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Woman aged 52 presenting symptoms such as ['No dehydration', 'disorientation', 'hypertension', 'Hypoglycaemia', 'weight loss', 'Ambiguous genitalia in females', 'Postnatal virilization in males and females', 'diarrhea', 'Dizziness', 'fatigue', 'vomiting', 'weakness', 'Muscle ache']

Disease Name: 11ß-hydroxylase Deficiency, symptoms: ['No dehydration', 'disorientation', 'hypertension', 'Hypoglycaemia', 'weight loss', 'Ambiguous genitalia in females', 'Postnatal virilization in males and females', 'diarrhea', 'Dizziness', 'fatigue', 'vomiting', 'weakness', 'Muscle ache'], Treatment: [{'medication': ['Hydrocortisone ']}, 'Vaginoplasty and\nclitoral recession'], Pathophysiology: Congenital adrenal hyperplasia (CAH) is a family of autosomal recessive disorders of cortisol biosynthesis.it occurs due to defect in CYP11B1 8q24.3gene.Cortisol deficiency increases secretion of corticotropin (adrenocorticotropic hormone [ACTH]), which, in turn, leads to adrenocortical hyperplasia and overproduction of intermediate metabolites., Epidemiology:nan, Complications:[], Diagnostics:['ACTH', 'Cortisol', 'Plasma Renin', 'serum potassium K+', 'SERUM ANDROGEN LEVEL'], Differential diagnosis:[], disease description:Congenital adrenal hyperplasia (CAH) is a family of autosomal recessive disorders of cortisol biosynthesis.it occurs due to defect in CYP11B1 8q24.3gene

Individual, 30 years old, with ['muscle weakness', 'Ambiguous genitalia in males', 'Sexual infantilism', 'decrease level of consciousness', 'breathlessness', 'Dizziness', 'headache', 'lethargy', 'vomiting']

Disease Name: 17a Hydroxylase/17,20- Lyase Deficiency, symptoms: ['muscle weakness', 'Ambiguous genitalia in males', 'Sexual infantilism', 'decrease level of consciousness', 'breathlessness', 'Dizziness', 'headache', 'lethargy', 'vomiting'], Treatment: [{'medication': ['Hydrocortisone ']}, 'sex hormone\nreplacement\nconsonant with sex\nof rearing', 'Orchidopexy or removal of\nintraabdominal\ntestes;'], Pathophysiology: Congenital adrenal hyperplasia (CAH) is a family of autosomal recessive disorders of cortisol biosynthesis.CYP17 10q24.3 gene defect is present., Epidemiology:nan, Complications:[], Diagnostics:['ACTH', 'Cortisol', 'TESTOSTERONE TEST', 'Plasma Renin', 'serum potassium K+', 'SERUM ESTROGEN LEVEL', 'Cortisol blood test'], Differential diagnosis:[], disease description:Congenital adrenal hyperplasia (CAH) is a family of autosomal recessive disorders of cortisol biosynthesis, where their is defect in CYP17 10q24.3 gene.

A 35-year-old patient experiencing ['Confusion', 'cyanosis', 'hypotonia', 'rapid breathing']

Disease Name: 2,4-dienoyl-coa Reductase, symptoms: ['Confusion', 'cyanosis', 'hypotonia', 'rapid breathing'], Treatment: nan, Pathophysiology: nan, Epidemiology:nan, Complications:[], Diagnostics:['Total and free carnitine', 'acyl:free carnitine ratio', 'urine organic acids', 'acylglycines'], Differential diagnosis:[], disease description:It is a Mitochondrial Fatty Acid Oxidation Disorders.In this disease their is defect in DECR1 gene

Suffering from ['developmental delay', 'hypotonia', 'intellectual disability', 'DELAYED SPEECH'] at 43

Disease Name: 2-aminoadipic Acidemia, symptoms: ['developmental delay', 'hypotonia', 'intellectual disability', 'DELAYED SPEECH'], Treatment: nan, Pathophysiology: nan, Epidemiology:nan, Complications:[], Diagnostics:nan, Differential diagnosis:[], disease description:nan

A 45-year-old suffering ['Ataxia', 'developmental delay', 'Hydrocephalus', 'Hyperlactataemia', 'hypertonia', 'metabolic acidosis', 'short stature']

Disease Name: 2-ketoglutarate Dehydrogenase Complex Deficiency , symptoms: ['Ataxia', 'developmental delay', 'Hydrocephalus', 'Hyperlactataemia', 'hypertonia', 'metabolic acidosis', 'short stature'], Treatment: nan, Pathophysiology: nan, Epidemiology:nan, Complications:[], Diagnostics:nan, Differential diagnosis:[], disease description:nan

Suffering from ['developmental delay', 'hypotonia', 'intellectual disability', 'DELAYED SPEECH'] at 30

Disease Name: 2-oxoadipic Acidemia, symptoms: ['developmental delay', 'hypotonia', 'intellectual disability', 'DELAYED SPEECH'], Treatment: nan, Pathophysiology: nan, Epidemiology:nan, Complications:[], Diagnostics:nan, Differential diagnosis:[], disease description:nan

A 41-year-old lady with symptoms like ['infertility', 'Acne', 'Hirsutism', '‘Daughter yaws’ are multiple lesions that develop in the secondary stage as the initial lesion heals, and they occur in successive crops.', '‘burning’ discomfort in the lesions', 'precocious adrenarche', 'Asymptomatic', 'menstrual irregularity']

Disease Name: 21-hydroxylase Deficiency,nonclassic Form, symptoms: ['infertility', 'Acne', 'Hirsutism', '‘Daughter yaws’ are multiple lesions that develop in the secondary stage as the initial lesion heals, and they occur in successive crops.', '‘burning’ discomfort in the lesions', 'precocious adrenarche', 'Asymptomatic', 'menstrual irregularity'], Treatment: [{'medication': ['Hydrocortisone ']}], Pathophysiology: Congenital adrenal hyperplasia (CAH) is a family of autosomal recessive disorders of cortisol biosynthesis.Cortisol deficiency increases secretion of corticotropin (adrenocorticotropic hormone [ACTH]), which, in turn, leads to adrenocortical hyperplasia and overproduction of intermediate metabolitesin this there is defect in CYP21 6p21.3gene., Epidemiology:nan, Complications:[], Diagnostics:['SERUM ANDROGEN LEVEL', '17-hydroxyprogesterone level in plasma'], Differential diagnosis:[], disease description:Congenital adrenal hyperplasia (CAH) is a family of autosomal recessive disorders of cortisol biosynthesis.

Symptoms reported by a 38-year-old: ['HEPATOMEGALY', 'coma', 'death', 'No dehydration', 'diarrhea', 'Hypoglycaemia', 'lethargy', 'metabolic acidosis', 'hypotonia', 'vomiting']

Disease Name: 3-hydroxy-3-methylglutaryl-coa Lyase Deficiency, symptoms: ['HEPATOMEGALY', 'coma', 'death', 'No dehydration', 'diarrhea', 'Hypoglycaemia', 'lethargy', 'metabolic acidosis', 'hypotonia', 'vomiting'], Treatment: [{'medication': ['Sodium bicarbonate ', 'Glucose/Dextrose']}, 'hydration,provision of adequate calories,Renal replacement therapy in patients\nwith severe recalcitrant hyperammonemia,Restriction of protein and fat intake is\nrecommended for long-term management.Oral administration of L -carnitine\n(50-100 mg/kg/24 hr) prevents secondary carnitine deficiency'], Pathophysiology: nan, Epidemiology:nan, Complications:['DILATED CARDIOMYOPATHY', 'Pancreatitis', 'seizures', 'intellectual disability', 'hepatic steatosis'], Diagnostics:['random blood sugar RBS', 'URINE R/M', 'URINE R/M', '24 Hrs Ambulatory pH Recording', 'LIVER BIOPSY', 'BLOOD KETONE (D3HB)', 'ammonia level'], Differential diagnosis:['medium chain acyl-CoA dehydrogenase deficiency', 'REYE SYNDROME'], disease description:This is a rare disorder ,approximately 30% develop symptoms in the 1st few days of life, and >60% of patients become symptomatic between 3 and 11 month of age. Infrequently, patients may remain asymptomatic until adolescence. With the addition of 3-HMG-CoA lyase deficiency to the newborn screening using C5-OH-carnitine, many infants are identified presymptomatically in the newborn period

At the age of 22, symptoms like ['diarrhea', 'Hypoglycaemia', 'lethargy', 'hypotonia', 'vomiting', 'poor appetite']

Disease Name: 3-hydroxyacyl-coa Dehydrogenase Deficiency, symptoms: ['diarrhea', 'Hypoglycaemia', 'lethargy', 'hypotonia', 'vomiting', 'poor appetite'], Treatment: nan, Pathophysiology: nan, Epidemiology:nan, Complications:[], Diagnostics:nan, Differential diagnosis:[], disease description:nan

Person at 19 with ['No dehydration', 'developmental delay', 'failure to thrive', 'long philtrum', 'low set ears', 'intellectual disability', 'diarrhea', 'lethargy', 'nausea']

Disease Name: 3-hydroxyisobutyric Aciduria, symptoms: ['No dehydration', 'developmental delay', 'failure to thrive', 'long philtrum', 'low set ears', 'intellectual disability', 'diarrhea', 'lethargy', 'nausea'], Treatment: nan, Pathophysiology: nan, Epidemiology:nan, Complications:[], Diagnostics:nan, Differential diagnosis:[], disease description:nan

Symptoms at 27 years: ['hypotonia']

Disease Name: 3-methyl-crotonyl-glycinuria, symptoms: ['hypotonia'], Treatment: nan, Pathophysiology: nan, Epidemiology:nan, Complications:[], Diagnostics:nan, Differential diagnosis:[], disease description:nan

Individual aged 34 with manifestations like ['cardiomyopathy', 'Deafness', 'developmental delay', 'DILATED CARDIOMYOPATHY', 'failure to thrive', 'hepatic dysfunction', 'Lactic acidosis', 'neutropenia', 'seizures', 'hypotonia', 'short stature']

Disease Name: 3-methylglutaconic Aciduria Type Ii, X-linked , symptoms: ['cardiomyopathy', 'Deafness', 'developmental delay', 'DILATED CARDIOMYOPATHY', 'failure to thrive', 'hepatic dysfunction', 'Lactic acidosis', 'neutropenia', 'seizures', 'hypotonia', 'short stature'], Treatment: nan, Pathophysiology: nan, Epidemiology:nan, Complications:[], Diagnostics:nan, Differential diagnosis:[], disease description:nan

A 18-year-old patient with ['hypertonia', 'nystagmus', 'intellectual disability', 'Growth retardation', 'ADDUCTED LIMB', 'DEVELOPMENTAL CATARACT', 'decreased testicle size', 'Spastic tetraplegia', 'Hypsarrhythmia', 'Dizziness', 'tingling of the extremities', 'Easy bruisability', 'EASY BLEEDING']

Disease Name: 3-phosphoglycerate Dehydrogenase (3-pgdh) Deficiency , symptoms: ['hypertonia', 'nystagmus', 'intellectual disability', 'Growth retardation', 'ADDUCTED LIMB', 'DEVELOPMENTAL CATARACT', 'decreased testicle size', 'Spastic tetraplegia', 'Hypsarrhythmia', 'Dizziness', 'tingling of the extremities', 'Easy bruisability', 'EASY BLEEDING'], Treatment: nan, Pathophysiology: nan, Epidemiology:nan, Complications:[], Diagnostics:nan, Differential diagnosis:[], disease description:nan

Symptoms reported by a 38-year-old female include ['muscle weakness', 'precocious adrenarche', 'Ambiguous genitalia in females and male', 'diarrhea', 'fainting', 'lethargy', 'vomiting', 'weight loss', 'Abdominal Pain', 'salt craving']

Disease Name: 3ß-hydroxysteroid Dehydrogenase Deficiency, Classic Form, symptoms: ['muscle weakness', 'precocious adrenarche', 'Ambiguous genitalia in females and male', 'diarrhea', 'fainting', 'lethargy', 'vomiting', 'weight loss', 'Abdominal Pain', 'salt craving'], Treatment: [{'medication': ['Fludrocortisone ', 'Hydrocortisone ', 'Estradiol cypionate ', 'Sodium chloride ', 'Testosterone ']}, 'Surgical correction of\ngenitals'], Pathophysiology: Congenital adrenal hyperplasia (CAH) is a family of autosomal recessive disorders of cortisol biosynthesis.HSD3B2 1p13.1 gene is affected. Cortisol deficiency increases secretion of corticotropin (adrenocorticotropic hormone [ACTH]), which, in turn, leads to adrenocortical hyperplasia and overproduction of intermediate metabolites., Epidemiology:nan, Complications:[], Diagnostics:['ACTH', 'Cortisol', 'SERUM Sodium Na+', 'TESTOSTERONE TEST', 'Plasma Renin', 'serum potassium K+', 'plasma DHEA SULFATE LEVEL', 'SERUM ESTRADIOL', 'ANDROSTENEDIONE'], Differential diagnosis:[], disease description:Congenital adrenal hyperplasia (CAH) is a family of autosomal recessive disorders of cortisol biosynthesis,where their is defect in HSD3B2 1p13.1 gene.

Person, 24 years old, presenting ['hyperreflexia', 'seizures', 'hypotonia', 'weak or high-pitched cry']

Disease Name: 4-aminobutyrate Aminotransferase Deficiency, Gaba-, symptoms: ['hyperreflexia', 'seizures', 'hypotonia', 'weak or high-pitched cry'], Treatment: nan, Pathophysiology: nan, Epidemiology:nan, Complications:[], Diagnostics:nan, Differential diagnosis:[], disease description:nan

Symptoms at 44: ['cyanosis', 'cryptorchidism', 'pseudohermaphroditism', 'Aphallia', 'Clitoromegaly', 'breathlessness']

Disease Name: 46,xy Disorders Of Sex Development (disorders Related To Androgen Excess), symptoms: ['cyanosis', 'cryptorchidism', 'pseudohermaphroditism', 'Aphallia', 'Clitoromegaly', 'breathlessness'], Treatment: nan, Pathophysiology: nan, Epidemiology:nan, Complications:[], Diagnostics:nan, Differential diagnosis:[], disease description:nan

A 32-year-old patient with ['fatigue', 'jaundice', 'splenomegaly', 'dyspnea', 'DARK URINE']

Disease Name: 5-nucleotidase Deficiency, symptoms: ['fatigue', 'jaundice', 'splenomegaly', 'dyspnea', 'DARK URINE'], Treatment: nan, Pathophysiology: nan, Epidemiology:nan, Complications:[], Diagnostics:nan, Differential diagnosis:[], disease description:nan

Symptoms reported at the age of 26: ['hyperthermia', 'drowsiness', 'Irritability']

Disease Name: 6-pyruvoyl-tetrahydropterin Synthase Deficiency, symptoms: ['hyperthermia', 'drowsiness', 'Irritability'], Treatment: nan, Pathophysiology: nan, Epidemiology:nan, Complications:[], Diagnostics:nan, Differential diagnosis:[], disease description:nan

Person at 41 years, dealing with ['anorexia', 'decreased appetite', 'malaise', 'vomiting', 'Abdominal Pain', 'abdominal distension', 'CHRONIC DIARRHEA', 'loss of appetite', 'fever', 'LOW GRADE FEVER', 'weight loss']

Disease Name: Abdominal Tuberculosis, symptoms: ['anorexia', 'decreased appetite', 'malaise', 'vomiting', 'Abdominal Pain', 'abdominal distension', 'CHRONIC DIARRHEA', 'loss of appetite', 'fever', 'LOW GRADE FEVER', 'weight loss'], Treatment: [{'medication': ['Rifampicin/Rifampin', 'Ethambutol ', 'Isoniazid ', 'Pyrazinamide ', 'Amikacin ', 'Ethionamide ', 'Levofloxacin ']}, 'As recommended by WHO and AAP, the standard therapy of intrathoracic tuberculosis (pulmonary disease and/or hilar lymphadenopathy) in children is a 6 mo regimen of isoniazid and rifampin supplemented in the 1st 2 mo of treatment by pyrazinamide and ethambutol. When directly observed therapy (DOT) is used, intermittent (twice or thrice weekly) administration of drugs after an initial period as short as 2 wk of daily therapy is as effective for drug-susceptible tuberculosis in children as daily therapy for the entire course', 'Surgery is indicated if there is bowel perforation, obstruction or massive hemorrhage.'], Pathophysiology: Esophageal TBEsophageal involvement in TB occurs rarely. It has been seen to occur due to spread from adjacent tissues. It usually involves the middle one-third of the esophagus, at the level of the carina.Gastric and Gastroduodenal TBDue to the protective fatty acid capsule of mycobacteria, proximal GIT lesions were thought to be rare. Additional factors that were thought to prevent TB in the stomach and duodenum were a high acid environment, rapid transit time, and a relative absence of lymphoid tissue. However, they have been reported in the stomach and duodenum.Gastrointestinal (GI) tuberculosis in this anatomic location may lead to gastric outlet obstruction and surgical obstructive jaundice.TB of the Small and Large IntestineFour major forms have been reported:Ulcerative – the most common form. Usually presents with superficial transverse ulcers. It is more likely to be seen in the small intestine.Hypertrophic – occurs as a hyperplastic reaction around the ulcer, producing an inflammatory mass. It is more likely to be seen in the cecum.Ulcero-hypertrophic – a combination of ulcerative and hypertrophic forms may occur.Fibrous stricturing – may lead to fibrosis and stricture formation, resulting in intestinal obstruction.Rectal and Anal TBTB involving the rectal and anal areas may present as multiple fistulae (mimicking Crohn disease), a non-healing lesion after recent anal surgery or a circumferential mass resembling rectal prolapse.Peritoneal TBPeritoneal TB usually occurs with other forms of abdominal TB, with peritoneal involvement occurring after the rupture of necrotic lymph nodes. Lymph nodes in the small bowel mesentery and the retroperitoneum are commonly involved, and these may caseate and calcify. Ascites is the most frequent manifestation.Peritoneal InvolvementTB peritonitis exists in 5 main forms:AsciticLoculated (encysted)Plastic (fibrous)PurulentNodular, Epidemiology:['5 percent of all cases of TB worldwide', '0.1% and 0.7% globally', 'good', 'If you have active TB, you can infect other people. For that reason, your doctor will tell you to stay home during the first few weeks of treatment, until you’re no longer contagious. During that time, you should avoid public places and people with weakened immune systems, like young children, the elderly, and people with HIV. You’ll have to wear a special mask if you have visitors or need to go to the doctor’s office.'], Complications:['genital tuberculosis', 'intestinal obstruction ', 'Mesentric Lymphadenitis', 'peritonitis'], Diagnostics:['HISTOPATHLOGY', 'Peritoneal/ascitic Fluid Examination', 'Real Time PCR For Mycobacterium Tuberculosis', 'CT Abdomen', 'TUBERCULIN SKIN TEST', 'USG GUIDED FNAC', 'CULTURE FROM Gastric TISSUE BIOPSY SPECIMEN'], Differential diagnosis:['Amoebiasis', 'CHRONIC DIARRHEA', 'Crohns Disease', 'peritonitis'], disease description:Abdominal tuberculosis (TB) includes involvement of the gastrointestinal tract, peritoneum, lymph nodes, and/or solid organs. The most common forms of disease include involvement of the peritoneum, intestine, and/or lymph nodes. TB of the abdomen may occur via reactivation of latent TB infection or by ingestion of tuberculous mycobacteria (as with ingestion of unpasteurized milk or undercooked meat). In the setting of active pulmonary TB or miliary TB, abdominal involvement may develop via hematogenous spread via contiguous spread of TB from adjacent organs (such as retrograde spread from the fallopian tubes) or via spread through lymphatic channels.

Woman aged 21 presenting symptoms such as ['pelvic pain', 'bleeding after sex', 'pallor', 'irregular menstrual bleeding', 'bleeding pv']

Disease Name: Abnormal Uterine Bleeding, symptoms: ['pelvic pain', 'bleeding after sex', 'pallor', 'irregular menstrual bleeding', 'bleeding pv'], Treatment: [{'medication': ['Progesterone ', 'Tranexamic acid ', 'Mefenamic acid ', 'Danazol', 'ORMELOXIFENE', 'GESTRINONE', 'combined oral contraceptives']}, 'Blood thinners and aspirin.\nHormone replacement therapy.\nTamoxifen (breast cancer drug).\nIntrauterine devices (IUDs).\nBirth control pills and injectables (NuvaRing, Depo-Provera, Implanon).'], Pathophysiology: Problems with ovulation—Lack of ovulation can cause irregular, sometimes heavy, menstrual bleeding. If you do not ovulate for several menstrual cycles, areas of the endometrium (the tissue that lines the uterus) can become too thick. This condition can occur during the first few years after you start having periods and during perimenopause. It also can occur in women with certain medical conditions, such as polycystic ovary syndrome (PCOS) and hypothyroidism.Fibroids and polyps—Fibroids are noncancerous growths that form from the muscle tissue of the uterus. Polyps are another type of noncancerous growth. They can be found inside the uterus or on the cervix. Both can cause irregular or heavy menstrual bleeding.Adenomyosis—In this condition, the endometrium grows into the wall of the uterus. Signs and symptoms may include heavy menstrual bleeding and menstrual pain that worsens with age.Bleeding disorders—When a woman’s blood does not clot properly, there can be heavy bleeding. You may have a bleeding disorder if you have had heavy periods since you first started menstruating. Other signs include heavy bleeding after childbirth or during surgery, gum bleeding after dental work, easy bruising, and frequent nosebleeds.Medications—Hormonal birth control methods can cause changes in bleeding, including breakthrough bleeding (bleeding at a time other than your period). Some medications, such as blood thinners and aspirin, can cause heavy menstrual bleeding. The copper intrauterine device (IUD) can cause heavier menstrual bleeding, especially during the first year of use.Cancer—Abnormal uterine bleeding can be an early sign of endometrial cancer. Most cases of endometrial cancer occur in women in their mid-60s who are past menopause. It usually is diagnosed at an early stage when treatment is most effective. A condition that can lead to endometrial cancer is called endometrial intraepithelial neoplasia (EIN). It also causes abnormal uterine bleeding. Treatment of this condition can prevent endometrial cancer.Other causes— Endometriosis and other problems related to the endometrium can cause heavy menstrual bleeding. Other causes of abnormal uterine bleeding include those related to pregnancy, such as ectopic pregnancy and miscarriage. Pelvic inflammatory disease (PID) also can be a cause. Sometimes, there is more than one cause., Epidemiology:['42.3% among women aged 40 to 44 years and 34.6% in women aged 45 to 49 years.', 'About 10–15% of women experience episodes of abnormal \nuterine bleeding (AUB) at sometime during the reproductive years of their lives', 'good', 'You can’t prevent many causes of abnormal uterine bleeding. But you can reduce your risk of certain conditions that lead to abnormal bleeding. For instance, maintaining a healthy weight plays a potential role in keeping your hormones balanced. Avoiding diets that contain a high amount of animal fat can reduce your risk of some cancers. Practicing safer sex can reduce your risk of certain sexually transmitted infections (STIs) that can cause abnormal uterine bleeding.'], Complications:['Endometrial cancer', 'shock', 'infertility', 'Hypotension', 'severe anaemia,'], Diagnostics:['ultrasound', 'COAGULATION PROFILE', 'endometrial histology'], Differential diagnosis:['abnormal uterine bleeding', 'adenomyosis', 'CANCER CERVIX', 'endometrium carcinoma', 'FIBROID UTERUS'], disease description:Abnormal uterine bleeding (AUB) is a common and debilitating condition with high direct and indirect effects. AUB can frequently co-exist with fibroids, but the relationship between the two remains incompletely understood and in many women the identification of fibroids may be incidental to a menstrual bleeding complaint. A structured approach for establishing the cause using the Fédération International de Gynécologie et d'Obstétrique (FIGO) PALM-COEIN (Polyp, Adenomyosis, Leiomyoma, Malignancy (and hyperplasia), Coagulopathy, Ovulatory disorders, Endometrial, Iatrogenic and Not otherwise classified) classification system will facilitate accurate diagnosis and inform treatment options.

A 52-year-old patient experiencing ['Anorectal pain', 'blood in stool', 'Localised pain', 'Redness', 'swelling', 'swelling', 'Tenderness on palpation']

Disease Name: Abscess, symptoms: ['Anorectal pain', 'blood in stool', 'Localised pain', 'Redness', 'swelling', 'swelling', 'Tenderness on palpation'], Treatment: ['antibiotics that are typically prescribed in this instance include:\n\nclindamycin\ncephalexin\ndicloxacillin\ndoxycycline\ntrimethoprim-sulfamethoxazole (Bactrim)', 'Incision and drainage'], Pathophysiology: Most abscesses are caused by a bacterial infection.When bacteria enter your body, your immune system sends infection-fighting white blood cells to the affected area.As the white blood cells attack the bacteria, some nearby tissue dies, creating a hole which then fills with pus to form an abscess. The pus contains a mixture of dead tissue, white blood cells and bacteria.Internal abscesses often develop as a complication of an existing condition, such as an infection elsewhere in your body. For example, if your appendix bursts as a result of appendicitis, bacteria can spread inside your tummy (abdomen) and cause an abscess to form., Epidemiology:['64%', '2.3 cases per 100,000 people', 'good', 'Washing your hands frequently.\nNot sharing towels, razors or toothbrushes.\nAvoiding nicking your skin while shaving.\nMaintaining a healthy diet.\nQuitting smoking.\nPracticing good dental hygiene.'], Complications:['gangrene', 'sepsis', 'MRSA, or methicillin-resistant Staphylococcus aureus, infection'], Diagnostics:['PUS CULTURE', 'Total Leucocyte Count (TLC)', 'X RAY', 'CT SCAN', 'USG'], Differential diagnosis:['B-cell pseudolymphomas usually present as solitary or multiple, itchy or asymptomatic, smooth surfaced or excoriated, dermal papules and nodules, which may also be subcutaneous', 'hidradenitis suppurativa', 'Panniculitis'], disease description:An abscess is a painful collection of pus, usually caused by a bacterial infection. Abscesses can develop anywhere in the body. This article focuses on 2 types of abscess: skin abscesses – which develop under the skin. internal abscesses – which develop inside the body, in an organ or in the spaces between organs.

Symptoms at 25 years: ['Learning difficulty', 'chewing movements', 'sudden discontinuation of the activity', 'eye fluttering', 'Behavioural DIsorder', 'abrupt lapse of awareness or consciousness']

Disease Name: Absence Seizures, symptoms: ['Learning difficulty', 'chewing movements', 'sudden discontinuation of the activity', 'eye fluttering', 'Behavioural DIsorder', 'abrupt lapse of awareness or consciousness'], Treatment: [{'medication': ['Valproic acid(sodium valproate)/ Divalproex Sodium', 'Ethosuximide ', 'Lamotrigine ']}, 'Effective agents include ethosuximide,\nsodium valproate, lamotrigine and benzodiazepines'], Pathophysiology: Seizures (convulsions, fits) are caused by abnormal electrical discharges from the brain resulting in abnormal involuntary, paroxysmal, motor, sensory, autonomic or sensorial activity. About 5 percent children experience convulsions during the first five years of life. Motor movements consisting of tonic and clonic components are the most commonly observed phenomenon, except in the newborn period. Several times, a child may present with a condition that can mimic or be misinterpreted as a seizure. These conditions include convulsive syncope with or without cardiac dysarrhythmia, decerebrate posturing, psychogenic events, dystonia and migraine. Seizures should be differentiated from these conditions as misdiagnosis can have significant therapeutic implications. Absence seizures start abruptly in childhood; the peak prevalence is between 6-8 yr. Absence seizures are not preceded by aura. The patients have a brief abrupt lapse of awareness or consciousness, sudden discontinuation of the activity being performed with staring spell, eye fluttering, or rhythmic movements. The seizure lasts less than 30 seconds. There is no loss of posture, incontinence of urine/ stools or breathing difficulty. Other neurological manifestations and postictal phenomena are absent and development is normal. Unaware of the nature of their illness, school teachers may consider them inattentive pupils. Hyperventilation for 3 min often precipitates the attacks. Absence seizures may occur in multiples, everyday. Attacks following in close succession indicate petit ma/ status or pyknolepsy. About half of patients become seizure free and the rest develop tonic-clonic fits. Learning disabilities and behavior disorders when present are probably related to associated conditions. EEG shows a characteristic 3 per second spike and slow wave pattern. Absence fits are distinguished from complex partial seizures by shorter duration (10 seconds), absence of aura and abrupt return of full consciousness., Epidemiology:['10%', 'between 0.7 and 4.6 per 100,000 in the general population and around 6 to 8 per 100,000 in the pediatric population younger than 15 years', 'GOOD', 'Get plenty of sleep each night.\n\nFind ways to manage your stress.\n\nEat a healthy diet.\n\nExercise regularly.'], Complications:['seizures', 'Behavioural DIsorder', 'Learning difficulty'], Diagnostics:['EEG', 'CT SCAN'], Differential diagnosis:['focal seizure', 'partial seizures'], disease description:Absence seizures start abruptly in childhood; the peak prevalence is between 6-8 yr.Someone having an absence seizure may look like he or she is staring blankly into space for a few seconds. Then, there is a quick return to a normal level of alertness. This type of seizure usually doesn't lead to physical injury. Absence seizures are not preceded by aura. The patients have a brief abrupt lapse of awareness or consciousness, sudden discontinuation of the activity being performed with staring spell, eye fluttering, or rhythmic movements. The seizure lasts less than 30 seconds. There is no loss of posture, incontinence of urine/ stools or breathing difficulty.

Suffering from ['shallow anterior chamber', 'FILAMENTARY KERATITIS', 'Perilimbal reddish blue zone', 'Caput medusae, i.e., a few prominent and enlarged vessels are seen in long-standing cases', 'Iris becomes atrophic', 'Pupil becomes fixed and dilated and gives a greenish hue', 'Optic disc shows glaucomatous optic atrophy', 'Painful blind eye', 'increased intraocular pressure', 'eye pain', 'headache', 'nausea', 'red eyes', 'vomiting', 'blurred vision', 'bullous keratopathy'] at 55

Disease Name: Absolute Primary Angle-closure Glaucoma, symptoms: ['shallow anterior chamber', 'FILAMENTARY KERATITIS', 'Perilimbal reddish blue zone', 'Caput medusae, i.e., a few prominent and enlarged vessels are seen in long-standing cases', 'Iris becomes atrophic', 'Pupil becomes fixed and dilated and gives a greenish hue', 'Optic disc shows glaucomatous optic atrophy', 'Painful blind eye', 'increased intraocular pressure', 'eye pain', 'headache', 'nausea', 'red eyes', 'vomiting', 'blurred vision', 'bullous keratopathy'], Treatment: ['Paracentesis', 'Systemic\n\nCarbonic anhydrase inhibitors – oral acetazolamide’s maximum IOP reduction is reached in 2-4 hours and lasts for 6-8 hours. Intravenous acetazolamide drops the IOP within 2 minutes with a peak effect noted by 10-15 minutes. In acute situations, a single dose of 500 mg acetazolamide should be given orally if the patient is not vomiting. Regular acetazolamide is preferred over the sustained-release sequel form because of quicker onset of action. If the patient is vomiting, acetazolamide can be given intravenously.\nOsmotic agents\nMannitol can decrease the IOP 30 mm Hg or more within 30 minutes of administration. The recommended intravenous dose is 0.5-1.5 g/kg body weight as a 15% or 20% solution, delivered at 3 to 5 mL/minute. Frail patients with cardiac or conditions may develop circulatory overload, pulmonary edema, congestive heart failure, and electrolyte imbalance. A rapid reduction in cerebral volume may result in subdural hematomas from vein rupture between the sagittal sinus and cortical surface. Therefore, patients receiving IV mannitol should be monitored in a hospital setting.\nOral osmotic agents:\nGlycerin: 1 to 1.5 g/kg body weight of a 50% solution. Onset of pressure reduction is typically 10 to 30 minutes. Avoid in diabetics because the increased caloric load can cause ketoacidosis.\nIsosorbide is commercially available as a 45% (45 g/100 mL) solution (Ismotic; Alcon Surgical). The recommended dose is 1 to 1.5 g/kg body weight. Its effect is similar to glycerin’s but is safe for use in diabetics because it is not metabolized.\nAlthough less common, oral agents can also cause subdural hematomas. Headache and gastrointestinal upset are common adverse reactions.', 'TOPICAL\nBeta blockers\nSelective alpha agonists\nCarbonic anhydrase inhibitors\nMiotics (e.g., pilocarpine 2%) may help break an early angle-closure attack, but may be ineffective if the iris is already ischemic. High-concentration miotics (e.g., pilocarpine 4%) should be avoided because of the potential for forward displacement iris-lens diaphragm.\nProstaglandin analogues – unreliable effect in acute attack because of slow onset of action \nHyperosmolar agent (e.g. 5% sodium chloride) – assists in clearing corneal edema\nPrednisolone 1% - decreases inflammation', 'Laser Iridotomy'], Pathophysiology: Primary angle closure glaucoma is caused by relative pupillary block in the majority of cases. In pupillary block, aqueous humor encounters increased resistance as it flows from the posterior to anterior chamber through the iris-lens channel. Some degree of relative pupillary block is present in most phakic eyes. The risk of pupillary block is highest with a mid-dilated pupil where there appears to be maximum contact between the iris and the lens. In eyes with angle closure, other factors exacerbate the block, such as the front lens surface being anterior to the plane of iris insertion into the ciliary body base. The increased pressure gradient across the pupil causes the peripheral iris to bow forward and cover some or all of the filtering portion of the trabecular meshwork, resulting in appositional angle closure. Peripheral anterior synechiae form after prolonged or repeated contacts of the peripheral iris with TM., Epidemiology:['0.6%', '17.14 million (95% CI = 14.28–22.85) for people older than 40 years old worldwide, with 12.30 million (95% CI = 10.54–17.57) in Asia', 'good', 'Laser iridotomy is also used to treat persons suspected of having primary angle closure in order to prevent the development of glaucoma, a condition in which the eye’s optic nerve is damaged, typically by fluid pressure buildup and, untreated, can result in permanent vision loss.\nThe best way to prevent an acute angle closure glaucoma attack is to get your eyes checked regularly, especially if you’re at high risk. Your doctor can keep tabs on pressure levels and how well fluid drains. If they think your risk is unusually high, they may suggest laser treatment to hold off an attack.'], Complications:['Loss of vision', 'central retinal artery occlusion', 'malignant glaucoma'], Diagnostics:['TONOMETRY TEST', 'slit-lamp biomicroscopic examination', 'Gonioscopic examination'], Differential diagnosis:['ANTERIOR UVEITIS (IRIDOCYCLITIS)', 'LENS-INDUCED (PHACOGENIC) GLAUCOMAS', 'neovascular glaucoma'], disease description:Primary Angle Closure Glaucoma is a condition in which elevation of intraocular pressure (IOP) occurs as a result of obstruction of aqueous outflow by partial or complete closure of angle by the peripheral iris. Primary angle closure glaucoma, if untreated, gradually passes into the final phase of absolute glaucoma.

Suffering from ['yellowish discoloration of eyes', 'yellowish discoloration of skin', 'jaundice', 'abdominal flatulance', 'bloating', 'epigastric pain', 'nausea', 'vomiting', 'dyspepsia', 'fatty food intolerance'] at 31

Disease Name: Acalculous Cholecystitis, symptoms: ['yellowish discoloration of eyes', 'yellowish discoloration of skin', 'jaundice', 'abdominal flatulance', 'bloating', 'epigastric pain', 'nausea', 'vomiting', 'dyspepsia', 'fatty food intolerance'], Treatment: ['Antibiotic agents for initial empiric treatment of acalculous cholecystitis\n\nMild to moderate infection :\tCefazolin, cefuroxime, and ceftriaxone\n\nSevere infection or high-risk factors such\nas advanced age, immunocompromise,\nand end-organ disease:\nImipenem-cilastatin, meropenem, doripenem,\npiperacillin-tazobactam, ciprofloxacin, levofloxacin,\nor cefepime, each in combination with metronidazole\n\nExtended-spectrum beta-lactamase\n(ESBL)-producing organisms: Imipenem-cilastatin, meropenem, doripenem, and\npiperacillin-tazobactam, each in combination with\nmetronidazole\n\nHealth care–associated infection of any\nseverity\tAdd vancomycin to appropriate regimen above.', 'Percutaneous US-guided/CT-guided or open cholecystostomy initially, later cholecystectomy is the treatment of choice'], Pathophysiology: Stasis of the gallbladder results in the build-up of intraluminal pressure. This eventually results in ischemia of the gallbladder wall and inflammation. This stasis can also lead to the colonization of bacteria which contributes to the inflammatory response. If the pressure is not relieved, the gallbladder wall will become progressively ischemic eventually resulting in gangrenous changes and perforation. This will lead to sepsis and shock. These findings are referred to as acute cholecystitis. Chronic acalculous cholecystitis usually presents more insidiously. Symptoms are more prolonged and may be less severe., Epidemiology:['0.2% to 0.4% of all critically ill patients', '5-10% of all cases of acute cholecystitis', 'bad', 'However, the definitive treatment of acalculous cholecystitis is cholecystectomy for patients who are able to tolerate surgery. In selected patients with acute acalculous cholecystitis (AAC), nonsurgical treatment (such as antibiotics or percutaneous cholecystostomy) may be an effective alternative to surgery.'], Complications:['gangrene', 'perforation', 'sepsis'], Diagnostics:['Endoscopic USG', 'ERCP', 'HIDA Cholescintigraphy', 'MRCP', 'USG ABDOMEN(W/A)', 'X RAY ABDOMEN', 'PERCUTANEOUS TRANSHEPATIC CHOLANGIOGRAPHY(PTC)'], Differential diagnosis:['ACALCULOUS CHOLECYSTITIS', 'ASCENDING CHOLANGITIS', 'CHOLANGIOCARCINOMA', 'CHOLECYSTOSES', 'CHOLEDOCHAL CYST', 'CHOLELITHIASIS', 'PRIMARY SCLEROSING CHOLANGITIS'], disease description:Acalculous cholecystitis is an acute necroinflammatory disease of the gallbladder with a multifactorial pathogenesis.

