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At 25, dealing with ['erythema', 'bullous stage is characterized by intense pruritus accompanied with widespread tense blisters and vesicles on apparently normal or erythematous skin', 'haemorrhagic crusts and urticated and infiltrated erythematosus plaques with an occasionally annular or figurate pattern are present', 'excoriation', 'Nikolsky sign is negative', 'blisters', 'crusting of the skin', 'pruritus', 'Urticarial skin lesions']

Disease Name: Bullous Pemphigoid, symptoms: ['erythema', 'bullous stage is characterized by intense pruritus accompanied with widespread tense blisters and vesicles on apparently normal or erythematous skin', 'haemorrhagic crusts and urticated and infiltrated erythematosus plaques with an occasionally annular or figurate pattern are present', 'excoriation', 'Nikolsky sign is negative', 'blisters', 'crusting of the skin', 'pruritus', 'Urticarial skin lesions'], Treatment: [{'medication': ['Doxycycline ', 'Dapsone ', 'Methotrexate', 'Azathioprine ', 'Prednisolone']}, 'Management algorithm for bullous pemphigoida\nLocalized and mild disease\n•\tLesional very potent topical corticosteroids 2×/day\nModerate diseaseb\nFirst line\n•\tVery potent topical corticosteroids on the whole body surface 2×/day\nSecond line\n•\tVery potent topical corticosteroids on the whole body surface 2×/day\nplus (in alphabetical order)\n•\tAzathioprine 2.5 mg/kg/day (with normal TPMT activity) \nor\n•\tDapsone 1.0–1.5 mg/kg/day or\n•\tDoxycycline 200 mg/day ± nicotinamide 2 g/day or\n•\tMethotrexate 10–20 mg/week or\n•\tMycophenolates (mofetil 2 g/day, gastro-resistant \nmycophenolic acid (Myfortic®) 1.44 g/day)\nor\n•\tPrednisolone 0.5 mg/kg/day tapering, with or without\n•\tAzathioprine, dapsone, doxycycline, methotrexate, \nmycophenolates (see earlier)\nExtensive disease\nFirst line\n•\tVery potent topical corticosteroids on the whole body surface 2×/day\nplus\n•\tAzathioprine, dapsone, doxycycline, methotrexate, \nmycophenolates \nor\n•\tVery potent topical corticosteroids on the whole body surface 2×/day\nplus\n•\tPrednisolone 0.5 mg/kg/day tapering, with or without\n•\tAzathioprine, dapsone, doxycycline, methotrexate, \nmycophenolates (see earlier)\nSecond line\n•\tIn case of insufficient response treat with oral prednisolone, \nincrease dose to 0.75 mg/kg/day and, if still insufficient, to \n1.0 mg/kg/day\nThird line\n•\t plus immunoadsorption, rituximab or IVIG'], Pathophysiology: The pathogenic importance of humoral and cellular autoimmunity against BP180 has clearly been demonstrated. Both Fc receptor independent and, importantly, Fc receptor mediated effects were shown to be essential for blister formation in BP using in vitro, ex vivo and various animal models. More specifically, complement activation at the DEJ and the activation of mast cells appeared to be crucial to attract neutrophils and macrophages at the DEJ. Subsequent release of reactive oxygen species and various proteases then induced dermal–epidermal splitting. Targeting mast cells, neutrophils, complement activation and the cytokine network may open novel therapeutic avenues for this disease. Autoantibodies In nearly all BP patients, autoantibodies bind to BP180 (also termed type XVII collagen, and BPAG2). The extracellular portion of the 16th non-collagenous domain (NC16A) located directly adjacent to the cellular membrane is the immunodominant region in BP and is recognized by autoantibodies in 75–90% of BP patients. Cellular immune response In contrast to the humoral immune response, the cellular immune response has been less widely studied in human BP. T- and B-cell reactivity against the NH2-terminal portion of the BP180 ectodomain is associated with severe BP, while the central portion is more frequently recognized in patients with limited disease. In contrast, combined T- and B-cell response against the COOH- and NH2-terminal globular domains of BP230 were found in less than 50%. The response to the BP180 ectodomain is restricted to the DQß1*0301 allele. Autoreactive T cells in BP patients produced a Th1/Th2 mixed cytokine profile. Cytokines and chemokines Elevated levels of IL-1ß, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-15, IL-16, IL-17, IL-21, eotaxin, monocyte chemotactic protein 4 (MCP-4), TNF-a and CCL-18 occur in the sera and/or blister fluids of BP patients. Serum levels of TNF-a, IL-6, IL-8, IL-15, IL-21 and CCL18 correlated with the extent of BP skin lesions pointing to a pathological relevance of these mediators. The assumption that Th2-type cytokines are important in human BP is supported by the increased frequency of cutaneous lymphocyte-associated antigen-positive IL-4- and IL-13-producing cells in the peripheral blood. More recently, the potential role of Th17 cells in BP was highlighted., Epidemiology:['reported incidence of BP ranges between 2.5 and 66', 'VARIABLE', 'Healthcare providers and medical researchers aren’t sure how to prevent bullous pemphigoid.\n\nAvoid sun exposure. Avoid prolonged sun exposure on any area of the skin affected by bullous pemphigoid.\nDress in loosefitting cotton clothes. This helps protect your skin.'], Complications:['neurological disturbances', 'Pulmonary Embolism', 'Psychiatric disorders', 'PULMONARY INFECTIONS'], Diagnostics:['ELISA', 'ELECTRON MICROSCOPY', 'Histopathological examination'], Differential diagnosis:['contact allergic dermatitis', 'Dermatitis herpetiformis', 'Epidermolysis bullosa', 'Epidermolysis bullosa acquisita', 'erythema multiforme', 'scabies dermatology', 'Urticaria'], disease description:BP is not only the most common disorder within the group of subepidermal immunobullous disorders but also represents the most frequent autoimmune blistering disease in general. It mainly affects elderly people although younger patients may also be affected and often starts with pruritus and urticated and erythematous lesions. Later, tense blisters are characteristic both on erythematous and on normal skin. Mucosal involvement only develops in a minority of patients and is not predominant. 

At the age of 19, symptoms like ['ENCEPHALITIS', 'LOW GRADE FEVER', 'abscesses', 'PNEUMONIA']

Disease Name: Burkholderia Infection, symptoms: ['ENCEPHALITIS', 'LOW GRADE FEVER', 'abscesses', 'PNEUMONIA'], Treatment: [{'medication': ['Sulfamethoxazole and Trimethoprim (Co-trimoxazole)', 'Ceftazidime ']}, 'Infections due to Bcc can be challenging to manage, as Bcc is intrinsically resistant to a number of commonly used antibiotics. Trimethoprim-sulfamethoxazole (TMP-SMX) and ceftazidime are considered first-line options for Bcc infections'], Pathophysiology: The exact pathophysiology of this syndrome is poorly understood, and the precise mortality rate in not known, although it is thought to approach 100%.Burkholderia organisms are found in soil and water. The germs can be spread through person-to-person contact. The initial symptoms may be a low-grade fever, progressing to much more serious conditions, including pneumonia and other lung disorders that can sometimes be deadly.Some strains of Burkholderia bacteria are spread from person to person or by contamination of disinfectants, including in hospital settings. Good personal hygiene, including frequent hand washing, and infection control measures in hospitals can lower the risk of disease transmission. Centers treating children with cystic fibrosis often try to limit contact with other youngsters infected with B cepacia., Epidemiology:['only 3 percent of respondents noted a Burkholderia cepacia complex infection.', 'poor', 'Good personal hygiene, including frequent hand washing, and infection control measures in hospitals can lower the risk of disease transmission.'], Complications:['death', 'lung damage'], Diagnostics:['SPUTUM CULTURE', 'PCR', 'Culture on blood agar'], Differential diagnosis:['PNEUMONIA', 'Pseudomonas infection', 'PULMONARY INFECTIONS', 'staphylococcal infections'], disease description:Burkholderia cepacia is an aerobic gram-negative bacillus found in various aquatic environments. B cepacia is an organism of low virulence and is a frequent colonizer of fluids used in the hospital (eg, irrigation solutions, intravenous fluids). B cepacia rarely causes infection in healthy hosts. Based on phenotypic and genotypic analyses, B cepacia is divided into 9 genomovars that constitute the B cepacia complex (BCC).

Symptoms reported by a 55-year-old: ['Night sweat', 'fever', 'Bruising', 'weight loss', 'shortness of breath', 'tiredness', 'painless swelling']

Disease Name: Burkitt's Lymphoma, symptoms: ['Night sweat', 'fever', 'Bruising', 'weight loss', 'shortness of breath', 'tiredness', 'painless swelling'], Treatment: ['Burkitt lymphoma is usually treated with a number of different chemotherapy drugs and a targeted immunotherapy drug called rituximab (Mabthera).\nDrug combinations for Burkitt lymphoma include:\n\nR-CODOX-M (rituximab, cyclophosphamide, vincristine, doxorubicin, and methotrexate)', 'You might have radiotherapy:\n\nto relieve symptoms if your lymphoma is pressing on an organ, causing a blockage (obstruction)\nbefore a stem cell or bone marrow transplant'], Pathophysiology: The MYC family is composed of regulator genes and oncogenes that encode transcription factors that regulate the cell cycle. Translocations of the c-MYC gene on chromosome 8 is the hallmark of BL, occurring in approximately 95% of cases. The t(8;14)(q24;q32) is the most common translocation in BL, occurring in 70% to 80%. The MYC oncogene is relocated to be juxtaposed to the promoter sequence of the immunoglobulin IgG heavy chain (IgH) gene leading to constitutive activation of MYC. Other translocations include t(2;8)(p12; q24) and t(8;22)(q24; q11). The collocation of the MYC oncogene to the heavy chain (14q32), kappa light chain (2p12) or lambda light chain (22q11) of the immunoglobulin gene results in the dysregulation of the MYC. The presence of an MYC rearrangement is not specific for BL.In addition to the characteristic translocation of c-MYC, many gene mutations have been identified, including truncating mutations of ARID1A, amplification of MCL1, truncating alterations of PTEN, NOTCH, and ATM; amplifications of RAF1, MDM2, KRAS, IKBKE, deletion of CDKN2A, and CCND3 activating mutations. In normal B-cells, MYC overexpression causes apoptosis via a p53-dependent pathway. In the neoplastic cells of BL, it is not uncommon for tumor suppressor gene TP53 to be mutated., Epidemiology:['Burkitt lymphoma is more common in males than females.', '3 to 6 cases per 100,000 children annually.', 'VARIABLE', 'There is no known prevention for Burkitt’s lymphoma. Using protection (condoms) during sex and avoiding intravenous drug use can effectively prevent HIV infection, which is associated with immunodeficiency-related Burkitt’s lymphoma.'], Complications:[], Diagnostics:['Complete Blood Count CBC', 'LDH', 'LYMPH NODE BIOPSY', 'PET SCAN', 'CT'], Differential diagnosis:['diffuse large B cell lymphoma'], disease description:Burkitt lymphoma (BL) is an aggressive non-Hodgkin B-cell lymphoma. The disease is associated with Epstein Barr virus (EBV), human immunodeficiency virus (HIV), and chromosomal translocations that cause the overexpression of oncogene c-myc. The World Health Organization (WHO) classifies BL into three clinical groups: endemic, sporadic and immunodeficiency-related. The endemic form is linked to malaria and EBV. The immunodeficiency-related variant is associated with HIV and to a lesser extent, organ transplantation.  With intense chemotherapy treatment disease prognosis is excellent in children but poor in adults.

Person aged 46 with manifestations like ['Oral irritation', 'burning sensation in the mouth', 'Numbness']

Disease Name: Burning Mouth Syndrome, symptoms: ['Oral irritation', 'burning sensation in the mouth', 'Numbness'], Treatment: [{'medication': ['Clonazepam', 'paroxetine', 'Gabapentin']}, 'Reassurance and highlighting that the symptoms are real\n•\t Sialogogue and oral lubricant\n•\t Clonazepam 1 mg sucked slowly has been shown to be \neffective in a randomized controlled trial lasting for 2 \nweeks. However, the tablets are small and difficult to suck. \nPatients often end up swallowing the tablets and hence getting exposed to systemic effects of the drug \n•\tLidocaine gel topically\n•\tBenzydamine mouth wash'], Pathophysiology: Burning mouth syndrome is most likely a form of neuropathic pain and a variety of hypotheses have been postulated. It is known that some individuals have increased numbers of taste buds (so- called supertasters). It is proposed that for patients with BMS, neuropathic changes inside the taste neuronal connections induce the burning sensation by removing the inhibitory control on somatic small-fibre afferents . BMS may be related to damage to the chorda tympani during the removal of wisdom teeth. Also, there is, according to some authors, evidence of neuropathic changes in the mucosa and/or in the central nervous system. The genetics of BMS are currently unknown., Epidemiology:['prevalence is about 1%', 'very difficult to establish the incidence', 'The prognosis is very variable. Spontaneous remiss', "There's no known way to prevent burning mouth syndrome. But you may be able to reduce your discomfort by not using tobacco, limiting acidic or spicy foods, not drinking carbonated beverages, and using stress management methods. Or these measures may prevent your discomfort from feeling worse."], Complications:['Dryness', 'taste disturbances'], Diagnostics:['Complete Blood Count CBC', 'BLOOD GLUCOSE', 'allergy skin test'], Differential diagnosis:['anemia', 'Aphthous stomatitis', 'candidiasis', 'GASTRO OESOPHAGEAL REFLUX DISEASE', 'gastrointestinal disorders', 'Geographic Tongue', 'Hypothyroidism', 'leukoplakia', 'Multiple Sclerosis', 'rheumatoid arthritis', 'scleroderma', 'Sjogren’s Syndrome', 'VITAMIN DEFICIENCIES'], disease description:Burning mouth syndrome (BMS) is a sensation of continuous burning, often accompanied by taste changes for which no dental or systematic cause can be found and in which there are no gross clinical signs.Burning mouth syndrome is a disorder particularly encountered in perimenopausal women. In general, there are no abnormal clinical signs and, as a consequence, it is poorly understood by health care professionals. Burning mouth syndrome most frequently affects middle-aged and older patients

Suffering from ['Tachycardia', 'compartment syndrome', 'Scarring', 'Fluid imbalance', 'severe pain', 'eschar formation', 'acute respiratory distress syndrome'] at 38

Disease Name: Burns, symptoms: ['Tachycardia', 'compartment syndrome', 'Scarring', 'Fluid imbalance', 'severe pain', 'eschar formation', 'acute respiratory distress syndrome'], Treatment: ['Open method with application of silver sulfadiazine without any \ndressings, used commonly in burns of face, head and neck. \nClosed method is with dressings done to soothen and to \nprotect the wound, to reduce the pain, as an absorbent. \nTangential excision of burn wound with skin grafting can be \ndone within 48 hours in patients with less than 25% burns. \nIt is usually done in deep dermal burn wherein dead dermis \nis removed layer by layer until fresh bleeding occurs. Later \nskin grafting is done', 'Admit the patient. \nMaintain airway, breathing, circulation (ABC). Emergency \nendotracheal intubation may be required in early period itself; \nin such situation succinylcholine should not be used. \nAssess the percentage, degree, and type of burn. \nKeep the patient in a clean environment. \nSedation and proper analgesia. \nPatient should be placed in burns unit (ideally air-conditioned) with barrier nursing, sterile clothes, bed sheets with \nall aseptic methods.', "Formulas to calculate the fluid replacement: \nATLS-10th-Edition\nAdults and older\nchildren (=14 years old)\n2 ml LR x kg x % TBSA\nChildren (<14 years old) 3 ml LR x kg x % TBSA\nInfants and young\nchildren (=30kg)\n3 ml LR x kg x % TBSA\nPlus a sugar-containing solution at\nmaintenance rate\nMaximum percentage considered is 50%. \nHalf the volume is given in first 8 hours, rest given in 16 \nhours. \nMuir and Burclay regime: For colloid after 12-24 hours. \n% Burns x Body weight in kg 1 R t· \n2 = a 10n \n3 Rations given in first 12 hours. \n2 Rations in second 12 hours. \n1 Ration in third 12 hours. \nB \n• Galveston regime (pediatric): \n5000 mUm2 burned+ 1500 mUm2 total \n• Modified Brooke formula: \nFirst 24 hours: RL: 4 ml/kg/% burns in 24 hours (first half in first \n8 hours) Colloid- none. \nSecond 24 hours: Crystalloids-to maintain urine output; \nColloids-0.3 ml to 0.5 ml/kg/burns in 24 hours; (Albumin in \nRl solution) (Albumin alone should be given with care if really \nindicated only}. \nEvan's formula: \nIn first 24 hours: Normal saline 1 mUkg/% burns; Colloids 1 mu \nkg/% burns; 5% dextrose in water, 2000 ml in adult. \nIn second 24 hours: Half of the volume used in first 24 hours."], Pathophysiology: Many things can cause a burn. Thermal sources, including fire, hot liquids, steam and contact with hot surfaces, are the most common causes of burns. Other causes include exposure to:Chemicals, such as cement, acids or drain cleaners.Radiation.Electricity.Sun (ultraviolet or UV light).• Thermal injury - Scald-spillage of hot liquids - Flame burns - Flash burns due to exposure of natural gas, alcohol, combustible liquids - Contact burns-contact with hot metals/objects/materials • Electrical injury • Chemical burns-acid/alkali • Cold injury-frost bite • Ionising radiation • Sun burns. Massive oedema in the body is due to altered pressure gradient because of the injury to basement membrane. Cardiac dysfunction is due to: Hypovolaemia. Release of cardiac depressants. Hormonal causes like catecholamines, vasopressin, angiotensins. Renal changes are due to: Release of ADH from posterior pituitary to cause maximum water reabsorption. Release of aldosterone from adrenals to cause maximum sodium reabsorption. Toxins released from the wound along with sepsis causes acute tubular necrosis. Myoglobin released from muscles (in case of electric injury or often from eschar) is most injurious to kidneys. Pulmonary changes are due to: Altered ventilation-perfusion ratio. Pulmonary oedema due to burn injury, fluid overload, inhalation injury. ARDS; Aspiration; Septicaemia. Metabolic Changes Hypermetabolic rate (BMR). Negative nitrogen balance; Electrolyte imbalance. Deficiencies of vitamins and essential elements. Metabolic acidosis due to hypoxia and lactic acid. I Sepsis in Burn Patient Focus may be at the burn site, catheter site, cannula/CVP line site, or respiratory infection. Low immunity, loss of proteins and immunoglobulins, loss of barrier causes sepsis. Opportunistic infection is also common. Associated conditions like diabetes, HIV infection, old age, respiratory diseases worsen the sepsis in burn injury. It may be local infection commonly by Staphylococcus aureus in early period, Pseudomonas, Candida, Aspergillus, herpes simplex virus in partial thickness nasolabial burns. It may be suppurative thrombophlebitis also. Systemic infection like pneumonia, bacteraemia, septicaemia can occur. Burns itself creates immunosuppression (cell-mediated immunity). Sepsis is identified by fever, lethargy, leucocytosis, thrombocytopenia., Epidemiology:['A total of 8,378,122 new cases (95% UI, 6,531,887–10,363,109cases) of burns were identified globally in 2019, which is almost evenly split between men and women, and most of the new cases were concentrated in the 10–19-year age group.', 'The estimated annual burn incidence in India is approximately 6-7 million per year.', 'depends on degree of burns', 'Burns have many accidental causes. You can take these steps to reduce the risk of burns:\n\nWear sunscreen.\nSet your home’s hot water heater below 120 degrees Fahrenheit.\nAlways test the water in a shower or bath before getting in or bathing a child.\nLock up chemicals, lighters and matches.\nUse the stove’s back burners as much as possible when cooking, turn handles of pots and pans where they won’t be bumped and don’t leave the stove unattended.\nDon’t hold a child when you’re near hot objects, such as the stove.\nSet safeguards around a fireplace and never leave a child unattended.\nInstall and regularly test smoke detectors in your home.\nStock your home with fire extinguishers and know how to use them.\nCover electrical outlets.'], Complications:['Bacterial infection'], Diagnostics:['Complete Blood Count CBC', 'Differential Leucocyte Count DLC', 'Total Leucocyte Count (TLC)', 'X RAY', 'COAGULATION PROFILE', 'Electrocardiography (EKG)'], Differential diagnosis:['Chemical burns', 'Sunburn'], disease description:Burns are tissue damage brought on by heat, chemicals, electricity, radiation or the sun. First-degree burns, and most second-degree burns, heal with at-home treatments. Third-degree burns can be life-threatening and require specialized medical care.1st-degree burn. This minor burn affects only the outer layer of the skin (epidermis). It may cause redness and pain.2nd-degree burn. This type of burn affects both the epidermis and the second layer of skin (dermis). It may cause swelling and red, white or splotchy skin. Blisters may develop, and pain can be severe. Deep second-degree burns can cause scarring.3rd-degree burn. This burn reaches to the fat layer beneath the skin. Burned areas may be black, brown or white. The skin may look leathery. Third-degree burns can destroy nerves, causing numbness.The Rule of Nines, also known as the Wallace Rule of Nines, is a tool used by trauma and emergency medicine providers to assess the total body surface area (TBSA) involved in burn patients. 

Symptoms at 26 years old: ['Tenderness', 'pain in elbow', 'Pain']

Disease Name: Bursitis, symptoms: ['Tenderness', 'pain in elbow', 'Pain'], Treatment: [{'medication': ['Hydrocortisone ']}, 'ANTI BACTERIAL DRUGS', 'excision of the bursa is required.'], Pathophysiology: two types. It is caused by excessive pressure or friction, occasionally due to a gouty deposit. Inflammation of the bursa results in the effusion of a clear fluid within the bursal sac. With prolonged inflammation, the sac gets thickened and may cause pressure erosion on the adjacent bone.Infective bursitis: Uncommonly, a bursa may get infected by a pyogenic or tubercular infection.It occurs commonly in trochanteric bursa or prepatellar bursa. Treatment is by surgical drainage and antibacterial drugs.. Prepatellar bursitis Housemaid's knee Infrapatellar bursitis Clergyman's knee Olecranon bursitis Student's elbow Ischial bursitis Weaver's bottom On lateral malleolus Tailor's ankle On great toe Bunion, Epidemiology:['GOOD'], Complications:[], Diagnostics:nan, Differential diagnosis:[], disease description:Inflammation may occur in a normally situated bursa or in an adventitious bursa. It may arise from mechanical irritation or from bacterial infection..

Symptoms at 54 years: ['exophytic and papillomatous pattern of growth', 'lymphadenopathy', 'growth on genitoanal region']

Disease Name: Buschke–löwenstein Tumour, symptoms: ['exophytic and papillomatous pattern of growth', 'lymphadenopathy', 'growth on genitoanal region'], Treatment: ['Topical, intralesional, or oral chemotherapy with fluorouracil (5-FU), podophyllin, cidofovir, interferon, and imiquimod, as well as systemic chemotherapeutic drugs e.g., bleomycin, cisplatin, and leucovorin have been used as neoadjuvant or adjuvant therapy and for treating tumor recurrences after surgery.Chemotherapy alone, however, has not shown promising results', 'laser treatment, interferon-a , radiotherapy or bleomycin have been deployed', 'Mohs surgery is the preferred technique as it allows tissue sparing while simultaneously enabling the surgeon to ensure tumor-free margins and spotting any SCC foci. If necessary, surgical defects can later be surgically reconstructed e.g., by using delayed split-thickness grafts. In most cases, GCBL recurrences are dealt with by radical surgery. Carbon dioxide/argon laser resection has also been used for recurrences.'], Pathophysiology: These terms have been used interchangeably for large verruciform tumours of the penis presenting with an exophytic and papillomatous pattern of growth. They are well differentiated, with low metastatic rate and better survival compared with usual squamous cell carcinoma. It is perhaps more accurate and more clinically useful to consider giant condyloma and the Buschke– Löwenstein tumour as synonymous or overlapping HPV-related entities. Verrucous carcinoma is HPV unrelated but associated with lichen sclerosus and more dangerous. The prognosis can be poor because verrucous carcinoma might continue to grow and invade locally, causing death by exsanguination from femoral arterial invasion or cachexia . Even with treatment, recurrence and progressive malignant transformation do occur so follow-up is necessary., Epidemiology:['0.1 %', 'poor', 'Instructions for patients in order to prevent or minimize further exposures to cadmium.\n\nStop smoking. Tobacco smoke contains cadmium and cadmium is absorbed into the system through the lungs.\nBe sure of adequate iron in the diet. People who are iron deficient will absorb more oral cadmium into their system.\nPractice good occupational hygiene if involved in work with cadmium or in hobbies involving cadmium exposure such as jewelry making or paints using cadmium.'], Complications:['Fistula', 'secondary infection'], Diagnostics:['BIOPSY FROM SKIN LESION'], Differential diagnosis:['ADENOCARCINOMA OF CERVIX', 'Genital warts', 'Hemorrhoids', 'Malignant melanoma', 'Squamous cell carcinoma', 'Syphilis'], disease description:Giant condylomata acuminata of Bushke-Löwenstein (GCBL) is a rare, slow-growing verrucous tumor of the penis and anogenital region which can grow up to twenty centimeters in size and can locally destroy contiguous structures. These terms have been used interchangeably for large verruciform tumours of the penis presenting with an exophytic and papillomatous pattern of growth. They are well differentiated, with low metastatic rate and better survival compared with usual squamous cell carcinoma. It is perhaps more accurate and more clinically useful to consider giant condyloma and the Buschke– Löwenstein tumour as synonymous or overlapping HPV-related entities. Verrucous carcinoma is HPV unrelated but associated with lichen sclerosus and more dangerous. Dramatic polypoid or cauliflower-like clinical lesions are encountered

A woman, 47 years old, with ['myalgia', 'fever with chills', 'hematemesis', 'Osteoporosis', 'diarrhea', 'nausea', 'respiratory problems', 'vomiting', 'hemoptysis', 'tenesmus'] issues

Disease Name: Cadmium Exposure, symptoms: ['myalgia', 'fever with chills', 'hematemesis', 'Osteoporosis', 'diarrhea', 'nausea', 'respiratory problems', 'vomiting', 'hemoptysis', 'tenesmus'], Treatment: ['The mainstay of management for most inhalation exposure victims is supportive treatment including\n\nfluid replacement,\nsupplemental oxygen, and\nmechanical ventilation.\nIn cases of ingestion, gastric decontamination by emesis or gastric lavage may be beneficial soon after exposure. Administration of activated charcoal has not been proven effective.'], Pathophysiology: Cadmium is known to increase oxidative stress by being a catalyst in the formation of reactive oxygen species, increasing lipid peroxidation, and depleting glutathione and protein-bound sulfhydryl groups. Cadmium also can stimulate the production of inflammatory cytokines and downregulates the protective function of nitric oxide formation., Epidemiology:['as high as 73.2% and much higher than 53% in U.S. general ..', 'variable', 'To Do : maintaining a clean work area free of dust,\nwashing hands well before smoking, eating, or drinking after work or during breaks. Not To Do : not tracking dust from the work area to the rest of the home,\nnot smoking in the work area,\nno eating or drinking in the work area, and'], Complications:['cardiomyopathy', 'gastroenteritis', 'kidney damage', 'Lung cancer', 'metabolic acidosis'], Diagnostics:['X RAY CHEST', 'LIVER FUNCTION TEST LFT', 'kidney function test KFT', 'SERUM ELECTROLYTE', 'BONE DENSITY'], Differential diagnosis:['acute respiratory distress syndrome', 'Arsenic poisoning', 'iron poisoning', 'Lead Poisoning', 'Mercury poisoning', 'pneumonitis'], disease description:Cadmium poisoning has been reported from many parts of the world. It is one of the global health problems that affect many organs and in some cases it can cause deaths annually. Long-term exposure to cadmium through air, water, soil, and food leads to cancer and organ system toxicity such as skeletal, urinary, reproductive, cardiovascular, central and peripheral nervous, and respiratory systems. Cadmium levels can be measured in the blood, urine, hair, nail and saliva samples. Patients with cadmium toxicity need gastrointestinal tract irrigation, supportive care, and chemical decontamination traditional-based chelation therapy with appropriate new chelating agents and nanoparticle-based antidotes.

Experiencing ['Slow growth rate', 'SOFT TISSUE SWELLING', 'Skin color changes.'] at 55 years old

Disease Name: Calcifying Aponeurotic Fibroma, symptoms: ['Slow growth rate', 'SOFT TISSUE SWELLING', 'Skin color changes.'], Treatment: ['. Treatment for this tumor consists of simple excision. There is a reasonably high incidence of local recurrence (approximately 50%) following excision. Local recurrence of this tumor is not destructive. Most recurrences are treated and cured by removal of the recurrent tumor. These lesions do not metastasize.'], Pathophysiology: Pathophysiologically, the condition is characterized by fibroblast proliferation with an indistinct border and calcification.CAF growth process is divided into two phases as follows. In the early phase, CAF is often not accompanied by calcification. In the latter phase, calcification and chondrocyte differentiation become clear., Epidemiology:['They usually occur in children and adolescents with a peak between the age of 5 and 15 years. Occasional cases in adults have been described. There is a male predilection 1-4.', 'occurs in the first or second decade of life', 'good', 'accurate preoperative diagnosis and complete excision are important to prevent the recurrence of the tumor after surgical removal.'], Complications:[], Diagnostics:['biopsy', 'MRI', 'USG'], Differential diagnosis:['ganglion cyst', 'Lipofibromatosis', 'Nodular fasciitis', 'Soft tissue chondroma', 'Synovial sarcoma'], disease description:Calcifying aponeurotic fibroma (CAF) is a rare benign tumor that typically develops in the fascia and tendons of young individuals. Pathologically, the condition is characterized by fibroblast proliferation with an indistinct border and calcification.

Symptoms at 28 years old: ['decreased appetite', 'fatigue', 'fever', 'weight loss', 'PAINLESS MASS', 'Asymptomatic', 'firm']

Disease Name: Calcifying Fibrous Tumour Giant Cell Angiofibroma, symptoms: ['decreased appetite', 'fatigue', 'fever', 'weight loss', 'PAINLESS MASS', 'Asymptomatic', 'firm'], Treatment: ['The majority of tumors tend to be indolent and slow-growing. Aggressive tumors occur at a rate of ~30% (range 10-57%) . Surgical resection is the treatment of choice .Chemotherapy and radiotherapy are used in the minority (<5%) of patients .', 'Surgical excision is the main treatment for patients with CFT.'], Pathophysiology: CFT originates from the subcutaneous and the deep soft tissue and macroscopically, it is a well-circumscribed, nonencapsulated mass, which has got a wide range of size and diameter (0.1–25cm) and can infiltrate the surrounding tissues. Microscopically, it is characterized by the presence of hypocellular, densely hyalinized collagen with psammomatous or dystrophic calcifications, a proliferation of (myo)fibroblastic spindle cells, mononuclear inflammatory infiltrate, and lymphoid aggregates such as focal plasmocytes, eosinophils, neutrophils, and mast cell infiltrations. Sometimes, lymph nodes can be found enlarged and positive for CFT., Epidemiology:['Calcifying fibrous tumor seems to have a female predilection (ratio 1:1.27).', '5th and 6th decades of life', 'variable'], Complications:['intraventricular haemorrhage', 'cognitive impairment'], Diagnostics:['biopsy', 'CT SCAN', 'immunohistochemistry'], Differential diagnosis:['fibromatosis', 'GASTROINTESTINAL STROMAL TUMORS', 'Inflammatory myofibroblastic tumour'], disease description:Calcifying fibrous tumor (CFT) is a rare benign lesion that is composed of abundant dense well-circumscribed hyalinized collagen with lymphoplasmatic infiltrate, spindle cells, lymphoid aggregates, and psammomatous or dystrophic calcifications.

Individual aged 26 dealing with ['Painful, often purpuric, areas on the lower abdomen, thighs or lower legs are the hallmarks of calciphylaxis', 'purpuric, ulcerating, necrotic, calcified plaques on the lower abdomen or thighs', 'livedo', 'NECROTIC LESIONS', 'lump on skin', 'ulceration', 'Purpuric skin lesions', 'painful lesions']

Disease Name: Calciphylaxis, symptoms: ['Painful, often purpuric, areas on the lower abdomen, thighs or lower legs are the hallmarks of calciphylaxis', 'purpuric, ulcerating, necrotic, calcified plaques on the lower abdomen or thighs', 'livedo', 'NECROTIC LESIONS', 'lump on skin', 'ulceration', 'Purpuric skin lesions', 'painful lesions'], Treatment: [{'medication': ['Sodium thiosulfate ']}, 'First line • Debride necrotic tissue', 'First line • Correct abnormalities of systemic calcium homeostasis • Optimize treatment of underlying renal/hepatic failure or malignancy • Treat septicaemia\n\nSecond line\n•\tIntravenous sodium thiosulphate (25 g three times per week)\n•\tThrombolysis and anticoagulation', 'Third line\n•\tParathyroidectomy'], Pathophysiology: The aetiology of calciphylaxis is uncertain. Abnormalities of systemic calcium homeostasis are common but not invariable. Coagulation abnormalities have been recorded, but not consistently. It is likely that the pathophysiology is multifactorial. It has been proposed that a final common pathway might be via receptor activator of nuclear factor b (RANK), RANK ligand and osteoprotogenerin, which appear to regulate extraskeletal mineralization. Parathyroid hormone, corticosteroids, aluminum, liver disease and various forms of inflammation can activate this system, which may have a role in calciphylaxis. Matrix Gla protein and fetuin A, which inhibit extraosseous calcification, may also be important. A potential role for warfarin could be explained by inhibition of vitamin K-dependent carboxylation of matrix Gla protein., Epidemiology:['prevalence of 4% and 1-year mortality of 45–80%', '35 cases per 10 000 patients in the United States', 'Calciphylaxis has a poor prognosis', 'Because the causes of calciphylaxis are not fully understood, it is harder to prevent it from happening. For that reason, healthcare providers often recommend minimizing use or exposure to sensitizers or triggers as much as possible. This includes things in your diet, personal care or hygiene items, medications, etc.'], Complications:['septicaemia'], Diagnostics:['HbA1c', 'Bacteria Culture Test', 'LIVER FUNCTION TEST LFT', 'biopsy', 'COAGULATION PROFILE', 'DOPPLER USG', 'skin lesion biopsy'], Differential diagnosis:['ANTIPHOSPHOLIPID SYNDROME', 'CELLULITIS', 'pyoderma gangrenosum', 'vasculitis'], disease description:Calciphylaxis is a life-threatening vasculopathy characterized by calcium deposition in the skin and subcutis both within vessels and in the surrounding tissues. Calciphylaxis is a serious, life-threatening thrombo-occlusive disorder most commonly seen in the setting of renal failure. The pathophysiology of this condition is poorly understood and there is no universally accepted treatment. Death usually results from either sepsis or systemic thrombosis.

Symptoms at 25: ['diarrhea', 'muscle pain', 'nausea', 'stomach cramps', 'LOW GRADE FEVER', 'vomiting']

Disease Name: Calicivirus Infection, symptoms: ['diarrhea', 'muscle pain', 'nausea', 'stomach cramps', 'LOW GRADE FEVER', 'vomiting'], Treatment: ["Oral rehydration solutions may be used. If you're not able to drink enough fluids to prevent dehydration", 'over-the-counter anti-diarrheal medication and medication to reduce nausea.'], Pathophysiology: Noroviruses are difficult to culture in a lab setting. Because of this, it has been difficult to predict exactly how norovirus infects and replicates in humans. Studies suggest that norovirus infection is multi-faceted, with the involvement of multiple cell types in the human gut. The predominant cell type lining the human gut is a single layer of intestinal epithelial cells called enterocytes. Lying deep to the enterocytes are numerous immune cells. Several studies have confirmed that norovirus infects and replicates in immune cells including macrophages, dendritic cells, and B cells. It is postulated that noroviruses have a way of bypassing enterocytes to enter the human hosts. Proposed mechanisms include entering through M cells, a specialized type of cell in the gut that overlies the Peyer patches and lymphoid follicles in the gut. M cells lack microvilli and do not secrete mucus, making it easier for the norovirus to enter the host and invade immune cells. However, although definitive data are lacking, other studies suggest norovirus may directly invade enterocytes lining the gut lumen. Furthermore, the role of the host’s pre-existing gut microflora in norovirus infection is being investigated. It has been proposed that norovirus interacts with bacteria in the gut to enhance infection and replication. The average time period from inoculation with the virus until clinical symptoms develop is 1.2 days, and symptoms of norovirus usually resolve within 1 to 3 days. Although symptoms may resolve, humans can continue to shed the virus in their stool for extended periods of time, up to 60 days in some cases. Immunocompromised patients can continue to shed the virus for months or years., Epidemiology:['estimated 21 million cases of gastrointestinal illness in the United States each year', 'incidence of norovirus to be 21,400 per 100,000 for children under 5 years of age', 'immunocompromised patients are at risk for increas', ".Wash your hands thoroughly with soap and water for at least 20 seconds.\n.Avoid contaminated food and water.\n.Cook seafood thoroughly.\n.Use caution when traveling. If you're traveling to areas with a high risk of norovirus infection,"], Complications:['Hemolytic Uremic Syndrome', 'hypokalemia', 'hyponatremia', 'metabolic alkalosis', 'Dehydration'], Diagnostics:['SEROLOGIC TEST', 'RAPID DIAGNOSTIC TEST', 'PCR for detection of virus in STOOL', 'PCR for detection of virus in vomitus'], Differential diagnosis:['Abdominal aortic aneurysm', 'ADENOVIRUS INFECTION', 'astrovirus infection', 'Bowel obstruction', 'Mesenteric ischemia', 'Norovirus infection', 'Pancreatitis', 'Pelvic Inflamatory Disease', 'recurrent urinary tract infections', 'ROTAVIRUS'], disease description:Noroviruses are nonenveloped, positive-sense, single-stranded RNA viruses belonging to the Caliciviridae viral family. The virus was first identified and named “Norwalk virus” when it was discovered as the cause of a 1968 outbreak of gastroenteritis in Norwalk, Ohio. Norovirus is a common cause of acute gastrointestinal illness worldwide. In developed countries with rotavirus vaccine programs, norovirus surpasses rotavirus as the most common cause of gastroenteritis in children. 

