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What is (are) Spinocerebellar ataxia 15 ?
|
Spinocerebellar ataxia 15 (SCA15) is a neurological condition characterized by slowly progressive gait and limb ataxia, often in combination with eye movement abnormalities and balance, speech and swallowing difficulties. The onset of symptoms typically occurs between ages 7 and 66 years. The ability to walk independently is often maintained for many years following onset of symptoms. SCA15 is caused by mutations in the ITPR1 gene. It is inherited in an autosomal dominant manner. Diagnosis is based on clinical history, physical examination, molecular genetic testing, and exclusion of other similar diseases. There is no effective treatment known to modify disease progression. Patients may benefit from occupational and physical therapy for gait dysfunction and speech therapy for dysarthria.
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What are the symptoms of Gracile bone dysplasia ?
|
What are the signs and symptoms of Gracile bone dysplasia? The Human Phenotype Ontology provides the following list of signs and symptoms for Gracile bone dysplasia. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormality of bone mineral density 90% Abnormality of the spleen 90% Bowing of the long bones 90% Decreased skull ossification 90% Micromelia 90% Narrow mouth 90% Recurrent fractures 90% Short philtrum 90% Short stature 90% Skeletal dysplasia 90% Slender long bone 90% Tented upper lip vermilion 90% Abnormality of pelvic girdle bone morphology 50% Abnormality of the clavicle 50% Abnormality of the fingernails 50% Abnormality of the helix 50% Abnormality of the metacarpal bones 50% Abnormality of the metaphyses 50% Abnormality of the ribs 50% Anteverted nares 50% Aplasia/Hypoplasia affecting the eye 50% Aplasia/Hypoplasia of the lungs 50% Aplasia/Hypoplasia of the thymus 50% Brachydactyly syndrome 50% Cloverleaf skull 50% Depressed nasal bridge 50% Enlarged thorax 50% Frontal bossing 50% Hypoplasia of penis 50% Intrauterine growth retardation 50% Low-set, posteriorly rotated ears 50% Malar flattening 50% Platyspondyly 50% Renal hypoplasia/aplasia 50% Respiratory insufficiency 50% Short distal phalanx of finger 50% Short nose 50% Short toe 50% Tapered finger 50% Wide nasal bridge 50% Abnormality of neuronal migration 7.5% Abnormality of the fontanelles or cranial sutures 7.5% Aplasia/Hypoplasia involving the nose 7.5% Aplasia/Hypoplasia of the eyebrow 7.5% Blepharophimosis 7.5% Blue sclerae 7.5% Cataract 7.5% Cleft palate 7.5% Cryptorchidism 7.5% Displacement of the external urethral meatus 7.5% Hepatomegaly 7.5% Hypertelorism 7.5% Hypotelorism 7.5% Iris coloboma 7.5% Microcornea 7.5% Muscular hypotonia 7.5% Oligohydramnios 7.5% Rocker bottom foot 7.5% Upslanted palpebral fissure 7.5% Asplenia 5% Aniridia - Ascites - Autosomal dominant inheritance - Failure to thrive - Flared metaphysis - Hydrocephalus - Hypocalcemia - Hypoplastic spleen - Micropenis - Microphthalmia - Prominent forehead - Seizures - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
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] |
What is (are) Optic atrophy 1 ?
|
Optic atrophy 1 is a condition that mainly affects vision, but may include other features. Vision loss typically begins within the first decade of life; severity varies widely among affected people (from nearly normal vision to complete blindness), even among members of the same family. Vision problems may include difficulty distinguishing colors, progressive narrowing of the field of vision (tunnel vision) and an abnormally pale appearance (pallor) of the optic nerve. Additional, less common abnormalities may include sensorineural hearing loss, ataxia, myopathy (muscle disease) and other neurological findings. It is usually caused by mutations in the OPA1 gene, although some individuals with optic atrophy 1 do not have identified mutations in this gene, in which case the cause of the condition is unknown. This condition is inherited in an autosomal dominant pattern but some cases result from a new mutation in the gene and occur in people with no history of the disorder in their family. Treatment focuses on individual symptoms when possible.
|
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[
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1,
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15
] |
What is (are) Lymphatic filariasis ?
|
Lymphatic filariasis is a parasitic disease caused by microscopic, thread-like worms that only live in the human lymph system, which maintains the body's fluid balance and fights infections. It is spread from person to person by mosquitoes. Most infected people are asymptomatic and never develop clinical symptoms. A small percentage of people develop lymphedema, which may affect the legs, arms, breasts, and genitalia; bacterial infections that cause hardening and thickening of the skin, called elephantiasis; hydrocele (swelling of the scrotum) in men; and pulmonary tropical eosinophilia syndrome. Treatment may include a yearly dose of medicine, called diethylcarbamazine (DEC); while this drug does not kill all of the adult worms, it prevents infected people from giving the disease to someone else.
|
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3095,
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What is (are) Wandering spleen ?
|
Wandering spleen is a rare condition that occurs when the spleen lacks one or more of the ligments that hold the spleen in its normal position in the upper left abdomen. If a person is born with this condition it is referred to as congenital wandering spleen. The condition is not hereditary. Acquired wandering spleen may occur during adulthood due to injuries or other underlying conditions that may weaken the ligaments that hold the spleen. Symptoms of wandering spleen may include englargement of the spleen (splenomegaly), abdominal pain, intestinal obstruction, nausea, vomiting, fever, and a lump in the abdomen or the pelvis. Some individuals with this condition do not have symptoms. Treatment for this condition involes removal of the spleen (splenectomy).
|
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What causes Tumor necrosis factor receptor-associated periodic syndrome ?
|
What causes tumor necrosis factor receptor-associated periodic syndrome (TRAPS)? TRAPS is a genetic condition caused by mutations in a gene called TNFRSF1A. This gene gives the body instructions to make a protein called tumor necrosis factor receptor 1 (TNFR1). This protein exists in cell membranes where it binds to another protein called tumor necrosis factor (TNF). The binding sends signals that tell the cells to trigger inflammation (producing immune system proteins) or self-destruct. Most TNFRSF1A gene mutations that cause TRAPS result in incorrectly-shaped TNFR1 proteins, which become trapped in cells and cannot reach the surface to bind with TNF. The trapped proteins then clump together and are thought to trigger other pathways involved in causing inflammation. Affected people typically have a mutation in only one of their 2 copies of the TNFRSF1A gene, so some normal TNFR1 proteins are still produced, leading to even more inflammation. This is what leads to excess inflammation in people with TRAPS. It is unclear if abnormalities in the cells' ability to self-destruct also plays a role in causing the features of TRAPS.
|
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] |
What are the symptoms of Macrothrombocytopenia progressive deafness ?
|
What are the signs and symptoms of Macrothrombocytopenia progressive deafness? The Human Phenotype Ontology provides the following list of signs and symptoms for Macrothrombocytopenia progressive deafness. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormal bleeding - Abnormality of the eye - Abnormality of the urinary system - Autosomal dominant inheritance - Bruising susceptibility - Giant platelets - Progressive sensorineural hearing impairment - Prolonged bleeding time - Thrombocytopenia - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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What is (are) Multi-Infarct Dementia ?
|
Multi-infarct dementia (MID) is a common cause of memory loss in the elderly. MID is caused by multiple strokes (disruption of blood flow to the brain). Disruption of blood flow leads to damaged brain tissue. Some of these strokes may occur without noticeable clinical symptoms. Doctors refer to these as silent strokes. An individual having asilent stroke may not even know it is happening, but over time, as more areas of the brain are damaged and more small blood vessels are blocked, the symptoms of MID begin to appear. MID can be diagnosed by an MRI or CT of the brain, along with a neurological examination. Symptoms include confusion or problems with short-term memory; wandering, or getting lost in familiar places; walking with rapid, shuffling steps; losing bladder or bowel control; laughing or crying inappropriately; having difficulty following instructions; and having problems counting money and making monetary transactions. MID, which typically begins between the ages of 60 and 75, affects men more often than women. Because the symptoms of MID are so similar to Alzheimers disease, it can be difficult for a doctor to make a firm diagnosis. Since the diseases often occur together, making a single diagnosis of one or the other is even more problematic.
|
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] |
What are the genetic changes related to Costeff syndrome ?
|
Mutations in the OPA3 gene cause Costeff syndrome. The OPA3 gene provides instructions for making a protein whose exact function is unknown. The OPA3 protein is found in structures called mitochondria, which are the energy-producing centers of cells. Researchers speculate that the OPA3 protein is involved in regulating the shape of mitochondria. OPA3 gene mutations that result in Costeff syndrome lead to a loss of OPA3 protein function. Cells without any functional OPA3 protein have abnormally shaped mitochondria. These cells likely have reduced energy production and die sooner than normal, decreasing energy availability in the body's tissues. It is unclear why the optic nerves and the parts of the brain that control movement are particularly affected.
|
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] |
Is corticosteroid-binding globulin deficiency inherited ?
|
This condition is reported to have an autosomal recessive pattern of inheritance, which means both copies of the gene in each cell have mutations. The parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene, but they typically do not show signs and symptoms of the condition. However, some people with only one SERPINA6 gene mutation may have symptoms such as fatigue or chronic pain. Alternatively, individuals with two SERPINA6 gene mutations may not have any features of the disorder. It is unclear why some people with mutations have features of the disorder and others do not.
|
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What are the treatments for X-linked sideroblastic anemia ?
|
These resources address the diagnosis or management of X-linked sideroblastic anemia: - Genetic Testing Registry: Hereditary sideroblastic anemia - MedlinePlus Encyclopedia: Anemia These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
|
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Is fatty acid hydroxylase-associated neurodegeneration inherited ?
|
This condition is inherited in an autosomal recessive pattern, which means both copies of the gene in each cell have mutations. The parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene, but they typically do not show signs and symptoms of the condition.
|
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What are the symptoms of Long QT syndrome 8 ?
|
What are the signs and symptoms of Long QT syndrome 8? The Human Phenotype Ontology provides the following list of signs and symptoms for Long QT syndrome 8. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Prolonged QT interval - Sudden death - Syndactyly - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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What is (are) autoimmune polyglandular syndrome, type 1 ?
