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Cutaneous Small-vessel Vasculitis

Disease Name : Cutaneous Small-vessel Vasculitis, Treatment : First line,Oral prednisolone 30–80 mg once daily, tapered over 2–3 weeks, ,often gives symptom control,Second line,Colchicine 0.6 mg twice daily has been shown to be of benefi t ,by anecdotal evidence and open-label studies. Dapsone ,50-150 mg daily may be advantageous in the treatment of CSVV,Third line,In patients with disease refractory to the above therapies-azathioprine,(1–2 mg/kg/day) and methotrexate (15–25 mg/week), Pathophysiology : Leukocytoclastic vasculitis with segmental inflammation in an angiocentric pattern, swelling of the endothelium, fibrinoid necrosis of vessel walls, extravasation of erythrocytes, and an infiltrate of neutrophils with karyorrhexis of the nuclei (i.e. leukocytoclasia) are major features of CSVV. In superficial dermal papillary vessels, IgM or complement C3 perivascular deposits are demonstrated in up to 80% of fresh lesions. Some studies state lower proportions, but this may depend on the timing of the biopsy and also because IgM is relatively poor at fixing complement. IgG is found less often., Epidemiology : 0.4–3.4 per million people with a female predominance, 10-30 cases per million people per year., VARAIBLE, NA, Complications : infection, Diagnostics : Complete Blood Count CBC, Differential Leucocyte Count DLC, Erythrocyte Sedimentation Rate (ESR), SERUM Creatinine, Total Leucocyte Count (TLC), ANCA, full thickness skin biopsy, Differential diagnosis : allergies, chemical exposures, infections, systemic vasculitides, disease description : Cutaneous small-vessel vasculitis (CSVV) refers to a group of disorders usually characterized by palpable purpura; it is caused by leukocytoclastic vasculitis of postcapillary venules. CSVV can be idiopathic or can be associated with a drug, infection, or underlying systemic disease.

Cutaneous Warts

Disease Name : Cutaneous Warts, Treatment : medication : Glutaraldehyde , Formaldehyde Solution , Cidofovir , Imiquimod , Salicylic acid , Fluorouracil , Zinc/Zinc Sulphate, Tretinoin, Vitamin D Substances, Acitretin, Treatments that are physician administered, more time consuming ,or expensive can be classed as second line. 1.Cryotherapy, 2.Laser, 3.Hyperthermia, 4.Surgery, 5.Photodynamic therapy, 6., First line,Topical treatments that can be used by the patient at home can be ,regarded as first line.1.Salicylic acid, 2.Glutaraldehyde, 3.Formalin, 4.Topical 5-fluorouracil, 5.Retinoic acid. Third line,Third line treatments include those that might be considered in ,situations of severe and recalcitrant infection and also those treatments with less evidence base that might be considered when first ,and second line treatments have produced no effect.,1.Podophyllin and podophyllotoxin, 2.Imiquimod, 3.Topical immunotherapy, 4.Intralesional immunotherapy, 5.Interferon, 6.H2 receptor antagonists, 7.Oral zinc, 8.Oral retinoids, 9.Intralesional bleomycin, 10. Cidofovir, 11.Psychological methods., Pathophysiology : Out of the 100 subtypes of HPV, a few of them have the propensity to induce cancer. These subtypes include HPV strains 6, 11, 16, 18, 31, and 35. Malignant transformation tends to occur in individuals with genital warts and those who are immunocompromised. HPV strains 5, 8, 20, and 47 also have malignant potential in individuals with epidermodysplasia verruciformis. Warts, in general, are benign, but there are reports that sometimes they may become malignant and develop into what is known as verrucous carcinoma. The verrucous carcinoma is a slow-growing tumor and is classified as a well-differentiated squamous cell malignancy that is often mistaken for a common wart. Even though it can occur on any part of the body, it is most common on the plantar surface. Verrucous cancer rarely spreads, but it is locally destructive., Epidemiology : 3.5% of adults and 33% of children, approximately 10% of the population. In school-aged children, the prevalence is as high as 10% to 20%, VARIABLE, There are ways to prevent warts or keep them from spreading to other parts of your body if you already have one. Follow these simple guidelines : ,,Wash your hands regularly, especially if you’ve been in contact with someone with warts.,Don’t pick at your warts.,Cover warts with a bandage.,Keep your hands and feet dry.,Wear shower shoes (flip-flops) when in a locker room or communal bathing facility., Complications : cancer, Diagnostics : HISTOPATHLOGY, biopsy, PCR, TISSUE HISTOLOGY, immunohistochemistry, DERMATOSCOPY, Differential diagnosis : Actinic keratosis : Arsenical keratosis, PUVA kera, Bowen disease, Lichen Planus, Molluscum Contagiosum, Seborrheic Keratoses, Squamous cell carcinoma, disease description : These small, noncancerous growths appear when your skin is infected with one of the many viruses of the human papillomavirus (HPV) family. The virus triggers extra cell growth, which makes the outer layer of skin thick and hard in that spot. While they can grow anywhere you have skin, youre more likely to get one on your hands or feet. The type of wart depends on where it is and what it looks like.