Person at 36 with manifestations like ['blisters', 'foot pain', 'thickened skin']

Disease Name: Callosities, Corns And Calluses, symptoms: ['blisters', 'foot pain', 'thickened skin'], Treatment: ['For soft corns, the use of a toe separator (felt, foam or silicone) \ncan provide rapid relief. Salicylic acid (10–20%) keratolytic preparations can be of some help.\n Extra \nwidth may be needed, especially with the toebox. A softer upper \nmay be needed. With marginal calluses, the shoe is likely to be too \nloose. The shoe may need to be adapted to receive an orthosis – a \ncushioning device designed to redistribute the mechanical forces \ncausing the callosity.', 'simple debridement in combination with a \ntopical application of 1% cantharidin, 30% salicylic acid and 5% \npodophyllin has been shown to treat calluses effectively, with a \n1.4% recurrence rate. This treatment, applied under occlusion, \nleads to blister formation in about 2 days, with the callus peeling off at day'], Pathophysiology: Calluses are due to lateral pressure combined with downward pressure on the skin, producing a reaction. If the process is too acute and severe, it exceeds the capacity of the skin to react and produces instead a blister, known as a “friciton blister.” The repeated friction and pressure of the skin overlying the bony prominences leads to a hyperkeratotic thickness. This latter is a protective body reaction that produces an excess of the horny epithelial layer to prevent skin ulceration. This explains the preferential location of corns next to the condyles of the metatarsals and phalanges, as well as the occurrence of corns in patients with a foot deformity., Epidemiology:['about 5% of people in the United States every year,', 'variable', 'Feet are an often overlooked part of the body until a problem develops. With a little bit of attention and care, most cases of corns or calluses can be prevented. Things to keep in mind include:\n\nWear shoes that are comfortable and fit well. Shoes should support your feet, be well-cushioned and have shock-absorbing soles. The toe area of shoes should have enough length and width so toes are not rubbing against the shoe or other toes. This would also mean avoiding high-heeled narrow-toed shoes that push the toes forward causing them to rub against the shoe or each other. Avoid hard-soled or leather-soled shoes unless they have enough padding (or you add padding) to cushion your feet.\nWear socks with your footwear. Make sure socks are snug enough that they don’t bunch up under your feet.\nUse cushioned or padded insoles. If you have had corns or calluses in the past, you may want to ask your doctor about customized insoles. These inserts can even out weight-bearing forces on the bottom of your foot to prevent calluses from forming. Also use lamb’s wool (not cotton) between your toes to relieve friction and soften corns.\nWear gloves when you are doing manual labor or working with heavy or rough materials that can damage the skin on your hands or fingers.\nInspect your feet daily and keep them clean. Wash your feet in warm soapy water, dry them and apply a moisturizing foot cream. This helps keep your skin soft and supple.\nKeep your toenails trimmed.\nDon’t walk barefoot.\nApply a daily foot powder to keep your feet dry if you have sweaty feet.'], Complications:['ulceration', 'osteomyelitis'], Diagnostics:['full thickness skin biopsy'], Differential diagnosis:['acanthosis nigricans', 'CALCINOSIS CUTIS', 'granuloma annulare', 'viral warts'], disease description:Corns and calluses are thick, hardened layers of skin that develop when the skin tries to protect itself against friction or pressure. They often form on feet and toes or hands and fingers. Calluses and corns on the feet are usually the result of deformity, sometimes associated with dynamic changes in the function of the foot. . They are often made worse or even caused by unsuitable footwear. Perhaps the most extreme example of footwear causing gross abnormalities is the Chinese foot-binding syndrome, although some western shoe fashions, such as ‘winkle-pickers’ and high- heeled shoes.

Individual, 37 years old, with ['diarrhea', 'stomach cramps', 'fever', 'vomiting']

Disease Name: Campylobacteriosis, symptoms: ['diarrhea', 'stomach cramps', 'fever', 'vomiting'], Treatment: ['Azithromycin (Zithromax, Zmax) is usually the first antibiotic your doctor will try.\nCiprofloxacin (Cetraxal, Ciloxan, Cipro) or levofloxacin (Levaquin) are other options.', 'Campylobacter infections are best treated with macrolide antibiotics'], Pathophysiology: Pathogenesis of Campylobacter jejuni show that for this organism to cause disease the susceptibility of the host and the relative virulence of the infecting strain are both important. Infection with C. jejuni results from the ingestion of contaminated food or water, and the infective dose can be as low as 800 organisms. To initiate infection the organism must penetrate the gastrointestinal mucus, which it does by using its high motility and spiral shape. The bacteria must then adhere to the gut enterocytes and once adhered can then induce diarrhoea by toxin release. C. jejuni releases several different toxins which vary from strain to strain, mainly enterotoxin and cytotoxins, and these correlate with the severity of the enteritis. During infection, levels of all immunoglobulin classes rise. Of these, IgA is the most important as it can cross the gut wall. IgA immobilises organisms, causing them to aggregate and activate complement, and also gives short-term immunity against the infecting strain of organism., Epidemiology:['800 to 1200 cases of Campylobacter are reported in Minnesota each year.', '1.3 million cases of Campylobacter infection each year in the United States alone.', 'variable', 'You can avoid getting food poisoning from Campylobacter with a bit of precaution. To avoid getting sick, wash your hands:\n\nAfter blowing your nose, coughing or sneezing.\nAfter using the toilet, changing diapers or cleaning up a child who used the bathroom.\nBefore and after taking care of someone who is sick.\nAfter petting cats and dogs or cleaning up their poop.\nAfter touching garbage.\nYou should disinfect toilets after use by someone who has diarrhea. If you have diarrhea, you should wash your hands frequently with warm, soapy water.\n\nWhen it comes to food safety, always wash your hands before handling food and after handling raw food. These tips also help:\n\nAvoid getting bacteria on other foods by using separate cutting boards for chicken/meat and vegetables.\nClean utensils and countertops with hot soapy water after contact with raw meat.\nCook meat (especially chicken) until there is no pink. If you go to a restaurant, send chicken back to the kitchen if it still has pink.\nDon’t drink water if you don’t know if it has been tested for purity — including water from streams.\nOnly drink pasteurized milk.'], Complications:['Irritable Bowel Syndrome', 'BARRETT ESOPHAGUS', 'Guillain-Barre Syndrome', 'paralysis'], Diagnostics:['STOOL CULTURE', 'RAPID DIAGNOSTIC TEST', 'PCR tests'], Differential diagnosis:['Clostridium difficile infection', 'Escherichia coli', 'inflammatory bowel syndrome', 'Shigellosis', 'viral gastroenteritis'], disease description:Campylobacteriosis is an infection caused by bacteria of the genus Campylobacter. These bacteria live in the intestines of healthy birds, and raw poultry meat commonly has Campylobacter on it. Campylobacter species represent one of the most common causes of bacterial diarrheal illness worldwide. According to the United States Centers for Disease Control, there are about 1.3 million cases of Campylobacter infection each year in the United States alone. This leads to an economic cost between $1.3 to 6.8 billion dollars annually in the United States .

Individual aged 24 dealing with ['spasticity', 'joint stiffness', 'poor weight gain', 'severe hypotonia', 'Gastroesophageal reflux disease (GERD)', 'contractures of tissue', 'persistent head lag', 'delayed milestones', 'Irritability', 'difficulty in swallowing', 'developmental delay', 'seizures', 'hypotonia']

Disease Name: Canavan Disease, symptoms: ['spasticity', 'joint stiffness', 'poor weight gain', 'severe hypotonia', 'Gastroesophageal reflux disease (GERD)', 'contractures of tissue', 'persistent head lag', 'delayed milestones', 'Irritability', 'difficulty in swallowing', 'developmental delay', 'seizures', 'hypotonia'], Treatment: ['No specific treatment is currently available.', 'Management included control of seizures, treatment for infection (if present), and follow up of growth index by the best feeding drive.'], Pathophysiology: The deficiency of the enzyme aspartoacylase leads to NAA accumulation in the brain, especially in white matter, and massive urinary excretion of this compound. Excessive amounts of NAA are also present in the blood and CSF. Brain biopsies of patients with Canavan disease show spongy degeneration of the myelin fibers, astrocytic swelling, and elongated mitochondria. There is striking vacuolization and astrocytic swelling in white matter. Electron microscopy reveals distorted mitochondria. As the disease progresses, the ventricles enlarge because of cerebral atrophy., Epidemiology:['1 in 6,400 to 13,500 people in the Ashkenazi Jewish population. T', 'most common in the Ashkenazi Jewish community', 'poor', 'You can’t prevent Canavan disease, but families can have DNA tests to see if they carry the genetic mutation. Both parents have to have the mutation in order for their baby to get the disease. Testing can help them make informed decisions about having children.'], Complications:['Swallowing defect'], Diagnostics:['CT BRAIN', 'MRI', 'NAA', 'Genotyping'], Differential diagnosis:['Adrenoleukodystrophy', 'ALEXANDER DISEASE', 'Metachromatic leukodystrophy (MLD)', 'PELIZAEUS-MERZBACHER DISEASE'], disease description:Canavan’s disease is a fatal illness that begins early in infancy and the major manifestation is white matter dysmyelination that are delineated as spongy degenerations.  Canavan disease is an autosomal recessive disorder. canavan disease is a neurological disorder in which the brain degenerates into spongy tissue full of small fluid-filled spaces. It is caused by a mutation in the ASPA gene which makes an enzyme called aspartoacylase. ?

Experiencing ['Irregular menstruation', 'pelvic pain', 'POSTCOITAL BLEEDING', 'pain during sex', 'FOUL SMELLING DISCHARGE'] at the age of 43, female

Disease Name: Cancer Cervix, symptoms: ['Irregular menstruation', 'pelvic pain', 'POSTCOITAL BLEEDING', 'pain during sex', 'FOUL SMELLING DISCHARGE'], Treatment: [{'medication': ['Ifosfamide /Isophosphamide', 'Cisplatin ', 'Carboplatin', 'Paclitaxel']}, 'Schauta’s operation', 'brachytherapy followed by external radiation', 'In Wertheim’s hysterectomy.\nIn Schauta’s vaginal hysterectomy (known as Mitra operation\nin India) and Taussig’s or laparoscopic lymphadenectomy.\nIn Primary radiotherapy.\nIn Combined surgery and radiotherapy. Injection of blue\ndye into the cervical tissue before surgery identifies\nlymph nodes. Negative sentinel lymph node (obturator\ngland) avoids pelvic lymphadenectomy.'], Pathophysiology: Cervical cancer begins when healthy cells in the cervix develop changes (mutations) in their DNA. A cell's DNA contains the instructions that tell a cell what to do.Healthy cells grow and multiply at a set rate, eventually dying at a set time. The mutations tell the cells to grow and multiply out of control, and they don't die. The accumulating abnormal cells form a mass (tumor). Cancer cells invade nearby tissues and can break off from a tumor to spread (metastasize) elsewhere in the body.It isn't clear what causes cervical cancer, but it's certain that HPV plays a role. HPV is very common, and most people with the virus never develop cancer. This means other factors — such as your environment or your lifestyle choices — also determine whether you'll develop cervical cancer., Epidemiology:['Prevalence rate is 2.3 million annually globally', '100,000 women develop invasive cancer every year', 'CANCEROUS', 'There are some things you can do to prevent cervical cancer. Receiving regular gynecological exams and getting Pap tests are the most important steps to take toward preventing cervical cancer. Other things you can do are:\n\nGet the HPV vaccine (if you are eligible).\nUse condoms or other barrier methods when you have sex.\nLimit your sexual partners.\nStop smoking and using tobacco products.'], Complications:['METASTASES AT DIFFERENT SITES'], Diagnostics:['HISTOPATHLOGY', 'PAP SMEAR', 'PCR For HPV', 'Colposcopy', 'PET SCAN', 'Sigmoidoscopy', 'biopsy', 'MRI', 'PROCTOSCOPY', 'CT SCAN', 'CYSTOSCOPY', 'FDG-PET', "SCHILLER'S IODINE TEST"], Differential diagnosis:['Cervicitis', 'endometrium carcinoma', 'Pelvic Inflamatory Disease', 'Primary melanoma', 'vaginitis'], disease description:Carcinoma of the cervix continues to be the most common genital cancer encountered in clinical practice in India (80%). Cervical cancer is cancer that starts in the cells of the cervix. The cervix is the lower, narrow end of the uterus (womb). The cervix connects the uterus to the vagina (birth canal). Cervical cancer usually develops slowly over time. Before cancer appears in the cervix, the cells of the cervix go through changes known as dysplasia, in which abnormal cells begin to appear in the cervical tissue. Over time, if not destroyed or removed, the abnormal cells may become cancer cells and start to grow and spread more deeply into the cervix and to surrounding areas.

A 46-year-old individual dealing with ['ear pain', 'Jaw pain', 'white patches on tongue & oral mucosa', 'soreness of mouth', 'red patch in mouth']

Disease Name: Cancer Floor Of Mouth, symptoms: ['ear pain', 'Jaw pain', 'white patches on tongue & oral mucosa', 'soreness of mouth', 'red patch in mouth'], Treatment: ['Small lesions without involvement of tongue, \nlingual gingiva or nodes can be treated by surgical excision \nor radiotherapy with equal results. Larger lesions with exten\x02sion to the tongue, gingiva or mandible require wide exci\x02sion including marginal or segmental mandibular resection. \nBlock dissection is indicated when cervical nodes show clini\x02cal evidence of metastases.'], Pathophysiology: The lesion is ulcerative or infiltrative type and spreads locally into the adjoining areas such as ventral aspect of the tongue, lingual gingiva, mandibular periosteum or deeply into the floor of mouth and submental space. Lymphatic metastases go to submandibular nodes. Lesions of the floor of mouth remain asymptomatic for a long time or cause soreness or irregularity in the floor of the mouth. A swelling in the submandibular region may be either due to obstructive enlargement of submandibular salivary gland or lymph node metastases and this may require differentiation., Epidemiology:['1 in 60 (1.7%) for men and 1 in 140 (0.71%) for women', '28-35% of all oral cancers.', 'POOR', 'Oral cancer can be prevented, and you can play an active role in preventing it. You can help prevent oral cancer with the following tips:\n\nIf you’re someone who smokes tobacco, chews tobacco or uses a water pipe, try stopping or cutting back. Talk to your doctor about smoking cessation programs.\nIf you’re someone who drinks alcohol, drink in moderation.\nRemember your sunscreen. Use UV-AB-blocking sunscreen on your face and sunblock.\nGet vaccinated for human papillomavirus.\nEat a well-balanced diet.\nHave regular dental check-ups. People between ages 20 and 40 should have an oral cancer screening every three years and annual exams after age 40.'], Complications:['vocal cord palsy', 'METASTASES AT DIFFERENT SITES'], Diagnostics:['biopsy', 'CT'], Differential diagnosis:['candidiasis', 'Erythroplakia', 'herpes labialis', 'HERPETIC GINGIVOSTOMATITIS', 'Human Papillomavirus Infections', 'LINGUAL THYROID', 'Lipoma', 'MEDIAN RHOMBOID GLOSSITIS', 'neurofibroma', 'RANULA', 'Salivary gland tumour'], disease description:Floor of the mouth cancer is a cancer that grows in the tissue under the tongue, near the lower jaw bone (mandible). Squamous cell carcinoma is the most common.  Typically, lesions start anteriorly near the opening of submandibular duct which may get obstructed, leading to enlargement of submandibular gland.

Person aged 51 with manifestations like ['lymphadenopathy', 'dysphagia', 'Halitosis', 'throat pain', 'hoarseness of voice', 'weight loss', 'stridor']

Disease Name: Cancer Larynx, symptoms: ['lymphadenopathy', 'dysphagia', 'Halitosis', 'throat pain', 'hoarseness of voice', 'weight loss', 'stridor'], Treatment: ['(b) Total laryngectomy\n3. Combined therapy. Surgery with pre- or postoperative\nradiotherapy\n4. Endoscopic resection with CO2 laser\n5. Organ preservation', '(a) Conservation laryngeal surgery\n(b) Total laryngectomy', 'Early Stage Laryngeal Cancer\n\nEarly-stage laryngeal cancers, inclusive of T1-2N0 disease, are treated successfully with a single, locally-directed treatment modality, whether local radiation therapy or surgery.\n\nT1-2N0 Glottic Cancer\n\nLocal radiation therapy or surgery is recommended, with a choice of modality highly dependent on provider experience and patient preference. Given the sparse lymphatic drainage of the true glottis, these modalities all share a common fundamental principle in that they only address the primary tumor. Level I data comparing the 2 approaches do not exist, but local control rates from retrospective experience are comparable between surgical approaches and RT. Voice-sparing surgery is an option in many, but not all, of these cancers. In one experience, total laryngectomy was the required surgical approach in 10% of T1 and 55% of T2 tumors. Other approaches include transoral laser excision, laryngofissure, and partial laryngectomy. Despite no randomized evidence comparing surgery and RT, there is randomized data demonstrating superior voice preservation with definitive RT versus transoral laser excision.\n\nT1-2N0, Selected T1-2N1/T3N0-1 Supraglottic Cancer\n\nSimilar to early-stage glottic cancers, supraglottic cancers can be managed with either larynx-sparing surgical or RT monotherapy, with demonstrated overall comparable efficacy. The major difference versus glottic cancers is the management of the neck given the risk of nodal metastases. Surgical approaches include endoscopic resection or partial supraglottic laryngectomy for T1-2 and low-volume T3 disease, with neck dissection often indicated T2 or T3 lesions. Adjuvant RT is given to many patients, with common indications including positive nodal disease, extracapsular extension, and positive margins. Definitive RT often entails the inclusion of at-risk cervical nodal stations, generally levels II to IV.\n\nLocally Advanced Laryngeal Cancers\n\nLocally-advanced cancers, inclusive of T3-4N1-3 disease, are more difficult to treat and typically involve combination therapy. These cancers, if surgically resectable, are not amenable to laryngeal preservation surgery, while definitive radiation concurrent with cisplatin chemotherapy remains an option for laryngeal preservation. In contrast to early-stage disease, the therapeutic approach to locally-advanced disease is based on level I evidence, with combined chemotherapy and radiation demonstrating both improved locoregional control and larynx-preservation. In the context of T4 disease, laryngectomy, and adjuvant RT has demonstrated similar locoregional control rates compared to chemoradiation and salvage surgery. Larynx-preserving chemoradiation is not recommended for T4 disease and associated with inferior survival.'], Pathophysiology: The vast majority of laryngeal cancers are well-differentiated squamous cell carcinoma. A minority of cases represent squamous cell variants, including verrucous carcinoma, sarcomatoid carcinoma, and neuroendocrine carcinoma. Verrucous and sarcomatoid carcinomas historically were regarded as radioresistant, though recent experience contradicts this notion. Patterns of spread depend on the location of the primary mass, and the inherent lymphatic supply at that location. Laryngeal cancers are divided into supraglottic, glottic, and subglottic subsites, with pathophysiology and treatment differing according to the subsite .The supraglottis is further subdivided into suprahyoid epiglottis, infrahyoid epiglottis, false vocal cords, aryepiglottic folds, and the arytenoids. Suprahyoid epiglottic tumors may grow exophytically and superiorly, at times becoming quite large before inducing symptoms. In other cases, they may invade inferiorly into the tip of the epiglottis and destroy associated cartilage. Lymphatic involvement is a pathologic hallmark of supraglottic cancers, in contrast to both glottic and subglottic cancers, with 55% of patients having clinical evidence of nodal metastasis at presentation, and 16% with contralateral involvement. In order of decreasing the risk of involvement, cancer principally spreads to levels II, II, and IV of the cervical nodal chain., Epidemiology:['3.29 new cases in males and 0.42 new cases in fema', 'ten times more common in males than in females (4.79% versus 0.47%', 'POOR', 'You can’t prevent all cancer. But you can lower your risk for developing cancer, including laryngeal cancer, with healthy behaviors:\n\nQuit smoking and avoid tobacco products.\nLimit alcohol consumption and get treatment for alcohol use disorder.\nEat a healthy diet.'], Complications:['mucositis'], Diagnostics:['biopsy', 'MRI', 'CHEST X RAY', 'CT SCAN', 'Indirect Laryngoscopy', 'Direct Laryngoscopy', 'Flexible Fiberoptic Laryngoscopy', 'Soft Tissue Radiograph', 'HISTORY TAKING'], Differential diagnosis:['BENIGN TUMORS', 'branchial cleft cyst', 'contact granuloma', 'HEMANGIOMA', 'HPV infection', 'laryngitis', 'Laryngocele', 'Sialadenitis', 'thyroglossal duct cyst'], disease description:Laryngeal cancer is cancer of the larynx, part of the throat. Cancer happens when specific cells grow uncontrollably. As the cells multiply, they invade and damage the body. In laryngeal cancer, these cancerous (malignant) cells start in the larynx (voice box).

Person aged 32 dealing with ['Complete destruction of the nail plate', 'most common is distal and lateral subungual onychomycosis', 'fragile small nails', 'nail discoloration', 'brittled nail']

Disease Name: Candida Onychomycosis, symptoms: ['Complete destruction of the nail plate', 'most common is distal and lateral subungual onychomycosis', 'fragile small nails', 'nail discoloration', 'brittled nail'], Treatment: [{'medication': ['Fluconazole ', 'Itraconazole ']}, 'In proven Candida onychomycosis, fluconazole or itraconazole \nproduce the best reponses.'], Pathophysiology: The pathophysiology of Candida onychomycosis involves the following processes:Nail Plate Invasion: Candida species invade the nail plate, which is composed of keratin. The invasion usually occurs through microscopic fissures or separations between the nail plate and the nail bed. Candida fungi can also enter the nail plate through trauma or damage to the nail, such as from injury or nail biting.Moisture and Warmth: Candida species thrive in warm, moist environments. Moisture and warmth provide an optimal environment for fungal growth and colonization. These conditions can be present in situations such as wearing tight shoes or socks for prolonged periods, excessive sweating, or inadequate drying of the feet or hands.Nail Plate Degradation: Candida fungi produce enzymes, such as proteases and keratinases, that break down and degrade the structural components of the nail plate, particularly keratin. This degradation weakens the nail plate, leading to thickening, discoloration, and deformity.Immune Response: The immune response to Candida onychomycosis varies depending on the individual's immune status. In individuals with intact immune function, the immune system mounts a response against the fungal infection, attempting to control and eliminate the Candida fungi. However, the immune response may not be fully effective in eradicating the infection, leading to persistent or recurrent episodes of onychomycosis.Predisposing Factors: Certain factors can increase the risk of Candida onychomycosis. These include underlying immunosuppression (e.g., HIV/AIDS, diabetes mellitus), peripheral vascular disease, chronic moisture exposure, nail trauma, poor hygiene, and frequent exposure to water or moist environments.Secondary Infection: In some cases, Candida onychomycosis can lead to secondary bacterial infection of the nail and surrounding tissues. The damaged nail plate and the presence of Candida create a favorable environment for bacterial colonization and infection., Epidemiology:['Prevalence estimates range from 1% to 8%,', '50% of all infections of the nails', 'good', 'There’s no way to guarantee you won’t get toenail fungus. But you can take several steps to help prevent it:\n\nAvoid going barefoot in communal areas such as public showers, locker rooms and swimming pools. Most people pick up fungus in these situations. It helps to wear flip flops in these public areas.\nIf you have a family member with foot fungus or nail fungus, try to use a different shower or wear flip flops in the shower to avoid coming in contact with it.\nTrauma due to accidental or aggressive clipping of the nails can turn into portals of entry for the fungus.\nClean your nail trimmer before using it.\nDon’t tear or rip your toenails on purpose.\nIf you have diabetes, follow all foot care recommendations from your healthcare provider.\nKeep your feet dry. Make sure to fully dry your feet after a shower.\nSoak toenails in warm water before cutting them. Or you can cut your nails after a shower or bath.\nTrim toenails straight across (don’t round the edges).\nWear shoes that fit correctly. They shouldn’t be too loose or tight around the toes.'], Complications:['sepsis', 'osteomyelitis'], Diagnostics:['FUNGAL CULTURE', 'MICROSCOPIC EXAMINATION with KOH'], Differential diagnosis:['adverse drug reaction', 'Contact dermatitis', 'ECZEMA', 'Hypothyroidism', 'Lichen Planus', 'psoriasis', 'yellow nail syndrome'], disease description:Candida onychomycosis is an infection of the nail plate caused by Candida species. Fungal nail infections, also known as “onychomycosis,” are very common. They may affect up to 14% of the general population. Fungal toenail infections are more common than fungal fingernail infections.

Person at 35 with ['nail tenderness', 'thick white pus may discharge', 'Nail dystrophy with buckling of the nail plate', 'nail discoloration', 'nail pain']

Disease Name: Candida Paronychia, symptoms: ['nail tenderness', 'thick white pus may discharge', 'Nail dystrophy with buckling of the nail plate', 'nail discoloration', 'nail pain'], Treatment: [{'medication': ['Fluconazole ', 'Itraconazole ']}, 'First line\n• Azole solution twice daily for 2–4 months depending on \nclinical response\n• Plus in chronic cases a medium strength topical steroid \napplied to the nail fold skin once daily\nOr\n• Itraconazole 100 mg daily for 1–2 months\n• Fluconazole 100 mg daily for 1–2 months\nSecond line\n• 4% thymol solution'], Pathophysiology: Candida species, not always C. albicans , can be isolated from the majority of cases of chronic paronychia. The yeast is thought to have an aetiological role in this condition, but bacteria and irritant or allergic contact dermatitis also play a part, although the contribution of each varies from patient to patient and with the chronicity of the disease. Predisposing factors: This condition is chiefly found among those whose hands are frequently immersed in water. In chefs and pastry cooks, the presence of organic debris such as flour and other carbohydrates may be equally important. Toenail folds are not usually affected. Some experimental confirmation of the role of Candida has been achieved by occluding the nail fold in the presence of the yeast, but fully developed, chronic paronychia has not been produced experimentally., Epidemiology:['Paronychia is more common in women than in men, with a female-to-male ratio of 3 to 1.', 'The incidence of chronic paronychia was highest among housewives (64%) i', 'good', 'To prevent paronychia:\n\nCare for the nails and the skin around the nails properly.\nAvoid damaging the nails or fingertips. Because the nails grow slowly, an injury can last for months.\nDo not bite or pick the nails.\nProtect the nails from exposure to detergents and chemicals by using rubber or plastic gloves. Gloves with cotton liners are best.\nBring your own manicure tools to nail salons. Do not allow the manicurist to work on your cuticles.'], Complications:['nail discoloration'], Diagnostics:['Gram Staining', 'FUNGAL CULTURE', 'Examination under Microscope'], Differential diagnosis:['CELLULITIS', 'Herpetic whitlow', 'Nail psoriasis', 'Onychomycosis', 'squamous cell carcinoma.'], disease description:Paronychia is an infection of the proximal and lateral fingernails and toenails folds, including the tissue that borders the root and sides of the nail. This condition can occur spontaneously or following trauma or manipulation. Paronychia is among the most common infections of the hand. Paronychia results from the disruption of the protective barrier between the nail and the nail fold, introducing bacteria and predisposing the area to infection. Acute paronychia is usually limited to one nail; however, if drug-induced, it can involve many nails.

Person, 28 years old, presenting ['erythema', 'DYSPAREUNIA', 'PRURITIS VULVA', 'vulval oedema']

Disease Name: Candidal Vulvo-vaginitis, symptoms: ['erythema', 'DYSPAREUNIA', 'PRURITIS VULVA', 'vulval oedema'], Treatment: [{'medication': ['Fluconazole ', 'Clotrimazole ', 'Miconazole']}, 'Acute candidal vulvovaginitis is treated with antifungal agents. Since most cases of candidal vulvovaginitis are secondary to C. albicans species, and since C. albicans does not have significant resistance to azole antifungals, these are the agents of choice for this disease. Antifungals may be taken orally as a single dose (fluconazole 150 mg) or can be applied intravaginally in a single day or 3-day regimens that are available over the counter. In patients with uncomplicated disease (those without immunosuppression or pregnancy who do not have recurrent candidal vulvovaginitis) either therapy is equally efficacious. Therefore, treatment decision may be made based on cost, patient preference, and drug interactions. If patients do not respond to standard therapy, cultures may be warranted to look for other species of candida, which are often resistant to azoles.\n\nPatients with complicated candidal vulvovaginitis, for example those patients who are .immunosuppressed, require longer therapy. Typically, therapy includes intravaginal azole therapy for at least 1 week, or oral treatment with fluconazole 150 mg (renally adjusted for CrCl <50 ml/min) once every 3 days for three doses. Patients with recurrent candidal vulvovaginitis may benefit from suppressive therapy with weekly oral fluconazole for 6 months. Pregnant patients should not be given oral antifungals. In these patients, a 7-day course of intravaginal therapy is appropriate. Fluconazole is considered safe in breastfeeding women.'], Pathophysiology: Candidal vulvovaginitis occurs when Candida species superficially penetrate the mucosal lining of the vagina and cause an inflammatory response. The dominant inflammatory cells are typically polymorphonuclear cells and macrophages. candida vulvovaginitis is a microbial disease and not all patients with detectable pathogen are symptomatic. Multiple risk factor and the imbalance in the protective vaginal defenses predispose patients to develop active disease. candida vaginal infections are more common in the reproductive age group because of the high concentration of estrogen as it increases the amount of gycogen in the vagina providing a carbon source for candida organisms to colonize . It also increases the adherence of candida to the vaginal epithelial cells., Epidemiology:['75% of women on at least one occasion over a lifetime.', '8% of women suffer recurrent candidal vulvovaginitis.', 'good', 'You can often prevent vaginal yeast infections by making a few lifestyle changes. These changes can include:\n\nNot douching — douching can kill bacteria that actually control fungus.\nAvoiding the use of feminine deodorants.\nNot using scented tampons or pads.\nChanging out of wet clothing, like bathing suits or gym clothes, as soon as you can.\nWearing cotton underwear and loose-fitting clothes.\nUsing water-based sexual lubricants.\nKeeping your blood sugar levels in a normal range if you have diabetes.'], Complications:['candidial infection'], Diagnostics:['VAGINAL SWAB CULTURE', 'MICROSCOPIC EXAMINATION OF TISSUE', "SABORAUD'S MEDIUM", "NICKERSON'S MEDIUM"], Differential diagnosis:['allergic reaction', 'Atopic dermatitis', 'Lichen simplex chronicus', 'Paget disease', 'psoriasis', 'Vulvodynia'], disease description:Vaginal complaints are common. Vulvovaginitis, or inflammation of the vulva and vagina, is most commonly secondary to infectious agents in reproductive-aged women. Candidal vulvovaginitis is responsible for about one-third of cases .Candida albicans causes vulvo-vaginitis and 75% of women will experience at least one episode. It is rare before menarche and is most prevalent in the third and fourth decades.

Individual aged 37 dealing with ['sore tongue', 'fever', 'skin infection', 'white patches on tongue & oral mucosa', 'painful intercourse', 'thick white discharge']

Disease Name: Candidiasis, symptoms: ['sore tongue', 'fever', 'skin infection', 'white patches on tongue & oral mucosa', 'painful intercourse', 'thick white discharge'], Treatment: [{'medication': ['Fluconazole ', 'Clotrimazole ']}, 'ANTI FUNGAL THERAPY ALONG WITH TOPICAL OINTMENTS'], Pathophysiology: Candida albicans cause thrush when normal host immunity is disturbed. The organism may overgrow on the oral mucosa causing desquamation of epithelial cells and accumulation of keratin, bacteria,  and necrotic tissue. This debris form a pseudo-membrane, which adheres closely to the mucosa. This membrane may rarely involve extensive areas of edema, ulceration, and necrosis of underlying mucosa .Neonates affected with thrush are usually colonized by C. albicans during passage through the affected vagina; with an active vaginal yeast infection, the chances of development of thrush in the neonate increase. There are three major routes by which Candida reaches the bloodstream: the most frequent route is via the gastrointestinal tract mucosal barrier, others being through an intravascular catheter and from a localized infection. Candida can pass into the bloodstream in neutropenic patients as well as in intensive care unit patients. They are also a part of the normal gut microflora, and any condition that may make a person immunocompromised can lead to candidiasis in the bloodstream. Candida growth of indwelling catheters, especially central lines, can occur at either the implantation site or the hub and lead to the next infection with Candida., Epidemiology:['20% IN AIDS,HOSPITAL PATIENTS', '25,000 cases of candidemia occur nationwide each year.', 'EXCELLENT', 'You can prevent candidiasis by:\n\nMaintaining good physical and oral hygiene.\nMinimizing unhealthy foods from your diet like refined carbohydrates and sugar.\nManaging your stress.\nTreating current medical conditions like diabetes, cancer or HIV.\nTalking with your healthcare provider about current medications you are taking that might cause candidiasis as a side effect.'], Complications:['death', 'Endocarditis', 'myocarditis', 'septicemia'], Diagnostics:['Gram Staining', 'FUNGAL CULTURE', 'BLOOD CULTURE', 'Examination under Microscope', 'PCR tests'], Differential diagnosis:['Abdominal Abscess', 'Aspergillosis', 'Cryptococcosis', 'erythema migrans', 'Erythroplakia', 'mucositis', 'Pustular psoriasis', 'septic shock'], disease description:Candida species as common human pathogens dates to the introduction of modern therapeutic approaches that suppress normal host-defense mechanisms. Of these relatively recent advances, the most important is the use of antibacterial agents that alter the normal human microbiota and allow nonbacterial species to become more prevalent in the commensal flora.

Suffering from ['borborygmi', 'MUSCLE WASTING', 'protein & electrolyte loss', 'CHRONIC DIARRHEA', 'vomiting', 'weight loss', 'Abdominal Pain', 'edema'] at the age of 51

Disease Name: Capillariasis, symptoms: ['borborygmi', 'MUSCLE WASTING', 'protein & electrolyte loss', 'CHRONIC DIARRHEA', 'vomiting', 'weight loss', 'Abdominal Pain', 'edema'], Treatment: ['Mebendazole 400 mg/day given in divided doses for 20 days for new\ncases and for 30 days for relapses of cases.\nAlbendazole has also been found effective in treating intestinal\ncapillariasis using the same dosage as Mebendazole.'], Pathophysiology: Capillariasis produces a progressive sprue-like illness. The intestinal capillariasis patients usually present watery diarrhea weight loss, abdominal pain, borborygmi, muscle wasting, weakness, edema and laboratory examination showed low levels of potassium and albumin in blood.Those patterns may result from C. philippinensis  secretion of a proteolytic substance or direct penetration of the intestinal wall that causes cellular injury and dysfunction .the destruction of the intestinal cell membrane may interrupt nutrient absorption that causes weight loss in intestinal capillariasis patients. Moreover, the intestinal cells’ destruction may lead to fluids, proteins and electrolytes loss because those intestinal cells are dysfunctional and cannot control fluids and electrolytes balance in the body that results in a low level of potassium and albumin in the blood of C. philippinensis infection patients., Epidemiology:['prevalences of 3–29%', 'good', 'In order to prevent both types of capillariasis, proper hygiene and disposal of fecal matter is important.\n\nSpecific latrines should be used that are both out of reach from animals and will not let fecal matter seep into the water or around the food supply.\nWashing your hands with soap and warm water after touching or working with soil and before handling food.\nTeach children the importance of washing hands to prevent infection.\nWash fruits and vegetables before eating them.\nDo not eat raw or undercooked fish.\nThe FDA recommends the following for fish preparation or storage to kill parasites.\n\nCooking\nCook fish adequately (to an internal temperature of at least 145° F [~63° C]).\nFreezing\nAt -4°F (-20°C) or below for 7 days (total time), or\nAt -31°F (-35°C) or below until solid, and storing at -31°F (-35°C) or below for 15 hours, or\nAt -31°F (-35°C) or below until solid and storing at -4°F (-20°C) or below for 24 hours.'], Complications:['cardiomyopathy', 'death', 'CACHEXIA'], Diagnostics:['STOOL ROUTINE/MICROSCOPIC', 'Intestinal Biopsy', 'SEROLOGIC TEST', 'STOOL EXAMINATION'], Differential diagnosis:['CHRONIC DIARRHEA', 'malabsorption syndrome'], disease description:Capillariasis is a parasitic disease in humans caused by two different species of capillarids: Capillaria hepatica and Capillaria philippinensis. C. hepatica is transferred through the fecal matter of infected animals and can lead to hepatitis. C.

Suffering from ['blue/black discoloration of the palate'] at 34

Disease Name: Capillary Hemangiomas, symptoms: ['blue/black discoloration of the palate'], Treatment: ['SURGICAL EXCISION'], Pathophysiology: Haemangiomas are the most common benign tumours of the parotid in children, predominantly affecting females. Most of them are discovered at birth, grow rapidly in the neonatal period and then involute spontaneously. Cutaneous haemangioma may coexist in 50% of the patients. They are soft and painless and increase in size with crying or straining. Overlying skin may show bluish discoloration. Surgical excision is indicated if they do not regress spontaneously., Epidemiology:nan, Complications:[], Diagnostics:['PHYSICAL EXAMINATION'], Differential diagnosis:[], disease description:Haemangiomas are the most common benign tumours of the parotid in children, predominantly affecting females. Most of them are discovered at birth, grow rapidly in the neonatal period and then involute spontaneously. Cutaneous haemangioma may coexist in 50% of the patients. They are soft and painless and increase in size with crying or straining. Overlying skin may show bluish discoloration. Surgical excision is indicated if they do not regress spontaneously.

A baby with ['Psychosis', 'convulsion', 'headache', 'lethargy', 'vomiting', 'refusal to eat', 'Body temperature dysregulation', 'respiratory difficulties', 'Feeding Difficulty', 'sleepiness', 'coma'], 4.69 years old

Disease Name: Carbamoyl Phosphate Synthetase Deficiency, symptoms: ['Psychosis', 'convulsion', 'headache', 'lethargy', 'vomiting', 'refusal to eat', 'Body temperature dysregulation', 'respiratory difficulties', 'Feeding Difficulty', 'sleepiness', 'coma'], Treatment: [{'medication': ['Sodium chloride ', 'Glucose/Dextrose', 'Sodium benzoate']}, 'Provide adequate calories, fluid'], Pathophysiology: Mutations in the CPS1  gene cause carbamoyl phosphate synthetase I deficiency. The CPS1 gene provides instructions for making the enzyme carbamoyl phosphate synthetase I. This enzyme participates in the urea cycle, which is a sequence of biochemical reactions that occurs in liver cells. The urea cycle processes excess nitrogen, generated when protein is broken down by the body, to make a compound called urea that is excreted by the kidneys. The specific role of the carbamoyl phosphate synthetase I enzyme is to control the first step of the urea cycle, a reaction in which excess nitrogen compounds are incorporated into the cycle to be processed.Carbamoyl phosphate synthetase I deficiency belongs to a class of genetic diseases called urea cycle disorders. In this condition, the carbamoyl phosphate synthetase I enzyme is at low levels (deficient) or absent, and the urea cycle cannot proceed normally. As a result, nitrogen accumulates in the bloodstream in the form of toxic ammonia instead of being converted to less toxic urea and excreted. Ammonia is especially damaging to the brain, and excess ammonia causes neurological problems and other signs and symptoms of carbamoyl phosphate synthetase I deficiency., Epidemiology:['1 : 1,300,000', 'Carbamoyl phosphate synthetase I deficiency is a rare disorder; its overall incidence is unknown. Researchers in Japan have estimated that it occurs in 1 in 800,000 newborns in that country.', 'variable', "This condition is inherited in an autosomal recessive pattern and therefore it can't be prevented. \nGenetic Counselling is advisable."], Complications:['death'], Diagnostics:['ammonia level', 'Urine orotic acid level', 'glutamine', 'alanine', 'citrulline', 'Arginine'], Differential diagnosis:['Argininosuccinate lyase deficiency/Argininosuccini', 'Citrullinemia type I (CTLN1)', 'Genetics of Methylmalonic acidemia', 'Genetics of Propionic acidemia', 'migraine', 'N-acetylglutamate synthetase deficiency'], disease description:CPS1 and NAGS deficiencies are inherited as an autosomal recessive trait;Carbamoyl phosphate synthetase I deficiency is an inherited disorder that causes ammonia to accumulate in the blood (hyperammonemia). Ammonia, which is formed when proteins are broken down in the body, is toxic if the levels become too high. The brain is especially sensitive to the effects of excess ammonia.

