umarjan11/Medical-qna huggingface dataset:
Question: Who is at risk for Parasites - Fascioliasis (Fasciola Infection)? ?

Answer: Fascioliasis occurs in many areas of the world and usually is caused by F. hepatica, which is a common liver fluke of sheep and cattle. In general, fascioliasis is more common and widespread in animals than in people. Even so, the number of infected people in the world is thought to exceed 2 million.
    
Fasciola hepatica is found in more than 50 countries, in all continents except Antarctica. It is found in parts of Latin America, the Caribbean, Europe, the Middle East, Africa, Asia, and Oceania. Fasciola gigantica is less widespread. Human cases have been reported in the tropics, in parts of Africa and Asia, and also in Hawaii.
    
In some areas where fascioliasis is found, human cases are uncommon (sporadic). In other areas, human fascioliasis is very common (hyperendemic). For example, the areas with the highest known rates of human infection are in the Andean highlands of Bolivia and Peru.
    
Special conditions are needed for fascioliasis to be present in an area, and its geographic distribution is very patchy (focal). The eggs passed in the stool of infected mammals have to develop (mature) in a suitable aquatic snail host to be able to infect another mammalian host. Requirements include sufficient moisture and favorable temperatures (above 50°F) that allow the development of miracidia, reproduction of snails, and larval development within the snails. These factors also contribute to both the prevalence and level (intensity) of infection. Prevalence is highest in areas where climatic conditions promote development of cercariae.
    
More on: Biology
    
Infective Fasciola larvae (metacercariae) are found in contaminated water, either stuck to (encysted on) water plants or floating in the water, often in marshy areas, ponds, or flooded pastures. People (and animals) typically become infected by eating raw watercress or other contaminated water plants. The plants may be eaten as a snack or in salads or sandwiches. People also can get infected by ingesting contaminated water, such as by drinking it or by eating vegetables that were washed or irrigated with contaminated water. Infection also can result from eating undercooked sheep or goat livers that contain immature forms of the parasite.
    
The possibility of becoming infected in the United States should be considered, despite the fact that few locally acquired cases have been documented. The prerequisites for the Fasciola life cycle exist in some parts of the United States. In addition, transmission because of imported contaminated produce could occur, as has been documented in Europe.
Question: What are the symptoms of Iron-Deficiency Anemia ?

Answer: The signs and symptoms of iron-deficiency anemia depend on its severity. Mild to moderate iron-deficiency anemia may have no signs or symptoms.
                
When signs and symptoms do occur, they can range from mild to severe. Many of the signs and symptoms of iron-deficiency anemia apply to all types of anemia.
                
Signs and Symptoms of Anemia
                
The most common symptom of all types of anemia is fatigue (tiredness). Fatigue occurs because your body doesn't have enough red blood cells to carry oxygen to its many parts.
                
Also, the red blood cells your body makes have less hemoglobin than normal. Hemoglobin is an iron-rich protein in red blood cells. It helps red blood cells carry oxygen from the lungs to the rest of the body.
                
Anemia also can cause shortness of breath, dizziness, headache, coldness in your hands and feet, pale skin, chest pain, weakness, and fatigue (tiredness).
                
If you don't have enough hemoglobin-carrying red blood cells, your heart has to work harder to move oxygen-rich blood through your body. This can lead to irregular heartbeats called arrhythmias (ah-RITH-me-ahs), a heart murmur, an enlarged heart, or even heart failure.
                
In infants and young children, signs of anemia include poor appetite, slowed growth and development, and behavioral problems.
                
Signs and Symptoms of Iron Deficiency
                
Signs and symptoms of iron deficiency may include brittle nails, swelling or soreness of the tongue, cracks in the sides of the mouth, an enlarged spleen, and frequent infections.
                
People who have iron-deficiency anemia may have an unusual craving for nonfood items, such as ice, dirt, paint, or starch. This craving is called pica (PI-ka or PE-ka).
                
