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Person, 41 years old, presenting ['Rashes', 'nephritis', 'ascites', 'jaundice', 'spider telangiectasias', 'splenomegaly', 'edema', 'ERYTHEMA NODUSUM', 'SICCA SYNDROME', 'amenorrhoea', 'fatigue', 'loss of appetite', 'malaise', 'anorexia', 'arthralgia', 'arthritis', 'maculopapular rash', 'skin acne', 'Generalised oedema', 'vasculitis']

Disease Name: Autoimmune Hepatitis, symptoms: ['Rashes', 'nephritis', 'ascites', 'jaundice', 'spider telangiectasias', 'splenomegaly', 'edema', 'ERYTHEMA NODUSUM', 'SICCA SYNDROME', 'amenorrhoea', 'fatigue', 'loss of appetite', 'malaise', 'anorexia', 'arthralgia', 'arthritis', 'maculopapular rash', 'skin acne', 'Generalised oedema', 'vasculitis'], Treatment: [{'medication': ['Mercaptopurine', 'Azathioprine ', 'Prednisolone']}, 'Prednisone at an initial dose of 1-2 mg/kg/24 hr is continued until\naminotransferase values return to less than twice the upper limit of normal. The\ndose should then be lowered in 5-mg decrements over 2-4 mo until a\nmaintenance dose of 0.1-0.3 mg/kg/24 hr is achieved. In patients who respond\npoorly, who experience severe side effects, or who cannot be maintained on lowdose steroids, azathioprine (1.5-2.0 mg/kg/24 hr, up to 100 mg/24 hr) can be\nadded, with frequent monitoring for bone marrow suppression. Measurement of\nthiopurine methyltransferase activity should be done prior to beginning\ntreatment with the thiopurine drugs azathioprine and 6-mercaptopurine. n patients with a mild and\nrelatively asymptomatic presentation, some favor a lower starting dose of\nprednisone (10-20 mg) coupled with the simultaneous early administration of\neither 6-mercaptopurine (1.0-1.5 mg/kg/24 hr) or azathioprine (1.5-2.0 mg/kg/24\nhr). Patients with primary sclerosing cholangitis/autoimmune hepatitis overlap\nsyndrome respond similarly to immunosuppressive therapy.There is a potential role for budesonide combined with\nazathioprine in treatment of noncirrhotic patients. Cyclosporine, tacrolimus,\nmycophenolate mofetil, and sirolimus have been used in the management of\ncases refractory to standard therapy.'], Pathophysiology: Autoimmune hepatitis arises in a genetically predisposed host after an unknown trigger leads to a T cell–mediated immune response targeting liver autoantigens. A dense portal mononuclear cell infiltrate invades the surrounding parenchyma and comprises T and B lymphocytes, macrophages, and plasma cells. The immunopathogenic mechanisms underlying autoimmune hepatitis are unsettled. Triggering factors can include molecular mimicry, infections, drugs, and the environment (toxins) in a genetically susceptible host. Several human leukocyte antigen class II molecules?particularly DR3, DR4, and DR7 isoforms?confer susceptibility to autoimmune hepatitis. Self-antigenic peptides are processed by populations of antigen-presenting cells and presented to CD4 and CD8 effector T cells. CD4+ T lymphocytes recognizing a self-antigenic liver peptide orchestrate liver injury. Cell-mediated injury by cytokines released by CD8+ cytotoxic T cells and/or antibody-mediated cytotoxicity can be operative. There is also evidence that regulatory T cells from patients with autoimmune hepatitis are impaired in their ability to control the proliferation of CD4 and CD8 effector cells. Cytochrome P450 2D6 is the main autoantigen in type 2 autoimmune hepatitis. Antibody-coated hepatocytes may be lysed by complement or Fc-bearing natural killer lymphocytes. Heterozygous mutations in the autoimmune regulator gene (AIRE), which encodes a transcription factor controlling the negative selection of autoreactive thymocytes, can be found in some children with autoimmune hepatitis types 1 and 2. AIRE mutations also cause autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (also called autoimmune polyendocrinopathy syndrome), in which autoimmune hepatitis occurs in approximately 20% of patients. Pathology The histologic features common to untreated cases include inflammatory infiltrates, consisting of lymphocytes and plasma cells that expand portal areas and often penetrate the lobule (interface hepatitis); moderate to severe piecemeal necrosis of hepatocytes extending outward from the limiting plate; variable necrosis, fibrosis, and zones of parenchymal collapse spanning neighboring portal triads or between a portal triad and central vein (bridging necrosis); and variable degrees of bile duct epithelial injury. Distortion of hepatic architecture can be severe; cirrhosis may be present in children at the time of diagnosis. Histologic features in acute liver failure may be obscured by massive necrosis and multilobular collapse. Other histologic features may suggest an alternative diagnosis: characteristic periodic acid–Schiff-positive, diastase-resistant granules are seen in a1 -antitrypsin deficiency, and macrovesicular and microvesicular steatosis is found in nonalcoholic steatohepatitis and often in Wilson disease. Bile duct injury can suggest an autoimmune cholangiopathy or an overlap syndrome. Ultrastructural analysis might suggest distinct types of storage disorders., Epidemiology:['31.2 cases per 100,000 persons in the United States.', '0.9-2/100,000 populations per year', 'Without treatment, life expectancy is 50%', 'In most cases autoimmune hepatitis cannot be prevented. Knowing the risk factors may help you detect and treat the disease early.'], Complications:['ascites', 'Hepatic cirrhosis', 'HEPATIC ENCEPHALOPATHY', 'splenomegaly', 'varices'], Diagnostics:['ANA', 'ELISA For IgG', 'LIVER BIOPSY', 'LIVER FUNCTION TEST LFT', 'LIVER ANTIBODIES', 'SERUM AMINOTRANSFERASE', 'MRI', 'SERUM GAMMAGLOBULIN LEVEL', 'antiactin (smooth muscle) antibody', 'liver-kidney microsomal antibody'], Differential diagnosis:['Hepatitis A', 'Hepatitis C', 'Hepatitis D', 'Hepatitis E', 'PRIMARY BILIARY CIRRHOSIS', 'PRIMARY SCLEROSING CHOLANGITIS', 'viral hepatitis'], disease description:Autoimmune hepatitis is a chronic hepatic inflammatory process manifested by elevated serum aminotransaminase concentrations, liver-associated serum autoantibodies, and/or hypergammaglobulinemia. The serological autoantibody profile defines 2 main types of autoimmune hepatitis: AIH type 1, with positivity for anti-nuclear antibodies (ANA) and/or anti–smooth muscle antibody (SMA) and AIH type 2, with positivity for anti–liver kidney microsomal type 1 antibody (anti-LKM-1).

Suffering from ['Bradycardia', 'peripheral edema', 'puffy face', 'Carpal tunnel syndrome', 'Goiter', 'Dry coarse skin', 'cool peripheral extremities', 'Diffuse alopecia', 'Delayed tendon reflex relaxation', 'constipation', 'dry skin', 'hair loss', 'impaired hearing', 'menorrhagia', 'weakness', 'weight gain', 'Poor memory', 'poor appetite', 'dyspnea', 'paresthesias', 'Hoarse voice', 'tiredness', 'feeling cold', 'Difficulty concentrating'] at the age of 46

Disease Name: Autoimmune Hypothyroidism, symptoms: ['Bradycardia', 'peripheral edema', 'puffy face', 'Carpal tunnel syndrome', 'Goiter', 'Dry coarse skin', 'cool peripheral extremities', 'Diffuse alopecia', 'Delayed tendon reflex relaxation', 'constipation', 'dry skin', 'hair loss', 'impaired hearing', 'menorrhagia', 'weakness', 'weight gain', 'Poor memory', 'poor appetite', 'dyspnea', 'paresthesias', 'Hoarse voice', 'tiredness', 'feeling cold', 'Difficulty concentrating'], Treatment: [{'medication': ['Levothyroxine/Tetra idothyronine']}], Pathophysiology: The development of Hashimoto disease is thought to be of autoimmune origin with lymphocyte infiltration and fibrosis as typical features. The current diagnosis is based on clinical symptoms correlating with laboratory results of elevated TSH with normal to low thyroxine levels. It is interesting to note, however, that there is little evidence demonstrating the role of antithyroid peroxidase (anti-TPO) antibody in the pathogenesis of autoimmune thyroid disease (AITD). Anti-TPO antibodies can fix complement and, in vitro, have been shown to bind and kill thyrocytes. However, to date, there has been no correlation noted in human studies between the severity of disease and the level of anti-TPO antibody concentration in serum. We do, however, know that positive serum anti-TPO antibody concentration is correlated with the active phase of the disease, Epidemiology:['bad', 'To Do : .Using insect repellent.\n.Wearing gloves when handling sick or dead animals.\n.Avoiding mowing over dead animals.\n.Wear long pants, long sleeves, and long socks to keep ticks and deer flies off your skin.\n.Don’t drink untreated surface water.\n.Use of masks during mowing and other landscaping activities may reduce your risk of inhaling the bacteria.\n.Cook game meat thoroughly before eating.\n.Not using bare hands to skin or dress wild animals.\n.Removing ticks promptly.\n.Wearing clothing that covers exposed skin (tight at the wrists and ankles)'], Complications:['coma', 'Myxedema'], Diagnostics:['Anti TPO Antibodies', 'Free T4', 'Serum Cholesterol Total', 'Serum Triglycerides', 'TG (Triglycerides Test)', 'Thyroid Stimulating Hormone TSH', 'USG Thyroid', 'hemoglobin HB', 'serum creatine phosphokinase'], Differential diagnosis:['metastatic thyroid carcinoma', 'toxic multinodular goiter'], disease description:Autoimmune hypothyroidism may be associated with a goiter (Hashimoto’s, or goitrous thyroiditis) or, at the later stages of the disease, minimal residual thyroid tissue (atrophic thyroiditis). Because the autoimmune process gradually reduces thyroid function, Although some patients may have minor symptoms, this state is called subclinical hypothyroidism. Later, unbound T4 levels fall and TSH levels rise further; symptoms become more readily apparent at this stage (usually TSH >10 mIU/L), which is referred to as clinical hypothyroidism or overt hypothyroidism there is a phase of compensation when normal thyroid hormone levels are maintained by a rise in TSH.

At 44 years old, experiencing ['arthritis', 'Glomerulonephritis', 'hepatitis', 'Urticaria', 'uveitis', 'vasculitis', 'Panniculitis', 'anemia', 'encephalopathy', 'headache', 'seizures', 'splenomegaly', 'HEPATOMEGALY']

Disease Name: Autoimmune Lymphoproliferative Syndrome (alps), symptoms: ['arthritis', 'Glomerulonephritis', 'hepatitis', 'Urticaria', 'uveitis', 'vasculitis', 'Panniculitis', 'anemia', 'encephalopathy', 'headache', 'seizures', 'splenomegaly', 'HEPATOMEGALY'], Treatment: [{'medication': ['Cyclophosphamide ', 'Methotrexate', 'Azathioprine ']}, 'There currently is no standard cure for ALPS. The disorder can be managed by treating low blood-cell counts (cytopenias) and other autoimmune diseases that occur in people with ALPS. The disease also can be managed by monitoring and treating complications, including the excessive production of a type of white blood cell called a lymphocyte (lymphoproliferation), enlarged spleen, and cancer of the lymph nodes (lymphoma).', 'Spleen removal, or splenectomy, may be necessary in rare cases.'], Pathophysiology: ALPS due to germline pathogenic variants in the Fas cell surface death receptor (FAS) gene that encodes an apoptosis-associated antigen (ALPS-FAS) is the most common and best-characterized type of ALPS, although it is nonetheless a rare condition. , Epidemiology:['annual incidence is approximately 10/100,000 and is increasing in developed countries.', 'variable', "It can't be prevented as this condition is inherited in an autosomal dominant pattern. \n\nGenetic counselling is advisable."], Complications:['lymphadenopathy', 'splenomegaly', 'HEPATOMEGALY'], Diagnostics:['Complete Blood Count CBC', 'GENRAL BLOOD PICTURE', 'GENETIC TESTING', 'GENETIC TESTING', 'MRI', 'CT SCAN'], Differential diagnosis:['Epstein-Barr Virus', 'WISKOTT-ALDRICH SYNDROME', 'X linked lymphoproliferative disease'], disease description:Autoimmune lymphoproliferative syndrome (ALPS) is a rare genetic disorder of the immune system. In ALPS, unusually high numbers of white blood cells called lymphocytes accumulate in the lymph nodes, liver, and spleen and can lead to enlargement of these organs.

Suffering from ['hypoparathyroidism', 'VITILIGO', 'candidiasis', 'Gonadal suppression', 'alopecia', 'Pernicious anaemia', 'oral candidiasis', 'MALABSORPTION', 'leukoplakia'] at 50

Disease Name: Autoimmune Polyendocrine Syndrome, symptoms: ['hypoparathyroidism', 'VITILIGO', 'candidiasis', 'Gonadal suppression', 'alopecia', 'Pernicious anaemia', 'oral candidiasis', 'MALABSORPTION', 'leukoplakia'], Treatment: [{'medication': ['Ketoconazole ']}, 'all patients with\nhypothyroidism and the possibility of APS should be screened\nfor adrenal insufficiency to allow treatment with glucocorticoids\nprior to the initiation of thyroid hormone replacement. Treatment\nof mucocutaneous candidiasis with ketoconazole in an individual\nwith subclinical adrenal insufficiency may also precipitate adrenal\ncrisis.', 'including glucocorticoids such as prednisone, cyclosporin, the calcineurin inhibitors tacrolimus and sirolimus, methotrexate, mycophenolate mofetil, and rituximab, a CD20 inhibitor; these are especially used for auto-immune hepatitis, enteropathy, tubulo-interstitial nephritis, interstitial lung disease and keratoconjunctivitis.\n\nmanagement of autoimmune polyendocrine syndromes includes hormonal replacement therapy as needed and treatment of complications.\n\nHormonal and vitamin (Vitamin D, B12) replacement should be implemented for the known hormonal deficiencies, and other deficiencies should be anticipated and screened for periodically, especially in those with circulating antibodies for components of adrenal steroidogenesis (21-hydroxyase, 17-hydroxylase), thyroid (TPO, TG antibodies) and calcium, phosphate, or parathyroid hormone levels as indicated.'], Pathophysiology: APS-1 (Online Mendelian Inheritance in Man [OMIM] 240300) has also been called autoimmune polyendocrinopathy–candidiasis–ectodermal dystrophy (APECED). Mucocutaneous candidiasis, hypoparathyroidism, and Addison’s disease form the three major components of this disorder. However, many other organ systems can be involved over time. APS-1 is rare, with fewer than 500 cases reported in the literature. The classical form of APS-1 is an autosomal recessive disorder caused by mutations in the AIRE gene (autoimmune regulator gene) found on chromosome 21. This gene is most highly expressed in thymic medullary epithelial cells (mTECs) where it appears to control the expression of tissue-specific self-antigens (e.g., insulin). Deletion of this regulator leads to decreased expression of tissue-specific self-antigens and is hypothesized to allow autoreactive T cells to avoid central deletion, which normally occurs during T cell maturation in the thymus. The AIRE gene is also expressed in epithelial cells found in peripheral lymphoid organs, but its role in these extrathymic cells remains controversial. To date, over 100 mutations have been described in this gene, and there is a higher frequency within certain ethnic groups including Iranian Jews, Sardinians, Finns, Norwegians, and Irish. Recently, several autosomal dominant mutations have been identified, and are localized primarily in the PHD1 domain of the AIRE gene, rather than the CARD region where the autosomal recessive mutations have been found. Individuals with this non-classical form of APS-1 may have a later onset of symptoms, and less aggressive disease, without the full spectrum of autoimmune components being expressed.When one of the component disorders is present, a second associated disorder occurs more commonly than in the general population. There is controversy as to which tests to use and how often to screen individuals for disease. A strong family history of autoimmunity should raise suspicion in an individual with an initial component diagnosis. The development of a rarer form of autoimmunity, such as Addison’s disease, should prompt more extensive screening for other linked disorders, as ~50% of Addison’s disease patients develop another autoimmune diseases during their lifetime. Circulating autoantibodies, as previously discussed, can precede the development of clinical disease by many years but would allow the clinician to follow the patient and identify the disease onset at its earliest time point. For each of the endocrine components of the disorder, appropriate autoantibody assays are listed and, if positive, should prompt physiologic testing to diagnose clinical or subclinical disease. For Addison’s disease, antibodies to 21-hydroxylase antibodies are highly diagnostic for risk of adrenal insufficiency. However, individuals may take many years to develop overt symptoms of hypoadrenalism. Screening of 21-hydroxylase antibody– positive patients can be performed measuring morning ACTH and cortisol on a yearly basis. Rising ACTH values over time or low morning cortisol in association with signs or symptoms of adrenal insufficiency should prompt testing via the cosyntropin stimulation test. T1D can be screened for by measuring autoantibodies directed against insulin, GAD65, IA-2, and ZnT8. Risk for progression to disease is based on the number of antibodies (=2 islet autoantibodies with normal glucose tolerance is now defined as stage 1 of T1D as the lifetime risk for developing clinical symptoms is nearly 100%), and metabolic factors (impaired oral glucose tolerance test). National Institutes of Health–sponsored trial groups such as Type 1 Diabetes TrialNet are screening first- and second-degree family members for these autoantibodies and identifying prediabetic individuals who may qualify for intervention trials to change the course of the disease prior to onset. Efforts are now underway to screen the general population for T1D risk with islet autoantibodies. Screening tests for thyroid disease can include anti–thyroid peroxidase (TPO) or anti-thyroglobulin autoantibodies or anti- TSH receptor antibodies for Graves’ disease. Yearly measurements of TSH can then be used to follow these individuals. Celiac disease can be screened for using the anti– tissue transglutaminase (tTg) antibody test. For those <20 years of age, testing every 1–2 years should be performed, whereas less frequent testing is indicated after the age of 20 because the majority of individuals who develop celiac disease have the antibody earlier in life. Positive tTg antibody test results should be confirmed on 2759 repeat testing, followed by small-bowel biopsy to document pathologic changes of celiac disease. Many patients have asymptomatic celiac disease that is nevertheless associated with osteopenia and impaired growth. If left untreated, symptomatic celiac disease has been reported to be associated with an increased risk of gastrointestinal malignancy, especially lymphoma, and osteoporosis later in life. The knowledge of the particular disease associations should guide other autoantibody or laboratory testing. A complete history and physical examination should be performed every 1–3 years including CBC, metabolic panel, TSH, and vitamin B12 levels to screen for most of the possible abnormalities. More specific tests should be based on specific findings from the history and physical examination., Epidemiology:["Can't be prevented as such because Autoimmune polyendocrine syndrome is an autosomal recessive genetic disorder. \n\nEffective measures for the secondary prevention of autoimmune polyendocrine syndrome (APS) includes patient education and periodic screening. Genetic counselling is advisable. \n\nThe last decade has unraveled new monogenic forms of APS and better diagnostic tools, both genetic tests and autoantibody analyses. Research in the next decades should focus on prevention and targeted treatment of autoimmune diseases."], Complications:['hepatitis', 'hypogonadism', 'MALABSORPTION', 'pernicious anemia'], Diagnostics:['ACTH', 'Blood Glucose test', 'Complete Blood Count CBC', 'ESTRADIOL', 'Hb', 'serum Vitamin B12 level', 'serum potassium K+', 'GENETIC TESTING', 'Serum FSH Level Test', 'serum phosphate', 'Blood smear', 'SERUM CALCIUM LEVEL', 'SERUM SODIUM LEVEL', 'THYROID PROFILE', 'ADRENAL FUNCTION TEST'], Differential diagnosis:['Congenital rubella', 'Hemochromatosis', 'hypogonadism', 'KEARNS-SAYRE SYNDROME'], disease description:Polyglandular deficiency syndromes have been given many different names, reflecting the wide spectrum of disorders that have been associated with these syndromes and the heterogeneity of their clinical presentations. The name used in this chapter for this group of disorders is autoimmune polyendocrine syndrome (APS). In general, these disorders are divided into two major categories, APS type 1 (APS-1) and APS type 2 (APS-2). Some groups have further subdivided APS-2 into APS type 3 (APS-3) and APS type 4 (APS-4) depending on the type of autoimmunity involved. For the most part, this additional classification does not clarify our understanding of disease pathogenesis or prevention of complications in individual patients. Importantly, there are many nonendocrine disease associations included in these syndromes, suggesting that although the underlying autoimmune disorder predominantly involves endocrine targets, it does not exclude other tissues.

Symptoms reported by a 24-year-old: ['angioedema', 'ECZEMA', 'erythema multiforme', 'fixed drug eruptions', 'Urticaria']

Disease Name: Autoimmune Progesterone Dermatitis, symptoms: ['angioedema', 'ECZEMA', 'erythema multiforme', 'fixed drug eruptions', 'Urticaria'], Treatment: ['General measures\nOral and topical corticosteroids\nAntihistamines\nOmalizumab\nSpecific treatments\nOral contraceptive pill\nGonadotrophin releasing hormones', 'Oral and topical corticosteroids\nAntihistamines\nOmalizumab', 'Oral contraceptive pill\nGonadotrophin releasing hormones\nTamoxifen\nProgesterone desensitisation by injection or intravaginal topical application', 'Oophorectomy'], Pathophysiology: Autoimmune progesterone dermatitis is predominantly a condition of young adult women with a mean age of onset of 27.3 years; it has also been reported in adolescents after the menarche and in older premenopausal women. It often, but not always, occurs in women who have previously received exogenous progestogens, such as the oral contraceptive pill or fertility treatments. It may present in pregnancy or the post-partum period. There is no genetic risk.The cause of autoimmune progesterone dermatitis is not known. Hypotheses include:Exogenous progestogens may trigger a type 1 (immediate) hypersensitivity reaction with the formation of progesterone-specific immunoglobulin E (IgE) antibodies and a mast cell-mediated response, which may target progesterone receptors expressed above the basal layer on keratinocytes.There may be a type 4 (delayed) hypersensitivity reaction to progestogens.Sensitised patients then have cyclical symptoms due to an ongoing autoimmune response to the elevated levels of progesterone seen in the luteal phase of the menstrual cycle.The cause in patients with no prior exposure to exogenous progestogens is unclear., Epidemiology:['The prevalence of autoimmune progesterone dermatitis is unclear, but about 80 cases have been reported i', 'variable'], Complications:['Abortion'], Diagnostics:['ELISA', 'Interferon-Gamma Release Assays', 'allergy skin test', 'intradermal saline injection (pathergy test'], Differential diagnosis:['allergic contact dermatitis', 'Atopic dermatitis', 'fixed drug eruptions', 'rosacea', 'Urticaria'], disease description:Autoimmune progesterone dermatitis (APD) is a rare form of hypersensitivity reaction to cyclic variation in progesterone levels in women of childbearing age [1]. The clinical presentation can range from urticaria, to stomatitis, to anaphylaxis [2-4].

Individual, 42 years old, with ['palpable abdominal mass', 'proteinuria', 'raised blood pressure', 'hematuria', 'headache', 'Urinary Tract Infection', 'flank pain']

Disease Name: Autosomal Dominant Polycystic Kidney Disease, symptoms: ['palpable abdominal mass', 'proteinuria', 'raised blood pressure', 'hematuria', 'headache', 'Urinary Tract Infection', 'flank pain'], Treatment: ['Treatment of ADPKD is primarily supportive. Control of blood pressure is\ncritical because the rate of disease progression in ADPKD correlates with the\npresence of hypertension. Angiotensin-converting enzyme inhibitors and/or\nangiotensin II receptor antagonists are agents of choice.'], Pathophysiology: Approximately 85% of patients with ADPKD have mutations that map to the PKD1 gene on the short arm of chromosome 16, which encodes polycystin, a transmembrane glycoprotein. Another 10–15% of ADPKD mutations map to the PKD2 gene on the long arm of chromosome 4, which encodes polycystin 2, a proposed nonselective cation channel. The majority of mutations appear to be unique to a given family. At present, a mutation can be found in 85% of patients with well-characterized disease. Approximately 8–10% of patients will have de novo, disease-causing mutations. Mutations of PKD1 are associated with more severe renal disease than mutations of PKD2 . The pathophysiology of the disease appears to be related to the disruption of normal multimeric cystoprotein complexes, with consequent abnormal intracellular signaling resulting in abnormal proliferation, tubular secretion, and cyst formation. Abnormal growth factor expression, coupled with low intracellular calcium and elevated cyclic adenosine monophosphate, appear to be important features leading to formation of cysts and progressive enlargement. Mutations in GANAB have been reported in PKD1- and PKD2- negative patients.ADPKD is a multiorgan disorder affecting many tissue types. Cysts may be asymptomatic but present within the liver, pancreas, spleen, and ovaries and when present help confirm the diagnosis in childhood. Intracranial aneurysms, which appear to segregate within certain families, have an overall prevalence of 15% and are an important cause of mortality in adults, but occasionally occur in children. Mitral valve prolapse is seen in approximately 12% of children; aortic and coronary artery aneurysms and aortic valve insufficiency are noted in affected adults. Hernias, bronchiectasis, and intestinal diverticula can also occur in these children., Epidemiology:['1/400 to 1/1000', 'poor', "If you have polycystic kidney disease and you're considering having children, a genetic counselor can help you assess your risk of passing the disease to your offspring.\n\nKeeping your kidneys as healthy as possible may help prevent some of the complications of this disease. One of the most important ways you can protect your kidneys is by managing your blood pressure.\n\nHere are some tips for keeping your blood pressure in check:\n\nTake the blood pressure medications prescribed by your doctor as directed.\nEat a low-salt diet containing plenty of fruits, vegetables and whole grains.\nMaintain a healthy weight. Ask your doctor what the right weight is for you.\nIf you smoke, quit.\nExercise regularly. Aim for at least 30 minutes of moderate physical activity most days of the week.\nLimit alcohol use."], Complications:['ANEURYSM', 'BRONCHIECTASIS', 'Hernia', 'MITRAL VALVE PROLAPSE'], Diagnostics:['ultrasound', 'GENETIC TESTING', 'MRI', 'CT SCAN', 'Renal ultrasonography'], Differential diagnosis:['Tuberous sclerosis', 'von Hippel Lindau disease'], disease description:Autosomal dominant polycystic kidney disease (ADPKD), also known as adultonset polycystic kidney disease, is the most common hereditary human kidney disease, with an incidence of 1/400 to 1/1,000. It is a systemic disorder withpossible cyst formation in multiple organs (liver, pancreas, spleen, brain) and the development of saccular cerebral aneurysms.Both kidneys are enlarged and show large cortical and medullary cysts originating from all regions of the nephron.

A baby, 4.9 years old, with symptoms including ['Neonates are born with armour-like skin (truncal plates with fissuring)', 'Bilateral ectropion and eclabium are present and hyperkeratotic skin may result in ears lacking retroaural folds.', 'neonate is encased in a shiny parchment-like membrane, which cracks within a few days after birth and usually peels off within the first 4 weeks of life', 'ectropion and everted lips of different degrees', 'Children are born as collodion babies involving the entire skin.', 'Shedding of the collodion membrane is followed by the development of large dark grey/brownish scales affecting the trunk and the scalp, but sparing the face and extremities', 'Ears are often deformed and small', 'hypohidrosis']

Disease Name: Autosomal Recessive Congenital Ichthyosis, symptoms: ['Neonates are born with armour-like skin (truncal plates with fissuring)', 'Bilateral ectropion and eclabium are present and hyperkeratotic skin may result in ears lacking retroaural folds.', 'neonate is encased in a shiny parchment-like membrane, which cracks within a few days after birth and usually peels off within the first 4 weeks of life', 'ectropion and everted lips of different degrees', 'Children are born as collodion babies involving the entire skin.', 'Shedding of the collodion membrane is followed by the development of large dark grey/brownish scales affecting the trunk and the scalp, but sparing the face and extremities', 'Ears are often deformed and small', 'hypohidrosis'], Treatment: [{'medication': ['Sodium chloride ', 'Urea ', 'Vitamin E / Tocopherol', 'Tretinoin', 'Glycerine/Glycerol', 'Macrogols/Polyethylene glycols', 'Propylene glycol']}, 'The aim is to hydrate the stratum corneum by elevating the moisture level of the skin. Urea-based ointments (up to 10%) and lactic acid based ointments (up to 12%) as well as glycerol- based ointments are widely used. Substances such as macrogol 400 or propylene glycol can decrease the scaling and work as keratolytics. In Sweden, an ointment combining 5% lactic acid with 20% propylene glycol in the fatty cream locobase was shown to be effective in a controlled study.'], Pathophysiology: Autosomal recessive congenital ichthyosis is associated with mutations in a plethora of genes, which encode proteins involved in lipid transport, such as ABCA12, in lipid biosynthesis such as CERS3, in fatty acid metabolism or have a role in assembling suprastructures such as the cornified envelope. A ‘unified field theory’ explaining how these various proteins interact with each other and result in a barrier defect and in hyperkeratosis is lacking., Epidemiology:['in the range of 1.6 : 100 000.', '1 in 200,000 births', 'variable', "Can't be prevented as it's an inherited disease. By definition, autosomal recessive congenital ichthyosis (ARCI) is inherited in an autosomal recessive manner.\n\n Although Genetic Counseling is advisable. \n\nGenetic counseling is the process of providing individuals and families with information on the nature, mode(s) of inheritance, and implications of genetic disorders to help them make informed medical and personal decisions."], Complications:['Blistering', 'infections', 'Dehydration'], Diagnostics:['Complete Blood Count CBC', 'GENETIC TESTING', 'TISSUE HISTOLOGY', 'SWEAT TEST'], Differential diagnosis:['Harlequin ichthyosis', 'Netherton syndrome (ichthyosis, bamboo hairs)', 'Sjögren syndrome'], disease description:ARCI includes all non-syndromic autosomal recessive congenital forms of ichthyosis without a tendency toward blistering. Thus the spectrum includes harlequin ichthyosis (HI), bathing suit ichthyosis (BSI), lamellar ichthyosis (LI), congenital ichthyosiform erythroderma (CIE), self-improving congenital ichthyosis (SICI), as well as transient manifestations, such as collodion baby.

A baby, 4.77 years old, with symptoms including ['kidney dysfunction', 'developmental delay', 'Feeding Difficulty', 'hypertension', 'hepatosplenomegaly', 'mass in the abdomen', 'PORTAL HYPERTENSION', 'flank pain', 'respiratory distress']

Disease Name: Autosomal Recessive Polycystic Kidney Disease, symptoms: ['kidney dysfunction', 'developmental delay', 'Feeding Difficulty', 'hypertension', 'hepatosplenomegaly', 'mass in the abdomen', 'PORTAL HYPERTENSION', 'flank pain', 'respiratory distress'], Treatment: ['The treatment of ARPKD is supportive. Aggressive ventilatory support is often\nnecessary in the neonatal period secondary to pulmonary hypoplasia,\nhypoventilation, and the respiratory illnesses of prematurity. Careful\nmanagement of hypertension (angiotensin-converting enzyme inhibitors, and\nother antihypertensive medications as needed), fluid and electrolyte\nabnormalities, osteopenia, and clinical manifestations of renal insufficiency are\nessential.'], Pathophysiology: Both kidneys are markedly enlarged and grossly show innumerable small cysts throughout the cortex and medulla. Microscopic studies demonstrate dilated, ectatic collecting ducts radiating from the medulla to the cortex. The development of progressive interstitial fibrosis and tubular atrophy during the advanced stages of the disease eventually leads to renal failure. ARPKD causes dual-organ disease; hence, the term ARPKD/congenital hepatic fibrosis. Liver involvement is characterized by a basic ductal plate abnormality that leads to bile duct proliferation and ectasia, as well as progressive hepatic fibrosis.Fibrocystin may form a multimeric complex with proteins of other primary genetic cystic diseases. It appears that altered intracellular signaling from these complexes, located at epithelial apical cell surfaces, intercellular junctions, and basolateral cell surfaces in association with the focal adhesion complex, is a critical feature of the disease pathophysiology. Over 300 mutations in PKHD1 (without identified specific hot spots) cause disease, and the same mutation can give variable degrees of disease severity in the same family. This clinical observation is consistent with preclinical datademonstrating many environmental and unknown genetic factors affecting disease expression. The false-negative rate for genetic diagnosis is approximately 10%. Limited available information suggests only a gross genotype–phenotype correlation: mutations that modify fibrocystin appear to cause less-severe disease than those that truncate fibrocystin., Epidemiology:['incidence of 1 : 10,000 to 1 : 40,000', 'poor', "Researchers have not yet found a way to prevent PKD. However, you may be able to slow PKD problems caused by high blood pressure, such as kidney damage. Aim for a blood pressure goal of less than 120/80. Work with a health care team to help manage your or your child's PKD."], Complications:['Acute Renal Failure', 'Chronic renal failure', 'Pulmonary disorders'], Diagnostics:['IVP', 'LIVER BIOPSY', 'USG ABDOMEN(W/A)', 'GENETIC TESTING', 'MRI', 'USG'], Differential diagnosis:['Autosomal dominant polycystic kidney disease', 'HYDRONEPHROSIS', 'Renal Vein Thrombosis', 'WILMS TUMOR'], disease description:Autosomal recessive polycystic kidney disease (ARPKD) (also known as ARPKD-congenital hepatic fibrosis [CHF]) is an autosomal recessive disorder occurring with an incidence of 1 : 10,000 to 1 : 40,000 and a gene carrier rate in the general population of 1/70. The gene for ARPKD (PKHD1 [polycystic kidney and hepatic disease 1]) encodes fibrocystin, a large protein (>4,000 amino acids) with multiple isoforms. ARPKD-congenital hepatic fibrosis [CHF]) is an autosomal recessive disorder Both kidneys are markedly enlarged and grossly show innumerable small cysts throughout the cortex and medulla. Microscopic studies demonstrate dilated, ectatic collecting ducts radiating from the medulla to the cortex. The development of progressive interstitial fibrosis and tubular atrophy during the advanced stages of the disease eventually leads to renal failure. ARPKD causes dual-organ disease; hence, the term ARPKD/congenital hepatic fibrosis. Liver involvement is characterized by a basic ductal plate abnormality that leads to bile duct proliferation and ectasia, as well as progressive hepatic fibrosis.

At 42 years old, experiencing ['headache', 'lightheadedness', 'sweating', 'Dizziness', 'chest heaviness', 'shortness of breath', 'weakness', 'dyspnea', 'syncope']

Disease Name: Av Junctional Tachycardia, symptoms: ['headache', 'lightheadedness', 'sweating', 'Dizziness', 'chest heaviness', 'shortness of breath', 'weakness', 'dyspnea', 'syncope'], Treatment: ['Electrolytes should be corrected in case of electrolyte abnormalities. Amiodarone is the drug of choice and is given as a loading dose followed by a maintenance infusion. It can be used alone but is often used with other medications, including propranolol and flecainide. Intravenous adenosine does not terminate this arrhythmia given the absence of AV nodal reentry in JET.\n\nIvabradine has also been seen as an effective medication for congenital JET. Multiple medications can increase the risk of sudden cardiac death due to proarrhythmic effects. In postoperative JET, induction of hypothermia can also control these arrhythmias. Magnesium sulfate infusion preoperatively can also decrease the risk of these arrhythmias. Postoperative JET usually resolves within 72 hours. Dexmedetomidine, propafenone, procainamide, and sotalol have also been used in treating postoperative JET. Catheter ablation has been reserved for refractory cases.', 'If your symptoms don’t get better, your doctor might suggest a procedure called catheter ablation. It’s also known as radiofrequency ablation. This is when doctors use radio waves to destroy a tiny bit of heart tissue in the area that might trigger your tachycardia. It takes 2 to 4 hours. You usually go home the same day.'], Pathophysiology: Enhanced and abnormal automaticity has been described as the primary pathophysiologic mechanism underlying congenital junctional ectopic tachycardia. This is why this arrhythmia is refractory to intravenous adenosine and direct current cardioversion. It does not involve AV nodal reentry, which differentiates it from AV nodal reentry supraventricular tachycardias. Multiple gene deletions have been proposed as the underlying genetic abnormality, which includes angiotensin-converting enzyme insertion/deletion and troponin-I interacting kinase. Troponin-I interacting kinase mutation has been implicated in dilated cardiomyopathy seen in patients with congenital JET, Epidemiology:['rare in adults, but more common in babies and children', 'variable', 'Your healthcare provider may be able to give you certain medicines before or during surgery to reduce your risk of junctional tachycardia. These medicines may include:\n\nMagnesium.\nPropranolol (Inderal®XL or InnoPran®XL).\nDexmedetomidine (sometimes used in children around the time of heart surgery).'], Complications:['heart failure', 'ventricular fibrillation', 'complete heart block'], Diagnostics:['2-D Echo', 'ECG', 'holter monitering'], Differential diagnosis:['Atrioventricular block (AV block)', 'sinus node dysfunction'], disease description:Junctional tachycardia is a form of supraventricular tachycardia, a type of racing pulse caused by a problem in the area between the upper and lower chambers of your heart. Junctional tachycardia (junctional ectopic tachycardia) is a rare heart rhythm that starts from a natural pacemaker, but not the one your heart normally uses. Usually, your heartbeat starts in your sinoatrial node and travel down through your heart. This is called normal sinus rhythm.

Suffering from ['bone pain', 'joint stiffness', 'limping'] at 42

Disease Name: Avascular Necrosis Of Bone, symptoms: ['bone pain', 'joint stiffness', 'limping'], Treatment: ['Cold packs.\nHeat treatment.\nRest\nPhysical therapy to ease joint tenderness and increase range of motion.\nWalking aids such as canes and crutches.', 'Nonsteroidal anti-inflammatory drugs (NSAIDs).', 'Core decompression: Your surgeon drills small holes (cores) in your affected bone to improve blood flow to the affected bone. This procedure might be combined with injections or bone grafts to promote healing.', 'Joint replacement: They replace your damaged joint with an artificial one. Hip replacements and knee replacements are 95% effective at relieving pain and restoring mobility in people with avascular necrosis.'], Pathophysiology: Avascular necrosis occurs when blood flow to a bone is interrupted or reduced. Reduced blood supply can be caused by:Joint or bone trauma. An injury, such as a dislocated joint, might damage nearby blood vessels. Cancer treatments involving radiation also can weaken bone and harm blood vessels.Fatty deposits in blood vessels. The fat (lipids) can block small blood vessels. This can reduce blood flow to bones.Certain diseases. Medical conditions, such as sickle cell anemia and Gaucher's disease, also can lessen blood flow to bone.Sometimes the cause of avascular necrosis not brought on by trauma isn't fully understood. Genetics combined with overuse of alcohol, certain medications and other diseases likely play a role., Epidemiology:['approximately 10000 to 20000 new cases reported each year in the United States alone.', '1.4% to 25% for symptomatic cases.', 'POOR', 'You might not be able to prevent avascular necrosis, but there are steps you can take to reduce your risk:\n\nQuit smoking.\nCut back on your alcohol intake.\nWatch your cholesterol levels.\nIf you take corticosteroids for a chronic medical condition, talk to your healthcare provider about reducing your dosage.'], Complications:['arthritis'], Diagnostics:['MRI', 'X RAY'], Differential diagnosis:['Osteoarthritis', 'OSTEOCHONDROSIS (OSTEOCHONDRITIS)', 'osteomyelitis', 'osteopenia', 'Osteoporosis', 'rheumatoid arthritis', 'Septic arthritis'], disease description:Avascular necrosis happens when something blocks the flow of blood to your bone tissue. Your bones are constantly changing as your skeletal system makes new bone tissue to replace aging bone tissue that eventually breaks down and dies.Think of this as a cycle — your body makes new tissue to replace the tissue that’s breaking down and dying. This pattern needs to happen correctly to keep your bones healthy and strong. Blood carries the nutrients and oxygen bones need to stay healthy and regenerate. Without blood flow, your skeletal system can't make new bone tissue fast enough. The dying bone begins to crumble and eventually collapses.