At the age of 52, symptoms like ['failure to thrive', 'Hypoglycaemia', 'neurological disturbances', 'hypotonia', 'developmental delay']

Disease Name: Carbohydrate Deficient Glycoprotein Syndrome, symptoms: ['failure to thrive', 'Hypoglycaemia', 'neurological disturbances', 'hypotonia', 'developmental delay'], Treatment: ['Occupational therapy, physical therapy, and speech therapy should be instituted. As the developmental gap widens between children with CDG and their unaffected peers, parents, educators, and therapists need continued counseling and support.', 'Oral infusion of mannose can be effective in type Ib disease.'], Pathophysiology: Over 130 types of CDG have been reported to date. Given the ubiquitous presence of glycosylation pathways, CDG are extremely diverse in their biochemical pathogenesis. Numerous proteins and lipids (i.e., sphingolipids and glycolipids) undergo glycosylation with monosaccharides and/or oligosaccharides, collectively termed glycans, in different cellular compartments. Their subcellular locations are diverse, but most defects occur within the ER or Golgi apparatus.Amongst proteins, glycans are described by their linkage to the polypeptide chain—N-glycans are attached to the amide group of asparagine while O-glycans are attached to the hydroxyl group of either serine or threonine. N-glycan synthesis requires the stepwise construction of nucleotide-linked sugars in the cytosol, assembly in the endoplasmic reticulum, and processing in the Golgi apparatus. In contrast, O-glycan synthesis requires assembly but no processing, therefore O-glycosylation defects occur predominantly in the Golgi apparatus., Epidemiology:['5:100,000 to 0.06:100,000 births worldwide', 'more than 1,000 individuals, but the real frequency is probably much higher.', 'variable', 'Not To Do : Acetominophen and other agents metabolized by the liver should be used with caution.'], Complications:['deep venous thrombosis', 'immunosuppression', 'renal compilcations'], Diagnostics:['biopsy', 'molecular genetic testing'], Differential diagnosis:['congenital malformation (a birth defect)', 'Metabolic disturbances', 'myopathy'], disease description:Carbohydrate-deficient glycoprotein syndrome consists of a group of disorders with multisystemic involvement and prominent neurologic symptoms. The full clinical spectrum continues to evolve, with four types currently recognized; type I is by far the most common. The clinical presentation of CDGS appears more severe in infants than in adults. Diagnosis is based on the clinical findings of characteristic fat distribution, neurologic impairment, and developmental delay, combined with the biochemical finding of cathodally migrating serum glycoproteins, transferrin in particular, on isoelectric focusing.

A 21-year-old suffering ['small fiery coal, and describes the painful hard red lump that is the initial stage of the infection', 'fever', 'It is at first smooth, dome-shaped and acutely tender.', 'malaise', 'pus formation']

Disease Name: Carbuncle, symptoms: ['small fiery coal, and describes the painful hard red lump that is the initial stage of the infection', 'fever', 'It is at first smooth, dome-shaped and acutely tender.', 'malaise', 'pus formation'], Treatment: ['After incision and drainage, oral antibiotics are typically initiated; this is of particular importance if the patient has any systemic symptoms or if there is any surrounding cellulitis. Common first-line oral antibiotics include dicloxacillin and cephalosporins. If MRSA is suspected or cultured, oral antibiotics such as clindamycin, tetracyclines, trimethoprim-sulphamethoxazole, linezolid, or glycopeptide may be used. Oral antibiotics can be further adjusted once bacterial culture sensitivities are known.\n\nTopical antibiotics such as clindamycin or mupirocin may be used as adjunctive therapy.Once the carbuncle has receded, it usually does not require further treatment. However, in recurrent or refractory cases, the lesion may need to be surgically excised.', 'Carbuncles are usually incised and drained (I&D), in-office, and under local anesthesia. The I&D is usually performed with a #11 scalpel blade, curette, and iodoform packing strips. The #11 blade is used to make an incision into the carbuncle cavity and pressure is manually applied to express the purulent material within. Bacterial culture and sensitivity are usually obtained from the purulent material at this step. Next, a curette or hemostat is used to break up any loculations that may be present, and another attempt to express material is made. Once the majority of purulent material has been expelled, the lesion is typically packed with iodoform strips or gauze to assist with further drainage. The packing is typically left in place for 24 to 48 hours and then removed.'], Pathophysiology: The term carbuncle is derived from the Latin word for a small fiery coal, and describes the painful hard red lump that is the initial stage of the infection. It is at first smooth, dome-shaped and acutely tender. It increases in size for a few days, to reach a diameter of 3–10 cm or occasionally more. Suppuration begins after some 5–7 days, and pus is discharged from the multiple follicular orifices. Necrosis of the intervening skin leaves a yellow slough surmounting a crateriform nodule. In some cases, the necrosis develops more acutely without a preliminary follicular discharge, and the entire central core of the lesion is shed, to leave a deep ulcer with a purulent floor. Most lesions are on the back of the neck, the shoulders or the hips and thighs, and although usually solitary, may be multiple or associated with one or more furuncles. Constitutional symptoms may accompany, or even precede by some hours, the development of the carbuncle. Fever may be high, and malaise and prostration may be extreme if the carbuncle is large or the patient’s general condition poor. In favourable cases, healing slowly takes place to leave a scar. In the frail and ill, death may occur from toxaemia or from metastatic infection., Epidemiology:['he incidence of boil or abscess was 450 per 100 000 person-years and increased slightly over the study period', 'GOOD', 'A boil or carbuncle can happen despite the best hygiene. However, you can prevent boils if you:\n\nAvoid close contact with someone who has a staph infection, boil or carbuncle.\nWash your hands frequently with antibacterial soaps and gels, which can help prevent the spread of bacteria.\nBathe regularly with soap.\nDon’t share or reuse washcloths, towels and sheets.'], Complications:['septicaemia', 'scar'], Diagnostics:['Microbiological skin swabs'], Differential diagnosis:['Anthrax', 'Arthropod bites', 'CELLULITIS', 'hidradenitis suppurativa', 'ORF', 'osteomyelitis'], disease description:A carbuncle is a deep infection of a group of contiguous follicles with S. aureus, accompanied by intense inflammatory changes in the surrounding and underlying connective tissues, including the subcutaneous fat. Introduction and general description Carbuncles tend to be larger than abscesses/boils as they represent a cluster of coalescing boils connected under the skin surface. Carbuncles usually occur in otherwise healthy individuals but are more common in the presence of diabetes, malnutrition, cardiac failure, drug addiction or severe generalized dermatoses, obesity and during prolonged steroid therapy. Patients who are S. aureus carriers in the anterior nares are also at greater risk of developing a carbuncle than non-carriers. Generally, carbuncles are not common as demonstrated in a military setting where carbuncles/furuncles accounted for only 6% of bacterial skin infections in the US armed forces compared to cellulitis accounting for about 50%. Carbuncles occur predominantly in middle or old age. Males are more commonly affected than females.

Person, 32 years old, presenting ['diarrhea', 'flushing', 'pruritus', 'Rashes', 'Tachycardia', 'tremor', 'fever', 'Abdominal Pain', 'anxiety', 'breathlessness', 'delusion', 'palpitations', 'SKIN LESIONS', 'wheezing']

Disease Name: Carcinoid Syndrome, symptoms: ['diarrhea', 'flushing', 'pruritus', 'Rashes', 'Tachycardia', 'tremor', 'fever', 'Abdominal Pain', 'anxiety', 'breathlessness', 'delusion', 'palpitations', 'SKIN LESIONS', 'wheezing'], Treatment: [{'medication': ['Octreotide ']}, 'There are different treatment modalities for carcinoid syndrome, which include somatostatin analogs, liver-directed treatment therapy, surgical debulking for early-stage low-grade neuroendocrine tumors, and chemotherapy for the treatment of poorly differentiated neuroendocrine tumors or refractory carcinoid syndrome', 'Surgery plays a vital role in the treatment of carcinoid syndrome with or without metastases. If possible, always consider surgical resection of the primary tumor as well as nodal and liver metastases to reduce the tumor burden.'], Pathophysiology: The pathophysiology of carcinoid syndrome is based on biologically active amines and peptides entering the systemic circulation and escaping the first-pass metabolism of the liver. Usually, these bioactive products are inactivated in the liver. However, in the cases of neuroendocrine tumors with liver metastasis, either these bioactive products directly enter into the systemic circulation, or they are not inactivated due to deranged liver function.Less frequently, carcinoid syndrome can occur without liver metastasis in conditions, such as primary gut tumor with widespread retroperitoneal nodal metastases, ovarian tumor, or bronchial carcinoid, which release bioactive amines directly into the systemic circulation., Epidemiology:['only about 10% will develop carcinoid syndrome.', '1.5-1.9 clinical cases per 100,000 population. The incidence in autopsy cases is higher at 650 cases per 100,000 population.', 'poor', 'While you can’t prevent carcinoid syndrome, you can take steps to prevent a serious form of carcinoid syndrome called carcinoid crisis.'], Complications:[], Diagnostics:['CT Abdomen', 'MRI Abdomen', 'urine analysis for serotonin', 'serum protein chromogranin A', 'urinary 5HIAA level', 'plasma serotonin level', 'serum 5HT level', 'platlet serotonin level', 'plasma neuron spesific anolase'], Differential diagnosis:['Anaphylaxis', 'angioedema', 'CELIAC DISEASE', 'Irritable Bowel Syndrome', 'Urticaria'], disease description:Carcinoid syndrome refers to a number of symptoms caused by the release of humoral factors such as polypeptides, prostaglandins, and biogenic amines. These are mostly released from neuroendocrine tumors that are well-differentiated and were previously known as carcinoid tumors. These tumors start in cells that make certain chemicals, and they release more of those chemicals into your bloodstream.

Symptoms reported at the age of 43: ['chest pain', 'nausea', 'rectal bleeding', 'vomiting', 'weight gain', 'PURPLE SKIN STRIAE', 'wheezing', 'shortness of breath', 'diarrhea', 'Flushing of the skin', 'Abdominal Pain', 'rectal pain']

Disease Name: Carcinoid Tumors, symptoms: ['chest pain', 'nausea', 'rectal bleeding', 'vomiting', 'weight gain', 'PURPLE SKIN STRIAE', 'wheezing', 'shortness of breath', 'diarrhea', 'Flushing of the skin', 'Abdominal Pain', 'rectal pain'], Treatment: ["Chemotherapy uses strong drugs to kill tumor cells. It can be given through a vein in your arm or taken as a pill. Chemotherapy is sometimes recommended for treating advanced carcinoid tumors that can't be removed with surgery.", 'Octreotide (Sandostatin, Bynfezia Pen) and lanreotide (Somatuline Depot) are given as injections under the skin. Side effects from either medication may include abdominal pain, bloating and diarrhea. Telotristat (Xermelo) is a pill that is sometimes used in combination with octreotide or lanreotide to further try to improve the symptoms of carcinoid syndrome.', 'When detected early, a carcinoid tumor may be removed completely using surgery. If carcinoid tumors are advanced when discovered, complete removal may not be possible. In some situations, surgeons may try to remove as much of the tumor as possible, to help control signs and symptoms.'], Pathophysiology: Carcinoid tumors are commonly classified based on their embryologic origins and the vascular supply of the GI tract into the foregut, midgut, and hindgut carcinoids. Functional carcinoids can secrete various vasoactive substances such as serotonin, histamine, tachykinins, and prostaglandins. Presentation with carcinoid syndrome usually indicates underlying hepatic metastatic disease, indicating a loss of the ability of the liver to inactivate these substances, but foregut carcinoids can release vasoactive amines directly into the systemic circulation and can present with carcinoid syndrome without liver metastases. Embryonic hindgut carcinoids are rarely associated with a hormonal syndrome ., Epidemiology:['1.5-1.9 clinical cases per 100,000 population', 'within the gastrointestinal tract, nearly 45% of carcinoids arise in the small intestine, making this the most common location for carcinoid tumors', 'poor', 'There aren’t any known ways to prevent carcinoid tumors. But scientists suspect smoking increases the risk of this type of cancer. Avoiding tobacco products or quitting smoking may help prevent the disease.'], Complications:['Carcinoid syndrome', 'Cushings syndrome'], Diagnostics:['PET SCAN', 'biopsy', 'ENDOSCOPY', 'MRI', 'X RAY', 'CT SCAN'], Differential diagnosis:['Anaphylaxis', 'angioedema', 'Mastocytosis', 'medullary carcinoma', 'Tumor lysis syndrome', 'Urticaria'], disease description:?Carcinoid tumors are rare, slow-growing neuroendocrine tumors arising from the enterochromaffin cells disseminated throughout the gastrointestinal and bronchopulmonary systems. Though they have been traditionally classified based upon the embryologic site of origin, morphologic pattern, and silver affinity, newer classification systems have been developed to emphasize the considerable clinical and histopathologic variability of carcinoid tumors found within each embryologic site of origin. 

A 19-year-old patient with ['jaundice', 'yellowish discoloration of eyes', 'Thrombophlebitis migrans', 'color of urine', 'epigastric pain', 'light coloured stool', 'loss of appetite', 'nausea', 'pruritus', 'scratch marks', 'steatorrhoea', 'Pain', 'weight loss', 'DARK URINE', 'diarrhea']

Disease Name: Carcinoma Of The Pancreas, symptoms: ['jaundice', 'yellowish discoloration of eyes', 'Thrombophlebitis migrans', 'color of urine', 'epigastric pain', 'light coloured stool', 'loss of appetite', 'nausea', 'pruritus', 'scratch marks', 'steatorrhoea', 'Pain', 'weight loss', 'DARK URINE', 'diarrhea'], Treatment: ['his method uses drugs that kill cancer cells', 'High-speed energy used to kill the cancer cells.', 'pancreatectomy'], Pathophysiology: Pancreatic cancer can be of adenocarcinoma origin, serous, seromucinous, or mucinous .More than 85% of pancreatic cancers are ductal adenocarcinomas. The remaining tumours constitute a variety of pathologies with individual characteristics. Endocrine tumours of the pancreas are rare. Ductal adenocarcinomas arise most commonly in the head of the gland. They are solid, scirrhous tumours , characterised by neoplastic tubular glands within a markedly desmoplastic fibrous stroma. Cystic tumours of the pancreas may be serous or mucinous. Serous cystadenomas are typically found in older women, and are large aggregations of multiple small cysts, almost like bubble wrap. They are benign. Mucinous tumours, on the other hand, have the potential for malignant transformation. They include mucinous cystic neoplasms (MCNs) and intraductal papillary mucinous neoplasms (IPMNs). MCNs are seen in perimenopausal women, show up as multilocular thick-walled cysts in the pancreatic body or tail, and, histologically, contain an ovarian-type stroma. IPMNs are more common in the pancreatic head and in older men, but an IPMN arising from a branch duct can be difficult to distinguish from an MCN., Epidemiology:['2–3% of all cancers', '10 cases per 100 000 population per year in UK', 'Poor', 'Don’t smoke. If you do smoke or use tobacco in any form, try to quit.\nTry to reach and maintain a normal weight by eating healthy and exercising.\nTry to avoid getting diabetes. If you have it, control your blood sugar levels'], Complications:['jaundice', 'Delayed gastric emptying'], Diagnostics:['CECT Abdomen', 'Endoscopic USG', 'ERCP', 'MRI Abdomen', 'USG ABDOMEN(W/A)', 'LIVER FUNCTION TEST LFT', 'MR ANGIOGRAPHY', 'TRANSDUODENAL FNA', 'TRANSGASTRIC FNA', 'TRUCUT BIOPSY', 'PERCUTANEOUS TRANSPERITONEAL BIOPSY', 'DIAGNOSTIC LAPAROSCOPY', 'LAPROSCOPIC USG', 'SERUM CA 19-9 LEVEL'], Differential diagnosis:['ANNULAR PANCREAS', 'CHOLANGIOCARCINOMA', 'cholecystitis', 'CHOLEDOCHAL CYST', 'Chronic Pancreatitis', 'GASTRIC CANCER', 'PEPTIC ULCER DISEASE'], disease description:Pancreatic cancer occurs when changes (mutations) in the pancreas cells lead them to multiply out of control. A mass of tissue can result. Sometimes, this mass is benign (not cancerous). In pancreatic cancer, however, the mass is malignant (cancerous).

Person at 29 with manifestations like ['Pain', 'dysuria', 'hematuria', 'Suprapubic pain', 'increased frequency of urination', 'painless heamaturia']

Disease Name: Carcinoma Bladder, symptoms: ['Pain', 'dysuria', 'hematuria', 'Suprapubic pain', 'increased frequency of urination', 'painless heamaturia'], Treatment: [{'medication': ['Cisplatin ', 'Methotrexate', 'Vinblastine suphate', 'Doxorubicin']}, 'Endoscopic surgery,Radiotherapy\nEXTERNAL BEAM RADIOTHERAPY'], Pathophysiology: UC develops via two distinct pathways, the first relates to papillary lesions, and the second relates to flat lesions. Copy number alterations and genetic instability correlate with tumor progression and poorer prognosis. Low-grade papillary tumors usually arise from simple hyperplasia and/or minimal dysplasia and are characterized by loss of heterozygosity (LOH) of chromosome 9 and activating mutations of fibroblast growth factor receptor 3 (FGFR3), telomerase reverse transcriptase (TERT), phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit alpha isoform (PIK3CA) and inactivating mutations of STAG2. Low-grade papillary non-muscle-invasive BC can progress to muscle-invasive BC as a result of gaining CDKN2A loss. Muscle-invasive BC arises from flat dysplasia or carcinoma in situ (CIS); the lesions show TP53 mutations and LOH of chromosome 9.  , Epidemiology:['about 61,700 in men and 19,480 in women', 'incidence of BC is twice as high in developing countries compared to developed countries', 'POOR', "there's no guaranteed way to prevent bladder cancer\n.Don't smoke\n.take caution around chemicals. \n.Choose a variety of fruits and vegetables."], Complications:['erectile dysfunction', 'URETHRAL STRICTURE', 'urine leakage'], Diagnostics:['CT Abdomen', 'Endoscopic USG', 'ERCP', 'HIDA Cholescintigraphy', 'MRCP', 'TISSUE BIOPSY', 'USG ABDOMEN(W/A)', 'X RAY ABDOMEN', 'MRI', 'CHOLENGIOGRAPHY', 'PERCUTANEOUS TRANSHEPATIC CHOLANGIOGRAPHY(PTC)', 'LAPROSCOPIC USG', 'CHOLEDOCHOSCOPY'], Differential diagnosis:['BENIGN PROSTATIC HYPERPLASIA', 'BLADDER DIVERTICULA', 'BLADDER EXSTROPHY', 'BLADDER OUTLET OBSTRUCTION', 'BLADDER STONE', 'CARCINOMA PROSTATE', 'hemorrhagic cystitis', 'PROSTATIC CALCULI', 'RENAL ECTOPIA', 'Urinary Tract Infection'], disease description:Bladder cancer is a relatively rare form of cancer that starts in the lining of your bladder. Your bladder is a small hollow organ that holds your pee (urine). Healthcare providers have many ways to treat bladder cancer, including surgery to remove bladder cancer.

Symptoms at 50 years: ['bleeding', 'trismus', 'Pain', 'swelling in mouth']

Disease Name: Carcinoma Buccal Mucosa, symptoms: ['bleeding', 'trismus', 'Pain', 'swelling in mouth'], Treatment: ['Radiotherapy to primary lesion \nand also nodes if bone is not involved', 'Stage I (T1N0). Surgical excision.\n(b) Stage II (T2 N0). (i) Radiotherapy to primary lesion\nand also nodes if bone is not involved. (ii) If bone\n(maxilla/mandible) is involved or growth infiltrates\nthe muscle, surgery is the treatment of choice. It involves\nexcision of the growth, marginal or segmental\nmandibulectomy (or partial maxillectomy) and reconstruction\nof the area with skin or mucosal flaps.\n(c) Stage III and IV. Surgical resection, reconstruction with\nskin and/or myocutaneous flaps and postoperative radiotherapy\nto the site of lesion and nodes. Surgical\nresection is combined with neck dissection if nodes\nare clinically palpable'], Pathophysiology: Most common site is the angle of mouth or the line of occlusion of upper and lower teeth. It may also arise from the buccal sulcus where “pan” or tobacco quid is kept. As the whole of buccal mucosa is “condemned,” carcinoma may be multicentric. Gross appearance. Lesion may be exophytic or ulceroinfiltrative; the latter may infiltrate deeply. Exophytic type may be associated with erythroleukoplakia . Buccal mucosa is also the most common site for verrucous carcinoma which is a white papillary growth with considerable keratinization. From its site of origin, the lesion may spread deeply involving submucosa. Involvement of buccinator muscle or anterior masseter causes trismus. Tumour may spread radially from its site of origin and involve angle of the mouth and lip anteriorly, retromolar trigone and medial pterygoid posteriorly, upper gingivobuccal sulcus and maxilla superiorly, lower gingivobuccal sulcus and alveolar ridge and gums inferiorly. Lymphatic spread. Nodal involvement occurs in about 50% of cases. Submandibular and later the upper jugular nodes may get involved. Upper jugular nodes may also be involved, directly skipping the submandibular group... Stage I (T1N0). Surgical excision. (b) Stage II (T2 N0). (i) Radiotherapy to primary lesion and also nodes if bone is not involved. (ii) If bone (maxilla/mandible) is involved or growth infiltrates the muscle, surgery is the treatment of choice. It involves excision of the growth, marginal or segmental mandibulectomy (or partial maxillectomy) and reconstruction of the area with skin or mucosal flaps. (c) Stage III and IV. Surgical resection, reconstruction with skin and/or myocutaneous flaps and postoperative radiotherapy to the site of lesion and nodes. Surgical resection is combined with neck dissection if nodes are clinically palpable ., Epidemiology:['approximately 10% of oral cancer cases diagnosed in the United States', 'poor', 'You can prevent buccal mucosa cancer by avoiding heavy alcohol use, quitting smoking and discontinuing use of other tobacco products.\n\nRoutine dental visits can also help you detect any changes in the lining of your mouth early, when cancer is most treatable.'], Complications:['dysphagia'], Diagnostics:['Prothrombin Time Test and INR (PT/INR)', 'Complete Blood Count CBC', 'LIVER FUNCTION TEST LFT', 'biopsy', 'CT SCAN', 'PHYSICAL EXAMINATION'], Differential diagnosis:['adenoid cystic carcinoma', 'Erythroplakia', 'leukoplakia', 'Metastatic tumours', 'MUCOEPIDERMOID CARCINOMA', 'squamous cell carcinoma.', 'Verrucous carcinoma'], disease description:Buccal mucosa cancer is a rare cancer that develops in the inner cheek in your mouth. It’s a type of head and neck cancer .The buccal mucosa extends from the inside of your lips and cheeks to just behind your last teeth. It’s a soft, wet mucous membrane that’s made up of several layers of tissue.

Symptoms reported at the age of 20: ['anemia', 'constipation', 'diarrhea', 'rectal bleeding', 'Abdominal Pain']

Disease Name: Carcinoma Colon, symptoms: ['anemia', 'constipation', 'diarrhea', 'rectal bleeding', 'Abdominal Pain'], Treatment: ['5 fluorouracil (5 FU) with folinic acid (leucoverin/LV) is the \nmost commonly used regime for 6 months as monthly cycles. \nFolinic acid potentiates the action of 5 FU. \nLevamisole 150 mg/day for 3 days given once in 15 days for \none year with intravenous 5 FU monthly for one year. \nlrinotecan/5 FU/LV-IFL regime is also used. \nFolinic acid (LV)/5 FU/oxaliplatin-FOLFOX regime is also \nused. It is becoming treatment of choice.', 'Right radical hemicolectomy with ilea-transverse \nanastomosis is done.\n An extended right hemicolectomy is the procedure done \nfor transverse colon growth which includes division \nof right colic.\nLeft radical hemicolectomy is done, where in left ½ of \ntransverse colon and descending colon is removed along \nwith lymph nodes.'], Pathophysiology: The transformation of the normal colonic epithelium to a precancerous lesion (adenoma) and ultimately to invasive carcinoma requires an accumulation of genetic mutations either somatic (acquired) and/or germline (inherited). The theory of colonic carcinogenesis features a clonal mutation evolution that gives a cell survival-immortality advantage and allows to develop more mutations providing other cancer hallmarks as proliferation, invasion, metastasis, and others. Clinical evidence has shown that CRCs frequently arise from adenomatous polyps that typically acquire dysplastic changes in a 10 to 15-year period before developing invasive carcinoma, and the early detection-removal of polyps will reduce the incidence of CRC. New evidence has exposed that hamartomatous and serrated polyps could lead to CRC. There are three major molecular pathways linked to CRC, chromosomal instability, mismatch repair, and hypermethylation., Epidemiology:['about 1 in 23 (4.3%) for men and 1 in 25 (4.0%)', 'POOR', 'You may not be able to prevent colon cancer, but you can reduce your risk of developing the condition by managing risk factors:\n\nAvoid tobacco. If you smoke and want help quitting, talk to a healthcare provider about smoking cessation programs.\nUse moderation when you drink beverages containing alcohol.\nMaintain a healthy weight.\nEat a healthy diet. Add fruit and vegetables to your diet and cut back on red meat processed foods, and high-fat and high-calorie foods. Drinking coffee may lower your risk of developing colon cancer.\nKeep track of your family medical history. Colon cancer can run in families. Tell your healthcare provider if your biological parents, siblings or children have colon cancer or an advanced polyp or if any of your family has cancer before age 45.\nFollow colon cancer screening guidelines. Ask your healthcare provider when you should have colon cancer screening. If you have chronic irritable bowel disease or a family history of colon cancer, your healthcare provider may recommend you start screening earlier than age 45.'], Complications:['Bowel obstruction', 'Metastasis'], Diagnostics:['STOOL CULTURE', 'Barium Imaging', 'colonoscopy'], Differential diagnosis:['Arteriovenous malformation', 'Crohn disease', 'Ileus', 'PAPILLOMA AND ADENOMA', 'Ulcerative Colitis'], disease description:Colon cancer develops from certain polyps or growths in the inner lining of your colon. Healthcare providers have screening tests that detect precancerous polyps before they can become cancerous tumors. Colon cancer that’s not detected or treated may spread to other areas of your body. Thanks to screening tests, early treatment and new kinds of treatment, fewer people are dying from colon cancer.

A 34-year-old patient with ['dysphagia', 'lymphadenopathy', 'Dental pain', 'FACIAL PARALYSIS', 'Skin ulceration']

Disease Name: Carcinoma Ex Pleomorphic Adenoma, symptoms: ['dysphagia', 'lymphadenopathy', 'Dental pain', 'FACIAL PARALYSIS', 'Skin ulceration'], Treatment: ['Adjuvant chemotherapy may be required in cases with distant metastases', 'Adjuvant radiotherapy should be considered in some cases, including :\nPositive surgical margins\nAdvanced stage\nBone, perineural or lymphovascular invasion\nInvolved cervical lymph nodes', 'Surgical excision with negative surgical margins is the mainstay of treatment'], Pathophysiology: Earliest change is malignant transformation of ductal epithelial cells associated with dysfunctional p53 protein.Subsequent progression to intracapsular carcinoma, minimally invasive carcinoma and widely invasive carcinoma Associated with: HER2 amplification Loss of PLAG1 expressionMyoepithelial carcinomas may progress by different mechanisms, Epidemiology:['approximately 6% of pleomorphic adenomas', 'incidence rate of 0.17 tumours per 1 million persons', 'Noninvasive or minimally invasive carcinoma ex ple'], Complications:["FREY'S SYNDROME", 'facial nerve palsy'], Diagnostics:['MRI', 'immunohistochemistry', 'Histopathological examination'], Differential diagnosis:['adenoid cystic carcinoma', 'De novo carcinoma', 'MUCOEPIDERMOID CARCINOMA', 'MYOEPITHELIOMA', 'Recurrent pleomorphic adenoma', 'Squamous cell carcinoma'], disease description:Carcinoma ex pleomorphic adenoma (Ca ex PA) is a carcinoma arising from a primary or recurrent benign pleomorphic adenoma. It often poses a diagnostic challenge to clinicians and pathologists. This study intends to review the literature and highlight the current clinical and molecular perspectives about this entity. The most common clinical presentation of CA ex PA is of a firm mass in the parotid gland. The proportion of adenoma and carcinoma components determines the macroscopic features of this neoplasm

A 55-year-old suffering ['nausea', 'mass in right upper abdomen which is hard and nontender (gallbladder mass).', 'anorexia', 'jaundice', 'Pain in right hypochondrium', 'ascites']

Disease Name: Carcinoma Gall Bladder, symptoms: ['nausea', 'mass in right upper abdomen which is hard and nontender (gallbladder mass).', 'anorexia', 'jaundice', 'Pain in right hypochondrium', 'ascites'], Treatment: ['Immunotherapy:\nPembrolizumab is a type of PD-1 inhibitor that may be used in patients whose cancer is locally advanced and cannot be removed by surgery or has spread to other parts of the body.\nDurvalumab is a type of PD-L1 inhibitor that is being studied in combination with chemotherapy in previously untreated patients whose cancer is locally advanced, recurrent, or has spread to other parts of the body.', 'Targeted therapy\nTargeted therapy is a type of treatment that uses drugs or other substances to identify and attack specific cancer cells. The following targeted therapies are being studied in patients with gallbladder cancer that is locally advanced and cannot be removed by surgery or has spread to other parts of the body:\n\nIvosidenib is a type of targeted therapy that blocks a specific mutation in a gene called IDH1. It works by slowing or stopping the growth of cancer cells.\nPemigatinib is a type of targeted therapy that blocks specific changes in a gene called FGFR2. This may help keep cancer cells from growing and may kill them.', '1.Cholecystectomy with resection of liver segments IV and V extended cholecystectomy with perihepatic nodal clearance. \nAt least 2 cm margin in the liver from the gallbladder bed \nshould be cleared.\n2.Open approach rather than laparoscopic is ideal for \ncarcinoma gallbladder.\n3.Hemihepatectomy with cholecystectomy with nodal clearance. \nDuring laparoscopic cholecystectomy, any suspicious of GB \ncancer, procedure should be converted into open cholecystectomy'], Pathophysiology: Longstanding cholelithiasis and cholecystitis give rise to metaplastic changes (intestinal or pseudopyloric types) in the gallbladder mucosa .Metaplasia (especially intestinal type) gives rise to epithelial dysplasia and carcinoma in situ .Progression from dysplasia to advanced gallbladder carcinoma takes around 15 years .The current hypothesis establishes that chronic inflammation of the bile duct tissue accumulates successive genomic mutations that lead to malignant transformation. The most common mutations described are the oncogenes K-ras and tumor suppressors beta-catenin (CTNNB1). This condition progresses from pre-neoplastic dysplasia to carcinoma in situ and, ultimately, to invasive cancer, following roughly 15 years of inflammation. Squamous cell carcinoma is rare in the gallbladder., Epidemiology:['1.2% of all cancer diagnoses', '3 per 100000 people', 'poor 5-year survival rate', 'Gallbladder cancer can’t be prevented. You can do your best to avoid risk factors of gallbladder cancer. For example, you can work with your healthcare provider to maintain a healthy weight for you. Still, there’s no guarantee that your actions will prevent gallbladder cancer.'], Complications:['Obstructive jaundice'], Diagnostics:['USG ABDOMEN(W/A)', 'biopsy', 'MRI', 'CT SCAN', 'CHOLANGIOGRAPHY'], Differential diagnosis:['ACALCULOUS CHOLECYSTITIS', 'Biliary colic', 'cholangitis', 'cholecystitis', 'EMPYEMA OF GALL BLADDER', 'TORSION OF THE GALL BLADDER'], disease description:Gallbladder cancer is an abnormal growth of cells that begins in the gallbladder. Gallbladder cancer begins in the innermost layer of your gallbladder, called the mucosal layer, and spreads outward. It often doesn’t cause signs or symptoms in the early stages. Instead, healthcare providers often find the cancer by chance after gallbladder surgery.

Person at 51 years, dealing with ['bad breath', 'dysarthria', 'teeth pain', 'superficial ulcer with rolled out edges']

Disease Name: Carcinoma Hard Palate, symptoms: ['bad breath', 'dysarthria', 'teeth pain', 'superficial ulcer with rolled out edges'], Treatment: ['Treatment. Small tumours are resected along with the\nunderlying bone, larger ones require partial maxillectomy.\nIf nodes are enlarged, block dissection is also combined.\nSurgical defect in the palate, left after excision of\nthe growth, is closed by a suitable prosthesis'], Pathophysiology: ?Cancer starts as a superficial ulcer with rolled out edges and gives no symptoms except painless irregularity on the palate felt by the tongue. It may spread to the gingiva, lip. Palatal pathogenesis is associated with an accumulation of genetic mutations and epigenetic anomalies in signaling pathways that promote uncontrolled cellular proliferation and cancer development. The genetic mutations associated with oral SCC are most often attributed to cigarette smoke, alcohol, and human papillomavirus. Additional factors that may play a role in SCC development include oral microorganisms, vitamin deficiencies, immunosuppression, and environmental pollutants., Epidemiology:['about 1 to 5% of oral cavity malignancies are located on the hard palate', 'bout 1 in 60 (1.7%) for men and 1 in 140 (0.71%) for women.', 'GOOD', 'You may not be able to prevent hard palate cancer. However, you may be able to reduce your risk by avoiding certain activities that increase your risk of developing the condition:\n\nIf you smoke cigarettes or use smokeless tobacco, try to quit. Talk to a healthcare provider about programs to help you stop using tobacco.\nIf you regularly drink beverages that contain alcohol, try to limit how much and how often you drink. If you think you may have an issue with alcohol, ask a provider for help.\nEat a healthy diet that includes fruit and vegetables.\nHave regular dental checkups. People between 20 and 40 should have oral cancer screenings every three years and annual exams after age 40.'], Complications:['Speech Difficulties', 'METASTASES AT DIFFERENT SITES'], Diagnostics:['FNAC', 'CT'], Differential diagnosis:['cancer of maxillary antrum', 'cancer of nose', 'cancer of nose', 'Ewing sarcoma', 'Palatal Abscess', 'Pleomorphic adenoma'], disease description:Hard palate cancer is a type of head and neck cancer that begins when cells that make up the bony part of the roof of the mouth grow out of control and form lesions or tumors.The hard palate creates a barrier between the mouth and the nasal cavity. Cancers that develop there tend to spread into the nasal cavity when they become more advanced.

Person aged 24 dealing with ['fatigue', 'jaundice', 'DARK URINE', 'Abdominal Pain', 'palpable abdominal mass', 'splenomegaly', 'HEPATOMEGALY', 'PALPABLE GALLBLADDER', 'weight loss']

Disease Name: Carcinoma Head Of Pancreas, symptoms: ['fatigue', 'jaundice', 'DARK URINE', 'Abdominal Pain', 'palpable abdominal mass', 'splenomegaly', 'HEPATOMEGALY', 'PALPABLE GALLBLADDER', 'weight loss'], Treatment: ['Adjuvant chemotherapy using gemcitabine-better but \ncostly; dose is 1000 mg/m2 surface area; 5-fluorouracil; \nmitomycin; vincristine, cisplatin, docetaxel, leucoverin, \nabraxane (paclitaxel protein bound, oxaliplatin are used along \nwith gemcitabine. \n, Different regimes are--fOLFIRINOX (oxaliplatin (Elox\x02atin), irinotecan (Camptosar), leucovorin, fluorouracil); \nGemzar (gemcitabine) + Abraxane (albumin bound \npaclitaxel); Gemzar + erlotanib (Tarceva, EGFR drug). \nRadioactive iodine seeds 1\n125 to the field are on trial. External \nradiotherapy 4000 cGy units to relieve pain and to reduce the \ntumour size.', "1.Whipple's operation.\n2.Traverso-Longmire pylorus preserving pancreaticoduodenectomy.\n3.Fortner's regional pancreatectomy (extended Whipple's).\n4.Total pancreatectomy is presently said to be better. \n5.Roux-en· Y choledochojejunostomy is ideal palliative \nprocedure along with gastrojejunostomy after doing \ncholecystectomy.\n6.ERCP and stenting is done to drain bile."], Pathophysiology: Pancreatic cancer can be of adenocarcinoma origin, serous, seromucinous, or mucinous .Pancreatic cancer is a fatal malignancies which is predominantly seen in men and at advanced age (40-85 years) and has an aggressive course. Its frequency is gradually increasing over the past years. It accounts for 2% of all cancers and 5% of cancer-related deaths. Pancreatic cancer takes the first place among asymptomatic cancers. Ninety percent of cases are adenocarcinomas. Ten percent of the patients have a familial disposition. The disease is very difficult to detect as it has no early signs and spreads rapidly to surrounding organs is one of the most deadly types of cancer., Epidemiology:['incidence is 9 new cases per 100000 people. Mean age \nis 60-65 years.', 'Not good', 'Stop smoking. \nMaintain a healthy weight.\nDrink alcohol in moderation, or quit drinking altogether.\nUse safety equipment if your work exposes you to toxins.'], Complications:['Bowel obstruction', 'jaundice', 'Delayed gastric emptying'], Diagnostics:['CA 19.9', 'Hb', 'SERUM Creatinine', 'CT Abdomen', 'Endoscopic USG', 'ERCP', 'MRCP'], Differential diagnosis:['acute cholecystitis', 'CHOLANGIOCARCINOMA', 'cholangitis', 'Chronic Pancreatitis', 'GASTRIC CANCER', 'PEPTIC ULCER DISEASE'], disease description:Pancreatic cancer begins in the tissues of your pancreas — an organ in your abdomen that lies behind the lower part of your stomach. Your pancreas releases enzymes that aid digestion and produces hormones that help manage your blood sugar.Several types of growths can occur in the pancreas, including cancerous and noncancerous tumors. The most common type of cancer that forms in the pancreas begins in the cells that line the ducts that carry digestive enzymes out of the pancreas (pancreatic ductal adenocarcinoma).