|
Autoimmune polyglandular syndrome, type 1 is an inherited condition that affects many of the body's organs. It is one of many autoimmune diseases, which are disorders that occur when the immune system malfunctions and attacks the body's tissues and organs by mistake. In most cases, the signs and symptoms of autoimmune polyglandular syndrome, type 1 begin in childhood or adolescence. This condition is characterized by three specific features: mucocutaneous candidiasis, hypoparathyroidism, and Addison disease. Affected individuals typically have at least two of these features, and many have all three. Mucocutaneous candidiasis is a fungal infection that affects the skin and mucous membranes, such as the moist lining of the nose and mouth. In children with autoimmune polyglandular syndrome, type 1, these infections last a long time and tend to recur. Many affected children also develop hypoparathyroidism, which is a malfunction of the parathyroid glands. These glands secrete a hormone that regulates the body's use of calcium and phosphorus. Hypoparathyroidism can cause a tingling sensation in the lips, fingers, and toes; muscle pain and cramping; weakness; and fatigue. The third major feature, Addison disease, results from a malfunction of the small hormone-producing glands on top of each kidney (adrenal glands). The main features of Addison disease include fatigue, muscle weakness, loss of appetite, weight loss, low blood pressure, and changes in skin coloring. Autoimmune polyglandular syndrome, type 1 can cause a variety of additional signs and symptoms, although they occur less often. Complications of this disorder can affect the skin and nails, the gonads (ovaries and testicles), the eyes, a butterfly-shaped gland at the base of the neck called the thyroid, and the digestive system. Type 1 diabetes also occurs in some patients with this condition.
|
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What are the symptoms of Hereditary hemorrhagic telangiectasia type 4 ?
|
What are the signs and symptoms of Hereditary hemorrhagic telangiectasia type 4? The Human Phenotype Ontology provides the following list of signs and symptoms for Hereditary hemorrhagic telangiectasia type 4. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Epistaxis 90% Telangiectasia of the skin 90% Cavernous hemangioma 50% Microcytic anemia 50% Migraine 50% Portal hypertension 50% Spontaneous hematomas 50% Visceral angiomatosis 50% Abnormality of coagulation 7.5% Abnormality of the retinal vasculature 7.5% Biliary tract abnormality 7.5% Cerebral ischemia 7.5% Cirrhosis 7.5% Congestive heart failure 7.5% Conjunctival telangiectasia 7.5% Esophageal varix 7.5% Gastrointestinal hemorrhage 7.5% Hematuria 7.5% Hemoptysis 7.5% Hepatic failure 7.5% Intestinal polyposis 7.5% Nephrolithiasis 7.5% Peripheral arteriovenous fistula 7.5% Pulmonary embolism 7.5% Pulmonary hypertension 7.5% Seizures 7.5% Thrombophlebitis 7.5% Visual impairment 7.5% Arteriovenous fistulas of celiac and mesenteric vessels - Autosomal dominant inheritance - Celiac artery aneurysm - Cerebral arteriovenous malformation - Cerebral hemorrhage - Cyanosis - Dyspnea - High-output congestive heart failure - Ischemic stroke - Lip telangiectasia - Mesenteric artery aneurysm - Nasal mucosa telangiectasia - Palate telangiectasia - Pulmonary arteriovenous malformation - Right-to-left shunt - Spinal arteriovenous malformation - Spontaneous, recurrent epistaxis - Subarachnoid hemorrhage - Tongue telangiectasia - Transient ischemic attack - Venous varicosities of celiac and mesenteric vessels - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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Is Hereditary leiomyomatosis and renal cell cancer inherited ?
|
How is hereditary leiomyomatosis and renal cell cancer inherited? Hereditary leiomyomatosis and renal cell cancer (HLRCC) is inherited in an autosomal dominant pattern, which means that having one mutated copy of the gene in each cell is enough to cause symptoms of the condition. In some cases, an affected person inherits the mutated copy of the gene from an affected parent. Other cases result from new mutations in the gene and that occur for the first time in in the affected individual. When an individual with an autosomal dominant condition has children, each child has a 50% (1 in 2) risk to inherit the mutated gene. This is the case regardless of which parent has the condition.
|
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What are the treatments for Colorectal Cancer ?
|
Even if the doctor removes all the cancer that can be seen at the time of the operation, many patients receive chemotherapy after surgery to kill any cancer cells that are left. Chemotherapy treatment after surgery -- to increase the chances of a cure -- is called adjuvant therapy. Researchers have found that patients who received adjuvant therapy usually survived longer and went for longer periods of time without a recurrence of colon cancer than patients treated with surgery alone. Patients age 70 and older benefited from adjuvant treatment as much as their younger counterparts. In fact, adjuvant therapy is equally as effective -- and no more toxic -- for patients 70 and older as it is for younger patients, provided the older patients have no other serious diseases. Adjuvant chemotherapy is standard treatment for patients whose cancer is operable and who are at high risk for a recurrence of the disease. Most cases of colon cancer occur in individuals age 65 and over. But studies have shown that older patients receive adjuvant chemotherapy less frequently than younger patients.
|
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What causes Hypotension ?
|
Conditions or factors that disrupt the body's ability to control blood pressure cause hypotension. The different types of hypotension have different causes.
Orthostatic Hypotension
Orthostatic hypotension has many causes. Sometimes two or more factors combine to cause this type of low blood pressure.
Dehydration (de-hi-DRA-shun) is the most common cause of orthostatic hypotension. Dehydration occurs if the body loses more water than it takes in.
You may become dehydrated if you don't drink enough fluids or if you sweat a lot during physical activity. Fever, vomiting, and severe diarrhea also can cause dehydration.
Orthostatic hypotension also may occur during pregnancy, but it usually goes away after birth.
Because an older body doesn't manage changes in blood pressure as well as a younger body, getting older also can lead to this type of hypotension.
Postprandial hypotension (a type of orthostatic hypotension) mostly affects older adults. Postprandial hypotension is a sudden drop in blood pressure after a meal.
Certain medical conditions can raise your risk of orthostatic hypotension, including:
Heart conditions, such as heart attack, heart valve disease, bradycardia (a very low heart rate), and heart failure. These conditions prevent the heart from pumping enough blood to the body.
Anemia.
Severe infections.
Endocrine conditions, such as thyroid disorders, Addison's disease, low blood sugar, and diabetes.
Central nervous system disorders, such as Parkinson's disease.
Pulmonary embolism.
Some medicines for high blood pressure and heart disease can raise your risk of orthostatic hypotension. These medicines include:
Diuretics, also called "water pills"
Calcium channel blockers
Angiotensin-converting enzyme (ACE) inhibitors
Angiotensin II receptor blockers
Nitrates
Beta blockers
Medicines for conditions such as anxiety, depression, erectile dysfunction, and central nervous system disorders also can increase your risk of orthostatic hypotension.
Other substances, when taken with high blood pressure medicines, also can lead to orthostatic hypotension. These substances include alcohol, barbiturates, and some prescription and over-the-counter medicines.
Finally, other factors or conditions that can trigger orthostatic hypotension include being out in the heat or being immobile for a long time. "Immobile" means you can't move around very much.
Neurally Mediated Hypotension
Neurally mediated hypotension (NMH) occurs when the brain and heart don't communicate with each other properly.
For example, when you stand for a long time, blood begins to pool in your legs. This causes your blood pressure to drop. In NMH, the body mistakenly tells the brain that blood pressure is high. In response, the brain slows the heart rate. This makes blood pressure drop even more, causing dizziness and other symptoms.
Severe Hypotension Linked to Shock
Many factors and conditions can cause severe hypotension linked to shock. Some of these factors also can cause orthostatic hypotension. In shock, though, blood pressure drops very low and doesn't return to normal on its own.
Shock is an emergency and must be treated right away. If a person has signs or symptoms of shock, call 911.
Some severe infections can cause shock. This is known as septic shock. It can occur if bacteria enter the bloodstream. The bacteria release a toxin (poison) that leads to a dangerous drop in blood pressure.
A severe loss of blood or fluids from the body also can cause shock. This is known as hypovolemic (HI-po-vo-LE-mik) shock. Hypovolemic shock can happen as a result of:
Major external bleeding (for example, from a severe cut or injury)
Major internal bleeding (for example, from a ruptured blood vessel or injury that causes bleeding inside the body)
Major loss of body fluids from severe burns
Severe swelling of the pancreas (an organ that produces enzymes and hormones, such as insulin)
Severe diarrhea
Severe kidney disease
Overuse of diuretics
A major decrease in the heart's ability to pump blood also can cause shock. This is known as cardiogenic (KAR-de-o-JEN-ik) shock.
A heart attack, pulmonary embolism, or an ongoing arrhythmia (ah-RITH-me-ah) that disrupts heart function can cause this type of shock.
A sudden and extreme relaxation of the arteries linked to a drop in blood pressure also can cause shock. This is known as vasodilatory (VA-so-DI-la-tory) shock. It can occur due to:
A severe head injury
A reaction to certain medicines
Liver failure
Poisoning
A severe allergic reaction (called anaphylactic (AN-a-fi-LAK-tik) shock)
|
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] |
How to diagnose Prostate Cancer ?
|
The doctor may order other exams, including ultrasound, MRI, or CT scans, to learn more about the cause of the symptoms. But to confirm the presence of cancer, doctors must perform a biopsy. During a biopsy, the doctor uses needles to remove small tissue samples from the prostate and then looks at the samples under a microscope. If a biopsy shows that cancer is present, the doctor will report on the grade of the tumor. Doctors describe a tumor as low, medium, or high-grade cancer, based on the way it appears under the microscope.
|
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What is (are) Leg Injuries and Disorders ?
|
Your legs are made up of bones, blood vessels, muscles, and other connective tissue. They are important for motion and standing. Playing sports, running, falling, or having an accident can damage your legs. Common leg injuries include sprains and strains, joint dislocations, and fractures. These injuries can affect the entire leg, or just the foot, ankle, knee, or hip. Certain diseases also lead to leg problems. For example, knee osteoarthritis, common in older people, can cause pain and limited motion. Problems in your veins in your legs can lead to varicose veins or deep vein thrombosis.
|
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Who is at risk for Smoking and Your Heart? ?
|
The chemicals in tobacco smoke harm your heart and blood vessels in many ways. For example, they:
Contribute to inflammation, which may trigger plaque buildup in your arteries.
Damage blood vessel walls, making them stiff and less elastic (stretchy). This damage narrows the blood vessels and contributes to the damage caused by unhealthy cholesterol levels.
Disturb normal heart rhythms.
Increase your blood pressure and heart rate, making your heart work harder thannormal.
Lower your HDL (good) cholesterol and raise your LDL (bad) cholesterol. Smoking also increases your triglyceride level. Triglycerides are a type of fat found in theblood.
Thicken your blood and make it harder for your blood to carry oxygen.
Smoking and Heart Disease Risk
Smoking is a major risk factor for coronary heart disease, a condition in which plaque builds up inside the coronary arteries. These arteries supply your heart muscle with oxygen-rich blood.
When plaque builds up in the arteries, the condition is called atherosclerosis.