Person at 36 with manifestations like ['Ring infiltrate', 'Ring abscess', 'Epithelial roughening', 'Pseudodendrites formation', 'Radial keratoneuritis', 'eye pain', 'sensation of a foreign body in the eye', 'blepharospasm', 'photophobia', 'WATERING EYE', 'blurred or unstable vision']

Disease Name: Acanthamoeba Keratitis, symptoms: ['Ring infiltrate', 'Ring abscess', 'Epithelial roughening', 'Pseudodendrites formation', 'Radial keratoneuritis', 'eye pain', 'sensation of a foreign body in the eye', 'blepharospasm', 'photophobia', 'WATERING EYE', 'blurred or unstable vision'], Treatment: [{'medication': ['Chlorhexidine ', 'Neomycin ', 'Itraconazole ', 'Ketoconazole ', 'Clotrimazole ']}, 'Initial Therapy\n\nChlorhexadine combined with Brolene\n\n\nSecond Line Therapies\n\nPHMB\n\nHexamidine\n\nPentamadine\n\n\nThird Line Therapies\n\nImidazoles\n\nNeomycin\n\nAdjunctive Therapies\n\nNSAIDs\nPrednisolone', 'Penetrating keratoplasty'], Pathophysiology: Acanthamoeba castellani, the causative organism is a free lying amoeba found in soil, fresh water well water, sea water, sewage and air. It exists in trophozoite and encysted forms. Mode of infection. Corneal infection with acanthamoeba results from direct corneal contact with any material or water contaminated with the organism. Following situations of contamination have been described: 1. Contact lens wearers using home-made saline (from contaminated tap water and saline tablets) is the commonest situation recognised for acanthamoeba infection in western countries. 2. Non-contact lens related situations include mild trauma associated with contaminated vegetable matter, salt water diving, wind blown contaminant and hot tub use. Trauma with organic matter and exposure to muddy water are the major (90% cases) predisposing factors in developing countries. 3. Opportunistic infection. Acanthamoeba keratitis can also occur as opportunistic infection in patients with herpetic keratitis, bacterial keratitis, bullous keratopathy and neuroparalytic keratitis., Epidemiology:['0.15 per million to 1.4 per million', 'one to two new cases per 1 million contact lens wearers annually', 'good', 'Avoiding contact with contaminated water, which could include freshwater lakes, rivers and hot springs.\nFilling your contact lens storage case with fresh solution each time you open it.\nNever sleeping in your contact lenses.\nNot showering, swimming or using a hot tub while wearing contact lenses.\nNot using another person’s contact lenses.\nReplacing contact lenses regularly, according to your healthcare provider’s recommendations.\nUsing only disinfecting solution (not saline solution) to rinse and store your contact lenses — never use tap water.\nVisiting your optometrist or ophthalmologist for regular exams.\nWashing your hands before touching your eyes or handling your contact lenses.'], Complications:['cataract', 'Glaucoma', 'Radial keratoneuritis', 'iris atrophy'], Diagnostics:['PCR', 'Calcofluor white (CFW) stain', 'Corneal biopsy', 'Confocal microscopy', 'Potassium hydroxide (KOH) mount', 'Lactophenol cotton blue stained', 'Culture on non-nutrient agar'], Differential diagnosis:['HERPES SIMPLEX KERATITIS', 'ROSACEA KERATITIS', 'superficial keratitis', 'Syphilitic Interstitial Keratitis'], disease description:Acanthamoeba keratitis has recently gained importance because of its increasing incidence, difficulty in diagnosis and unsatisfactory treatment. Acanthamoeba castellani, the causative organism is a free lying amoeba found in soil, fresh water, well water, sea water, sewage and air. Acanthamoeba keratitis can also occur as opportunistic infection in patients with herpetic keratitis, bacterial keratitis, bullous keratopathy and neuroparalytic keratitis.

Experiencing ['HEPATOMEGALY', 'anorexia', 'diaphoresis', 'jaundice', 'malaise', 'nausea', 'pallor', 'vomiting', 'Right upper quadrant pain', 'Abdominal Pain'] at 31 years old

Disease Name: Acanthomas, symptoms: ['HEPATOMEGALY', 'anorexia', 'diaphoresis', 'jaundice', 'malaise', 'nausea', 'pallor', 'vomiting', 'Right upper quadrant pain', 'Abdominal Pain'], Treatment: [{'medication': ['Acetylcysteine (N-acetylcysteine) ']}, 'Supportive treatment includes correction of hypoglycemia maintenance of hydration, electrolyte balance, treatment of\ncoagulopathy, hemodialysis for acute renal failure and\nmanagement of fulminant hepatic failure.'], Pathophysiology: Not well understood but somatic hotspot mutations in the Arg156 position of KRT10, also known to cause epidermolytic ichthyosis (germline)., Epidemiology:['4.5 cases per 100000', 'good'], Complications:['hyperpigmentation', 'hypopigmentation', 'infection', 'Scarring'], Diagnostics:['HISTOPATHLOGY', 'Protein', 'Dermoscopy'], Differential diagnosis:['Acute Pancreatitis', 'gastroenteritis', 'hepatorenal syndrome', 'Renal tubular necrosis', 'viral hepatitis', 'WILSONS DISEASE'], disease description:it is  a solitary, red or red-brown, dome-shaped papule or nodule. A peripheral, wafer-like scale collarette is classically described in a majority of lesions, but may not always be present. The surface may also have a crusted or moist appearance and may bleed with minor trauma.

Suffering from ['velvety, dark plaques are seen on the labia majora, extending into the inguinal folds', 'hyperpigmentation of the skin'] at 19

Disease Name: Acanthosis Nigricans, symptoms: ['velvety, dark plaques are seen on the labia majora, extending into the inguinal folds', 'hyperpigmentation of the skin'], Treatment: ['Keratolytics, retinoids and laser treatment have all been tried.\nThese may be irritant in the genital skin'], Pathophysiology: Associated diseases Acanthosis nigricans is associated with insulin resistance in almost all cases. In adults, it can be a cutaneous sign of an underlying malignancy, usually an adenocarcinoma. If linked with malignancy, the onset and progression is rapid and unusual sites such as the eyelids, lips and palms (tripe palms) may be involved., Epidemiology:['If linked with malignancy, the onset and progressi'], Complications:[], Diagnostics:['biopsy', 'INSULIN TOLERANCE TEST'], Differential diagnosis:['epidermal naevi'], disease description:Acanthosis nigricans is characterized by hyperpigmentation and thickening of the skin, particularly in the flexures.

Person at 38 with manifestations like ['anorexia', 'jaundice', 'pallor', 'Abdominal Pain', 'Right upper quadrant pain', 'diaphoresis', 'malaise', 'nausea', 'vomiting', 'HEPATOMEGALY']

Disease Name: Acetaminophen Poisoning, symptoms: ['anorexia', 'jaundice', 'pallor', 'Abdominal Pain', 'Right upper quadrant pain', 'diaphoresis', 'malaise', 'nausea', 'vomiting', 'HEPATOMEGALY'], Treatment: [{'medication': ['Acetylcysteine (N-acetylcysteine) ']}, 'HEMODIALYSIS in case of renal faliure', 'Patients who continue to have deterioration such as renal failure, metabolic acidosis, encephalopathy, and coagulopathy should consider transplant'], Pathophysiology: Hepatic damage after paracetamol overdose usually begins at > 150 mg/ kg and occurs due to formation of a highly reactive intermediate, N-acetyl-p-benzoquinoneimine. This is normally detoxified by endogenous glutathione. Overdose of paracetamol results in depletion of glutathione, allowing the intermediate metabolite to damage hepatocytes. The stages of paracetamol toxicity are as follows: Stage I (12-24 hr): Nausea, vomiting and cold sweats Stage II (24-48 hr): Clinical recovery with biochemical evidence of hepatorenal injury; elevation of hepatic transaminases to above 1 000 IU /1 is associated with serious hepatic damage Stage III (48-96 hr): Peak hepatotoxicity Stage IV (7-8 days): Recovery is heralded by return of consciousness and improvement in the hepatic function tests. Histological recovery may take up to 3 months. Death may occur within 2-7 days of ingestion. Overdosage is treated with N-acetylcysteine used orally within 16 hr after ingestion at doses indicated in Once hepatic failure occurs, the agent is contraindicated. The following are poor prognostic factors in patients with hepatic failure due to paracetamol: blood pH <7.3, prothrombin time > 100 sec, grade III or more hepatic encephalopathy, elevated serum bilirubin >4 mg/ dl and SGOT > 1000 IU /1. A ratio of factor VIII to factor V >30 is associated with poor outcome., Epidemiology:['It is responsible for 56,000 emergency department visits, 2600 hospitalizations, and 500 deaths per year in the United States. Fifty percent of these are unintentional overdoses.', 'DEPENDS ON SEVERITY OF SYMPTOMS', 'Not To Do : There is no need to adjust the dose for patients with alcoholism or the chronically ill, and it is safe in pregnancy. Repeat acetaminophen levels are also not needed after treatment has begun'], Complications:['acute generalised exanthematous pustulosis', 'acute liver failure', 'toxic epidermal necrolysis', 'Steven-Johnson syndrome'], Diagnostics:['Serum Bilirubin (Total )', 'PROTHROMBIN TIME(PT)', 'ASPARTATE AMINOTRANSFERASE (SGOT )', 'ALANINE TRANSAMINASE (SGPT)'], Differential diagnosis:['Acute Pancreatitis', 'gastroenteritis', 'hepatorenal syndrome', 'Renal tubular necrosis', 'viral hepatitis', 'WILSONS DISEASE'], disease description:This is the most common and safest analgesic and antipyretic used in children. The toxic dose is usually >200 mg/kg in children below 12-yr-old.

Symptoms at 37 years: ['BELCHING', 'chest pain', 'dysphagia', 'heartburn', 'regurgitation', 'weight loss', 'dyspepsia']

Disease Name: Achalasia, symptoms: ['BELCHING', 'chest pain', 'dysphagia', 'heartburn', 'regurgitation', 'weight loss', 'dyspepsia'], Treatment: ['Peroral endoscopic myotomy (POEM) is an effective minimally invasive alternative to laparoscopic Heller myotomy to treat achalasia at limited centers .Dissection of the circular fibers of the LES is achieved endoscopically, leading to relaxation of the LES', 'Pneumatic dilatation of the esophagus via endoscopy is the most cost-effective non-surgical therapy for achalasia. Dilatation of the esophagus is achieved by disrupting the circular fibers of the LES with air pressure using a graded dilator approach', 'Endoscopic injection of botulinum toxin can be used in high-risk patients or those who relapse after myotomy. Botulinum toxin, derived from Clostridium botulinum, is a potent biological neurotoxin known to block the release of acetylcholine at the level of the lower esophageal sphincter. This treatment is useful in patients who may not be candidates for surgery or dilatation or alternatively, as a bridge to more definitive therapy', 'Pharmacologic treatments include the administration of nitrates, calcium channel blockers, and phosphodiesterase-5 inhibitors to reduce the lower esophageal sphincter (LES) pressure.', '1.HELLER’S MYOTOMY.\n2.PNEUMATIC DILATATION.\n3.ENDOSCOPIC MYOTOMY'], Pathophysiology: It Is due to selective loss of inhibitory neurons in the lower part of the oesophagus Due to which there is failure of relaxation of lower esophageal sphincter and hence causes dysphagia. (difficulty in swallowing of food) Treatment is by either endoscopic dilatation, or endoscopic or surgical myotomy, Epidemiology:['prevalence of 10 cases per 100,000 individuals', 'an annual incidence of approximately 1.6 cases per 100,000 individuals', 'good', 'Many of the causes of achalasia cannot be prevented. However, treatment may help to prevent complications.'], Complications:['bloating', 'Esophageal Cancer', 'GASTRO OESOPHAGEAL REFLUX DISEASE', 'PERFORATION OF OESOPHAGUS', 'recurrence'], Diagnostics:['HISTOPATHLOGY', 'Barium Imaging', 'Upper GI Endoscopy', 'BARIUM ESOPHAGOGRAM', 'X RAY', 'HIGH RESOLUTION OESOPHAGEAL MANOMERTY(HROM)'], Differential diagnosis:['CARCINOMA OF THE OESOPHAGUS', 'CORROSIVE INJURY TO OESOPHAGUS', 'PERFORATION OF OESOPHAGUS'], disease description:Achalasia is a rare disorder that makes it difficult for food and liquid to pass from the swallowing tube connecting your mouth and stomach (esophagus) into your stomach. Achalasia occurs when nerves in the esophagus become damaged.

Symptoms at 42 years: ['Prominent phlebectasia may be seen on the volar aspects of the fingers, over the interphalangeal joints.', 'rapid bluish discoloration of the affected digit']

Disease Name: Achenbach Syndrome, symptoms: ['Prominent phlebectasia may be seen on the volar aspects of the fingers, over the interphalangeal joints.', 'rapid bluish discoloration of the affected digit'], Treatment: ['Rest the affected limb and cool the area to the reduce swelling. \nAvoid trigger activities.'], Pathophysiology: The pathophysiology of this syndrome is not entirely clear, but intermittent spontaneous hematoma formation is reported as its characteristic symptom. Achenbach syndrome is more predominant in the female population. There are no known risk factors such as trauma, drug use, bleeding disorders, or rheumatologic diseases associated with the etiology of this syndrome. Although the symptoms are alarming to patients, the condition itself is not accompanied by any significant complications.The etiology of the disease is not yet established. There is no reported association with trauma, occupation, exposure to warm or cold temperature, or body habitus. Increased vascular fragility, likely in the setting of minor trauma, causing capillary micro-haemorrhages has been proposed as the possible causation of the disease, although, many patients develop the condition with no identifiable trigger., Epidemiology:['12.4% in women and 1.2% in men', 'fewer than 100 cases have been reported', 'Complete resolution usually occurs within a few da', 'Because of its benign nature, no specific prevention has been proposed. Complete resolution usually occurs within a few days, but symptoms may last for a few months. Recurrent episodes occur for a variable period of time (months or years) without any apparent lasting sequelae.'], Complications:[], Diagnostics:['ANGIOGRAPHY'], Differential diagnosis:['Acrocyanosis', 'buerger disease', 'FROSTBITE', 'Raynaud’s syndrome'], disease description:This is a sudden, painful, bluish discoloration and swelling of a finger or fingers (or sometimes the palm of the hand), often after physical effort of gripping or twisting. Associated diseases Raynaud phenomenon may be associated

Person aged 42 dealing with ['breathing pattern is rapid and shallow', 'chest circumference abnormal', 'obstructive sleep apnea', 'Joint laxity', 'hypotonia.', 'spinal claudication', 'lower limb pain', 'paraesthesia.', 'Numbness', 'weakness', 'Spinal cord compression', 'sleep apnea', 'button nose', 'frontal bossing.', 'small nasal bridge', 'Recurrent infection', 'dyspnea', 'short limbs', 'KYPHOSCOLIOSIS', 'mid-face hypoplasia']

Disease Name: Achondroplasia, symptoms: ['breathing pattern is rapid and shallow', 'chest circumference abnormal', 'obstructive sleep apnea', 'Joint laxity', 'hypotonia.', 'spinal claudication', 'lower limb pain', 'paraesthesia.', 'Numbness', 'weakness', 'Spinal cord compression', 'sleep apnea', 'button nose', 'frontal bossing.', 'small nasal bridge', 'Recurrent infection', 'dyspnea', 'short limbs', 'KYPHOSCOLIOSIS', 'mid-face hypoplasia'], Treatment: ['Ventriculoperitoneal shunt may be required for increased intracranial pressure; suboccipital decompression as indicated for signs and symptoms of craniocervical junction compression; adenotonsillectomy, positive airway pressure, and, rarely, tracheostomy to correct obstructive sleep apnea; pressure-equalizing tubes for middle ear dysfunction; monitor and treat obesity; evaluation and treatment by an orthopedist if progressive bowing of the legs arises; spinal surgery may be needed for severe, persistent kyphosis; surgery to correct spinal stenosis in symptomatic adults.', 'Vosoritide, a C-type natriuretic peptide (CNP) analog, was recently approved to enhance height in individuals with achondroplasia from age five years until growth plates close.'], Pathophysiology: A point mutation in the gene coding for the transmembrane portion of FGFR3, which resides on the short arm of chromosome 4, results in achondroplasia.The point mutation arises from two possible base substitutions: a transition of c.1138G>A (guanine to adenine substitution is identified in approximately 98% of affected individuals) and a transversion of c.1138G>C (guanine to cytosine, seen in about 1% of affected individuals)These base substitutions cause the normal GGG codon to change to AGG or CGG, causing glycine to be replaced with arginine (p.Gly380Arg) in both situations, and subsequently affecting the transmembrane domain of FGFR3. Both substitutions confer a pathogenic variant of FGFR3, which leads to a gain-of-function mechanism of FGFR3 and subsequent quantitative growth plate and cartilage defects seen in achondroplasia.GFR3 normal function is to slow the formation of bone by inhibiting the proliferation of chondrocytes in the proliferative zone of the physis of long bones. The genetic mutation of FGFR3 (p.Gly380Arg) results in a gain-of-function, constitutive activation of the receptor protein, and a significant decrease in endochondral bone formation via increased inhibition of chondrocyte proliferation and differentiation.This process results in the clinical phenotypic features. There is associated increased mortality in childhood, likely due to FMS. The stenosis at the base of the skull can cause cervicomedullary myelopathy (compression of a portion of the brainstem and spinal cord that may cause central sleep apnea, difficulty walking, difficulty swallowing, weakness, numbness, and loss of bowel or bladder control). The average adult height in achondroplasia is approximately 4 feet for both sexes., Epidemiology:['1 in 20,000 live births.', 'incidence of 1/25 000.', 'good', "Since achondroplasia is a rare genetic condition that's often the result of a new gene mutation, there's no way to prevent those random cases. If a parent has achondroplasia, the chance to pass it on could be significantly decreased through preimplantation genetic testing."], Complications:['ear infection', 'Hydrocephalus', 'obesity', 'otitis media', 'Spinal stenosis', 'dental problem', 'Apnea'], Diagnostics:['GENETIC TESTING', 'X RAY'], Differential diagnosis:['HYPOCHONDROPLASIA', 'PSEUDOACHONDROPLASIA'], disease description:Achondroplasia is the most common skeletal dysplasia. The inheritance pattern is autosomal dominant but the majority (>80%) occur secondary to de novo mutation in the fibroblast growth factor receptor 3 (FGFR3) that is identical in 95% of patients with this condition. 

A 2.71-year-old baby suffering from ['neurological signs of deep coma', 'headache', 'failure to thrive', 'nausea', 'vomiting', 'poor feeding', 'rapid and labored respiration']

Disease Name: Acidosis In Children, symptoms: ['neurological signs of deep coma', 'headache', 'failure to thrive', 'nausea', 'vomiting', 'poor feeding', 'rapid and labored respiration'], Treatment: nan, Pathophysiology: nan, Epidemiology:nan, Complications:['seizures', 'shock', 'MULTIORGAN FAILURE'], Diagnostics:['ABG pH'], Differential diagnosis:['iron poisoning', 'Maple Syrup Urine Disease'], disease description:Metabolic acidosis occurs frequently in small children. Metabolic acidosis is an acid-base disorder characterized by a decrease in serum pH that results from either a primary decrease in plasma bicarbonate concentration ([HCO3-]) or an increase in hydrogen ion concentration ([H+]). It is not a disease but rather a biochemical abnormality.

A 31-year-old patient with ['nausea', 'vomiting', 'weight loss', 'Abdominal Pain']

Disease Name: Acinar Cell Cystadenocarcinoma Of Pancreas, symptoms: ['nausea', 'vomiting', 'weight loss', 'Abdominal Pain'], Treatment: [{'medication': ['Cisplatin ', 'Oxaliplatin', 'Irinotecan', 'Paclitaxel', 'Gemcitabine hydrochloride', 'Capecitabine', 'Docetaxel', 'Fluorouracil ']}], Pathophysiology: nan, Epidemiology:['< 1%', '<1%'], Complications:[], Diagnostics:nan, Differential diagnosis:[], disease description:Acinar cell cystadenocarcinoma is a rare malignant epithelial neoplasm of the pancreas with a diffusely cystic, gross architecture in which the cysts are lined with neoplastic epithelial cells that demonstrate evidence of pancreatic exocrine enzyme production.

Experiencing ['pus formation', 'Confusion', 'vomiting', 'fever', 'fever', 'wound infection'] at 35 years old

Disease Name: Acinetobacter Infections, symptoms: ['pus formation', 'Confusion', 'vomiting', 'fever', 'fever', 'wound infection'], Treatment: ['First-line antibiotics — Infections caused by antibiotic-susceptible Acinetobacter isolates may have several first-line therapeutic options, including broad-spectrum cephalosporins (ceftazidime or cefepime), piperacillin-tazobactam, ampicillin-sulbactam, carbapenems (eg, meropenem or imipenem-cilastatin), and fluoroquinolones (eg, ciprofloxacin).\nSecond-line antibiotics — In the setting of resistance to the first-line agents, therapeutic options are limited. Polymyxins (ie, polymyxin B and colistin) and certain tetracycline derivatives (ie, minocycline and tigecycline) are the main therapeutic options for extensively drug-resistant Acinetobacter.'], Pathophysiology: While it is believed that several factors may contribute to the virulence potential of A. baumannii, one factor in particular, OmpA, a member of the Outer membrane proteins (OMPs), has been determined to contribute significantly to the disease causing potential of the pathogen. A. baumannii OmpA bind to the host epithelia and mitochondria, once bound to the mitochondria, OmpA induces mitochondrial dysfunction and causes the mitochondria to swell. This is followed by the release of cytochrome c, a heme protein, which leads to the formation of apoptosome. These reactions all contribute to apoptosis of the cell.OmpA, being the most abundant surface protein on the pathogen, is also involved in resistance to complement and the formation of biofilms—two key stress survival strategies and potentially important virulence associated factors that help to promote bacterial survival both inside and outside the host. The ability of A. baumannii to form biofilms allows it to grow persistently in unfavorable conditions and environments. Indeed, A. baumannii has been shown to form biofilms on abiotic surfaces, which can include glass and equipment used in intensive care units, and/or on biotic surfaces such as epithelial cells. The most common factors that control biofilm formation can include nutrient availability, the presence of pili and outer membrane proteins and macromolecular secretions. Pili assembly and production of biofilm-associated protein (BAP) both contribute to the initiation of biofilm production and maturation after A. baumannii attach to particular surfaces.When pili attach to abiotic surfaces, they initiate the formation of microcolonies, followed by the full development of biofilm structures. BAP are present on the surface of bacterial cells and they contribute to biofilm development and maturation by stabilizing the mature biofilm on abiotic or biotic surfaces. Environmental signals, such as metal cations, also play a role in controlling the formation of biofilms, increasing the ability of A. baumannii to adhere to particular surfaces ., Epidemiology:['Careful attention to infection control procedures, such as hand hygiene and environmental cleaning, can reduce the risk of transmission.'], Complications:['Meningitis', 'VENTILATOR-ASSOCIATED PNEUMONIA'], Diagnostics:['BLOOD CULTURE test', 'Protein'], Differential diagnosis:['nosocomial pneumonia', 'Pseudomonas infection', 'wound infection'], disease description:Acinetobacter baumannii is a Gram-negative bacillus that is aerobic, pleomorphic and non-motile. An opportunistic pathogen, A. baumannii has a high incidence among immunocompromised individuals, particularly those who have experienced a prolonged (> 90 d) hospital stay.1 Commonly associated with aquatic environments,it has been shown to colonize the skin as well as being isolated in high numbers from the respiratory and oropharynx secretions of infected individuals. In recent years, it has been designated as a “red alert” human pathogen, generating alarm among the medical fraternity, arising largely from its extensive antibiotic resistance spectrum.

Person aged 40 with manifestations like ['Right-handed students may have predominantly left-handed facial acne from pressure of the left hand.', 'The resultant acne can be severe (e.g. acne conglobata occurred on the buttocks in a trans-Atlantic rower)', 'Acne']

Disease Name: Acne Mechanica, symptoms: ['Right-handed students may have predominantly left-handed facial acne from pressure of the left hand.', 'The resultant acne can be severe (e.g. acne conglobata occurred on the buttocks in a trans-Atlantic rower)', 'Acne'], Treatment: [{'medication': ['Salicylic acid ', 'Benzoyl peroxide ', 'Vitamin A (Retinol)']}, 'Devices in contact with the skin should be removed as soon as they \nare not in use. For example, sports equipment should be removed \nimmediately after the activity is over. Benzoyl peroxide, applied \nfor 5 min, can be used to clean the skin prior to being rinsed off . Topical retinoids may be applied at night . Other keratolytics may be useful, such as 3% salicylate and 8% resorcinol in 70% \nethanol.'], Pathophysiology: Friction with heat, increased humidity and maceration may cause an acneform folliculitis in susceptible individuals. The effect of occlusion has been proposed to lead to the rupture of microcomedones that are not ordinarily clinic., Epidemiology:['To Do : .Don’t eat raw or barely cooked eggs or meat.\n.Don’t eat or drink anything with unpasteurized milk or juice.\n.Don’t wash raw poultry, meat, or eggs before cooking.\n.Wash raw fruits and vegetables well, and peel them if possible.\n.Don’t prepare food for other people if you’re vomiting or have diarrhea.\n.Refrigerate food properly, both before cooking it and after serving it.\n.Wash your hands well with soap and warm water before and after handling food.\n.Don’t mix cooked food with raw food or use the same utensils to prepare them. For example, don’t use the same knife to cut raw chicken and then to slice mushrooms, and use different plates or cutting boards to slice them on.\n.Wash your hands with soap and water after touching animals, their toys, and their bedding.'], Complications:['Acne vulgaris'], Diagnostics:['Scrape Smear', 'PHYSICAL EXAMINATION'], Differential diagnosis:['Acne vulgaris', 'Herpes Zoster', 'Miliaria', 'Perioral dermatitis', 'rosacea'], disease description:Acne mechanica is a localized acneform eruption induced by occlusion or friction. Most cases of acne mechanica in the literature refer to patients who are using a medical device such as a prosthetic stump or crutches, or to athletes who are experiencing friction from the use of equipment and protective clothing.

Symptoms reported by a 29-year-old: ['NODULES', 'pustules', 'tender skin', 'comedonal acne', 'erythema', 'itching on face', 'pigment change', 'blackheads', 'whiteheads', 'atrophic scarring', 'seborrhoea']

Disease Name: Acne Vulgaris, symptoms: ['NODULES', 'pustules', 'tender skin', 'comedonal acne', 'erythema', 'itching on face', 'pigment change', 'blackheads', 'whiteheads', 'atrophic scarring', 'seborrhoea'], Treatment: ['Lesion removal:\nBoth open and closed comedones can be removed mechanically with comedone extractor and a fine needle or a pointed blade.\n\nAspiration of deep inflamed lesion may be needed in few cases which are followed by IL steroid injection in cysts and sinus tract.\n\n Phototherapy:\nvisible light-They are indicated for mild-to-moderate inflammatory acne. In vitro and in vivo exposure of acne bacteria to 405–420 nm of ultraviolet free blue light results in the photo-destruction through the effect on the porphyrin produced naturally by P. acne.\n\nPhotodynamic therapy:', 'Systemic antibiotics :\nTetracycline (500 mg–1 g/day), doxycycline (50–200 mg/day), minocycline (50–200 mg/day), lymecycline (150–300 mg/day), erythromycin (500 mg–1 g/day), co-trimoxazole, trimethoprim, and recently azithromycin (500 mg thrice weekly).\n\n\nHormonal therapy: \n\n Oral contraceptives: estrogen.\nSpironolactone.\nCyproterone acetate.\n Flutamide.\nOral isotretinoin :0.5–2 mg/kg/day, which is usually given for 20 weeks.', 'Topical therapy :\nBenzoyl peroxide concentrations (2.5–10%).\nTopical retinoids : Tretinoin, adapalene, tazarotene, isotretinoin, metretinide.\nTopical antibiotics:\nClindamycin and erythromycin.\nOther topical/new agents:\nTopical clindamycin and benzoyl peroxide\nSalicylic acid\nAzelaic acid\nLactic acid/Lactate lotion\nPicolinic acid gel 10%'], Pathophysiology: During puberty, under the influence of androgens, sebum secretion is increased as 5-alpha reductase converts testosterone to more potent DHT, which binds to specific receptors in the sebaceous glands increasing sebum production. This leads to an increased hyperproliferation of follicular epidermis, so there is retention of sebum. Distended follicles rupture and release pro-inflammatory chemicals into the dermis, stimulating inflammation. C. acnes, Staphylococcus epidermis, and Malassezia furfur induce inflammation and induce follicular epidermal proliferation.Factors aggravating acne include:Food with a high glycemic number like dairy products (which also contain hormones), junk food, and chocolates which cause insulin-like growth factors that stimulate follicular epidermal hyperproliferationOil-based cosmetics and facial massageA premenstrual flare-up in acne seems to follow edema of the pilosebaceous duct. This occurs in 70% of female patients.Severe anxiety and anger may aggravate acne, probably by stimulating stress hormones., Epidemiology:['The highest prevelence occurs in adolescence where', 'GOOD', 'You can’t completely prevent acne, especially during hormone changes, but you can reduce your risk of developing acne by: \n\nWashing your face daily with warm water and a facial cleanser.\nUsing an oil-free moisturizer.\nWearing “noncomedogenic” makeup products and removing makeup at the end of each day.\nKeeping your hands away from your face.'], Complications:['DEPRESSION', 'scar', 'Poor facial aesthetics'], Diagnostics:['skin lesion biopsy'], Differential diagnosis:['Acne conglobata', 'acne fulminans', 'Acneiform eruptions', 'folliculitis', 'Perioral dermatitis', 'Pyoderma faciale', 'rosacea', 'Sebaceous gland hyperplasia, adenoma and carcinoma', 'Syringomas', 'Tuberous sclerosis'], disease description:Acne vulgaris is an inflammatory disorder of the pilosebaceous unit, which runs a chronic course and it is self-limiting. Acne vulgaris is triggered by Cutibacterium acnes in adolescence, under the influence of normal circulating dehydroepiandrosterone (DHEA). It is a very common skin disorder which can present with inflammatory and non-inflammatory lesions chiefly on the face but can also occur on the upper arms, trunk, and back. Diagnosis can be easily made by examinig the patient.

Experiencing ['acne on face', 'painful lesions', 'whiteheads'] at 27 years old

Disease Name: Acneform Dermatitis, symptoms: ['acne on face', 'painful lesions', 'whiteheads'], Treatment: ['For any residual lesions, treatments that have been used to treat them include topical or oral antibiotics, drug withdrawal or use of topical or oral retinoids. If the cause is a fungal infection like pityrosporum folliculitis, then the use of a topical antifungal agent can be helpful like ciclopirox, econazole, and ketoconazole can be helpful'], Pathophysiology: Drug-induced acneThis acne can occur due to corticosteroids, anticonvulsants like phenytoin, antidepressants, the antipsychotics olanzapine and lithium, antituberculosis drugs like INH, thiourea, thiouracil, disulfiram, corticotropin, antifungals like nystatin and itraconazole, hydroxychloroquine, naproxen, mercury, amineptine, chemotherapy drugs, and epidermal growth factor receptor inhibitors.Antibiotics like penicillins and macrolides cause acute generalized pustular eruption without comedones. Patients are febrile with leukocytosis, Other antibiotics causing it include co-trimoxazole, doxycycline, ofloxacin, and chloramphenicol.Steroid acne presents as monomorphous papulopustules located mainly on the trunk and extremities, with less involvement of the face. Characteristically,  lesions appear after the administration of systemic corticosteroids. Topical corticosteroids may also cause acneiform eruption over skin under which the topical preparation is applied or in around the nose or mouth in the case of inhaled steroids.Occupational acneDue to occupational exposure from Chloracne. Chloraphthalene, chlorophenyl (used as conductors and insulator), and chlorophenols (used as insecticide and fungicide) can cause acneiform eruptions. Lesions are mainly comedones without inflammation. Exposure by inhalation, ingestion, or direct contact of contaminated compounds or foods induces a cutaneous eruption of polymorphous comedones and cysts which is called as chloracne. Associated skin findings include xerosis, and pigmentary changes are also seen. Internal organs like eyes, central nervous system and liver may also be affected. Some chloracnegens can be oncogenic.Chemicals that contain iodides, bromides, and other halogens can also induce an acneiform eruption similar to steroid acne, but iodide-induced eruption are more severe. All patients should be investigated for ophthalmic, neurologic, hepatic, and lipoprotein abnormalities.Chemical acneChemical like heavy oils, waxes, cutting oils, heavy coal tar derivatives like pitch and creosote, vegetable oil in cosmetics, and cheap pomade oils causes acneiform eruptions.Mechanical acnePressure and friction induce acneiform eruptions over the neck of violin players, under arm bands, bra straps and in orthopedic cases prolonged immobilization.Eosinophilic pustular folliculitis is a disease of allergic hypersensitivity. It appears as a recurrent pruritic papulopustular eruption on the face, trunk, and extremities.Rosacea appears similar to acne vulgaris with papulopustules on the face but also has facial flushing and telangiectasias. Is commonly seen in the white population. It is more common in women in the third and fourth decades of life. Associated eye changes include blepharitis, conjunctivitis, iritis, iridocyclitis, hypopyon iritis, and keratitis. Weather extremes, hot or spicy foods, alcohol, ingestion of a high-dose vitamin B6 and Demodex folliculorum mites can trigger the condition., Epidemiology:['50-100% of patients.', 'Acneiform eruption occurs in 45%–100% of EGFRI patients17 and always develops within the first 4 weeks of treatment. The incidence of acneiform eruption is higher for treatment with monoclonal antibodies than treatment with TKIs', 'good', '- Prevention of acneiform rash caused by EGFR inhibitors includes topical corticosteroids (hydrocortisone 2.5%, alclometasone) and oral antibiotics (minocycline, doxycycline, or antibiotics covering skin flora) twice daily for at least the first 6 weeks.\n\n- Do your best to avoid what triggers your dermatitis. That might be foods you’re sensitive or allergic to, chemicals that irritate your skin and/or soaps that do the same. Moisturize your skin regularly. Don’t overheat. Use a humidifier to keep the air from getting too dry. Try not to scratch. Reduce your stress.'], Complications:['folliculitis'], Diagnostics:['skin lesion biopsy'], Differential diagnosis:['Acne vulgaris', 'allergic contact dermatitis', 'folliculitis', 'milia', 'rosacea'], disease description:A skin condition that causes small, raised, acne-like bumps to form, usually on the face, scalp, chest, and upper back. The bumps on the affected skin are usually red and filled with pus and may crust over.

Individual aged 32 with manifestations like ['acne on face', 'acne on forehead', 'papules', 'PUSTULE']

Disease Name: Acneform Eruption, symptoms: ['acne on face', 'acne on forehead', 'papules', 'PUSTULE'], Treatment: ['For any residual lesions, treatments that have been used to treat acneiform eruptions include laser ablation, excision, topical or oral antibiotics, drug withdrawal or use of topical or oral retinoids. If the cause is a fungal infection like pityrosporum folliculitis, then the use of a topical antifungal agent can be helpful like ciclopirox, econazole, and ketoconazole can be helpful.Some patients with eosinophilic pustular folliculitis may benefit from a short course of oral indomethacin. Lesions that fail to respond to indomethacin may be treated with cyclosporine.Patients who have gram-positive organisms causing the skin lesions may also benefit from doxycycline.'], Pathophysiology: Drug-induced acneThis acne can occur due to corticosteroids, anticonvulsants like phenytoin, antidepressants, the antipsychotics olanzapine and lithium, antituberculosis drugs like INH, thiourea, thiouracil, disulfiram, corticotropin, antifungals like nystatin and itraconazole, hydroxychloroquine, naproxen, mercury, amineptine, chemotherapy drugs, and epidermal growth factor receptor inhibitors.Antibiotics like penicillins and macrolides cause acute generalized pustular eruption without comedones. Patients are febrile with leukocytosis, Other antibiotics causing it include co-trimoxazole, doxycycline, ofloxacin, and chloramphenicol.Steroid acne presents as monomorphous papulopustules located mainly on the trunk and extremities, with less involvement of the face. Characteristically,  lesions appear after the administration of systemic corticosteroids. Topical corticosteroids may also cause acneiform eruption over skin under which the topical preparation is applied or in around the nose or mouth in the case of inhaled steroids.Occupational acneDue to occupational exposure from Chloracne. Chloraphthalene, chlorophenyl (used as conductors and insulator), and chlorophenols (used as insecticide and fungicide) can cause acneiform eruptions. Lesions are mainly comedones without inflammation. Exposure by inhalation, ingestion, or direct contact of contaminated compounds or foods induces a cutaneous eruption of polymorphous comedones and cysts which is called as chloracne. Associated skin findings include xerosis, and pigmentary changes are also seen. Internal organs like eyes, central nervous system and liver may also be affected. Some chloracnegens can be oncogenic.Chemicals that contain iodides, bromides, and other halogens can also induce an acneiform eruption similar to steroid acne, but iodide-induced eruption are more severe. All patients should be investigated for ophthalmic, neurologic, hepatic, and lipoprotein abnormalities.Chemical acneChemical like heavy oils, waxes, cutting oils, heavy coal tar derivatives like pitch and creosote, vegetable oil in cosmetics, and cheap pomade oils causes acneiform eruptions.Mechanical acnePressure and friction induce acneiform eruptions over the neck of violin players, under arm bands, bra straps and in orthopedic cases prolonged immobilization.Eosinophilic pustular folliculitis is a disease of allergic hypersensitivity. It appears as a recurrent pruritic papulopustular eruption on the face, trunk, and extremities., Epidemiology:['To Do : Protective clothing and removal of the worker from unsuitable environment also help. Not To Do : Avoid the causative drug in drug-induced acne. Minimize contacts or friction which will prevent occupational and mechanical acne.'], Complications:['liver disorders', 'eye problem'], Diagnostics:['BIOPSY FROM SKIN LESION'], Differential diagnosis:['Acne vulgaris', 'allergic contact dermatitis', 'folliculitis', 'milia', 'rosacea', 'Syphilis'], disease description:Acneiform eruptions are a group of disorders that are characterized by papules and pustules resembling acne vulgaris. It has an acute onset and can affect any age group. The characteristic lesion may be a nodule, papule, pustular or cyst.

