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What are the genetic changes related to Guillain-Barr syndrome ?
Some studies show that normal variations in certain genes may be associated with an increased risk of developing Guillain-Barr syndrome; however, more research is necessary to identify and confirm associated genes. Many of the genes that may increase the risk of Guillain-Barr syndrome are involved in the immune system, and their roles in fighting infection may contribute to the development of the condition. Most people who develop Guillain-Barr syndrome have a bacterial or viral infection prior to developing the signs and symptoms of the condition. However, only a very small percentage of people who have an infection develop Guillain-Barr syndrome. In order to fight the infection, specialized immune cells produce proteins called antibodies that recognize specific proteins or molecules on the bacteria or virus (pathogen). Some research shows that antibodies that recognize molecules on some pathogens may also recognize proteins on the body's own nerves. As a result, the immune system attacks the nerves, causing inflammation and damaging the axons and myelin, which can lead to the signs and symptoms of Guillain-Barr syndrome.
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What is (are) Absence of the Septum Pellucidum ?
The septum pellucidum (SP) is a thin membrane located at the midline of the brain between the two cerebral hemispheres, or halves of the brain.. It is connected to the corpus callosum -- a collection of nerve fibers that connect the cerebral hemispherers. This rare abnormality accompanies various malformations of the brain that affect intelligence, behavior, and the neurodevelopmental process, and seizures may occur. Children who are born without this membrane and also have other abnormalities--pituitary deficiencies and abnormal development of the optic disk--have a disorder known as septo-optic dysplasia. More information about this condition can be located at the NINDS Septo-Optic Dysplasia Information Page.
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What are the stages of Ovarian Germ Cell Tumors ?
Key Points - After ovarian germ cell tumor has been diagnosed, tests are done to find out if cancer cells have spread within the ovary or to other parts of the body. - There are three ways that cancer spreads in the body. - Cancer may spread from where it began to other parts of the body. - The following stages are used for ovarian germ cell tumors: - Stage I - Stage II - Stage III - Stage IV After ovarian germ cell tumor has been diagnosed, tests are done to find out if cancer cells have spread within the ovary or to other parts of the body. The process used to find out whether cancer has spread within the ovary or to other parts of the body is called staging. The information gathered from the staging process determines the stage of the disease. Unless a doctor is sure the cancer has spread from the ovaries to other parts of the body, an operation called a laparotomy is done to see if the cancer has spread. The doctor must cut into the abdomen and carefully look at all the organs to see if they have cancer in them. The doctor will cut out small pieces of tissue so they can be checked under a microscope for signs of cancer. The doctor may also wash the abdominal cavity with fluid, which is also checked under a microscope to see if it has cancer cells in it. Usually the doctor will remove the cancer and other organs that have cancer in them during the laparotomy. It is important to know the stage in order to plan treatment. Many of the tests used to diagnose ovarian germ cell tumor are also used for staging. The following tests and procedures may also be used for staging: - PET scan (positron emission tomography scan): A procedure to find malignant tumor cells in the body. A small amount of radioactive glucose (sugar) is injected into a vein. The PET scanner rotates around the body and makes a picture of where glucose is being used in the body. Malignant tumor cells show up brighter in the picture because they are more active and take up more glucose than normal cells do. - MRI (magnetic resonance imaging): A procedure that uses a magnet, radio waves, and a computer to make a series of detailed pictures of areas inside the body. This procedure is also called nuclear magnetic resonance imaging (NMRI). - Transvaginal ultrasound exam: A procedure used to examine the vagina, uterus, fallopian tubes, and bladder. An ultrasound transducer (probe) is inserted into the vagina and used to bounce high-energy sound waves (ultrasound) off internal tissues or organs and make echoes. The echoes form a picture of body tissues called a sonogram. The doctor can identify tumors by looking at the sonogram. There are three ways that cancer spreads in the body. Cancer can spread through tissue, the lymph system, and the blood: - Tissue. The cancer spreads from where it began by growing into nearby areas. - Lymph system. The cancer spreads from where it began by getting into the lymph system. The cancer travels through the lymph vessels to other parts of the body. - Blood. The cancer spreads from where it began by getting into the blood. The cancer travels through the blood vessels to other parts of the body. Cancer may spread from where it began to other parts of the body. When cancer spreads to another part of the body, it is called metastasis. Cancer cells break away from where they began (the primary tumor) and travel through the lymph system or blood. - Lymph system. The cancer gets into the lymph system, travels through the lymph vessels, and forms a tumor (metastatic tumor) in another part of the body. - Blood. The cancer gets into the blood, travels through the blood vessels, and forms a tumor (metastatic tumor) in another part of the body. The metastatic tumor is the same type of tumor as the primary tumor. For example, if an ovarian germ cell tumor spreads to the liver, the tumor cells in the liver are actually cancerous ovarian germ cells. The disease is metastatic ovarian germ cell tumor, not liver cancer. The following stages are used for ovarian germ cell tumors: Stage I In stage I, cancer is found in one or both ovaries. Stage I is divided into stage IA, stage IB, and stage IC. - Stage IA: Cancer is found inside a single ovary. - Stage IB: Cancer is found inside both ovaries. - Stage IC: Cancer is found inside one or both ovaries and one of the following is true: - cancer is also found on the outside surface of one or both ovaries; or - the capsule (outer covering) of the ovary has ruptured (broken open); or - cancer cells are found in the fluid of the peritoneal cavity (the body cavity that contains most of the organs in the abdomen) or in washings of the peritoneum (tissue lining the peritoneal cavity). Stage II In stage II, cancer is found in one or both ovaries and has spread into other areas of the pelvis. Stage II is divided into stage IIA, stage IIB, and stage IIC. - Stage IIA: Cancer has spread to the uterus and/or fallopian tubes (the long slender tubes through which eggs pass from the ovaries to the uterus). - Stage IIB: Cancer has spread to other tissue within the pelvis. - Stage IIC: Cancer is found inside one or both ovaries and has spread to the uterus and/or fallopian tubes, or to other tissue within the pelvis. Also, one of the following is true: - cancer is found on the outside surface of one or both ovaries; or - the capsule (outer covering) of the ovary has ruptured (broken open); or - cancer cells are found in the fluid of the peritoneal cavity (the body cavity that contains most of the organs in the abdomen) or in washings of the peritoneum (tissue lining the peritoneal cavity). Stage III In stage III, cancer is found in one or both ovaries and has spread outside the pelvis to other parts of the abdomen and/or nearby lymph nodes. Stage III is divided into stage IIIA, stage IIIB, and stage IIIC. - Stage IIIA: The tumor is found in the pelvis only, but cancer cells that can be seen only with a microscope have spread to the surface of the peritoneum (tissue that lines the abdominal wall and covers most of the organs in the abdomen), the small intestines, or the tissue that connects the small intestines to the wall of the abdomen. - Stage IIIB: Cancer has spread to the peritoneum and the cancer in the peritoneum is 2 centimeters or smaller. - Stage IIIC: Cancer has spread to the peritoneum and the cancer in the peritoneum is larger than 2 centimeters and/or cancer has spread to lymph nodes in the abdomen. Cancer that has spread to the surface of the liver is also considered stage III ovarian cancer. Stage IV In stage IV, cancer has spread beyond the abdomen to other parts of the body, such as the lungs or tissue inside the liver. Cancer cells in the fluid around the lungs is also considered stage IV ovarian cancer.
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How many people are affected by Roberts syndrome ?
Roberts syndrome is a rare disorder; approximately 150 affected individuals have been reported.
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How to diagnose Prolactinoma ?
A doctor will test for prolactin blood levels in women with unexplained milk secretion, called galactorrhea, or with irregular menses or infertility and in men with impaired sexual function and, in rare cases, milk secretion. If prolactin levels are high, a doctor will test thyroid function and ask first about other conditions and medications known to raise prolactin secretion. The doctor may also request magnetic resonance imaging (MRI), which is the most sensitive test for detecting pituitary tumors and determining their size. MRI scans may be repeated periodically to assess tumor progression and the effects of therapy. Computerized tomography (CT) scan also gives an image of the pituitary but is less precise than the MRI. The doctor will also look for damage to surrounding tissues and perform tests to assess whether production of other pituitary hormones is normal. Depending on the size of the tumor, the doctor may request an eye exam with measurement of visual fields.
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How to diagnose Renal Artery Stenosis ?
A health care provider can diagnose RAS by listening to the abdomen with a stethoscope and performing imaging tests. When blood flows through a narrow artery, it sometimes makes a whooshing sound, called a bruit. The health care provider may place a stethoscope on the front or the side of the abdomen to listen for this sound. The absence of this sound, however, does not exclude the possibility of RAS. In some cases, RAS is found when a person has a test for another reason. For example, a health care provider may find RAS during a coronary angiogram for diagnosis of heart problems. A coronary angiogram is a procedure that uses a special dye, called contrast medium, and x rays to see how blood flows through the heart. The following imaging tests are used to diagnose RAS: - Duplex ultrasound. Duplex ultrasound combines traditional ultrasound with Doppler ultrasonography. Traditional ultrasound uses a device, called a transducer, that bounces safe, painless sound waves off organs to create an image of their structure. Doppler ultrasonography records sound waves reflected off of moving objects, such as blood, to measure their speed and other aspects of how they flow. The procedure is performed in a health care providers office, outpatient center, or hospital by a specially trained technician, and the images are interpreted by a radiologista doctor who specializes in medical imaging. Anesthesia is not needed. The images can show blockage in the renal artery or blood moving through nearby arteries at a lower-than-normal speed. Ultrasound is noninvasive and low cost. - Catheter angiogram. A catheter angiogram, also called a traditional angiogram, is a special kind of x ray in which a thin, flexible tube called a catheter is threaded through the large arteries, often from the groin, to the artery of interestin this case, the renal artery. The procedure is performed in a hospital or outpatient center by a radiologist. Anesthesia is not needed though a sedative may be given to lessen anxiety during the procedure. Contrast medium is injected through the catheter so the renal artery shows up more clearly on the x ray. Catheter angiogram is the gold standard for diagnosing RAS due to the high quality of the image produced. In addition, severe RAS can be treated during the same visit. However, a catheter angiogram is an invasive procedure, and a person may have side effects from the sedative or contrast medium or may have bleeding or injury to the artery from the catheter. The procedure is also more expensive than other imaging tests. - Computerized tomographic angiography (CTA) scan. CTA scans use a combination of x rays and computer technology to create images. The procedure is performed in an outpatient center or hospital by an x-ray technician, and the images are interpreted by a radiologist. Anesthesia is not needed. Contrast medium is injected into a vein in the persons arm to better see the structure of the arteries. CTA scans require the person to lie on a table that slides into a tunnel-shaped device where the x rays are taken. CTA scans are less invasive than catheter angiograms and take less time. However, the risks from the x-ray radiation still exist, and the test often requires more contrast medium than a catheter angiogram, so it may not be recommended for a person with poor kidney function. - Magnetic resonance angiogram (MRA). MRA uses radio waves and magnets to produce detailed pictures of the bodys internal organs and soft tissues without using x rays. The procedure is performed in an outpatient center or hospital by an x-ray technician, and the images are interpreted by a radiologist. Anesthesia is not needed though light sedation may be used for people with a fear of confined spaces. Contrast medium may be injected into a vein in the persons arm to better see the structure of the arteries. With most MRA scans, the person lies on a table that slides into a tunnel-shaped device that may be open ended or closed at one end; some newer machines are designed to allow the person to lie in a more open space. In addition to providing high-quality images noninvasively, MRA can provide a functional assessment of blood flow and organ function. However, the use of contrast medium for an MRA is not advised for people with poor kidney function because of the risk of complications to the skin and other organs if the kidneys do not remove the contrast medium well enough.
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Is Wolman 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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How to diagnose Mulibrey Nanism ?
Is genetic testing available for mulibrey nanism? Testing for the TRIM37 gene is available for carrier testing, confirming the diagnosis, and prenatal diagnosis. GeneTests lists the names of laboratories that are performing genetic testing for mulibrey nanism. To view the contact information for the clinical laboratories conducting testing, click here. Please note that most of the laboratories listed through GeneTests do not accept direct contact from patients and their families; therefore, if you are interested in learning more, you will need to work with a health care provider or a genetics professional.
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How many people are affected by ocular albinism ?
The most common form of this disorder, ocular albinism type 1, affects at least 1 in 60,000 males. The classic signs and symptoms of this condition are much less common in females.
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How many people are affected by Stormorken syndrome ?
Stormorken syndrome is a rare disorder. Approximately a dozen cases have been reported in the medical literature.
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How to prevent Mitral Valve Prolapse ?
You can't prevent mitral valve prolapse (MVP). Most people who have the condition are born with it. Complications from MVP, such as arrhythmias (irregular heartbeats) and infective endocarditis (IE), are rare. IE is an infection of the inner lining of your heart chambers and valves. People at high risk for IE may be given antibiotics before some types of surgery and dental work. Antibiotics can help prevent IE. Your doctor will tell you whether you need this type of treatment. People at high risk for IE may include those who've had valve repair or replacement or who have some types of underlying heart disease.
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What is (are) Allan-Herndon-Dudley syndrome ?
Allan-Herndon-Dudley syndrome is a rare disorder of brain development that causes moderate to severe intellectual disability and problems with movement. This condition, which occurs exclusively in males, disrupts development from before birth. Although affected males have impaired speech and a limited ability to communicate, they seem to enjoy interaction with other people. Most children with Allan-Herndon-Dudley syndrome have weak muscle tone (hypotonia) and underdevelopment of many muscles (muscle hypoplasia). As they get older, they usually develop joint deformities called contractures, which restrict the movement of certain joints. Abnormal muscle stiffness (spasticity), muscle weakness, and involuntary movements of the arms and legs also limit mobility. As a result, many people with Allan-Herndon-Dudley syndrome are unable to walk independently and become wheelchair-bound by adulthood.
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What are the genetic changes related to 18q deletion syndrome ?