Plaque narrows the arteries and reduces blood flow to your heart muscle. The buildup of plaque also makes it more likely that blood clots will form in your arteries. Blood clots can partially or completely block blood flow.
Over time, smoking contributes to atherosclerosis and increases your risk of having and dying from heart disease, heart failure, or a heartattack.
Compared with nonsmokers, people who smoke are more likely to have heart disease and suffer from a heart attack. The risk of having or dying from a heart attack is even higher among people who smoke and already have heart disease.
For some people, such as women who use birth control pills and people who have diabetes, smoking poses an even greater risk to the heart and blood vessels.
Smoking is a major risk factor for heart disease. When combined with other risk factorssuch as unhealthy blood cholesterol levels, high blood pressure, and overweight or obesitysmoking further raises the risk of heart disease.
Smoking and the Risk of Peripheral Artery Disease
Peripheral artery disease (P.A.D.) is a disease in which plaque builds up in the arteries that carry blood to your head, organs, and limbs. Smoking is a major risk factor for P.A.D.
P.A.D. usually affects the arteries that carry blood to your legs. Blocked blood flow in the leg arteries can cause cramping, pain, weakness, and numbness in your hips, thighs, and calf muscles.
Blocked blood flow also can raise your risk of getting an infection in the affected limb. Your body might have a hard time fighting the infection.
If severe enough, blocked blood flow can cause gangrene (tissue death). In very serious cases, this can lead to leg amputation.
If you have P.A.D., your risk of heart disease and heart attack is higher than the risk for people who dont have P.A.D.
Smoking even one or two cigarettes a day can interfere with P.A.D. treatments. People who smoke and people who have diabetes are at highest risk for P.A.D. complications, including gangrene in the leg from decreased blood flow.
Secondhand Smoke Risks
Secondhand smoke is the smoke that comes from the burning end of a cigarette, cigar, or pipe. Secondhand smoke also refers to smoke thats breathed out by a person who is smoking.
Secondhand smoke contains many of the same harmful chemicals that people inhale when they smoke. It can damage the heart and blood vessels of people who dont smoke in the same way that active smoking harms people who do smoke. Secondhand smoke greatly increases adults risk of heart attack and death.
Secondhand smoke also raises the risk of future coronary heart disease in children and teens because it:
Damages heart tissues
Lowers HDL cholesterol
Raises blood pressure
The risks of secondhand smoke are especially high for premature babies who have respiratory distress syndrome and children who have conditions such asasthma.
Cigar and Pipe Smoke Risks
Researchers know less about how cigar and pipe smoke affects the heart and blood vessels than they do about cigarette smoke.
However, the smoke from cigars and pipes contains the same harmful chemicals as the smoke from cigarettes. Also, studies have shown that people who smoke cigars are at increased risk of heart disease.
|
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] |
What is (are) Q fever ?
|
Q fever is a worldwide disease with acute and chronic stages caused by the bacteria known as Coxiella burnetii. Cattle, sheep, and goats are the primary reservoirs although a variety of species may be infected. Organisms are excreted in birth fluids, milk, urine, and feces of infected animals and are able to survive for long periods in the environment. Infection of humans usually occurs by inhalation of these organisms from air that contains airborne barnyard dust contaminated by dried placental material, birth fluids, and excreta of infected animals. Other modes of transmission to humans, including tick bites, ingestion of unpasteurized milk or dairy products, and human to human transmission, are rare. Humans are often very susceptible to the disease, and very few organisms may be required to cause infection. In less than 5% of cases the affected people with acute Q fever infection develop a chronic Q fever. Treatment of the acute form is made with antibiotics. The chronic form's treatment depend on the symptoms.
|
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Is 22q11.2 deletion syndrome inherited ?
|
The inheritance of 22q11.2 deletion syndrome is considered autosomal dominant because a deletion in one copy of chromosome 22 in each cell is sufficient to cause the condition. Most cases of 22q11.2 deletion syndrome are not inherited, however. The deletion occurs most often as a random event during the formation of reproductive cells (eggs or sperm) or in early fetal development. Affected people typically have no history of the disorder in their family, though they can pass the condition to their children. In about 10 percent of cases, a person with this condition inherits the deletion in chromosome 22 from a parent. In inherited cases, other family members may be affected as well.
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Who is at risk for Osteoporosis? ?
|
The more likely you are to fall, the higher your risk for a fracture. And more severe falls increase your risk for fractures. Factors that increase your risk of falling and of fracturing a bone include - decreased muscle strength - poor balance - impaired eyesight - impaired mental abilities - certain medications, such as tranquilizers and muscle relaxants - hazardous elements in your living environment, such as slippery throw rugs and icy sidewalks. decreased muscle strength poor balance impaired eyesight impaired mental abilities certain medications, such as tranquilizers and muscle relaxants hazardous elements in your living environment, such as slippery throw rugs and icy sidewalks.
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How many people are affected by Liddle syndrome ?
|
Liddle syndrome is a rare condition, although its prevalence is unknown. The condition has been found in populations worldwide.
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How many people are affected by FOXG1 syndrome ?
|
FOXG1 syndrome appears to be rare. At least 30 affected individuals have been described in the medical literature.
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What causes Problems with Taste ?
|
The most common causes of taste disorders are medications, infections, head trauma, and dental problems. Most people who have a problem with taste are taking certain medications or they have had a head or neck injury. Gum disease, dry mouth, and dentures can contribute to taste problems, too. Other causes are radiation therapy for head and neck cancers, smoking, and some surgeries.
|
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What are the symptoms of Adrenal Insufficiency and Addison's Disease ?
|
Adrenal Insufficiency
The most common symptoms of adrenal insufficiency are
- chronic, or long lasting, fatigue - muscle weakness - loss of appetite - weight loss - abdominal pain
Other symptoms of adrenal insufficiency can include
- nausea - vomiting - diarrhea - low blood pressure that drops further when a person stands up, causing dizziness or fainting - irritability and depression - craving salty foods - hypoglycemia, or low blood sugar - headache - sweating - irregular or absent menstrual periods - in women, loss of interest in sex
Hyperpigmentation, or darkening of the skin, can occur in Addisons disease, although not in secondary adrenal insufficiency. This darkening is most visible on scars; skin folds; pressure points such as the elbows, knees, knuckles, and toes; lips; and mucous membranes such as the lining of the cheek.
The slowly progressing symptoms of adrenal insufficiency are often ignored until a stressful event, such as surgery, a severe injury, an illness, or pregnancy, causes them to worsen.
Adrenal Crisis
Sudden, severe worsening of adrenal insufficiency symptoms is called adrenal crisis. If the person has Addisons disease, this worsening can also be called an Addisonian crisis. In most cases, symptoms of adrenal insufficiency become serious enough that people seek medical treatment before an adrenal crisis occurs. However, sometimes symptoms appear for the first time during an adrenal crisis.
Symptoms of adrenal crisis include
- sudden, severe pain in the lower back, abdomen, or legs - severe vomiting and diarrhea - dehydration - low blood pressure - loss of consciousness
If not treated, an adrenal crisis can cause death.
Get Treatment for Adrenal Crisis Right Away People with adrenal insufficiency who have weakness, nausea, or vomiting need immediate emergency treatment to prevent an adrenal crisis and possible death. An injection with a synthetic glucocorticoid hormone called a corticosteroid can save a persons life. People should make sure to have a corticosteroid injection with them at all times, and make sure their friends and family know how and when to give the injection. Read more under How is adrenal insufficiency treated?
|
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What are the treatments for Septo-optic dysplasia ?
|
Can septo-optic dysplasia be cured? There is no cure for septo-optic dysplasia. Treatment is symptomatic. Hormone deficiencies may be treated with hormone replacement therapy. The optical problems are generally not treatable. Vision, physical, and occupational therapies may be required.
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What is (are) hystrix-like ichthyosis with deafness ?
|
Hystrix-like ichthyosis with deafness (HID) is a disorder characterized by dry, scaly skin (ichthyosis) and hearing loss that is usually profound. Hystrix-like means resembling a porcupine; in this type of ichthyosis, the scales may be thick and spiky, giving the appearance of porcupine quills. Newborns with HID typically develop reddened skin. The skin abnormalities worsen over time, and the ichthyosis eventually covers most of the body, although the palms of the hands and soles of the feet are usually only mildly affected. Breaks in the skin may occur and in severe cases can lead to life-threatening infections. Affected individuals have an increased risk of developing a type of skin cancer called squamous cell carcinoma, which can also affect mucous membranes such as the inner lining of the mouth. People with HID may also have patchy hair loss caused by scarring on particular areas of skin.
|
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What causes Urinary Tract Infection In Adults ?
|
Most UTIs are caused by bacteria that live in the bowel. The bacterium Escherichia coli (E. coli) causes the vast majority of UTIs. Microbes called Chlamydia and Mycoplasma can infect the urethra and reproductive system but not the bladder. Chlamydia and Mycoplasma infections may be sexually transmitted and require treatment of sexual partners.
The urinary tract has several systems to prevent infection. The points where the ureters attach to the bladder act like one-way valves to prevent urine from backing up toward the kidneys, and urination washes microbes out of the body. In men, the prostate gland produces secretions that slow bacterial growth. In both sexes, immune defenses also prevent infection. But despite these safeguards, infections still occur. Certain bacteria have a strong ability to attach themselves to the lining of the urinary tract.
|
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what research (or clinical trials) is being done for Glossopharyngeal Neuralgia ?
|
The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes at the National Institutes of Health conduct research related to GN and support additional research through grants to major research institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure disorders such as GN.
|
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What is (are) Skin Cancer ?