Cyclosporiasis

Disease Name : Cyclosporiasis, Treatment : medication : Sulfamethoxazole , Trimethoprim , Trimethoprim/sulfamethoxazole (TMP/SMX), sold under the trade names Bactrim, Septra, and Cotrim, is the usual therapy for Cyclospora infection. No highly effective alternative antibiotic regimen has been identified yet for patients who do not respond to the standard treatment or have a sulfa allergy.,Most people who have healthy immune systems will recover without treatment. If not treated, the illness may last for a few days to a month or longer. Symptoms may seem to go away and then return one or more times (relapse). Anti-diarrheal medicine may help reduce diarrhea, but a health care provider should be consulted before such medicine is taken. People who are in poor health or who have weakened immune systems may be at higher risk for severe or prolonged illness., Pathophysiology : Parasite invasion and replication within enterocytes damages the small intestinal epithelium, leading to the disruption of the brush border, loss of membrane bound digestive enzymes, and intestinal villous blunting and atrophy. An influx of lymphocytes, plasma cells, and occasionally eosinophils occurs in the lamina propria. These changes have the overall effect of decreasing the small intestinal absorptive capacity, leading to decreased uptake of water, nutrients, and electrolytes., Epidemiology : The prevalence of infection in endemic areas is estimated at 2% to 18%, 2.80 per 100, 000 population), GOOD, Proper food handling is the best way to reduce your risk of cyclosporiasis. This helps you avoid ingesting food or water that could be contaminated. Not all disinfecting or sanitizing methods kill Cyclospora.,,Things you can do to avoid getting cyclosporiasis include : ,,Wash your hands with soap and water before, during and after food prep.,Thoroughly rinse or peel fresh fruits and vegetables before eating.,Don’t leave peeled, cooked or cut fruits and vegetables out of the refrigerator for more than two hours.,Store vegetables and fruit separately from raw meat, seafood and poultry.,Wash all food prep surfaces, dishes and utensils with hot water and detergent after use.,Don’t drink untreated water. Drink bottled water and use it for food prep if you’re not sure if the water is treated.,Avoid eating produce from areas where Cyclospora is common., Complications : cholecystitis, MALABSORPTION, Diagnostics : stool microscopy, STOOL ACID FAST STAIN, PCR for DNA IN STOOL SAMPLE, Differential diagnosis : Amoebiasis, Ascariasis, disease description : Cyclosporiasis is an intestinal illness caused by the microscopic parasite Cyclospora cayetanensis. People can become infected with Cyclospora by consuming food or water contaminated with the parasite. People living or traveling in countries where cyclosporiasis is endemic may be at increased risk for infection.

Cylindroma

Disease Name : Cylindroma, Treatment : . Topical salicylic acid has been used with some success in patients with multiple cylindromas, Surgery is the treatment of choice. Extensive involvement of the ,scalp may require wide excision and replacement of the whole ,area by a graft, Pathophysiology : The lesions may be familial and a suppressor gene (cylindromatosis gene, CYLD ) has been identified on chromosome 16q12–13, loss of which is associated with cylindroma development. Somatic mutations have also been identified in sporadic cases. The loss of this gene causes activation of necrosis factor ß (NF-ß), which is a transcription factor with antiapoptotic activity. Based on genetic studies and the identification of mutations in the same gene in the Brooke–Spiegler syndrome, multiple familial trichoepitheliomas and familial cylindromatosis, it is suggested that the three diseases have the same genetic basis and are phenotypic expressions of the same disease. Recently, it has been demonstrated that benign sporadic dermal cylindromas express the MYB-NFIB gene fusion, which is also expressed in adenoid cystic carcinomas of the breast, head and neck. Transition from cylindroma to spiradenoma in CYLD defective tumours associated with reduced DKK2 expression has been reported. Pathology The tumours have a rounded outline and are composed of closely set mosaic-like masses (‘jigsaw-puzzle’ appearance) and columns of cells that are invested by a hyaline basal membrane of variable thickness. Thin bands of stroma separate tumour lobules from one another. The cells are of two types : one large, with a moderate amount of cytoplasm and a vesicular nucleus; and the other small, with little cytoplasm and a compact nucleus. The small cells tend to be peripheral; they also surround duct- like spaces or masses of hyaline material within the tumour lobule. There are strong immunohistochemical similarities between cylindromas and spiradenomas, and they may coexist in the same individual. Malignant transformation is very rare and a sarcomatous component may exceptionally be seen. The lesions may be familial and a suppressor gene (cylindromatosis gene, CYLD ) has been identified on chromosome 16q12–13, loss of which is associated with cylindroma development. Somatic mutations have also been identified in sporadic cases. The loss of this gene causes activation of necrosis factor ß (NF-ß), which is a transcription factor with antiapoptotic activity. Based on genetic studies and the identification of mutations in the same gene in the Brooke–Spiegler syndrome, multiple familial trichoepitheliomas and familial cylindromatosis, it is suggested that the three diseases have the same genetic basis and are phenotypic expressions of the same disease. Recently, it has been demonstrated that benign sporadic dermal cylindromas express the MYB-NFIB gene fusion, which is also expressed in adenoid cystic carcinomas of the breast, head and neck. Transition from cylindroma to spiradenoma in CYLD defective tumours associated with reduced DKK2 expression has been reported. The tumours have a rounded outline and are composed of closely set mosaic-like masses (‘jigsaw-puzzle’ appearance) and columns of cells that are invested by a hyaline basal membrane of variable thickness. Thin bands of stroma separate tumour lobules from one another. The cells are of two types : one large, with a moderate amount of cytoplasm and a vesicular nucleus; and the other small, with little cytoplasm and a compact nucleus. The small cells tend to be peripheral; they also surround duct- like spaces or masses of hyaline material within the tumour lobule. There are strong immunohistochemical similarities between cylindromas and spiradenomas, and they may coexist in the same individual. Malignant transformation is very rare and a sarcomatous component may exceptionally be seen., Epidemiology : It involves females more frequently than males., 0.7% of all adnexal neoplasms, Lesions behave in a benign COURSE ., "Cant be prevented since its a genetic disorder. Although Genetic counselling is advisable.", Complications : post-surgical complications, Diagnostics : GENETIC TESTING, Differential diagnosis : Spiradenoma, disease description : A skin tumour traditionally regarded as showing sweat gland lineage with a characteristic histology that usually manifests as nodules or tumours of the scalp. The onset is usually in early adult life, but may be in childhood or adolescence. 