Person at 47 years, dealing with ['diplopia', 'Halitosis', 'paraesthesia', 'proptosis', 'OPHTHALMOPLEGIA', 'weight loss', 'lymphadenopathy', 'epistaxis', 'facial pain', 'nasal congestion', 'nasal discharge']

Disease Name: Carcinoma Maxilla, symptoms: ['diplopia', 'Halitosis', 'paraesthesia', 'proptosis', 'OPHTHALMOPLEGIA', 'weight loss', 'lymphadenopathy', 'epistaxis', 'facial pain', 'nasal congestion', 'nasal discharge'], Treatment: ['Although the management of a node-negative neck remains controversial, the presence of cervical nodal metastasis decreases survival by 50% and warrants therapeutic neck dissection followed by adjuvant radiotherapy. Reconstructive options range from a nonbiologic obturator (a modified denture that extends to replace the resected tissue) to complex, microvascular, free-tissue transfer (composite fibula, scapula, deep circumflex iliac artery, or soft-tissue rectus transfer), depending on the extent of resection as well as patient factors.'], Pathophysiology: The pathogenesis of maxillary sinus cancer varies somewhat according to the site of origin within the antrum. Neoplasms of the suprastructure tend to spread into the nasal cavity, ethmoid air cells, orbit, pterygopalatine fossa , infratemporal fossa , and through the skull base into the middle cranial fossa . Tumors originating from the infrastructure can be difficult to distinguish from those of the upper gum and hard palate. Neoplasms of the infrastructure tend to spread into the palate, alveolar process, gingivobuccal sulcus, soft tissue of the cheek, nasal cavity, masseter muscle , pterygopalatine space, and pterygoid fossa., Epidemiology:['90% to 95% of all malignant neoplasms of the oral cavity', '0.44% OF ALL BODY CANCER IN INDIA', 'poor', 'It is not possible to completely prevent these cancers. However, the avoidance of risk factors may help to an extent. But it is important to know that even in the absence of these causative factors, a person may acquire a maxillary sinus cancer. However cessation of smoking and tobacco abuse can certainly help.'], Complications:['headache', 'lump on face'], Diagnostics:['LIVER FUNCTION TEST LFT', 'CT SCAN', 'SERUM FERRITIN LEVEL', 'SERUM CALCIUM LEVEL'], Differential diagnosis:['adenoid cystic carcinoma', 'Metastasis', 'MUCOEPIDERMOID CARCINOMA', 'Ossifying fibromyxoid tumour (incl. atypical / mal', 'osteosarcoma', 'squamous cell carcinoma.'], disease description:Oral SCC is typically associated with the mandible or the maxilla but will slowly invade the underlying tissues after onset. Invasive maxillary SCC will exhibit a multitude of clinical signs and symptoms, which might mimic facial pain syndromes, including TN. 

Symptoms reported by a 33-year-old female include ['breast ulcer', 'indrawing of nipple', 'Axillary lymphadenopathy', 'peau d’orange appearance of skin', 'nipple discharge', 'breast lump', 'supraclavicular lymphadenopathy', 'PLEURAL EFFUSION', 'breast pain']

Disease Name: Carcinoma Of Breast, symptoms: ['breast ulcer', 'indrawing of nipple', 'Axillary lymphadenopathy', 'peau d’orange appearance of skin', 'nipple discharge', 'breast lump', 'supraclavicular lymphadenopathy', 'PLEURAL EFFUSION', 'breast pain'], Treatment: [{'medication': ['Anastrozole ', 'Tamoxifen citrate ', 'Raloxifene Hydrochloride']}, 'Chemotherapy, hormone therapy, and targeted therapy are the systemic therapies used in breast cancer management. A 25 percent reduction in the risk of relapse over a 10 to 15-year period using a first-generation chemotherapy regimen such as cyclophosphamide, methotrexate, and 5-fluorouracil (CMF) in a 6-month cycle. Anthracyclines (doxorubicin or epirubicin) and the newer agents such as the taxanes are modern regimens used for breast cancer. Three to 6-month period is used for adjuvant and neoadjuvant chemotherapy. Adjuvant treatment of early-stage HR+ breast cancer with tamoxifen for at least 5 years has been shown to reduce the recurrence rate by about half throughout the first 10 years and reduces breast cancer mortality by about 30% throughout the first 15 years.\nThe mainstay of treatment for most premenopausal women with HR+ tumors is tamoxifen. Some women may also benefit from surgical removal (oophorectomy) or chemical suppression of the ovaries, which are the main source of estrogen before menopause. Treatment guidelines recommend aromatase inhibitors (AIs) such as anastrozole should usually be included in the treatment of postmenopausal women with HR+ breast cancer. Targeted therapy is usually indicated in about 17% of breast cancers that overproduce the growth-promoting protein HER2/neu. Trastuzumab, the first approved drug, is a monoclonal antibody that directly targets the HER2 protein. It reduces the risk of recurrence and death by 52% and 33%, respectively, if combined with chemotherapy in HER2+ early breast cancer if compared to chemotherapy alone.', 'Radiation therapy has a significant role in local disease control. The risk of cancer recurrence decreases by about 50% at 10 years, and the risk of breast cancer death reduces by almost 20% at 15 years when radiation therapy follows BCS. However, radiation is not necessary for women 70 years of age and older with small, lymph node-negative, hormone receptor-positive (HR+) cancers because it has not been shown to improve survival in patients who take hormonal therapy for at least 5 years. Radiation therapy is beneficial in large tumors (greater to 5 cm) or if the tumor invades skin or chest wall and if there are positive lymph nodes. It can also be used as palliative therapy in advanced cases, such as a central nervous system (CNS) or bone metastasis. It can be delivered as external beam radiation, brachytherapy, or a combination of both.', 'Excisional biopsy and frozen section followed by definitive\nsurgery as required\n-Lumpectomy\n- Simple mastectomy\n- Radical mastectomy\n- Postoperative radiotherapy and chemotherapy', 'Surgery has a major role in the treatment of breast cancer. It is the basic way to use for local control of the disease. Radical mastectomy of Halsted, which removed the breast with axillary lymph node dissection and excision of both pectoralis muscles, is no longer recommended due to the high rate of morbidity without a survival benefit. Now, the modified radical mastectomy of Patey is more famous. It entails removing the whole breast tissue with a large part of the skin and the axillary lymph nodes. The pectoralis major and minor muscles are preserved. Breast-only removal without axillary dissection is referred to as simple mastectomy. This procedure can be performed in small tumors with negative sentinel lymph nodes. Breast-conserving surgery (BCS) is aimed at removing the tumor plus a rim of at least 1 cm of normal breast tissue (wide local excision). A quadrantectomy involves removing the entire segment of the breast that contains the tumor. The last 2 procedures are usually combined with axillary clearance through a separate incision. Axillary procedures may include sentinel lymph node biopsy, sampling, partial (II), or complete (III) axillary lymph node dissection. Lumpectomy is the removal of a benign mass without excision of the normal breast tissue.'], Pathophysiology: Breast cancer develops due to DNA damage and genetic mutations that can be influenced by exposure to estrogen. Sometimes there will be an inheritance of DNA defects or pro-cancerous genes like BRCA1 and BRCA2. Thus the family history of ovarian or breast cancer increases the risk for breast cancer development. In a normal individual, the immune system attacks cells with abnormal DNA or abnormal growth. This fails in those with breast cancer disease leading to tumor growth and spread.Breast cancer can be invasive or non-invasive according to its relation to the basement membrane. Noninvasive neoplasms of the breast are broadly divided into two major types, lobular carcinoma in situ (LCIS) and ductal carcinoma in situ (DCIS)., Epidemiology:['One in twenty-eight Indian women is likely to develop breast cancer during her lifetime.', '13.5% of all cancer and around 10.6% of all deaths.', '80% SURVIVAL RATE IN 5 YEARS PROGNOSIS', 'While you can’t prevent breast cancer altogether, there are certain things you can do to reduce your risk of discovering it at an advanced stage. For example:\n\nGet routine mammograms. The American Cancer Society recommends having a baseline mammogram at age 35, and a screening mammogram every year after age 40.\nExamine your breasts every month after age 20. You’ll become familiar with the contours and feel of your breasts and will be more alert to changes.\nHave your breasts examined by a healthcare provider at least once every three years after age 20, and every year after age 40. Clinical breast exams can detect lumps that mammograms may not find.'], Complications:['fatigue', 'infection', 'neuropathy', 'permanent scarring'], Diagnostics:['mammography', 'MRI', 'CYTOLOGY', 'DOPPLER USG', 'BIMANUAL EXAMINATION'], Differential diagnosis:['ACUTE MYELOID LEUKEMIA', 'BREAST ABSCESS', 'Fibroadenoma'], disease description:Breast cancer is the commonest cancer in a woman and accounts for 10% of all breast problems presenting at the clinic. Breast cancer originates in your breast tissue. It occurs when breast cells mutate (change) and grow out of control, creating a mass of tissue (tumor). Like other cancer breast cancer can invade and grow into the tissue surrounding your breast. It can also travel to other parts of your body and form new tumors.?

Symptoms reported by a 30-year-old: ['lip ulcer', 'weight loss', 'bleeding', 'cervical lymphadenopathy']

Disease Name: Carcinoma Of Lip, symptoms: ['lip ulcer', 'weight loss', 'bleeding', 'cervical lymphadenopathy'], Treatment: ['Radiotherapy also gives good results in early cases.', 'surgical excision with adequate safety\nmargin of healthy tissue and plastic repair of the defect.\nLymph node metastases require block dissection'], Pathophysiology: Mostly, it is squamous cell carcinoma, often seen in males in the age group of 40–70 years. Lower lip is more often involved. Site of predilection is between the midline and commissure of the lip. Lesion is of exophytic or ulcerative type. Lymph node metastases develop late. Submental and submandibular nodes are the first to be involved; other deep cervical nodes may also get involved late.Squamous cell carcinoma is the commonest histological tumour type in lip cancers, followed by basal cell carcinoma. The most common non-mucosal form of lip cancer arises from tumours of the minor salivary glands, with in converse to mucosal lip cancer the upper lip being more commonly involved than the lower., Epidemiology:['overall prevalence of lip cancer is 1–2%', '13.5 per 100 000', 'POOR', 'Reduce your risk for lip cancer by avoiding common risk factors:\n\nDon’t smoke. Tobacco use is the leading risk factor for lip cancer and cancers of the mouth. If you smoke, consider quitting.\nAvoid heavy alcohol use. If you drink, do so in moderation.\nUse proper sun protection. Apply lip balm with SPF any time you’re outside and wear sunscreen daily to prevent other types of skin cancer.\nReduce your risk for HPV. Practice safe sex and consider getting an HPV vaccine.\nUndergo routine oral cancer screenings. Your primary care physician or your dentist can perform these screenings to ensure that no abnormalities have developed.'], Complications:['lymphadenopathy', 'Metastatic tumours'], Diagnostics:['biopsy', 'MRI', 'CT SCAN', 'PHYSICAL EXAMINATION'], Differential diagnosis:['Actinic cheilitis (solar cheilosis)', 'Basal cell carcinoma', 'Mucocele', 'pyogenic granuloma', 'Squamous cell carcinoma', 'viral warts'], disease description:Lip cancer occurs on the skin of the lips. Lip cancer can occur anywhere along the upper or lower lip, but is most common on the lower lip. Lip cancer is considered a type of mouth (oral) cancer.Most lip cancers are squamous cell carcinomas, which means they begin in the thin, flat cells in the middle and outer layers of the skin called squamous cells.

A 18-year-old with ['ulceration of gingiva', 'epistaxis', 'facial pain', 'trismus', 'nasal discharge', 'proptosis', 'Dental pain', 'nasal obstruction', 'nasal stuffiness', 'facial paraesthesias', 'epiphora']

Disease Name: Carcinoma Of Maxillary Sinus, symptoms: ['ulceration of gingiva', 'epistaxis', 'facial pain', 'trismus', 'nasal discharge', 'proptosis', 'Dental pain', 'nasal obstruction', 'nasal stuffiness', 'facial paraesthesias', 'epiphora'], Treatment: ['Chemoradiation is a treatment that gives chemotherapy along with radiation therapy. The chemotherapy drug most often used is cisplatin. It may be given after surgery if there are cancer cells in the tissue around the removed tumour.', "Radiation therapy may be offered before or after surgery. Radiation therapy may be given after surgery if:\n\nthe tumour can't be completely removed\ncancer cells are in the tissue around the removed tumour\ncancer cells are around or near a nerve", 'lateral rhinotomy and total\nethmoidectomy. If cribriform plate is involved, anterior\ncranial fossa is exposed by a neurosurgeon and total exenteration\nof the growth in one piece is accomplished by\nwhat is called craniofacial resection.', 'The type of surgery done is a maxillectomy. A maxillectomy is a surgery where the bone and the soft tissue lining (the mucosa) of the maxillary sinus are removed. Reconstructive surgery is done either at the same time as the surgery to remove the cancer or at a later time.'], Pathophysiology: There is no universally accepted classification for maxillary carcinoma. 1. Ohngren’s classification. An imaginary plane is drawn, extending between medial canthus of eye and the angle of mandible. Growths situated above this plane (suprastructural) have a poorer prognosis than those below it (intrastructural). 2.  AJCC classification is only for squamous cell carcinoma and does not include nonepithelial tumours of lymphoid tissue, soft tissue, cartilage and bone. Histopathologically, squamous cell carcinoma is further graded into: (a) Well-differentiated, (b) Moderately differentiated and (c) Poorly differentiated. In histopathology, note should also be made of vascular or perineural invasion. 3. Lederman’s classification. It uses two horizontal lines of Sebileau; one passing through the floors of orbits and the other through floors of antra, thus dividing the area into: (a) Suprastructure. Ethmoid, sphenoid and frontal sinuses and the olfactory area of nose. (b) Mesostructure. Maxillary sinus and the respiratory part of nose. (c) Infrastructure. Containing alveolar process. This classification further uses vertical lines, extending down the medial walls of orbit to separate ethmoid sinuses and nasal fossa from the maxillary sinuses., Epidemiology:['(0.2%) of human malignant tumors', '10.3% incidence of nodal disease', '5 year survival is about 40–50%. However, advances', 'To help reduce the risk of getting cancer of the nasal cavity and nasopharynx:\n\nDo not smoke. If you currently smoke, quit. Avoid exposure to second hand smoke.\nBe aware of workplace health and safety rules and follow them.\nLimit your consumption of salted, preserved fish. It is especially important not to give these foods to very young children.\n\n\nThe following may help reduce the risk of developing cancer:\n\nChoose a healthy diet to achieve and maintain a healthy weight. Eat more vegetables, fruits and whole grains and eat less red and processed (e.g., bacon, sausage, luncheon meat, hot dogs) meats. These actions may reduce the risk of developing many types of cancer as well as other diseases.\nExercise regularly.\nDiscuss the risks and benefits of medical imaging, such as CT scans, with your health care provider to avoid unnecessary exposure to ionizing radiation. This is particularly important for children.\nTalk to your health care provider about recommended cancer screenings.'], Complications:['proptosis', 'METASTASES AT DIFFERENT SITES'], Diagnostics:['X RAY PNS(OF/OM)', 'biopsy', 'ENDOSCOPY', 'CT SCAN'], Differential diagnosis:['BENIGN TUMORS', 'lymphoma', 'MALIGNANCY', 'Nasopharyngeal carcinoma', 'UNILATERAL NASAL OBSTRUCTION'], disease description:It arises from the sinus lining and may remain silent for a long time giving only vague symptoms of “sinusitis.” It then spreads to destroy the bony confines of the maxillary sinus and invades the surrounding structures..Maxillary sinus squamous cell carcinoma is an aggressive tumor, usually diagnosed at an advanced stage and most patients present with very poor prognosis and survival rate. We report a case of the patient who presented with pain and swelling in the left maxillary region

Person at 26 with manifestations like ['foul smelling in ear', 'Hearing loss', 'vertigo', 'pain in ear', 'FACIAL PARALYSIS', 'BLOODY DISCHARGE']

Disease Name: Carcinoma Of Middle Ear And Mastoid, symptoms: ['foul smelling in ear', 'Hearing loss', 'vertigo', 'pain in ear', 'FACIAL PARALYSIS', 'BLOODY DISCHARGE'], Treatment: ['palliative measure\nwhen tumour involves cranial nerves (IXth to XIIth) or\nspreads into the cranial cavity or the nasopharynx', 'combination of surgery and radiotherapy gives better\nresults. Surgery consists of radical mastoidectomy, subtotal\nor total petrosectomy depending on the extent of\ntumour.'], Pathophysiology: It affects age group of 40–60 years and is slightly more common in females. Most cases (75%) have associated long-standing ear discharge. Chronic irritation may be the causative factor in such cases. Some cases are seen in radical mastoid cavities. Primary carcinoma of mastoid air cells is also seen in radium dial painters. Tumour may arise primarily from middle ear or be an extension of carcinoma of the deep meatus. Squamous cell variety is by far the most common. Adenocarcinoma may occasionally be seen; it arises from the glandular elements of middle ear., Epidemiology:['1:20,000', '1 case in 1 million', 'POOR', 'effectively treating all ear infection .'], Complications:['METASTASES AT DIFFERENT SITES'], Diagnostics:['biopsy', 'CT SCAN', 'hearing tests'], Differential diagnosis:['BENIGN TUMORS', 'CHOLESTEATOMA', 'CHRONIC OTITIS MEDIA', 'keratosis obliterans', 'otosclerosis', 'schwannoma (who grade 1)'], disease description:An ear tumor is a mass or lump of abnormal cells that forms in the ear. Most ear tumors are benign or not cancerous. But some ear tumors are malignant cancerousEar tumors can form in any part of the ear, including the inner ear, middle ear and outer ear. they may effect hearing

Suffering from ['fatigue', 'fever', 'weight loss', 'Abdominal Pain'] at the age of 40

Disease Name: Carcinoma Of The Collecting Ducts Of Bellini, symptoms: ['fatigue', 'fever', 'weight loss', 'Abdominal Pain'], Treatment: ['Nephrectomy in addition to chemotherapy / radiation may be associated with survival benefit. \nMay respond to palbociclib in metastatic disease bearing a CDKN2A homozygous deletion.'], Pathophysiology: Collecting (Bellini) duct carcinoma (CDC) of the kidney is a highly aggressive tumour with an extremely poor prognosis. It is a variety of renal cell carcinoma (RCC) arising from the distal segment of the collecting ducts of Bellini in the renal medulla, accounting for less than 2% of all renal masses. Mancilla-Jimenez and colleagues8 first observed the atypical hyperplastic changes of the adjacent collecting ducts epithelium in 3 out of 34 cases of papillary RCC in 1976. Fleming and Lewi described 6 cases of CDC and presented diagnostic criteria to recognize it as a unique pathological subtype of RCC.According to the International Society of Urological Pathology (ISUP) conference on renal neoplasia in Vancouver in 2013, CDC should include at least some of the lesions from the medullary region, have a predominant formation of tubules, have a desmoplastic stromal reaction, have high-grade cytologic features, have infiltrative growth patterns, have no other typical RCC subtypes or urothelial carcinoma., Epidemiology:['Rare (< 1% of kidney cancers)', 'M:F = 2:1', 'poor', 'Maintaining a healthy weight by exercising and choosing a diet high in fruits and vegetables may also reduce your chance of getting this disease.'], Complications:['Budd Chiari Syndrome', 'hyperglycemia', 'hypertension'], Diagnostics:['Cytogenetics', 'CT SCAN', 'Immunostaining', 'Immunostaining'], Differential diagnosis:['metastatic carcinoma', 'Papillary renal cell carcinoma', 'Renal medullary carcinoma', 'Urothelial carcinoma in situ - Non-invasive papill'], disease description:Carcinoma of renal medulla arising from the principal cells of the distal collecting ducts of Bellini. It is a variety if renal cell carcinoma(RCC) arising from the distal segment of the collecting ducts of bellini in the renal medula.

Individual, 27 years old, with ['HEART BURN', 'odynophagia', 'dysphagia', 'vomiting', 'regurgitation', 'hoarseness of voice', 'weight loss', 'Melena', 'ascites']

Disease Name: Carcinoma Of The Oesophagus, symptoms: ['HEART BURN', 'odynophagia', 'dysphagia', 'vomiting', 'regurgitation', 'hoarseness of voice', 'weight loss', 'Melena', 'ascites'], Treatment: ['Only as a palliative measure in the locally advanced or disseminated disease', 'Treatment of choice, surgery of upper two-thirds of oesophagus is difficult due \nto great vessels and involvement of mediastinal nodes.', 'Surgery is the preferred method of treatment for cancer of lower one-third. The affected segment, with a wide \nmargin of oesophagus proximally and the fundus of \nstomach distally, can be excised with primary reconstruction of the food channel.\nIn advanced lesions-\n1-A by-pass operation.\n2. Oesophageal intubation with Celestin or MousseauBarbin or a similar tube.\n3. Permanent gastrostomy or a feeding jejunostomy.\n4. Laser surgery'], Pathophysiology: Squamous cell cancer and adenocarcinoma are the most common types. Squamous cell carcinoma generally affects the upper two-thirds of the oesophagus and adenocarcinoma the lower third. Worldwide, squamous cell cancer is most common, but adenocarcinoma predominates in the west and is increasing in incidence.Esophageal squamous cell carcinoma arises from small polypoid excrescences, denuded epithelium, and plaques, commonly located at the mid-portion of the esophagus. The early lesion may be subtle, and tissue staining with Lugol’s iodine should be used to stain normal squamous epithelium containing glycogen from malignant squamous glycogen-deprived cells to facilitate diagnosis. Advance lesions are ulcerated, circumferential, infiltrate submucosa, and extend in a cephalad direction. Spread occurs via the lymphatic system to regional lymph nodes, but a third of patients will have distant metastases to liver, lung, and bone including invasion of malignant cells to the bone marrow., Epidemiology:['100 per 100,000 (1,11)', 'About 20,640 new esophageal cancer cases', '5-10% SURVIVAL OF 5 YRS', 'You may be able to reduce your risk by eating well so you’re at a weight that’s right for you and that you can maintain. You may also reduce your risk by avoiding activities such as using tobacco, frequently drinking lots of alcohol or working around certain solvents. Having an HPV infection is a risk factor for esophageal cancer. Ask your healthcare provider if you should receive the HPV vaccine.\n\nThere isn’t a recommended way to screen for esophageal cancer. But if you have Barrett’s esophagus or certain other conditions, your healthcare provider may recommend screening. Your healthcare provider may do an EGD to do this screening. If your healthcare provider recommends screening, they’ll let you know how often you should have screening.'], Complications:['hematemesis'], Diagnostics:['Upper GI Endoscopy', 'BARIUM SWALLOW', 'CT SCAN', 'BRONCHOSCOPY', 'CROSS SECTION CT SCAN', 'ENDOSONOGRAPHY'], Differential diagnosis:['ACHALASIA', 'Esophageal leiomyoma', 'esophageal stricture', 'GASTRIC CANCER', 'GASTRO OESOPHAGEAL REFLUX DISEASE', 'PERFORATION OF OESOPHAGUS'], disease description:Carcinoma of the oesophagus is the sixth most common cancer in the world. Esophageal cancer is cancer that occurs in the esophagus — a long, hollow tube that runs from your throat to your stomach. Your esophagus helps move the food you swallow from the back of your throat to your stomach to be digested.Esophageal cancer usually begins in the cells that line the inside of the esophagus. Esophageal cancer can occur anywhere along the esophagus. More men than women get esophageal cancer.

Experiencing ['DYSPAREUNIA', 'pain during erection', 'non retractile prepuce', 'Inguinal lymphadenopathy', 'ulceration on penis', 'penile bleeding', 'penile discharge'] at 36 years

Disease Name: Carcinoma Of The Penis, symptoms: ['DYSPAREUNIA', 'pain during erection', 'non retractile prepuce', 'Inguinal lymphadenopathy', 'ulceration on penis', 'penile bleeding', 'penile discharge'], Treatment: ['Radiotherapy may be offered as an adjunct to surgery or as definitive \nalternative treatment. Combination chemotherapy has been used \nfor palliation and adjuvant treatment of carcinoma of the penis', 'adequate surgical excision, including circumcision, for \ndisease of the penis. The penile surgery may need to be radical, \ntotal or partial, depending on location and extent. To conserve \ntissue and minimize residual sexual dysfunction, conservative \ntechniques are increasingly used, with narrow excisional margins \nand innovative plastic repair, as are laser treatment'], Pathophysiology: Penile cancers traditionally begin as small lesions, most commonly on the glans or prepuce. The appearance can vary greatly. Some appear as white grey exophytic masses growing out of the penile skin and others can be flat, reddish-colored, and ulcerated masses. These lesions grow slowly laterally along the surface of the penile skin and often cover the entire glans or prepuce before invading into the corpora and shaft of the penis. Growth rates of ulcerative versus exophytic lesions are similar, although ulcerative lesions appear to metastasize to lymph nodes (LNs) earlier. Penile lymphatics drain both the glans penis and shaft and drainage proceeds first to superficial inguinal LNs to deep inguinal LNs and then to external iliac LNs in the pelvis., Epidemiology:['fewer than 1 man in 100,000 each year', 'overall, the \nhighest incidence is in Africa, South America and Asia (2–4/100 000 \ninhabitants) and lowest in the USA and Europe (0.3–1/100 000)', 'bad', 'To reduce your risk of penile cancer, consider the following:\n\nWeigh the benefits of circumcision. Circumcising an infant reduces their risk of penile cancer as an adult. Research suggests less benefit if circumcision takes place after a person has become sexually active. It’s important to weigh the medical benefits of circumcision against other deciding factors, like religious beliefs and cultural and individual preferences. Talk through the benefits with your healthcare provider as you consider the best options for yourself or your newborn.\nGet treated for phimosis. Phimosis in uncircumcised adults has many potential causes, ranging from infections to poor hygiene. Identifying the cause and receiving prompt treatment can reduce your risk of penile cancer.\nGet the HPV vaccine. The Food and Drug Administration (FDA) has approved three vaccines for preventing high-risk HPV: Gardasil, Gardasil-9 and Cervarix. Ideally, you should get vaccinated between ages 9 and 26 or before you become sexually active. If you’re older than 26, speak to your healthcare provider about the potential benefits of vaccination.\nPractice safer sex. Condoms and dental dams can’t fully protect you from HPV infection. Still, using them consistently and correctly and limiting your number of sexual partners can reduce your risk of HPV infection.\nDon’t use tobacco products. Choosing not to smoke, dip, etc., reduces your risk of penile cancer and many other types of cancer.\nPractice good hygiene. Good hygiene is an important part of having a healthy penis. Cleaning your penis regularly with mild soap and warm water can wash away germs that can cause inflammation or infection. If you’re uncircumcised, pull back your foreskin and clean the head of your penis to prevent smegma build-up.'], Complications:['phlebitis', 'Pulmonary Embolism'], Diagnostics:['PET SCAN', 'biopsy', 'CT SCAN', 'USG', 'PHYSICAL EXAMINATION'], Differential diagnosis:['Basal cell carcinoma : Superficial,Nodular (solid)', 'Bowen disease', 'condyloma acuminatum', 'Genital warts', 'kaposi sarcoma', 'lichen sclerosus', 'melanoma', 'pyoderma gangrenosum'], disease description:Penile cancer is a rare cancer that forms in the penis, the male sex organ that passes sperm and urine from the body. The most common type of penile cancer is squamous cell carcinoma (cancer that begins in flat cells in the top layer of the skin). It usually forms on or under the foreskin (the loose skin covering the head of the penis)

Person, 51 years old, presenting ['painless nodule in the anterior neck', 'dysphagia', 'Hoarseness', 'neck swelling', 'neck lymphadenopathy', 'Cervical lymph node metastasis']

Disease Name: Carcinoma Of The Thyroid, symptoms: ['painless nodule in the anterior neck', 'dysphagia', 'Hoarseness', 'neck swelling', 'neck lymphadenopathy', 'Cervical lymph node metastasis'], Treatment: ['Thyroid Hormone Suppression Therapy\n\nThyroid hormone suppression therapy to suppress TSH and thereby potentially minimize its stimulation of thyroid cancer growth is recommended in most patients after surgery. For patients with ATA high-risk, the goal TSH should be no more than 0.1m IU/liter, and for patients in the intermediate-risk category, the goal TSH should be between 0.1 and 0.5 mIU/liter. For the ATA low-risk category, a goal TSH between 0.5 and 2.0 mIU/liter is acceptable', 'Depending on the clinical situation, adjunctive therapy with both TSH\nsuppression (dosing levothyroxine to lower serum TSH and deprive residual\nthyroid cancer cells of this growth factor) and 131 I therapy (to ablate the normal\nthyroid remnant and/or to treat residual thyroid cancer) may be recommended', 'Systemic Chemotherapy\n\nSystemic chemotherapy is usually only considered in a group of carefully selected patients with a high metastatic disease burden or rapidly progressive metastatic disease despite the above treatment (Iodide-refractory). Because of the significant adverse effects associated with such therapy, it should be considered only when the associated benefits exceed the risks', 'Radioiodine (RAI) Ablation Therapy\n\nRAI therapy after thyroidectomy is used for remnant ablation of normal residual thyroid tissue, as adjuvant therapy for subclinical micrometastases, or as treatment of apparent local or distant metastasis. High-risk and some selected intermediate-risk patients, per the ATA risk stratification system, will benefit from RAI ablation. Patients who are candidates for RAI therapy should maintain a low iodine diet for 1 to 2 weeks before the treatment to ensure iodine depletion of the cells; they should also be cautioned against large iodine administrations such as through iodinated contrast or amiodarone to improve the avidity of the thyroid follicular cells to iodine.'], Pathophysiology: At all ages, the vast majority of differentiated thyroid cancers are of follicular cell origin and, in North America, papillary carcinoma (85–90%) is the most common subtype. While their histologic features are similar, thyroid cancers of childhood are genetically distinct from their adult counterparts. Although about 70% of adults with papillary thyroid cancer exhibit pathogenic somatic mutations in BRAF or RAS, these mutations are uncommon in children with papillary thyroid cancer. In contrast, RET-PTC translocations, which result in chimeric proteins containing the tyrosine kinase domains of RET fused to the regulatory sequences of ubiquitously expressed genes such as H1 and ELE1, are often found in childhood thyroid cancers. After papillary thyroid cancer, follicular carcinoma (10%) is the next most common type of childhood thyroid cancer. Medullary carcinoma (2%) and anaplastic thyroid cancers are relatively rare. Of note, only thyroid cancers of follicular cell origin (papillary and follicular carcinomas) respond to the adjunctive therapies of 131 I therapy and thyrotropin (TSH) suppression. Up to 10% of cases of follicular cell–derived thyroid cancers are familial, and these are usually inherited in an autosomal dominant manner. Familial syndromes associated with an increased risk of thyroid neoplasia include PTEN hamartoma tumor syndromes (Cowden, Bannayan-Riley-Ruvalcaba, and Proteus syndromes) characterized by macrocephaly, mucocutaneous lesions (fibromas), and breast cancer and endometrial tumors; and familial adenomatous polyposis (mutation in the APC gene). Germline mutations in DICER1 are also a cause of pediatric thyroid neoplasia. The evaluation of a child with thyroid nodule should include a medical and family history to assess for features of these syndromes. The thyroid gland of children is very sensitive to exposure to external radiation, particularly at very young ages. There probably is no lower threshold dose; however, 1 Gy of radiation exposure results in a 7.7-fold increased relative risk of thyroid cancer.. . Most large groups of treated children have a 10–30% incidence of benign thyroid nodules and an increased incidence of thyroid cancer. The latter begins to appear within 3-5 yr after radiation treatment and reaches a peak in 15-25 yr. It is unknown whether there is a period after which no more tumors develop. Administration of 131 I for diagnostic or therapeutic purposes does not appear to increase the risk of thyroid cancer. Thyroid cancer has been reported in children with congenital goiter or ectopic thyroid tissue. In these patients and in children with autoimmune thyroiditis and hypothyroidism, chronic TSH stimulation may play a pathogenic role. It is unclear if the course of thyroid cancer differs in these patients compared to the general population. From a practical standpoint, nodules that are detected in the context of these disorders should be fully evaluated for cancer risk as in other children., Epidemiology:['1% to 4% of all malignancies and is the fifth most common cancer in women', '4-5 in 100,000 cases', 'VARIABLE', 'Many people develop thyroid cancer for no known reason, so prevention isn’t really possible. But if you know you’re at risk for thyroid cancer, you may be able to take these steps:\n\nPreventive (prophylactic) surgery: Genetic tests can determine if you carry an altered gene (a mutation) that increases your risk for medullary thyroid cancer or multiple endocrine neoplasia. If you have the faulty gene, you may opt to have preventive (prophylactic) surgery to remove your thyroid gland before cancer develops.\nPotassium iodide: If you’ve had radiation exposure during a nuclear disaster, such as the 2011 incident at Fukushima, Japan, taking potassium iodide within 24 hours of exposure can lower your risk of eventually getting thyroid cancer. Potassium iodide (Pima®) blocks your thyroid gland from absorbing too much radioiodine. As a result, your gland stays healthy.'], Complications:['METASTASES AT DIFFERENT SITES'], Diagnostics:['Complete Blood Count CBC', 'Thyroid Stimulating Hormone TSH', 'ultrasound', 'X RAY', 'CT SCAN', 'USG', 'PHYSICAL EXAMINATION'], Differential diagnosis:['cervical lymphadenopathy', 'Metastatic tumors', 'PAPILLARY CARCINOMA', 'THYROID NODULE'], disease description:hyroid cancer develops in your thyroid, a small, butterfly-shaped gland at the base of your neck. This gland produces hormones that regulate your metabolism Papillary: Up to 80% of all thyroid cancers are papillary. This cancer type grows slowly. Although papillary thyroid cancer often spreads to lymph nodes in your neck, the disease responds very well to treatment. Papillary thyroid cancer is highly curable and rarely fatal.Follicular: Follicular thyroid cancer accounts for up to 15% of thyroid cancer diagnoses. This cancer is more likely to spread to your bones and organs, like your lungs. Metastatic cancer (cancer that spreads) may be more challenging to treat.Medullary: About 2% of thyroid cancers are medullary. A quarter of people with medullary thyroid cancer have a family history of the disease. A faulty gene (genetic mutation) may be to blame.Anaplastic: This aggressive thyroid cancer is the hardest type to treat. It can grow quickly and often spreads into surrounding tissue and other parts of your body. This rare cancer type accounts for about 2% of thyroid cancer diagnoses.

At the age of 21, a woman dealing with ['pallor', 'CACHEXIA', 'aching pain and tenderness over one area.', 'The uterus may be separated from the mass felt per abdomen.', 'abdominal distension', 'respiratory distress', 'localized abdominal pain', 'jaundice', 'vaginal bleeding']

Disease Name: Carcinoma Ovary, symptoms: ['pallor', 'CACHEXIA', 'aching pain and tenderness over one area.', 'The uterus may be separated from the mass felt per abdomen.', 'abdominal distension', 'respiratory distress', 'localized abdominal pain', 'jaundice', 'vaginal bleeding'], Treatment: ['Carboplatin (CP) 400 mg/m2 or AUC 5 6 3 weeks\nPaclitaxel (T) 135 mg/m2 6 3 weeks', 'Genetic screening is offered for BRCA1 and \nBRCA2 for women with high risk for ovarian and breast \ncancer are offered 10–15%.\n\x03 Annual mammographic screening for women with \nstrong family history of breast cancer. \n\x03 Periodic screening for other malignancies (colono\x02scopy, endometrial biopsy) for women with Lynch II \nsyndrome. \n\x03 Combined oral contraceptive pills as a preventive \n(chemoprevention) measure is recommended to a \nwoman specially belonging to Lynch type II families.', 'Bilateral salpingo-oophorectomy in women \nfollowing completed child bearing with BRCA \nmutation can reduce the risk of ovarian cancer \nsignificantly.\nEarly laparotomy is indicated in following cases:\n– The ovary enlarges progressively beyond 8 cm \nwhile under observation.\n– Any symptomatic ovarian tumor regardless of size'], Pathophysiology: Ovarian cancer can be further classified into two subtypes- Type I or Type II tumors, the latter being a more fatal variant, thought to be caused by continuous ovarian cycles leading to inflammation and endometriosis. Type I tumor includes low-grade serous, endometrioid, clear-cell, and mucinous carcinomas, with the rare subtypes being seromucinous and Brenner tumors. Type I tumors mostly arise from atypical proliferative (borderline) tumors. Type II tumors include high-grade serous carcinoma, carcinosarcoma, and undifferentiated carcinoma, which mainly originate from serous tubal intraepithelial carcinoma. Type I tumors usually present at an early stage and are low grade except for clear cell, which is considered high grade. Their proliferative activity is usually low. They are diagnosed early and carry a good prognosis. In comparison, Type II tumors are high-grade tumors and almost always of advanced stage. They have high proliferative activity with rapid and aggressive progression and a high degree of chromosomal instability compared to type I with the presence of p53 mutations in most of the cases., Epidemiology:['ovarian cancer is 1 in 71, and 1 in 200 women', 'Approximately, 1 in \nevery 70 newborn females in the United States will live \nto develop ovarian cancer and 1 woman in 100 will die of \nthe disease. 20% of ovarian neoplasms are malignant. It is \nmore common amongst nulliparous', 'depending upon staging', 'There’s no way to prevent ovarian cancer completely. But knowing your biological family history can help you prepare for any heightened risk of developing ovarian cancer.\n\nIf you have a genetic mutation such as BRCA mutation, your healthcare provider may recommend risk-reducing surgery to remove your ovaries and tubes before they become cancerous. If you’re not sure if you have a BRCA or another mutation, ask your healthcare provider about genetic testing.'], Complications:['ascites', 'Bowel obstruction', 'pedal edema'], Diagnostics:['PET SCAN', 'MRI', 'CT SCAN'], Differential diagnosis:['BRENNER TUMOR', 'colon cancer', 'Endometriosis', 'Gastric adenocarcinoma', 'Peritoneal cyst', 'serous adenocarcinoma', 'Uterine fibroids'], disease description:Ovarian cancer is the leading cause of death in women diagnosed with gynecological cancers. It is also the fifth most frequent cause of death in women, in general..Ovarian cancer is a growth of cells that forms in the ovaries. The cells multiply quickly and can invade and destroy healthy body tissue.The female reproductive system contains two ovaries, one on each side of the uterus. The ovaries — each about the size of an almond — produce eggs (ova) as well as the hormones estrogen and progesterone.