Experiencing ['crusting of the skin', 'crusting of the skin', 'papules', 'blackheads', 'whiteheads', 'pustules'] at 22 years

Disease Name: Acneform Pustules, symptoms: ['crusting of the skin', 'crusting of the skin', 'papules', 'blackheads', 'whiteheads', 'pustules'], Treatment: ['Oral treatment - tetracycline, erythromycin, minocycline, doxycycline', 'The treatment of acneiform eruptions depends on the cause. In most cases, if the cause is an organism or a drug, then the exposure should be discontinued. Most patients recover within a few weeks. For any residual lesions, treatments that have been used to treat acneiform eruptions include laser ablation, excision, topical or oral antibiotics, drug withdrawal or use of topical or oral retinoids. If the cause is a fungal infection like pityrosporum folliculitis, then the use of a topical antifungal agent can be helpful like ciclopirox, econazole, and ketoconazole can be helpful.', 'Topical treatment - Salicyclic acid ,benzoyl peroxide,retinoids, clindamycin, erythromycin'], Pathophysiology: Acne pustules develop when the walls of an affected pore begin to break down. It becomes a red, swollen skin blemish called a papule. White blood cells gather on the papule to fight against infection as the pore breaks down. These cells form the pus you see inside the blemish.At this point, the papule becomes a pustule that is filled with sebum, bacteria, and cell debris. The bacteria associated with acne is Propionibacterium acnes., Epidemiology:["9.4% of the world's population with the highest prevalence in adolescents.", '58.0 per 10,000 person-years, higher in females vs. males', 'good', 'Preventing papules is difficult, if not impossible, during normal hormonal changes. But the following tips might help:\n\nWash your face daily with warm water and a mild facial cleanser.\nRoutinely use non-comedogenic (non-pore-clogging) moisturizer.\nYou don’t have to stop using makeup, but try to use “non-comedogenic” products and remove your makeup at the end of each day.\nRoutinely wash your hair.\nKeep hair products away from your face.\nKeep your hands away from your face.'], Complications:['hyperpigmentation', 'hypopigmentation', 'Scarring'], Diagnostics:['Bacterial Culture& Sensitivity Routine Aerobic', 'BIOPSY FROM SKIN LESION'], Differential diagnosis:['Acne vulgaris', 'folliculitis', 'milia', 'rosacea', 'Syphilis'], disease description:An acne pustule is a type of pimple. These bulging patches of skin are pores that have become clogged with pus, sebum (oil), and cell debris. They may also be called whiteheads, blemishes, and zits. Though pustules can appear anywhere on the body, they're usually found on the face, neck, shoulders, and back.

Suffering from ['Dizziness', 'Facial numbness', 'tinnitus', 'headache', 'Hearing loss', 'nausea', 'Numbness', 'paresthesia', 'vertigo', 'PAPPILOEDEMA', 'blurred or unstable vision'] at 55

Disease Name: Acoustic Neuroma, symptoms: ['Dizziness', 'Facial numbness', 'tinnitus', 'headache', 'Hearing loss', 'nausea', 'Numbness', 'paresthesia', 'vertigo', 'PAPPILOEDEMA', 'blurred or unstable vision'], Treatment: ['Conventional radiotherapy by external beam has no role in\nthe treatment of acoustic neuromas due to low tolerance\nof the central nervous system to radiation.\nX-knife or Gamma knife surgery. It is a form of stereotactic\nradiotherapy where radiation energy is converged on\nthe tumour, thus minimizing its effect on the surrounding\nnormal tissue', 'Surgical removal of the tumour is the treatment of choice.\nSurgical approach will depend upon the size of tumour.\nThe various approaches are:\n1. Middle cranial fossa approach.\n2. Translabyrinthine approach.\n3. Suboccipital (retrosigmoid) approach.\n4. Combined translabyrinthine-suboccipital approach'], Pathophysiology: It is a benign, encapsulated, extremely slow-growing tumour of the VIIIth nerve. Microscopically, it consists of elongated spindle cells with rod-shaped nuclei lying in rows or palisades. Bilateral tumours are seen in patients with neurofibromatosis.The tumour almost always arises from the Schwann cells of the vestibular, but rarely from the cochlear division of VIIIth nerve within the internal auditory canal. As it expands, it causes widening and erosion of the canal and then appears in the cerebellopontine angle. Here, it may grow anterosuperiorly to involve Vth nerve or inferiorly to involve the IXth, Xth and XIth cranial nerves. In later stages, it causes displacement of brainstem, pressure on cerebellum and raised intracranial tension. The growth of the tumour is extremely slow and the history may extend over several years. Depending on the size, the tumour is classified as: 1. Intracanalicular (when it is confined to internal auditory canal) 2. Small size (up to 1.5 cm) 3. Medium size (1.5–4 cm) 4. Large size (over 4 cm), Epidemiology:['1 in 100,000 people in the general population.', 'Acoustic neuromas (ANs) represent approximately 6% of all intracranial tumors and are thought to have an incidence of 0.3 to 1 per 100 000 population per year.', 'GOOD', 'You cannot prevent acoustic neuromas from developing. But you can reduce your risk of complications by paying attention to how you feel and function. If you notice any symptoms such as hearing loss, dizziness or ringing in your ears, don’t dismiss your concerns.\n\nTalk to your healthcare provider who can perform a full diagnosis and get to the bottom of your symptoms. The earlier an acoustic neuroma is detected, the better the chances for full tumor removal and hearing preservation.'], Complications:['balance disorder', 'Facial numbness', 'Hearing loss', 'Ringing in ear'], Diagnostics:['CSF EXAMINATION', 'Pure tone audiometry (PTA)', 'MRI', 'X RAY', 'CT SCAN', 'Speech Audiometry', 'ANGIOGRAPHY'], Differential diagnosis:['ANEURYSM', 'arachnoid cyst', 'cholesterol granuloma', 'CPA lipoma', 'Craniopharyngioma', 'Epidermoid cyst', 'facial nerve schwannoma', 'glomus jugulare', "meniere's disease", 'meningioma', 'Pituitary adenoma', 'trigeminal schwannoma'], disease description:Acoustic neuroma is also known as vestibular schwannoma, neurilemmoma or eighth nerve tumour.Acoustic neuroma constitutes 80% of all cerebellopontine angle tumours and 10% of all the brain tumours

Person aged 37 dealing with ['hearing impairment', 'Hearing loss', 'Acquired Atresia and Stenosis of Meatus']

Disease Name: Acquired Atresia And Stenosis Of Meatus, symptoms: ['hearing impairment', 'Hearing loss', 'Acquired Atresia and Stenosis of Meatus'], Treatment: ['METOPLASTY Using a postaural incision,\nscar tissue and thickened meatal skin are excised, bony\nmeatus is enlarged and the raw meatal bone is covered\nwith pedicled flaps from meatus or split-skin grafts.'], Pathophysiology: It can result from: (a) Infections, e.g. chronic otitis externa—an important cause (b) Trauma, e.g. lacerations, fracture of tympanic plate, surgery on ear canal or mastoid. (c) Burns—thermal or chemical. Treatment is meatoplasty. Using a postaural incision, scar tissue and thickened meatal skin are excised, bony meatus is enlarged and the raw meatal bone is covered with pedicled flaps from meatus or split-skin grafts., Epidemiology:['POOR'], Complications:['hearing impairment'], Diagnostics:['CT SCAN'], Differential diagnosis:[], disease description:It can result from: (a) Infections, e.g. chronic otitis externa—an important cause (b) Trauma, e.g. lacerations, fracture of tympanic plate, surgery on ear canal or mastoid. (c) Burns—thermal or chemical. Treatment is meatoplasty. Using a postaural incision, scar tissue and thickened meatal skin are excised, bony meatus is enlarged and the raw meatal bone is covered with pedicled flaps from meatus or split-skin grafts.

Woman aged 39 experiencing ['hepatosplenomegaly', 'telangiectasias', 'Hirsutism', 'fat loss occurs in face, trunk, abdomen and extremities', 'dark velvity patches on skin', 'hyperkeratosis of the palms and soles', 'hyperpigmentation', 'Acne', 'alopecia', 'prominent musculature', 'curly hair', 'protrusion of jaw and eyebrows']

Disease Name: Acquired Generalized Lipodystrophy, symptoms: ['hepatosplenomegaly', 'telangiectasias', 'Hirsutism', 'fat loss occurs in face, trunk, abdomen and extremities', 'dark velvity patches on skin', 'hyperkeratosis of the palms and soles', 'hyperpigmentation', 'Acne', 'alopecia', 'prominent musculature', 'curly hair', 'protrusion of jaw and eyebrows'], Treatment: ['4 months of twice-daily subcutaneous metreleptin injections were shown to be safe and effective.In patients \nwith hypertriglyceridaemia, fasting levels of plasma triglycerides \ndecreased by 83%. In these patients, fasting plasma triglycerides \nincreased soon after discontinuation of the injections and were \ncorrected once again after reinitiation of the therapy', 'filler injections, autologous adipose tissue \ntransfer and muscle tissue transfers may help correct volume \nlosses'], Pathophysiology: The mechanism of fat loss in AGL is unknown. Despite reports of a variety of preceding infections, it is not clear that these infections directly cause AGL. The classic complement pathway is postulated to be involved in the pathogenesis among AGL patients with autoimmune hepatitis and low serum complement . Antibody-mediated destruction or cell-mediated lysis of adipocytes has also been considered. The consequences are that there is an insufficient mass of adipose tissue to store excess energy, which is stored instead as triglyceride in the liver and skeletal muscle, and that there is a perpetual elevation of plasma free fatty acid (FFA), resulting in an impaired ß-cell response to glucose and insulin resistance. Low serum leptin and adiponectin levels, reflecting the low amount of body fat in these patients, may further contribute to severe insulin resistance and the metabolic complications observed in AGL., Epidemiology:['Acquired forms of lipodystrophy are often triggered by an infection or autoimmune condition. While some types of infection, such as chickenpox and whooping cough (pertussis), can be prevented with vaccinations, other infections that are associated with acquired lipodystrophy and autoimmune conditions aren’t preventable.'], Complications:['Acute Pancreatitis', 'Nephropathy', 'neuropathy', 'retinopathy', 'eruptive xanthomas', 'lipaemia retinalis', 'premature atherosclerosis', 'coronary heart disease'], Diagnostics:['Glucose Tolerance Test', 'HDL', 'Serum Triglycerides', 'Insulin in Blood test', 'MRI'], Differential diagnosis:['acquired partial lipodystrophy', 'autosomal dominant familial partial lipodystrophy', 'congenital generalized lipodystrophy', 'localized lipodystrophy', 'mandibuloacral dysplasia'], disease description:Acquired generalized lipodystrophy (AGL) is a rare disease characterized by a selective loss of adipose tissue from large regions of the body, occurring after birth.

Suffering from ['Fat loss occurs symmetrically,on the face and scalp, neck, shoulders, upper extremities, thoracic region and upper abdomen'] at 33

Disease Name: Acquired Partial Lipodystrophy, symptoms: ['Fat loss occurs symmetrically,on the face and scalp, neck, shoulders, upper extremities, thoracic region and upper abdomen'], Treatment: ['identification of neutralizing \nantibodies against C3 nephritic factors in intravenous immunoglobulin (IVIg) has led to treatment of patients who have C3 \nnephritic factors and type II MCGN with IVIg with encouraging \nresults', 'filler injections, autologous adipose tissue transfer \nand muscle tissue transfers'], Pathophysiology: There is evidence to support an autoimmune-mediated destruction of adipocytes in APL. Approximately 80–90% of APL patients have a serum immunoglobulin G named C3 nephritic factor. This blocks the degradation of the enzyme C3 convertase, which leads to excessive consumption of C3. As a result, serum C3 levels are low in more than 80% of APL patients. Levels of C1q, C4, C5 and C6 and factors B and P are usually normal, suggesting selective activation of the alternative complement pathway. Lysis of adipocytes may be related to the expression of several complement proteins such as factors D (adipsin), B, H and P. For example, in vitro studies suggest that the C3 nephritic factor causes lysis in adipocytes expressing factor D. Heterogenecity of factor D expression in adipose tissue in different anatomical locations has been postulated to explain the selective loss of upper body fat in APL., Epidemiology:['3.07 cases/million', '1 in 1 million people overall.', 'bad', 'You can’t prevent genetic forms of lipodystrophy because it’s the result of a genetic mutation that’s inherited. To understand your risk of having a child with a genetic condition, talk to your healthcare provider about genetic testing if you plan on becoming pregnant.\n\nAcquired forms of lipodystrophy are often triggered by an infection or autoimmune condition. While some types of infection, such as chickenpox and whooping cough (pertussis), can be prevented with vaccinations, other infections that are associated with acquired lipodystrophy and autoimmune conditions aren’t preventable.'], Complications:['acanthosis nigricans', 'diabetes mellitus', 'dyslipidaemia'], Diagnostics:['COMPLEMENT 3(C3) LEVEL', 'Glucose Tolerance Test', 'HDL', 'Serum Triglycerides', 'Insulin in Blood test', 'MRI', 'C3 nephritic factor'], Differential diagnosis:['Acquired generalized lipodystrophy', 'familial partial lipodystrophy'], disease description:Acquired partial lipodystrophy (APL) is a rare disease characterized by symmetrical fat loss, usually occurring before the age of 15 years.

Experiencing ['Keratotic dome-shaped papules', 'white patches on skin', 'Itching of the skin', 'pruritus', 'NODULES'] at 40 years

Disease Name: Acquired Perforating Dermatosis, symptoms: ['Keratotic dome-shaped papules', 'white patches on skin', 'Itching of the skin', 'pruritus', 'NODULES'], Treatment: [{'medication': ['Amitriptyline ', 'Rifampicin/Rifampin', 'Methotrexate', 'Isotretinoin', 'Vitamin D3/Tacalcitol']}, 'Topical retinoids, emollient creams,intralesional steroids and \ntopical steroids under occlusion', 'Narrow-band UVB \n, PUVA and photodynamic therapy'], Pathophysiology: The bulk of the coarse granular basophilic material which is extruded by TEE appears to derive from the nuclei of polymorphonuclear leukocytes. It has been suggested that lysosomal enzymes derived from leukocytes might be responsible for the altered staining of collagen fibres, the degradation of elastic fibres and the impairment of keratinocyte adhesion, which allows TEE of dermal components. Most patients have chronic renal disease and/or longstanding diabetes., Epidemiology:['there is no prevention.'], Complications:['infections'], Diagnostics:['HISTOPATHLOGY', 'Dermoscopy'], Differential diagnosis:['folliculitis', 'Molluscum Contagiosum', 'papular urticaria', 'prurigo nodularis', 'scabies'], disease description:An acquired disorder of transepidermal elimination of degenerate collagen, elastin and other connective tissue components. It is strongly associated with diabetes and chronic kidney disease.It is characterized by TEE of both collagen and elastin and presents as a chronic pruritic dermatosis with multiple keratotic crusted papules and nodules.

Person at 42 with ['cold extremities', 'sweating', 'cold clammy skin', 'bluish discoloration of the extremities']

Disease Name: Acrocyanosis, symptoms: ['cold extremities', 'sweating', 'cold clammy skin', 'bluish discoloration of the extremities'], Treatment: ['There is no effective medical treatment for acrocyanosis. Vasodilator \ntherapies, such as the calcium-channel antagonists, do not appear \nto be benefi cial. Drug-induced acrocyanosis will be improved by \ncessation of the culprit drug. Treatment of an underlying systemic \ndisorder may improve the appearance in secondary acrocyanosis.'], Pathophysiology: There is vasospasm of peripheral arterioles, aggravated by cold, and dilatation of the subpapillary venous plexus . The condition is most probably a primary vascular defect since studies have not demonstrated a deficit of neuronal supply to the cutaneous vessels. Decreased acral blood flow may be further compromised by plasma hyperviscosity. In ethylmalonic encephalopathy – a rare metabolic disorder with neuromotor delay, hyperlactic acidaemia and orthostatic acrocyanosis – a mutation has been demonstrated in ETHE1 , a gene encoding a mitochondrial matrix protein.Acrocyanosis can be diagnosed clinically by proper history and physical examination., Epidemiology:['The prognosis varies with the underlying disorder.', 'In older children and adults, keeping hands and feet warm and covering up their body parts can protect them from cold temperatures.\n\nSevere cases may be treated with medications, including alpha blockers or medicines that relax muscles and help small blood vessels to remain open.\n\nSecondary acrocyanosis symptoms resolve when the underlying condition is treated and managed'], Complications:['Gangrene of digits', 'gangrene of the extremities', 'ulceration'], Diagnostics:['ANA', 'Complete Blood Count CBC', 'DUPLEX ULTRASONOGRAPHY'], Differential diagnosis:['buerger disease', 'Raynaud’s syndrome'], disease description:Acrocyanosis is a persistent cyanotic or erythrocyanotic mottled discoloration of the hands and, less commonly, feet and face. Acrocyanosis may be idiopathic or secondary to a number of systemic disorders, including an underlying malignancy. Sometimes there is a family history, indicating a genetic basis. Rarely, it is drug induced. Age and sex Presentation is typically in adolescence, with a reported female preponderance

Symptoms reported by a 23-year-old: ['subcutaneous nodules', 'NODULES', 'plaques', 'paraesthesias', 'Gaiter-like sclerosis of the lower third of the leg', 'Morphoea of the trunk', 'painless nodules', 'acral pain', 'limitation of movement of the joints of the hands and feet, or of the shoulders']

Disease Name: Acrodermatitis Chronica Atrophicans, symptoms: ['subcutaneous nodules', 'NODULES', 'plaques', 'paraesthesias', 'Gaiter-like sclerosis of the lower third of the leg', 'Morphoea of the trunk', 'painless nodules', 'acral pain', 'limitation of movement of the joints of the hands and feet, or of the shoulders'], Treatment: ['First line\n•\tOral antibiotics (e.g. doxyxycline or amoxicillin)\nSecond line\n•\tIntravenous antibiotics (e.g. benzylpenicillin if significant \nsystemic manifestations)'], Pathophysiology: During the early stages, there is non-specific dermal oedema with perivascular inflammatory infiltration. Subsequently, the epidermis becomes atrophic and the epidermal appendages are destroyed. Beneath a subepidermal zone of degenerate connective tissue lies a dense, band-like infiltrate, predominantly consisting of lymphocytes, histiocytes and plasma cells. Ultimately, the infiltrate is reduced to narrow bands between collagen fibres. In some patients, scleroderma-like changes may develop, Epidemiology:['not good', "Avoid areas endemic for Lyme borreliosis.\nWhen walking in high grass or woodland, wear white clothes (so the tick can be seen more easily) with long sleeves, long trousers tucked into socks or long boots.\nUse repellents/insecticides.\nAfter returning from a walk in an endemic area, change your clothes and check your whole body carefully.\nThe next day, check your body for ticks again.\nRemove the tick as prompt removal decreases the risk of Lyme disease transmission. Disinfect the site. Use tweezers to carefully and steadily pull the tick out from the skin. Disinfect the site again. Wash your hands.\nWatch the site of the tick bite for several weeks. If a rash appears bigger than 5 cm or you have 'flu-like symptoms, consult your doctor."], Complications:['Squamous carcinoma in situ', 'lymphoma', 'LYME BORRELIOSIS'], Diagnostics:['HISTOPATHLOGY', 'Antibody Serology Tests', 'Immunoblotting'], Differential diagnosis:['erythema chronicum migrans', 'LYME BORRELIOSIS'], disease description:This is a late skin manifestation of Lyme borreliosis. It is characterized by the insidious onset of painless, dull-red nodules or plaques on the extremities, which slowly extend centrifugally for several months or years, leaving central areas of atrophy.

A 38-year-old patient experiencing ['Proximal muscle weakness', 'coarse facial features', 'erectile dysfunction', 'fatigue', 'large fleshy nose', 'visual disorders', 'joint pain', 'Oily skin', 'enlarged hand and feet', 'menstrual irregularity']

Disease Name: Acromegaly, symptoms: ['Proximal muscle weakness', 'coarse facial features', 'erectile dysfunction', 'fatigue', 'large fleshy nose', 'visual disorders', 'joint pain', 'Oily skin', 'enlarged hand and feet', 'menstrual irregularity'], Treatment: [{'medication': ['Pegvisomant ']}, '1-Somatostatin analogs (octreotide, Lanreotide, pasireotide)\n2-Dopamine receptor agonists (cabergoline, bromocriptine)\n3-GH-Receptor antagonist (pegvisomant)', 'Radiotherapy\n\nRadiotherapy is considered in those patients in whom medical management is not effective in controlling disease, recurrence after surgery, and again the failure of medical therapy. The patients treated with radiotherapy need to be closely monitored for hypopituitarism.\n\nConventional fractionated radiotherapy is often administered as an adjunct to surgery to prevent relapse or when surgery cannot bring the acceptable lowering of GH levels. It is associated with the risk of irradiating adjacent brain tissues. It is provided at small daily doses 5 days a week, usually for 5 to 6 weeks duration. Remission can take up to 10 years, and these patients require medical management in the interim.\nStereotactic radiosurgery: This is precision radiotherapy, directing high dose radiation to the tumor and minimizing risk to nearby healthy brain tissues. It is a single high dose of radiation. The adenoma needs to be multiple millimeters away from the optic chasm to avoid damage to utilize this technique.', 'Surgery is the treatment of choice for all microadenomas as well as macroadenomas, causing a mass effect. Debulking of macroadenomas without mass effect can also be done and has been described as a modality to allow for better response to medical treatment even if a surgical cure is not likely. The best predictors of surgical cure include smaller tumor size, lower levels of GH/IGF-1, and absence of invasion of surrounding structures such as the cavernous sinus.'], Pathophysiology: In pituitary adenomas, a mutation in the alpha subunit of the guanine nucleotide stimulatory protein is responsible for the excess growth hormone secretion.The mutation in the alpha subunit will lead to increase synthesis of cAMP which is responsible for the growth of certain cells.Increase synthesis of cAMP will result in the increase secretion of the growth hormone.Signal transduction and transcription (STAT) induce production of IGF-1 from liver, bone and pituitary gland.The IGF-1 is responsible for the acral features of acromegaly. IGF-1 causes the rapid increase in the hand and feet size, forehead protrusion, and jaw prominence.The high level of IGF-1 is responsible for the following pathologic processes:IGF-1 is responsible for the diabetes mellitus which is common in 20% of patients with acromegaly. IGF-1 interferes with insulin on its receptor which leads to insulin resistance and hyperglycemia.IGF-1 causes hypertrophy of the body organs like the heart (cardiomegaly) and tongue (macroglossia)., Epidemiology:['50 to 70 people per million.', 'good', 'Acromegaly cannot be prevented. Early treatment may prevent the disease from getting worse and help to avoid complications.\n\n Scientists aren’t sure what causes pituitary tumors that cause acromegaly to develop, though they think certain genetic factors may play a role.'], Complications:['cardiomyopathy', 'goitre', 'hypertension', 'Polyps', 'Osteoarthritis', 'Type 2 Diabetes Mellitus'], Diagnostics:['PROLACTIN', 'MRI PITUITERY', 'Serum GH', 'Serum IGF-1', 'XRAY long bones', 'Oral Glucose Tolerance Test'], Differential diagnosis:['Carney complex', 'McCune-Albright Syndrome', 'MULTIPLE ENDOCRINE NEOPLASIAS 1(MEN 1)', 'sotos syndrome'], disease description:Acromegaly is a rare disorder caused by excessive growth hormone production (GH), most commonly from an adenoma of the anterior pituitary gland. The resulting production of insulin-like growth factor 1 (IGF-1) causes the characteristic overgrowth of certain tissues resulting in coarsening of facial features, enlarging hands and feet, as well as effects on multiple systems throughout the body, including cardiovascular, rheumatologic, neurologic, pulmonary, neoplastic, and metabolic. 

Person at 54 with manifestations like ['skin over the distal phalanx becomes red and scaly, and pustules develop', 'nail folds and nail bed may be involved, leading to nail dystrophy', 'proximal edge of the lesion is bordered by a fringe of undermined epidermis, irregular, often sodden and sometimes preceded by a line of vesiculopustules.', 'nail plate may be completely destroyed', 'Itching of the skin', 'PUSTULE']

Disease Name: Acropustulosis, symptoms: ['skin over the distal phalanx becomes red and scaly, and pustules develop', 'nail folds and nail bed may be involved, leading to nail dystrophy', 'proximal edge of the lesion is bordered by a fringe of undermined epidermis, irregular, often sodden and sometimes preceded by a line of vesiculopustules.', 'nail plate may be completely destroyed', 'Itching of the skin', 'PUSTULE'], Treatment: [{'medication': ['Cyclosporine/Ciclosporine', 'Tacrolimus ', 'Adalimumab ', 'Calcipotriol', 'Acitretin']}, 'First line \n• Super-potent topical corticosteroid ± occlusion\n Second line \n• Acitretin\n• Ciclosporin\n Third line \n• Adalimumab'], Pathophysiology: The features are similar to those of generalized pustular psoriasis. In the epidermis, there are numerous subcorneal neutrophilic pustules and spongiform pustules with hypergranulosis and parakeratotic hyperkeratosis. There is a lymphocytic infiltrate in the dermis, which in chronic disease may become atrophic. Genetics: IL36RN has been sequenced in nine Europeans with acrodermatitis continua of Hallopeau. Two unrelated patients were found to have mutations (homozygous p.Ser113Leu in one and compound heterozygote p.Arg35Trp/p.Ser113Leu in the other). A Lebanese man with acrodermatitis continua of Hallopeau has been reported in whom a mutation in IL36RN was detected (homozygous p.Ser113Leu). His sister who had generalized pustular psoriasis (von Zumbusch) without acral involvement had the same IL36RN mutation, supporting the view that acrodermatitis continua of Hallopeau is a localized variant of generalized pustular psoriasis. Recently, germline mutations in AP1S3 were identified in four of seven unrelated individuals with acrodermatitis continua of Hallopeau and subsequently a small number of patients with generalized pustular psoriasis and palmoplantar pustulosis. AP1S3 encodes the s1C subunit of the adaptor protein complex 1, which is involved in vesicular transport between the transgolgi network and endosomes. The functional significance of these mutations is yet to be established but may involve impaired TLR3 signalling., Epidemiology:['Try to keep your child from scratching their lesions. Excessive scratching can lead to scarring. Cover your child’s feet with socks to protect their skin from scratching. Soft cotton gloves can sometimes keep them from scratching or rubbing their hands too much.\n\nIf acropustulosis develops along with scabies, treatment of scabies will be necessary too.'], Complications:['Scarring'], Diagnostics:['Bacterial Culture& Sensitivity Routine Aerobic'], Differential diagnosis:['Contact dermatitis', 'scleroderma'], disease description:This is a rare chronic sterile pustular eruption affecting initially the tips of the fingers or toes that tends slowly to extend locally but which may evolve into generalized pustular psoriasis. The distribution of lesions in acrodermatitis continua of Hallopeau is distinctive; as is the local destruction. This may be seen in children. It is rare in young adults and, unlike palmoplantar pustulosis, not infrequently begins in old age.

At 27 years old, experiencing ['Redness', 'swelling', 'Tenderness on palpation', 'crusted erosions']

Disease Name: Actinic Cheilitis (solar Cheilosis), symptoms: ['Redness', 'swelling', 'Tenderness on palpation', 'crusted erosions'], Treatment: [{'medication': ['Diclofenac ', 'Fluorouracil ', 'Tretinoin']}, 'Laser treatment: preferred non-surgical intervention (efficacy 93%, low recurrences)\nCO2 Laser: 10600 nm\nErbium Laser: 2940 nm.\n\nVermilionectomy/Surgical excision: preferred treatment for severe/refractory cases (efficacy near 100%, low recurrences).\n\nTopical Treatments: preferred treatment for patients with large areas of sun damage or those preferring medical intervention:\n5-FU\nImiquimod\nIngenol mebutate\nTrichloroacetic acid\nDiclofenac\n\nPhototherapy: while actinic cheilitis results from by UV light damaging epithelial DNA, light therapy at an increased intensity level that causes reactive oxygen species to destroy damaged skin cells .\n\nCryotherapy: liquid nitrogen physically destroys abnormal cells.\nElectrocautery/Curettage: physical destruction of the abnormal cells.\nPhotoprotection: reduce the progression.'], Pathophysiology: Those with fair skin have less melanin and innately less protection against UV rays. The physical properties of the lips, such as their shape and being a transition area from oral mucosa to skin with thinner epithelium, less sebaceous glands, and less melanin, contribute to less protection and increased exposure to UV radiation. Chronic exposure to UV light damages tumor suppressor gene p53 resulting in uncontrolled replication of defective cells, which is a common gene mutation found with increasing frequency as actinic cheilitis and actinic keratoses undergo malignant transformation to SCC. Although actinic cheilitis can affect both the upper and lower oral cutaneous mucosa, more light from the sun hits the lower lip, making this area especially prone to sun damage and an increased number of skin cancers., Epidemiology:['The prevalence of actinic cheilitis was 31.3%', 'actinic cheilitis can undergo malignant transforma', 'The best way to prevent actinic cheilitis and SCC is to protect your lips from the sun’s harmful rays year-round:\n\nApply lip balm that contains sunscreen regularly.\nLimit time in the sun, especially when it’s at peak solar strength.\nWear a hat with a brim that shades your lips.\nPeople with actinic cheilitis should have routine checkups to detect any changes that could be early warning signs of cancer. Most healthcare providers recommend yearly skin checks by a dermatologist (skin doctor) for such individuals.\n\nIn addition, smokers should quit smoking. Ask your healthcare provider for help with quitting.'], Complications:['squamous cell carcinoma.'], Diagnostics:['HISTOPATHLOGY', 'X RAY', 'ELECTRON MICROSCOPY'], Differential diagnosis:['Basal cell carcinoma', 'Discoid lupus erythematosus', 'Glandular cheilitis', 'herpes', 'herpes labialis', 'leukoplakia', 'Malignant melanoma', 'Squamous cell carcinoma'], disease description:Actinic cheilitis is a precancerous condition that can create rough, scaly, discolored patches on your lips. Prolonged sun exposure causes it, and usually affects your lower lip. It's also called: Actinic cheilosis.

Symptoms reported at the age of 51: ['on the neck -well-defined furrows into an irregular rhomboidal pattern seen', 'plaques on the face', 'thickened skin', 'Elastosis', 'NODULES']

Disease Name: Actinic Elastosis, symptoms: ['on the neck -well-defined furrows into an irregular rhomboidal pattern seen', 'plaques on the face', 'thickened skin', 'Elastosis', 'NODULES'], Treatment: ['Dermabrasion is a useful technique which offers good depth control.\nMicrodermabrasion has also been found to be effective but pushes up the cost of treatment as several sessions are necessary, and the time taken for improvement to be visible is increased .\n\nChemical peels for medium depth peeling .\n\nLaser resurfacing may be done using carbon dioxide or erbium:yttrium-aluminum-garnet (Er:YAG) laser, but at least three weeks must be provided for skin healing to occur. This may be cut down to one week if fractionated lasers are used.\n\nPhotodynamic therapy .', 'Topical application of retinoids, usually 0.025% at the beginning and building up to 0.05% for thicker skin, is performed every evening.\n\ntopical alphahydroxy acids (AHAs) given as 10% solution three times a week, building up to 15% and 20% .\n\nTopical imiqimod and fluorouracil have also been used to reduce the lines and furrows of solar elastosis.\n\nImiquimod is an immune response modifying agent; it may be used three times a week but stopped after four to six weeks.'], Pathophysiology: The appearance of solar elastosis is as patches of thick coarsely furrowed skin with a bumpy rough surface. It occurs most often over the sun-exposed areas of the face, lips, hands and forearms, ears and neck.The normal collagen and elastic fibers in the skin are degraded by ultraviolet rays, with the fibroblast responding to photodamage by oversecreting new tropoelastin. This elastic tissue is hyperplastic but has lost its normal orderly appearance. This is accompanied by the action of matrix metalloproteinases which degrade the surrounding tissue.The disruption of collagen and elastic tissues in the dermis causes the normal cellular structure to be lost, with excessive deposition of residual material which eventually results in vasodilatation. The normal dermal architecture is thus lost in the damaged region., Epidemiology:['10.2% in females and 26.5% in males.', 'incidence of 1 : 1250 is seen', 'good', 'People with solar elastosis should minimise or avoid exposure to its known precipitants:\n\ncareful sun protection measures with clothing and broad-spectrum high-protection sunscreens\ndiscontinue smoking and avoid exposure to passive smoking.\nAblative and non-ablative laser treatments, dermal fillers, and neurotoxin injections (botulinum toxin) have been used in an attempt to improve the cosmetic appearance of solar elastosis.'], Complications:['melanoma', 'Actinic keratoses', 'Basal cell carcinoma'], Diagnostics:['HISTOLOGIC EXAMINATION', 'full thickness skin biopsy'], Differential diagnosis:['Basal cell carcinoma', 'colloid milium', 'Diffuse plane xanthomatosis', 'Pseudoxanthoma elasticum'], disease description:Actinic elastosis is another component of hypertrophic skin photodamage. It is characterized clinically by yellowish discoloration and thickening of the skin, and histologically by a reduction in collagen and an accumulation of amorphous masses of degenerate elastic fibres in the papillary and upper reticular dermis

having ['excessive watering from eyes', 'lacrimal abscess', 'fistulae formation', 'painful swelling in the region of lacrimal sac', 'malaise', 'fever', 'pain in eyes', 'red eyes', 'WATERING EYE'] at the age of 45

Disease Name: Actinic Granuloma And Annular Elastolytic Giant Cell Granulomaa, symptoms: ['excessive watering from eyes', 'lacrimal abscess', 'fistulae formation', 'painful swelling in the region of lacrimal sac', 'malaise', 'fever', 'pain in eyes', 'red eyes', 'WATERING EYE'], Treatment: [{'medication': ['Cefixime ', 'Ceftriaxone ', 'Azithromycin ', 'Doxycycline ']}, '1. During cellulitis stage. It consists of systemic\nand topical antibiotics to control infection; and\nsystemic anti-inflammatory analgesic drugs and hot\nfomentation to relieve pain and swelling.\n2. During stage of lacrimal abscess. In addition to the\nabove treatment when pus starts pointing on the\nskin, it should be drained with a small incision.', 'Dacryocystorhinostomy (DCR), and Dacryocystectomy (DCT)'], Pathophysiology: Pathogenesis has not been clearly understood and is highly debatable. Several postulations have been put forward, a few of which include-1. O’BrienO’Brien’s Actinic hypothesis: Solar radiation is the initial trigger that selectively causes damage to the elastic tissue in the upper and mid-dermis. This degenerated tissue then becomes a target for an auto-immune cell-mediated response (predominantly CD4+ cells), that attempts to repair the damaged skin, but eventually leads to granulomatous inflammation instead. This theory is consistent with most of the findings seen in our patient- lesions in sun-exposed skin, improvement of lesions with stringent avoidance of sun exposure, fragmented elastic fibers ingested by giant cells, and presence of lymphocytes. 2. Inflammatory theory- arguably suggests that the elastic fiber destruction is caused by granulomatous inflammation itself, implying that inflammation is the inciting event; rather than actinic radiation.The four histopathologic variants-- Giant cell variant- Necrobiotic variant- Sarcoid variant- Histiocytic variant, Epidemiology:['GOOD', '- Sun-protective measures'], Complications:['conjunctivitis', 'orbital cellulitis', 'septicaemia', 'osteomyelitis', 'corneal ulceration', 'Lid abscess', 'Facial cellulitis and acute ethmoiditis'], Diagnostics:['X RAY ORBIT', 'CT SCAN', 'Nasal endoscopy', 'Dacryocystography', 'Fluorescein dye disappearance test (FDDT)'], Differential diagnosis:['Dacryoadenitis', 'granuloma annulare', 'Necrobiosis lipoidica', 'orbital cellulitis', 'periorbital cellulitis', 'Sebaceous cyst', 'sinusitis'], disease description:Annular elastolytic giant cell granuloma (AEGCG) is a rare, often self-limiting chronic inflammatory disorder mostly occurring in the sun-exposed areas such as the dorsum of hands, extensor surfaces of arms, face, anterior neck, and upper chest.