18q deletion syndrome is caused by a deletion of genetic material from the long (q) arm of chromosome 18. This chromosomal change is written as 18q-. The size of the deletion and its location on the chromosome vary among affected individuals. The signs and symptoms of 18q deletion syndrome, including the leukodystrophy that likely contributes to the neurological problems, are probably related to the loss of multiple genes on the long arm of chromosome 18. 18q deletion syndrome is often categorized into two types: individuals with deletions near the end of the long arm of chromosome 18 are said to have distal 18q deletion syndrome, and those with deletions in the part of the long arm near the center of chromosome 18 are said to have proximal 18q deletion syndrome. The signs and symptoms of these two types of the condition are overlapping, with certain features being more common in one form of the disorder than in the other. For example, hearing loss and heart abnormalities are more common in people with distal 18q deletion syndrome, while seizures occur more often in people with proximal 18q deletion syndrome. Researchers are working to determine how the loss of specific genes in these regions contributes to the various features of 18q deletion syndrome.
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What are the treatments for Albright's hereditary osteodystrophy ?
How might Albright's hereditary osteodystrophy be treated? Treatment with calcium and vitamin D supplements help maintain normal levels of calcium in the blood. If there are high levels of phosphate in the blood, it may be recommended to eat a low-phosphorous diet or take medications called phosphate binders to help lower the levels of phosphate. Examples of phosphate binders include calcium carbonate, calcium acetate, and sevelamer HCl.
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What is (are) Michels syndrome ?
Michels syndrome is an extremely rare disorder characterized by the eyelid triad of blepharophimosis (a narrowing of the eye opening), blepharoptosis and epicanthus inversus (an upward fold of the skin of the lower eyelid near the inner corner of the eye), skeletal defects including craniosynostosis, cranial asymmetry, abnormality of the occipital bone (at the base of the skull), and radioulnar synostosis, cleft lip and palate, and mental deficiency. Only 10 cases have been reported in the medical literature. While the underlying cause of this condition remains unknown, it is believed to be transmitted as an autosomal recessive trait. Based on phenotypic overlap and autosomal recessive inheritance, some researchers have suggested that Michels, Malpuech, Carnevale and Mingarelli syndromes represent a spectrum and should be referred to a 3MC syndrome (for Malpuech-Michels-Mingarelli-Carnevale).
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What is the outlook for Neurological Sequelae Of Lupus ?
The prognosis for lupus varies widely depending on the organs involved and the intensity of the inflammatory reaction. The course of lupus is commonly chronic and relapsing, often with long periods of remission. Most individuals with lupus do not develop serious health problems and have a normal lifespan with periodic doctor visits and treatments with various drugs.
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What are the symptoms of Olivopontocerebellar atrophy deafness ?
What are the signs and symptoms of Olivopontocerebellar atrophy deafness? The Human Phenotype Ontology provides the following list of signs and symptoms for Olivopontocerebellar atrophy 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) Cerebral cortical atrophy 90% Hearing impairment 90% Hyperreflexia 90% Incoordination 90% Ventriculomegaly 90% Aplasia/Hypoplasia of the cerebellum 50% Nystagmus 50% Chorioretinal coloboma 7.5% EEG abnormality 7.5% Hypertonia 7.5% Neurological speech impairment 7.5% Optic atrophy 7.5% Seizures 7.5% Strabismus 7.5% 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 Narcolepsy ?
The four major signs and symptoms of narcolepsy are extreme daytime sleepiness, cataplexy (muscle weakness) while awake, and hallucinations and sleep paralysis during sleep. If you have narcolepsy, you may have one or more of these symptoms. They can range from mild to severe. Less than one-third of people who have narcolepsy have all four symptoms. Extreme Daytime Sleepiness All people who have narcolepsy have extreme daytime sleepiness. This often is the most obvious symptom of the disorder. During the day, you may have few or many periods of sleepiness. Each period usually lasts 30minutes or less. Strong emotionssuch as anger, fear, laughter, or excitementcan trigger this sleepiness. People who have daytime sleepiness often complain of: Mental cloudiness or "fog" Memory problems or problems focusing Lack of energy or extreme exhaustion Depression Some people who have narcolepsy have episodes in which they fall asleep suddenly. This is more likely to happen when they're not activefor example, while reading, watching TV, or sitting in a meeting. However, sleep episodes also may occur in the middle of talking, eating, or another activity. Cataplexy also may occur at the same time. Cataplexy This condition causes loss of muscle tone while you're awake. Muscle weakness affects part or all of your body. Cataplexy may make your head nod or make it hard for you to speak. Muscle weakness also may make your knees weak or cause you to drop things you're holding. Some people lose all muscle control and fall. Strong emotionssuch as anger, surprise, fear, or laughteroften trigger cataplexy. It usually lasts a few seconds or minutes. During this time, you're usually awake. Cataplexy may occur weeks to years after you first start to have extreme daytime sleepiness. Hallucinations If you have narcolepsy, you may have vivid dreams while falling asleep, waking up, or dozing. These dreams can feel very real. You may feel like you can see, hear, smell, and taste things. Sleep Paralysis This condition prevents you from moving or speaking while falling asleep or waking up. However, you're fully conscious (aware) during this time. Sleep paralysis usually lasts just a few seconds or minutes, but it can be scary. Other Symptoms Most people who have narcolepsy don't sleep well at night. They may have trouble falling and staying asleep. Vivid, scary dreams may disturb sleep. Not sleeping well at night worsens daytime sleepiness. Rarely, people who fall asleep in the middle of an activity, such as eating, may continue that activity for a few seconds or minutes. This is called automatic behavior. During automatic behavior, you're not aware of your actions, so you don't do them well. For example, if you're writing before falling asleep, you may scribble rather than form words. If you're driving, you may get lost or have an accident. Most people who have this symptom don't remember what happened while it was going on. Children who have narcolepsy often have trouble studying, focusing, and remembering things. Also, they may seem hyperactive. Some children who have narcolepsy speed up their activities rather than slow them down. Children who have narcolepsy may have severe sleepiness. They may fall asleep while talking or eating, or during sporting events and social activities.
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How to diagnose Metabolic Syndrome ?
Your doctor will diagnose metabolic syndrome based on the results of a physical exam and blood tests. You must have at least three of the five metabolic risk factors to be diagnosed with metabolic syndrome. Metabolic Risk Factors A Large Waistline Having a large waistline means that you carry excess weight around your waist (abdominal obesity). This is also called having an "apple-shaped" figure. Your doctor will measure your waist to find out whether you have a large waistline. A waist measurement of 35 inches or more for women or 40 inches or more for men is a metabolic risk factor. A large waistline means you're at increased risk for heart disease and other health problems. A High Triglyceride Level Triglycerides are a type of fat found in the blood. A triglyceride level of 150 mg/dL or higher (or being on medicine to treat high triglycerides) is a metabolic risk factor. (The mg/dL is milligrams per deciliterthe units used to measure triglycerides, cholesterol, and blood sugar.) A Low HDL Cholesterol Level HDL cholesterol sometimes is called "good" cholesterol. This is because it helps remove cholesterol from your arteries. An HDL cholesterol level of less than 50 mg/dL for women and less than 40 mg/dL for men (or being on medicine to treat low HDL cholesterol) is a metabolic risk factor. High Blood Pressure A blood pressure of 130/85 mmHg or higher (or being on medicine to treat high blood pressure) is a metabolic risk factor. (The mmHg is millimeters of mercurythe units used to measure blood pressure.) If only one of your two blood pressure numbers is high, you're still at risk for metabolic syndrome. High Fasting Blood Sugar A normal fasting blood sugar level is less than 100 mg/dL. A fasting blood sugar level between 100125 mg/dL is considered prediabetes. A fasting blood sugar level of 126 mg/dL or higher is considered diabetes. A fasting blood sugar level of 100 mg/dL or higher (or being on medicine to treat high blood sugar) is a metabolic risk factor. About 85 percent of people who have type 2 diabetesthe most common type of diabetesalso have metabolic syndrome. These people have a much higher risk for heart disease than the 15 percent of people who have type 2 diabetes without metabolic syndrome.
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What causes Erythromelalgia ?
What causes erythromelalgia? About 15% of cases of erythromelalgia are caused by mutations in the SCN9A gene. The SCN9A gene gives instructions for making part of a sodium channel which carries sodium into cells and helps them make and transmit electrical signals. These sodium channels are found in nerve cells that transmit pain signals to the spine and brain. Mutations that cause erythromelalgia cause increased transmission of pain signals, leading to the signs and symptoms of the condition. In some of these cases, an affected individual inherits the mutation from an affected parent. In other cases, a new mutation occurs for the first time in an individual with no history of the condition in the family. In the remainder of cases, the exact underlying cause is not currently known. Evidence suggests that it results from abnormalities in the normal narrowing and widening of certain blood vessels, leading to abnormalities in blood flow to the hands and feet. There may be a variety of non-genetic causes, or mutations in other genes that have not yet been identified.
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What is (are) Lucey-Driscoll syndrome ?
Lucey-Driscoll syndrome, a form of transient familial hyperbilirubinemia, is a rare metabolic disorder that leads to very high levels of bilirubin in a newborn's blood. Babies with this disorder may be born with severe jaundice (yellow skin), yellow eyes and lethargy. It occurs when the body does not properly break down (metabolize) a certain form of bilirubin. If untreated, this condition can cause seizures, neurologic problems (kernicterus) and even death. Treatment for Lucey-Driscoll syndrome includes phototherapy with blue light (to treat the high level of bilirubin in the blood) and an exchange transfusion is sometimes necessary. Different inheritance patterns have been reported and in some cases, it occurs in individuals with no family history of the condition.
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How to diagnose Varicose Veins ?
Doctors often diagnose varicose veins based on a physical exam alone. Sometimes tests or procedures are used to find out the extent of the problem or to rule out other conditions. Specialists Involved If you have varicose veins, you may see a vascular medicine specialist or vascular surgeon. These doctors specialize in blood vessel conditions. You also may see a dermatologist. This type of doctor specializes in skin conditions. Physical Exam To check for varicose veins in your legs, your doctor will look at your legs while you're standing or sitting with your legs dangling. He or she may ask you about your signs and symptoms, including any pain you're having. Diagnostic Tests and Procedures Duplex Ultrasound Your doctor may recommend duplex ultrasound to check blood flow in your veins and to look for blood clots. Duplex ultrasound combines traditional with Doppler ultrasound. Traditional ultrasound uses sound waves to create apicture of the structures in your body, in this case the blood vessels and anything that may be blocking the flow of blood. Doppler ultrasound uses sound waves to create pictures of the flow or movement of the blood through theveins. The two types of ultrasound together paint a picture that helps your doctor diagnose your condition. During this test, a handheld device will be placed on your body and passed back and forth over the affected area. The device sends and receives sound waves. A computer will convert the sound waves into a picture of the blood flow in your arteries and veins. Angiogram Although it is not very common, your doctor may recommend an angiogram to get a more detailed look at the blood flow through your veins. For this procedure, dye is injected into your veins. The dye outlines your veins on x-ray images. An angiogram can help your doctor confirm whether you have varicose veins or another condition.
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How to prevent Hearing Loss ?
Researchers funded by the National Institutes of Health are studying the causes of hearing loss as well as new treatments. For example, they are studying ways to improve hearing aids so that you can hear certain sounds more clearly even when you are surrounded by background noise. They are also working to to improve cochlear implants and develop diagnostic methods to determine who would benefit from two versus one cochlear implant, especially in young children. Finding ways to improve access to accessible and affordable hearing health care, including screening and assessment, hearing aid selection and fitting, and rehabilitation of hearing loss, is also a goal of currently funded research.
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Is pulmonary veno-occlusive disease inherited ?
When caused by mutations in the EIF2AK4 gene, PVOD 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. In contrast, when caused by mutations in another gene, the condition can have an autosomal dominant pattern of inheritance, which means one copy of the altered gene in each cell is sufficient to cause the disorder. In these cases, one parent of an affected individual typically has increased blood pressure in the vessels of the lungs.
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Do you have information about Exercise and Physical Fitness
Summary : Regular physical activity is one of the most important things you can do for your health. It can help - Control your weight - Lower your risk of heart disease - Lower your risk for type 2 diabetes and metabolic syndrome - Lower your risk of some cancers - Strengthen your bones and muscles - Improve your mental health and mood - Improve your ability to do daily activities and prevent falls, if you're an older adult - Increase your chances of living longer Fitting regular exercise into your daily schedule may seem difficult at first. But even ten minutes at a time is fine. The key is to find the right exercise for you. It should be fun and should match your abilities. Centers for Disease Control and Prevention
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What are the symptoms of Duane syndrome type 2 ?
What are the signs and symptoms of Duane syndrome type 2? The Human Phenotype Ontology provides the following list of signs and symptoms for Duane syndrome type 2. 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) Ophthalmoparesis 90% Strabismus 90% Anteverted nares 50% Blepharophimosis 50% Deeply set eye 50% Amblyopia 48% Abnormal form of the vertebral bodies 7.5% Abnormal localization of kidney 7.5% Abnormality of the pupil 7.5% Aplasia/Hypoplasia of the iris 7.5% Aplasia/Hypoplasia of the radius 7.5% Aplasia/Hypoplasia of the thumb 7.5% Brachydactyly syndrome 7.5% Chorioretinal coloboma 7.5% Cleft palate 7.5% Cognitive impairment 7.5% External ear malformation 7.5% Hearing impairment 7.5% Heterochromia iridis 7.5% Microcephaly 7.5% Nystagmus 7.5% Optic atrophy 7.5% Ptosis 7.5% Seizures 7.5% Short neck 7.5% Talipes 7.5% Visual impairment 7.5% Wide nasal bridge 7.5% Autosomal dominant inheritance - Duane anomaly - 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 the outlook for Kearns-Sayre Syndrome ?
KSS is a slowly progressive disorder. The prognosis for individuals with KSS varies depending on the severity and the number of organs involved. Early diagnosis and periodic electrocardiogram (ECG) are important since heart block can cause death in 20 percent of patients. Early pacemaker implantation can be of great benefit and offer a longer life expectancy in many patients.
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How to diagnose Kidney Stones in Children ?