At 52 years old, experiencing ['dysphagia', 'Malnutrition', 'weight loss', 'Aphonia', 'voice change']

Disease Name: Carcinoma Postcricoid Region, symptoms: ['dysphagia', 'Malnutrition', 'weight loss', 'Aphonia', 'voice change'], Treatment: ['IN INITIAL CASES ONLY', 'laryngo-pharyngo-oesophagectomy with\nstomach pull-up or colon transposition to reconstruct\npharyngo-oesophageal segment', 'Surgical excision followed by postoperative radiation is the treatment of choice for cancers not amenable to a conservation protocol (ie, tumors destroying cartilage, tumors too bulky for control with primary radiation). The minimum operation recommended is a total laryngectomy and partial pharyngectomy, with a central (level 6) node dissection.'], Pathophysiology: Usually an ulcerative type of lesion arises from postcricoid region. Local spread often occurs in an annular fashion causing marked dysphagia. Growths may invade cervical oesophagus, arytenoids or recurrent laryngeal nerve at cricoarytenoid joint. Lymphatic spread involves paratracheal lymph nodes and may be bilateral due to the midline nature of lesions. They may not be clinically palpable. Clinical Features Females are usually affected, sometimes in the early age group of twenties and thirties. Progressive dysphagia is the predominant presenting symptom. This may cause progressive malnutrition and weight loss. Sometimes, voice change and aphonia may be produced due to infiltration of recurrent laryngeal nerve or posterior cricoarytenoid muscles affecting vocal cord mobility., Epidemiology:['incidence rate of about 5%', 'Prognosis is poor both with irradiation and surgic', 'Poor oral and dental hygiene.\nEnvironmental or occupational inhalants'], Complications:['Hypocalcemia', 'Hypothyroidism', 'Peripheral neuropathy'], Diagnostics:['Complete Blood Count CBC', 'BARIUM SWALLOW', 'ENDOSCOPY', 'CT SCAN'], Differential diagnosis:['Metastatic tumours', 'MUCOEPIDERMOID CARCINOMA', 'small cell carcinoma', 'squamous cell carcinoma.'], disease description:Postcricoid carcinoma is a rare but aggressive type of hypopharyngeal carcinoma with poor prognosis and high mortality; thus, it is indispensable to investigate the surgical efficacy and multimodal strategies. The postcricoid region is located behind the cricoarytenoid joint and the backside of the cricoid cartilage, connected to the esophagus at the lower edge [1]. The number of primary tumors from the postcricoid region is the least versus the other two types of hypopharyngeal carcinoma (pyriform sinus and posterior wall), with an incidence rate of about 5%

Symptoms at 28: ['ear pain', 'difficulty in swallowing', 'voice change', 'dysphagia', 'spitting of blood', 'palpable mass']

Disease Name: Carcinoma Posterior Pharyngeal Wall, symptoms: ['ear pain', 'difficulty in swallowing', 'voice change', 'dysphagia', 'spitting of blood', 'palpable mass'], Treatment: ['Early lesions, particularly exophytic, can be treated by\nradiotherapy with preservation of laryngeal function', 'Early small lesions can also be excised surgically via lateral\npharyngotomy and primary repair with equally good\nresults. Advanced lesions may require laryngopharyngectomy\nand block dissection of neck with repair of the food\nchannel.'], Pathophysiology: The exact pathogenesis is unknown. Growth is usually exophytic but may be ulcerative. It remains localized until late and then spreads to the prevertebral fascia, muscles and vertebrae. Lymphatic spread is usually bilateral due to midline nature of the lesion. Fifty per cent of the patients with cancer of posterior pharyngeal wall have nodal metastasis on their initial examination. Retropharyngeal nodes, though not clinically palpable, may also be involved., Epidemiology:['About 25% of oropharyngeal cancers occur in people under age 55', 'POOR', '.Don’t start smoking. If you smoke or use tobacco products, quit. Continuing to smoke greatly increased the risk of developing a second cancer in the mouth, throat or voice box or lung.\n.Eat a healthy, well-balanced diet and exercise regularly.\n.Avoid human papilloma virus (HPV) infection. Ask your doctor about the HPV vaccine.'], Complications:[], Diagnostics:['ENDOSCOPY', 'Soft Tissue Radiograph'], Differential diagnosis:['granulomatous infections', 'lichenoid', 'lymphoma', 'Metastatic tumours', 'oral candidiasis', 'squamous cell carcinoma.', 'tonsillitis'], disease description:This is the least common of laryngopharyngeal malignancy constituting only 10% of them. They are mostly seen in males above 50 years  of age.Hypopharyngeal carcinomas arising from the posterior pharyngeal wall are silent in the early stages and hence patients are likely to present with advanced disease. When cure is unlikely, adequate focus must be directed at maintaining quality of life

A 38-year-old female experiencing ['erectile dysfunction', 'anemia', 'BLADDER OUTLET OBSTRUCTION', 'haematuria', 'malaise', 'joint pain', 'pelvic pain']

Disease Name: Carcinoma Prostate, symptoms: ['erectile dysfunction', 'anemia', 'BLADDER OUTLET OBSTRUCTION', 'haematuria', 'malaise', 'joint pain', 'pelvic pain'], Treatment: [{'medication': ['Finasteride ', 'Tamsulosin ']}, 'Targeted therapy is a type of treatment that uses drugs or other substances to identify and attack specific cancer cells. Targeted therapies usually cause less harm to normal cells than chemotherapy or radiation therapy do.\n\nPARP inhibitors block an enzyme involved in many cell functions, including the repair of DNA damage. Blocking this enzyme may help keep cancer cells from repairing their damaged DNA, causing them to die. Olaparib is a PARP inhibitor used to treat patients', 'Abiraterone acetate can prevent prostate cancer cells from making androgens.\nOrchiectomy\nEstrogens\nLuteinizing hormone-releasing hormone agonists can stop the testicles from making testosterone. Examples are leuprolide, goserelin, and buserelin.', 'External radiation therapy .\nInternal radiation therapy .\nRadiopharmaceutical therapy uses a radioactive substance to treat cancer.', 'Open radical prostatectomy\nRadical laparoscopic prostatectomy\nRobot-assisted laparoscopic radical prostatectomy.\nPelvic lymphadenectomy.\nTransurethral resection of the prostate (TURP).'], Pathophysiology: It's not clear what causes prostate cancer.Doctors know that prostate cancer begins when cells in the prostate develop changes in their DNA. A cell's DNA contains the instructions that tell a cell what to do. The changes tell the cells to grow and divide more rapidly than normal cells do. The abnormal cells continue living, when other cells would die.Doctors know that prostate cancer begins when cells in the prostate develop changes in their DNA. A cell's DNA contains the instructions that tell a cell what to do. The changes tell the cells to grow and divide more rapidly than normal cells do. The abnormal cells continue living, when other cells would die.The accumulating abnormal cells form a tumor that can grow to invade nearby tissue. In time, some abnormal cells can break away and spread (metastasize) to other parts of the body.Risk factors.Factors that can increase your risk of prostate cancer include:Older age. Your risk of prostate cancer increases as you age. It's most common after age 50.Race. For reasons not yet determined, Black people have a greater risk of prostate cancer than do people of other races. In Black people, prostate cancer is also more likely to be aggressive or advanced.Family history. If a blood relative, such as a parent, sibling or child, has been diagnosed with prostate cancer, your risk may be increased. Also, if you have a family history of genes that increase the risk of breast cancer (BRCA1 or BRCA2) or a very strong family history of breast cancer, your risk of prostate cancer may be higher.Obesity. People who are obese may have a higher risk of prostate cancer compared with people considered to have a healthy weight, though studies have had mixed results. In obese people, the cancer is more likely to be more aggressive and more likely to return after initial treatment., Epidemiology:['1 in 456 men under age 50 will be diagnosed, the rate shoots up to 1 in 54 for ages 50 to 59', 'about 6 cases in 10 are diagnosed in men who are 65 or older, and it is rare in men under 40', 'POOR', 'Preventing prostate cancer isn’t possible. Still, taking these steps may reduce your risk:\n\nGet regular prostate screenings. Ask your healthcare provider how often you should get screened based on your risk factors.\nMaintain a healthy weight. Ask your provider what a healthy weight means for you.\nExercise regularly. The CDC recommends 150 minutes of moderate-intensity exercise each week, or a little more than 20 minutes daily.\nEat a nutritious diet. There’s no one diet to prevent cancer, but good eating habits can improve your overall health. Eat fruits, vegetables and whole grains. Avoid red meats and processed foods.\nQuit smoking. Avoid tobacco products. If you smoke, work with your provider on a smoking cessation program to kick the habit.'], Complications:['incontinence', 'infertility'], Diagnostics:['BONE SCAN', 'PET SCAN', 'USG KUB', 'MRI', 'SERUM PROSTATE SPECIFIC ANTIGEN(PSA)', 'CROSS SECTION CT SCAN', 'TRUS'], Differential diagnosis:['BENIGN PROSTATIC HYPERPLASIA', 'Bladder cancer', 'Cystitis', 'prostatic abscess', 'renal stones'], disease description:Prostate cancer is cancer that occurs in the prostate. The prostate is a small walnut-shaped gland in males that produces the seminal fluid that nourishes and transports sperm.Prostate cancer is one of the most common types of cancer. Many prostate cancers grow slowly and are confined to the prostate gland, where they may not cause serious harm.

Individual, 46 years old, with ['PALPABLE LYMPH NODE', 'dysphagia', 'odynophagia', 'laryngeal edema', 'hoarseness of voice', 'Referred otalgia', 'pricking sensation on swallowing']

Disease Name: Carcinoma Pyriform Sinus, symptoms: ['PALPABLE LYMPH NODE', 'dysphagia', 'odynophagia', 'laryngeal edema', 'hoarseness of voice', 'Referred otalgia', 'pricking sensation on swallowing'], Treatment: ['Early growth without nodes can be cured by radiotherapy\nwith the advantage of preserving the laryngeal\nfunction.Planned postoperative radiotherapy can be given rou\x02tinely to all cases. Patients with no palpable nodes (N0\nneck) can also be given radiotherapy avoiding block \ndissection.', 'If growth is limited to pyriform fossa and does not extend to postcricoid region, total laryngectomy and partial pharyngectomy is done.\nIf growth extends to postcricoid region, total laryngectomy and pharyngectomy is done along with block dissection. Pharyngo-oesophageal segment is reconstructed \nwith myocutaneous flaps or stomach pull-up.'], Pathophysiology:  1. Locally, the growth may spread upwards to the vallecula and base of tongue; downwards to postcricoid region; medially to aryepiglottic folds and ventricles. It may infiltrate into the thyroid cartilage, thyroid gland or may present as a soft tissue mass in the neck. 2. Lymphatic spread occurs early. Pyriform fossa has a rich lymphatic network. Seventy-five per cent of the patients have cervical nodal metastases when first seen, with half of them having bilateral involvement. Upper and middle group of jugular cervical nodes are often involved. Sometimes, nodes make their appearance long after the primary has been eradicated. 3. Distant metastases often occur late and may be seen in lung, liver and bones., Epidemiology:['male 93% and female 7%', '65-85% of hypopharyngeal carcinomas involve the pyriform sinuses', 'POOR', 'Maintain healthy life style.\nquit smoking.'], Complications:['METASTASES AT DIFFERENT SITES'], Diagnostics:['BARIUM SWALLOW', 'ENDOSCOPY', 'MRI', 'CT SCAN'], Differential diagnosis:['Metastatic lesion', 'Squamous cell carcinoma'], disease description:It constitutes 60% of all hypopharyngeal cancers, mostly affecting males above 40 years of age. Growth is either exophytic or ulcerative and deeply infiltrative. Because spread upwards to the vallecula and base of tongue; downwards to postcricoid region; medially to aryepiglottic folds and ventricles of the large size of the pyriform sinus, growths of this region remain asymptomatic for a long time. Metastatic neck nodes may be the first to attract attention.

Individual, 21 years old, with ['tenesmus', 'Altered bowel habit', 'Anorectal bleeding', 'Anorectal pain', 'diarrhea', 'CACHEXIA']

Disease Name: Carcinoma Rectum, symptoms: ['tenesmus', 'Altered bowel habit', 'Anorectal bleeding', 'Anorectal pain', 'diarrhea', 'CACHEXIA'], Treatment: ['5-Fluorouracil (5-FU) based regimens remain the first-line therapy and are associated with a 10% improvement in disease-free survival in patients with node-positive rectal cancer. Second-line therapies\ninclude oxaliplatin and irinotecan, and biological agents such as cetuximab.', '1-Anterior resection\n2- Transanal total mesorectal excision (taTME)\n3- Hartmann’s operation\n4-Abdominoperineal excision of the rectum\n5-Endoluminal stenting\n6-Palliative colostomy\n7- Pelvic exenteration'], Pathophysiology: The transformation of normal rectal or colonic epithelium to a precancerous lesion (adenomas) and ultimately to invasive carcinoma requires an accumulation of genetic mutations either somatic (acquired) and/or germline (inherited). The theory of colorectal carcinogenesis features a clonal mutation evolution that gives a cell survival-immortality advantage and allows for the development of more mutations providing for cancer hallmarks such as proliferation, invasion, metastasis, and others.  Clinical evidence has shown that colorectal cancer frequently arises from adenomatous polyps that typically acquire dysplastic changes over a 10 to 15 year period, leading to invasive carcinoma development. Thus, early detection and removal of polyps reduce the incidence of CRC. Alternative new evidence has demonstrated that hamartomatous and serrated polyps (in addition to adenomatous polyps) could lead to CRC.There are three major molecular pathways linked to CRC. These are chromosomal instability, mismatch repair, and hypermethylation. The chromosomal instability pathway is an accumulation of mutations unbalancing oncogene and tumor suppressor equilibrium, Epidemiology:['Approximately 18% of rectal cancer is earlier onset (age <50 years)', '1 million people every year', 'poor', 'While you can’t prevent rectal cancer altogether, there are steps you can take to reduce your risk. For example:\n\nStay at a healthy weight.\nExercise regularly.\nEat a healthy, well-balanced diet.\nAvoid drinking alcohol.\nDon’t smoke.'], Complications:['metastatic disease'], Diagnostics:['Complete Blood Count CBC', 'colonoscopy', 'TUMOR BIOPSY', 'MRI', 'PROCTOSCOPY'], Differential diagnosis:['Diarrhea or constipation', 'diverticulosis', 'fatty food intolerance', 'Hemorrhoids', 'INFLAMMATORY BOWEL DISEASES', 'Irritable Bowel Syndrome', 'RADIATION ENTERITIS'], disease description:Rectal cancer is cancer that begins in the rectum. The rectum is the last several inches of the large intestine. It starts at the end of the final segment of your colon and ends when it reaches the short, narrow passage leading to the anus.Cancer inside the rectum (rectal cancer) and cancer inside the colon (colon cancer) are often referred to together as "colorectal cancer."

A 19-year-old with ['heaviness in the scrotum', 'back pain', 'scrotal swelling']

Disease Name: Carcinoma Scrotum, symptoms: ['heaviness in the scrotum', 'back pain', 'scrotal swelling'], Treatment: ['seminoma responds well to chemotherapy', 'Orchiectomy'], Pathophysiology: Squamous carcinoma of the scrotum has been recognized in chimney sweeps (exposed to carcinogens in soot) , mule spinners (exposed to carcinogens in lubricating oils for the spinning jenny in the cloth industry), Persian nomads (who travelled with pots of burning charcoal between their legs) and Indian jute oil processors . Oil-mist exposure in industry continues to be widespread and, apart from scrotal cancer, has been associated with other cutaneous problems (such as contact dermatitis and oil acne) and respiratory diseases., Epidemiology:['0.3–1.5 cases per 1 000 000 males', 'prognosis for scrotal carcinoma is not good', 'Testicular cancer isn’t preventable, but you can perform testicular self-exams (TSE) to identify changes in your testicles that you should bring to your provider’s attention. Your provider should know about lumps, nodules, hardness or a testicle that’s become bigger or smaller.\n\nMany providers recommend performing a testicular self-exam monthly.'], Complications:['Cardiovascular Disease', 'hypogonadism', 'tinnitus', 'anxiety disorders'], Diagnostics:['Complete Blood Count CBC', 'TUMOR BIOPSY', 'MRI', 'scrotal usg'], Differential diagnosis:['adenofibroma', 'basal cell carcinoma(RODENT ULCER)', 'Extramammary Paget disease', 'HYDROCELE', 'Inguinal Hernias', 'kaposi sarcoma', 'Lung cancer', 'lymphoma', 'squamous intraepithelial neoplasia', 'Tuberculoma', 'VARICOCELE'], disease description:Squamous cell carcinoma (SCC) is the most common scrotal malignancy. Testicular cancer is a growth of cells that starts in the testicles. The testicles, which are also called testes, are in the scrotum. The scrotum is a loose bag of skin underneath the penis. The testicles make sperm and the hormone testosterone.Testicular cancer isn't a common type of cancer.

A 27-year-old with ['dysphagia', 'sore throat', 'trismus', 'pain in ear', 'bleeding from mouth', 'foul smell from mouth']

Disease Name: Carcinoma Tonsil And Tonsillar Fossa, symptoms: ['dysphagia', 'sore throat', 'trismus', 'pain in ear', 'bleeding from mouth', 'foul smell from mouth'], Treatment: ['COMBINATION THERAPY(Surgery may be combined\nwith pre- or postoperative radiation. Chemotherapy may\nbe given as an adjunct to surgery or radiation)', 'radiotherapy along with irradiation of cervical\nnodes.', 'Excision of the tonsil can be done for early\nsuperficial lesions. Larger lesions and those which invade\nbone require wide surgical excision with hemimandibulectomy\nand neck dissection'], Pathophysiology: The exact pathophysiology is unknown. Tumour may spread locally to soft palate and pillars, base of tongue, pharyngeal wall and hypopharynx. It may invade pterygoid muscles and mandible resulting in pain and trismus. Parapharyngeal space may also get invaded.  Fifty per cent of the patients have initial cervical node involvement at the time of presentation. Jugulodigastric nodes are the first to be involved. Distant metastases is seen in late cases. Clinical Features Persistent sore throat, difficulty in swallowing, pain in the ear or lump in the neck are the presenting symptoms. Later on, bleeding from the mouth, fetor oris and trismus may occur., Epidemiology:['23.1% of all malignancies of the oropharynx.', '1 in 60 chance that males will develop tonsil cancer in their lifetime', 'POOR', "To reduce your risk of tonsil cancer:\n\nDon't use tobacco. If you don't use tobacco, don't start. If you currently use tobacco of any kind, talk with your doctor about strategies to help you quit.\nLimit alcohol if you choose to drink. If you choose to drink alcohol, do so in moderation. For healthy adults, that means up to one drink a day for women and up to two drinks a day for men.\nGet regular dental care. During your appointment, your dentist will check your mouth for signs of cancer and precancerous changes.\nConsider the HPV vaccine. Receiving a vaccination to prevent HPV infection may reduce your risk of HPV-related cancers, such as tonsil cancer. Ask your doctor whether an HPV vaccine is appropriate for you."], Complications:['Cardiovascular Disease', 'METASTASES AT DIFFERENT SITES'], Diagnostics:['biopsy', 'X RAY', 'PALPATION'], Differential diagnosis:['lymphoma', 'Merkel Cell Carcinoma', 'Renal cell carcinoma', 'small cell carcinoma', 'Squamous cell carcinoma'], disease description:Tonsil cancer is an abnormal growth of cells that forms in a tonsil. Your tonsils are two oval-shaped pads in the back of your mouth that are part of your body's germ-fighting immune system.Tonsil cancer can cause difficulty swallowing and a sensation that something is caught in your throat.

having ['altered sensorium', 'pulsus paradoxus', 'soft or absent heart sound', 'JUGULAR VENOUS DISTENSION', 'PROMINENT x DESCENT', 'LOW ECG VOLTAGE', 'Hypotension', 'chest pain', 'Dizziness', 'palpitations', 'syncope', 'Breathing difficulty'] at the age of 52

Disease Name: Carcinosarcoma (malignant Mullerian Mixed Tumour), symptoms: ['altered sensorium', 'pulsus paradoxus', 'soft or absent heart sound', 'JUGULAR VENOUS DISTENSION', 'PROMINENT x DESCENT', 'LOW ECG VOLTAGE', 'Hypotension', 'chest pain', 'Dizziness', 'palpitations', 'syncope', 'Breathing difficulty'], Treatment: [{'medication': ['Lidocaine/Lignocaine', 'Amiodarone ', 'Adrenaline (Epinephrine)', 'Procainamide ', 'Noradrenaline/Norepinephrine', 'Atropine/ Atropine methonitrate']}, 'The treatment of cardiac tamponade is the removal of pericardial fluid to help relieve the pressure surrounding the heart. This can be done by performing a needle pericardiocentesis at the bedside, performed either using traditional landmark technique in a sub-xiphoid window or using a point-of-care echo to guide needle placement in real-time. Often the removal of the first small amounts of fluid can make a large improvement in hemodynamics, but leaving a catheter within the pericardium can allow for further drainage', 'Before rushing to decompression of the pericardium, the patient should be provided with oxygen, volume expansion and bed rest with legs elevated. If possible, positive pressure mechanical ventilation should be avoided as it may further decrease venous return and aggravate the symptoms.', 'Surgical options include creating a pericardial window or removing the pericardium. Emergency department resuscitative thoracotomy and the opening of the pericardial sac is a therapy that can be used in traumatic arrests with suspected or confirmed cardiac tamponade. These options are preferable to needle pericardiocentesis for traumatic pericardial effusions.'], Pathophysiology: 4 theories have been proposed (J Clin Pathol 2002;55:321):Collision theory: the sarcoma and carcinoma are two independent neoplasmsCombination theory: both components are derived from a single stem cell that undergoes divergent differentiation early in the evolution of the tumorConversion theory: the sarcomatous element derives from the carcinomatous element during the evolution of the tumorComposition theory: the spindle cell component is a pseudosarcomatous stromal reaction to the carcinomaCarcinomatous cells convert themselves to sarcomatous cells via epithelial to mesenchymal transition; this is supported by high epithelial to mesenchymal transition gene signature scores and is likely due to epigenetic alterations at microRNA promoters and histone gene mutations and amplifications., Epidemiology:['1–2% of uterine neoplasms', 'about two per 100,000 women develop UCS annually. Roughly only 35% of patients survive five years after diagnosis.', '5 year survival', "Many cases can't be prevented. Knowing your personal risk factors may help you get early diagnosis and treatment."], Complications:['bleeding', 'death', 'heart failure', 'shock', 'pulmonary edema'], Diagnostics:['MRI', 'CT SCAN', 'USG'], Differential diagnosis:['constrictive pericarditis', 'heart failure', 'PLEURAL EFFUSION', 'PNEUMOTHORAX', 'Pulmonary Embolism', 'shock'], disease description:A malignant mixed Mullerian tumour (MMMT), also termed uterine carcinosarcoma, is an extremely rare tumour, comprising only 1–2% of uterine neoplasms [1]. These tumours are a dedifferentiated or metaplastic form of endometrial carcinoma [2]. Based on recent data, this tumour is now considered to be uterine epithelial carcinoma rather than sarcoma [3, 4]. The management of MMMTs has seen several advances in recent decades. Despite the use of aggressive adjuvant therapy, only modest improvement in survival is noted over the last couple of decades

Symptoms at 51 years: ['Hypotension', 'bradyarrhythmia', 'unconsciousness', 'breathlessness', 'chest pain', 'Dizziness', 'fatigue', 'weakness']

Disease Name: Cardiac Arrest, symptoms: ['Hypotension', 'bradyarrhythmia', 'unconsciousness', 'breathlessness', 'chest pain', 'Dizziness', 'fatigue', 'weakness'], Treatment: [{'medication': ['Lidocaine/Lignocaine', 'Amiodarone ', 'Adrenaline (Epinephrine)', 'Procainamide ', 'Noradrenaline/Norepinephrine', 'Atropine/ Atropine methonitrate']}, 'An implantable cardioverter defibrillator (ICD).\nA subcutaneous cardioverter device (SCD).\nA wearable cardioverter device (WCD) may help people as they wait for a procedure to implant an ICD or SCD or for a heart transplant.', 'CPR, SHOCK BY defibrillator', 'Targeted temperature management (TTM) is necessary for all patients who cannot follow commands after their heartbeat returns. TTM helps protect the brain by lowering the body temperature using cooling blankets, cooling helmets, ice packs, or other methods.\nOxygen therapy can help get enough oxygen into your lungs so your organs can keep functioning as you recover.\nExtracorporeal membrane oxygenation (ECMO) treatment pumps blood through an artificial lung to add oxygen and remove carbon dioxide before returning the blood to your body. Read more about our study showing that ECMO life support may improve survival of patients who have an out-of-hospital cardiac arrest and do not respond to standard life support.'], Pathophysiology: The main cause of cardiac arrest is ventricular fibrillation or ventricular tachycardia, which are types of arrhythmias. Important risk factors include prior cardiac arrest, coronary heart disease, heart valve disease, congenital heart defects, and arrhythmias caused by faulty genes. However, half of cardiac arrests happen to people who did not know they had a heart problem., Epidemiology:['SCA accounts for 15-20% of all natural deaths in adults in the USA and Western Europe, and up to 50% of all cardiovascular deaths', 'This study found the annual incidence of SCD to be 53 per 1 lakh residents constituting 5.6% of total mortality.', 'poor', 'Treatments that can prevent cardiac arrest or lower your risk of a second episode include:\n\nImplantable cardioverter defibrillator (ICD).\nOther arrhythmia treatments in susceptible people.\nMedicines such as beta-blockers.\nFixing heart artery blockages with either coronary artery bypass surgery or angioplasty.'], Complications:['death', 'ventricular fibrillation', 'cardiopulmonary arrest'], Diagnostics:['ABG', 'Complete Blood Count CBC', 'ECG', 'Electrocardiography (EKG)'], Differential diagnosis:[], disease description:cardiac arrest is the abrupt loss of heart function, breathing and consciousness. The condition usually results from a problem with your heart's electrical system, which disrupts your heart's pumping action and stops blood flow to your body.Sudden cardiac arrest isn't the same as a heart attack, when blood flow to a part of the heart is blocked. However, a heart attack can sometimes trigger an electrical disturbance that leads to sudden cardiac arrest.If not treated immediately, sudden cardiac arrest can lead to death. Survival is possible with fast, appropriate medical care

Individual, 26 years old, with ['cyanosis', 'chest pain with dizziness', 'dyspnea', 'Asymptomatic', 'heart murmurs']

Disease Name: Cardiac Fibroma, symptoms: ['cyanosis', 'chest pain with dizziness', 'dyspnea', 'Asymptomatic', 'heart murmurs'], Treatment: ['Due to the rarity of cardiac fibromas (1 in 280,000 births), the best clinical management is not yet well defined, and it presents as a challenging entity for pediatric cardiologists. Suggestions for different management strategies exist in the literature including surgical resection, single ventricle palliation, cardiac transplant, and even conservative treatment with antiarrhythmic medications.', 'Medical management with amiodarone and beta-blockers seems to be effective. Small and apically located fibromas respond well to antiarrhythmic medications and are probably better managed without defibrillators. Surgical resection has shown to provide curative treatment, alleviating the need for a defibrillator and long-term antiarrhythmic medications.'], Pathophysiology: Here's a general overview of the pathophysiology of cardiac fibroma:Cellular Origin: Cardiac fibromas arise from the proliferation of fibroblasts, which are cells responsible for the production of connective tissue in the heart.Abnormal Growth: The fibroblasts within the myocardium undergo uncontrolled growth, leading to the formation of a mass or tumor. The tumor is composed of collagen fibers and other extracellular matrix components.Structural Disturbance: As the tumor grows, it can disrupt the normal architecture of the heart. It may involve any part of the heart, including the ventricles, atria, or septum (the dividing wall between the chambers).Mechanical Effects: Depending on the size and location, cardiac fibromas can cause mechanical complications. They can impede blood flow through the heart chambers, obstruct the valves, or distort the normal shape of the heart. These mechanical effects can lead to various symptoms, such as arrhythmias, heart murmurs, chest pain, or heart failure.Electrical Disturbances: Cardiac fibromas can disrupt the normal electrical conduction system of the heart. They may interfere with the generation and propagation of electrical signals, leading to abnormal heart rhythms or conduction abnormalities.Potential Complications: In some cases, cardiac fibromas can grow large enough to compress nearby structures, including blood vessels or coronary arteries. This compression can further compromise blood flow and lead to additional cardiac complications., Epidemiology:['prevalence of 1/31,000 to 1/164,000;', '1 in 280,000 births', 'GOOD', 'The approaches that inhibit myofibroblast formation have been demonstrated to prevent cardiac fibrosis, including systemic delivery of antifibrotic drugs, localized delivery of biomaterials, localized delivery of biomaterials and antifibrotic drugs, and localized delivery of cells using biomaterials. \n\nApply sunscreen, limit sun exposure, and avoid ionizing radiation.'], Complications:['death', 'fatality', 'heart failure'], Diagnostics:nan, Differential diagnosis:['HEMANGIOMA', 'lipoma', 'METASTASES AT DIFFERENT SITES', 'MYXOMA', 'Rhabdomyoma', 'rhabdomyosarcoma'], disease description:Cardiac fibromas are the second most common primary cardiac tumor after rhabdomyoma in children. They are primarily composed of connective tissue and fibroblast and although benign, can be symptomatic due to intracavitary obstruction, inflow and outflow tract obstruction, coronary artery compromise, thromboembolic events, conduction defects, and can also lead to sudden death.

Person at 28 with manifestations like ['altered sensorium', 'pulsus paradoxus', 'soft or absent heart sound', 'JUGULAR VENOUS DISTENSION', 'PROMINENT x DESCENT', 'LOW ECG VOLTAGE', 'Hypotension', 'chest pain', 'Dizziness', 'palpitations', 'syncope', 'Breathing difficulty']

Disease Name: Cardiac Tamponade, symptoms: ['altered sensorium', 'pulsus paradoxus', 'soft or absent heart sound', 'JUGULAR VENOUS DISTENSION', 'PROMINENT x DESCENT', 'LOW ECG VOLTAGE', 'Hypotension', 'chest pain', 'Dizziness', 'palpitations', 'syncope', 'Breathing difficulty'], Treatment: ['The treatment of cardiac tamponade is the removal of pericardial fluid to help relieve the pressure surrounding the heart. This can be done by performing a needle pericardiocentesis at the bedside, performed either using traditional landmark technique in a sub-xiphoid window or using a point-of-care echo to guide needle placement in real-time. Often the removal of the first small amounts of fluid can make a large improvement in hemodynamics, but leaving a catheter within the pericardium can allow for further drainage', 'Before rushing to decompression of the pericardium, the patient should be provided with oxygen, volume expansion and bed rest with legs elevated. If possible, positive pressure mechanical ventilation should be avoided as it may further decrease venous return and aggravate the symptoms.', 'Surgical options include creating a pericardial window or removing the pericardium. Emergency department resuscitative thoracotomy and the opening of the pericardial sac is a therapy that can be used in traumatic arrests with suspected or confirmed cardiac tamponade. These options are preferable to needle pericardiocentesis for traumatic pericardial effusions.'], Pathophysiology: Normally, a small, physiologic amount of fluid surrounds the heart within the pericardium. When the volume of fluid builds up fast enough, the chambers of the heart are compressed, and tamponade physiology develops rapidly with much smaller volumes. The classical example is the traumatic cardiac injury resulting in hemp-pericardium. Under this pressure, the chambers of the heart are unable to relax leading to decreased venous return, filling and cardiac output.Slow growing effusions, such as those due to autoimmune disease or neoplasms, allow for stretching of the pericardium, and effusions can become quite large before leading to tamponade physiology.The fluid may be hemorrhagic, serosanguineous or chylous. The underlying pathology behind cardiac tamponade is a decreased in diastolic filling, which leads to a decreased cardiac output. One of the first compensatory signs is tachycardia to overcome the reduced output. In addition, the compression also limits systemic venous return, impairing filling of the right atrium and ventricle., Epidemiology:['About 2 out of every 10,000 people get cardiac tamponade from other diseases.', '2 cases per 10,000 population', 'WITHOUT TREATMENT IT IS FATAL', 'Because either diseases or injuries can cause it, cardiac tamponade is extremely difficult to predict and prevent. However, it may be possible to avoid it with early detection and treatment of a pericardial effusion, especially after an injury or with conditions that you know you have.'], Complications:['bleeding', 'death', 'heart failure', 'shock', 'pulmonary edema'], Diagnostics:['ECG', 'X RAY CHEST', 'trans oesophageal 2D ECHO', 'USG', 'PHYSICAL EXAMINATION'], Differential diagnosis:['constrictive pericarditis', 'heart failure', 'PLEURAL EFFUSION', 'PNEUMOTHORAX', 'Pulmonary Embolism', 'shock'], disease description:Cardiac tamponade is a medical or traumatic emergency that happens when enough fluid accumulates in the pericardial sac compressing the heart and leading to a decrease in cardiac output and shock. The diagnosis of cardiac tamponade is a clinical diagnosis that requires prompt recognition and treatment to prevent cardiovascular collapse and cardiac arrest. The treatment of cardiac tamponade can be performed at the bedside or in the operating room

Person, 30 years old, presenting ['Rapid and weak pulse', 'S3 GALLOP', 'rapid breathing', 'Bradycardia', 'crackles', 'pale skin', 'cold clammy skin', 'low blood pressure', 'altered sensorium', 'breathlessness', 'sweating', 'decreased urine output']

Disease Name: Cardiogenic Shock, symptoms: ['Rapid and weak pulse', 'S3 GALLOP', 'rapid breathing', 'Bradycardia', 'crackles', 'pale skin', 'cold clammy skin', 'low blood pressure', 'altered sensorium', 'breathlessness', 'sweating', 'decreased urine output'], Treatment: ['REPERFUSION-REVASCULARIZATION,MECHANICAL CIRCULATORY SUPPORT,', 'Norepinephrine is preferred over dopamine in patients with severe hypotension (systolic blood pressure less than 70 mm Hg) or hypotension unresponsive to other medications as dopamine has been associated with higher rates of arrhythmias and a higher risk of mortality in this patient population.\nDobutamine is widely used, has beta-1 and beta-2 agonist properties, which can improve myocardial contractility, lower left ventricular end-diastolic pressure, and increased cardiac output.\nMilrinone, also a widely used inotrope, has been shown to reduce left ventricular filling pressures.\nSaline or lactated ringer solution greater than 200 ml per 15 to 30 minutes is indicated in patients with no signs of fluid overload.\nFibrinolytic therapy should be administered to patients who are unsuitable candidates for either percutaneous coronary intervention or coronary artery bypass graft if there are no contraindications. \nPatients with myocardial infarction or acute coronary syndrome are given aspirin and heparin. They have been shown to be effective in reducing mortality.\nDiuretics such as furosemide play a role in decreasing plasma volume and edema and thereby decreasing cardiac output and blood pressure.\nTherapeutic hypothermia is established for out-of-hospital cardiac arrest patients with shockable rhythm to prevent brain injury and improve survival.\nProcedures', 'VASOPRESSORS & IONOTROPES'], Pathophysiology: The understanding of the complex pathophysiology of CS has evolved over the past decades. In general, a profound depression of myocardial contractility results in a deleterious spiral of reduced cardiac output, low blood pressure, and ongoing myocardial ischemia, followed by further contractility reduction. This vicious cycle usually leads to death if not interrupted. CS can result in both acute and subacute derangements to the entire circulatory system. Hypoperfusion of vital organs and extremities remains a clinical hallmark. Although ineffective stroke volume is the inciting event, inadequate circulatory compensation also may contribute to shock. Initial peripheral vasoconstriction may improve coronary and peripheral perfusion at the cost of increased afterload. However, over the course of CS systemic inflammation response triggered by acute cardiac injury often induces pathologic vasodilatation. Inflammatory cytokines, endothelial and inducible nitric oxide synthase may augment NO production, accompanied by peroxynitrite, which has a negative inotropic effect and is cardiotoxic. Lactic acidosis and hypoxemia contribute to the vicious circle, as severe acidosis reduces the efficacy of endogenous and exogenous catecholamines. During ICU support bleeding and/ortransfusions may trigger inflammation and are usually associated with higher mortality., Epidemiology:['cardiogenic shock has a higher incidence in Elderly population\nPatient population with diabetes', '5–10%', 'GOOD', "Don't smoke, and avoid secondhand smoke\nMaintain a healthy weight\nEat less cholesterol and saturated fat.\nCut back on sugar.\nLimit alcohol."], Complications:['Cardiac arrest', 'death', 'renal failure', 'stroke', 'MULTIORGAN FAILURE'], Diagnostics:['2-D Echo', 'ECG', 'X RAY CHEST', 'SERUM LACTATE', 'CYSTATIN C'], Differential diagnosis:['Acute coronary syndromes', 'angina pectoris', 'aortic regurgitation', 'HAEMORRHAGES', 'Myocardial infarction', 'myocarditis', 'Pulmonary Embolism', 'septic shock', 'Systemic inflammatory response syndrome (SIRS)'], disease description:Cardiogenic shock is a life-threatening condition in which your heart suddenly can't pump enough blood to meet your body's needs. The condition is most often caused by a severe heart attack, but not everyone who has a heart attack has cardiogenic shock.Cardiogenic shock is rare. It's often deadly if not treated immediately. When treated immediately, about half the people who develop the condition survive.

Experiencing ['chest pain', 'Dizziness', 'fainting', 'fatigue', 'chest heaviness', 'dyspnea'] at 24 years

Disease Name: Cardiovascular Disorders, symptoms: ['chest pain', 'Dizziness', 'fainting', 'fatigue', 'chest heaviness', 'dyspnea'], Treatment: [{'medication': ['Clopidogrel ', 'Atorvastatin ']}, 'open-heart surgery'], Pathophysiology: Atherosclerosis is the pathogenic process in the arteries and the aorta that can potentially cause disease as a consequence of decreased or absent blood flow from stenosis of the blood vessels.It involves multiple factors dyslipidemia, immunologic phenomena, inflammation, and endothelial dysfunction. These factors are believed to trigger the formation of fatty streak, which is the hallmark in the development of the atherosclerotic plaque; a progressive process that may occur as early as in the childhood. This process comprises intimal thickening with subsequent accumulation of lipid-laden macrophages (foam cells) and extracellular matrix, followed by aggregation and proliferation of smooth muscle cells constituting the formation of the atheroma plaque. As this lesions continue to expand, apoptosis of the deep layers can occur, precipitating further macrophage recruitment that can become calcified and transition to atherosclerotic plaques., Epidemiology:['1 in every 4 deaths,', 'incidence is higher in men at younger ages.', 'You can reduce your cardiovascular risks by:\n\nAvoiding all tobacco products.\nManaging other health conditions, such as Type 2 diabetes, high cholesterol or high blood pressure.\nAchieving and maintaining a healthy weight.\nEating a diet low in saturated fat and sodium.\nExercising at least 30 to 60 minutes per day on most days.\nReducing and managing stress.'], Complications:['Aortic Dissection', 'sudden cardiac death', 'heart attacks'], Diagnostics:['CT SCAN', 'USG', 'stress test', 'Electrocardiography (EKG)', 'Ankle brachial pressure index'], Differential diagnosis:['Acute Pericarditis', 'angina pectoris', 'coronary artery vasospasm', 'DILATED CARDIOMYOPATHY', 'Giant cell arteritis', 'hypertension', 'hypertensive heart disease', 'Kawasaki Disease', 'myocarditis'], disease description:Cardiovascular disease is a group of diseases affecting your heart and blood vessels. These diseases can affect one or many parts of your heart and/or blood vessels. A person may be symptomatic (physically experiencing the disease) or asymptomatic (not feeling anything at all).Cardiovascular disease includes heart or blood vessel issues, including:Narrowing of the blood vessels in your heart, other organs or throughout your body.Heart and blood vessel problems present at birth.Heart valves that aren’t working right.Irregular heart rhythms.