A 51-year-old with ['papules with a rough horny surface', 'Hyperkeratotic spicules', 'plaques']

Disease Name: Actinic Keratosis: Arsenical Keratosis, Puva Kera, symptoms: ['papules with a rough horny surface', 'Hyperkeratotic spicules', 'plaques'], Treatment: ['Cryotherapy\nCurettage and electrodessication\nCarbon dioxide laser ablation\nTopical keratolytic agents- salicylic acid (5 to 10%), urea (10 to 20%)\nImiquimod 5% cream\nTopical 5-fluorouracil\nOral retinoids\nSurgical excision'], Pathophysiology: Though the exact pathomechanism underlying the premalignant and malignant manifestations of chronic arsenic exposure is unknown, there are several hypotheses that have been proposed and researched in several parts of the world. Arsenic metabolism in the body has a key role in most of these theories. Some such tested theories are as follows:Genetic polymorphism of enzymes involved in the metabolic pathway; arsenite methyltransferase (AS3MT) is the main mediator in the biomethylation of arsenic.Global DNA hypomethylation due to depletion of S-adenosylmethionine in cells during the process of arsenic biomethylation. This leads to aberrant gene expression in cells, resulting in carcinogenesis.Reactive oxygen species generated during the metabolism of arsenic causes oxidative DNA damage, resulting in chromosomal abnormalities and sister chromatic exchange., Epidemiology:['A greater incidence and prevalence of arsenic keratosis is reported from countries with documented environmental arsenic contamination, most commonly in groundwater. This includes Bangladesh, India, Taiwan, Mexico, Chile, Argentina, Japan, and China', 'bad', "Limit your time in the sun. Especially avoid time in the sun between 10 a.m. and 2 p.m. And avoid staying in the sun so long that you get a sunburn or a suntan.\nUse sunscreen. Before spending time outdoors, apply a broad-spectrum water-resistant sunscreen with a sun protection factor (SPF) of at least 30, as the American Academy of Dermatology recommends. Do this even on cloudy days.\n\nUse sunscreen on all exposed skin. And use lip balm with sunscreen on your lips. Apply sunscreen at least 15 minutes before going outside and reapply it every two hours — or more often if you're swimming or sweating.\n\nSunscreen is not recommended for babies under 6 months. Rather, keep them out of the sun if possible. Or protect them with shade, hats, and clothing that covers the arms and legs.\n\nCover up. For extra protection from the sun, wear tightly woven clothing that covers your arms and legs. Also wear a broad-brimmed hat. This provides more protection than does a baseball cap or golf visor.\nAvoid tanning beds. The UV exposure from a tanning bed can cause just as much skin damage as a tan from the sun.\nCheck your skin regularly and report changes to your health care provider. Examine your skin regularly, looking for the development of new skin growths or changes in existing moles, freckles, bumps and birthmarks. With the help of mirrors, check your face, neck, ears and scalp. Examine the tops and undersides of your arms and hands."], Complications:['squamous cell carcinoma.'], Diagnostics:['ARSENIC', 'ARSENIC', 'ARSENIC'], Differential diagnosis:['Actinic cheilitis (solar cheilosis)', 'Dermatophyte infections', 'Discoid Lupus Erythematosus.', 'Lichen Planus', 'porokeratosis', 'psoriasis', 'seborrhoeic', 'Squamous cell carcinoma', 'Verrucas: Verruca vulgaris, Verruca plantaris, Ver', 'viral warts'], disease description:Arsenical keratosis is an important cutaneous manifestation of chronic arsenic toxicity (CAT). As it is a common presenting complaint of CAT and a precancerous condition, awareness and a high degree of suspicion are required among clinicians for a prompt diagnosis and treatment.

Symptoms reported by a 19-year-old: ['Skin fissures', 'pruritus', 'ulceration', 'conjunctivitis', 'NODULES', 'itchy papule', 'crusting of the skin']

Disease Name: Actinic Prurigo, symptoms: ['Skin fissures', 'pruritus', 'ulceration', 'conjunctivitis', 'NODULES', 'itchy papule', 'crusting of the skin'], Treatment: ['Actinic prurigo treatment is with sunscreens, ß-carotene, psoralen \nand UVA (PUVA), and antihistamines. Oral thalidomide or pentoxifylline may be tried'], Pathophysiology: The pathophysiology of actinic prurigo remains largely unclear. Still, evidence suggests the disease process is driven by a delayed type-IV hypersensitive response to ultraviolet A and B (UVA and UVB) radiation in genetically predisposed individuals. Both TH1 and TH2 lymphocytic processes have been implicated in the disease process. Multiple studies note the presence of eosinophils and mast cells in the dermal layers of involved tissue, which suggests a type-IVb (TH2)-driven response specifically. TH2 lymphocytes secrete IL-4, IL-5, and IL-13, which promote IgE and IgG4 production by B cells. These immunoglobulins stimulate eosinophils and mast cells. Individuals with moderate to severe actinic prurigo have been found to have markedly elevated IgE levels, further supporting a type-IVb (TH2) hypersensitive reaction., Epidemiology:['rare', 'Actinic prurigo is a photodermatosis characterized', 'Minor cases of actinic prurigo can be treated with sun-avoidance alone. Proper sun protection includes avoiding sunlight by staying indoors or in shaded areas, wearing protective clothing, sunglasses, and wide-brim hats, and using a broad-spectrum sunscreen.'], Complications:['Contact dermatitis', 'infections', 'Impetigo'], Diagnostics:['biopsy'], Differential diagnosis:['porphyria', 'SYSTEMIC LUPUS ERYTHEMATOSUS'], disease description:Actinic prurigo is a photodermatosis characterized by symmetrical involvement of sun-exposed areas of the skin, lips and conjunctivae. Age Usually manifests during childhood. Associated diseases Commonly associated with cheilitis and conjunctivitis.

Woman aged 24 presenting symptoms such as ['breast deformity', 'mass lesion', 'lump', 'swelling', 'fever']

Disease Name: Actinomycosis Of Breast, symptoms: ['breast deformity', 'mass lesion', 'lump', 'swelling', 'fever'], Treatment: ['penicillin intravenously for two to six weeks, followed by oral therapy with penicillin or amoxicillin for 6 to 12 months [3]. Alternative antibacterial treatments include doxycycline, erythromycin or clindamycin'], Pathophysiology: Actinomycosis is a subacute to chronic, suppurative, granulomatous disease that tends to produce draining sinus tracts. Primary actinomycosis of the breast is an unusual condition where the most commonly isolated pathogen has been A. israelii. Possible causes of this condition include trauma, lactation and kissing . Actinomycosis of the breast usually presents as a recurrent abscess with fistulas. It may sometimes present as a breast lump that is difficult to distinguish from inflammatory carcinoma.Breast actinomycosis is primary when inoculation occurs through the nipple. Secondary actinomycosis of the breast refers to the extension of a pulmonary infection through the thoracic cage in a process that can affect the ribs, muscles and finally the breast.Breast actinomycosis may present as sinus tract or with mass-like features mimicking malignancy., Epidemiology:['good', 'Current guidelines recommend high dose of penicillin intravenously for two to six weeks, followed by oral therapy with penicillin or amoxicillin for 6 to 12 months . Alternative antibacterial treatments include doxycycline, erythromycin or clindamycin.'], Complications:['abscess', 'sinuses'], Diagnostics:['FNAC', 'mammography'], Differential diagnosis:['appendicitis', 'aspiration pneumonia', 'Brain Abscess', 'Crohn disease', 'Dental abscesses', 'diverticulosis', 'LUNG ABSCESS', 'PID', 'TUBERCULOSIS'], disease description:Actinomycosis is a slowly progressive infection caused by anaerobic bacteria, primarily from the genus Actinomyces. Primary actinomycosis of the breast is rare and presents as a mass like density which can mimic malignancy.

A 43-year-old female experiencing ['thoracic type of actinomycosis may simulate active tuberculosis with cough, haemoptysis, night sweats and weight loss', 'dull-red indurated nodule on the cheek or submaxillary region', 'NODULES', 'periodontal abscess', 'bone pain', 'chest pain', 'Night sweat', 'fever', 'Vaginal Discharge', 'hemoptysis', 'weight loss', 'Abdominal Pain', 'ABDOMINAL MASS', 'abnormal vaginal bleeding']

Disease Name: Actinomycosis, symptoms: ['thoracic type of actinomycosis may simulate active tuberculosis with cough, haemoptysis, night sweats and weight loss', 'dull-red indurated nodule on the cheek or submaxillary region', 'NODULES', 'periodontal abscess', 'bone pain', 'chest pain', 'Night sweat', 'fever', 'Vaginal Discharge', 'hemoptysis', 'weight loss', 'Abdominal Pain', 'ABDOMINAL MASS', 'abnormal vaginal bleeding'], Treatment: [{'medication': ['Imipenem ', 'Penicillin/Penicillin V/Phenoxymethylpenicillin', 'Chloramphenicol ', 'Erythromycin ', 'Tetracycline ']}, 'First line\n•\t10–12 million units of penicillin a day are administered \ni.v. for 12 h daily for 30–45 days\n•\tWide surgical excision of infected tissue then 2–5 million \nunits of penicillin given i.m. daily for 12–18 months, or \n5 million units of penicillin V given by mouth\nSecond line\n•\tTetracycline derivatives\n•\tErythromycin\n•\tChloramphenicol \n•\tImipenem \n•\tErythromycin'], Pathophysiology: Actinomyces are part of the normal flora of the human oral cavity, GI tract, and female urogenital tract. The organism is not virulent and only invades the body to cause deeper infections when there is tissue injury and a subsequent break in the normal mucosal barrier. Infection is mostly polymicrobial, with as many as 5 to 10 other bacterial species present. The infection is established with the help of a companion bacteria by inhibiting host defenses, reducing oxygen tension, or by producing a toxin that facilitates the inoculation of actinomycoses.Once mucosal barriers are breached, and infection is established, the human host responds by initiating an intense inflammatory response which is suppurative and granulomatous. The infection does not respect tissue planes and spreads contiguously. This results in draining sinus tracts, tiny yellow clumps called sulfur granules, and the result may be intense fibrosis of tissue., Epidemiology:['Actinomycosis is commonly found between 4th to 6th decade of life and very rare in infants and children.', 'annual incidence of 1/300 000 and a disease death rate of 0–28%', 'good', 'You can reduce your risk of cervicofacial actinomycosis (the most common type) by taking care of your dental health. This includes:\n\nAvoiding smoking and other tobacco products.\nBrushing your teeth at least twice a day with fluoride toothpaste.\nFlossing daily.\nUsing an antibacterial mouthwash.\nVisiting your dentist regularly. They can spot any potential issues with your teeth and gums early.\nOther forms of actinomycosis are hard to prevent, but they’re also uncommon.'], Complications:['Meningitis', 'Brain Abscess', 'Endocarditis', 'CNS infection', 'osteomyelitis', 'actinomycetoma', 'Hepatic actinomycosis', 'Disseminated actinomycosis'], Diagnostics:['HISTOPATHLOGY', 'PUS CULTURE', 'CT CHEST', 'HISTOLOGIC EXAMINATION'], Differential diagnosis:['ACTINOMYCOSIS OF BREAST', 'BREAST CYSTS ', 'CARCINOMA OF BREAST', 'HAEMATOMA OF BREAST', 'TUBERCULOSIS'], disease description:Actinomycosis is a rare subacute to chronic infection caused by the gram-positive filamentous non-acid fast anaerobic to microaerophilic bacteria, Actinomyces. The infection is usually a granulomatous and suppurative infection. The chronic form has multiple abscesses that form sinus tracts and are associated with sulfur granules. About 70% of infections are due to either Actinomyces israelii or Actinomyces gerencseriae.?

At the age of 43, symptoms like ['vomiting', 'fever', 'fever', 'Abdominal Pain', 'constipation']

Disease Name: Acute Appendicitis, symptoms: ['vomiting', 'fever', 'fever', 'Abdominal Pain', 'constipation'], Treatment: ["Appendectomy is a surgery to remove the appendix. Appendectomy can be performed as open surgery using one abdominal cut about 2 to 4 inches long. This is called laparotomy. The surgery also can be done through a few small abdominal cuts. This is called laparoscopic surgery. During a laparoscopic appendectomy, the surgeon places special tools and a video camera into your abdomen to remove your appendix.\n\nIn general, laparoscopic surgery allows you to recover faster and heal with less pain and scarring. It may be better for older adults and people with obesity.\n\nBut laparoscopic surgery isn't right for everyone. You may need an open appendectomy if your appendix has ruptured and infection has spread beyond the appendix, or you have an abscess. An open appendectomy allows your surgeon to clean the abdominal cavity.", 'OPEN APPENDECTOMY & Laproscopic appendectomy'], Pathophysiology: Obstruction of the appendiceal lumen is believed to be an important step in the development of appendicitis— at least in some cases. Here, obstruction leads to bacterial overgrowth and luminal distension, with an increase in intraluminal pressure that can inhibit the flow of lymph and blood. Then, vascular thrombosis and ischemic necrosis with perforation of the distal appendix may occur. Therefore, perforation that occurs near the base of the appendix should raise concerns about another disease process. Most patients who will perforate do so before they are evaluated by surgeons. Appendiceal fecaliths (or appendicoliths) are found in ~50% of patients with gangrenous appendicitis who perforate but are rarely identified in those who have simple disease. As mentioned earlier, the incidence of perforated, but not simple, appendicitis is increasing. The rate of perforated and nonperforated appendicitis is correlated in men but not in women. Together these observations suggest that the underlying pathophysiologic processes are different and that simple appendicitis does not always progress to perforation. It appears that some cases of simple acute appendicitis may resolve spontaneously or with antibiotic therapy with limited risk of recurrent disease. The use of antibiotics to treat uncomplicated appendicitis is currently being studied intensively. Preliminary data indicate that as many as 70% of patients who present with uncomplicated appendicitis based on computed tomography (CT) and who are treated with antibiotics alone will be free of recurrent disease for at least a year. These findings highlight the importance of clinical decision-making and risk assessment when deciding and discussing treatment options with patients who presumably have simple disease, for example, deciding who is an appropriate candidate for non-operative management and who is not. The latter is especially pertinent given the difficulty in assessing which patients might progress to perforation and which will not. Increasingly it appears that there are two broad categories of patients with appendicitis—those with complicated disease like gangrene or perforation and those without. When perforation occurs, the resultant leak may be contained by the omentum or other surrounding tissues to form an abscess. Free perforation normally causes severe peritonitis. These patients may also develop infective suppurative thrombosis of the portal vein and its tributaries along with intrahepatic abscesses. , Epidemiology:['~100 per 100,000 person- years', '233 per 100,000 population per year, with a lifetime incidence risk ranging from 6.7 to 8.6%', 'EXCELLENT', 'There’s no proven way to prevent appendicitis. Eating a high-fiber diet with lots of whole grains and fresh fruits and vegetables may help.'], Complications:['gangrene', 'peritonitis', 'sepsis'], Diagnostics:['C- REACTIVE PROTEIN TEST', 'CT Abdomen', 'BLOOD IN URINE TEST'], Differential diagnosis:['acute cholecystitis', 'Diabetic Ketoacidosis', 'ectopic pregnancy', 'enterocolitis', 'gastroenteritis', 'INFLAMMATORY BOWEL DISEASES', 'inflammatory bowel syndrome', 'intestinal obstruction ', 'INTUSSECEPTION', "MECKEL'S DIVERTICULUM", 'Mesentric Lymphadenitis', 'Pancreatitis', 'perforated peptic ulcer', 'PID', 'PNEUMONIA', 'Twisted Ovarian Cyst', 'Urinary Tract Infection', 'VOLVULUS'], disease description:Appendicitis is an inflammation of the appendix, a finger-shaped pouch that projects from your colon on the lower right side of your abdomen. Appendicitis causes pain in your lower right abdomen. However, in most people, pain begins around the navel and then moves.Appendicitis occurs more frequently in Westernized societies but its incidence is decreasing for uncertain reasons. Nevertheless, acute appendicitis remains the most common emergency general surgical disease affecting the abdomen.

Suffering from ['convulsion', 'hypertension', 'Tachycardia', 'bulbar palsy', 'respiratory paralysis', 'abnormal behaviour', 'constipation', 'hallucinations', 'hyponatremia', 'muscle pain', 'Numbness', 'vomiting', 'weakness', 'red urine', 'Abdominal Pain'] at 48

Disease Name: Acute Attacks Of Porphyria, symptoms: ['convulsion', 'hypertension', 'Tachycardia', 'bulbar palsy', 'respiratory paralysis', 'abnormal behaviour', 'constipation', 'hallucinations', 'hyponatremia', 'muscle pain', 'Numbness', 'vomiting', 'weakness', 'red urine', 'Abdominal Pain'], Treatment: ['Carbohydrate loading Adequate caloric support (carbohydrates and proteins) is essential to the treatment of AIP .\nMild attacks should initially be treated with oral glucose, but patients who are not tolerating oral glucose can be given glucose intravenously (300-500 g/day, preferably 10% dextrose in 0.45% saline) as a preferred source of energy , in order to down-regulate the activity of ALAS1 and prevent fasting.', "Injections of hemin (Panhematin), a medicine that is a form of heme, to limit your body's production of porphyrins.", 'Supportive treatment includes analgesia, sedatives and antiemetics (in each case\nusing drugs known to be safe in acute porphyria) and careful\nmanagement of fluid balance with rehydration and correction of\nhyponatraemia. The specific treatments are intravenous haematin\nor haem arginate (Normosang, Orphan Pharmaceuticals), which have now replaced carbohydrate as the treatment of choice. These\ndrugs suppress hepatic ALA synthase activity and so reduce ALA \nand PBG accumulation. Haem arginate is more effective when\ngiven earlier during an attack, increasing the importance of early\ndiagnosis. Advice from a specialist centre should be sought when\ntreating an acute attack.'], Pathophysiology: Impaired activity of PBG deaminase is associated with acute attacks. The deficiency can be primary (as in AIP) or secondary, the latter being due to inhibition of the enzyme by accumulated coproporphyrinogen and protoporphyrinogen (as in HC and VP). In the liver, haem is mostly incorporated into cytochrome P450 proteins, whose production is induced by many of the drugs and hormones metabolized by the P450 system. When a drug or hormone induces cytochrome P450, and hence acutely increases the hepatic requirement for haem, the inability of the pathway to respond adequately because of the PBG deaminase deficiency is exposed. This acute hepatic haemdeficiency in turn causes secondary accumulation of ALA and increased ALA synthase activity due to loss of end-product negative feedback. The symptoms of the acute attack result from neuronal dysfunction, the pathogenesis of which is not fully understood. Postulated mechanisms include disturbed metabolism of neurotransmitters (due to reduced activity of haem-containing hepatic tryptophan dioxygenase), direct neurotoxicity of accumulated ALA (which structurally resembles the neurotransmitter ?-aminobutyric acid) and acute haem deficiency within neurons., Epidemiology:['1–2 per 100 000 inhabitants', 'around 10% to 20%', 'good', 'Because genetic mutations cause most types of porphyria, the disorder can’t be prevented. However, you can avoid triggers that may cause symptoms. These triggers include smoking, alcohol consumption, and exposure to sunlight. Drugs that may need to be avoided include barbiturates, tranquilizers, birth control pills, and sedatives.'], Complications:['chronic kidney disease', 'hepatocellular carcinoma', 'hypertension'], Diagnostics:['SERUM Sodium Na+', 'Urine analysis', 'PBG in urine'], Differential diagnosis:['Acute lymphoblastic leukemia', 'anemia', 'Chronic Hepatitis B', 'Hepatitis C', 'Hodgkin lymphoma'], disease description:The porphyrias are a group of disorders caused by defects in the biosynthesis of haem. Their relevance to the skin arises from the phototoxic properties of the porphyrins, which accumulate in most porphyrias and cause photosensitivity. The majority of the porphyrias are inherited. Many of them affect other organs as well as the skin. 

Individual aged 39 dealing with ['mucopurulent discharge from the eyes', 'red eyes', 'Coloured halos', 'Conjunctival congestion', 'Flakes of mucopus seen in the fornices, canthi and lid margins', 'Chemosis (swelling of conjunctiva)', 'Cilia are usually matted together with yellow crusts', 'ocular discomfort', 'REDNESS OF EYE', 'sensation of a foreign body in the eye', 'grittiness in eyes', 'Sticking together of lid margins', 'blurred or unstable vision', 'PAPILLAE', 'petechial hemorrhage', 'eyelid oedema']

Disease Name: Acute Bacterial Conjunctivitis, symptoms: ['mucopurulent discharge from the eyes', 'red eyes', 'Coloured halos', 'Conjunctival congestion', 'Flakes of mucopus seen in the fornices, canthi and lid margins', 'Chemosis (swelling of conjunctiva)', 'Cilia are usually matted together with yellow crusts', 'ocular discomfort', 'REDNESS OF EYE', 'sensation of a foreign body in the eye', 'grittiness in eyes', 'Sticking together of lid margins', 'blurred or unstable vision', 'PAPILLAE', 'petechial hemorrhage', 'eyelid oedema'], Treatment: [{'medication': ['Ibuprofen ', 'Paracetamol/Acetaminophen', 'Chloramphenicol ', 'Ciprofloxacin ', 'Gentamicin ', 'Framycetin Sulfate ', 'Gatifloxacin ', 'Tobramycin sulfate ']}, '1. Topical antibiotics to control the infection constitute\nthe main treatment of acute bacterial conjunctivitis.\ntreatment\nmay be started with chloramphenicol (1%), or\ngentamicin (0.3%), or tobramycin 0.3% or framycetin\n0.3% eye drops 3–4 hourly in day and ointment used\nat night will not only provide antibiotic cover but also\nhelp to reduce the early morning stickiness. If the\npatient does not respond to these antibiotics, then\nthe quinolone antibiotic drops such as ciprofloxacin\n(0.3%), ofloxacin (0.3%), gatifloxacin (0.3%) or\nmoxifloxacin (0.5%) may be used.\n2. Irrigation of conjunctival sac with sterile warm\nsaline once or twice a day will help by removing the deleterious material'], Pathophysiology: Pathological changes of bacterial conjunctivitis consist of: 1. Vascular response. It is characterised by congestion and increased permeability of the conjunctival vessels associated with proliferation of capillaries. 2. Cellular response. It is in the form of exudation of polymorphonuclear cells and other inflammatory cells into the substantia propria of conjunctiva as well as in the conjunctival sac. 3. Conjunctival tissue repsonse. Conjunctiva becomes oedematous. The superficial epithelial cells degenerate, become loose and even desquamate. There occurs proliferation of basal layers of conjunctival epithelium and increase in the number of mucin-secreting goblet cells. 4. Conjunctival discharge. It consists of tears, mucus, inflammatory cells, desquamated epithelial cells, fibrin and bacteria. If the inflammation is very severe, diapedesis of red blood cells may occur and discharge may become blood stained. Severity of pathological changes varies depending upon the severity of inflammation and the causative organism. The changes are thus more marked in purulent conjunctivitis than mucopurulent conjunctivitis.Common variants include-Acute bacterial conjunctivitisIs the most common form of bacterial conjunctivitisIn children is often caused by Haemophilus influenzae, Streptococcus pneumoniae, or Moraxella catarrhalisIs typically self-limited within 1–2 weeks, but topical antibiotic therapy may reduce the duration of diseaseHyperacute bacterial conjunctivitisIs a very rare and severe type of conjunctivitis with rapid onset and progression, as well as severe symptoms, including massive exudate, severe chemosis, eyelid swelling, marked hyperemia, pain, and decreased visionCaused by Neisseria gonorrhoeae or Neisseria meningitidisRequires both parenteral and topical antibiotic therapyCan progress to corneal infiltrates, melting and perforation and vision loss if not treated promptly by an ophthalmologistChronic bacterial conjunctivitisDefined as symptoms lasting for at least 4 weeksCommon causes include by Staphylococcus aureus or Moraxella lacunataOften occurs with blepharitis (inflammation of the eyelid), which can cause flaky debris and warmth along the lidPeople with this condition should see an ophthalmologist, Epidemiology:nan, Complications:['blepharitis', 'blindness', 'superficial keratitis', 'superficial punctate epitheliopathy', 'marginal corneal ulceration'], Diagnostics:['NEUTROPHILS', 'conjunctival swab'], Differential diagnosis:['EPISCLERITIS', 'SCLERITIS'], disease description:Acute bacterial conjunctivitis is characterised by marked conjunctival hyperaemia and mucopurulent discharge from the eye. So, clinically, it is called acute mucopurulent conjunctivitis. It is the most common type of bacterial conjunctivitis. It can occur as sporadic and epidemics cases. Outbreaks of bacterial conjunctivitis, epidemics are quite frequent during monsoon season.

At the age of 24, symptoms like ['post nasal drip', 'facial pain', 'Halitosis', 'headache', 'nasal congestion', 'fever', 'nasal discharge', 'Nasal discomfort', 'HYPOSMIA', 'anosmia', 'nasal obstruction']

Disease Name: Acute Bacterial Rhinosinusitis, symptoms: ['post nasal drip', 'facial pain', 'Halitosis', 'headache', 'nasal congestion', 'fever', 'nasal discharge', 'Nasal discomfort', 'HYPOSMIA', 'anosmia', 'nasal obstruction'], Treatment: ['Mild disease and no recent antibiotic use:\nAmoxicillin-clavulanate potassium (Augmentin):\t500 mg every 8 hours, 875 mg every 12 hours.\n\t\t\t\nHigh dose (Augmentin XR):2,000 mg every 12 hours.\n\nAmoxicillin (Amoxil):500 mg every 8 hours, 875 mg every 12 hours.', 'Moderate disease or recent antibiotic use:\n\nGatifloxacin (Tequin):400 mg every 24 hours.\n\nLevofloxacin (Levaquin):500 mg every 24 hours.\n\nMoxifloxacin (Avelox)\t:400 mg every 24 hours.\nAmoxicillin-clavulanate (high dose):\t2,000 mg every 12 hours.', 'Oral decongestants\nPseudoephedrine (Sudafed)\t:0 mg every 6 hours or 120 mg every 12 hours.\nTopical decongestants:\nOxymetazoline (Afrin) :2 sprays every 12 hours.\nXylometazoline (Otrivin)\t:2 sprays every 8 hours.\nPhenylephrine (Neo-Synephrine) :2 sprays every 4 hours.', 'Topical anticholinergics:\nIpratropium (Atrovent) :0.06 percent\t2 sprays every 6 hours.\nAntihistamines:\nBrompheniramine (Dimetapp):8 to 12 mg every 12 hours.\nChlorpheniramine (Chlor-Trimeton):\t8 to 12 mg every 12 hours.\nDiphenhydramine (Benadryl):\t25 to 50 mg every 6 hours.'], Pathophysiology: This usually follows viral upper respiratory infection. The virus damages the cilia and epithelium, and causes oedema of the mucosa membrane and obstruction of sinus ostia with stasis of sinus secretion and subsequent bacterial infection. The most common bacteria responsible for RS are Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis and Staphylococcus aureus. Pathophysiology is an interplay of forces between pathogens and the host's immune responses and other structural predisposing factors., Epidemiology:['0.5% to 2% of all cases of viral upper respiratory tract infections (URI).', 'GOOD', 'Washing your hands well before and after eating and after using the bathroom.\nStaying away from sick people.\nTreating your allergies, possibly with nasal steroid therapy or immunotherapy (primarily known as allergy shots).\nKeeping your body and your immune system in good shape by eating well (lots of vegetables and fruits) and staying hydrated.\nUsing a humidifier if your house is dry or an air purifier. Make sure to clean your equipment regularly.\nIrrigating your nose when necessary with a saline rinse.\nLIVING WITH'], Complications:['Meningitis', 'orbital cellulitis', 'chronic rhinosinusitis', 'Subperiosteal abscess'], Diagnostics:['CT SCAN', 'Nasal endoscopy'], Differential diagnosis:['ADENOIDS', 'foreign body in nose', 'history of upper respiratory tract infection'], disease description:Acute bacterial rhinosinusitis (ABRS) is an infection of both your nasal cavity and sinuses. It is caused by bacteria. ABRS sets in when your nasal cavity and sinuses first become inflamed from another cause, often a viral infection.

A woman, 41 years old, with ['Changes in cervix', 'abdomen fullness', 'abdominal discomfort', 'backache', 'Vaginal Discharge', 'painful urination', 'intermenstrual bleeding', 'pain during sex', 'bleeding after sex'] issues

Disease Name: Acute Cervicitis, symptoms: ['Changes in cervix', 'abdomen fullness', 'abdominal discomfort', 'backache', 'Vaginal Discharge', 'painful urination', 'intermenstrual bleeding', 'pain during sex', 'bleeding after sex'], Treatment: [{'medication': ['Cefixime ', 'Ceftriaxone ', 'Azithromycin ', 'Doxycycline ']}, '1g single oral dose azithromycin PLUS either 800 mg cefixime in a single oral dose or 250 mg intramuscular ceftriaxone in a single dose\n100 mg oral doxycycline twice daily for 7 days PLUS either 800 mg cefixime in a single oral dose or 250 mg intramuscular ceftriaxone in a single dose\nFor severe allergy to penicillins/cephalosporins: 2g oral azithromycin in a single dose'], Pathophysiology: The pathophysiology of cervicitis depends on the etiological agent and the physiological state of the patient. Under the influence of estrogen, the normal vaginal epithelium cornifies, making it somewhat resistant to infectious agents. The endocervix is lined by columnar epithelium which is susceptible to infectious agents leading to cervicitis.Gonococcal cervicitis results after the exposure of the cervix to N. gonorrhea in seminal fluid during sexual intercourse. N. gonorrhea infectivity is facilitated by type IV pilus-mediated motility of the bacterium. In the presence of seminal fluid, the bacterial motility is characterized by high velocity, low directional persistence and enhanced microcolony formation. Once the pili are attached, local inflammation results from the release of neutrophilic cytokines, leading to purulent or mucopurulent discharge.C. trachomatis infection is often associated with intense lymphocytic and neutrophilic inflammatory reactions in the affected areas, and is occasionally associated with follicular aggregation of lymphocytes. The chronic course of chlamydial cervicitis is associated with low content of cytokines, mainly IL-1a, IL-1ß, and TNFa, and an elevated concentration of IL-8 in the pathogenesis.Inflammation and ulceration of the ectocervix is evident in herpetic cervicitis., Epidemiology:nan, Complications:['ectopic gestation', 'Premature rupture of membranes', 'infertility', 'CHRONIC PELVIC PAIN'], Diagnostics:['Complete Blood Count CBC', 'Gram Staining', 'PAP SMEAR', 'LESION TISSUE HISTOLOGY', 'USG'], Differential diagnosis:['ACUTE PID', 'Cystitis', 'Endometrial cancer', 'ENDOMETRITIS', 'gonorrhoea', 'vaginitis'], disease description:Cervicitis is an inflammation of the cervix, the lower, narrow end of the uterus that opens into the vagina. Acute cervicitis often follows sexually transmitted infections (Chlamydia trachomatis or gonorrhoea), septic abortion (criminal induced abortion) and puerperal sepsis.

Person at 36 years, dealing with ['abscess', 'ulcer on skin', 'cutaneous lesions consist of crops of minute bluish papules, vesicles, pustules or haemorrhagic lesions in a patient who is obviously ill', 'lesions can occur all over the body but are most frequently found on the trunk, thighs, buttocks and genitalia', 'SKIN LESIONS', 'red spot']

Disease Name: Acute Cutaneous Miliary Tuberculosis, symptoms: ['abscess', 'ulcer on skin', 'cutaneous lesions consist of crops of minute bluish papules, vesicles, pustules or haemorrhagic lesions in a patient who is obviously ill', 'lesions can occur all over the body but are most frequently found on the trunk, thighs, buttocks and genitalia', 'SKIN LESIONS', 'red spot'], Treatment: ['Treatment of cutaneous tuberculosis is the same as treatment of systemic tuberculosis. It also involves multidrug treatment. The drugs that are most commonly used are isoniazid, rifampicin, pyrazinamide, and ethambutol or streptomycin. The treatment consists of 2 phases.\n\nAn intensive phase that involves rapidly decreasing the burden of M. tuberculosis\nA continuation phase that is also called the sterilizing phase\nThe intensive phase of therapy lasts about 8 weeks. After this phase, the patient no longer remains infectious, but he or she still requires more treatment to eradicate the infection. The continuation phase is designed to eradicate remaining bacteria and lasts for 9 to 12 months. Cure of tuberculosis requires the patient to adhere to treatment strictly.'], Pathophysiology: Miliary tuberculosis follows generalised spread of tubercle bacilli via the bloodstream from an active internal focus of tuberculosis. It is seen mainly in children and immunocompromised patients. Skin involvement is called disseminated cutaneous tuberculosis or acute cutaneous miliary tuberculosis., Epidemiology:['1% to 1.5% of extrapulmonary tuberculosis,', 'Of all patients with TB, 1.5% are estimated to have miliary tuberculosis.', 'poor', 'You usually have to be in contact with someone with active TB for a long time before becoming infected. It helps to follow infection prevention guidelines like:\n\nWashing your hands thoroughly and often.\nCoughing into your elbow or covering your mouth when you cough.\nAvoiding close contact with other people.\nMaking sure you take all of your medication correctly.\nNot returning to work or school until you’ve been cleared by your healthcare provider.\nIn the hospital, the most important measures to stop the spread of TB are having proper ventilation and using the correct types of personal protective equipment.'], Complications:['hypersensitivity reactions', 'LUPUS VULGARIS', 'Scrofuloderma'], Diagnostics:['HISTOPATHLOGY', 'TUBERCULIN SKIN TEST', 'skin biopsy with immunohistochemistry', 'x ray lateral view'], Differential diagnosis:['acute respiratory distress syndrome', 'Leprosy (Hansen disease)', 'LUPUS VULGARIS', 'Sarcoidosis'], disease description:Acute miliary tuberculosis is due to the hematogenous spread of tubercle bacilli into the skin. Acute miliary tuberculosis of the skin is rare and is usually seen in advanced pulmonary or meningeal and disseminated tuberculosis. It affects infants and young children or immunosuppressed patients such as those with concurrent HIV infection or following viral infections such as measles or malnutrition.

Symptoms reported by a 49-year-old: ['headache', 'nausea', 'Rashes', 'Tachycardia', 'fever', 'low blood pressure', 'Breathing difficulty']

Disease Name: Acute Cytokine Release Syndrome, symptoms: ['headache', 'nausea', 'Rashes', 'Tachycardia', 'fever', 'low blood pressure', 'Breathing difficulty'], Treatment: ['The current generally accepted sequence of agents to manage severe or life-threatening CRS include: 1) tocilizumab with or without corticosteroids, 2) high-dose corticosteroids if not already employed, and 3) other agents such as siltuximab or multiple tocilizumab doses.'], Pathophysiology: Cytokine release syndrome (CRS) is a systemic inflammatory response that can be triggered by a variety of factors such as infections and certain drugs.The pathophysiology of CRS is only incompletely understood. CRS is usually due to on-target effects induced by binding of the bispecific antibody or CAR T cell receptor to its antigen and subsequent activation of bystander immune cells and non-immune cells, such as endothelial cells. Activation of the bystander cells results in the massive release of a range of cytokines. We know little about how the initial activation of CAR T cells results in the distortion of the cytokine network that drives the inflammatory process in CRS. Depending on a number of characteristics of the host, the tumor, and the therapeutic agent the administration of T cell-engaging therapies can set off an inflammatory circuit that overwhelms counter-regulatory homeostatic mechanisms and results in a cytokine storm that can have detrimental effects on the patient., Epidemiology:['18.5%', '42–100%, and 0–46% of patients develop severe CRS after CAR T-cell infusion', 'bad', 'It’s not possible to prevent CRS as a result of infection. But people receiving immunotherapy may be able to reduce their risk for CRS by decreasing their medication dosage.'], Complications:['death (in supratherapeutic doses)', 'Hypotension', 'Breathing difficulty'], Diagnostics:['Upper GI Endoscopy'], Differential diagnosis:['sepsis', 'systemic infection'], disease description:Cytokine release syndrome (CRS) is an acute systemic inflammatory syndrome characterized by fever and multiple organ dysfunction that is associated with chimeric antigen receptor (CAR)-T cell therapy, therapeutic antibodies, and haploidentical allogeneic transplantation.

