umarjan11/Medical-qna huggingface dataset:
Question: What is (are) Quitting Smoking for Older Adults ?

Answer: Quitlines are free, anonymous telephone counseling services. These programs have helped more than 3 million smokers. When you call a quitline, you talk to a trained counselor who can help you develop a strategy for quitting or help you stay on track. The counselor can provide material that could improve your chances of quitting. - You can call the National Cancer Institutes Smoking Quitline at (877) 44U-QUIT or (877) 448-7848 between 8:00 a.m. and 8:00 p.m. Eastern Time.  You can call the National Cancer Institutes Smoking Quitline at (877) 44U-QUIT or (877) 448-7848 between 8:00 a.m. and 8:00 p.m. Eastern Time. - You can also call your states quitline. Call (800) QUIT-NOW or (800) 784-8669 to be connected with free resources about quitting and counseling information in your state.  You can also call your states quitline. Call (800) QUIT-NOW or (800) 784-8669 to be connected with free resources about quitting and counseling information in your state. - If you are a veteran, you can call (855)-QUIT VET or (855) 784-8838 between 8:00 a.m. and 8:00 p.m. Eastern Time on Mondays through Fridays.  If you are a veteran, you can call (855)-QUIT VET or (855) 784-8838 between 8:00 a.m. and 8:00 p.m. Eastern Time on Mondays through Fridays. You can also check out SmokeFree 60Plus. a quit-smoking website for older adults developed by the National Cancer Institute.
Question: What are the symptoms of Familial visceral myopathy with external ophthalmoplegia ?

Answer: What are the signs and symptoms of Familial visceral myopathy with external ophthalmoplegia? The Human Phenotype Ontology provides the following list of signs and symptoms for Familial visceral myopathy with external ophthalmoplegia. 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 gastric mucosa 90% Decreased body weight 90% Malabsorption 90% Myopathy 90% Ptosis 90% Skeletal muscle atrophy 90% Abnormality of the mitral valve 7.5% Abdominal distention - Abdominal pain - Abnormality of metabolism/homeostasis - Autosomal recessive inheritance - External ophthalmoplegia - Gastroparesis - Malnutrition - Ophthalmoplegia - Peripheral neuropathy - Spontaneous esophageal perforation - 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 Distal myopathy with vocal cord weakness ?

Answer: What are the signs and symptoms of Distal myopathy with vocal cord weakness? The Human Phenotype Ontology provides the following list of signs and symptoms for Distal myopathy with vocal cord weakness. 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) Dementia 5% Distal sensory impairment 5% Abnormal lower motor neuron morphology - Abnormal upper motor neuron morphology - Abnormality of the nasopharynx - Adult onset - Amyotrophic lateral sclerosis - Aspiration - Autosomal dominant inheritance - Bowing of the vocal cords - Bulbar palsy - Bulbar signs - Decreased nerve conduction velocity - Distal muscle weakness - Dysarthria - Dysphagia - Elevated serum creatine phosphokinase - Hoarse voice - Hyperreflexia - Respiratory insufficiency due to muscle weakness - Rimmed vacuoles - Shoulder girdle muscle weakness - 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 Vitreoretinochoroidopathy dominant ?

Answer: What are the signs and symptoms of Vitreoretinochoroidopathy dominant? The Human Phenotype Ontology provides the following list of signs and symptoms for Vitreoretinochoroidopathy dominant. 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% Optic atrophy 50% Abnormal electroretinogram 7.5% Aplasia/Hypoplasia of the lens 7.5% Dyschromatopsia 7.5% Microphthalmia 7.5% Abnormality of chorioretinal pigmentation - Abnormality of color vision - Autosomal dominant inheritance - Glaucoma - Microcornea - Nyctalopia - Nystagmus - Pigmentary retinopathy - Pulverulent Cataract - Retinal arteriolar constriction - Retinal arteriolar occlusion - Retinal detachment - Strabismus - Vitreous hemorrhage - 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: How to diagnose Pyruvate dehydrogenase deficiency ?

Answer: Is genetic testing available for pyruvate dehydrogenase deficiency? Genetic testing is available for pyruvate dehydrogenase deficiency. GeneTests lists the names of laboratories that are performing genetic testing for pyruvate dehydrogenase deficiency. To view the contact information for the clinical laboratories conducting testing click here. Please note: 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. How is pyruvate dehydrogenase deficiency diagnosed? The diagnosis of pyruvate dehydrogenase (PDH) deficiency may be considered in any individual with early-onset neurological disease, especially if it appears to be associated with structural abnormalities in the brain and unexplained lactic acidosis. When lactic acid (also called lactate) and pyruvate in the blood do not seem to be significantly high, an important clue to the diagnosis may be high concentrations of lactate and/or pyruvate in the cerebrospinal fluid (the fluid that surrounds the brain and spinal cord). Additionally, magnetic resonance spectroscopy (MRS) of the brain may show concentrations of lactate in the central nervous system. Analysis of serum and urine amino acids usually shows hyperalaninemia (high levels of the amino acid alanine). When lactic acidosis is present, other disorders involving pyruvate abnormalities are part of the differential diagnosis. However, in all of these conditions, the diagnosis is based on specific laboratory tests. Specific enzyme tests have been designed which measure both the individual's overall PDH activity, as well as each separate component of the complex (because any defect in the complex may cause the condition). The vast majority of individuals with PDH deficiency are found to be deficient in the El enzyme, but abnormalities have also been detected in other components.
Question: What are the genetic changes related to Hermansky-Pudlak syndrome ?

