protocol is for at least four implants to be placed in a jaw. The back implants are typically angled approximately 30 to 45 degrees from the occlusion (biting plane). The implant is placed in front of the maxillary sinus in the upper jaw ( maxilla ), and in front of the mental nerve in the lower jaw ( mandible ). The head of the implant emerges in approximately the second premolar position. This will allow a molar tooth to be cantilevered posterior, resulting in a denture or bridge with approximately twelve teeth. [ 2 ]
|
https://en.wikipedia.org/wiki/All-on-4
|
AllTrials (sometimes called All Trials or AllTrials.net ) is a project advocating that clinical research adopt the principles of open research . The project summarizes itself as "All trials registered, all results reported": that is, all clinical trials should be listed in a clinical trials registry , and their results should always be shared as open data .
At the center of the organisation is a petition signed by over 85,000 individuals and
599 organisations (as of August 2015):
Thousands of clinical trials have not reported their results; some have not even been registered.
Information on what was done and what was found in these trials could be lost forever to doctors and researchers, leading to bad treatment decisions, missed opportunities for good medicine, and trials being repeated.
All trials past and present should be registered, and the full methods and the results reported.
We call on governments, regulators and research bodies to implement measures to achieve this.
Ben Goldacre , author of Bad Science and Bad Pharma , is a founder of the campaign and its most public spokesperson. In 2016, he participated in the launch of the OpenTrials database. [ 1 ]
AllTrials is an international initiative of Bad Science , BMJ , Centre for Evidence-based Medicine , Cochrane Collaboration , James Lind Initiative, PLOS and Sense about Science and is being led in the US by Sense about Science USA, Dartmouth's Geisel School of Medicine and the Dartmouth Institute for Health Policy & Clinical Practice. [ 2 ]
The project is a reaction to under-reporting of research. [ 3 ] [ 4 ] [ 5 ] [ 6 ]
A substantial proportion (estimates range from one-third to one-half) of medical research goes unpublished. [ 7 ] It has also been shown that negative findings are less likely to be published than positive ones, even in the absence of conflicts of interest. [ citation needed ]
Much medical research is done by the pharmaceutical industry, which have a conflict of interest reporting results which may hurt sales of their products. [ 8 ] There is a measurable funding bias in reporting; studies have shown that published drug studies funded by pharmaceutical companies are much more likely to support the use of the tested drug than studies with other funding. Industry-funded trials are also less likely to be published. [ 7 ] [ 9 ]
If the statistical methods used to analyse the trial are not chosen before the study it started, there is a danger that researchers will intentionally or unintentionally pick the method that gives the results they expect, or which gives the most significant results. This makes the analysis statistically invalid .
Not publishing trials which fail to find a clear effect exposes trial volunteers to pointless risk [ 10 ] and wastes research effort (as the same trial is repeated over and over). It also biases the medical literature, making it report effects where none exist (since, given enough trials, eventually one will find a difference by pure chance). [ 11 ]
Pre-trial registration makes non-publication and changes in analysis methods obvious to medical reviewers. It also enables authors of meta-studies to track down and analyse missing data. Finally, it lets doctors and patients know when a trial is looking for volunteers. [ 10 ]
There are other sources of bias, such as the conditions sometimes attached to funding by funding agencies with a financial interest in the trial's outcome. Medical researchers may be asked to agree to allow the funding agency to censor results. Some funding agencies may also refuse to give the medical researcher access to the raw data, giving them only the finished analysis, or even a draft paper, and asking them to put their name to it. This is not acceptable academic practice, and some academic journals require that authors sign a statement that they have not entered into such agreements. [ 8 ] [ 9 ]
Ben Goldacre , a physician and spokesperson for the campaign, would like to address the systematic flaws in clinical research which cause data to be lost after it is gathered. [ 12 ] [ 13 ] [ 14 ] [ 15 ] [ 16 ] [ 17 ] [ 18 ]
The campaign has been widely covered, and supported, in the academic press. The British Medical Journal and PLOS are founding members. Nature [ 19 ] and The Lancet [ 20 ] both published supportive articles in January 2014.
There has also been mainstream media coverage. [ 21 ]
There has been criticism from the Pharmaceutical Research and Manufacturers of America (PhRMA), with senior vice-president Matt Bennett saying that trial data disclosure measures which AllTrials has recommended to the European Medicines Agency "could risk patient privacy, lead to fewer clinical trials, and result in fewer new medicines to meet patient needs and improve health.". [ 22 ]
AllTrials have published a detailed statement [ 23 ] of exactly what they want to see published, which states "The AllTrials campaign is not calling for individual patient data to be made publicly available".