Some people who have iron-deficiency anemia develop restless legs syndrome (RLS). RLS is a disorder that causes a strong urge to move the legs. This urge to move often occurs with strange and unpleasant feelings in the legs. People who have RLS often have a hard time sleeping.
                
Iron-deficiency anemia can put children at greater risk for lead poisoning and infections.
                
Some signs and symptoms of iron-deficiency anemia are related to the condition's causes. For example, a sign of intestinal bleeding is bright red blood in the stools or black, tarry-looking stools.
                
Very heavy menstrual bleeding, long periods, or other vaginal bleeding may suggest that a woman is at risk for iron-deficiency anemia.
Question: What are the genetic changes related to Vohwinkel syndrome ?

Answer: The classic form of Vohwinkel syndrome is caused by mutations in the GJB2 gene. This gene provides instructions for making a protein called gap junction beta 2, more commonly known as connexin 26. Connexin 26 is a member of the connexin protein family. Connexin proteins form channels called gap junctions that permit the transport of nutrients, charged atoms (ions), and signaling molecules between neighboring cells that are in contact with each other. Gap junctions made with connexin 26 transport potassium ions and certain small molecules.  Connexin 26 is found in cells throughout the body, including the inner ear and the skin. In the inner ear, channels made from connexin 26 are found in a snail-shaped structure called the cochlea. These channels may help to maintain the proper level of potassium ions required for the conversion of sound waves to electrical nerve impulses. This conversion is essential for normal hearing. In addition, connexin 26 may be involved in the maturation of certain cells in the cochlea. Connexin 26 also plays a role in the growth, maturation, and stability of the outermost layer of skin (the epidermis).  The GJB2 gene mutations that cause Vohwinkel syndrome change single protein building blocks (amino acids) in connexin 26. The altered protein probably disrupts the function of normal connexin 26 in cells, and may interfere with the function of other connexin proteins. This disruption could affect skin growth and also impair hearing by disturbing the conversion of sound waves to nerve impulses.  The variant form of Vohwinkel syndrome, sometimes called loricrin keratoderma, is caused by mutations in the LOR gene. This gene provides instructions for making a protein called loricrin, which is involved in the formation and maintenance of the epidermis, particularly its tough outer surface (the stratum corneum). The stratum corneum, which is formed in a process known as cornification, provides a sturdy barrier between the body and its environment. Each cell of the stratum corneum, called a corneocyte, is surrounded by a protein shell called a cornified envelope. Loricrin is a major component of the cornified envelope. Links between loricrin and other components of the envelopes hold the corneocytes together and help give the stratum corneum its strength.  Mutations in the LOR gene change the structure of the loricrin protein; the altered protein is trapped inside the cell and cannot reach the cornified envelope. While other proteins can partially compensate for the missing loricrin, the envelope of some corneocytes is thinner than normal in affected individuals, resulting in ichthyosis and the other skin abnormalities associated with the variant form of Vohwinkel syndrome.
Question: How to diagnose Uterine Sarcoma ?

Answer: Tests that examine the uterus are used to detect (find) and diagnose uterine sarcoma. 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.    -  Pelvic exam: An exam of the vagina, cervix, uterus, fallopian tubes, ovaries, and rectum. A speculum is inserted into the vagina and the doctor or nurse looks at the vagina and cervix for signs of disease. A Pap test of the cervix is usually done. The doctor or nurse also inserts one or two lubricated, gloved fingers of one hand into the vagina and places the other hand over the lower abdomen to feel the size, shape, and position of the uterus and ovaries. The doctor or nurse also inserts a lubricated, gloved finger into the rectum to feel for lumps or abnormal areas.    -  Pap test: A procedure to collect cells from the surface of the cervix and vagina. A piece of cotton, a brush, or a small wooden stick is used to gently scrape cells from the cervix and vagina. The cells are viewed under a microscope to find out if they are abnormal. This procedure is also called a Pap smear. Because uterine sarcoma begins inside the uterus, this cancer may not show up on the Pap test.     -   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.     -   Dilatation and curettage : A procedure to remove samples of tissue from the inner lining of the uterus. The cervix is dilated and a curette (spoon-shaped instrument) is inserted into the uterus to remove tissue. The tissue samples are checked under a microscope for signs of disease. This procedure is also called a D&C.    -   Endometrial biopsy : The removal of tissue from the endometrium (inner lining of the uterus) by inserting a thin, flexible tube through the cervix and into the uterus. The tube is used to gently scrape a small amount of tissue from the endometrium and then remove the tissue samples. A pathologist views the tissue under a microscope to look for cancer cells.
Question: What are the symptoms of Tetrahydrobiopterin deficiency ?