The process of diagnosing any illness begins with consideration of the symptoms. Pain or bloody urine may be the first symptom. Urine, blood, and imaging tests will help determine whether symptoms are caused by a stone. Urine tests can be used to check for infection and for substances that form stones. Blood tests can be used to check for biochemical problems that can lead to kidney stones. Various imaging techniques can be used to locate the stone: - Ultrasound uses a device, called a transducer, that bounces safe, painless sound waves off organs to create an image of their structure. An abdominal ultrasound can create images of the entire urinary tract. The procedure is performed in a health care providers office, outpatient center, or hospital by a specially trained technician, and the images are interpreted by a radiologista doctor who specializes in medical imaging; anesthesia is not needed. The images can show the location of any stones. This test does not expose children to radiation, unlike some other imaging tests. Although other tests are more useful in detecting very small stones or stones in the lower portion of the ureter, ultrasound is considered by many health care providers to be the best screening test to look for stones. - Computerized tomography (CT) scans use a combination of x rays and computer technology to create threedimensional (3-D) images. A CT scan may include the injection of a special dye, called contrast medium. CT scans require the child to lie on a table that slides into a tunnel-shaped device where the x rays are taken. The procedure is performed in an outpatient center or hospital by an x-ray technician, and the images are interpreted by a radiologist; anesthesia is not needed. CT scans may be required to get an accurate stone count when children are being considered for urologic surgery. Because CT scans expose children to a moderate amount of radiation, health care providers try to reduce radiation exposure in children by avoiding repeated CT scans, restricting the area scanned as much as possible, and using the lowest radiation dose that will provide the needed diagnostic information. - X-ray machines use radiation to create images of the childs urinary tract. The images can be taken at an outpatient center or hospital by an x-ray technician, and the images are interpreted by a radiologist; anesthesia is not needed. The x rays are used to locate many kinds of stones. A conventional x ray is generally less informative than an ultrasound or CT scan, but it is less expensive and can be done more quickly than other imaging procedures.
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How many people are affected by pantothenate kinase-associated neurodegeneration ?
The precise incidence of this condition is unknown. It is estimated to affect 1 to 3 per million people worldwide.
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What are the genetic changes related to Lesch-Nyhan syndrome ?
Mutations in the HPRT1 gene cause Lesch-Nyhan syndrome. The HPRT1 gene provides instructions for making an enzyme called hypoxanthine phosphoribosyltransferase 1. This enzyme is responsible for recycling purines, a type of building block of DNA and its chemical cousin RNA. Recycling purines ensures that cells have a plentiful supply of building blocks for the production of DNA and RNA. HPRT1 gene mutations that cause Lesch-Nyhan syndrome result in a severe shortage (deficiency) or complete absence of hypoxanthine phosphoribosyltransferase 1. When this enzyme is lacking, purines are broken down but not recycled, producing abnormally high levels of uric acid. For unknown reasons, a deficiency of hypoxanthine phosphoribosyltransferase 1 is associated with low levels of a chemical messenger in the brain called dopamine. Dopamine transmits messages that help the brain control physical movement and emotional behavior, and its shortage may play a role in the movement problems and other features of this disorder. However, it is unclear how a shortage of hypoxanthine phosphoribosyltransferase 1 causes the neurological and behavioral problems characteristic of Lesch-Nyhan syndrome. Some people with HPRT1 gene mutations produce some functional enzyme. These individuals are said to have Lesch-Nyhan variant. The signs and symptoms of Lesch-Nyhan variant are often milder than those of Lesch-Nyhan syndrome and do not include self-injury.
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What are the genetic changes related to FG syndrome ?
Researchers have identified changes in five regions of the X chromosome that are linked to FG syndrome in affected families. Mutations in a gene called MED12, which is located in one of these regions, appear to be the most common cause of the disorder. Researchers are investigating genes in other regions of the X chromosome that may also be associated with FG syndrome. The MED12 gene provides instructions for making a protein that helps regulate gene activity. Specifically, the MED12 protein forms part of a large complex (a group of proteins that work together) that turns genes on and off. The MED12 protein is thought to play an essential role in development both before and after birth. At least two mutations in the MED12 gene have been found to cause FG syndrome. Although the mutations alter the structure of the MED12 protein, it is unclear how they lead to intellectual disability, behavioral changes, and the physical features associated with this condition.
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What are the treatments for Hydranencephaly ?
There is no definitive treatment for hydranencephaly. Treatment is symptomatic and supportive. Hydrocephalus may be treated with a shunt (a surgically implanted tube that diverts fluid from one pathway to another).
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What is (are) childhood myocerebrohepatopathy spectrum ?
Childhood myocerebrohepatopathy spectrum, commonly called MCHS, is part of a group of conditions called the POLG-related disorders. The conditions in this group feature a range of similar signs and symptoms involving muscle-, nerve-, and brain-related functions. MCHS typically becomes apparent in children from a few months to 3 years old. People with this condition usually have problems with their muscles (myo-), brain (cerebro-), and liver (hepato-). Common signs and symptoms of MCHS include muscle weakness (myopathy), developmental delay or a deterioration of intellectual function, and liver disease. Another possible sign of this condition is a toxic buildup of lactic acid in the body (lactic acidosis). Often, affected children are unable to gain weight and grow at the expected rate (failure to thrive). Additional signs and symptoms of MCHS can include a form of kidney disease called renal tubular acidosis, inflammation of the pancreas (pancreatitis), recurrent episodes of nausea and vomiting (cyclic vomiting), or hearing loss.
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What causes Amelogenesis imperfecta ?
What causes amelogenesis imperfecta? Amelogenesis imperfecta is caused by mutations in the AMELX, ENAM, and MMP20 genes. These genes provide instructions for making proteins that are essential for normal tooth development. These proteins are involved in the formation of enamel, which is the hard, calcium-rich material that forms the protective outer layer of each tooth. Mutations in any of these genes alter the structure of these proteins or prevent the genes from making any protein at all. As a result, tooth enamel is abnormally thin or soft and may have a yellow or brown color. Teeth with defective enamel are weak and easily damaged. In some cases, the genetic cause of amelogenesis imperfecta can not been identified. Researchers are working to find mutations in other genes that are responsible for this disorder. Click on each gene name to learn more about the role it plays in the development of tooth enamel.
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How many people are affected by spinocerebellar ataxia type 2 ?
The prevalence of SCA2 is unknown. This condition is estimated to be one of the most common types of spinocerebellar ataxia; however, all types of spinocerebellar ataxia are relatively rare. SCA2 is more common in Cuba, particularly in the Holgun province, where approximately 40 per 100,000 individuals are affected.
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What is (are) Adult neuronal ceroid lipofuscinosis ?
Adult neuronal ceroid lipofuscinosis is a rare condition that affects the nervous system. Signs and symptoms usually begin around age 30, but they can develop anytime between adolescence and late adulthood. There are two forms of adult neuronal ceroid lipofuscinosis that are differentiated by their underlying genetic cause, mode of inheritance and certain symptoms: Type A is characterized by a combination of seizures and uncontrollable muscle jerks (myoclonic epilepsy); dementia; difficulties with muscle coordination (ataxia); involuntary movements such as tremors or tics; and dysarthria. It is caused by changes (mutations) in the CLN6 or PPT1 gene and is inherited in an autosomal recessive manner. Type B shares many features with type A; however, affected people also experience behavioral abnormalities and do not develop myoclonic epilepsy or dysarthria. It can be caused by mutations in the DNAJC5 or CTSF gene and is inherited in an autosomal dominant manner. Treatment options for adult neuronal ceroid lipofuscinosis are limited to therapies that can help relieve some of the symptoms.
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What are the symptoms of Peripheral Artery Disease ?
Many people who have peripheral artery disease (P.A.D.) dont have any signs or symptoms. Even if you don't have signs or symptoms, ask your doctor whether you should get checked for P.A.D. if you're: Aged 70 or older Aged 50 or older and have a history of smoking or diabetes Younger than 50 and have diabetes and one or more risk factors for atherosclerosis Intermittent Claudication People who have P.A.D. may have symptoms when walking or climbing stairs, which may include pain, numbness, aching, or heaviness in the leg muscles.Symptoms also may include cramping in the affected leg(s) and in the buttocks, thighs, calves, and feet. Symptoms may ease after resting.These symptoms are called intermittent claudication. During physical activity, your muscles need increased blood flow. If your blood vessels are narrowed or blocked, your muscles won't get enough blood, which will lead to symptoms. When resting, the muscles need less blood flow, so the symptoms will go away. Other Signs and Symptoms Other signs and symptoms of P.A.D. include: Weak or absent pulses in the legs or feet Sores or wounds on the toes, feet, or legs that heal slowly, poorly, or not at all A pale or bluish color to the skin A lower temperature in one leg compared to the other leg Poor nail growth on the toes and decreased hair growth on the legs Erectile dysfunction, especially among men who have diabetes
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What is the outlook for Guillain-Barr Syndrome ?
Guillain-Barr syndrome can be a devastating disorder because of its sudden and unexpected onset. Most people reach the stage of greatest weakness within the first 2 weeks after symptoms appear, and by the third week of the illness 90 percent of all patients are at their weakest. The recovery period may be as little as a few weeks or as long as a few years. About 30 percent of those with Guillain-Barr still have a residual weakness after 3 years. About 3 percent may suffer a relapse of muscle weakness and tingling sensations many years after the initial attack.
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How to prevent Omsk Hemorrhagic Fever (OHF) ?
There is no vaccine currently available for OHF, but vaccines for tick-borne encephalitis disease (TBE) have been shown to confer some immunity and may be used for high-risk groups. Additionally, utilizing insect repellents and wearing protective clothing in areas where ticks are endemic is recommended.
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What is (are) Chronic Fatigue Syndrome (CFS) ?
Chronic fatigue syndrome, or CFS, is a devastating and complex disorder. People with CFS have overwhelming fatigue and a host of other symptoms that are not improved by bed rest and that can get worse after physical activity or mental exertion. They often function at a substantially lower level of activity than they were capable of before they became ill. Besides severe fatigue, other symptoms include muscle pain, impaired memory or mental concentration, insomnia, and post-exertion malaise lasting more than 24 hours. In some cases, CFS can persist for years. Researchers have not yet identified what causes CFS, and there are no tests to diagnose CFS. Moreover, because many illnesses have fatigue as a symptom, doctors need to take care to rule out other conditions, which may be treatable.
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What are the symptoms of Pfeiffer Mayer syndrome ?
What are the signs and symptoms of Pfeiffer Mayer syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Pfeiffer Mayer 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) Abnormal nasal morphology 90% Abnormality of the pinna 90% Cognitive impairment 90% Optic atrophy 90% Preaxial hand polydactyly 90% Short stature 90% Chorioretinal coloboma 50% Iris coloboma 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 is (are) Anemia in Chronic Kidney Disease ?
The kidneys are two bean-shaped organs, each about the size of a fist. They are located just below the rib cage, one on each side of the spine. Every day, the kidneys filter about 120 to 150 quarts of blood to produce about 1 to 2 quarts of urine. Healthy kidneys produce a hormone called erythropoietin (EPO). A hormone is a chemical produced by the body and released into the blood to help trigger or regulate particular body functions. EPO prompts the bone marrow to make red blood cells, which then carry oxygen throughout the body.
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Is Partington syndrome inherited ?
Is Partington syndrome inherited? Partington syndrome is inherited in an X-linked recessive manner. A condition is considered X-linked if the mutated gene that causes the condition is located on the X chromosome, one of the two sex chromosomes (the Y chromosome is the other sex chromosome). Women have two X chromosomes and men have an X and a Y chromosome. In X-linked recessive conditions, men develop the condition if they inherit one gene mutation (they have only one X chromosome). Females are generally only affected if they have two gene mutations (they have two X chromosomes), although some females may rarely have a mild form of the condition if they only inherit one mutation. A woman with an X-linked recessive condition will pass the mutation on to all of her sons and daughters. This means that all of her sons will have the condition and all of her daughters will be carriers. A man with an X-linked recessive condition will pass the mutation to all of his daughters (carriers) and none of his sons.
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What is (are) Popliteal pterygium syndrome ?
Popliteal pterygium syndrome is a condition that affects the development of the face, skin, and genitals. Most people with this disorder are born with a cleft lip and/or a cleft palate. Affected individuals may have depressions (pits) near the center of the lower lip and small mounds of tissue on the lower lip. In some cases, people with popliteal pterygium syndrome have missing teeth. Other features may include webs of skin on the backs of the legs across the knee joint, webbing or fusion of the fingers or toes (syndactyly), characteristic triangular folds of skin over the nails of the large toes, and tissue connecting the upper and lower eyelids or the upper and lower jaw. Affected individuals may also have abnormal genitals. This condition is inherited in an autosomal dominant fashion and is caused by mutations in the IRF6 gene.
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What are the treatments for Sickle Cell Disease ?