Cystathioninuria

Disease Name : Cystathioninuria, Treatment : supportive therapy, "The treatment, if any is available, varies depending on the category of cystathioninuria a patient has. The vitamin B6 – responsive form is best treated by an increased consumption of vitamin B6. This increased consumption helps with cystathionases altered ability to bind to the active form of vitamin B6.", Pathophysiology : The pathophysiology of cystathioninuria can be understood in the context of the normal metabolism of methionine, an essential amino acid. Methionine is initially converted to homocysteine, which is then either remethylated back to methionine or undergoes transsulfuration to form cysteine. The transsulfuration pathway involves the action of several enzymes, including CGL.In individuals with cystathioninuria, there is a defect in the CGL enzyme, leading to impaired transsulfuration and accumulation of cystathionine. This accumulation occurs because cystathionine is not effectively converted to cysteine and alpha-ketobutyrate.The exact mechanisms by which the deficiency or dysfunction of CGL leads to the symptoms of cystathioninuria are not fully understood. However, the accumulation of cystathionine can potentially disrupt cellular metabolism and affect various physiological processes., Epidemiology : 1-9/100000 (Canada, Canada), VARIABLE, NA., Complications : nephrolithiasis, Diagnostics : URINE R/M, ultrasound, Differential diagnosis : CYSTINURIA, EXTRAHEPATIC BILIARY ATRESIA, HEPATOBLASTOMA, HOMOCYSTINURIA, NEUROBLASTOMA, Pyridoxine deficiency, disease description : A rare inborn error of metabolism characterized by abnormal accumulation of plasma cystathionine and subsequent increased urinary excretion due to cystathionine gamma-lyase deficiency. The condition is considered benign without pathological relevance. Mode of inheritance is autosomal recessive.

Cystic Fibrosis

Disease Name : Cystic Fibrosis, Treatment : medication : Levofloxacin , Tobramycin sulfate , Colistin, Aztreonam, Antibiotics prevent or treat lung infections and improve lung function. Your doctor may prescribe oral, inhaled, or intravenous (IV) antibiotics.,Anti-inflammatory medicines, such as ibuprofen or corticosteroids, reduce inflammation. Inflammation causes many of the changes in cystic fibrosis, such as lung disease.,Bronchodilators relax and open airways. These treatments are taken by inhaling them.,CFTR modulators improve the function of the faulty CFTR protein. They improve lung function and help prevent lung problems and other complications. Examples include ivacaftor and lumacaftor.,Mucus thinners make it easier to clear the mucus from your airways., Pathophysiology : Cystic Fibrosis Transmembrane Conductance Regulator (CFTR)- CFTR is an integral membrane protein that functions as an epithelial anion channel. The ~1480-amino-acid molecule encodes a passive conduit for chloride and bicarbonate transport across plasma membranes of epithelial tissues, with direction of ion flow dependent on the electrochemical driving force. Gating of CFTR involves conformational cycling between an open and closed configuration and is augmented by hydrolysis of adenosine triphosphate (ATP). Anion flux mediated by CFTR does not involve active transport against a concentration gradient but utilizes the energy provided from ATP hydrolysis as a central feature of ion channel mechanochemistry and gating. CFTR is situated in the apical plasma membranes of acinar and other epithelial cells where it regulates the amount and composition of secretion by exocrine glands. In numerous epithelia, chloride and bicarbonate release is followed passively by the flow of water, allowing for mobilization and clearance of exocrine products. Along respiratory mucosa, CFTR is necessary to provide sufficient depth of the periciliary fluid layer (PCL), allowing normal ciliary extension and mucociliary transport. CFTR-deficient airway cells exhibit depleted PCL, causing ciliary collapse and failure to clear overlying mucus. In airway submucosal glands, CFTR is highly expressed in acini and may participate both in the formation of mucus and extrusion of glandular secretion onto the airway surface. In other exocrine glands characterized by abrogated mucus transport (e.g., pancreatic acini and ducts, as well as bile canaliculi, intestinal lumen), similar pathogenic mechanisms have been implicated. In these tissues, a driving force for apical chloride and/or bicarbonate secretion is believed to promote CFTR-mediated fluid and electrolyte release into the lumen, which confers proper rheology of mucins and other exocrine products. The CF airway is characterized by an aggressive, unrelenting, neutrophilic inflammatory response with release of proteases and oxidants leading to airway remodeling and bronchiectasis. Intense pulmonary inflammation is largely driven by chronic respiratory infection. Macrophages and other cells resident in CF lungs augment elaboration of proinflammatory cytokines, which contribute to innate and adaptive immune reactivity. CFTR-dependent abnormalities of airway surface fluid composition (e.g., pH) have been reported as contributors to impaired bacterial killing in CF lungs. The role of CFTR as a direct mediator of inflammatory responsiveness and/or pulmonary remodeling represents an important and topical area of investigation. with concomitant tissue injury., Epidemiology : 7.37 per 100, 000 population in the U.S. and in E.U., 1 in 2, 500 to 3, 500 white newborns., VARIABLE, You can’t prevent cystic fibrosis because it’s an inherited condition. If you or your partner have any kind of family history, you may want to speak to a genetic counselor before you decide to have children., Complications : sinusitis, infertility, Diagnostics : CT Thorax, DNA analysis for mutation, X RAY CHEST, SERUM ELECTROLYTE, PULMONARY FUNCTION TEST(PFT), Differential diagnosis : BRONCHIECTASIS, BRONCHIOLITIS, CIRRHOSIS, heart failure, disease description : Cystic fibrosis (CF) is an autosomal recessive exocrinopathy affecting multiple epithelial tissues. The gene product responsible for CF (the cystic fibrosis transmembrane conductance regulator CFTR) serves as an anion channel in the apical (luminal) plasma membranes of epithelial cells and regulates volume and composition of exocrine secretion. An increasingly sophisticated understanding of CFTR molecular genetics and membrane protein biochemistry has facilitated CF drug discovery, with a number of new agents recently approved or advancing through the clinical testing phase.