Symptoms at 50 years old: ['infertility']

Disease Name: Azoospermia, symptoms: ['infertility'], Treatment: ['If low hormone production is the main cause, you may be given hormone treatments. Hormones include follicle-stimulating hormone (FSH), human chorionic gonadotropin (HCG), clomiphene, anastrazole and letrozole.', 'If a varicocele is the cause of poor sperm production, the problem veins can be tied off in a surgical procedure, keeping surrounding structures preserved.', 'Obstructive azoospermia may be treated by either reconnecting or reconstructing the tubes or ducts that aren’t allowing the sperm to flow.'], Pathophysiology: The exact pathophysiology of azoospermia is not always known. However, in such cases, azoospermia mainly occurs due to abnormal ciliary function and poor mucus quality.Pretesticular causes are endocrinal abnormalities related to the hypothalamus, pituitary, and male gonads (testis). In addition, testicular causes usually involve disorders related to spermatogenesis. Posttesticular causes of azoospermia include any ductal obstruction at any site in the entire male reproductive tract., Epidemiology:['. Around 10 percent of infertile men and 1 percent of all men have azoospermia.', 'variable', 'There is no known way to prevent the genetic problems that cause azoospermia. If your azoospermia is not a genetic problem, doing the following can help lessen the chance of azoospermia:\n\nAvoid activities that could injure the reproductive organs.\nAvoid exposure to radiation.\nKnow the risks and benefits of medications that could harm sperm production.\nAvoid lengthy exposure of your testes to hot temperatures.'], Complications:['infertility'], Diagnostics:['usg testis', 'SEMEN ANALYSIS'], Differential diagnosis:['Congenital Adrenal Hyperplasia', 'cryptorchidism', 'epididymitis', 'Hyperprolactinemia', 'Kallmann Syndrome', 'Retrograde ejaculation', 'Sexual dysfunction', 'Spermatocele'], disease description:Azoospermia is the complete absence of spermatozoa in the ejaculate. It is the most severe and one of the leading causes of male infertility. The exact pathophysiology of azoospermia is not always known. Azoospermia can be due to pre-testicular, testicular, and post-testicular causes. It is also classified as obstructive azoospermia (OA) or non-obstructive azoospermia (NOA). Recent advances in evaluating and managing patients with decreased or absent sperm in the ejaculate have progressed significantly. In addition, the management of azoospermia has been drastically improved as assisted reproductive technology offers potentially successful treatments in couples having male factor infertility.

Individual, 47 years old, with ['peripheral edema', 'periorbital swelling', 'SIGN OF SEVERE ANEMIA']

Disease Name: Azotaemia, symptoms: ['peripheral edema', 'periorbital swelling', 'SIGN OF SEVERE ANEMIA'], Treatment: ['For prerenal causes, IV fluid hydration and possible vasopressor support are crucial to re-establish adequate perfusion to the kidneys to optimize and salvage the integrity of the renal vasculature and tubules. Intrinsic renal diseases are so multifaceted and variable. Cessation of the toxic substances, avoidance of further use and contrast, followed by hydration, can allow for recovery to the kidney structures. Hypertension and diabetes are two of the most common disease processes that can adversely affect renal vascular and tubular epithelium and renal interstitium if poorly managed. Therefore, optimizing blood pressure and hemoglobin A1c are crucial for renal protection. For port-renal azotemia, relief of any obstruction followed by hydration is the mainstay. A urologic evaluation might be necessary, along with catheter placement.'], Pathophysiology: The kidney receives about 25% of the body's cardiac output. Therefore are quite sensitive to any decrease in perfusion and oxygenation. In the setting of severe/prolonged decreased blood flow or hypoxia to these organs, it impairs cellular integrity and metabolism and ultimately vascular, glomerular, and tubular dysfunction. The damage is reflected by the glomerular filtration rate (GFR), which falls in the setting of injury. However, the GFR is not always correlated to the underlying condition, demonstrating the complexity of vascular and tubular processes in renal dysfunction., Epidemiology:['azotemia is quite common, responsible for 8% to 16% of hospital admissions', 'variable', 'The following tips can help you take care of your kidneys and prevent azotemia:\n\nUse certain medications sparingly. Some medications can damage your kidneys if you take them too often, including nonsteroidal anti-inflammatory drugs (NSAIDs), some antibiotics (penicillin, sulfonamides) and herbal supplements. Talk to a healthcare provider about what a safe dose is for you.\nTreat blood loss. A decrease in blood flow to your kidneys can cause prerenal azotemia. Make sure you apply pressure to and bandage any wounds. For a serious injury, seek medical attention.\nGet screened for kidney disease. If you have a biological family history of kidney disease, it’s a good idea to have a healthcare provider assess your risk.\nPrevent dehydration. Most adults need to drink about eight glasses of water per day. Your pee should be clear or pale yellow. If it’s darker than that, you should drink more water.\nDrink alcohol in moderation. Alcohol can damage your kidneys and affect how well they filter your blood. It can also cause dehydration. Women and people AFAB should limit their intake to one drink or less. Men and people AMAB should limit your intake to two drinks or less.\nFollow a diet that’s healthy for you. Eat lots of fruits, vegetables and whole grains. Limit the amount of salt you eat. You’re at a greater risk of developing stones if you eat a lot of salt (sodium).\nExercise regularly. You should exercise for at least 30 minutes five to seven days per week.\nQuit smoking. Smoking damages blood vessels, which can affect blood flow to your kidneys.'], Complications:['encephalopathy', 'nausea', 'Platelet dysfunction', 'vomiting'], Diagnostics:['BLOOD UREA NITROGEN ( BUN )', 'SERUM URIC ACID', 'URINE OSMOLALITY'], Differential diagnosis:['congestive heart failure (CHF)', 'GI bleed', 'ketoacidosis'], disease description:Azotemia is a biochemical abnormality, defined as elevation, or buildup of, nitrogenous products, creatinine in the blood, and other secondary waste products within the body.

Person at 25 with ['fatigue', 'weakness', 'glossitis', 'pallor', 'Tachycardia', 'Dizziness']

Disease Name: B12 Deficiency, symptoms: ['fatigue', 'weakness', 'glossitis', 'pallor', 'Tachycardia', 'Dizziness'], Treatment: [{'medication': ['Cyanocobalamin']}, "Treatment of vitamin B12 deficiency involves repletion with B12. However, depending on the etiology of the deficiency, the duration and route of treatment vary. In patients who are deficient due to a strict vegan diet, an oral supplement of B12 is adequate for repletion.\n\nIn patients with a deficiency in intrinsic factor, either due to pernicious anemia or gastric bypass surgery, a parenteral dose of B12 is recommended, as oral B12 will not be fully absorbed due to the lack of intrinsic factor. A dose of 1000 mcg of B12 via the intramuscular route is recommended once a month. In newly diagnosed patients, 1000 mcg of B12 is given intramuscularly once a week for four weeks to replenish stores before switching to once-monthly dosing. Studies have shown that at doses high enough to fully saturate intestinal B12 receptors, oral B12 is also effective, despite a lack of intrinsic factor.\n\nIn anyone at risk of developing a B12 deficiency, such as patients with Crohn's disease or celiac disease, routine monitoring of B12 should be performed. If the severity of the disease worsens and B12 levels begin to decline, treatment is then started. However, prophylactic treatment before B12 levels fall is not indicated"], Pathophysiology: The pathophysiology of this group of anemia is ineffective erythropoiesis secondary to intramedullary apoptosis of hematopoietic cell precursors, which results from DNA synthesis abnormalities. Both vitamin B12 and folate deficiencies may cause defective DNA synthesis. Subsequently, the nucleus and cytoplasm do not mature simultaneously. The cytoplasm (in which hemoglobin synthesis is unaltered) mature at the normal rate, and the nucleus (with impaired DNA synthesis) is not fully mature. The cells arrest in the DNA synthesis (S) phase and make DNA replication errors, which eventually leads to apoptotic cell death., Epidemiology:['The prognosis for megaloblastic anemia is favorabl', 'Take a balanced diet. Options for consuming vitamin B12 include: Animal food products: Red meat, fish, poultry, eggs, milk and other dairy products all contain vitamin B12'], Complications:['Ataxia', 'Memory loss', 'Peripheral neuropathy', 'vision abnormalities'], Diagnostics:['Peripheral Blood Smear', 'Schilling test'], Differential diagnosis:['aplastic anaemia', 'FOLATE DEFICIENCY'], disease description:Megaloblastic anemia is a condition in which the bone marrow produces unusually large, structurally abnormal, immature red blood cells (megaloblasts). Bone marrow, the soft spongy material found inside certain bones, produces the main blood cells of the body -red cells, white cells, and platelets.

Person at 36 years, dealing with ['Abdominal Pain', 'neck stiffness', 'sign of heart failure', 'Signs of renal failure', 'yellowish discoloration of eyes', 'photophobia', 'ecchymoses', 'petechiae', 'slight pharyngeal erythema', 'splinter haemmorhages', 'erythema migrans', 'chest pain', 'fatigue', 'malaise', 'nausea', 'sore throat', 'Tachycardia', 'vomiting', 'fever', 'dyspnea', 'arthralgia', 'weakness', 'weight loss']

Disease Name: Babesiosis, symptoms: ['Abdominal Pain', 'neck stiffness', 'sign of heart failure', 'Signs of renal failure', 'yellowish discoloration of eyes', 'photophobia', 'ecchymoses', 'petechiae', 'slight pharyngeal erythema', 'splinter haemmorhages', 'erythema migrans', 'chest pain', 'fatigue', 'malaise', 'nausea', 'sore throat', 'Tachycardia', 'vomiting', 'fever', 'dyspnea', 'arthralgia', 'weakness', 'weight loss'], Treatment: [{'medication': ['Quinine ', 'Atovaquone ', 'Azithromycin ', 'Clindamycin ']}, 'Most asymptomatic persons do not require treatment. Treatment decisions should be individualized, especially for patients who have (or are at risk for) severe or relapsing infection.\n\nFor ill patients, babesiosis usually is treated for at least 7-10 days with a combination of two prescription medications — typically either:\n\nAtovaquone PLUS azithromycin; OR\nClindamycin PLUS quinine (this combination is the standard of care for severely ill patients).'], Pathophysiology: Anemia is a key feature of the pathogenesis of babesiosis. Hemolytic anemia caused by rupture of infected RBCs generates cell debris that may accumulate in the kidney and cause renal failure. Anemia also results from the clearance of intact RBCs as they pass through the splenic red pulp and encounter resident macrophages. Babesia antigens expressed on the RBC membrane promote opsonization and facilitate uptake by splenic macrophages. In addition, RBCs are poorly deformable as a result of oxidation generated by the parasite and the host immune response and are filtered out as they attempt to squeeze across the venous vasculature. Bone marrow suppression due to cytokine production may also contribute to anemia. An appropriate immune response is necessary for the control and clearance of Babesia. Studies in laboratory mice have established that CD4+ T cells are critical for resistance to and resolution of B. microti infection. CD4+ T cells are a major source of interferon ? (IFN-?), and lack of this cytokine causes resistant mice to become highly susceptible to B. microti. IFN-? is central to host resistance in B. duncani infection, but natural killer cells are its main source. Several lines of evidence suggest that an excessive immune response contributes to pathogenesis. Blockade of tumor necrosis factor receptor p55 (TNFRp55) accelerates resolution of B. microti parasitemia. B. duncani infection is more severe than B. microti infection in rodents and is characterized by pulmonary inflammation. Tumor necrosis factor a is expressed around alveolar septa, whereas IFN-? is detected around pulmonary vessels. Blockade of either cytokine promotes the survival of mice infected with B. duncani., Epidemiology:['an overall pooled estimate (PE) of 2.23% (95% CI: 1.46-3.39) for Babesia infections in humans.', 'GOOD', 'Avoiding tick bites is the best way to prevent babesiosis if you live in or are traveling to an area where it exists. Some specific ways to reduce your risk of tick bites include:\n\nKeep grass shorter than 5 inches. Ticks wait on long grass to find a host to bite.\nStay on cleared paths while in wooded areas.\nUse bug sprays approved to keep ticks away (usually those with DEET).\nUse clothing to cover as much of your skin as possible when you’re in the woods or areas with long grass. You can buy clothing that’s pre-treated with tick-repellant if you’re in areas with ticks often.\nCheck yourself for ticks after you’ve been outside during warm months. If possible, have someone else check you in places you can’t see yourself (like your scalp and back).\nAsk your veterinarian about the best way to protect your pets from ticks. Check your pets for ticks often, especially after they’ve been outside.\nFollow directions for safely removing a tick if you find one on you.'], Complications:['acute respiratory failure', 'congestive heart failure (CHF)', 'DIC', 'liver failure', 'Spleen Infarction', 'kidney dysfunction'], Diagnostics:['ABG', 'Complete Blood Count CBC', 'Erythrocyte Sedimentation Rate (ESR)', 'Peripheral Blood Smear', 'SERUM Creatinine', 'IgG/IgM immunoblast', 'HIV serology', 'Urine analysis'], Differential diagnosis:['anemia', 'Colorado tick fever', 'Ehrlichiosis', 'Malaria', 'Q Fever', 'Rocky Mountain spotted fever', 'TYPHOID FEVER'], disease description:Babesiosis is a worldwide emerging tick-borne infectious disease caused by protozoan parasites of the genus Babesia that invade and eventually lyse red blood cells (RBCs). More than 100 Babesia species infect a broad array of wild and domestic animals, but only a few of these species have been identified as etiologic agents of human babesiosis. Most cases are due to Babesia microti and occur in the United States. The infection typically is mild or asymptomatic in young and otherwise healthy individuals but can be severe and sometimes fatal in the elderly and the immunocompromised.

Suffering from ['mucosal lesions', 'lesions are solitary or appear in crops, as small papules of dermal', 'fever', 'weight loss', 'bone pain', 'lymphadenopathy', 'skin eruptions'] at the age of 55

Disease Name: Bacillary Angiomatosis, symptoms: ['mucosal lesions', 'lesions are solitary or appear in crops, as small papules of dermal', 'fever', 'weight loss', 'bone pain', 'lymphadenopathy', 'skin eruptions'], Treatment: [{'medication': ['Azithromycin ', 'Doxycycline ']}, 'The drug of choice is macrolide erythromycin or doxycycline. In patients who are not able to tolerate erythromycin or doxycycline, azithromycin or clarithromycin may be used.\nIn patients who are immunosuppressed, therapy should be continued till the CD4 T-helper cell count normalizes. In HIV patients, antiretroviral therapy is essential however a case of immune reconstitution inflammatory syndrome has been reported. \nTherapy in HIV patients should be continued until the CD4 count remains above 200 cells/microliter for over six months.'], Pathophysiology: In nature, cats are the reservoir of B. henselae. Cats may have episodes of asymptomatic bacteremia where the bacteria have adapted to life within the erythrocytes. The infection is acquired by cats via cat fleas when they carry B henselae or B quintana.Transmission of the organisms to humans by cats occur when they scratch humans. The body louse Pediculus humanus transmits B. quintana to humans. 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. , Epidemiology:['2.5%', 'the incidence of bacillary angiomatosis was 1.2/1000 patients.', 'responds to antibiotic but recurance is common', 'Immunocompromised individuals should consider the potential risks of cat\nownership (AIII). Patients who want cats should acquire animals that are older than 1 year of age\nand in good health (BII). Cats should be acquired from a known environment, have a documented\nhealth history, and be free of fleas. Stray cats and cats with flea infestation should be avoided'], Complications:['encephalopathy', 'Endocarditis', 'gastrointestinal bleeding'], Diagnostics:['biopsy', 'PCR', 'Warthin–Starry staining'], Differential diagnosis:['epitheliod hemangioma', 'kaposi sarcoma', 'pyogenic granuloma', 'Sporotrichosis'], disease description:Bacillary angiomatosis is an uncommon disease found in AIDS patients and occasionally other patients with severe immunosuppression. It is characterized by the development of friable angiomatous papules and nodules. Two Bartonella spp. have been associated with this infection: B. henselae and B. quintana. The appearance of these lesions follows a septicaemia, which is usually mild and often passes unnoticed. The disease presents with small proliferative blood vessel containing lesions on the skin surface.Bacillary angiomatosis can occur in non-HIV patients such as transplant patients, who have chronic hepatitis B, patients with leukemia, and those on chemotherapy particularly when the CD4 T-helper cell counts are suppressed.

A 30-year-old individual dealing with ['vomiting', 'Abdominal Pain', 'diarrhea', 'nausea']

Disease Name: Bacillus Cereus Infection, symptoms: ['vomiting', 'Abdominal Pain', 'diarrhea', 'nausea'], Treatment: ['B. cereus infection is usually self-limited and does not require any targeted therapy. Treatment for most patients is symptomatic care with oral hydration. Most patients recover within 24 hours after symptom onset. Empiric antibiotic therapy for gastrointestinal syndromes secondary to B. cereus infections is not indicated. In severe cases, intravenous fluid hydration may be necessary.\ntreatment with vancomycin, gentamicin, chloramphenicol, or carbapenems should be considered.'], Pathophysiology: The pathogenicity of B. cereus, whether inside or outside the gastrointestinal (GI) tract, is associated with exoenzyme production. Among the secreted toxins are four hemolysins, three distinct phospholipases, and three pore-forming enterotoxins. The enterotoxins which activate the nod-like receptor protein-3 (NLRP3) are hemolysin BL (HBL), nonhemolytic enterotoxin (NHE), and cytotoxin K. In the small intestine, vegetative cells, ingested as viable cells or spores, produce and secrete a protein enterotoxin and induce a diarrheal syndrome. Cereulide is a plasmid-encoded cyclic peptide, which is produced in food products and ingested as a formed toxin. In rabbit ligated ileal-loop assays, culture filtrates of enterotoxigenic strains induced fluid accumulation and hemolytic, cytotoxic, dermonecrosis, and increased vascular permeability in rabbit skin.The enterotoxin is composed of a binding component (B) and two hemolytic components, designated HBL. In the diarrheal form of the disease, a nonhemolytic three-component enterotoxin, designated NHE, has been identified. The non-hemolytic enterotoxin (NHE) from Bacillus cereus activates the nod-like receptor protein-3 (NLRP3) inflammasome and pyroptosis. This leads to programmed cell death initiated by the activation of inflammatory caspases of the infected tissue., Epidemiology:['incidences of B. cereus from raw meat and meat products samples were 27.8 and 35 %, respectively', 'good', 'You can lower your risk of INTESTINAL Bacillus cereus by storing your food safely. Steps you can take include:\n\nCooling cooked foods that you won’t eat immediately to below 41 degrees Fahrenheit (41 F) within six hours.\nKeeping cold food refrigerated below 41 degrees Fahrenheit (41 F).\nKeeping hot food at temperatures above 135 degrees Fahrenheit (135 F).\nMaking sure reheated food reaches a temperature of at least 165 degrees Fahrenheit (165 F).\nThrowing out any food you think may contain bacteria.\n\nProper and frequent hand washing can reduce your risk of NON - INTESTINAL B. cereus. You can also reduce your risk by:\n\nGetting treatment for any conditions that compromise your immune system.\nNot using IV drugs.\nSeeking prompt care for any wounds or injuries.'], Complications:['CELLULITIS', 'gangrene', 'ASEPTIC MENINGITIS', 'septicemia'], Diagnostics:['BLOOD CULTURE test', 'SEROLOGIC TEST'], Differential diagnosis:['appendicitis', 'Bacterial infection', 'DIVERTICULITIS', 'Mesenteric ischemia', 'parasitic infections', 'ROTAVIRUS', 'viral infections'], disease description:Bacillus cereus is a toxin-producing facultatively anaerobic gram-positive bacterium. The bacteria are commonly found in the environment and can contaminate food. It can quickly multiply at room temperature with an abundantly present preformed toxin. When ingested, this toxin can cause gastrointestinal illness, which is the commonly known manifestation of the disease. Gastrointestinal (GI) syndromes associated with B. cereus include diarrheal illness without significant upper intestinal symptoms and a predominantly upper GI syndrome with nausea and vomiting without diarrhea. B. cereus has also been implicated in infections of the eye, respiratory tract, and wounds. The pathogenicity of B. cereus, whether intestinal or nonintestinal, is intimately associated with the production of tissue-destructive exoenzymes. Among these secreted toxins are hemolysins, phospholipases, and proteases.

Suffering from ['muscle spasm', 'fever', 'joint pain', 'Joint swelling', 'Tenderness', 'renal insufficiency'] at 25

Disease Name: Bacterial Arthritis, symptoms: ['muscle spasm', 'fever', 'joint pain', 'Joint swelling', 'Tenderness', 'renal insufficiency'], Treatment: [{'medication': ['Cefazolin ', 'Cefotaxime ', 'Vancomycin ', 'Levofloxacin ']}, 'Medical management of infectious arthritis should be focused on adequate and timely drainage of the infected synovial fluid; administration of appropriate antibiotic(s); and debridement of any associated osteomyelitis or soft tissue infection with immobilization of the joint to control pain. The major challenges are duration of oral and intravenous antibiotic administration, especially in the setting of PJI.\n\nAcute PJI (< 3 wks in duration) can be cured medically if it is of the early type or secondary to hematogenous spread without any evidence of periarticular soft-tissue involvement or joint instability. However, it is imperative to monitor therapy by repeat ultrasounds or other imaging studies of the joint, as well as inflammatory markers such as CRP.\n\nOverall, the mean length of hospitalization for septic arthritis is 11.5 days. However, outpatient antibiotic therapy in stable patients can significantly reduce hospital stays.'], Pathophysiology: Bacteria enter the joint from the bloodstream; from a contiguous site of infection in bone or soft tissue; or by direct inoculation during surgery, injection, animal or human bite, or trauma. In hematogenous infection, bacteria escape from synovial capillaries, which have no limiting basement membrane, and within hours provoke neutrophilic infiltration of the synovium. Neutrophils and bacteria enter the joint space ;later ,bacteria adhere to articular cartilage. Degradation of cartilage begins within 48 h as a result of increased intraarticular pressure, release of proteases and cytokines from chondrocytes and synovial macrophages,and invasion of the cartilage by bacteria and inflammatory cells. Histologic studies reveal bacteria lining the synovium and cartilage as well as abscesses extending into the synovium, cartilage, and—in severe cases—subchondral bone. Synovial proliferation results in the formation of a pannus over the cartilage, and thrombosis of inflamed synovial vessels develops. Bacterial factors that appear important in the pathogenesis of infective arthritis include various surface-associated adhesins in S. aureus that permit adherence to cartilage and endotoxins that promote chondrocyte-mediated breakdown of cartilage., Epidemiology:['4 to 12/100 000 person-years (PY)', 'variable', 'While not all cases of septic arthritis are preventable, there are a few things you can do to try to prevent getting it, including:\n\nMake sure cuts and wounds don’t get infected: If you have a cut or wound on your skin, keep it clean to prevent infection. If you are experiencing signs of an infection — such as redness, warmth and/or pus in or around your wound — contact your healthcare provider immediately.\nTry to manage your chronic health condition(s) well: If you have a chronic health condition such as diabetes or AIDS (acquired immunodeficiency syndrome), try to manage your condition as well as you can in order to stay healthy.\nPractice safe sex: Always follow safe sex practices, such as always using a condom or dental dam and talking with your sexual partner about past partners and STI (sexually transmitted infection) history.\nDon’t abuse drugs: Injection drug use can cause infections. Only take medications as prescribed by your healthcare provider.'], Complications:['avascular necrosis of bone', 'osteomyelitis', 'septicemia'], Diagnostics:['CRP', 'Erythrocyte Sedimentation Rate (ESR)', 'Total Leucocyte Count (TLC)', 'MRI', 'MRI', 'CT', 'X RAY', 'X RAY'], Differential diagnosis:['Acute Gout', 'avascular necrosis of bone', 'bacterial endocarditis', 'infections', 'monoarthritis', 'Osteoarthritis', 'pseudogout', 'rheumatoid arthritis', 'systemic lupus erythematosus (SLE)'], disease description:The term Septic Arthritis (SA) represents an invasion of a joint space by a variety of microorganisms, most commonly bacteria. Staphylococcus aureus, Neisseria gonorrhoeae, and other bacteria are the most common causes of infectious arthritis .Since acute bacterial infection can destroy articular cartilage rapidly, all inflamed joints must be evaluated without delay to exclude noninfectious processes and determine appropriate antimicrobial therapy and drainage procedures. For more detailed information on infectious arthritis caused by specific organisms, the reader is referred to the chapters on those organisms. Acute bacterial infection typically involves a single joint or a few joints.

At 29 years old, experiencing ['blepharospasm', 'Circumcorneal congestion', 'discharge from eyes', 'pain in eyes', 'REDNESS OF EYE', 'Defective vision', 'photophobia', 'FOREIGN BODY SENSATION IN EYE']

Disease Name: Bacterial Corneal Ulcer, symptoms: ['blepharospasm', 'Circumcorneal congestion', 'discharge from eyes', 'pain in eyes', 'REDNESS OF EYE', 'Defective vision', 'photophobia', 'FOREIGN BODY SENSATION IN EYE'], Treatment: ['Counseling and regular follow-up are important for a good postoperative outcome. The patient should instill hourly antibiotic eyedrops for 48 hours to 1 week. Based on the clinical response, the drug is tapered. In the case of a large ulcer involving the visual axis, it is always better to start two antibacterials hourly. If the response is good, the same drug is continued; in case of a poor response, it is better to revise the diagnosis. The adjuvants are added with the antibacterials for an additive effect and quick clinical response', 'Medical Treatment\n\nThe medical treatment should be immediately started once the patient presents to the clinician. The smear results are usually available within 1 hour. After obtaining the smear results, the patient should start on broad-spectrum antibiotic therapy, covering both gram-positive and negative bacteria. Once the culture results are available after 48 to 72 hours, the treatment must be switched to targeted antibacterial therapy. In peripheral ulcers not involving the visual axis (<3mm), monotherapy is initiated. In the case of larger and deep stromal ulcers, it is better to start two antibacterial to prevent irreversible vision-threatening sequelae.\nTopical Antibiotics\nCephalosporins\nThe most common drug implicated is topical cefazolin 5% (fortified). It is best suitable for non-penicillinase-producing gram-positive bacteria.\nAminoglycosides\nGlycopeptides\nFluoroquinolones\n\nCycloplegics\n\nLubricating Eye Drops\n\nThese drugs help epithelial healing, reduce irritation, wash away debris and necrotic enzymes, and smoothen the ocular surface and cornea. The commonly implicated drugs are topical 0.5% carboxymethylcellulose and 0.3% hydroxypropyl methylcellulose'], Pathophysiology: Pathophysiology of Focal Bacterial KeratitisThe development of bacterial keratitis progresses through four stagesStage of progressive infiltration-Stage of active ulcerationStage of regressionStage of cicatrizationThe final course of bacterial keratitis is dependent on the virulence of the offending bacteria, host defensive mechanisms, and the treatment receivedPathophysiology of Perforated Bacterial Corneal UlcerPerforation of bacterial corneal ulcers results from rapid keratolysis and a stromal melt, and the ulcerative process reaches up to the Descemet membrane (DM). The DM has high resistance, and when it bulges out, it results in the formation of Descemetocele. Any maneuver at this stage raising the intraocular pressure like sneezing, coughing, straining may perforate the ulcer. After perforation, there is an immediate gush of aqueous humor which reduces the intraocular pressure, the iris lens complex moves forward, and the patient is relieved of pain. The result of perforation depends upon the size and position of the defect. In cases with small perforation and opposite to iris tissue, it results in iris plugging and rapid healing. Hence, this results in the formation of adherent leucoma., Epidemiology:['19.31%', 'The annual incidence of corneal ulcers in the United States alone is estimated to be between 30000 and 75000,', 'variable', 'The best way to prevent a corneal ulcer is to see your eye care provider right away if you have an eye injury or think you have symptoms of a corneal ulcer.\n\nContact lens use is the highest risk factor for a corneal ulcer. With this in mind, some helpful tips for contact lens wearers include:\n\nAlways wash your hands before touching your eyes.\nProperly clean and disinfect your contact lenses before and after wearing them.\nDon’t sleep while wearing your contact lenses. Always take them out every night.\nDon’t swim or shower in your contacts.\nDon’t buy contacts from nonmedical sources.\nDon’t wear your contacts if your eyes are irritated.\nClean and sterilize your contact lens case with the proper solutions.\nBe aware of the increased risk of infection with extended wear lenses. Talk with your eye care provider or optician if you have questions.\nAsk your eye care provider when to throw out and replace your contacts.\nAlways wear protective eyewear if you work or have hobbies that put you at risk for an eye injury.'], Complications:['Secondary glaucoma', 'Perforation of corneal ulcer', 'Corneal scarring'], Diagnostics:['Microscopic Examination of SCRAPINGS', 'conjunctival swab', 'Corneal biopsy'], Differential diagnosis:['ACANTHAMOEBA KERATITIS', 'atopic keratoconjunctivitis', 'EXPOSURE KERATOPATHY', 'fungal keratitis', 'interstitial keratitis', 'MOOREN’S ULCER', 'Peripheral Ulcerative Keratitis', 'ROSACEA KERATITIS', 'viral keratitis'], disease description:Bacterial keratitis or corneal ulcer is a common sight-threatening ocular corneal pathology. In some cases, there is rapidly progressive stromal inflammation. If untreated can lead to progressive tissue destruction, corneal perforation, or extension of infection to adjacent tissue. Signs are more common than symptoms in bacterial keratitis.

At the age of 30, a woman dealing with ['Diffuse redness, tenderness, warmness and brawny induration in the breast', 'breast pain', 'Redness', 'fever', 'purulent discharge', 'swelling at breast', 'ulceration']

Disease Name: Bacterial Mastitis, symptoms: ['Diffuse redness, tenderness, warmness and brawny induration in the breast', 'breast pain', 'Redness', 'fever', 'purulent discharge', 'swelling at breast', 'ulceration'], Treatment: [{'medication': ['Amoxicillin and Clavulanic acid ', 'Flucloxacillin']}, 'Antibiotics- cephalosporins, flucloxacillin and amoxicillin', 'This is less commonly needed as prompt commencement of antibiotics and repeated aspiration is usually successful. Incision of a lactational abscess is necessary if there is marked skin thinning and can usually be performed under local anaesthesia if an analgesic cream such as EMLA (lidocaine) is applied\n30 minutes before surgery.The usual incision is sited in a radial direction over the affected segment, although if a circumareolar incision will allow adequate access to the affected area this is preferred because it gives a better cosmetic result. The incision passesthrough the skin and the superficial fascia. A long artery forceps\nis then inserted into the abscess cavity. Every part of the abscess is palpated against the point of the artery forceps and its jaws are opened. All loculi that can be felt are entered. Finally, the artery forceps having been withdrawn, a finger is introduced and any remaining septa are disrupted. The wound may then be lightly packed with ribbon gauze or a drain inserted to allow dependent drainage.'], Pathophysiology: AETIOLOGY Lactational mastitis is seen far less frequently than in former years. Most are caused by S. aureus and, if hospital acquired, are likely to be penicillin resistant. The intermediary is usually the infant; after the second day of life, 50% of infants harbour staphylococci in the nasopharynx. Although ascending infection from a sore and cracked nipple may initiate the mastitis, in many cases the lactiferous ducts will first become blocked by epithelial debris leading to stasis; this theory is supported by the relatively high incidence of mastitis in women with a retracted nipple. Once within the ampulla of the duct, staphylococci cause clotting of milk and, within this clot, organisms multiply, Epidemiology:['26.4%', 'one in four women breastfeeding during the first 26 weeks postpartum.', 'good', 'A good rule of thumb is to only pump what’s needed for your baby. If you’re feeding from your breast, don’t pump afterward to “drain” it.\n\nIt might be helpful to talk to a lactation consultant or attend a breastfeeding class to learn what a good latch looks like and feels like. A latch is how your baby nurses from your breasts. A good latch may help with mastitis because your body can naturally adjust your milk production to your baby’s milk intake.\n\nPeople who are breastfeeding can also take these steps to lower their chances of getting mastitis:\n\nDon’t wear tight-fitting bras.\nAvoid using nipple shells or other devices on your breasts.'], Complications:['BREAST ABSCESS', 'fistulae formation'], Diagnostics:['Complete Blood Count CBC', 'mammography', 'USG', 'Core cut Needle Biopsy', 'PHYSICAL EXAMINATION'], Differential diagnosis:['BREAST ABSCESS', 'CELLULITIS', 'DUCT ECTASIA/PERIDUCTAL MASTITIS', 'Inflammatory carcinoma ( BREAST )'], disease description:Lactational mastitis, also known as puerperal mastitis, is typically due to prolonged engorgement of milk ducts, with infectious components from the entry of bacteria through skin breaks. Patients can develop a focal area of erythema, pain, and swelling, and can have associated systemic symptoms, including fever. Commonly seen in lactating women. Usually up to 6 months of lactation period. It occurs in 3% of breastfeeding mothers

Person, 21 years old, presenting ['convulsion', 'projectile vomiting', 'tremor', 'BRUDZINSKI SIGN', 'coma', 'hypertonia', 'kernig sign positive', 'neck rigidity', 'tendon reflexes are exaggerated initially but later become sluggish or absent', 'Mental Confusion', 'drowsiness', 'headache', 'nausea', 'neck stiffness', 'seizures', 'vomiting', 'fever', 'Irritability', 'photophobia', 'cheyne-stokes respiration', 'hemiparesis', 'Papilloedema', 'hemiplegia', 'hemianopia', 'chills', 'rigor', 'paralysis']

Disease Name: Bacterial Meningitis, symptoms: ['convulsion', 'projectile vomiting', 'tremor', 'BRUDZINSKI SIGN', 'coma', 'hypertonia', 'kernig sign positive', 'neck rigidity', 'tendon reflexes are exaggerated initially but later become sluggish or absent', 'Mental Confusion', 'drowsiness', 'headache', 'nausea', 'neck stiffness', 'seizures', 'vomiting', 'fever', 'Irritability', 'photophobia', 'cheyne-stokes respiration', 'hemiparesis', 'Papilloedema', 'hemiplegia', 'hemianopia', 'chills', 'rigor', 'paralysis'], Treatment: [{'medication': ['Penicillamine ', 'Dexamethasone ', 'Ampicillin ', 'Cefotaxime ', 'Vancomycin ', 'Diazepam ']}, 'A combination \nof ampicillin (200 mg/kg) and chloramphenicol (100 mg/ \nkg/24 hr) for 10-14 days is also effective as initial empiric \nchoice.'], Pathophysiology: The infection spreads hematogenously to meninges from distant foci, e.g. pneumonia, empyema, pyoderma and osteomyelitis. Purulent meningitis may follow head injury. Rarely, the infection may extend from contiguous septic foci, e.g. infected paranasal sinuses, mastoiditis, osteomyelitis and fracture of the base of skull. Recurrent meningitis may be associated with pilonidal sinus, CSF rhinorrhea, traumatic lesions of the cribriform plate and ethmoidal sinus or congenital fistulae, besides immune deficiency disorders. Pathology The leptomeninges are infiltrated with inflammatory cells. The cortex of the brain shows edema, exudate and proliferation of microglia. Ependymal cells are destroyed and purulent exudate collects at the base of the brain, most marked in interpeduncular and chiasmatic cisterns. Exudates may block the foramina of Luschka and Magendie resulting in internal hydrocephalus. Thrombophlebitis of the cerebral vessels may occur leading to infarction and neurological sequelae. In cases of meningococcal meningitis, the illness may be fulminating and death may occur within a few hours because of endotoxic shock., Epidemiology:['1.33 cases per 100,000 population.', 'variable', "Common bacteria or viruses that can cause meningitis can spread through coughing, sneezing, kissing, or sharing eating utensils, a toothbrush or a cigarette.\n\nThese steps can help prevent meningitis:\n\nWash your hands. Careful hand-washing helps prevent the spread of germs. Teach children to wash their hands often, especially before eating and after using the toilet, spending time in a crowded public place or petting animals. Show them how to thoroughly wash and rinse their hands.\nPractice good hygiene. Don't share drinks, foods, straws, eating utensils, lip balms or toothbrushes with anyone else. Teach children and teens to avoid sharing these items too.\nStay healthy. Maintain your immune system by getting enough rest, exercising regularly, and eating a healthy diet with plenty of fresh fruits, vegetables and whole grains.\nCover your mouth. When you need to cough or sneeze, be sure to cover your mouth and nose.\nIf you're pregnant, take care with food. Reduce your risk of a listeria infection by cooking meat, including hot dogs and deli meat, to 165 degrees Fahrenheit (74 degrees Celsius). Avoid cheeses made from unpasteurized milk. Choose cheeses that are clearly labeled as being made with pasteurized milk.\n\n\nVaccinations - \nSome forms of bacterial meningitis are preventable with the following vaccinations:\n\n1. Haemophilus influenzae type b vaccine (Hib).\n2. Pneumococcal conjugate vaccine (PCV13 or PCV15).\n3. Pneumococcal polysaccharide vaccine (PPSV23). \n4. Meningococcal conjugate vaccine (MenACWY). \n5. Serogroup B meningococcal vaccine (MenB)."], Complications:['Hearing loss', 'seizures', 'cognitive impairment', 'FOCAL NEUROLOGICAL DEFICITS', 'recurrence'], Diagnostics:['CSF EXAMINATION', 'MRI', 'ELISA', 'TOTAL SERUM PROTEIN LEVEL'], Differential diagnosis:['ASEPTIC MENINGITIS', 'Brain Abscess', 'delirium tremens', 'ENCEPHALITIS', 'HERPES SIMPLEX', 'Leptospirosis', 'stroke', 'Subarachnoid Hemorrhage', 'TUBERCULAR MENINGITIS', 'VIRAL ENCEPHALITIS'], disease description:Bacterial meningitis is a bacterial infection of the meninges, which is the protective covering for the brain and spinal cord resulting in inflammation. It is a serious and life-threatening condition that requires prompt diagnosis and treatment,  Bacterial meningitis is caused by a bacterial infection of the meninges, resulting in inflammation. The infection is either community-acquired or nosocomial. Community-acquired bacterial meningitis is the result of the invasion of the bacteria into the meninges from bacteremia or direct extension from local infection

Symptoms at 41 years: ['Tenderness', 'malaise', 'swelling of parotid gland', 'swelling of parotid gland', 'fever', 'cervical lymphadenopathy']

Disease Name: Bacterial Sialadenitis, symptoms: ['Tenderness', 'malaise', 'swelling of parotid gland', 'swelling of parotid gland', 'fever', 'cervical lymphadenopathy'], Treatment: ['Acute sialadenitis: Most cases receive treatment with conservative medical management; this includes hydration, warm compresses, and massage, pain relief with analgesics (e.g., NSAIDs), sialogogues. Empiric antibiotic therapy starts with amoxicillin/clavulanate or clindamycin. Antibiotics selection should be according to culture and sensitivity reports. Intravenous antibiotics may be necessary for severe cases. If soft tissue swelling is significant, and there is no contraindication, corticosteroid therapy is an option. Rarely, acute suppurative sialadenitis can lead to abscess formation; surgical incision and drainage are indicated in these cases.\nChronic sialadenitis: Medical management is with hydration, oral hygiene, pain relief, sialogogues. In cases of infection, broad-spectrum antibiotics are added. In the case of sialolithiasis, salivary gland stone removal should take place, using interventional sialendoscopy or direct surgical removal.', 'EWSL under ultrasonic guidance is used for intraglandular duct stone removal.Recurrent sialadenitis (>3 episodes/year) or in chronic sclerosing sialadenitis: excision of the salivary gland is the recommendation.'], Pathophysiology: Major risk factors for sialadenitis include reduced salivary secretion and duct obstruction. Hyposecretion of saliva can occur in dehydrated people, postoperative patients, immunocompromised, and undernourished. Medications that decrease salivary flow like antihistaminics, diuretics,beta-blockers can predispose to sialadenitis. Decreased salivary production can occur in patients with a history of radiation to the head and neck region, long-standing xerostomia (e.g., Sjogren syndrome), and those with chronic illness. Salivary duct obstruction is usually due to sialolithiasis, ductal stricture, ductal foreign body, and external compression of the duct, Epidemiology:['0.01-0.02% of all hospital admissions.', 'The submandibular gland is suggested to account for approximately 10% of all cases of sialadenitis of the major salivary gland', 'variable4', 'You may not be able to prevent sialadenitis completely. But there are a few things you can do to reduce your risk:\n\nDrink plenty of water.\nPractice good oral hygiene.\nEat a diet that’s healthy for you.\nAvoid smoking and using other tobacco products.'], Complications:['Dental Caries', 'recurrence', 'Abscess formation'], Diagnostics:['Complete Blood Count CBC', 'Hb', 'PUS CULTURE', 'Total Leucocyte Count (TLC)', 'CT', 'FACIAL RADIOGRAPHY'], Differential diagnosis:['Pleomorphic adenoma', 'Sarcoidosis', 'Sjogren syndrome', 'SYSTEMIC LUPUS ERYTHEMATOSUS'], disease description:Acute ascending bacterial sialadenitis is historically described in dehydrated elderly patients following major surgery. Reduced salivary flow secondary to dehydration results in ascending infection via the parotid duct into the parotid parenchyma. The more common picture today is an acute bacterial parotitis associated with a salivary calculus

At the age of 43, a woman dealing with ['Vaginal Discharge', 'DYSPAREUNIA', 'Tenderness', 'burning sensation', 'vulval itching']

Disease Name: Bacterial Vaginosis, symptoms: ['Vaginal Discharge', 'DYSPAREUNIA', 'Tenderness', 'burning sensation', 'vulval itching'], Treatment: [{'medication': ['Cefixime ', 'Doxycycline ', 'Clindamycin ', 'Metronidazole ']}, 'Metronedazole 200 mg PO TID × 7 days\n Metronedazole gel (0.75%) 5 gm (1 full applicator) \nintravaginal once daily × 5 days\n? Clindamycin 2% 5 gm (1 full applicator) intravaginally \nbed time × 7 days\nVaginal application daily for 5 days is used to prevent \nobstetric complications. Sexual partner should be treated \nsimultaneously. Cure rate is 80%'], Pathophysiology: There is considerable decrease in lactobacilli in the normal vaginal discharge. The lactobacilli produce hydrogen peroxide toxic to other bacteria but a decrease in the former causes the increase in growth of the other anaerobic bacteria thereby causing vaginal discharge.It is a polymicrobial condition., Epidemiology:['20–30 % of women with vaginal discharge have BV', '10-25% and may be as high as 30-65%', 'GOOD', 'You can’t prevent bacterial vaginosis. However, taking these precautions could reduce your risk:\n\nAvoid douching. It changes the natural balance of bacteria in your vagina. Instead, practice healthy vaginal and vulvar care.\nAvoid vaginal contact with anything that has touched your anus. Things like toilet paper and sex toys could transfer bacteria found in your poop to your vagina. Make sure sexual toys are properly cleaned after every use.\nLimit your number of sex partners. Research shows you’re more likely to get BV if you have multiple sex partners.\nUse latex condoms or dental dams. Although it’s unclear why, research indicates that sexual activity is associated with BV.\nWear cotton or cotton-lined underwear. Bacteria thrive in moist environments. Cotton helps wick away moisture.'], Complications:['Pelvic Inflamatory Disease', 'Premature rupture of membranes', 'preterm labour'], Diagnostics:['Gram Staining', 'Total Leucocyte Count (TLC)', 'VAGINAL SWAB CULTURE', 'HANGING DROP EXAMINATION', 'WHIFF TEST'], Differential diagnosis:['HERPES SIMPLEX', 'Trichomoniasis', 'vaginal candidiasis'], disease description:Vaginosis (also known earlier as nonspecific vaginitis/ Gardnerella vaginalis/Corynebacterium vaginitis and anaerobic vaginitis) is associated with minimal inflammatory response, the vaginal fluid reveals few leucocytes. The concentration of bacteria is increased manifold (100–1000 fold) as compared to normal women.