Answer: At least nine genes are associated with Hermansky-Pudlak syndrome. These genes provide instructions for making proteins that are used to make four distinct protein complexes. These protein complexes play a role in the formation and movement (trafficking) of a group of cell structures called lysosome-related organelles (LROs). LROs are very similar to compartments within the cell called lysosomes, which digest and recycle materials. However, LROs perform specialized functions and are found only in certain cell types. LROs have been identified in pigment-producing cells (melanocytes), blood-clotting cells (platelets), and lung cells.  Mutations in the genes associated with Hermansky-Pudlak syndrome prevent the formation of LROs or impair the functioning of these cell structures. In general, mutations in genes that involve the same protein complex cause similar signs and symptoms. People with this syndrome have oculocutaneous albinism because the LROs within melanocytes cannot produce and distribute the substance that gives skin, hair, and eyes their color (melanin). Bleeding problems are caused by the absence of LROs within platelets, which affects the ability of platelets to stick together and form a blood clot. Mutations in some of the genes that cause Hermansky-Pudlak syndrome affect the normal functioning of LROs in lung cells, leading to pulmonary fibrosis.  Mutations in the HPS1 gene cause approximately 75 percent of the Hermansky-Pudlak syndrome cases from Puerto Rico. About 45 percent of affected individuals from other populations have mutations in the HPS1 gene. Mutations in the HPS3 gene are found in about 25 percent of affected people from Puerto Rico and in approximately 20 percent of affected individuals from other areas. The other genes associated with Hermansky-Pudlak syndrome each account for a small percentage of cases of this condition.  In some people with Hermansky-Pudlak syndrome, the genetic cause of the disorder is unknown.
Question: What are the genetic changes related to factor XIII deficiency ?

Answer: Inherited factor XIII deficiency results from mutations in the F13A1 gene or, less commonly, the F13B gene. These genes provide instructions for making the two parts (subunits) of a protein called factor XIII. This protein plays a critical role in the coagulation cascade, which is a series of chemical reactions that forms blood clots in response to injury. After an injury, clots seal off blood vessels to stop bleeding and trigger blood vessel repair. Factor XIII acts at the end of the cascade to strengthen and stabilize newly formed clots, preventing further blood loss.  Mutations in the F13A1 or F13B gene significantly reduce the amount of functional factor XIII available to participate in blood clotting. In most people with the inherited form of the condition, factor XIII levels in the bloodstream are less than 5 percent of normal. A loss of this protein's activity weakens blood clots, preventing the clots from stopping blood loss effectively.  The acquired form of factor XIII deficiency results when the production of factor XIII is reduced or when the body uses factor XIII faster than cells can replace it. Acquired factor XIII deficiency is generally mild because levels of factor XIII in the bloodstream are 20 to 70 percent of normal; levels above 10 percent of normal are usually adequate to prevent spontaneous bleeding episodes.  Acquired factor XIII deficiency can be caused by disorders including an inflammatory disease of the liver called hepatitis, scarring of the liver (cirrhosis), inflammatory bowel disease, overwhelming bacterial infections (sepsis), and several types of cancer. Acquired factor XIII deficiency can also be caused by abnormal activation of the immune system, which produces specialized proteins called autoantibodies that attack and disable the factor XIII protein. The production of autoantibodies against factor XIII is sometimes associated with immune system diseases such as systemic lupus erythematosus and rheumatoid arthritis. In other cases, the trigger for autoantibody production is unknown.
Question: What is (are) Urinary Incontinence in Children ?

Answer: Urinary incontinence is the loss of bladder control, which results in the accidental loss of urine. A child with UI may not stay dry during the day or night. Some UI is caused by a health problem such as
                
- a urinary tract infection (UTI)  - diabetes, a condition where blood glucose, also called blood sugar, is too high  - kidney problems  - nerve problems  - constipation, a condition in which a child has fewer than two bowel movements a week and stools can be hard, dry, small, and difficult to pass  - obstructive sleep apnea (OSA), a condition in which breathing is interrupted during sleep, often because of inflamed or enlarged tonsils  - a structural problem in the urinary tract
                
Most of the time, the exact cause of UI is not known, but it is often the result of more than one factor.
                