Health Maintenance To Prevent Complications Babies with sickle cell disease (SCD) should be referred to a doctor or provider group that has experience taking care of people with this disease. The doctor might be a hematologist (a doctor with special training in blood diseases) or an experienced general pediatrician, internist, or family practitioner. For infants, the first SCD visit should take place before 8 weeks of age. If someone was born in a country that doesnt perform newborn SCD screening, he or she might be diagnosed with SCD later in childhood. These people should also be referred as soon as possible for special SCD care. Examining the person Giving medicines and immunizations Performing tests Educating families about the disease and what to watch out for Preventing Infection In SCD, the spleen doesnt work properly or doesnt work at all. This problem makes people with SCD more likely to get severe infections. Penicillin In children with SCD, taking penicillin two times a day has been shown to reduce the chance of having a severe infection caused by the pneumococcus bacteria. Infants need to take liquid penicillin. Older children can take tablets. Many doctors will stop prescribing penicillin after a child has reached the age of 5. Some prefer to continue this antibiotic throughout life, particularly if a person has hemoglobin SS or hemoglobin S0 thalassemia, since people with SCD are still at risk. All people who have had surgical removal of the spleen, called a splenectomy, or a past infection with pneumococcus should keep taking penicillin throughout life. Immunizations People with SCD should receive all recommended childhood vaccines. They should also receive additional vaccines to prevent other infections. Pneumococcus. Even though all children routinely receive the vaccine against pneumococcus (PCV13), children with SCD should also receive a second kind of vaccine against pneumococcus (PPSV23). This second vaccine is given after 24 months of age and again 5 years later. Adults with SCD who have not received any pneumococcal vaccine should get a dose of the PCV13 vaccine. They should later receive the PPSV23 if they have not already received it or it has been more than 5 years since they did. A person should follow these guidelines even if he or she is still taking penicillin. Influenza. All people with SCD should receive an influenza shot every year at the start of flu season. This should begin at 6 months of age. Only the inactivated vaccine, which comes as a shot, should be used in people with SCD. Meningococcus. A child with SCD should receive this vaccine (Menactra or Menveo) at 2, 4, 6, and 1215 months of age. The child should receive a booster vaccine 3 years after this series of shots, then every 5 years after that. Screening Tests and Evaluations Height, Weight, Blood Pressure, and Oxygen Saturation Doctors will monitor height and weight to be sure that a child is growing properly and that a person with SCD is maintaining a healthy weight. Doctors will also track a persons blood pressure. When a person with SCD has high blood pressure, it needs to be treated promptly because it can increase the risk of stroke. Oxygen saturation testing provides information about how much oxygen the blood is carrying. Blood and Urine Testing People with SCD need to have frequent lab tests. Blood tests help to establish a persons baseline for problems like anemia. Blood testing also helps to show whether a person has organ damage, so that it can be treated early. Urine testing can help to detect early kidney problems or infections. Transcranial Doppler (TCD) Ultrasound Screening Children who have hemoglobin SS or hemoglobin S0 thalassemia and are between the ages of 2 and 16 should have TCD testing once a year. This study can find out whether a child is at higher risk for stroke. When the test is abnormal, regular blood transfusions can decrease the chances of having a stroke. The child is awake during the TCD exam. The test does not hurt at all. The TCD machine uses sound waves to measure blood flow like the ultrasound machine used to examine pregnant women. Eye Examinations An eye doctor, or ophthalmologist, should examine a persons eyes every 12 years from the age of 10 onwards. These exams can detect if there are SCD-related problems of the eye. Regular exams can help doctors find and treat problems early to prevent loss of vision. A person should see his or her doctor right away for any sudden change in vision. Pulmonary Hypertension Doctors have different approaches to screening for pulmonary hypertension. This is because studies have not given clear information as to when and how a person should receive the screening. People with SCD and their caretakers should discuss with their doctor whether screening makes sense for them. Cognitive Screening People with sickle cell disease can develop cognitive (thinking) problems that may be hard to notice early in life. Sometimes these problems are caused by silent strokes that can only be seen with magnetic resonance imaging (MRI) of the brain. People with SCD should tell their doctors or nurses if they have thinking problems, such as difficulties learning in school, slowed decision making, or trouble organizing their thoughts. People can be referred for cognitive testing. This testing can identify areas in which a person could use extra help. Children with SCD who have thinking problems may qualify for an Individualized Education Program, or IEP. An IEP is a plan that helps students to reach their educational goals. Adults may be able to enroll in vocational rehabilitation programs that can help them with job training. Education and Guidance Doctors and other providers will talk with people who have SCD and their caretakers about complications and also review information at every visit. Because there are a lot of things to discuss, new topics are often introduced as a child or adult reaches an age when that subject is important to know about. Doctors and nurses know that there is a lot of information to learn, and they dont expect people to know everything after one discussion. People with SCD and their families should not be afraid to ask questions. Topics that are usually covered include: Hours that medical staff are available and contact information to use when people with SCD or caretakers have questions A plan for what to do and where to get care if a person has a fever, pain, or other signs of SCD complications that need immediate attention How SCD is inherited and the risk of having a child with SCD The importance of regular medical visits, screening tests, and evaluations How to recognize and manage pain How to palpate (feel) a childs spleen. Because of the risk of splenic sequestration crisis, caretakers should learn how to palpate a childs spleen. They should try to feel for the spleen daily and more frequently when the child is ill. If they feel that the spleen is bigger than usual, they should call the care provider. Transitioning Care When children with SCD become adolescents or young adults, they often need to transition from a pediatric care team to an adult care team. This period has been shown to be associated with increased hospital admissions and medical problems. There seem to be many reasons for this. Some of the increased risk is directly related to the disease. As people with SCD get older, they often develop more organ damage and more disabilities. The shift in care usually occurs at the same time that adolescents are undergoing many changes in their emotional, social, and academic lives. The transition to more independent self-management may be difficult, and following treatment plans may become less likely. When compared with pediatrics, there are often fewer adult SCD programs available in a given region. This makes it more difficult for a person with SCD to find appropriate doctors, particularly those with whom they feel comfortable. To improve use of regular medical care by people with SCD and to reduce age-related complications, many SCD teams have developed special programs that the make transition easier. Such programs should involve the pediatric and the adult care teams. They should also start early and continue over several years. Managing Some Complications of SCD Acute Pain Each person with SCD should have a home treatment regimen that is best suited to their needs. The providers on the SCD team usually help a person develop a written, tailored care plan. If possible, the person with SCD should carry this plan with them when they go to the emergency room. When an acute crisis is just starting, most doctors will advise the person to drink lots of fluids and to take a non-steroidal anti-inflammatory (NSAID) pain medication, such as ibuprofen. When a person has kidney problems, acetaminophen is often preferred. If pain persists, many people will find that they need a stronger medicine. Combining additional interventions, such as massage, relaxation methods, or a heating pad, may also help. If a person with SCD cannot control the pain at home, he or she should go to an SCD day hospital/outpatient unit or an emergency room to receive additional, stronger medicines and intravenous (IV) fluids. Some people may be able to return home once their pain is under better control. In this case, the doctor may prescribe additional pain medicines for a short course of therapy. People often need to be admitted to the hospital to fully control an acute pain crisis. When taken daily, hydroxyurea has been found to decrease the number and severity of pain episodes. Chronic Pain Sometimes chronic pain results from a complication, such as a leg ulcer or aseptic necrosis of the hip. In this case, doctors try to treat the complication causing the pain. While chronic pain is common in adults with SCD, the cause is often poorly understood. Taking pain medicines daily may help to decrease the pain. Some examples of these medicines include: NSAID drugs, such as ibuprofen Duloxetine Gabapentin Amitriptyline Strong pain medicines, such as opiates Other approaches, such as massage, heat, or acupuncture may be helpful in some cases. Chronic pain often comes with feelings of depression and anxiety. Supportive counseling and, sometimes, antidepressant medicines may help. (See coping and emotional issues.) Severe Anemia People should see their doctors or go to a hospital right away if they develop anemia symptoms from a splenic sequestration crisis or an aplastic crisis. These conditions can be life-threatening, and the person will need careful monitoring and treatment in the hospital. A person also usually needs a blood transfusion. People with SCD and symptoms of severe anemia from other causes should also see a doctor right away. Infections Fever is a medical emergency in SCD. All caretakers of infants and children with SCD should take their child to their doctor or go to a hospital right away when their child has a fever. Adults with SCD should also seek care for fever or other signs of infection. All children and adults who have SCD and a fever (over 38.50 C or 101.30 F) must be seen by a doctor and treated with antibiotics right away. Some people will need to be hospitalized, while others may receive care and follow-up as an outpatient. Acute Chest Syndrome People with SCD and symptoms of acute chest syndrome should see their doctor or go to a hospital right away. They will need to be admitted to the hospital where they should receive antibiotics and close monitoring. They may need oxygen therapy and a blood transfusion. When taken daily, the medicine hydroxyurea has been found to decrease the number and severity of acute chest events. Clinical Stroke People with SCD who have symptoms of stroke should be brought to the hospital right away by an ambulance. If a person is having symptoms of stroke, someone should call 9-1-1. Symptoms of stroke may include: Weakness of an arm or leg on one side of the body Trouble speaking, walking, or understanding Loss of balance Severe headache If imaging studies reveal that the person has had an acute stroke, he or she may need an exchange transfusion. This procedure involves slowly removing an amount of the persons blood and replacing it with blood from a donor who does not have SCD or sickle cell trait. Afterward, the person may need to receive monthly transfusions or other treatments to help to prevent another stroke. Silent Stroke and Cognitive Problems Children and adults with SCD and cognitive problems may be able to get useful help based upon the results of their testing. For instance, children may qualify for an IEP. Adults may be able to enroll in vocational, or job, training programs. Priapism Sometimes, a person may be able to relieve priapism by: Emptying the bladder by urinating Taking medicine Increasing fluid intake Doing light exercise If a person has an episode that lasts for 4 hours or more, he should go to the hospital to see a hematologist and urologist. Pregnancy Pregnant women with SCD are at greater risk for problems. They should always see an obstetrician, or OB, who has experience with SCD and high-risk pregnancies and deliveries. The obstetrician should work with a hematologist or primary medical doctor who is well informed about SCD and its complications. Pregnant women with SCD need more frequent medical visits so that their doctors can follow them closely. The doctor may prescribe certain vitamins and will be careful to prescribe pain medicines that are safe for the baby. A pregnant woman with SCD may need to have one or more blood transfusions during her pregnancy to treat complications, such as worsening anemia or an increased number of pain or acute chest syndrome events. Hydroxyurea What Is Hydroxyurea? Hydroxyurea is an oral medicine that has been shown to reduce or prevent several SCD complications. This medicine was studied in patients with SCD because it was known to increase the amount of fetal hemoglobin (hemoglobin F) in the blood. Increased hemoglobin F provides some protection against the effects of hemoglobin S. Hydroxyurea was later found to have several other benefits for a person with SCD, such as decreasing inflammation. Use in adults. Many studies of adults with hemoglobin SS or hemoglobin S thalassemia showed that hydroxyurea reduced the number of episodes of pain crises and acute chest syndrome. It also improved anemia and decreased the need for transfusions and hospital admissions. Use in children. Studies in children with severe hemoglobin SS or S thalassemia showed that hydroxyurea reduced the number of vaso-occlusive crises and hospitalizations. A study of very young children (between the ages of 9 and 18 months) with hemoglobin SS or hemoglobin S thalassemia also showed that hydroxyurea decreased the number of episodes of pain and dactylitis. Who Should Use Hydroxyurea? Since hydroxyurea can decrease several complications of SCD, most experts recommend that children and adults with hemoglobin SS or S0 thalassemia who have frequent painful episodes, recurrent chest crises, or severe anemia take hydroxyurea daily. Some experts offer hydroxyurea to all infants over 9 months of age and young children with hemoglobin SS or S0 thalassemia, even if they do not have severe clinical problems, to prevent or reduce the chance of complications. There is no information about how safe or effective hydroxyurea is in children under 9 months of age. Some experts will prescribe hydroxyurea to people with other types of SCD who have severe, recurrent pain. There is little information available about how effective hydroxyurea is for these types of SCD. In all situations, people with SCD should discuss with their doctors whether or not hydroxyurea is an appropriate medication for them. Pregnant women should not use hydroxyurea. How Is Hydroxyurea Taken? To work properly, hydroxyurea should be taken by mouth daily at the prescribed dose. When a person does not take it regularly, it will not work as well, or it wont work at all. A person with SCD who is taking hydroxyurea needs careful monitoring. This is particularly true in the early weeks of taking the medicine. Monitoring includes regular blood testing and dose adjustments. What Are the Risks of Hydroxyurea? Hydroxyurea can cause the bloods white cell count or platelet count to drop. In rare cases, it can worsen anemia. These side effects usually go away quickly if a person stops taking the medication. When a person restarts it, a doctor usually prescribes a lower dose. Other short-term side effects are less common. It is still unclear whether hydroxyurea can cause problems later in life in people with SCD who take it for many years. Studies so far suggest that it does not put people at a higher risk of cancer and does not affect growth in children. But further studies are needed. Red Blood Cell Transfusions Doctors may use acute and chronic red blood cell transfusions to treat and prevent certain SCD complications. The red blood cells in a transfusion have normal hemoglobin in them. A transfusion helps to raise the number of red blood cells and provides normal red blood cells that are more flexible than red blood cells with sickle hemoglobin. These cells live longer in the circulation. Red blood cell transfusions decrease vaso-occlusion (blockage in the blood vessel) and improve oxygen delivery to the tissues and organs. Acute Transfusion in SCD Doctors use blood transfusions in SCD for complications that cause severe anemia. They may also use them when a person has an acute stroke, in many cases of acute chest crises, and in multi-organ failure. A person with SCD usually receives blood transfusions before surgery to prevent SCD-related complications afterwards. Chronic Transfusion Doctors recommend regular or ongoing blood transfusions for people who have had an acute stroke, since transfusions decrease the chances of having another stroke. Doctors also recommend chronic blood transfusions for children who have abnormal TCD ultrasound results because transfusions can reduce the chance of having a first stroke. Some doctors use this approach to treat complications that do not improve with hydroxyurea. They may also use transfusions in people who have too many side effects from hydroxyurea. What Are the Risks of Transfusion Therapy? Possible complications include: Hemolysis Iron overload, particularly in people receiving chronic transfusions (can severely impair heart and lung function) Infection Alloimmunization (can make it hard to find a matching unit of blood for a future transfusion) All blood banks and hospital personnel have adopted practices to reduce the risk of transfusion problems. People with SCD who receive transfusions should be monitored for and immunized against hepatitis. They should also receive regular screenings for iron overload. If a person has iron overload, the doctor will give chelation therapy, a medicine to reduce the amount of iron in the body and the problems that iron overload causes. Hematopoietic Stem Cell Transplantation At the present time, hematopoietic stem cell transplantation (HSCT) is the only cure for SCD. People with SCD and their families should ask their doctor about this procedure. What Are Stem Cells? Stem cells are special cells that can divide over and over again. After they divide, these cells can go on to become blood red cells, white cells, or platelets. A person with SCD has stem cells that make red blood cells that can sickle. People without SCD have stem cells that make red cells that usually wont sickle. What Stem Cells Are Used in HSCT? In HSCT, stem cells are taken from the bone marrow or blood of a person who does not have sickle cell disease (the donor). The donor, however, may have sickle cell trait. The donor is often the persons sister or brother. This is because the safest and most successful transplants use stem cells that are matched for special proteins called HLA antigens. Since these antigens are inherited from parents, a sister or brother is the most likely person to have the same antigens as the person with SCD. What Happens During HSCT? First, stem cells are taken from the donor. After this, the person with SCD (the recipient) is treated with drugs that destroy or reduce his or her own bone marrow stem cells. The donor stem cells are then injected into the persons vein. The injected cells will make a home in the recipients bone marrow, gradually replacing the recipients cells. The new stem cells will make red cells that do not sickle. Which People Receive HSCT? At the present time, most SCD transplants are performed in children who have had complications such as strokes, acute chest crises, and recurring pain crises. These transplants usually use a matched donor. Because only about 1 in 10 children with SCD has a matched donor without SCD in their families, the number of people with SCD who get transplants is low. HSCT is more risky in adults, and that is why most transplants are done in children. There are several medical centers that are researching new SCD HSCT techniques in children and adults who dont have a matched donor in the family or are older than most recipients. Hopefully, more people with SCD will be able to receive a transplant in the future, using these new methods. What Are the Risks? HSCT is successful in about 85 percent of children when the donor is related and HLA matched. Even with this high success rate, HSCT still has risks. Complications can include severe infections, seizures, and other clinical problems. About 5 percent of people have died. Sometimes transplanted cells attack the recipients organs (graft versus host disease). Medicines are given to prevent many of the complications, but they still can happen.