|
Skin cancer is the most common type of cancer in the U.S. It occurs in more than a million people each year, including many older people. There are three main types of skin cancer: basal cell carcinoma, squamous cell carcinoma, and melanoma. Of the three, melanoma is the most serious. The Body's Largest Organ The skin is the body's largest organ. It has two main layers: the inner layer, called the dermis, and the outer layer, called the epidermis. The dermis contains sweat glands, nerves, hair follicles, and blood vessels. The epidermis forms the protective, waterproof layer of the skin. The very top of the epidermis, which is called the stratum corneum, is made up of dead cells that have moved their way up through the other layers. The epidermis, or outer layer, is made up of three types of living cells: - Squamous cells are flat and form the top layer of living cells. - Basal cells are round and lie directly under squamous cells. - Melanocytes are specialized skin cells that produce pigment called melanin. Squamous cells are flat and form the top layer of living cells. Basal cells are round and lie directly under squamous cells. Melanocytes are specialized skin cells that produce pigment called melanin. The melanin pigment produced by melanocytes gives skin its color. It also protects the skin from ultraviolet (UV) ray damage from the sun by absorbing and scattering the energy. People with more melanin have darker skin and better protection from UV light. People with lighter skin (less melanin) are more vulnerable to damage from UV light. How Tumors Form Normally, cells in the body grow, divide, and produce more cells as needed. But sometimes the process goes wrong -- cells become abnormal and multiply in an uncontrolled way. These extra cells form a mass of tissue, called a growth or tumor. Tumors can be relatively harmless (benign) or cancerous (malignant). A malignant tumor can spread, damage healthy tissue, and make a person ill. Skin cancer occurs when abnormal cells form and multiply in an uncontrolled way in the epidermis, or abnormal cells from the epidermis invade the dermis of the skin. Basal cell carcinoma, squamous cell carcinoma, and melanoma are skin cancers that are named for the epidermal cells from which they develop. Basal Cell and Squamous Cell Carcinoma Basal cell and squamous cell carcinomas are very common in both older and younger people and are rarely life-threatening. Melanoma is a less common, yet more serious, type of skin cancer. Basal cell and squamous cell carcinomas are often called non-melanoma skin cancers or keratinocyte cancers. Melanoma Melanoma results from the uncontrolled growth of melanocytes and can occur anywhere on the body where melanocytes are located, including the skin, eyes, mouth and gastrointestinal tract. Men tend to develop melanoma more often on the trunk (the area from the shoulders to the hips) or the head and neck. Women more often develop melanoma on the extremities (arms and legs). Melanoma is found most often in adults, but can occur in children and teenagers. Melanoma is the most serious and most aggressive (fastest growing) form of skin cancer. An estimated 76,690 new cases of melanoma will be diagnosed in 2013. Because it is difficult to adequately treat melanoma after it has spread, the disease is expected to claim the lives of approximately 9,480 Americans in 2013. Can Skin Cancer Be Treated? Most basal cell and squamous cell skin cancers can be cured if found and treated early. Melanoma can often be treated effectively if caught in time.
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what research (or clinical trials) is being done for Spinal Cord Injury ?
|
The National Institute of Neurological Disorders and Stroke (NINDS) conducts spinal cord research in its laboratories at the National Institutes of Health (NIH) and also supports additional research through grants to major research institutions across the country. Advances in research are giving doctors and patients hope that repairing injured spinal cords is a reachable goal. Advances in basic research are also being matched by progress in clinical research, especially in understanding the kinds of physical rehabilitation that work best to restore function. Some of the more promising rehabilitation techniques are helping spinal cord injury patients become more mobile.
|
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What is (are) Kleefstra syndrome ?
|
Kleefstra syndrome is a disorder that involves many parts of the body. Characteristic features of Kleefstra syndrome include developmental delay and intellectual disability, severely limited or absent speech, and weak muscle tone (hypotonia). Affected individuals also have an unusually small head size (microcephaly) and a wide, short skull (brachycephaly). Distinctive facial features include eyebrows that grow together in the middle (synophrys), widely spaced eyes (hypertelorism), a sunken appearance of the middle of the face (midface hypoplasia), nostrils that open to the front rather than downward (anteverted nares), a protruding jaw (prognathism), rolled out (everted) lips, and a large tongue (macroglossia). Affected individuals may have a high birth weight and childhood obesity. People with Kleefstra syndrome may also have structural brain abnormalities, congenital heart defects, genitourinary abnormalities, seizures, and a tendency to develop severe respiratory infections. During childhood they may exhibit features of autism or related developmental disorders affecting communication and social interaction. In adolescence, they may develop a general loss of interest and enthusiasm (apathy) or unresponsiveness (catatonia).
|
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What are the treatments for Laron syndrome ?
|
How might Laron syndrome be treated? There is currently no cure for Laron syndrome. Treatment is primarily focused on improving growth. The only specific treatment available for this condition is subcutaneous injections of insulin-like growth factor 1 (a growth-promoting hormone), often called IGF-1. IGF-1 stimulates linear growth (height) and also improves brain growth and metabolic abnormalities caused by long-term IGF-1 deficiency. It has also been shown to raise blood glucose levels, reduce cholesterol, and increase muscle growth. IGF-1 and GH levels should be closely monitored in people undergoing this treatment because overdosage of IGF-I causes a variety of health problems.
|
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What are the symptoms of Neurofibromatosis-Noonan syndrome ?
|
What are the signs and symptoms of Neurofibromatosis-Noonan syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Neurofibromatosis-Noonan syndrome. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormality of the helix 90% Abnormality of the pulmonary valve 90% Aplasia/Hypoplasia of the abdominal wall musculature 90% Cafe-au-lait spot 90% Cognitive impairment 90% Hypertelorism 90% Hypertrophic cardiomyopathy 90% Low-set, posteriorly rotated ears 90% Ptosis 90% Short stature 90% Webbed neck 90% Abnormality of coagulation 50% Abnormality of the lymphatic system 50% Abnormality of the thorax 50% Cryptorchidism 50% Feeding difficulties in infancy 50% Lisch nodules 5% Autosomal dominant inheritance - Axillary freckling - Cubitus valgus - Delayed speech and language development - Depressed nasal bridge - Epicanthus - Hypoplasia of midface - Inguinal freckling - Low posterior hairline - Low-set ears - Macrocephaly - Malar flattening - Muscle weakness - Neurofibromas - Optic glioma - Pectus excavatum of inferior sternum - Posteriorly rotated ears - Prominent nasolabial fold - Pulmonic stenosis - Scoliosis - Secundum atrial septal defect - Short neck - Specific learning disability - Superior pectus carinatum - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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] |
Is Chronic inflammatory demyelinating polyneuropathy inherited ?
|
Is chronic inflammatory demyelinating polyneuropathy (CIDP) inherited? CIDP is not known to be inherited and is considered an acquired disorder. No clear genetic predisposition or other predisposing factors for CIDP have been identified.
|
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What are the treatments for X-linked chondrodysplasia punctata 1 ?
|
These resources address the diagnosis or management of X-linked chondrodysplasia punctata 1: - Gene Review: Gene Review: Chondrodysplasia Punctata 1, X-Linked - Genetic Testing Registry: Chondrodysplasia punctata 1, X-linked recessive These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
|
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Who is at risk for Adult Non-Hodgkin Lymphoma? ?
|
Age, gender, and a weakened immune system can affect the risk of adult non-Hodgkin lymphoma. Anything that increases your risk of getting a disease is called a risk factor. Having a risk factor does not mean that you will get cancer; not having risk factors doesnt mean that you will not get cancer. Talk with your doctor if you think you may be at risk. These and other risk factors may increase the risk of certain types of adult non-Hodgkin lymphoma: - Being older, male, or white. - Having one of the following medical conditions: - An inherited immune disorder (such as hypogammaglobulinemia or Wiskott-Aldrich syndrome). - An autoimmune disease (such as rheumatoid arthritis, psoriasis, or Sjgren syndrome). - HIV/AIDS. - Human T-lymphotrophic virus type I or Epstein-Barr virus infection. - Helicobacter pylori infection. - Taking immunosuppressant drugs after an organ transplant.
|
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What are the symptoms of Inguinal Hernia ?
|
The first sign of an inguinal hernia is a small bulge on one or, rarely, on both sides of the grointhe area just above the groin crease between the lower abdomen and the thigh. The bulge may increase in size over time and usually disappears when lying down.
Other signs and symptoms can include
- discomfort or pain in the groinespecially when straining, lifting, coughing, or exercisingthat improves when resting - feelings such as weakness, heaviness, burning, or aching in the groin - a swollen or an enlarged scrotum in men or boys
Indirect and direct inguinal hernias may slide in and out of the abdomen into the inguinal canal. A health care provider can often move them back into the abdomen with gentle massage.
|
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What are the treatments for Marden-Walker syndrome ?
|
How might Marden-Walker syndrome be treated? Very little information is available regarding the treatment of Marden-Walker syndrome. In general, treatment is symptomatic, with a multidisciplinary approach. The team of providers may include a regular pediatrician, a geneticist, a neurologist, an orthopedist and/or a physical medicine specialist. Special diets and feeding techniques may be of benefit. Early childhood intervention services may help with developmental problems. Other treatments are dependent upon the specific symptoms present in each patient.
|
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What are the genetic changes related to congenital deafness with labyrinthine aplasia, microtia, and microdontia ?
|
LAMM syndrome is caused by mutations in the FGF3 gene, which provides instructions for making a protein called fibroblast growth factor 3 (FGF3). By attaching to another protein known as a receptor, the FGF3 protein triggers a cascade of chemical reactions inside the cell that signal the cell to undergo certain changes, such as dividing or maturing to take on specialized functions. During development before birth, the signals triggered by the FGF3 protein stimulate cells to form the structures that make up the inner ears. The FGF3 protein is also involved in the development of many other organs and structures, including the outer ears and teeth. FGF3 gene mutations involved in LAMM syndrome alter the FGF3 protein. The altered protein likely has reduced or absent function and is unable to stimulate signaling. The loss of FGF3 function impairs development of the ears and teeth, which leads to the characteristic features of LAMM syndrome.
|
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What is (are) Anthrax ?
|
Anthrax is a disease caused by Bacillus anthracis, a germ that lives in soil. Many people know about it from the 2001 bioterror attacks. In the attacks, someone purposely spread anthrax through the U.S. mail. This killed five people and made 22 sick. Anthrax is rare. It affects animals such as cattle, sheep, and goats more often than people. People can get anthrax from contact with infected animals, wool, meat, or hides. It can cause three forms of disease in people. They are - Cutaneous, which affects the skin. People with cuts or open sores can get it if they touch the bacteria. - Inhalation, which affects the lungs. You can get this if you breathe in spores of the bacteria. - Gastrointestinal, which affects the digestive system. You can get it by eating infected meat. Antibiotics often cure anthrax if it is diagnosed early. But many people don't know they have anthrax until it is too late to treat. A vaccine to prevent anthrax is available for people in the military and others at high risk. NIH: National Institute of Allergy and Infectious Diseases
|
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What are the symptoms of Negative rheumatoid factor polyarthritis ?
|
What are the signs and symptoms of Negative rheumatoid factor polyarthritis? The Human Phenotype Ontology provides the following list of signs and symptoms for Negative rheumatoid factor polyarthritis. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Autoimmune antibody positivity - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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What are the genetic changes related to mal de Meleda ?