Answer: What are the signs and symptoms of Tetrahydrobiopterin deficiency? Infants with tetrahydrobiopterin (BH4) deficiency typically appear normal and healthy at birth. Neurological signs and symptoms usually become apparent over time, and can range from mild to severe. These may include abnormal muscle tone; poor sucking and coordination; seizures; and delayed motor development. Other manifestations may include decreased spontaneous movements and difficulty swallowing. Without early and appropriate treatment, signs and symptoms progress and affected individuals may experience irreversible intellectual disability, behavioral problems, an inability to control body temperature, and even death in severe cases. The Human Phenotype Ontology provides the following list of signs and symptoms for Tetrahydrobiopterin deficiency. 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) Cognitive impairment 90% Microcephaly 90% Abnormality of eye movement - Ataxia - Autosomal recessive inheritance - Bradykinesia - Cerebral calcification - Choreoathetosis - Dysphagia - Dystonia - Episodic fever - Excessive salivation - Hyperkinesis - Hyperphenylalaninemia - Hyperreflexia - Hypertonia - Infantile onset - Intellectual disability - Intellectual disability, progressive - Irritability - Lethargy - Limb hypertonia - Motor delay - Muscular hypotonia - Muscular hypotonia of the trunk - Myoclonus - Parkinsonism - Poor suck - Progressive neurologic deterioration - Rigidity - Seizures - Severe muscular hypotonia - Small for gestational age - Somnolence - Transient hyperphenylalaninemia - Tremor - Variable expressivity - 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.
Question: What are the symptoms of Maternally inherited diabetes and deafness ?

Answer: What are the signs and symptoms of Maternally inherited diabetes and deafness? The Human Phenotype Ontology provides the following list of signs and symptoms for Maternally inherited diabetes and 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) Abnormality of the macula 90% Chorioretinal abnormality 90% Constipation 90% Diabetes mellitus 90% Malabsorption 90% Sensorineural hearing impairment 90% Abnormality of lipid metabolism 50% Aplasia/Hypoplasia of the cerebellum 50% Arrhythmia 50% Congestive heart failure 50% Glomerulopathy 50% Hypertension 50% Hypertrophic cardiomyopathy 50% Muscle weakness 50% Myalgia 50% Ophthalmoparesis 50% Proteinuria 50% Cataract 7.5% Incoordination 7.5% Renal insufficiency 7.5% Retinopathy 7.5% Visual impairment 7.5% Ptosis 5% Dysarthria - External ophthalmoplegia - Hyperglycemia - Mitochondrial inheritance - Pigmentary retinal degeneration - Retinal degeneration - Seizures - Type II diabetes mellitus - Unsteady gait - Vertigo - 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. When do the diabetes and hearing loss associated with MIDD typically develop? In MIDD, the diabetes and hearing loss usually develop in mid-adulthood, although the age that they occur varies from childhood to late adulthood. Typically, hearing loss occurs before diabetes.
Question: What causes Heart Block ?

Answer: Heart block has many causes. Some people are born with the disorder (congenital), while others develop it during their lifetimes (acquired).
                
Congenital Heart Block
                
One form of congenital heart block occurs in babies whose mothers have autoimmune diseases, such as lupus. People who have these diseases make proteins called antibodies that attack and damage the body's tissues or cells.
                
In pregnant women, antibodies can cross the placenta. (The placenta is the organ that attaches the umbilical cord to the mother's womb.) These proteins can damage the baby's heart and lead to congenital heart block.
                