Cysticercosis

Disease Name : Cysticercosis, Treatment : medication : Albendazole , Praziquantel , Cerebral disease is treated with praziquantel 50 mg/kg daily for 10 days, under steroid cover. Steroids should be used to decrease the inflammation associated with the dying organisms. Patients may also require antiepileptic therapy if they present with seizures. Adult tapeworms are treated with praziquantel in a dose of 10 mg/kg once. Obstructive lesions of the brain require surgical relief., Individual subcutaneous cysts may be removed surgically if desired., Pathophysiology : Cysticercosis is a parasitic infection caused by the larval stage of the tapeworm Taenia solium. The pathophysiology of cysticercosis involves the complex interactions between the parasite, the host immune response, and the affected organs.When a person ingests the eggs of Taenia solium, the larvae can hatch in the intestines and penetrate the intestinal wall. From there, they can migrate to various organs, most commonly the central nervous system (neurocysticercosis), but also the muscles, eyes, and other tissues.The larvae develop into cysticerci, which are fluid-filled sacs containing the larval form of the parasite. These cysts can vary in size and location and may cause different symptoms depending on their location., Epidemiology : approximately 10 to 20 percent of individuals have evidence of neurocysticercosis on computed tomography scans, primarily in the form of calcified lesions, VARIABLE, Safe food and water preparation and hand washing are the most important things you can do to help prevent cysticercosis.,,Wash your hands with soap and water frequently, especially after using the bathroom, after changing diapers, before eating and before preparing food.,Wash fruits and vegetables thoroughly or peel before eating.,Wash cutting boards, counters, dishes and utensils with soapy water after use.,Don’t drink untreated water.,If you’re traveling to a place where you don’t know if the water is treated, drink bottled or boiled water only. Boil water for one minute before allowing to cool and then drinking.,Filter drinking water with an “absolute 1 micron or less” filter (found at camping supply stores), then dissolve iodine tablets into filtered water before drinking., Complications : headache, seizures, Diagnostics : Antibody Serology Tests, CT HEAD, stool microscopy, X RAY, TISSUE HISTOLOGY, Differential diagnosis : Brain Abscess, Tuberculoma, disease description : Cysticercosis is a parasitic tissue infection caused by larval cysts of the tapeworm Taenia solium. These larval cysts infect brain, muscle, or other tissue, and are a major cause of adult onset seizures in most low-income countries. A person gets cysticercosis by swallowing eggs found in the feces of a person who has an intestinal tapeworm.

Cystinuria

Disease Name : Cystinuria, Treatment : nan, Pathophysiology : nan, Epidemiology : nan, Complications : nan, Diagnostics : nan, Differential diagnosis : nan, disease description : nan

Cystitis

Disease Name : Cystitis, Treatment : medication : Codeine , Potassium/Potassium Salts, Ciprofloxacin , Norfloxacin , Nitrofurantoin , large ,quantities of fluids by mouth, at least 2.5 L every 24 h. ,Plain water, alkaline drinks, milk and weak tea should be ,given, Pathophysiology : Method of infection of the bladder is by a descending infection from the kidney, such as may occur with renal tuberculosis and chronic pyelonephritis. Organisms may also reach the bladder from adjacent structures such as an inflamed cervix and parametric infections. The bladder may perhaps be infected by way of the bloodstream, and in other cases by lymphatic spread from the genitalia or the bowel. The organisms found in urine in cystitis are E. coli, streptococci, staphylococci, Bacillus proteus, the tubercle bacilli and occasionally other organisms, such as Pseudomonas pyocyanea. Gonococcal cystitis is relatively rare and almost invariably follows instrumentation. The organism which is found most frequently is E. coli. This organism is now supposed to attack the bladder secondarily to an original infection by other organisms and subsequently to overgrow and replace the primary infection. On the other hand, it is well established that cystitis due to a primary E. coli infection is occasionally encountered.., Epidemiology : Almost 30% of the women will experience at least one episode of cystitis during their life span. Of these 30%, 20% of these women will have recurrent cystitis., The incidence of cystitis in women is 5-7 per year per 100, 000 while that in same age men is 50-80 per 100000., GOOD, Women should wipe from front to back after a bowel movement to prevent the spread of bacteria from feces. In addition, taking showers instead of baths may also help. Make sure to wash skin gently in the genital area.,,Women should empty their bladders after sexual intercourse, and drink water. Finally, avoid any products that irritate the area., Complications : Urinary Tract Infection, Diagnostics : Complete Blood Count CBC, PUS CULTURE, URINE C/S, Differential diagnosis : Pyelonephritis, disease description : Cystitis is inflammation of the bladder, usually caused by a bladder infection.Its a common type of urinary tract infection (UTI), particularly in women, and is usually more of a nuisance than a cause for serious concern. Mild cases will often get better by themselves within a few days.