Person at 23 with manifestations like ['dry eyes', 'weak thready pulse', 'vomiting', 'Irritability', 'abdominal distension', 'dry oral mucosa', 'sunken fontanelles', 'sunken eyes', 'doughy skin', 'lethargy', 'nausea', 'Restlessness', 'loose motion', 'fever', 'Abdominal Pain']

Disease Name: Acute Diarrhoeal Disease, symptoms: ['dry eyes', 'weak thready pulse', 'vomiting', 'Irritability', 'abdominal distension', 'dry oral mucosa', 'sunken fontanelles', 'sunken eyes', 'doughy skin', 'lethargy', 'nausea', 'Restlessness', 'loose motion', 'fever', 'Abdominal Pain'], Treatment: [{'medication': ['Potassium/Potassium Salts', 'Ondansetron ', 'Oral Rehydration Salts ', 'Zinc/Zinc Sulphate', 'Probiotics/Lactic-acid producing organisms', 'Racecadotril']}, 'Treatment Plan A: Treatment of "No Dehydration"\n\nSuch children may be treated at home after explanation\nof feeding and the danger signs to the mother/ caregiver.\nThe mother may be given WHO ORS for use at home. Danger signs requiring medical attention\nare those of continuing diarrhea beyond 3 days, increased\nvolume/ frequency of stools, repeated vomiting, increasing\nthirst, refusal to feed, fever or blood in stools.\n\nTreatment Plan B: Treatment of\n"Some Dehydration"\ni. The daily fluid requirements in children are calculated\nas follows:\nUp to 10 kg = 100 ml/kg\n10-20 kg = 50 ml/kg\n>20 kg = 20 ml/kg\nAs an example, the daily fluid requirement in a child\nweighing 15 kg will be 1250 ml (first 10 kg, 10 x 100 =\n1000 ml; another 5 kg, 5 x 50 = 250 ml, total 1000 + 250\n= 1250 ml).\nii. Deficit replacement or rehydration therapy is calculated\nas 75 ml/kg of ORS, to be given over 4 hr. If ORS cannot\nbe taken orally then nasogastric tube can be used.\nIf after 4 hr, the child still has some dehydration then\nanother treatment with ORS (as in rehydration therapy)\nis to be given. This therapy is effective in 95% cases.\nOral rehydration therapy may be ineffective in children\nwith a high stool purge rate of >5 ml/kg body weight/\nhr, persistent vomiting >3 per hr, paralytic ileus and\nincorrect preparation of ORS (very dilute solution).\niii. Maintenance fluid therapy to replace losses. This phase\nshould begin when signs of dehydration disappear,\nusually within 4 hr. ORS should be administered in\nvolumes equal to diarrheal losses, usually to a maximum\nof 10 ml/kg per stool.\n\nTreatment Plan C: Children with "Severe\nDehydration"\nIntravenous fluids should be started immediately using\nRinger lactate with 5% dextrose. Normal saline or plain\nRinger solution may be used as an alternative, but 5%\ndextrose alone is not effective. A total of 100 ml/kg of\nfluid is given, over 6 hr in children <12 months and over\n3 hr in children >12 months as shown below.\nORS solution should be started simultaneously if the\nchild can take orally. If IV fluids cannot be given (for\nreasons of access, logistic availability or during transport),\nnasogastric feeding is given at 20 ml/kg/hr for 6 hr (total\n120 ml/kg). The child should be reassessed every 1-2 hr;\nif there is repeated vomiting or abdominal distension, the\noral or nasogastric fluids are given more slowly. If there\nis no improvement in hydration after 3 hr, IV fluids should\nbe started as early as possible.'], Pathophysiology: Diarrhoea is usually a symptom of an infection in the intestinal tract, which can be caused by a variety of bacterial, viral and parasitic organisms. Infection is spread through contaminated food or drinking-water, or from person-to-person as a result of poor hygiene. Infection: Diarrhoea is a symptom of infections caused by a host of bacterial, viral and parasitic organisms, most of which are spread by faeces-contaminated water. Infection is more common when there is a shortage of adequate sanitation and hygiene and safe water for drinking, cooking and cleaning. Rotavirus and Escherichia coli, are the two most common etiological agents of moderate-to-severe diarrhoea in low-income countries. Other pathogens such as cryptosporidium and shigella species may also be important. Location-specific etiologic patterns also need to be considered.Malnutrition: Children who die from diarrhoea often suffer from underlying malnutrition, which makes them more vulnerable to diarrhoea. Each diarrhoeal episode, in turn, makes their malnutrition even worse. Diarrhoea is a leading cause of malnutrition in children under five years old.Source: Water contaminated with human faeces, for example, from sewage, septic tanks and latrines, is of particular concern. Animal faeces also contain microorganisms that can cause diarrhoea.Other causes: Diarrhoeal disease can also spread from person-to-person, aggravated by poor personal hygiene. Food is another major cause of diarrhoea when it is prepared or stored in unhygienic conditions. Unsafe domestic water storage and handling is also an important risk factor. Fish and seafood from polluted water may also contribute to the disease., Epidemiology:['525,000 children under-5 years die due to diarrhea every year, roughly 2195 every day [1]. This represents 8% of all deaths and is the second leading cause of death among children under-5 years old', 'Globally, there are nearly 1.7 billion cases of childhood diarrhoeal disease every year', 'DEPENDS ON SEVERITY OF SIGNS AND SYMPTOMS', 'There are a few ways you can decrease your chances of having diarrhea, including:\n\n1. Avoiding infections with good hygiene habits: Washing your hands with soap and water after using the bathroom, as well as cooking, handling, and eating, is an important way to prevent diarrhea. \n\n2. Getting your vaccinations: Rotavirus, one of the causes of diarrhea, can be prevented with the rotavirus vaccine. \n\n3. Storing food properly: By keeping your food stored at the right temperatures, not eating things that have gone bad, cooking food to the recommended temperature and handling all foods safely, you can prevent diarrhea.\n\n4. Watching what you drink when you travel: Traveler’s diarrhea can happen when you drink water or other drinks that haven’t been treated correctly. This is most likely to happen in developing countries. To avoid getting diarrhea there are a few tips to follow. Watch what you drink. Don’t drink tap water, use ice cubes, brush your teeth with tap water, or consume unpasteurized milk, milk products or unpasteurized juices.\n\n5. You should also be careful when trying local foods from street vendors, eating raw or undercooked meats (and shellfish), as well as raw fruits and vegetables. When in doubt, drink bottled water or something that’s been boiled first (coffee or tea).'], Complications:['No dehydration', 'paralytic ileus', 'septicaemia', 'Electrolyte disturbances including profound hypokalaemia', 'Malnutrition'], Diagnostics:['ECG', 'SERUM ELECTROLYTE', 'serum potassium K+', 'stool microscopy'], Differential diagnosis:['abdominal tuberculosis', 'appendicitis', 'CARCINOID TUMORS', 'CELIAC DISEASE', 'Crohns Disease', 'Digestion and Absorption of food', 'dysentery', 'fatty food intolerance', 'giardiasis', 'TYPHOID FEVER'], disease description:Diarrhea is defined as a change in consistency and frequency of stools, i.e. liquid or watery stools, that occur >3 times a day. If there is associated blood in stools, it is termed dysentery.I n the vast majority of cases, these acute episodes subside within 7 days. Acute diarrhea may persist for >2 weeks in 5-15% cases, which is labeled as persistent diarrhea. 

Symptoms at 31: ['lethargy', 'persistent irritability', 'meningeal signs', 'Ataxia', 'headache', 'seizures', 'vomiting', 'fever', 'encephalopathy', 'visual loss']

Disease Name: Acute Disseminated Encephalomyelitis (adem), symptoms: ['lethargy', 'persistent irritability', 'meningeal signs', 'Ataxia', 'headache', 'seizures', 'vomiting', 'fever', 'encephalopathy', 'visual loss'], Treatment: [{'medication': ['Prednisolone', 'Methyl prednisolone ']}, 'high-dose intravenous steroids are commonly employed (typically, methylprednisolone 20-30 mg/kg per day for 5 days with a maximum dose of 1000 mg per day) followed by an oral prednisolone taper of 1-2 mg/kg/day (maximum 40-60 mg/day) over 4-6 wk.\n\nintravenous immunoglobulin (usually 2 g/kg administered over 2-5 days)\n\nplasmapheresis (typically 5-7 exchanges administered every other day) for refractory or severe cases'], Pathophysiology: ADEM appears to be an immune reaction to the infection. In this reaction, the immune system, instead of fighting off the infection, causes inflammation in the central nervous system. Inflammation is defined as the body's complex biological response to harmful stimuli, such as infectious agents, damaged cells, or irritants. Inflammation is a protective attempt to remove the injurious stimuli and initiate the healing process. In the case of ADEM, the immune response is also responsible for demyelination, a process in which the myelin that covers many nerve fibers is stripped off.Molecular mimicry induced by infectious exposure or vaccine has been thought to trigger production of CNS autoantigens, although causality has never been proven. Many patients experience a transient febrile illness in the month prior to ADEM onset. Preceding infections associated with ADEM include influenza, Epstein-Barr virus, cytomegalovirus, varicella, enterovirus, measles, mumps, rubella, herpes simplex, and Mycoplasma pneumoniae. Postvaccination ADEM has been reported following immunizations for rabies, smallpox, measles, mumps, rubella, Japanese encephalitis B, pertussis, diphtheria–polio–tetanus, and influenza, although the risk of ADEM postvaccination is significantly lower than following the infection itself., Epidemiology:['1 in 125,000-250,000 individuals affected by ADEM each year', 'incidence ranges from 0.1-0.6 per 100,000 per year', 'GOOD', 'Because the exact cause isn’t clear, there’s no known prevention method.\n\nAlways report neurological symptoms to your doctor. It’s important to get a proper diagnosis. Treating inflammation in the central nervous system early can help prevent more severe or lasting symptoms.'], Complications:['neurological deficit', 'raised intracranial pressure'], Diagnostics:['CSF EXAMINATION', 'EEG', 'CT HEAD', 'MRI', 'CT SCAN'], Differential diagnosis:['ASEPTIC MENINGITIS', 'Brucellosis', 'Cerebral venous thrombosis', 'LEUKODYSTROPHY', 'mitochondrial disorders', 'Multiple Sclerosis', 'vasculitis'], disease description:ADEM is an inflammatory, demyelinating event of early childhood presenting with an acute onset of polyfocal neurologic deficits, accompanied by encephalopathy and changes compatible with demyelination on brain MRI.

Suffering from ['fever', 'Excessive bleeding', 'Vaginal Discharge', 'pelvic pain'] at 29 years old, female

Disease Name: Acute Endometritis, symptoms: ['fever', 'Excessive bleeding', 'Vaginal Discharge', 'pelvic pain'], Treatment: [{'medication': ['Amoxicillin and Clavulanic acid ', 'Doxycycline ', 'Levofloxacin ']}, 'Doxycycline 100 mg every 12 hours + metronidazole 500 mg every 12 hours. Doxycycline is not contraindicated in breastfeeding mothers if its use is for less than three weeks.\nLevofloxacin 500 mg every 24 hours + metronidazole 500 mg every 8 hours. Levofloxacin should be avoided in breastfeeding mothers.\nAmoxicillin-clavulanate 875 mg/125 mg every 12 hours.'], Pathophysiology: Endometritis results from the ascension of bacteria from the cervix and vagina into the uterus. The uterus does not harbour microorganisms until the amniotic sac ruptures, which thus provides passage for bacteria to ascend into the uterus. Microorganisms tend to harbour in an endometrium that is then devitalized and injured (such as in case of a caesarean section or uterine surgery). In any pelvic procedure, if proper asepsis is not maintained or if the woman has an untreated vaginal infection prior to a pelvic intervention such as dilatation, curettage, or endometrial aspiration, then the risk of endometritis is higher.Acute infections can be caused by both aerobes and anaerobes. Post-caesarean section endometritis is generally due to Streptococcus pyogenes and Staphylococcus aureus infection. Chlamydia endometritis has a late presentation and generally manifests seven days after delivery. Acute Endometritis is characterized in histopathology by micro-abscesses in the endometrium and presence of neutrophils in the superficial epithelium and in the lumen of the glands of the endometrium. Group A streptococcus endometritis presents with pain, diarrhoea and vaginal discharge, and may progress to sepsis, toxic shock and necrotising fasciitis. Therefore, these patients should be treated with utmost care. , Epidemiology:['PID most commonly affects younger adults and teenagers, 15 to 29 years of age.', 'there is an incidence of 1% to 2%. Risk factors, however, can increase this rate to a 5% to 6% risk of infection following vaginal delivery.', 'GOOD', 'Since untreated STIs often cause endometritis, the best prevention is to:\n\nFollow safe sex practices (use condoms).\nTreat STIs promptly.\nGet regular screenings for STIs.\nEncourage your sexual partners to get regular screenings for STIs.\nPeople having a C-section should have antibiotics before the procedure to prevent infection.'], Complications:['peritonitis', 'septicaemia', 'THROMBOPHLEBITIS', 'Cervicitis', 'SALPINGITIS'], Diagnostics:['HISTOPATHLOGY', 'Total Leucocyte Count (TLC)', 'USG ABDOMEN(W/A)', 'NUCLEIC ACID AMPLIFICATION TEST NAAT'], Differential diagnosis:['appendicitis', 'DIVERTICULITIS', 'Ectopic pregnency', 'Endometriosis', 'Irritable Bowel Syndrome', 'Pelvic Inflamatory Disease', 'Urinary Tract Infection'], disease description:Endometritis is caused by an infection in the uterus. It can be due to chlamydia, gonorrhea, tuberculosis, or a mix of normal vaginal bacteria. It is more likely to occur after miscarriage or childbirth. Acute endometritis is caused by septic abortion, puerperal sepsis and acute gonorrhoea. In all three conditions, the other clinical features tend to overshadow the inflammation of the endometrium of the uterus.

Experiencing ['crackles', 'Tachycardia', 'tachypnoea', 'poor appetite', 'weight loss', 'chest pain', 'fatigue', 'myalgia', 'fever', 'night sweats', 'dyspnea', 'Abdominal Pain'] at 33 years old

Disease Name: Acute Eosinophilic Pneumonia, symptoms: ['crackles', 'Tachycardia', 'tachypnoea', 'poor appetite', 'weight loss', 'chest pain', 'fatigue', 'myalgia', 'fever', 'night sweats', 'dyspnea', 'Abdominal Pain'], Treatment: [{'medication': ['Methyl prednisolone ']}, 'Treatment has uniformly been the use of a corticosteroid (e.g.,\nmethylprednisolone 1-2 mg/kg/day) either intravenously or orally for 2-4 wk. A\nminimum or maximum treatment time has not been determined. Rare fatalities\nhave been reported. Complete recovery has been seen in days with resolution of\npleural effusions within the 4 wk treatment time.'], Pathophysiology: Eosinophilic lung disease, regardless of the stage of disease or etiology, shows mixed cellular infiltration of the alveoli and interstitial spaces with a predominance of eosinophils when transbronchial biopsy or open lung biopsy is performed. This may be accompanied by a fibrinous exudate with intact lung architecture. Other findings include eosinophilic microabscesses, a nonnecrotizing nongranulomatous vasculitis, and occasional multinucleated giant cells again without granuloma formation. Eosinophils are filled with numerous toxic granules. Evidence of eosinophil degranulation may be found by electron microscopy, biopsy, urine excretion, and BAL fluid. Most commonly, eosinophil-derived neurotoxin, leukotriene E4 , other granule proteins, such as major basic protein, Charcot Leyden crystals, or proinflammatory cytokines, are identified and support the evidence that eosinophils are not only present but contributing to the disease process. A unique and dramatic presentation of the eosinophilic pneumonias is AEP. AEP mimics infectious pneumonia or acute respiratory distress syndrome with its rapid onset and marked hypoxemia.  Although this disease has been labeled as idiopathic, there have been identifiable exposures (e.g., 1,1,1-trichloroethane or Scotchgard). Numerous reports link the onset of smoking tobacco, change in smoking frequency, reinitiation of smoking in young male adolescents or adults, and even massive secondary smoke exposure as critical associations with onset of AEP., Epidemiology:['0% to 2.5%', '0.54 cases per 100,000 population per year', 'GOOD', "Your ability to reduce your risk of developing eosinophilic pneumonia depends on what caused the condition. Allergies are the most common cause of high eosinophil levels and may be passed down in families (inherited). Medication can help prevent or control your immune system's allergic reactions.\n\nA healthy lifestyle, which includes reducing or quitting smoking, can also help reduce your overall risk of disease. Your healthcare provider can discuss options to help you reduce your risk of developing eosinophilic pneumonia."], Complications:['respiratory failure'], Diagnostics:['Arterial Blood Gas Analysis(ABG)', 'EOSINOPHILS - ABSOLUTE COUNT', 'HISTOPATHLOGY', 'HRCT Thorax', 'CHEST X RAY', 'BRONCHOALVEOLAR LAVAGE'], Differential diagnosis:['PNEUMONIA'], disease description:A unique and dramatic presentation of the eosinophilic pneumonias is AEP. AEP mimics infectious pneumonia or acute respiratory distress syndrome with its rapid onset and marked hypoxemia. In pediatrics, this disease most frequently occurs in the teenage population. Overall, young adults most commonly contract this idiopathic disease.

Person, 22 years old, presenting ['breathlessness', 'Grunting', 'sore throat', 'fever', 'difficulty in swallowing', 'stridor']

Disease Name: Acute Epiglottitis (syn Supraglottic Laryngitis), symptoms: ['breathlessness', 'Grunting', 'sore throat', 'fever', 'difficulty in swallowing', 'stridor'], Treatment: ['Adequate hydration. Patient may require parenteral fluids.Humidification and oxygen. Patient may require mist \ntent or a croupette.', 'Antibiotics. Ampicillin or third generation cephalosporin are effective against H. influenzae and are given by \nparenteral route (i.m. or i.v.) without waiting for results \nof throat swab and blood culture. Steroids. Hydrocortisone or dexamethasone is given in \nappropriate doses i.m. or i.v. They relieve oedema and \nmay obviate need for tracheostomy.', 'Intubation or tracheostomy. It may be required for respiratory obstruction'], Pathophysiology: Epiglottitis is most frequently caused by infection, although caustic ingestion, thermal injury, and local trauma are important noninfectious etiologies. Infectious epiglottitis is a cellulitis of the epiglottis, aryepiglottic folds, and other adjacent tissues. It results from bacteremia and/or direct invasion of the epithelial layer by the pathogenic organism. The posterior nasopharynx is the primary source of pathogens in epiglottitis. Microscopic trauma to the epithelial surface (eg, mucosal damage during a viral infection or from food during swallowing) may be a predisposing factor. Less frequently, noninfectious conditions cause local burns or ecchymosis of the epiglottis and adjacent structures., Epidemiology:['People can take a number of measures to limit dryness and irritation to the vocal cords and help reduce the risk of laryngitis:\n\navoiding clearing the throat\ntaking steps to prevent upper respiratory tract infections, such as practicing good hygiene and avoiding contact with people who have contagious infections\nquitting smoking and avoiding secondhand smoke where possible\nlimiting or eliminating alcohol and caffeine intake, as these can increase the risk of dehydration\ntaking precautions to avoid reflux, such as avoiding eating late at night, not chewing gum, and elevating while sleeping'], Complications:['septicaemia'], Diagnostics:['X RAY NECK LATERAL', 'Indirect Laryngoscopy', 'Oral cavity examination'], Differential diagnosis:['ACUTE LARYNGO-TRACHEO-BRONCHITIS'], disease description:It is an acute inflammatory condition confined to supraglottic structures, i.e. epiglottis, aryepiglottic folds and arytenoids. There is marked oedema of these structures which may obstruct the airway.

Person at 38 with manifestations like ['odynophagia', 'Red swollen epiglottis', 'dysphagia', 'sore throat', 'fever', 'stridor']

Disease Name: Acute Epiglottits, symptoms: ['odynophagia', 'Red swollen epiglottis', 'dysphagia', 'sore throat', 'fever', 'stridor'], Treatment: [{'medication': ['Hydrocortisone ', 'Adrenaline (Epinephrine)', 'Amoxicillin and Clavulanic acid ', 'Ampicillin ']}, 'TRACHEOSTOMY', 'Empiric combination antibiotic therapy with a third-generation cephalosporin and an antistaphylococcal agent is usually recommended.Vancomycin is the antistaphylococcal agent of choice in patients with epiglottitis complicated by sepsis, those with concomitant meningitis, or those from areas with an increased prevalence of clindamycin-resistant methicillin-resistant S aureus. Patients with a penicillin allergy should be treated with vancomycin and a quinolone antibiotic agent. Antibiotics should be altered as culture sensitivities are identified by lab and adjusted to ensure completion of a 10-day course.\n\ncorticosteroids are to be used, the recommended course of treatment in adults is IV dexamethasone 4 to 10 mg as an initial bolus with a repeated IV dose of 4 mg every 6 hours along with close observation of the airway.'], Pathophysiology: It is an infectious process that leads to edema and increase in weight and mass of the epiglottis is more likely to cause symptoms in a child - the pliancy of the cartilage allows a ball-valve effect, where each inspiration pulls an edematous epiglottis over the laryngeal airway, causing symptoms. In adults, whose cartilages are stiffer, an isolated epiglottic infection and the resultant increase in epiglottic mass may be resisted by the more rigid laryngeal/epiglottic cartilage; but an infection that encompasses more of the tissues of the supraglottis, leading to edema, can lead to symptoms and an unstable airway.H. influenzae and other, infections of the epiglottis can lead to marked edema and swelling 0f the epiglottis and supraglottis of patients of any age. This edema can rapidly spread to adjacent structures leading to the rapid development of airway obstruction symptoms. While H. influenzae remains the most common pathogen in both adults and children, other organisms such as S. pneumoniae, S. aureus, and beta-hemolytic Streptococcus sp. are important pathogens also in both adults and children. In immunocompromised patients, the list of potential causes is much longer and must include Mycobacterium tuberculosis, as well as a litany of others, though the relative frequencies remain the same., Epidemiology:['the incidence in adults has remained stable. Additionally, the age of children who have had epiglottitis has increased from three years old to six to twelve years old in the post-vaccine era', 'good', 'While you can’t prevent epiglottitis altogether, there are things you can do to significantly reduce your risk:\n\nMake sure vaccinations are up to date. In children, the best prevention is to ensure all childhood immunizations are up to date. Children have undeveloped immune systems. This makes them more vulnerable to infections, including Hib bacteria.\nPractice good hygiene. Wash your hands frequently, and avoid placing fingers in your eyes, nose and mouth.\nProtect yourself from infection. Take necessary precautions around people who are coughing and sneezing.\nAvoid injury to your throat. Drinking hot liquids or smoking can increase your risk of epiglottitis.'], Complications:['abscess', 'CELLULITIS', 'septicaemia', 'cervical adenitis', 'empyema'], Diagnostics:['HISTOPATHLOGY', 'Indirect Laryngoscopy', 'Soft Tissue Lateral View Neck Radiographs'], Differential diagnosis:['ACUTE LARYNGO-TRACHEO-BRONCHITIS', 'angioedema', 'diphtheria', 'foreign body', 'Peritonsillar abscess', 'retropharyngeal abscess'], disease description:It is an acute inflammatory condition confined to supraglottic structures, i.e. epiglottis, aryepiglottic folds and arytenoids. There is marked oedema of these structures which may obstruct the airway. It is a serious condition and affects children of 2–7 years of age but can also affect adults. H. influenzae B is the most common organism responsible for this condition in children.

Symptoms at 30 years: ['bad breath', 'post nasal drip', 'facial swelling', 'oedema of the lids', 'sore throat', 'nasal discharge', 'Pain']

Disease Name: Acute Ethmoid Sinusitis, symptoms: ['bad breath', 'post nasal drip', 'facial swelling', 'oedema of the lids', 'sore throat', 'nasal discharge', 'Pain'], Treatment: [{'medication': ['Ephedrine ', 'Phenylephrine ']}, 'A nebulizer can treat many sphenoid sinusitis symptoms like postnasal drip or nasal congestion. They moisturize and provide relief from pain and irritation. Systemic or topical decongestants, hot fermentation, steam inhalation, and steroid nasal sprays can also help the situation.\n\nantibiotics because it often involves infection with bacteria.', 'Endoscopic transnasal sphenoidotomy is one of the most reliable surgical procedures and is considered the gold standard for treating chronic sphenoid sinusitis. The endoscopic method aids better visualization and has faster healing and a higher success rate. Microscopic sphenoidotomy and balloon-assisted endoscopic sphenoidotomy are other methods to treat sphenoid sinusitis surgically. A sphenoidotomy aims to improve sinus drainage and reduce pressure on your optic nerve (which could cause vision problems). It can be done by removing bone or tissue, blocking the sinus openings, or widening them.'], Pathophysiology: The most common cause of acute sinusitis is an upper respiratory tract infection (URTI) of viral origin. The viral infection can lead to inflammation of the sinuses that usually resolves without treatment in less than 14 days. If symptoms worsen after 3 to 5 days or persist for longer than 10 days and are more severe than normally experienced with a viral infection, a secondary bacterial infection is diagnosed. The inflammation can predispose to the development of acute sinusitis by causing sinus ostial blockage. Although inflammation in any of the sinuses can lead to blockade of the sinus ostia, the most commonly involved sinuses in both acute and chronic sinusitis are the maxillary and the anterior ethmoid sinuses. The anterior ethmoid, frontal, and maxillary sinuses drain into the middle meatus, creating an anatomic area known as the ostiomeatal complex The nasal mucosa responds to the virus by producing mucus and recruiting mediators of inflammation, such as white blood cells, to the lining of the nose, which cause congestion and swelling of the nasal passages. The resultant sinus cavity hypoxia and mucus retention cause the cilia—which move mucus and debris from the nose—to function less efficiently, creating an environment for bacterial growth.If the acute sinusitis does not resolve, chronic sinusitis can develop from mucus retention, hypoxia, and blockade of the ostia. This promotes mucosal hyperplasia, continued recruitment of inflammatory infiltrates, and the potential development of nasal polyps. However, other factors can predispose to sinusitis , Epidemiology:['Approximately 6% to 7% of children with respiratory symptoms have acute rhinosinusitis. An estimated 16% of adults are diagnosed', '1 out of every 7 adults in the United States, with more than 30 million individuals diagnosed each year.', 'good', 'Do not smoke. Smoking is not good for you or for people around you, since this can cause mucous to become clogged in the nose/sinuses. Avoid being around second-hand smoke, as well as other triggers like animal dander, dust, mold and pollen. \n\nTake pains to prevent sinus and other infections by:\n\nWashing your hands well before and after eating and after using the bathroom.\nStaying away from sick people.\nTreating your allergies, possibly with nasal steroid therapy or immunotherapy (primarily known as allergy shots).\nKeeping your body and your immune system in good shape by eating well (lots of vegetables and fruits) and staying hydrated.\nUsing a humidifier if your house is dry or an air purifier. Make sure to clean your equipment regularly.\nIrrigating your nose when necessary with a saline rinse.'], Complications:['Meningitis', 'CAVERNOUS SINUS THROMBOSIS', 'orbital cellulitis', 'seizures', 'visual defects'], Diagnostics:['X RAY', 'CT SCAN'], Differential diagnosis:['allergies', 'Brain Abscess', 'Common Cold', 'migraine', 'rhinitis medicamentosa', 'Tension-Type Headaches'], disease description:Ethmoid sinusitis is the inflammation of a specific group of sinuses — the ethmoid sinuses — which sit between the nose and eyes. The ethmoid sinuses are hollow spaces in the bones around the nose. They have a lining of mucus to help prevent the nose from drying out. Acute ethmoiditis is often associated with infection of other sinuses. Ethmoid sinuses are more often involved in infants and young children.

Individual aged 21 with manifestations like ['post nasal drip', 'frontal headache', 'oedema of the lids', 'nasal discharge', 'Tenderness']

Disease Name: Acute Frontal Sinusitis, symptoms: ['post nasal drip', 'frontal headache', 'oedema of the lids', 'nasal discharge', 'Tenderness'], Treatment: [{'medication': ['Phenylephrine ']}, 'Amoxicillin-clavulanate as empirical first line therapy in adults and children with severe or worsening symptom of acute sinusitis.\nMacrolides are not recommended due to high rates of resistance among S. pneumonia (30 %).\nTMP/SMX is also not recommended due to high rates of resistance among both S pneumonia and H influenza (30–40 %).\nSecond generation oral cephalosporins are not recommended for monotherapy due to variable rates of resistance among S pneumoniae .\nIn adult patients allergic to penicillin, either doxycycline or a respiratory fluoroquinolone (levofloxacin or moxifloxacin) may be used.\nIn children, combination therapy of oral third generation cephalosporin (cefixime or cefpodoxime) and clindamycin is recommended.\nRoutine coverage of MRSA is not recommended.\nRecommended treatment duration in uncomplicated ABRS is 5–7 days in adults and 10–14 days in children.'], Pathophysiology: The main cause of acute frontal sinusitis is mucus buildup due to sinus inflammation. Several factors may influence the amount of mucus being produced and your frontal sinus’ ability to drain the mucus:VirusesThe common cold virus is the most frequent cause of acute frontal sinusitis. When you have a cold or flu virus, it increases the amount of mucus your sinuses produce. That makes them more likely to clog and become inflamed.BacteriaYour sinonasal cavity is filled with tiny hairs called cilia that help block organisms from entering the sinuses. These cilia aren’t 100 percent effective. Bacteria can still enter your nose and travel to the sinus cavities. A bacterial infection in the sinuses will often follow a viral infection, since it’s easier for bacteria to grow in the mucus-rich environment caused by a viral infection such as the common cold. Bacterial infections usually cause the most severe symptoms of acute sinusitis.Nasal polypsPolyps are abnormal growths in your body. Polyps in the frontal sinuses may block the sinuses from filtering air and increase the amount of mucus buildup.Deviated nasal septumPeople who have a deviated nasal septum can’t breathe equally through both sides of their nose. A lack of proper air circulation can cause inflammation if the tissues of the frontal sinuses become compromised., Epidemiology:['Approximately 6% to 7% of children with respiratory symptoms have acute rhinosinusitis. An estimated 16% of adults are diagnosed', '1 out of every 7 adults in the United States, with more than 30 million individuals diagnosed each year', 'GOOD', 'Good personal hygiene is essential in reducing the risk of sinus infections. This includes regular hand-washing, especially:\n\nbefore and after eating\nwhile cooking\nwhile taking care of children\nafter using the bathroom\nAvoid common allergens, such as tobacco products, smoke, pollution, and dust, as these can trigger respiratory reactions.\n\nMaintaining a healthful lifestyle that includes regular physical activity and well-balanced meals goes a long way toward keeping the immune system healthy and reducing the risk of sinus infections.'], Complications:['Meningitis', 'CAVERNOUS SINUS THROMBOSIS', 'orbital cellulitis', 'osteomyelitis', 'SUBDURAL ABSCESS'], Diagnostics:['X Ray skull', 'CT SCAN'], Differential diagnosis:['allergies', 'Common Cold', 'migraine', 'nasal discharge', 'rhinitis medicamentosa'], disease description:Acute frontal sinusitis is defined as an acute bacterial infection of the frontal sinus cavity. Among all of the paranasal sinuses, acute bacterial infections localized to the frontal sinus are most commonly associated with intracranial complications.

Individual aged 31 dealing with ['erythema', 'headache', 'pruritic skin rash', 'fever', 'PUSTULE']

Disease Name: Acute Generalised Exanthematous Pustulosis, symptoms: ['erythema', 'headache', 'pruritic skin rash', 'fever', 'PUSTULE'], Treatment: [{'medication': ['Diphenhydramine ', 'Prednisolone', 'paracetamol']}, 'immediate cessation of the offending drug', 'Treatment is then based around relieving symptoms with moisturisers, topical corticosteroids, oral antihistamines, and analgesics until the rash resolves. Systemic therapy is rarely indicated.'], Pathophysiology: GEP has been classified as a T cell-related sterile neutrophilic inflammatory response (type IVd reaction). The activation, proliferation and migration of drug-specific cluster of differentiation (CD) 4 and CD8 T cells play an important role in the development of AGEP , as supported by the use of patch tests  and in vitro tests . It is supposed that drug-specific cytotoxic T cells and cytotoxic proteins such as granzyme B and perforin induce the apoptosis of keratinocytes, leading to subcorneal vesicles . Recently, it has also been shown that, besides in toxic epidermal necrolysis (TEN), granulysin is also expressed by CD4 and CD8 T cells and natural killer (NK) cells in different drug reactions including AGEP, suggesting that granulysin may also play a role in the pathogenesis of AGEP . Furthermore, in vitro tests have shown that drug-specific T cells in AGEP patients produced significantly more chemokine (C-X-C motif) ligand 8 (CXCL8)/IL-8, a potent neutrophil chemotactic chemokine . CXCL8/IL-8 is thought to play a central role in the formation of pustules by recruitment of neutrophils. The increased levels of IL-17 and IL-22 as well as granulocyte-macrophage colony-stimulating factor (GM-CSF) in AGEP patients may also participate in the strong neutrophilic activity by the synergistic effect on the production of CXCL8/IL-8 and the prevention of apoptosis of the neutrophils . Recent studies also described a higher level of IL-17 expression by neutrophils, mast cells (MC), and macrophages, and a lower level by T cells, in AGEP patients, indicating that innate cells may also be involved in the pathogenesis of AGEP . Furthermore, a deficiency in the IL36-Ra in some AGEP patients seems to play a role, leading to the increased expression of various proinflammatory cytokines and chemokines such as IL-1, IL-6, IL-12, IL-23, IL-17, tumor necrosis factor alpha (TNFa) and CXCL8/IL-8, which can further enhance neutrophilic recruitment and activation., Epidemiology:['1–5 patients per million per year', 'bad', 'Primarily involves withdrawal of the causative medicine.\nPatients with AGEP should avoid re-exposure to the causative medicine.'], Complications:['toxic epidermal necrolysis', 'organ dysfunction'], Diagnostics:['CRP', 'EOSINOPHILS - ABSOLUTE COUNT', 'Erythrocyte Sedimentation Rate (ESR)', 'HISTOPATHLOGY', 'NEUTROPHILS'], Differential diagnosis:['infection', 'inflammation', 'neutrophilic dermatosis', "Stevens-Johnson's syndrome"], disease description:Acute generalized exanthematous pustulosis (AGEP) (also known as pustular drug eruption and toxic pustuloderma) is a rare skin reaction that in 90% of cases is related to medication administration. AGEP is characterized by sudden skin eruptions that appear on average five days after a medication is started. These eruptions are pustules, i.e. small red white or red elevations of the skin that contain cloudy or purulent material (pus). 

Suffering from ['bad breath', 'swollen gums', 'Tender gums', 'dark gums'] at the age of 18

Disease Name: Acute Gingivitis, symptoms: ['bad breath', 'swollen gums', 'Tender gums', 'dark gums'], Treatment: ['deep cleaning teeth', 'Root planing.\nLasers', 'A dental professional may initially carry out scaling. This is so they can remove excess plaque and tartar. This can be uncomfortable, especially if the tartar buildup is extensive or the gums are sensitive.\n\nOnce they have cleaned a person’s teeth, the dental professional will explain the importance of oral hygiene and how to brush and floss effectively.\n\nThey may recommend follow-up appointments to monitor a person’s plaque and tartar. This will allow the dental professional to catch and treat any recurrences quickly.\n\nFixing any damaged teeth also contributes to oral hygiene. Some dental problems, such as crooked teeth, badly fitted crowns, or bridges, may make it harder to remove plaque and tartar properly. They can also irritate the gums.'], Pathophysiology: Pathophysiologically, gingivitis has been divided into initial, early, and established stages, and periodontitis has been indicated as the advanced stage.Initial LesionThis stage is characterized by an acute exudative inflammatory response, a raised gingival fluid flow, and the migration of neutrophils from the blood vessel of the subgingival plexus located in the gingival connective tissue to the gingival sulcus. An alteration of the matrix of the connective tissue located next to vessels results in the accumulation of fibrin in the area. The initial lesion is seen within four days of the initiation of plaque accumulation. There is a destruction of collagen caused by collagenase and other enzymes secreted by the neutrophils. About 5% to 10% of the connective tissue is occupied by the inflammatory infiltrate in this stageEarly LesionThe early lesion is consistent with delayed hypersensitivity. It usually appears after one week from the beginning of plaque deposition. In this stage, the clinical signs of gingivitis, such as redness and bleeding from the gingiva start appearing. The inflammatory cells that predominate in this lesion are lymphocytes accounting for 75% of the total, and macrophages. A small number of plasma cells are also seen. Along with the inflammatory infiltration that occupies 5% to 15% of the connective tissue of the gingival margin, there is loss of collagen in the affected area that reaches 60% to 70%. Furthermore, the local fibroblasts undergo a series of pathological changes, and the gingival fluid flow and the number of leukocytes migrating to the region continue to increase. Neutrophils and mononuclear cells are also increased in the junctional epithelium. The duration of the early lesion has not yet been determined, it can remain for more time than previously expectedThere is increased collagenolytic activity in this stage along with a rise in the number of macrophages, plasma cells, T and B lymphocytes. However, the predominant cells are plasma cells and B lymphocytes. In this stage, a small gingival pocket lined with a pocket epithelium is created. The lesion exhibits a high degree of organization. It has been suggested that the severity of gingivitis correlates with a growth in the B cells and plasma cells population, and a decrease in the number of T cells.An established lesion may follow two paths, it can either remain stable for months or years; or progress to a more destructive lesion, which appears to be related to a change in the microbial flora or infection of the gingiva. This stage has shown to be reversible after an effective periodontal therapy that results in an increase in the number of microorganisms associated with periodontal health that directly correlates with a reduction in the plasma cells and lymphocytes This stage is a transition to periodontitis. It is characterized by attachment loss that is irreversible. The inflammatory changes and the bacterial infection starts affecting the supporting tissues of the teeth and the surrounding structures such as gingival, periodontal ligament, and alveolar bone resulting in their destruction and may eventually result in tooth loss., Epidemiology:['9-17% of children aged 3-11 years have gingivitis. At puberty, prevalence rises to 70-90%', 'good', 'You can reduce your risk for gingivitis with good oral hygiene:\n\nBrush thoroughly twice a day — once when you wake up and once before you go to bed.\nManage diabetes if you have it.\nDon’t smoke or use other tobacco products.\nFloss every day to remove bacteria between your teeth.\nLimit food and drinks containing alcohol and excess sugar.\nSee a dentist at least once a year for checkups, and more often if you have any symptoms.\nIf people in your family have gum disease, you may face a greater risk of developing it. You may need more checkups and cleanings to prevent gum disease. Ask your dentist about a cleaning schedule that’s right for you.'], Complications:['Chronic Gingivitis', 'periodontitis'], Diagnostics:['PHYSICAL EXAMINATION', 'Oral cavity examination'], Differential diagnosis:['Acute Periodontitis'], disease description:Gingivitis is a common and mild form of gum disease (periodontal disease) that causes irritation, redness and swelling (inflammation) of your gingiva, the part of your gum around the base of your teeth. It's important to take gingivitis seriously and treat it promptly. Gingivitis can lead to much more serious gum disease called periodontitis and tooth loss.