|
Mal de Meleda is caused by mutations in the SLURP1 gene. This gene provides instructions for making a protein that interacts with other proteins, called receptors, and is likely involved in signaling within cells. Studies show that the SLURP-1 protein can attach (bind) to nicotinic acetylcholine receptors (nAChRs) in the skin. Through interaction with these receptors, the SLURP-1 protein is thought to be involved in controlling the growth and division (proliferation), maturation (differentiation), and survival of skin cells. Mutations in the SLURP1 gene lead to little or no SLURP-1 protein in the body. It is unclear how a lack of this protein leads to the skin problems that occur in mal de Meleda. Researchers speculate that without SLURP-1, the activity of genes controlled by nAChR signaling is altered, leading to overgrowth of skin cells or survival of cells that normally would have died. The excess of cells can result in skin thickening. It is unclear why skin on the hands and feet is particularly affected.
|
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What is (are) Niemann-Pick disease type A ?
|
Niemann-Pick disease is an inherited condition involving lipid metabolism, which is the breakdown, transport, and use of fats and cholesterol in the body. In people with this condition, abnormal lipid metabolism causes harmful amounts of lipids to accumulate in the spleen, liver, lungs, bone marrow, and brain. Niemann-Pick disease type A appears during infancy and is characterized by an enlarged liver and spleen (hepatosplenomegaly), failure to gain weight and grow at the expected rate (failure to thrive), and progressive deterioration of the nervous system. Due to the involvement of the nervous system, Niemann-Pick disease type A is also known as the neurological type. There is currently no effective treatment for this condition and those who are affected generally do not survive past early childhood. Niemann-Pick disease type A is caused by mutations in the SMPD1 gene. It is inherited in an autosomal recessive pattern.
|
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What are the treatments for Dextrocardia with situs inversus ?
|
How might dextrocardia with situs inversus be treated? Treatment typically depends on the heart or physical problems the person may have in addition to dextrocardia with situs inversus. For example, infants born with congenital heart defects or other organ malformations may require surgery. The management of people affected by Kartagener syndrome typically includes measures to enhance clearance of mucus, prevent respiratory infections, and treat bacterial infections. GeneReviews offers more specific information on the treatment of Kartagener syndrome and other types of primary ciliary dyskinesia. Please click on the link to access this resource.
|
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What are the genetic changes related to multiple sulfatase deficiency ?
|
Multiple sulfatase deficiency is caused by mutations in the SUMF1 gene. This gene provides instructions for making an enzyme called formylglycine-generating enzyme (FGE). This enzyme is found in a cell structure called the endoplasmic reticulum, which is involved in protein processing and transport. The FGE enzyme modifies other enzymes called sulfatases, which aid in breaking down substances that contain chemical groups known as sulfates. These substances include a variety of sugars, fats, and hormones. Most SUMF1 gene mutations severely reduce the function of the FGE enzyme or lead to the production of an unstable enzyme that is quickly broken down. The activity of multiple sulfatases is impaired because the FGE enzyme modifies all known sulfatase enzymes. Sulfate-containing molecules that are not broken down build up in cells, often resulting in cell death. The death of cells in particular tissues, specifically the brain, skeleton, and skin, cause many of the signs and symptoms of multiple sulfatase deficiency. Research indicates that mutations that lead to reduced FGE enzyme function are associated with the less severe cases of the condition, whereas mutations that lead to the production of an unstable FGE enzyme tend to be associated with the more severe cases of multiple sulfatase deficiency.
|
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What is (are) Hutchinson-Gilford progeria syndrome ?
|
Hutchinson-Gilford progeria syndrome is a genetic condition characterized by the dramatic, rapid appearance of aging beginning in childhood. Affected children typically look normal at birth and in early infancy, but then grow more slowly than other children and do not gain weight at the expected rate (failure to thrive). They develop a characteristic facial appearance including prominent eyes, a thin nose with a beaked tip, thin lips, a small chin, and protruding ears. Hutchinson-Gilford progeria syndrome also causes hair loss (alopecia), aged-looking skin, joint abnormalities, and a loss of fat under the skin (subcutaneous fat). This condition does not disrupt intellectual development or the development of motor skills such as sitting, standing, and walking. People with Hutchinson-Gilford progeria syndrome experience severe hardening of the arteries (arteriosclerosis) beginning in childhood. This condition greatly increases the chances of having a heart attack or stroke at a young age. These serious complications can worsen over time and are life-threatening for affected individuals.
|
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Is Felty's syndrome inherited ?
|
Is Felty's syndrome inherited? It has not been concluded that Felty's syndrome is an inherited condition; most individuals with Felty's syndrome have not had a history of the condition in their family. However, there have been a few reports of the condition appearing to be familial. Furthermore, although the condition itself may not be inherited, some of the risk factors associated with Felty's syndrome may have genetic components. One study found that a family history of rheumatoid arthritis was more common in patients with Felty's syndrome and that there was a strong association with HLA-DR4 (an immune system gene common in individuals with RA). The authors also stated that there was an increased frequency of another gene as well, suggesting that certain other immune system genes may interact with HLA-DR4 and contribute to individuals developing Felty's syndrome. In another report, the authors described a family in which 3 siblings had Felty's syndrome. All of the siblings shared a specific haplotype (a group of immune system genes that may be inherited together). The authors stated that they believe this supports the theory that multiple genetic factors are involved in family members being predisposed to Felty's syndrome. An earlier article described a family in which the mother and 2 of her 5 children had Felty's syndrome, which suggested autosomal dominant inheritance (which has not otherwise been reported).
|
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What causes Chronic inflammatory demyelinating polyneuropathy ?
|
What causes chronic inflammatory demyelinating polyneuropathy (CIDP)? The exact underlying cause of CIDP is unknown, but there is evidence to support that it is related to the immune system and may have multiple triggers. It is thought to be caused by an abnormal immune response in which the immune system mistakenly attacks and damages the myelin sheath (the covering that protects nerve fibers) of the peripheral nerves. However, no specific provoking antigens or other predisposing factors for CIDP have been identified. In several case reports, treatment with tumor necrosis factor-alpha inhibitors has been associated with the subsequent development of chronic demyelinating neuropathies.
|
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What are the treatments for X-linked infantile nystagmus ?
|
These resources address the diagnosis or management of X-linked infantile nystagmus: - Gene Review: Gene Review: FRMD7-Related Infantile Nystagmus - Genetic Testing Registry: Infantile nystagmus, X-linked - MedlinePlus Encyclopedia: Nystagmus These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
|
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What are the treatments for Systemic capillary leak syndrome ?
|
How might systemic capillary leak syndrome be treated? Unfortunately, there is no cure for systemic capillary leak syndrome at this time. However, recent studies suggest that taking medication known as beta-adrenergic agonists (including terbutaline) or undergoing immunoglobulin intravenous (IV) therapy may reduce the frequency of attacks and may increase survival in individuals affected with this condition.
|
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What are the genetic changes related to congenital hyperinsulinism ?
|
Congenital hyperinsulinism is caused by mutations in genes that regulate the release (secretion) of insulin, which is produced by beta cells in the pancreas. Insulin clears excess sugar (in the form of glucose) from the bloodstream by passing glucose into cells to be used as energy. Gene mutations that cause congenital hyperinsulinism lead to over-secretion of insulin from beta cells. Normally, insulin is secreted in response to the amount of glucose in the bloodstream: when glucose levels rise, so does insulin secretion. However, in people with congenital hyperinsulinism, insulin is secreted from beta cells regardless of the amount of glucose present in the blood. This excessive secretion of insulin results in glucose being rapidly removed from the bloodstream and passed into tissues such as muscle, liver, and fat. A lack of glucose in the blood results in frequent states of hypoglycemia in people with congenital hyperinsulinism. Insufficient blood glucose also deprives the brain of its primary source of fuel. Mutations in at least nine genes have been found to cause congenital hyperinsulinism. Mutations in the ABCC8 gene are the most common known cause of the disorder. They account for this condition in approximately 40 percent of affected individuals. Less frequently, mutations in the KCNJ11 gene have been found in people with congenital hyperinsulinism. Mutations in each of the other genes associated with this condition account for only a small percentage of cases. In approximately half of people with congenital hyperinsulinism, the cause is unknown.
|
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What is (are) core binding factor acute myeloid leukemia ?
|
Core binding factor acute myeloid leukemia (CBF-AML) is one form of a cancer of the blood-forming tissue (bone marrow) called acute myeloid leukemia. In normal bone marrow, early blood cells called hematopoietic stem cells develop into several types of blood cells: white blood cells (leukocytes) that protect the body from infection, red blood cells (erythrocytes) that carry oxygen, and platelets (thrombocytes) that are involved in blood clotting. In acute myeloid leukemia, the bone marrow makes large numbers of abnormal, immature white blood cells called myeloid blasts. Instead of developing into normal white blood cells, the myeloid blasts develop into cancerous leukemia cells. The large number of abnormal cells in the bone marrow interferes with the production of functional white blood cells, red blood cells, and platelets. People with CBF-AML have a shortage of all types of mature blood cells: a shortage of white blood cells (leukopenia) leads to increased susceptibility to infections, a low number of red blood cells (anemia) causes fatigue and weakness, and a reduction in the amount of platelets (thrombocytopenia) can result in easy bruising and abnormal bleeding. Other symptoms of CBF-AML may include fever and weight loss. While acute myeloid leukemia is generally a disease of older adults, CBF-AML often begins in young adulthood and can occur in childhood. Compared to other forms of acute myeloid leukemia, CBF-AML has a relatively good prognosis: about 90 percent of individuals with CBF-AML recover from their disease following treatment, compared with 25 to 40 percent of those with other forms of acute myeloid leukemia. However, the disease recurs in approximately half of them after successful treatment of the initial occurrence.
|
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What is (are) Narcolepsy ?
|
Narcolepsy (NAR-ko-lep-se) is a disorder that causes periods of extreme daytime sleepiness. The disorder also may cause muscle weakness.
Most people who have narcolepsy have trouble sleeping at night. Some people who have the disorder fall asleep suddenly, even if they're in the middle of talking, eating, or another activity.
Narcolepsy also can cause:
Cataplexy (KAT-ah-plek-se). This condition causes a sudden loss of muscle tone while you're awake. Muscle weakness can affect certain parts of your body or your whole body. For example, if cataplexy affects your hand, you may drop what you're holding. Strong emotions often trigger this weakness. It may last seconds or minutes.
Hallucinations (ha-lu-sih-NA-shuns). These vivid dreams occur while falling asleep or waking up.
Sleep paralysis (pah-RAL-ih-sis). This condition prevents you from moving or speaking while waking up and sometimes while falling asleep. Sleep paralysis usually goes away within a few minutes.
Overview
The two main phases of sleep are nonrapid eye movement (NREM) and rapid eye movement (REM). Most people are in the NREM phase when they first fall asleep. After about 90 minutes of sleep, most people go from NREM to REM sleep.
