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Symptoms at 37: ['movement disorders', 'Memory disturbances', 'headache', 'seizures']

Disease Name: Anaplastic Oligoastrocytoma, symptoms: ['movement disorders', 'Memory disturbances', 'headache', 'seizures'], Treatment: ['tandard of care for 1p/19q co-deleted oligodendroglial tumors should be the combination of CHT and radiotherapy (RT). In OA, a favourable prognosis was associated to young age, grade II and extent of resection'], Pathophysiology: Anaplastic oligoastrocytoma is a brain tumor that forms when two types of cells in the brain, called oligodendrocytes and astrocytes, rapidly increase in number to form a mass. These brain cells are known as glial cells, which normally protect and support nerve cells in the brain. Because an oligoastrocytoma is made up of a combination of two cell types, it is known as a mixed glioma. An oligoastrocytoma is described as anaplastic when the tumor grows quickly and the cancer cells within the tumor have the potential to spread into surrounding brain tissue or to more distant parts of the body. The exact cause of this condition is unknown., Epidemiology:['about 9.4% of all primary brain and central nervous system tumors and 5%–18% of all glial neoplasms', 'variable', 'there is no way to prevent'], Complications:['coma', 'Hydrocephalus', 'venous thromboembolism', 'Metastasis', 'intracranial hemorrhage'], Diagnostics:['HISTOPATHLOGY', 'CT SCAN'], Differential diagnosis:['anaplastic astrocytoma', 'infection', 'inflammation', 'Metastatic tumours', 'oligodendroglioma (who grade 2)'], disease description:Anaplastic oligoastrocytoma is a brain tumor that forms when two types of cells in the brain, called oligodendrocytes and astrocytes, rapidly increase in number to form a mass. These brain cells are known as glial cells, which normally protect and support nerve cells in the brain. Because an oligoastrocytoma is made up of a combination of two cell types, it is known as a mixed glioma. An oligoastrocytoma is described as anaplastic when the tumor grows quickly and the cancer cells within the tumor have the potential to spread into surrounding brain tissue or to more distant parts of the body. 

Suffering from ['behavioural disturbances', 'headache', 'impaired memory', 'language impairment', 'seizures'] at the age of 48

Disease Name: Anaplastic Oligodendroglioma, symptoms: ['behavioural disturbances', 'headache', 'impaired memory', 'language impairment', 'seizures'], Treatment: ['Chemotherapy: Anti-cancer drugs destroy cancer cells throughout the body. Most chemotherapy is injected into a vein or taken in pill form. Doctors may recommend chemotherapy before or after radiation therapy to kill cancer cells left behind after surgery or radiation.', 'Clinical trials: If all treatments have been tried and failed, you and your healthcare provider may want to look into clinical trials. You may meet entry criteria to join a clinical trial. You can use this site to learn more about treatments being investigated. Visit clinicaltrials.gov.', 'radiation or chemotherapy with temozolomide or a chemotherapy with Procarbazine, CCNU and Vincristine (PCV) has been shown to be effective and was the most commonly used chemotherapy regimen used for treating anaplastic oligodendrogliomas', 'Surgery: When oligodendroglioma develops in an accessible area, surgeons remove the tumor. They work very carefully to remove as much of the tumor as possible without damaging surrounding healthy tissue. In some cases, it is not possible to remove the entire tumor through surgery alone.'], Pathophysiology: The kinds of oligodendrogliomas are:Grade 2 (low grade) oligodendroglioma: These benign tumors grow slowly. They can be present for years before causing symptoms. They are usually confined to nearby tissue only.Grade 3 (high grade) anaplastic oligodendroglioma: These tumors are malignant and can spread quickly to other areas of the central nervous system.The tumors begin in cells of the brain called oligodendrocytes. Oligodendrocytes are a type of cell called glial cells.Glial cells are glue-like cells that surround nerve cells and help them function. When these cells grow uncontrollably, a tumor forms. Oligodendroglioma is a type of tumor called a glioma, named for the type of cell –glial cells– from which it develops.Doctors suspect that in some cases, a chromosome abnormality may be the cause. Missing chromosomes (parts of your genes) can cause cells to grow into a tumor., Epidemiology:['around 5% of all central nervous system neuroepithelial tumors. . About 1,000 oligodendrogliomas are diagnosed per year in the United States.', 'variable', 'You cannot prevent oligodendrogliomas. You can reduce your risk for the tumor by limiting your exposure to radiation from X-rays.'], Complications:['hearing disturbances', 'nausea', 'vomiting', 'vision abnormalities'], Diagnostics:['HISTOPATHLOGY', 'MRI', 'CT SCAN'], Differential diagnosis:['anaplastic astrocytoma', 'anaplastic ganglioglioma', 'dysembryoplastic neuroepithelial tumour (who grade', 'ependymoma', 'Glioblastoma multiforme'], disease description:Oligodendroglioma is a tumor that forms in the brain. These uncommon tumors usually develop in either the frontal or temporal lobes of the brain, but in rare cases, they can form in the spinal cord. Oligodendrogliomas develop from cells called oligodendrocytes. Oligodendrocytes create a substance that protects nerves in the brain and helps them function.Oligodendrogliomas can be malignant (cancer) or benign (non cancer). 

having ['Pain', 'weight loss', 'Numbness', 'weakness', 'fever'] at the age of 31

Disease Name: Anca Small-vessel Vasculitis, symptoms: ['Pain', 'weight loss', 'Numbness', 'weakness', 'fever'], Treatment: [{'medication': ['Cyclophosphamide ', 'Azathioprine ', 'Methyl prednisolone ']}, 'induction of remission, maintenance of remission, and treatment of relapse.11 Current induction therapy often consists of cyclophosphamide (Cytoxan) and corticosteroids. For aggressive disease, use of high-dose intravenous methylprednisolone for three days is recommended, combined with intravenous or oral cyclophosphamide.11 Tapering doses of prednisone should follow, along with cyclophosphamide maintenance for 12 to 18 months. The lowest dosage of steroids that controls the disease should be used, and infection should be considered if the symptoms appear to exacerbate. For patients in sustained remission at 12 months, the use of all medications may be gradually discontinued. Patients whose symptoms are under good control must, nevertheless, be closely followed at six-month intervals for signs and symptoms of relapse. During treatment with these agents, complete blood counts and liver function tests should be performed periodically.\n\nOther treatment regimens that may be of benefit include methotrexate, azathioprine (Imuran), trimethoprim-sulfamethoxazole (Bactrim, Septra), plasma exchange, cyclosporine (Sandimmune), intravenous im-munoglobulin, and monoclonal antibodies.\n\nDuring the use of potentially ulcerogenic immunosuppressive therapy, patients may be given H2-blockers or proton-pump inhibitors. Prophylactic treatment with fluconazole (Diflucan) orally for fungal infection may be considered, as well as trimethoprim-sulfamethoxazole (480 mg) three times weekly for prophylactic treatment of patients with pneumocystis carinii prophylaxis.'], Pathophysiology: It is still unknown how the antineutrophilic cytoplasmic antibody (ANCA) antibodies develop. Some studies suggest a genetic role. In two studies, there was an association between the anti-PR3-ANCA and HLA-DP, PRTN3 (the gene encoding proteinase-3), and anti-MPO ANCA was associated mainly with HLA-DQ polymorphisms.Some studies link the development of ANCA antibodies to environmental causes or infections, proposing the molecular mimicry model.In vitro studies showed that neutrophils are initially primed (partially stimulated) with TNF-alpha, lipopolysaccharide (LPS), or complement (C5a), then it will be activated once it is bound to the ANCA. After activation, it will degranulate and mediate endothelial cell damage.Other studies showed that ANCA activates intracellular signaling pathways leading to altered adhesion molecule expression, which facilitates neutrophil adhesion and transmigration to the vascular endothelium, Epidemiology:['male to female ratio of 2:1', 'incidence of 5 to 10 cases per million and a peak incidence in middle age', 'good', 'By reducing inflammation, they can reduce the damage caused by the immune system .'], Complications:['Osteoporosis', 'Scarring', 'kidney faliure'], Diagnostics:['ANA', 'Complete Blood Count CBC', 'CRP', 'Erythrocyte Sedimentation Rate (ESR)', 'Hb', 'Renal Biopsy', 'SERUM Creatinine', 'anti-proteinase 3 (PR3)', 'X RAY CHEST', 'cANCA', 'pANCA', 'CT SCAN'], Differential diagnosis:["Behcet's syndrome/disease", 'Goodpasture syndrome', 'HENOCH-SCHONLEIN PURURA', 'lymphoma', 'rheumatoid arthritis', 'systemic lupus erythematosus (SLE)'], disease description:Antineutrophilic cytoplasmic antibody (ANCA) associated vasculitides are a heterogeneous group of rare autoimmune conditions that causes an inflammation of blood vessels with various manifestations. It includes three main diseases, which are granulomatosis with polyangiitis (GPA; formerly known as Wegener granulomatosis), eosinophilic granulomatosis with polyangiitis (EGPA; previously known as Churg-Strauss syndrome), and microscopic polyangiitis (MPA). Other ANCA-associated diseases are drug-induced vasculitis and renal limited vasculitis.

Suffering from ['balance disorder', 'developmental delay', 'movement disorders', 'hypotonia', 'delayed milestones', 'Ataxia', 'mid face hypoplasia', 'seizures', 'Sleep disturbances', 'tremor'] at 20

Disease Name: Ancylostomiasis, symptoms: ['balance disorder', 'developmental delay', 'movement disorders', 'hypotonia', 'delayed milestones', 'Ataxia', 'mid face hypoplasia', 'seizures', 'Sleep disturbances', 'tremor'], Treatment: [{'medication': ['Albendazole ', 'Mebendazole ', 'Pyrantel Pamoate']}, 'Feeding Difficulties - Sucking might be ineffective, so breastfeeding is not possible sometimes. The use of special nipples is advised, monitoring weight gain and referral to specialized teams for advice and training on feeding.\nGastroesophageal Reflux - Administration of magnesium carbonate and aluminum hydroxide in upright .positioning.\nConstipation - Increased fluid intake. Jelly can be used as an alternative. A diet rich in fiber and laxatives can also be used.\nObesity - Regular checkup of weight and BMI. Also, regular exercise is advised.\nDiet -The ketogenic diet is helpful and is effective.The most effective drugs are sodium valproate, clonazepam, and phenobarbital'], Pathophysiology: The hookworm species that reach maturity in the human intestine have similar life cycles. Eggs passed in the stool hatch in 1 to 2 days (if they are deposited in a warm, moist place on loose soil) and release rhabditiform larvae, which molt once to become slender filariform larvae in 5 to 10 days. The larvae can survive 3 to 4 weeks if environmental conditions are favorable. Filariform larvae penetrate human skin when people walk barefoot on or otherwise come into direct contact with infested soil.The larvae reach the lungs via blood vessels, penetrate into pulmonary alveoli, ascend the bronchial tree to the epiglottis, and are swallowed. The larvae develop into adults in the small bowel; there, they attach to the wall, feeding on blood. Adult worms may live = 2 years., Epidemiology:['more than 1.5 billion people worldwide', 'poor', 'You should avoid walking barefoot in places where the soil or sand may be infected. In these areas, don’t touch the ground with your bare hands. Sit on a tarp or other barrier instead of sitting on the bare earth.\n\nTake these precautions in regions where people:\n\nGo to the bathroom outdoors.\nFertilize gardens or farmland with human feces.'], Complications:['iron deficiency anemia', 'Nutritional deficiencies'], Diagnostics:['EEG', 'GENETIC TESTING', 'CT/MRI', 'X RAY'], Differential diagnosis:['allergic dermatitis', 'Gastrointestinal infection', 'inflammatory bowel syndrome', 'iron deficiency anemia', 'malabsorption syndrome'], disease description:Ancylostoma duodenale, the human hookworm, is the most common parasitic infection in countries with poor access to adequate water, sanitation, and hygiene. Ancylostomiasis  is caused when hookworms, present in large numbers, produce an iron deficiency anemia by sucking blood from the host's intestinal walls. 

Person aged 34 with manifestations like ['intellectual disability', 'intention tremor', 'Ataxia', 'fatigue', 'irregular heart beat', 'lightheadedness', 'Neurological symptoms', 'shortness of breath']

Disease Name: Anemia Due To Disorder Of Glutathione Metabolism, symptoms: ['intellectual disability', 'intention tremor', 'Ataxia', 'fatigue', 'irregular heart beat', 'lightheadedness', 'Neurological symptoms', 'shortness of breath'], Treatment: ['Genetic counseling should be offered to affected individuals and their families.', 'The treatment of glutathione synthetase deficiency is directed toward the specific symptoms that are apparent in each individual. Treatment will include sodium bicarbonate to correct the metabolic acidosis. Initially, this may require parenteral (e.g. intravenous) therapy. Eventually, affected individuals can be treated with sodium bicarbonate or citrate, delivered through the mouth (orally). Supplemental therapy with vitamins E and C, which have antioxidant properties, may also be given.\n\nDrugs that precipitate hemolysis in glucose-6-phosphate dehydrogenase deficiency should be avoided. (For more information on this disorder and such drugs, choose “glucose 6 phosphate dehydrogenase deficiency” as your search term in the NORD Rare Disease Database.)'], Pathophysiology: The GSS alterations that cause glutathione synthetase deficiency are inherited in an autosomal recessive manner. Most such genetic diseases are determined by the status of the two copies of a gene, one received from the father and one from the mother. Recessive genetic disorders occur when an individual inherits two copies of an abnormal gene for the same trait, one from each parent. If an individual inherits one normal gene and one gene for the disease, the person will be a carrier for the disease but usually will not show symptoms. The risk for two carrier parents to both pass the altered gene and have an affected child is 25% with each pregnancy. The risk to have a child who is a carrier like the parents is 50% with each pregnancy. The chance for a child to receive normal genes from both parents is 25%. The risk is the same for males and females. The GSS gene contains instructions for making the enzyme glutathione synthetase. This enzyme is required for the body to create the small protein molecule glutathione. An alteration in the GSS gene leads to deficiency of or glutathione synthetase, which, in turn, leads to a lack of glutathione, which is a peptide molecule that plays a crucial role in many cellular processes. Cellular processes are activities that go on inside of a cell that are vital for proper health and development., Epidemiology:['about 400 million people are affected by this deficiency.', 'variable', 'To Do : general population, the use of a live-attenuated zoster vaccine (Zostavax, Merck) has been shown to decrease the risk for herpes zoster development by about 50%.\n.This vaccine is a one-time subcutaneous injection.\n.'], Complications:['death', 'jaundice', 'weakness'], Diagnostics:['PLATELET COUNT', 'Serum Alkaline Phosphatase ALP', 'alanine transaminase (ALT)', 'White Blood Cell count WBC', 'ASPARTATE AMINOTRANSFERASE (SGOT )'], Differential diagnosis:['aplastic anaemia', 'GI bleed', 'Hemolytic anemia', 'Hemolytic anemia', 'iron deficiency anemia', 'MEGALOBLASTIC ANAEMIA', 'PEPTIC ULCER DISEASE', 'Pernicious anaemia', 'sickel cell disease', 'Thalassemia'], disease description:Anemia due to disorders of glutathione metabolism is a group of red cell disorders caused by inherited abnormality of enzymes of glutathione metabolism.Mild glutathione synthetase deficiency usually results in the destruction of red blood cells (hemolytic anemia). In addition, affected individuals may release large amounts of a compound called 5-oxoproline in their urine (5-oxoprolinuria). This compound builds up when glutathione is not processed correctly in cells.

Experiencing ['splenomegaly', 'Sluggishness', 'poor feeding', 'jaundice', 'pale skin', 'Bruises', 'HEPATOMEGALY'] at the age of 2.44, baby

Disease Name: Anemia In Newborn, symptoms: ['splenomegaly', 'Sluggishness', 'poor feeding', 'jaundice', 'pale skin', 'Bruises', 'HEPATOMEGALY'], Treatment: [{'medication': ['Folic acid / Vitamin B9', 'Iron ']}, 'BLOOD TRANSFUSION,EXCHANGE TRANSFUSION, NUTRITIONAL SUPPORT'], Pathophysiology: Anemia in the newborn infant may be due to any one of the three pathologies: (a) Physiologic anemia of infancy is due to shorter life span of RBCs and less erythropoietin production; (b) Loss of RBCs (Hemorrhagic anemia); (c) Destruction of RBCs (Hemolytic anemia) or (d) Under production of RBCs (Hypoplastic anemia)., Epidemiology:['a prevalence of 29.2 and 20.8% among male and female newborn', 'GOOD', "You can often prevent iron-deficiency anemia through screening and taking iron supplements.Watch how much cow's milk your child drinks. Feeding your toddler too much cow's milk (more than 32 ounces a day) can prevent the absorption of iron from other foods and limit the intake of other foods that are rich in iron."], Complications:['developmental delay', 'Mental Disorder', 'Hydrops fetalis'], Diagnostics:['Complete Blood Count CBC', 'Hb', 'COAGULATION PROFILE', 'Blood smear'], Differential diagnosis:['Glucose 6-phasphate dehydrogenase deficiency', 'Glutamine synthetase deficiency', 'hereditary spherocytosis', 'Pyruvate kinase (PK) deficiency'], disease description:At birth normal values of hemoglobin (central venous) in infants > 34 weeks gestation are 14–20 g/dL with an average value of 17 g/dL. Central venous hemoglobin level < 13 g/dL in an infant of > 34 weeks gestation is considered anemia .Babies who have anaemia  have a red blood cell count that is lower than normal. Red blood cells carry oxygen throughout the body.

Suffering from ['anorexia', 'pallor', 'stomatitis', 'lassitude', 'palpitations', 'weakness', 'Giddiness', 'dyspnea', 'crepitations in chest', 'systolic murmur', 'breathlessness', 'indigestion'] at 22

Disease Name: Anemia In Pregnancy, symptoms: ['anorexia', 'pallor', 'stomatitis', 'lassitude', 'palpitations', 'weakness', 'Giddiness', 'dyspnea', 'crepitations in chest', 'systolic murmur', 'breathlessness', 'indigestion'], Treatment: [{'medication': ['Folic acid / Vitamin B9', 'Ferrous Sulphate ', 'Iron ']}, 'PARENTERAL IRON & BLOOD TRANSFUSION'], Pathophysiology: Maternal plasma volume increases by about 40–50%. RBC volume increases by 20%. There is relative fall in the level of hemoglobin and hematocrit during pregnancy. All these values return to normal by 6 weeks postpartum. In addition, there is marked demand of extra iron during pregnancy especially in the second half. Even an adequate diet cannot provide the extra demand of iron. Thus, there always remains a physiological iron deficiency state during pregnancy. As a result, there is not only a fall in hemoglobin concentration and hematocrit value in the second half of pregnancy but there is also associated low serum iron, increased iron binding capacity and increased rate of iron absorption as found in iron deficiency anemia. Thus, the fall in the hemoglobin concentration during pregnancy is due to combined effect of hemodilution and negative iron balance. The anemia is normocytic and normochromic in type. Normal blood values in non-pregnant and pregnant state.. CRiTERia OF PHySiOLOgiCaL anEMia: The lower limit of physiological anemia during the second half of pregnancy should fulfill the following hematological values: (1) Hb-10 gm% (2) RBC-3.2 million/mm3 (3) PCV-32%. (4) Peripheral smear showing normal morphology of the RBC with central pallor. ERyTHROPOiESiS: In adults, erythropoiesis is confined to the bone marrow. Red blood cells are formed through stages of pronormoblasts normoblasts reticulocytes to mature non-nucleated erythrocytes. The average life span of red blood cells is about 120 days after which the RBC degenerate and the hemoglobin is broken down into hemosiderin and bile pigment. For proper erythropoiesis, adequate nutrients are needed. These are minerals, vitamins, proteins and hormones. Inadequate reserve or increased demand or deficient supply of any of the constituents interferes with the normal erythropoiesis. (A) Minerals: (i) Iron is essential element in the synthesis of hemoglobin (ii) Traces of copper and cobalt are also required in the synthesis.(B)Vitamins: The specific vitamins that are required in the maturation process are vitamin B12, folic acid and vitamin C. Folic acid and vitamin B12 are essential in the synthesis of nucleoprotein, particularly of erythropoietic cells. Vitamin B12 acts at an early stage in the synthesis of RNA but folic acid acts at a later stage in the synthesis of DNA. Thus, deficiency of Vitamin B12 results in defective synthesis of both RNA and DNA, while the deficiency of the folic acid results in defective synthesis of DNA only. Vitamin C is essential for conversion of folic acid to folinic acid.(C) Proteins: The proteins supply the amino acid for the synthesis of globin moiety. (D) Erythropoietin: The hormone is responsible for increase in red cells volume, by stimulating the stem cells in the bone marrow. Increased secretion of erythropoietin is brought about mostly by placental lactogen and also by progesterone. Erythropoietin is produced by the kidneys (90%) and the liver (10%)., Epidemiology:['prevalence of anemia in pregnancy is 42% worldwide', 'GOOD', 'To Do : IRON & FOLIC ACID SUPPLEMENTATION'], Complications:['heart failure', 'infection', 'pre eclampsia', 'Pulmonary Embolism', 'shock', 'UTERINE INERTIA'], Diagnostics:['serum Folic Acid', 'Hematocrit HCT', 'HISTOPATHLOGY', 'MCH', 'MCHC', 'MCV', 'SERUM IRON', 'TIBC', 'serum Vitamin B12 level', 'hemoglobin HB', 'Microcyte', 'SERUM FERRITIN LEVEL'], Differential diagnosis:['Bone marrow failure', 'enzyme deficiency', 'HEMOGLOBINEMIA', 'Hemolytic anemia', 'hemorrhage', 'INBORN ERRORS OF METABOLISM', 'Nutritional deficiencies'], disease description:Anemia is when you don’t have enough red blood cells to carry oxygen throughout your body. When your body doesn’t get enough oxygen from your blood, it can’t function properly. A person who has anemia during pregnancy is considered anemic.The red blood cells (RBCs) contain an important protein called hemoglobin. This protein holds oxygen and helps your red blood cells carry oxygen from your lungs to your body. It also helps carry carbon dioxide from your body to your lungs so you can breathe it out.. It’s common for women to become anemic during pregnancy because they don’t have enough iron and other vitamins.

A 52-year-old patient with ['fatigue', 'leg fatigue', 'tiredness', 'backache', 'PALENESS OF BODY', 'weakness', 'pica']

Disease Name: Anemia Of Chronic Disease, symptoms: ['fatigue', 'leg fatigue', 'tiredness', 'backache', 'PALENESS OF BODY', 'weakness', 'pica'], Treatment: ['Chronic anemia is managed predominantly in outpatient settings. They need hospitalization if:\n\nPatient is symptomatic\nThere is a significant drop in hemoglobin/HCT\nTransfusion is needed\nExtensive investigations are needed\nIf hemoglobin is less than 7 g/dL or if a patent is symptomatic, transfusion of packed red blood cells (PRBC) are indicated.\n\nTransfusions should be performed with caution in patients with volume overload status like end-stage renal disease (on hemodialysis) and congestive heart failure (CHF).\n\nOther treatments include treating underlying conditions as below.\n\nIron deficiency anemia: Intravenous (IV) iron versus oral iron\nVitamin B12 and folic acid deficiency with B12 and folic acid supplementation\nTreating underlying bone marrow disorders\nEPO injections in chronic kidney disease patients\nSynthroid in patients with hypothyroidism\nAvoiding any culprit medications\nTreatment of GI causes of blood loss (PPI for gastritis and PUD)\nRegulation of menstrual cycles in patients with menorrhagia\nAdmission if:\n\nThe patient has acute bleeding with hypovolemia, tachycardia and altered mental status\nPresence of pancytopenia\nNon-compliant patients or those who require extensive workup'], Pathophysiology: The conditions associated with ACD share features of acute or chronic immune activation, with immune mechanisms significantly contributing to the observed anaemia. Indeed, anaemias associated with other conditions such as heart failure, old age and obesity may also be caused, at least in part, by subtle proinflammatory changes. The low serum levels of iron usually seen in patients with ACD are now known to be mediated by the polypeptide hepcidin, which is produced in the liver and plays a key role in iron balance and transport. Production of hepcidin is increased by inflammatory cytokines, particularly interleukin (IL) 6, as well as in conditions of iron overload, whereas levels reduce in iron deficiency. Hepcidin acts by binding to ferroportin and blocking iron export from macrophages and hepatocytes. At the same time, iron absorption by duodenal enterocytes is downregulated. The combined effect is to produce a state of ‘functional iron deficiency’ (FID). In ACD, the normal response of increasing production of erythropoietin (EPO) in response to decreasing levels of haemoglobin (Hb) is blunted, possibly mediated through increased levels of IL-1 and tumour necrosis factor alpha (TNF-a). At the same time, EPO-induced proliferation and differentiation of early erythroid precursors is reduced. Finally, limited evidence supports a reduction in red cell survival in patients with ACD., Epidemiology:['consecutive hospitalized elderly patients with anemia, 70% of patients were found to have anemia of chronic disease.', '40% of children 6–59 months of age, 37% of pregnant women, and 30% of women 15–49 years of age worldwide are anaemic', 'variable', 'Anemia of chronic disease happens because you have a chronic illness that affects your red blood cell levels. You may not be able to prevent anemia, but you can help your overall health by eating a healthy diet that includes:\n\nLean protein including chicken, turkey and beans.\nDark leafy greens like spinach and kale.\nIron-fortified bread and cereal.\nVitamin supplements including B12, folate and iron.'], Complications:['angina', 'Arrhythmias', 'multiple-organ system failure', 'renal failure', 'cognitive impairment'], Diagnostics:['Complete Blood Count CBC', 'HISTOPATHLOGY', 'SERUM IRON'], Differential diagnosis:['blood disorder', 'Hemolytic anemia', 'infection', 'iron deficiency anemia', 'nephritis', 'sickle cell anemia', 'Thalassemia', 'Vitamin B12 deficiency'], disease description:Anemia of chronic disease (ACD), sometimes known as anemia of inflammation, is the second most common form of anemia worldwide and is seen in a variety of conditions, including cancer, autoimmune conditions and infections.

having ['chest pain', 'Dizziness', 'fatigue', 'headache', 'lethargy', 'weakness', 'shortness of breath'] at the age of 38

Disease Name: Anemia, symptoms: ['chest pain', 'Dizziness', 'fatigue', 'headache', 'lethargy', 'weakness', 'shortness of breath'], Treatment: [{'medication': ['Iron ']}, 'Iron-deficiency anemia: Iron supplements and dietary changes can help, and a doctor will identify and address the cause of any excessive bleeding if present.\nVitamin deficiency anemia: Treatments can include dietary supplements and vitamin B12 injections.\nThalassemia: Treatments includeTrusted Source folic acid supplements, iron chelation, and, for some people, blood transfusions and bone marrow transplants.\nAnemia due to chronic disease: The doctor will focus on managing the underlying condition.\nAplastic anemia: Treatment for aplastic anemia involves blood transfusions or bone marrow transplants.\nSickle cell anemia: Doctors treat this with oxygen therapy, pain relief medication, and intravenous fluids. They may also prescribe antibiotics, folic acid supplements, blood transfusions, and a cancer drug called hydroxyureaTrusted Source.\nHemolytic anemia: The treatment plan may include immunosuppressant drugs, treatments for infections, and plasmapheresis, which filters the blood.'], Pathophysiology: The pathophysiology of anemia varies greatly depending on the primary cause. For instance, in acute hemorrhagic anemia, it is the restoration of blood volume with intracellular and extracellular fluid that dilutes the remaining red blood cells (RBCs), which results in anemia. A proportionate reduction in both plasma and red cells results in falsely normal hemoglobin and hematocrit. RBC are produced in the bone marrow and released into circulation. Approximately 1% of RBC are removed from circulation per day. Imbalance in production to removal or destruction of RBC leads to anemia. The main mechanisms involved in anemia are listed below:1. Increased RBC destructionBlood lossAcute- hemorrhage, surgery, trauma, menorrhagiaChronic- heavy menstrual bleeding, chronic gastrointestinal blood losses [6] (in the setting of hookworm infestation, ulcers, etc.), urinary losses (BPH, renal carcinoma, schistosomiasis)Hemolytic anemiaAcquired- immune-mediated, infection, microangiopathic, blood transfusion-related, and secondary to hypersplenismHereditary- enzymopathies, disorders of hemoglobin (sickle cell), defects in red blood cell metabolism (G6PD deficiency, pyruvate kinase deficiency), defects in red blood cell membrane production (hereditary spherocytosis and elliptocytosis)2. Deficient/defective erythropoiesisMicrocyticNormocytic, normochromicMacrocytic, Epidemiology:['prevalence is more than 20% of individuals who are older than the age of 85', 'common disease affecting up to one-third of the global population', 'GOOD', 'You can’t prevent some kinds of anemia, such as sickle cell anemia, hemolytic anemia or aplastic anemia. People with chronic diseases who may develop anemia should watch for anemia symptoms. And you can prevent nutritional anemias by eating a healthy diet.'], Complications:['Arrhythmias', 'death', 'mental disturbances', 'Myocardial infarction', 'weakness'], Diagnostics:['Complete Blood Count CBC', 'Peripheral Blood Smear'], Differential diagnosis:['Adrenal crisis', 'HIV', 'Myxedema', 'renal failure', 'TUBERCULOSIS'], disease description:Anemia is described as a reduction in the proportion of the red blood cells. Anemia is not a diagnosis, but a presentation of an underlying condition. Whether or not a patient becomes symptomatic depends on the etiology of anemia, the acuity of onset, and the presence of other comorbidities, especially the presence of cardiovascular disease. Most patients experience some symptoms related to anemia when the hemoglobin drops below 7.0 g/dL.

Symptoms reported by a 34-year-old: ['Hypopituitarism', 'cleft palate', 'absence of cranial vault', 'angiomatous, brain tissue']

Disease Name: Anencephaly, symptoms: ['Hypopituitarism', 'cleft palate', 'absence of cranial vault', 'angiomatous, brain tissue'], Treatment: ['IF DETECTED BEFORE 20 WEEKS-TERMINATION TO BE DONE'], Pathophysiology: Folate is a coenzyme that facilitates the transfer of one-carbon units, which are then in various reactions, such as purine and pyrimidine synthesis, as well as methylation reactions. Folate deficiency is an important nutritional risk factor known to contribute to the development of the disease. A deficiency in folate can result from a variety of causesAnti-epileptic drugs (AEDs) are a known cause of NTDs. Use of AEDs, such as valproate, carbamazepine, and phenytoin, alters folate absorption, leading to decreased levels of folate in the blood. Of note, valproate is considered the most teratogenic AEDs, especially when combined with lamotrigine.Other folic acid antagonists include trimethoprim (an antibiotic used to treat infections, such as malaria), triamterene (a potassium-sparing diuretic), and aspirin (an over-the-counter anti-coagulant).Diabetes complicates pregnancies by increasing the risk of the fetus developing congenital birth defects (diabetic embryopathy). This complication is because high blood sugar causes dysfunction during organogenesis.The mechanism behind this is that hyperglycemia causes a disturbance in protein folding and promotes apoptosis in embryonic cells. The misfolded proteins aggregate and are unable to be degraded properly. The aggregates then accumulate in the cytosol and disrupt organelle function, leading to the creation of reactive oxygen species (ROS). Oxidative stress causes intracellular signaling to become disrupted, and cells are unable to function properly.Hyperthermia during the first trimester can alter anterior neural tube closure and correlates with anencephaly. Possible causes of hyperthermia in the mother include the use of saunas or hot tubs, exercising in an environment with increased temperatures, and febrile illness.Excess Vitamin A has shown to be teratogenic in pregnant rats due to decreased protein synthesis. Increases in Vitamin A prevent the anterior neural tube from closing, leading to the development of anencephaly or other NTDs., Epidemiology:['1 in 1,000 births', 'POOR', 'Although it isn’t always possible to prevent anencephaly, you may be able to reduce your chance of having a child with the condition. To lower your risk, you should:\n\n1. Get plenty of folic acid.\n2. Avoid certain medications. \n3. Stay out of saunas and hot tubs.\n4. Manage your health.'], Complications:['polyhydramnios', 'preterm labour', 'MALPRESENTATION', 'POST MATURITY'], Diagnostics:['HISTOPATHLOGY', 'USG'], Differential diagnosis:['microcephaly'], disease description:The anomaly results from deficient development of the vault of the skull and brain tissue, but the facial portion is normal. The pituitary gland is often absent or hypoplastic. Typically, there is marked diminution of the size of the adrenal glands probably secondary to the absence of the pituitary gland.

At the age of 43, symptoms like ['erythema', 'macules', 'NODULES', 'plaques', 'Urticarial rashes']

Disease Name: Anetoderma, symptoms: ['erythema', 'macules', 'NODULES', 'plaques', 'Urticarial rashes'], Treatment: [{'medication': ['Benzathine benzylpenicillin ']}, 'Established lesions can be excised for definitive treatment but will leave a permanent scar. Laser treatment may improve lesion appearance according to limited case reports\n\nOther treatments that have been used with no studied efficacy include cryotherapy, intralesional steroids, colchicine, hydroxychloroquine, vitamin E, oral penicillin G, epsilon-aminocaproic acid, aspirin, niacin, dapsone, and phenytoin.', 'Colchicine has been shown to prevent new primary anetoderma lesions from forming. In secondary anetoderma, controlling the causative dermatoses should theoretically prevent new lesions from forming.\n\nOther treatments that have been used with no studied efficacy include cryotherapy, intralesional steroids, colchicine, hydroxychloroquine, vitamin E, oral penicillin G, epsilon-aminocaproic acid, aspirin, niacin, dapsone, and phenytoin.'], Pathophysiology: The exact pathophysiology of anetoderma is not certain. In all types of anetoderma, there is a decrease in elastic tissue hypothesized to be from a decrease in the production of elastin, an increase in elastin degradation through an increase in elastolytic enzymes, a decrease in elastolytic enzyme inhibitors, or increased elastin phagocytosis. In penicillamine drug-induced anetoderma, aldol cross-linking is inhibited, which does not allow elastic fibers to develop normally. It has been hypothesized in anetoderma of prematurity that tissue hypoxia secondary to adhesive medical devices causes degradation of elastin by producing an increase in the expression of matrix metalloproteinases., Epidemiology:['. Cases have been reported from all age ranges, but it most commonly occurs in adults 20 to 40 years old. Anetoderma is more common in females than males and has not been found to have a racial predilection.', 'poor', 'Colchicine has been shown to prevent new primary anetoderma lesions from forming.\nTo date, no effective treatment is available for anetoderma. Therapeutic options that have been used but have not shown consistent results include intralesional steroids, as well as systemic penicillin G, aspirin, phenytoin, dapsone, vitamin E, and niacin. Anecdotal reports have described topical epsilon-aminocaproic acid (an antifibrinolytic) and oral colchicine as potential treatments to prevent the development of new lesions.'], Complications:['Abortion', 'Thrombotic complications', 'superficial phlebitis'], Diagnostics:['MRI', 'antiphospholipid antibodies'], Differential diagnosis:['Aquired cutis laxa', 'atrophic scars', 'Extragenital lichen sclerosus', 'Focal dermal hypoplasia'], disease description:The term anetoderma (anetos: slack) refers to a circumscribed area of slack skin associated with a loss of dermal substance on palpation and a loss of elastic tissue on histological examination. ‘Primary’ anetoderma implies that there is no associated localized underlying cutaneous disease, whereas ‘secondary’ anetoderma can be attributed to some associated condition

Person at 53 with manifestations like ['DEFORMITY', 'Pain', 'fracture']

Disease Name: Aneurysmal Bone Cyst, symptoms: ['DEFORMITY', 'Pain', 'fracture'], Treatment: ['The most common treatment for an aneurysmal bone cyst, this is an operation during which the cyst is scraped out of the bone with a special instrument called a curette that has a scoop, loop, or ring at its tip. The procedure itself is called curettage.\n\nThe remaining cavity is then packed with donor bone tissue (called an allograft), bone chips taken from another bone (autograft), or other materials.'], Pathophysiology: Researchers believe aneurysmal bone cysts to be due to a vascular malformation, with the definitive cause being unknown. The current thinking is that the vascular malformations lead to increased pressure and expansion in the bone itself, causing erosion and resorption of the involved bone. The majority of primary aneurysmal bone cysts lesions possess a t(16,17) gain-of-function translocation that upregulates the TRE17/USP6 oncogene, which halts osteoblastic maturation., Epidemiology:['1% to 6%', '0.14 per 10 people.', 'good', 'Since providers don’t know the exact cause of aneurysmal bone cysts, there’s no way to prevent them.'], Complications:['bleeding', 'infection', 'Pulmonary Embolism', 'osteomyelitis'], Diagnostics:['HISTOPATHLOGY', 'MRI', 'X RAY', 'CT SCAN'], Differential diagnosis:['Chondroblastoma', 'fibrous dysplasia', 'Giant cell tumour'], disease description:Aneurysmal bone cysts are non-malignant, tumor-like, vascular lesions that can grow aggressively, be locally destructive, and weaken bones to the point of pathologic fracture. They are more common in pediatric patients and can cause significant morbidity, especially if they involve the growth plate of bones. This activity reviews the evaluation and treatment of aneurysmal bone cysts and highlights the role of the an interprofessional healthcare team in evaluating and treating patients with this condition.

