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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).