Person, 33 years old, presenting ['diarrhea', 'tenesmus', 'Abdominal Pain']

Disease Name: Bacteroides Infection, symptoms: ['diarrhea', 'tenesmus', 'Abdominal Pain'], Treatment: ['Bacteroides fragilis is resistant to penicillin due to the production of beta-lactamase. Cefoxitin, moxifloxacin, and clindamycin have low levels of susceptibility for Bacteroides fragilis, whereas Piperacillin/tazobactam, meropenem, and metronidazole have high susceptibility rates.\neravacycline, a novel fluorocycline antibiotic, has been evaluated against complicated mixed aerobic/anaerobic intra-abdominal infections.'], Pathophysiology: Bacteroides fragilis is usually a commensal organism that, when the mucosal barrier becomes disrupted, results in abscess formation and bacteremia. Bacteroides species have involvement in the prolongation of the intrinsic pathway of clotting in human blood. Both B. fragilis and B. thetaiotaomicron cause the release of significant levels of bradykinin in human plasma, a mechanism that will provide the bacteria with an opportunity to spread by inhibition of clot formation.Bacteroides fragilis virulence is mostly by toxin production. Enterotoxigenic Bacteroides fragilis (ETBF) strains are strains of B. fragilis that secrete an enterotoxin termed the B. fragilis toxin (BFT) and may have a role in inflammatory diarrhea and flare-ups of inflammatory bowel disease.Outer-membrane vesicles (OMVs) are vesicles that bud out of the outer membrane of bacteria and are commonly produced by gram-negative bacteria and may play a role in trafficking bacterial biochemicals. Elhenawy et al. .demonstrated the preferential packing of acidic glycosidases and proteases into Bacteroide's outer membrane vesicles and proposed that OMVs contribute to the establishment and balance of the gut microbiota., Epidemiology:['49.9%', 'variable', 'Preventative measures of B. fragilis infections includes administration of antibiotics prior to abdominal or pelvic surgery.\n\nBacteroides infection can also be prevented by initial treatment with gentamicin, an antibiotic which targets facultative anaerobes such as E. coli but not Bacteroides. Because Bacteroides fragilis infection depends also on the existence of a facultative anaerobe, this antibiotic can be another preventative measure taken to prevent severe anaerobic infections involving B. fragilis. This method, however, does not stop the later development of Bacteroides abscesses. Therefore a more effective treatment combines both gentamicin with clindamycin, an antibiotic that is effective against Bacteroides, prevents the initial infection and later development of abdominal abscesses.'], Complications:['Dental Caries', 'TUBO OVARIAN ABSCESS'], Diagnostics:['Automated Anaerobic Bacterial Culture', 'Fine-needle aspiration biopsy'], Differential diagnosis:['infection', 'MALIGNANCY', 'Trauma', 'ulcer'], disease description:Anaerobes are bacteria that do not require oxygen to live. Anaerobes usually fit into two groups based on their gram stain into gram-positive and gram-negative and into cocci and bacilli based on their morphology. Of these, notable pathogenic gram-negative bacillus-shaped strains are Prevotella, Fusobacterium, Bacteroides, and Porphyromonas. Bacteroides species are important clinical pathogens and are present in most anaerobic infections, with an associated mortality of approximately 19%. Bacteroides fragilis is an obligate anaerobic gram-negative bacillus. The human colon has the greatest population of bacteria in the body (over ten organisms per gram of wet weight), and the largest part of these organisms are anaerobes; of these, approximately 25% are species of Bacteroides. Bacteroides fragilis is part of the normal microbiota of the human colon. Disruption of the mucosal surface either by inflammation, trauma, or surgery and spread of Bacteroides fragilis to the bloodstream or surrounding tissues results in clinically significant infection.

Suffering from ['diarrhea', 'vomiting', 'blood in stool', 'Abdominal Pain', 'DYSENTRY', 'weight loss'] at 50

Disease Name: Balantidiasis, symptoms: ['diarrhea', 'vomiting', 'blood in stool', 'Abdominal Pain', 'DYSENTRY', 'weight loss'], Treatment: [{'medication': ['Metronidazole ', 'Tetracycline ']}, 'The antibiotic drug most commonly used to treat balantidiasis is Tetracycline. Tetracycline is the antibiotic of choice, but it is not recommended for pregnant women and children under eight. When Tetracycline cannot be given, drugs like Iodoquinol or Metronidazole are given. It is not necessary to isolate a person with balantidiasis. The feces (stool) of infected individuals must be disposed of and should be taken care that they do not come into contact with drinking water or food supplies. Metronidazole is administered for five days, and Tetracycline dosage is for ten days, whereas Iodoquinol is given for twenty days. The other drugs which are used are Doxycycline and Ampicillin.'], Pathophysiology: Balantidiasis is a protozoan infection caused by infection with Balantidium coli. Balantidium coli exists in either of two developmental stages: trophozoites and cysts. In the trophozoite form, they can be oblong or spherical, and are typically 30 to 150 µm in length and 25 to 120 µm in width. It is its size at this stage that allows Balantidium coli to be characterized as the largest protozoan parasite of humans. Trophozoites possess both a macronucleus and a micronucleus, and both are usually visible. The macronucleus is large and sausage-shaped while the micronucleus is less prominent. At this stage, the organism is not infective but it can replicate by transverse binary fission.In its cyst stage, the parasite takes on a smaller, more spherical shape, with a diameter of around 40 to 60 µmUnlike the trophozoite, whose surface is covered only with cilia, the cyst form has a tough wall made of one or more layers. The cyst form also differs from the trophozoite form because it is non-motile and does not undergo reproduction. Instead, the cyst is the form that the parasite takes when it causes infection., Epidemiology:['prevalence of 1%', 'good', 'Balantidium coli infection can be prevented when traveling by following good hygiene practices. Wash your hands with soap and warm water after using the toilet, changing diapers, and before handling food. Teach children the importance of washing hands to prevent infection. Wash all fruits and vegetables with clean water when preparing or eating them, even if they have a removable skin.'], Complications:['CHRONIC DIARRHEA'], Diagnostics:['stool microscopy', 'ENDOSCOPY'], Differential diagnosis:['Amebiasis', 'colitis', 'DYSENTRY', 'Shigellosis', 'Yersinia enterocolitica'], disease description:Balantidium (=Neobalantidium) (=Balantioides) coli, a large ciliated protozoan, is the only ciliate known to be capable of infecting humans. It is often associated with swine, the primary reservoir host. Recent molecular analyses have suggested the need for taxonomic revision, and it is now sometimes referred to as Neobalantidium coli or Balantioides coli, although this nomenclature has neither been resolved nor widely adopted in the medical community. Balantidium coli occurs worldwide. Because pigs are the primary reservoir, human infections occur more frequently in areas where pigs are raised and sanitation is inadequate.

Suffering from ['band-shaped opacity in the interpalpebral zone with a clear interval between the ends of the band and the limbus', 'CORNEAL OPACITY', 'Visual impairment'] at 45

Disease Name: Band Shape Keratopathy, symptoms: ['band-shaped opacity in the interpalpebral zone with a clear interval between the ends of the band and the limbus', 'CORNEAL OPACITY', 'Visual impairment'], Treatment: ['1. Chelation, i.e., chemical removal of deposited\ncalcium salts is an effective treatment. First of\nall, corneal epithelium is scraped under local\nanaesthesia. Then 0.01 molar solution of EDTA\n(chelating agent) is applied to the denuded\ncornea with the help of a cotton swab for about\n10 minutes. This removes most of the deposited\ncalcium. Pad and bandage is then applied for 2–3\ndays to allow the epithelium to regenerate.', '1. Phototherapeutic keratectomy (PTK) with excimer\nlaser is very effective in clearing the cornea.\n2. Keratoplasty may be performed when the band\nkeratopathy is obscuring useful vision.'], Pathophysiology: Band shape keratopathy (BSK) is essentially a degenerative change associated with deposition of calcium salts in Bowman’s membrane, most superficial part of stroma and in deeper layers of epithelium.  • Ocular diseases complicated by band keratopathy include chronic uveitis in adults, children with Still’s disease, phthisis bulbi, chronic glaucoma, chronic keratitis and ocular trauma. • Age-related BSK is common and affects otherwise healthy cornea. • Primary BSK is familial. • Metabolic conditions rarely associated with BSK include hypercalcaemia, hyperphosphataemia, hyperuricemia and chronic renal failure. It typically presents as a band-shaped opacity in the interpalpebral zone with a clear interval between the ends of the band and the limbus. The condition begins at the periphery and gradually progresses towards the centre. The opacity is beneath the epithelium which usually remains intact. Surface of this opaque band is stippled due to holes in the calcium plaques in the area of nerve canals of Bowman’s membrane. In later stages, transparent clefts due to cracks or tears in the calcium plaques may also be seen., Epidemiology:['0.47% in children (age: <16 years) and 0.31% in adults.', 'good', 'You may be able to reduce your risk of developing band keratopathy by managing your overall health and your eye health.\n\nThis can include:\n\nManaging chronic conditions like high blood pressure, high cholesterol or diabetes.\nEating healthy foods.\nGetting regular activity.\nReaching and maintaining a healthy weight for you.\nHaving regular medical checkups as well as regular appointments with an eye care provider.'], Complications:['infection', 'VISION DEFICITS', 'CORNEAL EDEMA', 'Corneal scarring'], Diagnostics:['Slit lamp examination', 'ophthalmoscopy'], Differential diagnosis:['corneal degeneration', 'Crohns Disease', 'interstitial keratitis', 'WILSONS DISEASE'], disease description:Band shape keratopathy (BSK) is essentially a degenerative change associated with deposition of calcium salts in Bowman’s membrane, most superficial part of stroma and in deeper layers of epithelium. Band keratopathy, also called calcific band keratopathy, involves calcium deposits that collect in layers of your eye’s cornea. This can happen when calcium levels in your body are unbalanced. The usual treatment is chelation.

Person aged 31 dealing with ['aspiration pneumonia', 'Shallow respiration', 'Bradycardia', 'cyanosis', 'hypothermia', 'raised intracranial pressure', 'vertigo', 'Oliguria', 'Confusion', 'disorientation', 'slurred speech']

Disease Name: Barbiturate Poisoning, symptoms: ['aspiration pneumonia', 'Shallow respiration', 'Bradycardia', 'cyanosis', 'hypothermia', 'raised intracranial pressure', 'vertigo', 'Oliguria', 'Confusion', 'disorientation', 'slurred speech'], Treatment: [{'medication': ['Activated charcoal ']}, 'Treatment of barbiturate toxicity remains supportive as there is no specific antidote for overdose. The first step in treatment, as with any overdose, is assessing the patient’s airway, breathing, and circulation. With significant sedation and respiratory depression, intubation and mechanical ventilation may become necessary.\n Early treatment with activated charcoal may be useful and can be given via nasogastric tube. Patients will likely need to be admitted or observed. During recovery, the patient should receive counseling about the dangers of barbiturate misuse. Long-term barbiturate use can cause tolerance and physical dependence. Therefore, withdrawal symptoms can occur with abrupt discontinuation.\nOther options for managing barbiturate toxicity include forced alkaline diuresis and hemodialysis for severe cases.', 'Bemegride (Megimide) is a central nervous system stimulant that increases respiration and can be used as a treatment for depressant toxicity.'], Pathophysiology: Barbiturates act on GABA-A receptors by increasing the amount of time the chloride ion channel is opened, which increases the affinity of the receptor for GABA. GABA is the primary inhibitory neurotransmitter of the central nervous system, which acts to reduce neuronal activity. In contrast to benzodiazepines, they also act to increase chloride influx in the absence of GABA, which accounts for their ability to significantly depress the central nervous system and contribute to their toxicity., Epidemiology:['good with early care', 'If you are using barbiturates, consider taking steps to reduce your risk of overdose:\n\nTake all medications as prescribed.\nAvoid mixing barbiturates with other drugs and alcohol.\nConsult with a medical professional if you feel that you need changes made to your medication regimen.\nAvoid taking other people’s prescription medications, which may be prescribed at different dosages.\nDiscuss any other prescription or illicit drugs you are taking with your doctor.'], Complications:['coma', 'respiratory depression', 'Hypotension'], Diagnostics:['Plasma barbiturate concentration'], Differential diagnosis:['cardiogenic shock', 'DEPRESSION', 'ENCEPHALITIS', 'Hemorrhagic Stroke (HS)', 'Hypoglycaemia', 'hypothermia', 'Myxedema'], disease description:Barbiturate overdose can be intentional or unintentional. A barbiturate overdose occurs when someone takes more than the normal or recommended amount of this medicine. This can be by accident or on purpose. An overdose is life threateningDecreased use of this controlled substance has led to a decrease in barbiturate-related fatalities. However, this medication should still be considered in cases of suspected overdose in patients with respiratory depression.

Individual aged 35 dealing with ['oedema', 'Urticaria', 'maculopapular eruption', 'arthralgia', 'myalgia', 'Rashes', 'fever']

Disease Name: Barmah Forest Virus, symptoms: ['oedema', 'Urticaria', 'maculopapular eruption', 'arthralgia', 'myalgia', 'Rashes', 'fever'], Treatment: ['Treatment: \nThere is no specific drug treatment for Barmah Forest virus infection. Treatment involves managing the symptoms that develop. Your doctor will advise on treatment for joint and muscle pains. A combination of plenty of rest, and gentle exercise are important to keep joints moving and to prevent overtiredness but medication may sometimes be necessary'], Pathophysiology: Barmah Forest virus infection is spread by mosquitoes from infected animals to humans. Native animals, such as wallabies and kangaroos, are thought to be the main animals involved in the cycle of infection. When a female mosquito feeds on the blood of an infected animal, the mosquito may become infected with the virus. The virus may subsequently be passed on to humans or other animals when the mosquito feeds again.Barmah Forest virus infection is spread by mosquitoes from infected animals to humans. Native animals, such as wallabies and kangaroos, are thought to be the main animals involved in the cycle of infection. When a female mosquito feeds on the blood of an infected animal, the mosquito may become infected with the virus. The virus may subsequently be passed on to humans or other animals when the mosquito feeds again., Epidemiology:['With »15,000 laboratory-confirmed cases over the last decade', 'good', 'There is no preventive vaccine available. Your only protection against Barmah Forest virus and the most effective way to prevent other mosquito-borne diseases is is by avoiding mosquito bites and removing mosquito breeding sites around your home and property.'], Complications:['arthritis'], Diagnostics:['Antibody Serology Tests', 'ELISA FOR ANTIBODY TITRE'], Differential diagnosis:['Chikungunya', 'Epstein-Barr Virus', 'Influenza', 'rheumatoid arthritis', 'Ross River virus', 'Zika Virus Disease'], disease description:Barmah Forest virus disease is caused by an alphavirus, which is spread by mosquitoes. Symptoms usually begin to appear between 7 to 10 (but up to 21) days after becoming infected, however many people infected with Barmah Forest virus will never develop any symptoms.The illness presents with arthralgia and myalgia and occasionally fever, but these general symptoms may be absent. The rash, which occurs in about 90% and may be the presenting feature, is often florid and generalized. It is maculopapular but may be vesicular. Facial urticaria and oedema may be seen.Barmah Forest virus was first identified near the Murray River in New South Wales, Australia. The illness it causes is similar to, but milder than, Ross River virus. The infection is endemic in northern Queensland, Australia, where the incidence of the disease is increasing.

Symptoms reported by a 53-year-old female include ['fever', 'unilateral vulval swelling', 'pain in vulva', 'Vaginal Discharge', 'DYSPAREUNIA']

Disease Name: Bartholin Abscess, symptoms: ['fever', 'unilateral vulval swelling', 'pain in vulva', 'Vaginal Discharge', 'DYSPAREUNIA'], Treatment: [{'medication': ['Diclofenac ', 'Cefixime ']}, 'Home remedies\nHome remedies can provide relief from the symptoms of a Bartholin’s abscess, but they do not usually cure the condition.\n\nThe following home treatments may alleviate pain and swelling in the short-term:\n\nSitz bath\nSitz baths can ease pain and discomfort. They may also help very small abscesses to rupture and drain.\n\nTo take a sitz bath, fill a bathtub with several inches of warm water. Sit down in the water for 15 minutes.\n\nRepeat this treatment several times daily for at least 3–4 days, or until symptoms subside or a person seeks medical treatment.\n\nTopical treatments\nAccording to some people, natural topical treatments can provide relief from Bartholin’s abscesses. There is no scientific evidence to support the use of these remedies.\n\nPopular topical treatments include:\n\nTea tree oil: Applying a mixture of tea tree oil and castor oil to the abscess may encourage drainage. Tea tree oil has natural antibacterial properties. Use gauze to apply the mixture and place a hot compress on top of the gauze. Hold in place for 15 minutes.\nApple cider vinegar (ACV): Typically, people who use ACV to treat a Bartholin’s abscess dilute it and apply it to the cyst with a cotton ball', 'Most cases of Bartholin’s abscess require draining. If an abscess develops again, a doctor may recommend marsupialization. In rare cases, a surgeon may remove the glands.\n\nSurgical drainage\nThe doctor may use a local anesthetic to numb the area or a general anesthetic to put the person to sleep.\n\nMarsupialization\nA procedure called marsupialization can help prevent recurrent Bartholin’s abscesses.\n\nFirst, the doctor will make a small incision in the abscess so that it can drain. They will then use stitches at each side of the incision to create a permanent opening. The opening is typically less than a quarter-inch wide. Sometimes, the doctor may insert a catheter for a few days to speed up the drainage process.\n\nMarsupialization is usually successful. Only 5–15% of Bartholin’s cysts come back after the procedure.\n\nGland removal\nIf abscesses still recur after marsupialization, a doctor may recommend the removal of the Bartholin’s glands. However, most doctors consider this a last resort, and it is rarely necessary.\n\nHowever, if a person does require surgery, the procedure takes place in the hospital under general anesthesia. As with all surgeries, there is a risk of bleeding, infection, and other complications.'], Pathophysiology: Cysts are common complications of the Bartholin's gland, affecting the ductal region due to outlet blockage . When the Bartholin's gland duct orifice becomes obstructed, the glands produce a build-up of mucus. This build-up leads to a cystic dilation of the duct and cyst formation. Infection of this cyst is likely to result in Bartholin's gland abscess. Duct cyst is not required for the development of abscess. The abscesses are almost three times more common than duct cysts . Bartholin's abscess cultures often show polymicrobial infection.Lesions in the Bartholin's gland can occur in the form of carcinomas, a rare type of gynecological tumor that accounts for 2-7% of vulvar carcinomas. This type of vulvar growth is carefully monitored among postmenopausal women who are more prone to Bartholin's malignancy . The median age at which Bartholin's gland cancer is diagnosed is 57 years old and carcinoma incidence is highest among women in their 60's. The 2 common types, adenocarcinoma and squamous cell carcinoma, account for 80-90% of primary cases. The remaining 10-20% of cases include transitional, adenoid-cystic or undifferentiated carcinomas . Human papillomavirus is only related to squamous cell lesions. Benign tumors are rarer than carcinomas., Epidemiology:['2% of women', 'fair', 'It is not always possible to prevent a Bartholin’s abscess from developing. To reduce the risk::\n\nUse condoms to avoid STIs, such as chlamydia and gonorrhea.\nGet regular checkups to test for STIs.\nPractice good genital hygiene and only clean the outside of the vagina.\nTake probiotic supplements to support the urinary tract and vagina.\nDrink plenty of fluids throughout the day.'], Complications:['bleeding', 'CELLULITIS', 'DYSPAREUNIA'], Diagnostics:['Complete Blood Count CBC', 'MRI', 'PHYSICAL EXAMINATION'], Differential diagnosis:['CELLULITIS', 'epidermal cysts', "Gartner's Cyst", 'Sebaceous cyst'], disease description:Bartholin abscess is formed when its duct gets blocked by inflammation due to infection or by inspissated secretions..It appears as a swelling on the inside of the anterior two-thirds and posterior one-thirds of the labia majora.History and physical examination are important in diagnosis. so diagnosis is generally clinical.

A 52-year-old lady with symptoms like ['Redness', 'fluctuant mass', 'unilateral vulval swelling', 'Vaginal Discharge', 'DYSPAREUNIA']

Disease Name: Bartholin Cyst, symptoms: ['Redness', 'fluctuant mass', 'unilateral vulval swelling', 'Vaginal Discharge', 'DYSPAREUNIA'], Treatment: [{'medication': ['Diclofenac ', 'Cefixime ']}, 'Sitz baths\nMarsupialization', 'Antibiotics', 'Asymptomatic Bartholin cysts do not require further treatment. Bartholin cysts or abscesses that are spontaneously draining may be managed conservatively with sitz baths and analgesics.\n\nAlthough no modality of treatment, surgical or conservative, is superior to any other in terms of recurrence rate, first-time Bartholin abscesses may be treated with incision and drainage with Word catheter placement due to ease and effectiveness of treatment.\n\nAllergy history should be obtained before beginning the procedure as the Word catheter stem is composed of latex, and marsupialization is the procedure of choice in those with latex allergies.\n\nAlthough this is not a sterile procedure, a mask with a face shield and a gown are recommended.\n\nIncision and drainage with Word catheter are performed by first cleaning the region with povidone-iodine and anesthetizing the location where the incision will be made with 3 mL of 1% lidocaine. A small, approximately 3 mm, a vertical incision should be made with a scalpel along the mucosal surface of the labia minora to avoid obvious scarring and to reduce the risk of Word catheter displacement. Purulent discharge evacuated may be sent to the lab for cultures, and biopsy may also be performed at this time. Word catheter is then inserted with the balloon tip sitting within the abscess cavity. Inflate the balloon tip with 3 to 5mL of saline water. For comfort and to reduce the chance of displacement, the external portion of the Word catheter is pushed into the vagina. Word catheters should be left in place for at least 4 weeks for appropriate drainage and tract epithelization.\n\nIncision and Drainage with Word catheter placement may be attempted a second time for recurrent Bartholin abscess with the addition of antibiotics. Antibiotics should cover staphylococcal, specifically methicillin-resistant Staphylococcus aureus, and streptococcal species as well as enteric gram-negative aerobes, including Escherichia coli. Antibiotic choices include trimethoprim-sulfamethoxazole alone, amoxicillin-clavulanate plus clindamycin, or cefixime plus clindamycin. Referral to gynecology for marsupialization may also be considered at this time.\n\nAntibiotic therapy should be considered for those who have failed initial I&D (incision and drainage) with Word catheter placement, patients with systemic symptoms including fever, patients who have suspected sepsis, and those considered at high risk for recurrence.\n\nMarsupialization is performed by a gynecologist in the operating room, and for this reason, incision and drainage with Word catheter placement are usually attempted first. Marsupialization is performed by creating a 2-cm incision lateral to the hymenal ring, everting the edges with forceps, and suturing the edges onto the epithelial surface with interrupted absorbable sutures.\n\nOther less common procedures include silver nitrate ablation,carbon dioxide laser vaporization, Jacobi ring placement , and Bartholin gland excision as a last resort when other modalities have failed.\n\nWomen who are pregnant and have Bartholin abscesses should be treated in the same manner as nonpregnant women, with the exception of Bartholin gland excision due to the increased risk of bleeding.'], Pathophysiology: Bartholin abscess is formed when its duct gets blocked by inflammation or inspissated with secretions., Epidemiology:['about 2% of all women at some time in their life', 'low (0.13%) during pregnancy.', 'good', "Healthcare providers don't know why most Bartholin cysts occur, so you usually can't prevent them. You can reduce your risk of developing a cyst caused by STIs (sexually transmitted infections) by using a condom during sex. Good hygiene practices can help prevent infection of a cyst before it forms an abscess.\n\nYou can’t prevent a Bartholin cyst from developing, but you can reduce your risk for complications that cause infections like maintaining good hygiene practices and wearing condoms during sex."], Complications:['BARTHOLIN ABSCESS', 'Haemorrhage', 'recurrance'], Diagnostics:['TISSUE BIOPSY', 'MRI', 'USG'], Differential diagnosis:['Choriocarcinoma', 'Endometriosis', 'Fibroadenoma', 'Fibroma', 'folliculitis', 'hematomas', 'inclusion cyst', 'lipoma', 'squamous cell carcinoma.', 'Syringoma'], disease description:A Bartholin gland cyst is usually a unilateral, asymptomatic blockage of the Bartholin gland that may be incidentally discovered during a pelvic exam or imaging studies. A Bartholin gland cyst is a benign blockage of the Bartholin gland that is usually unilateral, asymptomatic, and maybe incidentally found during a pelvic exam or imaging studies.  Medical history and  a pelvic exam helps in diagnosis.

Person aged 48 dealing with ['tenderness of wrist', 'difficulty in movement', 'localized swelling', 'DEFORMITY', 'pain in wrist']

Disease Name: Barton's Fracture, symptoms: ['tenderness of wrist', 'difficulty in movement', 'localized swelling', 'DEFORMITY', 'pain in wrist'], Treatment: ["Volar Approach for Volar Barton's Fracture \n\nA Volar T-buttress plate is used for the fixation of volar rim fracture. In contrast to the principle of fixation, the plate is applied on the volar surface rather than the tensile/dorsal surface due to less soft tissue irritation. Henry's approach or trans-FCR approach is used to approach volar barton fracture. Henry's approach includes the interval between the flexor carpi radialis tendon and the radial artery, while the fracture is approached through the tendon sheath of the flexor carpi radialis tendon in the trans-FCR approach. The dissection is done radial to flexor carpi radialis to prevent injury to the palmar cutaneous branch of the median nerve. Flexor carpi radialis, the flexor digitorum superficialis, and profundus tendons are retracted towards the ulnar side. in order to prevent the possible denervation of the muscle, avoid radial retraction of the flexor pollicis longus. The volar radiocarpal ligaments that stabilize the wrist are preserved as the pronator quadratus is lifted off from the radial side. Every effort should be made to stabilize the volar lunate facet fragment to prevent carpal subluxation and instability. This may require an extension of the volar incision that incorporates a carpal tunnel release or a separate ulnar incision is made to stabilize the lunate facet fragment. A volar barton's fracture with dorsal rim fracture of the distal radius requires a well-contoured volar plate to prevent dorsal angulation of distal radius articular surface and poor wrist functional outcome.Following surgery, the wrist is immobilized in a splint for five to ten days and then active wrist mobility is started.\n\nDorsal Approach for Dorsal Barton's Fracture\n\nA preoperative CT scan is required for the evaluation of fracture patterns and the level of comminution. The dorsal approach is used for dorsal barton and fragment-specific fixation of distal radius fracture through the 3rd dorsal compartment. A 5-6 cm longitudinal incision is made along the lister tubercle. The extensor pollicis longus tendon is retracted radially after incising the roof of the 3rd dorsal compartment. Subperiosteal dissection is done in the 2nd and 4th dorsal compartments to expose the distal radius. To prevent postoperative wrist pain, the posterior interosseous nerve is sacrificed proximally or preserved by dissecting it in a subperiosteal fashion in the 4th compartment. In order to prevent radiocarpal instability, the scapholunate ligament is preserved while performing a dorsal wrist capsulotomy. The dorsal capsule is incised vertically along the skin incision. The dorsal barton fracture is reduced with traction and dorsiflexion maneuver. The dorsal buttress plate or locking plate is used to stabilize the fracture and maintain articular congruity.\n\nK-wires have been used along with a spanning external fixator for barton fracture with a success rate of 80-90%.The disadvantages of K-wire fixation are mal-reduction, tendon penetration of wires, and pin site infection. The overall success rate with the plating system is 90-95% however it is associated with wound-related complications. The long-term outcome depends upon the level of fracture comminution, joint arthrosis, and range of motion wrist exercises postoperatively. If volar Barton fractures do not include carpal subluxation, closed reduction with the cast is advised. However, a 2mm articular step warrants operative fixation"], Pathophysiology: A Barton fracture is a compression injury with a marginal shearing fracture of the distal radius. The most common cause of this injury is a fall on an outstretched, pronated wrist. The compressive force travels from the hand and wrist through the articular surface of the radius, resulting in a triangular portion of the distal radius being displaced dorsally along with the carpus. Multiple stabilizing structures help to maintain the relationship between the radius and the carpal bones, including the extrinsic radiocarpal ligaments, the joint capsule, and the scaphoid and lunate fossa of the radius., Epidemiology:['prevalence of 17.5%', 'good', "Be extra careful when you're playing sports, working manual labor, riding a motorcycle or climbing something high like a ladder. If you’re at higher risk for osteoporosis, eliminate tripping hazards in your home. Be sure to always use your cane or walker if you use one."], Complications:['Complex Regional Pain Syndrome', 'Carpal tunnel syndrome', 'NERVE INJURY'], Diagnostics:['X RAY AP VIEWS', 'X RAY', 'x ray lateral view'], Differential diagnosis:["COLLES' FRACTURE", "SMITH'S FRACTURE (Reverse of Colles' Fracture)"], disease description:This is an intra-articular fracture of the distal radius. Here, the fracture extends from the articular surface of the radius to either its anterior or posterior cortices. The small distal fragment gets displaced and carries with it, the carpals. Depending upon the displacement, there is a volar Barton's fracture (anterior type), and a dorsal Barton's fracture (posterior type).

Person at 32 years, dealing with ['drooping mouth', 'metabolic alkalosis', 'protruding ears', 'large eyes with strabismus', 'Dehydration', 'Dizziness', 'muscle cramps', 'weakness', 'Hypotension', 'failure to thrive']

Disease Name: Bartter Syndrome, symptoms: ['drooping mouth', 'metabolic alkalosis', 'protruding ears', 'large eyes with strabismus', 'Dehydration', 'Dizziness', 'muscle cramps', 'weakness', 'Hypotension', 'failure to thrive'], Treatment: [{'medication': ['Indomethacin ']}, 'A saline infusion may be needed in the neonatal period. The target is to normalize potassium levels in serum which can be achieved with oral potassium supplementation such as KCL 25 to 100 mmol/day. ACE inhibitors and angiotensin receptor blockers (ARB) help decrease elevated angiotensin II and aldosterone levels, limit proteinuria, and increase serum potassium in some cases. Other options include amiloride 5 to 40 mg/day, spironolactone, NSAID (indomethacin 1-3 mg/kg/24 hours) to antagonize increased urine PGE2 levels. Magnesium supplementation should be considered, as hypomagnesemia may aggravate potassium wasting.\n\nTubular abnormalities usually are resolved after kidney transplantation with no recurrence.'], Pathophysiology: The biochemical features of Bartter syndrome, hypokalemic hypochloremic metabolic alkalosis with hypercalciuria, resemble those seen with chronic use of loop diuretics and reflect a defect in sodium, chloride, and potassium transport in the ascending loop of Henle. The loss of sodium and chloride, with resultant volume contraction, stimulates the renin–angiotensin II–aldosterone axis. Aldosterone promotes sodium uptake and potassium secretion, exacerbating the hypokalemia. It also stimulates hydrogen ion secretion distally, worsening the metabolic alkalosis. Hypokalemia stimulates prostaglandin synthesis, which further activates the renin–angiotensin II–aldosterone axis. Bartter syndrome has been associated with at least five distinct genetic defects in loop of Henle transporters. Each contributes, in some manner, to sodium and chloride transport. Mutations in the genes that encode the Na+ /K+ /2Cl-transporter (NKCC2, the site of action of furosemide), the luminal potassium channel (ROMK), combined chloride channel (CLC-Ka, CLC-Kb), or subunit of chloride channels (barttin) cause neonatal Bartter syndrome. Isolated defects in the genes that produce a specific basolateral chloride channel (ClC-Kb) cause classic Bartter syndrome., Epidemiology:['1 in 1,000,000 individuals', 'good', "This condition is inherited in an autosomal recessive pattern and thus, it can't be prevented. \nAlthough Genetic Counselling is advisable."], Complications:['Arrhythmias', 'Chronic renal failure', 'interstitial nephritis'], Diagnostics:['ABG', 'URINARY POTASSIUM K+', 'URINARY SODIUM Na+', 'Plasma Aldosterone', 'Plasma Renin', 'serum potassium K+', 'SERUM CHLORIDE VALUE', 'URINARY CALCIUM CA++', 'SERUM PROSTAGLANDINS LEVEL'], Differential diagnosis:['CYSTIC FIBROSIS', 'Gitelman Syndrome', 'h/o Drug intake', 'hypokalemia', 'hypomagnesemia', 'pyloric stenosis', 'vomiting'], disease description:Bartter syndrome is an autosomal recessive disorder of salt reabsorption resulting in extracellular fluid volume depletion with low/normal blood pressure. It is characterized by several electrolyte abnormalities including low potassium and chloride and, in few cases, hypomagnesemia. Other abnormalities include high renin, secondary hyperaldosteronism, and elevated levels of prostaglandin E2. Acid-base manifestation is typically metabolic alkalosis.Types of Bartters syndrome-Type I results from mutations in the sodium chloride/potassium chloride cotransporter gene (NKCC2)Type II results from mutations in the ROMK gene Type III results from mutations in the chloride channel gene (CLC-Kb)Type IV results from the loss-of-function mutations in gene encoding barttin Type V results from mutations in extracellular calcium ion-sensing receptor and in the genes that encode the chloride channel subunits, ClC-Ka and ClC-Kb

Symptoms at 54 years old: ['PAINLESS MASS']

Disease Name: Basal Cell Adenoma, symptoms: ['PAINLESS MASS'], Treatment: ['All variants of basal cell adenomas are treated by local excision or resection of involved lobe except the membranous type which requires extensive surgery due to increased recurrence rate (24%).'], Pathophysiology: Four histological patterns of basal cell adenoma are observed: Solid (sheets of basaloid cells separated by collagenous stroma), trabecular (nests and cords of basaloid cells separated by cellular stoma), tubular (glandular formations) and membranous (thick bands of hyaline material at the periphery of basaloid cells). Peripheral palisading is a prominent feature within the nests. Mitoses are occasional. Capsular or vascular invasion, necrosis and chondroid matrix are absent., Epidemiology:['seen predominantly in women over 50 years of age', 'representing 1–3% of all salivary gland neoplasms', 'variable'], Complications:['recurrence', 'skin cancer'], Diagnostics:['FNAC', 'MRI', 'CT'], Differential diagnosis:['Basal cell adenocarcinoma', 'MONOMORPHIC ADENOMA', 'Pleomorphic adenoma', 'WARTHIN TUMOUR'], disease description:Basal cell adenoma (BCA) of the salivary gland is a rare neoplasm consists of a monomorphic population of basaloid epithelial cells, and it accounts for approximately 1–2 % of all salivary gland tumors. Its most frequent location is the parotid gland. It usually appears as a firm and mobile slow-growing mass. Histologically, isomorphic cells in nests and interlaced trabecules with a prominent basal membrane are observed. In contrast to pleomorphic adenoma, it tends to be multiple and its recurrence rate after surgical excision is high.