Symptoms reported by a 30-year-old: ['fatigue', 'hypertension', 'edema', 'hematuria', 'foamy urine', 'muscle cramps']

Disease Name: Acute Glomerulonephritis, symptoms: ['fatigue', 'hypertension', 'edema', 'hematuria', 'foamy urine', 'muscle cramps'], Treatment: ['High-dose corticosteroids,\nRituximab (a monoclonal antibody that causes the lysis of B-lymphocytes),\nCytotoxic agents (e.g., cyclophosphamide, along with glucocorticoids are of value in severe cases of post-streptococcal glomerulonephritis),\nPlasma exchange (glomerular proliferative nephritis, pauci-immune glomerulonephritis – used temporarily till chemotherapy takes effect)'], Pathophysiology: The underlying pathogenetic mechanism common to all of these different varieties of glomerulonephritis (GN) is immune-mediated, in which both humoral as well as cell-mediated pathways are active. The consequent inflammatory response, in many cases, paves the way for fibrotic events that follow.The targets of immune-mediated damage vary according to the type of GN. For instance, glomerulonephritis associated with staphylococcus shows IgA and C3 complement deposits.One of the targets is the glomerular basement membrane itself or some antigen trapped within it, as in post-streptococcal disease.[16] Such antigen-antibody reactions can be systemic, with glomerulonephritis occurring as one of the components of the disease process, such as in systemic lupus erythematosus (SLE) or IgA nephropathy.On the other hand, in small vessel vasculitis, cell-mediated immune reactions are the main culprit instead of antigen-antibody reactions. Here, T lymphocytes and macrophages flood the glomeruli with resultant damage.These initiating events activate common inflammatory pathways, i.e., the complement system and coagulation cascade. The generation of pro-inflammatory cytokines and complement products, in turn, results in the proliferation of glomerular cells. Cytokines such as platelet-derived growth factor (PDGF) are also released, ultimately causing glomerulosclerosis. This event is seen in those situations where the antigen is present for longer periods, for example, in hepatitis C viral infection. When the antigen is rapidly cleared, as in post-streptococcal GN, the resolution of inflammation is more likely., Epidemiology:['WHO estimates that 472,000 patients are affected globally with APSGN each year, and results in 5,000 deaths annually', 'Sporadic cases of acute nephritis often progress to a chronic form. This progression occurs in as many as 30% of adult patients and 10% of pediatric patients. GN is the most common cause of chronic renal failure (25%).', 'variable', 'There is no proven way to prevent glomerulonephritis, though some practices may help:\n\nEat a healthy, unprocessed food.\nManage high blood pressure with a low salt diet, exercise and medication.\nPrevent infections by practicing good hygiene and safe sex. Also avoid using needles for illegal drugs and tattoos.\nSee a healthcare provider whenever you think you have an infection like strep throat.'], Complications:['chronic kidney disease', 'Pulmonary Embolism', 'renal failure', 'DVT'], Diagnostics:['Complete Blood Count CBC', 'Renal Biopsy', 'ANTISTREPTOLYSIN O (ASO) TITRE', 'kidney function test KFT', 'SERUM ELECTROLYTE', 'ELECTRON MICROSCOPY', 'Urine analysis', 'Renal ultrasonography', 'autoantibody test'], Differential diagnosis:['acute kidney injury', 'Lupus Nephritis', 'Tension-Type Headaches', 'vascular headache'], disease description:Glomerulonephritis is inflammation of the tiny filters in the kidneys (glomeruli). The excess fluid and waste that glomeruli remove from the bloodstream exit the body as urine. Glomerulonephritis can come on suddenly (acute) or gradually (chronic).

Experiencing ['erythematous blanching macules develop on the palms, soles', 'bullae', 'anorexia', 'nausea', 'vomiting', 'Abdominal Pain', 'burning sensation', 'generalized erythroderma', 'morbilliform exanthem', 'dark stools', 'diarrhea', 'pruritus'] at 22 years

Disease Name: Acute Graft-versus-host Disease, symptoms: ['erythematous blanching macules develop on the palms, soles', 'bullae', 'anorexia', 'nausea', 'vomiting', 'Abdominal Pain', 'burning sensation', 'generalized erythroderma', 'morbilliform exanthem', 'dark stools', 'diarrhea', 'pruritus'], Treatment: [{'medication': ['Mycophenolate mofetil/ Mycophenolate sodium', 'Etanercept ', 'Prednisolone', 'Sirolimus / Rapamycin', 'Alemtuzumab']}, 'Treatment ladder \nStage 2–4 aGvHD\n First line \n• Corticosteroids, e.g. prednisolone 1 mg/kg oral or IV\n• Oral calcineurin inhibitors \n Second line \n• Extracorporeal photopheresis \n• Mycophenolate mofetil\n• Etanercept \n• mTOR inhibitors, e.g. sirolimus\n• Anti-interleukin 2 receptor antibodies \n Third line \n• Mesenchymal stromal cells\n• Alemtuzumab\n• Pentostatin \n Future treatments/trials \n• Anti-thymocyte globulin (if not given during preconditioning)\n• T-regulatory adoptive immunotherapy strategies'], Pathophysiology: The pathophysiology of aGvHD is well understood and has been elucidated using animal models, supported by some experimental human studies . It is likely that aGvHD arises from a three-stage process: • First, toxicity from conditioning chemotherapy or radiotherapy causes tissue damage in the host, resulting in the release of numerous inflammatory cytokines, termed ‘a cytokine storm’.• Second, mature donor lymphocytes from the graft are recruited by these cytokines leading to activation and proliferation of donor lymphocytes when contact is made with host and donor antigen-presenting cells (APCs) expressing disparate host antigens (such as minor histocompatibility antigens (MiHC)). • Third, alloreactive T cells expand to form cytotoxic effector T cells that, in turn, induce further tissue injury and release more inflammatory cytokines. Acute GvHD often occurs 2–4 weeks after HSCT but can present any time after transplantation. Pruritus or a burning sensation can precede the skin eruption. Patients may report oral or genital ulceration. Profuse diarrhoea points to GI tract involvement, as do symptoms of nausea, anorexia, vomiting and abdominal pain. Cholestatic symptoms of pale urine, dark stools and right upper quadrant tenderness may also be reported., Epidemiology:['The incidence of chronic GVHD ranges from 6% to 80%', 'bad', "Tissue typing labs have been developing and using more precise DNA level tests to enable your BMT Team to select the best HLA matched donor for you.\nWe try to lower your risk of developing GvHD by giving you preventive (prophylactic) medicines to suppress the immune system after your transplant. These medicines will decrease the ability of your donor's cells to start an immune response against your own tissues.\n\nFungal, bacterial, and viral infections are major risks with this prophylactic medicine regimen, since your immune system will be suppressed and have a decreased ability to fight infection. You will be on prophylactic antibiotics, antifungals and antiviral medicines to decrease infection risks."], Complications:['weight loss', 'secondary infection', 'organ failure', 'Dehydration'], Diagnostics:['EOSINOPHILS', 'skin biopsy with immunohistochemistry'], Differential diagnosis:['drug-induced liver injury', 'engraftment syndrome', 'fixed drug eruptions', 'PEPTIC ULCER DISEASE', 'Viral exanthem', 'viral hepatitis'], disease description:Graft-versus-host disease (GvHD) is a multiorgan disease process that results from the action of donor-derived immunocompetent T lymphocytes against antigens expressed on the cells of the immunocompromised recipient host. The main organs affected are the skin, liver and gastrointestinal (GI) tract.

A 19-year-old with ['Redness', 'fever', 'Tenderness', 'lymphadenopathy', 'malaise', 'sensation of warmth', 'swelling', 'severe pain']

Disease Name: Acute Haematogenous Osteomyelitis, symptoms: ['Redness', 'fever', 'Tenderness', 'lymphadenopathy', 'malaise', 'sensation of warmth', 'swelling', 'severe pain'], Treatment: [{'medication': ['Cefotaxime ', 'Fusidic acid ', 'Flucloxacillin']}, '1- SURGICAL DRAINAGE\n2- SPLINTAGE'], Pathophysiology: ACUTE OSTEOMYELITIS IN CHILDREN The earliest change in the metaphysis is an acute inflammatory reaction with vascular congestion, exudation of fluid and infiltration by polymorphonuclear leucocytes. The intraosseous pressure rises rapidly, causing intense pain, obstruction to blood flow and intravascular thrombosis. Even at an early stage, the bone tissue is threatened by impending ischaemia and resorption due to a combination of phagocytic activity and the local accumulation of cytokines, growth factors, prostaglandin and bacterial enzymes. By the second or third day, pus forms within the bone and forces its way along the Volkmann canals to the surface where it produces a subperiosteal abscess. This is much more evident in children, because of the relatively loose attachment of the periosteum, than in adults. From the subperiosteal abscess, pus can spread along the shaft, to re-enter the bone at another level or burst into the surrounding soft tissues. The developing physis acts as a barrier to direct spread towards the epiphysis, but where the metaphysis is partly intracapsular (e.g. at the hip, shoulder or elbow) pus may discharge through the periosteum into the joint. The rising intraosseous pressure, vascular stasis, small-vessel thrombosis and periosteal stripping increasingly compromise the blood supply; by the end of a week there is usually microscopic evidence of bone death. Bacterial toxins and leucocytic enzymes also may play their part in the advancing tissue destruction. With the gradual ingrowth of granulation tissue the boundary between living and devitalized bone becomes defined. Pieces of dead bone may separate as sequestra varying in size from mere spicules to large necrotic segments of the cortex in neglected cases. Macrophages and lymphocytes arrive in increasing numbers and the debris is slowly removed by a combination of phagocytosis and osteoclastic resorption. A small focus in cancellous bone may be completely resorbed, leaving a tiny cavity, but a large cortical or cortico-cancellous sequestrum will remain entombed, inaccessible to either final destruction or repair., Epidemiology:['8–10 per 100 000 in developed countries & up to 80 per 100 000, in developing countries. Incidence of septic arthritis is half of overall arthritis incidence.', 'GOOD', 'It’s important to clean and treat wounds to keep out bacteria and prevent infections. If you’ve had a recent bone break or surgery, or have an artificial joint, contact your healthcare provider at the first sign of any infection. But in many instances, there isn’t anything you can do to prevent osteomyelitis.'], Complications:['arthritis', 'Bone disorders', 'metastatic disease', 'pathological fracture', 'CHRONIC OSTEOMYELITIS'], Diagnostics:['CRP', 'Erythrocyte Sedimentation Rate (ESR)', 'Gram Staining', 'HISTOPATHLOGY', 'PUS CULTURE', 'Radionuclide Imaging technique', 'White Blood Cell count WBC', 'BLOOD CULTURE', 'MRI', 'X RAY', 'CT SCAN', 'USG'], Differential diagnosis:['ACUTE SUPPURATIVE ARTHRITIS', 'CELLULITIS', "Gaucher's Disease", 'Painful Crisis of Sickle Cell Anemia', 'rheumatoid arthritis'], disease description:Acute haematogenous osteomyelitis is mainly a disease of children. When adults are affected, it is usually because their resistance is lowered. Trauma may determine the site of infection, possibly by causing a small haematoma or fluid collection in a bone, in patients with concurrent bacteraemia.Acute haematogenous osteomyelitis shows a characteristic progression marked by inflammation, suppuration, bone necrosis, reactive new bone formation and, ultimately, resolution and healing or else intractable chronicity. However, the pathological picture varies considerably, depending on the patient’s age, the site of infection, the virulence of the organism and the host response.

Symptoms at 18: ['eyelid oedema', 'Conjunctival congestion', 'Chemosis of conjunctiva', 'Pre-auricular lymphadenopathy', 'multiple haemorrhages in bulbar conjunctiva', 'fine epithelial keratitis', 'eye pain', 'REDNESS OF EYE', 'photophobia', 'WATERING EYE', 'transient blurring of vision']

Disease Name: Acute Haemorrhagic Conjunctivitis, symptoms: ['eyelid oedema', 'Conjunctival congestion', 'Chemosis of conjunctiva', 'Pre-auricular lymphadenopathy', 'multiple haemorrhages in bulbar conjunctiva', 'fine epithelial keratitis', 'eye pain', 'REDNESS OF EYE', 'photophobia', 'WATERING EYE', 'transient blurring of vision'], Treatment: ['• No specific effective curative treatment is known.\nHowever, broad-spectrum antibiotic eyedrops\nmay be used to prevent secondary bacterial\ninfections.\n• Usually the disease has a self-limiting course of 7\ndays. Supportive treatment for amelioration of symptoms\nis the only treatment required and includes:\n• Cold compresses, and sun glasses to decrease glare,\n• Decongestant and lubricant tear drops to decrease\ndiscomfort'], Pathophysiology: The disease is caused by picornaviruses (enterovirus type 70) which are RNA viruses of small (pico) size. The disease is very contagious and is transmitted by direct hand-to-eye contact. Incubation period of EHC is very short (1–2 days)., Epidemiology:['good', 'To Do : • Frequent handwashing,\n• Relative isolation of infected individual,\n• Avoiding eye rubbing and common use of towel or\nhandkerchief sharing, and\n• Disinfection of ophthalmic instruments and\nclinical surfaces after examination of a patient is\nessential.'], Complications:['KERATITIS', 'multiple haemorrhages in bulbar conjunctiva'], Diagnostics:['ophthalmoscopy'], Differential diagnosis:[], disease description:It is an acute inflammation of conjunctiva characterised by multiple conjunctival haemorrhages, conjunctival hyperaemia and mild follicular hyperplasia.

At the age of 52, symptoms like ['fatigue', 'nausea', 'poor appetite', 'Abdominal Pain', 'bloating', 'light coloured stool', 'itching', 'WEAKNESS OF MUSCLES']

Disease Name: Acute Hepatic Failure, symptoms: ['fatigue', 'nausea', 'poor appetite', 'Abdominal Pain', 'bloating', 'light coloured stool', 'itching', 'WEAKNESS OF MUSCLES'], Treatment: [{'medication': ['Adrenaline (Epinephrine)', 'Dopamine ', 'Buprenorphine']}, 'ALF toxin removal\n•\nPlasma exchange\n•\nHemodialysis\n•\nHemofiltration\n•\nCharcoal hemoperfusion\n•\nHemodiabsorption\nToxin removal with hepatic cell assistance\n•\nExtracorporeal perfusion with animal or human liver\n•\nArtificial liver support systems using hepatocytes\n.\nHepat Assist\n.\nELAD system\n.\nGerlach system\n.\nBAL system\n•\nHepatocyte transplantation\n•\nMolecular Adsorption Recirculating System (MARS)', 'Liver transplant'], Pathophysiology: The pathophysiology depends on the etiology of the ALF. Most cases of ALF (except acute fatty liver of pregnancy and Reye syndrome) will have massive hepatocyte necrosis and/or apoptosis leading to liver failure. Hepatocyte necrosis occurs due to ATP depletion causing cellular swelling and cell membrane disruption. The pathophysiology of cerebral edema and hepatic encephalopathy is seen in ALF is multi-factorial and includes altered blood-brain barrier (BBB) secondary to inflammatory mediators leading to microglial activation, accumulation of glutamine secondary to ammonia crossing the BBB and subsequent oxidative stress leading to depletion of adenosine triphosphate (ATP) and guanosine triphosphate (GTP). This ultimately leads to astrocyte swelling and cerebral edema., Epidemiology:['incidence of less than 10 cases per million population in the developed world.', 'poor', "Follow instructions on medications. If you take acetaminophen or other medications, check the package insert for the recommended dosage, and don't take more than that. If you already have liver disease, ask your health care provider if it is safe to take any amount of acetaminophen.\nTell your provider about all your medicines. Even over-the-counter and herbal medicines can interfere with prescription drugs you're taking.\nDrink alcohol in moderation, if at all. If you choose to drink alcohol, do so in moderation. For healthy adults, that means up to one drink a day for women and up to two drinks a day for men.\nAvoid risky behavior. Get help if you use illicit intravenous drugs. Don't share needles. Use condoms during sex. If you get tattoos or body piercings, make sure the shop you choose is clean and safe. Don't smoke.\nGet vaccinated. If you have chronic liver disease, a history of any type of hepatitis infection or an increased risk of hepatitis, talk to your provider about getting the hepatitis B vaccine. A vaccine also is available for hepatitis A.\nAvoid contact with other people's blood and body fluids. Accidental needle sticks or improper cleanup of blood or body fluids can spread hepatitis viruses. Sharing razor blades or toothbrushes also can spread infection.\nDon't eat wild mushrooms. It can be difficult to tell the difference between a poisonous mushroom and one that is safe to eat.\nTake care with aerosol sprays. When you use an aerosol cleaner, make sure the room is ventilated, or wear a mask. Take similar protective measures when spraying insecticides, fungicides, paint and other toxic chemicals. Follow product instructions carefully.\nWatch what gets on your skin. When using insecticides and other toxic chemicals, cover your skin with gloves, long sleeves, a hat and a mask.\nMaintain a healthy weight. Obesity can cause a condition called nonalcoholic fatty liver disease, which may include fatty liver, hepatitis and cirrhosis."], Complications:['GI bleed', 'HEPATIC ENCEPHALOPATHY', 'infections', 'Coagulopathy', 'intravascular coagulation', 'pulmonary edema', 'pulmonary infarction'], Diagnostics:['HISTOPATHLOGY', 'Prothrombin Time PC INR', 'USG ABDOMEN(W/A)', 'LIVER FUNCTION TEST LFT'], Differential diagnosis:['acetaminophen poisoning', 'bacillus cereus infection', 'Ebola-Marburg Viral Disease', 'Galactosemia', 'HELLP SYNDROME', 'hereditary fructose intolerance(deficency of fruct', 'Tyrosinemia'], disease description:Acute liver failure is loss of liver function that occurs rapidly — in days or weeks — usually in a person who has no preexisting liver disease. It's most commonly caused by a hepatitis virus or drugs, such as acetaminophen. Acute liver failure is less common than chronic liver failure, which develops more slowly.

Experiencing ['decreased appetite', 'nausea', 'vomiting', 'Yellow skin discoloration', 'Abdominal Pain', 'yellow intensification in the colour of urine', 'clay coloured stool'] at 38 years old

Disease Name: Acute Hepatitis, symptoms: ['decreased appetite', 'nausea', 'vomiting', 'Yellow skin discoloration', 'Abdominal Pain', 'yellow intensification in the colour of urine', 'clay coloured stool'], Treatment: [{'medication': ['Cholestyramine/Colestyramine']}, 'Supportive treatment for symptoms', 'Treatment with N-acetylcysteine is also recommended for all patients with acute liver failure except ischemic hepatitis, with or without evidence of acetaminophen overdose'], Pathophysiology: Under ordinary circumstances, none of the hepatitis viruses is known to be directly cytopathic to hepatocytes. Evidence suggests that the 0 1 2 3 4 5 6 12 24 36 48 60 120 Anti-HCV HCV RNA ALT Months after exposure clinical manifestations and outcomes after acute liver injury associated with viral hepatitis are determined by the immunologic responses of the host. Among the viral hepatitides, the immunopathogenesis of hepatitis B and C has been studied most extensively. Hepatitis B For HBV, the existence of inactive hepatitis B carriers with normal liver histology and function suggests that the virus is not directly cytopathic. The fact that patients with defects in cellular immune competence are more likely to remain chronically infected rather than to clear HBV supports the role of cellular immune responses in the pathogenesis of hepatitis B–related liver injury. The model that has the most experimental support involves cytolytic T cells sensitized specifically to recognize host and hepatitis B viral antigens on the liver cell surface. Nucleocapsid proteins (HBcAg and possibly HBeAg), present on the cell membrane in minute quantities, are the viral target antigens that, with host antigens, invite cytolytic T cells to destroy HBV-infected hepatocytes. Differences in the robustness and broad polyclonality of CD8+ cytolytic T cell responsiveness; in the level of HBV-specific helper CD4+ T cells; in attenuation, depletion, and exhaustion of virus-specific T cells; in viral T cell epitope escape mutations that allow the virus to evade T cell containment; and in the elaboration of antiviral cytokines by T cells have been invoked to explain differences in outcomes between those who recover after acute hepatitis and those who progress to chronic hepatitis, or between those with mild and those with severe (fulminant) acute HBV infection. Although a robust cytolytic T cell response occurs and eliminates virus-infected liver cells during acute hepatitis B, >90% of HBV DNA has been found in experimentally infected chimpanzees to disappear from the liver and blood before maximal T cell infiltration of the liver and before most of the biochemical and histologic evidence of liver injury. This observation suggests that components of the innate immune system and inflammatory cytokines, independent of cytopathic antiviral mechanisms, participate in the early immune response to HBV infection; this effect has been shown to represent elimination of HBV replicative intermediates from the cytoplasm and covalently closed circular viral DNA from the nucleus of infected hepatocytes. In turn, the innate immune response to HBV infection is mediated largely by natural killer (NK) cell cytotoxicity, activated by immunosuppressive cytokines (e.g., interleukin [IL] 10 and transforming growth factor [TGF] ß), reduced signals from inhibitory receptor expression (e.g., major histocompatibility complex), or increased signals from activating receptor expression on infected hepatocytes. In addition, NK cells reduce helper CD4+ cells, which results in reduced CD8+ cells and exhaustion of the virus-specific T cell response to HBV infection. Ultimately, HBV-HLA–specific cytolytic T cell responses of the adaptive immune system are felt to be responsible for recovery from HBV infection. As noted above, precore genetic mutants of HBV have been associated with the more severe outcomes of HBV infection (severe chronic and fulminant hepatitis), suggesting that, under certain circumstances, relative pathogenicity is a property of the virus, not the host. Although the precise mechanism of liver injury in HBV infection remains elusive, studies of nucleocapsid proteins have shed light on the profound immunologic tolerance to HBV of babies born to mothers with highly replicative (HBeAg-positive), chronic HBV infection. In HBeAg-expressing transgenic mice, in utero exposure to HBeAg, which is sufficiently small to traverse the placenta, induces T cell tolerance to both nucleocapsid proteins. An important distinction should be drawn between HBV infection acquired at birth, common in endemic areas, such as East Asia, and infection acquired in adulthood, common in the West. Infection in the neonatal period is associated with the acquisition of what appears to be a high level of immunologic tolerance to HBV and absence of an acute hepatitis illness, but the almost invariable establishment of chronic, often lifelong infection., Epidemiology:['During 2020, 44 states reported 2,157 acute hepatitis B cases resulting in an estimated 14,000 infections. After a decade of stable rates, the rate of acute hepatitis B abruptly decreased by 32%', 'The incidence of Hepatitis A virus (HAV) has significantly decreased by approximately 95% since the introduction of the hepatitis A vaccine in 1995', 'GOOD', "There are many ways you can reduce your chances of getting hepatitis:\n\nGet the vaccines for hepatitis A and hepatitis B.\nUse a condom during sex.\nDon't share needles to take drugs.\nPractice good personal hygiene such as thorough hand-washing with soap and water.\nDon't use an infected person's personal items.\nTake precautions when getting any tattoos or body piercings.\nTake precaution when traveling to areas of the world with poor sanitation. (Make sure to get your vaccines.)\nDrink bottled water when traveling."], Complications:['HEPATIC ENCEPHALOPATHY', 'hyperbilirubinemia', 'liver failure', 'Coagulopathy'], Diagnostics:['HISTOPATHLOGY', 'PT/PC/INR', 'SERUM Creatinine', 'USG ABDOMEN(W/A)', 'Viral Markers TEST', 'T2 WEIGHTED CONTRAST MRI'], Differential diagnosis:['Acute Hepatitis', 'Congestive heart failure', 'Hepatic artery thrombosis', 'NON FUNCTIONAL ENDOCRINE PANCREATIC TUMORS', 'sepsis', 'Systemic hypotension'], disease description:Acute viral hepatitis is a systemic infection affecting the liver predominantly. Almost all cases of acute viral hepatitis are caused by one of five viral agents: hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis C virus (HCV), the HBV-associated delta agent or hepatitis D virus (HDV), and hepatitis E virus (HEV).

A 18-year-old patient with ['KERATITIS', 'Pre-auricular lymphadenopathy', 'pain in eyes', 'red eyes', 'glare and light sensitivity', 'blurred vision']

Disease Name: Acute Herpetic Conjunctivitis, symptoms: ['KERATITIS', 'Pre-auricular lymphadenopathy', 'pain in eyes', 'red eyes', 'glare and light sensitivity', 'blurred vision'], Treatment: ['Acyclovir and Ganciclovir specifically inhibit thymidine kinase and polymerase and are least toxic. Topical Acyclovir 3% ointment, Ganciclovir 3% gel, and Trifluridine 1% solutions are used regularly at five times/day. Oral preparations are Acyclovir 400 mg 5 times/day and Valacyclovir 500 mg thrice daily. Intravenously Acyclovir 10mg/kg thrice daily is the usual dosage. Corticosteroids are the mainstay of treatment for stromal keratitis and Keratouveitis. 1% prednisolone acetate or 0.1% dexamethasone are commonly used under antiviral cover to prevent recurrence and reactivation of HSV infection.', 'Primary herpetic infection is usually self-limiting.\n• The topical antiviral drugs control the infection\neffectively and prevent recurrences.\n• Supportive treatment for amelioration of symptoms\nis the only treatment required and includes:\n• Cold compresses, and sun glasses to decrease glare,\n• Decongestant and lubricant tear drops to decrease\ndiscomfort.'], Pathophysiology: The disease is commonly caused by herpes simplex virus type 1 and spreads by kissing or other close personal contacts. HSV type 2 associated with genital infections, may also involve the eyes in adults as well as children, though rarely. Acute herpetic follicular conjunctivitis is usually a unilateral affection with an incubation period of 3–10 days. It may occur in two clinical forms—typical and atypical. • In typical form, the follicular conjunctivitis is usually associated with other lesions of primary infection such as vesicular lesions of face and lids. • In atypical form, the follicular conjunctivitis occurs without lesions of the face, eyelid and the condition then resembles epidemic keratoconjunctivitis. The condition may evolve through phases of nospecific hyperaemia, follicular hyperplasia and pseudomembrane formation.• Corneal involvement, though rare, is not uncommon in primary herpes. It may be in the form of fine or coarse epithelial keratitis or typical dendritic keratitis. • Preauricular lymphadenopathy occurs almost always., Epidemiology:['1.3 - 4.8%', 'good', 'Wash your hands often with soap and water, and help young children do the same. Wash hands especially well after touching someone with pink eye or their personal items.\nAvoid touching or rubbing your eyes. This can worsen the condition or spread it to your other eye.\nAvoid sharing personal items, such as makeup, eye drops, towels, bedding, contact lenses and containers, and eyeglasses.\nDo not use the same eye products for your infected and non-infected eyes.\nStop wearing contact lenses until your eye doctor says it’s okay.\nClean, store, and replace your contact lenses as instructed by your eye doctor.'], Complications:['CORNEAL ULCER', 'Corneal perforation'], Diagnostics:['PCR FOR HSV 1&2 DNA', 'ELISA', 'DIRECT FLORESCENT ANTIBODY TESTING', 'CYTOLOGY', 'Tzanck smear', 'Viral cultures'], Differential diagnosis:['ACANTHAMOEBA KERATITIS', 'HERPES ZOSTER OPHTHALMICUS', 'herpetic keratitis', 'Sjogren syndrome'], disease description:Acute herpetic follicular conjunctivitis is always an accompaniment of the ‘primary herpetic infection’, which mainly occurs in small children and in adolescents.

A 24-year-old with ['tremor', 'constipation', 'muscle weakness', 'nausea', 'Pain in extremities', 'dysuria', 'excess sweating', 'hypertension', 'Tachycardia', 'Confusion', 'diarrhea', 'muscle pain', 'seizures', 'Tingling', 'vomiting', 'Red or brown color urine', 'Abdominal Pain', 'anxiety']

Disease Name: Acute Intermittent Porphyria, symptoms: ['tremor', 'constipation', 'muscle weakness', 'nausea', 'Pain in extremities', 'dysuria', 'excess sweating', 'hypertension', 'Tachycardia', 'Confusion', 'diarrhea', 'muscle pain', 'seizures', 'Tingling', 'vomiting', 'Red or brown color urine', 'Abdominal Pain', 'anxiety'], Treatment: ['Intravenous administration of heme is the specific therapy. It replenishes the hepatocyte heme pool and down-regulates ALAS1, resulting in reduced production of porphyrin precursors and corresponding improvement in symptoms. Heme not only controls hepatic ALAS1 by down-regulating ALAS1 transcription but also by inducing mRNA destabilization or by blocking the mitochondrial import of the mature enzyme.'], Pathophysiology: Acute attacks of acute intermittent porphyria are more frequent in women, especially in the post-pubertal age group. The acute attacks of AIP are typically triggered by certain factors, which include several drugs, infection, fasting, alcohol, steroid hormones, as stated above.In acute intermittent porphyria, the neurologic damage occurs due to the accumulation of the porphyrin precursors, porphobilinogen, and aminolevulinic acid (ALA). The AIP-associated neurological damage manifests as peripheral and autonomic neuropathies and psychiatric manifestations.The exact mechanism by which elevated levels of porphobilinogen and ALA lead to symptomatic disease remains enigmatic because most patients with the genetic defect do not present with symptoms despite excessive porphyrin secretion., Epidemiology:['1 in 10,000', 'good', 'Prevention of attacks includes eliminating precipitating factors, heme prophylaxis and liver transplantation. New treatment options include givosiran (siRNA) to down-regulate ALA synthase-1 (ALAS1) and the messenger RNA of PBGD (PBGD mRNA) delivered to the liver cells of patients with AIP.'], Complications:['hepatocellular carcinoma', 'foot drop', 'end stage renal disease'], Diagnostics:['Hb', 'ALA', 'Cytogenetics', 'XRAY ABDOMEN'], Differential diagnosis:['acute cholecystitis', 'Acute Pyelonephritis', 'appendicitis', 'delirium', 'esophagitis', 'Fibromyalgia', 'Guillain-Barre Syndrome', 'hypertensive crisis', 'Lead Poisoning', 'Ovarian Cyst', 'panic attacks', 'peritonitis', 'PID'], disease description:Acute intermittent porphyria is a rare autosomal dominant disease characterized by a deficiency of hydroxymethylbilane synthase (HMBS). It presents with abdominal pain, nausea, vomiting, peripheral neuropathy, and seizures.

Suffering from ['Tachycardia', 'Hypotension', 'bowel sound is absent', 'Oliguria', 'abdomen tightness', 'abdominal distension', 'constipation', 'nausea', 'vomiting', 'anorexia', 'Abdominal Pain', 'fever'] at 25

Disease Name: Acute Intestinal Obstruction, symptoms: ['Tachycardia', 'Hypotension', 'bowel sound is absent', 'Oliguria', 'abdomen tightness', 'abdominal distension', 'constipation', 'nausea', 'vomiting', 'anorexia', 'Abdominal Pain', 'fever'], Treatment: ['Aggressive intravenous fluid therapy and correction of electrolyte imbalance are crucial in the initial management of acute SBO. A Foley catheter and occasionally central venous or even a swan ganz catheter are needed to monitor fluid resuscitation. Blood tests identify electrolyte imbalance, elevated leukocyte count, abnormal liver function tests, elevated amylase level, acidosis, anemia, and bleeding tendency. A nasogastric tube allows decompression of the stomach and prevents aspiration. There is no convincing evidence that long intestinal tube is more efficacious than nasogastric tubes in decompression of SBO (Stage C). Plain radiograph of the abdomen is the initial diagnostic test and luminal contrasts tests are used selectively. The indications of CT scan are expanding and benefits of its early utilization are becoming more apparent .', 'Neostigmine is an acetylcholinesterase inhibitor that increases cholinergic (parasympathetic) activity, which can stimulate colonic motility.'], Pathophysiology: The normal physiology of the small intestine consists of the digestion of food and the absorption of nutrients. The large bowel continues to aid in digestion and is responsible for vitamin synthesis, water absorption, and bilirubin breakdown. Any obstructive mechanism will hinder these physiologic components. Obstruction causes dilation of the bowel proximal to the transition point and collapses distally. A result of partial or complete blockage of digested products during obstruction is emesis. Frequent emesis can lead to fluid deficits and electrolyte abnormalities. As the condition is left untreated and worsens, a bowel wall edema forms, and third-spacing begins. A serious and life-threatening complication of bowel obstruction is strangulation. Strangulation is more commonly seen in closed-loop obstructions. If the strangulated bowel is not treated promptly, it eventually becomes ischemic, and tissue infarction occurs. Tissue infarction progresses to bowel necrosis, perforation, and sepsis/septic shock. , Epidemiology:['the prevalence of intestinal obstruction was 21.8 % and 4.8 % among patients admitted for acute abdomen surgery and total surgical admissions, respectively. The mortality rate was 2.5 % (6 of 262)', 'bad', 'Healthy lifestyle choices are a great way to lower the risk of bowel obstruction. Even low levels of exercise will help keep the bowels healthy.\nDietary and lifestyle changes\nSimple changes to a person’s diet and lifestyle can help them digest food more easily and lower the impact of bowel obstructions.\n\nDietary changes that may help a person who has bowel obstructions include:\n\neating smaller portions more often\navoiding large amounts of high fiber foods, such as whole grain cereals and nuts\nfocusing on eating soft or liquid meals\nlimiting the intake of caffeine, which can irritate the bowels\navoiding tough or stringy foods, such as celery or dried meat\nExercising regularly and staying hydrated can also aid regular digestive function.'], Complications:['death', 'intestinal perforation', 'peritonitis', 'sepsis'], Diagnostics:['Total Leucocyte Count (TLC)', 'CT Abdomen', 'serum potassium K+', 'SERUM CHLORIDE VALUE', 'X RAY ABDOMEN', 'BUN / SR.CREATININE RATIO'], Differential diagnosis:['CARCINOID TUMORS', 'CARCINOMA COLON', 'CARCINOMA RECTUM', 'GASTRIC CANCER', 'GASTRINOMA(ZOLLINGER ELLISON SYNDROME)', 'GASTROINTESTINAL STROMAL TUMORS', 'INTUSSUSSEPTION', 'MAILGNANT LYMPHOMA'], disease description:Acute intestinal obstruction occurs either mechanically from blockage or from intestinal dysmotility when there is no blockage. In the latter instance, the abnormality is described as being functional. Mechanical bowel obstruction may be caused by extrinsic processes, intrinsic abnormalities of the bowel wall, or intraluminal abnormalities

At 53, dealing with ['small pupil', 'eyes redness', 'pain in eyes', 'photophobia', 'WATERING EYE', 'glare', 'headache', 'blurred or unstable vision']

Disease Name: Acute Iritis, symptoms: ['small pupil', 'eyes redness', 'pain in eyes', 'photophobia', 'WATERING EYE', 'glare', 'headache', 'blurred or unstable vision'], Treatment: [{'medication': ['Cyclophosphamide ', 'Prednisolone', 'Tropicamide']}, 'Treatment is primarily aimed at reducing inflammation and pain and preventing complications'], Pathophysiology: Eye pain is thought to be due to irritation of the ciliary nerves and ciliary muscle spasms. Photophobia is caused by irritation of the trigeminal nerve from the ciliary spasm.[38] Increased permeability of blood vessels in the anterior chamber allows proteinaceous transudate ("flare") and WBCs ("cells"), the characteristic 'flare and cells' seen with the slit lamp. In traumatic uveitis, there can be microbial contamination and retention of necrotic debris at the site of trauma, resulting from a florid inflammatory response in the anterior segment of the eye. In infectious uveitis, the pathophysiological mechanism is immune-mediated destruction of foreign antigens that may cause damage to the uveal tissue, vessels, and cells.[40] There is immune complex deposition inside the uveal tract in autoimmune uveitic conditions, a form of hypersensitivity reaction.Uveal inflammation behaves similarly to inflammation in other body tissues, i.e., having a vascular and cellular response. But due to excessive vascularity and looseness of uveal tissue, there is heightened vascular response. Pathophysiologically, the uveal inflammation is subdivided into purulent (suppurative) and nonpurulent (non-suppurative) types., Epidemiology:['121 per 100,000.', '25-52 cases per 100,000 persons per year.', 'Good', "There is not much you can do to prevent iritis. If you have an autoimmune condition, taking your medicines as prescribed may help prevent iritis. You may reduce your chance for problems if you see your eye care provider at the first sign of symptoms. Keep any follow-up appointments to make sure your iritis responds to treatment.\n\nIf you have certain health conditions, you may need regular eye exams to check for early signs of iritis. For example, if you have juvenile idiopathic arthritis, you will need regular screenings. That's because vision loss is often the first symptom. Going to all your screening visits may help prevent problems from iritis"], Complications:['optic nerve atrophy', 'catastrophic permanent vision loss'], Diagnostics:['Slit lamp examination', 'Slit lamp examination'], Differential diagnosis:['acute angle-closure glaucoma', 'conjunctivitis', 'corneal abrasion', 'CORNEAL ULCER', 'dry eyes', 'EPISCLERITIS', 'Intraocular foreign body', 'Subconjunctival hemorrhages', 'ulcerative keratitis'], disease description:Acute anterior uveitis, also known as iritis, is the inflammation of the anterior or posterior chamber and iris. It is not a true ocular emergency, and with proper treatment and follow-up, it has a good prognosis. 