Symptoms at 46 years: ['disorientation', 'fatigue', 'seizures', 'vomiting', 'developmental delay', 'Hypoglycaemia', 'irregular heart beat', 'Irritability', 'HEPATOMEGALY', 'Hypotension', 'lethargy']

Disease Name: Carnitine Acylcarnitine Translocase, symptoms: ['disorientation', 'fatigue', 'seizures', 'vomiting', 'developmental delay', 'Hypoglycaemia', 'irregular heart beat', 'Irritability', 'HEPATOMEGALY', 'Hypotension', 'lethargy'], Treatment: ["Carnitine supplementation: Carnitine is a natural substance that plays a vital role in fatty acid metabolism. In CACTD, supplementation with L-carnitine may be recommended to improve the transport of fatty acids and support energy production. The dosage and frequency of carnitine supplementation will depend on the individual's needs and should be determined by a healthcare professional experienced in metabolic disorders.", 'Genetic counseling: Since CACTD is an inherited condition, genetic counseling should be offered to affected individuals and their families. Genetic counseling can provide information about the inheritance pattern, the risk of having affected children, and available testing options.'], Pathophysiology: Mutations in the SLC25A20 gene cause CACT deficiency. This gene provides instructions for making a protein called carnitine-acylcarnitine translocase (CACT). This protein is essential for fatty acid oxidation, a multistep process that breaks down (metabolizes) fats and converts them into energy. Fatty acid oxidation takes place within mitochondria,  which are the energy-producing centers in cells. A group of fats called long-chain fatty acids must be attached to a substance known as carnitine to enter mitochondria. Once these fatty acids are joined with carnitine, the CACT protein transports them into mitochondria. Fatty acids are a major source of energy for the heart and muscles. During periods of fasting, fatty acids are also an important energy source for the liver and other tissues., Epidemiology:['CACT deficiency is very rare; at least 30 cases have been reported.', 'variable', "This condition is inherited in an autosomal recessive pattern. And therefore, it can't be prevented. \nAlthough Genetic counselling is advisable."], Complications:['coma', 'liver failure'], Diagnostics:['LIVER FUNCTION TEST LFT', 'GENETIC TESTING', 'ammonia level', 'Total and free carnitine', 'acylcarnitine profile'], Differential diagnosis:['Carnitine palmitoyltransferase 2 deficiency', 'Hyperammonemia', 'Hypoglycaemia'], disease description:It is a Mitochondrial Fatty Acid Oxidation Disorders,in which CACT SLC25A20 gene defect occursCarnitine-acylcarnitine translocase (CACT) deficiency is a condition that prevents the body from using certain fats for energy, particularly during periods without food (fasting).

Individual aged 21 with manifestations like ['Irritability', 'Hypoglycaemia', 'EXERCISE INTOLERANCE', 'lethargy', 'muscle pain', 'seizures', 'weakness', 'red urine']

Disease Name: Carnitine Palmitoyl Transferase-ii, symptoms: ['Irritability', 'Hypoglycaemia', 'EXERCISE INTOLERANCE', 'lethargy', 'muscle pain', 'seizures', 'weakness', 'red urine'], Treatment: ['CPT II deficiency is inherited in an autosomal recessive manner. At conception, each sib of an affected individual has a 25% chance of being affected, a 50% chance of being a carrier, and a 25% chance of being unaffected and not a carrier. Heterozygotes (carriers) are usually asymptomatic; however, manifesting carriers have been reported. Prenatal testing for a pregnancy at increased risk for one of the severe forms of the disease is possible either by molecular genetic testing of CPT2, if the two pathogenic variants in the family are known, or by assay of CPT II enzyme activity.', 'Treatment of manifestations: High-carbohydrate (70%) and low-fat (<20%) diet to provide fuel for glycolysis; use of carnitine to convert potentially toxic long-chain acyl-CoAs to acylcarnitines; avoidance of known triggers.\nPrevention of primary manifestations: Infusions of glucose during intercurrent infections to prevent catabolism; frequent meals; avoiding extended fasting and prolonged exercise.\n\nPrevention of secondary complications: Providing adequate hydration during an attack of rhabdomyolysis and myoglobinuria to prevent renal failure.'], Pathophysiology: Carnitine palmitoyltransferase II (CPT II) deficiency is a disorder of long-chain fatty-acid oxidation. The three clinical presentations are lethal neonatal form, severe infantile hepatocardiomuscular form, and myopathic form (which is usually mild and can manifest from infancy to adulthood). While the former two are severe multisystemic diseases characterized by liver failure with hypoketotic hypoglycemia, cardiomyopathy, seizures, and early death, the latter is characterized by exercise-induced muscle pain and weakness, sometimes associated with myoglobinuria. The myopathic form of CPT II deficiency is the most common disorder of lipid metabolism affecting skeletal muscle and the most frequent cause of hereditary myoglobinuria. Males are more likely to be affected than females., Epidemiology:['1-9 / 100 000', 'bad , Babies with the lethal neonatal form of CPT2', "This condition is inherited in an autosomal recessive pattern and therefore, it can't be prevented.\n Although Genetic counselling is advisable."], Complications:['renal failure'], Diagnostics:['Urinary Myoglobin level', 'Total and free carnitine', 'molecular genetic testing'], Differential diagnosis:['Carnitine-acylcarnitine translocase deficiency', 'Glutaric aciduria type 2'], disease description:It is a Mitochondrial Fatty Acid Oxidation Disorders, where their is defect in CPT-II geneCarnitine palmitoyltransferase II (CPT II) deficiency is a disorder of long-chain fatty-acid oxidation. The three clinical presentations are lethal neonatal form, severe infantile hepatocardiomuscular form, and myopathic form (which is usually mild and can manifest from infancy to adulthood). While the former two are severe multisystemic diseases characterized by liver failure with hypoketotic hypoglycemia, cardiomyopathy, seizures, and early death, the latter is characterized by exercise-induced muscle pain and weakness, sometimes associated with myoglobinuria. The myopathic form of CPT II deficiency is the most common disorder of lipid metabolism affecting skeletal muscle and the most frequent cause of hereditary myoglobinuria. Males are more likely to be affected than females.

Person aged 18 dealing with ['EXERCISE INTOLERANCE', 'Hypoglycaemia', 'lethargy', 'muscle pain', 'seizures', 'weakness', 'Irritability', 'red urine']

Disease Name: Carnitine Palmitoyltransferase 2 Deficiency, symptoms: ['EXERCISE INTOLERANCE', 'Hypoglycaemia', 'lethargy', 'muscle pain', 'seizures', 'weakness', 'Irritability', 'red urine'], Treatment: ['CPT II deficiency is inherited in an autosomal recessive manner. At conception, each sib of an affected individual has a 25% chance of being affected, a 50% chance of being a carrier, and a 25% chance of being unaffected and not a carrier. Heterozygotes (carriers) are usually asymptomatic; however, manifesting carriers have been reported. Prenatal testing for a pregnancy at increased risk for one of the severe forms of the disease is possible either by molecular genetic testing of CPT2, if the two pathogenic variants in the family are known, or by assay of CPT II enzyme activity.', 'Treatment of manifestations: High-carbohydrate (70%) and low-fat (<20%) diet to provide fuel for glycolysis; use of carnitine to convert potentially toxic long-chain acyl-CoAs to acylcarnitines; avoidance of known triggers. Prevention of primary manifestations: Infusions of glucose during intercurrent infections to prevent catabolism; frequent meals; avoiding extended fasting and prolonged exercise. Prevention of secondary complications: Providing adequate hydration during an attack of rhabdomyolysis and myoglobinuria to prevent renal failure.'], Pathophysiology: Carnitine palmitoyltransferase II (CPT II) deficiency is a disorder of long-chain fatty-acid oxidation. The three clinical presentations are lethal neonatal form, severe infantile hepatocardiomuscular form, and myopathic form (which is usually mild and can manifest from infancy to adulthood). While the former two are severe multisystemic diseases characterized by liver failure with hypoketotic hypoglycemia, cardiomyopathy, seizures, and early death, the latter is characterized by exercise-induced muscle pain and weakness, sometimes associated with myoglobinuria. The myopathic form of CPT II deficiency is the most common disorder of lipid metabolism affecting skeletal muscle and the most frequent cause of hereditary myoglobinuria. Males are more likely to be affected than females., Epidemiology:['1-9 / 100 000', 'bad', "This condition is inherited in an autosomal recessive pattern and therefore it can't be prevented. \nAlthough Genetic counselling is advisable."], Complications:['renal failure'], Diagnostics:['Urinary Myoglobin level', 'Total and free carnitine', 'molecular genetic testing'], Differential diagnosis:['Carnitine-acylcarnitine translocase deficiency', 'Glutaric aciduria type 2', 'mitochondrial disorders'], disease description:It is a Mitochondrial Fatty Acid Oxidation Disorders, where their is defect in CPT-II geneCarnitine palmitoyltransferase II (CPT II) deficiency is a disorder of long-chain fatty-acid oxidation. The three clinical presentations are lethal neonatal form, severe infantile hepatocardiomuscular form, and myopathic form (which is usually mild and can manifest from infancy to adulthood). While the former two are severe multisystemic diseases characterized by liver failure with hypoketotic hypoglycemia, cardiomyopathy, seizures, and early death, the latter is characterized by exercise-induced muscle pain and weakness, sometimes associated with myoglobinuria. The myopathic form of CPT II deficiency is the most common disorder of lipid metabolism affecting skeletal muscle and the most frequent cause of hereditary myoglobinuria. Males are more likely to be affected than females.

Symptoms at 42: ['developmental delay', 'disorientation', 'fatigue', 'Hypoglycaemia', 'irregular heart beat', 'seizures', 'vomiting', 'Irritability', 'HEPATOMEGALY', 'Hypotension', 'Microcephaly–capillary malformation syndrome']

Disease Name: Carnitine-acylcarnitine Translocase Deficiency, symptoms: ['developmental delay', 'disorientation', 'fatigue', 'Hypoglycaemia', 'irregular heart beat', 'seizures', 'vomiting', 'Irritability', 'HEPATOMEGALY', 'Hypotension', 'Microcephaly–capillary malformation syndrome'], Treatment: ['SUPPORTIVE THERAPY'], Pathophysiology: Mutations in the SLC25A20 gene cause CACT deficiency. This gene provides instructions for making a protein called carnitine-acylcarnitine translocase (CACT). This protein is essential for fatty acid oxidation, a multistep process that breaks down (metabolizes) fats and converts them into energy. Fatty acid oxidation takes place within mitochondria,  which are the energy-producing centers in cells. A group of fats called long-chain fatty acids must be attached to a substance known as carnitine to enter mitochondria. Once these fatty acids are joined with carnitine, the CACT protein transports them into mitochondria. Fatty acids are a major source of energy for the heart and muscles. During periods of fasting, fatty acids are also an important energy source for the liver and other tissues., Epidemiology:['CACT deficiency is very rare; at least 30 cases have been reported.', 'variable', "This condition is inherited in an autosomal recessive pattern. And therefore, it can't be prevented. \nAlthough Genetic counselling is advisable."], Complications:['coma', 'liver failure'], Diagnostics:['GENETIC TESTING', 'Total and free carnitine', 'acylcarnitine profile'], Differential diagnosis:['Hyperammonemia', 'Hypoglycaemia'], disease description:It is a Mitochondrial Fatty Acid Oxidation Disorders,in which CACT SLC25A20 gene defect occursCarnitine-acylcarnitine translocase (CACT) deficiency is a condition that prevents the body from using certain fats for energy, particularly during periods without food (fasting).

Individual aged 51 dealing with ['developmental delay', 'Myoclonic Seizures', 'hypotonia', 'intellectual disability', 'DELAYED INTELLECTUAL DEVELOPMENT', 'muscle weakness']

Disease Name: Carnosinuria/carnosinemia/carnosinase Deficiency, symptoms: ['developmental delay', 'Myoclonic Seizures', 'hypotonia', 'intellectual disability', 'DELAYED INTELLECTUAL DEVELOPMENT', 'muscle weakness'], Treatment: ['The treatment of carnosinemia is symptomatic and supportive as there has not been an effective drug treatment thus far. A vegetarian diet will reduce the amount of carnosine and anserine presented to the body, and may lower serum carnosine levels. However, it remains unclear whether this will have any effect of symptoms or progression of the disease.'], Pathophysiology: Carnosinase, the enzyme responsible for degrading histidine-containing dipeptides, such as carnosine, anserine and homocarnosine, is encoded by the CNDP1 gene. Loss of carnosinase function has been reported in a small number of patients with highly elevated blood carnosine concentrations, but it is unclear whether the variety of clinical symptoms in these individuals is causally related to carnosinase deficiency.Carnosinemia is thought to be inherited in an autosomal recessive inheritance pattern.Recessive genetic disorders occur when an individual inherits an abnormal gene from each parent. If an individual receives one normal gene and one abnormal gene for the disease, the person will be a carrier for the disease, but usually will not show symptoms. The risk for two carrier parents to both pass the abnormal gene and, therefore, have an affected child is 25% with each pregnancy. The risk to have a child who is a carrier, like the parents, is 50% with each pregnancy. The chance for a child to receive normal genes from both parents is 25%. The risk is the same for males and females., Epidemiology:['Carnosinemia is a very rare disorder that affects males and females in equal numbers. Approximately 30 individuals with carnosinemia have been reported in the medical literature world-wide.', 'variable', 'When carnosinase is deficient, carnosine levels rise in the blood and urine.\n\nA strict meat-free diet can help with symptoms, but it will not cure the disease. A vegetarian diet lowers serum carnosine levels by reducing the amount of carnosine and anserine supplied to the body.'], Complications:['Slow growth rate', 'DELAYED INTELLECTUAL DEVELOPMENT'], Diagnostics:['EEG', 'Amino acid level in blood'], Differential diagnosis:['Gaba-transaminase deficiency'], disease description:Carnosinemia is a very rare inherited metabolic disorder characterized by developmental delays and seizures. Symptoms can begin during infancy and may include drowsiness, seizures that may be accompanied by involuntary jerking muscle movements of the arms, legs, or head (myoclonic seizures), and intellectual disability.

Symptoms reported at the age of 42: ['cholangitis', 'jaundice', 'fever', 'Abdominal Pain', 'sepsis', 'hepatic failure']

Disease Name: Carolis Disease, symptoms: ['cholangitis', 'jaundice', 'fever', 'Abdominal Pain', 'sepsis', 'hepatic failure'], Treatment: ['Antibiotics for cholangitis; endoscopic stenting \nas initial measure only; hepatectomy. Liver transplantation \nis final need in most of the patients. Condition carries high \nmortality.', 'The mainstay of therapy is supportive and individualized according to the presentation. Cholangitis due to biliary obstruction is treated with antibiotics that cover gram-negative rods and anaerobic rods. Adequate biliary drainage may be required in the form of biliary stent placement through ERCP or IR-guided percutaneous trans-hepatic catheter (PTC) placement. PTC is usually more effective at draining intra-hepatic obstruction and patients sometimes require indwelling catheters with periodic flushing and changing of the catheter. Ursodeoxycholic acid is used to treat severe cholestasis. Some authors have recommended segmentectomy, lobectomy, or hepaticojejunostomy depending on the range of cystic formation for the treatment of Caroli disease.'], Pathophysiology: Caroli disease is a genetic disorder involving a mutation of the PKHD1 gene that is also responsible for the fibrocystin protein. It is a large gene present on chromosome 6p12 and is expressed primarily in the kidney and with lower levels in the liver and pancreas. More than 100 mutations in this gene have been recorded., Epidemiology:['in approximately 1 in 10,000 live birth', 'Peak incidence is in early adult life, and more than 80% of patients present before turning 30 years of age.', 'good', 'The aim is to prevent recurrent ascites and variceal bleeding'], Complications:['abscess', 'CHOLANGIOCARCINOMA', 'cholangitis'], Diagnostics:['CT Abdomen', 'ERCP', 'MRCP', 'LIVER FUNCTION TEST LFT'], Differential diagnosis:['cholangitis', 'CHOLEDOCHAL CYST', 'POLYCYSTIC LIVER DISEASE', 'PRIMARY SCLEROSING CHOLANGITIS'], disease description:Caroli disease is a rare genetic condition that causes the bile ducts in the liver to be wider than usual. Widening (dilation) of the bile ducts in the liver (intrahepatic bile ducts) can cause bile duct stones to form, which can lead to yellowing of the skin (jaundice) and flu-like symptoms. People with Caroli disease can have many episodes of these symptoms over their lifetime.It is congenital, nonfamilial, multiple, irregular, dilatations of the intrahepatic ducts with stenotic segments in between. It is associated with congenital hepatic fibrosis and medullary sponge kidney. It can also be included under type V choledochal cyst.

Person aged 54 with manifestations like ['Carotid arterial bruit', 'conjunctival chemosis', 'headache', 'proptosis', 'OPHTHALMOPLEGIA', 'pulsatile tinnitus']

Disease Name: Carotid-cavernous Fistula, symptoms: ['Carotid arterial bruit', 'conjunctival chemosis', 'headache', 'proptosis', 'OPHTHALMOPLEGIA', 'pulsatile tinnitus'], Treatment: ['Compression treatment: For low flow fistulas, this conservative therapy is the least invasive alternative that involves compression of the cervical carotid multiple times a day for 4 to 6 weeks to promote thrombosis of the fistula. This is done by applying pressure to the neck by the opposite hand since any cortical ischemia resulting from the compression would cause the hand to fall away from the neck. Closure with conservative management can be expected in only 30% of all cases.', 'A carotid-cavernous fistula requires a definitive\ntreatment, which currently involves endovascular\ntechnique. The fistula can usually be occluded with a\nballoon or coil without sacrifice of the carotid artery.'], Pathophysiology: There are two type of carotid-cavernous fistula: High-flow fistula: These are secondary to trauma or iatrogenic and present acutely with pain, proptosis (often pulsatile exophthalmos). Chemosis, congestion, bruit, ophthalmoplegia (III-VI nerve palsies), headache, and objective pulsatile tinnitus. The classical triad of presentation is proptosis, chemosis, and bruit. It presents within days or weeks following trauma. Low-flow fistula: These develop spontaneously in elder women, during pregnancy or in those with hyperplastic tissue. These typically present slowly with less pronounced symptoms., Epidemiology:['commonly present in young males and tend to be high flow', 'The incidence is less than 1%,', 'GOOD', 'Avoid contact sports\nControl high blood pressure\nMaintain regular follow up with an ophthalmologist'], Complications:['proptosis', 'OPHTHALMOPLEGIA'], Diagnostics:['CT Angio', 'TONOMETRY TEST', 'CT SCAN', 'Carotid Angiography', 'cerebral angiography', 'cerebral angiography'], Differential diagnosis:['CAVERNOUS SINUS THROMBOSIS'], disease description:Carotid cavernous fistula (CCFs) is an abnormal shunt from the carotid artery to the cavernous sinus. The symptomatology of CCFs depends on the involvement of the important neural and vascular structures in the cavernous sinus. These structures include cranial nerves III (oculomotor nerve), IV (trochlear nerve), V1 (ophthalmic nerve), V2 (maxillary nerve), and VI (abducens nerve). CCFs can be classified based on the hemodynamic properties, the etiology, or the anatomy of the shunt.

Suffering from ['malaise', 'fever', 'HEPATOMEGALY', 'anemia'] at 47

Disease Name: Carrión’s Disease (oroya Fever And Verruga Peruana, symptoms: ['malaise', 'fever', 'HEPATOMEGALY', 'anemia'], Treatment: [{'medication': ['Chloramphenicol ', 'Ciprofloxacin ', 'Rifampicin/Rifampin', 'Streptomycin ']}, 'TREATMENT OF MANIFESTATIONS-In the newborn. Hypoplastic anemia may require repeated blood transfusions; congenital megacolon or Hirschsprung disease may require surgical resection.\nIn childhood. Surgery may be needed to fuse unstable cervical vertebrae and/or to treat progressive kyphoscoliosis that compromises lung function in AD; corrective osteotomies may be required to treat progressive varus deformity associated with ligament laxity in the knees. Pubertal maturation may be delayed and may require hormonal induction.'], Pathophysiology: Cartilage-hair hypoplasia is caused by mutations in the RMRP gene. Unlike many genes, the RMRP gene does not contain instructions for making a protein. Instead, a molecule called a noncoding RNA, a chemical cousin of DNA, is produced from the RMRP gene. This RNA attaches (binds) to several proteins, forming an enzyme complex called mitochondrial RNA-processing endoribonuclease, or RNase MRP., Epidemiology:['1 in 1,300 newborns', 'In people of Finnish descent, its incidence is approximately 1 in 20,000. Outside of these populations, the condition is rare, and its specific incidence is not known. It has been reported in individuals of European and Japanese descent.', 'good'], Complications:['opportunistic infections', 'lymphoma'], Diagnostics:['LIVER FUNCTION TEST LFT', 'plain radiograph', 'Giemsa-stained'], Differential diagnosis:['Epstein-Barr Virus', 'Malaria', 'skeletal abnormalities', 'TYPHOID FEVER', 'Zika Virus Disease'], disease description:Cartilage-hair hypoplasia (CHH) is an unusual form of short-limbed dwarfism with frequent and severe infections. It occurs with a high frequency among the Amish and Finnish people.Cartilage-hair hypoplasia is a disorder of bone growth characterized by short stature (dwarfism) with other skeletal abnormalities; fine, sparse hair hypotrichosis and abnormal immune system function (immune deficiency) that can lead to recurrent infections.

At 36 years old, experiencing ['light hair and eyebrows', 'nail deformity', 'short limbs', 'hypopigmentation of the hair and skin', 'short stature', 'hyperextensible joints of hands and feet but an inability to extend the elbows completely', 'light hair', 'short, pudgy hands']

Disease Name: Cartilage Hair Hypoplasia, symptoms: ['light hair and eyebrows', 'nail deformity', 'short limbs', 'hypopigmentation of the hair and skin', 'short stature', 'hyperextensible joints of hands and feet but an inability to extend the elbows completely', 'light hair', 'short, pudgy hands'], Treatment: ['TREATMENT OF MANIFESTATIONS-In the newborn. Hypoplastic anemia may require repeated blood transfusions; congenital megacolon or Hirschsprung disease may require surgical resection.\nIn childhood. Surgery may be needed to fuse unstable cervical vertebrae and/or to treat progressive kyphoscoliosis that compromises lung function in AD; corrective osteotomies may be required to treat progressive varus deformity associated with ligament laxity in the knees. Pubertal maturation may be delayed and may require hormonal induction.'], Pathophysiology: Cartilage-hair hypoplasia is caused by mutations in the RMRP gene. Unlike many genes, the RMRP gene does not contain instructions for making a protein. Instead, a molecule called a noncoding RNA, a chemical cousin of DNA, is produced from the RMRP gene. This RNA attaches (binds) to several proteins, forming an enzyme complex called mitochondrial RNA-processing endoribonuclease, or RNase MRP., Epidemiology:['1 in 1,300 newborns', 'In people of Finnish descent, its incidence is approximately 1 in 20,000. Outside of these populations, the condition is rare, and its specific incidence is not known. It has been reported in individuals of European and Japanese descent.', 'variable'], Complications:['opportunistic infections'], Diagnostics:['LIVER FUNCTION TEST LFT', 'X RAY', 'plain radiograph'], Differential diagnosis:['HYPOCHONDROPLASIA', 'lymphoma', 'severe combined immunodeficiency (SCID)', 'skeletal abnormalities'], disease description:Cartilage-hair hypoplasia (CHH) is an unusual form of short-limbed dwarfism with frequent and severe infections. It occurs with a high frequency among the Amish and Finnish people.Cartilage-hair hypoplasia is a disorder of bone growth characterized by short stature (dwarfism) with other skeletal abnormalities; fine, sparse hair hypotrichosis and abnormal immune system function (immune deficiency) that can lead to recurrent infections.

Suffering from ['woolly hair', 'cardiomyopathy', 'heart failure'] at 33

Disease Name: Carvajal-huerta Syndrome, symptoms: ['woolly hair', 'cardiomyopathy', 'heart failure'], Treatment: ['Implantation of automatic cardioverter defibrillator for prevention of sudden cardiac death, antiarrhythmic drugs for prevention of ventricular tachycardia, and treatment of congestive heart failure are possible treatment modalities.', 'Emollients, topical keratolytics, tazarotene 0.05%, and tretinoin 0.1% can be tried for palmoplantar keratoderma.', 'Heart transplantation can be considered for end-stage disease.'], Pathophysiology: Recessive desmoplakin (DSP) mutations producing a premature stop codon and leading to a truncated protein cause this disorder. Other genetic defects in DSP have been found to generate a wide range of phenotypes. A 10 amino-acid insertion in DSP exerting a dominant negative effect on desmosomal assembly has been found to be associated with cardiomyopathy, and mild hyperkeratosis of the elbows and knees. Heterozygous carriers of the missense mutation p.S299R showed isolated arrhythmogenic right ventricular cardiomyopathy without cutaneous phenotype. Complete loss of the tail domain of desmoplakin presents as acantholytic epidermolysis bullosa. Hence, dosage of desmoplakin is critical in maintaining epidermal integrity as illustrated by compound heterozygote patients carrying one null allele and one missense mutation, who developed pronounced skin fragility and alopecia without cardiac anomalies., Epidemiology:['up to 1 in every 1000 people', 'variable', 'Implantation of automatic cardioverter defibrillator for prevention of sudden cardiac death.'], Complications:['sudden cardiac death'], Diagnostics:['X RAY', 'CARDIAC MRI', 'HISTOLOGIC EXAMINATION', 'Transthoracic echocardiography (TTE)'], Differential diagnosis:['Nonischemic dilated cardiomyopathy'], disease description:The disease represents a cardiocutaneous syndrome with NEPPK, woolly hair and dilated cardiomyopathy. Carvajal syndrome also known as ‘Striate palmoplantar keratoderma with woolly hair and cardiomyopathy is a cutaneous condition inherited in an autosomal recessive pattern due to a defect in desmoplakin gene. The skin disease presents as a striate palmoplantar keratoderma particularly at sites of pressure. The patient is at risk of sudden cardiac death due to dilated cardiomyopathy associated with this entity.

Experiencing ['palpable lymphadenopathy', 'anorexia', 'arthralgia', 'arthritis', 'malaise', 'Night sweat', 'seizures', 'fever', 'weight loss', 'ERYTHEMATOUS PAPULE OR PUSTULE', 'Abdominal Pain', 'backache'] at 24 years old

Disease Name: Cat Scratch Disease, symptoms: ['palpable lymphadenopathy', 'anorexia', 'arthralgia', 'arthritis', 'malaise', 'Night sweat', 'seizures', 'fever', 'weight loss', 'ERYTHEMATOUS PAPULE OR PUSTULE', 'Abdominal Pain', 'backache'], Treatment: [{'medication': ['Azithromycin ']}, 'nti-inflammatory medicine like ibuprofen (Advil, Motrin, Nuprin) or naproxen (Aleve, Anaprox, Naprosyn) sodium to ease swelling and pain. A hot compress can help, too.', 'Suppurative nodes should be drained by large-bore needle aspiration\nand not by incision and drainage in order to avoid chronic\ndraining tracts'], Pathophysiology: The clinical hallmark is lymphadenopathy at the site of inoculation. In the immunocompetent host, a granulomatous response ensues. The immunocompromised host may develop a vascular-proliferative response. Affected lymph nodes become enlarged and tender over one to two weeks. Cat scratch disease is a common cause of chronic lymphadenopathy as well, which may spread beyond the site of inoculation. Cat scratch disease can disseminate to the eye, liver, spleen, and central nervous system (CNS)., Epidemiology:['Fifty-five percent of cases are in children younger than 18 years of age', 'incidence is ~4–10 cases per 100,000 population', 'not specific', 'If you’re around cats, there are a few simple things you can do to help prevent cat scratch disease:\n\nTry to avoid cat bites or scratches.\nWash your hands after playing with, picking up or petting cats or kittens.\nKeep your cats indoors to help reduce the risk of flea bites.\nDon’t pet or pick up stray cats or kittens.\nDon’t let cats lick scratches or wounds.\nAsk your veterinarian how to protect your cat from fleas.\nIf you have a compromised immune system, adopt a cat over a year old rather than a kitten.'], Complications:['Endocarditis', 'Neuroretinitis', 'osteomyelitis', "Parinaud's oculoglandular syndrome"], Diagnostics:['HISTOPATHLOGY', 'Immunofluorescence', 'PCR', 'ELISA', 'SERUM IMMUNOGLOBULINS'], Differential diagnosis:['kaposi sarcoma', 'Leishmaniasis', "lyme's disease", 'lymphadenitis', 'Lymphogranuloma Venereum', 'Nocardiosis', 'Sarcoidosis', 'Sporotrichosis', 'Syphilis', 'Toxoplasmosis'], disease description:Cat scratch fever, also called cat scratch disease (CSD), is a bacterial infection. The disease gets its name because people contract it from cats infected with Bartonella henselae bacteria.B. henselae is the principal etiologic agent of CSD. Rare cases have been associated with Afipia felis and other Bartonella species.

Experiencing ['Oedema in mastoid region', 'TOXEMIA', 'Pupils may be fixed and dilated', 'OPHTHALMOPLEGIA', 'eye pain', 'headache', 'visual disturbances', 'vomiting', 'fever'] at 52 years old

Disease Name: Cavernous Sinus Thrombosis, symptoms: ['Oedema in mastoid region', 'TOXEMIA', 'Pupils may be fixed and dilated', 'OPHTHALMOPLEGIA', 'eye pain', 'headache', 'visual disturbances', 'vomiting', 'fever'], Treatment: ['1. Antibiotics are the sheet anchor of treatment.\nMassive doses of modern potent broad spectrum\nantibiotics should be injected intravenously.\n2. Analgesics and anti-inflammatory drugs control\npain and fever.\n3. Anticoagulants’ role is controversial.'], Pathophysiology: Septic thrombosis of the cavernous sinus is a disastrous sequela, resulting from spread of sepsis travelling along its tributaries from the infected sinuses, teeth, ears, nose, and skin of the face. Very rarely cavernous sinus thrombosis may also occur after trauma (head injury). Cavernous sinus thrombosis is described along with infections of the orbit as it also manifests as acute inflammatory type of proptosis. Communications of cavernous sinus and sources of infection. 1. Anteriorly, the superior and inferior ophthalmic veins drain in the sinus. These veins receive blood from face, nose, paranasal sinuses and orbits. Therefore, infection to cavernous sinus may spread from infected facial wounds, erysipelas, squeezing of stye, furuncles, orbital cellulitis and sinusitis. 2. Posteriorly, the superior and inferior petrosal sinuses leave it to join the lateral sinus. Labyrinthine veins opening into the inferior petrosal sinuses bring infections from the middle ear. Mastoid emissary veins may spread infection from the mastoid air cells. 3. Superiorly, the cavernous sinus communicates with veins of the cerebrum and may be infected from meningitis and cerebral abscesses. 4. Inferiorly, the sinus communicates with pterygoid venous plexus. 5. Medially, the two cavernous sinuses are connected with each other by transverse sinuses which account for transfer of infection from one side to the other., Epidemiology:['approximately 1% to 4% of cerebral venous and sinus thrombosis', '0.2 to 1.6 per 100,000 per year.', 'poor', 'You can do a lot to prevent stroke by leading a heart healthy lifestyle:\n\nEat a low-fat diet, including lots of fruits and vegetables.\nGet daily exercise.\nAvoid cigarette smoke.\nControl chronic health conditions, such as diabetes.'], Complications:['death', 'meningeal signs', 'pulmonary infarction', 'fits'], Diagnostics:['FUNDOSCOPY', 'CT HEAD', 'BLOOD CULTURE', 'MRI ANGIOGRAPHY'], Differential diagnosis:['Meningioma', 'orbital cellulitis', 'Sarcoidosis', 'Syphilis', 'TUBERCULOSIS'], disease description:Cavernous sinus thrombosis (CST) is a rare, life-threatening disorder that can complicate facial infection, sinusitis, orbital cellulitis, pharyngitis, or otitis or following traumatic injury or surgery, especially in the setting of a thrombophilic disorder. Early recognition of cavernous sinus thrombosis which, often presents with fever, headache, eye findings such as periorbital swelling, and ophthalmoplegia, is critical for a good outcome. Despite modern treatment with antibiotics and anticoagulation, the risk of long-term sequelae, such as vision, diplopia, and stroke, remains significant .

Symptoms at 32 years: ['Tachycardia', 'Hypotension', 'jaundice', 'nausea', 'pruritus', 'vomiting', 'fever', 'Abdominal Pain', 'clay coloured stool', 'ALTERED MENTAL STATUS']

Disease Name: Cbd Stone, symptoms: ['Tachycardia', 'Hypotension', 'jaundice', 'nausea', 'pruritus', 'vomiting', 'fever', 'Abdominal Pain', 'clay coloured stool', 'ALTERED MENTAL STATUS'], Treatment: ['The treatment for choledocholithiasis is the removal of the obstructing stones via endoscopic means. An ERCP can be performed under general anesthesia, with the patient in either prone, left lateral, or supine position, though prone is the most common position used. The endoscopist will then place a duodenoscope into the second portion of the duodenum and advance a catheter and guidewire into the common bile duct. A sphincterotome then is used to cut the papilla, using cautery, and enlarge the ampulla of Vater. Often, the stones will be released with this maneuver.', 'There are no medications that will cure choledocholithiasis. However, a one-time dose of 50 mg to 100 mg rectal indomethacin can be used to prevent post-procedure pancreatitis if the pancreatic duct was manipulated during an ERCP. Antibiotics are typically not needed for choledocholithiasis unless the patient also has associated cholecystitis or cholangitis.'], Pathophysiology: Bile made in the liver and stored in the gallbladder can lead to gallstone formation. In some patients with gallstones, the stones will pass from the gallbladder into the cystic duct and then into the common bile duct. Most of the choledocholithiasis cases are secondary to the gallstones passage from the gallbladder into the CBD.Primary choledocholithiasis which is the formation of stones within the common bile duct is seen less commonly. Primary choledocholithiasis occurs in the setting of bile stasis, which results in intraductal stone formation. The size of the bile duct increases with age. Older adults with dilated bile ducts and biliary diverticula are at risk for the formation of primary bile duct stones. Less common sources of choledocholithiasis include complicated Mirizzi syndrome or hepatolithiasis. Bile flow is obstructed by stones within the common bile duct, which leads to obstructive jaundice and possibly hepatitis. The stagnant bile can also lead to bactibilia and ascending cholangitis., Epidemiology:['10–15% of the adult population', '5% to 20% at the time of cholecystectomy in patients with cholelithiasis.', 'GOOD', 'As cholesterol gallstones are the most common type, you may be able to reduce your risk by reducing cholesterol in your blood through dietary and lifestyle changes. Healthcare providers also recommend that you avoid “yo-yo” dieting and lose weight gradually. Losing too quickly can encourage gallstones.'], Complications:['renal failure', 'sepsis'], Diagnostics:['Total Leucocyte Count (TLC)', 'Cranial Ultrasonography', 'MRCP', 'USG ABDOMEN(W/A)', 'LIVER FUNCTION TEST LFT', 'CT SCAN'], Differential diagnosis:['acute cholecystitis', 'bile duct cystadenocarcinoma', 'CHOLEDOCHAL CYST', 'PEPTIC ULCER DISEASE'], disease description:Choledocholithiasis is the presence of stones within the common bile duct (CBD). It is estimated that common bile duct stones are present in anywhere from 1-15% of patients with cholelithiasis. The present-day treatment of bile duct stones is endoscopic retrograde cholangiopancreatography (ERCP), or in some cases, laparoscopic cholecystectomy with bile duct exploration. In most US centers, when bile duct stones present, ERCP is usually followed by laparoscopic cholecystectomy.

Suffering from ['MUSCLE WASTING', 'Irritability', 'Osteoporosis', 'abdominal distension', 'anaemia', 'pathological fracture', 'amenorrhoea', 'anorexia', 'CHRONIC DIARRHEA', 'constipation', 'DELAYED DENTITION', 'diarrhea', 'enamel hypoplasia', 'failure to thrive', 'muscle weakness', 'Numbness', 'Tingling', 'Malnutrition', 'weight loss', 'DELAYED PUBERTY', 'vesicular eruption', 'growth abnormality', 'Bleeding tendencies', 'skin abnormalities', 'iron deficiency anemia', 'Ataxia', 'Peripheral neuropathy', 'seizures', 'vomiting', 'Generalised oedema'] at 18 years old, female

Disease Name: Celiac Disease, symptoms: ['MUSCLE WASTING', 'Irritability', 'Osteoporosis', 'abdominal distension', 'anaemia', 'pathological fracture', 'amenorrhoea', 'anorexia', 'CHRONIC DIARRHEA', 'constipation', 'DELAYED DENTITION', 'diarrhea', 'enamel hypoplasia', 'failure to thrive', 'muscle weakness', 'Numbness', 'Tingling', 'Malnutrition', 'weight loss', 'DELAYED PUBERTY', 'vesicular eruption', 'growth abnormality', 'Bleeding tendencies', 'skin abnormalities', 'iron deficiency anemia', 'Ataxia', 'Peripheral neuropathy', 'seizures', 'vomiting', 'Generalised oedema'], Treatment: ['The only treatment for CD is lifelong strict adherence to a gluten-free diet. This\nrequires a wheat-, barley-, and rye-free diet.\nAvoid all foods containing wheat, rye, and barley gluten (pure oats usually safe).\nAvoid malt unless clearly labeled as derived from corn.\nUse only rice, corn, maize, buckwheat, millet, amaranth, quinoa, sorghum, potato or potato starch, soybean,\ntapioca, and teff, bean, and nut flours.\nWheat starch and products containing wheat starch should only be used if they contain <20 ppm gluten and are\nmarked “gluten free.”\nRead all labels and study ingredients of processed foods.\nBeware of gluten in medications, supplements, food additives, emulsifiers, or stabilizers.\nLimit milk and milk products initially if there is evidence of lactose intolerance.\nAvoid all beers, lagers, ales, and stouts (unless labeled gluten free).\nWine, most liqueurs, ciders, and spirits, including whiskey and brandy, are allowed.'], Pathophysiology: A peptide derived from gluten called gliadin causes damage to the small intestine. There is local inflammation, and the process leads to the destruction of the small intestinal villi.  This destruction, in turn, leads to the decreased functionality of the intestinal surface and malabsorption. The lack of nutrient absorption impacts directly on the digestive system but also indirectly on all the systems of the body. This impact results in generally poor health and is the reason why celiac disease can have signs and symptoms arising from almost any system of the body, not just the gastrointestinal system, Epidemiology:['1% prevalence', 'incidence is greater among people with autoimmune disorders like type 1 diabetes', 'DEPENDS ON SEVERITY OF SYMPTOMS', 'Celiac disease cannot necessarily be prevented, but it can be successfully managed and improved with the right diet and behaviors.\n\nIf you are diagnosed with celiac disease, you may be able to prevent it from causing further damage to your small intestine. This can be achieved by eating a healthy and strict gluten-free diet. Researchers say a gluten-free diet may even reverse damage to the small intestine caused by celiac disease.'], Complications:['bleeding diathesis', 'Epilepsy', 'failure to thrive', 'iron deficiency anemia', 'Osteoporosis', 'seizures'], Diagnostics:['serum Folic Acid', 'SERUM IRON', 'serum Vitamin B12 level', 'SERUM VITAMIN D3 LEVEL', 'tTG serology', 'serum IgA anti endomyseal antibody', 'GENETIC TESTING', 'ENDOSCOPY', 'SEROLOGIC TEST'], Differential diagnosis:['Bacterial Gastroenteritis', 'Crohns Disease', 'Hypocalcemia', 'iron deficiency anemia', 'Irritable Bowel Syndrome', 'MALABSORPTION', 'viral gastroenteritis'], disease description:Celiac disease is an enteropathy of the small intestine. It is triggered by exposure to gluten in the diet of susceptible people. The susceptibility is genetically determined. The condition is chronic, and currently, the only treatment consists of permanent exclusion of gluten from the food intake.Patients with celiac disease can present with diarrhea and failure to thrive; some may be asymptomatic.