Dreaming occurs during the REM phase of sleep. During REM, your muscles normally become limp. This prevents you from acting out your dreams. (For more information about sleep cycles, go to the National Heart, Lung, and Blood Institute's "Your Guide to Healthy Sleep.")
People who have narcolepsy often fall into REM sleep quickly and wake up directly from it. As a result, they may have vivid dreams while falling asleep and waking up.
Hypocretin (hi-po-KREET-in), a chemical in the brain, helps promote wakefulness. Most people who have narcolepsy have low levels of this chemical. What causes these low levels isn't well understood.
Researchers think that certain factors may work together to cause a lack of hypocretin. These factors may include heredity, infections, brain injuries, and autoimmune disorders. (Autoimmune disorders occur if the body's immune system mistakenly attacks the body's cells and tissues.)
Outlook
Narcolepsy symptoms usually begin during the teen or young adult years. People who have narcolepsy may find it hard to function at school, work, home, and in social situations because of extreme tiredness.
Narcolepsy has no cure, but medicines, lifestyle changes, and other therapies can improve symptoms. Research is ongoing on the causes of narcolepsy and new ways to treat it.
|
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How to diagnose Familial Mediterranean fever ?
|
How is familial Mediterranean fever (FMF) diagnosed? In making a diagnosis of FMF, doctors take all of these factors into account: Whether the person has the clinical symptoms common for the disease and whether the symptoms are recurrent. How he or she responds to colchicine treatment. Usually a positive family history in people of Middle Eastern ancestry. The results of genetic testing. Also helpful in establishing a correct diagnosis of FMF is the person's ancestry. Testing for the following can also be helpful: Elevated white blood cell count, which is an indication of an immune response. Elevated erythrocyte sedimentation rate (ESR), which is an indication of an inflammatory response. Elevated plasma fibrinogen, which helps stop bleeding. An elevated amount would indicate that something might be wrong with this mechanism. Elevated serum haptoglobin, which would indicate that red blood cells are being destroyed, a common occurrence in rheumatic diseases, such as FMF. Elevated C-reactive protein, which is a special type of protein, produced by the liver, that is only present during episodes of acute inflammation. Elevated albumin in the urine, which is demonstrated by urinalysis. The presence of the protein albumin in the urine can be a symptom of kidney disease, along with microscopic hematuria (very small - microscopic - amounts of blood or blood cells in the urine), during attacks. Is genetic testing for familial Mediterranean fever (FMF) available? Yes. The Genetic Testing Registry (GTR) provides information about the genetic testing for this condition. We strongly recommend that you work with a genetics professional if you wish to pursue genetic testing.
|
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Is Glutaric acidemia type I inherited ?
|
How is glutaric acidemia type I inherited? Glutaric acidemia type I is inherited in an autosomal recessive manner. This means that both copies of the responsible gene in each cell must have mutations for a person to be affected. The parents of a person with an autosomal recessive condition typically each carry one mutated copy of the gene and are referred to as carriers. Carriers of an autosomal recessive condition typically are unaffected and have no signs or symptoms. When two carrier parents have children, each child has a 25% (1 in 4) chance to be affected, a 50% (1 in 2) chance to be an unaffected carrier like each parent, and a 25% chance to be unaffected and not be a carrier.
|
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What are the symptoms of Methylmalonic acidemia with homocystinuria, type cblJ ?
|
What are the signs and symptoms of Methylmalonic acidemia with homocystinuria, type cblJ? The Human Phenotype Ontology provides the following list of signs and symptoms for Methylmalonic acidemia with homocystinuria, type cblJ. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Atria septal defect 5% Cerebral atrophy 5% Coarctation of aorta 5% Cryptorchidism 5% Decreased methionine synthase activity 5% Decreased methylcobalamin 5% Gastroesophageal reflux 5% Hypertelorism 5% Pulmonary hypertension 5% Wide intermamillary distance 5% Abnormal posturing - Anemia - Autosomal recessive inheritance - Congenital onset - Decreased adenosylcobalamin - Feeding difficulties - Growth delay - Homocystinuria - Hyperhomocystinemia - Inguinal hernia - Lethargy - Methylmalonic acidemia - Methylmalonic aciduria - Muscular hypotonia - Neutropenia - Tachypnea - Thrombocytopenia - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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What are the symptoms of Breast Cancer ?
|
When breast cancer first develops, there may be no symptoms at all. But as the cancer grows, it can cause changes that women should watch for. You can help safeguard your health by learning the following warning signs of breast cancer. - a lump or thickening in or near the breast or in the underarm area - a change in the size or shape of the breast - ridges or pitting of the breast; the skin looks like the skin of an orange - a change in the way the skin of the breast, areola, or nipple looks or feels; for example, it may be warm, swollen, red, or scaly - nipple discharge or tenderness, or the nipple is pulled back or inverted into the breast. a lump or thickening in or near the breast or in the underarm area a change in the size or shape of the breast ridges or pitting of the breast; the skin looks like the skin of an orange a change in the way the skin of the breast, areola, or nipple looks or feels; for example, it may be warm, swollen, red, or scaly nipple discharge or tenderness, or the nipple is pulled back or inverted into the breast. You should see your doctor about any symptoms like these. Most often, they are not cancer, but it's important to check with the doctor so that any problems can be diagnosed and treated as early as possible.
|
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How many people are affected by proopiomelanocortin deficiency ?
|
POMC deficiency is a rare condition; approximately 50 cases have been reported in the medical literature.
|
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What are the genetic changes related to Beare-Stevenson cutis gyrata syndrome ?
|
Mutations in the FGFR2 gene cause Beare-Stevenson cutis gyrata syndrome. This gene produces a protein called fibroblast growth factor receptor 2, which plays an important role in signaling a cell to respond to its environment, perhaps by dividing or maturing. A mutation in the FGFR2 gene alters the protein and promotes prolonged signaling, which is thought to interfere with skeletal and skin development. Some individuals with Beare-Stevenson cutis gyrata syndrome do not have identified mutations in the FGFR2 gene. In these cases, the cause of the condition is unknown.
|
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What are the genetic changes related to acatalasemia ?
|
Mutations in the CAT gene can cause acatalasemia. This gene provides instructions for making the enzyme catalase, which breaks down hydrogen peroxide molecules into oxygen and water. Hydrogen peroxide is produced through chemical reactions within cells. At low levels, it is involved in several chemical signaling pathways, but at high levels it is toxic to cells. If hydrogen peroxide is not broken down by catalase, additional reactions convert it into compounds called reactive oxygen species that can damage DNA, proteins, and cell membranes. Mutations in the CAT gene greatly reduce the activity of catalase. A shortage of this enzyme can allow hydrogen peroxide to build up to toxic levels in certain cells. For example, hydrogen peroxide produced by bacteria in the mouth may accumulate in and damage soft tissues, leading to mouth ulcers and gangrene. A buildup of hydrogen peroxide may also damage beta cells of the pancreas, which release a hormone called insulin that helps control blood sugar. Malfunctioning beta cells are thought to underlie the increased risk of type 2 diabetes mellitus in people with acatalasemia. It is unclear why some people have no health problems associated with a loss of catalase activity. Many people with reduced catalase activity do not have an identified mutation in the CAT gene; in these cases, the cause of the condition is unknown. Researchers believe that other genetic and environmental factors can also influence the activity of catalase.
|
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What are the treatments for atopic dermatitis ?
|
These resources address the diagnosis or management of atopic dermatitis: - American Academy of Dermatology: Atopic Dermatitis: Tips for Managing These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
|
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] |
How to diagnose Urinary Tract Infections in Children ?
|
Only a health care provider can determine whether a child has a UTI.
A urine sample will be collected and examined. The way urine is collected depends on the childs age:
- If the child is not yet toilet trained, the health care provider may place a plastic collection bag over the childs genital area. The bag will be sealed to the skin with an adhesive strip. If this method is used, the bag should be removed right after the child has urinated, and the urine sample should be processed immediately. Because bacteria from the skin can contaminate this sample, the methods listed below are more accurate. - A health care provider may need to pass a small tube called a catheter into the urethra of an infant. Urine will drain directly from the bladder into a clean container. - Sometimes the best way to collect a urine sample from an infant is by placing a needle directly into the bladder through the skin of the lower abdomen. Getting urine through a catheter or needle will ensure that the urine collected does not contain bacteria from the skin. - An older child may be asked to urinate into a container. The sample needs to come as directly into the container as possible to avoid picking up bacteria from the skin or rectal area.
Some of the urine will be examined with a microscope. If an infection is present, bacteria and sometimes pus will be found in the urine. A urine culture should also be performed on some of the urine. The culture is performed by placing part of the urine sample in a tube or dish with a substance that encourages any bacteria present to grow. Once the bacteria have multiplied, which usually takes 1 to 3 days, they can be identified.
The reliability of the culture depends on how the urine is collected and how long the urine stands before the culture is started. If the urine sample is collected at home, it should be refrigerated as soon as it is collected. The container should be carried to the health care provider or lab in a plastic bag filled with ice.
The health care provider may also order a sensitivity test, which tests the bacteria for sensitivity to different antibiotics to see which medication is best for treating the infection.
|
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] |
Is Wolff-Parkinson-White syndrome inherited ?
|
Is Wolff-Parkinson-White syndrome inherited?
|
[
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] |
How to prevent Polycythemia Vera ?
|
Primary polycythemia (polycythemia vera) can't be prevented. However, with proper treatment, you can prevent or delay symptoms and complications.
Sometimes you can prevent secondary polycythemia by avoiding things that deprive your body of oxygen for long periods. For example, you can avoid mountain climbing, living at a high altitude, or smoking.
People who have serious heart or lung diseases may develop secondary polycythemia. Treatment for the underlying disease may improve the secondary polycythemia. Following a healthy lifestyle to lower your risk of heart and lung diseases also will help you prevent secondary polycythemia.
|
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What are the treatments for Chorea-acanthocytosis ?
|
How is chorea-acanthocytosis treated? There are currently no treatments to prevent or slow the progression of chorea-acanthocytosis; treatment is symptomatic and supportive. Management may include: botulinum toxin for decreasing the oro-facio-lingual dystonia; feeding assistance; speech therapy; mechanical protective devices; splints for foot drop; phenytoin, clobazam, and valproate for seizure management; antidepressant or antipsychotic medications; dopamine antagonists such as atypical neuroleptics or tetrabenazine; and standard treatment for cardiomyopathy. Surveillance includes monitoring of nutritional status and adaptation of diet to assure adequate caloric intake, cardiac evaluations every five years, and EEG every third year.
|
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What causes Nephrotic Syndrome in Adults ?
|
Nephrotic syndrome can be caused by diseases that affect only the kidneys, such as focal segmental glomerulosclerosis (FSGS) or membranous nephropathy. Diseases that affect only the kidneys are called primary causes of nephrotic syndrome. The glomeruli are usually the targets of these diseases for reasons that are not fully understood. In FSGSthe most common primary cause of nephrotic syndromescar tissue forms in parts of the glomeruli. In membranous nephropathy, immune molecules form harmful deposits on the glomeruli.