A 34-year-old individual dealing with ['balance disorder', 'developmental delay', 'movement disorders', 'delayed milestones', 'Ataxia', 'mid face hypoplasia', 'seizures', 'hypotonia', 'Sleep disturbances', 'tremor', 'hypotonia']

Disease Name: Angelman Syndrome, symptoms: ['balance disorder', 'developmental delay', 'movement disorders', 'delayed milestones', 'Ataxia', 'mid face hypoplasia', 'seizures', 'hypotonia', 'Sleep disturbances', 'tremor', 'hypotonia'], Treatment: ['Feeding Difficulties - Sucking might be ineffective, so breastfeeding is not possible sometimes. The use of special nipples is advised, monitoring weight gain and referral to specialized teams for advice and training on feeding.\nGastroesophageal Reflux - Administration of magnesium carbonate and aluminum hydroxide in upright .positioning.\nConstipation - Increased fluid intake. Jelly can be used as an alternative. A diet rich in fiber and laxatives can also be used.\nObesity - Regular checkup of weight and BMI. Also, regular exercise is advised.\nDiet -The ketogenic diet is helpful and is effective.The most effective drugs are sodium valproate, clonazepam, and phenobarbital'], Pathophysiology: The findings of Angelman syndrome (AS) are mostly limited to the nervous system because physiologically paternal UBE3A is only imprinted in the brain. So if there is a pathologic loss of function mutation of maternal UBE3A, mainly the brain is affected.UBE3A codes for a ubiquitin ligase called E6-associated protein (E6-AP). E6-AP is critical for the functioning of the ubiquitin-proteasome pathway, which is essential for the normal functioning of neurons and synaptic plasticity. Loss of function mutation of E6-AP causes impaired ubiquitin-proteasome degradation of many proteins. Many targets of E6-AP that have been identified are p53, p27, Arc, and ephexin5. P53 and p27 are crucial for the regulation of cell survival in the nervous system. Elevation of Arc levels increases the internalization of surface AMPA receptors causing impairment of post-synaptic excitatory transmission. Increased expression of ephexin5, which regulates synapse formation, caused decreased synapse formation. Together with increased levels of Arc and ephexin5 cause decreased experience-dependent synapse remodeling. This gives rise to neurologic deficits.Mouse models of AS with UBE3A knockout of the maternal gene have shown ataxia, seizures, decreased size of the brain, motor abnormalities. These models have also demonstrated deficits in hippocampal long term potentiation (LTP), which explains deficits in memory and learning in AS patients.Also, several of these experiments have shown abnormal dendritic morphology and decreased spine density. This might also explain the motor and cognitive deficits in AS.There are mainly four mechanisms that cause loss of function of UBE3A. These are deletion, mutation, imprinting, and uniparental disomy.The most severe symptoms are seen in the deletion subtype, out of which class 1 has the worst clinical phenotype. These include global developmental delay, microcephaly, and seizures, no speech, and oculocutaneous hypopigmentation. Increased susceptibility to seizures is seen since some of the GABA genes are deleted in deletion mutations. The deletion of OCA1 genes in combination with the regulatory effect of UBE3A on MC1R might explain oculocutaneous hypopigmentation, Epidemiology:['1 in 12,000 to 20,000 people', 'People with Angelman syndrome tend to live close t', 'Unfortunately, in most cases, there’s no way to prevent Angelman syndrome since it occurs as a result of spontaneous (random) genetic abnormalities while the fetus is developing in the uterus. In most cases, this happens without a known cause.\n\nA small percentage of people with Angelman syndrome inherit the condition. If you plan on having a biological child, talk with your healthcare provider about genetic testing to understand your risk of having a child with a genetic condition or a condition that can be caused by an inherited genetic mutation.'], Complications:['Ataxia', 'developmental delay', 'Seizure disorders'], Diagnostics:['EEG', 'GENETIC TESTING', 'CT/MRI', 'MRI'], Differential diagnosis:['Autism spectrum disorder', 'fragile x syndrome', 'Prader-Willi syndrome', 'RETT SYNDROME'], disease description:Angelman syndrome is a rare neurogenic disorder. It is a classic example of genomic imprinting, where the expression of a genomic region differs depending on the chromosome's parent of origin. AS is a neurodevelopmental disorder affecting mostly the nervous system that manifests with intellectual and developmental disabilities, a puppet-like ataxic movement and phenotype, as well as sleep disorders, and hyperactivity

Suffering from ['bleeding', 'anemia', 'brisk bleed'] at 37

Disease Name: Angiodysplasia, symptoms: ['bleeding', 'anemia', 'brisk bleed'], Treatment: ['Endoscopy or colonoscopy - If angiodysplasia is present on endoscopy or colonoscopy then different techniques can be used to treat angiodysplasia which is as follows \n\nArgon plasma coagulation ablation - Most commonly used intervention.High-frequency energy transmitted to tissues by ionized gas. It requires thorough bowel preparation to avoid a colonic gas explosion. It has comparatively more risk of bowel perforation in the upper GI tract.\nElectrocoagulation - Uses bipolar or heater probe coagulation. It is more suitable for the lower GI tract.\nEndoscopic clips and band ligation - These are mechanical methods to treat angiodysplasia. Band ligation is an option in the stomach and small bowel angiodysplasia treatment.\nInjection sclerotherapy - It includes injecting a sclerosant to obliterate angiodysplasia and other vascular lesions of the upper and lower GI tract. Commonly used sclerosants are ethanolamine or sodium tetradecyl sulfate. Endoscopic ligation, endoscopic resection, and photocoagulation are also some other techniques that are being used in the treatment of angiodysplasia endoscopically.', 'Incidental angiodysplasia- Incidental angiodysplasia should not have treatment if there is no history of GI bleeding or unexplained iron deficiency anemia. The future risk of incidental angiodysplasia-related bleeding is unknown, and the recommendation is based solely on expert opinions.\n\nNonbleeding angiodysplasia in a patient with GI bleeding - In these patients, angiodysplasia should have treatment, which again has its basis on expert opinions.\n\nActively bleeding angiodysplasia- In most patient’s management should follow a similar path as in managing upper and lower GI bleeding for other reasons, which is hemodynamic resuscitation, frequent complete blood count monitoring, and blood transfusion if needed. Treatment decisions should be dependent on hemodynamic stability and whether the patient is actively bleeding or not.\n\nHemodynamically unstable patient - In an unstable patient with active bleeding intravenous fluid resuscitation should be started immediately. If the patient is obtunded with a thready pulse, hypoxic, having active hematemesis, and unable to protect the airway, then they need to be intubated and admitted in the intensive care unit for frequent CBC monitoring and blood transfusion as required. An endoscopy or colonoscopy should be done if possible, but it may not be possible if the patient is actively bleeding. In that case, surgery or radiology intervention with angiography is usually required.\n\nHemodynamically stable patient - In patients with stable vitals, an endoscopy or colonoscopy should be done within 24 hours based on characteristics of bleeding. If the test reveals no identified source, then the next diagnostic modality is chosen on the fact whether the bleeding is active or not.\nAngiogenesis inhibitors - Thalidomide and bevacizumab have been described with success in the treatment of gastrointestinal vascular malformation, including angiodysplasia.\nHormone therapy - Few studies have evaluated treatment with estrogen with or without progesterone in chronic obscure GI bleeding.\nOctreotide – Octreotide seems to be effective in the treatment of refractory angiodysplasia related GI bleeding, as mentioned in some case series and meta-analysis. Octreotide with twice-daily subcutaneous injections with dose 50 to 100 mcg and long-acting form, octreotide-LAR, which is given intramuscularly once a month is an option.'], Pathophysiology: Histologically, it resembles telangiectasia and development is related to age and strain on the bowel wall. It is a degenerative lesion, acquired, probably resulting from chronic and intermittent contraction of the colon that is obstructing the venous drainage of the mucosa. As time goes by the veins become more and more tortuous, while the capillaries of the mucosa gradually dilate and precapillary sphincter becomes incompetent. Thus is formed an arteriovenous malformation characterized by a small tuft of dilated vessels. Although angiodysplasia is probably quite common, the risk of bleeding is increased in disorders of coagulation. A classic association is Heyde's syndrome (coincidence of aortic valve stenosis and bleeding from angiodysplasia) In this disorder, von Willebrand factor (vWF) is proteolysed due to high shear stress in the highly turbulent blood flow around the aortic valve. vWF is most active in vascular beds with high shear stress, including angiodysplasias, and deficiency of vWF increases the bleeding risk from such lesion., Epidemiology:['0.8% in healthy patients older than 50 years who are undergoing screening colonoscopy.', 'GOOD', 'There is no known prevention.'], Complications:['aortic stenosis', 'iron deficiency anemia', 'strictures'], Diagnostics:['Complete Blood Count CBC', 'HISTOPATHLOGY', 'SERUM IRON', 'colonoscopy', 'CT ANGIOGRAPHY', 'CT SCAN', 'ANGIOGRAPHY', 'TECHNETIUM 99'], Differential diagnosis:['colitis', 'colon cancer', 'Diverticulosis of colon', 'PEPTIC ULCER DISEASE'], disease description:Angiodysplasia is a vascular malformation that commonly causes haemorrhage from the colon in patients over the age of 60 years. The malformations consist of dilated tortuous submucosal veins.. Angiodysplasia is an abnormal, tortuous, dilated small blood vessel in the mucosal and submucosal layers of the GI tract. It is the most common vascular abnormality in the GI tract.

Symptoms at 53 years: ['Tenderness', 'Pain']

Disease Name: Angioleiomyoma, symptoms: ['Tenderness', 'Pain'], Treatment: ['Excision of an angioleiomyoma is simple and is the treatment of choice.'], Pathophysiology: Benign dermal / subcutaneous neoplasm arising in vascular smooth muscle; there is strong overlap with myopericytoma and these lesions are considered to be part of the same spectrum of disease.Histogenesis is uncertain.Minor trauma, venous stasis and hormonal changes, especially estrogen are usually implicated., Epidemiology:['angioleiomyoma has a female preponderance', 'roughly 5% among all soft tissue tumors', 'good', 'NA'], Complications:['post-surgical complications'], Diagnostics:['HISTOPATHLOGY', 'MRI', 'CT SCAN', 'USG', 'TECHNETIUM 99'], Differential diagnosis:['angiolipoma', 'Fibroma', 'Giant cell tumor of bone', 'Glomus tumour (and variants)', 'HEMANGIOMA', 'lipoma', 'Synovial sarcoma'], disease description:Angioleiomyoma is a rare, benign, smooth muscle tumor arising from the tunica media of veins and is seldom diagnosed before surgery. Angioleiomyoma can be found throughout the body but occurs most frequently in the lower extremities. It commonly arises in the dermis or subcutaneous tissue.Two types are described: isolated angiomyolipoma and angiomyolipoma that is associated with tuberous sclerosisRenal AML can be classified according to amount of fat as fat rich, fat poor, or fat invisible.

A 39-year-old with ['Tenderness', 'Skin discoloration', 'lump']

Disease Name: Angiolipoma, symptoms: ['Tenderness', 'Skin discoloration', 'lump'], Treatment: ['Ablation therapy: During ablation therapy, healthcare providers use energy (radiofrequency waves), heat or cold gas to destroy angiomyolipomas.\nArterial embolization: Your provider makes a small incision in your inner thigh and uses a thin tube (catheter) to insert tiny beads. These beads block blood flow to the angiomyolipoma to shrink it, reduce its blood flow and minimize the risk of bleeding.\nComplete nephrectomy: During a nephrectomy, surgeons remove the entire kidney that contains the angiomyolipoma.\nPartial nephrectomy: Surgeons remove the part of your kidney that contains the angiomyolipoma but not the entire kidney. You might have open partial nephrectomy or robotic partial nephrectomy.'], Pathophysiology: Angiolipomas are encapsulated. They consist of mature adipose tissue intermingled with a prominent vascular component usually more prominent in the periphery of tumour lobules. Some of the blood vessels contain fibrin thrombi. Cases with a prominent vascular component obscuring the adipocytic component have been termed ‘cellular angiolipomas’. Genetics  and cytogenetic studies have consistently shown no karyotypic abnormality. This is a unique finding in adipocytic tumours, which has given rise to arguments regarding its pathogenesis. It has been proposed that the lesion is primarily a vascular tumour and that it should be named lipoangioma., Epidemiology:['A male predominance is observed.', 'They are rare in children, the middle aged and the elderly.', 'good', 'Because healthcare providers don’t know what causes angiolipomas, it may not be possible to prevent them. However, you may lower your risk of developing angiolipomas by:\n\nAdopting healthy lifestyle habits that decrease your chances of getting diabetes.\nAvoiding minor, repetitive injuries.\nHaving surgery to remove angiolipomas completely so they don’t come back.'], Complications:['PELVIC HEMATOMA', 'Cystic degeneration', 'post-surgical complications'], Diagnostics:['biopsy', 'MRI', 'CT SCAN', 'ANGIOGRAPHY', 'PHYSICAL EXAMINATION'], Differential diagnosis:['Angioleiomyoma', 'HEMANGIOMA', 'lipoma', 'Liposarcoma', 'Spiradenoma'], disease description:Angiolipoma is a benign tumour composed of mature white adipose tissue admixed with a variable amount of thin-walled vessels.An angiolipoma is a small, benign, rubbery tumor that contains blood vessels and grows under your skin. Angiolipomas usually develop in young adults between the ages of 20 and 30. They most often appear in your forearms, and they can be painful if touched

A 20-year-old patient with ['fever', 'weight loss', 'anemia']

Disease Name: Angiomatoid Fibrous Histiocytoma, symptoms: ['fever', 'weight loss', 'anemia'], Treatment: ['If the tumor is located in an area that makes surgical removal challenging (such as your head or neck) — or if the tumor has spread to distant areas of your body — then chemotherapy or radiation therapy may be recommended.', 'Angiomatoid fibrous histiocytoma treatment usually involves surgical removal of the tumor.'], Pathophysiology: Histiocytomas develop when histiocytes (normal immune cells found in various parts of your body) grow rapidly and produce more histiocytes. AFH has been linked to genetics, inherited conditions and radiation treatment, but the exact cause is unknown.Angiomatoid fibrous histiocytomas generally occur in the dermis (skin) of your arms and legs. In extremely rare cases, AHF can develop in the somatic soft tissues, including your brain, lung, mediastinum (the part of your body that contains your heart and thymus gland) and omentum (the fold of tissue that connects your stomach to your other abdominal organs).Angiomatoid fibrous histiocytomas are often benign soft tissue tumors, meaning they’re noncancerous. But they can be malignant (cancerous) soft tissue tumors in some cases. When tumors are malignant, they might be called soft tissue sarcomas. Overall, AFH is considered a low-grade malignant tumor. This means there’s a low probability that it’ll spread to other parts of your body., Epidemiology:['It makes up approximately 0.3% of soft tissue tumors.', 'AFH is rare.', 'good', 'There’s no known way to prevent angiomatoid fibrous histiocytoma.'], Complications:['weakness', 'post-surgical complications'], Diagnostics:['MRI', 'NEEDLE BIOPSY', 'MICROSCOPIC EXAMINATION'], Differential diagnosis:['aneurysmal fibrous histiocytoma', 'Fibrosarcoma', 'hematomas', 'inflammatory myofibroblastic tumor'], disease description:Angiomatoid fibrous histiocytoma (AFH) is a rare type of soft tissue tumor. It commonly affects your extremities, such as your arms, legs, hands or feet.A histiocytoma is a tumor that contains normal immune cells (histiocytes) that have traveled from one area of your body to another. The term “angiomatoid” describes the vascular-like appearance of the tumor. “Fibrous” refers to the ropey, sinewy nature of the mass.

A 20-year-old individual dealing with ['bone pain', 'swelling', 'hyperpigmented macules']

Disease Name: Angiomatosis, symptoms: ['bone pain', 'swelling', 'hyperpigmented macules'], Treatment: ['Complete resection is preferred in local angiomatosis while radiotherapy or interferon a2a is the treatment of choice in extensive angiomatosis.'], Pathophysiology: Once Bartonella species are inoculated by blood-sucking arthropods or penetrate the skin after exposure to cat, the gram-negative bacteria attach themselves to a variety of host cells, which include erythrocytes, monocytes, macrophages, and dendritic cells. The endothelial cell is an important target for B. quintana but not so much for B. henselae. There are several mechanisms employed by Bartonella species to enter the host cells and are the result of complex interactions at the cell surface between the bacterial and host cell proteins. Therefore, Bartonella species are highly host-specific. First, adhesion of the bacteria to the host cell membrane is followed by uptake of groups of Bartonella in a vacuole by the host cell. In a second mechanism, bacteria accumulate on the host cell surface and induce self-phagocytosis. This process results in phagosome where Bartonella species must survive the harsh environment resisting enzymes of oxidative stress. Both are well-equipped to deal with intracellular oxidative stress and produce heat shock proteins. A third mechanism is specific for entry into the erythrocytes, which involves secretion of a protein called deformin. Deformin causes, invaginations of the erythrocyte membrane providing entry points for these bacteria which are adept at rearranging the cell cytoskeleton once they are attached to the cell surface. These bacteria are the carpenters of the bacterial world.[9]Bartonella is the only genus known to release factors that stimulate endothelial cells to produce angiopoietin-2 and epidermal production of vascular endothelial growth factor. BadA protein on the cell surface of B. henselae is responsible for adhesion to endothelial cells and fibronectin. BadA protein is responsible for promoting angiogenesis in B. henselae infections. BadA protein is also known to promote angiogenesis via inducible hypoxia factor-1 (IHF-1). Expression of outer membrane proteins (Vomp) is responsible for promoting vascular growth in the case of B. quintana.The ability to enter the erythrocytes protects these species from the host’s adaptive and innate immune response. The CD4 T-helper cells produce interferon gamma and TNF alpha, which are responsible for eliminating the bacteria. The Bartonella species are capable of attenuating the host immune response thereby establishing a chronic asymptomatic carrier state. An asymptomatic carrier state caused by B. quintana exemplifies this in homeless patients., Epidemiology:['2.5%', 'variable. Although the disorder is treatable and ', 'Prevention of bacillary angiomatosis associated with B henselae infection includes avoidance of contact with cats and control of flea infestations in cats.\n\nPreventive measures associated with B quintana infection are as follows:\n\nDelousing procedures, such as the use of permethrin dusting powder (1%; 30-50 g per adult)\n\nTreatment of clothing and bedding\n\nIn addition, macrolides for Mycobacterium avium-intracellulare prophylaxis in patients infected with HIV are protective against bacillary angiomatosis.'], Complications:['post-surgical complications'], Diagnostics:['X RAY', 'DOPPLER USG'], Differential diagnosis:['angiolipoma', 'epitheliod hemangioma', 'kaposi sarcoma', 'pyogenic granuloma'], disease description:Figure 1. A: Erythematous lesion on the front right leg with purpuric lesion. B: The back of the right leg. C: Leg ulceration progressed. D, E: Histopathologic examination demonstrates a diffuse proliferation of benign endothelial cells in the papillary and reticular dermis. There is scant formation of small vascular lumina with occasional extravasating erythrocytes and no evidence of cholesterol emboli or vasculitis (A and B, hematoxylin–eosin stain; original magnification: A, 40×; B, 400×). F: Positive immunohistochemical staining using anti-CD31 antibody confirBacillary angiomatosis (epithelioid angiomatosis) is an uncommon disease characterized by neovascular proliferation in the skin or the internal organs (peliosis) due to an infection with Bartonella henselae or Bartonella quintana. It commonly occurs in immunocompromised as well as immunocompetent patients. 

A 30-year-old with ['abdominal distension', 'diarrhea', 'nausea', 'Rashes', 'vomiting', 'blood in stool', 'itching', 'Abdominal Pain', 'mucus in stool']

Disease Name: Angiomyofibroblastoma, symptoms: ['abdominal distension', 'diarrhea', 'nausea', 'Rashes', 'vomiting', 'blood in stool', 'itching', 'Abdominal Pain', 'mucus in stool'], Treatment: [{'medication': ['Oxytetracycline ']}, 'Treatment is by surgical excision'], Pathophysiology: Its pathogenesis is uncertain; may arise from subepithelial stroma or a perivascular stem cell., Epidemiology:['Only about 70 cases of vulvar AMFB have been reported in women outside China.', 'good'], Complications:['allergic reaction', 'intestinal perforation'], Diagnostics:['HISTOPATHLOGY', 'Color Doppler', 'MRI', 'USG'], Differential diagnosis:['Cellular angiofibroma', 'GASTROINTESTINAL STROMAL TUMORS', 'lipoma'], disease description:Angiomyofibroblastoma is a rare mesenchymal benign tumor that frequently occurs in young- to middle-aged women, arising from the genital tract. There are many overlapping radiological and immunohistochemical features with other stromal cell lesions, making the diagnosis difficult.

A 22-year-old patient experiencing ['renal failure', 'urinary tract infections', 'palpable mass', 'flank pain', 'hematuria', 'anemia']

Disease Name: Angiomyolipoma, symptoms: ['renal failure', 'urinary tract infections', 'palpable mass', 'flank pain', 'hematuria', 'anemia'], Treatment: ['Arterial embolization: Your provider makes a small incision in your inner thigh and uses a thin tube (catheter) to insert tiny beads. These beads block blood flow to the angiomyolipoma to shrink it, reduce its blood flow and minimize the risk of bleeding.', 'Ablation therapy: During ablation therapy, healthcare providers use energy (radiofrequency waves), heat or cold gas to destroy angiomyolipomas.', 'Complete nephrectomy: During a nephrectomy, surgeons remove the entire kidney that contains the angiomyolipoma.\nPartial nephrectomy: Surgeons remove the part of your kidney that contains the angiomyolipoma but not the entire kidney. You might have open partial nephrectomy or robotic partial nephrectomy.', 'Excision'], Pathophysiology: Renal angiomyolipoma is caused by a genetic mutation to the TSC1 or TSC2 gene (tumor suppressor genes). They are responsible for producing tuberin, a protein that helps control cells’ growth and size. When the TSC genes mutate or change, it affects the production of tuberin, and cells may grow out of control.There are three types of AML kidney, based on the type of cells and tissue the tumor contains:Classic (triphasic) AMLs: Most angiomyolipomas (AMLs) contain three types of tissue — blood vessels, fat and smooth muscle tissue.Monophasic AMLs: Some AMLs contain almost all of one type of tissue, such as smooth muscle or fat.Epithelioid angiomyolipomas: These angiomyolipomas are mostly made up of cells that line your kidney’s blood vessels (epithelioid cells). These tumors may be more likely to become cancer., Epidemiology:['67% for patients with TSC', '4.6%', 'variable', 'There are no strategies to prevent the genetic mutations that lead to renal angiomyolipoma.\n\nBut if you have certain other medical conditions, you should have imaging tests regularly to catch AML early:\n\nLymphangioleiomyomatosis.\nNeurofibromatosis type 1.\nTuberous sclerosis complex.\nvon Hippel-Lindau disease.'], Complications:['skin problem', 'Neurological symptoms', 'cognitive impairment'], Diagnostics:['MRI', 'CT SCAN'], Differential diagnosis:['Oncocytoma', 'Renal cell carcinoma', 'WILMS TUMOR'], disease description:Angiomyolipoma is a condition in which benign tumors form in your kidney. You may have no symptoms, or you may have anemia, fever, pain or high blood pressure. Tumors that grow may need treatment such as embolization or surgery to reduce the risk of bleeding.

Individual, 23 years old, with ['bruise on skin', 'swelling']

Disease Name: Angiosarcoma Of Soft Tissue, symptoms: ['bruise on skin', 'swelling'], Treatment: ['Metastatic disease: Metastatic disease is treated with chemotherapy. Cytotoxic agents, targeted therapy, and Immune checkpoint inhibitors are being explored in treating metastatic disease. \nCytotoxic chemotherapy- anthracycline-based regimens are usually the first line of treatment in a patient with any STS. However, in patients with AS, paclitaxel is an effective drug with comparable response rates to anthracyclines.\nAnthracyclines- In patients with STS, the response rate is between 16-36%. In most cases, a combination with another drug, ifosfamide, certainly increases toxicity but may not benefit the outcome. Liposomal doxorubicin has also shown therapeutic responses in patients with AS.\nTaxanes: The antiangiogenic properties of taxanes make them useful in patients with AS. After numerous retrospective studies reporting benefits in AS, a small phase II prospective study (ANGIOTAX study) showed an ORR of 17%. However, two of the five patients with responses underwent surgery and achieved a complete pathological response.Since then, multiple studies have confirmed the activity of weekly paclitaxel in patients with AS.Paclitaxel is administered as 80mg/m2 on days 1, 8, 15 of a 28-day cycle.\nOther cytotoxic drugs like Ifosfamdie, Gemcitabine, Cisplatin are also active in patients with AS; however, they are usually not used as the first line of treatment.\nTargeted therapy\nAnti-VEGF molecule- Since AS is a malignancy arising from vascular endothelium, anti-VEGF therapy, particularly bevacizumab, gained a lot of attention for metastatic AS. However, a prospective phase II study failed to show any benefit.\nTyrosine Kinase inhibitors (TKI)- Several TKI (Sorafenib, Pazopanib, Axitinib, and regorafenib) have been tested in patients with AS. The drugs mainly target either VEGF or PDGFRA, which are critical to the growth of AS. Unfortunately, none of these drugs showed a beneficial response, despite clinical activity in patients with AS.\nImmune checkpoint inhibitors (ICI). \nRecent data suggest that ICI may be active in patients with AS. This is yet to be tested in a prospective trial.', 'Non-metastatic disease:\nLocal surgery with R0 resection is the treatment of choice.', 'Recently used in unresectable tumors,', 'Surgical resection is the main treatment modality, in addition to chemotherapy and radiotherapy'], Pathophysiology: Upregulation of vascular specific receptor tyrosine kinases, including TIE1, KDR, TEK and FLT.Angiosarcoma happens when the cells in the inner lining of your blood vessels change from normal to abnormal cells. Unlike normal cells, the abnormal cells don’t die but continue to churn out abnormal cells that eventually become masses or tumors. The abnormal cells keep on growing from your affected blood vessels, sometimes spreading to other areas of your body.Researchers believe these tumors start forming when something changes in your blood vessel and/or lymph vessels’ genetic code. They’ve also identified several risk factors that may increase the chance you’ll develop angiosarcoma. Those risk factors are:Having radiation therapy, particularly if you received radiation therapy for breast cancer. Researchers believe there’s a link between radiation therapy and angiosarcoma that can develop many years after you’ve received radiation therapy.Being exposed to chemicals, including polyvinyl chloride, arsenic and thorium dioxide.Having chronic lymphedema. Approximately 5% of all angiosarcomas are linked to a form of chronic lymphedema called Stewart-Treves syndrome.Familial syndromes. About 3% of all angiosarcomas affect people who have conditions caused by genetic disorders., Epidemiology:['Angiosarcomas make up about 1% to 2% of all sarcomas. They are most common in people over the age of 70 but can happen at any age', 'Around 2% of soft tissue sarcomas in general and 5.4% of cutaneous soft tissue sarcomas are angiosarcomas .', 'bad', 'Researchers have identified several activities and medical conditions that might increase your risks for developing angiosarcoma. For example, you may reduce your risk by protecting your skin from the sun and limiting your exposure to certain chemicals. Some risk factors you can’t avoid, such as inheriting a genetic condition or needing radiation therapy for cancer.'], Complications:['thrombocytopenia', 'Skin ulceration'], Diagnostics:['PET SCAN', 'CT SCAN', 'CT SCAN', 'immunohistochemistry', 'immunohistochemistry', 'Histopathological examination', 'molecular testing'], Differential diagnosis:['benign hemangioma', 'EPITHELIOID HEMANGIOENDOTHELIOMA', 'kaposi sarcoma', 'Metastatic tumours'], disease description:Angiosarcoma is a malignant neoplasm showing morphological or immunophenotypic evidence of endothelial differentiation. Because angiosarcoma arises from your blood vessels, you can develop an angiosarcoma almost anywhere in your body. That said, angiosarcoma most commonly affects your skin, breasts, liver or head and neck.

Individual aged 32 dealing with ['Excoriation of the skin around the angles', 'eyes irritation', 'collection of dirty-white foamy discharge at the angles', 'Redness in the angles of eyes', 'Hyperaemia of bulbar conjunctiva', 'Foamy mucopurulent discharge', 'ocular discomfort', 'burning sensation in eyes']

Disease Name: Angular Bacterial Conjunctivitis, symptoms: ['Excoriation of the skin around the angles', 'eyes irritation', 'collection of dirty-white foamy discharge at the angles', 'Redness in the angles of eyes', 'Hyperaemia of bulbar conjunctiva', 'Foamy mucopurulent discharge', 'ocular discomfort', 'burning sensation in eyes'], Treatment: [{'medication': ['Oxytetracycline ']}, 'A. Prophylaxis includes treatment of associated nasal\ninfection and good personal hygiene.\nB. Curative treatment consists of:\n1. Oxytetracycline (1%) eye ointment, 2–3 times a day\nfor 9–14 days will eradicate the infection.\n2. Zinc lotion instilled in day time and zinc oxide\nointment at bed time inhibits the proteolytic\nferment and thus helps in reducing the\nmaceration.'], Pathophysiology: The causative organism, i.e., MA bacillus produces a proteolytic enzyme which acts by macerating the epithelium. This proteolytic enzyme collects at the angles by the action of tears and thus macerates the epithelium of the conjunctiva, lid margin and the skin, the surrounding angles of eye. The maceration is followed by vascular and cellular responses in the form of mild grade chronic inflammation. Skin may show eczematous changes. Direct transmission of pathogens onto the conjunctiva leads to infectious conjunctivitis. Conjunctivitis can occur when the epithelial layer of the eye is compromised, or there is disruption in overall defense mechanisms. An immunocompromised state may also predispose to bacterial conjunctivitis, Epidemiology:['135 cases per 10,000 population annually, constituting approximately 1% of all primary care consultations.07-Feb-2023', 'GOOD', 'Avoid touching or rubbing your eyes. This can worsen the condition or spread it to your other eye.\nWith clean hands, wash any discharge from around your eye(s) several times a day using a clean, wet washcloth or fresh cotton ball. Throw away cotton balls after use, and wash used washcloths with hot water and detergent, then wash your hands again with soap and warm water.\nClean eyeglasses, being careful not to contaminate items (like hand towels) that might be shared by other people.'], Complications:['blindness', 'Corneal perforation', 'corneal ulceration'], Diagnostics:['Gram Staining', 'fluid microbiological culture', 'PCR', 'PHYSICAL EXAMINATION'], Differential diagnosis:['ACUTE IRIDOCYCLITIS', 'allergic rhinitis', 'blepharitis', 'CHALAZION', 'dry eye syndrome', 'KERATITIS', 'VIRAL CONJUNCTIVITIS'], disease description:Conjunctivitis, also informally known as "pink eye," makes up the majority of ophthalmologic disorders seen at primary care clinics. Patients present complaining of eye redness, which may or may not be accompanied by pain, itching, and discharge. Dilation of conjunctival blood vessels secondary to viral or bacterial infection, chemical exposures, or allergies results in the redness seen on the examination, While viral and allergic conjunctivitis occurs more frequently, bacterial conjunctivitis is responsible for increased morbidity and provides a more challenging clinical scenario for physicians

Symptoms at 39 years: ['erythema', 'Skin fissures', 'oedema']

Disease Name: Angular Cheilitis, symptoms: ['erythema', 'Skin fissures', 'oedema'], Treatment: [{'medication': ['Miconazole']}, 'Dentures should be removed from the mouth at night and stored in \na candidacidal solution such as hypochlorite. Denture-related sto\x02matitis should be treated with an antifungal. Miconazole may be \npreferable treatment for candidosis (cream applied locally, together \nwith the oral gel) as it has some Gram-positive bacteriostatic action.'], Pathophysiology: Predisposing factors Most cases are due to mechanical and/or infective causes or dry mouth but nutritional or immune defects are also causes. • Infective agents are the major cause. • Immune deficiency , such as diabetes and HIV infection, may present with angular stomatitis. Outbreaks of acute pustular and fissured cheilitis may occur in children, particularly if they are malnourished, and in some cases streptococci or staphylococci have appeared to be causative. • Mechanical factors in edentulous patients who do not wear a denture or who have inadequate dentures, and also as a normal consequence of the ageing process, produce an oblique curved fold and keep the small area of skin constantly macerated. The recurrent trauma of dental fl ossing is a very rare cause of angular cheilitis. • Nutritional defi ciencies , particularly defi ciencies of ribofl avin, folate, iron and general protein malnutrition, may produce smooth shiny red lips associated with angular stomatitis, a combination called cheilosis. Crohn disease or orofacial granulomatosis may be found in some. • Hyposalivation , such as after drug therapy, irradiation or in Sjögren syndrome may predispose. Pathology Infl ammation. Causative organisms Candida and/or staphylococci are isolated from most patients , especially if there is HIV infection. Permanent cure can be achieved only by eliminating the Candida beneath the upper denture . Candidosis was probably responsible for some of the cases of cheilitis attributed to allergy to denture materials, since contamination of denture material by Candida may cause false-positive patch- test reactions. Agents causing hyposalivation (e.g. irradiation, chemotherapy or anticholinergic drugs) can predispose to infections., Epidemiology:['Common.', 'Common.'], Complications:['Denture-related stomatitis'], Diagnostics:nan, Differential diagnosis:[], disease description:Angular cheilitis is a common skin condition affecting the corners of your mouth. It leads to painful, cracked sores. People often confuse angular cheilitis with cold sores. Unlike cold sores, angular cheilitis isn’t contagious. This condition usually goes away with special skin ointments, medication or diet changes.

Symptoms at 44 years old: ['plaques', 'cracking at angle of mouth']

Disease Name: Angular Stomatitis, symptoms: ['plaques', 'cracking at angle of mouth'], Treatment: ['Fungicidal Medications\n\nFungal infections require topical fungicidal medications applied to the labial commissures, usually 3 times daily for 2 weeks.\n\nNystatin 100,000 units/mL ointment topically twice per day (BID)\nGentian violet solution topically BID to 3 times per day (TID) is effective in children if a purple discoloration is acceptable\nKetoconazole 2% cream topically\nClotrimazole 1% cream topically\nMiconazole 2% cream topically (with or without hydrocortisone 1%): Mixed staphylococcal and candidal infections respond best to this treatment because of its inherent gram-positive bacteriostatic activity, thus being used as first-line treatment by some providers\nIodoquinol 1% cream topically BID to TID, usually combined with hydrocortisone 1% cream'], Pathophysiology: Most cases of angular cheilitis (AC) are ultimately due to physical maceration at the angular commissures due to overexposure to saliva. The digestive enzymes in saliva can act even on body tissues if allowed prolonged contact. Continued saliva exposure induces contact dermatitis and eczematous reaction at the commissures. The compromised integrity of the stratum corneum epithelium allows local commensal organisms to infect the area. Frequently, colonizing Candida albicans establishes and invades the susceptible tissue. This may then allow bacterial superinfection with staph and strep species. Thus, risk factors are those that increase saliva retention at the commissures, increase exposure to culprit microbes, cause direct tissue inflammation, or inhibit wound healing and immunity. Non-infectious causes of AC are further discussed in the etiology section., Epidemiology:['To Do : Dental\n\nA dentist should refit ill-fitting dentures or other dental apparati to restore facial contour. As the functional reservoir of Candida, treat dentures with an antifungal and cleaned frequently. In chronically debilitated patients, a cannula incorporated into the dentures can channel salivary flow into the oropharynx.\n\nSometimes, malocclusion persists despite dental realignment or is not a viable option for a patient. Other times, depressions at the commissures exist and are amenable to dermal filler therapy. Injectable fillers (collagen, hyaluronic acid) or surgical implants can change mouth shape and restore commissural anatomy. This makes saliva less likely to accumulate at the fissures. A practitioner who is well-versed in the administration of fillers should apply these fillers since the purpose is beyond the normal cosmetic application. Not To Do : Elimination of Behavioral Practices that Contribute to AC\n\nTobacco smoking\nLip licking'], Complications:['atrophy'], Diagnostics:nan, Differential diagnosis:['Atopic dermatitis', 'seborrhoeic dermatitis'], disease description:Angular stomatitis describes an inflammatory skin process of variable etiology occurring at the labial commissure, the angle of the mouth.

Person at 31 with manifestations like ['mucus in stool', 'abdominal distension', 'diarrhea', 'nausea', 'Rashes', 'vomiting', 'blood in stool', 'itching', 'Abdominal Pain']

Disease Name: Anisakiasis, symptoms: ['mucus in stool', 'abdominal distension', 'diarrhea', 'nausea', 'Rashes', 'vomiting', 'blood in stool', 'itching', 'Abdominal Pain'], Treatment: ['Endoscopic removal of the larvae\nPossibly albendazole\nEndoscopic removal of the larvae is curative.', 'Treatment of presumptive anisakiasis with albendazole 400 mg orally twice a day for 6 to 21 days may be effective'], Pathophysiology: Anisakis species have complex life cycles which pass through a number of hosts through the course of their lives. Eggs hatch in seawater, and larvae are eaten by crustaceans, usually euphausids. The infected crustaceans are subsequently eaten by fish or squid, and the nematodes burrow into the wall of the gut and encyst in a protective coat, usually on the outside of the visceral organs, but occasionally in the muscle or beneath the skin. The life cycle is completed when an infected fish is eaten by a marine mammal, such as a whale, seal, sea lion, dolphin or another animal like a seabird or shark. The nematode excysts in the intestine, feeds, grows, mates, and releases eggs into the seawater in the host's feces. As the gut of a marine mammal is functionally very similar to that of a human, Anisakis species are able to infect humans who eat raw or undercooked fish.Anisakiasis is a human parasitic infection of the gastrointestinal tract caused by the consumption of raw or undercooked seafood containing larvae of the nematode Anisakis simplex. The first case of human infection by a member of the family Anisakidae was reported in the Netherlands by Van Thiel, who described the presence of a marine nematode in a patient suffering from acute abdominal pain. It is frequently reported in areas of the world where fish is consumed raw, lightly pickled, or salted.Within a few hours of ingestion, the parasitic worm tries to burrow though the intestinal wall, but since it cannot penetrate it, it gets stuck and dies. The presence of the parasite triggers an immune response; immune cells surround the worms, forming a ball-like structure that can block the digestive system, causing severe abdominal pain, malnutrition, and vomiting. Occasionally, the larvae are regurgitated. If the larvae pass into the bowel or large intestine, a severe eosinophilic granulomatous response may also occur one to two weeks following infection, causing symptoms mimicking Crohn's disease ., Epidemiology:['d between 18 and 20 cases per 100,000 inhabitants/year for method 2 and method 1, respectively.', 'good', 'Do not eat raw or undercooked fish or squid.\n\nThe FDA recommends the following for seafood preparation or storage to kill parasites.\n\nCooking (Seafood in General)\nCook seafood adequately (to an internal temperature of at least 145° F [~63° C]).\nFreezing (Fish)\nAt -4°F (-20°C) or below for 7 days (total time), or\nAt -31°F (-35°C) or below until solid, and storing at -31°F (-35°C) or below for 15 hours, or\nAt -31°F (-35°C) or below until solid and storing at -4°F (-20°C) or below for 24 hours.'], Complications:['abscess', 'allergic reaction', 'intestinal perforation', 'small bowel obstruction'], Diagnostics:['ENDOSCOPY', 'CT SCAN'], Differential diagnosis:['appendicitis', 'DUODENAL ULCER', 'gastric ulcer', 'gastroenteritis', 'INFLAMMATORY BOWEL DISEASES', 'PEPTIC ULCER DISEASE', 'TUBERCULOSIS'], disease description:Anisakis is a genus of parasitic nematodes that have life cycles involving fish and marine mammals. They are infective to humans and cause anisakiasis. People who produce immunoglobulin E in response to this parasite may subsequently have an allergic reaction, including anaphylaxis, after eating fish infected with Anisakis species.A history of eating undercooked fish or squid is helpful for diagnosis.

Symptoms at 20 years: ['diplopia', 'Asthenopia (tiredness of eyes relieved by closing the eyes)', 'ANISOMETROPIA', 'Difficulty in depth perception']

Disease Name: Aniseikonia, symptoms: ['diplopia', 'Asthenopia (tiredness of eyes relieved by closing the eyes)', 'ANISOMETROPIA', 'Difficulty in depth perception'], Treatment: ['1. Optical aniseikonia may be corrected by aniseikonic\nglasses, contact lenses or intraocular lenses or other\nrefractive surgery depending upon the situation.\n2. Retinal aniseikonia may be corrected by treating\nthe cause.\n3. Cortical aniseikonia is very difficult to treat.'], Pathophysiology: Pathophysiologically,1. Optical aniseikonia may occur due to either inherent or acquired anisometropia of high degree. 2. Retinal aniseikonia may develop due to: displacement of retinal elements towards the nodal point in one eye due to stretching or oedema of the retina. 3. Cortical aniseikonia implies asymmetrical simultaneous perception inspite of equal size of images formed on the two retinae. Clinical types Clinically, aniseikonia may be of different types: 1. Symmetrical aniseikonia a. Spherical, image may be magnified or minified equally in both meridians. b. Cylindrical, image is magnified or minified symmetrically in one meridian. 2. Asymmetrical aniseikonia a. Prismatic. In this image, difference increases progressively in one direction. b. Pincushion. In this image, distortion increases progressively in both directions, as seen with high plus correction in aphakia. c. Barrel distortion. In this image, distortion decreases progressively in both directions, as seen with high minus correction. d. Oblique distortion. In this, the size of image is same, but there occurs an oblique distortion of shape., Epidemiology:['5-10% of the population above the age of twenty', 'good', 'prevent the measurement of aniseikonia, as most common techniques require direct comparisons of images seen by each eye.'], Complications:['amblyopia', 'Visual impairment', 'Strabismus', 'Asthenopia (tiredness of eyes relieved by closing the eyes)'], Diagnostics:['RETINOSCOPY', 'autorefractometry', 'Eikonometry'], Differential diagnosis:['ANISOMETROPIA', 'hallucinations', 'Intermittent diplopia'], disease description:Aniseikonia at a young age can result in amblyopia .Aniseikonia at a later age can cause asthenopia, headache, diplopia, dizziness, nervousness, imbalance, nausea, spectacle intolerance, ocular suppression, and distorted space perception. It is thought that over 0.75% of aniseikonia can start to cause symptoms, that at 1 to 3% definite symptoms are present, and that more than 5% of aniseikonia is incompatible with binocular vision.

At 18 years old, experiencing ['Alternate vision occurs when one eye is hypermetropic and the other myopic', 'physical signs']

Disease Name: Anisometropia, symptoms: ['Alternate vision occurs when one eye is hypermetropic and the other myopic', 'physical signs'], Treatment: ['1. Spectacles. The corrective spectacles can be\ntolerated up to a maximum difference of 4D. After\nthat there occurs diplopia.\n2. Contact lenses are advised for higher degrees of\nanisometropia.\n3. Aniseikonic glasses are also available, but their\nclinical results are often disappointing.\n4. Other modalities of treatment include:\n• Intraocular lens–implantation for uniocular\naphakia.', '• Refractive corneal surgery for unilateral high\nmyopia, astigmatism and hypermetropia.\n• Phakic Refractive Lenses (PRL) and Refractive\nLens Exchange (RLE) are quite useful in very high\ndegree anisometropia.'], Pathophysiology: Age-related ocular changes, such as cataracts, can lead to refractive changes due to refraction index alteration associated with lens opacification. The asymmetric occurrence of this phenomenon can cause anisometropia in the older population, whereas most of the anisometropia in younger subjects are attributed to the difference in axial length. Despite the documented association between anisometropia and interocular axial length growth asymmetries, evidence on the exact mechanism correlating these two conditions are lacking. A significant reduction in the visual input in one eye due to evident structural abnormalities, such as congenital cataracts, ptosis, or retinal alterations, like in prematurity, can induce axial elongation, but other mechanisms must be involved in the absence of evident structural alterations Anisometropia is often, but not always, associated with amblyopia. These two conditions are commonly found during school vision screening., Epidemiology:['The prevalence of anisometropia is 0 to 28%', 'GOOD', 'There’s currently no way to prevent refractive errors.'], Complications:['amblyopia'], Diagnostics:['RETINOSCOPY', 'autorefractometry', 'Maddox rod test', 'Cover tests'], Differential diagnosis:['cataracts', 'IMMATURE CATARACT'], disease description:Anisometropia is a condition of asymmetric refraction between the two eyes. This condition is defined by a difference of 1 or more diopter in spherical equivalent. Its diagnosis and treatment in the first years of life are essential to optimize children's visual development and binocular function. Anisometropia is a condition of refractive interocular asymmetry and is usually referred only to as the clinically significant differences between the right and the left eye. According to studies conducted in different regions, the incidence of this common refractive abnormality ranges from 3.79% to 21.8% ,A difference of 1 diopter or more in spherical equivalent (SE) is usually reported to define this condition.