Cystoid Macular Edema

Disease Name : Cystoid Macular Edema, Treatment : medication : Ranibizumab , Bevacizumab , Dexamethasone , Nepafenac , Systemic therapy : The majority of the patients develop macular edema secondary to systemic health conditions like diabetes mellitus, high blood pressure, dyslipidemia, or inflammatory conditions. Therefore, systemic treatment is of prime importance., Ocular laser : The various types of laser treatment include : ,Focal laser (Original ETDRS), Grid laser (Original ETDRS), Modified ETDRS grid laser (mETDRS), Mild macular laser photocoagulation (MMG)., Pathophysiology : A delicate exchange of homeostatic mechanisms is in place with the vitreous, retina, retinal pigment epithelium (RPE), and choroid receiving their circulation through the retinal and choroidal vasculature.A variety of risk factors may disrupt the normal interactions affecting the retinal environment. There is an intrinsic balance amongst the osmotic force, hydrostatic force, capillary permeability, and tissue compliance that occur within the vasculature. Specifically, the capillary filtration rate should equal the rate of fluid removal from extracellular retinal tissue, such as glial and RPE cells. Once these forces are disrupted an imbalance occurs and accumulation of fluid is seen in cystoid spaces within the inner layers of the retina, most commonly the outer plexiform layer (OPL). The OPL is more prone to fluid collection due to the watershed area that exists between the retinal and choroidal circulation, especially within the central retina due to its anatomical avascular zone. Accumulation of the fluid commonly occurs in the Henle’s fiber layer causing the classic petaloid pattern.Specifically, a common factor that can cause CME is vitreomacular traction (VMT). VMT can cause stress at the Muller cell end-feet, exerting tractional forces and contributing to the release of inflammatory factors such as basic fibroblastic grown factor (bFGF), vascular endothelial growth factor (VEGF), and platelet-derived growth factor (PDGF). This results in blood-retinal barrier breakdown from separation of the retina and RPE, lysis of muller cells, leakage and edema. However, typically CME associated with VMT does not demonstrate leak on FFA., Epidemiology : 49%, incidence of 0.1–2.35%, GOOD, Optimal prevention of PCME starts preoperatively with a personalized risk assessment. Diabetes mellitus, retinal vein occlusion, epiretinal membrane, macular hole, and uveitis are the most important risk factors for developing cystoid macular edema after cataract surgery. Topical NSAIDs either in addition to, or instead of, topical corticosteroids reduce the risk of developing PCME. ,,Additional intravitreal corticosteroid and antivascular endothelial growth factor injections have been studied in patients with diabetes. Timely diagnosis and treatment of PCME is essential. Topical NSAIDs solely, or in addition to corticosteroids, improve visual acuity in patients with PCME. Oral acetazolamide and intravitreal dexamethasone implants have been used in refractory cases., Complications : endophthalmitis, Scarring, Diagnostics : Optical coherence tomography (OCT), Slit lamp examination, ELECTRORETINOGRAPHY, Fundus fluorescein angiography (FFA), Differential diagnosis : berlins edema, CENTRAL SEROUS CHORIORETINOPATHY, disease description : Cystoid Macular Edema (CME) as retinal thickening of the macula due to a disruption of the normal blood-retinal barrier; this causes leakage from the perifoveal retinal capillaries and accumulation of fluid within the intracellular spaces of the retina, primarily in the outer plexiform layer.

Cysts Of Conjunctiva

Disease Name : Cysts Of Conjunctiva, Treatment : During excision of cyst conjunctiva along with tenon’s was held with non-traumatic forceps gently above the cyst, a small incision was given and the blunt tip of scissors introduced between cyst and tenon’s to separate the cyst from the surrounding tissue. Conjunctiva above the cyst was left as such, which helped to hold the cyst firmly during blunt dissection.,Conjunctival cysts need a careful surgical excision. The excised cyst should always be subjected to histopathological examination., Pathophysiology : Inclusion cysts : Inclusion cysts happen when a layer of your conjunctiva folds over onto itself. A cyst forms around the bump and fills with fluid as a response to the irritation. More than 80% of conjunctival cysts are inclusion cysts.Retention cysts : Retention cysts form when one of the tiny ducts in your conjunctiva gets clogged by something like an allergen, dust or debris. A cyst forms around the blockage filled with cells and fluid from your lymphatic system., Epidemiology : between 1% and 7.7, GOOD, You can’t prevent a conjunctival cyst from forming. In general, make sure you always wear protective eyewear and proper safety equipment while working with tools or doing any activity that could injure your eyes., Complications : discomfort, proptosis, Diagnostics : HISTOPATHLOGY, Slit lamp examination, ultrasound, biopsy, Differential diagnosis : dermoid cyst, Sebaceous cyst, disease description : Conjunctival cysts are noncancerous growths on the conjunctiva — the thin membrane that covers the white of your eye. Some cysts go away on their own without treatment. But, even if you need it removed, a conjunctival cyst shouldn’t have any long-term impact on your eyeball or vision.