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What is (are) Non-A-E hepatitis ?
Non-A-E hepatitis, sometimes referred to as hepatitis X, is a disease of the liver that is diagnosed when there is swelling of the liver (hepatitis) but examination and testing does not identify a cause. Symptoms of non-A-E hepatitis may include feeling tired or unwell (malaise), nausea, vomiting, pain in the abdomen, and fever. Non-A-E hepatitis usually goes away on its own, but it can become a chronic condition in a small proportion (12%) of affected individuals. The cause of non-A-E hepatitis is currently unknown.
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How to diagnose Rheumatic Fever ?
How is rheumatic fever diagnosed? A diagnosis of rheumatic fever is usually based on the following: Characteristic signs and symptoms identified by physical examination and/or specialized testing such as a blood test, chest X-ray and echocardiogram Confirmation of group A Streptococcus bacterial infection with a throat culture or blood tests The diagnosis can also be supported by blood tests that confirm the presence of certain proteins that increase in response to inflammation (called acute-phase reactants) and tend to be elevated in rheumatic fever. Additional tests may be recommended to rule out other conditions that cause similar features.
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What are the symptoms of Ulna metaphyseal dysplasia syndrome ?
What are the signs and symptoms of Ulna metaphyseal dysplasia syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Ulna metaphyseal dysplasia 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 hip bone 90% Abnormality of the metaphyses 90% Abnormality of the ulna 90% Aplasia/Hypoplasia of the radius 90% Delayed skeletal maturation 90% Abnormal form of the vertebral bodies 50% Abnormality of the fibula 50% Abnormality of the metacarpal bones 50% Short stature 50% Abnormality of the voice 7.5% Depressed nasal ridge 7.5% Microdontia 7.5% Nephrolithiasis 7.5% Abnormality of the vertebral column - Autosomal dominant inheritance - Coxa valga - Hypercalcemia - 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 Whipple Disease ?
A person with Whipple disease and malabsorption may need - a diet high in calories and protein - vitamins - nutritional supplements
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What causes Weill-Marchesani syndrome ?
What causes Weill-Marchesani syndrome? Weill-Marchesani syndrome is usually caused by mutations in the ADAMTS10 gene. Two families have been found with mutations in different genes, one with a mutation in FBN1 and one with a mutation in LTBP2.
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What are the treatments for Thalassemia ?
How might thalassemia be treated? The best treatment options depend on the severity of thalassemia. People affected by a mild form often need little to no treatment, while people with intermediate to severe thalassemias may require frequent blood transfusions, iron chelation therapy (treatments to remove excess iron from the body), and/or folic acid supplementation. For more information on the treatment of thalassemia, please click here.
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What is the outlook for Metachromatic Leukodystrophy ?
The prognosis for MLD is poor. Most children within the infantile form die by age 5. Symptoms of the juvenile form progress with death occurring 10 to 20 years following onset. Those persons affected by the adult form typically die withing 6 to 14 years following onset of symptoms.
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How many people are affected by congenital dyserythropoietic anemia ?
Several hundred cases of CDA have been reported worldwide. CDA type II is the most common form of the disorder, with more than 300 reported cases. CDA type III is the rarest form; it has been described in only a few families from Sweden, Argentina, and the United States. The incidence of CDA type I is unknown. Because CDA is so rare and its signs and symptoms overlap with those of other disorders, many cases likely remain undiagnosed or are incorrectly diagnosed as other disorders.
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What is (are) Bursitis ?
A bursa is a small, fluid-filled sac that acts as a cushion between a bone and other moving parts, such as muscles, tendons, or skin. Bursitis occurs when a bursa becomes inflamed. People get bursitis by overusing a joint. It can also be caused by an injury. It usually occurs at the knee or elbow. Kneeling or leaning your elbows on a hard surface for a long time can make bursitis start. Doing the same kinds of movements every day or putting stress on joints increases your risk. Symptoms of bursitis include pain and swelling. Your doctor will diagnose bursitis with a physical exam and tests such as x-rays and MRIs. He or she may also take fluid from the swollen area to be sure the problem isn't an infection. Treatment of bursitis includes rest, pain medicines, or ice. If there is no improvement, your doctor may inject a drug into the area around the swollen bursa. If the joint still does not improve after 6 to 12 months, you may need surgery to repair damage and relieve pressure on the bursa. NIH: National Institute of Arthritis and Musculoskeletal and Skin Diseases
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What are the symptoms of Congenital toxoplasmosis ?
What are the signs and symptoms of Congenital toxoplasmosis? The Human Phenotype Ontology provides the following list of signs and symptoms for Congenital toxoplasmosis. 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 retinal pigmentation 90% Premature birth 90% Visual impairment 50% Anemia 7.5% Aplasia/Hypoplasia affecting the eye 7.5% Ascites 7.5% Cardiomegaly 7.5% Cerebral calcification 7.5% Cognitive impairment 7.5% Diarrhea 7.5% Elevated hepatic transaminases 7.5% Hearing impairment 7.5% Hepatomegaly 7.5% Hydrocephalus 7.5% Hypermelanotic macule 7.5% Intrauterine growth retardation 7.5% Lymphadenopathy 7.5% Microcephaly 7.5% Muscular hypotonia 7.5% Nystagmus 7.5% Seizures 7.5% Thrombocytopenia 7.5% Ventriculomegaly 7.5% 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 Brachydactyly type B inherited ?
How is brachydactyly type B inherited? Brachydactyly type B is caused by mutations in the ROR2 gene. It is inherited in an autosomal dominant fashion, which means one copy of the altered gene in each cell is sufficient to cause the disorder. Individuals with brachydactyly type B have a 50% chance of passing on this condition to their children.
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How many people are affected by spondylocostal dysostosis ?
Spondylocostal dysostosis is a rare condition, although its exact prevalence is unknown.
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How to diagnose Diverticular Disease ?
Diverticulosis Health care providers often find diverticulosis during a routine x ray or a colonoscopy, a test used to look inside the rectum and entire colon to screen for colon cancer or polyps or to evaluate the source of rectal bleeding. Diverticular Disease Based on symptoms and severity of illness, a person may be evaluated and diagnosed by a primary care physician, an emergency department physician, a surgeon, or a gastroenterologista doctor who specializes in digestive diseases. The health care provider will ask about the persons health, symptoms, bowel habits, diet, and medications, and will perform a physical exam, which may include a rectal exam. A rectal exam is performed in the health care providers office; anesthesia is not needed. To perform the exam, the health care provider asks the person to bend over a table or lie on one side while holding the knees close to the chest. The health care provider slides a gloved, lubricated finger into the rectum. The exam is used to check for pain, bleeding, or a blockage in the intestine. The health care provider may schedule one or more of the following tests: - Blood test. A blood test involves drawing a persons blood at a health care providers office, a commercial facility, or a hospital and sending the sample to a lab for analysis. The blood test can show the presence of inflammation or anemiaa condition in which red blood cells are fewer or smaller than normal, which prevents the bodys cells from getting enough oxygen. - Computerized tomography (CT) scan. A CT scan of the colon is the most common test used to diagnose diverticular disease. CT scans use a combination of x rays and computer technology to create three-dimensional (3D) images. For a CT scan, the person may be given a solution to drink and an injection of a special dye, called contrast medium. CT scans require the person to lie on a table that slides into a tunnel-shaped device where the x rays are taken. The procedure is performed in an outpatient center or a hospital by an x-ray technician, and the images are interpreted by a radiologista doctor who specializes in medical imaging. Anesthesia is not needed. CT scans can detect diverticulosis and confirm the diagnosis of diverticulitis. - Lower gastrointestinal (GI) series. A lower GI series is an x-ray exam that is used to look at the large intestine. The test is performed at a hospital or an outpatient center by an x-ray technician, and the images are interpreted by a radiologist. Anesthesia is not needed. The health care provider may provide written bowel prep instructions to follow at home before the test. The person may be asked to follow a clear liquid diet for 1 to 3 days before the procedure. A laxative or enema may be used before the test. A laxative is medication that loosens stool and increases bowel movements. An enema involves flushing water or laxative into the rectum using a special squirt bottle. These medications cause diarrhea, so the person should stay close to a bathroom during the bowel prep. - For the test, the person will lie on a table while the radiologist inserts a flexible tube into the persons anus. The colon is filled with barium, making signs of diverticular disease show up more clearly on x rays. - For several days, traces of barium in the large intestine can cause stools to be white or light colored. Enemas and repeated bowel movements may cause anal soreness. A health care provider will provide specific instructions about eating and drinking after the test. - Colonoscopy. The test is performed at a hospital or an outpatient center by a gastroenterologist. Before the test, the persons health care provider will provide written bowel prep instructions to follow at home. The person may need to follow a clear liquid diet for 1 to 3 days before the test. The person may also need to take laxatives and enemas the evening before the test. - In most cases, light anesthesia, and possibly pain medication, helps people relax for the test. The person will lie on a table while the gastroenterologist inserts a flexible tube into the anus. A small camera on the tube sends a video image of the intestinal lining to a computer screen. The test can show diverticulosis and diverticular disease. - Cramping or bloating may occur during the first hour after the test. Driving is not permitted for 24 hours after the test to allow the anesthesia time to wear off. Before the appointment, people should make plans for a ride home. Full recovery is expected by the next day, and people should be able to go back to their normal diet.
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What are the symptoms of Triple A syndrome ?
What are the signs and symptoms of Triple A syndrome? Triple A syndrome is characterized by three specific features: achalasia, Addison disease, and alacrima (reduced or absent ability to secrete tears). Achalasia is a disorder that affects the ability to move food through the esophagus, the tube that carries food from the throat to the stomach. It can lead to severe feeding difficulties and low blood sugar (hypoglycemia). Addison disease, also known as primary adrenal insufficiency, is caused by abnormal function of the small hormone-producing glands on top of each kidney (adrenal glands). The main features of Addison disease include fatigue, loss of appetite, weight loss, low blood pressure, and darkening of the skin. The third major feature of triple A syndrome is alacrima. Most people with triple A syndrome have all three of these features, although some have only two. Many of the features of triple A syndrome are caused by dysfunction of the autonomic nervous system. This part of the nervous system controls involuntary body processes such as digestion, blood pressure, and body temperature. People with triple A syndrome often experience abnormal sweating, difficulty regulating blood pressure, unequal pupil size (anisocoria), and other signs and symptoms of autonomic nervous system dysfunction (dysautonomia). People with this condition may have other neurological abnormalities such as developmental delay, intellectual disability, speech problems (dysarthria), and a small head size (microcephaly). In addition, affected individuals commonly experience muscle weakness, movement problems, and nerve abnormalities in their extremities (peripheral neuropathy). Some develop optic atrophy, which is the degeneration (atrophy) of the nerves that carry information from the eyes to the brain. Many of the neurological symptoms of triple A syndrome worsen over time. Adults may exhibit progressive neural degenearation, parkinsonism features and cognitive impairment. People with triple A syndrome frequently develop a thickening of the outer layer of skin (hyperkeratosis) on the palms of their hands and the soles of their feet. Other skin abnormalities may also be present in people with this condition. Alacrima is usually the first noticeable sign of triple A syndrome, as it becomes apparent early in life that affected children produce little or no tears while crying. Individuals typically develop Addison disease and achalasia during childhood or adolescence, and most of the neurologic features of triple A syndrome begin during adulthood. The signs and symptoms of this condition vary among affected individuals, even among members of the same family. The Human Phenotype Ontology provides the following list of signs and symptoms for Triple A 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) Generalized hyperpigmentation 90% Primary adrenal insufficiency 90% Seizures 90% Palmoplantar keratoderma 50% Short stature 50% Visual impairment 50% Anterior hypopituitarism 7.5% Developmental regression 7.5% Hyperreflexia 7.5% Incoordination 7.5% Iris coloboma 7.5% Microcephaly 7.5% Muscular hypotonia 7.5% Optic atrophy 7.5% Respiratory insufficiency 7.5% Sensorineural hearing impairment 7.5% Abnormality of visual evoked potentials - Achalasia - Adrenocorticotropin (ACTH) receptor (ACTHR) defect - Anisocoria - Ataxia - Autosomal recessive inheritance - Babinski sign - Childhood onset - Dysarthria - Dysautonomia - Hyperpigmentation of the skin - Hypocortisolemia - Intellectual disability - Motor axonal neuropathy - Muscle weakness - Orthostatic hypotension - Palmoplantar hyperkeratosis - Progressive - 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 Coronary Heart Disease ?