Symptoms at 51 years: ['ptosis', 'squint', 'ocular cyst', 'eyelid excursion']

Disease Name: Ankyloblepharon, symptoms: ['ptosis', 'squint', 'ocular cyst', 'eyelid excursion'], Treatment: [{'medication': ['Imiquimod ', 'Podophyllum resin/Podophyllum']}, 'Lids should be separated by excision of adhesions between the lid margins and kept apart during the healing process. When adhesions extend to the angles, epithelial grafts should be given to prevent recurrences.['], Pathophysiology: Congenital ankyloblepharonDuring fetal development, eyelid margins remain fused until the fifth gestational month, and may not be completely separated until the seventh month of gestation. Congenital ankyloblepharon occurs when the lid margins fail to separate at birth. The exact etiology of this condition is unknown. The currently accepted theory is that this condition is due to temporary epithelial arrest and rapid mesenchymal proliferation, allowing union of eyelids at abnormal positions.Acquired ankyloblepharonAcquired ankyloblepharon may occur due to trauma or inflammatory conditions. It may be associated with symblepharon also. The following conditions cause ankyloblepharon:[3]Chemical burns, thermal burns, or trauma to the eyesCicatrising diseases such as Stevens–Johnson syndrome or cicatricial ocular pemphigoidInflammatory diseases such as herpes simplex infection or ulcerative blepharitisTrachomaCicatricial conjunctivitisMucous membrane pemphigoid: ocular form of mucous membrane pemphigoid may cause ankyloblepharon (4th stage of foster grading system)., Epidemiology:['1 in 70,000 newborns worldwide.', 'good', 'Detailed systemic assessment by an experienced pediatrician is essential to rule out coexisting pathology and proper management of congenital ankyloblepharon.'], Complications:['amblyopia'], Diagnostics:['PCR'], Differential diagnosis:['Lymphogranuloma Venereum', 'Symblepharon', 'Verrucous carcinoma'], disease description:Ankyloblepharon describes direct fusion of the lids. It is a rare congenital abnormality, in which single or multiple strands of fine connective tissue join the upper and lower lids anywhere along the lid but never at the lateral or medial canthus . These strands are extensible, and by forcibly opening the lids their length can be almost doubled. The tissue invariably arises from the grey line, anterior to the meibomian gland orifices and posterior the cilia?

Suffering from ['non protuded tongue', 'Speech Difficulties', 'DEFECTIVE SPEECH'] at 37

Disease Name: Ankylogossia, symptoms: ['non protuded tongue', 'Speech Difficulties', 'DEFECTIVE SPEECH'], Treatment: ["Frenotomy:\n\nA simple surgical procedure called a frenotomy can be done with or without anesthesia in the hospital nursery or doctor's office.\n\nThe doctor examines the lingual frenulum and then uses sterile scissors to snip the frenulum free. The procedure is quick and discomfort is minimal since there are few nerve endings or blood vessels in the lingual frenulum.\n\nIf any bleeding occurs, it's likely to be only a drop or two of blood. After the procedure, a baby can breast-feed immediately.\n\n\nA more extensive procedure known as a frenuloplasty might be recommended if additional repair is needed or the lingual frenulum is too thick for a frenotomy.\n\nFRENULOPLASTY:\nA frenuloplasty is done under general anesthesia with surgical tools. After the frenulum is released, the wound is usually closed with sutures that absorb on their own as the tongue heals."], Pathophysiology: There is no standard definition of ankyloglossia, and multiple classifications exist. When examined, the ‘free tongue’ length in newborns should be greater than 16 mm. Measurements of less than 11 mm indicate moderate ankyloglossia and less than 7 mm indicates severe ankyloglossia. However, this measurement may not be useful in infants. The term posterior ankyloglossia is used when the frenulum is attached at the middle to the posterior aspect of the undersurface of the tongue. Taking into consideration the anatomy and function, there are many assessment tools for classification.One of them is the Hazelbaker Assessment for Lingual Frenulum Function. This tool uses a scoring system using anatomy and function.Anatomy: Appearance of tongue when lifted, elasticity of frenulum, length of lingual frenulum when tongue lifted, attachment of lingual frenulum to tongue and attachment of lingual frenulum to inferior alveolar ridgeFunction: Lateralization, lift of tongue, extension of the tongue, spread, cupping of tongue, peristalsis, snap-backIt consists of 10 points for frenulum appearance and 14 points for tongue function., Epidemiology:['The incidence of ankyloglossia in the newborn well-baby population is 4.8%', 'GOOD', 'Since people are born with tongue-tie, there’s no way to prevent it. For more severe cases of tongue-tie, early diagnosis and treatment are key to a successful recovery.'], Complications:['Speech Difficulties', 'poor oral nutrition'], Diagnostics:['PHYSICAL EXAMINATION'], Differential diagnosis:['LINGUAL THYROID', 'Lymphatic malformation', 'macroglossia', 'RANULA'], disease description:Ankyloglossia, also known as tongue-tie, is a short lingual frenum that interferes with normal tongue movement. Prevalence has been estimated to be from less than 1% to 10%. This significant wide range can be attributable to the lack of diagnostic criteria for tongue-tie

Experiencing ['back lower stiffness', 'back pain', 'heel pain'] at 28 years old

Disease Name: Ankylosing Spondilitis, symptoms: ['back lower stiffness', 'back pain', 'heel pain'], Treatment: [{'medication': ['Indomethacin ', 'NSAID']}, 'No specific therapy is available. Aim is to control\nthe pain and maintain maximum degree of joint\nmobility. This can readily be achieved by life long\npursuit of a structured exercise programme. In\nsome cases surgical intervention is required.', 'physiotherapy\n– this\nconsists of proper posture guidance, heat therapy\nand mobilisation exercises; (iii) radiotherapy – in\nsome resistant cases; and (iv) yoga therapy.', "Pain killer:\nNon-steroidal anti-inflammatory drugs (NSAIDs):\nibuprofen\nnaproxen\ndiclofenac\n\nCodeine.\n\nAnti-TNF medicine\nIf your symptoms cannot be controlled using NSAIDs and exercising and stretching, anti-tumour necrosis factor (TNF) medicine may be recommended. TNF is a chemical produced by cells when tissue is inflamed.\n\nAnti-TNF medicines are given by injection and work by preventing the effects of TNF, as well as reducing the inflammation in your joints caused by ankylosing spondylitis.\n\nMonoclonal antibody treatment\nMonoclonal antibodies, such as secukinumab and ixekizumab, may be offered to people with AS who do not respond to NSAIDs or anti-TNF medicine, or as an alternative to anti-TNF medicine.\nJAK inhibitors\nJAK inhibitors such as upadacitinib are a new type of medicine that may be offered to people with AS who do not respond to anti-TNF medicine or cannot take it.\nCorticosteroids\nCorticosteroids have a powerful anti-inflammatory effect and can be taken as injections by people with AS.\n\nIf a particular joint is inflamed, corticosteroids can be injected directly into the joint. You'll need to rest the joint for up to 48 hours after the injection.\n\nIt's usually recommended to limit corticosteroid injections to no more than 3 times in one year, with at least 3 months between injections in the same joint.\n\nDisease-modifying anti-rheumatic drugs (DMARDs)\nDisease-modifying anti-rheumatic drugs (DMARDs) are an alternative type of medicine often used to treat other types of arthritis.\n\nDMARDs may be prescribed for AS, although they're only beneficial in treating pain and inflammation in joints in areas of the body other than the spine.\n\nSulfasalazine and methotrexate are the main DMARDs", 'Operative methods: Role of operative treatment is\nin correction of kyphotic deformities of the spine by\nspinal osteotomy, and joint replacement for cases\nwith hip or knee joint ankylosis.'], Pathophysiology: Ankylosing spondylitis (AS) is a chronic inflammatory disease with an insidious onset. Progressive musculoskeletal, and often extraskeletal, signs and symptoms are characteristic of the disease. The rate of progression can vary from one patient to the next. The primary pathology of spondyloarthropathies is enthesitis with chronic inflammation, including CD4 and CD8 T lymphocytes and macrophages.Cytokines, particularly tumor necrosis factor-a (TNF-a) and transforming growth factor-ß (TGF-ß), are also important in the inflammatory process by leading to inflammation, fibrosis, and ossification at sites of enthesitis.Ankylosing spondylitis (AS) is a chronic inflammatory disease with an insidious onset. Progressive musculoskeletal, and often extraskeletal, signs and symptoms are characteristic of the disease. The rate of progression can vary from one patient to the next. The primary pathology of spondyloarthropathies is enthesitis with chronic inflammation, including CD4 and CD8 T lymphocytes and macrophages.Cytokines, particularly tumor necrosis factor-a (TNF-a) and transforming growth factor-ß (TGF-ß), are also important in the inflammatory process by leading to inflammation, fibrosis, and ossification at sites of enthesitis., Epidemiology:['0.2-0.5%', '0.4-14 per 100,000 person-years.', 'good', 'Because ankylosing spondylitis has no known cause, there isn’t any way to prevent it.'], Complications:['aortic regurgitation', 'iritis', 'mood disorders', 'pulmonary fibrosis', 'psoriasis'], Diagnostics:['Erythrocyte Sedimentation Rate (ESR)', 'Hb', 'HLA B 27 TYPING', 'X RAY CHEST', 'X RAY PELVIS', 'MRI', 'X RAY', 'x ray lumber spine'], Differential diagnosis:['rheumatoid arthritis', 'Spinal stenosis'], disease description:Ankylosing spondylitis (AS) is a chronic, inflammatory disease of the axial spine that can manifest with various clinical signs and symptoms. Chronic back pain and progressive spinal stiffness are the most common features of the disease. Involvement of the spine and sacroiliac (SI) joints, peripheral joints, digits, entheses are characteristic of the disease. Impaired spinal mobility, postural abnormalities, buttock pain, hip pain, peripheral arthritis, enthesitis, and dactylitis ("sausage digits") are all associated with AS.

Individual aged 50 with manifestations like ['Polycyclic, annular, erythematous plaques that may expand by up to 2–3 mm per day with central clearing.', 'ring shaped or annular lesions']

Disease Name: Annular Erythema Of Infancy, symptoms: ['Polycyclic, annular, erythematous plaques that may expand by up to 2–3 mm per day with central clearing.', 'ring shaped or annular lesions'], Treatment: [{'medication': ['Tacrolimus ']}, 'First line \n• Any associated infection should be treated \n Second line \n• Topical corticosteroids\n Third line \n• Topical tacrolimus'], Pathophysiology: Annular erythema of infancy is a benign disease of early infancy characterized by urticarial papules that enlarge peripherally, forming 2–3 cm rings or arcs with firm, raised, cord-like or urticarial borders.4–6 Adjacent lesions become confluent, forming arcuate and polycyclic lesions (Fig. 19-1). Neither vesiculation nor scaling is present at the border. The eruption is asymptomatic. Individual lesions resolve spontaneously without a trace within several days, but new lesions continue to appear in a cyclical fashion until complete resolution within the first year of life.The cause of annular erythema is unknown, and there are no associated systemic findings. Histologic studies reveal a superficial and deep, dense, perivascular infiltrate of mono-nuclear cells and eosinophils. No flame figures are observed. The epidermis is normal or mildly spongiotic., Epidemiology:['self-limiting', 'Family members of the infected neonates must be examined and treated accordingly. Fomite and environmental decontamination should be considered too.'], Complications:['purpura', 'thromboembolic disorders'], Diagnostics:['HISTOPATHLOGY', 'Skin Biopsy With Immunofluorescence', 'Microscopic Examination of SCRAPINGS', 'direct microscopy'], Differential diagnosis:['erythema migrans', 'Mycosis fungoides', 'psoriasis', 'Tinea corporis dermatology', 'Urticaria'], disease description:Annular erythema of infancy is a benign disease of early infancy characterized by urticarial papules that enlarge peripherally, forming 2–3 cm rings or arcs with firm, raised, cord-like or urticarial borders. Adjacent lesions become confluent, forming arcuate and polycyclic lesions.The diagnosis of annular erythema is made clinically and may be confirmed by histopathology.

At the age of 48, symptoms like ['jaundice', 'weight loss', 'abdominal distension', 'nausea', 'vomiting', 'Abdominal Pain']

Disease Name: Annular Pancreas, symptoms: ['jaundice', 'weight loss', 'abdominal distension', 'nausea', 'vomiting', 'Abdominal Pain'], Treatment: ['Duodenoduodenostomy-ideal. \nDuodenojejunostomy.'], Pathophysiology: The pathophysiology of annular pancreas is explained by the direct impact of the migratory defect during embryogenesis. Duodenal obstruction is secondary to a mechanical defect, which can be extrinsic from the encasement of the duodenum or intrinsic from scarring, stenosis, or the presence of duodenal webs. The pathogenesis of pancreatitis in AP is unclear. Pancreatitis, when it occurs, is usually confined to the annulus and the adjoining pancreatic head sparing the body and tail of the gland which is likely secondary to fibrosis resulting in the inability of the pancreatic secretions to pass through the annular duct and increased intrinsic susceptibility of the annular pancreatic tissue to damage. Peptic ulcer disease may be related to gastric stasis and antral overdistension with resulting hypergastrinemia. Biliary ductal dilation is attributed likely due to the progression of chronic pancreatitis resulting in fibrosis or ductal compression by the annular gland., Epidemiology:['Older studies have reported the prevalence of AP in three of 20,000 autopsies and three of 24,519 surgical cases', 'variable', "There's no possible way to prevent the annular pancreas from happening. It's a condition that happens during development in the womb. However, you can take steps to ensure you have a healthy pregnancy for a healthy baby.\n\nSome things you can do to help you have a healthy pregnancy and baby are:\n\nMake sure you keep up with a healthy diet, including fruits, whole grains, and vegetables.\nVisit your doctor regularly for prenatal checkups.\nDon’t smoke.\nDon't take over-the-counter medications.\nAvoid alcohol.\nStay hydrated."], Complications:['Pancreatitis', 'Fistula'], Diagnostics:['Barium Imaging', 'MRCP', 'X RAY ABDOMEN', 'CT SCAN'], Differential diagnosis:['CARCINOMA OF THE PANCREAS', 'CHOLEDOCHAL CYST', 'CHOLELITHIASIS', 'GASTRIC OUTLET OBSTRUCTION', 'GASTRITIS', 'GASTRO OESOPHAGEAL REFLUX DISEASE', 'PEPTIC ULCER DISEASE'], disease description:Annular pancreas (AP) is a rare congenital anomaly characterized by partial or complete circumferential encasement of the second part of the duodenum by a band of pancreatic tissue during embryogenesis. It is usually located above the papilla of Vater in approximately 85% of diagnosed cases .Based on the morphologic distribution of pancreatic tissue, AP has been classified into a complete or incomplete type. Complete type AP shows pancreatic parenchyma or annular duct completely encircling the second part of the duodenum confirmed by macroscopic inspection, and incomplete type AP demonstrates partial circumferential encasement of the duodenum by pancreatic tissue confirmed by endoscopic retrograde cholangiopancreatography (ERCP) or surgical evaluation

Symptoms at 29 years: ['SKIN LESIONS', 'Warts', 'mass']

Disease Name: Ano-genital Warts, symptoms: ['SKIN LESIONS', 'Warts', 'mass'], Treatment: [{'medication': ['Imiquimod ', 'Podophyllum resin/Podophyllum']}, 'First line\n•\tPodophyllotoxin\n•\tImiquimod\nSecond line\n•\t Cryotherapy\n•\t Surgery\n•\tLaser\n•\t Caustics\n•\tPhotodynamic therapy\nThird line\n•\tInterferon', 'Physical (Surgical) Removal or Destruction\n\nDirect surgical excision or physically destructive therapies are considered more effective on keratinized warts, especially if they are larger in size.\n\nSimple surgical excision under local anesthesia is simple and direct but will leave a scar and requires a small surgical procedure.\n\nLiquid nitrogen cryosurgery ablation is inexpensive, considered safe for use during pregnancy, and does not usually cause much scarring but requires cryosurgical equipment and training. It may require anesthesia due to pain and multiple treatments are often necessary. \n\nElectrocauterization is considered effective but causes scarring and requires some level of anesthesia.\n\nLaser vaporization has minimal bleeding but may be somewhat less effective than other ablative techniques. It is typically used for extensive areas of genital wart involvement, is relatively expensive, and may cause a plume of virus-containing smoke.\n\nSurgical removal under general anesthesia may be necessary for more extensive lesions, intra-anal warts, or in children. \n\nPhotodynamic therapy with a photosensitizing agent (such as aminolevulinic acid) has demonstrated efficacy in eliminating external warts. The aminolevulinic acid is applied topically or directly intralesionally.'], Pathophysiology: Genital warts show extreme acanthosis and papillomatosis, but the horny layer is parakeratotic and not very thick. Koilocytes may be limited in distribution and not found in all sections. The epidermal processes are wide and rounded, with a well-defined lower border. The connective tissue is frequently very oedematous and the capillaries tortuous and increased. Causative organisms The low-risk HPVs are most often the cause of ano-genital warts, most commonly HPV-6 (in about 45–90%) or HPV-11 and less frequently other types as indicated in. HPV-1 and HPV-2 may occur in genital warts. In children, warts in the ano-genital area are often more hyperkeratotic than in adults and may be caused by HPV types associated with cutaneous disease as well as HPV-6 and -11. Studies involving HPV typing of childhood ano-genital warts have produced somewhat varying conclusions, but overall, approximately 50% have been found to harbour mucosogenital HPV with the cutaneous types 2, 27 and 57 also commonly detected., Epidemiology:['0.13%-5.1%', '2.9% of the US male population will have genital HPV', 'recurrence after clinical cure', 'Condoms - \nData are conflicting but there is evidence of protection against anogenital warts and condom use is generally advised.\n\nVaccination - \nThere are two HPV vaccines available in the UK: Cervarix and Gardasil. \n\nHPV vaccines are highly effective at preventing the infection of susceptible women with the HPV types covered by the vaccine.'], Complications:['SEXUALLY TRANSMITTED DISEASE', 'Malignant transformation'], Diagnostics:['biopsy', 'PHYSICAL EXAMINATION'], Differential diagnosis:['GENITAL HERPES', 'HERPES SIMPLEX', 'Lichen Planus', 'Molluscum Contagiosum', 'Seborrheic Keratoses', 'Syphilis'], disease description:Genital warts (condyloma acuminatum) are the clinical manifestations of a sexually transmitted infection caused by some types of human papillomavirus (HPV), Warts are a recognized symptom of genital HPV infections. About 90% of those exposed who contract HPV will not develop genital warts. Only about 10% who are infected will transmit the virus. HPV types 6 and 11 cause genital warts. There are over 100 different known types of HPV viruses. HPV is spread through direct skin-to-skin contact with an infected individual, usually during sex. While some types of HPV cause cervical and anal cancer, these are not the same viral types that cause genital warts. It is possible to be infected with different types of HPV at the same time.

Suffering from ['small eyes', 'born without one or both eyes', 'blindness', 'eyes deformity'] at 51

Disease Name: Anophthalmia And Microphthalmia, symptoms: ['small eyes', 'born without one or both eyes', 'blindness', 'eyes deformity'], Treatment: ['no treatment available'], Pathophysiology: The precise pathogenesis of anophthalmia and microphthalmia remains unknown. Mann suggested anophthalmia has its genesis early in gestation as a result of failure of development of the anterior neural tube (secondary anophthalmia) or optic pit(s) to enlarge and form optic vesicle(s) (primary anophthalmia). A third category, consecutive or degenerative anophthalmia was applied to cases where optic vesicles have degenerated and disappeared subsequent to formation. Observations of optic nerves, chiasm, and/or tracts with anophthalmia may indicate the regression of a partially developed eye rather than aplasia of the optic vesicle(s), a view supported by observations in an apparently anophthalmic orbit of extraocular muscle insertion into a fibrous mass, possibly representing an aborted eye. Following observations that the posterior segment of microphthalmic eyes are more affected than the anterior.Weiss and colleagues suggested that post-natal ocular growth is crucial and speculated that decreased size of the optic cup, altered proteoglycans in the vitreous, low intraocular pressure and abnormal growth factor production may all or in part have a bearing on the pathogenesis of simple microphthalmia; whilst inadequate production of secondary vitreous may result in complex microphthalmia. Some cases of microphthalmia may be associated with a cyst; these are believed to result from failure of the optic fissure to close. , Epidemiology:['The prevalence of microphthalmia is 1:7,000, anophthalmia is 1:30,000', '1 in 5,200 to 1 in 10,000 infants born each year in the U.S.', 'poor', 'There’s no way to completely eliminate your risk of microphthalmia and anophthalmia, but there are ways to make pregnancy safer:\n\nSee a healthcare provider before you get pregnant and work together so you can be as healthy as possible before and during your pregnancy. This talk should include details on what types of vaccinations you might need to be up-to-date before you get pregnant.\nMake sure you get prenatal care (care before birth) early and consistently. Always go to your appointments, even if you feel fine.\nTalk to your provider about the medications and over-the-counter products you take to make sure that they are compatible with a healthy pregnancy. This includes prescription products and supplements. You must talk to your provider if you take isotretinoin and thalidomide.\nYour provider may suggest genetic testing before you get pregnant after discussing your medical history and your family history.\nAvoid harmful chemicals.'], Complications:['ptosis'], Diagnostics:['GENETIC TESTING', 'USG', 'PHYSICAL EXAMINATION'], Differential diagnosis:['cataracts', 'microcornea'], disease description:Microphthalmia and anophthalmia are both congenital conditions that affect the eyes. A congenital condition is one that you have when you’re born. Conditions that are a result of problems with fetal development are sometimes called birth defects. You may hear some people say that anophthalmia and microphthalmia are examples of “eye birth defects.”Microphthalmia means that one eye or both eyes don’t develop fully so they are small and disorganized. Bilateral microphthalmia is the term for when the condition affects both eyes. Unilateral microphthalmia is the term for when the condition affects only one eye. Anophthalmia means that one or both eyes don’t develop at all so they are missing. In bilateral anophthalmia, both eyes are missing. In unilateral anophthalmia, one eye is missing.

Symptoms at 46 years old: ['induration', 'Tenderness', 'blood in stool', 'painful urination', 'bleeding', 'swelling', 'fever', 'Perianal irritation', 'Perianal pain']

Disease Name: Anorectal Absess, symptoms: ['induration', 'Tenderness', 'blood in stool', 'painful urination', 'bleeding', 'swelling', 'fever', 'Perianal irritation', 'Perianal pain'], Treatment: ['As with all abscesses, the “gold standard” is drainage. Office drainage of an uncomplicated anorectal abscess may suffice. A small incision\nclose to the anal verge is made, and a Mallenkot drain is advanced into the abscess cavity. For patients who have a complicated abscess\nor who are diabetic or immunocompromised, drainage should be performed in an operating room under anesthesia. These patients are at greater risk for developing necrotizing fasciitis'], Pathophysiology: An anorectal abscess is an abnormal fluid-containing cavity in the anorectal region. Anorectal abscess results from an infection involving the glands surrounding the anal canal. Normally, these glands release mucus into the anal canal, which aids in defecation. When stool accidentally enters the anal glands, the glands become infected and an abscess develops. Anorectal abscesses are perianal in 40–50% of patients, ischiorectal in 20–25%, intersphincteric in 2–5%, and supralevator in 2.5%., Epidemiology:['37% of patients developed chronic anal fistula or recurrent sepsis', 'GOOD', 'Prevention or prompt treatment of STDs may prevent an anorectal abscess from forming. Use condoms during intercourse, including anal sex, to prevent such infections.\n\nIn infants and toddlers, frequent diaper changes and proper cleaning during diaper changes can help prevent both anal fissures and abscesses.'], Complications:['FISTULA-IN-ANO', 'infections', 'Pain'], Diagnostics:['CT SCAN', 'PHYSICAL EXAMINATION'], Differential diagnosis:['Abdominal Pain', 'Acute proctitis', 'ANAL FISSURE', 'Bartholin Cyst Abscess', 'Hemorrhoids', 'INFLAMMATORY BOWEL DISEASES', 'POST ANAL DERMOID', 'RECTAL PROLAPSE'], disease description:An anorectal abscess is a collection of pus in the area of the anus and rectum. Common causes of anorectal abscess include: Blocked glands in the anal area. Infection of an anal fissure. Sexually transmitted infection (STD)

Person, 29 years old, presenting ['hepatosplenomegaly', 'pancytopenia', 'telangiectasias', 'petechiae', 'amenorrhoea', 'anorexia', 'Confusion', 'Dizziness', 'fainting', 'headache', 'hypercholesterolaemia', 'Hypoglycaemia', 'dryness of hair', 'weight loss', 'tiredness', 'blurred vision', 'lanugo hair']

Disease Name: Anorexia Nervosa, symptoms: ['hepatosplenomegaly', 'pancytopenia', 'telangiectasias', 'petechiae', 'amenorrhoea', 'anorexia', 'Confusion', 'Dizziness', 'fainting', 'headache', 'hypercholesterolaemia', 'Hypoglycaemia', 'dryness of hair', 'weight loss', 'tiredness', 'blurred vision', 'lanugo hair'], Treatment: ['Medically unstable (bradycardia, dehydration, hypoglycemia or poorly controlled diabetes, hypokalemia or other electrolyte imbalances indicative of refeeding syndrome, hypothermia, hypotension, organ compromise requiring acute treatment)', 'Outpatient treatment includes intensive therapy (2 to 3 hours per weekday) and partial hospitalization (6 hours per day). Pediatric patients benefit from family-based psychotherapy to explore underlying dynamics and restructure the home environment.'], Pathophysiology: Studies demonstrate biological factors play a role in the development of anorexia nervosa in addition to environmental factors. Genetic correlations exist between educational attainment, neuroticism, and schizophrenia. Patients with anorexia nervosa have altered brain function and structure there are deficits in neurotransmitters dopamine (eating behavior and reward) and serotonin (impulse control and neuroticism), differential activation of the corticolimbic system (appetite and fear), and diminished activity among the frontostriatal circuits (habitual behaviors). Patients have co-morbid psychiatric disorders such as major depressive disorder and generalized anxiety disorder., Epidemiology:['Lifetime prevalence is 0.3% to 1% (European studies have demonstrated a prevalence of 2% to 4%), irrespective of culture, ethnicity, and race', 'around 6% of the total population,', 'variable', 'Although it might not be possible to prevent all cases of anorexia, it’s helpful to start treatment as soon as someone begins to have symptoms.\n\nIn addition, teaching and encouraging healthy eating habits and realistic attitudes about food and body image also might help prevent the development or worsening of eating disorders. If your child or family member decides to become vegetarian or vegan, for instance, it’s worth seeing a dietitian versed in eating disorders and touching base with your pediatrician or healthcare provider to make sure that this change occurs without a loss in nutrients.'], Complications:['amenorrhoea', 'constipation', 'hypothermia', 'Osteoporosis', 'renal failure'], Diagnostics:['ABG', 'Complete Blood Count CBC', 'SERUM VITAMIN D3 LEVEL', 'ECG', 'SERUM ELECTROLYTE', 'SERUM CORTISOL LEVEL'], Differential diagnosis:['ACHALASIA', 'cancer', 'CELIAC DISEASE', 'hyperthyroidism', 'Irritable Bowel Syndrome', 'MALABSORPTION', 'Mesentric Ischemia'], disease description:Anorexia nervosa is an eating disorder defined by restriction of energy intake relative to requirements, leading to a significantly low body weight. Patients will have an intense fear of gaining weight and distorted body image with the inability to recognize the seriousness of their significantly low body weight.Diagnosis is generally clinical.A healthcare provider can diagnose a person with anorexia based on the criteria for anorexia nervosa listed in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) published by the American Psychiatric Association. The three criteria for anorexia nervosa under the DSM-5 include:Restriction of calorie consumption leading to weight loss or a failure to gain weight resulting in a significantly low body weight based on that person’s age, sex, height and stage of growth.Intense fear of gaining weight or becoming “fat.”Having a distorted view of themselves and their condition. In other words, the individual is unable to realistically assess their body weight and shape believes their appearance has a strong influence on their self-worth and denies the medical seriousness of their current low body weight and/or food restriction.

At the age of 24, symptoms like ['Numbness', 'localized swelling', 'DEFORMITY', 'restricted joint movement', 'severe pain']

Disease Name: Anterior Dislocation Of The Hip, symptoms: ['Numbness', 'localized swelling', 'DEFORMITY', 'restricted joint movement', 'severe pain'], Treatment: ['1- closed reduction\n2- open reduction', 'Anterior hip dislocation is commonly reduced by inline traction and external rotation, with an assistant pushing on the femoral head or pulling the femur laterally to assist reduction.'], Pathophysiology: Epstein classification of anterior hip dislocationsType 1: Superior dislocations1A: No associated fracture1B: Associated fracture or impaction of the femoral head1C: Associated fracture of the acetabulumType 2: Inferior dislocations2A: No associated fracture2B: Associated fracture or impaction of the femoral head2C: Associated fracture of the acetabulumComprehensive classification of hip dislocationsThis system includes both anterior and posterior dislocations and incorporated pre- and –post findings.Type I: No significant associated fracture, no clinical instability after reductionType II: Irreducible dislocation (after attempt under general anesthesia) without significant femoral head or acetabular fractureType III: Unstable hip after reduction or with incarcerated fragments of cartilage, labrum, or boneType IV: Associated acetabular fracture requiring reconstruction to restore hip stability or joint congruityType V: Associated femoral head or neck injury, Epidemiology:['Over 90% were treated with a closed reduction, and approximately 70% were reduced within 12 hours.', 'good', 'Safety: Since hip dislocation usually results from an accident, common safety guidelines are the best prevention. Always wear your seatbelt in the car and wear protective gear when participating in contact sports. Take precautions when using a ladder or workplace equipment, too.\nConditioning: If you’ve previously dislocated your hip, it might be more prone to dislocating again. You can help reinforce your joint by strengthening your hip tendons and muscles through physical therapy and keeping them conditioned through regular exercise.\nHip dysplasia care: Children with hip dysplasia should be treated while their skeletons are still growing to prevent future injury.'], Complications:['avascular necrosis of bone', 'Sciatica', 'Chondrolysis of articular cartilage'], Diagnostics:['X RAY AP VIEWS', 'X RAY', 'CT SCAN', 'x ray lateral view'], Differential diagnosis:['FEMORAL NECK FRACTURE', 'pelvis injury'], disease description:Hip dislocations after trauma are frequently encountered in the emergency setting. A significant force is generally required to dislocate a hip as this ball and socket joint is quite stable due to its bony structure and the associated muscular and ligamentous attachments. Due to the required force, hip dislocations often are associated with other significant injuries; for example, fractures are found in over 50% of these patients. The majority of all hip dislocations are due to motor vehicle accidents. Posterior hip dislocations are the most common type, with anterior occurring only about 10% of the time. These injuries are true orthopedic emergencies and should be reduced expediently. The majority will resolve with a closed reduction in the emergency department

Suffering from ['Posterior corneal opacity', 'Small and medium Keratic precipitates', 'Aqueous flare', 'Changes in depth and shape of anterior chamber', 'Changes in the angle of anterior chamber', 'Koeppe’s nodules in iris', 'Busacca’s nodules in iris', 'Neovascularisation of iris', 'Pupillary reaction sluggish', 'Cystoid macular oedema', 'polychromatic luster and bread-crumb appearance of the early posterior subcapsular opacities', 'Corneal oedema', 'Circumcorneal congestion', 'festooned pupil', 'posterior synechiae', 'Mutton fat Keratic precipitates', 'Fine Keratic precipitates', 'Old Keratic precipitates', 'Aqueous cells in anterior chamber', 'eye pain', 'Lacrimation', 'REDNESS OF EYE', 'blepharospasm', 'photophobia', 'Defective vision'] at 30

Disease Name: Anterior Uveitis (iridocyclitis), symptoms: ['Posterior corneal opacity', 'Small and medium Keratic precipitates', 'Aqueous flare', 'Changes in depth and shape of anterior chamber', 'Changes in the angle of anterior chamber', 'Koeppe’s nodules in iris', 'Busacca’s nodules in iris', 'Neovascularisation of iris', 'Pupillary reaction sluggish', 'Cystoid macular oedema', 'polychromatic luster and bread-crumb appearance of the early posterior subcapsular opacities', 'Corneal oedema', 'Circumcorneal congestion', 'festooned pupil', 'posterior synechiae', 'Mutton fat Keratic precipitates', 'Fine Keratic precipitates', 'Old Keratic precipitates', 'Aqueous cells in anterior chamber', 'eye pain', 'Lacrimation', 'REDNESS OF EYE', 'blepharospasm', 'photophobia', 'Defective vision'], Treatment: [{'medication': ['Timolol ', 'Naproxen ', 'Dexamethasone ', 'Azithromycin ', 'Erythromycin ', 'Methotrexate', 'Azathioprine ', 'Prednisolone', 'Atropine/ Atropine methonitrate', 'Phenylbutazone']}, 'a. Local therapy: 1. Cycloplegic drugs. These are very useful and most\neffective during acute phase of iridocyclitis. 2. Corticosteroids, administered locally, are very\neffective in cases of iridocyclitis. 3. Broad spectrum antibiotic drops, though of no use\nin iridocyclitis, are usually prescribed with topical\nsteroid preparations to provide an umbrella cover\nfor them. b. Systemic therapy\n1. Corticosteroids. When administered systemically\nthey have a definite role in nongranulomatous\niridocyclitis, where inflammation, most of the times,\nis due to antigen-antibody reaction. 2. Non-steroidal anti-inflammatory drugs (NSAIDs)\nsuch as aspirin can be used where steroids\nare contraindicated. 3. Immunosuppressive drugs. These should be used\nonly in desperate and extremely serious cases\nof uveitis, in which vigorous use of steroids have\nfailed to resolve the inflammation and there is\nan imminent danger of blindness. 4. Azithromycin or tetracycline or erythromycin\nshould be considered to treat chlamydial infection\nin patients and their sexual partners with Reiter’s\nsyndrome having urethritis and iritis. c. Physical measures:\n1. Hot fomentation. 2. Dark goggles. Specific treatment of the cause: a full course of antitubercular drugs for\nunderlying Koch’s disease, adequate treatment for\nsyphilis, toxoplasmosis, etc., when detected should\nbe carried out. Treatment of complications: 1. Inflammatory glaucoma (hypertensive uveitis).\nIn such cases, drugs to lower intraocular pressure\nsuch as 0.5% timolol maleate eyedrops twice\na day and tablet acetazolamide (250 mg thrice\na day) should be added, over and above the\nusual treatment of iridocyclitis. Pilocarpine and\nlatanoprost eye drops are contraindicated in\ninflammatory glaucoma.', '1. Postinflammatory glaucoma due to ring synechiae\nis treated by laser iridotomy. Surgical iridectomy may\nbe done when laser is not available. However, surgery\nshould be performed in a quiet eye under high doses\nof corticosteroids. 2. Complicated cataract requires lens extraction\nwith guarded prognosis in spite of all precautions.\nPresence of fresh KPs is considered a contraindication\nfor intraocular surgery.\n3. Retinal detachment of exudative type usually settles\nitself if uveitis is treated aggressively. A tractional\ndetachment requires vitrectomy and management\nof complicated retinal detachment, with poor visual\nprognosis.\n4. Phthisis bulbi especially when painful, requires\nremoval by enucleation operation.'], Pathophysiology: The pathophysiology of uveitis in general is not well understood.  Groups have hypothesized that trauma to the eye can cause cell injury or death which leads to the release of inflammatory cytokines leading to a post-traumatic uveitis.  Uveitis caused by inflammatory diseases is thought to be due to molecular mimicry, where an infectious agent cross-reacts with ocular-specific antigens.  Vision-threatening inflammation is mediated by CD4 Th1 cells.  Normally, only activated lymphocytes are allowed past the blood-retina barrier, thus decreasing sensitization of naïve T cells to ocular proteins. Researchers have proposed there is molecular mimicry between retinal S-Ag peptides and a peptide from disease associated HLA-B antigens, which leads to targeting of ocular proteins and inflammatory response., Epidemiology:['Prevalence rates for 2006 and 2007 came in at 57.5 and 58 respectively per 100,000 persons', '15% to 20% of children', 'good', 'Recognize early symptoms of uveitis\n Quit smoking\nHave enough rest and relaxation.\nEat a healthy and balanced diet for uveitis'], Complications:['Loss of vision', 'Secondary glaucoma', 'complicated cataract', 'festooned pupil', 'phthisis bulbi', 'IOP is markedly lowered', 'Cyclitic membrane', 'Choroiditis', 'Retinal complications', 'Papillitis (inflammation of the optic disc)', 'Band-shaped keratopathy'], Diagnostics:['ANTI NUCLEAR ANTI BODY(ANA)', 'Complete Blood Count CBC', 'Erythrocyte Sedimentation Rate (ESR)', 'SERUM URIC ACID', 'MRI Head', 'CT Thorax', 'X RAY CHEST', 'STOOL EXAMINATION', 'BLOOD GLUCOSE', 'Urine analysis', 'ophthalmoscopy', 'slit-lamp biomicroscopic examination'], Differential diagnosis:['acute angle-closure glaucoma', 'bilateral granulomatous panuveitis', 'conjunctivitis', 'corneal abrasions'], disease description:uveitis is a term used to describe inflammatory processes of the portion of the eye known as the uvea, which is composed of the iris, ciliary body, and the choroid; however, any area of the eye can be inflammed.  Uveitis can be further subdivided into anterior, intermediate, posterior, and panuveitis based on the primary anatomical location of the inflammation in the eye. Symptoms and consequences can range from pain and conjunctival injection to complete vision loss. Anterior uveitis is epitomized by the anterior segment being the predominate site of inflammation. Intermediate uveitis is defined by inflammation of the vitreous cavity and pars plana, while posterior uveitis involves the retina and choroid. Inflammation in panuveitis includes all layers.