A 2012 editorial published by senior regulators from the European Medicines agency [ 24 ] largely agreed with AllTrials, saying "We consider it neither desirable nor realistic to maintain the status quo of limited availability of regulatory trials data". They were also of the opinion that adequate standards for protection of personal data could be written. However, they warned that third party reanalysis was neither a guarantee of quality nor of lack of conflict of interest, which, in the worst case, could lead to negative public health consequences. [ citation needed ]
They suggested that reanalyses should therefore be subject to the same regulations as sponsor analyses, such as registering analysis plans. They argued against completely unrestricted access to data, but in favor of broader access. [ 24 ] AllTrials is not calling for completely unrestricted access to raw data, [ 23 ] so the scope of disagreements is limited to what restrictions should be in place.
The campaign is an initiative of Sense about Science , [ 25 ] Centre for Evidence Based Medicine , The Dartmouth Institute for Health Policy and Clinical Practice , [ 26 ] James Lind Alliance , Cochrane Collaboration , [ 27 ] [ 28 ] BMJ Group , PLOS , [ 29 ] and Bad Science . The petition statement of AllTrials has been signed by organizations including Wellcome Trust , [ 30 ] British Library , Medical Research Council (UK) , British Heart Foundation , Institute for Quality and Efficiency in Health Care , National Institute for Health and Care Excellence , BioMed Central , [ 31 ] National Physicians Alliance , Royal Society of Medicine , Health Research Authority , American Medical Student Association , GlaxoSmithKline , [ 32 ] and others.
As of May 2017, The AllTrials petition has been signed by 90,282 people and 721 organisations. [ 33 ] In October 2016, AllTrials published a road map detailing steps that various types of organisations can take to get more trials registered and more results reported. [ 34 ]
85 investors with >€3.5 trillion (£2.45trn; $3.83trn) of investments have supported AllTrials (as of July 2015), with Peter van der Werf of RobecoSAM saying: "We deem this to be a financially material factor and encourage all companies to gain credibility regarding their approach to clinical trial transparency by signing up to the AllTrials principles.". [ 35 ] The Laura and John Arnold Foundation provided early and ongoing financial support. [ 36 ]
The original policy of the Coalition for Epidemic Preparedness Innovations required that funded parties pre-register any trials in a clinical trials registry , publish results within a year of study completion (except with compelling reason and permission of CEPI), publish results in open-access articles, and have mechanisms for securely sharing underlying data and results, including negative results, in a way that preserves trial volunteer privacy. In May 2018 the CEPI proposed changing the policy to remove these provisions. [ 37 ] The policy was changed by the CEPI in December 2018. [ 38 ] [ 39 ]
The European Federation of Pharmaceutical Industries and Associations and Pharmaceutical Research and Manufacturers of America have expressed interest in lobbying against the campaign. [ 40 ] Campaign supporters criticized Hoffmann-La Roche 's plans to be more open but not to the extent requested by AllTrials. [ 41 ] [ 42 ]
|
https://en.wikipedia.org/wiki/AllTrials
|
All in the Mind is a half-hour magazine radio programme about psychology and psychiatry , broadcast in weekly episodes on Radio 4 and produced by the BBC's Science Unit. [ 1 ] It is currently presented by Claudia Hammond . [ 2 ] Former presenters have included Raj Persaud , [ 3 ] Kwame McKenzie , Tanya Byron , [ 4 ] and the first presenter of the series, Anthony Clare .
The programme is typically broadcast at 9 pm on a Tuesday, with a repeat the next day (Wednesday) at 3:30 pm.
Episode descriptions are largely as provided by the BBC. [ 5 ]
|
https://en.wikipedia.org/wiki/All_in_the_Mind_(BBC_radio)
|
The incidence of life-threatening hypersensitivity reactions occurring during surgery and anesthesia is around one in 10,000 procedures. [ 1 ] Severe allergic reactions to anesthetic medications are rare and are usually attributable to factors other than the anesthetic. Neuromuscular blocking agents , natural rubber latex , and antibiotics are the most common causes of serious allergic reactions during surgery. [ 2 ] The mortality rate from these reactions ranges between 3-9%. [ 3 ]
Successful immediate treatment requires prompt recognition by the attending anesthetist , or in the US, the attending anesthesiologist or nurse anesthetist. Anesthetists are trained to recognise if an allergic reaction is occurring. The identification of a complication is made by the recognition of issues such as low blood pressure, hives, wheezing, rash, swelling around the eyes or in the mouth and throat and other breathing difficulties. [ 4 ] Adrenaline (epinephrine) remains the mainstay of treatment, with corticosteroids and antihistamines providing limited benefit in the acute situation.