Cyto Megalovirus Infection

Disease Name : Cyto Megalovirus Infection, Treatment : medication : Valganciclovir , Ganciclovir , Foscarnet , Most CMV infections do not require specific therapy, but in life-,threatening situations or when CMV retinitis threatens sight, ,two antiviral agents – ganciclovir and foscarnet – have been used ,with some success. Valganciclovir, a prodrug of ganciclovir, is used as prophylactic treatment in CMV antibody-negative ,transplant recipients receiving a solid organ from a CMV-positive ,donor and has also been reported to be effective as treatment for ,acute or recurrent CMV disease., Pathophysiology : Congenital CMV infection Primary CMV infection in the first or second trimester of pregnancy can have multiple effects on the fetus. In its most severe form, there are hepatosplenomegaly, jaundice and purpura. Most cases die within 2 months and survivors usually have severe neurological damage especially deafness. There may be erythropoietic tissue in the dermis derived from undifferentiated dermal mesenchyme; this presents as purple or red papules or nodules lasting 4–6 weeks (‘blueberry muffin’ lesions). Vesicles occur very rarely in congenital CMV disease. CMV can present as a congenital infection where there is underlying immune defect., Epidemiology : People who are pregnant and people with a compromised immune system can reduce their risk of CMV by avoiding contact with other people’s body fluids. Specific ways to reduce your risk include : ,,Don’t share food or forks, spoons, cups or other eating utensils with a child.,Don’t put a child’s pacifier in your mouth.,Wash your hands after changing a diaper or helping a child go to the bathroom. Use warm water and soap.,Use a condom when having oral, anal or vaginal sex, even if you always have sex with the same partner.,If you’ve received an organ transplant, your provider may treat you with antiviral medications to prevent CMV. They may monitor your blood for infections so that they can treat you as soon as possible if you do get infected., Complications : ENCEPHALITIS, erythema multiforme, neurological deficit, Diagnostics : SEROLOGIC ESSAY, PCR, Viral cultures, Differential diagnosis : nan, disease description : Cytomegalovirus infections are common throughout the world and are usually inapparent. Primary infection is followed by lifelong carriage of the virus with intermittent shedding in various secretions. This may be increased by physiological stimuli such as pregnancy, and by immune suppression due to disease or therapy as in AIDS and transplant recipients, respectively.

Cytopenia

Disease Name : Cytopenia, Treatment : nan, Pathophysiology : nan, Epidemiology : nan, Complications : nan, Diagnostics : nan, Differential diagnosis : nan, disease description : nan

D-2-hydroxyglutaric Aciduria

Disease Name : D-2-hydroxyglutaric Aciduria, Treatment : There is no specific treatment for D-2-hydroxyglutaric aciduria. Management mainly involves control of seizures when they are present., Pathophysiology : The D2HGDH and L2HGDH genes provide instructions for making enzymes that are found in, which are the energy-producing centers within cells. The enzymes break down compounds called D-2-hydroxyglutarate and L-2-hydroxyglutarate, respectively, as part of a series of reactions that produce energy for cell activities. Mutations in either of these genes lead to a shortage of functional enzyme, which allows D-2-hydroxyglutarate or L-2-hydroxyglutarate to build up in cells. At high levels, these compounds can damage cells and lead to cell death. Brain cells appear to be the most vulnerable to the toxic effects of these compounds, which may explain why the signs and symptoms of D-2-HGA type I and L-2-HGA primarily involve the brain., Epidemiology : D-2-HGA and L-2-HGA have each been reported to affect fewer than 150 individuals worldwide., "D-2-HGA type I, L-2-HGA, and combined D, L-2-HGA all have an autosomal recessive pattern and therefore, it cant be prevented. ,,Although Genetic counselling is advisable.", Complications : seizures, hypotonia, Feeding Difficulty, Diagnostics : molecular genetic testing, Differential diagnosis : nan, disease description : 2-hydroxyglutaric aciduria is a condition that causes progressive damage to the brain. The major types of this disorder are called D-2-hydroxyglutaric aciduria (D-2-HGA), L-2-hydroxyglutaric aciduria (L-2-HGA), and combined D, L-2-hydroxyglutaric aciduria (D, L-2-HGA).The main features of D-2-HGA are delayed development, seizures, weak muscle tone (hypotonia), and abnormalities in the largest part of the brain (the cerebrum), which controls many important functions such as muscle movement, speech, vision, thinking, emotion, and memory. Researchers have described two subtypes of D-2-HGA, type I and type II. The two subtypes are distinguished by their genetic cause and pattern of inheritance, although they also have some differences in signs and symptoms. Type II tends to begin earlier and often causes more severe health problems than type I. Type II may also be associated with a weakened and enlarged heart, a feature that is typically not found with type I.

D-glyceric Acidemia Primary Hyperoxaluria

Disease Name : D-glyceric Acidemia Primary Hyperoxaluria, Treatment : high oral fluid intake (2-3 L/m2,/24,hr while controlling for fluid balance), urine alkalinization, phosphate,supplementation, monitoring of vitamin C and vitamin D intake, and avoidance,of drugs that increase urinary calcium excretion (e.g., loop diuretics) are,recommended, Organ transplantation has emerged as the most definitive treatment. The,decision to undergo kidney, liver, or liver-kidney transplant is complex and may,vary, Pathophysiology : This rare condition is caused by a deficiency of the glyoxylate reductase– hydroxypyruvate reductase enzyme complex. A deficiency in the activity of this complex results in an accumulation of two intermediate metabolites, hydroxypyruvate (the ketoacid derivative of serine) and glyoxylic acid. Both these compounds are further metabolized by LDH to L -glyceric acid and oxalic acid, respectively. A high prevalence of this disorder is reported in the Saulteaux-Ojibway Indians of Manitoba. Primary hyperoxaluria type 2 results in the deposition of calcium oxalate in the renal parenchyma and urinary tract. Renal stones presenting with renal colic and hematuria may develop before age 2 yr. Renal failure is less common in this condition than in primary hyperoxaluria type 1., Epidemiology : 1 in 58, 000 individuals worldwide., 1-2/10 000 000 per year, variable, there are no known prevention methods, Complications : renal disease, Diagnostics : DNA analysis for mutation, LIVER BIOPSY, kidney biopsy, Urine analysis, molecular testing, blood test, Differential diagnosis : nan, disease description : This rare condition is caused by a deficiency of the glyoxylate reductase– hydroxypyruvate reductase enzyme complex. A deficiency in the activity of this complex results in an accumulation of two intermediate metabolites, hydroxypyruvate (the ketoacid derivative of serine) and glyoxylic acid. Both these compounds are further metabolized by LDH to L -glyceric acid and oxalic acid, respectively. A high prevalence of this disorder is reported in the Saulteaux-Ojibway Indians of Manitoba