A 36-year-old suffering ['erythema', 'Bulla formation', 'papules', 'regional adenopathy', 'diarrhea', 'dysphagia', 'haematemesis', 'Abdominal Pain', 'gastrointestinal disorders', 'respiratory disorders']

Disease Name: Anthrax, symptoms: ['erythema', 'Bulla formation', 'papules', 'regional adenopathy', 'diarrhea', 'dysphagia', 'haematemesis', 'Abdominal Pain', 'gastrointestinal disorders', 'respiratory disorders'], Treatment: [{'medication': ['Amoxicillin and Clavulanic acid ', 'Ciprofloxacin ', 'Doxycycline ', 'PENICILLIN G']}, 'For most cases, early treatment with oral ciprofloxacin or doxycycline for 60 days is given. Oral amoxicillin may be used following \nclinical improvement since penicillin will ensure that cutaneous \nanthrax lesions are culture negative within 24 h. An alternative is \nintravenous penicillin G given for 7–10 days, in a dose of 4 million units 6 hourly for the first 3–4 days. \nIf the patient is already \nseverely toxic when treatment is started, intravenous fluids and \ncorticosteroids are advisable.'], Pathophysiology: The pathogenesis of anthrax follows the route of infection with three primary forms in humans: cutaneous, GI, and inhalational.Inhalational anthrax leads to accumulation of B. anthracis spores within the lung alveoli. The spores are engulfed by immune cells (macrophages, neutrophils, dendritic cells) and transported to regional lymph nodes where the bacteria germinate, multiply, and begin toxin production.  This results in systemic clinical illness, and pathologically to toxin-induced cell damage and cell death.  As the disease progresses, bloodstream infection occurs leading to septic shock.  Patients can present suddenly and may deteriorate rapidly.   Cutaneous anthrax results from inoculation of B. anthracis spores through the abraded skin into subcutaneous tissues. The bacteria subsequently germinate and multiply locally and begin toxin production.  This leads to the characteristic edema and cutaneous ulceration. GI anthrax occurs due to ingestion of contaminated meat, with spores introduced into the gastrointestinal tract, causing bacterial replication, mucosal ulcerations, and bleeding. , Epidemiology:['Anthrax occurs worldwide, and the world health organization (WHO) estimates the annual global incidence of between 2000 and 20,000 cases', 'In severe untreated cases, malaise, high fever, to', 'The anthrax vaccine is 90% effective at preventing infection. \n\nThe anthrax vaccine isn’t available to the general public. If you’re traveling to an area known to have anthrax problems, you should not:\n\nEat raw or undercooked meat.\nHandle or buy souvenirs made with animal hide or hair.\nPet or touch animals.'], Complications:['Cutaneous eruptions', 'Haemorrhage'], Diagnostics:['Antibody Serology Tests', 'PCR', 'X RAY', 'ANTHRAX blood test', 'anthraxin skin test'], Differential diagnosis:['community-acquired pneumonia', 'Ecthyma', 'Respiratory syncytial virus', 'staphylococcal infections', 'tularemia', 'VACCINIA'], disease description:The bacteria Bacillus anthracis causes anthrax. The bacteria is a small aerobic or facultatively-anaerobic, gram-positive or gram-variable, encapsulated, spore-forming rod. The organism produces toxins which are important for clinical virulence. It grows well on blood agar resulting in large, irregular-shaped colonies. The origin of the name comes from the Greek word "anthrakis," meaning black, in reference to the necrotic lesion seen in cutaneous anthrax.Although B. anthracis is generally an environmentally-stable and ubiquitous organism in nature, it has also been recognized as a potential pathogen that could be used as a biologic weapon.Anthrax can affect the skin or internal organs. When inhaled, anthrax is usually fatal. Symptoms usually appear several days after the infection and this makes it difficult to track the organism

Person at 34 years, dealing with ['Genital lesions', 'tense blister on skin', 'oral lesions']

Disease Name: Anti-p200 Pemphigoid, symptoms: ['Genital lesions', 'tense blister on skin', 'oral lesions'], Treatment: [{'medication': ['Doxycycline ', 'Dapsone ', 'Azathioprine ', 'Prednisolone', 'Oxytetracycline ']}, 'First line\n•\tVery potent topical corticosteroids on the whole body surface or\n•\tPrednisolone 0.5 mg/kg/day tapering\nplus\n•\tDapsone 1.0–1.5 mg/kg/day or\n•\tAnti-inflammatory antibiotics, e.g. doxycycline 200 mg/\nday, oxytetracycline 2 g/day ± nicotinamide 2 g/day or\nSecond line\n•\tPrednisolone 0.5 mg/kg/day tapering plus\n•\tAzathioprine 2.5 mg/kg/day (with normal TPMT activity)\nThird line\n•\tAddition of IVIG or immunoadsorption'], Pathophysiology: The C terminus of laminin gamma1 has been described as immunodominant region in anti-p200 pemphigoid. About a third of sera additionally react with epitopes outside the 245 C-terminal amino acids while in 10% of sera, no reactivity with laminin gamma1 can be found. Most autoantibodies belong to the IgG4 subclass, an individual patient with exclusive IgA autoantibodies against the p200 antigen but unreactive with laminin gamma1 has been reported. Intermolecular epitope spreading appears to be relatively frequent in anti-p200 pemphigoid with various reports of concomitant autoantibody reactivity against BP180, BP230, laminin 332 and type VII collagen, respectively. To investigate the role of IL-8 in the neutrophil infiltration frequently seen in the patients’ upper dermis by histopathology, Iwata et al. determined the IL-8 release of cultured human keratinocytes in response to anti-p200 pemphigoid IgG. In contrast to BP-IgG, incubation with anti-p200 IgG did not result in the secretion of IL-8. These results point to different mechanisms of neutrophil accumulation in skin lesions in the two pemphigoid diseases., Epidemiology:['0.0419 per 1000 person-years', 'variable'], Complications:['sepsis', 'viral infections', 'Bacterial infection'], Diagnostics:['Antibody Serology Tests', 'ELISA', 'BIOPSY FROM SKIN LESION', 'WESTERN BLOT TEST'], Differential diagnosis:['Bullous pemphigoid', 'Linear IgA disease'], disease description:`Anti-p200 pemphigoid is a rare subepidermal autoimmune bullous disease (AIBD) initially described in 1996.. This novel disease, presumed to be a subset of pemphigoid, was characterized by autoantibodies targeting a 200-kDa protein localized within the lower lamina lucida of the basement membrane zone (BMZ). Their sera bound to the dermal side of salt-split skin by indirect immunofluorescence (IIF) microscopy. Subsequent studies demonstrated that sera from 90% of anti-p200 pemphigoid patients recognized laminin ?1, which C-terminus was identified as an immunodominant region and utilized for immunoblotting and ELISA for diagnosis.

Symptoms at 44 years old: ['dry cough', 'fatigue', 'loss of appetite', 'weakness', 'burning micturation', 'blood in urine', 'edema', 'hemoptysis', 'shortness of breath', 'hematuria', 'dyspnea', 'fever', 'Oliguria', 'blood in vomiting']

Disease Name: Antiglomerular Basement Membrane Disease, symptoms: ['dry cough', 'fatigue', 'loss of appetite', 'weakness', 'burning micturation', 'blood in urine', 'edema', 'hemoptysis', 'shortness of breath', 'hematuria', 'dyspnea', 'fever', 'Oliguria', 'blood in vomiting'], Treatment: [{'medication': ['Cyclophosphamide ', 'Prednisolone']}, 'Plasmapheresis, which removes harmful antibodies to help reduce inflammation in the kidneys and lungs.\nCorticosteroid medicines (such as prednisone) and other drugs, which suppress or quiet the immune system.\nMedicines such as angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs), which help control blood pressure.\nDialysis, which may be done if kidney failure can no longer be treated.\nA kidney transplant, which may be done when your kidneys no longer function.'], Pathophysiology: Goodpasture syndrome is due to circulating autoantibodies directed at the glomerular basement membrane. The resulting crescentic glomerulonephritis is the result of the antigen-antibody complexes that form at the basement membrane.The autoantibodies activate the complement system in the basement membrane, causing tissue injury. This binding of autoantibodies can be seen as a linear deposition of immunoglobulins along the basement membrane. The inflammatory response in that area results in the typical picture of glomerulonephritis.The alveolar basement membrane shares the same collagen target as that of the glomerulus. The main component of the basement membrane is type 4 collagen, which can be expressed as six different chains, from alpha 1 to alpha 6. Despite the presence of circulating antibodies in anti-glomerular basement membrane disease, pulmonary symptoms are not always observed. An inciting lung injury seems to make pulmonary symptoms more likely.In a healthy individual, the alveolar endothelium acts as a barrier to the anti-basement membrane antibodies. However, if an insult results in increased permeability of the alveolar capillaries, it leads to the trespassing of autoantibodies, which then bind to the basement membrane, Epidemiology:['1 in 1 million new cases being reported per year.', 'variable', 'You may not be able to prevent Goodpasture syndrome. But you can lower your risk by avoiding tobacco and chemicals that may trigger the disorder.\n\nHealthcare providers can do a blood test to check for the HLA-DR15 antigen. If you know you have the HLA-DR15 antigen, ask your provider about regular checkups to monitor your health. If you smoke, talk to your provider about how to quit smoking.'], Complications:['chronic kidney disease', 'pulmonary haemorrhage', 'Rapidly Progressive (Crescentic) Glomerulonephriti'], Diagnostics:['Arterial Blood Gas Analysis(ABG)', 'ABG', 'SERUM Creatinine', 'ELISA for anti GBM antibody', 'western blotting for anti GBM antibody', 'immunoflorescence for anti IgG', 'CT SCAN', 'kidney biopsy'], Differential diagnosis:['ACUTE GLOMERULONEPHRITIS', 'acute kidney injury', 'Churg-Strauss Syndrome', 'IgA Nephropathy', 'Microscopic polyangiitis', 'Precipitate or aggravate systemic lupus erythematosus', 'thrombotic thrombocytopenic purpura', 'Wegener granulomatosis'], disease description:Goodpasture syndrome refers to an anti-glomerular basement membrane (anti-GBM) disease that involves both the lungs and kidneys, often presenting as pulmonary hemorrhage and glomerulonephritis. However, some clinicians may interchangeably use several terms, including anti-glomerular basement membrane disease, Goodpasture syndrome, and Goodpasture disease.

Woman aged 40 experiencing ['stroke', 'Rashes', 'thrombocytopenia', 'miscarriages']

Disease Name: Antiphospholipid Syndrome, symptoms: ['stroke', 'Rashes', 'thrombocytopenia', 'miscarriages'], Treatment: [{'medication': ['Heparin ', 'Clopidogrel ', 'Hydroxychloroquine ']}, 'First line \n• Anticoagulation (heparin/warfarin) in the non-pregnant \npatient \n• Heparin ± low-dose aspirin to be considered in the \n pregnant patient \n Second line \n• Oral direct thrombin and anti-factor Xa inhibitors \n• Combination antiaggregant therapy (low-dose aspirin plus \nclopidogrel or dipyridamole)\n• Low-dose aspirin combined with hydroxychloroquine in \nthose with SLE\n Third line \n• Immunomodulatory therapies: plasmapheresis, intravenous human IgG and rituximab\n• In refractory cases, plasmapheresis'], Pathophysiology: Many mechanisms for thrombosis in APLS have been suggested, such as increased expression of tissue factor on monocytes and endothelial cells , interference in the protein C anticoagulant pathway, inhibition of fibrinolysis and inhibition of annexin V binding to phospholipids. B2GPI (apolipoprotein H) is a cofactor required for APA to bind to cardiolipin. These findings suggested that APA are directed against a complex antigen that includes B2GPI. Genetics Hudson et al. found a possible linkage between the HLA-DRB1*14 allele on chromosome 6p21.3 and familial primary APLS. A meta-analysis recently showed that the B2GPI Val/Leu(247) polymorphism was associated with susceptibility to APLS and thrombosis and with anti-B2GPI positivity. Patients have one or more clinical episodes of arterial, venous or small vessel thrombosis. Venous thrombosis in APLS is most commonly lower limb deep-vein thrombosis or pulmonary embolism but any part of the venous system may be involved, including superficial, portal, renal, mesenteric and intracranial veins. The most frequent site of arterial thrombosis in APLS is in the cerebral vasculature resulting in transient cerebral ischaemia/stroke. Myocardial infarction is less common, although subclinical myocardial ischaemia may be underrecognized. Pregnancy morbidity consists of: 1 One or more unexplained deaths of a normal fetus after the 10th week of gestation. 2 One or more preterm births of a normal fetus before the 34th week of gestation because of: (i) eclampsia; or (ii) recognized features of placental insufficiency. 3 Three or more unexplained consecutive spontaneous miscarriages before the 10th week of gestation (with maternal anatomical and parental chromosomal causes excluded)., Epidemiology:['The true prevalence of the syndrome is unclear', '0.0419 per 1000 person-year', 'POOR', 'While researchers aren’t sure what exactly causes antiphospholipid syndrome, the following things are considered risk factors for developing it:\n\nBeing female: Approximately 70% of people who have antiphospholipid syndrome are female.\nHaving other autoimmune disorders: Approximately 30% to 40% of people who have lupus (systemic lupus erythematosus or SLE), an autoimmune disorder, have antiphospholipid syndrome.\nHaving a rheumatic disorder: Rheumatic disorders affect your joints, bones or muscles. People who have a rheumatic disorder are more likely to have antiphospholipid syndrome.\nHaving a family history of antiphospholipid syndrome: The syndrome sometimes runs in families.'], Complications:['Chorea', 'haemolytic anaemia', 'thrombocytopenia', 'VALVULAR HEART DISEASE', 'MULTIORGAN FAILURE'], Diagnostics:['APTT', 'ANTIGEN DETECTION ELISA', 'MRI'], Differential diagnosis:['Disseminated Intravascular Coagulation (DIC)', 'Infective endocarditis', 'thrombocytopenia', 'thrombosis', 'thrombotic thrombocytopenic purpura'], disease description:The antiphospholipid syndrome (APLS) is an autoimmune disease with clinical features of thrombosis (venous, arterial and microvascular) and pregnancy complications, which include recurrent fetal loss, preterm delivery and placental insufficiency. The condition is associated with a spectrum of autoantibodies directed against the cellular phospholipid component (hence the term ‘antiphospholipid antibodies’ or APA); most commonly: lupus anticoagulant, anticardiolipin and anti-ß2 -glycoprotein I (anti-B2GPI).

Person at 34 with manifestations like ['obstructive sleep apnea', 'nasal discharge', 'hoarseness of voice', 'nasal obstruction', 'epistaxis', 'SNORING']

Disease Name: Antrochoanal Polyp, symptoms: ['obstructive sleep apnea', 'nasal discharge', 'hoarseness of voice', 'nasal obstruction', 'epistaxis', 'SNORING'], Treatment: ['endoscopic\nsinus surgery. It has superseded earlier operations\nof simple polypectomy and Caldwell–Luc operation performed\nfor recurring cases'], Pathophysiology: Exact cause is unknown. Nasal allergy coupled with sinus infection is incriminated. Antrochoanal polypi are seen in children and young adults. Usually they are single and unilateral. Unilateral nasal obstruction is the presenting symptom. Obstruction may become bilateral when polyp grows into the nasopharynx and starts obstructing the opposite choana. Voice may become thick and dull due to hyponasality. Nasal discharge, mostly mucoid, may be seen on one or both sides. As the antrochoanal polyp grows posteriorly, it may be missed on anterior rhinoscopy. When large, a smooth greyish mass covered with nasal discharge may be seen. It is soft and can be moved up and down with a probe. A large polyp may protrude from the nostril and show a pink congested look on its exposed part. Posterior rhinoscopy may reveal a globular mass filling the choana or the nasopharynx. A large polyp may hang down behind the soft palate and present in the oropharynx. Examination of the nose with an endoscope may reveal a choanal or antrochoanal polyp hidden posteriorly in the nasal cavity., Epidemiology:['4-6% of all nasal polyps that affect the general population;', '4-6% of all nasal polyps and displays both analogies and differences with bilateral nasal polyposis.', 'GOOD', 'The strategies include the following:\n\nFollow your doctor’s instructions on taking your allergy and asthma medications.\nAvoid breathing airborne allergens or irritants that lead to inflammation of your nose and sinus cavities.\nPractice good hygiene.\nUse a humidifier in your home to help moisten your breathing passages.\nUse a saline nasal rinse or spray to remove allergens or other irritants that may cause nasal polyps.'], Complications:['infection', 'NASAL BLOCKAGE'], Diagnostics:['X RAY PNS(OF/OM)', 'X Ray skull', 'X RAY', 'Non contrast CT scan', 'NASAL EXAMINATION', 'rhinoscopy'], Differential diagnosis:['deviated nasal septum', 'FURUNCLE', 'INVERTED PAPILLOMA', 'nasal foreign bodies', 'RHINOLITH', 'sinusitis'], disease description:This polyp arises from the mucosa of maxillary antrum near its accessory ostium, comes out of it and grows in the choana and nasal cavity. Thus it has three parts. 1. Antral, which is a thin stalk. 2. Choanal, which is round and globular. 3. Nasal, which is flat from side to side..

A 24-year-old patient experiencing ['Tachycardia', 'Abdominal Pain', 'back pain', 'chest pain', 'pulsatile abdominal mass', 'dysphagia', 'dyspnea']

Disease Name: Aortic Aneurysm, symptoms: ['Tachycardia', 'Abdominal Pain', 'back pain', 'chest pain', 'pulsatile abdominal mass', 'dysphagia', 'dyspnea'], Treatment: [{'medication': ['Atorvastatin ', 'Propranolol ', 'Telmisartan ', 'Ramipril ']}, 'Aspirin, may be recommended, especially if you have other cardiovascular risks. This medicine may increase the risk external linkof bleeding.\nBlood pressure medicinesexternal link lower blood pressure. These medicines include beta blockers, angiotensin-converting enzyme (ACE) inhibitors, and angiotensin receptor blockers (ARBs).\nStatins control cholesterol levels.', 'Open surgical repair is the most common type of surgery. You will be asleep during the procedure. Your doctor first makes a large cut in your stomach area or chest, depending on the location of the aneurysm. Then, the aneurysm is removed and a graft is sewn in its place. This graft is typically a tube made of leak-proof polyester. Recovery time for open surgical repair is about a month.\nEndovascular aneurysm repair (EVAR) is done by cardiac catheterization and is less invasive than open surgical repair. This is because the cut is smaller, and you usually need less recovery time. EVAR is used to repair abdominal aortic aneurysms more often than thoracic aortic aneurysms. During the procedure, your surgical team makes a small cut, usually in the groin, then guides a stent graft — a tube covered with fabric — through your blood vessels up to the aorta. The stent graft then expands and attaches to the aortic walls. A seal forms between the stent graft and the vessel wall to prevent blood from entering the aortic aneurysm.'], Pathophysiology: Aortic aneurysms result from conditions that cause degradation or abnormal production of the structural components of the aortic wall elastin and collagen. The causes of aortic aneurysms may be broadly 1917 categorized as degenerative disorders, genetic or developmental diseases, vasculitis, infections, and trauma. Inflammation, oxidative stress, proteolysis, and biomechanical wall stress contribute to the degenerative processes that characterize most aneurysms of the abdominal and descending thoracic aorta. These are mediated by B cell and T cell lymphocytes, macrophages, inflammatory cytokines, and matrix metalloproteinases that degrade elastin and collagen and alter the tensile strength and ability of the aorta to accommodate pulsatile stretch. The associated histopathology demonstrates destruction of elastin and collagen, decreased vascular smooth muscle, in-growth of new blood vessels, and inflammation. Factors associated with degenerative aortic aneurysms include aging, cigarette smoking, hypercholesterolemia, hypertension, and male sex. The most common pathologic condition associated with degenerative aortic aneurysms is atherosclerosis. Many patients with aortic aneurysms have coexisting risk factors for atherosclerosis, as well as atherosclerosis in other blood vessels. Medial degeneration, previously designated cystic medial necrosis, is the histopathologic term used to describe the degeneration of collagen and elastic fibers in the tunica media of the aorta as well as the loss of medial cells that are replaced by multiple clefts of mucoid material,such as proteoglycans. Medial degeneration characteristically affects the proximal aorta, results in circumferential weakness and dilation, and leads to the development of fusiform aneurysms involving the ascending aorta and the sinuses of Valsalva. This pathologic condition occurs in patients with Marfan’s syndrome, Loeys-Dietz syndrome, Ehlers-Danlos syndrome type IV, hypertension, congenital bicuspid aortic valves, Turner’s syndrome, and familial thoracic aortic aneurysm syndromes; sometimes it appears as an isolated condition in patients without any other apparent disease. Familial clusterings of aortic aneurysms occur in 20% of patients, suggesting a hereditary basis for the disease. Mutations of the gene that encodes fibrillin-1 are present in patients with Marfan’s syndrome. Fibrillin-1 is an important component of extracellular microfibrils, which support the architecture of elastic fibers and other connective tissue. Deficiency of fibrillin-1 in the extracellular matrix leads to excessive signaling by transforming growth factor ß (TGF-ß). Loeys- Dietz syndrome is caused by mutations in the genes that encode TGF-ß receptors 1 (TGFBR1) and 2 (TGFBR2). Increased signaling by TGF-ß and mutations of TGFBR1, TGFBR2, TGFBR3, as well as TGFB2 and TGFB3, may cause thoracic aortic aneurysms. Mutations of SMAD3, which encodes a downstream signaling protein involved with TGF binding to its receptors, have been described in a syndrome of thoracic aortic aneurysm; craniofacial, skeletal, and cutaneous anomalies; and osteoarthritis. Mutations of the genes encoding the smooth muscle– specific alpha-actin (ACTA2), smooth muscle cell–specific myosin heavy chain 11 (MHC11), and myosin light chain kinase (MYLK) and mutations of TGFBR2 and SMAD3 have been reported in some patients with nonsyndromic familial thoracic aortic aneurysms. Mutations of type III procollagen have been implicated in Ehlers-Danlos type IV syndrome. The infectious causes of aortic aneurysms include syphilis, tuberculosis, and other bacterial infections. Syphilis is a relatively uncommon cause of aortic aneurysm. Syphilitic periaortitis and mesoaortitis damage elastic fibers, resulting in thickening and weakening of the aortic wall. Approximately 90% of syphilitic aneurysms are located in the ascending aorta or aortic arch., Epidemiology:['2.5 to 6.5 aneurysms per 1000 person-years', 'GOOD', 'Having high blood pressure, high cholesterol or using tobacco products increases your risk of developing an aortic aneurysm. You can reduce your risk by maintaining a healthy lifestyle. This includes:\n\nEating a heart-healthy diet.\nGetting regular exercise.\nMaintaining a healthy weight.\nQuitting smoking and using tobacco products.'], Complications:['heart failure'], Diagnostics:['ultrasound', 'X RAY CHEST', 'MRI', 'DIGITAL PERCUTANEOUS SUBTRACTION ANGIOGRAPHY(DSA)', 'CT SCAN'], Differential diagnosis:['stroke'], disease description:An aortic aneurysm is a bulge that occurs in the wall of the major blood vessel (aorta) that carries blood from the heart to the body. Aortic aneurysms can occur anywhere in the aorta and may be tube-shaped (fusiform) or round (saccular).Aortic aneurysms include:Abdominal aortic aneurysm. An abdominal aortic aneurysm occurs along the part of the aorta that passes through the abdomen.Thoracic aortic aneurysm. A thoracic aortic aneurysm occurs along the part of the aorta that passes through the chest cavity.

A 37-year-old suffering ['dysphagia', 'Abdominal Pain', 'hypertension', 'loss of pulses', 'intrascapular pain', 'left haemothorex', 'hematuria', 'diastolic murmur', 'chest pain', 'Pain', 'breathlessness', 'diaphoresis', 'vomiting', 'wide pulse pressure', 'pericardial rub', 'tachypnoea', 'pulmonary edema', 'syncope', 'weakness', 'blood in urine', 'dyspnea', 'bowel ischaemia']

Disease Name: Aortic Dissection, symptoms: ['dysphagia', 'Abdominal Pain', 'hypertension', 'loss of pulses', 'intrascapular pain', 'left haemothorex', 'hematuria', 'diastolic murmur', 'chest pain', 'Pain', 'breathlessness', 'diaphoresis', 'vomiting', 'wide pulse pressure', 'pericardial rub', 'tachypnoea', 'pulmonary edema', 'syncope', 'weakness', 'blood in urine', 'dyspnea', 'bowel ischaemia'], Treatment: [{'medication': ['Amlodipine ']}, 'Emergency surgical correction is the preferred treatment for Stanford type A (DeBakey type I and II) ascending aortic dissection. It is also preferred for complicated Stanford type B (DeBakey type III) aortic dissections with clinical or radiologic evidence of the following conditions:\n\nPropagation (increasing aortic diameter)\nIncreasing size of hematoma\nCompromise of major branches of the aorta\nImpending rupture\nPersistent pain despite adequate pain management\nBleeding into the pleural cavity\nDevelopment of saccular aneurysm', 'Those involving the ascending aorta usually require surgical intervention.'], Pathophysiology: The aortic wall consists of three layers: the intima, media, and adventitia. Constant exposure to high pulsatile pressure and shear stress leads to a weakening of the aortic wall in susceptible patients resulting in an intimal tear. Following this rent, blood flows into the intima-media space, creating a false lumen. Most of these tears take place in the ascending aorta, usually in the right lateral wall where the greatest shear force on the aorta occurs. An AAD can propagate anterograde and/or retrograde and depending on the direction the dissection travels, cause branch obstruction that produces ischemia of affected territory (coronary, cerebral, spinal, or visceral), and for proximal type A AADs can instigate acute tamponade, aortic regurgitation or aortic rupture.In an AAD, the true lumen is lined by the intima whereas the false lumen is within the media. In most cases, the true lumen is smaller than the false lumen. Overtimes, the blood flowing through the false lumen leads to the development of an aneurysm with the potential for rupture. The three common sites for AAD are as follows:Nearly 2-2.5 cm above the aortic root (the most common site)Just distal to the origin of the left subclavian arteryIn the aortic arch, Epidemiology:['5-30 cases per 1 million people per year', 'variable', 'Many of the factors that increase the risk of developing aortic dissection can’t be changed, such as being born with certain heart conditions, connective tissue disorders, or genetic triggers associated with having a family history of aortic dissection. However, like many other medical diseases and conditions, you can decrease some of your risks by changing the risk factors that can be modified. These risks include:\n\nLowering high blood pressure to the goal of 120/80 mm/Hg with medication, dietary changes and other measures recommended by your healthcare provider.\nQuitting smoking/using tobacco products and maintaining a healthy weight.\nWearing your seat belt to prevent injury to your chest in case of an accident.\nSeeing your provider for regularly scheduled check-ups and any other times you experience a change in your health.\nIt’s important for first-degree relatives of a person who has had an aortic dissection to be screened for their risk of aortic disease. They can be closely followed and treated before an aortic event occurs.'], Complications:['cardiac tamponade', 'kidney damage', 'stroke'], Diagnostics:['MRI CHEST', 'CT SCAN', 'TOE'], Differential diagnosis:['aortic regurgitation', 'aortic stenosis', 'cardiac tamponade', 'Myocardial infarction', 'Pulmonary Embolism', 'THORACIC AORTIC ANEURYSMS'], disease description:This occurs when a defect or flap occurs in the intima of the aorta, resulting in blood tracking into the aortic tissues splitting the medial layer and creating a false lumen. It most commonly occurs in the ascending aorta or, less often, just distal to the left subclavian artery. It is also more common in men, typically those aged 50–70 years, and in Afro-Caribbean patients.

At 41, dealing with ['basal crepts', 'murmurs of mitral and tricuspid regurgitation', 'Tender Hepatomegaly', 'PLEURAL EFFUSION', 'prominent pulsation', 'visible arterial pulsations over extremity vessels (dancing peripheral arteries)', 'visible pulsations of the abdominal aorta', 'pulse pressure is wide', 'Arteriolar pulsations may be seen over the nail bed, uvula, lips, ear lobes and in the eye grounds', 'combination of systolic and diastolic murmurs is the Duroziez sign', 'chest pain', 'heat intolerance', 'sweating', 'Abdominal Pain', 'cheyne-stokes respiration', 'heart murmur', 'hypertension', 'increased jugular venous pressure', 'murmur', 'nocturia', 'pedal edema', 'presacral edema', 'S3 may be audible', 'WATER HAMMER PULSE', 'wide pulse pressure', 'pulmonary edema', 'exertional dyspnea', 'ORTHOPNEA', 'PND(PAROXYSMAL NOCTURNAL DYSPNEA)', 'HEPATOMEGALY', 'Duroziez sign', 'Nodding of head may be present with each systole (de Musset sign)', 'Prominent carotid pulsations (Corrigan sign)', 'fatigue', 'palpitations', 'anorexia', 'breathlessness', 'Mental Confusion', 'nausea']

Disease Name: Aortic Regurgitation, symptoms: ['basal crepts', 'murmurs of mitral and tricuspid regurgitation', 'Tender Hepatomegaly', 'PLEURAL EFFUSION', 'prominent pulsation', 'visible arterial pulsations over extremity vessels (dancing peripheral arteries)', 'visible pulsations of the abdominal aorta', 'pulse pressure is wide', 'Arteriolar pulsations may be seen over the nail bed, uvula, lips, ear lobes and in the eye grounds', 'combination of systolic and diastolic murmurs is the Duroziez sign', 'chest pain', 'heat intolerance', 'sweating', 'Abdominal Pain', 'cheyne-stokes respiration', 'heart murmur', 'hypertension', 'increased jugular venous pressure', 'murmur', 'nocturia', 'pedal edema', 'presacral edema', 'S3 may be audible', 'WATER HAMMER PULSE', 'wide pulse pressure', 'pulmonary edema', 'exertional dyspnea', 'ORTHOPNEA', 'PND(PAROXYSMAL NOCTURNAL DYSPNEA)', 'HEPATOMEGALY', 'Duroziez sign', 'Nodding of head may be present with each systole (de Musset sign)', 'Prominent carotid pulsations (Corrigan sign)', 'fatigue', 'palpitations', 'anorexia', 'breathlessness', 'Mental Confusion', 'nausea'], Treatment: ['Mild to moderate AR is well tolerated for years. There is\nrole for therapy with calcium channel blockers.', 'Aortic valve repair. To repair an aortic valve, surgeons may separate valve flaps (cusps) that have fused, reshape or remove excess valve tissue so that the cusps can close tightly, or patch holes in a valve. Doctors may use a catheter procedure to insert a plug or device to repair a leaking replacement aortic valve.\nAortic valve replacement. In aortic valve replacement, your surgeon removes the damaged valve and replaces it with a mechanical valve or a valve made from cow, pig or human heart tissue (biological tissue valve). Transcatheter aortic valve replacement (TAVR) is a minimally invasive heart procedure to replace a narrowed aortic valve with a biological tissue valve.'], Pathophysiology: AR is a backward leak from the aorta into the left ventricle during diastole. This increases the volume of blood reaching the left ventricle. The left ventricle increases in size to accommodate the extra volume. The size of the left ventricle is thus directly related to the degree of aortic leak, unless there is myocardial disease. Because of the backward flow of blood the forward flow is impaired. This is compensated by peripheral vasodilatation as well as increased ejection from the left ventricle during early part of the systole. However, significant AR results in low forward output. Signs of wide pulse pressure in the form of exaggerated arterial and arteriolar pulsations are present unless the AR is mild. Slowing of heart rate increases the diastolic period and increases the regurgitant volume of blood in AR. With good left ventricular myocardial function, even moderate AR is tolerated well for long periods. If the left ventricular myocardium is failing the left ventricular diastolic pressure goes up and results in an increase in left atrial pressure and pulmonary congestion., Epidemiology:['GOOD', 'You can’t always prevent heart valve disease. But you can lower your risk by:\n\nAvoiding tobacco products.\nAvoiding recreational drugs.\nGetting the amount of exercise your healthcare provider recommends.\nSeeing a provider right away when you’re sick or have an infection.\nTaking your medications, including those that treat high blood pressure.'], Complications:['death', 'heart failure', 'pulmonary congestion'], Diagnostics:['HISTOPATHLOGY', '2-D Echo', 'ECG', 'CHEST X RAY', 'X RAY', 'Electrocardiography (EKG)'], Differential diagnosis:['Acute coronary syndromes', 'heart failure', 'Infective endocarditis', 'mitral regurgitation', 'mitral stenosis', 'Myocardial infarction', 'THYROTOXICOSIS', 'tricuspid stenosis'], disease description:Aortic valve involvement in RHD results in AR. Clinically pure AR, without associated mitral valve disease, is rare and occurs in 5 to 8% patients. Pathologically pure rheumatic aortic valve disease is almost unknown. Aortic valve disease is more common in boys compared to girls. The main symptom is palpitation, related to the large stroke volume. With mild to moderate AR the forward flow can be raised effectively on exercise. Thus fatigue is not an early symptom.

A 54-year-old individual dealing with ['burning sensation in the mouth', 'sore mouth', 'lymphadenopathy', 'ulcer']

Disease Name: Aphthous Ulcer, symptoms: ['burning sensation in the mouth', 'sore mouth', 'lymphadenopathy', 'ulcer'], Treatment: [{'medication': ['Lidocaine/Lignocaine', 'Lugols solution (5% Iodine + 10% Potassium iodide)', 'Tetracycline ']}], Pathophysiology: They are recurrent and superficial, usually involving movable mucosa, i.e. inner surfaces of lips, buccal mucosa, tongue, floor of mouth and soft palate, while sparing mucosa of the hard palate and gingivae. In the minor form, which is more common, ulcers are 2-10 mm in size and multiple with a central necrotic area and a red halo. They heal in about 2 weeks without leaving a scar. In the major form, ulcer is very big, 2-4 cm in size and heals with a scar but is soon followed by another ulcer. Aetiology of aphthous ulcers is unknown. It may be an autoimmune process, nutritional deficiency (vitamin B12, folic acid and iron), viral or bacterial infection, food allergies or due to hormonal changes or stress. Aphthous ulcers can be differentiated from viral ulcers by their frequent recurrence, involvement of movable mucosa as on the soft palate or cheek, and the absence of constitutional symptoms like fever, malaise and enlargement of cervical nodes., Epidemiology:['Approximately 1% of American children may have recurrent aphthous ulcers, with onset before age 5 years.', 'GOOD', 'Regular brushing after meals and flossing once a day can keep your mouth clean and free of foods that might trigger a sore.\n Have a balanced diet with all vitamins'], Complications:['CELLULITIS', 'dental infections'], Diagnostics:['serum Vitamin B12 level', 'Helicobacter pylori (H. pylori) TEST', 'buccal examination'], Differential diagnosis:['HERPES SIMPLEX', 'ORAL CAVITY CANCER'], disease description:They are recurrent and superficial, usually involving movable mucosa, i.e. inner surfaces of lips, buccal mucosa, tongue, floor of mouth and soft palate, while sparing mucosa of the hard palate and gingivae. In the minor form, which is more common, ulcers are 2-10 mm in size and multiple with a central necrotic area and a red halo. Diagnosis of aphthous stomatitis is clinical, and laboratory testing is usually unnecessary.

Symptoms at 47: ['localized pain', 'localized swelling', 'LOCALIZED TENDERNESS']

Disease Name: Apical Subungual Infection, symptoms: ['localized pain', 'localized swelling', 'LOCALIZED TENDERNESS'], Treatment: ['In the early stage, the infection can\nbe aborted by conservative treatment, but once\nsuppuration occurs, drainage is required. For\ndrainage, a small V-shaped piece is removed\nfrom the centre of the free edge of the nail along\nwith a little wedge of the full thickness of the skin\noverlying the abscess.', 'Paronychias are usually either treated with incision and drainage or antibiotics. If there is inflammation with no definite abscess, treatment can include warm soaks with water or antiseptic solutions (chlorhexidine, povidone-iodine) and antibiotics. Warm soaks should be for 10 to 15 minutes, multiple times a day. There is not strong evidence recommending topical vs. oral antibiotics, and this may be physician-dependent based on experience. Antibiotic used should have staph aureus coverage. Topical antibiotics used may be a triple antibiotic ointment, bacitracin, or mupirocin. In patients failing topical treatment or more severe cases, oral antibiotics are an option; dicloxacillin (250mg four times a day) or cephalexin (500mg three to four times a day). Indications for antibiotics with anaerobic coverage include patients where there is a concern for oral inoculation; this would require the addition of clindamycin or amoxicillin-clavulanate. If the patient has risk factors for MRSA (including but not limited to: recent hospitalization, recent surgery, ESRD on hemodialysis, HIV/AIDS, IVDU, resident of long term care facility), chose an antibiotic with the appropriate coverage. Options include trimethoprim/sulfamethoxazole DS (1 to 2 tablets twice a day), clindamycin (300 to 450mg four times a day) or doxycycline (100mg twice a day)'], Pathophysiology: This infection affects the tissues of the terminal phalanx's periosteum and nailplate.   It   happens   as   a   result   of   a   splinter   or   pinprick   under   the  nail.   Littleedoema is present, and the lesion is exceedingly painful. The area that is most tender is directly below the nail's free edge. At the nail's free edge, the pus breaks the surface., Epidemiology:['35% of these disorders. The infection is more common in women than in men, with a female-to-male ratio of 3:1.', 'GOOD'], Complications:['infection', 'swelling', 'Pain'], Diagnostics:['PUS CULTURE', 'Total Leucocyte Count (TLC)'], Differential diagnosis:['CELLULITIS', 'ingrowing toenail', 'Onychomycosis', 'Paronychia', 'pyogenic granuloma', 'Trauma'], disease description:This is an infection of the tissues between the nail plate and the periosteum of the terminal phalanx. It results from a pin-prick or splinter beneath the nail. The lesion is excruciatingly painful with little swelling. Tenderness is maximum just beneath the free edge of the nail. The pus comes to the surface at the free edge of the nail.

Experiencing ['lymphadenopathy', 'ecchymoses', 'Severe Pallor', 'dyspnea', 'pallor', 'petechiae', 'bleeding', 'bleeding gums', 'breathlessness', 'fatigue', 'infection', 'lassitude', 'nose bleeding', 'oozing from gums', 'fever', 'Bruising', 'weight loss'] at 39 years

Disease Name: Aplastic Anaemia, symptoms: ['lymphadenopathy', 'ecchymoses', 'Severe Pallor', 'dyspnea', 'pallor', 'petechiae', 'bleeding', 'bleeding gums', 'breathlessness', 'fatigue', 'infection', 'lassitude', 'nose bleeding', 'oozing from gums', 'fever', 'Bruising', 'weight loss'], Treatment: ['Supportive care should be instituted with packed red cells\nfor severe anemia, platelets transfusions for severe\nthrombocytopenia and antibiotics for management of\ninfections. Hematopoietic stem cell transplant (HSCT) is\nthe only definitive therapy. Criteria for referral for HSCT\ninclude: (i) young age; (ii) severe aplastic anemia; and\n(iii) availability of matched sibling. Patients with severe\nacquired aplastic anemia who cannot undergo HSCT may\nbenefit from infusions of antithymocyte globulin (ATC)\nor antilymphocyte globulin (ALG) along with oral\ncyclosporine. Patients with neutropenia with infection\nshould receive a trial of granulocyte colony stimulating\nfactor (G-CSF). However, G-CSF should be discontinued\nafter seven days even if neutrophil count does not\nimprove, since its prolonged use carries the risk of\nmalignant transformation.'], Pathophysiology: Aplastic anemia comprises a group of disorders of the hematopoietic stem cells resulting in the suppression of one or more of erythroid, myeloid and megakaryocytic cell lines. The condition may be inherited or acquired. Hematopoietic stem cells may be deficient due to (i) an acquired injury from viruses, toxins or chemicals; (ii) abnormal marrow microenvironment; (iii) immunologic suppression of hematopoiesis (mediated by antibodies or cytotoxic T cells); and (iv) mutations in genes controlling hematopoiesis resulting in inherited bone marrow failure syndromes. Physical examination in case of severe anemia reveals pallor and/or signs of congestive heart failure. Ecchymoses, petechiae, gum bleeding and nose bleeds are associated with thrombocytopenia. Fever, pneumonia or sepsis may occur due to neutropenia. Inherited bone marrow failure syndromes, usually diagnosed in childhood or as young adults, may be associated with characteristic congenital physical anomalies, positive family history or neonatal thrombocytopenia., Epidemiology:['2-6 individuals per million populations', '1.5 to about seven cases per million inhabitants/year, and from 25–60 years, respectively.', 'DEPENDS ON SEVERITY OF SYMPTOMS', 'There is no guaranteed way to prevent aplastic anemia.'], Complications:['Bleeding complications', 'cardiac failure', 'infections'], Diagnostics:['Hb', 'Peripheral Blood Smear', 'PLATELET COUNT', 'Reticulocyte Count', 'NEUTROPHILS'], Differential diagnosis:['Acute lymphoblastic leukemia', 'Acute Myeloid Leukemia (AML)', 'MEGALOBLASTIC ANAEMIA', 'multiple myeloma', 'myelodysplastic syndrome (MDS)', "non-hodgkin's lymphoma", 'thrombocytopenia'], disease description:Aplastic anemia comprises a group of disorders of the hematopoietic stem cells resulting in the suppression of one or more of erythroid, myeloid and megakaryocytic cell lines. The condition may be inherited or acquired. In developed countries, bone marrow failure due to hypoplastic or aplastic anemia affects 2-6 individuals per million populations. Although precise information is lacking, the prevalence is estimated to be higher in India.

A 23-year-old patient with ['absent respiration', 'hypothermia', 'pallor', 'hypotonia', 'seizures', 'shock', 'INTRACRANIAL HAEMORRHAGE', 'Bradycardia', 'cyanosis']

Disease Name: Apnea Of Prematurity, symptoms: ['absent respiration', 'hypothermia', 'pallor', 'hypotonia', 'seizures', 'shock', 'INTRACRANIAL HAEMORRHAGE', 'Bradycardia', 'cyanosis'], Treatment: [{'medication': ['caffeine ', 'Aminophylline ', 'Doxapram ']}, 'Prone position Prone positioning can improve thoracoabdominal synchrony and stabilize the chest wall without affecting breathing pattern or SpO2. Several studies have demonstrated that prone position reduces AOP. Extension of the neck 15° from the prone position is referred to as the head elevated tilt position, which has been found to decrease episodes of oxygen desaturation by 48.5%. A more comfortable three-stair-position that maintains the head and abdomen in a horizontal position was reported to improve apnea, bradycardia, and desaturation. However, head elevated tilt position has not been shown to work in combination with pharmacologic therapy. Recently, two randomized controlled trials investigated the effect of three different postural interventions on the incidence of bradycardia and desaturation. The researchers found that the effect of head elevated tilt position and three-stair-position interventions following aminophylline treatment was similar to standard prone positioning and only decreased the rate of desaturation by 12%. Thus, in infants receiving other effective treatment, neither head elevated tilt position nor three-stair-position resulted in a further improvement in AOP. Since head elevated tilt position and three-stair-position are easy to provide, it should be considered as a first-line intervention in infants with AOP.\nContinuous positive airway pressure and nasal intermittent positive pressure ventilation CPAP at 4–6 cmH2O has proven a safe and effective therapy for AOP over the past 35 years. CPAP delivers a continuous distending pressure via the infant’s pharynx to the airways to prevent both pharyngeal collapse and alveolar atelectasis. Therefore, CPAP can enhance functional residual capacity and reduce the work of breathing, improving oxygenation and decreasing bradycardia. CPAP works effectively to reduce the incidence of obstruction, but it has no clear efficacy in central AOP.\nAn extension of CPAP is the administration of NIPPV. Systematic meta-analysis has shown it to be effective in preventing extubation failure and for the treatment of AOP. A randomized crossover trial found that variable-flow nasal continuous positive airway pressure (NCPAP) is more effective in treating AOP than a conventional ventilator using NIPPV mode. In a word, reduced work of breathing may be the key to improving AOP, which can be achieved via either synchronized NIPPV or variable-flow NCPAP devices.'], Pathophysiology: While AOP is a developmental disorder, the reasons behind the propensity for apnea in immature infants are not entirely clear. Although the pathogenesis of AOP is poorly understood, the immature pulmonary reflexes and breathing responses to hypoxia and hypercapnia likely contribute to the occurrence or severity of AOP. It may also be exacerbated by a number of coexisting factors or disease states. Severe apnea that lasts longer than 20 s is usually associated with bradycardia or desaturation, which may lead to disturbances of cerebral hemodynamics and possibly affect neurodevelopmental outcome. However, it is difficult to prove a link between apnea and poor neurodevelopmental outcomes due to a number of comorbidities and confounding factors affecting neurological development in premature infants. Therefore, evaluating the consequences of AOP on long-term neurodevelopment remains a challenge., Epidemiology:['The incidence of AOP is inversely correlated with gestational age and birth weight. Seven percent of neonates born at 34 to 35 weeks gestation, 15% at 32 to 33 weeks, 54% at 30 to 31 weeks [50], and nearly all infants born at <29 weeks gestation or <1,000 g exhibit AOP.'], Complications:['cerebral palsy', 'delayed motor development'], Diagnostics:nan, Differential diagnosis:[], disease description:Apnea of prematurity (AOP) is a common problem affecting premature infants, likely secondary to a “physiologic” immaturity of respiratory control that may be exacerbated by neonatal disease. These include altered ventilatory responses to hypoxia, hypercapnia, and altered sleep states, while the roles of gastroesophageal reflux and anemia remain controversial.