Person aged 38 dealing with ['crackles', 'hypoalbuminemia', 'Tachycardia', 'reduced jvp', 'Hypotension', 'cardiac gallop', 'arthritis', 'facial edema', 'fatigue', 'history of protracted hypotension', 'history of recent phayngitis', 'dry oral mucosa', 'hypertension', 'periorbital swelling', 'sunken fontanelles', 'Oliguria', 'edema', 'hematuria', 'Palpable abdominal massor flank mass', 'Confusion', 'nausea', 'blood in urine', 'decreased urine output', 'history of vomiting and diarrhea', 'breathlessness', 'Rashes', 'Nephrotoxic drugs']

Disease Name: Acute Kidney Injury, symptoms: ['crackles', 'hypoalbuminemia', 'Tachycardia', 'reduced jvp', 'Hypotension', 'cardiac gallop', 'arthritis', 'facial edema', 'fatigue', 'history of protracted hypotension', 'history of recent phayngitis', 'dry oral mucosa', 'hypertension', 'periorbital swelling', 'sunken fontanelles', 'Oliguria', 'edema', 'hematuria', 'Palpable abdominal massor flank mass', 'Confusion', 'nausea', 'blood in urine', 'decreased urine output', 'history of vomiting and diarrhea', 'breathlessness', 'Rashes', 'Nephrotoxic drugs'], Treatment: [{'medication': ['Furosemide ', 'Dopamine ', 'Bumetanide ', 'Mannitol ']}, 'Dialysis, Peritoneal dialysis, Continuous renal replacement therapy (CRRT).', 'Determination of the volume status is of critical importance when initially evaluating a patient with AKI. If there is no evidence of volume overload or cardiac failure, the intravascular volume should be expanded by intravenous administration of isotonic saline, 20 mL/kg over 30 min. \n\n\n\n\n\n\n\n\nAnuria/oliguria Volume overload with evidence of hypertension and/or pulmonary edema refractory to diuretic therapy Persistent hyperkalemia Severe metabolic acidosis unresponsive to medical management Uremia (encephalopathy, pericarditis, neuropathy) Calcium:phosphorus imbalance, with hypocalcemic tetany that cannot be controlled by other measures.'], Pathophysiology: The pathogenesis of AKI is etiology-driven. The common endpoint in all types of acute tubular necrosis is a cellular insult either secondary to ischemia or direct toxins, which results in effacement of the brush border and eventually cell death, thus shutting down the function of tubular cells. Intratubular obstruction by pigments such as myoglobin or crystals such as uric acid in tumor lysis syndrome or immunoglobulin light chains, as seen in monoclonal gammopathy, may also lead to the same result. On the other hand, the mechanism of injury in glomerulonephritis may be due to direct immune-mediated injury of the vessels or immune complex deposition leading to an immune response and damage to the glomeruli., Epidemiology:['common problem afflicting all ages.', '2–5%', 'DEPENDS UP ON UNDERLYING ETIOLOGY', 'Though kidney failure and CKD aren’t reversible, you can take steps to help preserve your kidney function. Healthy habits and routines may slow down how quickly your kidneys lose their ability to function.\n\nIf you have CKD or kidney failure, it’s a good idea to:\n\nMonitor your kidney function.\nKeep your blood sugar levels in normal range if you have diabetes.\nKeep your blood pressure levels in a normal range.\nAvoid using tobacco products.\nAvoid foods high in protein and sodium.\nGo to every regularly scheduled appointment with your healthcare provider.'], Complications:['Arrhythmias', 'hyperkalemia', 'hypertension', 'hyponatremia', 'metabolic acidosis', 'nausea', 'Neuromuscular irritability', 'pulmonary edema'], Diagnostics:['BLOOD UREA NITROGEN ( BUN )', 'COMPLEMENT 3(C3) LEVEL', 'Hb', 'PLATELET COUNT', 'RBC Count', 'SERUM Creatinine', 'UREA CREATININE', 'ECG', 'USG KUB', 'serum potassium K+', 'serum albumin', 'White Blood Cell count WBC', 'CHEST X RAY', 'CT SCAN', 'serum phosphate', 'Urine analysis'], Differential diagnosis:['Chronic renal failure', 'Dehydration', 'Diabetic Ketoacidosis', 'gastrointestinal bleeding', 'heart failure', 'RENAL CALCULI', 'sickle cell anemia', 'urinary tract infections', 'URINARY TRACT OBSTRUCTION'], disease description:Acute kidney injury (AKI) has been traditionally defined as an abrupt loss of kidney function leading to a rapid decline in the glomerular filtration rate (GFR), accumulation of waste products such as blood urea nitrogen (BUN) and creatinine, and dysregulation of extracellular volume and electrolyte homeostasis. 

Individual, 21 years old, with ['Hennebert’s sign', 'Hearing loss', 'nausea', 'vertigo', 'vomiting', 'SENSORINEURAL HEARING LOSS', 'tinnitus', 'fullness in ear']

Disease Name: Acute Labyrinthitis, symptoms: ['Hennebert’s sign', 'Hearing loss', 'nausea', 'vertigo', 'vomiting', 'SENSORINEURAL HEARING LOSS', 'tinnitus', 'fullness in ear'], Treatment: ['Corticosteroid medicines (to help reduce nerve inflammation)\nAntiviral medicines.\nAntibiotics (if there are signs of a bacterial infection)\nMedicines to take for a short time that control nausea and dizziness (such as diphenhydramine and lorazepam)', 'i.v. penicillin and \nsteroids.'], Pathophysiology: Labyrinthitis is an inflammation of the membranous labyrinth. It can be caused by viruses, bacteria, or systemic diseases. In rare cases, it can result in labyrinthitis ossificans, wherein pathological new bone formation occurs within the membranous labyrinth. Vestibular neuritis (also termed vestibular neuronitis) is often used interchangeably with labyrinthitis as the symptoms and clinical picture are extremely similar. However, true vestibular neuritis is inflammation confined to the vestibular nerve itself, without membranous labyrinth inflammation.Viral LabyrinthitisThe most common cause of labyrinthitis is secondary to a viral upper respiratory tract infection.Bacterial LabyrinthitisBacterial labyrinthitis typically arises from either bacterial meningitis (20% of children with bacterial meningitis will develop auditory or vestibular symptoms) or otitis media.Autoimmune LabyrinthitisLabyrinthitis has been demonstrated to be a rare complication of both polyarteritis nodosa and granulomatosis with polyangiitis.HIV/ SyphilisBoth syphilis and HIV have been associated with labyrinthitis. However, there is limited research as to whether the inflammation is caused by opportunistic infections as a result of the HIV-related immunosuppression or the virus itself., Epidemiology:['3.5 cases per 100,000', 'good', 'Because labyrinthitis is usually an underlying symptom of other conditions, the best way to avoid it is to wash your hands regularly and take proper precautions during cold and flu season.'], Complications:['balance disorder', 'Deafness', 'tinnitus', 'Visual impairment'], Diagnostics:['MRI'], Differential diagnosis:['acute labyrinthitis', 'acute vestibular neuronitis', "meniere's disease", 'Multiple Sclerosis'], disease description:Labyrinthitis is an inner ear infection characterized by inflammation of the labyrinth. The labyrinth is the inner ear system responsible for your hearing and sense of balance. When your labyrinth or one of the nerves inside your labyrinth is inflamed or irritated, hearing and balance can be affected. This is because your brain tries to make sense of mismatched information between your healthy labyrinth or nerve and your infected one.

Person at 20 years, dealing with ['hyperaemia', 'malaise', 'sore throat', 'fever', 'hoarseness of voice', 'cough']

Disease Name: Acute Laryngitis, symptoms: ['hyperaemia', 'malaise', 'sore throat', 'fever', 'hoarseness of voice', 'cough'], Treatment: ['Voice rest: This is the single most important factor. Use of voice during laryngitis results in incomplete or delayed recovery. Complete voice rest is recommended although it is almost impossible to achieve. If the patient needs to speak, the patient should be instructed to use a "confidential voice;" that is, a normal phonatory voice at low volume without whispering or projecting.\nSteam Inhalation: Inhaling humidified air enhances moisture of the upper airway and helps in the removal of secretions and exudates.\nAvoidance of irritants: Smoking and alcohol should be avoided. Smoking delays prompt resolution of the disease process.\nDietary modification: dietary restriction is recommended for patients with gastroesophageal reflux disease. This includes avoiding caffeinated drinks, spicy food items, fatty food, chocolate, peppermint. Another important lifestyle modification is the avoidance of late meals. The patient should have meals at least 3 hours before sleeping. The patient should drink plenty of water. These dietary measures have been shown to be effective in classic GERD, though their efficacy in LPR is disputed, they are often still employed.\n\nMedications: Antibiotics prescription for an otherwise healthy patient with acute laryngitis is currently unsupported; however for high-risk patients and patients with severe symptoms antibiotics may be given. .\nFungal laryngitis can be treated with the use of oral antifungal agents such as fluconazole. Treatment is usually required for three weeks period and may be repeated if needed.'], Pathophysiology: The infectious type is more common and usually follows upper respiratory infection. To begin with, it is viral in origin but soon bacterial invasion takes place with Streptococcus pneumoniae, Haemophilus influenzae and haemolytic Streptococci or Staphylococcus aureus. Exanthematous fevers like measles, chickenpox and whooping cough are also associated with laryngitis. The noninfectious type is due to vocal abuse, allergy, thermal or chemical burns to larynx due to inhalation or ingestion of various substances, or laryngeal trauma such as endotracheal intubation. Laryngeal appearances vary with severity of disease. In early stages, there is erythema and oedema of epiglottis, aryepiglottic folds, arytenoids and ventricular bands, but the vocal cords appear white and near normal and stand out in contrast to surrounding mucosa, betraying the degree of hoarseness patient has. Later, hyperaemia and swelling increase. Vocal cords also become red and swollen. Subglottic region also gets involved. Sticky secretions are seen between the cords and interarytenoid region. In case of vocal abuse, submucosal haemorrhages may be seen in the vocal cords., Epidemiology:['Yearly incidence has been reported in one study as 3.47 per 1,000; lifetime incidence is said to be up to 21%', 'GOOD', 'Though you can’t always prevent laryngitis, there are a few things you can do to reduce your risk. For example:\n\nAvoid smoking\nEat a well-balanced diet\nDon’t clear your throat\nAvoid spicy foods\nLimit caffeine and alcohol\nDrink lots of water\nWash your hands frequently'], Complications:['dysphonia', 'Respiratory Distress Syndrome', 'airway obstruction'], Diagnostics:['Laryngoscopy'], Differential diagnosis:['ACUTE LARYNGITIS', 'Epiglottitis', 'infectious mononucleosis', 'Laryngeal Diphtheria', 'laryngopyocoele', 'laryngo-tracheo-bronchitis', 'spasmodic'], disease description:Laryngitis refers to inflammation of the larynx. This is often due to an acute viral infection, which is typically a mild and self-limiting condition that lasts for a period of 3 to 7 days. There are non-infectious causes and more serious conditions that can present with acute laryngeal symptoms.

having ['nasal congestion', 'fever', 'hoarseness of voice', 'stridor', 'cough', 'rhinorrhoea'] at the age of 49

Disease Name: Acute Laryngo-tracheo-bronchitis, symptoms: ['nasal congestion', 'fever', 'hoarseness of voice', 'stridor', 'cough', 'rhinorrhoea'], Treatment: [{'medication': ['Hydrocortisone ', 'Adrenaline (Epinephrine)', 'Ampicillin ']}, "The goal of treatment is to decrease airway obstruction. Treatment includes nebulized epinephrine, corticosteroids, and at least 3 hours of observation after the last dose of epinephrine. Supplemental oxygen via blow by or nasal cannula can also be used for hypoxic patients with croup.\n\nNebulized Epinephrine\n\nRacemic epinephrine 2.25% 0.05 mL/kg nebulized with a maximum of 5 mL or L-epinephrine 0.5 mL/kg nebulized with a maximum of 5 mL is reserved for moderate and severe croup. Admit patients requiring more than 1 to 2 doses of nebulized epinephrine in the emergency department.\n\nCorticosteroids\n\nRegardless of severity, all patients with croup benefit from oral steroids. Dexamethasone 0.15 mg/kg to 0.6 mg/kg by mouth with a maximum of 10 mg as a one-time dose is the typical dose (the intravenous dose can be given by mouth).\n\nObservation\n\nPatients with croup should be observed for a minimum of 3 hours after the completion of each dose of nebulized racemic epinephrine. Watch for worsening or recurrence of symptoms, including persistent stridor at rest, increased work of breathing, and hypoxia, during the observation period. Admit patients requiring more than one or two doses of nebulized epinephrine in the emergency department.\n\nHeliox\n\nSeveral trials have been conducted on helion in the management of croup, and the results are mixed. Overall, there is no harm from trying heliox because most anecdotal reports indicate that it helps ease breathing.\n\nIntubation\n\nIntubation is reserved for severe cases of croup not responding to medical treatment. The endotracheal tube size should be smaller than typical for the patient's age and size to avoid trauma to the already edematous airway."], Pathophysiology: Inhalation of the virus causing croup first infects the nasal and pharyngeal mucosal epithelia, then spreads to the subglottic space. For children 8 years and younger, the subglottic space is the most narrow part of the airway. The cricoid cartilage forms a complete cartilaginous ring that is nonexpanding. This inability of the cricoid to expand leads to a significant narrowing of the subglottic region secondary to the inflamed mucosa. When the child cries or becomes agitated, further dynamic obstruction can occur at and below the cartilaginous ring. These factors lead to the common high-pitched stridor heard at rest and when the patient becomes agitated. Extension into the bronchi, as occurs with laryngotracheobronchitis, can lead to wheezing, crackles, air trapping, and increased tachypnea; a clinical picture that can be confused with acute asthma., Epidemiology:['4 to 23 percent [', '3.47 per 1,000 people.', 'good', 'Croup can spread by physical contact or through the air. To help prevent its spread:\n\nWash and dry your hands thoroughly after caring for your child.\nWash toys between each use.\nEncourage your child to cover their mouth and nose when coughing and sneezing.\nKeep your child home from school or daycare when they’re ill or if outbreaks occur.\nThrow used tissues away.'], Complications:['otitis media', 'PNEUMOTHORAX', 'Dehydration', 'secondary bacterial infections'], Diagnostics:['X RAY'], Differential diagnosis:['cholangitis', 'CHOLEDOCHAL CYST', 'Epiglottitis', 'foreign body', 'HEMANGIOMA', 'Peritonsillar abscess', 'retropharyngeal abscess'], disease description:Laryngotracheobronchitis, as the name implies, refers to inflammation of the larynx, trachea, and bronchi. Cases of laryngotracheobronchitis can be more severe than laryngotracheitis as the former extends into the lower airway. Both may be difficult to distinguish clinically. 

Suffering from ['ascites', 'jaundice', 'abdominal distension', 'anorexia', 'Mental Confusion', 'disorientation', 'lethargy', 'malaise', 'nausea', 'vomiting', 'Yellow skin discoloration', 'Confusional state', 'yellow discolouration of sclera', 'Abdominal Pain', 'asterexis', 'Bleeding complications', 'hematemesis', 'comatose patients', 'blood in stool', 'blood in vomiting', 'stupor', 'seizures'] at the age of 32

Disease Name: Acute Liver Failure, symptoms: ['ascites', 'jaundice', 'abdominal distension', 'anorexia', 'Mental Confusion', 'disorientation', 'lethargy', 'malaise', 'nausea', 'vomiting', 'Yellow skin discoloration', 'Confusional state', 'yellow discolouration of sclera', 'Abdominal Pain', 'asterexis', 'Bleeding complications', 'hematemesis', 'comatose patients', 'blood in stool', 'blood in vomiting', 'stupor', 'seizures'], Treatment: [{'medication': ['Phenytoin ', 'Lactulose ', 'Pantoprazole ', 'Cloxacillin Sodium ', 'Cefotaxime ', 'Mannitol ']}, 'Elective intubation and ventilation is beneficial in subjects with stage 3 hepatic\nencephalopathy or more. The hemodynamics need to be\nassessed and supported.', 'The management of liver failure in children is based on:\n(i) diagnosis of etiology as it influences the prognosis and\nmanagement; (ii) assessment of severity of liver failure\nand timely liver transplantation if indicated; and\n(iii) anticipation, prevention and treatment of complications.\nPatients should be treated and monitored closely\nin an intensive care unit.'], Pathophysiology: The mechanisms that lead to acute hepatic failure are poorly understood. It is unknown why only approximately 1–2% of patients with viral hepatitis experience liver failure. Massive destruction of hepatocytes might represent both a direct cytotoxic effect of the virus and an immune response to the viral antigens. Of patients with HBV-induced liver failure, – become negative for serum hepatitis B surface antigen within a few days of presentation and often have no detectable HBV antigen or HBV DNA in serum. These findings suggest a hyperimmune response to the virus that underlies the massive liver necrosis. Formation of hepatotoxic metabolites that bind covalently to macromolecular cell constituents is involved in the liver injury produced by drugs such as acetaminophen and isoniazid; acute hepatic failure can follow depletion of intracellular substrates involved in detoxification, particularly glutathione. Whatever the initial cause of hepatocyte injury, various factors can contribute to the pathogenesis of liver failure, including impaired hepatocyte regeneration, altered parenchymal perfusion, endotoxemia, and decreased hepatic reticuloendothelial function., Epidemiology:['HIGH MORTALITY 60-70%', "Follow instructions on medications. If you take acetaminophen or other medications, check the package insert for the recommended dosage, and don't take more than that. If you already have liver disease, ask your health care provider if it is safe to take any amount of acetaminophen.\nTell your provider about all your medicines. Even over-the-counter and herbal medicines can interfere with prescription drugs you're taking.\nDrink alcohol in moderation, if at all. If you choose to drink alcohol, do so in moderation. For healthy adults, that means up to one drink a day for women and up to two drinks a day for men.\nAvoid risky behavior. Get help if you use illicit intravenous drugs. Don't share needles. Use condoms during sex. If you get tattoos or body piercings, make sure the shop you choose is clean and safe. Don't smoke.\nGet vaccinated. If you have chronic liver disease, a history of any type of hepatitis infection or an increased risk of hepatitis, talk to your provider about getting the hepatitis B vaccine. A vaccine also is available for hepatitis A.\nAvoid contact with other people's blood and body fluids. Accidental needle sticks or improper cleanup of blood or body fluids can spread hepatitis viruses. Sharing razor blades or toothbrushes also can spread infection.\nDon't eat wild mushrooms. It can be difficult to tell the difference between a poisonous mushroom and one that is safe to eat.\nTake care with aerosol sprays. When you use an aerosol cleaner, make sure the room is ventilated, or wear a mask. Take similar protective measures when spraying insecticides, fungicides, paint and other toxic chemicals. Follow product instructions carefully.\nWatch what gets on your skin. When using insecticides and other toxic chemicals, cover your skin with gloves, long sleeves, a hat and a mask.\nMaintain a healthy weight. Obesity can cause a condition called nonalcoholic fatty liver disease, which may include fatty liver, hepatitis and cirrhosis."], Complications:['Azotaemia', 'HEPATIC ENCEPHALOPATHY', 'infections', 'metabolic acidosis', 'renal failure', 'Coagulation disorders'], Diagnostics:['Anti HEV IgM Antibody ELISA', 'Complete Blood Count CBC', 'anti-HAV IgM', 'LIVER FUNCTION TEST LFT', 'SERUM ELECTROLYTE', 'COAGULATION PROFILE', 'BLOOD GLUCOSE', 'ammonia level'], Differential diagnosis:['ACUTE VIRAL HEPATITIS', 'alcoholic cirrhosis', 'AUTOIMMUNE HEPATITIS', 'cholecystitis', 'CHOLELITHIASIS', 'Galactosemia', 'HELLP SYNDROME', 'Tyrosinemia I,II,III'], disease description:Liver failure refers to a clinical state resulting from hepatocyte dysfunction or necrosis and not a specific disease etiology. It may occur de novo in normal children without any evidence of pre-existing liver disease where it is known as acute liver failure (ALF). Acute liver failure. An international normalized ratio 2:1.5 with hepatic encephalopathy or an international normalized ratio 2:2 without hepatic encephalopathy along with biochemical evidence of liver injury in the absence of underlying chronic liver disease is considered as acute liver failure. The presence of hepatic encephalopathy is not essential for diagnosis of ALF in children. All international normalized prothrombin values refer to that measured after 8 hr of parenteral vitamin K administration. This definition has evolved with the understanding that detection of mild grades of hepatic encephalopathy in small children is difficult and any behavioral change or irritability in this age group may not be necessarily due to hepatic encephalopathy.

Individual aged 51 with manifestations like ['SIGN OF SEVERE ANEMIA', 'tachypnoea', 'testicular enlargement', 'respiratory distress', 'Conjunctival vascular congestion', 'purpura', 'splenomegaly', 'HEPATOMEGALY', 'fatigue', 'pallor', 'lymphadenopathy', 'joint pain']

Disease Name: Acute Lymphoblastic Leukemia, symptoms: ['SIGN OF SEVERE ANEMIA', 'tachypnoea', 'testicular enlargement', 'respiratory distress', 'Conjunctival vascular congestion', 'purpura', 'splenomegaly', 'HEPATOMEGALY', 'fatigue', 'pallor', 'lymphadenopathy', 'joint pain'], Treatment: [{'medication': ['Cyclophosphamide ', 'Methotrexate', 'Mercaptopurine', 'Vincristine', 'L-asparaginase/Asparaginase/Calasparagase Pegol/Colaspase/Crisantaspase/Pegaspargase', 'Prednisolone', 'Daunorubicin (Daunomycin)']}, 'regimens include vincristine, prednisone, L-asparaginase and an anthracycline, with remission achieved in 95-98% of cases. The induction therapy lasts for 4-6 weeks. CNS Preventive Therapy CNS prophylaxis has enabled increased survival rates in leukemia. Most children in the past received a combination of intrathecal methotrexate and cranial irradiation. \n In order to achieve effective CNS prophylaxis while minimizing neurotoxicity, experts now recommend a lower dose of cranial irradiation with intrathecal methotrexate. Intensification (Consolidation) Therapy There is clear evidence that intensification has improved the longterm survival in patients with ALL, especially those with high-risk disease. Commonly used agents for intensification therapy include high dose methotrexate, L-asparaginase, epipodophyllotoxin, cyclophosphamide and cytarabine.'], Pathophysiology: Leukemia is a malignancy that arises from clonal proliferation of abnormal hematopoietic cells leading to disruption of normal marrow function leading to marrow failure. The clinical manifestations of leukemia are the result of the unregulated proliferation of the malignant clone and bone marrow failure. Genetic abnormalities found in the leukemic clone greatly impact the therapy and prognosis of ALL. Conventional cytogenetics and fluorescence in situ hybridization should be performed on the bone marrow specimen to look for common genetic alterations in ALL. The presence of hyperdiploidy (chromosome number >50, DNA index >1.16) is associated with good prognosis in contrast to the poor prognosis in patients with hypodiploidy. Specific chromosomal translocations in ALL, including t(8;14, associated with Burkitt leukemia) in B cell ALL, t(4;11) in infant leukemia and t(9;22) translocation, that forms the Philadelphia chromosome, are associated with a poor prognosis., Epidemiology:['3-4 cases per 100,000 children below 15 yr of age', 'POOR', 'No, it can’t. Children with ALL develop the condition because of genetic changes that happened before they were born. But adults with ALL may be able to lower their risk by avoiding carcinogens, including tobacco and toxic chemicals.'], Complications:['avascular necrosis of bone', 'cardiomyopathy', 'congestive heart failure (CHF)', 'lymphadenopathy', 'splenomegaly', 'HEPATOMEGALY', 'neurocognitive disorders'], Diagnostics:['BONE MARROW ASPIRATION', 'CSF EXAMINATION', 'HISTOPATHLOGY', 'Peripheral Blood Smear', 'USG ABDOMEN(W/A)', 'LIVER FUNCTION TEST LFT', 'SERUM ELECTROLYTE', 'White Blood Cell count WBC', 'MRI', 'CHEST X RAY', 'COAGULATION PROFILE', 'EOSINOPHILS'], Differential diagnosis:['Acute Myeloid Leukemia (AML)', 'anemia', 'Epstein-Barr Virus', 'infectious mononucleosis', 'Leukocytosis', 'NEUROBLASTOMA', "NON HODGKIN'S LYMPHOMA", 'osteomyelitis', 'PARVOVIRUS B19', 'RETINOBLASTOMA', 'rhabdomyosarcoma'], disease description:ALL is the most common childhood malignancy accounting for one-fourth of all childhood cancers and three-fourths of all newly diagnosed patients with acute leukemia. Leukemia is a malignancy that arises from clonal proliferation of abnormal hematopoietic cells leading to disruption of normal marrow function leading to marrow failure.

Person at 43 with manifestations like ['Hearing loss', 'MASTOID TENDERNESS', 'Sagging of posterosuperior meatal wall', 'Perforation of tympanic membrane.', 'Swelling over the mastoid.', 'ear discharge', 'fever', 'PAIN BEHIND EAR']

Disease Name: Acute Mastoiditis, symptoms: ['Hearing loss', 'MASTOID TENDERNESS', 'Sagging of posterosuperior meatal wall', 'Perforation of tympanic membrane.', 'Swelling over the mastoid.', 'ear discharge', 'fever', 'PAIN BEHIND EAR'], Treatment: [{'medication': ['Amoxicillin and Clavulanic acid ', 'Ampicillin ', 'Chloramphenicol ']}, 'Myringotomy. When pus is under tension it is relieved\nby wide myringotomy (see operative surgery). Early cases\nof acute mastoiditis respond to conservative treatment\nwith antibiotics alone or combined with myringotomy\nCortical Mastoidectomy. It is indicated when there is:\n(a) Subperiosteal abscess.\n(b) Sagging of posterosuperior meatal wall.\n(c) Positive reservoir sign, i.e. meatus immediately fills\nwith pus after it has been mopped out'], Pathophysiology: Two main pathological processes are responsible: 1. Production of pus under tension. 2. Hyperaemic decalcification and osteoclastic resorption of bony walls. Extension of inflammatory process to mucoperiosteal lining of air cell system increases the amount of pus produced due to large surface area involved. Drainage of this pus, through a small perforation of tympanic membrane and/or eustachian tube, cannot keep pace with the amount being produced. Swollen mucosa of the antrum and attic also impede the drainage system resulting in accumulation of pus under tension. Hyperaemia and engorgement of mucosa causes dissolution of calcium from the bony walls of the mastoid air cells (hyperaemic decalcification). Both these processes combine to cause destruction and coalescence of mastoid air cells, converting them into a single irregular cavity filled with pus (empyema of mastoid). Pus may break through mastoid cortex leading to subperiosteal abscess which may even burst on surface leading to a discharging fistula., Epidemiology:['approximately 25%', 'Its incidence is variously reported in different countries, varying in pediatric age from1. 2 to 6.1 per 100,000 children aged 0-14 years, per year', 'GOOD', 'You may not be able to prevent mastoiditis, but there are things you can to do protect yourself and your child:\n\nThe pneumococcus bacteria causes several infections, including middle ear infections that can lead to mastoiditis. The U.S. Centers for Disease Control and Prevention (CDC) recommend children up to age 2 receive pneumococcal vaccinations.\nIf you or your child do develop ear issues, talk to a healthcare provider about any steps you should take to reduce the chance you or your child will develop mastoiditis.\nTake steps to prevent middle ear infections.'], Complications:['abscess', 'acute labyrinthitis', 'Chronic and Recurrent Meningitis', 'Hydrocephalus', 'petrositis', 'THROMBOPHLEBITIS', 'FACIAL PARALYSIS'], Diagnostics:['Complete Blood Count CBC', 'Erythrocyte Sedimentation Rate (ESR)', 'Erythrocyte Sedimentation Rate (ESR)', 'HISTOPATHLOGY', 'X RAY PNS(OF/OM)', 'culture & sensitivity for ear discharge', 'Mastoid X-Ray', 'Mastoid X-Ray'], Differential diagnosis:['acute mastoiditis', "Ewing's sarcoma", 'Furunculosis of meatus', 'Infected sebaceous cyst', 'Myofibroma / Myofibromatosis', 'OTITIS EXTERNA'], disease description:Inflammation of mucosal lining of antrum and mastoid air cell system is an invariable accompaniment of acute otitis media and forms a part of it. The term “mastoiditis” is used when infection spreads from the mucosa, lining the mastoid air cells, to involve bony walls of the mastoid air cell system.

Person, 35 years old, presenting ['headache', 'malaise', 'fever', 'bodyache', 'nasal discharge', 'Pain', 'post nasal drip']

Disease Name: Acute Maxillary Sinusitis, symptoms: ['headache', 'malaise', 'fever', 'bodyache', 'nasal discharge', 'Pain', 'post nasal drip'], Treatment: [{'medication': ['Ephedrine ', 'Oxymetazoline ', 'Amoxicillin and Clavulanic acid ', 'Ampicillin ', 'Doxycycline ', 'Erythromycin ', 'Clotrimazole ']}, 'Steam inhalation. Steam alone or medicated with menthol or Tr. Benzoin Co. provides symptomatic relief and \nencourages sinus drainage.Hot fomentation. Local heat to the affected sinus is often \nsoothing and helps in the resolution of inflammation.', '1. Antimicrobial drugs,2. Nasal decongestant drops,3. Analgesics.', 'Antral lavage.It is done \nonly when medical treatment has failed and that too only \nunder cover of antibiotics.'], Pathophysiology: Acute inflammation of sinus mucosa causes hyperaemia, exudation of fluid, outpouring of polymorphonuclear cells and increased activity of serous and mucous glands. Depending on the virulence of organisms, defenses of the host and capability of the sinus ostium to drain exudates, the disease may be mild (nonsuppurative) or severe (suppurative). Initially the exudates is serous; later it may become mucopurulent or purulent . Severe infections cause destruction of mucosal lining. Failure of the ostium to drain results in empyema of the sinus and destruction of its bony walls leading to complications. Dental infections are very fulminating and soon result in suppurative sinusitis. 1.Most commonly, it is viral rhinitis which spreads to involve the sinus mucosa. This is followed by bacterial invasion. 2. Diving and swimming in contaminated water. 3. Dental infections are important source of maxillary sinusitis. Roots of premolar and molar teeth are related to the floor of sinus and may be separated only by a thin layer of mucosal covering. Periapical dental abscess may burst into the sinus; or the root of a tooth, during extraction, may be pushed into the sinus. In case of oroantral fistula, following tooth extraction, bacteria from oral cavity enter the maxillary sinus. 4. Trauma to the sinus such as compound fractures, penetrating injuries or gunshot wounds may be followed by sinusitis., Epidemiology:['6% to 7% of children with respiratory symptoms have acute rhinosinusitis. An estimated 16% of adults are diagnosed with ABRS annually', 'the incidence of acute sinusitis ranges from 15 to 40 episodes per 1000 patients per year,', 'GOOD', 'Do not smoke. Smoking is not good for you or for people around you, since this can cause mucous to become clogged in the nose/sinuses. Avoid being around second-hand smoke, as well as other triggers like animal dander, dust, mold and pollen. Take pains to prevent sinus and other infections by:\n\nWashing your hands well before and after eating and after using the bathroom.\nStaying away from sick people.\nTreating your allergies, possibly with nasal steroid therapy or immunotherapy (primarily known as allergy shots).\nKeeping your body and your immune system in good shape by eating well (lots of vegetables and fruits) and staying hydrated.\nUsing a humidifier if your house is dry or an air purifier. Make sure to clean your equipment regularly.\nIrrigating your nose when necessary with a saline rinse.'], Complications:['orbital cellulitis', 'osteomyelitis', 'ACUTE FRONTAL SINUSITIS'], Diagnostics:['X Ray skull', 'MRI', 'CT SCAN'], Differential diagnosis:['Brain Abscess', 'Meningitis', 'Tension-Type Headaches', 'toothache', 'vascular headache'], disease description:Acute maxillary sinusitis is characterized by facial pain, localized to the cheek, but also in the frontal area or the teeth, that is made worse by stooping down or straining. The pain can be unilateral or bilateral, and tenderness may overlie the sinus It is usually an acute condition, but chronic sinusitis may also develop following an acute episode and may persist or recur if drainage from the antrum to the nasal cavity is poor or when a foreign body is retained??

At the age of 19, symptoms like ['HEPATOMEGALY', 'bone pain', 'fatigue', 'malaise', 'splenomegaly', 'weight loss', 'anemia']

Disease Name: Acute Myeloid Leukemia (aml), symptoms: ['HEPATOMEGALY', 'bone pain', 'fatigue', 'malaise', 'splenomegaly', 'weight loss', 'anemia'], Treatment: [{'medication': ['Pentoxifylline/Oxpentifylline', 'Cytosine arabinoside (Cytarabine)', 'Daunorubicin (Daunomycin)', 'Cladribine']}, 'The most commonly used induction regimens (for patients other\nthan those with APL) consist of combination chemotherapy with\ncytarabine and an anthracycline (e.g., daunorubicin, idarubicin).\nIn adults, cytarabine used at standard dose (100–200 mg/m2\n) is\nadministered as a continuous intravenous infusion for 7 days. With\ncytarabine, anthracycline therapy generally consists of daunorubicin\n(60–90 mg/m2\n) or idarubicin (12 mg/m2\n) intravenously on days\n1, 2, and 3 (the 7 and 3 regimen). Other agents can be added (e.g.,\ncladribine) when 60 mg/m2\n of daunorubicin is used. With the 7 and\n3 regimen, it is now clearly established that 45 mg/m2\n dosing of\ndaunorubicin results in inferior outcomes; patients should receive\nhigher doses as described.\n Conventional therapy for older patients is similar to that for\nyounger: the 7 and 3 regimen with standard-dose cytarabine and\nidarubicin (12 mg/m2\n), or daunorubicin (60 mg/m2\n, or 90 mg/\nm2\n for those <65 years). For patients aged >65 years, high-dose\ndaunorubicin (90 mg/m2\n) has increased toxicity and is not recommended. Older patients and those with adverse-risk genetics may\nreceive lower intensity therapy with a hypomethylating agent\n(decitabine or azacitidine), clofarabine, or preferably investigational therapy .\nWith the 7 and 3 regimen, 60–80% of younger and 33–60%\nof older patients (among those who are candidates for intensive\ntherapy) with primary AML achieve CR. Of patients who do not\nachieve CR, most have drug-resistant leukemia, although induction\ndeath is more frequent with advancing age and medical comorbidity. Patients with refractory disease after induction should be\nconsidered for salvage treatments, preferentially on clinical trials,\nbefore receiving allogeneic hematopoietic stem cell transplantation\n(HCT) that is usually reserved for patients in or near CR.'], Pathophysiology: The PML/RARa protein heterodimerizes with the retinoid X receptor (RXR), the resulting PML/RARa-RXR complex binds to retinoic acid-responsive elements in target genes, resulting in cessation of myeloid differentiation at the promyelocytic stage. The excessive promyelocytes express tissue factor (TF) which forms a complex with factor VII and activates factor X and IX and result in a pro-coagulant state. The immature promyelocytes also cannot build defenses against infections, rendering patients immunosuppressed.There are also certain fusions that make this leukemia insensitive to retinoic acid and chemotherapy., Epidemiology:['about 1% of cancers', '~1.2% of all cancer cases.', 'good', 'No, you can’t prevent acute myeloid leukemia. Experts know that genetic mutations cause acute myeloid leukemia but they don’t know what triggers them. They do know about risk factors that may cause AML. Risk factors you can modify include:\n\nSmoking, including exposure to second-hand smoke. If you smoke, try to quit. If you live or work around someone who smokes, try to limit how much time you spend with them when they’re smoking.\nLong-term exposure to certain carcinogenic chemicals, particularly benzene and formaldehyde. If you work around these carcinogens, be sure you follow all safety precautions, such as wearing protective clothing.'], Complications:['gastrointestinal haemorrhage', 'immunosuppression', 'pulmonary haemorrhage', 'INTRACRANIAL HAEMORRHAGE'], Diagnostics:['BONE MARROW BIOPSY', 'BONE MARROW ASPIRATION', 'ABG', 'Prothrombin Time Test and INR (PT/INR)', 'Complete Blood Count CBC', 'LDH', 'Peripheral Blood Smear', 'SERUM Creatinine', 'SERUM URIC ACID', 'ECG', 'SERUM ELECTROLYTE', 'serum calcium Ca++', 'X RAY', 'IMMUNOHISTOCHEMICAL METHOD', 'CT SCAN'], Differential diagnosis:['Acute lymphoblastic leukemia', 'anemia', 'aplastic anaemia', 'Bone marrow failure', 'CHRONIC MYELOID LEUKEMIA', 'MEGALOBLASTIC ANAEMIA', 'NEUROBLASTOMA', 'rhabdomyosarcoma'], disease description:Acute myeloid leukemia (AML) is a neoplasm characterized by infiltration of the blood, bone marrow, and other tissues by proliferative, clonal, poorly differentiated cells of the hematopoietic system.   Acute myeloid leukemia (AML) is a malignant disease of the bone marrow in which hematopoietic precursors are arrested in an early stage of development. Most AML subtypes are distinguished from other related blood disorders by the presence of more than 20% blasts in the bone marrow.