A 29-year-old individual dealing with ['a slightly raised thread-like margin or a ‘whipcord’ edge, which is irregular in outline and may be defi cient at part of the circumference', 'longitudinal melanonycha', 'black lesion with raised border', 'ulceration', 'NODULES']

Disease Name: Basal Cell Carcinoma, symptoms: ['a slightly raised thread-like margin or a ‘whipcord’ edge, which is irregular in outline and may be defi cient at part of the circumference', 'longitudinal melanonycha', 'black lesion with raised border', 'ulceration', 'NODULES'], Treatment: [{'medication': ['Imiquimod ']}, 'Intralesional interferon a-2b.\nTopical 5-fl uorouracil (5-FU)', 'Superfi cial and electron beam radiotherapy or brachytherapy are\neffective therapeutic strategies in primary or surgically recurrent\nBCC as well as high-risk BCC in patients who are unwilling or\nunable to tolerate surgery', 'Adequate excision is vital and Mohs micrographic surgery is the\ntreatment of choice'], Pathophysiology: The tumour cells resemble those of the basal layer of the epidermis and the matrix cells of the appendages, in the relatively small amount of cytoplasm they possess and in their ability to interact with the dermis adjacent to them. Their nuclei are compact, rather darkly staining and closely set. Their cytoplasm stains poorly and the cell margins are rather indistinct. Adjacent cells are connected by bridges. The sparsity of keratin fibrils gives these connections a different appearance from the ‘prickles’ of the Malpighian layer, but the presence of desmosomes and tonofibrils has been shown by electron microscopy. The interaction with the dermis, which is one of the principal functions of the normal epidermal basal cell, produces the characteristic marginal palisade of tumour cells and the well-organized stroma that surrounds it. The dependence of the tumour on its stroma has been shown by transplantation experiments. The cells within the palisade usually show little evidence of organization or differentiation. Mitotic fi gures may be frequent, and it is speculated that the combination of large numbers of mitoses and a slow growth rate result from a high rate of apoptosis. Data on cell kinetics indicate that a considerable proportion of cells in the tumour die fairly rapidly. In some tumours, the cells may become acantholytic and amyloid may be identifi ed. n early lesions, the tumour buds can be seen arising from the epidermis. In very small lesions, multiple buds have been seen. These very soon become confl uent, and the three-dimensional examination of superfi cial BCC shows a coherent margin of tumour with a reticular pattern of growth along the interpapillary ridges and larger, more discrete masses centrally. As the tumour progresses, the masses extend into the dermis, and may separate from each other and from their point of origin. Growth in one area may be accompanied by involution of the tumour in nearby areas leaving an atrophic epidermis. A common site of origin in humans and in the experimental tumours of the rat is the junction between a pilosebaceous duct and the epidermis. From here, the tumour may extend along the epidermis and down the duct. It is diffi cult to prove a purely adnexal origin for BCC, but some lesions behave as though this were so. In all considerations about the origin of the tumour, one must remember that the tumour can either sever its connection with epithelial structures or establish a secondary connection to structures to which it has grown close. The variability of the natural history of BCCs is refl ected in its pattern of growth. Most tumours are composed of rounded expansile islands. These throw out small buds that grow in the same way to produce multilobular masses with thin strands or septa of fi brous tissue penetrating them. Genetics Naevoid BCC syndrome (NBCCS; syn. Gorlin syndrome, MIM 109400; is an autosomal dominant disorder with distinct clinical features including palmoplantar pits, odontogenic cysts, calcifi cation of the falx cerebri, skeletal abnormalities, medulloblastomas and multiple BCC. Insight into the molecular pathogenesis of BCC derives from the study of patients with NBCCS which results from germline mutations in PTCH1 , a segment polarity gene (9q22.3) with tumour suppressor functions. PTCH1 was originally identifi ed in the fruitfl y Drosophila melanogaster, and is known to play a critical role in vertebrate development. PTCH1 encodes a 12-pass putative transmembrane protein, Patched-1 (Ptch-1) which acts like the receptor of the diffusible morphogen protein sonic hedgehog (SHH). Ptch-1 acts as a tumour suppressor, repressing the G-protein- coupled receptor smoothened (Smo). Loss-of-function mutations of PTCH1 result in reduced suppression of Smo which activates the Gli family of transcription factors and promotes their importation into the nucleus resulting in sustained activation of target genes. Gli proteins are bound by Sufu, loss of which produces constitutive activation of Gli. Atypical protein kinase C iota/lambda (aPKC-?/?), a novel Gli regulator, and its polarity signalling partners colocalize at the centrosome and form a complex with missing-in-metastasis (MIM), a scaffolding protein that potentiates Hh signalling. Activated aPKC-?/? is upregulated in SMO-inhibitor-resistant tumours and targeting aPKC-?/? suppresses signalling and growth of resistant BCC cell lines. Somatic PTCH1 mutations have a high frequency in familial BCC. Sporadic BCC tumours also demonstrate loss of function of PTCH1 in 80–90% and SMO in 10–20% of cases. The melanocortin-1 receptor ( MC1R ) gene variants ASIP and TYR are associated with fair skin, red hair and melanoma risk. Recent evidence suggests that they may also be independent risk factors for BCC. Similarly, the role of the p53 tumour suppressor gene has been examined as 50% of BCC carry a p53 mutation. Both cytochrome P450s (CYP) and glutathione S-transferases (GST) catalyse the detoxication of the products of oxidative stress. Environmental factors The mechanism of UV radiation induced mutagenesis has been extensively studied. Both UVB and UVA radiation are mutagenic; however, UVB radiation causes direct DNA and RNA damage by inducing covalent bond formation between adjacent pyrimidines. This leads to the generation of mutagenic photoproducts, e.g. cyclopyrimidine dimers (TT) and pyrimidine–pyrimidine adducts., Epidemiology:['33-39% for men and 23-28% for women.', 'Inadequate excision accounts for a high recurrence'], Complications:[], Diagnostics:['biopsy', 'CT/MRI', 'MRI', 'Dermoscopy'], Differential diagnosis:['Actinic keratosis: Arsenical keratosis, PUVA kera', 'Bowen disease', 'Chronic paronychia', 'Cutaneous T-cell lymphoma', 'Malignant melanoma', 'Molluscum Contagiosum', 'mycotic infection', 'psoriasis', 'Sebaceous hyperplasia', 'Squamous cell carcinoma'], disease description:Basal cell carcinoma (BCC), previously known as basal cell epithelioma, is the most common cancer in Humans. BCC mostly arises on sun-damaged skin and rarely develops on the mucous membranes or palms and soles. Basal cell carcinoma is usually a slow-growing tumor for which metastases are rare. Although rarely fatal, BCC can be highly destructive and disfigure local tissues when treatment is inadequate or delayed. On clinical examination, BCC usually appears as flesh- or pink-colored, pearly papules with overlying ulceration or telangiectatic vessels. BCC occurs on the head or neck in the majority of cases, but can involve the trunk and extremities.

Symptoms reported at the age of 18: ['irregular mass', 'painful swelling']

Disease Name: Basaloid Squamous Cell Carcinoma, symptoms: ['irregular mass', 'painful swelling'], Treatment: [{'medication': ['Bevacizumab ', 'Ifosfamide /Isophosphamide', 'Cisplatin ', 'Carboplatin', 'Mitomycin', 'Topotecan ', 'Irinotecan', 'Paclitaxel', 'Gemcitabine hydrochloride', 'Docetaxel', 'Fluorouracil ']}, 'Combining systemic chemotherapy with locoregional radiation is a logical approach to treatment, especially for the BSCC, given its tendency to metastasize early after definitive therapy.', 'In resectable lesions with no evidence of metastasis, complete surgical excision, supplemented by postoperative radiotherapy is considered most accepted.'], Pathophysiology: Etiology and pathogenesis of basaloid cell carcinoma is similar to conventional squamous carcinoma. Most patients have a long history of smoking and alcohol drinking. Histologically, BSCC shows a biphasic pattern of basaloid and squamous components, with a predominating basaloid component (80%–90%)., Epidemiology:['BSCC is a rare variant of squamous cell carcinoma with a frequency of >1% of all squamous cell carcinoma.', 'its prognosis is unfavorable'], Complications:['Metastasis'], Diagnostics:['Immunostaining'], Differential diagnosis:['adenoid cystic carcinoma', 'Basal cell adenocarcinoma', 'small cell carcinoma', 'squamous cell carcinoma.'], disease description:Basaloid squamous cell carcinoma (BSCC) is a rare and aggressive variant of oral squamous cell carcinoma with a predilection for the tongue and in other locations, such as floor of the mouth, palate, retromolar trigone, and gingival mucosa.

Experiencing ['hyperkeratosis', 'palm dryness', 'Shedding of the collodion membrane is followed by the development of large dark grey/brownish scales affecting the trunk and the scalp, but sparing the face and extremities', 'hypohidrosis', 'Children are born as collodion babies involving the entire skin.'] at 52 years

Disease Name: Bathing Suit Ichthyosis, symptoms: ['hyperkeratosis', 'palm dryness', 'Shedding of the collodion membrane is followed by the development of large dark grey/brownish scales affecting the trunk and the scalp, but sparing the face and extremities', 'hypohidrosis', 'Children are born as collodion babies involving the entire skin.'], Treatment: ['moisturizing the skin, reducing fluid loss, and preventing infections.'], Pathophysiology: Bathing suit ichthyosis was found to be due to peculiar missense mutations in TGM1 that render the enzyme TG1 temperature sensitive. Recombinant expression of the TGM1 mutations in BSI showed that they exhibit a marked shift in temperature optimum from 37°C to 31°C. Deficient activity of BSI mutants could be rescued and even reconstituted by decreasing the temperature to below 33°C. All BSI mutations showed an activity above 10% at their temperature optimum at 31°C and a dramatic decrease at 37°C. It is of note that the vast majority of BSI-causing mutations affect arginine residues, e.g. p.Arg315His, and often affects exons 5, 6 or 7. A few of these patients heal eventually completely and could also be regarded as examples of SICI., Epidemiology:['1 in 200 000 births', 'variable', 'NOT KNOWN'], Complications:['infections'], Diagnostics:['PCR AMPLIFICATION OF DNA'], Differential diagnosis:['Ichthyosis vulgaris', 'psoriasis', 'severe congenital ichthyosis', 'X-linked ichthyosis (XLI)'], disease description:Bathing suit ichthyosis is a peculiar type of Autosomal recessive congenital ichthyosis (ARCI) first recognized in South African Bantu of the Nguni ethnic group. While children are born as collodion babies, they later develop a lamellar type of ichthyosis that spares the face and the extremities, and follows the distribution pattern of bathing suits.

Symptoms at 41 years: ['blindness', 'chest pain', 'coma', 'Loss of muscle tone', 'HEPATOMEGALY', 'tiredness', 'cough', 'nausea']

Disease Name: Baylisascaris Infection, symptoms: ['blindness', 'chest pain', 'coma', 'Loss of muscle tone', 'HEPATOMEGALY', 'tiredness', 'cough', 'nausea'], Treatment: ['No drugs have been shown to be totally effective for the treatment of Baylisascaris infection. In cases where suspicion of exposure is high, immediate treatment with albendazole (25-50 mg/kg per day by mouth for 10 – 20 days) may be appropriate. Treatment is successful when administered soon after exposure to abort the migration of larvae.'], Pathophysiology: Raccoons are the primary, or definitive, host of Baylisascaris procyonis, a roundworm. Raccoons become infected with Baylisascaris in one of the following two ways:By eating infectious eggs during foraging, feeding, and grooming.By eating rodents, rabbits, and birds that are infected with the larvae of Baylisascaris.Infected raccoons have been found throughout the United States, mainly in the Midwest, Northeast, Middle Atlantic, and West Coast.Raccoons are peridomestic animals, which means they live in or around areas where people live. Roundworm eggs are passed in the feces of infected raccoons. Raccoons defecate in communal sites, called latrines. Raccoon latrines are often found at bases of trees, in unsealed attics, or on flat surfaces such as logs, tree stumps, rocks, decks, and rooftops. As more raccoons move into populated areas, the number and density of their latrines will increase.The worms develop to maturity in the raccoon intestine, where they produce millions of eggs that are passed in the feces. Eggs that are excreted by raccoons are not immediately infectious. These eggs must develop in the environment for 2 to 4 weeks, after which the eggs are able to cause infection. The eggs are resistant to most environmental conditions and with adequate moisture, can survive for years.While raccoons are the roundworm’s primary host, other types of animals can become infected. Birds and small mammals, such as rodents and rabbits, are susceptible to the parasite. Unlike raccoons, these animals sometimes show signs of infection, such as muscle spasms, tremors, and progressive weakness; infection can lead to death. Predator animals, including dogs, may become infected by eating an animal that has been infected with Baylisascaris. In some dogs, Baylisascaris may develop to adult worms and pass eggs in the dogs’ feces.Young children are at risk for Baylisascaris infection as they may be more likely to put contaminated fingers, soil, or objects into their mouths., Epidemiology:['Cases have been reported in California, Illinois, Louisiana, Massachusetts, Michigan, Minnesota, Missouri, New York, Oregon, Washington and Pennsylvania. As of 2018, there were 23 published human neurological cases in the US; six of the infected persons died.', 'variable', 'Care should be taken to avoid contaminating hands and clothes. Treat decks, patios, and other surfaces with boiling water or a propane flame-gun (exercise proper precautions). Prompt removal and destruction of raccoon feces.'], Complications:['ENCEPHALITIS'], Diagnostics:['CSF EXAMINATION', 'MRI Brain', 'TISSUE BIOPSY', 'SEROLOGIC TEST'], Differential diagnosis:['Ascariasis', 'Echinococcosis', 'Strongyloidiasis', 'toxocara endophthamitis'], disease description:Baylisascaris infection is caused by a roundworm found in raccoons. This roundworm can infect people as well as a variety of other animals, including dogs. Human infections are rare, but can be severe if the parasites invade the eye (ocular larva migrans), organs (visceral larva migrans) or the brain (neural larva migrans).

Suffering from ['pigmentation of the skin and subcutaneous tissue', 'pus formation', 'Tender wound', 'fever', 'ulcer', 'Warm Skin'] at 29

Disease Name: Bedsores, symptoms: ['pigmentation of the skin and subcutaneous tissue', 'pus formation', 'Tender wound', 'fever', 'ulcer', 'Warm Skin'], Treatment: [{'medication': ['Amoxicillin and Clavulanic acid ']}, 'Cause should be treated correction of diabetes and anaemia.Nutritional supplementation.Rest antibiotics slough excision,regular dressings. Vacuum-assisted closure (VAC). Once ulcer granulates well, flap cover or skin grafting is done.Excision of the ulcer and skin grafting.Flaps-local rotation or other flaps (transposition flaps). ,, Cultured muscle interposition. ,.. Proper care: Change in position once in 2 hours; lifting the limb upwards for 1 0 seconds once in 1 0 minutes.'], Pathophysiology: It is due to-impaired nutrition; defective blood supply; neurological deficit, pressure, anaemia, injury, moisture. It is common in patients with orthopaedic and head injuries, comatose and stroke patients, old age and tetanus patients. Sites: Over the ischial tuberosity; sacrum; heel; heads of metatarsals; buttocks; shoulder; occiput. Due to the presence of neurological deficit, trophic ulcer is also called as neurogenic ulcer/neuropathic ulcer. Initially it begins as callosity due to repeated trauma and pressure, under which suppuration occurs and gives way through a central hole which extends down into the deeper plane up to the underlying bone as perforating ulcer (penetrating ulcer'). Bedsores are trophic ulcers. Nonblanching erythema--early superficial ulcer Partial thickness skin loss-late superficial ulcer • Full thickness skin loss extending into subcutaneous tissue but not through fascia-early deep ulcer • Full thickness skin loss with fascia and underlying structures like muscle/tendon/bone, etc.-late deep ulcer, Epidemiology:['of 5 to 9% and more than 70% occurring in patients over 70 years of age.', '0.4 to 38.0% in major hospitals, 2.2 to 23.9% in those on long-term care and 0 to 17% in home care settings.', 'variable', 'To Do : use of water bed/air bed/ripple bed/air-fluid \nflotation bed and pressure dispersion cushions to the \naffected area; urinary and faecal care; hygiene; psychological counselling. Regular skin observation; keeping \nskin clean and dry (using regular use of talcum powder); \noil massaging of the skin and soft tissues using clean, \nabsorbent porous clothing; control and prevention of \nsepsis helps in the management.\n\nshift body weight frequently,Keep skin clean and dry.'], Complications:['CELLULITIS', 'Bone infection'], Diagnostics:['random blood sugar RBS', 'Differential Leucocyte Count DLC', 'PUS CULTURE', 'Total Leucocyte Count (TLC)'], Differential diagnosis:['CELLULITIS', 'DIABETIC GANGRENE', 'DRY GANGRENE', 'NECROTISING FASCIITIS', 'osteomyelitis', 'pyoderma gangrenosum', 'THROMBOPHLEBITIS', 'TRAUMATIC FAT NECROSIS'], disease description:Pressure sore is tissue necrosis and ulceration due to prolonged pressure. Blood flow to the skin stops once external pressure becomes more than 30 mmHg (more than capillary occlusive pressure) and this causes tissue hypoxia, necrosis and ulceration. It is more prominent between bony prominence and an external surface. Sites: Over the ischial tuberosity; sacrum; heel; heads of metatarsals; buttocks; shoulder; occiput. MOST COMMON SITES ARE Tailbone or buttocks , Heels Shoulder blades and spine Risk factors Immobility Incontinence Poor nutrition and hydration

Experiencing ['bronchospasm', 'diarrhea', 'pruritus', 'laryngeal edema', 'Hypotension', 'erythema at sting site', 'swelling at sting site', 'headache', 'vomiting', 'shock'] at 49 years old

Disease Name: Bees, Wasps And Ants (hymenoptera), symptoms: ['bronchospasm', 'diarrhea', 'pruritus', 'laryngeal edema', 'Hypotension', 'erythema at sting site', 'swelling at sting site', 'headache', 'vomiting', 'shock'], Treatment: [{'medication': ['Adrenaline (Epinephrine)', 'Chlorpheniramine/ Pheniramine Maleate / Dexchlorpheniramine Maleate']}, 'first aid-\nWash the site with soap and water.\nRemove the stinger using gauze wiped over the area or by scraping a fingernail over the area.\nNever squeeze the stinger or use tweezers.\nApply ice to reduce swelling.\nDo not scratch the sting as this may increase swelling, itching, and risk of infection.', 'The application \nof a potent topical corticosteroid to the sting site before the area is \ncooled with wet dressings or cool packs is usually recommended. Oral antihistamine and/or systemic corticosteroids may be \nrecommended even if there are no controlled studies; it is considered that this therapy should be initiated as soon as possible after \nthe sting.\n\nThe treatment of choice for anaphylaxis is intramuscular epinephrine (adrenaline) (in adults, a dose of 0.5 mL 1 : 1000 solution should be administered, and repeated after about 5 min in \nthe absence of clinical improvement or if deterioration occurs after \nthe initial treatment), followed by chlorpheniramine (10–20 mg, \nintramuscular or slow intravenous) and hydrocortisone (100–\n500 mg, intramuscular or slow intravenous).'], Pathophysiology: The composition of venoms is complex. Pharmacologically active and antigenic substances are both present, and an individual’s reaction to the sting is determined partly by the quantity of the former, and partly by the degree of acquired hypersensitivity to the latter. Hymenoptera venom contains vasoactive amines, small polypeptides and larger protein molecules. The components of vespid (wasps, yellow-jackets and hornets) venoms include histamine, serotonin, mast cell degranulating peptide, wasp kinin, phospholipases, hyaluronidase and antigen 5. The three major allergens in vespid venoms are phospholipases, hyaluronidase and antigen 5. The venom of the honeybee contains histamine, mast cell degranulating peptide, melittin, phospholipase A2, hyaluronidase and acid phosphatase. The three proteins in honeybee venom which are important allergens are phospholipase A2, hyaluronidase and acid phosphatase. In addition, the polypeptide melittin is also antigenic. Bumblebee venom appears to be chemically and antigenically related to honeybee venom. Allergy to Hymenoptera venom is mediated by IgE antibodies. The antigenic substances in the venom of many Hymenoptera are more liable to induce high degrees of hypersensitivity of the immediate type than are the antigens of most other insects. Several risk factors are associated with the occurrence of severe systemic anaphylactic sting reactions: vespid stings, older age, elevated tryptase concentration, male patient, specific medication (angiotensin-converting inhibitors) and mastocytosis. Preceding less severe systemic reaction may also predispose the patient to more severe reactions., Epidemiology:['between 5 and 7.5% of Americans are hypersensitive to insect stings.', 'VARIABLE', 'Wear light-colored, smooth-finished clothing.\nAvoid perfumed soaps, shampoos, and deodorants. ...\nWear clean clothing and bathe daily. ...\nWear clothing to cover as much of the body as possible.\nAvoid flowering plants when possible.\nKeep work areas clean.'], Complications:['hypersensitivity reactions', 'Anaphylaxis'], Diagnostics:['Complete Blood Count CBC', 'allergy skin test'], Differential diagnosis:['abscess', 'Anaphylaxis', 'angioedema', 'CELLULITIS', 'folliculitis', 'food allergies'], disease description: Humans are frequently stung by these insects, with reactions varying from local discomfort to fatal anaphylaxis. The Hymenoptera are readily recognized by the narrow waist (isthmus) connecting the abdomen to the thorax. Hymenopteran stings only cause local inflammation in most people. However, they also account for the largest percentage of envenomation-related deaths in the United States. Most deaths result from immediate hypersensitivity reactions and anaphylaxis. This activity reviews Hymenoptera stings and highlights the role of the interprofessional team in its management.

Symptoms at 31: ['erythema nodosum', 'floaters in eyes', 'Macular edema', 'Genital ulceration', 'SKIN LESIONS', 'Central scotoma', 'swollen optic disc', 'chest pain', 'Confusion', 'diarrhea', 'Joint pain/Arthritis', 'nausea', 'Ocular irritation', 'pain in eyes', 'REDNESS OF EYE', 'seizures', 'fever', 'blood in sputum', 'retro-orbital pain', 'glare and light sensitivity', 'Abdominal Pain', 'decreased visual acuity', 'painful urination', 'blurred vision', 'painless loss of vision', 'reduced color vision']

Disease Name: Behçet Disease, symptoms: ['erythema nodosum', 'floaters in eyes', 'Macular edema', 'Genital ulceration', 'SKIN LESIONS', 'Central scotoma', 'swollen optic disc', 'chest pain', 'Confusion', 'diarrhea', 'Joint pain/Arthritis', 'nausea', 'Ocular irritation', 'pain in eyes', 'REDNESS OF EYE', 'seizures', 'fever', 'blood in sputum', 'retro-orbital pain', 'glare and light sensitivity', 'Abdominal Pain', 'decreased visual acuity', 'painful urination', 'blurred vision', 'painless loss of vision', 'reduced color vision'], Treatment: [{'medication': ['Colchicine ', 'Cyclosporine/Ciclosporine', 'Prednisolone', 'Thalidomide']}, 'Mucocutaneous Manifestations\n\nIsolated oral and genital aphthae:\n\nInitial treatment with topical triamcinolone acetonide cream 3 to 4 times a day until the pain from the ulcer is relieved\nTopical sucralfate 1g/5mL four times daily with or as an alternative to topical corticosteroids.\nTopical anesthetics, generally not as effective as steroids or sucralfate, can also provide temporary relief\n Prevention of recurrent oral and genital ulcers:\n\nColchicine 1 to 2 mg/day in divided doses\nFirst-line drug \nDoses in the range of 1.2 to 1.8 mg can be used when 0.5 mg tablets are unavailable.\nMore effective in genital ulcers.\nHas a narrow therapeutic index.\nCytopenias are a significant side effect.\nApremilast is titrated at a rate of 10 mg daily over six days to attain a maintenance dose of 30 mg twice daily.\nMore effective in oral ulcers.\nAdverse events include nausea, diarrhea, and headache.\nMultiple lesions or isolated oral aphthae or genital ulcers are refractory to the therapy mentioned above:\n\nPrednisone 15 mg/day, tapering to 10 mg/day after one week and completing the course over a two- to three-week period\nLow-dose prednisone (e.g., 5 mg/day) with a prolonged course may be used in case of recurrent oral aphthae.', 'When all the treatment mentioned above fails:\n\nAzathioprine\nThe initial dose of azathioprine is 50 mg daily.\nAs tolerated, increase the daily dose by 50 mg every four weeks.\nThe target dose is 2.5 mg/kg/day.\nComplete blood count (CBC) is monitored every two weeks initially till the maximum required dose is achieved and then every 6 to 12 weeks.\nA lower dose is used in case of renal compromise.\nGenetic testing for thiopurine methyltransferase is advised before starting therapy. A deficiency of thiopurine methyltransferase can cause an increased risk of developing severe, potentially life-threatening bone marrow toxicity with conventional doses of azathioprine or mercaptopurine.\nIt can be combined with tumor necrosis factor (TNF)-alpha inhibitors (infliximab, adalimumab, etanercept)[\nInterferon\nInterferon alfa-2a and Interferon alfa-2b (generally given 3 to 6 million units three times weekly)\nCutaneous lesions (except erythema nodosum and pyoderma gangrenosum):\n\nMild:\nColchicine 1 to 2 mg daily in divided dose\nLesions unresponsive to colchicine:\nPrednisolone up to 40 mg/day initially and a maintenance dose of 5 and 10 mg/day\nErythema nodosum:\n\nInitial therapy is a combination of oral prednisone (40 to 60 mg daily) and azathioprine.\nThe initial dose of azathioprine is 50 mg daily.\nAs tolerated, increase the daily dose by 50 mg every four weeks.\nThe target dose is 2.5 mg/kg/day.\nComplete blood count (CBC) is monitored every two weeks initially till the maximum required dose is achieved and then every 6 to 12 weeks.\nThe initial prednisone dose is administered for one month and then tapered gradually to complete the course over three to four months.\nPyoderma gangrenosum (PG):\n\nExtensive debridement is discouraged.\nSterile saline or a mild antiseptic for wound care\n Mild, localized PG:\nTopical corticosteroid (high potency or superpotent) or topical tacrolimus (0.03% to 0.3%)\nMore extensive or rapidly progressing PG:\nSystemic glucocorticoids\nOral prednisolone (0.5 to 1.5 mg/kg per day) or its equivalent is started initially, with a maximum daily dose of 60 mg.\nIntravenous pulse therapy with 1 g methylprednisolone daily for one to five days can be started initially for very aggressive or painful disease.\nTaper off glucocorticoids within 4 to 10 weeks and monitor closely for continued improvement or adverse effects.\nSystemic cyclosporine\nAlternative for glucocorticoid intolerant or glucocorticoid unresponsive cases.\nInitiated at a dose of 4 to 5 mg/kg and subsequently tapered as tolerated\nTreatment is limited to less than one year due to side effects, such as hypertension and renal toxicity.'], Pathophysiology: The etiology and pathogenesis of this syndrome remain obscure. The disease appears to be in the crossroads of autoinflammatory and autoimmune disorders. The main pathologic lesion is systemic perivasculitis with early neutrophil infiltration and endothelial swelling. In some patients, diffuse inflammatory disease, involving all layers of large vessels and resulting to formation of pseudoaneurysms suggests vasculitis of vasa vasorum. Apart from activated neutrophils, increased numbers of infiltrating TH1, TH17, cytotoxic CD8+, and  T cells are observed, supporting a link between innate and adaptive autoreactive immune response. Circulating autoantibodies against a-enolase of endothelial cells, selenium binding protein, and anti-Saccharomyces cerevisiae antibodies have been observed, but their pathogenic role remains unclear. A recent genome-wide association study confirmed the known association of Behçet’s syndrome with HLA-B*51 and identified a second, independent association within the major histocompatibility complex (MHC) class I region. In addition, an association with interleukin (IL) 10 and the IL-23R–IL-12RB2 locus was also observed. Interestingly, the disease-associated IL-10 variant was correlated with diminished mRNA expression and low protein production., Epidemiology:['Fewer than 100 thousand cases per year (India)', 'GOOD', "The inflammation associated with Behcet's disease can be reduced by drugs that prevent your immune system from attacking healthy tissues."], Complications:['blindness', 'decreased visual acuity', 'coronary arterial aneurysms', 'miscarriages'], Diagnostics:['Skin Prick test', 'intradermal saline injection (pathergy test'], Differential diagnosis:['INFLAMMATORY BOWEL DISEASES', 'Multiple Sclerosis', 'Recurrent aphthous stomatitis', "Reiter's syndrome", 'Sarcoidosis', "Stevens-Johnson's syndrome", 'systemic lupus erythematosus (SLE)', 'viral infections'], disease description:Behçet’s syndrome is a multisystem disorder presenting with recurrent oral and genital ulcerations as well as ocular involvement. The diagnosis is clinical and based on internationally agreed diagnostic criteria.. The syndrome affects young males and females from the Mediterranean region, the Middle East, and the Far East. The frequency of Behçet’s syndrome increases from north to south Europe. Males and females are affected equally. Males often have more severe disease. The syndrome is rare in Sub-Saharan Africa. Behçet's disease (BD) is usually diagnosed between the second and fourth decades. Onset after 50 years of age is extremely rare.

Symptoms at 18: ['lymphadenopathy', 'PERIOSTITIS', 'swollen lymphnodes', 'primary lesion is a papule or small ulcer,usually occurs in the mouth.', 'bone pain', 'plaques', 'MACULAR RASH', 'ulceration', 'papules', 'Condylomata lata']

Disease Name: Bejel, symptoms: ['lymphadenopathy', 'PERIOSTITIS', 'swollen lymphnodes', 'primary lesion is a papule or small ulcer,usually occurs in the mouth.', 'bone pain', 'plaques', 'MACULAR RASH', 'ulceration', 'papules', 'Condylomata lata'], Treatment: [{'medication': ['Penicillin/Penicillin V/Phenoxymethylpenicillin', 'Azithromycin ']}, 'It responds to parenteral penicillin and azithromycin'], Pathophysiology: Histopathological features of lesions resemble those of venereal syphilis. Likewise serological reactions are identical to those seen in venereal syphilis. The primary lesion, which is frequently a papule or small ulcer, usually occurs in the mouth, where it often goes undetected, or on the nipples of breastfeeding women nursing infected children. Secondary lesions, which are similar to those of venereal syphilis, include mucous patches on the buccal mucosa or lips, a generalized popular or macular rash, condylomata lata and generalized lymphadenopathy; painful periostitis may affect the legs and hands. Untreated, secondary lesions last for 6–9 months. The late (tertiary) stage is characterized by gummata of the nasopharynx that may result in destruction of the nose (gangosa), gummatous or plaque-like lesions in the skin, periostitis and bony gummata., Epidemiology:['prevalence of bejel is usually common in areas with a dry climatic condition.', 'variable', 'The World Health Organization (WHO) has worked with many countries to prevent this and other diseases, and the number of cases of bejel has been reduced somewhat. Widespread use of penicillin has been responsible for reducing the number of existing cases, but the only way to eliminate bejel is by improving living and sanitation conditions and through continuing health education. Since the disease is very contagious, public health personnel must seek out and treat infected children and their contacts in order to prevent additional case .'], Complications:['neurological disturbances', 'Cardiovascular disturbances', 'HIV infection and AIDS', 'tumors'], Diagnostics:['SEROLOGIC TEST'], Differential diagnosis:['Atopic dermatitis', 'Cutaneous Leishmaniasis', 'GENITAL HERPES', 'Syphilis', 'Yaws'], disease description:Endemic syphilis is a rare disease caused by Treponema pallidum subspecies endemicum. It occurs predominantly in the southern border of the Sahara desert and parts of the Middle East. It is still seen occasionally and usually in remote communities isolated from medical care. It is presumed to be spread by non-sexual contact.

Symptoms at 32 years: ['eyeball turns up and out (Bell phenomenon)', 'drooping of the mouth to the affected side', 'facial asymmetry', 'abscence of nasolabial fold', 'loss of wrinkles on forehead on affected side', 'wide palpabral fissure', 'ear pain', 'loss of taste', 'DROOLING OF SALIVA', 'unable to close his eye.', 'Tears flow down from the eye', 'noise intolerance']

Disease Name: Bell’s Palsy, symptoms: ['eyeball turns up and out (Bell phenomenon)', 'drooping of the mouth to the affected side', 'facial asymmetry', 'abscence of nasolabial fold', 'loss of wrinkles on forehead on affected side', 'wide palpabral fissure', 'ear pain', 'loss of taste', 'DROOLING OF SALIVA', 'unable to close his eye.', 'Tears flow down from the eye', 'noise intolerance'], Treatment: [{'medication': ['Prednisolone']}, 'Reassurance', 'Physiotherapy or massage of the facial muscles gives\npsychological support to the patient. It has not been\nshown to influence recovery. Active facial movements\nare encouraged when there is return of some movement\nto the facial muscles', 'Corticosteroids are the main treatment with a common regimen consisting of 60 mg to 80 mg a day for approximately 1 week. There is also some evidence stating corticosteroids and antivirals combined improved the outcome of BP compared with corticosteroids alone', 'Nerve decompression'], Pathophysiology: 1. Viral Infection. Most of the evidence supports the viral aetiology due to herpes simplex, herpes zoster or the Epstein–Barr virus. Other cranial nerves may also be involved in Bell palsy which is thus considered a part of the total picture of polyneuropathy. 2. Vascular Ischaemia. It may be primary or secondary. Primary ischaemia is induced by cold or emotional stress. Secondary ischaemia is the result of primary ischaemia which causes increased capillary permeability leading to exudation of fluid, oedema and compression of microcirculation of the nerve. 3. Hereditary. The fallopian canal is narrow because of hereditary predisposition and this makes the nerve susceptible to early compression with the slightest oedema. Ten per cent of the cases of Bell palsy have a positive family history.4. Autoimmune Disorder. T-lymphocyte changes have been observed., Epidemiology:['The annual incidence is 15 to 20 per 100,000 with 40,000 new cases each year', '85-90%of the patients recovers', "Bell's palsy cannot usually be prevented"], Complications:['visual loss', 'damage to the facial nerve', 'Abnormal growth of nerve fibers'], Diagnostics:['Complete Blood Count CBC', 'ELECTROMYOGRAPHY', 'Otoscopy', 'MRI', 'PHYSICAL EXAMINATION'], Differential diagnosis:['intracranial hemorrhage', 'Lyme disease', 'Meningioma', 'neurosyphilis', 'ramsay hunt syndrome', 'Sarcoidosis', 'stroke'], disease description:BELLS PALSY is defined as idiopathic, peripheral facial paralysis or paresis of acute onset. Both sexes are affected with equal frequency. Any age group may be affected though incidence rises with increasing age. A positive family history is present in 6–8% of patients. Risk of Bell palsy is more in diabetics (angiopathy) and pregnant women (retention of fluid).

Symptoms at 26 years old: ['dysphagia', 'painless, slow-growing mass that is firm or hard.', 'dyspnoea']

Disease Name: Benign Fibrous Histiocytoma, symptoms: ['dysphagia', 'painless, slow-growing mass that is firm or hard.', 'dyspnoea'], Treatment: ['The treatment of choice is radical excision of the tumour with adequate free margins'], Pathophysiology: Fibrous histiocytomas represent a classical entity for diagnosis. They are mesenchymal in origin. The tumor mimics various other forms of dermatofibromas and aggressive malignant fibrous histiocytoma. The tumor most frequently occurs in dermis but is also found in soft tissue and parenchymal organs. The BFH usually originates in sun exposed areas of skin and orbital tissues., Epidemiology:['Very rare', '1% of the benign bone tumors', 'good', 'Because exact histiocytoma causes are unclear, it may not be possible to fully prevent it from occurring. However, you can reduce the risk of many sarcomas by making healthy lifestyle choices, like eating a balanced diet, exercising regularly and avoiding tobacco products'], Complications:['recurrance'], Diagnostics:['ultrasound', 'MRI', 'X RAY', 'Dermoscopy'], Differential diagnosis:['dermatofibroma', 'dermatofibrosarcoma protuberans', 'Malignant fibrous histiocytoma', 'neurofibroma', 'Spindle cell lipoma'], disease description:Benign fibrous histiocytoma (BFH) is a mesenchymal tumor composed of fibroblasts and histiocytes arising in cutaneous and non cutaneous soft tissues [1]. Cutaneous BHF commonly originate in sun exposed areas of skin. Non cutaneous BFH comprises 1 % of all benign FH lesions [2]. Mean age of patients is 55 years with a range from 12 to 71 years. In the oral cavity the most common site is buccal mucosa and appears to originate from the tongue, gums, upper lip and bone ?

Woman aged 40 presenting symptoms such as ['Dysmenorrhoea', 'menorrhagia', 'Urinary Tract Infection', 'Irregular menstruation', 'infertility', 'hematuria', 'Abdominal Pain', 'increased frequency of urination']

Disease Name: Benign Gynecological Diseases, symptoms: ['Dysmenorrhoea', 'menorrhagia', 'Urinary Tract Infection', 'Irregular menstruation', 'infertility', 'hematuria', 'Abdominal Pain', 'increased frequency of urination'], Treatment: nan, Pathophysiology: nan, Epidemiology:nan, Complications:[], Diagnostics:nan, Differential diagnosis:[], disease description:Benign Gynaecological problems are important because they cause symptoms of offensive odour, irritation and sometimes pain. They are common problems and interfere with normal life. Many women often ignore their symptoms or try and treat themselves. There are many benign gynaecological conditions and they cannot all be covered in detail here. Some of these conditions include:Vaginal infectionsBenign ovarian cystsVulval Dystrophy

A 33-year-old patient experiencing ['difficulty in swallowing', 'Bulla formation', 'Oral ulcers', 'sore throat', 'Ocular symptoms']

Disease Name: Benign Mucous Membrane Pemphigoid, symptoms: ['difficulty in swallowing', 'Bulla formation', 'Oral ulcers', 'sore throat', 'Ocular symptoms'], Treatment: [{'medication': ['Triamcinolone ', 'Human normal immunoglobulin ', 'Betamethasone ', 'Clobetasol propionate ']}, 'For mild disease, corticosteroids and doxycycline plus nicotinamide\nFor severe disease, systemic immunosuppression\nTreatment of mucous membrane pemphigoid is similar to that for bullous pemphigoid. Topical or intralesional corticosteroids and a combination of oral doxycycline 100 mg orally twice a day and nicotinamide 500 mg orally 3 times a day may be useful for milder cases.\n\nSevere disease may require systemic immunosuppression with dapsone or prednisone or sometimes high-dose prednisone with immunosuppressants (eg, azathioprine, mycophenolate, cyclophosphamide, rituximab) and IV immune globulin.'], Pathophysiology: Circulating IgG and/or IgA autoantibodies against components of the basement membrane zone found in MMP patients’ serum indicate MMP is mediated by a humoral immune response. Loss of immunologic tolerance to structural proteins in the BMZ results in development of autoantibodies., Epidemiology:['about 2/million inhabitants/year in central Europe.', 'GOOD', 'NOT KNOWN'], Complications:['erosions', 'ulceration', 'Scarring'], Diagnostics:['Immunofluorescence', 'buccal examination'], Differential diagnosis:['Human herpesvirus 8 infection', 'Lichen Planus', 'severe erythema multiforme', 'Stevens–Johnson syndrome/toxic epidermal necrolysi'], disease description:Mucous membrane pemphigoid (MMP) is a heterogeneous group of chronic, autoimmune subepithelial blistering diseases which predominantly involves the mucous membranes and occasionally the skin. Mucosal lesions involve cheek, gingivae and palate. Although the oral and ocular mucosae are the most common sites affected, the nasopharynx, esophagus, larynx and anogenital region may also be involved. Lesion starts as a bulla filled with clear or haemorrhagic fluid which ruptures to form superficial ulceration covered with shaggy collapsed mucosa.

A woman, 40 years old, with ['abdominal swelling', 'increased micturition frequency', 'sense of pelvic pressure', 'menstrual irregularities', 'oedema', 'Abdominal Pain'] issues

Disease Name: Benign Ovarian Tumors, symptoms: ['abdominal swelling', 'increased micturition frequency', 'sense of pelvic pressure', 'menstrual irregularities', 'oedema', 'Abdominal Pain'], Treatment: ['Observation of selected cysts', 'Sometimes surgery (cystectomy or oophorectomy)\nMany functional cysts < 5 cm resolve without treatment; serial ultrasonography is done to document resolution. If asymptomatic women of reproductive age have simple, thin-walled cystic adnexal masses 5 to 8 cm (usually follicular) without characteristics of cancer, expectant management with repeated ultrasonography is appropriate. Benign tumors require treatment.\n\nMasses with radiographic characteristics of cancer are excised laparoscopically or by laparotomy.\n\nIf technically feasible, surgeons aim to preserve the ovaries (eg, by cystectomy).\n\nOophorectomy is done for the following:\n\nFibromas that cannot be removed by cystectomy\nCystadenomas\nCystic teratomas > 10 cm\nCysts that cannot be surgically removed separately from the ovary\nMost cysts that are detected in postmenopausal women and that are > 5 cm'], Pathophysiology: Ovarian tumours, even bilateral, do not generally affect the menstrual cycles. The only tumours causing menorrhagia are granulosa and theca cell tumours by virtue of their oestrogen hormone secretion. Similarly, masculinizing tumours cause amenorrhoea and virilization. Postmenopausal bleeding occurs in benign Brenner and feminizing tumours. The ovarian tumour placed in the uterovesical pouch anterior to the uterus and those impacted in the pouch of Douglas may cause increase in frequency of micturition and even retention. Pressure on the rectum is hardly ever noticed. Mammoth tumours such as mucinous tumours may cause dyspnoea and palpitation, and bilateral pitting oedema of the feet. Normally, benign ovarian tumours cause no abdominal pain and are comfortably placed in the abdominal cavity which is distensible. The mammoth tumour may however cause abdominal discomfort and difficulty in walking. Acute abdominal pain develops if the ovarian tumour undergoes torsion, rupture or haemorrhage. An infected dermoid cyst is likely to develop pain and fever. With torsion, the woman develops acute abdominal pain, vomiting and at times low-grade fever. The patient may be in shock, with thready pulse. The abdomen is distended, and moves poorly with respiration. The cyst is tense and tender. Immediate laparotomy is required to remove the tumour. The germ cell tumours occurring in adolescent and young women grow rapidly and cause abdominal pain, which may be the first symptom noticed by these young girls., Epidemiology:['68.6% in perimenopausal and 31.4% in postmenopausal women', 'COMMON', 'GOOD', 'AVOID SMOKING \nEAT HEALTHY DIET \nREGULAR EXERCISE'], Complications:['MALIGNANCY'], Diagnostics:['CA 125', 'HCG', 'CT SCAN', 'USG', 'BIMANUAL EXAMINATION'], Differential diagnosis:['Brenner tumour', 'dermoid cyst', 'ectopic pregnancy', 'ENDOMETRITIS', 'FIBROID UTERUS', 'Fibroma', 'mucinous cystadenoma', 'OVARIAN CANCER', 'Ovarian Cyst', 'PID', 'TUBO OVARIAN ABSCESS'], disease description:Although benign ovarian cysts frequently produce enormous tumours, they cause relatively few symptoms. Indeed, in innocent ovarian tumours, the patient’s attention is first directed to the abdominal swelling. Benign ovarian tumors usually grow slowly and rarely become malignant. They include the following:Benign cystic teratomas: These tumors are also called dermoid cysts because although derived from all 3 germ cell layers, they consist mainly of ectodermal tissue.Fibromas: These slow-growing connective tissue tumors are usually < 7 cm in diameter.Cystadenomas: These tumors are most commonly serous or mucinous.