Congenital heart defects also may cause congenital heart block. These defects are problems with the heart's structure that are present at birth. Often, doctors don't know what causes these defects.
                
Acquired Heart Block
                
Many factors can cause acquired heart block. Examples include:
                
Damage to the heart from a heart attack. This is the most common cause of acquired heart block.
                
Coronary heart disease, also called coronary artery disease.
                
Myocarditis (MI-o-kar-DI-tis), or inflammation of the heart muscle.
                
Heart failure.
                
Rheumatic (roo-MAT-ik) fever.
                
Cardiomyopathy (KAR-de-o-mi-OP-a-the), or heart muscle diseases.
                
Other diseases may increase the risk of heart block. Examples include sarcoidosis (sar-koy-DOE-sis) and the degenerative muscle disorders Lev's disease and Lenegre's disease.
                
Certain types of surgery also may damage the heart's electrical system and lead to heart block.
                
Exposure to toxic substances and taking certain medicinesincluding digitalis, beta blockers, and calcium channel blockersalso may cause heart block. Doctors closely watch people who are taking these medicines for signs of problems.
                
Some types of heart block have been linked to genetic mutations (changes in the genes).
                
An overly active vagus nerve also can cause heart block. You have one vagus nerve on each side of your body. These nerves run from your brain stem all the way to your abdomen. Activity in the vagus nerve slows the heart rate.
                
In some cases, acquired heart block may go away if the factor causing it is treated or resolved. For example, heart block that occurs after a heart attack or surgery may go away during recovery.
                
Also, if a medicine is causing heart block, the disorder may go away if the medicine is stopped or the dosage is lowered. Always talk with your doctor before you change the way you take your medicines.
Question: What are the treatments for What I need to know about Living with Kidney Failure ?

Answer: Kidney failure means your kidneys no longer work well enough to do their job. You need treatment to replace the work your damaged kidneys have stopped doing. The treatments for kidney failure are
                
- hemodialysis  - peritoneal dialysis  - a kidney transplant
                
Your kidneys filter wastes and extra fluid from your blood to keep you healthy. The wastes and extra fluid become urine that is stored in your bladder until you urinate. When your kidneys fail, dialysis can take over a small part of the work your damaged kidneys can no longer do. You can make treatments work better by
                
- sticking to your treatment schedule  - taking all medicines your doctor prescribes  - following a special diet that keeps wastes from building up in your blood  - being active most days of the week
                
Hemodialysis
                
Hemodialysis is a treatment for kidney failure. Hemodialysis uses a machine to filter your blood outside your body. First, a dialysis nurse places two needles into your arm. A pump on the hemodialysis machine draws your blood through one of the needles into a tube. The tube takes the blood to a filter, called a dialyzer. Inside the dialyzer, your blood flows through thin fibers that are like straws. The wastes and extra fluid leave the blood through tiny holes in the fibers. Then, a different tube carries the filtered blood back to your body through the second needle.
                
More information is provided in the NIDDK health topics, Treatment Methods for Kidney Failure: Hemodialysis and Home Hemodialysis.
                
Peritoneal Dialysis
                
catheter
                
Treatment Methods for Kidney Failure: Peritoneal Dialysis
                
Kidney Transplant
                
A kidney transplant places a healthy kidney from another person into your body. The kidney may come from someone who has just died. Your doctor will place your name on a waiting list for a kidney. A family member or friend might be able to give you a kidney. Then you dont have to wait.
                
The new kidney takes over filtering your blood. The damaged kidneys usually stay where they are. The new kidney is placed in the front lower abdomen, on one side of the bladder. Your body normally attacks anything that shouldnt be there, such as bacteria. Your body will think the new kidney shouldnt be there. You will take medicines called immunosuppressants to keep your body from attacking the new kidney.
                
More information is provided in the NIDDK health topic, Treatment Methods for Kidney Failure: Transplantation.
                
*See the Pronunciation Guide for tips on how to say the the words in bold type.