Woman aged 20 experiencing ['breast tenderness', 'NODULES', 'breast lump']

Disease Name: Apocrine Carcinoma, symptoms: ['breast tenderness', 'NODULES', 'breast lump'], Treatment: ['Wide excision and close follow-up are required. Based on the similarities between breast and apocrine carcinoma it may be of benefit \nto treat patients with high-risk tumours and positivity for steroid \nreceptors with medications such as tamoxifen'], Pathophysiology: Three histological patterns may be seen: tubular, tubulopapillary and solid. The degree of differentiation varies, and the diagnosis is often diffi cult in poorly differentiated tumours. Mitotic figures, local invasion and nuclear pleomorphism all suggest a malignant lesion. The most specific pathological feature is the presence of decapitation secretion. Some cases are associated with prominent pagetoid spread, particularly those presenting on genital skin. Tumour cells are positive for gross cystic disease fluid protein-15 (GCDFP-15), and they show positivity for oestrogen, progesterone and androgen receptors in up to a third of f cases. Recently, it is suggested that an immunohistochemical panel of adipophilin, ER, PR, HER2, cytokeratin 5/6 and mammaglobin may be helpful in distinguishing cutaneous apocrine carcinoma from mammary apocrine carcinoma as the former is positive for these markers whilst the latter tends to be negative. A histologically distinctive variant of apocrine carcinoma has been described as cribiform apocrine carcinoma. The designation as malignant is surprising as this tumour shows little cytological atypia, low mitotic activity, does not tend to recur and no metastases have been reported, Epidemiology:['Apocrine carcinoma affects a wide age range of patients from 19 to 92 years, with the reported mean age varying from 53 to 62. Using strict morphologic criteria, apocrine carcinoma is rare and constitutes less than 1% of all breast cancers.', 'Apocrine carcinoma is a rare malignant sweat gland tumor that has been reported in approximately 200 cases.', 'Patients with grade 3 tumours have a poor prognos', 'NA'], Complications:['post-surgical complications'], Diagnostics:['HER 2 NEU'], Differential diagnosis:['Metaplastic carcinomas: Pure epithelial metaplasti', 'Oncocytic carcinoma', 'phyllodes tumor', 'Secretory carcinoma', 'squamous cell carcinoma.'], disease description:A malignant adnexal carcinoma showing clear evidence of apocrine differentiation – large cells with abundant pink cytoplasm and decapitation secretion. Age Patients are middle aged or elderly. Sex There is a slight predilection for females.

A 34-year-old patient experiencing ['papules', 'itching', 'Hair loss in the axillae']

Disease Name: Apocrine Miliaria, symptoms: ['papules', 'itching', 'Hair loss in the axillae'], Treatment: ['First Line\n\nFirst-line treatments include topical and oral retinoids, topical benzoyl peroxide, topical clindamycin, intralesional or topical corticosteroids (TCS), topical calcineurin inhibitors (CNIs), and oral contraceptives.These are the initial choices because of availability, easy administration, and low risk for serious side effects. There has been no establishment of optimal regimens. Recurrence is possible after discontinuing treatment.\n\nLow potency topical corticosteroids (TCS) are best (less risk of skin atrophy, striae, fissuring), usually twice daily until symptoms improve and then may decrease to daily use two to three times per week.\nTopical clindamycin twice daily. Patients may see improvement in the first few weeks. Te mechanism is unclear.\nTopical CNIs reduce inflammation akin to TCS without the risk of cutaneous atrophy. Both pimecrolimus and tacrolimus use have resulted in moderate to near-complete clearance.\nTopical retinoids - Both tretinoin and adapalene are options. These are thought to reduce follicular occlusion and secondary ductal occlusion. Skin irritation is an issue. Patients may tolerate application every other day instead of daily may be better tolerated.\nOral isotretinoin has shown decent results in anecdotal reports.\nSecond Line and Novel Treatments\n\nThese are better for cases that are severe and/or refractory to the first-line therapies. These include:', 'Second line-\tUltraviolet light', 'electrocautery,\nsurgical excision of the affected skin or subcutaneous removal of \nthe apocrine glands'], Pathophysiology: The condition occurs as a result of apocrine sweat duct occlusion by aggregates of epithelial cells of the apocrine or apoeccrine secretory cells. The earliest pathological sign is a small vesicle in the apocrine duct. Later, the apocrine glands are seen to be enlarged, and as a consequence of repeated inflammatory events, perifollicular xanthomatosis with perifollicular foam cells expressing CD68 may develop, Epidemiology:['The exact prevalence and incidence are unknown, as it is a rare disorder.', 'variable', 'The prevention and treatment of miliaria primarily consists of controlling heat and humidity so that sweating is not stimulated. Measures may involve treating a febrile illness; removing occlusive clothing; limiting activity; providing air conditioning; or, as a last resort, having the patient move to a cooler climate.'], Complications:['hyperpigmented skin discoloration'], Diagnostics:['HISTOPATHLOGY', 'skin biopsy with immunohistochemistry', 'Dermoscopy'], Differential diagnosis:['acanthosis nigricans', "Darier's disease", 'folliculitis', 'milia', 'Pseudofolliculitis', 'Syringomas'], disease description:Apocrine miliaria is a disorder of the apocrine glands comparable to prickly heat of the eccrine glands, and caused by obliteration of the apocrine duct at the infundibulum. It usually presents with an itchy papular eruption in the axillae, ano-genital area or on the areolae of the nipple.

Symptoms at 39: ['hypernatremia', 'hypertension', 'hypokalemia']

Disease Name: Apparent Mineralocorticoid Excess Syndrome, symptoms: ['hypernatremia', 'hypertension', 'hypokalemia'], Treatment: ['administration of exogenous corticoids to block ACTH and suppress the endogenous secretion of cortisol.', 'blockade of the mineralocorticoid receptor by spironolactone (2-10 mg/kg/day), combined with thiazides to help to normalize blood pressure and reduce hypercalciuria and nephrocalcinosis.'], Pathophysiology: Apparent mineralocorticoid excess is an autosomal recessive disorder causing hypertension (high blood pressure), hypernatremia (increased blood sodium concentration) and hypokalemia (decreased blood potassium concentration). It results from mutations in the HSD11B2 gene, which encodes the kidney isozyme of 11ß-hydroxysteroid dehydrogenase type 2. In an unaffected individual, this isozyme inactivates circulating cortisol to the less active metabolite cortisone. The inactivating mutation leads to elevated local concentrations of cortisol in the aldosterone sensitive tissues like the kidney. Cortisol at high concentrations can cross-react and activate the mineralocorticoid receptor due to the non-selectivity of the receptor, leading to aldosterone-like effects in the kidney. This is what causes the hypokalemia, hypertension, and hypernatremia associated with the syndrome. Patients often present with severe hypertension and end-organ changes associated with it like left ventricular hypertrophy, retinal, renal and neurological vascular changes along with growth retardation and failure to thrive. In serum both aldosterone and renin levels are low., Epidemiology:['Fewer than 1,000 people in the U.S.', 'AME is exceedingly rare, with fewer than 100 cases recorded worldwide', 'with appropriate treatment appears to be good.', 'Low Sodium diet.'], Complications:['hypertension', 'hypoaldosteronism', 'hypokalaemia'], Diagnostics:['Cortisol', 'GENETIC TESTING'], Differential diagnosis:["Liddle's syndrome"], disease description:A rare form of pseudohyperaldosteronism characterized by very early-onset and severe hypertension, associated with low renin levels and hypoaldosteronism.

having ['headache', 'lymphadenopathy', 'pharyngitis', 'Rashes', 'fever', 'Oral ulcers'] at the age of 23

Disease Name: Apthous Stomatis, symptoms: ['headache', 'lymphadenopathy', 'pharyngitis', 'Rashes', 'fever', 'Oral ulcers'], Treatment: ['Many treatment options are available for aphthous stomatitis, including topical agents such as local anesthetics (benzocaine), coating or occlusive agents (bismuth subsalicylate, sucralfate, 2-octyl cyanoacrylate, and various bioadherent emollient pastes), antiseptics (chlorhexidine gluconate and hydrogen peroxide), anti-inflammatory agents such as glucocorticosteroids (clobetasol, dexamethasone, fluocinonide, and triamcinolone), amlexanox and metalloprotease inhibitors (antimicrobials tetracycline, doxycycline, or minocycline), honey, and immunomodulatory agents (amlexanox, colchicine, cyclosporine, cyclophosphamide, dapsone, methotrexate, montelukast, thalidomide, or retinoids).'], Pathophysiology: Aphthous ulcerations are initially and primarily the result of T cell-mediated immune dysfunction but also may involve neutrophil and mast cell-mediated destruction of the mucosal epithelium. Lesions can have alterations in several intercellular mediators, such as elevations in interferon gamma, tumor necrosis factor-alpha, and interleukins (IL)-2, IL-4 and IL-5, as well as various adhesion molecules involved in cell communication and epithelial integrity. This inflammatory process results in a pseudomembrane containing fibrinous exudate, bacteria, inflammatory cells, and necrotic mucosal cells.??, Epidemiology:['Recurrent aphthous ulcers affect 2-66% of the international population', 'GOOD', 'Patient education is important to prevent recurrence of aphthous ulcerations.\n\nPractice good oral hygiene and avoidance of local trauma or oral hygiene products of known sensitivity.\nConsider taking dietary supplements with iron, zinc, or vitamins B1, B2, B6, B12, or C if a vitamin or mineral deficiency is identified.\nOnly individuals diagnosed with celiac disease should choose a gluten-free diet.\nAvoid known trigger foods, emotional or physiologic stress whenever possible.'], Complications:['dysphagia', 'infection'], Diagnostics:['Complete Blood Count CBC', 'Complete Blood Count CBC', 'serum Vitamin B12 level'], Differential diagnosis:['Contact dermatitis', 'HERPES SIMPLEX', 'Irritant contact dermatitis', 'Lichen Planus'], disease description:Aphthous stomatitis is a common ailment, idiopathic in nature, with recurrent painful aphthous ulcers (commonly termed "canker sores") on the non-keratinized oral mucous membranes. 

Person aged 35 with manifestations like ['lymphadenopathy', 'pharyngitis', 'Rashes', 'throat pain', 'fever']

Disease Name: Arcanobacterium Haemolytic Infection, symptoms: ['lymphadenopathy', 'pharyngitis', 'Rashes', 'throat pain', 'fever'], Treatment: ['first-line therapy for deep soft-tissue infections should be intravenous penicillin or cephalosporins. In cases of treatment failure or beta-lactam allergies, macrolides are a good alternative.\n\nAdditionally, for patients with beta-lactam allergies, antibiotics such as vancomycin, fluoroquinolones, clindamycin, and doxycycline should be considered. In addition to medical management with antibiotics, patients with systemic infections may require vasopressors, fluid resuscitation, and surgical intervention as needed.'], Pathophysiology: Cultures of A. haemolyticum can be detected as a part of normal skin flora and pharynx of healthy individuals. This causes difficulty in the early detection of the pathogen since the organism is often overlooked as the cause of symptoms during an infection. In symptomatic patients, A. haemolyticum has been cultured as the sole pathogen or as a part of a polymicrobial infection.There are two biotypes of A. haemolyticum: smooth and rough. In the smooth-type form, even colonies on a growth medium are beta-hemolytic, beta-glucuronidase negative, and ferment sucrose and trehalose. Smooth-type colonies are more commonly associated with soft-tissue infections. The rough-type form uneven colonies on a growth medium, are non-hemolytic, beta-glucuronidase positive, and do not ferment sucrose and trehalose. Rough-type colonies are more commonly associated with pharyngitis., Epidemiology:['haemolyticum is responsible for 0.5% - 2.5% of all bacterial pharyngitis', 'good', 'there are no known preventive methods'], Complications:['Brain Abscess', 'Endocarditis', 'Bacteremia'], Diagnostics:['BLOOD CULTURE test'], Differential diagnosis:['acute pharyngitis', 'scarlet fever'], disease description:Arcanobacterium haemolyticum is a gram-positive, facultative anaerobic, branching bacillus. The first cases ascribed to this pathogen were described in 1946 and caused ulcerative skin lesions among American soldiers in the Pacific Islands. Today, infections by A. haemolyticum are rare but most commonly cause pharyngitis in adolescents and young adults or skin and soft-tissue infections in immunocompromised populations.Though cases of systemic infections such as meningitis or bacteremia are uncommon, A. haemolyticum should remain on the differential to enable the early recognition, management, and treatment of disease associated with the pathogen.The classic presentation of pharyngeal disease may commonly be mistaken for streptococcal infections. Patients present with a sore throat, pharyngeal erythema, fever, exanthema, and swollen lymph nodes. The natural history of the disease may be self-limiting or require antibiotic treatment

Individual aged 53 dealing with ['Change in eye colour']

Disease Name: Arcus Senilis, symptoms: ['Change in eye colour'], Treatment: ['Arcus senilis in of themselves do not warrant treatment, as they are clinically insignificant and asymptomatic; however, if after further assessment an underlying disorder is found to be the cause of the arcus the disorder should be treated, i.e. if a patient is found to have underlying hypercholesteremia this condition should be addressed through environmental, and pharmacologic treatment options'], Pathophysiology: This is a lipoid infiltration of the cornea seen in the elderly. It is almost universally present to some extent in people who are above 60 years of age. It commences as a crescentic grey line or whitish arc concentric with the upper and lower margins of the cornea, the extremities of which finally meet so that an opaque line, thicker above and below, is formed completely round the cornea. It is characterized by being separated from the margin by a narrow zone of comparatively clear cornea, being sharply defined on the peripheral side, fading off on the central. It is never more than about 1 mm broad, is of no importance either from the point of view of vision or of the vitality of the cornea and is unrelated to secondary forms of hypercholesterolaemia., Epidemiology:['the prevalence of corneal arcus in men (47.76%) was higher than in women (40.84%', '44.28%', 'good', 'You can’t stop arcus senilis from forming when it’s the result of aging. But you can take steps to keep cholesterol levels in line as you go through life. Here are some things you can do:\n\nDon’t smoke. Make plans to quit if you do smoke.\nFind ways to add physical activity in your days.\nTry to reach and maintain a healthy weight.\nFollow a heart-healthy food plan, such as the Mediterranean diet.'], Complications:['coronary artery disease'], Diagnostics:['ophthalmoscopy'], Differential diagnosis:['hypercholesterolaemia', 'impaired lipid metabolism'], disease description:This is a lipoid infiltration of the cornea seen in the elderly. It is almost universally present to some extent in people who are above 60 years of age.

having ['facial flushing', 'lymphadenopathy', 'sore throat', 'conjunctival redness', 'Oral ulcers', 'malaise', 'fever', 'Body Ache'] at the age of 42

Disease Name: Argentine Hemorrhagic Fever, symptoms: ['facial flushing', 'lymphadenopathy', 'sore throat', 'conjunctival redness', 'Oral ulcers', 'malaise', 'fever', 'Body Ache'], Treatment: ['consists of the early transfusion of immune plasma in standardized doses of neutralizing antibodies.', 'Patient management included supportive care and combination therapy with ribavirin and favipiravir.'], Pathophysiology: The incubation period is usually from 6 to 14 days. Most infections with Junin virus (80%) result in clinical disease. Three phases are recognized in the illness: prodromal, neurological–hemorrhagic, and convalescence Prodromal phase: This phase lasts for the first week from onset of symptoms. The onset is insidious, with chills, malaise, anorexia, headache, myalgia centered particularly over the lower back, and moderate hyperthermia (38–39 °C). Other common symptoms include retro-orbital pain, nausea or vomiting, epigastric pain, photophobia, dizziness, constipation or mild diarrhea. Physical examination reveals flushing of the face, neck and upper chest; conjunctival congestion and periorbital edema.Neurologic–hemorrhagic phase: Around 20–30% of the cases with AHF between 8 and 12 days after onset of symptoms enter in this phase, presenting severe hemorrhagic or neurologic manifestations, shock and superimposed bacterial infections. Hemorrhagic signs include hematemesis, melena, hemoptysis, epistaxis, hematomas, metrorrhagia and hematuria.Convalescence phase: Surviving cases experience a prolonged, protracted convalescence that lasts from 1 to 3 months. Patients experience asthenia, irritability, memory changes and hair loss. Around 10% of the cases treated with immune plasma develop a late neurological syndrome (LNS).Convalescence phase: Surviving cases experience a prolonged, protracted convalescence that lasts from 1 to 3 months. Patients experience asthenia, irritability, memory changes and hair loss. Around 10% of the cases treated with immune plasma develop a late neurological syndrome (LNS)., Epidemiology:['Estimated risk population of 5 million.', 'It is found mostly in people who reside or work in rural areas; 80% of those infected are males between 15 and 60 years of age.', 'variable', 'The Candid #1 vaccine for AHF was created in 1985 by Argentine virologist Dr. Julio Barrera Oro.\nCandid #1 has been applied to adult high-risk population and is 95.5% effective'], Complications:['internal bleeding', 'MULTIORGAN FAILURE'], Diagnostics:['REVERSE TRANSCRIPTASE PCR FOR VIRAL NUCLEIC ACID'], Differential diagnosis:['Dengue with warning signs', 'hepatitis', 'infectious mononucleosis', 'Leptospirosis', 'Rickettsial Infection', 'TYPHOID FEVER'], disease description:Argentine hemorrhagic fever (AHF) or O'Higgins disease, also known in Argentina as mal de los rastrojos (stubble disease) is a hemorrhagic fever and zoonotic infectious disease occurring in Argentina. It is caused by the Junín virus.(an arenavirus, closely related to the Machupo virus, causative agent of Bolivian hemorrhagic fever). Its vector is the drylands vesper mouse, a rodent found in Argentina and Paraguay.

Symptoms at 53 years: ['Ataxia', 'growth retardation in children', 'hyperactivity', 'spasticity']

Disease Name: Argininemea, symptoms: ['Ataxia', 'growth retardation in children', 'hyperactivity', 'spasticity'], Treatment: ['Conservative treatment, i.e., intravenous (IV) fluids : sodium phenylacetate or sodium benzoate, along with restriction of protein intake, and the introduction of non-protein calorie sources like fats and carbohydrates.', 'Liver transplantation can be considered as an ultimate treatment to reduce recurrent hyperammonemia.'], Pathophysiology: Arginase, commonly found in liver, erythrocytes, and salivary glands, catalyzes the fifth and last reaction of the urea cycle, hydrolyzing L-arginine into ornithine and urea. Its deficiency or absence, causes accumulation of arginine, reversibly translating into ammonia overproduction at different levels and expressions after 1 to 3 years of life; although, a few cases have been reported in early infancy. Orotic acid accumulation can be found, given that reduction of ornithine impairs ornithine transcarbamylase activity, creating a backup or overflow of carbamyl phosphate, which is subsequently shunted to the pyrimidine synthetic path. , Epidemiology:['incidence ranges from 0.5 to 1 per 1,000,000', 'poor', 'You can’t prevent since it’s a genetic condition. If you plan on becoming pregnant and want to understand the risks of having a child with a genetic condition, talk to your provider about genetic testing.'], Complications:['Cerebral oedema', 'neurotoxicity', 'spasticity', 'brain damage'], Diagnostics:['SERUM ARGININE'], Differential diagnosis:['Citrullinaemia type1', 'Hyperargininemia', 'Ornithine transcarbamylase deficiency', 'Urea Cycle Defects'], disease description:Argininemia is an autosomal recessive disorder causing hyperammonemia secondary to arginine accumulation. It is a disorder first noticed in children with growth reduction, slowing cognition, and milestone development. Arginase deficiency (argininemia) is an autosomal recessive metabolic disorder characterized by hyperammonemia secondary to arginine accumulation. Ammonia levels can vary according to the patient’s current age and status, presenting initially with slow growth, followed by developmental delay and cognitive problems. When improperly treated, it may lead to regression. 

Person, 32 years old, presenting ['coma', 'seizures', 'lethargy', 'Somnolence', 'tachypnoea', 'vomiting', 'refusal to feed']

Disease Name: Argininosuccinate Lyase Deficiency/argininosuccini, symptoms: ['coma', 'seizures', 'lethargy', 'Somnolence', 'tachypnoea', 'vomiting', 'refusal to feed'], Treatment: nan, Pathophysiology: Deficiency of ASL results in an accumulation of argininosuccinic acid in tissues, and excretion of argininosuccinic acid in urine leading to the condition argininosuccinic aciduria, ASA.ASA is an autosomal recessive disorder and is the second most common urea cycle disorder. In addition to the accumulation of argininosuccinic acid, ASL deficiency results in decreased synthesis of arginine which is in common with all UCDs except argininemia. Arginine is not only the precursor for the synthesis of urea and ornithine as part of the urea cycle but it is also the substrate for the synthesis of nitric oxide, polyamines, proline, glutamate, creatine and agmatine. Hence, while ASL is the only enzyme in the body able to generate arginine, at least four enzymes use arginine as substrate: arginine decarboxylase, arginase, nitric oxide synthetase (NOS) and arginine/glycine aminotransferase. In the liver, the main function of ASL is ureagenesis, and hence, there is no net synthesis of arginine. In contrast, in most other tissues, its role is to generate arginine that is designated for the specific cell’s needs., Epidemiology:nan, Complications:[], Diagnostics:nan, Differential diagnosis:[], disease description:nan

Individual aged 48 with manifestations like ['respiratory alkalosis', 'coma', 'vomiting', 'seizures']

Disease Name: Argininosuccinic Aciduria (argininosuccinate Lyase Deficiency), symptoms: ['respiratory alkalosis', 'coma', 'vomiting', 'seizures'], Treatment: ['Genetic counseling\nASA is inherited in an autosomal recessive manner; where both parents are unaffected carriers, the risk of disease transmission is 25%.', 'Prenatal diagnosis is possible in families with a known disease causing mutation on both alleles.', "During an acute hyperammonemic episode, oral proteins must be avoided (for 24-48 hours' maximum) and intravenous (I.V.) lipids, glucose and insulin (if needed) should be given to promote anabolism. I.V. nitrogen scavenging therapy (with sodium benzoate and/or sodium phenylacetate/phenylbutyrate) should normalize ammonia levels, but if unsuccessful or in case of severe hyperammonemic encephalopathy, hemodialysis is recommended."], Pathophysiology: Mutations in the ASL gene cause argininosuccinic aciduria. This condition belongs to a class of genetic diseases called urea cycle disorders because they are caused by problems with a process in the body called the urea cycle. The urea cycle is a sequence of reactions that occurs in liver cells. This cycle breaks down excess nitrogen, which is made when protein is used by the body, to make a compound called urea. Urea is removed from the body in urine. Breaking down excess nitrogen and excreting it as urea prevents it from accumulating in the body as ammonia.The ASL gene provides instructions for making an enzyme called argininosuccinate lyase, which is needed for the fourth step of the urea cycle. The specific role of the argininosuccinate lyase enzyme is to start the reaction in which the amino acid arginine, a building block of proteins, is produced from argininosuccinate, the molecule that carries the waste nitrogen collected earlier in the urea cycle. The arginine is later broken down into urea, which is excreted, and ornithine, which restarts the urea cycle.In people with argininosuccinic aciduria, argininosuccinate lyase is dysfunctional or missing. As a result, the urea cycle cannot proceed normally, arginine is not produced, and nitrogen is not broken down efficiently. The excess nitrogen accumulates in the blood in the form of ammonia. This buildup of ammonia damages the brain and other tissues and causes neurological problems and other signs and symptoms of argininosuccinic aciduria. It is unclear how a lack of arginine contributes to the features of this condition., Epidemiology:['Ranges between 1/70,000-218,000 worldwide.', 'Poor', 'Using chorionic villus sampling, prenatal diagnosis is possible as early as 11-12 weeks’ gestation. It is essential to establish the nature of the mutation in the parents first, given the large number of private mutations known to occur. This should be discussed with any family with one or more affected first-degree relatives.'], Complications:['coma', 'death', 'seizures'], Diagnostics:['plasma ammonia', 'molecular genetic testing', 'citrulline'], Differential diagnosis:['Carbamoyl phosphate synthetase (CPS) deficiency', 'Citrullinaemia type1', 'N-acetylglutamate synthetase deficiency', 'Ornithine transcarbamylase (OTC) deficiency'], disease description:A rare, genetic disorder of urea cycle metabolism typically characterized by either a severe, neonatal-onset form that manifests with hyperammonemia accompanied with vomiting, hypothermia, lethargy and poor feeding in the first few days of life, or late-onset forms that manifest with stress- or infection-induced episodic hyperammonemia or, in some, behavioral abnormalities and/or learning disabilities, or chronic liver disease. Patients often manifest liver dysfunction.

Individual, 43 years old, with ['coma', 'Confusion', 'developmental delay', 'seizures', 'vomiting', 'SKIN LESIONS']

Disease Name: Argininosuccinic Aciduria (arginsa)/argininosuccin, symptoms: ['coma', 'Confusion', 'developmental delay', 'seizures', 'vomiting', 'SKIN LESIONS'], Treatment: ['Treatment involves dietary protein restriction and drugs (sodium \nbenzoate and/or sodium phenylbutyrate). l-arginine is also given \nto correct the defi ciency of this amino acid and to facilitate the \nexcretion of ammonia (incorporated into argininosuccinic acid). \nThese measures prevent hyperammonaemia and lead to resol\x02ution of the trichorrhexis nodosa.'], Pathophysiology: Episodes of encephalopathy in ASA are primarily caused by hyperammonaemia. It has been suggested that the trichorrhexis nodosa may be due to chronic arginine defi ciency. This seems unlikely as arginine defi ciency occurs in most urea cycle disorders but abnormal hair is only found in ASA. Argininosuccinate lyase stabilizes nitric oxide synthase and some of the long-term complications may be due to nitric oxide defi ciency . Genetics This is an autosomal recessive disorder caused by mutations in the ASL gene., Epidemiology:['Its incidence is approximately one in 70 000', 'Prognosis Even with treatment, most patients hav', 'To Do : dietry protien restriction'], Complications:[], Diagnostics:['URINE ANALYSIS (Protein)'], Differential diagnosis:[], disease description:Argininosuccinic aciduria (ASA) is a rare urea cycle disorder. It may present acutely,with hyperammonaemia, or chronically, with learning diffi culties and trichorrhexis nodosa.

A 40-year-old woman suffering from ['macromastia', 'Gynecomastia', 'Irregular menstruation', 'growth abnormality']

Disease Name: Aromatase Excess Syndrome, symptoms: ['macromastia', 'Gynecomastia', 'Irregular menstruation', 'growth abnormality'], Treatment: ['Several treatments have been found to be effective in managing AEXS, including aromatase inhibitors and gonadotropin-releasing hormone analogues in both sexes, androgen replacement therapy with non-aromatizable androgens such as DHT in males, and progestogens (which, by virtue of their antigonadotropic properties at high doses, suppress estrogen levels) in females. In addition, male patients often seek bilateral mastectomy, whereas females may opt for breast reduction if warranted.'], Pathophysiology: Rearrangements of genetic material involving the CYP19A1 gene cause aromatase excess syndrome. The CYP19A1 gene provides instructions for making an enzyme called aromatase. This enzyme converts a class of hormones called androgens, which are involved in male sexual development, to different forms of estrogen. In females, estrogen guides female sexual development before birth and during puberty. In both males and females, estrogen plays a role in regulating bone growth. The condition can result from several types of genetic rearrangements involving the CYP19A1 gene. These rearrangements alter the activity of the gene and lead to an increase in aromatase production. In affected males, the increased aromatase and subsequent conversion of androgens to estrogen are responsible for the gynecomastia and limited bone growth characteristic of aromatase excess syndrome. Increased estrogen in females can cause symptoms such as irregular menstrual periods and short stature., Epidemiology:['The prevalence of aromatase excess syndrome is unknown; more than 20 cases have been described in the medical literature.', 'variable', '1. Losing excess body fat. \n2. Increasing zinc, selenium, and magnesium intake to inhibit aromatase. \n3. Increasing the intake of foods containing natural aromatase inhibitors, including mushrooms, celery, carrots, spinach, and grapes.'], Complications:['hypoaldosteronism', 'macromastia'], Diagnostics:['GENETIC TESTING'], Differential diagnosis:['Endometriosis', 'Polycystic Ovarian Disease', 'Uterine fibroids'], disease description:Aromatase excess syndrome is a condition characterized by elevated levels of the female sex hormone estrogen in both males and females. Males with aromatase excess syndrome experience breast enlargement (gynecomastia) in late childhood or adolescence.

Symptoms reported by a baby aged 4.87 include ['Miosis', 'ptosis', 'hypotonia', 'difficulty in walking', 'Muscle Stiffness', 'DROOLING OF SALIVA', 'Hypotension', 'abnormal rotation of eyeballs', 'fainting', 'lack of energy', 'nasal congestion', 'agitation', 'Irritability', 'poor feeding', 'athetosis', 'developmental delay', 'Sleep disturbances']

Disease Name: Aromatic L-amino Acid Decarboxylase (aadc) Deficiency, symptoms: ['Miosis', 'ptosis', 'hypotonia', 'difficulty in walking', 'Muscle Stiffness', 'DROOLING OF SALIVA', 'Hypotension', 'abnormal rotation of eyeballs', 'fainting', 'lack of energy', 'nasal congestion', 'agitation', 'Irritability', 'poor feeding', 'athetosis', 'developmental delay', 'Sleep disturbances'], Treatment: ['The pattern of inheritance is autosomal recessive; where both parents are unaffected carriers, there is a 25% risk of transmitting the disease to offspring. Genetic counseling about inheritance, risk of reoccurrence and disease is very important for affected families.', 'Treatment with dopamine agonists and MAO inhibitors is beneficial'], Pathophysiology: Aromatic L-amino acid decarboxylase (AADC), coded by the DDC gene (7p12.2-p12.1), is the final enzyme in the biosynthesis of the monoamine neurotransmitters serotonin and dopamine; dopamine is the precursor for norepinephrine and epinephrine. Subsequently, AADC enzyme deficiency results in a severe combined deficiency of serotonin, dopamine, norepinephrine and epinephrine., Epidemiology:['between 1:64,000 and 1:90,000 births in the USA, 1:116,000 in the European Union, 1:162,000 in Japan and 1:32,000 in Taiwan', 'The prognosis mainly depends on the disease severi', "It can't be prevented as it is an inherited disorder. Although Non-drug therapies, such as physiotherapy, occupational therapy, and speech therapy, can help AADC patients build muscle strength, find alternative ways to perform daily tasks, and overcome difficulties with speaking or eating."], Complications:['lack of coordination', 'muscle weakness'], Diagnostics:['CSF EXAMINATION', 'AMNIOTIC FLUID EXAMINATION'], Differential diagnosis:[], disease description:A rare, severe, genetic neurometabolic disorder associated with clinical manifestations related to impaired synthesis of dopamine, noradrenaline, adrenaline and serotonin.

A 31-year-old suffering ['absent pulses', 'presence of bruit', 'INTERMITTENT CLAUDICATION', 'foot pain', 'IMPAIRED GAIT', 'hair loss', 'MUSCLE ATROPHY']

Disease Name: Arterial Thromboembolism, symptoms: ['absent pulses', 'presence of bruit', 'INTERMITTENT CLAUDICATION', 'foot pain', 'IMPAIRED GAIT', 'hair loss', 'MUSCLE ATROPHY'], Treatment: ['Anticoagulants (commonly referred to as “blood thinners”) are the medications most commonly used to treat DVT or PE. Although called blood thinners, these medications do not actually thin the blood.\n...\nAnticoagulants\nWarfarin,\nDabigatran,\nRivaroxaban,\nApixaban, and.\nEdoxaban.\n\nThrombolytics\nThrombolytics (commonly referred to as “clot busters”) work by dissolving the clot. They have a higher risk of causing bleeding compared to the anticoagulants, so they are reserved for severe cases.', 'Inferior vena cava filter\nWhen anticoagulants cannot be used or don’t work well enough, a filter can be inserted inside the inferior vena cava (a large vein that brings blood back to the heart) to capture or trap an embolus (a clot that is moving through the vein) before it reaches the lungs.\nThrombectomy/Embolectomy\nIn rare cases, a surgical procedure to remove the clot may be necessary. Thrombectomy involves removal of the clot in a patient with DVT. Embolectomy involves removal of the blockage in the lungs caused by the clot in a patient with PE.'], Pathophysiology: Embolic vessel occlusion The majority of arterial emboli originate in the left heart where they form secondary to structural or functional abnormalities. Most other emboli originate from the arterial tree itself. In general, emboli that originate more proximally in relation to the heart have more potential targets available to them. Thus clots originating in the heart or the aortic arch can potentially embolize to any arterial branch in the body. Conversely, atherosclerotic plaque formed in more distal arteries such as the carotids are far more likely to embolize to the brain - causing strokes or transient ischemic attacks (TIA's), while plaques in the infra-renal aorta are far more likely to cause lower extremity ischemia. Retrograde embolization may occasionally occur during the late diastolic flow reversal seen with decreased heart rates. This process is believed to allow large descending aortic plaques to cause strokes. The ultimate probability of an embolus reaching any specific arterial bed is determined by the relative amount of blood flow that bed receives and the anatomy of the arterial branches supplying that area. Larger emboli tend to lodge at points of acute narrowing such as arterial bifurcations or areas of luminal stenosis, whereas smaller emboli may travel distally to lodge in tiny arterioles. Although arterial embolic disease shares many features with arterial thrombosis, there are important distinctions. Differentiating an acute embolic event from an acute thrombotic event is in fact one of the conundrums faced by medical practitioners. Both processes typically affect individuals with risk factors for heart disease and peripheral arterial disease. Often, embolic and thrombotic diseases may coexist in the same patient. In situations such as limb ischemia, making the correct diagnosis early may allow for expedited care. Acuity of presentation is perhaps the most important distinction between the two processes. Because arterial thrombosis is a gradual process that presents with ischemia in its late stages, patients often have time to develop collateral flow to the ischemic region. However, individuals with embolic ischemia usually do not have time to build collateral circulation and therefore often present with more sudden and severe symptoms such as threatened limb loss. Cardiac sources of arterial emboli As noted above, most arterial emboli originate in the heart. In the past, valvular damage from rheumatic heart disease (RHD) was responsible for most cardiac embolic sources. However, as the incidence of RHD has decreased and the population ages, AF has become the most common source of arterial emboli. The most frequent manifestations of cardiac embolic events are strokes and transient ischemic events. Clots formed in the left side of the heart also account for 55-87% of emboli to peripheral arteries and most emboli to the viscera. Long-term systemic anticoagulation, typically with a vitamin K antagonist such as warfarin, greatly reduces the probability of cardiac thrombus formation in high risk patients. Unfortunately, many patients worldwide are not adequately treated, putting them at high risk for arterial thromboembolism. During AF stasis of blood in the left atrium predisposes to clot formation within the left atrial appendage. These thrombi can range in size from a few millimeters to 4cm and are found in 5 to 14% of patients with AF lasting more than two days. Generally, all patients with AF due to valvular pathology such as mitral stenosis (except those with a strong counter-indication) should be anti-coagulated due to their high risk for stroke and other embolic events., Epidemiology:['variable', "It's not possible to prevent blood clots entirely, but you can reduce your risk by lowering your risk of atherosclerosis.\n\nThe main things you can do are:\n\nstop smoking\neat a healthy, balanced diet\nexercise regularly\nmaintain a healthy weight – find advice about losing weight\ncut down on your alcohol consumption\nIf you're at a high risk of getting a blood clot, your doctor may also recommend taking medicines such as:\n\nstatins to manage high cholesterol\nmedicines for high blood pressure\nmedicines to reduce the risk of your blood clotting. For example, an anticoagulant such as warfarin and an antiplatelet such as low-dose aspirin or clopidogrel"], Complications:['heart failure', 'stroke', 'transient ischaemic attacks', 'organ failure', 'organ dysfunction'], Diagnostics:['Complete Blood Count CBC', 'CT Angio', 'MRI', 'CT SCAN', 'CT SCAN'], Differential diagnosis:['Atherosclerosis', 'Myocardial infarction', 'myocarditis', 'PERIPHERAL ARTERY DISEASE', 'PNEUMOTHORAX', 'vasculitis'], disease description:Arterial embolism results when a mass of tissue or a foreign substance travels through the vascular tree, ultimately lodging in a distal artery where it obstructs blood flow. Arterial thrombosis is a blood clot in an artery, which can be very serious because it can stop blood reaching important organs. Arteries are blood vessels that carry blood from the heart to the rest of the body and the heart muscle.

At the age of 32, symptoms like ['nausea', 'vomiting', 'Excessive warmth in the area', 'loss of consciousness', 'seizures', 'swelling', 'Unusual pain', 'neurological deficit']

Disease Name: Arterio Venous Malformation, symptoms: ['nausea', 'vomiting', 'Excessive warmth in the area', 'loss of consciousness', 'seizures', 'swelling', 'Unusual pain', 'neurological deficit'], Treatment: ['Medications can help manage symptoms such as seizures, headaches and back pain.', 'Sclerotherapy, embolization and \nsurgery.'], Pathophysiology: Arteriovenous malformations consist of arteries connecting directly to veins without the intervening capillary bed. Where they connect is called the nidus. The feeding arteries have a deficient muscularis layer and the draining veins dilate due to the high-velocity blood flow they receive. It is not known how these abnormal connections arise. It is postulated that during early fetal development there of a failure of regression of arteriovenous channels in the primitive plexus that allows these lesions to form which may be due to an aberration in the transforming growth factor ß signalling pathway, Epidemiology:['the point prevalence in adults is ~18/100 000', '1.34 per 100,000 person-years, although the actual prevalence rate is higher due to clinically silent disease, as only 12% of AVMs are estimated to become symptomatic.', 'variable', 'No, AVMs can’t be prevented because researchers believe they’re congenital, meaning you’re born with them. But if you develop any of the symptoms listed in this article, see your healthcare provider right away. Responding quickly to developing symptoms is the best approach.'], Complications:['Haemorrhage', 'ischaemia', 'difficulty in breathing', 'Impaired vision', 'Chronic venous insufficiency', 'Cosmetic deformity', 'Limb growth asymmetry', 'High output cardiac failure'], Diagnostics:['Complete Blood Count CBC', 'Color Doppler', 'ultrasound', 'CT SCAN', 'Magnetic Resonance Arteriography'], Differential diagnosis:['capillary malformations', 'Cerebral venous thrombosis', 'cluster headache', 'intracranial hemorrhage', 'kaposi sarcoma', 'migraine', 'Vascular tumours'], disease description:An arteriovenous malformation (AVM) is an abnormal tangle of blood vessels connecting arteries and veins, which disrupts normal blood flow and oxygen circulation.Arteries are responsible for taking oxygen-rich blood from the heart to the brain. Veins carry the oxygen-depleted blood back to the lungs and heart.Arteriovenous malformations are fast-flow vascular lesions composed of malformed arterial and venous vessels connected directly to one another without an intervening capillary bed. Dermatologists are more likely to encounter arteriovenous malformations when the vasculature affected involves the skin or mucosal surfaces or as an association of hereditary haemorrhagic telangiectasia.