Suffering from ['nocturia', 'urinary hesitancy', 'Urinary Tract Infection', 'urinary urgency', 'POOR FLOW OF URINE', 'INTERMITTENT STREAM', 'DRIBBLING', 'SENSATION OF POOR BLADDER EMPTYING', 'URGE INCONTINENCE', 'NOCTURNAL INCONTINENCE', 'increased frequency of urination'] at 50

Disease Name: Benign Prostatic Hyperplasia, symptoms: ['nocturia', 'urinary hesitancy', 'Urinary Tract Infection', 'urinary urgency', 'POOR FLOW OF URINE', 'INTERMITTENT STREAM', 'DRIBBLING', 'SENSATION OF POOR BLADDER EMPTYING', 'URGE INCONTINENCE', 'NOCTURNAL INCONTINENCE', 'increased frequency of urination'], Treatment: [{'medication': ['Finasteride ', 'Tamsulosin ', 'paracetamol']}, 'Lifestyle Changes\nA health care provider may recommend lifestyle changes for men whose symptoms are mild or slightly bothersome. Lifestyle changes can include\n\nreducing intake of liquids, particularly before going out in public or before periods of sleep\navoiding or reducing intake of caffeinated beverages and alcohol\navoiding or monitoring the use of medications such as decongestants, antihistamines, antidepressants, and diuretics', 'Transurethral needle ablation. This procedure uses heat generated by radiofrequency energy to destroy prostate tissue. A urologist inserts a cystoscope through the urethra to the prostate. A urologist then inserts small needles through the end of the cystoscope into the prostate. The needles send radiofrequency energy that heats and destroys selected portions of prostate tissue.\n\nTransurethral microwave thermotherapy. This procedure uses microwaves to destroy prostate tissue. A urologist inserts a catheter through the urethra to the prostate, and a device called an antenna sends microwaves through the catheter to heat selected portions of the prostate. The temperature becomes high enough inside the prostate to destroy enlarged tissue. \n\nHigh-intensity focused ultrasound. For this procedure, a urologist inserts a special ultrasound probe into the rectum, near the prostate. Ultrasound waves from the probe heat and destroy enlarged prostate tissue.\n\nTransurethral electrovaporization. For this procedure, a urologist inserts a tubelike instrument called a resectoscope through the urethra to reach the prostate. An electrode attached to the resectoscope moves across the surface of the prostate and transmits an electric current that vaporizes prostate tissue. \n\nWater-induced thermotherapy. This procedure uses heated water to destroy prostate tissue. A urologist inserts a catheter into the urethra so that a treatment balloon rests in the middle of the prostate.\n\nProstatic stent insertion. This procedure involves a urologist inserting a small device called a prostatic stent through the urethra to the area narrowed by the enlarged prostate.', 'Alpha blockers. These medications relax the smooth muscles of the prostate and bladder neck to improve urine flow and reduce bladder blockage:\n\nterazosin (Hytrin)\ndoxazosin (Cardura)\ntamsulosin (Flomax)\nalfuzosin (Uroxatral)\nsilodosin (Rapaflo)\nPhosphodiesterase-5 inhibitors. Urologists prescribe these medications mainly for erectile dysfunction. Tadalafil (Cialis) belongs to this class of medications and can reduce lower urinary tract symptoms by relaxing smooth muscles in the lower urinary tract. Researchers are working to determine the role of erectile dysfunction drugs in the long-term treatment of benign prostatic hyperplasia.\n\n5-alpha reductase inhibitors. These medications block the production of DHT, which accumulates in the prostate and may cause prostate growth:\n\nfinasteride (Proscar)\ndutasteride (Avodart)\nThese medications can prevent progression of prostate growth or actually shrink the prostate in some men. Finasteride and dutasteride act more slowly than alpha blockers and are useful for only moderately enlarged prostates.\n\nCombination medications. Several studies, such as the Medical Therapy of Prostatic Symptoms (MTOPS) study, have shown that combining two classes of medications, instead of using just one, can more effectively improve symptoms, urinary flow, and quality of life. The combinations include\n\nfinasteride and doxazosin\ndutasteride and tamsulosin (Jalyn), a combination of both medications that is available in a single tablet\nalpha blockers and antimuscarinics', 'Surgery to remove enlarged prostate tissue includes\n\ntransurethral resection of the prostate (TURP)\nlaser surgery\nopen prostatectomy\ntransurethral incision of the prostate (TUIP)\n\n\nTURP. With TURP, a urologist inserts a resectoscope through the urethra to reach the prostate and cuts pieces of enlarged prostate tissue with a wire loop. Special fluid carries the tissue pieces into the bladder, and the urologist flushes them out at the end of the procedure. TURP is the most common surgery for benign prostatic hyperplasia and considered the gold standard for treating blockage of the urethra due to benign prostatic hyperplasia.\n\nLaser surgery. With this surgery, a urologist uses a high-energy laser to destroy prostate tissue. The urologist uses a cystoscope to pass a laser fiber through the urethra into the prostate. The laser destroys the enlarged tissue.\n\nOpen prostatectomy. In an open prostatectomy, a urologist makes an incision, or cut, through the skin to reach the prostate. The urologist can remove all or part of the prostate through the incision. This surgery is used most often when the prostate is greatly enlarged, complications occur, or the bladder is damaged and needs repair.\n\nTUIP. A TUIP is a surgical procedure to widen the urethra. During a TUIP, the urologist inserts a cystoscope and an instrument that uses an electric current or a laser beam through the urethra to reach the prostate. The urologist widens the urethra by making a few small cuts in the prostate and in the bladder neck.'], Pathophysiology: BPH affects both glandular epithelium and connective tissue stroma to variable degrees. These changes are similar to those occurring in breast dysplasia , in which adenosis, epitheliosis and stromal proliferation are seen in differing proportions. BPH typically affects the submucous group of glands in the transitional zone, forming a nodular enlargement. Eventually, this overgrowth compresses the PZ glands into a false capsule and causes the appearance of the typical ‘lateral’ lobes. When BPH affects the subcervical CZ glands, a ‘middle’ lobe develops that projects up into the bladder within the internal sphincter. Sometimes, both lateral lobes also project into the bladder, so that when viewed from within, the sides and back of the internal urinary meatus are surrounded by an intravesical prostatic collar. Effects of benign prostatic hyperplasia It is important to realise that the relationship between anatomical prostatic enlargement, lower urinary tract symptoms (LUTS) and urodynamic evidence of bladder outflow obstruction (BOO) is complex. Pathophysiologically, BOO may be caused in part by increased smooth muscle tone, which is under the control of a-adrenergic agonists.Anatomically, the effects are as follows:  Urethra. The prostatic urethra is lengthened, sometimes to twice its normal length, but it is not narrowed anatomically. The normal posterior curve may be so exaggerated that it requires a curved catheter to negotiate it. When only one lateral lobe is enlarged, distortion of the prostatic urethra occurs. Bladder. If BPH causes BOO, the musculature of the bladder hypertrophies to overcome the obstruction and appears trabeculated. Significant BPH is associated with increased blood flow, and the resultant veins at the base of the bladder are apt to cause haematuria. ->Lower urinary tract symptoms ->Bladder outflow obstruction, Epidemiology:['10 million cases per year INDIA', '8% in the fourth decade of life, 50% in the sixth decade of life, and 80% in the ninth decade of life', 'GOOD', 'Regular exercise and maintaining a healthy weight can reduce the risk of developing BPH'], Complications:['BLADDER STONE', 'incomplete bladder emptying'], Diagnostics:['URINE R/M', 'USG ABDOMEN(W/A)', 'MRI', 'SERUM PROSTATE SPECIFIC ANTIGEN(PSA)', 'SERUM PROSTATE SPECIFIC ANTIGEN(PSA)', 'URINE FLOW RATE', 'TRANSRECTAL USG', 'CYSTOSCOPY', 'CYSTOSCOPY'], Differential diagnosis:['Bladder cancer', 'CARCINOMA PROSTATE', 'INTERSTITIAL CYSTITIS', 'neurogenic bladder disorders', 'PROSTATIC CALCULI', 'URETHRAL STRICTURE', 'Urinary Tract Infection'], disease description:Benign prostatic hyperplasia (BPH) — also called prostate gland enlargement — is a common condition as men get older. An enlarged prostate gland can cause uncomfortable urinary symptoms, such as blocking the flow of urine out of the bladder. It can also cause bladder, urinary tract or kidney problemsHormones Serum testosterone levels slowly but significantly decrease with advancing age; however, levels of oestrogenic steroids are not decreased equally. According to this theory, the prostate enlarges because of increased oestrogenic effects. It is likely that the secretion of intermediate peptide growth factors plays a part in the development of BPH.

Experiencing ['FATTY MASS AROUND NECK', 'DEFORMITY', 'fatty mass'] at 50 years

Disease Name: Benign Symmetrical Lipomatosis, symptoms: ['FATTY MASS AROUND NECK', 'DEFORMITY', 'fatty mass'], Treatment: ['Fibrate has been claimed to stop the growth \nor even reduce the volume of fatty masses in BSL patients', 'lipectomy and liposuction'], Pathophysiology: While many theories on the pathogenesis of BSL exist, a role for brown fat in BSL has garnered attention. Although, grossly and histologically, the accumulated adipose tissue in BSL is indistinguishable from mature fat, ultrastructural analysis of adipose tissue deposits in BSL suggests that it resembles brown fat. Further support for the role of brown fat in BSL came from another study that demonstrated mRNA expression of brown adipose tissue-specific uncoupling protein-1 (UCP-1) in a lipoma of a patient with BSL, but not in the normal subcutaneous fat from the same patient. Brown fat hypertrophy has been proposed to result from functional sympathetic denervation, or from alterations in the synthesis of intracellular cyclic adenosine monophosphate (cAMP) under noradrenergic stimulation. Lipomatous tissue in BSL consists of small adipocytes with no atypical features and a slight increase in vascular and fibrous elements. The lipomas are typically not encapsulated and may infiltrate across fasciomuscular and neurovascular planes. Genetic alternations in mitochondrial DNA have been demonstrated in BSL patients. Most reported BSL cases have been sporadic, although a very small number of familial cases exist for which autosomal recessive inheritance has been proposed., Epidemiology:['less than 300 cases reported in the literature', 'variable', 'The cause of the disease remains unknown, but its incidence strongly correlates with alcohol use disorder; abstinence from alcohol prevents disease progression'], Complications:['nerve compression'], Diagnostics:['MRI', 'CHEST X RAY'], Differential diagnosis:['Dercum disease', 'Liposarcoma', 'Neurofibromatosis'], disease description:Benign symmetrical lipomatosis (BSL) is an uncommon condition characterized by multiple, symmetrical, unencapsulated fatty tissue deposits involving multiple areas of the body, particularly the neck, shoulder girdle and the proximal upper and lower extremities.

Symptoms reported at the age of 53: ['polypoid, cauliflower-like growth of granulation tissue on conjunctiva', 'resemble the cocks comb type of conjunctival tubercular lesion', 'Lacrimation', 'Eye irritation', 'FOREIGN BODY SENSATION IN EYE']

Disease Name: Benign Tumours Of Conjunctiva, symptoms: ['polypoid, cauliflower-like growth of granulation tissue on conjunctiva', 'resemble the cocks comb type of conjunctival tubercular lesion', 'Lacrimation', 'Eye irritation', 'FOREIGN BODY SENSATION IN EYE'], Treatment: ['COMPLETE SURGICAL EXCISION'], Pathophysiology: Neoplasms can arise in the conjunctiva from both its epithelial and stromal structures. These are similar clinically and histopathologically to tumors that arise from other mucous membranes in the body. However, unlike other mucous membranes in the body, the conjunctiva is partially exposed to sunlight, which may be a factor in the development of some tumors. Similarly, the cornea can develop epithelial tumors, but corneal stromal tumors are uncommon., Epidemiology:['fair', 'Since the sun is a risk factor, the use of glasses with filters can help prevent some tumours.\n\nAlthough most conjunctival tumours are benign, some of them can be premalignant (precursors to malignancy). Undergoing regular ophthalmic examinations or visiting an ophthalmologist as soon as a new lesion appears are the best ways of detecting them early.'], Complications:['AMPUTATION'], Diagnostics:['CT', 'Incisional biopsy'], Differential diagnosis:['BACILLARY ANGIOMATOSIS', 'HEMANGIOMA', 'Lymphangioma', 'papilloma', 'PINGUECULA', 'Pterygium', 'Subconjunctival hemorrhages'], disease description:1. Simple granuloma. It consists of an extensive polypoid, cauliflower-like growth of granulation tissue. Simple granulomas are common following squint surgery, as foreign body granuloma and following inadequately scraped chalazion. ¦¦Treatment consists of complete surgical removal. 2. Papilloma. It is a benign polypoid tumour usually occurring at inner canthus, fornices or limbus. It may resemble the cocks comb type of conjunctival tubercular lesion. It has a tendency to undergo malignant change and hence needs complete excision. 3. Fibroma. It is a rare soft or hard polypoid growth usually occurring in lower fornix.Diagnosis is generally clinical.

A 52-year-old with ['wheezing', 'chest pain', 'hemoptysis', 'dyspnea']

Disease Name: Benign Tumours Of Lung , symptoms: ['wheezing', 'chest pain', 'hemoptysis', 'dyspnea'], Treatment: ['In many cases, doctor may simply observe a suspicious lung nodule with multiple chest X-rays over several years. However, your doctor may suggest a biopsy or removal of an entire nodule in situations like these:\n\nYou are a smoker and the nodule is large.\nYou have symptoms.\nA scan suggests the nodule might be cancerous.\nThe nodule has grown.\nA biopsy can often be done with small incisions and a short hospital stay. If your nodule is benign, you will not need any further treatment, except to manage any underlying problems or complications related to the nodule such as pneumonia or an obstruction.'], Pathophysiology: Since many tumors comes under this entity specific pathophysiology is difficult to explain.Here are some types of- BENIGN TUMOURS OF LUNGHamartomas are the most common type of benign lung tumor and the third most common cause of solitary pulmonary nodules. These firm marble-like tumors are made up of tissue from the lung's lining as well as tissue such as fat and cartilage. They are usually located in the periphery of the lung.Bronchial adenomas make up about half of all benign lung tumors. They are a diverse group of tumors that arise from mucous glands and ducts of the windpipe or large airways of the lung. A mucous gland adenoma is an example of a true benign bronchial adenoma.Rare neoplasms may include chondromas, fibromas, or lipomas -- benign tumors made up of connective tissue or fatty tissue , Epidemiology:['At least 60% of pulmonary nodules seen on chest X-rays turn out to be benign', 'good', "There's no sure way to prevent lung cancer, but you can reduce your risk if you:\n\n1. Don't smoke - If you've never smoked, don't start. Talk to your children about not smoking so that they can understand how to avoid this major risk factor for lung cancer.\n\n2. Stop smoking. Stop smoking now. Quitting reduces your risk of lung cancer, even if you've smoked for years.\n\n3. Avoid secondhand smoke. If you live or work with a smoker, urge him or her to quit. At the very least, ask him or her to smoke outside. \n\n4. Test your home for radon. Have the radon levels in your home checked, especially if you live in an area where radon is known to be a problem.\n\n5.Avoid carcinogens at work. Take precautions to protect yourself from exposure to toxic chemicals at work. \n\n6. Eat a diet full of fruits and vegetables. Choose a healthy diet with a variety of fruits and vegetables. \n\n7. Exercise most days of the week. If you don't exercise regularly, start out slowly. Try to exercise most days of the week."], Complications:['Atelectasis', 'PNEUMONIA', 'Recurrent infection', 'hemoptysis', 'cough with sputum'], Diagnostics:['PET SCAN', 'X RAY CHEST', 'CT', 'BRONCHOSCOPY', 'CT GUIDED BIOPSY'], Differential diagnosis:['granular cell tumour', 'Hamartoma', 'leiomyoma', 'lipoma', 'neurofibroma', 'Papillomas: Squamous cell papilloma and verruca vu', 'PRIMARY LUNG CANCER'], disease description:A benign lung tumor is an abnormal growth of tissue that serves no purpose and is found not to be cancerous. Benign lung tumors may grow from many different structures in the lung.Benign lung nodules and tumors usually cause no symptoms. This is why they are almost always found accidentally on a chest X-ray or CT scan.The causes of benign lung tumors and nodules are poorly understood. But in general, they often result from problems like these:Inflammation from infections such as:An infectious fungus (histoplasmosis, coccidioidomycosis, cryptococcosis, or aspergillosis, for example)Tuberculosis (TB)A lung abscessRound pneumonia (rare in adults)

At 27, dealing with ['Tenderness', 'swelling at the base of thumb', 'pain at base of thumb']

Disease Name: Bennett's Fracture, symptoms: ['Tenderness', 'swelling at the base of thumb', 'pain at base of thumb'], Treatment: ['1- Accurate reduction and restoration of the smooth\njoint surface\n2- Closed reduction and percutaneous K-wire\nfixation\n3- Open reduction and internal fixation', 'Surgical treatment of Bennett fractures is varied but generally consists of either closed reduction with percutaneous pinning or open reduction with either pins or interfragmentary screws. All methods of fixation have been shown to be effective in case reviews and series. Treating with closed reduction with intermetacarpal fixation from the first to the second metacarpal and/or to the trapezium is usually effective in reducing the first metacarpal shaft subluxation. If it is decided to treat this fracture with open reduction, it is most commonly performed through a Wagner incisio'], Pathophysiology: The fracture pattern is distinct. The base of the first metacarpal is fractured with intraarticular extension due to the palmar ulnar fragment of the first metacarpal held in place by its ligamentous attachment to the trapezium (known as the anterior oblique ligament) during the axial loading with the rest of the metacarpal moving in the opposite direction and the main fracture line occurring along this point of weakness. Due to this fracture, the first metacarpal shaft subluxes dorsally, proximally, and radially due to the pull of the abductor pollicis longus, extensor pollicis longus, extensor pollicis brevis, and the adductor pollicus brevis, which remain attached to the fracture fragment., Epidemiology:["The overall incidence of Bennett's fracture is 1.4%", 'good', 'Get enough calcium and vitamin D and eat a well balanced diet.\nEngage in regular exercise.\nEat foods that are good for bone health, such as fruits and vegetables.\nAvoid smoking and limit alcohol to 2-3 drinks per day.'], Complications:['Osteoarthritis'], Diagnostics:['X RAY AP VIEWS', 'X RAY', 'x ray lateral view'], Differential diagnosis:["ROLANDO'S FRACTURE"], disease description:It is an oblique intra-articular fracture of the base of the first metacarpal with subluxation or dislocation of the metacarpal. It is sustained as a result of a longitudinal force applied to the thumb. Bennett fracture is the most common fracture involving the base of the thumb. This fracture refers to an intraarticular fracture that separates the palmar ulnar aspect of the first metacarpal base from the remaining first metacarpal.The injury is typically caused by axial loading on a partially flexed metacarpal and may be associated with other carpal bone fractures or ligament injuries.Radiographs are essential in the evaluation of these injuries and in helping to plan a surgical approach for reduction, as these fractures are considered unstable. The surgical treatment is varied for these fractures. It may consist of closed reduction with percutaneous pinning or open reduction with either pins or inter-fragment pinning. If there is a good alignment of the fracture fragments at postsurgical fixation, clinical outcomes are generally good.

A 28-year-old patient experiencing ['loss of foveal contour', 'metamorphopsia', 'Hyphema', 'Central scotoma', 'visual field defects', 'VISION DEFICITS']

Disease Name: Berlins Edema, symptoms: ['loss of foveal contour', 'metamorphopsia', 'Hyphema', 'Central scotoma', 'visual field defects', 'VISION DEFICITS'], Treatment: [{'medication': ['Nepafenac ']}, 'Expectant – resolution within weeks to months', 'There is no approved or commonly used medical treatment for commotio retinae. However, in cases that do not resolve spontaneously, high dose IV steroids have been anecdotally shown to reduce retinal swelling and improve visual acuity'], Pathophysiology: The pathogenesis of Berlin's edema is uncertain; but one possible factor is breakdown of the blood-retinal barrier. Berlin initially postulated that areas of retinal opacification or whitening corresponded to regions of extracellular edema in the neurosensory retina. However, this proved controversial in the years that followed as there were some who believed that the underlying mechanism was secondary to intracellular edema . Photoreceptor outer segment disruption was another proposed etiology . In both experimental models and in vivo studies, the primary injury was found to occur at the level of the photoreceptor outer segments. These regions of outer segment disruption corresponded to the areas of whitening visualized on exam, and were thought to be secondary to increased scattering of light by photoreceptor disruption and disorientation., Epidemiology:['approximately 4.9 per 1,000 individuals', 'good', 'Primary prevention includes protective eye wear for athletes. 2-mm polycarbonate lenses in normal streetwear is recommended for low impact sports. Impact resistant sports frames with a 3-mm polycarbonate lens are recommended for moderate to high impact sports. Face masks attached to a helmet should be used in the highest risk sports including ice and field hockey, football, baseball, and lacrosse'], Complications:['cataract formation', 'retinal tear'], Diagnostics:['Optical coherence tomography (OCT)', 'Optical coherence tomography (OCT)', 'ELECTRORETINOGRAPHY', 'Fundus examination'], Differential diagnosis:['macular hole', 'RETINAL DETACHMENT', 'retinal ischemia'], disease description:Commotio Retinae or Berlin’s Oedema is grey-white discolouration of the retina due to disruption of outer segment photoreceptor layer following blunt trauma. This is caused due to contrecoup injury. Shock waves caused due to impact traverses the fluid- filled eye and then strike retina.Commotio retinae may involve any part of retina and may be accompanied by choroidal rupture or retinal haemorrhage. Macular oedema reduces central vision, but vision usually improves as the oedema resolves. After an acute attack of oedema, there may be scarring of retina with pigment dispersal. Vision may be acutely reduced or normal depending upon whether the macula is involved or not. It may permanently reduce vision if the fovea centralis is involved.The diagnosis of commotio retinae is clinical and relies on funduscopic examination.

Symptoms at 27 years: ['nasal congestion', 'Polyps', 'anosmia', 'WATERY DISCHARGE', 'headache']

Disease Name: Bilateral Ethmoidal Polypi, symptoms: ['nasal congestion', 'Polyps', 'anosmia', 'WATERY DISCHARGE', 'headache'], Treatment: ['Early polypoidal changes with oedematous mucosa\nmay revert to normal with antihistaminics and control\nof allergy.\n2. A short course of steroids may prove useful in case of\npeople who cannot tolerate antihistaminics', 'functional endoscopic sinus surgery (FESS).,Polypectomy,Intranasal ethmoidectomy,Extranasal ethmoidectomy,Transantral ethmoidectomy'], Pathophysiology: Pathogenesis involves nasal mucosa, particularly in the region of middle meatus and turbinate, becomes oedematous due to collection of extracellular fluid causing polypoidal change. Polypi which are sessile in the beginning become pedunculated due to gravity and excessive sneezing. In early stages, surface of nasal polypi is covered by ciliated columnar epithelium like that of normal nasal mucosa but later it undergoes a metaplastic change to transitional and squamous type on exposure to atmospheric irritation. Submucosa shows large intercellular spaces filled with serous fluid. There is also infiltration with eosinophils and round cells., Epidemiology:['It is\ncommon in Westernized societies, with up to one third of the\npopulation affected', '1-4%.', 'good', 'Manage allergies and asthma\nAvoid nasal irritants\nPractice good hygiene\nHumidify your home\nUse a nasal rinse'], Complications:['obstructive sleep apnea', 'sinusitis', 'Asthma like symptoms'], Diagnostics:['MRI', 'CT SCAN', 'HISTOLOGIC EXAMINATION', 'NASAL EXAMINATION'], Differential diagnosis:['acute rhinitis', 'allergic rhinitis', 'chronic rhinosinusitis', 'CYSTIC FIBROSIS', 'Granulomatosis with polyangiitis', 'nasal polyps', 'rhinitis medicamentosa', 'septal abscess'], disease description:Ethmoidal polyps are multiple, bilateral, painless, pearly white, grape like masses arising from the ethmoidal air cells. Ethmoidal air cells are multiple air cells present on medial to the eyes.Aetiology of nasal polypi is very complex and not wellunderstood. They may arise in inflammatory conditions of nasal mucosa (rhinosinusitis), disorders of ciliary motility or abnormal composition of nasal mucus (cystic fibrosis).

Individual, 33 years old, with ['Speech Difficulties', 'difficulty in opening mouth', 'obstructive sleep apnea', 'DEFORMITY']

Disease Name: Bilateral Tm Joint Ankylosis, symptoms: ['Speech Difficulties', 'difficulty in opening mouth', 'obstructive sleep apnea', 'DEFORMITY'], Treatment: ['Post-operative early physiotherapy', 'The treatment plan included bilateral condylectomy with coronoidectomy through a combination of endaural and rhytidectomy incision and interpositional grafting with temporalis myofascial flap. Reconstruction of the TMJ was done with specially designed stainless steel partial condylar prosthesis.'], Pathophysiology: Temperomandibular joint ankylosis can be defined as an ‘inability to open the mouth due to either a fibrous or bony union between the head of the condyle and the glenoid fossa.Any condition that gives rise to osseous or fibrous adhesion between the surfaces of the temporomandibular joint is a true ankylosis as compared to false ankylosis which results from pathologic condition not directly related to the joint., Epidemiology:['unilateral TMJ ankylosis (74%) was more prevalent as compared to bilateral TMJ ankylosis (26%)', 'variable', 'NOT KNOWN. BUT PREVENTION OF TRAUMA IN EARLY CHILDHOOD IS IMPORTANT.'], Complications:['deformity of face', 'Speech Difficulties', 'Feeding Difficulty'], Diagnostics:['CT', 'CT SCAN'], Differential diagnosis:['Giant cell arteritis', "lyme's disease", 'migraine', 'Trauma'], disease description:Ankylosis is the fusion of joint surfaces by bone or fibrous tissue. Temporomandibular joint (TMJ) ankylosis may cause difficulty in chewing, speech, oral hygiene maintenance, and esthetic disfigurement. This condition can be unilateral or bilateral, complete or incomplete. TMJ ankylosis may occur due to various factors, such as trauma, local and systemic inflammatory conditions, neoplasms, and TMJ infection. Trauma due to forceps delivery causing bilateral TMJ ankylosis is rare. We report a case with difficulty in mouth opening, eating, speech, oral hygiene maintenance, facial disfigurement as a result of bilateral TMJ ankylosis caused due to trauma by forceps delivery. This report implores upon preventing such disabling complications due to forceps delivery.Classification of TMJ Ankylosis based on Joint mobility by Sawhney CP Type Features Type I Visible and significantly deformed head of the condylar process, with the fibro-adhesions making TMJ movement impossible Type II Consolidation of the deformed head of the condylar process and articular surface occurs mostly at the edges and in the anterior and posterior parts of the structures, and the medial part of the surface of the condylar head remain undamaged Type III The ankylotic mass involves the mandibular ramus and zygomatic arch; an atrophic and displaced fragment of the anterior part of the condylar head is in a medial location Type IV TMJ is completely obliterated by bony ankylotic mass growing between the mandibular ramus and cranial base

At the age of 41, symptoms like ['nausea', 'vomiting', 'fever', 'biliary pain', 'appendicitis']

Disease Name: Biliary Ascariasis, symptoms: ['nausea', 'vomiting', 'fever', 'biliary pain', 'appendicitis'], Treatment: [{'medication': ['Albendazole ']}, 'The patients with HBA are to be hospitalized without delay because in them the worm load is usually high. In addition, co-existing mechanical intestinal obstruction are common (especially in young children) but may also follow deworming during or after institution of treatment. It must be remembered that excretion products of the worms can cause marked bowel contraction.[81] Similarly, associated acute pancreatitis may complicate the clinical course and there is a definite mortality risk in those with hemorrhagic pancreatitis.\n\nPure biliary ascariasis have a negligible mortality <2%. The principles of treatment of biliary ascariasis are:\nTreatment of cholangitis or cholecystitis by conservative means.\nOral administration of anthelminthics, which allows the paralyzed worms to be expelled by normal intestinal activity.\nEndoscopic and Surgical treatment.'], Pathophysiology: Man is infected by ingesting food, raw vegetables or water contaminated by mature ova. Children are mostly infected by contaminated fingers, toys and soil. To complete their life cycle, the worms leave the human body as eggs and re-infect it as larvae. The eggs hatch in the duodenum after being stimulated by gastric juice and the resultant rhabditiform larvae migrate to the cecum. They penetrate the epithelium to reach the portal vein and then the liver. Some will migrate through the hepatic veins or the lymphatics to be carried to heart and lungs. There they cross the capillary wall into the alveolar space and reach the bronchial tree. They molt twice during this journey and ascend to the larynx and hypopharynx before being swallowed .In the upper gastrointestinal tract, they attain sexual maturity by 2-3 months and molt again to become adult worms. The adult worm resides in the jejunum as a facultative anaerobic organism, with a life-span of 6-18 months. Since adult worms do not multiply inside their host, manifestation of clinical disease depends on their absolute number. Female worms are bigger; approximately 20-40 cm and can produce a large number of eggs daily (~240,000/female) which pass out in the feces. in the soil the fertilized eggs require 10-15 days to become infectious. Clay soil favors their survival. The eggs are resistant to cold weather, chemical water purifiers, disinfectants and can remain viable and infectious for up to 10 year smaking eradication difficult., Epidemiology:['0.31% in male patients and 0.55% in female patients)', "Twenty-five per cent of the world's population is estimated to be infested (0.8–1.22 billion people)", 'variable', '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:['LIVER ABSCESS', 'strictures', 'empyema'], Diagnostics:['EOSINOPHILS - ABSOLUTE COUNT', 'STOOL CULTURE', 'MRCP', 'ultrasound', 'CT', 'CHEST X RAY', 'STOOL EXAMINATION'], Differential diagnosis:['cholangitis', 'EXTRAHEPATIC BILIARY ATRESIA', 'hepatitis', 'PRIMARY BILIARY CIRRHOSIS'], disease description:The roundworm Ascaris lumbricoides commonly infests the intestines of inhabitants of Asia, Africa and Central America. It may enter the biliary tree through the ampulla of Vater and cause biliary pain.Hepato-biliary ascariasis (HBA) is becoming a common entity now than in the past owing to the frequent usage of ultrasonograms and endoscopic diagnostic procedures in the clinical practice.

Person aged 29 dealing with ['jaundice', 'nausea', 'pruritus', 'fever', 'dyspepsia', 'Abdominal Pain']

Disease Name: Biliary Cystadenocarcinoma, symptoms: ['jaundice', 'nausea', 'pruritus', 'fever', 'dyspepsia', 'Abdominal Pain'], Treatment: ['Surgical removal of the tumor by complete excision is often the treatment of choice. The overall prognosis is considered better than for other malignant tumors of the liver.\n\tRight hepatic segmentectomy (segment V) with cholecystectomy.', 'treated by marsupialization, internal Roux-en-Y drainage, aspiration, sclerosis, or partial resection. All of these methods have been associated with high rates of complication, including sepsis, continued growth, and progress to malignancy. With total ablation, there are reports of lower rates of long-term complications.'], Pathophysiology: Cystadenocarcinomas arise from the intrahepatic bile duct and are composed of multiloculated mucin producing epithelial cells. Malignant polypoid tumors and associated mesenchymal “ovarilan-like” stroma are classically seen. , Epidemiology:['There is recognized increased female predilection.', 'The incidence of biliary cystadenomas is 1 in 20,000–100,000, while the risk of malignant transformation to adenocarcinoma has been reported to be as high as 20–23%', 'fair', 'The recommended management of suspicious liver cysts is complete surgical resection. Less invasive methods to include interval followup'], Complications:['intraabdominal abscess'], Diagnostics:['CECT Abdomen', 'CECT', 'ERCP', 'CT SCAN', 'CELIAC ANGIOGRAPHY'], Differential diagnosis:['CHOLANGIOCARCINOMA', 'hepatocellular carcinoma', 'HYDATID LIVER DISEASE', 'intraductal papillary mucinous adenoma', 'LIVER ABSCESS'], disease description:Biliary cystadenocarcinoma is a very rare cystic tumor that arises in the liver or, less frequently, in the extrahepatic biliary system. It has been shown to arise in congenital liver cysts, bile ducts, biliary cystadenoma, in the context of fibro-polycystic disease and in the hepatoduodenal ligament.

having ['jaundice', 'pruritus', 'Abdominal Pain'] at the age of 24

Disease Name: Biliary Papillomatosis, symptoms: ['jaundice', 'pruritus', 'Abdominal Pain'], Treatment: ['Due to the high risk of malignant transformation and the high rate of local recurrence of biliary papillomatosis, radical excision is typically the recommended treatment. When lesions are confined to a single hepatic lobe, as in the present case, partial hepatectomy is advocated', 'exploratory laparotomy using a left reverse L-shaped incision was performed.'], Pathophysiology: ?The pathogenesis of biliary papillomatosis remains to be elucidated, however bile stasis and recurrent infection induced by hepatolithiasis or clonorchiasis likely contribute to the chronic inflammation and subsequent mucosal changes that lead to biliary papillomatosis., Epidemiology:['more common in men (male-to-female ratio, 2:1).', '1.2 TO 1.36 / 100,000', 'The recurrence rate is estimated from 20% to 60%,', 'Not known'], Complications:['Malignant transformation'], Diagnostics:['ERCP', 'MRI', 'CT', 'USG'], Differential diagnosis:['Caroli disease', 'CHOLEDOCHAL CYST', 'hepatocellular carcinoma'], disease description:Biliary papillomatosis, or intraductal papillary neoplasm of the bile duct, is a rare disease of the biliary tract characterized by the distinctive papillary proliferation of bile duct epithelial cells.  The pathogenesis of biliary papillomatosis remains to be elucidated, however bile stasis and recurrent infection induced by hepatolithiasis or clonorchiasis likely contribute to the chronic inflammation and subsequent mucosal changes that lead to biliary papillomatosis. Although it is histologically categorized as benign, biliary papillomatosis should be considered to be a premalignant lesion, due to the fact that malignant transformation has been observed in 35% of cases at the time of presentation or at subsequent follow-up 

Person aged 26 with manifestations like ['conjunctivitis', 'Irritability', 'REDNESS OF EYE', 'lethargy', 'Loss of hair', 'Rashes', 'seizures', 'hypotonia', 'Periorificial facial dermatitis']

Disease Name: Biotin Deficiency, symptoms: ['conjunctivitis', 'Irritability', 'REDNESS OF EYE', 'lethargy', 'Loss of hair', 'Rashes', 'seizures', 'hypotonia', 'Periorificial facial dermatitis'], Treatment: [{'medication': ['BIOTIN (Vitamin B7)']}, 'Biotin deficiency management essentially means treating the cause. Lifelong treatment with biotin supplements is required in patients with genetic disorders disrupting biotin metabolism, such as holocarboxylase synthetase deficiency and biotinidase deficiency. If the deficiency is related to excess consumption of raw eggs, it should be stopped, and biotin replacement should ensue. Change anticonvulsants if the deficiency is because of the use of a particular anticonvulsant. Similarly, those on prolonged oral antibiotic therapy may benefit from biotin supplementation.\n\nOral biotin supplements have high bioavailability. Usually, a dose of 5 mg/day is given regardless of the etiology of biotin deficiency.'], Pathophysiology: Biotin (B7) has a key role in cellular energy metabolism, including ATP production and regulation of oxidative stress, since it is a crucial cofactor for five carboxylases that works for mitochondrial metabolism of glucose, fatty acids, and amino acids. Holocarboxylase synthetase plays a vital role in protein biotinylation, and protein biotinidase is essential for the release of biotin from biotinylated peptides.Current evidence shows a vital role of biotin in gene expression and chromatin structure. Approximately 2000 genes have been identified so far that are biotin-dependent. Biotin is attached to histones, and this histone biotinylation appears to work in transcriptional repression of genes and thus maintain genome stability, Epidemiology:['1 in 1, 37,000 and 1 in 1, 10,000 respectively.', 'good', 'have a balanced diet'], Complications:['candidiasis'], Diagnostics:['DNA analysis for mutation'], Differential diagnosis:['Hyperammonemia', 'inborn error of metabolism'], disease description:Biotin (vitamin H or vitamin B7) is a B-complex vitamin that acts as an essential coenzyme for five carboxylases: pyruvate carboxylase, 3-methylcrotonyl-CoA carboxylase, propionyl-CoA carboxylase, and coenzyme for acetyl-CoA carboxylases 1 and 2.These carboxylases help in several chemical processes in the cell, including gluconeogenesis, amino acid metabolism, and fatty acid synthesis.

At the age of 33, symptoms like ['SENSORINEURAL HEARING LOSS', 'Alopecia Areata', 'Ataxia', 'developmental delay', 'hair loss', 'Hearing loss', 'Skin rashes', 'difficulty in breathing', 'seizures', 'hypotonia']

Disease Name: Biotinidase Deficiency, symptoms: ['SENSORINEURAL HEARING LOSS', 'Alopecia Areata', 'Ataxia', 'developmental delay', 'hair loss', 'Hearing loss', 'Skin rashes', 'difficulty in breathing', 'seizures', 'hypotonia'], Treatment: [{'medication': ['BIOTIN (Vitamin B7)']}], Pathophysiology: Pathogenesis involves impaired biotinidase activity which results in biotin deficiency .The gene for biotinidase (BTD) is located on chromosome 3p25.1, Epidemiology:['1 per 137,400 population;', 'good', 'there are no known prevention methods'], Complications:['Ataxia', 'alopecia'], Diagnostics:['MRI Brain', 'SERUM LACTIC ACID LEVEL', 'serum biotinidase'], Differential diagnosis:['Bacterial infection', 'BIOTIN DEFICIENCY', 'fungal infections', 'Infantile spasm', 'Meningitis', 'Neuromyelitis Optica', 'Optic Atrophy', 'seborrheic dermatitis', 'Sensorineural deafness'], disease description:Biotinidase deficiency is an inherited disorder in which the body is unable to recycle the vitamin biotin. If this condition is not recognized and treated, its signs and symptoms typically appear within the first few months of life, although it can also become apparent later in childhood.

Individual aged 48 dealing with ['grandiosity', 'Difficulty in sleeping', 'hypomania', 'mania', 'loss of judgement & reasoning', 'HOPELESSNESS', 'elation', 'increased energy', 'worthlessness', 'DEPRESSION', 'Difficulty concentrating']

Disease Name: Bipolar Disorder, symptoms: ['grandiosity', 'Difficulty in sleeping', 'hypomania', 'mania', 'loss of judgement & reasoning', 'HOPELESSNESS', 'elation', 'increased energy', 'worthlessness', 'DEPRESSION', 'Difficulty concentrating'], Treatment: [{'medication': ['Valproic acid(sodium valproate)/ Divalproex Sodium', 'Lamotrigine ', 'Carbamazepine', 'Lithium carbonate ']}], Pathophysiology: Genetic predisposition to bipolar disorder is evident from family studies; the concordance rate for monozygotic twins approaches 80%. A number of risk genes that have been identified to date overlap with those conveying risk for other psychiatric disorders, such as schizophrenia and autism, implying some degree of shared pathophysiology. Replicated loci include the alpha subunit of the L-type calcium channel (CACNA1C), teneurin transmembrane protein 4 (ODZ4), ankryn 3 (ANK3), neurocan (NCAN), and tetratricopeptide repeat and ankyrin repeat containing 1 (TRANK1). No clear biomarkers have been identified, but there is evidence for circadian rhythm dysregulation and oxidative stress, mitochondrial, and endoplasmic reticulum abnormalities., Epidemiology:['~1.5% of the population', 'An estimated 4.4% of U.S. adults experience bipolar disorder at some time in their lives.', 'very poor, patient may attempt suicide', "To help prevent a manic episode, avoid triggers such as caffeine, alcohol or drug use, and stress. Exercise, eat a balanced diet, get a good night's sleep, and keep a consistent schedule. This can help reduce minor mood swings that can lead to more severe episodes of mania."], Complications:['conduct disorder', 'SUICIDAL TENDENCY'], Diagnostics:['HISTORY TAKING', 'PHYSICAL EXAMINATION'], Differential diagnosis:['hyperthyroidism', 'Hypothyroidism', "lyme's disease", 'Major depressive disorder', 'Multiple Sclerosis', 'neurosyphilis', 'Obsessive-compulsive disorder (OCD)', 'Schizophrenia', 'severe anxiety', 'systemic lupus erythematosus (SLE)', 'THYROTOXICOSIS'], disease description:Bipolar disorder is characterized by unpredictable swings in mood from mania (or hypomania) to depression. Some patients suffer only from recurrent attacks of mania, which in its pure form is associated with increased psychomotor activity; excessive social extroversion; decreased need for sleep; impulsivity and impaired judgment; and expansive, grandiose, and sometimes irritable mood . In severe mania, patients may experience delusions and paranoid thinking indistinguishable from schizophrenia. 