D-glyceric Acidemia

Disease Name : D-glyceric Acidemia, Treatment : nan, Pathophysiology : The enzyme glycerate kinase catalyses the enzymatic conversion of D-glyceric acid to 2-phosphoglycerate. This enzymatic conversion is an intermediary reaction found in several metabolic pathways, particularly in the breakdown of fructose, Epidemiology : Extremely rare disorder with fewer than 10 cases reported in the medical literature., Complications : nan, Diagnostics : plasma D-glyceric acid, Differential diagnosis : Renal disorders, disease description : A rare inborn error of metabolism characterized by abnormal urinary excretion of D-glyceric acid due to D-glycerate kinase deficiency. Reported manifestations are highly variable and include a severe encephalopathic picture, chronic metabolic acidosis, developmental delay, intellectual disability, microcephaly, seizures, behavioral abnormalities, as well as only mild speech delay and apparently normal development.

D-glycerol 1-phosphate

Disease Name : D-glycerol 1-phosphate, Treatment : nan, Pathophysiology : D-Glycerol 1-phosphate is a molecule that plays a role in certain metabolic pathways, particularly in the synthesis of lipids and glycerolipids. However, it is important to note that D-Glycerol 1-phosphate is not typically associated with a specific pathophysiological condition or disease. It is a relatively less-studied molecule compared to other metabolites.Glycerolipid metabolism : D-Glycerol 1-phosphate serves as an intermediate in the biosynthesis of glycerolipids, which are important components of cell membranes and energy storage molecules. In this context, disruptions or abnormalities in the metabolism of D-Glycerol 1-phosphate could potentially affect the synthesis and homeostasis of glycerolipids, leading to lipid-related disorders or dysfunctions.Glycerol metabolism : D-Glycerol 1-phosphate can also be involved in the breakdown of glycerol, a process known as glycerolysis. Glycerol is an important energy source and is derived from the breakdown of triglycerides in adipose tissue. Alterations in the metabolism of D-Glycerol 1-phosphate may impact glycerol metabolism, potentially leading to abnormalities in energy balance or lipid-related disorders.Possible genetic disorders : Although rare, there are genetic disorders that involve defects in the enzymes or transporters associated with D-Glycerol 1-phosphate metabolism. For example, mutations in the glycerol kinase gene (GK) have been associated with glycerol kinase deficiency, a condition characterized by the inability to phosphorylate glycerol to form D-Glycerol 1-phosphate. This deficiency can lead to elevated levels of glycerol in the blood and urine, resulting in clinical symptoms such as intellectual disability, seizures, and glyceroluria., Epidemiology : unknown, variable, Complications : nan, Diagnostics : molecular genetic testing, Differential diagnosis : nan, disease description : Glycerol-3-phosphate dehydrogenase (GlpD) is an essential membrane enzyme, functioning at the central junction of respiration, glycolysis, and phospholipid biosynthesis. Its critical role is indicated by the multitiered regulatory mechanisms that stringently controls its expression and function. Once expressed, GlpD activity is regulated through lipid-enzyme interactions in Escherichia coli.

Dacryoadenitis

Disease Name : Dacryoadenitis, Treatment : When pus is,formed, incision and drainage should be carried out., systemic antibiotic, analgesic and anti-inflammatory,drugs along with hot fomentation, Pathophysiology : I. Acute dacryoadenitis It may develop as a primary inflammation of the gland or secondary to some local or systemic infection. Dacryoadenitis secondary to local infections occurs in trauma, erysipelas of the face, conjunctivitis (especially gonococcal and staphylococcal) and orbital cellulitis. Dacryoadenitis secondary to systemic infections is associated with mumps, influenza, infectious mononucleosis and measles.Acute inflammation of the palpebral part is characterised by a painful swelling in the lateral part of the upper lid. The lid becomes red and swollen with a typical S-shaped curve of its margin. Acute orbital dacryoadenitis produces some painful proptosis in which the eyeball moves down and in. A fistula in the upper and lateral quadrant of the upper lid may develop as a complication of suppurative dacryoadenitis. II. Chronic dacryoadenitis It is characterised by engorgement and simple hypertrophy of the gland. Chronic dacryoadenitis may occur : • As sequelae to acute inflammation; • In association with chronic inflammations of conjunctiva and; • Due to systemic diseases such as tuberculosis, syphilis and sarcoidosis. (i) a painless swelling in upper and outer part of lid associated with ptosis; (ii) eyeball may be displaced down and in; and (iii) diplopia may occur in up and out gaze. On palpation, a firm lobulated mobile mass may be felt under the upper and outer rim of the orbit., Epidemiology : Not reported., GOOD, The best way to prevent acute dacryoadenitis is to wash your hands frequently, especially before you touch your eyes. When you rub your eyes or touch your nose or mouth, any germs on your hands can enter your body through mucous membranes in your eyes, nose or mouth. Wash your hands with clean, running water, lather them with soap and scrub for at least 20 seconds.,,If you have an autoimmune disease, it might be impossible to prevent chronic dacryoadenitis. Your provider will tell you how to manage your symptoms as they come and go (recur)., Complications : THYROID EYE DISEASE, Diagnostics : ANTI NUCLEAR ANTI BODY(ANA), Complete Blood Count CBC, FNAC, biopsy, CT SCAN, Differential diagnosis : CHALAZION, MALIGNANCY, orbital cellulitis, THYROID EYE DISEASE, disease description : Dacryoadenitis is the SWELLINGS OF LACRIMAL GLAND. Dacryoadenitis may be acute or chronic. i.Acute Dacryoadenitis : It may develop as a primary inflammation of the gland or secondary to some local or systemic infection. II. Chronic dacryoadenitis It is characterised by engorgement and simple hypertrophy of the gland.Inflammation of the gland can be due to infectious or inflammatory sources but may be idiopathic. Viral dacryoadenitis is self-resolving, while bacterial sources may require antibiotic administration. Inflammatory causes may respond to steroids, or demonstrate a chronic relapsing course requiring long-term treatment to maintain remission.