Individual, 47 years old, with ['splinter haemmorhages', 'Cotton wool spots', 'RAPD', 'hemianopia', 'anorexia', 'diplopia', 'headache', 'malaise', 'night sweats', 'weight loss', 'visual loss', 'tenderness of the temporal arteries and scalp.', 'Jaw claudication, characterized by pain on speaking or chewing, is pathognomonic of GCA', 'Optic disc oedema', 'Peripapillary pallor and oedema deep to retina', 'fever']

Disease Name: Arteritic Anterior Ischaemic Optic Neuropathy, symptoms: ['splinter haemmorhages', 'Cotton wool spots', 'RAPD', 'hemianopia', 'anorexia', 'diplopia', 'headache', 'malaise', 'night sweats', 'weight loss', 'visual loss', 'tenderness of the temporal arteries and scalp.', 'Jaw claudication, characterized by pain on speaking or chewing, is pathognomonic of GCA', 'Optic disc oedema', 'Peripapillary pallor and oedema deep to retina', 'fever'], Treatment: [{'medication': ['Methyl prednisolone ']}, 'Goal of treatment is to prevent visual loss in the\nfellow eye, apart from avoiding systemic vascular\ncomplications.\nCorticosteroids, started immediately, as follows,\nconstitute the main treatment.\n• Methylprednisolone 1 gm/day, intravenously for\n3–5 days followed by\n• Prednisolone per oral 80 mg/day to be tapered\nevery week by 10 mg. Daily maintenance therapy\nof 10 mg may have to be continued for 1–2 years'], Pathophysiology: Anterior ischemic optic neuropathy (AION) is thought to be an ischemic process affecting the posterior circulation of the globe, principally vessels (ie, short posterior ciliary arteries) supplying the optic nerve at its exit from the eye. Only glial cells support the optic disc at this site, and it is the only portion of the optic nerve in which swelling can occur. More posterior ischemia results in a similar condition, without visible swelling, and is termed posterior ischemic optic neuropathy.Early observations of optic disc photographs suggested that patients with congenitally smaller discs and having smaller or nonexistent optic nerve cups have an anatomical predisposition for nonarteritic anterior ischemic optic neuropathy (NAION). As an ischemic episode evolves, the swelling compromises circulation within a presumable already more compact disc, with a spiral of ischemia and swelling resulting in further neuronal damage. This type of structural/ischemic spiral is less implicated in the arteritic type of AION, in which the entire ophthalmic arterial circulation to the eye and orbit may be compromised. , Epidemiology:['annual incidence of 2.3 – 10.2/100,000 in the United States (U.S.).', 'variable', 'Managing the risk factors associated with NA-AION is an important preventive measure.\n\nIn addition, people who have risk factors should avoid the use of blood pressure-lowering medications or erectile dysfunction drugs before bedtime. The combination of such drugs along with the normal drop in blood pressure while sleeping could be enough to interrupt blood supply to the optic nerve.\n\nFor A-AION, continued use of corticosteroids is recommended to avoid further loss of vision. Close follow-up with a rheumatologist is needed.'], Complications:['visual loss', 'decreased visual acuity'], Diagnostics:['CRP', 'Erythrocyte Sedimentation Rate (ESR)', 'FUNDOSCOPY', 'VISUAL ACUITY TEST', 'MRI', 'Perimetry', 'Fundus fluorescein angiography (FFA)', 'Temporal artery biopsy'], Differential diagnosis:['ocular hypotony', 'papilledema'], disease description:Anterior Ischaemic Optic Neuropathy (AION) refers to ischaemic damage to the optic nerve head from occlusion of the short posterior ciliary arteries. It is of two types: • Arteritic anterior ischaemic optic neuropathy (AAION), and • Non-arteritic anterior ischaemic optic neuropathy (NAAION). Etiology Arteritic anterior ischaemic optic neuropathy (AAION), results from inflammatory and thrombic occlusion of short posterior ciliary arteries caused by Giant Cell Arteritis (GCA). It usually occurs in older patients (mean age 70 years) and accounts for only 5–10% cases of AION.

Suffering from ['fatigue', 'weight loss', 'diarrhea', 'vomiting', 'Abdominal Pain'] at the age of 43

Disease Name: Ascariasis, symptoms: ['fatigue', 'weight loss', 'diarrhea', 'vomiting', 'Abdominal Pain'], Treatment: ['People who are treated for roundworms should be checked again in 3 months. This involves examining the stools to check for eggs of the worm. If eggs are present, treatment should be given again.', 'Anthelmintic medications (drugs that remove parasitic worms from the body), such as albendazole and mebendazole, are the drugs of choice for treatment of Ascaris infections, regardless of the species of worm. Infections are generally treated for 1–3 days. The drugs are effective and appear to have few side effects.', 'If there is a blockage of the intestine caused by a large number of worms, a procedure called endoscopy may be used to remove the worms. In rare cases, surgery is needed.'], Pathophysiology: Infection occurs when the host ingests eggs found in stool-contaminated soil. Once in the duodenum, larvae are released and enter the circulation via the enteric mucosa. Once in the capillaries (venous, arterial or lymphatic), it reaches the liver via the portal vein and then the lungs within the first week. In the lung, they damage the alveolar membrane and mature in the alveolus. Eventually, the larvae are expectorated and swallowed, reentering the gastrointestinal tract. Once in the small intestine lumen, the larvae mature into adult worms in about 20 days. When the adult female and male worms are present, they copulate, and the female can produce approximately 200,000 eggs per day. They are later eliminated in the feces of the soil. In the appropriate conditions of a moist, shady, and warm environment, the eggs mature to infective form in two to eight weeks and remain viable for up to 17 months. They can be ingested and restart the infective cycle, Epidemiology:['Approximately one billion people worldwide', 'poor', 'Take steps to prevent ascariasis:\n\nDon’t touch soil that might be contaminated with human feces, including feces used to fertilize crops.\nWash hands with soap and water before preparing food.\nTeach children to wash hands frequently.\nWash, peel and/or cook any raw vegetables and fruits, especially if they grew in manure-fertilized soil.\nDon’t defecate outdoors except in latrines that have proper sewage disposal.'], Complications:['intestinal functional disturbances', 'obstruction', 'Nutritional deficiencies'], Diagnostics:['stool microscopy', 'MRI', 'X RAY', 'CT SCAN', 'USG'], Differential diagnosis:['Acute Pancreatitis', 'Asthma', 'cholangitis', 'cholecystitis', 'Hookworm Infestation', 'small bowel obstruction'], disease description:Ascariasis is an infection of the small intestine caused by Ascaris lumbricoides, which is a species of roundworm. Roundworms are a type of parasitic worm. Infections caused by roundworms are fairly common. Ascariasis is the most common roundworm infection. About 10 percent of the developing world is infected with intestinal worms, according to the World Health Organization .

Person, 24 years old, presenting ['Abdominal Pain', 'abdomen tightness', 'rigor', 'jaundice', 'fever']

Disease Name: Ascending Cholangitis, symptoms: ['Abdominal Pain', 'abdomen tightness', 'rigor', 'jaundice', 'fever'], Treatment: ['Percutaneous transhepatic biliary drainage :\nPTBD is a valuable tool in treating patients with cholangitis. Care must be taken, however, in avoiding injection of contrast into the biliary system with pressure during the procedure in the setting of acute cholangitis because it will exacerbate septicemia. The primary aim of emergency PTBD is to establish drainage rather than definitive cholangiography in the acute phase of cholangitis. In recent reported series, emergency PTBD for patients with acute cholangitis could achieve a successful biliary drainage rate close to 100% with a complication rate less than 10% and mortality around 5%. The major advantage of PTBD compared with surgery or endoscopic treatment is that there is no need for systemic sedation or anesthesia, which can result in hemodynamic instability and respiratory complications. \n\n Endoscopic drainage:\n\nendoscopic sphincterotomy and stone extraction is done', 'reasonable choice for initial antibiotic treatment of acute cholangitis is ticarcillin and clavulanante (Timentin) or piperacillin and tazobactam (Tazocin). About 90% of patients with acute cholangitis respond to antibiotics and other supportive treatment within 24 to 48 hours.', 'Surgical interventions for drainage include stone extraction, T-tube insertion, transhepatic intubation of bile duct or bilio-enteric bypass.'], Pathophysiology: Acute cholangitis is a condition caused by acute inflammation and infection of the biliary duct system as well as the obstruction of biliary flow that leads to increased bacteria and endotoxins in the vascular and lymphatic drainage systems. Normally as bile flows through the biliary duct system, the bile duct epithelium secretes IgA, which is an anti-adherent factor towards bacteria to flush out the ducts. However, when the intra-biliary pressure exceeds the bacteriostatic abilities of the biliary epithelium, this leads to increased inflammation and infection, leading to potentially fatal complications such as biliary septicemia and hepatic abscesses.As for biliary obstruction, which is most commonly due to underlying mechanical cholestasis such as choledocholithiasis, it is partially believed that the cholesterol bile ductal stones are colonized by a biofilm by a bacterial pathogen and upon multiplication is thought to lead to obstruction-induced mucosa inflammatory cytokine production. Primary bile duct stones are thought to be caused by the biliary infection itself, with both processes leading to ascending infection throughout the biliary system., Epidemiology:['there are less than 200,000 cases of acute cholangitis annually.', 'good', 'Treatment of gallstones, tumors, and infestations of parasites may reduce the risk for some people. A metal or plastic stent that is placed in the bile system may be needed to prevent the infection from returning.'], Complications:['Acute Renal Failure', 'liver failure', 'Pancreatitis', 'portal vein thrombosis', 'septicemia', 'multiple organ failure'], Diagnostics:['random blood sugar RBS', 'Complete Blood Count CBC', 'CRP', 'Erythrocyte Sedimentation Rate (ESR)', 'ERCP', 'MRCP', 'CT SCAN', 'MR CHOLENGIOGRAPHY MRC', 'USG'], Differential diagnosis:['acute cholecystitis', 'CHOLANGIOCARCINOMA', 'CIRRHOSIS', 'DIVERTICULITIS', 'hepatitis', 'liver failure', 'Pancreatitis', 'PRIMARY SCLEROSING CHOLANGITIS', 'pyogenic hepatic abscess'], disease description:Acute cholangitis, also known as ascending cholangitis, is a life-threatening condition caused by an ascending bacterial infection of the biliary tree. Choledocholithiasis is the most common cause, with infection-causing stones in the common bile duct leading to partial or complete obstruction of the biliary system. The diagnosis is made by clinical presentation, abnormal laboratory results, and imaging studies implying infection and biliary obstruction.

Symptoms at 40 years old: ['puddle sign', 'dyspnea', 'abdominal distension', 'Dullness on percussion', 'shifting dullness']

Disease Name: Ascites, symptoms: ['puddle sign', 'dyspnea', 'abdominal distension', 'Dullness on percussion', 'shifting dullness'], Treatment: [{'medication': ['Furosemide ', 'Spironolactone ', 'Octreotide ']}, 'Refractory cases may require large volume paracentesis or transjugular\nintrahepatic portosystemic shunting.', 'For most patients, treatment consists of dietary sodium restriction and diuretic\ntherapy with spironolactone, with the addition of furosemide in more severe\ncases. Supplemental albumin can also aid in ascitic fluid mobilization'], Pathophysiology: Ascites is a consequence of increased hydrostatic and osmotic pressures within the hepatic and mesenteric capillaries resulting in transfer of fluid from the blood vessels to the lymphatics that overcomes the drainage capacity of the lymphatic system. Ascites can also be associated with nephrotic syndrome and other urinary tract abnormalities, metabolic diseases (such as lysosomal storage diseases), congenital or acquired heart disease, and hydrops fetalis. Factors favoring the intraabdominal accumulation of fluid include decreased plasma colloid (albumin) osmotic pressure, increased capillary hydrostatic pressure, increased ascitic colloid osmotic fluid pressure, and decreased ascitic fluid hydrostatic pressure. Abnormal renal sodium retention plays a central role., Epidemiology:['DEPENDS UP ON UNDERLYING CAUSE', 'To Do : SALT RESTRICTION'], Complications:['SPONTANEOUS BACTERIAL PERITONITIS'], Diagnostics:['USG ABDOMEN(W/A)', 'serum-ascitis albumen gradient SAAG'], Differential diagnosis:['Intestinal Lymphangiectasia'], disease description:Ascites is the pathologic accumulation of fluid within the peritoneal cavity. Multiple causes of ascites have been described in different age groups. In children, hepatic and renal disease are the most common causes, but ascites can also be caused by cardiac disease, trauma, infection, or neoplasia.

Individual, 23 years old, with ['fatigue', 'vomiting', 'headache', 'loss of appetite', 'fever with chills', 'stomach pain']

Disease Name: Aseptic Meningitis, symptoms: ['fatigue', 'vomiting', 'headache', 'loss of appetite', 'fever with chills', 'stomach pain'], Treatment: ['Early recognition of the most plausible cause of meningitis is crucial to begin treatment as soon as possible. Initial stabilization of the patient is necessary, and intravenous fluids for 48 hours have been proven beneficial', 'Typically, doctors use an antibiotic called ceftriaxone to treat pneumococcal meningitis. Other antibiotics used include:\n\npenicillin\nbenzylpenicillin\ncefotaxime\nchloramphenicol\nvancomycin'], Pathophysiology: Viruses are the most common etiology for aseptic meningitis, but other causes can be divided into two main categories: infectious and non-infectious. This fact leads us to state that aseptic meningitis and viral meningitis are not interchangeable terms. Manifestations may differ based on the underlying cause and the host's immune status, placing patients with deficient humoral immunity at a higher risk of negative outcomes, including neonates and patients with agammaglobulinemia.In terms of infectious causes, these include viruses, bacteria, fungi, and parasites, the most common agent being viral. More than half the cases encompassed enteroviruses (Coxsackie and ECHO viruses), followed by herpes simplex virus-2, West Nile virus, and varicella-zoster. Other associated viruses include respiratory viruses (adenovirus, influenza virus, rhinovirus), mumps virus, arbovirus, HIV, and lymphocytic choriomeningitis., Epidemiology:['The male-to-female ratio was 2 to 1.', 'l incidence is 11 per 100,000 people per year', 'poor', 'You and your children should get vaccinated for viruses that cause aseptic meningitis, such as chickenpox and mumps. It’s also important to practice good hygiene to reduce your risk of getting meningitis. Wash your hands before meals and after using the restroom, and teach your children to do the same. Always cover your mouth before sneezing or coughing. You should also avoid sharing drinks or food with others, especially when you’re in a group setting.\n\nYou can also prevent meningitis by making sure you get plenty of rest, maintain a healthy diet, and avoid contact with others who have symptoms of a cold or the flu.'], Complications:['Hearing loss', 'Mumps', 'status epilepticus', 'meningoencephalitis', 'cranial nerve palsies'], Diagnostics:['Erythrocyte Sedimentation Rate (ESR)', 'lumbar puncture', 'CT SCAN', 'PCR tests', 'EBV test'], Differential diagnosis:['Brain Abscess', 'BRAIN TUMOURS', 'intracranial hemorrhage', 'leukemia', 'PNEUMONIA', 'TUBERCULOSIS', 'Urinary Tract Infection'], disease description:Aseptic meningitis is a term used to define inflammation of the brain linings, called meninges, due to various etiologies with negative cerebrospinal fluid (CSF) bacterial cultures. Many studies and books determine it by showing CSF pleocytosis of more than five cells/mm3.  It is one of the most common, usually benign, inflammatory disorders of the meninges.Viruses are the most common etiology for aseptic meningitis, but other causes can be divided into two main categories: infectious and non-infectious

Suffering from ['shock', 'chest pain', 'difficulty in breathing', 'fever', 'wheezing', 'COUGHING'] at 43

Disease Name: Aspergillosis, symptoms: ['shock', 'chest pain', 'difficulty in breathing', 'fever', 'wheezing', 'COUGHING'], Treatment: [{'medication': ['Gentian Violet ', 'Amphotericin B ']}, 'Voriconazole: IV: 6 mg/kg Q12 × 24 h, 4 mg/kg Q12 starting Day 2\nPO: 200 mg Q12 h.\n\nIsavuconazole:IV: 200 mg Q8 h × 48 h, 200 mg daily starting Day 3\nPO: 200 mg Q8 h for 48 h, 200 mg daily starting Day 3.\n\nPosaconazole:IV: 300 mg Q12 × 24 h, 300 mg daily starting Day 2\nDelayed-release: 300 mg Q12 ×24 h, 300 mg daily starting Day 2\nOral suspension: 200 mg TID.'], Pathophysiology: In an otherwise immunocompetent person, Aspergillus conidia are inhaled and taken up by phagocytes in the lungs. The conidia germinate into hyphae at body temperature. In immunocompetent hosts, phagocytes secrete mediators such as beta-D-glucan which activate neutrophils. Neutrophils kill the invasive hyphae, and the Aspergillus infection is kept at bay. If any of these mechanisms are impaired in an immunocompromised patient, the infection may be allowed to spread ., Epidemiology:['1-4 million people worldwide', 'incidence of aspergillosis in patients undergoing bone marrow transplantation can be as high as 10% to 20%', 'good', 'It’s hard to avoid Aspergillus molds. If you’re at high risk for infection, talk to your provider about the best ways to protect yourself. Your provider might:\n\nPrescribe an antifungal medicine to prevent infection.\nTest you for signs of infection to make sure you get treated early.\nYou might be able to reduce your exposure to fungi by:\n\nAvoiding areas with lots of dust or mold, such as construction sites or compost piles.\nAvoiding activities such as gardening or lawn mowing. If you might be exposed to airborne dust or mold, wear an N95 face mask.'], Complications:['bleeding', 'death', 'Endocarditis', 'respiratory failure', 'hemoptysis', 'wheezing', 'Lung Fibrosis'], Diagnostics:['FUNGAL STAIN', 'X RAY CHEST'], Differential diagnosis:['acute respiratory distress syndrome', 'Asthma', 'Bacterial pneumonia', 'BRONCHIECTASIS', 'BRONCHOGENIC CARCINOMA', 'Chronic Obstructive Pulmonary Disease', 'Heart transplantation', 'Interstitial Lung Disease', 'Liver transplantation', 'LUNG ABSCESS', 'mucormycosis', 'PNEUMONIA', 'Pulmonary Embolism', 'Sarcoidosis'], disease description:Aspergillus is a fungus found throughout the world that can cause infection in primarily immunocompromised hosts and individuals with the underlying pulmonary disease. Many different species of Aspergillus can cause infection. There are three major types of bronchopulmonary Aspergillus infections: invasive aspergillosis, chronic aspergillosis, and allergic aspergillosis. Aspergillosis infection can also manifest as sinus disease in immunocompromised hosts. If left untreated, invasive aspergillosis can have mortality approaching 100%. In cases of suspected invasive aspergillosis, an extensive diagnostic workup is necessary, but treatment should be initiated early to reduce morbidity and mortality.

A 42-year-old patient experiencing ['Atelectasis', 'polydactyly', 'Micromelia', 'fever', 'respiratory failure']

Disease Name: Asphyxiating Thoracic Dystrophy, symptoms: ['Atelectasis', 'polydactyly', 'Micromelia', 'fever', 'respiratory failure'], Treatment: ['Treatment is based on managing respiratory infections and monitoring renal and hepatic function regularly. The risk of severe respiratory infections diminishes after age two.\n\nThe vertical expandable prosthetic titanium rib (VEPTR) was approved by the FDA in 2004 as a treatment for thoracic insufficiency syndrome (TIS) in pediatric patients. TIS is a congenital condition where severe deformities of the chest, spine, and ribs prevent normal breathing and lung development. The VEPTR is an implanted, expandable device that helps straighten the spine and separate ribs so that the lungs can grow and fill with enough air to breathe. The length of the device can be adjusted as the patient grows. For treatment of spondylothoracic dysplasia, ribs are separated on each side of the chest and VEPTRs are placed on each side of the chest.'], Pathophysiology: It is estimated that 70 percent of affected individuals have mutations in one these genes. Mutations in these genes result in abnormal cilia proteins that affect bone development. ATD is inherited in an autosomal recessive pattern. Recessive genetic disorders occur when an individual inherits a non-working gene from each parent. If an individual receives one working gene and one non-working gene for the disease, the person will be a carrier for the disease, but usually will not show symptoms. The risk for two carrier parents to both pass the non-working gene and, therefore, have an affected child is 25% with each pregnancy. The risk to have a child who is a carrier, like the parents, is 50% with each pregnancy. The chance for a child to receive working genes from both parents is 25%. The risk is the same for males and females., Epidemiology:['1 in 100,000 to 130,000 people.', 'The incidence of ATD is about 1 in 100,000 to 150,000 live births.', 'variable', "This condition is inherited in an autosomal recessive pattern, which means both copies of the gene in each cell have mutations. And thus, it can't be prevented. \n\n- Genetic counselling is advisable."], Complications:['Shortening of the leg', 'kidney disease', 'short stature'], Diagnostics:['X RAY', 'X RAY', 'molecular genetic testing'], Differential diagnosis:['Achondroplasia', 'Cartilage hair hypoplasia', 'dysplasia', 'Hypophosphatasia'], disease description:Asphyxiating thoracic dystrophy (ATD) is a very rare form of skeletal dysplasia that primarily affects development of the bone structure of the chest (thorax) resulting in a very narrow and bell-shaped chest.

Experiencing ['crackles', 'bronchial breath sound', 'Decreased tactile fremitus', 'Dull on percussion', 'hypoxaemia', 'fever', 'dyspnea'] at 54 years old

Disease Name: Aspiration Pneumonia, symptoms: ['crackles', 'bronchial breath sound', 'Decreased tactile fremitus', 'Dull on percussion', 'hypoxaemia', 'fever', 'dyspnea'], Treatment: ["The treatment varies between aspiration pneumonia and aspiration pneumonitis. The patient's position should be adjusted, followed by the suction of oropharyngeal contents with the placement of the nasogastric tube. In patients who are not intubated, humidified oxygen is administered, and the head end of the bed should be raised by 45 degrees. Close monitoring of the patient's oxygen saturation is important and immediate intubation with mechanical ventilation should be provided if hypoxia is noted. Flexible bronchoscopy is usually indicated for large volume aspiration to clear the secretion and also for obtaining the sample of bronchoalveolar lavage for quantitative bacteriological studies.", 'antibiotics are initiated immediately even though they are not required in aspiration pneumonitis to prevent the progression of the disease. The choice of antibiotics for community-acquired aspiration pneumonia are ampicillin-sulbactam or a combination of metronidazole and amoxicillin. In patients with penicillin allergy, clindamycin is preferred. However, in hospital-acquired aspiration pneumonia, antibiotics are needed that cover resistant gram-negative bacteria and S. aureus, so the use of a combination of vancomycin and piperacillin-tazobactam is most widely used.'], Pathophysiology: In normal healthy adults, the mucociliary mechanism and alveolar macrophages act as defenses in clearing micro aspirations from the oropharyngeal secretions. The pathological process of aspiration pneumonia occurs when the normal defense mechanisms fail in a predisposed individual. The entry of fluid into the bronchi and alveolar space triggers an anti-inflammatory reaction with the release of proinflammatory cytokines, tumor necrosis factor-alpha, and interleukins. Inoculation of organisms of common flora from the oropharynx and esophagus results in the infectious process. Mendelson first studied the pathophysiology of aspiration pneumonitis by inducing gastric contents in the rabbit’s lung and comparing it to 0.1 N hydrochloric acid. Later studies conducted in rats using diluted hydrochloric acid demonstrated the biphasic response with the initial corrosive phase by acidic pH followed by a neutrophil-mediated inflammatory response. Inoculation of normal oropharyngeal flora in the aspirate results in the infectious process and results in aspiration pneumonia. If the bacterial load of aspirate is low normal host defenses will clear the secretions and prevent infection., Epidemiology:['The prevalence of undiagnosed dysphagia in community dwelling elders, a major risk factor for aspiration pneumonia, can be up to 15% . This prevalence increases to 31% in those living in nursing homes', 'incidence of aspiration pneumonia to be 9.8%, with 12 out of 123 patients developing aspiration pneumonia after extubation', 'The prognosis is dependent on the patient age and ', 'Things that you can do to reduce your risk of aspiration pneumonia include the following:\n\nAvoid drinking alcohol to excess and using recreational drugs. These can affect your ability to swallow.\nStay upright when you are eating.\nChew slowly and completely.\nIf you have problems swallowing (things often “go down the wrong pipe”), talk to your healthcare provider. They might need to change or adjust your diet or medication. They can also order tests or refer you to a speech professional or swallowing specialist.\nDon’t smoke or use nicotine products.\nTake good care of your teeth.'], Complications:['acute respiratory distress syndrome', 'respiratory failure', 'LUNG ABSCESS', 'empyema'], Diagnostics:['X RAY CHEST', 'X RAY', 'BRONCHOSCOPY'], Differential diagnosis:['acute respiratory distress syndrome', 'bronchitis', 'Chronic Obstructive Pulmonary Disease', 'mycoplasma pnemonia', 'PNEUMONIA', 'septic shock'], disease description:The infectious pulmonary process that occurs after abnormal entry of fluids into the lower respiratory tract is termed aspiration pneumonia. The aspirated fluid can be oropharyngeal secretions, particulate matter, or can also be gastric content. The term aspiration pneumonitis refers to inhalational acute lung injury that occurs after aspiration of sterile gastric contents. 

Symptoms reported at the age of 45: ['finger pulps are dry and cracked, producing distorted prints and retaining a prolonged depression after pressure (‘parchment pulps’)', 'crazy-paving pattern on legs', 'DRY SCALY SKIN', 'Irritation in this form of eczema is often intense, and worse with changes of temperature, particularly on undressing at night.', 'surface of the backs of the hands is marked in a criss-cross fashion']

Disease Name: Asteatotic Eczema, symptoms: ['finger pulps are dry and cracked, producing distorted prints and retaining a prolonged depression after pressure (‘parchment pulps’)', 'crazy-paving pattern on legs', 'DRY SCALY SKIN', 'Irritation in this form of eczema is often intense, and worse with changes of temperature, particularly on undressing at night.', 'surface of the backs of the hands is marked in a criss-cross fashion'], Treatment: [{'medication': ['Pimecrolimus']}, 'Eliminate or reduce the use of soap on the involved areas; use only in the perineum and axillae. Avoid harsh skin cleansers. Apply petrolatum-based emollients following bathing, and use moisturizing agents liberally. Apply topical steroid ointments with or without polyethylene occlusion', 'Second line \n• Emollients, with or without urea, bath oil and soap substitute \n Third line \n• Mild topical corticosteroids; a randomized, vehicle- \ncontrolled trial of 40 patients with asteatotic eczema found\npimecrolimus 1% cream to be effective after 4 four weeks\nof treatment'], Pathophysiology: At present, the relevant factors in the production of asteatotic eczema can be considered to be: (i) a naturally ‘dry’ skin and a lifelong tendency to chapping; (ii) a further reduction in lipid with age, illness, malnutrition or hormonal decline; (iii) increased transpiration relative to the environmental water content; (iv) loss of integrity of the water reservoir of the horny layer; (v) chapping and degreasing (and perhaps cell damage) by industrial or domestic cleansers or solvents; (vi) low environmental humidity and dry, cold winds increasing convection loss; and (vii) repeated minor trauma leading to inflammation and further disorganization of the surface aqueous/lipid balance. Percutaneous absorption through the degreased and damaged epidermis is increased, and contact irritants and sensitizers may further damage and irritate the skin. Although the condition is thought to be due to a decrease in skin surface lipid, the exact pathogenesis of the skin changes is obscure. The amino acid content of the skin is lower in more severe cases. A decrease in the keratohyaline-derived natural moisturizers may also be important. Hyposteatosis occurs in many conditions of maldevelopment, malnutrition and atrophy of the skin, but does not necessarily lead to eczema. The part played by the loss of fluid from the skin has been underrated in the past. The relationship between the transpiration rate and the lipid layer has been the subject of many studies., Epidemiology:['7.3% of adults in the U.S. Of those affected with the disease, about 40% have moderate or severe symptoms.', 'relapsing each winter and clearing in the summer, ', 'There are steps you can take that may prevent eczema flare-ups and outbreaks, including:\n\nMoisturize your skin regularly or when your skin becomes dry. Seal in moisture after a bath or shower by immediately applying moisturizer to your skin.\nTake baths or showers with warm, not hot, water.\nStay hydrated and drink at least eight glasses of water each day. Water helps keep your skin moist.\nWear loose clothes made of cotton and other natural materials. Wash new clothing before wearing it. Avoid wool or synthetic fibers.\nManage your stress and emotional triggers. See a psychiatrist for medication and a therapist for counseling if you’re experiencing symptoms of poor mental/emotional health.\nUse a humidifier if dry air makes your skin dry.\nAvoid irritants and allergens.'], Complications:['Skin fissures', 'infection', 'secondary infection'], Diagnostics:['Skin Biopsy With Immunofluorescence', 'Patch Test'], Differential diagnosis:['allergic contact dermatitis', 'CELLULITIS', 'Contact dermatitis', 'Irritant contact dermatitis', 'Myxedema', 'nummular dermatitis', 'stasis dermatitis'], disease description:This is eczema developing in very dry skin, usually in the elderly. Asteatotic eczema usually affects the legs, arms and hands of elderly people in the context of dry skin. A characteristic ‘crazy- paving’ pattern is observed on the legs in particular, resulting in the synonym of eczéma craquelé. It may flare during winter due to a reduction in humidity associated with central heating. Management centres on the restoration of skin hydration.

Individual, 47 years old, with ['chest tightness', 'fatigue', 'Tachycardia', 'shortness of breath']

Disease Name: Asthma, symptoms: ['chest tightness', 'fatigue', 'Tachycardia', 'shortness of breath'], Treatment: [{'medication': ['Beclometasone ', 'Ipratropium bromide ', 'Montelukast ', 'Theophylline ', 'Salmeterol']}, 'Allergy medications may help if your asthma is triggered or worsened by allergies. These include:\n\nAllergy shots (immunotherapy). Over time, allergy shots gradually reduce your immune system reaction to specific allergens. You generally receive shots once a week for a few months, then once a month for a period of three to five years.\nBiologics. These medications — which include omalizumab (Xolair), mepolizumab (Nucala), dupilumab (Dupixent), reslizumab (Cinqair) and benralizumab (Fasenra) — are specifically for people who have severe asthma.', "Long-term asthma control medications, generally taken daily, are the cornerstone of asthma treatment. These medications keep asthma under control on a day-to-day basis and make it less likely you'll have an asthma attack. Types of long-term control medications include:\n\nInhaled corticosteroids. These medications include fluticasone propionate (Flovent HFA, Flovent Diskus, Xhance), budesonide (Pulmicort Flexhaler, Pulmicort Respules, Rhinocort), ciclesonide (Alvesco), beclomethasone (Qvar Redihaler), mometasone (Asmanex HFA, Asmanex Twisthaler) and fluticasone furoate (Arnuity Ellipta).\n\nYou may need to use these medications for several days to weeks before they reach their maximum benefit. Unlike oral corticosteroids, inhaled corticosteroids have a relatively low risk of serious side effects.\n\nLeukotriene modifiers. These oral medications — including montelukast (Singulair), zafirlukast (Accolate) and zileuton (Zyflo) — help relieve asthma symptoms.\n\nMontelukast has been linked to psychological reactions, such as agitation, aggression, hallucinations, depression and suicidal thinking. Seek medical advice right away if you experience any of these reactions.\n\nCombination inhalers. These medications — such as fluticasone-salmeterol (Advair HFA, Airduo Digihaler, others), budesonide-formoterol (Symbicort), formoterol-mometasone (Dulera) and fluticasone furoate-vilanterol (Breo Ellipta) — contain a long-acting beta agonist along with a corticosteroid.\nTheophylline. Theophylline (Theo-24, Elixophyllin, Theochron) is a daily pill that helps keep the airways open by relaxing the muscles around the airways. It's not used as often as other asthma medications and requires regular blood tests.", "Quick-relief (rescue) medications are used as needed for rapid, short-term symptom relief during an asthma attack. They may also be used before exercise if your doctor recommends it. Types of quick-relief medications include:\n\nShort-acting beta agonists. These inhaled, quick-relief bronchodilators act within minutes to rapidly ease symptoms during an asthma attack. They include albuterol (ProAir HFA, Ventolin HFA, others) and levalbuterol (Xopenex, Xopenex HFA).\n\nShort-acting beta agonists can be taken using a portable, hand-held inhaler or a nebulizer, a machine that converts asthma medications to a fine mist. They're inhaled through a face mask or mouthpiece.\n\nAnticholinergic agents. Like other bronchodilators, ipratropium (Atrovent HFA) and tiotropium (Spiriva, Spiriva Respimat) act quickly to immediately relax your airways, making it easier to breathe. They're mostly used for emphysema and chronic bronchitis, but can be used to treat asthma.\nOral and intravenous corticosteroids. These medications — which include prednisone (Prednisone Intensol, Rayos) and methylprednisolone (Medrol, Depo-Medrol, Solu-Medrol) — relieve airway inflammation caused by severe asthma. They can cause serious side effects when used long term, so these drugs are used only on a short-term basis to treat severe asthma symptoms."], Pathophysiology: The pathology of asthma has been revealed through examining the lungs of patients who have died of asthma and from bronchial biopsies. The airway mucosa is infiltrated with activated eosinophils and T lymphocytes, and there is activation of mucosal mast cells. The degree of inflammation is poorly related to disease severity and may even be found in atopic patients without asthma symptoms. This inflammation is usually reduced by treatment with ICS. There are also structural changes in the airways (often termed remodeling). A characteristic finding is thickening of the basement membrane due to subepithelial collagen deposition. This feature is also found in patients with eosinophilic bronchitis presenting as cough who do not have asthma and is, therefore, likely to be a marker of eosinophilic inflammation in the airway as eosinophils release fibrogenic mediators. The epithelium is often shed or friable, with reduced attachments to the airway wall and increased numbers of epithelial cells in the lumen.The airway wall itself may be thickened and edematous, particularly in fatal asthma. Another common finding in fatal asthma is occlusion of the airway lumen by a mucous plug, which is comprised of mucous glycoproteins secreted from goblet cells and plasma proteins from leaky bronchial vessels ). There is also vasodilation and increased numbers of blood vessels (angiogenesis). Direct observation by bronchoscopy indicates that the airways may be narrowed, erythematous, and edematous. The pathology of asthma is remarkably uniform in different phenotypes of asthma, including atopic (extrinsic), non-atopic (intrinsic), occupational, aspirin-sensitive, and pediatric asthma. These pathologic changes are found in all airways, but do not extend to the lung parenchyma; peripheral airway inflammation is found particularly in patients with severe asthma. The involvement of airways may be patchy and this is consistent with bronchographic findings of uneven narrowing of the airways., Epidemiology:['~300 million people worldwide, with ~250,000 death', '4.8 million children under the age of 18 with asthma.', 'variable', 'If your healthcare provider says you have asthma, you’ll need to figure out what triggers an attack. Avoiding the triggers can help you avoid an attack. You can’t prevent yourself from getting asthma, though.'], Complications:['fatigue', 'PNEUMONIA', 'respiratory failure'], Diagnostics:['DUST ALLERGY', 'CT CHEST', 'CHEST X RAY', 'PULMONARY FUNCTION TEST(PFT)', 'methacholine challenge test', 'Bronchial challenge test', 'spirometry'], Differential diagnosis:['Aspergillosis', 'BRONCHIECTASIS', 'BRONCHIOLITIS', 'Chronic Obstructive Pulmonary Disease', 'Chronic Sinusitis', 'Churg-Strauss Syndrome', 'CYSTIC FIBROSIS', 'Gastroesophageal reflux disease (GERD)', 'Pulmonary Embolism', 'Sarcoidosis', 'upper respiratory tract irritation'], disease description:Asthma is a syndrome characterized by airflow obstruction that varies markedly, both spontaneously and with treatment. Asthmatics harbor a special type of inflammation in the airways that makes them more responsive than nonasthmatics, leading to excessive narrowing with consequent reduced airflow and symptomatic wheezing and dyspnea. Narrowing of the airways is usually reversible, but in some patients with chronic asthma there may be an element of irreversible airflow obstruction. Asthma is a he

Experiencing ['abdominal discomfort', 'headache', 'anxiety', 'diarrhea', 'malaise', 'nausea', 'vomiting', 'fever'] at 20 years

Disease Name: Astrovirus Infection, symptoms: ['abdominal discomfort', 'headache', 'anxiety', 'diarrhea', 'malaise', 'nausea', 'vomiting', 'fever'], Treatment: ['fluid rehydration therapy and immunoglobulin treatment for immunocompromised individuals'], Pathophysiology: In calves, astrovirus infection was localized to the dome epithelial cells overlying Peyer's patches. These cells appeared flat or rounded and released cells were identified in the intestinal lumen. Astrovirus infection in calves was shown to be specifically targeted to M cells and led to the sloughing of necrotic M cells into the intestinal lumen. Enterocytes were never observed to be infected. Specific tropism of the virus for immune cells suggests that astrovirus may have an immunomodulatory role in calves. While the virus replicated in these animals and could be detected in their feces, the calves displayed no clinical signs. In most bovine studies, viral infection is asymptomatic, although changes in the feces from solid and brown to soft and yellow were noted in one study. Mild villus atrophy and slight changes in villus-to-crypt ratios have been noted but no changes in xylose absorption were observed. Despite the lack of symptoms, viral shedding continued until the termination of the experiment., Epidemiology:['mostly in young children and immunocompromised adults', 'Astrovirus infections occur worldwide, and their incidence in children with gastroenteritis in both developing and developed countries ranges from 2 to 9%', 'variable', 'There are things you can do to avoid getting or spreading astrovirus:\n\nWash your hands thoroughly, especially after using the bathroom or changing diapers.\nDo not share utensils or cups if you or people around you are sick or have diarrhea.\nStay home from work or school if you are ill.\nAvoid handling and preparing food while ill or recovering from illness.\nUse antiseptic disinfectants to clean surfaces, especially in the bathroom and kitchen.'], Complications:['interstitial nephritis', 'INTUSSUSSEPTION'], Diagnostics:['RT PCR', 'ELECTRON MICROSCOPY'], Differential diagnosis:['Norovirus infection', 'Rota virus'], disease description:Astroviruses are enteric viruses first identified in the feces of children with diarrhea. Detection was originally based on a five- to six-pointed star morphology of virions by electron microscopy (EM). However, only about 10% of viral particles display these structures; the remaining 90% of particles have a smooth surface and a size similar to other small, round-structured viruses like picornaviruses and caliciviruses. Thus, accurate diagnostics were difficult to obtain and the true prevalence of astrovirus within a population was difficult to assess. Development of much more sensitive detection techniques like real time reverse transcription-polymerase chain reaction (RT-PCR), cell culture RT-PCR, and astrovirus-specific enzyme-linked immunosorbent assays (ELISAs) have made detection more accurate and specific, even allowing diagnosis of specific serotypes.

Person aged 23 dealing with ['Chorea', 'seizures', 'Respiratory infections', 'unsteadiness', 'Discoloration of skin', 'Ataxia', 'nystagmus']

Disease Name: Ataxia-telangiectasia, symptoms: ['Chorea', 'seizures', 'Respiratory infections', 'unsteadiness', 'Discoloration of skin', 'Ataxia', 'nystagmus'], Treatment: ['Chemotherapy treatment for cancer.', 'Avoiding overexposure to sunlight to control dilated blood vessels (telangiectasia).', 'Physical therapy to strengthen muscles.', 'Receiving gammaglobulin injections for respiratory infections.\nReceiving immunoglobulin therapy to address a weakened immune system.\nTaking antibiotics to treat infections.\nTaking diazepam to control slurred speech and involuntary muscle movem'], Pathophysiology: Mutations of the ATM gene are responsible for A-T. Nonsense, frameshift, missense, and insertion-deletion mutations of the ATM gene associated with A-T have been described. In the majority of cases, mutations lead to a truncated and thus nonfunctional protein. Compound heterozygous mutations are not infrequent as well. ATM is involved in many different molecular mechanisms. The protein is most important for cellular DNA repair, cell cycle control, and cellular response to external triggers, such as oxidative damage, ionizing radiation, and alkylating agents. The protein itself is a serine/threonine kinase affecting many different downstream targets that are involved in those pathways important for cellular protection against toxic insults. The loss of function of the ATM protein is therefore responsible for the aberrant proliferation of cells due to the unrepaired double-strand DNA breaks, increasing the cancer risk and the radiosensitivity. Also, the impairment of cell cycle control can cause malformations, such as gonadal dysgenesis, which is found in patients with A-T. Moreover, ATM is important also for immunoglobulin production and lymphoid cell survival. This explains why ATM mutations are responsible for a higher risk of tumors of the lymphatic system and autoimmune manifestations. The mechanism underlying the formations of telangiectasia remains unknown. This condition results in dilated blood vessels and is one of the hallmarks of the disorder., Epidemiology:['Thirty-five percent of children experienced astrovirus infections.', 'The incidence of A-T ranges from 1:40,000 to 1:100,000.', 'variable', 'Since ataxia-telangiectasia is the result of a genetic mutation, there is no way to prevent it from occurring. You can take steps to reduce your risk of having a child with a genetic condition by avoiding smoking and avoiding exposure to chemicals. If you plan on becoming pregnant, talk with your healthcare provider about genetic testing to understand your risk of having a child with a genetic condition like ataxia-telangiectasia.'], Complications:['MALIGNANCY', 'cognitive impairment'], Diagnostics:['HISTOPATHLOGY', 'GENETIC TESTING', 'MRI', 'MRI', 'BLOOD MICROSCOPY'], Differential diagnosis:['Acute Disseminated Encephalomyelitis (ADEM)', 'mitochondrial disorders', 'Urea Cycle Defects', 'VITAMIN E DEFICIENCY'], disease description:Ataxia telangiectasia (Louis-Bar Syndrome) is a rare autosomal recessive condition characterized by cutaneous telangiectasias, cerebellar atrophy with progressive ataxia, and a higher incidence of malignancy, immune deficiency, radiosensitivity, recurrent sinopulmonary infections, and elevated levels of alpha-fetoprotein (AFP) in serum.