Nephrotic syndrome can also be caused by systemic diseases, which are diseases that affect many parts of the body, such as diabetes or lupus. Systemic diseases that affect the kidneys are called secondary causes of nephrotic syndrome. More than 50 percent of nephrotic syndrome cases in adults have secondary causes, with diabetes being the most common.1
|
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What is (are) nephronophthisis ?
|
Nephronophthisis is a disorder that affects the kidneys. It is characterized by inflammation and scarring (fibrosis) that impairs kidney function. These abnormalities lead to increased urine production (polyuria), excessive thirst (polydipsia), general weakness, and extreme tiredness (fatigue). In addition, affected individuals develop fluid-filled cysts in the kidneys, usually in an area known as the corticomedullary region. Another feature of nephronophthisis is a shortage of red blood cells, a condition known as anemia. Nephronophthisis eventually leads to end-stage renal disease (ESRD), a life-threatening failure of kidney function that occurs when the kidneys are no longer able to filter fluids and waste products from the body effectively. Nephronophthisis can be classified by the approximate age at which ESRD begins: around age 1 (infantile), around age 13 (juvenile), and around age 19 (adolescent). About 85 percent of all cases of nephronophthisis are isolated, which means they occur without other signs and symptoms. Some people with nephronophthisis have additional features, which can include liver fibrosis, heart abnormalities, or mirror image reversal of the position of one or more organs inside the body (situs inversus). Nephronophthisis can occur as part of separate syndromes that affect other areas of the body; these are often referred to as nephronophthisis-associated ciliopathies. For example, Senior-Lken syndrome is characterized by the combination of nephronophthisis and a breakdown of the light-sensitive tissue at the back of the eye (retinal degeneration); Joubert syndrome affects many parts of the body, causing neurological problems and other features, which can include nephronophthisis.
|
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What are the genetic changes related to tuberous sclerosis complex ?
|
Mutations in the TSC1 or TSC2 gene can cause tuberous sclerosis complex. The TSC1 and TSC2 genes provide instructions for making the proteins hamartin and tuberin, respectively. Within cells, these two proteins likely work together to help regulate cell growth and size. The proteins act as tumor suppressors, which normally prevent cells from growing and dividing too fast or in an uncontrolled way. People with tuberous sclerosis complex are born with one mutated copy of the TSC1 or TSC2 gene in each cell. This mutation prevents the cell from making functional hamartin or tuberin from the altered copy of the gene. However, enough protein is usually produced from the other, normal copy of the gene to regulate cell growth effectively. For some types of tumors to develop, a second mutation involving the other copy of the TSC1 or TSC2 gene must occur in certain cells during a person's lifetime. When both copies of the TSC1 gene are mutated in a particular cell, that cell cannot produce any functional hamartin; cells with two altered copies of the TSC2 gene are unable to produce any functional tuberin. The loss of these proteins allows the cell to grow and divide in an uncontrolled way to form a tumor. In people with tuberous sclerosis complex, a second TSC1 or TSC2 mutation typically occurs in multiple cells over an affected person's lifetime. The loss of hamartin or tuberin in different types of cells leads to the growth of tumors in many different organs and tissues.
|
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What is (are) Developmental Disabilities ?
|
Developmental disabilities are severe, long-term problems. They may be physical, such as blindness. They may affect mental ability, such as learning disorders. Or the problem can be both physical and mental, such as Down syndrome. The problems are usually life-long, and can affect everyday living. There are many causes of developmental disabilities, including - Genetic or chromosome abnormalities. These cause conditions such as Down syndrome and Rett syndrome. - Prenatal exposure to substances. Drinking alcohol when pregnant can cause fetal alcohol spectrum disorders. - Certain viral infections during pregnancy - Preterm birth Often there is no cure, but treatment can help the symptoms. Treatments include physical, speech, and occupational therapy. Special education classes and psychological counseling can also help. NIH: National Institute of Child Health and Human Development
|
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What causes Heart Block ?
|
Heart block has many causes. Some people are born with the disorder (congenital), while others develop it during their lifetimes (acquired).
Congenital Heart Block
One form of congenital heart block occurs in babies whose mothers have autoimmune diseases, such as lupus. People who have these diseases make proteins called antibodies that attack and damage the body's tissues or cells.
In pregnant women, antibodies can cross the placenta. (The placenta is the organ that attaches the umbilical cord to the mother's womb.) These proteins can damage the baby's heart and lead to congenital heart block.
Congenital heart defects also may cause congenital heart block. These defects are problems with the heart's structure that are present at birth. Often, doctors don't know what causes these defects.
Acquired Heart Block
Many factors can cause acquired heart block. Examples include:
Damage to the heart from a heart attack. This is the most common cause of acquired heart block.
Coronary heart disease, also called coronary artery disease.
Myocarditis (MI-o-kar-DI-tis), or inflammation of the heart muscle.
Heart failure.
Rheumatic (roo-MAT-ik) fever.
Cardiomyopathy (KAR-de-o-mi-OP-a-the), or heart muscle diseases.
Other diseases may increase the risk of heart block. Examples include sarcoidosis (sar-koy-DOE-sis) and the degenerative muscle disorders Lev's disease and Lenegre's disease.
Certain types of surgery also may damage the heart's electrical system and lead to heart block.
Exposure to toxic substances and taking certain medicinesincluding digitalis, beta blockers, and calcium channel blockersalso may cause heart block. Doctors closely watch people who are taking these medicines for signs of problems.
Some types of heart block have been linked to genetic mutations (changes in the genes).
An overly active vagus nerve also can cause heart block. You have one vagus nerve on each side of your body. These nerves run from your brain stem all the way to your abdomen. Activity in the vagus nerve slows the heart rate.
In some cases, acquired heart block may go away if the factor causing it is treated or resolved. For example, heart block that occurs after a heart attack or surgery may go away during recovery.
Also, if a medicine is causing heart block, the disorder may go away if the medicine is stopped or the dosage is lowered. Always talk with your doctor before you change the way you take your medicines.
|
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What is (are) Familial pemphigus vulgaris ?
|
Familial pemphigus vulgaris refers to a cluster of pemphigus vulgaris within a family. Pemphigus vulgaris is a rare autoimmune condition that is characterized by blisters and sores on the skin and mucus membranes. Although the exact cause of familial pemphigus vulgaris is unknown, autoimmune conditions generally occur when the body's immune system mistakenly attacks healthy tissue (in this case, the skin and mucus membranes). Most cases of pemphigus vulgaris occur sporadically in people with no family history of the condition; however, rare reports exist of "familial" cases which affect more than one member of a single family. In these cases, the underlying genetic cause is unknown, although an association between pemphigus vulgaris and certain HLA antigens has been identified. Treatment generally includes medications and other strategies to decrease blister formation, prevent infections and promote healing.
|
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] |
What causes Lipedema ?
|
What causes lipedema? The cause of lipedema is unknown. Hormones appear to play a role, especially considering that the condition occurs almost entirely in females and often develops after puberty or other periods of hormone change (e.g., pregnancy, menopause). Although people who are obese may be overrepresented among those with lipedema, persons of normal weight are also commonly affected. As a result, obesity alone is unlikely to be a major determinant of this syndrome. Many people with lipedema have a family history of similarly enlarged legs. At this time the role of genetics in the causation of lipedema is unknown.
|
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What is (are) Large granular lymphocyte leukemia ?
|
Large granular lymphocyte (LGL) leukemia is a rare cancer of a type of white blood cells called lymphocytes. LGL leukemia causes a slow increase in white blood cells called T lymphocytes, or T cells, which originate in the lymph system and bone marrow and help to fight infection. This disease usually affects people in their sixties. Symptoms include anemia; low levels of platelets (thrombocytopenia) and infection-fighting neutrophils (neutropenia) in the blood; and an enlarged spleen. About one-third of patients are asymptomatic at the time of diagnosis. The exact cause of LGL leukemia is unknown. Doctors can diagnose this disease through a bone marrow biopsy, or by using a specialized technique in which various types of blood or bone marrow cells are separated, identified, and counted.
|
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What are the genetic changes related to familial adenomatous polyposis ?
|
Mutations in the APC gene cause both classic and attenuated familial adenomatous polyposis. These mutations affect the ability of the cell to maintain normal growth and function. Cell overgrowth resulting from mutations in the APC gene leads to the colon polyps seen in familial adenomatous polyposis. Although most people with mutations in the APC gene will develop colorectal cancer, the number of polyps and the time frame in which they become malignant depend on the location of the mutation in the gene. Mutations in the MUTYH gene cause autosomal recessive familial adenomatous polyposis (also called MYH-associated polyposis). Mutations in this gene prevent cells from correcting mistakes that are made when DNA is copied (DNA replication) in preparation for cell division. As these mistakes build up in a person's DNA, the likelihood of cell overgrowth increases, leading to colon polyps and the possibility of colon cancer.
|
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What are the genetic changes related to Lynch syndrome ?
|
Variations in the MLH1, MSH2, MSH6, PMS2, or EPCAM gene increase the risk of developing Lynch syndrome. The MLH1, MSH2, MSH6, and PMS2 genes are involved in the repair of mistakes that occur when DNA is copied in preparation for cell division (a process called DNA replication). Mutations in any of these genes prevent the proper repair of DNA replication mistakes. As the abnormal cells continue to divide, the accumulated mistakes can lead to uncontrolled cell growth and possibly cancer. Mutations in the EPCAM gene also lead to impaired DNA repair, although the gene is not itself involved in this process. The EPCAM gene lies next to the MSH2 gene on chromosome 2; certain EPCAM gene mutations cause the MSH2 gene to be turned off (inactivated), interrupting DNA repair and leading to accumulated DNA mistakes. Although mutations in these genes predispose individuals to cancer, not all people who carry these mutations develop cancerous tumors.
|
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] |
What is (are) Bladder Cancer ?
|
The bladder is a hollow organ in your lower abdomen that stores urine. Bladder cancer occurs in the lining of the bladder. It is the sixth most common type of cancer in the United States. Symptoms include - Blood in your urine - A frequent urge to urinate - Pain when you urinate - Low back pain Risk factors for developing bladder cancer include smoking and exposure to certain chemicals in the workplace. People with a family history of bladder cancer or who are older, white, or male have a higher risk. Treatments for bladder cancer include surgery, radiation therapy, chemotherapy, and biologic therapy. Biologic therapy boosts your body's own ability to fight cancer. NIH: National Cancer Institute
|
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What is (are) Common variable immunodeficiency ?