A common symptom of coronary heart disease (CHD) is angina. Angina is chest pain or discomfort that occurs if an area of your heart muscle doesn't get enough oxygen-rich blood. Angina may feel like pressure or squeezing in your chest. You also may feel it in your shoulders, arms, neck, jaw, or back. Angina pain may even feel like indigestion. The pain tends to get worse with activity and go away with rest. Emotional stress also can trigger the pain. Another common symptom of CHD is shortness of breath. This symptom occurs if CHD causes heart failure. When you have heart failure, your heart can't pump enough blood to meet your bodys needs. Fluid builds up in your lungs, making it hard to breathe. The severity of these symptoms varies. They may get more severe as the buildup of plaque continues to narrow the coronary arteries. Signs and Symptoms of Heart Problems Related to Coronary Heart Disease Some people who have CHD have no signs or symptomsa condition called silent CHD. The disease might not be diagnosed until a person has signs or symptoms of a heart attack, heart failure, or an arrhythmia (an irregular heartbeat). Heart Attack A heart attack occurs if the flow of oxygen-rich blood to a section of heart muscle is cut off. This can happen if an area of plaque in a coronary artery ruptures (breaks open). Blood cell fragments called platelets stick to the site of the injury and may clump together to form blood clots. If a clot becomes large enough, it can mostly or completely block blood flow through a coronary artery. If the blockage isnt treated quickly, the portion of heart muscle fed by the artery begins to die. Healthy heart tissue is replaced with scar tissue. This heart damage may not be obvious, or it may cause severe or long-lasting problems. Heart With Muscle Damage and a Blocked Artery The most common heart attack symptom is chest pain or discomfort. Most heart attacks involve discomfort in the center or left side of the chest that often lasts for more than a few minutes or goes away and comes back. The discomfort can feel like uncomfortable pressure, squeezing, fullness, or pain. The feeling can be mild or severe. Heart attack pain sometimes feels like indigestion or heartburn. The symptoms of angina can be similar to the symptoms of a heart attack. Angina pain usually lasts for only a few minutes and goes away with rest. Chest pain or discomfort that doesnt go away or changes from its usual pattern (for example, occurs more often or while youre resting) might be a sign of a heart attack. If you dont know whether your chest pain is angina or a heart attack, call 911. All chest pain should be checked by a doctor. Other common signs and symptoms of a heart attack include: Upper body discomfort in one or both arms, the back, neck, jaw, or upper part of the stomach Shortness of breath, which may occur with or before chest discomfort Nausea (feeling sick to your stomach), vomiting, light-headedness or fainting, or breaking out in a cold sweat Sleep problems, fatigue (tiredness), or lack of energy For more information, go to the Health Topics Heart Attack article. Heart Failure Heart failure is a condition in which your heart can't pump enough blood to meet your bodys needs. Heart failure doesn't mean that your heart has stopped or is about to stop working. The most common signs and symptoms of heart failure are shortness of breath or trouble breathing; fatigue; and swelling in the ankles, feet, legs, stomach, and veins in the neck. All of these symptoms are the result of fluid buildup in your body. When symptoms start, you may feel tired and short of breath after routine physical effort, like climbing stairs. For more information, go to the Health Topics Heart Failure article. Arrhythmia An arrhythmia is a problem with the rate or rhythm of the heartbeat. When you have an arrhythmia, you may notice that your heart is skipping beats or beating too fast. Some people describe arrhythmias as a fluttering feeling in the chest. These feelings are called palpitations (pal-pih-TA-shuns). Some arrhythmias can cause your heart to suddenly stop beating. This condition is called sudden cardiac arrest (SCA). SCA usually causes death if it's not treated within minutes. For more information, go to the Health Topics Arrhythmia article.
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What is (are) renal hypouricemia ?
Renal hypouricemia is a kidney (renal) disorder that results in a reduced amount of uric acid in the blood. Uric acid is a byproduct of certain normal chemical reactions in the body. In the bloodstream it acts as an antioxidant, protecting cells from the damaging effects of unstable molecules called free radicals. However, having too much uric acid in the body is toxic, so excess uric acid is removed from the body in urine. People with renal hypouricemia have little to no uric acid in their blood; they release an excessive amount of it in the urine. In many affected individuals, renal hypouricemia causes no signs or symptoms. However, some people with this condition develop kidney problems. After strenuous exercise, they can develop exercise-induced acute kidney injury, which causes pain in their sides and lower back as well as nausea and vomiting that can last several hours. Because an excessive amount of uric acid passes through the kidneys to be excreted in urine in people with renal hypouricemia, they have an increased risk of developing kidney stones (nephrolithiasis) formed from uric acid crystals. These uric acid stones can damage the kidneys and lead to episodes of blood in the urine (hematuria). Rarely, people with renal hypouricemia develop life-threatening kidney failure.
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What are the genetic changes related to mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes ?
MELAS can result from mutations in one of several genes, including MT-ND1, MT-ND5, MT-TH, MT-TL1, and MT-TV. These genes are found in the DNA of cellular structures called mitochondria, which convert the energy from food into a form that cells can use. Although most DNA is packaged in chromosomes within the nucleus, mitochondria also have a small amount of their own DNA, known as mitochondrial DNA or mtDNA. Some of the genes related to MELAS provide instructions for making proteins involved in normal mitochondrial function. These proteins are part of a large enzyme complex in mitochondria that helps convert oxygen, fats, and simple sugars to energy. Other genes associated with this disorder provide instructions for making molecules called transfer RNAs (tRNAs), which are chemical cousins of DNA. These molecules help assemble protein building blocks called amino acids into full-length, functioning proteins within mitochondria. Mutations in a particular transfer RNA gene, MT-TL1, cause more than 80 percent of all cases of MELAS. These mutations impair the ability of mitochondria to make proteins, use oxygen, and produce energy. Researchers have not determined how changes in mtDNA lead to the specific signs and symptoms of MELAS. They continue to investigate the effects of mitochondrial gene mutations in different tissues, particularly in the brain.
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What is (are) cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy ?
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy, usually called CADASIL, is an inherited condition that causes stroke and other impairments. This condition affects blood flow in small blood vessels, particularly cerebral vessels within the brain. The muscle cells surrounding these blood vessels (vascular smooth muscle cells) are abnormal and gradually die. In the brain, the resulting blood vessel damage (arteriopathy) can cause migraines, often with visual sensations or auras, or recurrent seizures (epilepsy). Damaged blood vessels reduce blood flow and can cause areas of tissue death (infarcts) throughout the body. An infarct in the brain can lead to a stroke. In individuals with CADASIL, a stroke can occur at any time from childhood to late adulthood, but typically happens during mid-adulthood. People with CADASIL often have more than one stroke in their lifetime. Recurrent strokes can damage the brain over time. Strokes that occur in the subcortical region of the brain, which is involved in reasoning and memory, can cause progressive loss of intellectual function (dementia) and changes in mood and personality. Many people with CADASIL also develop leukoencephalopathy, which is a change in a type of brain tissue called white matter that can be seen with magnetic resonance imaging (MRI). The age at which the signs and symptoms of CADASIL first begin varies greatly among affected individuals, as does the severity of these features. CADASIL is not associated with the common risk factors for stroke and heart attack, such as high blood pressure and high cholesterol, although some affected individuals might also have these health problems.
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What are the symptoms of Autosomal recessive Charcot-Marie-Tooth disease with hoarseness ?
What are the signs and symptoms of Autosomal recessive Charcot-Marie-Tooth disease with hoarseness? The Human Phenotype Ontology provides the following list of signs and symptoms for Autosomal recessive Charcot-Marie-Tooth disease with hoarseness. 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) Onion bulb formation 7.5% Areflexia - Autosomal recessive inheritance - Axonal degeneration/regeneration - Decreased motor nerve conduction velocity - Decreased number of peripheral myelinated nerve fibers - Distal amyotrophy - Distal muscle weakness - Distal sensory impairment - Flexion contracture - Neonatal onset - Pes cavus - Spinal deformities - Split hand - Vocal cord paresis - 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) leukocyte adhesion deficiency type 1 ?
Leukocyte adhesion deficiency type 1 is a disorder that causes the immune system to malfunction, resulting in a form of immunodeficiency. Immunodeficiencies are conditions in which the immune system is not able to protect the body effectively from foreign invaders such as viruses, bacteria, and fungi. Starting from birth, people with leukocyte adhesion deficiency type 1 develop serious bacterial and fungal infections. One of the first signs of leukocyte adhesion deficiency type 1 is a delay in the detachment of the umbilical cord stump after birth. In newborns, the stump normally falls off within the first two weeks of life; but, in infants with leukocyte adhesion deficiency type 1, this separation usually occurs at three weeks or later. In addition, affected infants often have inflammation of the umbilical cord stump (omphalitis) due to a bacterial infection. In leukocyte adhesion deficiency type 1, bacterial and fungal infections most commonly occur on the skin and mucous membranes such as the moist lining of the nose and mouth. In childhood, people with this condition develop severe inflammation of the gums (gingivitis) and other tissue around the teeth (periodontitis), which often results in the loss of both primary and permanent teeth. These infections often spread to cover a large area. A hallmark of leukocyte adhesion deficiency type 1 is the lack of pus formation at the sites of infection. In people with this condition, wounds are slow to heal, which can lead to additional infection. Life expectancy in individuals with leukocyte adhesion deficiency type 1 is often severely shortened. Due to repeat infections, affected individuals may not survive past infancy.
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What is (are) Branchiooculofacial syndrome ?
Branchiooculofacial syndrome (BOFS) is a very rare genetic disorder that is apparent at birth. Only about 50 cases of BOFS had been reported in the medical literature. Like its name implies, BOFS is characterized by skin defects, eye abnormalities, and distinctive facial features. Among the reported cases thus far, the symptoms may vary from mild to severe. BOFS is caused by mutations in the TFAP2A gene and inherited as an autosomal dominant trait.
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Is autosomal recessive congenital methemoglobinemia 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 trisomy 13 ?
These resources address the diagnosis or management of trisomy 13: - Genetic Testing Registry: Complete trisomy 13 syndrome - MedlinePlus Encyclopedia: Trisomy 13 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 is (are) Limited systemic sclerosis ?
Systemic sclerosis ine scleroderma is a type of systemic scleroderma that is characterized by Raynaud's phenomenon and the buildup of scar tissue (fibrosis) on one or more internal organs but not the skin. While the exact cause of sine scleroderma is unknown, it is believed to originate from an autoimmune reaction which leads to the overproduction of collagen (a tough protein which normally strengthens and supports connective tissues throughout the body). When fibrosis affects internal organs, it can lead to impairment or failure of the affected organs. The most commonly affected organs are the esophagus, heart, lungs, and kidneys. Internal organ involvement may be signaled by heartburn, difficulty swallowing (dysphagia), high blood pressure (hypertension), kidney problems, shortness of breath, diarrhea, or impairment of the muscle contractions that move food through the digestive tract (intestinal pseudo-obstruction).
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What are the genetic changes related to thrombotic thrombocytopenic purpura ?
Mutations in the ADAMTS13 gene cause the familial form of thrombotic thrombocytopenic purpura. The ADAMTS13 gene provides instructions for making an enzyme that is involved in the normal process of blood clotting. Mutations in this gene lead to a severe reduction in the activity of this enzyme. The acquired form of thrombotic thrombocytopenic purpura also results from a reduction in ADAMTS13 enzyme activity; however, people with the acquired form do not have mutations in the ADAMTS13 gene. Instead, their immune systems often produce specific proteins called autoantibodies that block the activity of the enzyme. A lack of ADAMTS13 enzyme activity disrupts the usual balance between bleeding and clotting. Normally, blood clots form at the site of an injury to seal off damaged blood vessels and prevent excess blood loss. In people with thrombotic thrombocytopenic purpura, clots form throughout the body as platelets bind together abnormally and stick to the walls of blood vessels. These clots can block small blood vessels, causing organ damage and the other features of thrombotic thrombocytopenic purpura. Researchers believe that other genetic or environmental factors may contribute to the signs and symptoms of thrombotic thrombocytopenic purpura. In people with reduced ADAMTS13 enzyme activity, factors such as pregnancy, surgery, and infection may trigger abnormal blood clotting and its associated complications.
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What is (are) task-specific focal dystonia ?
Task-specific focal dystonia is a movement disorder that interferes with the performance of particular tasks, such as writing, playing a musical instrument, or participating in a sport. Dystonias are a group of movement problems characterized by involuntary, sustained muscle contractions, tremors, and other uncontrolled movements. The term "focal" refers to a type of dystonia that affects a single part of the body, such as the hand or jaw. Researchers have described several forms of task-specific focal dystonia. The most common is writer's cramp, in which muscle cramps or spasms in the hand, wrist, or forearm interfere with holding a pen or pencil. Writer's cramp begins in the hand used for writing (the dominant hand) and is usually limited to that task, but with time it can spread to the other hand and affect other fine-motor activities such as shaving or typing. Musician's dystonia is a form of task-specific focal dystonia characterized by muscle cramps and spasms that occur while playing a musical instrument. This condition can affect amateur or professional musicians, and the location of the dystonia depends on the instrument. Some musicians (such as piano, guitar, and violin players) develop focal hand dystonia, which causes loss of fine-motor control in the hand and wrist muscles. This condition reduces finger coordination, speed, and endurance while playing. Musicians who play woodwind or brass instruments can develop what is known as embouchure dystonia. This condition causes muscle cramps or spasms involving the lips, tongue, or jaw, which prevents normal positioning of the mouth around the instrument's mouthpiece. Musician's dystonia often occurs only when playing a particular instrument. However, over time focal hand dystonia may impair other activities, and embouchure dystonia can worsen to affect eating and speech. Task-specific focal dystonia can affect people who play sports and engage in other occupations involving repetitive, highly practiced movements. For example, some golfers experience involuntary jerking of the wrists during putting, a condition known informally as "the yips." Cramps and spasms of the hand and arm muscles can also affect tennis players, billiards players, dart throwers, and other athletes. Additionally, task-specific dystonia has been reported in tailors, shoemakers, hair stylists, and people who frequently type or use a computer mouse. The abnormal movements associated with task-specific focal dystonia are usually painless, although they can cause anxiety when they interfere with musical performance and other activities. Severe cases can cause professional disability.