Experiencing ['headache', 'myalgia', 'sore throat', 'fever', 'Respiratory disturbance', 'diarrhea', 'nausea', 'vomiting'] at 27 years

Disease Name: Bird Flu, symptoms: ['headache', 'myalgia', 'sore throat', 'fever', 'Respiratory disturbance', 'diarrhea', 'nausea', 'vomiting'], Treatment: [{'medication': ['Rimantadine Hydrochloride ', 'Amantadine ', 'Oseltamivir ']}, 'In the hepatic lobes, enucleation must be the objective. The technique used should be personalised taking into account the placement and the patient in context.', 'Treatment must be surgical whenever possible, due to a potential malignant degeneration of these lesions. The technique chosen for bile duct sites is complete resection of the bile duct, associating cholecystectomy and reconstruction with hepatic-jejunostomy in Roux-en-Y.'], Pathophysiology: The binding of avian influenza viruses (AIVs) to human cells is mostly via specific receptors found more commonly in the respiratory tract. The pathophysiology of avian influenza and that of normal influenza are different. Avian influenza involves more of the lower airways than human influenza. This involvement is probably due to differences in the hemagglutinin protein and the types of sialic acid residues to which the protein binds. Avian viruses prefer sialic acid alpha (2-3) galactose, which, in humans, is found in the terminal bronchi and alveoli. But human viruses prefer sialic acid alpha (2-6) galactose, which appears on epithelial cells in the upper respiratory tract. Interestingly, the receptors preferred by most AIVs, especially H7N9, are also found in the human eye, which may explain the conjunctival symptoms often seen with AIV infection.Once the AIV has entered the host cell, replication may be prolonged relative to endemic human influenza viruses. In the 1997 H5N1 outbreak, the median time from infection to the detection of the virus was 6.5 days, and in some patients, no virus was detectable for up to 16 days.Host immune response plays a role in pathogenicity, as inflammatory markers appear to be higher in patients who experience a more severe disease course, and the presence of inflammatory cells in damaged alveoli in post-mortem patient evaluation seems to support this suggestion. The most common pathological organ failure in AIV-infected individuals is respiratory failure due to primary viral pneumonia, which appears to commonly be due to viral replication and host immune response producing diffuse alveolar damage as well as alveolar hemorrhage. There is some additional information in mouse studies that the virus may replicate and produce apoptosis in pre-Botzinger complex neurons, which are responsible for generating respiratory rhythm, and the damage caused to these neurons likely produces some of the ataxic breathing a respiratory collapse found in AIV infection., Epidemiology:['873 humans have been infected with H5N1 avian flu over the past 20 years, and 458 have died', 'True incidence is unknown at the present time. However, if individuals are infected, the current case-fatality rate for avian flu is thought to be greater than 50% in humans', 'fair', 'To Do : Wash your hands\nflu shot Not To Do : Avoid domesticated birds'], Complications:['death', 'PNEUMONIA', 'respiratory failure', 'kidney dysfunction'], Diagnostics:['Complete Blood Count CBC', 'Erythrocyte Sedimentation Rate (ESR)', 'Immunofluorescence', 'fluid culture'], Differential diagnosis:['Asthma', 'Bacterial pneumonia', 'Chronic Obstructive Pulmonary Disease', 'Pulmonary Embolism', 'Streptococcal infections'], disease description:Avian influenza or bird flu refers to the disease caused by infection with avian (bird) influenza (flu) Type A viruses. These viruses naturally spread among wild aquatic birds worldwide and can infect domestic poultry and other bird and animal species. Bird flu viruses do not normally infect humans.

Experiencing ['fatigue', 'hemolysis', 'jaundice', 'myoglobinuria', 'pale skin', 'seizures', 'stroke', 'Pain', 'cramping', 'dyspnea', 'splenomegaly'] at 46 years old

Disease Name: Bisphosphoglycerate Mutase Deficiency, symptoms: ['fatigue', 'hemolysis', 'jaundice', 'myoglobinuria', 'pale skin', 'seizures', 'stroke', 'Pain', 'cramping', 'dyspnea', 'splenomegaly'], Treatment: ['Treated with the protein synthesis inhibitor cycloheximide'], Pathophysiology: BPGM deficiency is a very rare disorder that results in reduced levels of 2,3-BPG.As a result, the oxygen affinity of hemoglobin is increased, causing a decrease in tissue oxygenation and, consequently, erythrocytosis. Only three families with BPGM deficiency have been described. Four mutations have been identified in BPGM. BPGM deficiency appears to be an autosomal recessive disorder, although some heterozygous individuals also display increased hemoglobin concentrations., Epidemiology:['variable', 'there are no known prevention methods'], Complications:['Hemolytic anemia'], Diagnostics:nan, Differential diagnosis:['autoimmune haemolytic anaemia', 'GLUCOSE-6-PHOSPHATE DEHYDOGENASE DEFICIENCY', 'Hemolytic Uremic Syndrome', 'paroxysmal nocturnal hemoglobinuria'], disease description:A rare, autosomal recessive, inherited disorder caused by mutation of the BPGM gene. It is characterized by hemolytic anemia and splenomegaly.

A 55-year-old patient with ['dysuria', 'difficulty in urinating', 'muscle pain', 'fever', 'Breathing difficulty', 'cough', 'seizures', 'liver damage']

Disease Name: Bk Virus Infection, symptoms: ['dysuria', 'difficulty in urinating', 'muscle pain', 'fever', 'Breathing difficulty', 'cough', 'seizures', 'liver damage'], Treatment: ['There is currently no specific anti-viral therapy to treat BKV-associated diseases. Indeed, the usual clinical approach consists of a gradual reduction of immunosuppression, guided by consecutive measurements of BKV presence in plasma by qRT-PCR'], Pathophysiology: Potential factors that contribute to the pathogenesis of BKVN may be a combination of (1) ineffective immune surveillance by the host T lymphocytes, (2) the absence of previous humoral immunity to BKV(3) molecular sequence variability of the virus, and (4) alloimmune activation These details have been reviewed elsewhere and are also discussed next.Occurrence of BKVN in renal transplant recipients as opposed to liver and heart transplant recipients unveils a potential role of alloimmune activation in renal grafts with BKV activation and frank nephritis. Awadalla et al. showed that the occurrence of BKVN correlates with a higher degree of HLA mismatches, which postulates the role of alloimmune activation. Investigators from Emory University showed using a mouse polyoma transplant model that polyoma viral nephritis occurs only in the presence of alloimmune activation. Thus, subclinical alloimmune activation in renal grafts may trigger BKV replication and nephritis and explains why this is specific to renal grafts., Epidemiology:['BKVN affects up to 10% of renal transplanted recipients, and results in graft loss in up to 50% of those affected.', '. The incidence of BKVN is 1–10% and graft loss occurs in from 10% to 80% of cases.', 'good', 'routine, regular screening posttransplantation to detect either BKV viruria or viremia. Patients who are persistently positive should undergo a reduction in immunosuppression with the aim of reducing viral replication and preventing the progression to BKV nephropathy (preemptive therapy).'], Complications:['graft loss'], Diagnostics:['kidney biopsy', 'PCR tests'], Differential diagnosis:['acute tubular necrosis(Kidney)', 'Cytomegalovirus (CMV)', 'interstitial nephritis', 'Urinary Tract Infection'], disease description:Poliomavirus BK virus (BKV) is highly infective, causing asymptomatic infections during childhood. After the initial infection, a stable state of latent infection is recognized in kidney tubular cells and the uroepithelium with negligible clinical consequences. BKV is an important risk factor for BKV-associated diseases, and, in particular, for BKV-associated nephropathy (BKVN) in renal transplanted recipients (RTRs).

Suffering from ['blue black pigmentation'] at 51

Disease Name: Black Heel And Palm, symptoms: ['blue black pigmentation'], Treatment: ['The condition is asymptomatic, and its importance lies in its \nresemblance to malignant melanoma. When in doubt as to the \ndiagnosis, carefully paring away the stratum corneum is generally \nsufficient to remove the pigment.'], Pathophysiology: Black heel occurs when the repeated shearing force of the epidermis sliding over the dermal papillae results in damage to the papillary dermal capillaries, resulting in intraepidermal haemorrhage. Pathology Extravasated erythrocytes may be found in the dermal papillae , but often the histological changes are limited to the stratum corneum, where amorphous yellow-brown material may be found in rounded collections having undergone transepidermal elimination. This material is often negative with Perls’ stain (which stains haemosiderin) but gives a positive benzidine reaction, showing that it is derived from haemoglobin, Epidemiology:nan, Complications:[], Diagnostics:['full thickness skin biopsy', 'Direct illumination-SLIT LAMP EXAMINATION'], Differential diagnosis:[], disease description:Pigmentation of the heel or palm secondary to extravasation of red blood cells.The condition results from shear–stress rupture of the papillary capillaries, for example during violent sport, particularly where repeated jumping and sudden stopping or twisting of the heel occurs. Similar circumstances explain the occurrence on the palm. Age Young adolescents may be more prone, in addition to athletes and sportspersons. Sex Either sex may be affected.

Symptoms at 18 years: ['Black piedra is characterized by the presence of firmly adherent, black, gritty, hard nodules on the hairs of the scalp, or less frequently of the beard, moustache or pubic area.']

Disease Name: Black Piedra, symptoms: ['Black piedra is characterized by the presence of firmly adherent, black, gritty, hard nodules on the hairs of the scalp, or less frequently of the beard, moustache or pubic area.'], Treatment: [{'medication': ['Terbinafine ']}, 'Shaving the head of all the hair is the best way to get rid of this fungal infection. However, this option may not be acceptable to females for aesthetic reasons.\n\nTopical antifungal agents in the form of cream or shampoos are effective; 2% ketoconazole or 2% miconazole shampoo applied once a week for three weeks is effective. Non-surfactant-based leave-on lotions are also an option. Ciclopirox (0.77%) lotion or 1 to 1.5% shampoo have also been used successfully.\n\nOlder treatments include benzoic acid compound (BPC) ointment or a 1 to 2000 solution of mercury perchloride act as antifungal preparations for application to the hair after shampooing.\n\nOral antifungals such as terbinafine and itraconazole have been used successfully in cases resistant to topical medications.', 'To prevent recurrence, \nantifungal preparations such as benzoic acid ointment compound \nBPC can be applied. Treatment success with terbinafi ne has been \nreported.'], Pathophysiology: Black piedra is characterized by the presence of firrmly adherent, black, gritty, hard nodules on the hairs of the scalp, or less frequently of the beard, moustache or pubic area. The nodules vary in size from microscopic to 1 mm or more in diameter, and their thickness often tapers, either from one end to the other or from the middle to the edge. They are usually multiple, and oval or elongate in shape. Subcuticular fungal growth may rupture the cuticle, and the fungus may then grow on the outside of the cuticle, completely surrounding the hair shaft. Because the fungus grows into the hair shaft, the hair may fracture easily., Epidemiology:['s common in hot and humid countries like South American countries and Southeast Asian countries', 'good', 'avoid sharing combs, hats, and hair ornaments and avoid activities like swimming in stagnant water'], Complications:['alopecia', 'Pediculosis'], Diagnostics:['FUNGAL CULTURE', 'Potassium hydroxide (KOH) mount', 'direct microscopy'], Differential diagnosis:['Monilethrix', 'PEDICULOSIS PUBIS', 'White piedra'], disease description:This is a fungal infection confi ned to the hair shafts and resulting in the formation of hard, dark, superfi cial nodules thereon. Black piedra is caused by the fungus Piedraia hortae . The infection was thought to be more common in males than females, but one study showed no signifi cant difference between the sexes.

A 44-year-old patient with ['Abdominal Pain', 'BLADDER STONE', 'urinary frequency', 'urinary urgency', 'fever']

Disease Name: Bladder Diverticula, symptoms: ['Abdominal Pain', 'BLADDER STONE', 'urinary frequency', 'urinary urgency', 'fever'], Treatment: [{'medication': ['Levofloxacin ']}, 'Bladder diverticulectomy is usually done as an elective case. Surgery is generally indicated as described above when the bladder diverticulum becomes symptomatic. Most of the time, those symptoms are related to the poor emptying function of the diverticulum and urinary stasis. A detailed preoperative assessment is taken before surgery to decide the suitability of treatment for each individual.\n\nThe current minimal invasive treatment options available for diverticula removal are endoscopic resection, injecting bulking agents at the neck of the bladder, and fulguration.'], Pathophysiology: Bladder diverticula, an out-pouching of the bladder, may occur congenitally or as a result of various bladder conditions and/or surgery. Although bladder diverticula are rare and often asymptomatic, severe complications including frequent recurring urinary tract infections may arise depending on the patient., Epidemiology:['They appear in approximately 15% of patients with obstructive conditions of the lower urinary tract', '1.7%', 'GOOD', 'Not known'], Complications:['BLADDER STONE', 'HYDRONEPHROSIS', 'Recurrent infection'], Diagnostics:['X-RAY Abdomen', 'CT', 'PRESSURE FLOW URODYNAMIC STUDY', 'CYSTOSCOPY'], Differential diagnosis:['BLADDER EXSTROPHY', 'BLADDER OUTLET OBSTRUCTION', 'lymphocele', 'URETEROCELE'], disease description:The normal intravesical pressure during voiding is about 35–50 cmH2O; however, pressures as great as 150 cmH2O may be reached by a hypertrophied bladder endeavouring to force urine past an obstruction. This pressure causes the lining between the inner layer of hypertrophied muscle to protrude, forming multiple saccules. If one or more, but usually one saccule is forced through the bladder wall, it becomes a diverticulum. Congenital diverticula are the result of a developmental defect.

A 54-year-old patient experiencing ['Recurrent infection', 'cryptorchidism', 'A fleshy, red mass prolapsing out of the suprapubic region', 'dorsal chordee', 'continuous urine leakage from the mass']

Disease Name: Bladder Exstrophy, symptoms: ['Recurrent infection', 'cryptorchidism', 'A fleshy, red mass prolapsing out of the suprapubic region', 'dorsal chordee', 'continuous urine leakage from the mass'], Treatment: [{'medication': ['Levofloxacin ']}, 'Preoperative Care of the Exposed Bladder\n\nCovering of the bladder plate with a non-adherent wrap or film not only avoids trauma and bleeding by the diaper but also prevents the formation of polyps. A polypoidal bladder is always difficult to close. Various films, wraps, and dressings have been used for the protection of the bladder plate. A clear plastic wrap or a saran wrap is the most commonly used.\nOsteotomy: due to abnormalities of the bony pelvis, there is tension on the bladder and the abdominal wall following turn-in.', 'Surgical Treatment: surgical treatment of classical bladder exstrophy not only involves the bladder closure, but it also includes procedures such as epispadias repair, bladder neck reconstruction, bladder augmentation, and ureteric reimplantation. Additionally, the abnormalities in the bony pelvis and the pelvic floor need to be addressed along with exstrophy repair. Various procedures have been described for bladder exstrophy. They fall into two main categories: the reconstructive procedures and the diversion procedures. The modern approaches focus mainly on the reconstructive procedure; however, the Mainz group in Germany has favored the diversion procedures and has highlighted different aspects from time to time. The major goals of exstrophy repair include the closure of the bladder and creating a receptacle for storage that grows with the child, preservation of the upper tract function, and reconstruction of the genitalia providing good functional outcomes in terms of continence and sexual function.'], Pathophysiology: Bladder-exstrophy-epispadias-complex (BEEC) depicts a spectrum of birth defects, ranging from epispadias to cloacal exstrophy at the milder and the most severe ends of the spectrum. The classical bladder exstrophy is characterized by abnormalities involving the lower urinary tract, abdominal wall, bony pelvis, genitalia, pelvic floor, spine, and the anus.As a general rule, all the structures, including the bladder, urethra, vagina, and rectum, are displaced anteriorly in bladder exstrophy. The distorted anatomy of the bony pelvis in bladder exstrophy needs a special mention. The 'open book configuration' of the pelvis is an appropriate term for its description. The main abnormalities in the bony pelvis include pubic diastasis, shorter anterior segments, and outward rotation of the anterior and posterior segments.In children with exstrophy, the pubic diastasis is around 4 cm at birth and increases to around 8 cm by the age of 10 years. Contrary to this, in a normal human, the distance is less than 1 cm at all ages. It has been postulated that a disruption in the symphyseal ligaments might be responsible for this. Secondly, the anterior segments of the bony pelvis are approximately 30% shorter. However, the dimensions of the posterior segments of the bony pelvis are within normal limits. Both, the anterior and posterior segments of the bony pelvis, are also externally rotated., Epidemiology:['prevalence is approximately 2 per 100,000 births', '3.3 cases per 100,000 live births. The male-to-female ratio is 2.3:1.', 'fair', 'Because there is no clear cause of bladder exstrophy, parents can’t do anything to prevent it. Parents with known risk factors should speak with their healthcare provider about potential testing and treatment plans.'], Complications:['infection', 'Painful micturition'], Diagnostics:['USG KUB', 'X RAY', 'CT SCAN'], Differential diagnosis:['BLADDER DIVERTICULA', 'Omphalocele'], disease description:Bladder exstrophy is a rare congenital anomaly characterized by a spectrum of anomalies involving the ventral body wall, urinary tract, genitalia, bony pelvis, spine, anus, etc. Its diagnosis is clinical and does not require any additional investigations.Although multiple theories highlighting the etiology and pathogenesis of bladder exstrophy have been published, the exact cause still eludes us. Of all these theories, the one by Marshall and Muecke is the most accepted. An abnormally large cloacal membrane causes a wedge effect and prevents the medial migration of the mesenchymal tissue. As a result, the lower abdominal wall is not well-formed. A subsequent rupture of the cloacal membrane results in herniation of all the contents and leading to the clinical picture of bladder-exstrophy-epispadias complex.The most common complications of the surgical treatment of bladder exstrophy are wound dehiscence and bladder dehiscence. Complete dehiscence can cause bladder prolapse. It can be prevented by adequate mobilization of the flaps and by incorporating osteotomy during bladder turn-in, thus reducing the tension over the abdominal wall and bladder plate.

A 44-year-old individual dealing with ['dysuria', 'incomplete bladder emptying', 'increased urgency', 'HESITANCY', 'Abdominal Pain', 'increased frequency of urination']

Disease Name: Bladder Outlet Obstruction, symptoms: ['dysuria', 'incomplete bladder emptying', 'increased urgency', 'HESITANCY', 'Abdominal Pain', 'increased frequency of urination'], Treatment: [{'medication': ['Tamsulosin ', 'Prazosin ', 'Indoramin ', 'paracetamol']}], Pathophysiology: This condition is common in aging men. It is often caused by enlarged prostate. Bladder stones and bladder cancer are also more commonly seen in men than women. As a man ages, the chances of getting these diseases increase greatly.Other common causes of BOO include:Pelvic tumors (cervix, prostate, uterus, rectum)Narrowing of the tube that carries urine out of the body from the bladder (urethra), due to scar tissue or certain birth defectsLess common causes include:Cystocele (when the bladder falls into the vagina)Foreign objectsUrethral or pelvic muscle spasmsInguinal (groin) hernia, Epidemiology:['1 in 4,000 to 5,000 births', '1 in 4,000 to 5,000 births and is more common in males', 'variable', 'If the condition that blocks your bladder neck is preventable, then the bladder outlet obstruction might be preventable, too.'], Complications:['kidney damage', 'urine leakage', 'Urinary infection ', 'bladder dysfunction'], Diagnostics:['URINE CULTURE', 'USG KUB', 'CT SCAN', 'URINE FLOW RATE', 'PRESSURE FLOW URODYNAMIC STUDY', 'RETROGRADE CYSTOGRAPHY', 'VOIDING CYSTOGRAM'], Differential diagnosis:['BLADDER EXSTROPHY', 'BLADDER STONE'], disease description:Bladder outlet obstruction (BOO) is a blockage at the base of the bladder. It reduces or stops the flow of urine into the urethra. The urethra is the tube that carries urine out of the body.Bladder outlet obstruction (BOO) is when the neck at the very bottom of your bladder gets blocked. The neck is where your bladder connects to your urethra, which carries urine (pee) out of your body. A blockage stops or slows down the flow of pee. Possible blockages include scar tissue, bladder stones, a large gland, cancer or a tumor.

Experiencing ['urine leakage', 'fever', 'Pain', 'hematuria', 'incomplete bladder emptying', 'increased frequency of urination'] at 21 years old

Disease Name: Bladder Stone, symptoms: ['urine leakage', 'fever', 'Pain', 'hematuria', 'incomplete bladder emptying', 'increased frequency of urination'], Treatment: [{'medication': ['Cefazolin ', 'Ceftriaxone ', 'Vancomycin ', 'Levofloxacin ']}, 'Medical Therapy\n\nDissolution of bladder stones, particularly uric acid, can sometimes be accomplished with oral alkalinizing agents alone if the higher pH level necessary (usually 6.5 to 7) can be maintained long enough. This is typically done with oral potassium citrate, which can be supplemented with sodium bicarbonate if necessary. For most patients, this will require roughly 60 mEq per day of potassium citrate. Serum potassium levels and urinary pH levels should be checked periodically while on this therapy. The dosage of potassium citrate should be titrated and adjusted to maintain the optimal pH level.', "A transurethral cystolitholapaxy is the most common procedure used to treat adults with bladder stones.\n\nThe surgeon inserts a small, rigid tube with a camera at the end (a cystoscope) into your urethra and up into your bladder. The camera is used to help locate the bladder stones.\n\nA crushing device, lasers or ultrasound waves transmitted from the cystoscope can be used to break up the stones into smaller fragments, which can be washed out of your bladder with fluids.\n\nA transurethral cystolitholapaxy is carried out under either a local anaesthetic or a general anaesthetic, so you shouldn't feel any pain during the procedure.\n\nThere's a risk of developing an infection during the procedure, so you may be given antibiotics as a precaution. There's also a small risk of injury to the bladder."], Pathophysiology: Most vesical calculi are mixed. An oxalate calculus is a primary calculus that grows slowly; usually, it is of moderate size and solitary, and its surface is uneven . Although calcium oxalate is white, the stone is usually dark brown or black because of the incorporation of blood pigment. Uric acid calculi are round or oval and smooth, and vary in colour from yellow to brown. They occur in patients with gout but are also found in patients with ileostomies or bladder outflow obstruction. A cystine calculus occurs only in the presence of cystinuria and is radio-opaque because of its high sulfur content. A triple phosphate calculus is composed of ammonium, magnesium and calcium phosphates and occurs in urine infected with urea-splitting organisms. It tends to grow rapidly. In some instances it occurs on a nucleus of one of the other types of calculus; more rarely it occurs on a foreign body . It is dirty white in colour and of chalky consistency. A bladder stone is usually free to move in the bladder and it gravitates to the lowest part of the bladder. Less commonly, the stone is wholly or partially in a diverticulum, where it may be hidden from view., Epidemiology:['approximately 5% of all urinary tract stones, yet are responsible for 8% of urolithiasis-related mortalities in developed nations.', 'GOOD', 'You may not be able to prevent bladder stones. But you can lower your risk by drinking plenty of water. Water dilutes minerals in your pee, so they’re less likely to clump together and form bladder stones. Talk to a healthcare provider about how much water you should drink every day.\n\nIt’s a good idea to talk to a healthcare provider if you’re over 50 and have an enlarged prostate. They may recommend specific techniques or medications to help empty your bladder.\n\nYou can also help lower your risk of developing certain types of stones by modifying your diet or taking specific medications.'], Complications:['HYDRONEPHROSIS', 'obstruction', 'urinary tract infections'], Diagnostics:['IVP', 'USG KUB', 'X RAY', 'CYSTOSCOPY'], Differential diagnosis:['BENIGN PROSTATIC HYPERPLASIA', 'BLADDER OUTLET OBSTRUCTION', 'clots', 'Urinary Tract Infection', 'urothelial carcinoma'], disease description:Bladder stones are hard masses of minerals in your bladder. They develop when the minerals in concentrated urine crystallize and form stones. This often happens when you have trouble completely emptying your bladder.Small bladder stones may pass without treatment, but sometimes bladder stones need medications or surgery. Left untreated, bladder stones may lead to infections and other complicationsA primary bladder stone is one that develops in sterile urine; it often originates in the kidney. A secondary stone occurs in the presence of infection, outflow obstruction, impaired bladder emptying or a foreign body.

Person at 29 with ['Lacrimation', 'swelling', 'Pain', 'Redness', 'photophobia', 'IRRITATION IN EYES']

Disease Name: Blepharitis, symptoms: ['Lacrimation', 'swelling', 'Pain', 'Redness', 'photophobia', 'IRRITATION IN EYES'], Treatment: [{'medication': ['Doxycycline ', 'Minocycline ', 'Moxifloxacin ']}, 'Anterior Blepharitis: bathing of the eyes with 1:4 baby shampoo or\nwith warm 3% bicarbonate of soda lotion.\nPosterior Blepharitis: Treatment is again by warm compresses and lid\nmassage, together with doxycycline or minocycline for\n6 weeks.'], Pathophysiology: Blepharitis (blef-uh-RYE-tis) is inflammation of the eyelids. Blepharitis usually affects both eyes along the edges of the eyelids.Blepharitis commonly occurs when tiny oil glands near the base of the eyelashes become clogged, causing irritation and redness. Several diseases and conditions can cause blepharitis.Blepharitis is often a chronic condition that's difficult to treat. Blepharitis can be uncomfortable and unsightly. But it usually doesn't cause permanent damage to your eyesight, and it's not contagious., Epidemiology:['more than 25 million Americans suffer from blepharitis', 'excellent', 'Many blepharitis cases aren’t preventable. Some risk factors for blepharitis, such as certain skin conditions, are beyond your control. Here are some steps you can take every day to help with the symptoms:\n\nKeep your hands, face and scalp clean.\nTry not to touch your itchy eyes or your face. Use a clean tissue if you must touch them.\nRemove all eye makeup before bedtime.\nWipe away excess tears or eye drops with a clean tissue.\nWear glasses instead of contact lenses until the condition clears.\nUse artificial tears if you have dry eyes and your provider agrees.\nUse anti-dandruff shampoo to wash your hair.\nReplace eye makeup — eyeliner, eye shadow, mascara — because they may have bacteria in the containers. You want to avoid reinfection.'], Complications:['conjunctivitis', 'ECTROPION', 'madarosis', 'trichiasis', 'tylosis'], Diagnostics:['PUS CULTURE', 'Total Leucocyte Count (TLC)', 'PHYSICAL EXAMINATION'], Differential diagnosis:['bacterial conjunctivitis', 'bacterial keratitis', 'Basal cell carcinoma', 'CHALAZION', 'dry eye syndrome', 'trichiasis'], disease description:This is a chronic inflammation of the margins of the lids, appearing as a simple hyperaemia or as a true inflammation, which may occur in two forms: anterior and posterior. The anterior form may be (i) seborrhoeic or squamous; and (ii) ulcerative. The causes of blepharitis are very varied. The condition may follow chronic conjunctivitis due to staphylococci carried to the lid margins by infected fingers. Occasionally, parasites cause blepharitis—blepharitis acarica, due to Demodex folliculorum, and phthiriasis palpebrarum, due to the crab louse, very rarely to the head louse.

Suffering from ['pigmentation on skin', 'eyelid laxity', 'wrinkling', 'painless eyelid swelling'] at 19

Disease Name: Blepharochalasis, symptoms: ['pigmentation on skin', 'eyelid laxity', 'wrinkling', 'painless eyelid swelling'], Treatment: ['The treatment of BS should be aimed to reduce the swelling during the acute episodes and to correct the sequelae in the quiescent stage.\n\nThere are no well-defined protocols to treat inflammatory attacks. Several authors report good results with the use of steroids, both systemic and topical. However, there are only a few reports based on case series and suggest only some improvement. Considering the potential side effects of steroids, especially if administered systematically, this treatment is not accepted as a general rule for treating the BS, although it could be considered in certain cases. Other immunosuppressant agents have been tried topically, such as tacrolimus.', 'Surgical options for the complications discussed above include blepharoplasty, levator aponeurosis dehiscence repair, eyelid tightening, canthal tendon reattachment, and fat grafting. Surgeons should be conser\xadvative when excising prolapsed orbital fat, given that fat atrophy is part of the natural history of this disease'], Pathophysiology: In the early stages, there may be a mild dermal lymphocytic infiltrate, and in the later stages the elastic fibres in the lids fragment and decrease. Normal elastin gene expression suggests other factors may be involved in elastic fibre loss. IgA deposition may be detected on fibres, implying an immunopathogenic mechanism may be relevant Genetics Some pedigrees show autosomal dominance, although most cases are sporadic, Epidemiology:['This hospital-based study showed that blepharochalasis was much less common in males (27.96%) than in females (72.04%)', 'Poor due recurrance of complications', 'Not known'], Complications:['discolouration of skin', 'ptosis', 'dermatochalasis'], Diagnostics:['HISTORY TAKING', 'PHYSICAL EXAMINATION'], Differential diagnosis:['allergic reaction', 'angioedema', 'CHALAZION', 'dermatochalasis', 'dermatochalasis', 'EHLERS-DANLOS SYNDROME', 'stye'], disease description:Blepharochalasis is a rare syndrome consisting of recurrent bouts of upper eyelid edema associated with thinning, stretching, and fine wrinkling of the involved skin. The lower eyelids are not commonly involved. These episodes often result in eyelid skin redundancy.

At 38, dealing with ['TELECANTHUS', 'short palpebral fissures', 'ptosis']

Disease Name: Blepharophimosis, symptoms: ['TELECANTHUS', 'short palpebral fissures', 'ptosis'], Treatment: ["Treatment goals include surgical eyelid repair for normal visual development and improved cosmesis, alleviating neck strain from chin-up posture, and addressing primary ovarian insufficiency and infertility in females with BPES type I. Management begins with a pediatric ophthalmologist's determination of amblyopia, strabismus, and refractive error. Referral to an oculoplastic surgeon should be made to evaluate the degree of ptosis, blepharophimosis, and epicanthus inversus.\n\nHistorically, correcting eyelids was performed as a 2-stage surgery at 3 to 5 years old. A medial canthoplasty via the Mustarde technique or double-opposing z-plasty to repair epicanthus inversus and telecanthus, followed by frontalis suspension for ptosis repair six to twelve months later. If ptosis and medial canthoplasty were performed simultaneously, the tightened vertical and horizontal tissues would pull against each other in opposite directions, limiting their effect versus if performed separately."], Pathophysiology: The phenotype of BPES can be traced back to dysfunction or absence of the FOXL2 gene product.  FOXL2 is a single gene exon expressed in the mesenchyme of developing eyelids and ovaries. It is the only known gene directly implicated in the BPES phenotype. FOXL2 codes for a transcription factor that regulates the expression of various other genes, including those involved in inflammation, transcription, proteolysis, apoptosis, and detoxification of reactive oxygen species.FOXL2 expression can be altered by intragenic mutations, larger genomic deletions involving the FOXL2 gene, and even genomic alterations outside of the FOXL2 locus. Intragenic mutations account for about 72% of mutations in BPES and can manifest as nonsense, frameshift, missense, or in-frame mutations. Nonsense and frameshift mutations severely impair gene function, but the effect of missense mutations can vary. The location of the missense mutation plays a role in its pathogenic potential. Mutations in the forkhead domain, the region of the protein that binds to DNA, are likely to be pathogenic. In-frame mutations tend to manifest as poly-alanine expansions. These expansions are caused by slippage of DNA polymerase when duplicating trinucleotide repeats and account for about 31% of all intragenic mutations in BPES overall. Large genomic deletions involving FOXL2 region account for about 10% of the genetic defects in BPES. Genomic alterations in loci outside of the FOXL2 region have also been found to account for about 4% of the known genetic defects in BPES. These remote alterations affect the transcription of FOXL2 by impacting distant regulatory elements. , Epidemiology:['1 in 50,000 births.', 'GOOD', 'There’s no real way to lower your risk of blepharophimosis syndrome. If the syndrome runs in your family, you may want to consider genetic counseling.'], Complications:['Visual impairment'], Diagnostics:['VISUAL ACUITY TEST', 'GENETIC TESTING'], Differential diagnosis:['Dubowitz syndrome', 'Hereditary Congenital Ptosis', 'Noonan syndrome', 'Williams syndrome'], disease description:In this condition the extent of the palpebral fissure is decreased. It appears contracted at the outer canthus.Blepharophimosis, ptosis, and epicanthus inversus syndrome (BPES) is a rare developmental condition affecting the eyelids and ovary. Typically, four major facial features are present at birth: narrow eyes, droopy eyelids, an upward fold of skin of the inner lower eyelids and widely set eyes.

Symptoms at 48 years: ['pain in finger', 'fever', 'tense bullae at finger']

Disease Name: Blistering Distal Dactylitis, symptoms: ['pain in finger', 'fever', 'tense bullae at finger'], Treatment: ['If bullae are tense and tender, incision and drainage followed by wet dressing are recommended. Bullae may also be deflated with a sterile needle, leaving the blister roof intact. Wet compresses are helpful for rapid resolution of the bulla followed by topical antibiotics. BDD can coexist with and may be secondary to clinically indiscernible bacterial infections of the upper and lower respiratory or gastrointestinal tract, which underlines the need for systemic antibiotic therapy.', 'If bullae are tense, they may be disrupted gently with a sterile needle, \nleaving the blister roof intact . A course of ß-lactamase-resistant \nantibiotics (flucloxacillin, dicloxacillin, cloxacillin, temocillin) is\nusually effective. Topical therapy with wet dressings may be \nhelpful.'], Pathophysiology: Causative organisms Group A streptococci and other organisms have been identified, including group B streptococci and staphylococci. More recently S. aureus has been noted to be implicated in adults. A large blister or blisters containing thin seropurulent fluid forms on the distal phalanx, usually of a finger, and typically on the palmar pad, although it may extend to the nail folds, and more proximal involvement of the palmar skin is sometimes seen . An upper respiratory tract infection is some times present. One recurrent case occurred beside an ingrowing toenail., Epidemiology:['GOOD', 'BDD usually resolves rapidly with the appropriate antibiotics and local dressing without any complications or sequelae. There is a report of digital amputation post BDD which emphasizes the need to treat infections aggressively, especially in HIV positive individuals.'], Complications:['osteomyelitis'], Diagnostics:['Bacteria Culture Test', 'fluid gram staining'], Differential diagnosis:['Ankylosing spondylitis', 'axial spondyloarthritis', 'Chronic gout', 'Gout', 'Histoplasmosis', 'Osteoarthritis', 'PLANTAR FASCIITIS', 'PSORIATIC ARTHRITIS'], disease description:A distinct entity presenting with localized group A ß-haemolytic Streptococcus infection of the distal phalanx usually in a child. Bistering distal dactylitis manifests as multiple bullae on the volar aspects of the hands and fingers usually in young children. Lesions appear over a few days and may leave superficial erosions secondary to usually streptococcal but also staphylococcal infections. Children between the ages of 2 and 16 years of age are most commonly affected but there are cases reported in adults. Rarely cases have been reported in children a few months of age.BDD presents as a single, or sometimes multiple, oval-shaped tense bullae containing seropurulent fluid on an erythematous base over the palmar aspect of the finger which may extend dorsally to involve lateral nail folds. The lesions usually range in size from 10 mm to 30 mm. Darkening of the skin may be noticed a few days before the actual onset of the blisters. The bull progresses to form bullae with central erosions or simple erosion with adherent layers of skin.

Symptoms reported by a 48-year-old: ['paresthesia', 'proptosis', 'Limitation of upward gaze', 'diplopia']

Disease Name: Blow Out Fracture Of Orbit, symptoms: ['paresthesia', 'proptosis', 'Limitation of upward gaze', 'diplopia'], Treatment: ["During postoperative care, the examiner should watch out for postoperative complications such as infection, visual, or central nervous system (CNS) symptoms. The patient's head should be elevated to reduce the edema, and cool compresses can be placed over the closed eyelid to reduce pain and swelling. The patient's visual acuity ad pupillary function should be periodically assessed; if any changes are noticed, the surgeon should be immediately notified", '*prophylactic antibiotic therapy to prevent infection.\n*Corticosteroids may help reduce the edema in some cases', 'In general, surgery should be undertaken within 14 days to prevent fibrosis. Most surgeons wait 24-72 hours to allow the edema to subside before undertaking surgery. \nThe goal of surgery is to restore herniated structures into the orbital cavity. The surgery may be done via a transconjunctival or transmaxillary approach. Today there are endoscopic techniques to manage orbital fracture. Several types of implants are also available for reconstruction of the orbit, but these should be avoided in the presence of an obvious infection.'], Pathophysiology: In most cases, orbital blowout fractures are secondary to an explosive increase in the intraorbital pressure. The kinetic energy from the impact is transmitted to all the adjacent structures within the bony socket. The majority of fractures tend to occur in the posterior medial area, where the bones are thin., Epidemiology:['10% of all facial fractures', 'variable', 'preventing blunt trauma to the midface'], Complications:['enophthalmos', 'Loss of vision'], Diagnostics:['VISUAL ACUITY TEST', 'CT SCAN'], Differential diagnosis:['sixth nerve palsy', 'Traumatic diplopia'], disease description:Fractures of the orbital floor and the medial orbital wall (blowout fractures) are common midface injuries. Orbital fractures have a distinct trauma mechanism and are complex due to the complex anatomy of the bony and soft tissue structures involved. The common mechanisms are falls, high-velocity ball-related sports, traffic accidents, and interpersonal violence.Orbital fractures are more common in males than in females and most often occur in men, ages 21  to 30.

Experiencing ['NODULES'] at 41 years old

Disease Name: Blue Nevus, symptoms: ['NODULES'], Treatment: [{'medication': ['Cisplatin ', 'Vincristine', 'Dacarbazine']}, 'The definitive treatment of blue nevus is excision, though it is appropriate to monitor stable lesions clinically. In rare cases, blue nevus may recur at sites of prior excision. Though excision is considered curative, the appearance of recurrent blue nevus at a prior site should warrant biopsy and/or re-excision as it could represent emerging malignant blue nevus or other melanoma'], Pathophysiology: The exact etiology of blue nevus is unclear. Some postulate that components of blue nevus are remnants of migrating neural crest melanocytes during development. Others theorize that they arise from specific stem cells within the dermis.The proliferation of melanocytes in the dermis and surrounding melanophages containing abundant melanin pigment create a distinctive blue hue. The characteristic blue color results from reflection, rather than absorption, of shorter wavelengths of light corresponding to the color blue by dermal melanin. This phenomenon is known as the Tyndall effect., Epidemiology:['3–5% in Asians, compared to only 1–2% in Caucasians', 'good', 'not known'], Complications:['melanoma'], Diagnostics:['biopsy', 'Dermoscopy'], Differential diagnosis:['dermatofibroma'], disease description:The term "blue nevus" describes a group of skin lesions characterized by dermal proliferation of melanocytes presenting as blue to black nodules on the head, extremities, or buttocks. In most cases, they are acquired and present as a solitary lesion but may also be congenital and appear at multiple sites. Blue nevi may present as a solitary, well-demarcated, blue to black nodule or confluence of nodules at a single site or maybe diffusely distributedThe diagnosis of blue nevus is generally clinical, made grossly, or with the use of a dermatoscope.