At 33, dealing with ['Well circumscribed mass']

Disease Name: Cellular Angiofibroma, symptoms: ['Well circumscribed mass'], Treatment: ['Excision with negative margins.\nUsually does not recur.'], Pathophysiology: Pathophysiology is poorly understood. Etiopathologically, it is suggested that these lesions are stem cell–derived, with a capacity for adipose and myofibroblastic differentiation in accordance with the influence of hormones, microenvironments, cytokines and growth factors. , Epidemiology:['incidence in the 5th decade of life in women, whereas men are usually affected in the 7th decade', 'variable', 'Surgery is often used to remove the tumor.'], Complications:[], Diagnostics:['Colposcopy', 'Cytogenetics', 'MRI', 'USG', 'Immunostaining', 'Immunostaining'], Differential diagnosis:['Angiomyofibroblastoma', 'fibroepithelial polyp', 'leiomyoma', 'Myxoid liposarcoma', 'schwannoma'], disease description:Cellular angiofibroma represents a rare benign mesenchymal tumor, occurring mainly in the superficial soft tissue of the genital region. The involvement of 13q14 in some cases confirmed the morphological suggested link with spindle cell lipoma and mammary-type myofibroblastoma

Symptoms reported by a 38-year-old female include ['ascites', 'pelvic pain', 'Abdominal Pain']

Disease Name: Cellular Fibroma, symptoms: ['ascites', 'pelvic pain', 'Abdominal Pain'], Treatment: ['Surgical excision (salpingo-oophorectomy, oophorectomy or ovarian sparing procedure with or without hysterectomy depending on patient’s age).\nCellular fibromas require long term follow up, particularly in the setting of ovarian surface involvement, intraoperative rupture or extraovarian spread.'], Pathophysiology: Pathophysiology involves neoplastic transformation of ovarian stromal cells due to hereditary or sporadic genetic abnormalities., Epidemiology:['30-40 % of all normal children.', 'Most common ovarian stromal tumor\n~4% of all ovarian tumors', 'poor', 'You can’t prevent fibromas caused by genetics or unknown reasons. For tumors caused by trauma or irritation, you can take precautions to lower your risk.'], Complications:['FIBROID UTERUS', 'infertility'], Diagnostics:['CA 125', 'Cytogenetics', 'MRI', 'CT SCAN', 'CT SCAN', 'USG', 'ELECTRON MICROSCOPY', 'Immunostaining', 'Immunostaining'], Differential diagnosis:['fibromatosis', 'Fibrosarcoma', 'leiomyoma', 'Sclerosing stromal tumour'], disease description:Cellular fibroblastic tumors of the ovary are currently classified as either cellular fibroma (CF) or fibrosarcoma. The former are characterized by bland nuclei, 3 or fewer mitotic figures per 10 high-power fields (MFs/10 HPFs), and a low malignant potential, whereas fibrosarcomas usually have severe nuclear atypia, > or = 4 MFs/10 HPFs, and an aggressive clinical course. The prognosis of cellular fibromatous tumors with > or = 4 MFs/10 HPFs and low-grade cytology is not established and it is the purpose of this study to investigate that aspect

A 53-year-old suffering ['fever', 'Irritability', 'failure to thrive', 'polyuria', 'increased thirst', 'NOCTURNAL ENURESIS', 'polydipsia', 'Weight disturbances', 'increased frequency of urination']

Disease Name: Cellulitis And Erysipelas, symptoms: ['fever', 'Irritability', 'failure to thrive', 'polyuria', 'increased thirst', 'NOCTURNAL ENURESIS', 'polydipsia', 'Weight disturbances', 'increased frequency of urination'], Treatment: [{'medication': ['vassopresin']}, 'Patients with both central and NDI\nshould ingest a diet without excessive solute (e.g., sodium chloride) to help\ndecrease urine output when vasopressin action wanes.', 'Treatment of central DI in older children is best accomplished with the use of\nDDAVP. The intranasal preparation of DDAVP (10 µg/0.1\nmL) can be administered by rhinal tube (allowing dose titration) or by nasal\nspray (10 µg/puff). Oral dosages of\n25-300 µg every 8-12 hr are safe and effective in children. A typical dosage for intravenous vasopressin therapy is 1.5\nmU/kg/hr, which results in a blood vasopressin concentration of approximately\n10 pg/mL. \nVasopressin concentrations >1,000 pg/mL should be avoided because\nthey can cause cutaneous necrosis, rhabdomyolysis, cardiac rhythm\ndisturbances, and hypertension.'], Pathophysiology: Central DI can result from multiple etiologies, including genetic mutations in the vasopressin gene; trauma (accidental or surgical) to vasopressin neurons; congenital malformations of the hypothalamus or pituitary; neoplasms; infiltrative, autoimmune, and infectious diseases affecting vasopressin neurons or fiber tracts; and increased metabolism of vasopressin. In approximately 10% of children with central DI, the etiology is idiopathic. Other pituitary hormone deficiencies may be present. Over time, up to 35% of those with idiopathic central DI will develop other hormone deficiencies or have an underlying etiology identified. Autosomal dominant central DI usually occurs within the first 5 yr of life and results from mutations in the vasopressin gene, AVP . A number of mutations can cause gene-processing defects in a subset of vasopressin-expressing neurons, which have been postulated to result in endoplasmic reticulum stress and cell death. Wolfram syndrome, which includes DI, diabetes mellitus, optic atrophy, and deafness, also results in vasopressin deficiency. Mutations in 2 genes, which give rise to endoplasmic reticulum proteins, are associated with this condition. Congenital brain abnormalities such as optic nerve hypoplasia syndrome with agenesis of the corpus callosum, the Niikawa- Kuroki syndrome, holoprosencephaly, and familial pituitary hypoplasia with absent stalk may be associated with central DI and defects in thirst perception (adipsia). Empty sella syndrome, possibly resulting from unrecognized pituitary infarction, can be associated with DI in children. Trauma to the base of the brain and neurosurgical intervention in the region of the hypothalamus or pituitary are common causes of central DI. The triphasic response following surgery refers to an initial phase of transient DI, lasting 12- 48 hr, followed by a 2nd phase of syndrome of inappropriate antidiuretic hormone secretion (SIADH), lasting up to 10 days, which may be followed by permanent DI. The initial phase may be the result of local edema interfering with normal vasopressin secretion; the 2nd phase results from unregulated vasopressin release from dying neurons, whereas in the 3rd phase, permanent DI, results if more than 90% of the neurons have been destroyed. Given the anatomic distribution of vasopressin neurons over a large area within the hypothalamus, tumors causing DI must either be very large and infiltrative or be strategically located near the base of the hypothalamus, where vasopressin axons converge before their entry into the posterior pituitary. Germinomas and pinealomas typically arise in this region and are among the most common primary brain tumors associated with DI. Germinomas can be very small and undetectable by MRI for several years following the onset of polyuria. Quantitative measurement of a-fetoprotein and ß-human chorionic gonadotropin, often secreted by germinomas, should be performed in children with idiopathic or unexplained DI, in addition to serial MRI scans. Craniopharyngiomas and optic gliomas can also cause central DI when they are very large, although this is more often a postoperative complication of the treatment for these tumors. Hematologic malignancies, such as acute myelocytic leukemia, can cause DI via infiltration of the pituitary stalk and sella. Langerhans cell histiocytosis  and lymphocytic hypophysitis are common types of infiltrative disorders causing central DI, with hypophysitis as the cause in 50% of cases of “idiopathic” central DI. Infections involving the base of the brain, including meningitis (meningococcal, cryptococcal, listerial,  toxoplasmal), congenital cytomegalovirus infection, and nonspecific inflammatory diseases of the brain may give rise to central DI that is often transient. Drugs associated with the inhibition of vasopressin release include ethanol, phenytoin, opiate antagonists, halothane, and a-adrenergic agents., Epidemiology:['1 in 25,000 people, or about 0.004% of the global population.', 'GOOD', 'Many of the cases may not be preventable. Prompt treatment of infections, tumors, and injuries may reduce risk.'], Complications:['headache', 'hypernatremia', 'kidney damage', 'Tachycardia', 'weight loss', 'brain damage', 'Hypotension', 'Temperature'], Diagnostics:['ABG', 'SERUM Osmolality', 'SERUM Sodium Na+', 'URINE OSMOLALITY', 'MRI Brain', 'serum potassium K+', 'plasma creatinine'], Differential diagnosis:['deep vein thrombosis', 'Erysipelas', 'Necrotizing fasciitis', 'Septic arthritis'], disease description:Central diabetes insipidus (CDI) is a rare condition in which your body doesn’t have enough antidiuretic hormone (ADH, or vasopressin), which causes you to pee large volumes of urine and become very thirsty. Your hypothalamus produces ADH, but your pituitary gland stores and releases it. You can get central diabetes insipidus if your pituitary gland or hypothalamus is damaged.

Person at 20 with manifestations like ['Tachycardia', 'vesicles', 'Hypotension', 'Warm Skin', 'bullae', 'erythema', 'lymphadenopathy', 'fever', 'LOCALIZED TENDERNESS', 'diffuse swelling of the skin']

Disease Name: Cellulitis, symptoms: ['Tachycardia', 'vesicles', 'Hypotension', 'Warm Skin', 'bullae', 'erythema', 'lymphadenopathy', 'fever', 'LOCALIZED TENDERNESS', 'diffuse swelling of the skin'], Treatment: [{'medication': ['Amoxicillin and Clavulanic acid ']}, 'Elevation of limb or part to reduce oedema so as to increase \nthe circulation and bandaging.', 'Antibiotics-penicillins, cephalosporins. \nDressing (often glycerine dressing is used as it reduces the \noedema because of its hygroscopic action glycerine magnesium sulphate dressing'], Pathophysiology: Cellulitis is characterized by erythema, warmth, edema, and tenderness to palpation resulting from cytokine and neutrophil response from bacteria breaching the epidermis. The cytokines and neutrophils are recruited to the affected area after bacteria have penetrated the skin leading to an epidermal response. This response includes the production of antimicrobial peptides and keratinocyte proliferation and is postulated to produce the characteristic exam findings in cellulitis. Group A Streptococci, the most common bacteria to cause cellulitis, can also produce virulence factors such as pyrogenic exotoxins (A, B, C, and F) and streptococcal superantigen that can lead to a more pronounced and invasive disease., Epidemiology:['approximately 50 cases per 1000 patient-years', 'most often occurs in middle-aged and older adults.', 'good', 'You can reduce your risk of developing cellulitis by:\n\nCleaning your wounds or sores with antibacterial soap and water.\nApplying an antibiotic ointment on your wounds or sores.\nCovering your wounds or sores with a bandage to prevent dirt or bacteria from entering the area.\nRefraining from touching or rubbing your affected areas.\nGetting medical attention right away for any deep cuts or puncture wounds.'], Complications:['Endocarditis', 'osteomyelitis', 'Bacteremia'], Diagnostics:['Blood Glucose test', 'Total Leucocyte Count (TLC)', 'HISTORY TAKING', 'PHYSICAL EXAMINATION'], Differential diagnosis:['Diabetes mellitus type 1', 'nocturia', 'polydipsia'], disease description:Cellulitis  is a common, potentially serious bacterial skin infection. The affected skin is swollen and inflamed and is typically painful and warm to the touch.Cellulitis usually affects the lower legs, but it can occur on the face, arms and other areas. The infection happens when a break in the skin allows bacteria to enter.Left untreated, the infection can spread to the lymph nodes and bloodstream and rapidly become life-threatening. 

Person aged 43 with manifestations like ['fever', 'Irritability', 'failure to thrive', 'NOCTURNAL ENURESIS', 'polydipsia', 'polyuria', 'Weight disturbances']

Disease Name: Central Diabetes Insipidus, symptoms: ['fever', 'Irritability', 'failure to thrive', 'NOCTURNAL ENURESIS', 'polydipsia', 'polyuria', 'Weight disturbances'], Treatment: [{'medication': ['vassopresin']}, 'Patients with both central and NDI\nshould ingest a diet without excessive solute (e.g., sodium chloride) to help\ndecrease urine output when vasopressin action wanes.', 'Treatment of central DI in older children is best accomplished with the use of\nDDAVP. The intranasal preparation of DDAVP (10 µg/0.1\nmL) can be administered by rhinal tube (allowing dose titration) or by nasal\nspray (10 µg/puff). Oral dosages of\n25-300 µg every 8-12 hr are safe and effective in children. A typical dosage for intravenous vasopressin therapy is 1.5\nmU/kg/hr, which results in a blood vasopressin concentration of approximately\n10 pg/mL. \nVasopressin concentrations >1,000 pg/mL should be avoided because\nthey can cause cutaneous necrosis, rhabdomyolysis, cardiac rhythm\ndisturbances, and hypertension.'], Pathophysiology: Central DI can result from multiple etiologies, including genetic mutations in the vasopressin gene; trauma (accidental or surgical) to vasopressin neurons; congenital malformations of the hypothalamus or pituitary; neoplasms; infiltrative, autoimmune, and infectious diseases affecting vasopressin neurons or fiber tracts; and increased metabolism of vasopressin. In approximately 10% of children with central DI, the etiology is idiopathic. Other pituitary hormone deficiencies may be present. Over time, up to 35% of those with idiopathic central DI will develop other hormone deficiencies or have an underlying etiology identified. Autosomal dominant central DI usually occurs within the first 5 yr of life and results from mutations in the vasopressin gene, AVP . A number of mutations can cause gene-processing defects in a subset of vasopressin-expressing neurons, which have been postulated to result in endoplasmic reticulum stress and cell death. Wolfram syndrome, which includes DI, diabetes mellitus, optic atrophy, and deafness, also results in vasopressin deficiency. Mutations in 2 genes, which give rise to endoplasmic reticulum proteins, are associated with this condition. Congenital brain abnormalities such as optic nerve hypoplasia syndrome with agenesis of the corpus callosum, the Niikawa- Kuroki syndrome, holoprosencephaly, and familial pituitary hypoplasia with absent stalk may be associated with central DI and defects in thirst perception (adipsia). Empty sella syndrome, possibly resulting from unrecognized pituitary infarction, can be associated with DI in children. Trauma to the base of the brain and neurosurgical intervention in the region of the hypothalamus or pituitary are common causes of central DI. The triphasic response following surgery refers to an initial phase of transient DI, lasting 12- 48 hr, followed by a 2nd phase of syndrome of inappropriate antidiuretic hormone secretion (SIADH), lasting up to 10 days, which may be followed by permanent DI. The initial phase may be the result of local edema interfering with normal vasopressin secretion; the 2nd phase results from unregulated vasopressin release from dying neurons, whereas in the 3rd phase, permanent DI, results if more than 90% of the neurons have been destroyed. Given the anatomic distribution of vasopressin neurons over a large area within the hypothalamus, tumors causing DI must either be very large and infiltrative or be strategically located near the base of the hypothalamus, where vasopressin axons converge before their entry into the posterior pituitary. Germinomas and pinealomas typically arise in this region and are among the most common primary brain tumors associated with DI. Germinomas can be very small and undetectable by MRI for several years following the onset of polyuria. Quantitative measurement of a-fetoprotein and ß-human chorionic gonadotropin, often secreted by germinomas, should be performed in children with idiopathic or unexplained DI, in addition to serial MRI scans. Craniopharyngiomas and optic gliomas can also cause central DI when they are very large, although this is more often a postoperative complication of the treatment for these tumors. Hematologic malignancies, such as acute myelocytic leukemia, can cause DI via infiltration of the pituitary stalk and sella. Langerhans cell histiocytosis  and lymphocytic hypophysitis are common types of infiltrative disorders causing central DI, with hypophysitis as the cause in 50% of cases of “idiopathic” central DI. Infections involving the base of the brain, including meningitis (meningococcal, cryptococcal, listerial, toxoplasmal), congenital cytomegalovirus infection, and nonspecific inflammatory diseases of the brain may give rise to central DI that is often transient. Drugs associated with the inhibition of vasopressin release include ethanol, phenytoin, opiate antagonists, halothane, and a-adrenergic agents., Epidemiology:['prevalence was 7 in 10 000', '1 in 25,000 people or about 0.004% of the global population', 'GOOD', 'Unfortunately, most cases of central diabetes insipidus (CDI) can’t be prevented. Risk factors for developing CDI include:\n\nBrain surgery.\nFamily history of diabetes insipidus and/or Wolfram syndrome.\nHead injury.\nInfection of the brain.'], Complications:['hypernatremia', 'kidney damage', 'Tachycardia', 'weight loss', 'brain damage', 'Hypotension'], Diagnostics:['ABG', 'SERUM Osmolality', 'SERUM Sodium Na+', 'MRI Brain', 'serum potassium K+', 'plasma creatinine'], Differential diagnosis:['Diabetes mellitus type 1', 'nocturia', 'polyuria'], disease description:Central diabetes insipidus (CDI) is a rare condition in which your body doesn’t have enough antidiuretic hormone (ADH, or vasopressin), which causes you to pee large volumes of urine and become very thirsty. Your hypothalamus produces ADH, but your pituitary gland stores and releases it. You can get central diabetes insipidus if your pituitary gland or hypothalamus is damaged.

having ['localized swelling', 'Stiffness of joint', 'Tenderness', 'External rotation of the leg, the patella facing outwards', 'Shortening of the leg', 'severe pain'] at the age of 47

Disease Name: Central Fracture-dislocation Of The Hip, symptoms: ['localized swelling', 'Stiffness of joint', 'Tenderness', 'External rotation of the leg, the patella facing outwards', 'Shortening of the leg', 'severe pain'], Treatment: ['1- skeletal traction is applied distally and laterally\n2- continuous traction\n3- surgical reconstruction of the acetabular floor', 'Operative treatment for central acetabular fractures dislocation includes conservative treatment with skeletal traction, open reduction with internal fixation and total hip arthroplasty. Hip arthroplasty with fixation of acetabulum fracture is helpful in elderly patients in view of high risk of avascular necrosis.'], Pathophysiology: Central dislocation of femoral head was reported as a result of axial loading the. femur in abduction. When an impact occurs, the force is usually transmitted from the femoral head to the acetabular columns and walls. Therefore, most quadrilateral plate fractures are associated with acetabular anterior and/or posterior column fractures . Elementary pattern of the acetabular rim are : anterior wall, anterior column, posterior wall, posterior column, and transverse . A severe blow to the lateral aspect of the hip especially when it is abducted may drive the femoral head centrally trough a comminuted fracture in the medial wall of the acetabulum , Epidemiology:['occurs in 3.8% of patients when followed for ten years', 'less than 10%', 'GOOD', '1. Safety: Since hip dislocation usually results from an accident, common safety guidelines are the best prevention. Always wear your seatbelt in the car and wear protective gear when participating in contact sports. Take precautions when using a ladder or workplace equipment, too.\n2. Conditioning: If you’ve previously dislocated your hip, it might be more prone to dislocating again. You can help reinforce your joint by strengthening your hip tendons and muscles through physical therapy and keeping them conditioned through regular exercise.\n3. Hip dysplasia care: Children with hip dysplasia should be treated while their skeletons are still growing to prevent future injury.'], Complications:['myositis', 'stiffness'], Diagnostics:['X RAY AP VIEWS', 'X RAY PELVIS', 'CT SCAN'], Differential diagnosis:['FEMORAL NECK FRACTURE', 'pathological fracture', 'Torticollis'], disease description:Hip dislocations are traumatic hip injuries that result in femoral head dislocation from the acetabular socket.Diagnosis can be made with hip radiographs to determine the direction of dislocation and CT scan studies to assess for associated injuries. Treatment is urgent reduction to minimize risk of avascular necrosis followed by CT scan to assess for associated injuries that may require surgical treatment (loose bodies, femoral head fractures, acetabular fractures).

Suffering from ['seizures', 'weakness', 'Memory disturbances', 'headache', 'nausea', 'vomiting', 'VISION DEFICITS'] at the age of 38

Disease Name: Central Neurocytoma (who Grade 2), symptoms: ['seizures', 'weakness', 'Memory disturbances', 'headache', 'nausea', 'vomiting', 'VISION DEFICITS'], Treatment: ['Although chemotherapy is not a primary treatment modality for CN, chemotherapy has been used as an adjuvant or salvage therapy for recurrent CNs or inoperable patients.', 'Surgical management with a gross-total resection (GTR) is currently the gold standard treatment for CNs, which often has excellent prognosis and minimizes the chances of CN recurrence.'], Pathophysiology: Central neurocytomas demonstrate neuronal differentiation and histologically appear similar to oligodendrogliomas which, historically, resulted in many tumors erroneously categorized.The initial description classified them as WHO grade 1 lesions. However, this was upgraded in 1993 to WHO grade 2 as it was recognized that at least some of these tumors exhibited more aggressive behavior., Epidemiology:['CN remains relatively rare, comprising about 0.1–0.5% of all brain tumors', 'Most common neoplasm of septum pellucidum in young adults but still < 1% of all CNS tumors', 'variable', 'To protect function as much as possible, complete tumor resection should be the first choice of treatment for CN.'], Complications:['headache', 'seizures', 'vomiting'], Diagnostics:['MRI', 'CT SCAN', 'CYTOLOGY', 'ELECTRON MICROSCOPY', 'Immunostaining', 'Immunostaining'], Differential diagnosis:['choroid plexus papilloma (who grade 1)', 'ependymoma', 'GLIOMA]', 'oligodendroglioma (who grade 2)', 'subependymoma (who grade 1)'], disease description:CN is a benign tumor of the central nervous system that is classified as a grade II tumor by the World Health Organization (WHO) CN may increase the intracranial pressure by obstructing the interventricular foramen, which can lead to hydrocephalus . Patients may also experience nausea, vomiting, headache, seizures, decreased consciousness, weakness, and memory or vision problems ?

Woman aged 38 experiencing ['mass lesion', 'nipple mass', 'nipple discharge', 'breast lump']

Disease Name: Central Papilloma, symptoms: ['mass lesion', 'nipple mass', 'nipple discharge', 'breast lump'], Treatment: ['cryotherapy or laser surgery.', 'Treatment of intraductal papilloma involves surgical excision and complete removal of the tumor. This is due to the possibility of upgrading to atypical ductal hyperplasia or DCIS upon excision. Surgical excision, in the form of lumpectomy with complete removal of the papilloma, is recommended'], Pathophysiology: Here are some key points about the pathophysiology of central papilloma:Epithelial Origin: Central papillomas are thought to arise from the surface epithelium lining the nasal cavity and paranasal sinuses. The epithelial cells undergo changes that lead to the development of papillary growth patterns and invaginations into the underlying tissues.Human Papillomavirus (HPV) Infection: Although most nasal papillomas are not associated with HPV infection, a subset of cases has been linked to certain types of HPV, particularly HPV types 6 and 11. HPV-related papillomas tend to have a higher recurrence rate and may exhibit more aggressive behavior.Chronic Inflammation: Chronic inflammation of the nasal cavity and paranasal sinuses is believed to play a role in the development of central papilloma. Factors such as chronic sinusitis, allergies, and exposure to irritants or pollutants may contribute to the inflammatory process. Inflammation can lead to cellular changes and abnormal growth patterns.Genetic and Molecular Alterations: Genetic and molecular changes have been identified in central papillomas, although the specific mechanisms are not fully understood. Studies have suggested alterations in certain genes, including tumor suppressor genes and oncogenes, as well as dysregulation of signaling pathways involved in cell proliferation and differentiation.Local Invasion and Recurrence: Central papillomas have a tendency to invade adjacent structures, such as the nasal bones, sinuses, and skull base. The tumor's invasive nature can make complete surgical removal challenging and contribute to the high recurrence rate seen with this condition. Incomplete removal or residual tumor cells left behind after surgery can lead to regrowth of the tumor., Epidemiology:['5% of benign breast lesions', 'approximately 2-3% in humans.', 'variable', 'There is no known way to prevent intraductal papilloma. Breast self-exams and screening mammograms can help detect the disease early.'], Complications:['Bleeding complications', 'infections', 'Scarring'], Diagnostics:['Cytogenetics', 'mammography', 'MRI', 'usg breast', 'Immunostaining'], Differential diagnosis:['Adenomyoepithelioma', 'Intraductal papillary carcinoma', 'Invasive ductal carcinoma, not otherwise specified', 'Invasive papillary carcinoma'], disease description:An intraductal papilloma is a benign tumor that grows inside the breast duct. A central intraductal papilloma develops in a large duct just below the nipple, usually as a single growth, although it’s possible to have more than one.

A 21-year-old female experiencing ['early closure of the epiphyses', 'testicular enlargement', 'breast enlargement', 'Emotional behavior and mood swings', 'short stature', 'growth spurt', 'pubic or underarm hair', 'early menstruation']

Disease Name: Central Precocious Puberty, symptoms: ['early closure of the epiphyses', 'testicular enlargement', 'breast enlargement', 'Emotional behavior and mood swings', 'short stature', 'growth spurt', 'pubic or underarm hair', 'early menstruation'], Treatment: [{'medication': ['Leuprolide ', 'Triptorelin ', 'Goserelin ']}, 'The observation that the pituitary gonadotropic cells require pulsatile, rather\nthan continuous, stimulation by GnRH to maintain the ongoing release of\ngonadotropins provides the rationale for using GnRH agonists for treatment of\nCPP. By virtue of being more potent, and having a longer duration of action than\nnative GnRH, these GnRH agonists (after a brief period of stimulation)\ndesensitize the gonadotropic cells of the pituitary to the stimulatory effect of\nendogenous GnRH and effectively halt the progression of central sexual\nprecocity.\nLong-acting formulations of GnRH agonists, which maintain fairly constant\nserum concentration of the drug for weeks or months, constitute the preparations\nof choice for treatment of CPP. In the United States, the available preparations\ninclude: (a) leuprolide acetate (Lupron Depot Ped), in a dose of 0.2-0.3 mg/kg (7.5-15 mg) intramuscularly once every 4 wk; (b) longer-acting preparations of\ndepot-leuprolide, allowing for injections (11.25 or 30 mg IM) every 90 days; (c)\nhistrelin (Supprelin LA), a subcutaneous 50-mg implant with effects lasting at\nleast 12 mo; and (d) triptorelin (Triptodur), 22.5 mg IM every 6 months. Other\npreparations such as goserelin acetate (Zoladex ) are approved for treatment of\nprecocious puberty in other countries. Recurrent sterile fluid collections at the\nsites of injections are an uncommon local side effect and occur in less than 1–3%\nof patients treated with depot-leuprolide. Breakage or malfunction of the\nhistrelin implant is very rare.'], Pathophysiology: Sexual development may begin at any age and generally follows the sequence observed in normal puberty. In females, early menstrual cycles may be more irregular than they are with normal puberty. The initial cycles are usually anovulatory, but pregnancy has been reported as early as 5.5 yr of age. In males, testicular biopsies have shown stimulation of all elements of the testes, and spermatogenesis has been observed as early as 5-6 yr of age. In affected females and males, height, weight, and height velocity are accelerated. The increased rate of bone maturation results in early closure of the epiphyses, and compromised adult height, particularly if puberty begins at a very early age. Historically, approximately 30% of females and an even larger percentage of males achieved a height below the 5th percentile as adults without treatment. Mental development is usually compatible with chronological age. Emotional behavior and mood swings are common, but serious psychological problems are rare. Although the clinical course is variable, 3 main patterns of pubertal progression can be identified. Most females (particularly those younger than 6 yr of age at the onset) and a large majority of males have rapidly progressive puberty, characterized by rapid physical and osseous maturation, leading to a loss of height potential. An increasing percentage of females (older than 6 yr of age at the onset with an idiopathic form), and rarely males, have a slowly progressive variant, characterized by parallel advancement of osseous maturation and linear growth, with preserved height potential. Very rarely, central puberty may regress spontaneously (unsustained CPP). This variability in the natural course of sexual precocity underscores the need for longitudinal observation at the onset of sexual development, before treatment is considered., Epidemiology:['A high prevalence of CPP has been reported in female', '1:5,000 to 1:10,000 children.', 'variable', "Central precocious puberty follows an autosomal dominant pattern and therefore, it can't be prevented. \nAlthough Genetic counselling is advisable."], Complications:['Bleeding complications'], Diagnostics:['SERUM TESTOSTERONE LEVEL', 'SERUM ESTRADIOL', 'Serum LH Level Test', 'TESTICULAR BIOPSY'], Differential diagnosis:['Congenital Adrenal Hyperplasia', 'Leydig cell tumour', 'McCune-Albright Syndrome', 'Ovarian Cyst'], disease description:CPP is defined by the onset of breast development before the age of 8 yr in females and by the onset of testicular development (volume = 4 mL) before the age of 9 yr in males, as a result of the early activation of the hypothalamic pituitary-gonadal axis. It occurs 5- to 10-fold more frequently in females than in males and is usually sporadic. Although at least 90% of females have an idiopathic form, a structural central nervous system (CNS) abnormality may occur in 25–75% of males with CPP. Genetic forms of CPP, such as the paternally transmitted type due to a mutation of the MKRN3 gene, have been recently described. 

A 31-year-old with ['Small yellow grey elevations', 'Foveal reflex is absent or distorted', 'Subretinal deposists', 'Multifocal pigmentary changes', 'metamorphopsia', 'Relative positive scotoma', 'micropsia', 'VISION DEFICITS', 'Black spots in front of eyes', 'sudden painless loss of vision', 'distortion of vision']

Disease Name: Central Serous Chorioretinopathy, symptoms: ['Small yellow grey elevations', 'Foveal reflex is absent or distorted', 'Subretinal deposists', 'Multifocal pigmentary changes', 'metamorphopsia', 'Relative positive scotoma', 'micropsia', 'VISION DEFICITS', 'Black spots in front of eyes', 'sudden painless loss of vision', 'distortion of vision'], Treatment: ['• Discontinuation of steroids, if possible, should be\ndone at the earliest.\n• Life style changes to reduces stress in life, should\nbe adopted.', 'Laser photocoagulation is indicated in following\ncases:• Long-standing cases (more than 6 months).\n• Patients having recurrent CSR with visual loss.\n• Patients having permanent loss of vision in the\nother eye due to this condition.', 'Anti-VEGF can be considered if CNV develops', 'Photodynamic therapy (PDT) may be beneficial\nfor those with severe disease not amenable to\nconventional laser treatment, e.g., with sub-foveal\nleaks and chronic cases.'], Pathophysiology: Pathogenesis is not known exactly. Various theories have been postulated. Presently, the most accepted theory is of ‘choroidal vascular hyperpermeability’. This theory correlates the clinical findings with indocyanine green (ICG) angiography findings. It proposes that sympathetic drive, sympathomimetics and corticosteroids alter the choroidal vascular permeability either directly or indirectly by affecting its autoregulation. This, in turn, increases the tissue hydrostatic pressure in the choroid causing pigment epithelial defect (PED) resulting in a breach in the outer blood retinal barrier. Leakage of fluid across this area results in development of localized serous detachment of neurosensory retina. Clinical course CSR is usually self-limiting but often recurrent. Three patterns are known: Acute classic CSCR is characterized by short clinical course with spontaneous resolution within 3–6 months with near normal visual recovery. Recurrences are known in 30–50% of all the cases. Chronic CSCR, also termed as diffuse retinal pigment epitheliopathy (DRPE), is seen in few cases. It is characterized by a chronic course lasting more than 12 months, typically affecting individuals above 50 years of age. Such cases may have permanent visual impairment due to progressive RPE atrophy and photoreceptor degeneration. Bullous CSCR is rare presentation characterized by larger and more numerous areas of serous retinal and RPE detachments often confused with bullous retinal detachment., Epidemiology:['Prevalence of CSCR was 1.7%.', 'incidence of 9.9 per 100000 in men and 1.7 per 100000 in women.', 'poor', 'There are no known ways to prevent central serous retinopathy, although some lifestyle changes can reduce your risk for the condition or improve your symptoms as you wait for it to clear up. For example, your eye doctor may recommend that you:\n\nStop taking steroid drugs with the help of your prescribing physician, if possible.\nGet treatment for steroid drug abuse, if their use is not prescribed.\nFind ways to lower your stress levels. Mindfulness or breathing exercises, yoga, and other physical practices are often recommended.\nEat a healthy diet and get regular exercise to manage your stress levels.\nGet enough sleep to reduce your overall stress and boost well-being.'], Complications:['Bleeding complications', 'hyperglycemia', 'Osteoporosis'], Diagnostics:['FUNDOSCOPY', 'Optical coherence tomography (OCT)', 'indocyanine green angiography', 'Fundus fluorescein angiography (FFA)'], Differential diagnosis:['age related macular degeneration', 'Choroidal neovascularization', 'Diabetic Retinopathy', 'macular hole', 'rhegmatogenous retinal detachment'], disease description:Central serous chorioretinopathy (CSCR) is characterised by spontaneous serous detachment of neurosensory retina in the macular region, with or without retinal pigment epithelium detachment.

A woman, 47 years old, with ['lymphadenopathy', 'Tenderness on palpation', 'acanthosis nigricans', 'plaque involving the groin (80%), axillae (20%) or neighbouring regions', 'mild discomfort', 'Regional lymph nodes are enlarge', 'periphery of the atrophic plaque is typically erythematous while the centre is of normal colour or may have a violaceous or bluish hue', 'failure to thrive', 'menstrual irregularities'] issues

Disease Name: Centrifugal Lipodystrophy, symptoms: ['lymphadenopathy', 'Tenderness on palpation', 'acanthosis nigricans', 'plaque involving the groin (80%), axillae (20%) or neighbouring regions', 'mild discomfort', 'Regional lymph nodes are enlarge', 'periphery of the atrophic plaque is typically erythematous while the centre is of normal colour or may have a violaceous or bluish hue', 'failure to thrive', 'menstrual irregularities'], Treatment: [{'medication': ['Ibuprofen ', 'Chloroquine ', 'Penicillin/Penicillin V/Phenoxymethylpenicillin', 'Betamethasone ', 'Vitamin A (Retinol)', 'Vitamin E / Tocopherol', 'Methyl prednisolone ', 'Pimecrolimus']}, 'topical dimethyl sulfoxide', 'Psoralen with UVA'], Pathophysiology: The cause of CLD is unknown. It has been suggested that apoptosis may play a part in the fatty tissue degeneration of CLD but it is unclear if this is a primary event. Fibrous long-spacing collagen has been observed on ultrastructural studies of lesional skin, although the relation of their presence to disease pathogenesis remains to be elucidated. So far, no abnormalities of serum leptin levels have been reported., Epidemiology:['approximately 170 cases', '1 case per 12 million persons.', 'fair', 'In most cases, lipodystrophy isn’t preventable.\n\nYou can’t prevent genetic forms of lipodystrophy because it’s the result of a genetic mutation that’s inherited. \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:['ulceration'], Diagnostics:['cholesterol test', 'molecular genetic testing'], Differential diagnosis:['Acquired partial lipodystrophy', 'AUTOIMMUNE POLYGLANDULAR SYNDROME', 'Cushings syndrome', 'Metabolic syndrome', 'Polycystic Ovarian Disease'], disease description:Centrifugal lipodystrophy (CLD) is a form of localized lipodystrophy in which atrophic plaque.The condition predominantly affects children who are otherwise well.  Centrifugal lipodystrophy is a rare, acquired, localized lipodistrophy characterized by single or, occasionally, multiple, centrifugally progressive, asymptomatic to sometimes mildly tender, hypopigmented, lipoatrophic skin depressions with weakly erymatheous inflammatory borders, typically associated with regional ipsilateral lymph nodes swelling. Lesions typically occur on lower trunk (in particular groin and abdomen region), followed by upper trunk (axilla and neighboring regions) and, rarely, neck and head. It is usually not associated with systemic disease and is typically self-resolving.

Symptoms at 49 years old: ['muscle weakness', 'hypotonia']

Disease Name: Centronuclear Myopathy, symptoms: ['muscle weakness', 'hypotonia'], Treatment: ['Genetic counseling.\nX-MTM is inherited in an X-linked manner. The risk to sibs of a male proband depends on the carrier status of the mother. If the mother is a carrier, each sib has a 50% chance of inheriting the MTM1 pathogenic variant. Males who inherit the variant will be affected; females who inherit the variant will be carriers and will generally not be affected. To date, there are no reported males with incomplete penetrance. In simplex cases (i.e., a single occurrence in a family), there is a probability of 80%-90% that a woman is a carrier if her son has a confirmed MTM1 pathogenic variant. Thus, about 10%-20% of males who represent simplex cases have a de novo pathogenic variant in MTM1 and a mother who is not a carrier. Germline mosaicism has been reported. Carrier testing of at-risk female relatives and prenatal testing for a pregnancy at risk are possible if the MTM1 pathogenic variant has been identified in an affected male relative.', 'Surveillance: Annual pulmonary assessment; polysomnography every one to three years; routine examination for scoliosis; annual ophthalmologic examinations to evaluate for ophthalmoplegia, ptosis, and myopia; routine assessment for dental malocclusion.', 'Treatment of manifestations: Treatment is supportive. Management optimally involves a team of specialists with expertise in the long-term care of children and/or adults with neuromuscular disorders, often including a pulmonologist, neurologist, physical therapist and/or rehabilitation medicine specialist, and clinical geneticist. Tracheostomy, G-tube feeding, and assistive communication devices are often required. Ophthalmologists, orthopedists, and orthodontists should address specific medical complications related to the underlying myopathy.'], Pathophysiology: Approximately 80% of affected males present with severe (classic) X-MTM characterized by polyhydramnios, decreased fetal movement, and neonatal weakness, hypotonia, and respiratory failure. Motor milestones are significantly delayed and most individuals fail to achieve independent ambulation. Weakness is profound and often involves facial and extraocular muscles. Respiratory failure is nearly uniform, with most individuals requiring 24-hour ventilatory assistance. It is estimated that at least 25% of boys with severe X-MTM die in the first year of life, and those who survive rarely live into adulthood.Males with mild or moderate X-MTM (~20%) achieve motor milestones more quickly than males with the severe form; many ambulate independently, and may live into adulthood. Most require gastrostomy tubes and/or ventilator support. In all subtypes of X-MTM, the muscle disease is not obviously progressive. Female carriers of X-MTM are generally asymptomatic, although manifesting heterozygotes are increasingly being identified. In affected females, symptoms range from severe, generalized weakness presenting in childhood, with infantile onset similar to affected male patients, to mild (often asymmetric) weakness manifesting in adulthood. Affected adult females may experience progressive respiratory decline and ultimately require ventilatory support., Epidemiology:['2/100000', 'around 1:25,000', 'This is the result of a genetic change (mutation), the disorder can’t be prevented. If you’re concerned about having a baby with a genetic condition, you should talk with your healthcare provider about genetic counseling and possible genetic testing.'], Complications:['Bone deformities'], Diagnostics:['Muscle Biopsy', 'GENETIC TESTING'], Differential diagnosis:['Congenital myopathies', 'Duchenne muscular dystrophy', 'Spinal Muscular Atrophies'], disease description:Myotubular myopathy is the most common and severe form of centronuclear myopathy, a type of inherited myopathy that causes problems with the tone and contraction of skeletal muscles.