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How to diagnose Pancreatic Neuroendocrine Tumors (Islet Cell Tumors) ?
Lab tests and imaging tests are used to detect (find) and diagnose pancreatic NETs. The following tests and procedures may be used: - Physical exam and history : An exam of the body to check general signs of health, including checking for signs of disease, such as lumps or anything else that seems unusual. A history of the patients health habits and past illnesses and treatments will also be taken. - Blood chemistry studies : A procedure in which a blood sample is checked to measure the amounts of certain substances, such as glucose (sugar), released into the blood by organs and tissues in the body. An unusual (higher or lower than normal) amount of a substance can be a sign of disease. - Chromogranin A test: A test in which a blood sample is checked to measure the amount of chromogranin A in the blood. A higher than normal amount of chromogranin A and normal amounts of hormones such as gastrin, insulin, and glucagon can be a sign of a non-functional pancreatic NET. - Abdominal CT scan (CAT scan): A procedure that makes a series of detailed pictures of the abdomen, taken from different angles. The pictures are made by a computer linked to an x-ray machine. A dye may be injected into a vein or swallowed to help the organs or tissues show up more clearly. This procedure is also called computed tomography, computerized tomography, or computerized axial tomography. - MRI (magnetic resonance imaging): A procedure that uses a magnet, radio waves, and a computer to make a series of detailed pictures of areas inside the body. This procedure is also called nuclear magnetic resonance imaging (NMRI). - Somatostatin receptor scintigraphy : A type of radionuclide scan that may be used to find small pancreatic NETs. A small amount of radioactive octreotide (a hormone that attaches to tumors) is injected into a vein and travels through the blood. The radioactive octreotide attaches to the tumor and a special camera that detects radioactivity is used to show where the tumors are in the body. This procedure is also called octreotide scan and SRS. - Endoscopic ultrasound (EUS): A procedure in which an endoscope is inserted into the body, usually through the mouth or rectum. An endoscope is a thin, tube-like instrument with a light and a lens for viewing. A probe at the end of the endoscope is used to bounce high-energy sound waves (ultrasound) off internal tissues or organs and make echoes. The echoes form a picture of body tissues called a sonogram. This procedure is also called endosonography. - Endoscopic retrograde cholangiopancreatography (ERCP): A procedure used to x-ray the ducts (tubes) that carry bile from the liver to the gallbladder and from the gallbladder to the small intestine. Sometimes pancreatic cancer causes these ducts to narrow and block or slow the flow of bile, causing jaundice. An endoscope is passed through the mouth, esophagus, and stomach into the first part of the small intestine. An endoscope is a thin, tube-like instrument with a light and a lens for viewing. A catheter (a smaller tube) is then inserted through the endoscope into the pancreatic ducts. A dye is injected through the catheter into the ducts and an x-ray is taken. If the ducts are blocked by a tumor, a fine tube may be inserted into the duct to unblock it. This tube (or stent) may be left in place to keep the duct open. Tissue samples may also be taken and checked under a microscope for signs of cancer. - Angiogram : A procedure to look at blood vessels and the flow of blood. A contrast dye is injected into the blood vessel. As the contrast dye moves through the blood vessel, x-rays are taken to see if there are any blockages. - Laparotomy : A surgical procedure in which an incision (cut) is made in the wall of the abdomen to check the inside of the abdomen for signs of disease. The size of the incision depends on the reason the laparotomy is being done. Sometimes organs are removed or tissue samples are taken and checked under a microscope for signs of disease. - Intraoperative ultrasound : A procedure that uses high-energy sound waves (ultrasound) to create images of internal organs or tissues during surgery. A transducer placed directly on the organ or tissue is used to make the sound waves, which create echoes. The transducer receives the echoes and sends them to a computer, which uses the echoes to make pictures called sonograms. - Biopsy : The removal of cells or tissues so they can be viewed under a microscope by a pathologist to check for signs of cancer. There are several ways to do a biopsy for pancreatic NETs. Cells may be removed using a fine or wide needle inserted into the pancreas during an x-ray or ultrasound. Tissue may also be removed during a laparoscopy (a surgical incision made in the wall of the abdomen). - Bone scan : A procedure to check if there are rapidly dividing cells, such as cancer cells, in the bone. A very small amount of radioactive material is injected into a vein and travels through the blood. The radioactive material collects in bones where cancer cells have spread and is detected by a scanner. Other kinds of lab tests are used to check for the specific type of pancreatic NETs. The following tests and procedures may be used: Gastrinoma - Fasting serum gastrin test: A test in which a blood sample is checked to measure the amount of gastrin in the blood. This test is done after the patient has had nothing to eat or drink for at least 8 hours. Conditions other than gastrinoma can cause an increase in the amount of gastrin in the blood. - Basal acid output test: A test to measure the amount of acid made by the stomach. The test is done after the patient has had nothing to eat or drink for at least 8 hours. A tube is inserted through the nose or throat, into the stomach. The stomach contents are removed and four samples of gastric acid are removed through the tube. These samples are used to find out the amount of gastric acid made during the test and the pH level of the gastric secretions. - Secretin stimulation test : If the basal acid output test result is not normal, a secretin stimulation test may be done. The tube is moved into the small intestine and samples are taken from the small intestine after a drug called secretin is injected. Secretin causes the small intestine to make acid. When there is a gastrinoma, the secretin causes an increase in how much gastric acid is made and the level of gastrin in the blood. - Somatostatin receptor scintigraphy: A type of radionuclide scan that may be used to find small pancreatic NETs. A small amount of radioactive octreotide (a hormone that attaches to tumors) is injected into a vein and travels through the blood. The radioactive octreotide attaches to the tumor and a special camera that detects radioactivity is used to show where the tumors are in the body. This procedure is also called octreotide scan and SRS. Insulinoma - Fasting serum glucose and insulin test: A test in which a blood sample is checked to measure the amounts of glucose (sugar) and insulin in the blood. The test is done after the patient has had nothing to eat or drink for at least 24 hours. Glucagonoma - Fasting serum glucagon test: A test in which a blood sample is checked to measure the amount of glucagon in the blood. The test is done after the patient has had nothing to eat or drink for at least 8 hours. Other tumor types - VIPoma - Serum VIP (vasoactive intestinal peptide) test: A test in which a blood sample is checked to measure the amount of VIP. - Blood chemistry studies: A procedure in which a blood sample is checked to measure the amounts of certain substances released into the blood by organs and tissues in the body. An unusual (higher or lower than normal) amount of a substance can be a sign of disease. In VIPoma, there is a lower than normal amount of potassium. - Stool analysis : A stool sample is checked for a higher than normal sodium (salt) and potassium levels. - Somatostatinoma - Fasting serum somatostatin test: A test in which a blood sample is checked to measure the amount of somatostatin in the blood. The test is done after the patient has had nothing to eat or drink for at least 8 hours. - Somatostatin receptor scintigraphy: A type of radionuclide scan that may be used to find small pancreatic NETs. A small amount of radioactive octreotide (a hormone that attaches to tumors) is injected into a vein and travels through the blood. The radioactive octreotide attaches to the tumor and a special camera that detects radioactivity is used to show where the tumors are in the body. This procedure is also called octreotide scan and SRS.
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What is (are) Kidney Stones in Adults ?
The urinary tract is the bodys drainage system for removing wastes and extra water. The urinary tract includes two kidneys, two ureters, a bladder, and a urethra. The kidneys are two bean-shaped organs, each about the size of a fist. They are located near the middle of the back, just below the rib cage, one on each side of the spine. Every day, the two kidneys process about 200 quarts of blood to produce about 1 to 2 quarts of urine, composed of wastes and extra water. The urine flows from the kidneys to the bladder through tubes called ureters. The bladder stores urine until releasing it through urination. When the bladder empties, urine flows out of the body through a tube called the urethra at the bottom of the bladder.
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What causes McCune Albright syndrome ?
What causes McCune Albright syndrome? McCune Albright syndrome (MAS) is caused by a change (mutation) in the GNAS gene. This gene provides instructions for making part of a protein that ultimately influences many cell functions by regulating hormone activity. GNAS gene mutations that cause MAS result in a protein that causes the enzyme adenylate cyclase to be constantly turned on. This, in turn, leads to over-production of several hormones, resulting in the signs and symptoms of MAS.
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What are the treatments for Amyloidosis and Kidney Disease ?
A health care provider treats dialysis-related amyloidosis with - medication therapy - newer, more effective hemodialysis filters - surgery - a kidney transplant The goal of medication therapy and the use of newer, more effective hemodialysis filters is to reduce amyloid protein levels in the blood. Medication therapy can help reduce symptoms such as pain and inflammation. A health care provider may treat a person with dialysis-related amyloidosis who has bone, joint, and tendon problems, such as bone cysts and carpal tunnel syndrome, using surgery. Dialysis-related amyloidosis has no cure; however, a successful kidney transplant may stop the disease from progressing. More information is provided in the NIDDK health topic, Treatment Methods for Kidney Failure: Transplantation.
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Is mitochondrial complex III deficiency inherited ?
Mitochondrial complex III deficiency is usually 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. In some cases caused by mutations in the MT-CYB gene, the condition is not inherited; it is caused by new mutations in the gene that occur in people with no history of the condition in their family. Other cases caused by mutations in the MT-CYB gene are inherited in a mitochondrial pattern, which is also known as maternal inheritance. This pattern of inheritance applies to genes contained in mtDNA. Because egg cells, but not sperm cells, contribute mitochondria to the developing embryo, children can only inherit disorders resulting from mtDNA mutations from their mother. These disorders can appear in every generation of a family and can affect both males and females, but fathers do not pass traits associated with changes in mtDNA to their children.
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What are the treatments for spinocerebellar ataxia type 6 ?
These resources address the diagnosis or management of SCA6: - Gene Review: Gene Review: Spinocerebellar Ataxia Type 6 - Genetic Testing Registry: Spinocerebellar ataxia 6 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 Alzheimer's Disease ?
Currently, no treatment can stop Alzheimer's disease. However, four medications are used to treat its symptoms. These medicines may help maintain thinking, memory, and speaking skills for a limited time. They work by regulating certain chemicals in the brain. Most of these medicines work best for people in the early or middle stages of the disease. For people with mild or moderate Alzheimer's, donepezil (Aricept), rivastigmine (Exelon), or galantamine (Razadyne) may help. Donepezil is also approved to treat symptoms of moderate to severe Alzheimer's. Another drug, memantine (Namenda), is used to treat symptoms of moderate to severe Alzheimer's, although it also has limited effects. All of these medicines have possible side effects. Learn how Alzheimers medications work, how to take them, and where to find more information. Certain medicines and other approaches can help control the behavioral symptoms of Alzheimer's disease. These symptoms include sleeplessness, agitation, wandering, anxiety, anger, and depression. See more about medications used to treat behavioral symptoms. Some medicines must be used with caution.
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What are the genetic changes related to glycogen storage disease type VI ?
Mutations in the PYGL gene cause GSDVI. The PYGL gene provides instructions for making an enzyme called liver glycogen phosphorylase. This enzyme is found only in liver cells, where it breaks down glycogen into a type of sugar called glucose-1-phosphate. Additional steps convert glucose-1-phosphate into glucose, a simple sugar that is the main energy source for most cells in the body. PYGL gene mutations prevent liver glycogen phosphorylase from breaking down glycogen effectively. As a result, liver cells cannot use glycogen for energy. Since glycogen cannot be broken down, it accumulates within liver cells, causing these cells to become enlarged and dysfunctional.
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What are the genetic changes related to congenital myasthenic syndrome ?
Mutations in many genes can cause congenital myasthenic syndrome. Mutations in the CHRNE gene are responsible for more than half of all cases. A large number of cases are also caused by mutations in the RAPSN, CHAT, COLQ, and DOK7 genes. All of these genes provide instructions for producing proteins that are involved in the normal function of the neuromuscular junction. The neuromuscular junction is the area between the ends of nerve cells and muscle cells where signals are relayed to trigger muscle movement. Gene mutations lead to changes in proteins that play a role in the function of the neuromuscular junction and disrupt signaling between the ends of nerve cells and muscle cells. Disrupted signaling between these cells results in an impaired ability to move skeletal muscles, muscle weakness, and delayed development of motor skills. The respiratory problems in congenital myasthenic syndrome result from impaired movement of the muscles of the chest wall and the muscle that separates the abdomen from the chest cavity (the diaphragm). Mutations in other genes that provide instructions for proteins involved in neuromuscular signaling have been found to cause some cases of congenital myasthenic syndrome, although these mutations account for only a small number of cases. Some people with congenital myasthenic syndrome do not have an identified mutation in any of the genes known to be associated with this condition.
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What are the treatments for Roberts syndrome ?
These resources address the diagnosis or management of Roberts syndrome: - Gene Review: Gene Review: Roberts Syndrome - Genetic Testing Registry: Roberts-SC phocomelia syndrome - MedlinePlus Encyclopedia: Contracture deformity - MedlinePlus Encyclopedia: Microcephaly 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 is the outlook for Generalized Gangliosidoses ?
Children with early infantile GM1 often die by age 3 from cardiac complications or pneumonia. Children with the early-onset form of Tay-Sachs disease may eventually need a feeding tube and often die by age 4 from recurring infection. Children with Sandhoff disease generally die by age 3 from respiratory infections.
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what research (or clinical trials) is being done for Dystonias ?
The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to dystonia in its laboratories at the National Institutes of Health (NIH) and also supports additional dystonia research through grants to major research institutions across the country. Scientists at other NIH Institutes (National institute on Deafness and Other Communications Disorders, National Eye Institute, and Eunice Kennnedy Shriver National Institute on Child Health and Human Development) also support research that may benefit individuals with dystonia. Investigators believe that the dystonias result from an abnormality in an area of the brain called the basal ganglia, where some of the messages that initiate muscle contractions are processed. Scientists at the NINDS laboratories have conducted detailed investigations of the pattern of muscle activity in persons with dystonias. Studies using EEG analysis and neuroimaging are probing brain activity. The search for the gene or genes responsible for some forms of dominantly inherited dystonias continues.