Person, 28 years old, presenting ['diarrhea', 'vomiting', 'stomach pain', 'headache', 'fever', 'joint pain', 'PAINFUL EYE MOVEMENT']

Disease Name: Bolivian Hemorrhagic Fever, symptoms: ['diarrhea', 'vomiting', 'stomach pain', 'headache', 'fever', 'joint pain', 'PAINFUL EYE MOVEMENT'], Treatment: ['While no specific treatment exists for most viral hemorrhagic fevers, the antiviral drug ribavirin (Rebetol, Virazole) might shorten the course of some infections and prevent complications in some people'], Pathophysiology: Following aerosol exposure virus particles are likely engulfed by alveolar macrophages leading to the first cellular infection. The incubation period for BHF is 3 to 16 days following exposure. Previously, exposure was believed to consistently lead to disease development as there were a low number of serum samples collected with antibodies specific to BHF who did not report disease development during the 1959 to 1964 outbreak. Recent serum sampling has detected a number of people with detectable IgG antibodies who never reported disease manifestations similar to BHF. These unpublished samplings may imply a number of possibilities; the first that MACV may be less lethal than identified in the initial outbreak, that MACV may be more widespread than previously thought within the Beni district, or that MACV virulence has reduced since the original outbreak in the 1960s. The prodromal phase of BHF is similar to that of Argentine hemorrhagic fever (AHF) caused by Junin virus (JUNV), with the onset of fever, malaise, myalgia, headache, and anorexia. This develops into severe symptoms including vomiting, hypersensitivity, and early signs of vascular damage. Laboratory findings of clinical samples include leukopenia, thrombocytopenia, and proteinuria during the first few days following hospitalization., Epidemiology:['The percentages of suspected infection ranged from 55 to 93 per cent. No human cases of Bolivian hemorrhagic fever have been registered since 1974', 'variable with mortality rate of 25 to 35%'], Complications:['internal bleeding'], Diagnostics:['ELISA For IgG', 'RT PCR'], Differential diagnosis:['Ebola virus disease (EVD)', 'Influenza', 'Lassa fever', 'Malaria', 'Marburg hemorrhagic fever', 'Rocky Mountain spotted fever', 'TYPHOID FEVER', 'yellow fever'], disease description:Bolivian hemorrhagic fever (BHF) or Machupo hemorrhagic fever (ICD-10 ) was first identified in 1959 as a sporadic hemorrhagic illness in rural areas of Beni department, Bolivia . BHF is a potentially severe febrile illness caused by Machupo virus (a member of the family Arenaviridae). Clusters of BHF patients were noted the same year and by 1962 BHF was recognized as a new epidemic infectious disease. In 1963, the etiological agent, the Machupo virus was first isolated from patients with acute hemorrhagic fever in San Joaquin, Bolivia.

Individual aged 53 with manifestations like ['painful papule without sinus formation', 'abscesses', 'ulcer']

Disease Name: Botryomycosis, symptoms: ['painful papule without sinus formation', 'abscesses', 'ulcer'], Treatment: [{'medication': ['Erythromycin ', 'Fusidic acid /Sodium Fusidate', 'Flucloxacillin']}, 'First line:\nFor S. aureus infections, flucloxacillin or erythromycin are usual.\nSecond line:\nSometimes an alternative approach such as flucloxacillin and \nfusidic acid can be used for very extensive lesions. The response \nis often determined by the presence or absence of underlying predisposing disease'], Pathophysiology: A history of injury is common in skin cases, and the literature relating to experimental models as well as some early case reports stresses the importance of a foreign body as well as infection. The size of bacterial inoculation may be crucial; a delicate balance between host and pathogen has been regarded as significant. Causative organisms: Most common Staphylococcus aureus, but other bacteria can be associated. The resemblance to actinomycosis is also evident clinically. Most lesions are on the limbs, but other sites including the perianal region and the face have been affected. In the primary cutaneous form, single or multiple abscesses of skin and subcutaneous tissues break down to discharge serous fluid through multiple sinuses, and heal after a course of many months to leave atrophic scars. The general condition may remain good. Patients may present with a smaller painful papule without sinus formation., Epidemiology:['approximately 200 cases reported', 'good'], Complications:['immunosuppression'], Diagnostics:['Gram Staining', 'Bacteria Culture Test', 'MICROSCOPIC EXAMINATION'], Differential diagnosis:['Actinomycosis', 'Folliculitis and furunculosis', 'Mycetoma'], disease description:Botryomycosis is a chronic granulomatous reaction to bacterial infection, containing granules resembling the sulphur granules of actinomycosis. Most cases of botryomycosis are caused by Staphylococcus aureus, but from some a pure culture of Pseudomonas has been obtained. Botryomycosis may develop in the skin or elsewhere and a variety of underlying predisposing factors have been described.

At the age of 21, symptoms like ['proteinuria', 'hematuria', 'small macular lesions that progress into papules and then pustules on a purpuric base', 'arthralgia', 'EPISCLERITIS', 'Gastrointestinal upset', 'myalgia', 'fever']

Disease Name: Bowel-associated Dermatitis–arthritis Syndrome, symptoms: ['proteinuria', 'hematuria', 'small macular lesions that progress into papules and then pustules on a purpuric base', 'arthralgia', 'EPISCLERITIS', 'Gastrointestinal upset', 'myalgia', 'fever'], Treatment: [{'medication': ['Mycophenolate mofetil/ Mycophenolate sodium', 'Colchicine ', 'Ciprofloxacin ', 'Erythromycin ', 'Dapsone ', 'Metronidazole ', 'Tetracycline ']}, 'First line:\n Manifestations of BADAS may often be controlled by the use of\nsystemic tetracycline, metronidazole, ciprofloxacin or erythromycin; this further suggests the important role of bacterial colonization in triggering the systemic response in BADAS.\n\nSecond line\n Systemic corticosteroids are typically unnecessary for the treatment of BADAS but may be justified depending on the degree of skin, joint or systemic symptoms, or to concurrently treat \nIBD. Other treatments including oral colchicine, dapsone and mycophenolate have been used; systemic immunosuppressants may need to be combined with an appropriate\nantibiotic.'], Pathophysiology: Pathophysiology involves blood vessel damage secondary to bowel flora antigen associated circulating immune complexes is thought to be the pathogenesis of the cutaneous lesions. In these patients, peptidoglycans from gastrointestinal flora may be the antigenic trigger for immune complex mediated vessel damage. Therapeutic response to antimicrobials in some cases supports this concept, and immune complexes have been demonstrated. Predisposing factors BADAS may be related to jejuno-ileal bypass, gastric resection, blind loops (Bilroth II or Roux-en-Y), defunctioning ileo-anal pouch procedures, and bilio-pancreatic diversion. It has also been related to other bowel disease: ulcerative colitis , Crohn disease, diverticulitis of the colon, jejunal diverticula, appendicitis and achalasia of the cardia. In some cases, there are combined causes (e.g. surgery for IBD). In most instances related to surgery, the loop of bypassed bowel, or a blind loop, is contiguous with the intestine, but may be separated as a defunctioning segment of bowel., Epidemiology:['The syndrome can occur in up to 20% of patients who have undergone jejunoileal bypass surgery', 'good', 'NOT KNOWN'], Complications:['Liver dysfunction', 'RENAL CALCULI', 'Hyperuricemia with fever', 'TENOSYNOVITIS'], Diagnostics:['URINE MICROALBUMIN', 'URINE ANALYSIS (Color)', 'CT'], Differential diagnosis:['Behcet’s Disease'], disease description:Bowel-associated dermatitis–arthritis syndrome (BADAS) is defined by the presence of pustular vasculitic lesions associated with blind loops of bowel or other causes of stasis of bowel content.

Person at 22 with manifestations like ['LESIONS', 'solitary plaque', 'LESIONS', 'scaling of skin']

Disease Name: Bowen Disease, symptoms: ['LESIONS', 'solitary plaque', 'LESIONS', 'scaling of skin'], Treatment: [{'medication': ['Diclofenac ', 'Tazarotene']}, 'topical 5% 5-fl uorouracil, 5% imiquimod\ncream or PDT would be the treatments of choice', 'PDT gave superior cosmetic results compared with cryotherapy \nor 5-fl uorouracil', 'Radiotherapy using both high- and low-dose regimens has been\nreported with equal efficacy but the evidence in trials remains\npoor'], Pathophysiology: Several large studies have identified a link between Bowen disease and ingestion of arsenic, which can pre-date the onset of disease by several decades. Historically, arsenic was found in Fowler’s solution used to treat psoriasis and Gay’s solution used to treat asthma. Agricultural workers may be exposed to arsenic salts used in fungicide, weedkiller, sheep dip or pesticide. In some countries, notably parts of Argentina, Bangladesh and Taiwan, the water supply has been contaminated in the past . The use of arsenic has diminished and is now much less of a concern in the Western world. Immunosuppression following solid-organ transplant, haematological malignancies, in particular chronic lymphocytic leukaemia or HIV, increases the risk of developing SCC and pre- malignant skin conditions but the exact risk for Bowen disease has not been determined. There are reports, however, of multiple areas of Bowen disease occurring in a younger age group in those on immunosuppression following solid-organ transplantation. There are also reports of Bowen disease following therapeutic and other ionizing radiation and following skin injury or chronic inflammation, such as lupus vulgaris and chronic lupus erythematosus. Bowen disease is characterized by full-thickness epidermal dysplasia and disordered differentiation with loss of epithelial polarity. The intraepidermal portion of cutaneous adnexae is generally affected. Parakeratosis and acanthosis are usually present and keratinocytes show variable pleomorphism, nuclear hyperchromasia and nuclear enlargement. Cells keratinise prematurely. Clear cell change may be observed due to increased intracytoplasmic glycogen, which can be highlighted by a PAS stain. Giant forms and multinucleate cells may be seen and mitotic figures can be frequent. The dermal–epidermal junction remains distinct. HPV-associated viral cytopathic changes are frequently seen particularly, but not exclusively, in lesions from genital skin. The papillary dermis shows an inflammatory cell infiltrate that is frequently quite dense and vascular ectasia is often present and may be conspicuous. The dermal inflammatory cell infiltrate may have a band-like distribution mimicking lichenoid dermatoses. Causative organisms Viral agents have been implicated in the aetiology of Bowen disease. Interest has centred around HPV with reports of a number of HPV types present. HPV DNA has been demonstrated in extragenital Bowen disease in varying amounts from 4.8% to 60%. Larger studies have failed to confirm these findings, except for HPV16 and HPV18, which are both commoner in anogenital Bowen disease and HPV16 has also been implicated in 60% of palmoplantar and periungual lesions. Environmental factors Bowen disease is more common on light-exposed sites such as the lower legs, suggesting a relationship with chronic UV damage from solar or iatrogenic source., Epidemiology:['unknown', 'In the white North American population it is reported to range from 14.9/100 000 to 27.8/100 000', 'excellent, except in SCC transformation', "The most effective method of reducing your risk of Bowen's disease, as well as other more serious types of skin cancer, is to limit your exposure to the sun."], Complications:['squamous cell carcinoma.'], Diagnostics:['X RAY AP VIEWS', 'full thickness skin biopsy', 'Dermoscopy'], Differential diagnosis:['Actinic keratosis: Arsenical keratosis, PUVA kera', 'Asteatotic eczema', 'Basal cell carcinoma', 'Lichen simplex', 'Lichen simplex chronicus', 'plaque psoriasis', 'Pompholyx eczema', 'psoriasis', 'squamous cell carcinoma', 'tinea corporis'], disease description:it can be pigmented or verrucous. It is commonly located on the lower limbs and on the head and neck. But BD is also seen subungual or periungual, palmar, genital and perianal. Usually BD is a solitary lesion, but in 10% to 20% it occurs at multiple sites. Bowen’s disease (squamous cell carcinoma in situ) has a 3%–5% risk to develop into invasive squamous cell carcinoma

At 39 years old, experiencing ['aphasia', 'nausea', 'neurological deficit', 'Irritability', 'nystagmus', 'papilledema', 'raised intracranial pressure', 'ipsilateral ataxia', 'dysmetria', 'drowsiness', 'severe headache', 'vomiting', 'visual defects', 'LOW GRADE FEVER', 'hemiparesis', 'Signs of meningeal irritation']

Disease Name: Brain Abscess, symptoms: ['aphasia', 'nausea', 'neurological deficit', 'Irritability', 'nystagmus', 'papilledema', 'raised intracranial pressure', 'ipsilateral ataxia', 'dysmetria', 'drowsiness', 'severe headache', 'vomiting', 'visual defects', 'LOW GRADE FEVER', 'hemiparesis', 'Signs of meningeal irritation'], Treatment: [{'medication': ['Meropenem ', 'Cefepime Hydrochloride ', 'Ceftriaxone ', 'Cefotaxime ', 'Vancomycin ', 'Metronidazole ']}, 'Medical therapy alone is not optimal for treatment of brain\nabscess and should be reserved for patients whose abscesses are\nneurosurgically inaccessible, for patients with small (<2–3 cm) or\nnonencapsulated abscesses (cerebritis), and for patients whose condition is too tenuous to allow performance of a neurosurgical\nprocedure. All patients should receive a minimum of 6–8 weeks of\nparenteral antibiotic.\nGlucocorticoids should not be given routinely to patients with\nbrain abscesses. Intravenous dexamethasone therapy (10 mg every\n6 h) is usually reserved for patients with substantial periabscess edema and associated mass effect and increased ICP. Dexamethasone should be tapered as rapidly as possible to avoid delaying the natural process of encapsulation of the abscess.', 'Aspiration and drainage of the abscess under stereotactic guidance\nare beneficial for both diagnosis and therapy. Empirical antibiotic\ncoverage should be modified based on the results of Gram’s stain and\nculture of the abscess contents. Complete excision of a bacterial abscess\nvia craniotomy or craniectomy is generally reserved for multiloculated\nabscesses or those in which stereotactic aspiration is unsuccessful.'], Pathophysiology: The intact brain parenchyma is relatively resistant to infection. Once bacteria have established infection, brain abscess frequently evolves through a series of stages, influenced by the nature of the infecting organism and by the immunocompetence of the host. The early cerebritis stage (days 1–3) is characterized by a perivascular infiltration of inflammatory cells, which surround a central core of coagulative necrosis. Marked edema surrounds the lesion at this stage. In the late cerebritis stage (days 4–9), pus formation leads to enlargement of the necrotic center, which is surrounded at its border by an inflammatory infiltrate of macrophages and fibroblasts. A thin capsule of fibroblasts and reticular fibers gradually develops, and the surrounding area of cerebral edema becomes more distinct than in the previous stage. The third stage, early capsule formation (days 10–13), is characterized by the formation of a capsule that is better developed on the cortical than on the ventricular side of the lesion. This stage correlates with the appearance of a ring-enhancing capsule on neuroimaging studies. The final stage, late capsule formation (day 14 and beyond), is defined by a well-formed necrotic center surrounded by a dense collagenous capsule. The surrounding area of cerebral edema has regressed, but marked gliosis with large numbers of reactive astrocytes has developed outside the capsule. This gliotic process may contribute to the development of seizures as a sequela of brain abscess., Epidemiology:['incidence of ~0.3–1.3:100,000 persons per year.', 'variable', 'You can reduce the risk of developing a brain abscess by getting treated for infections or health problems that can cause them.\n\nSome people, including those with certain heart disorders, may receive antibiotics before dental or other procedures to help reduce the risk of infection.'], Complications:['Meningitis', 'increased intracranial pressure', 'neurological deficit', 'seizures', 'ventriculitis after intrathecal', 'septicemia'], Diagnostics:['BLOOD CULTURE test', 'CRP', 'CSF EXAMINATION', 'Erythrocyte Sedimentation Rate (ESR)', 'Total Leucocyte Count (TLC)', 'CT HEAD', 'MRI', 'CT'], Differential diagnosis:['BACTERIAL MENINGITIS', 'Brain tumors', 'Demyelination', 'ENCEPHALITIS', 'Meningitis.', 'SUBDURAL ABSCESS', 'unexplained fever'], disease description:A brain abscess is a focal, suppurative infection within the brain parenchyma, typically surrounded by a vascularized capsule.A brain abscess is a pus-filled swelling in the brain. It usually occurs when bacteria or fungi enter the brain tissue after an infection or severe head injury.

Individual aged 55 with manifestations like ['Bradycardia', 'hypertension', 'nystagmus', 'raised intracranial pressure', 'vomiting', 'speech changes', 'Bell’s palsy', 'Ataxia', 'headache', 'respiratory difficulties', 'Personality change', 'Visual impairment']

Disease Name: Brain Tumours, symptoms: ['Bradycardia', 'hypertension', 'nystagmus', 'raised intracranial pressure', 'vomiting', 'speech changes', 'Bell’s palsy', 'Ataxia', 'headache', 'respiratory difficulties', 'Personality change', 'Visual impairment'], Treatment: ['Chemotherapy may also be used concurrently\nwith radiation therapy as a radiation sensitizer for some\ntumors. Newer agents such as antiangiogenic drugs and\ninhibitors of tyrosine kinases, histone deacetylases and\nthe sonic hedgehog pathway are under investigation for\nbrain tumors.', 'Radiation therapy utilizing photons is most commonly used for treating brain\ntumors.', 'Complete\nsurgical resection without damaging the critical structures\nof the brain is usually the desired goal.'], Pathophysiology: Exposure of CNS to significant doses of radiation and presence of certain genetic syndromes increases the risk of developing brain tumors. Meningiomas and malignant gliomas arise within the radiation field several years or decades after radiation therapy. Children who have received cranial or craniospinal radiation for treatment of ALL are at risk for developing these tumors. Several genetic syndromes predispose to developing CNS tumors . Of these NFl is the most common disorder. Approximately 15% of patients with NFl develop optic gliomas during their lifetime. Optic gliomas in patients with NFl have a more benign course and may even regress spontaneously. However, the majority of pediatric CNS tumors are sporadic and have no known cause. Infratentorial tumors are more common than supratentorial tumors in children and hence more likely to develop acute or chronic hydrocephalus. Recurrent headaches that are worse at night or early morning and worsen with lying down, early morning vomiting, vision loss, features of VI nerve palsy or sunset sign are indicative of raised intracranial pressure. Acute increase in intracranial pressure may present with Cushing triad of hypertension, bradycardia and altered respiration. Diencephalic syndrome (emaciation, euphoria and emesis) is associated with tumors in the diencephalon. Parinaud's syndrome of supranuclear upgaze palsy with pupils reactive to accommodation but not to direct light is associated with tumors of pineal region or upper brainstem. Seizures are very rarely associated with tumors. Low grade tumors of cerebral cortex may present with seizures as the main manifestation. Frontal lobe tumors present with personality changes, seizures and headaches. Tumors in the temporal lobe cause seizures and speech changes. Suprasellar tumors are associated with endocrinopathies and visual changes. Tumors compressing or involving the hypothalamicpituitary axis present with endocrinopathies. Tumor should always be ruled out in a new onset diabetes insipid us. Tumors involving the thalamus lead to motor and sensory deficits. Tectal plate (on top of brainstem) and pineal tumors cause obstructive hydrocephalus. Multiple cranial nerve deficits are classic presentation of brainstem gliomas. Nystagmus, ataxia and vomiting because of increased intracranial pressure are typically present with cerebellar tumors. Spinal tumors may cause back pain, scoliosis, numbness, weakness and impairment of bladder /bowel function., Epidemiology:['less than 1%', 'VARIABLE', 'Unfortunately, you can’t prevent a brain tumor. You can reduce your risk of developing a brain tumor by avoiding environmental hazards such as smoking and excessive radiation exposure.\n\nIf you have a first-degree biological relative (sibling or parent) who has been diagnosed with a brain tumor, it’s important to tell your healthcare provider. They may recommend genetic counseling to see if you have an inherited genetic syndrome that’s associated with brain tumors.'], Complications:['seizures', 'vision abnormalities'], Diagnostics:['MRI Head', 'CT HEAD', 'MRI'], Differential diagnosis:['Arteriovenous Malformation (AVM)', 'Brain Abscess', 'Meningitis', 'Neurofibromatosis', 'neurosyphilis', 'stroke', 'von Hippel Lindau disease'], disease description:A brain tumor is a growth of abnormal cells in the tissues of the brain. Brain tumors can be benign, with no cancer cells, or malignant, with cancer cells that grow quickly. Some are primary brain tumors, which start in the brain Tumors of the central nervous system are the second most common neoplasms in children in the developed countries. They account for 25% of all childhood cancers. Medulloblastomas are the most common malignant brain tumors in children.

Person, 21 years old, presenting ['visual field defects', 'painless loss of vision', 'sudden loss of vision']

Disease Name: Branch Retinal Artery Occlusion , symptoms: ['visual field defects', 'painless loss of vision', 'sudden loss of vision'], Treatment: [{'medication': ['Acetazolamide', 'Apraclonidine ']}, 'Medical therapy\nAntiplatelet therapy as needed\nIntravitreal anti-VEGF therapy for neovascular complications.', 'Surgery\nSurgical or LASER (Nd-YAG) embolectomy has been tried with variable success. Systemic evaluation is the most important part of management.\nCarotid endarterectomy when indicated\nLaser photocoagulation of ischemic retina for neovascular complications.'], Pathophysiology: Most commonly, BRAO results from an embolus. Emboli typically originate within vessels upstream where they dislodge and travel within the circulatory system to ultimately become lodged downstream in a vessel with a smaller lumen. The most common include cholesterol emboli from aorto-carotid atheromatous plaques, platelet-fibrin emboli from thrombotic disease, and calcific emboli from cardiac valvular disease. Various other endogenous emboli as well as exogenous emboli and nonembolic causes have been reported.Ischemia of the inner layers of the retina leads to intracellular edema as a result of cellular injury and necrosis. This intracellular edema has the ophthalmoscopic appearance of grayish whitening of the superficial retina. Primate studies have shown that complete occlusion of arterial supply to the retina results in reversible ischemic injury in up to 97 minutes. This may help explain why patients may give a history of transient loss of vision prior to an episode of BRAO. Possibly, these episodes are secondary to emboli transiently becoming lodged, causing temporary occlusions and then reperfusing the retina as the emboli are released., Epidemiology:['BRAOs account for 38%, and cilioretinal artery occlusions account for 5%.', 'VERY GOOD', 'Given its association with systemic disorders which result in luminal narrowing of blood vessels, primary prevention of BRAO should be aimed at chronic management of conditions such as hypertension, hypercholesterolemia, and diabetes mellitus. Smoking cessation counseling should be offered to prevent BRAO and myriad other medical conditions.'], Complications:['stroke'], Diagnostics:['Complete Blood Count CBC', 'Erythrocyte Sedimentation Rate (ESR) test', 'MRI', 'MRI', 'Transesophageal echocardiography (TEE)', 'Fluorescein angiography', 'Fundus examination', 'fasting glucose'], Differential diagnosis:['berlins edema', 'CRAO (Central retinal artery occlusion)'], disease description:The central retinal artery, a branch of the ophthalmic artery, enters the eye through the optic disc and divides into multiple branches to perfuse the inner layers of the retina. A branch retinal artery occlusion (BRAO) occurs when one of these branches of the arterial supply to the retina becomes occluded.

Experiencing ['FLAME SHAPED HAEMORRHAGE AND DOT BLOT HAEMORRHAGE', 'RETINAL EDEMA AND SOFT EXUDATES', 'visual field defects', 'hypertension', 'Visual impairment'] at 48 years

Disease Name: Branch Retinal Vein Occlusion , symptoms: ['FLAME SHAPED HAEMORRHAGE AND DOT BLOT HAEMORRHAGE', 'RETINAL EDEMA AND SOFT EXUDATES', 'visual field defects', 'hypertension', 'Visual impairment'], Treatment: ['Pharmacologic management of BRVO involves intravitreal injections of anti-VEGF therapy and/or corticosteroids. For anti-VEGF injections, one study showed patients with BRVO who were injected monthly with either 0.5 or 0.3 mg of ranibizumab versus those receiving sham injections showed greater than 15% improvement in best-corrected visual acuity (BCVA) from baseline at 12 months.', 'When iris neovascularization occurs, which it does in about 2% of patients, scatter photocoagulation has been shown to be beneficial in reducing the risk of neovascular glaucoma. Pars plana vitrectomy may be indicated for eyes that develop non-clearing vitreous hemorrhage or retinal detachment.'], Pathophysiology: The loss of vision in BRVO is caused by macular edema which can have multiple pathophysiologic mechanisms. Patients with long-standing systemic arterial hypertension undergo retinal artery arteriosclerosis that results in thickening of the arterial wall clinically evident as “silver and copper” wiring appearance. Retinal arteries and veins share a common adventitial sheath; therefore, thickening of the arterial wall that can compress the retinal vein at a point where they cross resulting in turbulent blood flow and potential thrombus formation.Japanese ophthalmologist Yoshizo Koyanagi was the first to associate the mechanical nature of BRVO and arteriovenous knicking in 1928. Another mechanism of BRVO is thrombus formation due to hypercoagulability secondary to increased acute phase reactants or other clotting disorders such as resistance to activated protein C, deficiency of Protein C and S, deficiency of antithrombin III, a genetic mutation in prothrombin gene, antiphospholipid antibodies, and hyperhomocysteinemia., Epidemiology:['0.5% to 1.2%', 'good', 'Retinal vein occlusion is a sign of a general blood vessel (vascular) disease. Measures used to prevent other blood vessel diseases may decrease the risk for retinal vein occlusion.\n\nThese measures include:\n\nEating a low-fat diet\nGetting regular exercise\nMaintaining an ideal weight\nNot smoking\nAspirin or other blood thinners may help prevent blockages in the other eye.\n\nControlling diabetes may help prevent retinal vein occlusion.'], Complications:['RETINAL DETACHMENT', 'Neovascularization'], Diagnostics:['Blood Glucose test', 'Complete Blood Count CBC', 'PT/PC/INR', 'Optical coherence tomography (OCT)', 'Optical coherence tomography (OCT)', 'Fundus examination'], Differential diagnosis:['Diabetic and non diabetic nephropathy', 'HYPERTENSIVE RETINOPATHY'], disease description: BRVO can have multiple underlying causes, including age, hypertension, diabetic retinopathy, or hypercoagulability. Branch retinal vein occlusion can be subdivided into major BRVO (retinal vein occlusion) and macular BRVO (macular vein occlusion). Regardless of the underlying cause, BRVO refers to the obstruction of a branch of the retinal vein at an arteriovenous crossing. This compression of the vein is thought to cause turbulent blood flow that leads to thrombus formation.The quadrant of the retina most commonly affected is the superotemporal quadrant in 63% to 66% of eyes affected with BRVO. Inferotemporal retina involvement constitutes 22% to 43% of eyes affected with BRVO. Nasal involvement is rare and is usually asymptomatic until neovascularization causes vitreous hemorrhage.

Person at 31 years, dealing with ['Bleeding complications', 'conjunctivitis', 'liver damage', 'fever', 'malaise', 'muscle pain', 'tremor', 'weakness', 'joint pain', 'stomach pain']

Disease Name: Brazilian Hemorrhagic Fever, symptoms: ['Bleeding complications', 'conjunctivitis', 'liver damage', 'fever', 'malaise', 'muscle pain', 'tremor', 'weakness', 'joint pain', 'stomach pain'], Treatment: ['Transfusions for bleeding disorders', 'Fluid and electrolytes maintenance', 'Oxygen and blood pressure maintenance'], Pathophysiology: Pathogens implicated in viral hemorrhagic fevers are able to replicate within macrophages and dendritic cells, allowing for rapid dissemination within the host. Macrophages are triggered to release cytokines and chemokines, which cause increased vascular permeability and a procoagulant state ., Epidemiology:['less than 10 reported cases of each', 'variable', 'Due to scarcity of knowledge about the virus and its reservoir, there is not much information about how to prevent this infection. Currently, there are also no approved vaccines available to prevent this infection.\n\nHowever, certain general preventive measures used for other arenaviruses can be helpful, and these include:\n\nAvoiding exposure to rodents and their body fluids and droppings\nRodent control using rodenticide and rodent traps in and around homes\nAvoiding contact with body fluids (e.g., saliva, blood, respiratory secretions, semen, urine, etc.) of affected individuals, both sick and recovering, until their tests are negative for the virus\nStrictly isolating suspected or confirmed individuals with the disease\nFollowing all infection-control procedures in healthcare and other settings, including the use of protective clothing, masks, and gloves\nBeing careful while handling rodents and patient samples, especially during research\nOther preventative measures may include:\n\nFrequent handwashing\nEnsuring proper disposal of contaminated materials\nAvoiding or limiting travel to the endemic regions in Brazil, especially the forested areas'], Complications:['severe bleeding', 'hypovolaemic shock', 'multiple organ failure'], Diagnostics:['Protein', 'PCR', 'Viral cultures'], Differential diagnosis:['Lassa fever', 'pyrexia', 'systemic lupus erythematosus (SLE)', 'TYPHOID FEVER', 'yellow fever'], disease description:Brazilian Hemorrhagic Fever is an emerging viral illness in certain regions of Brazil in South America. It is one of the South American hemorrhagic fevers which was discovered in 1990 that reemerged in 2020It is caused by Sabiá virus (SABV) which is an RNA virus belonging to Arenaviridae family of viruses and clade B of South American hemorrhagic fever arenaviruses. It is a newly emerged virus and due to lack of immunity in the human population, it has a potential to cause severe life-threatening diseaseRodents are the likely natural reservoirs of the virus. They carry the virus asymptomatically without being affected and transmit the virus to humans. However, the exact (rodent) species that transmit the virus is yet to be identified.

A 36-year-old woman suffering from ['FLUSHED BREAST', 'breast tenderness', 'fever', 'BRAWNY EDEMA', 'swelling at breast']

Disease Name: Breast Abscess, symptoms: ['FLUSHED BREAST', 'breast tenderness', 'fever', 'BRAWNY EDEMA', 'swelling at breast'], Treatment: ['Pain control with NSAIDs and/or prescription narcotics should also be considered.', 'Incision and drainage are the standard of care for breast abscesses. If the patient is seen in a primary care setting by a provider that is not comfortable in performing these procedures, the patient may be started on antibiotics and referred to a general surgeon for definitive treatment. Needle aspiration may be attempted for abscesses smaller than 3 cm or in lactational abscesses.'], Pathophysiology: The breast contains breast lobules, each of which drains to a lactiferous duct, which in turn empties to the surface of the nipple. There are lactiferous sinuses which are reservoirs for milk during lactation. The lactiferous ducts undergo epidermalization where keratin production may cause the duct to become obstructed, and in turn, can result in abscess formation. Abscesses associated with lactation usually begin with abrasion or tissue at the nipple, providing an entry point for bacteria. The infection often presents in the second postpartum week and is often precipitated in the presence of milk stasis. The most common organism known to cause a breast abscess is S. aureus, but in some cases, Streptococci, and Staphylococcus epidermidis may also be involved. Women are encouraged to continue breastfeeding or using a breast pump to continue draining milk from the affected ducts., Epidemiology:['0.4 to 11 percent of lactating mothers', 'GOOD', 'Primary prevention of breast abscess relies on mitigation of the risk factors and improving patient hygiene particularly in lactating patients. It relies especially on the mother and infant hygiene. Breastfeeding is advised to be continued after the abscess drainage to prevent recurrence.\n\nBreast abscess primary prevention measures include the following:\n\nPatients should be taught to keep the nipple area clean especially if there is injury\nComplete emptying of the breast after feeding the infant in order to prevent milk stasis\nKeep the infant in good contact during breastfeeding\nAvoid dehydration in the nipple and the surrounding to prevent cracking\nKeep the infant clean\nInfection control through washing hands frequently\nIt is advised to continue breastfeeding after the drainage to prevent recurrence and help healing.'], Complications:['CELLULITIS', 'cracked nipple', 'MASTITIS'], Diagnostics:['Complete Blood Count CBC', 'usg breast'], Differential diagnosis:['breast cancer.', 'CELLULITIS', 'Fibroadenoma', 'GALACTOCOELE', 'MASTITIS'], disease description:A breast abscess is a painful build-up of Breast abscesses are a common problem, especially in lactating women. Most breast abscesses are benign. However, when a non-lactating patient presents with a breast abscess, a more nefarious etiology such as an inflammatory carcinoma should be considered. Non-lactating patients presenting with breast abscess should also be screened for new-onset diabetes.pus in the breast caused by an infection. It mainly affects women who are breastfeeding.

Woman aged 33 experiencing ['breast tenderness', 'breast discharge', 'mastalgia', 'swelling at breast']

Disease Name: Breast Cysts , symptoms: ['breast tenderness', 'breast discharge', 'mastalgia', 'swelling at breast'], Treatment: ['A solitary cyst or small collection of cysts can be aspirated. If \nthey resolve completely, and if the fluid is not blood-stained, \nno further treatment is required. However, 30% will recur and \nrequire reaspiration. Cytological examination of cyst fluid is \nno longer practised routinely. If there is a residual lump or if \nthe fluid is blood-stained, a core biopsy or local excision for \nhistological diagnosis is advisable, which is also the case if \nthe cyst reforms repeatedly.'], Pathophysiology: Cysts seem to form as a result of fibrosis in breast tissue development and subsequent failure in the continuous process of the lobule and terminal ductule formation. The physical mechanism is that fibrosis causes thickening of the epithelium, and thus the developing lobule involutes early in its development. This causes the typical surrounding stroma to disappear and the adjoining ductule to break down, resulting in an aberrant epithelial lined fold, which becomes walled off entirely. The epithelial fold becomes dilated with epithelial acinar secretions and matures into a self-contained fluid-filled cavity. , Epidemiology:['The prevalence of benign breast disease is approximately 68% among all breast diseases.', 'good', 'You can’t prevent breast cysts. But regular self-exams and routine mammograms are good ways to manage overall breast health. Never assume a new lump is “just a cyst.” It’s always better to contact a healthcare provider for an exam.'], Complications:['hematomas', 'MASTITIS'], Diagnostics:['mammography', 'usg breast', 'usg breast', 'MRI BREAST', 'NEEDLE BIOPSY', 'CYTOLOGY', 'LARGE NEEDLE BIOPSY WITH VACCUM SYSTEMS'], Differential diagnosis:['ACTINOMYCOSIS OF BREAST', 'adenoid cystic carcinoma', 'CARCINOMA OF BREAST', 'HAEMATOMA OF BREAST'], disease description: Breast cysts are part of a larger benign disease process known as fibrocystic disease of the breast. This disease process is a wide spectrum of both fibrous and cystic changes in the breast tissue.The simple breast cyst forms as an aberration in the natural breast development and is composed of an epithelium lined fluid-filled cavity within the surrounding breast parenchyma. They can vary from small microcysts to large macrocysts and can be single or multiple. These cysts can be entirely asymptomatic and only discovered incidentally, or can be symptomatic, presenting as lumps, pain, or associated nipple discharge. Many studies report that in women, the lifetime prevalence of fibrocystic breast disease might be between 70% and 90%.The etiology of breast cysts is unknown. However, most breast cysts are associated with the aberration of normal development and involution (ANDI).

A 29-year-old woman suffering from ['swelling in abdomen', 'vaginal bleeding', 'Abdominal Pain']

Disease Name: Brenner Tumour, symptoms: ['swelling in abdomen', 'vaginal bleeding', 'Abdominal Pain'], Treatment: ['No adjuvant treatment for benign or borderline Brenner tumors.\nAdjuvant chemotherapy for advanced stage malignant Brenner tumors.', 'Oophorectomy'], Pathophysiology: The exact pathogenesis is unknown. Cell of origin of Brenner tumors is controversial; they may arise from Walthard rests., Epidemiology:['He mean age of patients with the noninvasive form ', '3.2% of ovarian epithelial neoplasms', 'Approximately 80% of malignant Brenner tumors are ', 'NA'], Complications:['TORSION'], Diagnostics:['Frozen Section', 'CT', 'Immunostaining', 'Immunostaining'], Differential diagnosis:['Adult granulosa cell tumour', 'CARCINOID TUMORS', 'Ovarian fibroma', 'Squamous cell carcinoma'], disease description:Brenner tumor is a rare ovarian tumor that is a part of the surface epithelial group of ovarian neoplasm. It is usually asymptomatic and most of the times it is an incidental pathological finding. Here we present a case of benign Brenner tumor of ovary treated surgically.Tumor composed of transitional / urothelial-like epithelium, typically embedded in fibromatous stroma.Benign, borderline and malignant variants are recognized, based on the growth pattern and cytological features of the epithelial cells.

Symptoms at 48 years: ['leg tenderness', 'leg pain', 'LOW GRADE FEVER']

Disease Name: Brodie’s Abscess, symptoms: ['leg tenderness', 'leg pain', 'LOW GRADE FEVER'], Treatment: ['Surgical evacuation and\ncurettage is performed under antibiotic cover. If\nthe cavity is large, it is packed with cancellous\nbone chips.'], Pathophysiology: A Brodie abscess is a subacute osteomyelitis, which may persist for years before progressing to a chronic, frank osteomyelitis. Classically, this may present after progression to a draining abscess extending from the tibia out through the skin. Occasionally acute osteomyelitis may be contained to a localized area and walled off by fibrous and granulation tissue.The most frequent causative organism is Staphylococcus aureus., Epidemiology:['The prevalence of acute primary hematogenous osteomyelitis in children is estimated to be between 1 and 13 per 100,000', 'GOOD', 'Reducing your risk of infection will also help your risk of developing osteomyelitis. In general, take precautions to avoid cuts, scrapes and animal scratches or bites, which give germs easy access to your body.'], Complications:['atrophy'], Diagnostics:['X RAY'], Differential diagnosis:['Eosinophilic Granuloma (Histiocytosis X)', 'Ewing sarcoma', 'osteosarcoma', 'sarcoma'], disease description:Brodie’s abscess is defined as a subacute or acute chronic osteomyelitis of the bone. It is an uncommon condition, usually mistaken for being a bone tumor , and has been frequently observed to involve the metaphysis of bones (especially tibia) . it is a special type of osteomyelitis in which the body’s defense mechanisms have been able to contain the infection so as to create a chronic bone abscess containing pus or jelly-like granulation tissue surrounded by a zone of sclerosis.Common sites are the upper end of the tibia and lower-end of the femur. It is usually located at the metaphysis.

Symptoms at 20 years old: ['cyanosis', 'barrel shaped chest', 'fatigue', 'tachypnoea', 'rhonchi', 'wheezing', 'breathlessness', 'dry cough']

Disease Name: Bronchial Asthma, symptoms: ['cyanosis', 'barrel shaped chest', 'fatigue', 'tachypnoea', 'rhonchi', 'wheezing', 'breathlessness', 'dry cough'], Treatment: [{'medication': ['Fluticasone ', 'Budesonide ', 'Ketotifen Fumarate ', 'Salbutamol/ Albuterol', 'Montelukast ', 'Theophylline ']}, 'The medications used for longterm\ntreatment of asthma include bronchodilators, steroids,\nmast cell stabilizers, leukotriene modifiers and theophylline'], Pathophysiology: Airway obstruction in asthma is caused by (i) edema and inflammation of mucous membrane lining the airways, (ii) excessive secretion of mucus, inflammatory cells and cellular debris and (iii) spasm of the smooth muscle of bronchi. Obstruction is diffuse but not uniform. Asthma has been classified as extrinsic (IgE mediated, triggered by allergens) and intrinsic (non IgE mediated, triggered by infection). Inhalation of an allergen leads to a biphasic response with early and late reactions ultimately causing bronchoconstriction. Early reaction starts within 10 minutes of the exposure to allergen. It is characterized by release of histamine, leukotrienes C,D,E, prostaglandins, platelet activating factor and bradykinin from the mast cells following the interaction of allergen with specific mast cell bound IgE. All these substances cause bronchoconstriction, mucosal edema and mucus secretion which manifests as airway obstruction. This phase is inhibited by Beta 2 agonist drugs. Late phase occurs in about two-third of patients. It develops 3-4 hours later with peak at 8-12 hours. Again there is a release of mast cell mediators. This phase is not prevented by premedication with Beta 2 agonist drugs. However, it is inhibited by premedication with steroids suggesting that airway narrowing is mainly due to an inflammatory reaction and mucosal edema. This phase presents as clinical asthma. Airway resistance is increased more so during exhalation because airways close prematurely during expiration. As a result lungs are hyperinflated; elasticity and frequency-dependent compliance of the lungs are reduced. Breathing involves more work resulting in dyspnea. Perfusion of inadequately ventilated lungs causes low Pa02 In early stages of illness PaC02 also falls because of hyperventilation caused by dyspnea. When obstruction becomes more severe, alveolar hypoventilation supervenes. This leads to retention of C02 with a rise of PaC02.With the exhaustion of buffer mechanisms, pH of blood falls (respiratory acidemia). Bronchial hyperresponsiveness and asthma: Bronchial hyperresponsiveness is one of the most characteristic features of asthma. This is attributed to one or more of the following abnormalities: i. defect in the airway, ii. abnormal neural control of the airways, and iii. bronchial inflammation It is suggested that an imbalance between excitatory (cholinergic, alpha-adrenergic and non-cholinergic) and inhibitory mechanisms (adrenergic and non-adrenergic) increases bronchial reactivity. Bronchoconstriction results from increased cholinergic activity causing bronchial smooth muscle to contract and bronchodilatation results from non-adrenergic system and endogenous catecholamines acting on the beta adrenergic receptors and prostaglandin E2. There are both inhibitory and excitatory nonadrenergic non-cholinergic nerves which secrete certain neuropeptides. Two of these have been well studied. Vasoactive intestinal peptides (VIP) relax smooth muscles of bronchi while substance-P increases smooth muscle tone, mucus hypersecretion and microvascular leakage., Epidemiology:['overall prevalence of 2.05%', 'GOOD', '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:['Cardiac arrhythmias', 'cyanosis', 'clubbing', 'barrel shaped chest'], Diagnostics:['EOSINOPHILS - ABSOLUTE COUNT', 'Radioallergosorbent test (RAST)', 'CHEST X RAY', 'PULMONARY FUNCTION TEST(PFT)'], Differential diagnosis:['Aspergillosis', 'BRONCHIOLITIS', 'Chronic Obstructive Pulmonary Disease', 'Chronic Sinusitis', 'CONGENITAL MALFORMATION', 'CYSTIC FIBROSIS', 'foreign body', 'pneumonitis', 'pulmonary eosinophilia', 'Sarcoidosis'], disease description:Bronchial asthma is a disease characterized by an increased responsiveness of the airways to various stimuli. It manifests by widespread narrowing of the airways causing paroxysmal dyspnea, wheezing or cough. The diffuse obstruction to the airflow is reversible in a large majority of cases, either spontaneously or in response to treatment. Bronchial reactivity is a necessary component of asthma.