Subsequent investigation aims to determine the responsible agent to allow its future avoidance. Skin testing is often useful to identify potentially cross-reactive compounds and appropriate therapeutic alternatives. This is done weeks after the initial reaction to allow the immune system to reset itself. However, skin testing can be misleading in giving false positive and false negative results.
Although complications during anesthesia are rare, potentially life-threatening consequences may occur if an anaphylactic reaction develops. The severity of the reaction whilst under anesthesia is because the anesthetist is only made aware of the allergy when it is severe enough to compromise the cardiovascular system and the respiratory system. At this stage, there is little time to manage the situation and recognise the severity of the condition. [ 5 ]
The immediate management of the issue consists of three processes:
Since the full withdrawal of the offending substance is near impossible, the administration of adrenaline is the main treatment to counteract the effects. Once the patient is stable they will need close observation for 24 hours. [ 5 ]
This surgery article is a stub . You can help Wikipedia by expanding it .
|
https://en.wikipedia.org/wiki/Allergic_reactions_to_anesthesia
|
The Alliance for Heart Failure is a coalition of charities, patient groups, professional bodies, public sector organisations and corporate members working together to raise the profile of heart failure within the UK Government , the National Health Service , and media . It was formed in October 2015.
The Alliance for Heart Failure's mission is to achieve better outcomes for people with heart failure by ensuring timely diagnosis and access to the right care and support.
Current members of the Alliance for Heart Failure are:
The co-chairs are Preeti Minhas from Health Education for Health and Richard Corder from Cardiovascular Care Partnership . They have a 12-month tenure. Day-to-day decisions are made by a steering committee.
The Alliance for Heart Failure is supported and funded by AstraZeneca UK , Boehringer Ingelheim Limited , Medtronic Limited , Novartis Pharmaceuticals UK Ltd , and Roche Diagnostics Ltd . Funders are not responsible for any of the materials produced by the Alliance for Heart Failure, which are created independently by the Alliance's Secretariat.
Heart Failure: A call to action was published on 22 February 2021. The report evaluates the progress made since the 2016 All Party Parliamentary Group ‘Focus on Heart Failure’ report and makes ten new recommendations to improve heart failure care and patient outcomes.
The report also calls for urgent action to meet the growing demand from a rising number of heart failure cases following the impact of the COVID-19 pandemic [1] [2] .
Heart Failure: A call to action was developed with input from heart failure specialists, patient groups, and professional organisations.
In 2016, the All Party Parliamentary Group on Heart Disease, chaired by Stuart Andrew MP , held an inquiry into living with heart failure . Written and oral evidence was provided by patients, healthcare professionals, and commissioners. The Inquiry's report, Focus on Heart Failure , was published in September 2016 and made ten recommendations for improving heart failure services.
Nine members of the Alliance for Heart Failure were co-opted onto an advisory panel for the inquiry. The panel had ten members in total.
The National Heart Failure Audit which analysed data from 2020 to 2021, highlighted a serious issue with access to echocardiography services, a vital diagnostic tool for heart failure, as well as a problem with follow up specialist care and cardiac rehabilitation for those living long-term with the illness. It also highlighted the chronic challenge of training and developing echocardiographers to ensure sufficient resources to meet demand in the future.
The Alliance for Heart Failure responded to the report stating that longstanding issues have been exacerbated, rather than caused, by the COVID-19 pandemic.
The National Heart Failure Audit (2017–18), published on 12 September 2019, reported that mortality among patients admitted to hospital remained high overall at 10.1% compared to 9.4% in the previous audit. However, the number of patients seen by heart failure specialists increased to over 82% (from 80% in the last audit), while more than 88% of patients get an echocardiogram. Rates still remain higher for those admitted to Cardiology (92%), however this has decreased since the last report (96%). The rate on General Medical wards remained the same at 84%. The report also recorded an increase in the prescription of key disease-modifying medicines for patients since last year.
The Alliance for Heart Failure responded positively to the report but called for the regional variation in patient service to be urgently addressed.
The National Confidential Enquiry into Patient Outcome and Death (NCEPOD) , published on 22 November 2018, recommended improvements in the process of care for patients with acute heart failure who died while admitted to hospital as an emergency. Responding to the report , the Alliance for Heart Failure said that it reinforces the need for urgent action to improve heart failure services, and the important role of heart failure specialist nurses, as part of a full multi-disciplinary heart failure team, in maximising outcomes for patients.
|
https://en.wikipedia.org/wiki/Alliance_for_Heart_Failure
|
Subsets and Splits
No community queries yet
The top public SQL queries from the community will appear here once available.