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What are the symptoms of Factor V Leiden thrombophilia ?
What are the signs and symptoms of factor V Leiden thrombophilia? Individuals affected by factor V Leiden thrombophilia have an increased risk of developing blood clots. The severity of factor V Leiden thrombophilia is extremely variable. Many individuals with the factor V Leiden allele never develop a blood clot. Although most individuals with factor V thrombophilia do not experience their first thrombotic event until adulthood, some have recurrent thromboembolism before age 30 years. The chance a person will develop a blood clot is affected by the number of factor V Leiden mutations, the presence of coexisting genetic abnormalities, and non-genetic risk factors. Non-genetic risk factors include surgery, long periods of not moving (like sitting on a long airplane ride), birth control pills and other female hormones, childbirth within the last 6 months, and traumas or fractures. Individuals who inherit one copy of the factor V Leiden mutation have a fourfold to eightfold increase in the chance of developing a clot. Homozygotes (people who inherit two factor V Leiden mutations) may have up to 80 times the usual risk of developing a blood clot. Considering that the risk of developing an abnormal blood clot averages about 1 in 1,000 per year in the general population, the presence of one copy of the factor V Leiden mutation increases that risk to 4 to 8 in 1,000, and having two copies of the mutation may raise the risk as high as 80 in 1,000. People with factor V Leiden have an increased chance of having a blood clot that forms in large veins in the legs (deep venous thrombosis, or DVT) or a clot that travels through the bloodstream and lodges in the lungs (pulmonary embolism, or PE). Symptoms of deep vein thrombosis usually include leg pain, tenderness, swelling, increased warmth or redness in one leg. The symptoms of pulmonary embolism usually include cough, chest pain, shortness of breath or rapid heartbeat or breathing. To learn more about the symptoms of DVT and PE, click here.
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What is (are) ornithine translocase deficiency ?
Ornithine translocase deficiency is an inherited disorder that causes ammonia to accumulate in the blood. Ammonia, which is formed when proteins are broken down in the body, is toxic if the levels become too high. The nervous system is especially sensitive to the effects of excess ammonia. Ornithine translocase deficiency varies widely in its severity and age of onset. An infant with ornithine translocase deficiency may be lacking in energy (lethargic) or refuse to eat, or have poorly controlled breathing or body temperature. Some babies with this disorder may experience seizures or unusual body movements, or go into a coma. Episodes of illness may coincide with the introduction of high-protein formulas or solid foods into the diet. In most affected individuals, signs and symptoms of ornithine translocase deficiency do not appear until later in life. Later-onset forms of ornithine translocase deficiency are usually less severe than the infantile form. Some people with later-onset ornithine translocase deficiency cannot tolerate high-protein foods, such as meat. Occasionally, high-protein meals or stress caused by illness or periods without food (fasting) may cause ammonia to accumulate more quickly in the blood. This rapid increase of ammonia may lead to episodes of vomiting, lack of energy (lethargy), problems with coordination (ataxia), confusion, or blurred vision. Complications of ornithine translocase deficiency may include developmental delay, learning disabilities, and stiffness caused by abnormal tensing of the muscles (spasticity).
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How many people are affected by MEGDEL syndrome ?
MEGDEL syndrome is a rare disorder; its prevalence is unknown. At least 40 affected individuals have been mentioned in the medical literature.
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What are the symptoms of Priapism ?
What are the signs and symptoms of Priapism? The Human Phenotype Ontology provides the following list of signs and symptoms for Priapism. 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 dominant inheritance - Priapism - 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 the outlook for Laryngeal Cancer ?
Certain factors affect prognosis (chance of recovery) and treatment options. Prognosis (chance of recovery) depends on the following: - The stage of the disease. - The location and size of the tumor. - The grade of the tumor. - The patient's age, gender, and general health, including whether the patient is anemic. Treatment options depend on the following: - The stage of the disease. - The location and size of the tumor. - Keeping the patient's ability to talk, eat, and breathe as normal as possible. - Whether the cancer has come back (recurred). Smoking tobacco and drinking alcohol decrease the effectiveness of treatment for laryngeal cancer. Patients with laryngeal cancer who continue to smoke and drink are less likely to be cured and more likely to develop a second tumor. After treatment for laryngeal cancer, frequent and careful follow-up is important.
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Is Anencephaly inherited ?
Is anencephaly inherited? Most cases of anencephaly are sporadic, which means they occur in people with no family history of anencephaly or other neural tube defects (NTDs). In some cases, it may be associated with a chromosome abnormality, a severe malformation syndrome, or disruption of the amniotic membrane. A small portion of cases have appeared to be familial, but it often does not have a clear inheritance pattern. In isolated populations, anencephaly has been suspected to be due to a single gene. In Iranian Jews, who have high rates of consanguinity (mating with family members), it is inherited in an autosomal recessive manner. Parents who have had a child with anencephaly are at an increased risk to have another affected child (compared with the risk in the general population). Because most cases are believed to be multifactorial (due to interaction of genetic and environmental factors), the recurrence risk is estimated to be between 2% and 5% after a single case. If anencephaly is known to be associated with an underlying disorder, the recurrence risk may depend on that of the underlying disorder. For women who have previously had a fetus or infant with anencephaly, the Centers for Disease Control and Prevention (CDC) recommends increasing the intake of folic acid to 4mg per day beginning at least one month prior to conception. People who have had a pregnancy or child with anencephaly or another NTD, and have questions about future risk, are encouraged to speak with a genetic counselor or other genetics professional.
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How many people are affected by hyperkalemic periodic paralysis ?
Hyperkalemic periodic paralysis affects an estimated 1 in 200,000 people.
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What causes Fibrolamellar carcinoma ?
What causes fibrolamellar carcinoma? The exact underlying cause of fibrolamellar carcinoma (FLC) is poorly understood. Other forms of liver cancer are often associated with liver cirrhosis (scarring of the liver) which may be caused by alcohol abuse; autoimmune diseases of the liver; Hepatitis B or C viral infections; chronic inflammation of the liver; and/or hemochromatosis. However, FLC typically occurs in the absence of underlying liver inflammation or scarring; thus, specific risk factors for this condition remain unidentified. Recent research suggests that a deletion on chromosome 19 may play a key role in the formation of FLC. This deletion is called a "somatic mutation" since it is only present in the cells of the liver. Somatic mutations accumulate during a person's lifetime and are not inherited or passed on to future generations.
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Is succinate-CoA ligase deficiency 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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How to diagnose Childhood Brain Stem Glioma ?
Tests that examine the brain are used to detect (find) childhood brain stem glioma. The following tests and procedures may be used: - Physical exam and history : An exam of the body to check general signs of health, including checking for signs of disease, such as lumps or anything else that seems unusual. A history of the patients health habits and past illnesses and treatments will also be taken. - Neurological exam : A series of questions and tests to check the brain, spinal cord, and nerve function. The exam checks a persons mental status, coordination, and ability to walk normally, and how well the muscles, senses, and reflexes work. This may also be called a neuro exam or a neurologic exam. - MRI (magnetic resonance imaging) with gadolinium : A procedure that uses a magnet, radio waves, and a computer to make a series of detailed pictures of areas inside the brain. A substance called gadolinium is injected into a vein. The gadolinium collects around the cancer cells so they show up brighter in the picture. This procedure is also called nuclear magnetic resonance imaging (NMRI). - A biopsy may be done to diagnose certain types of brain stem glioma. If the MRI scan looks like the tumor is a DIPG, a biopsy is usually not done and the tumor is not removed. If the MRI scan looks like a focal brain stem glioma, a biopsy may be done. A part of the skull is removed and a needle is used to remove a sample of the brain tissue. Sometimes, the needle is guided by a computer. A pathologist views the tissue under a microscope to look for cancer cells. If cancer cells are found, the doctor will remove as much tumor as safely possible during the same surgery. The following test may be done on the tissue that was removed: - Immunohistochemistry : A test that uses antibodies to check for certain antigens in a sample of tissue. The antibody is usually linked to a radioactive substance or a dye that causes the tissue to light up under a microscope. This type of test may be used to tell the difference between brain stem glioma and other brain tumors.
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What is (are) Psoriasis ?
Psoriasis (sow RYE uh sis) is a chronic skin disease. Chronic means that it lasts a long time, often a lifetime. Psoriasis affects more than 5 million adults in the United States. It appears about equally in males and females. Psoriasis occurs when the skin cells grow too quickly. The body does not shed these excess cells and they build up on the surface of the skin, forming thick, scaly patches. Types of Psoriasis Psoriasis occurs in five different forms that affect both men and women. Most people have only one type of psoriasis at a time. Sometimes, one type of psoriasis will disappear and another will appear. Here is a brief overview of the different forms of psoriasis. - Is the most common form - appears as raised red patches covered in silvery white scales - usually shows up on the scalp, knees, elbows and lower back - patches may itch or be painful and can also crack and bleed. Is the most common form appears as raised red patches covered in silvery white scales usually shows up on the scalp, knees, elbows and lower back patches may itch or be painful and can also crack and bleed. - is the second most common form of psoriasis - usually begins in childhood or early adulthood - appears as small red spots on the skin. is the second most common form of psoriasis usually begins in childhood or early adulthood appears as small red spots on the skin. - appears as red sores in body folds, such as the groin and under the breasts - is more common in people who are overweight - often occurs along with another form of psoriasis. appears as red sores in body folds, such as the groin and under the breasts is more common in people who are overweight often occurs along with another form of psoriasis. - features white blisters surrounded by red skin - mainly affects adults - may occur all over the body, but usually affects one area. features white blisters surrounded by red skin mainly affects adults may occur all over the body, but usually affects one area. - is the rarest and most dangerous form of psoriasis - is characterized by inflammation - usually affects most of the body. is the rarest and most dangerous form of psoriasis is characterized by inflammation usually affects most of the body.
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What is (are) Reye's Syndrome ?
Reye's syndrome (RS) is primarily a children's disease, although it can occur at any age. It affects all organs of the body but is most harmful to the brain and the liver--causing an acute increase of pressure within the brain and, often, massive accumulations of fat in the liver and other organs. RS is defined as a two-phase illness because it generally occurs in conjunction with a previous viral infection, such as the flu or chicken pox. The disorder commonly occurs during recovery from a viral infection, although it can also develop 3 to 5 days after the onset of the viral illness. RS is often misdiagnosed as encephalitis, meningitis, diabetes, drug overdose, poisoning, sudden infant death syndrome, or psychiatric illness. Symptoms of RS include persistent or recurrent vomiting, listlessness, personality changes such as irritability or combativeness, disorientation or confusion, delirium, convulsions, and loss of consciousness. If these symptoms are present during or soon after a viral illness, medical attention should be sought immediately. The symptoms of RS in infants do not follow a typical pattern; for example, vomiting does not always occur. Epidemiologic evidence indicates that aspirin (salicylate) is the major preventable risk factor for Reye's syndrome. The mechanism by which aspirin and other salicylates trigger Reye's syndrome is not completely understood. A "Reye's-like" illness may occur in children with genetic metabolic disorders and other toxic disorders. A physician should be consulted before giving a child any aspirin or anti-nausea medicines during a viral illness, which can mask the symptoms of RS.
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What is (are) Diabetes ?
Prediabetes means your blood glucose levels are higher than normal but not high enough for a diagnosis of diabetes. In 2012, about 86 million people in the U.S. had prediabetes, and 51% of those 65 or older had prediabetes. People with prediabetes are at an increased risk for developing type 2 diabetes and for heart disease and stroke. The good news is that if you have prediabetes, you can reduce your risk of getting type 2 diabetes. With modest weight loss and moderate physical activity, you can delay or prevent type 2 diabetes. Learn more about prediabetes here.
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What are the symptoms of Nephrotic Syndrome in Adults ?
In addition to proteinuria, hyperlipidemia, edema, and hypoalbumina, people with nephrotic syndrome may experience - weight gain - fatigue - foamy urine - loss of appetite
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What are the symptoms of What I need to know about Kidney Stones ?
You may have a kidney stone if you - have pain while urinating - see blood in your urine - feel a sharp pain in your back or lower abdomenthe area between your chest and hips The pain may last for a short or long time. You may have nausea and vomiting with the pain. If you have a small stone that passes on its own easily, you may not have symptoms at all.
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What is the outlook for Childhood Brain and Spinal Cord Tumors ?
Certain factors affect prognosis (chance of recovery). The prognosis (chance of recovery) depends on the following: - Whether there are any cancer cells left after surgery. - The type of tumor. - Where the tumor is in the body. - The child's age. - Whether the tumor has just been diagnosed or has recurred (come back).
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What are the genetic changes related to intranuclear rod myopathy ?
Intranuclear rod myopathy is caused by a mutation in the ACTA1 gene. This gene provides instructions for making a protein called skeletal alpha ()-actin, which is part of the actin protein family. Actin proteins are important for cell movement and the tensing of muscle fibers (muscle contraction). Thin filaments made up of actin molecules and thick filaments made up of another protein called myosin are the primary components of muscle fibers and are important for muscle contraction. Attachment (binding) and release of the overlapping thick and thin filaments allows them to move relative to each other so that the muscles can contract. ACTA1 gene mutations that cause intranuclear rod myopathy result in the accumulation of rods of skeletal -actin in the nucleus of muscle cells. Normally, most actin is found in the fluid surrounding the nucleus (the cytoplasm), with small amounts in the nucleus itself. Researchers suggest that the ACTA1 gene mutations that cause intranuclear rod myopathy may interfere with the normal transport of actin between the nucleus and the cytoplasm, resulting in the accumulation of actin in the nucleus and the formation of intranuclear rods. Abnormal accumulation of actin in the nucleus of muscle cells and a corresponding reduction of available actin in muscle fibers may impair muscle contraction and lead to the muscle weakness seen in intranuclear rod myopathy. In some people with intranuclear rod myopathy, no ACTA1 gene mutations have been identified. The cause of the disorder in these individuals is unknown.
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