Individual aged 39 with manifestations like ['cyanosis', 'pallor', 'tachypnoea', 'USE OF ACCESSORY MUSCLES OF RESPIRATION', 'fatigue', 'loss of appetite', 'Irritability', 'Recurrent infection', 'crackles', 'POSTURAL VARIATION', 'clubbing', 'wheezing', 'breathlessness', 'sputum production', 'fever', 'poor weight gain', 'blood in sputum']

Disease Name: Bronchiectasis, symptoms: ['cyanosis', 'pallor', 'tachypnoea', 'USE OF ACCESSORY MUSCLES OF RESPIRATION', 'fatigue', 'loss of appetite', 'Irritability', 'Recurrent infection', 'crackles', 'POSTURAL VARIATION', 'clubbing', 'wheezing', 'breathlessness', 'sputum production', 'fever', 'poor weight gain', 'blood in sputum'], Treatment: ['mucolytic administration,\naerosolization of bronchodilators and hyperosmolar agents (e.g.,\nhypertonic saline), and chest physiotherapy (e.g., postural drainage,\ntraditional mechanical chest percussion via hand clapping to the\nchest, or use of devices such as an oscillatory positive expiratory\npressure flutter valve or a high-frequency chest wall oscillation\nvest)', 'control of\nactive infection and improvements in secretion clearance and bronchial\nhygiene so as to decrease the microbial load within the airways and minimize the risk of repeated infections'], Pathophysiology: The most widely cited mechanism of infectious bronchiectasis is the “vicious cycle hypothesis,” in which susceptibility to infection and poor mucociliary clearance result in microbial colonization of the bronchial tree. Some organisms, such as Pseudomonas aeruginosa, exhibit a particular propensity for colonizing damaged airways and evading host defense mechanisms. Impaired mucociliary clearance can result from inherited conditions such as CF or dyskinetic cilia syndrome, and it has been proposed that a single severe infection (e.g., pneumonia caused by Bordetella pertussis or Mycoplasma pneumoniae) can result in significant airway damage and poor secretion clearance. The presence of the microbes incites continued chronic inflammation, with consequent damage to the airway wall, continued impairment of secretions and microbial clearance, and ongoing propagation of the infectious/ inflammatory cycle. Moreover, it has been proposed that mediators released directly from bacteria can interfere with mucociliary clearance. Classic studies of the pathology of bronchiectasis from the 1950s demonstrated significant small-airway wall inflammation and larger-airway wall destruction as well as dilation, with loss of elastin, smooth muscle, and cartilage. It has been proposed that inflammatory cells in the small airways release proteases and other mediators, such as reactive oxygen species and proinflammatory cytokines, that damage the larger-airway walls. Furthermore, the ongoing inflammatory process in the smaller airways results in airflow obstruction. It is thought that antiproteases, such as a1 antitrypsin, play an important role in neutralizing the damaging effects of neutrophil elastase and in enhancing bacterial killing. Bronchiectasis and emphysema have been observed in patients with a1 antitrypsin deficiency. Proposed mechanisms for noninfectious bronchiectasis include immune-mediated reactions that damage the bronchial wall (e.g., those associated with systemic autoimmune conditions such as Sjögren’s syndrome and rheumatoid arthritis). Traction bronchiectasis refers to dilated airways arising from parenchymal distortion as a result of lung fibrosis (e.g., postradiation fibrosis or idiopathic pulmonary fibrosis)., Epidemiology:['reached 1200 per 100,000 inhabitants among those aged 40 years', '30 to 40 per 100,000 individuals.', 'GOOD', 'You can reduce your risk of developing bronchiectasis by managing your lung health:\n\nMake sure you and your family are up-to-date on recommended vaccinations. Pertussis, the flu, pneumococcal disease, measles and staph infections can all cause or worsen bronchiectasis.\nWork with your healthcare provider to treat any ongoing health conditions, especially ones that affect your lungs. Keep your appointments and stick to your treatment plan. Talk to your provider if you feel like medications or therapies aren’t working.\nAvoid breathing in things that can hurt your lungs, like cigarette smoke, vaping, fumes and gases.'], Complications:['Chronic Obstructive Pulmonary Disease', 'recurrent chest infection'], Diagnostics:['AFB SMEAR', 'Complete Blood Count CBC', 'X RAY', 'BRONCHOSCOPY', 'SPUTUM CYTOLOGY'], Differential diagnosis:['aspiration pneumonia', 'Asthma', 'Bacterial pneumonia', 'CYSTIC FIBROSIS', 'emphysema', 'Gastroesophageal reflux disease (GERD)', 'PNEUMONIA', 'TUBERCULOSIS'], disease description:Bronchiectasis refers to an irreversible airway dilation that involves the lung in either a focal or a diffuse manner and that classically has been categorized as cylindrical or tubular (the most common form), varicose, or cystic. Bronchiectasis is a condition where damage causes the tubes in your lungs (airways) to widen or develop pouches. It makes it hard to clear mucus out of your lungs and can cause frequent infections. Coughing a lot with pus and mucus is the main symptom of bronchiectasis. Bronchiectasis can’t be cured but can be managed with treatment.

Symptoms at 21 years: ['tachypnoea', 'crackles', 'running nose', 'wheezing', 'paroxysmal cough', 'fever']

Disease Name: Bronchiolitis, symptoms: ['tachypnoea', 'crackles', 'running nose', 'wheezing', 'paroxysmal cough', 'fever'], Treatment: [{'medication': ['Salbutamol/ Albuterol']}, 'The treatment of children with viral bronchiolitis is supportive management.\nThose who are experiencing respiratory distress (hypoxia, inability to feed,\napnea, extreme tachypnea) should be hospitalized. High-flow nasal cannula is a noninvasive mode of oxygen\ndelivery capable of providing some positive end expiratory pressure, particularly\nin young children.'], Pathophysiology: The pathophysiology of acute bronchiolitis is characterized by bronchiolar obstruction with edema, mucus, and cellular debris. Resistance in the small air passages is increased during both inspiration and exhalation, but because the radius of an airway is smaller during expiration, the resultant respiratory obstruction leads to expiratory wheezing, air trapping, and lung hyperinflation. If obstruction becomes complete, trapped distal air will be resorbed and the child will develop atelectasis. Hypoxemia is a consequence of ventilation-perfusion mismatch. With severe obstructive disease hypercapnia can develop. Acute bronchiolitis is usually preceded by exposure to contacts with a minor respiratory illness within the previous week. The infant first develops signs of upper respiratory tract infection with sneezing and clear rhinorrhea. This may be accompanied by diminished appetite and fever. Gradually, respiratory distress ensues, with paroxysmal cough, dyspnea, and irritability. The infant is often tachypneic, which can interfere with feeding. Apnea may precede lower respiratory signs early in the disease, particularly with very young infants. Term infants at a postconceptual age of <44 wk and preterm infants at postconceptual age <48 wk are at highest risk for apneic events., Epidemiology:[', the incidence has been reported to be about 11% to 15%. Depending on the severity of the infection, there are at least 5 hospitalizations for every 1000 children younger than 2 years of age.', 'GOOD', 'Bronchiolitis can be spread by small children through close contact, saliva and mucus. The best way to prevent infection is to avoid others who are sick, and practice good hand washing. Until your child is better, keep him or her home from daycare and be sure to wash toys between uses. Do not share cups, forks or spoons.\n\nIn some cases, children may be given the RSV antibody palivizumab (Synagis®) to prevent RSV infections. This might happen if your healthcare provider thinks that your child is at a higher risk of having serious complications. Your child might be one of these if they have congenital heart defects or were very premature.\n\nAs with any type of medication, you should discuss palivizumab with your doctor so you understand what it is supposed to do, how and how often it is given and what the side effects might be. Also, you might want to check with your insurance provider to check on costs.'], Complications:['Asthma', 'Bronchopulmonary dysplasia'], Diagnostics:['Complete Blood Count CBC', 'immunoflorescence for anti IgG', 'X RAY', 'CHEST RADIOGRAPH'], Differential diagnosis:['Asthma', 'Bacterial pneumonia', 'Chronic Obstructive Pulmonary Disease', 'Croup', 'CYSTIC FIBROSIS', 'heart failure', 'pertussis', 'TUBERCULOSIS'], disease description:Acute bronchiolitis is a diagnostic term used to describe the clinical picture produced by several different viral lower respiratory tract infections in infants and very young children. The respiratory findings observed in bronchiolitis include tachypnea, wheezing, crackles, and rhonchi which result from inflammation of the small airways. Despite its commonality, a universal set of diagnostic criteria for bronchiolitis does not exist, with significant disagreement about the upper age limit for appropriate use of the diagnosis. Some clinicians restrict the term to children younger than 1 yr, and others extend it to the age of 2 yr or beyond.

A 45-year-old individual dealing with ['rhinitis', 'fever', 'crackles', 'wheezing', 'chest pain', 'dry cough', 'malaise']

Disease Name: Bronchitis, symptoms: ['rhinitis', 'fever', 'crackles', 'wheezing', 'chest pain', 'dry cough', 'malaise'], Treatment: ["Because most cases of bronchitis are caused by viral infections, antibiotics aren't effective. However, if your doctor suspects that you have a bacterial infection, he or she may prescribe an antibiotic.\n\nIn some circumstances, your doctor may recommend other medications, including:\n\nCough medicine. If your cough keeps you from sleeping, you might try cough suppressants at bedtime.\nOther medications. If you have allergies, asthma or chronic obstructive pulmonary disease (COPD), your doctor may recommend an inhaler and other medications to reduce inflammation and open narrowed passages in your lungs.", 'There is no specific therapy for acute bronchitis. The disease is self-limited, and\nantibiotics, although often prescribed, do not hasten improvement. Cough suppressants can relieve symptoms but can also increase the risk\nof suppuration and inspissated secretions and therefore should be used\njudiciously.'], Pathophysiology: The tracheobronchial epithelium is invaded by the infectious agent, leading to activation of inflammatory cells and release of cytokines. Constitutional symptoms including fever and malaise follow. The tracheobronchial epithelium can become significantly damaged or hypersensitized, leading to a protracted cough lasting 1-3 wk. The child first presents with nonspecific upper respiratory infectious symptoms, such as rhinitis. Three to 4 days later, a frequent, dry, hacking cough develops, which may or may not be productive. After several days, the sputum can become purulent, indicating leukocyte migration but not necessarily bacterial infection. Many children swallow their sputum which can produce emesis. Chest pain may be a prominent complaint in older children and is exacerbated by coughing. The mucus gradually thins, usually within 5-10 days, and then the cough gradually abates. The entire episode usually lasts about 2 wk and seldom longer than 3 wk. Chronic bronchitis is well recognized in adults, formally defined as 3 mo or longer of productive cough each year for 2 or more yr. The disease can develop insidiously, with episodes of acute obstruction alternating with quiescent periods. Some predisposing conditions can lead to progression of airflow obstruction or chronic obstructive pulmonary disease, with smoking as the major factor (up to 80% of patients have a smoking history). Other conditions include air pollution, occupational exposures, and repeated infections. In children, cystic fibrosis, bronchopulmonary dysplasia, and bronchiectasis must be ruled out., Epidemiology:['It is estimated that every year, 5% of the general population reports an episode of acute bronchitis.', 'GOOD', 'The best way to reduce your risk of bronchitis is to avoid getting sick from viruses and other causes of lung irritation. Specific ways to reduce your risk include:\n\nTry to avoid being around other people if you or they may be sick. This is especially true in the winter months when people gather indoors.\nAvoid smoke and other irritants.\nIf you have asthma or allergies, avoid any triggers (including pets, dust and pollen).\nRun a humidifier. Moist air is less likely to irritate your lungs.\nGet plenty of rest.\nEat a healthy diet.\nWash your hands often with soap and water. If you’re not able to use soap and water, use a hand sanitizer that contains alcohol.\nMake sure you are up-to-date on flu and pneumonia vaccines.'], Complications:['PNEUMONIA'], Diagnostics:['CHEST X RAY', 'PULMONARY FUNCTION TEST(PFT)', 'X RAY', 'sputum microscopy'], Differential diagnosis:['allergy', 'BRONCHIECTASIS', 'BRONCHIOLITIS', 'Chronic Obstructive Pulmonary Disease', 'Congenital heart disease', 'CYSTIC FIBROSIS', 'Gastroesophageal reflux disease (GERD)', 'Influenza', 'sinusitis', 'TUBERCULOSIS'], disease description: Acute bronchitis is a syndrome, usually viral in origin, with cough as a prominent feature. Acute bronchitis often follows a viral upper respiratory tract infection. It is more common in the winter when respiratory viral syndromes predominate. The tracheobronchial epithelium is invaded by the infectious agent, leading to activation of inflammatory cells and release of cytokines. Constitutional symptoms including fever and malaise follow. The tracheobronchial epithelium can become significantly damaged or hypersensitized, leading to a protracted cough lasting 1-3 wk. Chronic bronchitis is well recognized in adults, formally defined as 3 months or longer of productive cough each year for 2 or more yr. The disease can develop insidiously, with episodes of acute obstruction alternating with quiescent periods.

Person at 55 with ['cyanosis', 'oxygen dependence', 'dyspnea', 'Hypoxia', 'respiratory distress', 'tachypnoea', 'breathlessness', 'pulmonary hypertension']

Disease Name: Bronchopulmonary Dysplasia, symptoms: ['cyanosis', 'oxygen dependence', 'dyspnea', 'Hypoxia', 'respiratory distress', 'tachypnoea', 'breathlessness', 'pulmonary hypertension'], Treatment: [{'medication': ['Furosemide ', 'caffeine ', 'Azithromycin ', 'Vitamin A (Retinol)']}, 'Corticosteroids: Systemic corticosteroids have been used in BPD to improve lung function, reduce inflammation and reduce the need for mechanical ventilation. However, concerns about long term neurodevelopmental outcomes have led to recommendations to restrict their use to infants with severe BPD who remain ventilator dependent with high oxygen needs.\nDiuretics: Thiazides and loop diuretics are the most commonly used diuretics in the setting to improve short term pulmonary mechanics of BPD. These agents are most commonly used in infants who are ventilator dependent with increasing requirement of positive end-expiratory pressure despite fluid restriction. A systemic review of available literature does not show any improvement in long term clinical outcome in infants with established or developing BPD.\nBronchodilators:- administration of beta-2 agonists can decrease airway resistance and improve compliance. However, their routine use is not recommended in BPD as it has not been shown to improve long term outcomes. Their use should be restricted to manage acute episodes of bronchoconstriction in older infants who remain ventilator dependent.'], Pathophysiology: Injury from mechanical ventilation and reactive oxygen species to premature lungs in the presence of antenatal factors predisposing the lungs to BPD form the basis of pathogenesis of BPD in preterm neonates. This myriad of events leads to an exaggerated inflammatory response with an increase in proinflammatory cytokines like interleukin(IL)-6, IL 8, tumor necrosis factor alpha etc along with growth factors (transforming growth factor ) and angiogenic factors (vascular endothelial growth factor, angiopoietin 2) which ultimately results in aberrant tissue repair and arrest in lung development. Dysregulated vascular and arrested alveolar development form the basis of the pathology seen in “new BPD.”, Epidemiology:['The annual incidence in the first year of life is about 11 cases/100 children.', 'variable', 'To help prevent BPD:\n\nPrevent premature delivery whenever possible. If you are pregnant or thinking about getting pregnant, get prenatal care to help keep you and your baby healthy.\nIf your baby is on breathing support, ask the provider how soon your baby can be weaned from the ventilator.\nYour baby may receive surfactant to help keep the lungs open.'], Complications:['pulmonary hypertension', 'systemic hypertension'], Diagnostics:['Arterial Blood Gas Analysis(ABG)', 'CT Thorax'], Differential diagnosis:['Atelectasis', 'hypertension', 'patent ductus arteriosus', 'PNEUMONIA'], disease description:Bronchopulmonary dysplasia is one of the most common causes of morbidity and mortality in preterm infants. Despite significant advances in preterm infant care over the past few decades, the prevalence of this condition remains high. BPD is the result of a newborn's lungs not developing normally while the baby is growing in the womb, or not developing fully if the baby was born premature. Babies with BPD have fragile lungs that can be easily irritated or inflamed after birth.

A 22-year-old patient with ['hepatosplenomegaly', 'lymphadenopathy', 'arthralgia', 'fatigue', 'fever', 'headache', 'Muscle ache', 'poor appetite']

Disease Name: Brucellosis, symptoms: ['hepatosplenomegaly', 'lymphadenopathy', 'arthralgia', 'fatigue', 'fever', 'headache', 'Muscle ache', 'poor appetite'], Treatment: [{'medication': ['Doxycycline ', 'Sulfamethoxazole + Trimethoprim {Co-trimoxazole } ']}, 'Treatment of human brucellosis (adult or pediatric) is\nalways with a combination of antibiotics for 6 weeks as\nall monotherapies and short treatments are characterized\nby unacceptably high relapse rates. The standard regime is a\ncombination of doxycycline with streptomycin for 3 weeks\nfollowed by doxycycline and rifampicin to complete 3\nmore weeks. For children less than 8 yr of age combinations\ncontaining rifampicin and TMP-SMZ with or\nwithout aminoglycosides are recommended. Regimes\ncontaining macrolides and quinolones are also being\nevaluated. Treatment is prolonged for endocarditis and\nneurobrucellosis.'], Pathophysiology: Brucella species are intracellular gram-negative coccobacilli. The classification of brucella species is based on its preferred hosts namely B. melitensis (sheep and goats), B. abortus (cattle), B. suis (pigs), B. canis (dogs). Brucellosis is a zoonosis and transmission to humans can occur through the consumption of infected unpasteurized milk and animal products, through direct contact with infected animal parts such as placenta, by inoculation of skin and mucous membranes, and by inhalation of infected aerosolized particles. The vast majority of cases worldwide are attributed to B. melitensis. Human brucellosis can be an acute illness (<2 months), subacute illness (2-12 months) or chronic illness (>1 yr). The incubation period is usually between 7 days and 3 months. A history of exposure to animals especially drinking unpasteurized milk without proper boiling is present. Fever can be continuous or intermittent and persist for several months due to partial response to antibiotics. Fever is usually accompanied by profuse sweating, joint pains (particularly knee) and hepatosplenomegaly and less common lymphadenopathy. In untreated cases complications such as spondylitis, osteoarthritis, meningoencephalitis, brain abscess, pneumonia and endocarditis can occur., Epidemiology:['approximately 500,000 cases are reported annually', 'GOOD', 'There is no vaccine available for brucellosis. However, you can reduce your risk if you avoid eating or drinking unpasteurized milk, cheese and ice cream when you travel. Hunters should wear rubber gloves when handling the internal organs of animals.'], Complications:['Brain Abscess', 'Endocarditis', 'PNEUMONIA', 'Osteoarthritis', 'spondylitis'], Diagnostics:['BLOOD CULTURE test', 'Hb', 'PLATELET COUNT', 'serum igG igM', 'LIVER FUNCTION TEST LFT', 'White Blood Cell count WBC', 'MRI'], Differential diagnosis:['Brain Abscess', 'Cat scratch disease', 'Cystitis', 'enteric fever', 'epididymitis', 'HIV infection and AIDS', 'Malaria', 'Meningitis', 'osteomyelitis', 'Sarcoidosis', 'TUBERCULOSIS', 'Urinary Tract Infection', 'viral hepatitis'], disease description:Brucellosis is a bacterial infection that spreads from animals to people. Most commonly, people are infected by eating raw or unpasteurized dairy products. Sometimes, the bacteria that cause brucellosis can spread through the air or through direct contact with infected animals.Signs and symptoms of brucellosis may include fever, joint pain and fatigue. The infection can usually be treated with antibiotics. However, treatment takes several weeks to months, and the infection can recur.

Experiencing ['diarrhea', 'flushing', 'headache', 'sweating', 'Autism spectrum disorder', 'Behavioural DIsorder'] at 53 years

Disease Name: Brunner Syndrome, Maoa Deficiency, symptoms: ['diarrhea', 'flushing', 'headache', 'sweating', 'Autism spectrum disorder', 'Behavioural DIsorder'], Treatment: ['serotonin reuptake inhibitor, dietary modifications and avoidance of medications contraindicated in patients on monoamine oxidase inhibitors'], Pathophysiology: Monoamine oxidase A deficiency is caused by mutations in the MAOA gene. This gene provides instructions for making an enzyme called monoamine oxidase A. This enzyme breaks down chemicals called monoamines, including serotonin, epinephrine, and norepinephrine. These particular monoamines act as neurotransmitters, which transmit signals between nerve cells in the brain. Monoamine oxidase A helps break down the neurotransmitters when signaling is no longer needed. Signals transmitted by serotonin regulate mood, emotion, sleep, and appetite. Epinephrine and norepinephrine control the body's response to stress. Monoamine oxidase A also helps break down monoamines found in the diet.Mutations in the MAOA gene reduce monoamine oxidase A activity, which causes serotonin and other neurotransmitters to build up in the brain. It is unclear how this buildup leads to the signs and symptoms of monoamine oxidase A deficiency. Researchers suspect that high levels of serotonin may impair an affected individual's ability to control his impulses, leading to aggressive outbursts. In addition, the outbursts may be an overreaction to stress, possibly due to the impaired breakdown of epinephrine and norepinephrine., Epidemiology:['. Only about a third of people in Western populations have the low-activity form of MAOA', 'variable', "This condition is inherited in an X-linked recessive pattern and therefore, it can't be prevented. \nAlthough Genetic counselling is advisable."], Complications:['intellectual disability'], Diagnostics:['Urine analysis'], Differential diagnosis:['Attention Deficit-hyperactivity disorder (ADHD)', 'Autism spectrum disorder'], disease description:Brunner syndrome is a recessive X-linked disorder characterized by impulsive aggressiveness and mild mental retardation associated with MAOA deficiency.This condition is inherited in an X-linked recessive pattern. The gene associated with this condition is located on the X chromosome, which is one of the two sex chromosomeMonoamine oxidase A deficiency is thought to be very rare. Its prevalence is unknown.

A 42-year-old individual dealing with ['chills', 'gastrointestinal disorders', 'headache', 'leg pain', 'high fever', 'swollen lymphnodes', 'respiratory difficulties']

Disease Name: Bubonic Plague, symptoms: ['chills', 'gastrointestinal disorders', 'headache', 'leg pain', 'high fever', 'swollen lymphnodes', 'respiratory difficulties'], Treatment: [{'medication': ['Ciprofloxacin ', 'Doxycycline ', 'Gentamicin ']}], Pathophysiology: ??Although other means of contraction exist, Yersinia Pestis classically travels from enzootic rodent to a flea vector, in whom it forms a blockage in the gastrointestinal tract. This blockage causes flea to feed more often and regurgitate Y. Pestis into the host with each bite.  Following entering the host, Y. Pestis has many means of avoiding the immune system and typically travels to lymph nodes to propagate within macrophages.  Due to the pathophysiologic involvement of lymph nodes, 80 to 95% of Y. pestis infections present as the suppurative adenitis known as bubonic plague ., Epidemiology:['1,000 and 2,000 cases each year are reported to the World Health Organization (WHO), though the true number is likely much higher.', 'prognosis of all presentations of plague is poor. ', 'Make your home and yard inhospitable to rodents (mice, rats, squirrels) and other wild animals.\nDon’t leave places for them to hide or food for them to eat. This means cleaning up clutter, brush and other items and being careful when feeding animals.\nUse flea control products for your pets, especially those who are allowed to roam freely. \n.Take sick pets to the veterinarian immediately.\n.Don’t let pets who roam freely sleep in your bed.\n.Wear protective clothing — especially gloves — if you handle dead animals.\n.Use insect repellent if you go into wooded locations or other places that may expose you to fleas. Look for repellents that use DEET or permethrin.'], Complications:['Meningitis', 'death', 'gangrene'], Diagnostics:['Complete Blood Count CBC', 'TISSUE SMEAR', 'lymph node examination'], Differential diagnosis:['Anthrax', 'Brucellosis', 'Chancroid', 'Disseminated Intravascular Coagulation (DIC)', 'lymphadenitis', 'lymphadenopathy', 'Malaria', 'Rocky Mountain spotted fever', 'septic shock', 'Syphilis', 'Systemic inflammatory response syndrome (SIRS)', 'tularemia', 'typhus'], disease description:Plague is an infectious disease caused by a specific type of bacterium called Yersinia pestis. Y. pestis can affect humans and animals and is spread mainly by fleas. Bubonic plague is one type of plague. It gets its name from the SWOLLEN LYMPH NODES (buboes) caused by the disease. The nodes in the armpit, groin and neck can become as large as eggs and can ooze pus.

A 21-year-old suffering ['Abdominal Pain', 'ascites', 'splenomegaly', 'Tender Hepatomegaly', 'HEPATOMEGALY', 'abdominal distension', 'anorexia', 'jaundice', 'yellowish discoloration of eyes', 'pedal edema', 'Severe abdominal pain', 'nausea', 'vomiting']

Disease Name: Budd Chiari Syndrome, symptoms: ['Abdominal Pain', 'ascites', 'splenomegaly', 'Tender Hepatomegaly', 'HEPATOMEGALY', 'abdominal distension', 'anorexia', 'jaundice', 'yellowish discoloration of eyes', 'pedal edema', 'Severe abdominal pain', 'nausea', 'vomiting'], Treatment: ['Goals of Treatment \n\nRelieving obstruction \nCorrecting underlying conditions \nMonitoring liver deterioration\n Treatment of Budd-Chiari Syndrome\n\nAnticoagulants are the mainstay of treatment. They are started initially with low-molecular-weight heparin and then transitioned to warfarin, which is continued lifelong. PT/INR should be monitored and should be kept in the therapeutic range for patients on warfarin.\nOther treatment options include thrombolysis and stenting, as well as placement of a transjugular intrahepatic portosystemic shunt in acute forms of BCS, which fail to respond.\nSurgical decompression can also be considered in acute forms if other therapies fail.\nLiver transplantation: In patients who fail all therapies or who have developed decompensated cirrhosis, liver transplantation may be an option. The ten-year survival rate ranges from 69-84% as per two reported studies.'], Pathophysiology: Budd–Chiari syndrome (BCS) is a condition principally affecting young females, in which the venous drainage of the liver is occluded by hepatic venous thrombosis or obstruction from a venous web. As a result of venous outflow obstruction, the liver becomes acutely congested, with the development of impaired liver function and, subsequently, portal hypertension, ascites and oesophageal varices. In an acute thrombosis, the patient may rapidly progress to fulminant liver failure but, in the majority of cases, abdominal discomfort and ascites are the main presenting features. If chronic, the liver progresses to established cirrhosis. The cause of the venous thrombosis needs to be established, and an underlying myeloproliferative disorder or procoagulant state is commonly found, such as antithrombin 3, protein C or protein S deficiency. The diagnosis is commonly suspected in a patient presenting with ascites, in whom a CT scan shows a large congested liver or a small cirrhotic liver in which there is gross enlargement of segment I (the caudate lobe); this feature results from preservation and hypertrophy of the segment with direct venous drainage to the IVC in the face of atrophy of the rest of the liver due to venous obstruction. IVC compression or occlusion from the segment I hypertrophy is also a common feature, as is portal vein thrombosis., Epidemiology:['between 1/50,000 and 1/100,000.', 'May be fatal'], Complications:['ascites', 'PORTAL HYPERTENSION', 'oesophageal varices'], Diagnostics:['CT Abdomen', 'USG ABDOMEN(W/A)', 'LIVER FUNCTION TEST LFT', 'SERUM ANTITHROMBIN III LEVEL', 'SERUM PROTEIN C LEVEL', 'SERUM PROTEIN S LEVEL', 'DOPPLER USG'], Differential diagnosis:['appendicitis', 'CAROLIS DISEASE', 'chronic granulomatous disease', 'Cytomegalovirus (CMV) infection', 'INTUSSUSSEPTION', 'pancreatic pseudocyst', 'Pancreatitis', 'POLYCYSTIC LIVER DISEASE', 'PRIMARY BILIARY CIRRHOSIS', 'PRIMARY SCLEROSING CHOLANGITIS'], disease description:Budd–Chiari syndrome (BCS) is a condition principally affecting young females, in which the venous drainage of the liver is occluded by hepatic venous thrombosis or obstruction from a venous web. As a result of venous outflow obstruction, the liver becomes acutely congested, with the development of impaired liver function and, subsequently, portal hypertension, ascites and oesophageal varices. 

Symptoms reported at the age of 28: ['gangrene', 'ulceration', 'Thrombophlebitis migrans', 'Pain', 'blackening of distal part', 'rest pain', 'claudication']

Disease Name: Buerger Disease, symptoms: ['gangrene', 'ulceration', 'Thrombophlebitis migrans', 'Pain', 'blackening of distal part', 'rest pain', 'claudication'], Treatment: [{'medication': ['Aspirin/Acetylsalicylic acid']}, 'Patient is in supine position, legs elevated to 45 degree. Time taken \nfor blanchi ng is observed and for 2 more minutes limb is kept \nelevated. Patient is made to sit in high sitting position with limb \nin lowered position for 2 minutes. Lastly patient is made in supine \nposition for 5 minutes. This seq uence is done 5 times/session with \n3 sessions a day.', 'Low dose of aspirin 75 mg once a day-antithrombin activity. \nProstacyclins, ticlopidine, praxilene, carnitine. \nClopidogrel 75 mg; atorvastatin 1 0 mg; parvostatin 40 mg; \nci/ostazo/e 100 mg bid- is a phosphodiesterase inhibitor \nwhich improves circulation (ideal drug). \nHowever, graded injection of xanthine nocotinate \n3000 mg from day 1 to 9000 mg on day 5 is often practiced \nto promote ulcer healing', '1.Omentoplastyto revascularise the affected limb. \n2.Profundaplasty.\n3.Lumbar sympathectomy.\n4.Amputations are done at different levels depending on site, \nseverity and extent of vessel occlusion.\n5.lzarov method of bone lengthening helps in improving the \nrest pain and claudication'], Pathophysiology: Smoke contains carbon monoxide and nicotinic acid . Carboxyhaemoglobin Causes initially vasospasm and hyperplasia of intima . Thrombosis and so obliteration of vessels occur, commonly medium-sized vessels are involved. Panarteritis is common Usually involvement is segmental ventually artery, vein and nerve are together involved. Nerve involvement causes rest pain , Patient presents with features of ischaemia in the limb Once blockage occurs, plenty of collaterals open up depending on the site of blockage either around knee joint or around buttock Once collaterals open up, through these collaterals, blood supply is maintained to the ischaemic area  It is called as compensatory peripheral vascular disease , If patient continues to smoke, disease progresses into the collaterals, blocking them eventually, leading to severe ischaemia and is called as decompensatory peripheral vascular disease. It is presently called as critical limb ischaemia. It causes rest pain, ulceration, gangrene., Epidemiology:['the prevalence has reduced to approximately 12.6-20 cases per 100,000 population', '45 to 63% in India, 16 to 66% in Korea and Japan, and 80% among Ashkenazi Jews', 'variable', 'To avoid getting Buerger’s disease, don’t smoke or use tobacco of any kind. You should avoid nicotine patches and marijuana as well.'], Complications:['gangrene', 'infection', 'ulceration'], Diagnostics:['pulmonary angiography', 'compression USG', 'DUPLEX ULTRASONOGRAPHY', 'ASCENDING VENOGRAPHY', 'MR VENOGRAPHY', 'CT PULMONARY ANGIOGRAM'], Differential diagnosis:['Atherosclerosis', 'Diabetes mellitus type 1', 'Diabetes mellitus type 2', 'DIABETIC GANGRENE', 'FROSTBITE', 'Giant cell arteritis', 'Polyarteritis Nodosa', 'Raynaud phenomenon', 'scleroderma', 'systemic lupus erythematosus (SLE)'], disease description:It is a disease very commonly seen in young and middle-aged males; seen in smokers and tobacco users; not usually seen in females due to genetic reasons (but can occur in females very rarely).Almost always starts in lower limb, may start on one side and later on the other side. Upper limb involvement occurs only after lower limb is diseased. Only upper limb involvemnt can occur (not uncommon) but it is rare. It is nonatherosclerotic inflammatory disorder involving medium sized and distal vessels with cell mediated sensitivity to type I and type 111 collagen.

having ['blisters', 'papules', 'lymphadenopathy', 'malaise', 'fever'] at the age of 48

Disease Name: Buffalopox, symptoms: ['blisters', 'papules', 'lymphadenopathy', 'malaise', 'fever'], Treatment: ['Localized milkers nodes were usually treated symptomatically by applying protective bandages with desiccating ointments, powders and local antibiotics to prevent secondary infection.', 'Treatment is supportive.'], Pathophysiology: Predisposing factors Infection is more common in those who have not received smallpox vaccination. Buffalopoxvirus is an orthopoxvirus. The appearance of lesions is often accompanied by fever, malaise and local lymphadenopathy. Lesions are most common at sites of contact or contamination such as the hands, forearms and face. They start as papules and evolve into blisters before then crusting and sometimes ulcerating. Healing, often with scarring, is complete in a month., Epidemiology:['prevalence rate of 10.13%', 'bad'], Complications:['corneal damage'], Diagnostics:['PCR'], Differential diagnosis:['COWPOX', 'ORF', 'skin infection'], disease description:Buffalopox is caused by buffalopox virus (BPXV); it is a Poxviridae for which the natural host is buffalo. It mainly infects buffalo but has been known to infect cows and humans. It is classified in the Orthopoxvirus (OPV) genus and the subfamily Chordopoxvirinae. The appearance of buffalopox follows a pattern and is described as emerging and re-emerging, it commonly occurs in sporadic and epidemic forms in domestic and commercial farm settings.

Suffering from ['pruritic maculopapular lesion', 'visible as a haemorrhagic punctum', 'itching'] at the age of 45

Disease Name: Bugs Bite, symptoms: ['pruritic maculopapular lesion', 'visible as a haemorrhagic punctum', 'itching'], Treatment: ['Topical \nsteroids are used to relieve symptoms. Systemic antihistamines may be helpful in cases of severe pruritus. Secondary \nbacterial infections may require topical or systemic antibiotics, \ndepending on the severity.'], Pathophysiology: Bedbugs normally feed at night, usually about an hour before dawn, but they may feed during the day if circumstances are favourable. They usually fear light and avoid glossy surfaces. During the day, they hide in dark places such as crevices in furniture and mattresses or peeling wallpaper. Searching for a food source is erratic, and is probably at random at distances greater than a few centimetres, but in the final approach to the host, both temperature and odour play a part in guiding the bug. Feeding time is relatively short (3–12 min). During feeding, the bedbug injects saliva containing an anticoagulant and anaesthetic. Recently, a study demonstrates that allergens causing itching and skin lesions are most likely contained in the saliva of bedbugs. Interestingly, bedbugs without salivary glands attempted to feed but were unable to do so, indicating that saliva is necessary for the feeding process. Furthermore, bedbug saliva was potent enough to cause pruritus and lesion development in a human volunteer by topical application alone, without breaking the skin., Epidemiology:['the crude rate of bite and sting injuries was 340.1 (95% CI, 232.9–447.3) per 100,000 persons per year', 'good', 'To Do : It is classically recommended to wash mattress \ncovers and bed linen at 60°C.'], Complications:['secondary infection'], Diagnostics:['allergy skin test'], Differential diagnosis:['Bedbug bite', 'Chigger bite', 'erythema multiforme', 'Flea bites', 'Ticks (Acari) bite'], disease description:A bite is when an insect (like a mosquito, flea, or bedbug) uses its mouth to break a person's skin, usually so it can feed. Insect bites usually itch. A sting is when an insect uses another body part, such as a barbed stinger at its tail end, to pierce the skin and inject venom (like a poison).

A 31-year-old patient experiencing ['regional lymphadenopathy', 'vesicles', 'PUSTULE']

Disease Name: Bullous Impetigo, symptoms: ['regional lymphadenopathy', 'vesicles', 'PUSTULE'], Treatment: ['Mupirocin, retapamulin, and fusidic acid are the treatments of choice.\n\nSystemic antibiotics should be prescribed for all cases of bullous impetigo and cases of non-bullous impetigo with more than five lesions, deep tissue involvement, systemic signs of infection, lymphadenopathy or lesions in the oral cavity. Beta-lactamase-resistant antibiotics such as cephalosporins, amoxicillin-clavulanate, dicloxacillin are the treatment of choice. Cephalexin is commonly used. If culture confirms an infection solely caused by streptococci, oral penicillin is the preferred therapy.', 'Topical antibiotics alone or in conjunction with systemic antibiotics are used to treat impetigo. Antibiotic coverage should cover both S aureus and S pyogenes (i.e. GABHS).'], Pathophysiology: Any disturbance of the skin barrier leads to access to fibronectin receptors by GABHS and S aureus which require fibronectin for colonization. Trauma, cuts, insect bites, surgery, atopic dermatitis, burns, and varicella are common mechanisms of skin breakdown. Once a lesion is present, self-inoculation to other sites is very common. Malnutrition, immunosuppression, daycare attendance, overcrowding, diabetes, and poor hygiene make one more susceptible to impetigo.Triggers that breakdown skin and increase susceptibility to impetigo include:VaricellaHerpesScratchingLiceBurnsTraumaInsect bites, Epidemiology:['11.2% GLOBALLY', 'GOOD', 'People can get impetigo more than once. Having impetigo does not protect someone from getting it again in the future. There are no vaccines to prevent group A strep infections, but there are things you can do to help protect yourself and others.\n\nTo help prevent group A step infections, you should:\n\nClean and care for wounds\nWash your hands and laundry often\nTake antibiotics, if prescribed'], Complications:['renal compilcations', 'staphylococcal infections', 'hematuria', 'Staphylococcal scalded skin syndrome'], Diagnostics:['ANTISTREPTOLYSIN O (ASO) TITRE', 'full thickness skin biopsy'], Differential diagnosis:['Atopic dermatitis', 'candidiasis', 'HERPES SIMPLEX', 'Irritant contact dermatitis', 'scabies', 'Varicella zoster'], disease description:Impetigo is a common infection of the superficial layers of the epidermis that is highly contagious and most commonly caused by gram-positive bacteria. It most commonly presents as erythematous plaques with a yellow crust and may be itchy or painful.  The lesions are highly contagious and spread easily. Impetigo is a disease of children who reside in hot humid climates. The infection may be bullous or nonbullous. The infection typically affects the face but can also occur in any other part of the body that has an abrasion, laceration, insect bite or other trauma.The neonate is peculiarly liable to the development of bullous impetigo, which is most often caused by phage group II strains of S. aureus . The disorder in neonates differs in no significant way from that in older children and adults, although it was formerly distinguished by the rather confusing term pemphigus neonatorum.