Symptoms at 39 years old: ['angina', 'angina pectoris', 'apical beat may be difficult to palpate', 'hyper or hypotension', 'pallor', 'syncope', 'tachycardi or bradycardia', 'lightheadedness', 'Restlessness', 'palpitations', 'increased pulse rate', 'S3 and S4 gallop', 'chest pain', 'chest tenderness', 'shortness of breath', 'sweating', 'systolic murmur', 'anxiety', 'breathlessness', 'vomiting']

Disease Name: Acute Myocardial Infarction, symptoms: ['angina', 'angina pectoris', 'apical beat may be difficult to palpate', 'hyper or hypotension', 'pallor', 'syncope', 'tachycardi or bradycardia', 'lightheadedness', 'Restlessness', 'palpitations', 'increased pulse rate', 'S3 and S4 gallop', 'chest pain', 'chest tenderness', 'shortness of breath', 'sweating', 'systolic murmur', 'anxiety', 'breathlessness', 'vomiting'], Treatment: [{'medication': ['Glyceryl trinitrate (nitroglycerin) ', 'Enalapril Maleate', 'Streptokinase ', 'Heparin ', 'Atorvastatin ', 'Metoprolol ', 'Ramipril ', 'Morphine', 'Aspirin/Acetylsalicylic acid']}, 'A number of different medications can also be used to treat a heart attack:\n\nBlood thinners, such as aspirin, are often used to break up blood clots and improve blood flow through narrowed arteries.\nThrombolytics are often used to dissolve clots.\nAntiplatelet drugs, such as clopidogrel, can be used to prevent new clots from forming and existing clots from growing.\nNitroglycerin can be used to widen your blood vessels.\nBeta-blockers lower your blood pressure and relax your heart muscle. This can help limit the severity of damage to your heart.\nACE inhibitors can also be used to lower blood pressure and decrease stress on the heart.\nPain relievers may be used to reduce any discomfort you may feel.\nDiuretics can help decrease fluid buildup to ease the workload of the heart.', 'Heart attacks require immediate treatment, so most treatments begin in the emergency room. Treatment may include taking medications to resolve blood clots, reduce pain, or slow down your heart rate.\n\nThe doctor may also send you to undergo a minimally invasive procedure called percutaneous coronary intervention (PCI), formerly referred to as an angioplasty with a stent. This procedure is used to unblockTrusted Source the arteries that supply blood to the heart.', 'Another procedure your doctor may want you to undergo is a bypass surgery, which is usedTrusted Source to form new passages for blood to flow to the heart.', 'During the procedure, your surgeon will insert a long, thin tube called a catheter through your artery to reach the blockage. They will then inflate a small balloon attached to the catheter in order to reopen the artery, allowing blood flow to resume.\n\nYour surgeon may also place a small, mesh tube called a stent at the site of the blockage. The stent can prevent the artery from closing again.\n\nYour doctor may also want to perform a coronary artery bypass graft (CABG). In this procedure, your surgeon will restore blood flow by rerouting your veins and arteries so the blood can move around the blockage.\n\nA CABG is sometimes done immediately after a heart attack. In most cases, however, it’s performed several days after the incident so your heart has time to heal.'], Pathophysiology: Myocardial infarction is defined as sudden ischemic death of myocardial tissue. In the clinical context, myocardial infarction is usually due to thrombotic occlusion of a coronary vessel caused by rupture of a vulnerable plaque. Ischemia induces profound metabolic and ionic perturbations in the affected myocardium and causes rapid depression of systolic function. Prolonged myocardial ischemia activates a "wavefront" of cardiomyocyte death that extends from the subendocardium to the subepicardium. Mitochondrial alterations are prominently involved in apoptosis and necrosis of cardiomyocytes in the infarcted heart. The adult mammalian heart has negligible regenerative capacity, thus the infarcted myocardium heals through formation of a scar. Infarct healing is dependent on an inflammatory cascade, triggered by alarmins released by dying cells. Clearance of dead cells and matrix debris by infiltrating phagocytes activates anti-inflammatory pathways leading to suppression of cytokine and chemokine signaling. Activation of the renin-angiotensin-aldosterone system and release of transforming growth factor-ß induce conversion of fibroblasts into myofibroblasts, promoting deposition of extracellular matrix proteins. Infarct healing is intertwined with geometric remodeling of the chamber, characterized by dilation, hypertrophy of viable segments, and progressive dysfunction. This review manuscript describes the molecular signals and cellular effectors implicated in injury, repair, and remodeling of the infarcted heart, the mechanistic basis of the most common complications associated with myocardial infarction, and the pathophysiologic effects of established treatment strategies. Moreover, we discuss the implications of pathophysiological insights in design and implementation of new promising therapeutic approaches for patients with myocardial infarction., Epidemiology:['Acute myocardial infarctions are one of the leading causes of death in the developed world, with prevalence approaching three million people worldwide', '64.37/1000', 'variable', 'In general, there are many things that you can do that may prevent a heart attack. However, some factors beyond your control — especially your family history — can still lead to a heart attack despite your best efforts. Still, reducing your risk can postpone when you have a heart attack and reduce the severity if you have one.\n\nAlthough there are several risk factors that you can’t control, there are many ways you can help yourself and reduce your risk of a heart attack. These include:\n\nSchedule a checkup\nQuit tobacco products\nExercise regularly\nEat a healthy diet\nMaintain a weight that’s healthy for you\nManage your existing health conditions\nReduce your stress\nKeep all your medical appointments\nTake your medications as prescribed'], Complications:['Arrhythmias', 'cardiogenic shock', 'heart block', 'heart failure'], Diagnostics:['CPK', 'HISTOPATHLOGY', 'SERUM TROPONIN T(TROP T)', 'SERUM TROPONIN- I(TROP I)', '2-D Echo', 'ECG'], Differential diagnosis:['acute cholecystitis', 'Acute Pericarditis', 'Aortic Dissection', 'Asthma', 'Gastroesophageal reflux disease (GERD)', 'myocarditis', 'PNEUMOTHORAX', 'Pulmonary Embolism', 'stable angina pectoris'], disease description:A heart attack (medically known as a myocardial infarction) is a deadly medical emergency where your heart muscle begins to die because it isn’t getting enough blood flow. This is usually caused by a blockage in the arteries that supply blood to your heart. If blood flow isn’t restored quickly, a heart attack can cause permanent heart damage and death.

Individual aged 54 with manifestations like ['headache', 'fever', 'WATERING EYE', 'tiredness', 'stuffy nose', 'Dryness of the mouth', 'pain on swallowing', 'pyrexia', 'sore throat', 'Burning sensation of the throat', 'cervical lymphadenopathy', 'cough', 'itching in eyes']

Disease Name: Acute Nasopharyngitis, symptoms: ['headache', 'fever', 'WATERING EYE', 'tiredness', 'stuffy nose', 'Dryness of the mouth', 'pain on swallowing', 'pyrexia', 'sore throat', 'Burning sensation of the throat', 'cervical lymphadenopathy', 'cough', 'itching in eyes'], Treatment: ['decongestants, like pseudoephedrine (Sudafed)\ndecongestants combined with antihistamines (Benadryl D, Claritin D)\nnonsteroidal anti-inflammatory drugs, like aspirin or ibuprofen (Advil, Motrin)\nmucus thinners, like guaifenesin (Mucinex)\nlozenges to soothe a sore throat\ncough suppressant for severe cough, such as dextromethorphan (Robitussin, Zicam, Delsym) or codeine\nzinc supplements, which should be taken at the first sign of symptoms\nnasal spray, such as fluticasone propionate (Flonase)\nantiviral medication if you have an infection with influenza'], Pathophysiology: Acute infection of the nasopharynx may be an isolated infection confined to this part only or be a part of the generalized upper airway infection. It may be caused by viruses (common cold, influenza, parainfluenza, rhino or adenovirus) or bacteria (especially streptococcus, pneumococcus or Haemophilus influenzae). More than 200 viruses can cause nasopharyngitis, but the rhinovirus is the most common one, as it accounts for 10–40% of colds.The condition is highly contagious. People can catch it through droplets from a person with a cold that spread through touch or inhalation., Epidemiology:['adults get 2-3 common cold bouts per year and children get 6-10 infections per year', 'GOOD', 'The best way to treat a cold is to prevent one from happening in the first place. Here are some tips for preventing a cold:\n\nWash your hands often with soap, especially when around others with colds.\nWash or disinfect commonly used items, like toys, doorknobs, phones, and faucet handles.\nUse a hand sanitizer when you don’t have access to soap and water.\nUse your own pen to sign receipts in stores.\nSneeze into a tissue or your sleeve, and cover your mouth when you cough to stop the spread of the virus.\nGet a flu shot.\nSome evidence also suggests that taking a garlic supplement with 180 milligrams of allicin for 3 months, or taking 0.25 grams of vitamin C daily, may help prevent colds.'], Complications:['bronchitis', 'otitis media', 'PNEUMONIA', 'sinusitis', 'Croup'], Diagnostics:['HISTOPATHLOGY', 'X RAY NECK LATERAL', 'PHYSICAL EXAMINATION'], Differential diagnosis:['ACUTE SPHENOID SINUSITIS', 'infection', 'Influenza', 'non allergic rhinitis'], disease description:Acute infection of the nasopharynx may be an isolated infection confined to this part only or be a part of the generalized upper airway infection. It may be caused by viruses (common cold, influenza, parainfluenza, rhino or adenovirus) or bacteria (especially streptococcus, pneumococcus or Haemophilus influenzae).

Person aged 34 with manifestations like ['bleeding', 'malaise', 'Mouth ulceration', 'pyrexia', 'soreness', 'Halitosis']

Disease Name: Acute Necrotizing (ulcerative) Gingivitis And Noma, symptoms: ['bleeding', 'malaise', 'Mouth ulceration', 'pyrexia', 'soreness', 'Halitosis'], Treatment: [{'medication': ['Metronidazole ']}, 'Treatment of the acute phase aims to halt tissue destruction and to control the patient\'s discomfort. This involves gentle, ultrasonic debridement of superficial gingival plaques and calculi along with localized oxygen therapy, directed at necrotic lesions. The use of 0.12% chlorhexidine gluconate mouth rinse should be considered, a suggested regimen being twice a day for 30 days.\n\nMetronidazole (250 mg 3 times a day) is a common first drug choice due to its activity against anaerobes. Penicillin, tetracyclines, clindamycin, amoxicillin, and amoxicillin with clavulanate have been shown to produce "acceptable" results and are considered on a case-by-case basis. Oral penicillin, for example, was demonstrated in one study to show significant clinical improvement in three to six days.', 'Gingivectomy and/or gingivoplasty procedures can treat any superficial craters.'], Pathophysiology: Physiologic factors that play a main role in ANUG include psychological stress, poor diet, insufficient sleep, alcohol, tobacco, poor oral hygiene, preexisting gingivitis, and HIV infection. These factors have been shown to impair the host immune response, which facilitates bacterial pathogenicity. Psychological stress reduces the gingival microcirculation and salivary flow and increases adrenocortical secretions, which can modify the function of polymorphonuclear leukocytes and lymphocytes. This alters the immune response as well as the patient's behavior and mood, resulting in insufficient oral hygiene, malnutrition, and increased tobacco consumption. Similarly, poor diet results in increased histamine concentration and increased capillary permeability of the gingiva, which leads to decreased PMN leukocyte chemotaxis., Epidemiology:['uncommon', 'may lead to noma if left untreated', '- Improved oral hygiene\n- Mouth rinses\n- Regular dental check-up, preferably every six months\n- Reduce stress'], Complications:['stomatitis', 'periodontitis'], Diagnostics:['HISTOPATHLOGY', 'RBC Count', 'White Blood Cell count WBC', 'X RAY', 'BACTERIOLOGY'], Differential diagnosis:['HIV', 'infectious mononucleosis', 'Primary herpetic gingivostomatitis'], disease description:Acute necrotizing (ulcerative) gingivitis (ANUG) is typically an acute gingival ulceration, rarely complicated by gangrenous stomatitis (when it is called noma), although this is increasingly reported in HIV disease. ANUG is uncommon, typically seen in students, malnutrition or in confl ict situations. Noma is a serious destructive necrosis affecting the soft tissues and bones of the mouth and adjoining orofacial areas. Noma is seen predominantly in sub-Saharan Africa, where the estimated frequency in some communities varies from 1 to 7 cases per 1000 population. Age. ANUG is typically seen in children or adolescents, but may occur in young adults

Person aged 52 dealing with ['ear discharge', 'ear itching', 'Hearing loss', 'Tissue fibrosis', 'fever']

Disease Name: Acute Necrotizing Otitis Media, symptoms: ['ear discharge', 'ear itching', 'Hearing loss', 'Tissue fibrosis', 'fever'], Treatment: [{'medication': ['Amoxicillin and Clavulanic acid ', 'Ampicillin ']}, 'Ciprofloxacin (Cipro):750 mg orally every 12 hours.\nTicarcillin-clavulanate potassium (Timentin):3 g IV every 4 hours.\nPiperacillin-tazobactam (Zosyn):4 to 6 g IV every 4 to 6 hours.\nCeftazidime (Fortaz):2 g IV every 8 hours', 'Cortical mastoidectomy may be indicated if\nmedical treatment fails to control or the condition gets\ncomplicated by acute mastoiditis'], Pathophysiology: It is a variety of acute suppurative otitis media, often seen in children suffering from measles, scarlet fever or influenza. Causative organism is ß-haemolytic streptococcus. There is rapid destruction of whole of tympanic membrane with its annulus, mucosa of promontory, ossicular chain and even mastoid air cells. There is profuse otorrhoea. In these cases, healing is followed by fibrosis or ingrowth of squamous epithelium from the meatus (secondary acquired cholesteatoma). , Epidemiology:['0.25% per annum', 'incidence increased 1142 per cent within the 16-year period, from 123 recorded cases in 2002 to 1405 cases in 2017. This correlates with an increasing prevalence of diabetes, an ageing population and likely increased physician awareness of necrotising otitis externa', 'GOOD', "To Do : HYGIENE MAINTAINENCE\n\nHere are some ways to reduce risk of ear infections in you or your child:\n\nDon’t smoke. Studies have shown that second-hand smoking increases the likelihood of ear infections. Be sure no one smokes in the house or car — especially when children are present — or at your day care facility.\nControl allergies. Inflammation and mucus caused by allergic reactions can block the eustachian tube and make ear infections more likely.\nPrevent colds. Reduce your child's exposure to colds during the first year of life. Don’t share toys, foods, drinking cups or utensils. Wash your hands frequently. Most ear infections start with a cold. If possible, try to delay the use of large day care centers during the first year.\nBreastfeed your baby. Breastfeed your baby during the first 6 to 12 months of life. Antibodies in breast milk reduce the rate of ear infections.\nBottle feed baby in upright angle. If you bottle feed, hold your baby in an upright angle (head higher than stomach). Feeding in the horizontal position can cause formula and other fluids to flow back into the eustachian tubes. Allowing an infant to hold his or her own bottle also can cause milk to drain into the middle ear. Weaning your baby from a bottle between nine and 12 months of age will help stop this problem.\nWatch for mouth breathing or snoring. Constant snoring or breathing through the mouth may be caused by large adenoids. These may contribute to ear infections. An exam by an otolaryngologist, and even surgery to remove the adenoids (adenoidectomy), may be necessary.\nGet vaccinations. Make sure your child’s immunizations are up to date, including yearly influenza vaccine (flu shot) for those 6 months and older. Ask your doctor about the pneumococcal, meningitis and other vaccines too. Preventing viral infections and other infections help prevent ear infections."], Complications:['abscess', 'Necrosis of soft tissue and bone', 'Perforated ear drum'], Diagnostics:['HISTOPATHLOGY', 'HISTOPATHLOGY', 'Mastoid X-Ray'], Differential diagnosis:['CHRONIC OTITIS MEDIA', 'Herpes Zoster', 'OTITIS MEDIA WITH EFFUSION'], disease description:It is a variety of acute suppurative otitis media, often seen in children suffering from measles, scarlet fever or influenza. Causative organism is ß-haemolytic streptococcus. There is rapid destruction of whole of tympanic membrane with its annulus, mucosa of promontory, ossicular chain and even mastoid air cells. There is profuse otorrhoea. In these cases, healing is followed by fibrosis or ingrowth of squamous epithelium from the meatus (secondary acquired cholesteatoma).

Experiencing ['dysphagia', 'heartburn', 'retrosternal discomfort', 'difficulty in swallowing', 'blood in vomiting', 'Regurgitation of gastric contents'] at 24 years

Disease Name: Acute Oesophagitis, symptoms: ['dysphagia', 'heartburn', 'retrosternal discomfort', 'difficulty in swallowing', 'blood in vomiting', 'Regurgitation of gastric contents'], Treatment: ['Avoid spicy foods such as those with pepper, chili powder, curry and nutmeg.\nAvoid acidic foods and beverages such as tomatoes, oranges, grapefruits and their juices. Instead, try nectars and imitation fruit drinks with vitamin C.\nInclude more soft foods such as applesauce, cooked cereals, mashed potatoes, custards, puddings and high-protein shakes in your diet.\nTake small bites and chew your food thoroughly.\nAvoid alcohol and tobacco.', 'Treatment depends on the etiology but core principles of treatment in addition to etiology specific treatment include acid suppression with PPI or H2 blockers, lifestyle modification, liquid to soft or puree diet to allow adequate time for healing and dietary modification. If the etiology appears to be acid reflux based on history then the use of H2 blockers twice a day or proton-pump inhibitors daily is indicated initially. Patient should also be advised of lifestyle and dietary modifications which include weight loss, elevating the head end of bed (patient with nocturnal symptoms of cough, hoarseness, sore throat), elimination of some dietary triggers such as fatty food, chocolate, carbonated drinks, spicy food, smoking, and alcohol. If the etiology is medication-induced esophagitis, the medication should be stopped if possible and if necessary then should be switched to any other alternatives. The patient should be instructed to take pills with 4 oz of water and remain upright for 30 min after taking the pills. For eosinophilic esophagitis treatment include acid suppression, topical or systemic steroids either topical budesonide or fluticasone and dietary modification if a food allergy is suspected. If etiology is infectious, target therapy is indicated. For C. Albicans, oral fluconazole is the drug of choice. For HSV esophagitis, treatment is oral or intravenous acyclovir and Foscarnet for those who are non-responders. CMV esophagitis is treated with Gancyclovir or Valganciclovir. Treatment of complications like stenosis or stricture may require endoscopic dilation. Addition of topical anesthesia like topical lidocaine (e.g. GI cocktail) and opioids may help in ulcers related pain. NSAIDs must be avoided as it may exacerbate symptoms.'], Pathophysiology: Infections in the esophagus also can cause esophagitis. They usually occur in people with a weak immune system. Esophagitis from infections is common in people who have HIV infection, use steroid medicines long-term, have had organ transplants, or have been treated with chemotherapy for cancer.Only a few types of infection are common in the esophagus, such as:Even in someone who already has a herpes infection in the mouth, it rarely spreads down to the esophagus if the immune system is normal.yeastherpes virus (HSV)cytomegalovirus (CMV), Epidemiology:['8.8%', 'The estimated incidence is 0.35 per 100,000 population', 'GOOD', "Do not eat foods that may increase reflux. Eating or drinking large amounts of certain foods may worsen your symptoms of gastroesophageal reflux. These may include alcohol, caffeine, chocolate and mint-flavored foods.\nUse good pill-taking habits. Always take a pill with plenty of water. Don't lie down for at least 30 minutes after taking a pill.\nLose weight. Talk to your health care provider about an appropriate diet and exercise routine to help you lose weight and maintain a healthy weight.\nIf you smoke, quit. Talk to your provider if you need help ending a smoking habit.\nTry not to stoop or bend, especially soon after eating.\nDo not lie down after eating. Wait at least three hours after eating to lie down or go to bed.\nRaise the head of your bed. Place wooden blocks under your bed to elevate your head. Aim for an elevation of 6 to 8 inches (15 to 20 centimeters). If it's not possible to elevate your bed, insert a wedge between your mattress and box spring to elevate your body from the waist up. Raising your head by using only pillows isn't effective."], Complications:['PERFORATION OF OESOPHAGUS', 'strictures', 'Malnutrition', 'BARRETT ESOPHAGUS'], Diagnostics:['HISTOPATHLOGY', 'Barium Imaging', 'Upper GI Endoscopy', 'ESOPHAGOSCOPY', 'HISTORY TAKING'], Differential diagnosis:['ACHALASIA', 'PEPTIC ULCER DISEASE', 'PNEUMONIA', 'Pulmonary Embolism'], disease description:It is acute inflammation of the oesophagus and can be due to (i) ingestion of hot liquids, (ii) ingestion of caustic or corrosive agents, (iii) laceration due to swallowed foreign body, or trauma of oesophagoscopy, (iv) monilial infection of oesophagus from thrush in the oral cavity and (v) systemic disorder like pemphigus.The average age at diagnosis ranges between 30 and 50 years and suggests that EoE is a disease of the middle-aged man.

Experiencing ['fever', 'localized pain', 'localized swelling', 'LOCALIZED TENDERNESS', 'fatigue', 'painful swelling', 'difficulty in movement'] at 28 years

Disease Name: Acute Osteomyelitis, symptoms: ['fever', 'localized pain', 'localized swelling', 'LOCALIZED TENDERNESS', 'fatigue', 'painful swelling', 'difficulty in movement'], Treatment: ['If the child is brought within 48 hours of the onset of symptoms: Treatment consists of rest, antibiotics and general building-up of the patient. The limb is put to rest in a splint or by traction.In children less than 4 months of age, a combination of Ceftriaxone and Vancomycin in appropriate dose is preferred. In older children, a combination of Ceftriaxone and Cloxacillin is given. b) If the child is brought after 48 hours of the onset of symptoms: Surgical exploration and drainage is the mainstay of treatment at this stage. A drill hole is made in the bone in the region of the metaphysis.The wound is closed over a sterile suction drain. Rest, antibiotics and hydration are continued post-operatively.Antibiotics are continued for 6 weeks.', 'Staphylococcus aureus penicillin-sensitive\n\nTreatment of choice is penicillin G 4 million units every 6 hours\n\nAlternative regimens are a first-generation cephalosporin, e.g., cefazolin 2 g IV every 8 hours, clindamycin 900 mg IV every 8 hours, vancomycin 15 mg/kg IV every 12 hours, oxacillin or nafcillin 2 g IV every 4 hours\n\nStaphylococcus aureus penicillin-resistant\n\nTreatment of choice is nafcillin 2 gm IV every 4 hours\n\nAlternative therapies are cefazolin, clindamycin, or vancomycin (doses as above)\n\nStaphylococcus aureus methicillin-resistant\n\nTreatment of choice is vancomycin IV\n\nAn alternative regimen is linezolid 600 mg IV every 12 hours.\n\nStreptococci (group A, B, Beta hemolytic, Streptococcus pneumoniae)\n\nTreatment of choice is penicillin G 4 million units every 6 hours\n\nAlternative regimens include ceftriaxone 2 gm IV daily, clindamycin IV, vancomycin IV, cefazolin IV (doses as above)\n\nEnterobacteriaceae quinolone sensitive\n\nTreatment of choice is ciprofloxacin 400 mg IV twice per day (bid) or 750 mg orally (PO) bid, levofloxacin 500 to 750 mg PO or IV daily\n\nAlternative regimens include ceftriaxone 2g IV daily, cefepime 2 gm IV every 12 hours, ceftazidime 2 gm IV every 8 hours\n\nEnterobacteriaceae, quinolone-resistant (Escherichia coli)\n\nTreatment of choice is piperacillin/tazobactam 3.375 g IV every 8 hours, Ticarcillin/clavulanate 3.1 gm IV every 4 hours\n\nAn alternative regimen is ceftriaxone 2 g IV daily\n\nPseudomonas aeruginosa\n\nTreatment of choice is cefepime 2 gm IV every 12 hours, ceftazidime 2 gm IV every 8 hours\n\nAlternative regimens include meropenem 1 gm IV every 8 hours, Imipenem 500 mg IV every 6 hours, ciprofloxacin 400 mg IV every 12 hours, or 750 mg PO daily\n\nEnterococci\n\nTreatment of choice is penicillin G 4 million units every 6 hours\n\nAlternatively, vancomycin 15 mg/kg every 12 hours, daptomycin 6 mg/kg IV daily, linezolid 600 mg IV or PO every 12 hours\n\nAnaerobes\n\nTreatment of choice is clindamycin 900 mg IV every 8 hours, ticarcillin/clavulanate 3.1 gm IV every 4 hours\n\nAlternatively, metronidazole 500 mg IV every 8 hours (for gram-negative anaerobes)'], Pathophysiology:  Staphylococcus aureus is the commonest causative organism. Others are Streptococcus and Pneumococcus. These organisms reach the bone via the blood circulation. Primary focus of infection is generally not detectable.The bacteria, as they pass through the bone, get lodged in the metaphysis. Lower femoral metaphysis is the commonest site. The other common sites are the upper tibial, upper femoral and upper humeral metaphyses.  The host bone initiates an inflammatory reaction in response to the bacteria. This leads to bone destruction and production of an inflammatory exudate and cells (pus). Once sufficient pus forms in the medullary cavity, it spreads in the following directions. a) Along the medullary cavity- Blood supply to a segment of the bone is thus cut off. b) Out of the cortex: Pus travels along Volkmann’s canals and comes to lie sub-periosteally. A segment of bone is thus rendered avascular (sequestrum). c) In other directions: The epiphyseal plate is resistant to the spread of pus. At times it may be affected by the inflammatory process., Epidemiology:['2 to 5 out of every 10,000 people', '13 per 100,000 in children and approximately 90 per 100,000 in adults.', 'not specific', 'It’s important to clean and treat wounds to keep out bacteria and prevent infections. If you’ve had a recent bone break or surgery, or have an artificial joint, contact your healthcare provider at the first sign of any infection. But in many instances, there isn’t anything you can do to prevent osteomyelitis.'], Complications:['Septic arthritis', 'pathological fracture', 'CHRONIC OSTEOMYELITIS', 'BONE DEFORMITY', 'systemic infection'], Diagnostics:['Erythrocyte Sedimentation Rate (ESR)', 'HISTOPATHLOGY', 'Total Leucocyte Count (TLC)', 'BONE SCAN', 'X RAY'], Differential diagnosis:['BURSITIS', 'rheumatic disorder', 'SCURVY', 'Septic arthritis'], disease description:This can be primary (haematogenous) or secondary (following an open fracture or bone operation). Haematogeous osteomyelitis is the commonest, and is often seen in children.

Experiencing ['pus ear discharge', 'ear pain', 'hearing impairment', 'fever'] at 47 years

Disease Name: Acute Otitis Media, symptoms: ['pus ear discharge', 'ear pain', 'hearing impairment', 'fever'], Treatment: [{'medication': ['Ephedrine ', 'Amoxicillin and Clavulanic acid ', 'Ampicillin ', 'Erythromycin ', 'Pseudoephedrine', 'Sulfamethoxazole + Trimethoprim {Co-trimoxazole } ']}, 'analgesics and antibacterials', 'Myringotomy. It is incising the drum to evacuate\npus and is indicated when (i) drum is bulging and there is\nacute pain, (ii) there is an incomplete resolution despite\nantibiotics when drum remains full with persistent conductive\nhearing loss and (iii) there is persistent effusion\nbeyond 12 weeks.'], Pathophysiology: The most common infecting organisms are Streptococcus pneumoniae and Haemophilus influenzae. 1. Stage of Tubal Occlusion. Oedema and hyperaemia of nasopharyngeal end of eustachian tube blocks the tube leading to absorption of air and negative intratympanic pressure. There is retraction of tympanic membrane with some degree of effusion in the middle ear but fluid may not be clinically appreciable. Symptoms. Deafness and earache are the two symptoms but they are not marked. There is generally no fever. Signs. Tympanic membrane is retracted with handle of malleus assuming a more horizontal position, prominence of lateral process of malleus and loss of light reflex. Tuning fork tests show conductive deafness. 2. Stage of Presuppuration. If tubal occlusion is prolonged, pyogenic organisms invade tympanic cavity causing hyperaemia of its lining. Inflammatory exudate appears in the middle ear. Tympanic membrane becomes congested. Symptoms. There is marked earache which may disturb sleep and is of throbbing nature. Deafness and tinnitus are also present, but complained only by adults. Usually, child runs high degree of fever and is restless. Signs. To begin with, there is congestion of pars tensa. Leash of blood vessels appear along the handle of malleus and at the periphery of tympanic membrane imparting it a cart-wheel appearance. Later, whole of tympanic membrane including pars flaccida becomes uniformly red. Tuning fork tests will again show conductive type of hearing loss. 3. Stage of Suppuration. This is marked by formation of pus in the middle ear and to some extent in mastoid air cells. Tympanic membrane starts bulging to the point of rupture. Symptoms. Earache becomes excruciating. Deafness increases, child may run fever of 102–103 °F. This may be accompanied by vomiting and even convulsions. Signs. Tympanic membrane appears red and bulging with loss of landmarks. Handle of malleus may be engulfed by the swollen and protruding tympanic membrane and may not be discernible. A yellow spot may be seen on the tympanic membrane where rupture is imminent. 4. Stage of Resolution. The tympanic membrane ruptures with release of pus and subsidence of symptoms. Inflammatory process begins to resolve. If proper treatment is started early or if the infection was mild, resolution may start even without rupture of tympanic membrane. Symptoms. 5. Stage of Complication. If virulence of organism is high or resistance of patient poor, resolution may not take place and disease spreads beyond the confines of middle ear. It may lead to acute mastoiditis, subperiosteal abscess, facial paralysis, labyrinthitis, petrositis, extradural abscess, meningitis, brain abscess or lateral sinus thrombophlebitis., Epidemiology:['The overall incidence rate of AOM episodes as diagnosed by a physician during the prospective study was 256/1000 person-years', 'GOOD', 'To Do : Ear Toilet. If there is discharge in the ear, it is dry mopped\nwith sterile cotton buds and a wick moistened\nwith antibiotic may be inserted.\n6. Dry Local Heat. Helps to relieve pain.'], Complications:['acute labyrinthitis', 'Brain Abscess', 'petrositis', 'THROMBOPHLEBITIS', 'acute mastoiditis', 'CHRONIC OTITIS MEDIA', 'FACIAL PARALYSIS'], Diagnostics:['HISTOPATHLOGY', 'Otoscopy', 'X RAY', 'CT SCAN', 'Tuning Fork Tests'], Differential diagnosis:['allergic rhinitis', 'bullous myringitis', 'CHOLESTEATOMA', 'fever', 'FURUNCLE(LOCALISED ACUTE OTITIS EXTERNA)', 'Gastroesophageal reflux disease (GERD)', 'Haemophilus influenzae', 'hearing impairment', 'Human Parainfluenza virus infection', 'leukemia', 'lungs disease', 'NASOPHARYNGEAL CANCER', 'OTITIS EXTERNA', 'primary ciliary dyskinesia', 'ramsay hunt syndrome', 'serous otitis media', "wegener's granulomatosis"], disease description:Acute otitis media (AOM) is characterised by purulent fluid in the middle ear. The tympanic membrane bulges. The child suffers extreme pain until the tympanic membrane bursts.It is the second most common pediatric diagnosis in the emergency department following upper respiratory infections. Although acute otitis media can occur at any age, it is most commonly seen between the ages of 6 to 24 months. 

Person aged 18 dealing with ['Hypotension', 'Cullens sign', 'increased pulse rate', 'rigidity', 'Tachycardia', 'epigastric pain', 'erythematous rashes', 'Abdominal Pain', 'pain in abdomen radiating to back', "Grey Turner's sign", 'fever', 'nausea', 'vomiting', 'PLEURAL EFFUSION']

Disease Name: Acute Pancreatitis, symptoms: ['Hypotension', 'Cullens sign', 'increased pulse rate', 'rigidity', 'Tachycardia', 'epigastric pain', 'erythematous rashes', 'Abdominal Pain', 'pain in abdomen radiating to back', "Grey Turner's sign", 'fever', 'nausea', 'vomiting', 'PLEURAL EFFUSION'], Treatment: ['IV fluids. Pancreatitis is dehydrating, and hydration is very important for healing.\nTube feeding. If you’re unable to tolerate food by mouth, your doctors may administer food via a tube placed through your nose or stomach to help you get enough nutrition.\nParenteral nutrition: In very severe cases, your doctors may elect to provide nutrition through an intravenous line.\nPain relief. You’ll have medication through an IV directly to your bloodstream or by mouth.', 'Endoscopic retrograde cholangiopancreatography (ERCP). This procedure goes inside your bile ducts with an endoscope — a thin, flexible catheter with a camera attached. \n\nGallbladder removal surgery. Once gallstones have brought you to the hospital, the chance of them causing you trouble again is high. Gallbladder removal is the standard treatment for gallstones that cause complications. It can usually be done through minimally invasive (laparoscopic) surgery.'], Pathophysiology: After an initial insult, such as ductal disruption or obstruction, there is premature activation of trypsinogen to trypsin within the acinar cell. Trypsin then activates other pancreatic proenzymes, leading to autodigestion, further enzyme activation, and release of active proteases. Lysosomal hydrolases colocalize with pancreatic proenzymes within the acinar cell. Pancreastasis (similar in concept to cholestasis) with continued synthesis of enzymes occurs. Lecithin is activated by phospholipase A2 into the toxic lysolecithin. Prophospholipase is unstable and can be activated by minute quantities of trypsin. After the insult, cytokines and other proinflammatory mediators are released. The healthy pancreas is protected from autodigestion by pancreatic proteases that are synthesized as inactive proenzymes; digestive enzymes that are segregated into secretory granules at pH 6.2 by low calcium concentration, which minimizes trypsin activity; the presence of protease inhibitors both in the cytoplasm and zymogen granules; and enzymes that are secreted directly into the ducts. Histopathologically, interstitial edema appears early. Later, as the episode of pancreatitis progresses, localized and confluent necrosis, blood vessel disruption leading to hemorrhage, and an inflammatory response in the peritoneum can develop. The diagnosis of pancreatitis in children is made when 2 of 3 of the following are present: abdominal pain; serum amylase and/or lipase activity at least 3 times greater than the upper limit of normal; and imaging findings characteristic of, or compatible with, AP., Epidemiology:['4.9 to 35 per 100,000 population', '30.0 per 100 000 population and the mortality rates at 30 days and 60 days were 5.6% and 6.4%', 'GOOD', 'Not all causes are preventable, but you can reduce your risk by moderating your alcohol consumption. You can reduce your risk of gallstones, the other leading cause, by reducing cholesterol. If you’ve had acute pancreatitis, you can help prevent it from happening again by quitting alcohol and smoking. If you’ve had gallstone pancreatitis, removing your gallbladder can prevent it from recurring.'], Complications:['acute respiratory distress syndrome', 'hyperglycemia', 'Hypocalcemia', 'pancreatic pseudocyst', 'renal failure', 'shock', 'SPLENIC RUPTURE', 'CHRONIC PLEURAL EFFUSIONS'], Diagnostics:['HISTOPATHLOGY', 'CT Abdomen', 'USG ABDOMEN(W/A)', 'X RAY CHEST', 'SERUM LIPASE', 'X RAY ABDOMEN', 'COAGULATION PROFILE', 'BLOOD GLUCOSE'], Differential diagnosis:['Acute Hepatitis', 'Aortic Dissection', 'appendicitis', 'Bowel obstruction', 'bowel perforation', 'cholangitis', 'CHOLELITHIASIS', 'Diabetic Ketoacidosis', 'GASTRITIS', 'intestinal obstruction ', 'Mesenteric ischemia', 'Myocardial infarction', 'PEPTIC ULCER DISEASE', 'peritonitis', 'Renal colic'], disease description:Acute pancreatitis (AP), the most common pancreatic disorder in children, is increasing in incidence, and 50 or more cases are usually seen in major pediatric centers per year. In children, blunt abdominal injuries, multisystem disease such as the hemolytic uremic syndrome and inflammatory bowel disease, biliary stones or microlithiasis (sludging), and drug toxicity are the most common etiologies. 

Symptoms reported by a 36-year-old: ['swelling at nail fold', 'redness at nail fold', 'tenderness at nail fold', 'local pain']

Disease Name: Acute Paronychia, symptoms: ['swelling at nail fold', 'redness at nail fold', 'tenderness at nail fold', 'local pain'], Treatment: ['Paronychias are usually either treated with incision and drainage or antibiotics. If there is inflammation with no definite abscess, treatment can include warm soaks with water or antiseptic solutions (chlorhexidine, povidone-iodine) and antibiotics. Warm soaks should be for 10 to 15 minutes, multiple times a day. There is not strong evidence recommending topical vs. oral antibiotics, and this may be physician-dependent based on experience. Antibiotic used should have staph aureus coverage. Topical antibiotics used may be a triple antibiotic ointment, bacitracin, or mupirocin. In patients failing topical treatment or more severe cases, oral antibiotics are an option; dicloxacillin (250mg four times a day) or cephalexin (500mg three to four times a day). Indications for antibiotics with anaerobic coverage include patients where there is a concern for oral inoculation; this would require the addition of clindamycin or amoxicillin-clavulanate. If the patient has risk factors for MRSA (including but not limited to: recent hospitalization, recent surgery, ESRD on hemodialysis, HIV/AIDS, IVDU, resident of long term care facility), chose an antibiotic with the appropriate coverage. Options include trimethoprim/sulfamethoxazole DS (1 to 2 tablets twice a day), clindamycin (300 to 450mg four times a day) or doxycycline (100mg twice a day)', 'If an abscess is present, the infection will require drainage. Incision and drainage are usually with a #11 scalpel, and the blade is inserted under the eponychial fold (lateral nail fold) until pus begins to drain. Local or digital block anesthetic is generally helpful to allow comfort to ensure complete drainage. An abscess requires irrigation with normal saline, and if the abscess and incision site is large, the clinician can pack it with plain gauze for continued drainage.'], Pathophysiology: Paronychia results from the disruption of the protective barrier between the nail and the nail fold, which is the cuticle. Trauma (including manicures and pedicures), infections (including bacterial, viral, and fungal), structural abnormalities, and inflammatory diseases (ex. psoriasis) are predisposing factors. Organisms will enter the moist nail crevice, which leads to colonization of the area. The majority of acute paronychias are due to trauma, nail-biting, aggressive manicuring, artificial nails, and may involve a retained foreign body. Infections are most commonly the result of Staphylococcus aureus. Streptococci and Pseudomonas are more common in chronic infections., Epidemiology:['the most common hand infection in the United States, representing 35% of these disorders', 'GOOD', 'To prevent a nail infection, you should:\n\nAvoid biting or chewing on your nails or hangnails. Don’t pick at your cuticles.\nBe careful not to cut your nails too short. When trimming cuticles, avoid cutting too close to the nail fold.\nMaintain good hygiene by washing your hands and keeping your nails clean. Use gentle soaps that are not irritating to your skin.\nUse lotion on your nail fold and cuticles if your skin is dry. Excessive dryness can cause the skin to crack.\nWear waterproof gloves if you work with chemicals or your hands will be wet for a long period.'], Complications:['CELLULITIS', 'nail discoloration', 'nail dystrophy'], Diagnostics:['X RAY', 'PHYSICAL EXAMINATION'], Differential diagnosis:['CELLULITIS', 'Herpetic whitlow', 'Nail psoriasis', 'Onychomycosis'], disease description:Paronychia is an infection of the proximal and lateral toenail and fingernail folds which may occur spontaneously or following trauma or manipulation. It is one of the most common infections of the hand. Paronychia results from the disruption of the protective barrier between the nail and the nail fold, introducing bacteria and predisposing the area to infection. Acute paronychia is usually limited to one nail; however, if drug-induced, it can involve many nails.