Suffering from ['Areflexia', 'dysarthria', 'dystonia', 'extensor plantar response', 'gait disorders', 'night blindness of eyes', 'nystagmus', 'pendular tendon jerks', 'low muscle tone', 'intention tremor', 'Hearing loss', 'Positive babinski sign', 'slurred speech', 'difficulty in walking', 'CLUMSINESS', 'delayed motor development', 'Abnormal gait', 'falling to one side'] at 30

Disease Name: Ataxia, symptoms: ['Areflexia', 'dysarthria', 'dystonia', 'extensor plantar response', 'gait disorders', 'night blindness of eyes', 'nystagmus', 'pendular tendon jerks', 'low muscle tone', 'intention tremor', 'Hearing loss', 'Positive babinski sign', 'slurred speech', 'difficulty in walking', 'CLUMSINESS', 'delayed motor development', 'Abnormal gait', 'falling to one side'], Treatment: [{'medication': ['Rituximab', 'Human normal immunoglobulin ', 'Arginine or L-arginine', 'Vitamin B2 (Riboflavin) ', 'Vitamin B3/Nicotinic acid (Niacin)/Nicotinamide', 'Vitamin E / Tocopherol', 'BIOTIN (Vitamin B7)']}], Pathophysiology: Signs and symptoms of ataxia include clumsiness, difficulty walking or sitting, falling to one side, slurred speech, low muscle tone, intention tremor, dizziness, delayed motor development, or a combination of these. Genetic or chronic causes of cerebellar ataxia are often characterized by a long duration of symptoms, a positive family history, muscle weakness and abnormal gait, abnormal tone and strength, abnormal deep tendon reflexes, pes cavus, and sensory defects. Distinguishing ataxia from vestibular dysfunction may be difficult; however, labyrinth disorders are often characterized by severe vertigo, nausea and vomiting, position-induced vertigo, and a severe sense of unsteadiness. Congenital anomalies of the posterior fossa, including the Dandy-Walker malformation, Chiari malformation, and encephalocele, are prominently associated with ataxia because of their destruction or abnormal development of the cerebellum. MRI is the method of choice for investigating congenital abnormalities of the cerebellum, vermis, and related structures. Agenesis of the cerebellar vermis presents in infancy with generalized hypotonia and decreased deep tendon reflexes. Delayed motor milestones and truncal ataxia are typical. Joubert syndrome and related disorders are autosomal recessive disorders marked by developmental delay, hypotonia, abnormal eye movements, abnormal respirations, and a distinctive malformation of the cerebellum and brainstem that manifests as the “molar tooth sign” on axial MRI. Mutations in more than 21 different genes are associated with Joubert syndrome, but only approximately 50% of cases have a demonstrated causal mutation. The major infectious or postinfectious causes of ataxia include acute cerebellar ataxia, infectious cerebellitis, and acute labyrinthitis. Acute cerebellar ataxia occurs primarily in children 1-3 yr of age and is a diagnosis of exclusion. The condition often follows a viral illness, such as varicella virus, coxsackievirus, or echovirus infection, by 2-3 wk. It is thought to represent an autoimmune response to the viral agent affecting the cerebellum. The onset is typically sudden, and the truncal ataxia can be so severe that the child is unable to stand or sit. Vomiting may occur initially, but fever and nuchal rigidity are absent due to the lack of meningeal involvement. Horizontal nystagmus is evident in approximately 50% of cases, and, if the child is able to speak, dysarthria may be impressive. Examination of the cerebrospinal fluid is typically normal at the onset of ataxia, but a mild lymphocytic pleocytosis (10- 30/mm3 ) is not unusual. Later in the course, the cerebrospinal fluid protein undergoes a moderate elevation. The ataxia begins to improve in a few weeks but may persist for as long as 3 mo and rarely longer than that. The incidence of acute cerebellar ataxia appears to have declined with increased rates of vaccination against varicella. The prognosis for complete recovery is excellent. A small number of patients have long-term sequelae, including behavioral and speech disorders, as well as ataxia and incoordination. Acute cerebellitis, in contrast, is a more severe form of cerebellar ataxia characterized by abnormalities on MRI scans, more severe symptoms, and a worse long-term prognosis. Infectious agents include Epstein-Barr virus, mycoplasma, mumps, and influenza virus. Cerebellar abscesses can also occur with bacterial infections. In many, the etiology is unknown, but autoimmune cerebellitis may represent some of these unknown cases. Clinically, patients may present with ataxia, increased intracranial pressure from obstructive hydrocephalus, headache, and fever. Acute labyrinthitis may be difficult to differentiate from acute cerebellar ataxia in a toddler. The condition is associated with middle ear infections and presents with intense vertigo, vomiting, and abnormalities in labyrinthine function. Toxic causes of ataxia include alcohol, thallium (which is used occasionally in homes as a pesticide), dextromethorphan, and the anticonvulsants, particularly phenytoin and carbamazepine when serum levels exceed the usual therapeutic range. Brain tumors, including tumors of the cerebellum and frontal lobe, may present with ataxia. Cerebellar tumors cause ataxia because of direct disruption of cerebellar function or indirectly because of increased intracranial pressure from compression of the fourth ventricle. Frontal lobe tumors may cause ataxia as a consequence of destruction or interruption of the association fibers connecting the frontal lobe with the cerebellum, or because of increased intracranial pressure. Neuroblastoma may be associated with a paraneoplastic encephalopathy characterized by progressive ataxia, myoclonic jerks, and opsoclonus (nonrhythmic, conjugate horizontal and vertical oscillations of the eyes). Several metabolic disorders are characterized by ataxia, including abetalipoproteinemia, arginosuccinic aciduria, and Hartnup disease. Abetalipoproteinemia (Bassen-Kornzweig disease) is an autosomal recessive disorder caused by a mutation in the microsomal triglyceride transfer protein (MTP). This disorder begins in childhood with steatorrhea and failure to thrive. A blood smear shows acanthocytosis, which consists of spiculated red blood cells. Serum chemistries reveal decreased levels of cholesterol and triglycerides and absent serum ß-lipoproteins. Neurologic signs become evident by late childhood and consist of ataxia, retinitis pigmentosa, peripheral neuritis, abnormalities of position and vibration sense, muscle weakness, and intellectual disability. Vitamin E is undetectable in the serum of patients with neurologic symptoms. In addition, ataxia may be one manifestation of a mitochondrial disorder; these include MERFF (myoclonic epilepsy with ragged red fibers), Kearns-Sayre syndrome, POLG1 mutations, and Charlevoix-Saguenay syndrome. Degenerative diseases of the central nervous system represent an important group of ataxic disorders of childhood because of the genetic consequences and poor prognosis. Ataxia-telangiectasia, an autosomal recessive condition, is the most common of the degenerative ataxias and is heralded by ataxia beginning at approximately age 2 yr and progressing to loss of ambulation by adolescence. Ataxia-telangiectasia is caused by mutations in the ATM gene located at 11q22- q23. ATM is a phosphytidylinositol-3 kinase that phosphorylates proteins involved in DNA repair and cell-cycle control. Oculomotor apraxia of horizontal gaze, defined as difficulty shifting the gaze from one object to another and overshooting the target with lateral movement of the head, followed by refixating the eyes, is a frequent finding. In addition, strabismus, hypometric saccade pursuit abnormalities, and nystagmus are often seen. Ataxiatelangiectasia may present with chorea rather than ataxia. The telangiectasia becomes evident by mid-childhood and is found on the bulbar conjunctiva, over the bridge of the nose, and on the ears and exposed surfaces of the extremities. Examination of the skin shows a loss of elasticity. Abnormalities of immunologic function that lead to frequent sinopulmonary infections include decreased serum and secretory immunoglobulin (Ig) A, as well as diminished IgG2 , IgG4 , and IgE levels in more than 50% of patients. Children with ataxiatelangiectasia have a 50- to 100-fold increased risk of developing lymphoreticular tumors (lymphoma, leukemia, and Hodgkin disease), as well as brain tumors. Additional laboratory abnormalities include an increased incidence of chromosome breaks, particularly of chromosome 14, and elevated levels of a- fetoprotein. Death typically results from infection or tumor dissemination. Friedreich ataxia is inherited as an autosomal recessive disorder involving the spinocerebellar tracts, dorsal columns in the spinal cord, pyramidal tracts, and cerebellum and medulla. Most patients are homozygous for a GAA trinucleotide repeat expansion in the noncoding region of the gene coding for the mitochondrial protein frataxin. Mutations cause oxidative injury associated with excessive iron deposits in mitochondria. The onset of ataxia is somewhat later than in ataxia-telangiectasia but usually occurs before the age of 10. The ataxia is slowly progressive and involves the lower extremities to a greater degree than the upper extremities. Examination will demonstrate a positive Romberg test and absent deep tendon reflexes (particularly at the ankle); the plantar response is typically extensor (Babinski sign). Patients develop a characteristic explosive, dysarthric speech, and nystagmus is present in most children. Although patients may appear apathetic, their intelligence is preserved. They may have significant weakness of the distal musculature of the hands and feet. Marked loss of vibration and joint position sense is common and is caused by degeneration of the posterior columns. Friedreich ataxia is also characterized by skeletal abnormalities, including high-arched feet (pes cavus) and hammertoes, as well as progressive kyphoscoliosis. Results of electrophysiologic studies, including visual, auditory brainstem, and somatosensory-evoked potentials, are often abnormal. Hypertrophic cardiomyopathy with progression to intractable congestive heart failure is the cause of death for most patients. Several forms of spinocerebellar ataxia are similar to Friedreich ataxia but are less common. Roussy-Levy disease has, in addition to ataxia, atrophy of the muscles of the lower extremity with a pattern of wasting similar to that observed in Charcot-Marie-Tooth disease. Ramsay Hunt syndrome has an associated myoclonic epilepsy. There are more than 20 dominantly inherited spinocerebellar ataxias, some of which present in childhood. These include those associated with CAG (polyglutamine) trinucleotide repeats and noncoding microsatellite expansions. Dominantly inherited episodic ataxias caused by potassium or calcium channel dysfunction present as episodes of ataxia and muscle weakness. Some of these disorders may respond to acetazolamide. The dominantly inherited olivopontocerebellar atrophies include ataxia, cranial nerve palsies, and abnormal sensory findings in the second or third decade, but can present in children with rapidly progressive ataxia, nystagmus, dysarthria, and seizures. Additional degenerative ataxias include Pelizaeus-Merzbacher disease, neuronal ceroid lipofuscinoses, and late-onset GM2 gangliosidosis. Rare forms of progressive cerebellar ataxia have been described in association with vitamin E deficiency. A number of autosomal dominant progressive spinocerebellar ataxias have been defined at the molecular level, including those caused by unstable trinucleotide repeat expansions., Epidemiology:['EXCELLENT'], Complications:['Speech disorders', 'Behavioural DIsorder'], Diagnostics:['MRI Brain'], Differential diagnosis:['Adrenoleukodystrophy', 'cerebral palsy', 'ENCEPHALITIS', 'Gaucher Disease', 'Krabbe Disease', 'Leigh syndrome', 'Maple Syrup Urine Disease', 'Refsum disease', 'Zellweger Syndrome'], disease description:Ataxia is the inability to make smooth, accurate, and coordinated movements. It occurs because of a dysfunction of the cerebellum, its inputs or outputs, its sensory pathways in the posterior columns of the spinal cord, or a combination of these. Ataxias may be generalized but can also primarily affect the gait, the hands and arms, or the trunk; they may be acute or chronic, or acquired or genetic.

At 48 years old, experiencing ['Tachycardia', 'PLEURAL EFFUSION', 'chest pain', 'fever', 'dyspnea', 'cyanosis', 'DECREASED BREATH SOUNDS', 'low oxygen saturation']

Disease Name: Atelectasis, symptoms: ['Tachycardia', 'PLEURAL EFFUSION', 'chest pain', 'fever', 'dyspnea', 'cyanosis', 'DECREASED BREATH SOUNDS', 'low oxygen saturation'], Treatment: ['Treatment depends on the cause of the collapse: 1.Pleural effusion or pneumothorax- Relieve compression. 2. Mucus plug- Tracheal or bronchoscopic aspiration\nContinuous positive airway pressure. 3. Foreign body- Bronchoscopic examination. 4. Asthma- Bronchodilator and corticosteroid treatment\nRecombinant human deoxyribonuclease (off label use)\nHypertonic saline with or without bronchodilator. 5. Neuromuscular diseases- Intermittent positive pressure breathing\nMechanical insufflator–exsufflator\nNoninvasive bi-level positive pressure ventilation. 6. Cystic fibrosis- Airway clearance therapies\nHypertonic saline with or without bronchodilator. Hypertonic saline solution increases mucociliary clearance in patients with\nasthma, bronchiectasis, and cystic fibrosis and infants with acute bronchiolitis.'], Pathophysiology: The causes of atelectasis can be divided into 5 groups . Respiratory syncytial virus and other viral infections, including influenza viruses in young children can cause multiple areas of atelectasis. Mucous plugs are a common predisposing factor to atelectasis. Massive collapse of one or both lungs is most often a postoperative complication but occasionally results from other causes, such as trauma, asthma, pneumonia, tension pneumothorax , aspiration of foreign material , paralysis, or after extubation. Massive atelectasis is usually produced by a combination of factors, including immobilization or decreased use of the diaphragm and the respiratory muscles, obstruction of the bronchial tree, and abolition of the cough reflex. Symptoms vary with the cause and extent of the atelectasis. A small area is likely to be asymptomatic. When a large area of previously normal lung becomes atelectatic, especially when it does so suddenly, dyspnea accompanied by rapid shallow respirations, tachycardia, cough, and often cyanosis occurs. If the obstruction is removed, the symptoms disappear rapidly. Although it was once believed that atelectasis alone can cause fever, studies have shown no association between atelectasis and fever. Physical findings include limitation of chest excursion, decreased breath sound intensity, and coarse crackles. Breath sounds are decreased or absent over extensive atelectatic areas., Epidemiology:["The incidence of atelectasis in patient's undergoing general anesthesia is 90%", 'DEPENDS UPON UNDERLYING ETIOLOGY', 'Here are some ways to reduce the risk of atelectasis:\n\nGet up and walk around, perform breathing exercises and use an incentive spirometer after surgery as directed by your healthcare provider.\nIf you have any underlying conditions that can cause atelectasis, follow your provider’s recommendations for treating that condition.\nDon’t smoke or quit smoking.\nKeep small objects away from children to reduce their risk of inhaling them.'], Complications:['collapse', 'cyanosis', 'pulmonary fibrosis'], Diagnostics:['CT CHEST', 'CHEST X RAY', 'BRONCHOSCOPY', 'Aspiration for Culture & sensitivity', 'spirometry'], Differential diagnosis:['Asbestosis', 'ascites', 'BRONCHIAL ASTHMA', 'community-acquired pneumonia', 'CYSTIC FIBROSIS', 'IDIOPATHIC PULMONARY FIBROSIS', 'LUNG ABSCESS', 'PNEUMONIA', 'Pulmonary Embolism', 'respiratory failure'], disease description:Atelectasis is the incomplete expansion or complete collapse of air-bearing tissue, resulting from obstruction of air intake into the alveolar sacs. Segmental, lobar, or whole lung collapse is associated with the absorption of air contained in the alveoli, which are no longer ventilated.

Person at 31 with ['unconsciousness', 'HEAD DROP', 'SUDDEN LOSS OF POSTURAL MUSCLE TONE']

Disease Name: Atonic Seizures, symptoms: ['unconsciousness', 'HEAD DROP', 'SUDDEN LOSS OF POSTURAL MUSCLE TONE'], Treatment: [{'medication': ['Valproic acid(sodium valproate)/ Divalproex Sodium', 'Topiramate ', 'Lorazepam ', 'Levetiracetam ', 'Lamotrigine ']}, 'When medicines don’t work, dietary therapies (ketogenic, low glycemic, or modified Atkins diet), vagus nerve stimulation, or the split-brain operation (callosotomy) may help.\nWhich therapy to try depends in part on whether seizures start in one area or both sides of the brain.', 'A variety of seizure medicines can be used to treat these seizures, including valproic acid, topiramate, zonisamide, levetiracetam, lamotrigine, clonazepam, chlorazepate, lorazepam, clobazam, rufinamide, felbamate, and sometimes others.\nHowever, medicines often have limited effectiveness against atonic seizures.\nSince atonic seizures are common in people with Lennox-Gastaut syndrome, some new seizure medicines specific for this syndrome may help.', 'Brain surgery may be another treatment option for some individuals. Doctors may recommend surgery for uncontrolled atonic seizures if the seizure remains in one focal area of the brain. The surgery removes the seizure focus, which usually stops the seizures. As the procedure removes the part of the brain where the seizures originate, it is not an effective treatment for those who have atonic seizures that spread throughout the entire brain.'], Pathophysiology: There are two types of atonic seizures: focal and generalized. Focal seizures affect a small area of the brain and may only lead to muscle weakness in one area of the body.Conversely, generalized seizures can begin throughout both halves of the brain, affecting a more significant proportion of the body. When an atonic seizure involves the entire brain, doctors call it a generalized onset atonic seizure. These seizures begin with a sudden drop of the head, trunk, or whole body.Atonic seizures are most common in children. Although they may sometimes last into a person’s adult years, many children do outgrow them.Sometimes, atonic seizures are linked to Lennox-Gastout syndrome, which is a severe form of childhood epilepsy that causes frequent and multiple types of seizures. Children living with Lennox-Gastout syndrome often also have developmental and behavioral issues.Multiple factors, including rapid breathing and flickering lights, can trigger seizures in people with this form of epilepsy., Epidemiology:['1 to 2 out of 100 (1 to 2%) of all childhood-onset epilepsies', 'variable', 'Various medicines can treat atonic seizures, although they may not be helpful for everyone. The options to prevent or stop seizures include anti-seizure medications, which some may refer to as anti-epileptic drugs. It may take some trial and error to find the best drug and dosage amount.'], Complications:['injury'], Diagnostics:['random blood sugar RBS', 'Complete Blood Count CBC', 'CSF EXAMINATION', 'SERUM Sodium Na+', 'EEG', 'MRI Brain', 'PET SCAN', 'serum potassium K+', 'serum calcium Ca++', 'CT BRAIN'], Differential diagnosis:['migraine', 'syncope', 'transient ischaemic attacks', 'vertigo'], disease description:Atonic seizures are characterized by sudden loss of postural muscle tone lasting 1–2 s. Consciousness is briefly impaired, but there is usually no postictal confusion. A very brief seizure may cause only a quick head drop or nodding movement, whereas a longer seizure will cause the patient to collapse. 

A 18-year-old suffering ['crusting of the skin', 'erythematous rashes', 'Lichenification', 'Eczematous skin lesions', 'pruritus of the skin']

Disease Name: Atopic Dermatitis, symptoms: ['crusting of the skin', 'erythematous rashes', 'Lichenification', 'Eczematous skin lesions', 'pruritus of the skin'], Treatment: [{'medication': ['Diphenhydramine ', 'Fluticasone ', 'Cyclosporine/Ciclosporine', 'Tacrolimus ', 'Methotrexate', 'Azathioprine ', 'Betamethasone ', 'Clobetasol propionate ', 'Hydroxyzine']}, 'The treatment of AD requires a systematic, multifaceted approach that\nincorporates skin moisturization, topical antiinflammatory therapy, identification\nand elimination of flare factors and, if necessary, systemic\ntherapy.\n Moisturizers are first-line therapy. Lukewarm soaking baths or showers\nfor 15-20 min followed by the application of an occlusive emollient to retain\nmoisture provide symptomatic relief. Topical corticosteroids are the cornerstone of antiinflammatory treatment for\nacute exacerbations of AD.'], Pathophysiology: AD is associated with multiple phenotypes and endotypes that have overlapping clinical presentations. Atopic eczema is associated with IgE-mediated sensitization (at onset or during the course of eczema) and occurs in 70–80% of patients with AD. Nonatopic eczema is not associated with IgE-mediated sensitization and is seen in 20–30% of patients with AD. Both forms of AD are associated with eosinophilia. In atopic eczema, circulating T cells expressing the skin homing receptor cutaneous lymphocyte-associated antigen produce increased levels of T-helper type 2 (Th2) cytokines, including interleukin (IL)-4 and IL-13, which induce isotype switching to IgE synthesis. Another cytokine, IL-5, plays an important role in eosinophil development and survival. Nonatopic eczema is associated with lower IL-4 and IL-13 but increased IL-17 and IL-23 production than in atopic eczema. Age and race have also been found to affect the immune profile in AD. Compared with the skin of healthy individuals, both unaffected skin and acute skin lesions of patients with AD have an increased number of cells expressing IL-4 and IL-13. Chronic AD skin lesions, by contrast, have fewer cells that express IL-4 and IL-13, but increased numbers of cells that express IL-5, granulocyte-macrophage colony-stimulating factor, IL-12, and interferon (IFN)-? than acute AD lesions. Despite increased type 1 and type 17 immune responses in chronic AD, IL-4 and IL-13 as well as other type 2 cytokines (e.g. TSLP, IL- 31, IL-33) predominate and reflect increased numbers of Type 2 innate lymphoid cells and Th2 cells. The infiltration of IL-22–expressing T cells correlates with severity of AD, blocks keratinocyte differentiation, and induces epidermal hyperplasia. The importance of IL-4 and IL-13 in driving severe persistent AD has been validated by multiple clinical trials now demonstrating that biologics blocking IL-4 and IL-13 action lead to clinical improvement in moderate to severe AD. In healthy people the skin acts as a protective barrier against external irritants, moisture loss, and infection. Proper function of the skin depends on adequate moisture and lipid content, functional immune responses, and structural integrity. Severely dry skin is a hallmark of AD. This results from compromise of the epidermal barrier, which leads to excess transepidermal water loss, allergen penetration, and microbial colonization. Filaggrin , a structural protein in the epidermis, and its breakdown products are critical to skin barrier function, including moisturization of the skin. Genetic mutations in the filaggrin gene (FLG) family have been identified in patients with ichthyosis vulgaris (dry skin, palmar hyperlinearity) and in up to 50% of patients with severe AD. FLG mutation is strongly associated with development of food allergy and eczema herpeticum. Nonetheless, up to 60% of carriers of a FLG mutation do not develop atopic diseases. Cytokines found in allergic inflammation, such as IL-4, IL-13, IL-22, IL-25, and tumor necrosis factor, can also reduce filaggrin and other epidermal proteins and lipids. AD patients are at increased risk of bacterial, viral, and fungal infection related to impairment of innate immunity, disturbances in the microbiome, skin epithelial dysfunction, and overexpression of polarized immune pathways, which dampen host antimicrobial responses., Epidemiology:['GOOD', 'To Do : Maintain cool temperature in bedroom, and avoid too many bed covers.\nIncrease emollient use with cold weather.\nClothing: Avoid skin contact with irritating fibers (wool, large-fiber\ntextiles).\nAvoid wall-to-wall carpeting.\nRemove dust with a wet sponge.\nClose windows during peak pollen season on warm and dry\nweather days, and restrict, if possible, time outdoors.\nBreastfeeding may be beneficial. Not To Do : Do not use tight and too-warm clothing, to avoid excessive\nsweating.'], Complications:['exfoliative dermatitis', 'KERATOCONUS', 'atopic keratoconjunctivitis'], Diagnostics:['Complete Blood Count CBC', 'serum IgE level', 'Skin Prick test', 'EOSINOPHILS'], Differential diagnosis:['allergic contact dermatitis', 'Bacterial infection', 'Contact dermatitis', 'Histiocytosis X', 'HYPER-IgE SYNDROME', 'Impetigo', 'scabies', 'seborrhoeic dermatitis'], disease description:Atopic dermatitis (AD) , or eczema, is the most common chronic relapsing skin disease seen in infancy and childhood. It affects 10–30% of children worldwide and frequently occurs in families with other atopic diseases. Infants with AD are predisposed to development of food allergy, allergic rhinitis, and asthma later in childhood, a process called the atopic march . AD is a complex genetic disorder that results in a defective skin barrier, reduced skin innate immune responses, and polarized adaptive immune responses to environmental allergens and microbes that lead to chronic skin inflammation.

At the age of 44, symptoms like ['balaclava pattern of rashes', 'DRY SCALY SKIN', 'dry skin', 'itching on face', 'Itching of the skin', 'Rashes', 'wheezing']

Disease Name: Atopic Eczema, symptoms: ['balaclava pattern of rashes', 'DRY SCALY SKIN', 'dry skin', 'itching on face', 'Itching of the skin', 'Rashes', 'wheezing'], Treatment: ['Severity Clear Mild Moderate Severe\nTreatment for body Emollients Emollients\nMild potency topical corticosteroids\nEmollients\nModerate potency topical corticosteroids \n(use for axillae and groin flares for \n7–14 days only)\nNight time sedating antihistamines (if \nsleep disturbed)\nOral antibiotics (if clinically infected)\nEmollients\nPotent topical corticosteroids (use for \naxillae and groin flares for 7–14 days \nonly)\nNight time sedating antihistamines (if \nsleep disturbed)\nOral antibiotics (if clinically infected)\nTreatment for face and neck Emollients Emollients alone or mild potency \ntopical corticosteroids\nEmollients\nMild potency topical corticosteroids\nNight time sedating antihistamines (if \nsleep disturbed)\nOral antibiotics (if clinically infected)\nEmollients\nFor severe flares, use moderate potency \ntopical corticosteroids for 3–5 days only\nNight time sedating antihistamines (if \nsleep disturbed)\nOral antibiotics (if clinically infected)'], Pathophysiology: The pathophysiology of atopic dermatitis is complex and multifactorial, involving elements of barrier dysfunction, alterations in cell mediated immune responses, IgE mediated hypersensitivity, and environmental factors. Loss of function mutations in filaggrin have been implicated in severe atopic dermatitis due to a potential increase in trans-epidermal water loss, pH alterations, and dehydration. Other genetic changes have also been identified which may alter the skin's barrier function, resulting in an atopic dermatitis phenotype. The imbalance of Th2 to Th1 cytokines observed in atopic dermatitis can create alterations in the cell mediated immune responses and can promote IgE mediated hypersensitivity, both of which appear to play a role in the development of atopic dermatitis. One must additionally take into consideration the role of the environment on the causation of atopic dermatitis and the impact of chemicals such as airborne formaldehyde, harsh detergents, fragrances, and preservatives. Use of harsh alkaline detergents in skin care products may also unfavorably alter the skin's pH causing downstream changes in enzyme activity and triggering inflammation. Environmental pollutants can trigger responses from both the innate and adaptive immune pathways., Epidemiology:["Developing a basic skin care routine may help prevent eczema flares. The following tips may help reduce the drying effects of bathing:\n\nMoisturize your skin at least twice a day. Creams, ointments, shea butter and lotions seal in moisture. Choose a product or products that work well for you. Ideally, the best one for you will be safe, effective, affordable and unscented.\n\nUsing petroleum jelly on your baby's skin may help prevent development of atopic dermatitis.\n\nTake a daily bath or shower. Use warm, rather than hot, water and limit your bath or shower to about 10 minutes.\nUse a gentle, nonsoap cleanser. Choose a cleanser that's free of dyes, alcohols and fragrance. For young children, you usually need only warm water to get them clean — no soap or bubble bath needed. Soap can be especially irritating to the skin of young children. For people of any age, deodorant soaps and antibacterial soaps can remove too much of the skin's natural oils and dry the skin. Don't scrub the skin with a washcloth or loofah.\nPat dry. After bathing, gently pat the skin with a soft towel. Apply moisturizer while your skin is still damp (within three minutes).\nThe triggers for atopic dermatitis vary widely from person to person. Try to identify and avoid irritants that trigger your eczema. In general, avoid anything that causes an itch because scratching often triggers a flare.\n\nCommon triggers for atopic dermatitis include:\nRough wool fabric\nDry skin\nSkin infection\nHeat and sweat\nStress\nCleaning products\nDust mites and pet dander\nMold\nPollen\nSmoke from tobacco\nCold and dry air\nFragrances\nOther irritating chemicals\nInfants and children may have flares triggered by eating certain foods, such as eggs and cow's milk. Talk with your child's health care provider about identifying potential food allergies.\n\nOnce you understand what triggers your eczema, talk with your health care provider about how to manage your symptoms and prevent flares."], Complications:['fungal infections', 'viral infections', 'Bacterial infection'], Diagnostics:['serum IgE level'], Differential diagnosis:['Agammaglobulinaemia', 'Anhidrotic ectodermal dysplasia', 'Ataxia telangiectasia', 'Hypereosinophilic syndrome', 'HYPER-IgE SYNDROME', 'Netherton syndrome (ichthyosis, bamboo hairs)', 'Phenylketonuria', 'Wiskott–Aldrich syndrome (infections and thrombocytopenia'], disease description:AE is an itchy, chronic or chronically relapsing inflammatory skin condition that often starts in early childhood (usually before 2 years of age).The rash is characterized by erythema, itchy papules/papulovesicles (occasionally vesicles in infants) which may become excoriated and lichenified , and typically has a flexural distribution.

Symptoms reported at the age of 35: ['ECZEMA', 'The latter are characterized by small erythematous papules disseminated on the trunk and limbs as well as typical prurigo nodules, mostly located on the shins and arms', 'dry skin', 'itching', 'Eczematous skin lesions']

Disease Name: Atopic Eruption Of Pregnancy, symptoms: ['ECZEMA', 'The latter are characterized by small erythematous papules disseminated on the trunk and limbs as well as typical prurigo nodules, mostly located on the shins and arms', 'dry skin', 'itching', 'Eczematous skin lesions'], Treatment: ['asic treatment with emollients together with topical corticos\x02teroids for several days will usually lead to quick improvement \nof skin lesions. Severe cases may require a short course of sys\x02temic corticosteroids and antihistamines. Phototherapy (UVB) \nis a safe additional tool, particularly for severe cases in early \npregnancy.', 'First line \n• Topical emollients \n• Topical corticosteroids (see section on general treatment \nguidance) \n• Oral antihistamines: loratadine and cetirizine \n Second line \n• Narrow-band UVB phototherapy \n Third line \n• Prednisolone \n• Azathioprine'], Pathophysiology: The pathogenesis of AEP is thought to be triggered by pregnancy- specific immunological changes: a reduced cellular immunity and reduced production of Th1 cytokines (IL-2, interferon-?, IL-12) in contrast to the dominant humoral immunity and increased secretion of Th2 cytokines (IL-4, IL-10) . Thus the exacerbation of pre- existing atopic eczema and the first manifestation of atopic skin changes can be explained by the dominant Th2 immune response that is typical for pregnancy, Epidemiology:['common', 'Maternal prognosis is good even in severe cases as'], Complications:[], Diagnostics:['HISTOPATHLOGY', 'DIRECT IMMUNOFLORESCENCE ASSAY', 'INDIRECT IMMUNOFLORESCENCE ASSAY', 'SERUM SPECIFIC IgE TESTING'], Differential diagnosis:['folliculitis', 'intrahepatic cholestasis', 'Polymorphic eruption of pregnancy'], disease description:Atopic eruption of pregnancy (AEP) is a benign pruritic disorder of pregnancy that includes eczematous and/or papular lesions in patients with an atopic diathesis, once the other dermatoses of pregnancy have been excluded. It is the most common dermatosis in pregnancy, accounting for 50% of patients. It usually starts early on in pregnancy, with 75% of cases presenting before the third trimester, and a tendency to recur in subsequent pregnancies

Symptoms at 40 years old: ['itching in eyes', 'WATERING EYE']

Disease Name: Atopy And Atopic Eye Disease, symptoms: ['itching in eyes', 'WATERING EYE'], Treatment: [{'medication': ['Ketotifen Fumarate ', 'Sodium Cromoglycate ', 'Dexamethasone ', 'Prednisolone']}, 'Herpetic blepharitis may require treatment with local aciclovir \nointment, and corneal involvement may require systemic aciclovir therapy combined with appropriate topical steroid', 'allergen avoidance, use of cold compresses, \nand lubrication with preservative-free artificial tears are helpful. \n Addition of a potent topical antihistamine (levocabastine or emadastine) or a systemic antihistamine may \nhelp relieve itch in some patients. Long-term systemic antihistamine intake can lead to dry eye, the clinical features of which \ncan complicate the ocular allergy features'], Pathophysiology: Predisposing factors A personal or family history of atopy Pathology Recent advances in our understanding of the atopic eye diseases have come from investigation of the humoral mediators of inflammation in the tears and analysis of the cellular components by immunostaining and in situ hybridization of conjunctival biopsies. These techniques have shown that SAC and PAC are primarily type I IgE-mediated hypersensitivity responses whereas the others show varying degrees of a coexisting type IV hypersensitivity response and also involve the production of cytokines by various effector cells. Seasonal allergic conjunctivitis and PAC show mast cells and eosinophils in the conjunctival mucosa and submucosa with high levels of locally produced IgE to specific allergens being present in the tears. Symptoms are due to release of histamine and other inflammatory agents by mast cells which lead to dilatated blood vessels, irritated nerve endings and increased secretion of tears. The diseases can be mimicked by topical instillation of allergens and is blocked by drugs that are active against mast cells. The pathogenesis of AKC and VKC involves both IgE-mediated type I and non-IgE-mediated type IV hypersensitivity responses, with the production of various cytokines by effector cells. These lead to the more severe inflammatory changes that cause corneal damage. AKC and VKC show the cellular components present in SAC and PAC but also increased fibroblast activity with connective tissue hyperplasia, CD4+ lymphocytes and plasma cells together with different subsets of mast cells. The T cells are probably important inducers of the cellular inflammatory response in these diseases. Differences in AKC and VKC phenotypes may be explained by differences in the predominance of T-helper subsets; the Th1 subset involved in delayed hypersensitivity responses and inactivated by ciclosporin is more predominant in AKC than VKC in which the Th2 subset predominate with a B-cell helper role. Mast cells and eosinophils are found in larger numbers in VKC than AKC and functional heterogeneity in their populations may also be determinants of disease phenotypes. Eosinophils play a central role in atopic eye diseases and it appears that the level of eosinophil activation rather than the absolute numbers is relevant to the development of corneal disease. Eosinophils elaborate a host of cytokines and release cationic proteins including major basic protein which is epitheliotoxic and has been identified in the tears of VKC. It is probably a major factor responsible for the development of corneal epithelial erosions and macroerosions. The presence of the latter, with the mucous and debris present in acute exacerbations of keratopathy, accounts for the formation of plaque. Basophils have also been found to contribute to the atopic eye diseases through IgE-induced release of chemical mediators., Epidemiology:['The incidence of allergic conditions has increased', 'The symptoms of Atopic keratoconjunctivitis tend to begin before a person reaches their late 20s and can persist into the fourth or fifth decade of a person’s life.\n\nTreatments can control the symptoms and prevent further damage to the eyes. With the correct treatment, a person can have no symptomsTrusted Source and experience an improvement in their quality of life. A person can also manage their symptoms by avoiding contact with known allergens that worsen the symptoms of AKC.\n\nIf a person does not receive appropriate treatment, they may develop corneal involvement in one or both eyes, which can result in sight loss.'], Complications:['cataract', 'Glaucoma', 'KERATOCONUS'], Diagnostics:['serum IgE level', 'biopsy', 'Conjunctival cytology'], Differential diagnosis:['rosacea', 'Sjogren’s Syndrome'], disease description:The atopic eye diseases comprise a group of disorders that have in common a papillary conjunctivitis and evidence of a type I allergic mechanism. They include the milder conditions of seasonal allergic conjunctivitis (SAC) and perennial allergic conjunctivitis (PAC) and the more severe atopic keratoconjunctivitis (AKC), atopic blepharoconjunctivitis (ABC) and vernal keratoconjunctivitis The atopic eye diseases all involve immunoglobulin E (IgE) mediated hypersensitivity responses although each disease hasspecific immunogenic pathways. Ocular involvement in atopic patients ranges from 15 to 40% but is generally mild with features of SAC or PAC. Only a very small proportion of patients with atopic eczema have significant ocular disease

A 48-year-old patient with ['hearing impairment', 'fullness in ear']

Disease Name: Atresia Of External Canal, symptoms: ['hearing impairment', 'fullness in ear'], Treatment: ['REPAIR'], Pathophysiology: Congenital atresia of the meatus may occur alone or in association with microtia. When it occurs alone, it is due to failure of canalization of the ectodermal core that fills the dorsal part of the first branchial cleft. The outer meatus, in these cases, is obliterated with fibrous tissue or bone while the deep meatus and the tympanic membrane are normal. Atresia with microtia is more common. It may be associated with abnormalities of the middle ear, internal ear and other structures., Epidemiology:['1 in 10,000–20,000 live births', 'POOR', 'NA'], Complications:['Hearing loss', 'speech defect'], Diagnostics:['CT SCAN', 'PHYSICAL EXAMINATION'], Differential diagnosis:['Goldenhar syndrome', 'Treacher Collins syndrome'], disease description:Atresia of the external ear canal may be congenital or acquired. Congenital atresia presents a more complex problem. If it is bilateral, a severe hearing impairment exists from birth, with consequent tardy development of the child. A speech defect is coexistent.

Suffering from ['crepts present in chest', 'Dizziness', 'EXERCISE INTOLERANCE', 'palpitations', 'syncope', 'easy fatigability', 'IMPAIRED CARDIAC FUNCTION'] at 40

Disease Name: Atrial Fibrillation, symptoms: ['crepts present in chest', 'Dizziness', 'EXERCISE INTOLERANCE', 'palpitations', 'syncope', 'easy fatigability', 'IMPAIRED CARDIAC FUNCTION'], Treatment: [{'medication': ['Amiodarone ', 'Diltiazem ', 'Digoxin ', 'Heparin ', 'Metoprolol ', 'Rivaroxaban', 'Dabigatran Etexilate']}, 'surgical ablation of AF'], Pathophysiology: There are a wide variety of pathophysiological mechanisms that play a role in the development of atrial fibrillation (AF); however, it is cardiac remodeling that accounts for most of them. Cardiac remodeling, particularly of atria, results in structural and electrical changes that eventually become the cause of deranged rhythm in AF. Structural remodeling is caused by the changes in myocytes and the extracellular matrix, and fibrous tissue deposition also plays a major role in some etiologies. On the other hand, tachycardia and shortening of the refractory period lead to electrical remodeling.Most commonly, hypertension, structural, valvular, and ischemic heart disease illicit the paroxysmal and persistent forms of atrial fibrillation, but the underlying pathophysiology is not well understood. Some research has shown evidence of genetic causes of atrial fibrillation involving chromosome 10 (10q22-q24) that consists of a mutation in the gene, alpha-subunit of the cardiac Ik5, which is responsible for pore formation. This is a gain of function mutation, allowing for more pores, increasing the activity within the ion channels of the heart, and thus affecting the stability of the membrane and reducing its refractory time., Epidemiology:['5/100', 'More than 454,000 hospitalizations with AFib as the primary diagnosis happen each year in the United States.', 'bad', 'To Do : REGULAR EXERCISE, CONTROL BP Not To Do : AVOID EXCESSIVE ALCOHOL'], Complications:['heart failure', 'hypertension', 'Diabetes mellitus type 1', 'blood clot formation'], Diagnostics:['Thyroid Stimulating Hormone TSH', 'ECG', 'X RAY CHEST', 'trans oesophageal 2D ECHO', 'STRESS TEST (TREADMILL TEST TMT)'], Differential diagnosis:['atrial flutter', 'atrial tachycardia', 'FOCAL ATRIAL TACHYCARDIA', 'paroxysmal supraventricular tachycardia', 'Wolff-Parkinson-White syndrome'], disease description:ATRIAL FIBRILLATION IS CHARACTERIZED BY DISORGANISED ,RAPID AND RAPID ATRIAL ACTIVATION WITH LOSS OF ATRIAL CONTRACTION AND WITH AN IRREGULAR VENTRICULAR RATE . IN AN UNTREATED PATIENT THE VENTRICULAR RATE ALSO TENDS TO BE RAPID AND IRREGULAR BETWWEN(100 -120) BEATS PER MINUTE IT MAY EXCEED TO 200 BEATS PER MINUTE.