Individual, 39 years old, with ['macular erythema', 'papules closely resemble small insect bites', 'Itching of the skin', 'maculopapular rash', 'first sign of an infection is the development of a tingling sensation after contact with water', 'localised swelling']

Disease Name: Cercarial Dermatitis Dermatology, symptoms: ['macular erythema', 'papules closely resemble small insect bites', 'Itching of the skin', 'maculopapular rash', 'first sign of an infection is the development of a tingling sensation after contact with water', 'localised swelling'], Treatment: [{'medication': ['Hydrocortisone ', 'Hydroxyzine']}, '•\tAntipruritic cream (1% hydrocortisone) applied to the \naffected area twice daily × 1 week\n•\t Hydroxyzine 25 mg PO every 6 h as required for \npruritus × 1 week'], Pathophysiology: The pathogenesis of cercarial dermatitis is not completely understood, although the kinetics of the clinical response suggest that sensitization is involved. The first phase of epidermal penetration is accompanied by dermal oedema, which is followed by a brisk neutrophil reaction. Attempts to find common features connecting the likely locations for cercarial infections have not been entirely successful. It is apparent, however, that areas endemic for cercarial dermatitis usually have abundant submerged vegetation harbouring the intermediate hosts. Hot spells of weather have also been associated with a higher risk of the development of symptoms. Clinical variants: 1 Fresh-water avian cercarial dermatitis. This follows penetration of the skin by cercariae of avian blood flukes. The intermediate hosts are fresh-water molluscs. The flukes belong to the genera Trichobilharzia, Gigantobilharzia and Ornithobilharzia. The condition has been described from many different parts of the world including North America, particularly the lakes region of the USA, Canada, Europe, Africa and the Far East. In some countries, it affects patients with particular occupations such as rice farmers working in the paddyfields. 2 Sea-water avian cercarial dermatitis. This follows invasion of the skin by blood flukes whose definitive hosts are sea birds. While it is recorded less frequently than infections caused by fresh-water species, it accounts for the condition, seen in the Atlantic seaboard of the USA, known as clam-digger’s itch. The intermediate hosts are marine molluscs. The term ‘sea-bather’s eruption’ is used to describe a variety of different rashes that may develop after sea bathing. It is likely that it includes a number of different conditions from jellyfish dermatitis to eruptions due to toxic algae. A sea water form of cercarial dermatitis is therefore one cause of sea-bather’s eruption. 3 Fresh-water mammalian cercarial dermatitis. This has been reported mainly from the Far East, and the definitive hosts for the schistosomes in this condition are mammals such as water buffaloes., Epidemiology:['2310 population studied, 139 of them (6.1%) were infected to cecarial dermatitis.', '6.8 episodes per 100 water-exposure days', 'good', 'There are a few things you can do to reduce your risk of getting swimmer’s itch, including:\n\n1. Rinse off with clean water after swimming.\n2. Choose where you swim carefully.\n3. Do not feed birds or animals near where you are swimming.\n4. Do not swim or wade in or near marshy areas.\n5. If possible, try not to swim or wade in shallow water or by the shoreline.'], Complications:['Asthma', 'skin infection', 'food allergies'], Diagnostics:['allergy skin test'], Differential diagnosis:['Contact dermatitis', 'insect bites', 'schistosomiasis', 'skin eruptions'], disease description:Swimmer’s itch (cercarial dermatitis) is a temporary, non-contagious itchy rash that appears on your skin and is caused by a certain parasite found in fresh water (lake or pond water) or salt water (ocean water). If you swim in water that’s infested with the parasite, it can burrow (dig) into your skin.  Body has an allergic reaction to it, causing a rash. The parasites cannot survive in human skin, so they die shortly after burrowing into your skin. The rash usually gets better after a few days, but it can last for up to two weeks.

At 31 years old, experiencing ['headache', 'Memory loss', 'neck pain', 'vertigo']

Disease Name: Cerebellar Liponeurocytoma (who Grade 2), symptoms: ['headache', 'Memory loss', 'neck pain', 'vertigo'], Treatment: ['Cerebellar liponeurocytomas can be cured with complete resection and adjuvant radiotherapy.\n recurrence is common with incomplete resection followed by radiotherapy or with complete resection without adjuvant radiotherapy.', 'suboccipital craniectomy'], Pathophysiology: Pathophysiology is unknown. As the name implies, the vast majority of cases of liponeurocytoma arise in the cerebellum . However, up to a fifth of reported cases have been supratentorial, around or within the ventricular system., Epidemiology:['42 cases of liponeurocytoma reported in the literature. The patients’ ages ranged from 4 to 69 years, with a median of 49 years.', 'poor', 'Genetic counseling and testing.\nRegular health check-ups might help those individuals with a history of the condition in the immediate family, in order to help diagnose the tumor early.\nAvoiding cigarette smoke inhalation.'], Complications:['coma', 'Dementia'], Diagnostics:['MRI Brain', 'PET SCAN', 'CT', 'ELECTRON MICROSCOPY', 'Immunostaining'], Differential diagnosis:['central neurocytoma (who grade 2)', 'dysembryoplastic neuroepithelial tumour (who grade', 'gangliocytoma', 'medulloblastoma', 'oligodendroglioma (who grade 2)'], disease description:Well differentiated neurocytic neoplasm composed principally of neurocytes admixed with lipidized cells.Corresponds to WHO grade II,  cerebellar liponeurocytoma  also known as neurolipocytomas , are rare tumors of the cerebellum with neurocytic differentiation and abundant intracellular lipid. They are considered WHO grade 2 tumors .

A baby with ['Ataxia', 'hypotonia', 'visual changes', 'Abnormal gait', 'abnormal motor response', 'abnormally persistent neonatal reflexes', 'seizures', 'Strabismus', 'hearing disturbances', 'intellectual disability', 'Feeding Difficulty'], 2.7 years old

Disease Name: Cerebral Palsy, symptoms: ['Ataxia', 'hypotonia', 'visual changes', 'Abnormal gait', 'abnormal motor response', 'abnormally persistent neonatal reflexes', 'seizures', 'Strabismus', 'hearing disturbances', 'intellectual disability', 'Feeding Difficulty'], Treatment: [{'medication': ['Baclofen ', 'Levodopa ', 'Diazepam ']}, 'Symptomatic treatment is prescribed\nfor seizures. Tranquilizers are administered for behavior\ndisturbances and muscle relaxants may be used for improving\nmuscle function. Baclofen and tizanidine help to reduce\nspasticity. Diazepam may ameliorate spasticity and\nathetosis. Dantrolene sodium helps in relaxation of skeletal\nmuscles. Dynamic contractures can be managed with\nbotulinum toxin injection or alternatively nerve block with\nphenol.', 'Tendon, muscle and bony surgeries\nmay be required. Light weight splints may be required\nfor tight tendo-Achilles and cortical thumb.'], Pathophysiology: Factors may operate prenatally, during delivery or in the postnatal period. Cerebral malformations, perinatal hypoxia, birth trauma, chorioamnionitis, prothrombotic factors, acid base imbalance, indirect hyperbilirubinemia, metabolic disturbances and intrauterine or acquired infections may operate. Most infants have multiple risk factors. Prematurity is an important risk factor for spastic diplegia while term weight babies get quadriparesis or hemiparesis. The mechanism of CP in a large proportion of cases remains unclear and primary neurological aberrations may be unfolded in future. The importance of role of birth asphyxia has been questioned by recent data and asphyxia may be manifestation of the brain damage rather than the primary etiology. A variety of pathological lesions such as cerebral atrophy, porencephaly, periventricular, leukomalacia, basal ganglia thalamic and cerebellar lesions may be observed. Types of Cerebral Palsy 1.Spastic Cerebral Palsy This is the commonest form (65%) and is topographically classified into spastic quadriparesis, diplegia or hemiparesis. Early diagnostic features of neural damage include abnormally persistent neonatal reflexes, feeding difficulties, persistent cortical thumb after 3 months age and a firm grasp. On vertical suspension, the infant goes into scissoring due to adductor spasm with an extensor posture and does not flex his knees or thigh. The stretch tendon reflexes are always brisk. They have variable degrees of mental and visual handicaps, seizures and behavioral problems. Spastic quadriparesis is more common in term babies Spastic diplegia is commoner in preterm babies and is associated with periventricular leukomalacia. Spastic hemiplegia is usually recognized after 4-6 months age. 2.Hypotonic (Atonic) Cerebral Palsy Despite pyramidal involvement, these patients are atonic or hypotonic. Tendon reflexes are normal or brisk and Babinski response is positive. They are often severely mentally retarded. In cerebellar involvement, hypotonia is not associated with exaggerated reflexes. Muscles may show fiber disproportion and delayed CNS maturation is common. 3.Extrapyramldal CP This form accounts for 30% of cases. The clinical manifestations include athetosis, choreiform movements, dystonia, tremors and rigidity. Arms, leg, neck and trunk may be involved. Mental retardation and hearing deficits may be present. High tone audiometry should be performed. Cerebral damage following bilirubin ence-phalopathy is one of the causes. 4.Cerebellar Involvement This form is seen in less than 5% of the patients. There is hypotonia and hyporeflexia. Ataxia and intention tremors appear by the age of 2 yr. Nystagmus is unusual; mental status may be near normal in some of these patients. 5.Mixed Type A proportion of the patients have features of diffuse neurological involvement of the mixed type., Epidemiology:['cerebral palsy increases with declining gestational age', '1-2 per 100 live births', 'GOOD', 'CP happens for reasons that are unpredictable and that aren’t generally preventable. Because of that, it’s impossible to prevent it.\n\nWhile it isn’t preventable, there are ways to reduce the risks of your baby developing CP from certain causes.\n\n1. Magnesium sulfate for babies born prematurely.\n2. Cooling therapy for babies experiencing asphyxia.\n3. Prescription caffeine for premature babies.\n4. Corticosteroids during premature labor.'], Complications:['coma', 'Eye disorder', 'seizures', 'Speech disorders'], Diagnostics:['CT BRAIN', 'MRI'], Differential diagnosis:['Adrenoleukodystrophy', 'ATAXIA-TELANGIECTASIA', 'BRAIN TUMOURS', 'Glutaric aciduria', 'Hereditary Spastic Paraplegia', 'Hydrocephalus', 'Lesch-Nyhan syndrome', 'Metachromatic leukodystrophy (MLD)', 'neurological deficit', 'PELIZAEUS-MERZBACHER DISEASE', 'Pyruvate dehydrogenase deficiency', 'RETT SYNDROME', 'Tethered Cord', 'Zellweger Syndrome'], disease description:Cerebral palsy (CP) is defined as a nonprogressive neuromotor disorder of cerebral origin. It includes heterogeneous clinical states of variable etiology and severity ranging from minor incapacitation to total handicap. Most of the cases have multiple neurological deficits and variable mental handicap. The term does not include progressive, degenerative or metabolic disorders of the nervous system.

Symptoms reported by a 35-year-old: ['Memory loss', 'CORNEAL OPACITY', 'tendon xanthomas', 'diplopia', 'Coloured halos', 'blurred or unstable vision', 'Forgetfulness', 'cataract', 'dystonia', 'Ataxia', 'behavioural disturbances', 'visual disturbances', 'agitation', 'shortness of breath', 'hallucinations']

Disease Name: Cerebrotendinous Xanthomatosis, symptoms: ['Memory loss', 'CORNEAL OPACITY', 'tendon xanthomas', 'diplopia', 'Coloured halos', 'blurred or unstable vision', 'Forgetfulness', 'cataract', 'dystonia', 'Ataxia', 'behavioural disturbances', 'visual disturbances', 'agitation', 'shortness of breath', 'hallucinations'], Treatment: [{'medication': ['Chenodeoxycholic acid/ Chenodiol']}, 'treatment of choice in CTX is CDCA replacement therapy to inhibit the flux of cholesterol into the bile acid synthesis pathway and reduce the generation of toxic metabolites.\n hypercholesterolemia is not controlled with CDCA treatment alone, 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase inhibitors may be added. HMG-CoA reductase inhibitors (ie, statins) have well-established efficacy and safety in patients with hypercholesterolemia and have also been used alone and in combination with CDCA to treat CTX.'], Pathophysiology: It is caused by tissue accumulation of bile acid intermediates shunted into cholestanol, resulting from mutations in the gene for sterol 27-hydroxylase. This enzyme is necessary for normal mitochondrial synthesis of bile acids in the liver., Epidemiology:['Currently there is no consensus on the prevalence of CTX, one estimate being <5/100,000 worldwide.', '1 in 72,000 to 1 in 150,000.', 'Prevention of primary manifestations: Early treatment with CDCA in presymptomatic individuals appears to prevent clinical manifestations.\n\nSurveillance: Annual cholestanol plasma concentration, neurologic and neuropsychological evaluation, brain MRI, echocardiogram, and assessment of bone density.'], Complications:['Ataxia'], Diagnostics:['2-D Echo', 'ECG', 'GENETIC TESTING', 'MRI', 'PULMONARY FUNCTION TEST(PFT)', 'serum cholesterol'], Differential diagnosis:['Ataxia', 'CHRONIC DIARRHEA', 'eruptive xanthomas', 'Hereditary Spastic Paraplegia', 'Neonatal cholestasis', 'Sitosterolaemia', 'Smith-Lemli-Opitz syndrome', 'xanthoma'], disease description:Cerebrotendinous xanthomatosis (CTX)  is a rare autosomal-recessive lipid storage disease caused by mutations in the CYP27A1 gene; this gene codes for the mitochondrial enzyme sterol 27-hydroxylase, which is involved in bile acid synthesis. The CYP27A1 gene is located on chromosome 2q33-qter and contains nine exons. A CYP27A1 mutation leads to decreased synthesis of bile acid, excess production of cholestanol, and consequent accumulation of cholestanol in tissues.This autosomal recessive disorder presents clinically in late adolescent .

Symptoms at 47: ['aphasia', 'Dizziness', 'headache', 'Numbness']

Disease Name: Cerebrovascular Disease, symptoms: ['aphasia', 'Dizziness', 'headache', 'Numbness'], Treatment: ['Microsurgery for minimally invasive direct operation on the delicate cerebral blood vessels\nEndovascular neurosurgery for minimally invasive treatments from within the cerebral blood vessels', 'Stenting, using a small metallic tube or mesh to widen narrowed arteries and improve blood flow\nEmbolization, an umbrella term for endovascular procedures that block off an abnormality such as an aneurysm, arteriovenous malformation, fistula or tumor\nClipping, sealing off an aneurysm with a clip\nCoiling, filling an aneurysm with small metal coils that cause the blood inside it to clot\nFlow diversion, implanting a high surface-area stent that directs blood flow away from an aneurysm\nBypass surgery, rerouting the blood around an occlusion, tumor or damaged blood vessel'], Pathophysiology: Ischemic Stroke:Ischemic stroke occurs when a blood vessel supplying the brain becomes blocked, leading to reduced blood flow and inadequate oxygen supply. The most common cause of ischemic stroke is atherosclerosis, which is the buildup of fatty plaques within the arteries. Hemorrhagic Stroke:Hemorrhagic stroke occurs when a blood vessel in the brain ruptures, causing bleeding into the surrounding brain tissue., Epidemiology:['prevalence of stroke ranged from 44.29 to 559/100,000 persons in different parts of the country during the past decade.', '105 to 152/100,000 persons per year', 'variable', 'Although cerebrovascular disease is a fairly common medical condition, there are things you can do to help prevent it.\n\nSeveral health behaviors are associated with reducing stroke risk:\n\nnot smoking, or stopping if you do\nfollowing a healthy, balanced diet\ncontrolling your high blood pressure\nlowering your blood cholesterol\nexercising\nlosing weight if you’re overweight\nbeing aware of the risks of any type of hormone replacement therapy\nvisiting your doctor regularly for annual checkups\nlowering your stress levels\nreducing the amount of alcohol you drink\nPreventing cerebrovascular disease is always the best goal.'], Complications:[], Diagnostics:['MRI', 'CT SCAN'], Differential diagnosis:['Brain Abscess', 'ENCEPHALITIS', 'hypoglycemia', 'hyponatremia', 'syncope'], disease description:Cerebrovascular disease is a term for conditions that affect blood flow to your brain. Conditions include stroke, brain aneurysm, brain bleed and carotid artery disease. These conditions are medical emergencies and need prompt treatment, such as medications and surgery. Though disability or death may occur, some people make a full recovery.

Symptoms at 49: ['Dizziness', 'syncope', 'tinnitus', 'weakness', 'OTALGIA']

Disease Name: Ceruminoma, symptoms: ['Dizziness', 'syncope', 'tinnitus', 'weakness', 'OTALGIA'], Treatment: ['POST OPEARATIVELY', 'wide surgical excision'], Pathophysiology: The exact cause of ceruminoma is unknown, and there are no specific risk factors identified. However, certain factors may increase the likelihood of developing ceruminoma, including exposure to chemicals, chronic ear infections, and genetic predisposition. It typically occurs in adults, with a higher incidence in males., Epidemiology:['0.5-2% cases reported', 'GOOD', 'To Do : CLEANING OF EAR WAX\n wide local excision to remove all tumor with negative margins is essential to prevent recurrence'], Complications:['hearing loss & deafness'], Diagnostics:['HISTOPATHLOGY', 'CT SCAN'], Differential diagnosis:['Basal cell carcinoma', 'CHOLESTEATOMA', 'OTITIS EXTERNA', 'PAROTID GLAND TUMOURS', 'Pleomorphic adenoma', 'Squamous cell carcinoma'], disease description:It is a tumour of modified sweat glands which secrete cerumen. It presents as a smooth, firm, skin-covered polypoid swelling in outer part of the meatus, generally attached to the posterior or inferior wall. It obstructs the meatus leading to retention of wax and debris. Malignant type outnumbers the benign by 2:1 ratio

A 42-year-old female experiencing ['Abortion', 'backache', 'Vaginal Discharge', 'RECURRENT MISCARRIAGE']

Disease Name: Cervical Incompetence, symptoms: ['Abortion', 'backache', 'Vaginal Discharge', 'RECURRENT MISCARRIAGE'], Treatment: [{'medication': ['Progesterone ', 'Metformin ', 'Doxycycline ', 'Erythromycin ', 'Aspirin/Acetylsalicylic acid']}, 'BED REST & TENDER CARE AT HOME & ASSURANCE', 'METROPLASTY', 'Cerclage operation\nMcDONALD’S OPERATION'], Pathophysiology: History—Repeated midtrimester painless cervical dilatation (without apparent cause) and escape of liquor amnii followed by painless expulsion of the products of conception are very much suggestive. Internal examination: (i) Interconceptional period—Bimanual examination reveals presence of unilateral or bilateral tear and/or gaping of the cervix up to the internal os. INVESTIGATIONS: Interconceptional period: (i) Passage number 6–8 Hegar dilator beyond the internal os without any resistance and pain and absence of internal os snap on its withdrawal specially in premenstrual period indicate incompetence. (ii) Premenstrual hysterocervicography shows funnel-shaped shadow. The internal os is supposed to be tight due to action of progesterone during this phase of cycle. Similar funnel-shaped (iii) During pregnancy—(a) Clinical (speculum): Painless cervical shortening and dilatation. (b) Sonography: Short cervix < 25 mm; Funneling of the internal os > 1 cm. (c) Speculum examination: Detection of dilatation of internal os with herniation of the membrane..., Epidemiology:['POOR'], Complications:[], Diagnostics:['BLOOD GROUP', 'VDRL', 'TVS (Transvaginal ultrasound)', 'USG', 'HYSTEROSALPINGOGRAPHY', 'BLOOD GLUCOSE', 'THYROID PROFILE', 'ENDOCERVICAL SWAB', 'hysterocervicography'], Differential diagnosis:[], disease description:nan

Woman aged 29 presenting symptoms such as ['uterine bleeding', 'menstrual disturbances', 'Redness', 'Vaginal Discharge', 'POSTCOITAL BLEEDING', 'SWELLING IN CERVIX', 'Hyperplasia']

Disease Name: Cervical Polyp, symptoms: ['uterine bleeding', 'menstrual disturbances', 'Redness', 'Vaginal Discharge', 'POSTCOITAL BLEEDING', 'SWELLING IN CERVIX', 'Hyperplasia'], Treatment: ["Asymptomatic polyps usually don't need any intervention, but there are some exceptions. Symptomatic, large, or atypical polyps usually warrant removal. Some techniques for polyp management include polypectomy for polyps with slender pedicles, which consists in grasping the base of the polyp with a ring forceps and twisting and rotating it until it comes of off; for smaller polyps, punch biopsy forceps are used, and polyps with a thick stalk usually require electrosurgical excision or hysteroscopic removal.", 'avulsion or by torsion'], Pathophysiology: Mucous polyp arise from the mucous membrane of the cervical canal. They form a swelling about the size of a pea, and in rare cases may become as big as 2 cm in diameter. To the naked eye, a mucous polypus is a red vascular swelling which bleeds easily on touch and is covered by smooth glistening epithelium bathed in clear mucus. The polypus is pedunculated, the pedicle being attached to the mucous membrane of the cervical canal. The swelling is soft, smooth and slippery to touch. It is not uncommon for the polyp to be multiple so that two or three may be seen in the neighbourhood of the external os. In most cases, the polyp can be detected by palpation but small sessile polyp can be detected only by speculum examination. Histologically the polyp have a typical appearance. The surface epithelium is the high columnar type similar to that of the endocervical canal. Glands found in the stroma are racemose in type and are lined by tall columnar epithelium. The stroma is extremely vascular, containing a large number of dilated capillaries with round-celled infiltration near the lower pole of the polypus. One of the most constant features of mucous polyp of the cervix is that the surface epithelium in the region of the lower pole shows well-marked squamous metaplasia, and the squamous epithelium may penetrate into the depth of the glands. The mucous polyp should be regarded as being produced by hyperplasia of the mucous membrane of the cervical canal which becomes thrown into folds and finally one of the folds, projecting into the cervical canal, assumes the characteristics of a polypus. Mucous polyp usually occur in women during the childbearing period of life, but they develop also in women of menopausal age and are occasionally seen in women past the menopause. Mucous polyp cause an increased vaginal discharge, and as they bleed easily the patient may complain of irregular and post coital bleed., Epidemiology:['prevalence of cervical polyps is between 2 to 5 % of women', 'cervical polyps is approximately 1.5–10% in the general population.', 'GOOD', 'Cervical polyps are hard to prevent, but you can take certain steps to reduce your risk of infection like practicing safe sex (using a condom). Other causes of cervical polyps are out of your control. Getting regular pelvic exams and Pap tests is the best way to find and treat polyps before symptoms start.'], Complications:['infections', 'increased risk of infection or malignancy', 'hemorrhage'], Diagnostics:['HISTOPATHLOGY', 'USG', 'SPECULUM EXAMINATION'], Differential diagnosis:['adenomyosis', 'cervical ectropion', 'cervical tumours', 'ectopic pregnancy', 'ENDOMETRIAL HYPERPLASIA', 'Endometriosis', 'SEXUALLY TRANSMITTED DISEASE', 'Uterine fibroids'], disease description:Cervical polyps are benign growths, usually protruding from the surface of the cervical canal. They commonly occur during the reproductive years, especially after the age of 20.The cervical polyps may vary in size, shape, and origin. They can present as single or multiple, tear-shaped or lobular, cherry-red, or greyish-white in color, depending on the vascularity of the lesion. The size of the cervical polyp is typically less than three cm in diameter; however, as mentioned earlier, they can vary in size and can be large enough to fill the vagina or be present at the introitus.

Person, 26 years old, presenting ['Numbness', 'Tingling', 'Asymptomatic', 'cramps or pain after exercising', 'Pain in Arm', 'WEAKNESS OF UPPER EXTREMITY']

Disease Name: Cervical Rib And Thoracic Outlet Syndrome , symptoms: ['Numbness', 'Tingling', 'Asymptomatic', 'cramps or pain after exercising', 'Pain in Arm', 'WEAKNESS OF UPPER EXTREMITY'], Treatment: ['‘shrugging the shoulder’ exercises., avoidance of carrying\nheavy objects like shopping bag, bucket full of\nwater, suitcase etc. Occasionally, surgical excision of\nthe first rib may be required to relieve compression\non the neurovascular bundle of the upper limb', 'surgical excision of\nthe first rib may be required to relieve compression\non the neurovascular bundle of the upper limb.'], Pathophysiology: In 90 per cent of cases, there are no symptoms; an extra rib is detected on an X-ray made for some other purpose. In others, it produces symptoms after the age of 30 years, probably because with declining youth the shoulders sag, increasing the angulation of the neurovascular structures of the upper limb as they come out of the neck. It is more often symptomatic in females. A patient may present with the following symptoms: a) Neurological symptoms: Tingling and numbness along the distribution of the lowest part of the brachial plexus (T1 dermatome), along the medial border of the forearm and hand, is the commonest complaint. There may be weakness and wasting of the hand muscles and clumsiness in the use of the hand. b) Vascular symptoms: These are uncommon. Compression of the subclavian artery may result in an aneurysm distal to constriction. This is a potential source of tiny emboli to the hand and may cause gangrene of the finger tips. There may be a history of pain in the upper limb on using the arm or elevating the hand (claudication). c) Local symptoms: Occasionally, the patient presents with a tender supraclavicular lump (the anterior end of the cervical rib) which, on palpation, is bony hard and fixed., Epidemiology:['occurring in 0.05% to 3.0% of the population.', 'GOOD', 'To Do : ‘shrugging the shoulder’ exercises., avoidance of carrying heavy objects like shopping bag, bucket full of water, suitcase etc. Occasionally, surgical excision of the first rib may be required to relieve compression on the neurovascular bundle of the upper limb'], Complications:['Pulmonary Embolism', 'hemorrhage'], Diagnostics:['MRI', 'X RAY'], Differential diagnosis:['Carpal tunnel syndrome', 'CLAVICLE FRACTURE', 'VASCULAR DISORDER'], disease description:This is an additional rib which arises from the 7th cervical vertebra. It is usually attached to the first rib close to the insertion of the scalenus anterior muscle, and is present in less than 0.5 per cent of the population. It may be a complete rib, but more often it is present posteriorly for a short distance only; the anterior part being just a fibrous band. The cervical rib is usually unilateral and is more common on the right side.

Individual aged 31 with manifestations like ['vertigo', 'nausea', 'neck pain', 'Numbness', 'WEAKNESS OF UPPER EXTREMITY', 'lack of coordination', 'difficulty in walking']

Disease Name: Cervical Spondylosis, symptoms: ['vertigo', 'nausea', 'neck pain', 'Numbness', 'WEAKNESS OF UPPER EXTREMITY', 'lack of coordination', 'difficulty in walking'], Treatment: ['• Analgesics\n• Hot fomentation\n• Rest to the neck in a cervical collar\n• Traction to the neck if there is stiffness\n• Anti-emetics, if there is giddiness'], Pathophysiology: The pathogenesis of cervical spondylosis involves a degenerative cascade that produces biomechanical changes in the cervical spine, manifesting as secondary compression of neural and vascular structures. An increase in the keratin-chondroitin ratio prompts changes to the proteoglycan matrix resulting in loss of water, protein, and mucopolysaccharides within the intervertebral disc. Desiccation of the disc causes the nucleus pulposus to lose its elasticity as it shrinks and becomes more fibrous. As the nucleus pulposus loses its ability to maintain weight-bearing loads effectively, it begins to herniate through the fibers of the annulus fibrosus and contributes to the loss of disc height, ligamentous laxity, and buckling, and compression of the cervical spine. With further disc desiccation, the annular fibers become more mechanically compromised under compressive loads, producing significant alterations in the load distribution along the cervical spine. The result is a reversal of the normal cervical lordosis. Progression of the kyphosis causes the annular and Sharpey’s fibers to peel off from the vertebral body edges, resulting in reactive bone formation. These bone spurs or osteophytes can form along the ventral or dorsal margins of the cervical spine, which can then project into the spinal canal and intervertebral foramina ., Epidemiology:['95% prevalence by age 65 years.', '1-year incidence ranges from 4.8% to 79.5%', 'GOOD', 'There is no way to prevent cervical spondylosis as this condition is a normal, age-related deterioration (“wear and tear”) of the joint space and disks in your neck.\nIf you do have a job or a hobby that results in a lot of time spent looking overhead, downward or having your head in an awkward posture, take many short breaks in your day (if possible). Learn proper stretching and strengthening exercises from your healthcare provider or physical therapist.'], Complications:['muscle pain', 'Pulmonary Embolism'], Diagnostics:['X-Ray Spine', 'X RAY'], Differential diagnosis:['Adhesive capsulitis', 'AMYOTROPHIC LATERAL SCLEROSIS', 'Carpal tunnel syndrome', 'Fibromyalgia', 'fracture', 'Guillain-Barre Syndrome', 'Multiple Sclerosis', 'osteomyelitis', 'Vitamin B12 deficiency'], disease description:Cervical spondylosis is the degeneration of the bones and disks in the neck. This condition can lead to a variety of problems, including herniated disks and bone spurs. Cervical spondylosis is a term that encompasses a wide range of progressive degenerative changes that affect all the components of the cervical spine (i.e., intervertebral discs, facet joints, joints of Luschka , ligamenta flava, and laminae). It is a natural process of aging and presents in the majority of people after the fifth decade of life.

Suffering from ['edema', 'painful urination', 'pain during sex', 'Vaginal Discharge', 'Mucopurulent discharge', 'cervical tenderness'] at 52 years old, female

Disease Name: Cervicitis, symptoms: ['edema', 'painful urination', 'pain during sex', 'Vaginal Discharge', 'Mucopurulent discharge', 'cervical tenderness'], Treatment: ['1st choice: azithromycin 1 g p.o. in a single dose and either cefixime 800 mg p.o. in a single dose or ceftriaxone 250 mg IM in a single dose\n2nd choice: doxycycline 100 mg p.o. b.i.d. for 7 days and either cefixime 800 mg p.o. in a single dose or ceftriaxone 250 mg IM in a single dose\nFor patients with a history of allergic reaction to cephalosporins or history of severe or very severe delayed or immediate reaction to penicillins: Azithromycin 2 g p.o. in a single dose', 'Appropriate antibiotics should be prescribed. General \nmeasures are to be taken as outlined in acute pelvic \ninfection'], Pathophysiology: The endocervical infection usually follows child-birth, abortion, or any operation on cervix. The responsible organisms are pyogenic. Other common pathogens are: Gonococcus, Chlamydia trachomatis, Trichamonas, Bacterial vaginosis, Mycoplasma and HPV, the first one being less common nowadays. The organisms gain entry into the glands of the endocervix and produce acute inflammatory changes. The infection may be localized or spread upwards to involve the tube or sidewards involving the parametrium., Epidemiology:['4 to 5 times more common than gonococcal cervicitis', 'highest incidence is in sexually active women aged 15 to 24', 'good', 'Though you can’t always prevent cervicitis, you can reduce your risk by practicing safe sex. Using condoms every time you have intercourse will drastically reduce your risk of sexually transmitted infections.'], Complications:['Pulmonary Embolism', 'infertility'], Diagnostics:['NUCLEIC ACID AMPLIFICATION TEST NAAT', 'ENDOCERVICAL SWAB', 'MICROSCOPIC EXAMINATION'], Differential diagnosis:['Acute Pyelonephritis', 'bacterial vaginosis', 'candidiasis', 'Chancroid', 'Chlamydial Infections', 'Contact dermatitis', 'ectopic pregnancy', 'ENDOMETRITIS', 'genitourinary tract infection', 'gonorrhea infection', 'Human Papillomavirus Infections', 'OVARIAN CANCER', 'PID', 'Trichomoniasis', 'Urinary Tract Infection', 'uterine cancer', 'vaginitis'], disease description:Cervicitis is a clinical syndrome characterized by inflammation of primarily the columnar epithelium of the uterine endocervix. It can be acute or chronic, with acute having infectious causes, and chronic having mostly non-infectious sources. The clinical spectrum of the disease varies widely, from asymptomatic cases to patients with mucopurulent cervical discharge and systemic signs. 

Symptoms reported by a 26-year-old: ['Dizziness', 'raised intracranial pressure', 'unilateral or bilateral ataxia', 'constipation', 'diarrhea', 'nausea', 'seizures', 'Abdominal Pain']

Disease Name: Cestode Disease, symptoms: ['Dizziness', 'raised intracranial pressure', 'unilateral or bilateral ataxia', 'constipation', 'diarrhea', 'nausea', 'seizures', 'Abdominal Pain'], Treatment: ['Praziquantal is the treatment of choice.\nAlbendazole or praziquantal can be used for neurocysticercosis.'], Pathophysiology: Humans are the only definitive host for the adult stage of T. saginata and T. asiatica. The tapeworms, which can reach 8 m in length with 1000–2000 proglottids, inhabit the upper jejunum. The scolex of T. saginata has four prominent suckers, whereas T. asiatica has an unarmed rostellum. Each gravid segment has 15–30 uterine branches (in contrast to 8–12 for T. solium). The eggs are indistinguishable from those of T. solium; they measure 30–40 µm, contain the oncosphere, and have a thick brown striated shell. Eggs deposited on vegetation can live for months or years until they are ingested by cattle or other herbivores (T. saginata) or pigs (T. asiatica). The embryo released after ingestion invades the intestinal wall and is carried to striated muscle or viscera, where it transforms into the cysticercus. When ingested in raw or undercooked meat, the cysticercus evaginates and forms a tapeworm in the human intestines. Over ~2 months, the adult worm matures and begins to produce eggs., Epidemiology:['Up to 20 million humans are estimated to be infected worldwide.', '1,000 new cases of cysticercosis', 'GOOD', "Risk is low in the developed world, but traveling in developing countries and experimenting with raw and undercooked meats can increase your risk. To prevent tapeworm infection, follow these guidelines:\n\n1. Safe hygiene practices - Wash your hands with soap and water after using the toilet or interacting with animals and before handling food.\n\n2. Safe water practices - When water sources are untreated, boil for one minute before drinking. \n\n3. Safe meat preparation - Use a food thermometer when cooking meat. You should cook whole cuts to an internal temperature of at least 145 degrees Fahrenheit, then let them sit for three minutes before eating.\n\n4. Safe fish preparation - Cook large freshwater fish, such as salmon, to an internal temperature of 145 degrees Fahrenheit. If you’re eating fish raw, it's safest to freeze it first."], Complications:['Epilepsy', 'headache', 'Hydrocephalus'], Diagnostics:['EOSINOPHILS - ABSOLUTE COUNT', 'serum IgE level', 'STOOL CULTURE', 'XRAY long bones', 'stool microscopy'], Differential diagnosis:['abscess', 'Anaphylaxis', 'appendicitis', 'Aspergillosis', 'Biliary colic', 'Brain Abscess', 'Echinococcosis', 'ENCEPHALITIS', 'lymphoma', 'Meningitis', 'Multiple Sclerosis', 'Sarcoidosis', 'Syphilis', 'TUBERCULOSIS'], disease description:Cestodes are flat, parasitic, hermaphroditic tapeworms with complex life cycles that infect animals, including humans. Although there are multiple species of cestodes, this will focus on three particular species that cause human disease: Taenia solium (pork tapeworm), Taenia saginata (beef tapeworm), and Diphyllobothrium (fish tapeworm) .

Person at 35 years, dealing with ['nodule in eyelid', 'Reddish purple area seen on the palpebral conjunctiva', 'Painless swelling in the eyelid', 'Mild heaviness in the lid', 'WATERING EYE', 'blurred or unstable vision']

Disease Name: Chalazion, symptoms: ['nodule in eyelid', 'Reddish purple area seen on the palpebral conjunctiva', 'Painless swelling in the eyelid', 'Mild heaviness in the lid', 'WATERING EYE', 'blurred or unstable vision'], Treatment: [{'medication': ['Triamcinolone ', 'Tetracycline ']}, 'A marginal chalazion is better treated\nby diathermy.', 'Hot\nfomentation, topical antibiotic eyedrops and oral\nanti-inflammatory drugs. Intralesional injection of long-acting steroid\n(triamcinolone)', 'Incision and curettage'], Pathophysiology: Chalazion are inflammatory lesions that form when lipid breakdown products leak into surrounding tissue and incite a granulomatous inflammatory response. For this reason, a chalazion is also called a conjunctival granuloma. Meibomian glands are embedded in the tarsal plate of the eyelids; therefore, edema due blockage of these glands is ordinarily contained to the conjunctival portion of the lid. On occasion, a chalazion may enlarge and break through the tarsal plate to the external portion of the lid. Chalazia due to blockage of Zeis glands are usually located along the lid margin., Epidemiology:['prevalence rate of 0.57%', '0.95% (2656/280,034) in children and 0.51% (8614/1,702,024) in adults', 'GOOD', 'You may be able to avoid getting a chalazion by following good hygiene. Some essential elements of good hygiene include:\n\n1. Hand-washing.\n2. Contact lens care.\n3. Face-washing.\n4. Makeup hygiene.'], Complications:['infection', 'MALIGNANCY'], Diagnostics:['biopsy'], Differential diagnosis:['blepharitis', 'chronic dacryocystitis', 'Dacryoadenitis', 'Leishmaniasis', 'stye', 'trichiasis', 'tumors'], disease description:A chalazion is a red bump on your eyelid. It is sometimes called an eyelid cyst or a meibomian cyst. It slowly forms when an oil gland (called a meibomian) becomes blocked.At first, the chalazion may be painful, but after a little time, it usually doesn’t hurt. A chalazion usually forms on the upper eyelids but may occasionally form on the lower eyelid.

Symptoms at 42: ['regional lymphadenopathy', 'lesion, which is usually solitary, is often situated around the eyelids or near the mouth, or occasionally on the genitalia']

Disease Name: Chancriform Pyoderma, symptoms: ['regional lymphadenopathy', 'lesion, which is usually solitary, is often situated around the eyelids or near the mouth, or occasionally on the genitalia'], Treatment: ['Treatment with antibiotics shortens the duration but the response \nin our experience is not dramatic.'], Pathophysiology: Pathophysiology- The aetiology is uncertain, but a necrotizing reaction to a strain of Staphylococcus aureus, inoculated by minor trauma, has been suspected. The lesion, which is usually solitary, is often situated around the eyelids or near the mouth, or occasionally on the genitalia. A sharply marginated ulcer, sometimes exceeding 1 cm in diameter, with an indurated base and a bright-red areola, enlarges slowly for a few days. The regional lymph nodes are enlarged and tender., Epidemiology:['3 to 10 cases per million population per year.', 'less than 5% of cases occur in children.', 'Without treatment - poor prognosis', 'If you have the condition, try to avoid injuring your skin'], Complications:['Crohns Disease'], Diagnostics:['Skin test'], Differential diagnosis:['Leishmaniasis', 'lymphadenopathy', 'MYCOBACTERIUM TUBERCULOSIS', 'syphilis', 'vaccination'], disease description:This uncommon condition occurs more often in children than in adults. Chronic pyoderma reminiscent of syphilitic primary (chancre). Chancriform pyoderma is a rare, rapidly enlarging papule or pustule that progresses to a painless ulcer. It may become chronic, lasting for several months while relapsing a few times. Its etiology remains unclear.