|
Common variable immunodeficiency (CVID) is a group of disorders in which the immune system cannot make antibodies against agents that cause infection (such as bacteria). CVID is characterized by low levels of most or all of the immunoglobulin (Ig) classes. This causes affected people to get frequent infections, particularly in the sinuses, lungs, and digestive tract. Symptoms most commonly begin in early adulthood but have been found in children as young as age two. While in most cases the cause of CVID is unknown, it has been associated with changes (mutations) in at least 10 genes. About 10% of cases are due to mutations in the TNFRSF13B gene. Treatment for CVID includes Ig replacement therapy, which stops the cycle of recurrent infections.
|
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Is multiminicore disease inherited ?
|
This condition is inherited in an autosomal recessive pattern, which means both copies of the gene in each cell have mutations. The parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene, but they typically do not show signs and symptoms of the condition.
|
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What are the treatments for GM3 synthase deficiency ?
|
These resources address the diagnosis or management of GM3 synthase deficiency: - American Epilepsy Society: Find a Doctor - Clinic for Special Children (Strasburg, Pennsylvania) - Genetic Testing Registry: Amish infantile epilepsy syndrome These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
|
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What are the symptoms of Intellectual disability - athetosis - microphthalmia ?
|
What are the signs and symptoms of Intellectual disability - athetosis - microphthalmia? The Human Phenotype Ontology provides the following list of signs and symptoms for Intellectual disability - athetosis - microphthalmia. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormality of movement 90% Abnormality of thumb phalanx 90% Broad forehead 90% Chin dimple 90% Cognitive impairment 90% Facial cleft 90% Frontal bossing 90% Hypertelorism 90% Hypertonia 90% Hypoplasia of the ear cartilage 90% Large earlobe 90% Malar flattening 90% Microcephaly 90% Reduced number of teeth 90% Scoliosis 90% Single transverse palmar crease 90% Supernumerary nipple 90% Telecanthus 90% Abnormality of the palate 50% Abnormality of the thorax 50% Aplasia/Hypoplasia affecting the eye 50% Blue sclerae 50% Camptodactyly of finger 50% Facial asymmetry 50% Iris coloboma 50% Lip pit 50% Mandibular prognathia 50% Preauricular skin tag 50% Seizures 50% Strabismus 50% Tapered finger 50% The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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What are the symptoms of Optic atrophy 6 ?
|
What are the signs and symptoms of Optic atrophy 6? The Human Phenotype Ontology provides the following list of signs and symptoms for Optic atrophy 6. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Autosomal recessive inheritance - Infantile onset - Optic atrophy - Photophobia - Red-green dyschromatopsia - Slow progression - Visual impairment - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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What are the treatments for Zollinger-Ellison Syndrome ?
|
A health care provider treats Zollinger-Ellison syndrome with medications to reduce gastric acid secretion and with surgery to remove gastrinomas. A health care provider sometimes uses chemotherapymedications to shrink tumorswhen tumors are too widespread to remove with surgery.
Medications
A class of medications called proton pump inhibitors (PPIs) includes
- esomeprazole (Nexium) - lansoprazole (Prevacid) - pantoprazole (Protonix) - omeprazole (Prilosec or Zegerid) - dexlansoprazole (Dexilant)
PPIs stop the mechanism that pumps acid into the stomach, helping to relieve peptic ulcer pain and promote healing. A health care provider may prescribe people who have Zollinger-Ellison syndrome higher-than-normal doses of PPIs to control the acid production. Studies show that PPIs may increase the risk of hip, wrist, and spine fractures when a person takes them long term or in high doses, so its important for people to discuss risks versus benefits with their health care provider.
Surgery
Surgical removal of gastrinomas is the only cure for Zollinger-Ellison syndrome. Some gastrinomas spread to other parts of the body, especially the liver and bones. Finding and removing all gastrinomas before they spread is often challenging because many of the tumors are small.
Chemotherapy
Health care providers sometimes use chemotherapy drugs to treat gastrinomas that cannot be surgically removed, including
- streptozotocin (Zanosar) - 5-fluorouracil (Adrucil) - doxorubicin (Doxil)
|
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What causes Harlequin ichthyosis ?
|
What causes harlequin ichthyosis? Harlequin ichthyosis is caused by mutations in the ABCA12 gene. This gene provides instructions for making a protein that is essential for the normal development of skin cells. This protein plays a major role in the transport of fats (lipids) in the outermost layer of skin (the epidermis). Some mutations in the ABCA12 gene prevent the cell from making any ABCA12 protein, while others lead to the production of an abnormally small version of the protein that cannot transport lipids properly. A loss of functional ABCA12 protein disrupts the normal development of the epidermis, resulting in the hard, thick scales characteristic of harlequin ichthyosis.
|
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What is (are) Dowling-Degos disease ?
|
Dowling-Degos disease is a skin condition characterized by a lacy or net-like (reticulate) pattern of abnormally dark skin coloring (hyperpigmentation), particularly in the body's folds and creases. Other features may include dark lesions on the face and back that resemble blackheads, red bumps around the mouth that resemble acne, depressed or pitted scars on the face similar to acne scars but with no history of acne, cysts within hair follicles (pilar cysts) on the scalp, and rarely, patches of skin that are unusually light in color (hypopigmented). Symptoms typically develop in late childhood or in adolescence and progress over time. While the skin changes caused by Dowling-Degos disease can be bothersome, they typically don't cause health problems. Dowling-Degos disease is caused by mutations in the KRT5 gene. This condition is inherited in an autosomal dominant pattern.
|
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What are the symptoms of Wolff-Parkinson-White syndrome ?
|
What are the signs and symptoms of Wolff-Parkinson-White syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Wolff-Parkinson-White syndrome. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Arrhythmia 90% Cardiomyopathy - Palpitations - Paroxysmal atrial fibrillation - Paroxysmal supraventricular tachycardia - Prolonged QRS complex - Shortened PR interval - Stroke - Sudden cardiac death - Ventricular preexcitation with multiple accessory pathways - Wolff-Parkinson-White syndrome - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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What are the symptoms of Tyrosinemia type 3 ?
|
What are the signs and symptoms of Tyrosinemia type 3? The Human Phenotype Ontology provides the following list of signs and symptoms for Tyrosinemia type 3. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) 4-Hydroxyphenylacetic aciduria - 4-Hydroxyphenylpyruvic aciduria - Abnormality of the liver - Autosomal recessive inheritance - Hypertyrosinemia - Intellectual disability, mild - Seizures - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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What to do for Urinary Incontinence in Children ?
|
Eating, diet, and nutrition have not been shown to play a role in causing or preventing UI in children, though ensuring sufficient fluid intake throughout the day and avoiding caffeine intake may be helpful.
|
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What is the outlook for Ataxia Telangiectasia ?
|
Average lifespan has been improving for years, for unknown reasons, and varies with the severity of the underlying mutations, ATM (ataxia-telangiectasia mutated) protein levels, and residual ATM kinase activity. Some individuals with later onset of disease and slower progression survive into their 50s.
|
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What is (are) Smoking and the Digestive System ?
|
Smoking contributes to many common disorders of the digestive system, such as heartburn and gastroesophageal reflux disease (GERD), peptic ulcers, and some liver diseases. Smoking increases the risk of Crohns disease, colon polyps, and pancreatitis, and it may increase the risk of gallstones.
|
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Is Medium-chain acyl-coenzyme A dehydrogenase deficiency inherited ?
|
How is medium-chain acyl-coenzyme A dehydrogenase (MCAD) deficiency inherited? Medium-chain acyl-coenzyme A dehydrogenase deficiency (MCADD) is inherited in an autosomal recessive manner. This means that both copies of the responsible gene in each cell must have mutations for a person to be affected. Usually, the parents of a person with an autosomal recessive condition each have one mutated copy of the gene and are referred to as carriers. Carriers typically do not have any signs or symptoms of the condition. When two carriers of an autosomal recessive condition have children, each child has a 25% (1 in 4) chance to be affected, a 50% (1 in 2) chance to be a carrier like each parent, and a 25% chance to be unaffected and not be a carrier.
|
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What are the treatments for spastic paraplegia type 11 ?
|
These resources address the diagnosis or management of spastic paraplegia type 11: - Gene Review: Gene Review: Spastic Paraplegia 11 - Genetic Testing Registry: Spastic paraplegia 11, autosomal recessive - Spastic Paraplegia Foundation, Inc.: Treatments and Therapies These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
|
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What are the treatments for 22q11.2 deletion syndrome ?
|
These resources address the diagnosis or management of 22q11.2 deletion syndrome: - Gene Review: Gene Review: 22q11.2 Deletion Syndrome - Genetic Testing Registry: Asymmetric crying face association - Genetic Testing Registry: DiGeorge sequence - Genetic Testing Registry: Opitz G/BBB syndrome - Genetic Testing Registry: Shprintzen syndrome These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
|
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Is mucopolysaccharidosis type I inherited ?
|
This condition is inherited in an autosomal recessive pattern, which means both copies of the gene in each cell have mutations. The parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene, but they typically do not show signs and symptoms of the condition.
|
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What is the outlook for Multiple System Atrophy ?
|
The disease tends to advance rapidly over the course of 5 to 10 years, with progressive loss of motor skills, eventual confinement to bed, and death. There is no remission from the disease. There is currently no cure.
|
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Is Andersen-Tawil syndrome inherited ?
|
This condition is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder. In some cases, a person with Andersen-Tawil syndrome inherits the mutation from one affected parent. Other cases result from new mutations in the KCNJ2 gene. These cases occur in people with no history of the disorder in their family.
|
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What is (are) Aicardi-Goutieres syndrome type 2 ?
|
Aicardi-Goutieres syndrome is an inherited condition that mainly affects the brain, immune system, and skin. It is characterized by early-onset severe brain dysfunction (encephalopathy) that usually results in severe intellectual and physical disability. Additional symptoms may include epilepsy, painful, itchy skin lesion (chilblains), vision problems, and joint stiffness. Symptoms usually progress over several months before the disease course stabilizes. There are six different types of Aicardi-Goutieres syndrome, which are distinguished by the gene that causes the condition: TREX1, RNASEH2A, RNASEH2B, RNASEH2C, SAMHD1, and ADAR genes. Most cases are inherited in an autosomal recessive pattern, although rare autosomal dominant cases have been reported. Treatment is symptomatic and supportive.
|
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