A 40-year-old suffering ['Tachycardia', 'palpitations', 'dyspnea', 'EXERCISE INTOLERANCE', 'chest discomfort']

Disease Name: Atrial Flutter, symptoms: ['Tachycardia', 'palpitations', 'dyspnea', 'EXERCISE INTOLERANCE', 'chest discomfort'], Treatment: [{'medication': ['Ibutilide Fumarate ', 'Procainamide ']}, 'Medicines for the treatment of atrial flutter include:\n\nMedicines to slow down your heart rate: Calcium channel blockers and beta-blockers.\nMedicines to stop the abnormal rhythm: Antiarrhythmic drugs.', 'Procedures to treat atrial flutter include:\n\nCardioversion via electrical shock.\nCatheter ablation, a procedure a provider can use to destroy the tissue that’s creating abnormal signals.\nTemporary change in your pacemaker or implantable cardioverter defibrillator (ICD) setting.'], Pathophysiology: Typical Atrial Flutter Typical atrial flutter is the most common type of atrial flutter and is a macroreentrant atrial tachycardia that uses the CTI as an essential part of the circuit. The Todaro tendon, crista terminalis, the inferior vena cava, the tricuspid valve annulus, and the coronary sinus os delineate the circuit. These structures are essential to provide the pathway length for the flutter system. The CTI provides the slow conduction pathway, and it presents in the lateral aspect of the younger patient and the medial aspect in the older patients. The mechanism of slow conduction is not well understood but might be related to anisotropic fiber orientation. With aging and atrial dilation, occurs fibrosis of the atrial tissue and produce non-uniform anisotropic conduction through the CTI. The crista terminalis is a functional barrier that induces a transverse conduction block, steep slope, and arborization that allows the circuit to exist. The mechanism of arrhythmia is a macro-reentry activation of the right atrium from the interatrial septum and along the crista terminalis with passive activation of the left atrium via the coronary sinus muscular connection. As this cycle occurs in the atrium, conduction is determined by the atrioventricular node mechanism to conduct the atrial impulse. Commonly the atrioventricular conduction will be 2 to 1 with an atrial rate of 300 beats per minute with a ventricular rate of 150 beats per minute, but this can be variable depending on the underlying parasympathetic stimulus or refractoriness of the atrioventricular node. The absence of an isoelectric line between P waves or QRS complexes is due to the constant cycling of the circuit or atrial activation. The reason behind the existence of the circuit might relate to the nature of the anatomical structures that are circumscribing the circuit. The crista terminalis thickness might have the capacity to block conduction, as well as the low voltage of the CTI, can be signs of arrhythmogenesis and poor conduction in the right atrium. Atypical Atrial Flutter Atypical atrial flutter or other macroreentrant atrial tachycardia has a circuit configuration different from the typical right atrial flutter circuit. Electrophysiologic studies and intracardiac mapping are the only means to determine the exact mechanism or area generating the atrial flutter. Different from typical atrial flutter, the presence of atypical atrial flutter is related to structural heart diseases as prior cardiac surgery or ablation procedures. When the atrial flutter is determined to come from the right atrium but not associated with the CTI system, the circuit can be in the superior vena cava and part of the terminal crest. When prior surgery or intervention occurred, the presence of scar can often become arrhythmogenic, and the center of the circuit and the onset of the arrhythmia mostly occur after several years of the procedure, likely secondary to remodeling. In patients without prior cardiac intervention, the atrial flutter circuit can be low voltage areas like the lateral right atrium, this might be secondary to fibrosis due to chronic atrial high pressures, or cardiomyopathy that can produce fibrosis of the myocardium and creating low voltage areas that allow atrial flutter to occur. Left atrial flutter can be associated with surgical atriotomy scars or areas of prior ablations, combined with areas of low voltage. Electrophysiologic studies and mapping of the right and left atrium are necessary to determine the specific location and mechanism of the arrhythmia to guide the ablation. In the presence of an intra-atrial septal macro-reentrant system, the success rate is low when compared with the free wall atrial tachycardias., Epidemiology:['The prevalence of atrial fibrillation increases with age, as follows: 25-35 years: 2-3 cases per 1000 population. 55-64 years: 30-90 cases per 1000 population. 65-90 years: 50-90 cases per 1000 population.', 'variable', 'Prevention of atrial flutter focuses on controlling or preventing the risk factors.\n\nStay at a healthy weight.\nDrink alcohol only in moderation, if at all.\nStop tobacco use.\nControl high blood pressure and diabetes.'], Complications:['haemodynamic disturbances', 'Embolic events'], Diagnostics:['Thyroid Stimulating Hormone TSH', 'ECG', 'X RAY CHEST', 'holter monitering'], Differential diagnosis:['atrial fibrillation', 'atrial tachycardia'], disease description:Atrial flutter, a supraventricular arrhythmia, is one of the most common rhythm disturbances of the heart. It is characterized by a fast atrial rate with a fixed or variable ventricular rate. There are several atrial contractions to one ventricular contraction and symptoms include fatigue, palpitations, and syncope.

Person at 26 years, dealing with ['cardiac tamponade', 'heart murmur', 'arthralgia', 'breathlessness', 'malaise', 'syncope', 'fever', 'weight loss', 'CACHEXIA']

Disease Name: Atrial Myxoma, symptoms: ['cardiac tamponade', 'heart murmur', 'arthralgia', 'breathlessness', 'malaise', 'syncope', 'fever', 'weight loss', 'CACHEXIA'], Treatment: ['Surgical excision using cardiopulmonary bypass is indicated regardless of tumor size, and is generally curative. Myxomas recur in\n12–22% of familial cases but in only 1–2% of sporadic cases. Tumor recurrence most likely results from multifocal lesions in the former setting and incomplete tumor resection in the latter.'], Pathophysiology: Myxomas are the most common type of primary cardiac tumor in adults, accounting for one-third to one-half of all cases at postmortem examination, and approximately three-quarters of the tumors treated surgically. They occur at all ages, most commonly in the third through sixth decades, with a female predilection. Approximately 90% of myxomas are sporadic; the remainder are familial with autosomal dominant transmission. The familial variety often occurs as part of a syndrome complex (Carney complex) that includes (1) myxomas (cardiac, skin, and/or breast), (2) lentigines and/or pigmented nevi, and (3) endocrine overactivity (primary nodular adrenal cortical disease with or without Cushing’s syndrome, testicular tumors, and/or pituitary adenomas with gigantism or acromegaly). Certain constellations of findings have been referred to as the NAME syndrome (nevi, atrial myxoma, myxoid neurofibroma, and ephelides) or the LAMB syndrome (lentigines, atrial myxoma, and blue nevi), although these syndromes probably represent subsets of the Carney complex. The genetic basis of this complex has not been elucidated completely; however, inactivating mutations in the tumor-suppressor gene PRKAR1A, which encodes the protein kinase A type I-a regulatory subunit, have been identified in ~70% of patients with Carney complex. Pathologically, myxomas are gelatinous structures that consist of myxoma cells embedded in a stroma rich in glycosaminoglycans. Most sporadic tumors are solitary, arise from the interatrial septum in the vicinity of the fossa ovalis (particularly in the left atrium), and are often pedunculated on a fibrovascular stalk. In contrast, familial or syndromic tumors tend to occur in younger individuals, are often multiple, may be ventricular in location, and are more likely to recur after initial resection. Myxomas commonly present with obstructive signs and symptoms. The most common clinical presentation mimics that of mitral valve disease: either stenosis owing to tumor prolapse into the mitral orifice or regurgitation resulting from tumor-induced valvular trauma or distortion. Ventricular myxomas may cause outflow tract obstruction similar to that caused by subaortic or subpulmonic stenosis. The symptoms and signs of myxoma may be sudden in onset or positional in nature,owing to the effects of gravity on tumor position. A characteristic lowpitched sound, a “tumor plop,” may be appreciated on auscultation during early or mid-diastole and is thought to result from the impact of the tumor against the mitral valve or ventricular wall. Myxomas also may present with peripheral or pulmonary embolic phenomenon (resulting from embolization of tumor fragments or tumor-associated thrombus) or with constitutional signs and symptoms, including fever, weight loss, cachexia, malaise, arthralgias, rash, digital clubbing, and Raynaud’s phenomenon. Laboratory abnormalities, such as hypergammaglobulinemia, anemia, polycythemia, leukocytosis, elevated erythrocyte sedimentation rate, elevated C-reactive protein level, thrombocytopenia, and thrombocytosis are often present. These features account for the frequent misdiagnosis of patients with myxomas as having endocarditis, collagen vascular disease, or a paraneoplastic syndrome., Epidemiology:['< 5 per 10,000.', 'Primary tumors of the heart are rare entities with an estimated incidence of less than 0.03% of which 75% are benign and half of them are myxomas.', 'GOOD', 'People with myxomas generally have a good outlook. Surgery can usually remove myxomas and prevent them from coming back.\n\nBut about 1% to 2% of people develop new myxomas within 10 to 15 years of their surgery. Recurrence is more common among people who have Carney’s complex.\n\nThis is why your healthcare provider will recommend routine imaging tests if you have a history of myxomas. These tests can detect the formation of new myxomas and lower your risk of future complications.\n\nPeople who’ve had myxomas face a greater risk of atrial arrhythmias (rhythm problems in the upper chambers of your heart). Your healthcare provider will discuss your risk and prescribe medication if needed.'], Complications:['mitral regurgitation', 'mitral stenosis', 'tricuspid regurgitation'], Diagnostics:['CRP', 'Differential Leucocyte Count DLC', 'Erythrocyte Sedimentation Rate (ESR)', 'Hb', 'RBC Count', 'THROMBOCYTE COUNT', 'CT SCAN', 'Transthoracic echocardiography (TTE)', 'Transesophageal echocardiography (TEE)', 'Cardiac MRI with gadolinium contrast', 'Gated cardiac CT', 'Nuclear Imaging (including 18F-fluorodeoxyglucose positron emission tomography [FDG-PET])'], Differential diagnosis:['mitral regurgitation', 'mitral stenosis', 'Pulmonary Embolism', 'tricuspid regurgitation', 'tricuspid stenosis'], disease description:Cardiac tumors can be broadly classified into those that arise primarily in the heart and those that reflect metastatic disease from a distant primary source. Primary cardiac tumors can be further divided into those that are pathologically benign and those that are malignant. Overall, primary cardiac tumors are relatively uncommon, whereas secondary involvement of the heart or pericardium occurs in as many as 20% of patients with end-stage metastatic cancer. While patients with cardiac tumors may present with a variety of symptoms, many patients are asymptomatic at the time of diagnosis as the tumor may be identified incidentally on imaging studies performed for other reasons. Such findings need to be differentiated from other cardiac masses such as vegetation, thrombus, or myocardial hypertrophy. Echocardiography is usually the initial method of evaluation of cardiac tumors; however, a variety of imaging modalities are now available and a multimodality approach is often necessary for accurate diagnosis and clarification of treatment options.

A 32-year-old with ['cyanosis', 'dyspnea', 'Recurrent infection']

Disease Name: Atrial Septal Defects, symptoms: ['cyanosis', 'dyspnea', 'Recurrent infection'], Treatment: nan, Pathophysiology: nan, Epidemiology:nan, Complications:[], Diagnostics:['2-D Echo', 'Coronary Angiography', 'CT Thorax', 'ECG'], Differential diagnosis:['mitral regurgitation', 'tricuspid atresia'], disease description:nan

Symptoms at 28: ['may be normal or tachycardia', 'ejection click', 'failure to thrive', 'pedal edema', 'Tachyarrythmia', 'breathlessness', 'EXERCISE INTOLERANCE', 'dyspnea', 'wide fixed splitting of s2']

Disease Name: Atrial Septal Defect, symptoms: ['may be normal or tachycardia', 'ejection click', 'failure to thrive', 'pedal edema', 'Tachyarrythmia', 'breathlessness', 'EXERCISE INTOLERANCE', 'dyspnea', 'wide fixed splitting of s2'], Treatment: [{'medication': ['Furosemide ', 'Digoxin ', 'Aspirin/Acetylsalicylic acid']}, 'Most fossa ovalis defects with good margins can be closed\npercutaneously in the catheterization laboratory with\nocclusive devices. Others require surgical closure. Closure\nis recommended before school entry to prevent late\ncomplications. Small defects ( <8 mm) can be observed.\nSpontaneous closure is well recognized in small defects\nthat are diagnosed in infancy or early childhood .'], Pathophysiology: The physiology of ASD is that of a pre-tricuspid shunt. The enlarged right ventricle results in a parasternal impulse. The ejection systolic murmur originates from the pulmonary valve because of the increased blood flow. An increased flow through the tricuspid valve may result in a soft delayed diastolic rumble at the lower left sternal border. The overload of the right ventricle due to an increase in venous return prolongs the time required for its emptying resulting in delayed P2. This delay also results from the prolonged 'hang-out' interval because of the very low resistance in the pulmonary circulation. Additionally, since the two atria being linked via the large ASD, inspiration does not produce any net pressure change between them and respiration related fluctuations in systemic venous return to the right side of the heart are abolished; thereby the fixed S2. The electrocardiogram of ostium secundum ASD is characterized by right axis deviation and right ventricular hypertrophy. The characteristic configuration of the lead Vl is rsR' seen in almost 90% patients . Presence of left axis deviation beyond -30° suggests ostiurn prim um ASD. The chest X-ray shows mild to moderate cardiomegaly, right atrial and right ventricular enlargement, prominent main pulmonary artery segment, a relatively small aortic shadow and plethoric lung fields. The left atrium does not enlarge in size in atrial septal defect, unless associated with other anomalies like mitral regurgitation. Echocardiogram shows increased size of the right ventricle with paradoxical ventricular septal motion. 2D echo in subcostal view often best identifies the defect. The echocardiogram allows decision regarding suitability of catheter closure, based on measurements of the defect and the adequacy of margins., Epidemiology:['The prevalence of CHDs in adults was 2.4 per 1000 individuals in a cohort, with atrial septal defect (44.5%) being the most frequent defect.', '1 to 2 per 1000 live births', 'GOOD', "There’s no specific way to prevent atrial septal defects. They develop when a fetus is still in the uterus. But prenatal care may impact a fetus'schances of having congenital heart disease. If you’re pregnant or planning a pregnancy, it’s important to:\n\nQuit smoking and using tobacco products.\nAvoid drinking alcohol.\nAvoid secondhand smoke.\nAvoid using recreational drugs, especially cocaine.\nTalk with your provider about any prescription medications you’re taking and how those might affect your pregnancy.\nGenetic testing may be helpful if you or other biological family members have congenital heart disease."], Complications:['Arrhythmias', 'heart failure', 'PULMONARY ARTERIAL HYPERTENSION'], Diagnostics:['ECG', 'trans thoracic 2D ECHO', 'CARDIAC CATHETERIZATION', 'CHEST X RAY', 'CT SCAN', 'CARDIAC MRI'], Differential diagnosis:['FALLOTS TETRALOGY', 'VENTRICULAR SEPTAL DEFECTS'], disease description:Atrial septal defect (ASD) account for as an isolated anomaly 5-10% of all CHD. Based on anatomy, ASD is classified as follows: Fossa ova/is ASD. They are located in the central portion of atrial septum, in the position of foramen ovale. These defects are amenable to closure in the catheterization laboratory. Sinus venosus ASD. These are located at junction of superior vena cava and right atrium. These defects do not have a superior margin because the superior vena cava straddles the defect. These defects are associated with anomalous drainage of one or more right pulmonary veins. Ostium primum ASD. These defects are created by failure of septum primum, and are in lower part of the atrial septum; inferior margin of ASD is formed by the atrioventricular valve. Coronary sinus ASD. An unroofed coronary sinus is a rare communication between the coronary sinus and the left atrium, which produces features similar to other types of ASD.

Symptoms reported by a baby aged 2.8 include ['altered sensorium', 'systolic murmur apical mid-diastolic murmurs', 'chest pain', 'fatigue', 'Tachycardia', 'Night terrors', 'dyspnea', 'Dizziness', 'syncope']

Disease Name: Atrioventricular Block (av Block), symptoms: ['altered sensorium', 'systolic murmur apical mid-diastolic murmurs', 'chest pain', 'fatigue', 'Tachycardia', 'Night terrors', 'dyspnea', 'Dizziness', 'syncope'], Treatment: [{'medication': ['Atropine/ Atropine methonitrate']}, 'In general, patients that present with first-degree or second-degree Mobitz type 1 AV block do not require treatment. Any provoking medications can be removed, and patients can be monitored on an outpatient basis. However, patients with higher degrees of AV block (Mobitz type 2 AV block, 3rd degree) tend to have severe damage to the conduction system. They are at a much greater risk of progressing into asystole, ventricular tachycardia, or sudden cardiac death. Hence, they require urgent admission for cardiac monitoring, backup temporary cardiac pacing, and insertion of a permanent pacemaker.'], Pathophysiology: First degree AV block can originate from various locations within the conduction system. The levels of conduction delay include the atrium, AV node (most common in first-degree heart block), Bundle of His, bundle branches, fascicles, Purkinje system. Mobitz type I second degree AV block usually occurs within the AV block while Mobitz type II second degree AV block mainly originates from conduction system disease below the level of the AV node (in the bundle of His and in the bundle branches). In third-degree AV block, no atrial impulses could reach the ventricle- it can occur in the AV node or in the infranodal specialized conduction system., Epidemiology:['the prevalence of third-degree AV block is 0.04%', '0.02%', 'variable', 'Some cases of heart block may be congenital (present at birth). But most heart block develops after birth. Some causes can’t be prevented. We also know that the risk of heart block increases with age and so does heart disease. Some causes of heart disease are preventable.\n\nSteps you can take to keep your heart and body as healthy as possible include:\n\nLead a heart-healthy lifestyle, which includes eating a heart healthy diet, exercising regularly, getting an adequate amount of sleep each night, reducing stress, limiting alcohol and stopping smoking and use of illicit drugs.\nTalk with your healthcare provider about reviewing medications and other supplements you are taking to determine if any change the normal levels of potassium, calcium and magnesium – substances in your body that play a role with your heart’s electrical system. Your provider can change your medication to a different drug class if needed.'], Complications:['infection', 'stroke'], Diagnostics:['ECG', 'ECG', 'CHEST X RAY'], Differential diagnosis:['Cardiac ischemia', 'hyperkalemia', 'Myocardial infarction'], disease description:Atrioventricular (AV) conduction is evaluated by assessing the relationship between the P waves and QRS complexes. Normally, there is a P wave that precedes each QRS complex by a fixed PR interval of 120 to 200 milliseconds. AV block represents a delay or disturbance in the transmission of an impulse from the atria to the ventricles. This can be due to an anatomical or functional impairment in the heart’s conduction system. This disruption in normal electrical activity can be transient or permanent, and then further characterized as delayed, intermittent, or absent. In general, there are three degrees of AV nodal blocks: first degree, second degree (Mobitz type 1 or 2), and third-degree.

Symptoms at 24 years old: ['dry and glazed pharyngeal mucosa often covered with crusts', 'dryness of throat', 'FOUL SMELLING DISCHARGE', 'dry cough']

Disease Name: Atrophic Pharyngitis, symptoms: ['dry and glazed pharyngeal mucosa often covered with crusts', 'dryness of throat', 'FOUL SMELLING DISCHARGE', 'dry cough'], Treatment: [{'medication': ['Iodine (Sodium iodide,potassium iodide) ']}, 'crusts can\nbe removed by spraying the throat with alkaline solution,\nor pharyngeal irrigation. Mandl’s paint applied locally\nhas a soothing effect.'], Pathophysiology: Bacteria and viruses can cause direct invasion of the pharyngeal mucosa. Certain viruses like rhinovirus can cause irritation secondary to nasal secretions. In almost all cases, there is a local invasion of the pharyngeal mucosa which also results in excess secretion and edema., Epidemiology:['0.3 to 1 percent of the population i', '15 to 25 cases per 1000 children per year.', 'GOOD', 'Viral infections like colds and flu often cause sore throats. You can reduce your sore throat by protecting yourself against colds and flu. Some ways to do that include:\n\nWashing your hands often, using soap and water or alcohol-based hand sanitizers.\nAvoid people who are sneezing and coughing.\nIf you do spend time with people who are sneezing and coughing, avoid sharing food, drink or utensils.\nBe vaccinated against flu.'], Complications:['ACUTE RHEUMATIC FEVER', 'otitis media', 'sinusitis', 'Epiglottitis'], Diagnostics:['Oral cavity examination'], Differential diagnosis:['allergic rhinitis', 'chronic tonsillitis', 'diphtheria', 'Epiglottitis', 'Gastroesophageal reflux disease (GERD)', 'Peritonsillar abscess', 'Sjogren’s Syndrome', 'smoking'], disease description:It is a form of chronic pharyngitis often seen in patients of atrophic rhinitis. Pharyngeal mucosa along with its mucous glands shows atrophy. Scanty mucus production by glands leads to formation of crusts, which later get infected giving rise to foul smell..

Person at 24 with manifestations like ['roomy nasal cavity', 'epistaxis', 'anosmia', 'FOUL SMELLING DISCHARGE', 'hearing impairment', 'NASAL BLOCKAGE']

Disease Name: Atrophic Rhinitis, symptoms: ['roomy nasal cavity', 'epistaxis', 'anosmia', 'FOUL SMELLING DISCHARGE', 'hearing impairment', 'NASAL BLOCKAGE'], Treatment: [{'medication': ['Oestradiol/Oestrogen', 'Sodium bicarbonate ', 'Streptomycin ', 'Iodine (Sodium iodide,potassium iodide) ', 'Glycerine/Glycerol']}, 'Nasal irrigation and removal of crusts,25% glucose in glycerine,Local antibiotics,Oestradiol spray,Systemic use of streptomycin,', 'Young’s operation,Narrowing the nasal cavities'], Pathophysiology: Ciliated columnar epithelium is lost and is replaced by stratified squamous type. There is atrophy of seromucinous glands, venous blood sinusoids and nerve elements. Arteries in the mucosa, periosteum and bone show obliterative endarteritis. The bone of turbinates undergoes resorption causing widening of nasal chambers. Paranasal sinuses are small due to their arrested development., Epidemiology:['0.3%–1.0% of the population', '0.3 to 1 percent of the population', "There isn't a cure for atrophic rhinitis, but trea", 'Unfortunately, there isn’t any way to prevent atrophic rhinitis.'], Complications:['anosmia'], Diagnostics:['SERUM IRON', 'Vitamin A', 'plain radiograph', 'vitamin d', 'PHYSICAL EXAMINATION', 'NASAL EXAMINATION'], Differential diagnosis:['allergic rhinitis', 'Chronic Sinusitis', 'nasal polyps', 'rhinitis', 'RHINOSCLEROMA'], disease description:It is a chronic inflammation of nose characterized by atrophy of nasal mucosa and turbinate bones. The nasal cavities are roomy and full of foul-smelling crusts. Atrophic rhinitis is of two types: primary and secondary.

Individual aged 19 with manifestations like ['MUSCLE TWICHINGS', 'GENERALIZED,SLOW SPIKE & SLOW WAVE PATTERN.', 'stare', 'SEIZURE ACCOMPANIED WITH MORE OBVIOUS MOTOR SIGNS', 'LAPSE OF CONSIOUSNESS IS PROLONGED', 'developmental delay']

Disease Name: Atypical Absence Seizures, symptoms: ['MUSCLE TWICHINGS', 'GENERALIZED,SLOW SPIKE & SLOW WAVE PATTERN.', 'stare', 'SEIZURE ACCOMPANIED WITH MORE OBVIOUS MOTOR SIGNS', 'LAPSE OF CONSIOUSNESS IS PROLONGED', 'developmental delay'], Treatment: [{'medication': ['Valproic acid(sodium valproate)/ Divalproex Sodium', 'Topiramate ', 'Lamotrigine ']}, 'The first-line treatment for absence epilepsy is ethosuximide. A randomized controlled trial performed in 2010 that included 446 children with CAE showed that ethosuximide and valproic acid were superior to lamotrigine [10]. However, this study had a low seizure-free rate with 53% of patients in the ethosuximide group, 58% on the valproic acid group, and 29% of patients taking lamotrigine. The group that received valproic acid had significantly lower scores on attentional measures as compared to the ethosuximide and lamotrigine groups. For this reason, ethosuximide is the preferred agent for the treatment of absence epilepsy. An study showed that only one quarter of children with absence epilepty became seizure free with levetiracetam. Whne effective, leveteriacetam can control absence epilepsy at a relatively low dose (usually less then 40 mg/kg/day)'], Pathophysiology: Although some of the pathways involved in the development of absence seizures have been described, their pathophysiological mechanisms are yet to be fully understood. The cortico-thalamic-cortical circuit is considered to play a major role in the pathophysiology of absence seizures. Some of the neurons involved in the cortico-thalamic-cortical system include: Cortical glutamatergic neurons are originating on cortical layer VI and projecting to the nucleus reticularis of the thalamus. Thalamic relay neurons that have excitatory projections to cortical pyramidal neurons. Neurons from the thalamic nucleus reticularis containing inhibitory GABA-ergic projections that connect with other neurons from the same nucleus, and with thalamic relay neurons. These neurons do not connect directly with the cortex. Neurons from the thalamic nucleus reticularis can fire in an oscillatory pattern (for example, rhythmic bursts involved in the generation of sleep spindles) or continuously in single spikes (tonic firing during wakefulness). Shifts between these two firing patterns in the thalamic nucleus reticularis are modulated by spikes present in thalamocortical networks and neurons from the thalamic nucleus reticularis. These are mediated through low-threshold transient calcium channels known as T-type channels. After depolarization, T-type channels briefly allow calcium inflow before becoming inactivated. Reactivation requires a relatively long hyperpolarization facilitated by GABA-B receptors. Therefore, abnormal oscillatory rhythms can originate from T-type channel abnormalities, or from the increased GABA-B activity. As explained by the genetics of absence epilepsy, genes coding for T-type calcium channels and for GABA receptors have been associated with the etiopathogenesis of this type of epilepsy. Medications that suppress T-type calcium channels, such as ethosuximide and valproate, are effective anti-absence drugs. Conversely, medications that increase GABA-B activity (e.g., vigabatrin) exacerbate the frequency of absence seizures. In contrast, GABA-A agonists (e.g., benzodiazepines), that preferentially enhance GABA-ergic activity in neurons from the thalamic nucleus reticularis, can suppress absence seizures., Epidemiology:['The incidence of absence seizures is between 0.7 and 4.6 per 100,000 in the general population and around 6 to 8 per 100,000 in the pediatric population younger than 15 years', 'variable', 'Unfortunately, there isn’t a way to prevent absence seizures, since genetics are thought to play a role in their cause.'], Complications:['Lennox-Gastaut Syndrome'], Diagnostics:['CSF EXAMINATION', 'SERUM Sodium Na+', 'EEG', 'PET SCAN', 'serum potassium K+', 'serum calcium Ca++', 'MRI'], Differential diagnosis:['focal seizure', 'sleep disorders'], disease description:Absence seizures are brief seizures during which the patient is unresponsive. They are generally seen in children between 4 and 12 years of age.Here are some characteristic features of Atypical absence seizures:The person will stare (just like in absence seizure) but they may be able to respond a bit.Eye blinking, chewing movements, lip smacking, or slight jerking movements of the lips may occur.There may be rubbing of the fingers or hands or other small hand movements.Symptoms of absence seizures can be difficult to pick up in a person with other cognitive or behavioral problems. It may be hard to tell what is due to a seizure or from other behaviors.These seizures may begin and end gradually. This is different from the sudden start and stop of a typical absence seizure.Falling during the seizure is also more common than it is during typical absence seizures.Atypical absence seizures usually last 5 to 30 seconds, most often more than 10 seconds.

Individual, 52 years old, with ['Polyps']

Disease Name: Atypical Adenomatous Hyperplasia, symptoms: ['Polyps'], Treatment: ['1 colectomy with ileorectal anastomosis (IRA);\n2 restorative proctocolectomy with an ileal pouch–anal \nanastomosis (RPC);\n3 total proctectomy and end ileostomy.'], Pathophysiology: nan, Epidemiology:['POOR'], Complications:[], Diagnostics:['Sigmoidoscopy', 'XRAY ABDOMEN'], Differential diagnosis:['adenocarcinoma in situ'], disease description:Familial adenomatous polyposis (FAP) is defined clinically by the presence of more than 100 colorectal adenomas, but is also characterised by duodenal adenomas and multiple extraintestinal manifestations (Summary box 70.1). Over 80% of cases come from patients with a positive family history. The remainder arise as a result of new mutations in the adenomatous polyposis coli (APC) gene on the short arm of chromosome 5. FAP is inherited as an autosomal dominant condition and is consequently equally likely in men and women. The lifetime risk of colorectal cancer is 100% in patients with FAP. FAP can also be associated with benign mesodermal tumours such as desmoid tumours and osteomas. Epidermoid cysts can also occur (Gardner’s syndrome); desmoid tumours in the abdomen spread locally to involve the intestinal mesentery and, although non-metastasising, they may become unresectable. Up to 50% of patients with FAP have congenital hypertrophy of the retinal pigment epithelium (CHRPE), which can be used to screen affected families if genetic testing is unavailable.

Symptoms at 50 years old: ['The most common sites where naevi develop are the inner aspects of the labia majora, the labia minora and the clitoris.', 'Asymptomatic']

Disease Name: Atypical Genital Naevi, symptoms: ['The most common sites where naevi develop are the inner aspects of the labia majora, the labia minora and the clitoris.', 'Asymptomatic'], Treatment: ['Treatment should be aimed at complete removal by excision, preferably at the time of initial detection or biopsy. In particular, small and partial biopsies should be avoided because they may be associated with sampling error, and visualization of the deeper aspects of the tumor is necessary for adequate diagnosis.'], Pathophysiology: The histological features of these lesions can be difficult to interpret. They may be asymmetrical with the junctional component often involving the adnexae and exhibiting large nests of cells. The naevoid cells are atypical with this cytological atypia visible in both junctional and dermal parts. Dermal mitoses may be evident., Epidemiology:['The prevalence of atypical nevi in white populations has been reported to be as high as 17%', '2% to 18% of the population.', 'variable', 'In addition to limiting your exposure to sunlight and using sunscreen every day, examining your moles increases the chances of early detection and treatment of melanoma and other types of skin cancers.\n\nAwareness and recognition of this group of melanocytic lesions is important to avoid over diagnosis as melanoma with subsequent wide excision and possibly sentinel lymph node biopsy.'], Complications:[], Diagnostics:['HISTOLOGIC EXAMINATION'], Differential diagnosis:['Genital warts', 'lichen sclerosus', 'melanoma', 'Molluscum Contagiosum', 'Seborrheic Keratoses'], disease description:Atypical genital nevi are rare melanocytic lesions that most commonly arise on the vulva of young women. They are currently regarded as nevi of special sites, in that despite histologically worrisome features, their clinical behavior is reportedly benign.

Person aged 23 with manifestations like ['palpable mass', 'BLOODY DISCHARGE', 'nipple discharge']

Disease Name: Atypical Papilloma, symptoms: ['palpable mass', 'BLOODY DISCHARGE', 'nipple discharge'], Treatment: ['Atypical hyperplasia is generally treated with surgery to remove the abnormal cells and to make sure no in situ or invasive cancer also is present in the area. Doctors often recommend more-intensive screening for breast cancer and medications to reduce your breast cancer risk.'], Pathophysiology: Pathophysiology is unknown but intraductal papilloma might originate from bipotent progenitor cells that differentiate as luminal and myoepithelial cells., Epidemiology:['Intraductal papillomas are relatively rare, with an incidence of 2–3%.', 'with an incidence of 2–3%', 'variable', 'NA'], Complications:['bleeding', 'infection', 'cancer'], Diagnostics:['mammography', 'usg breast', 'MRI BREAST', 'Fine-needle aspiration biopsy'], Differential diagnosis:['Adenomyoepithelioma', 'Atypical ductal hyperplasia'], disease description:Atypical papilloma  is benign intraductal proliferation of epithelial cells with fibrovascular cores and underlying myoepithelial cells. Intraductal papilloma can be associated with another condition called atypical hyperplasia. Atypical cells mean that the cells are not entirely normal. Hyperplasia means the cells in the breast increase in number. Normal cells go through quite a few changes before they become cancerous. 

Individual, 38 years old, with ['failure to thrive', 'lethargy', 'vomiting', 'cranial nerve palsies']

Disease Name: Atypical Teratoid/rhabdoid Tumour (who Grade 4), symptoms: ['failure to thrive', 'lethargy', 'vomiting', 'cranial nerve palsies'], Treatment: ['Surgery, high dose chemotherapy with radiation.'], Pathophysiology: Heterogeneous mass with mixed cystic and solid components, often hyperdense on CT, hypointense/heterogeneous on T2, heterogeneous enhancement, may contain hemorrhage or Ca++Often hyperintense on DWI due to increased cellularityCalcifications seen in up to 40%Fairly even split between posterior fossa and supratentorial region (roughly 40–45% each), both in ~10%Propensity for leptomeningeal metastases, so entire spine imaging preoperative is required, Epidemiology:['Age typically < 3 years; rare in children aged > 6 years', 'Accounts for 1 - 2% of all pediatric brain tumors and is very rare in adults', 'variable', 'NA'], Complications:['MALIGNANCY'], Diagnostics:['Cytogenetics', 'MRI', 'CT SCAN', 'Immunostaining'], Differential diagnosis:['cns primitive neuroectodermal tumour (pnet) (who g', 'ependymoma', 'medulloblastoma (who grade 4)', 'Teratoma'], disease description:Atypical teratoid/rhabdoid tumors are aggressive neoplasms of the central nervous system occurring mainly in the early childhood and rarely in adults. . This tumor is mainly composed of rhabdoid cells, with the addition or not of areas demonstrating characteristics of primitive neuroectodermal tumor, epithelial tissue, neoplastic mesenchyme and neuronal or glial differentiation

Suffering from ['AUTOIMMUNE HEPATITIS', 'Hemolytic anemia', 'Hypothyroidism', 'nephrotic syndrome', 'purpura', 'anemia', 'anorexia', 'MALABSORPTION', 'weight loss', 'short stature', 'arthritis', 'CHRONIC DIARRHEA', 'diarrhea', 'failure to thrive'] at 49

Disease Name: Autoimmune Enteropathy, symptoms: ['AUTOIMMUNE HEPATITIS', 'Hemolytic anemia', 'Hypothyroidism', 'nephrotic syndrome', 'purpura', 'anemia', 'anorexia', 'MALABSORPTION', 'weight loss', 'short stature', 'arthritis', 'CHRONIC DIARRHEA', 'diarrhea', 'failure to thrive'], Treatment: [{'medication': ['Cyclosporine/Ciclosporine', 'Cyclophosphamide ', 'Azathioprine ', 'Prednisolone']}, 'Many patients with AIE develop malnutrition, which must be addressed as part of the treatment plan. A trial of oral nutritional supplementation may be successful. However, for many patients with AIE, total parenteral nutrition is required. In addition, medical therapy is commonly used, most typically with corticosteroids (budesonide and prednisone). However, some patients are refractory to corticosteroids, and in these patients immunosuppressive therapy with azathioprine, 6-mercaptopurine, cyclosporine, tacrolimus, mycophenolate mofetil, sirolimus, infliximab, and rituximab has been described'], Pathophysiology: Evidence demonstrates that an autoimmune response is involved in the pathophysiology of AIE. The innate immune system involves the intestinal epithelium, which is a natural barrier to both food borne and environmental antigens. Proper functioning of the thymus is important for a healthy immune system. When the thymus malfunctions, “self reactive” T cells are produced, leading to “anti-self B cells,” further contributing to an autoimmune response.Both IPEX and AIE are thought to be caused by an autoimmune response involving CD4+ T cells, but differ in their mechanism. IPEX is caused when T lymphocytes lose their regulatory function and activate an immune response that causes direct damage to the enterocytes, whereas enteropathy in AIE is a result in part of a humoral immune response involving anti-enterocyte antibodies (AEA), which are found in the majority of those affected, and anti-globlet cell antibodies. In one study, 22/26 cases of AIE (85%) had detectable AEA antibodies, which was similar to the findings in a more recent study, which reported AEA antibodies in 13 of 15 patients (87%)., Epidemiology:['prevalence of up to 29% in epidemiological studies', 'variable', 'Use nutrients such as fish oil, vitamin C, vitamin D, and probiotics to help calm your immune response naturally.\nExercise regularly — it’s a natural anti-inflammatory.\nPractice deep relaxation like yoga, deep breathing, biofeedback, or massage, because stress worsens the immune response.'], Complications:['infections', 'weight loss'], Diagnostics:['Complete Blood Count CBC', 'HISTOPATHLOGY', 'Small Bowel Biopsy', 'Upper GI Endoscopy'], Differential diagnosis:['CHRONIC DIARRHEA', 'severe malnutrition', 'weight loss'], disease description:Autoimmune Enteropathy (AIE) is a rare condition characterized by intractable diarrhea, histologic changes on small intestinal biopsy, failed response to dietary manipulation that also may present with extra-intestinal manifestations. 

Suffering from ['Tachycardia', 'tachypnoea', 'Hypotension', 'fever'] at the age of 44

Disease Name: Autoimmune Haemolysis, symptoms: ['Tachycardia', 'tachypnoea', 'Hypotension', 'fever'], Treatment: ['The rate of splenectomy is about 10-15% of all AIHA cases but is nowadays decreasing given the availability of equally effective second-line medical treatments, primarily rituximab. It is worth reminding that splenectomy is usually ineffective in CAD since most RBC destruction occurs in the liver [20,21]. An interesting recently reported finding is the emergence of long-lived autoreactive plasma cells in the spleen of primary wAIHA patients treated with rituximab'], Pathophysiology: The most frequent autoantibodies against RBCs are IgG, which mainly determine extravascular hemolysis through the ADCC in the reticuloendothelial system (spleen and to a lesser extent liver). The IgG subclass influences the degree to which these antibodies shorten RBC survival: IgG1 is the most commonly encountered subclass and together with IgG3 shortens the half-life more efficiently than IgG2 and IgG4. Autoantibodies of this class are mostly directed against epitopes of the Rh system. They generally react at 37 °C and, therefore, are responsible for the warm forms of AIHA . IgG are able to activate the complement cascade, with the exception of IgG2 and IgG4 subclasses. IgA autoantibodies are generally associated with IgG and only rarely reported as the sole causative agent of AIHA.IgM are pentameric autoantibodies able to dramatically fix complement compared with other isotypes, thus prevalently causing intravascular hemolysis, and to a lesser extent C3d-mediated extravascular lysis (mainly in the liver). Autoantibodies of this class are directed against the I/i system. Their optimal temperature of reaction is 4 °C, and thus they are responsible for the cold forms of AIHA . However, the thermal amplitude of IgM autoantibodies ranges from 0 to 34 °C, and those with a thermal activity close to physiological temperatures (warm IgM) are the most harmful autoantibodies, able to cause severe forms of AIHA with a reported mortality rate of about 20% . In fact, it is worth reminding that the amount of RBC destruction by intravascular hemolysis has been calculated in 200 ml of RBCs in 1 h, whereas by extravascular hemolysis it is 10-fold lesser (0.25 ml RBCs/kg/h, i.e., for a patient weighing 70 kg = 17.5 ml RBCs/h = 420 ml RBCs .Anti-RBC antibodies are usually detected by the direct antiglobulin test (DAT) or Coombs test, generally performed by the traditional tube agglutination technique with polyspecific antisera. Nowadays the use of monospecific anti-IgG, anti-IgM, and anti-C3 antisera is recommended to define the class of the autoantibody and its thermal amplitude. It is worth mentioning a simple test, the spontaneous agglutination of RBCs at 20 °C, a characteristic feature indicating the presence of cold IgM autoantibodies. According to DAT results and to the thermal characteristics of the autoantibody, AIHAs are usually classified in two main groups: wAIHA (~70% of cases), which displayed IgG only or IgG plus C3d on erythrocytes, and CAD (~20% of patients), which showed C3d only, along with high serum titer of cold agglutinins of I specificity. There are few cases (7-8% of all AIHAs), which showed a DAT positive for IgG and C3d, with the coexistence of warm autoantibodies and high-titer cold agglutinins (mixed AIHA). However, there is increasing evidence of atypical cases of difficult classification - mainly DAT-negative - which are frequently severe and refractory/relapsed after several therapy lines, and may have a fatal outcome . DAT-negative cases may be caused by warm IgM autoantibodies, which can be identified by the dual direct antiglobulin test (DDAT) . It is worth mentioning the Donath-Landsteiner autoantibody, a bithermic hemolysin able to fix complement at cold temperatures and to determine RBCs lysis at 37 °C, that is directed against the erythrocyte P antigen and responsible of paroxysmal cold hemoglobinuria, which is rather common in children (30% of cases) but rare in adults (<1% of all AIHA cases), Epidemiology:['one to three cases per 100,000 population per year', 'variable', 'It’s not always possible to prevent autoimmune hemolytic anemia. But if you have a viral infection or use medications that are commonly linked to AIHA, then your healthcare provider can monitor your situation in an effort to reduce your risk of developing the condition.'], Complications:['Arrhythmias', 'Cardiomyopathies', 'heart failure'], Diagnostics:['Complete Blood Count CBC', 'COOMB TEST DIRECT', 'Peripheral Blood Smear', 'Reticulocyte Count', 'serum haptoglobin', 'bilirubin TEST'], Differential diagnosis:['chronic lymphocytic leukaemia', 'GASTRIC CANCER', 'lung cancer.', 'microangiopathic hemolytic anemia', 'pernicious anemia', 'rheumatoid arthritis', 'systemic lupus erythematosus (SLE)'], disease description:Autoimmune hemolytic anemia (AIHA) occurs when your immune system mistakes red blood cells as unwanted substances. As a result, your body produces antibodies that destroy red blood cells, which can lead to a low amount of red blood cells (known as anemia).AIHA is highly manageable, but it can be fatal if left untreated. Immediate intervention is essential.