Although UI affects many children, it usually disappears naturally over time. UI after age 3the age when most children achieve daytime drynessmay cause great distress and embarrassment. Many children experience occasional UI, and treatment is available for most children who have a hard time controlling their bladder. Thus, caregivers of children who wet the bed or have accidents during the day should approach this problem with understanding and patience.
                
The age at which children achieve dryness varies. Wetting in younger children is common and not considered UI, so daytime UI is not usually diagnosed until age 5 or 6, and nighttime UI is not usually diagnosed until age 7.
                
Enuresis   Urinary incontinence is also called enuresis. Types of enuresis include the following:   - Primary enuresis is wetting in a child who has never been consistently dry.   - Secondary enuresis is wetting that begins after at least 6 months of dryness.   - Nocturnal enuresis is wetting that usually occurs during sleep, also called nighttime UI.   - Diurnal enuresis is wetting when awake, also called daytime UI.
Question: What causes Shingles ?

Answer: Caused By A Virus Shingles is caused by a virus called varicella-zoster virus -- the one that gave you chickenpox when you were a child. As you recovered from chickenpox, the sores healed and the other symptoms went away, but the virus remained. It is with you for life. The virus hides out in nerve cells, usually in the spine. But it can become active again. Somehow, the virus gets a signal that your immunity has become weakened. This triggers the reactivation. When the virus becomes active again, it follows a nerve path called a dermatome. The nerve path begins at specific points in the spine, continues around one side of the body, and surfaces at the nerve endings in the skin. The pattern of the rash reflects the location of that nerve path. Risk Factors The leading risk factor for shingles is a history of having had chickenpox. One out of every five people who have had chickenpox is likely to get shingles. Another risk factor is aging. As we age, our natural immunity gradually loses its ability to protect against infection. The shingles virus can take advantage of this and become active again. Conditions that weaken the immune system can also put people at risk for shingles. Shingles is especially dangerous for anyone who has had cancer, radiation treatments for cancer, HIV/AIDS, or a transplant operation. Stress is another factor that may contribute to outbreaks. While stress alone does not cause the outbreaks, shingles often occurs in people who have recently had a stressful event in their lives. Most cases of shingles occur in adults. Only about 5 percent of cases occur in children. With children, immune deficiency is the primary risk factor, but children who had chickenpox before they were one year old may also get shingles before they become adults. There have been studies of adults who had chickenpox as children and were later exposed to children who had chickenpox. Interestingly, that exposure apparently boosted the adult's immunity, which actually helped them avoid getting shingles later in life.
Question: What are the symptoms of Diabetes insipidus nephrogenic mental retardation and intracerebral calcification ?

Answer: What are the signs and symptoms of Diabetes insipidus nephrogenic mental retardation and intracerebral calcification? The Human Phenotype Ontology provides the following list of signs and symptoms for Diabetes insipidus nephrogenic mental retardation and intracerebral calcification. 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 metabolism/homeostasis 90% Abnormality of the antihelix 90% Carious teeth 90% Cerebral calcification 90% Cognitive impairment 90% Hypoplasia of the zygomatic bone 90% Increased number of teeth 90% Limitation of joint mobility 90% Short stature 90% Abnormality of the genital system 50% Conductive hearing impairment 50% Nephrogenic diabetes insipidus - 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 Histidinuria renal tubular defect ?

Answer: What are the signs and symptoms of Histidinuria renal tubular defect? The Human Phenotype Ontology provides the following list of signs and symptoms for Histidinuria renal tubular defect. 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) Aminoaciduria 90% Cerebral cortical atrophy 90% Cognitive impairment 90% Delayed skeletal maturation 90% Hypoglycemia 90% Hypoplastic toenails 90% Long philtrum 90% Macrotia 90% Sensorineural hearing impairment 90% Ventriculomegaly 90% Wide nasal bridge 90% Autosomal recessive inheritance - Generalized myoclonic seizures - Histidinuria - Impaired histidine renal tubular absorption - Intellectual disability - Rounded middle phalanx of finger - Short middle phalanx of finger - Smooth philtrum - 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 Sillence syndrome ?

Answer: What are the signs and symptoms of Sillence syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Sillence 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 thumb phalanx 90% Camptodactyly of finger 90% Scoliosis 90% Tall stature 90% Abnormality of pelvic girdle bone morphology 50% Anonychia 50% Epicanthus 50% Single transverse palmar crease 50% Narrow face 7.5% Aplasia of the middle phalanx of the hand - Autosomal dominant inheritance - Bilateral single transverse palmar creases - Broad foot - Chess-pawn distal phalanges - Distal symphalangism (hands) - Flat acetabular roof - Pes cavus - Short 1st metacarpal - Thoracolumbar scoliosis - Type A1 brachydactyly - 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.