De Quervains Tenosynovitis

Disease Name : De Quervains Tenosynovitis, Treatment : medication : Hydrocortisone , Applying ice to your thumb and wrist area to reduce swelling., REST, CREPE BANDAGE, local infiltration of,hydrocortisone, chronic case may,need slitting and excision of a part of the tendon,sheath., Pathophysiology : The combination of mechanical stress and inflammation results in the following pathophysiological changes : Tendon Thickening : The APL and EPB tendons become thickened due to the chronic inflammation and increased production of collagen fibers. This thickening narrows the tendon sheath, limiting the movement of the tendons within the sheath.Synovial Sheath Inflammation : The synovial sheath, which surrounds the tendons, becomes inflamed and produces excess synovial fluid. The increased fluid further restricts the movement of the tendons, causing pain and discomfort.Pain and Tenderness : The thickened tendons and inflamed sheath can compress the surrounding nerves, leading to pain and tenderness over the radial aspect of the wrist and base of the thumb. The pain is typically exacerbated with thumb and wrist movements or with grasping objects.Limited Range of Motion : The combination of tendon thickening and synovial inflammation restricts the gliding motion of the tendons, resulting in a limited range of motion of the thumb and wrist., Epidemiology : 2% in the general population. This frequency increases by fivefold or more in individuals with diabetes mellitus., 0.31 per 1000 in U.S. workers, GOOD, The best way to prevent de Quervain’s tenosynovitis is to avoid overusing your thumbs and wrists : ,,Learn the proper technique and wear proper protective equipment for sports, work and any physical activity.,Ease into new exercises or activities to avoid injury.,Take breaks if you’re doing a repetitive task.,Don’t “play through the pain” if your wrist hurts during or after physical activity.,Give your body time to rest and recover after intense activity., Complications : nan, Diagnostics : X-RAY AFFECTED JOINT, MRI, Differential diagnosis : BURSITIS, Carpal tunnel syndrome, CELLULITIS, gonorrhoea, Infective endocarditis, rheumatoid arthritis, disease description : This is a condition characterised by pain and swelling over the radial styloid process. It results from inflammation of the common sheath of abductor pollicis longus and extensor pollicis brevis tendons. It is associated with repetitive wrist motion, specifically motion requiring thumb radial abduction and simultaneous extension and radial wrist deviation. On examination, the tenderness is localised to the radial styloid process. Pain is aggravated by adducting the thumb across the palm and forcing ulnar deviation and on asking the patient to perform radial deviation against resistance (Finkelsteins test). There may be a palpable thickening of the sheath..

Deaf Child

Disease Name : Deaf Child, Treatment : Parental Guidance, Hearing Aids, Development of Speech and Language, Education of the Deaf, Vocational Guidance, Pathophysiology : Hearing loss in a child may develop from causes before birth (prenatal), during birth (perinatal) or thereafter (postnatal). A. PRENATAL CAUSES They may pertain to the infant or the mother. 1. INFANT FACTORS. An infant may be born with inner ear anomalies due to genetic or nongenetic causes. Anomalies may affect inner ear alone (nonsyndromic) or may form part of a syndrome (syndromic). Anomalies affecting the inner ear may involve only the membranous labyrinth or both the membranous and bony labyrinths. They include : (a) Scheibe dysplasia. It is the most common inner ear anomaly. Bony labyrinth is normal. Superior part of membranous labyrinth (utricle and semicircular ducts) is also normal. Dysplasia is seen in the cochlea and saccule; hence also called cochleosaccular dysplasia. It is inherited as an autosomal recessive nonsyndromic trait. (b) Alexander dysplasia. It affects only the basal turn of membranous cochlea. Thus only high frequencies are affected. Residual hearing is present in low frequencies and can be exploited by amplification with hearing aids. (c) Bing-Siebenmann dysplasia. There is complete absence of membranous labyrinth. (d) Michel aplasia. There is complete absence of bony and membranous labyrinth. Even the petrous apex is absent but external and middle ears may be completely unaffected. No hearing aids or cochlear implantation can be used. (e) Mondini dysplasia. Only basal coil is present or cochlea is 1.5 turns. There is incomplete partition between the scalae due to absence of osseous spiral lamina. Condition is unilateral or bilateral. This deformity may be seen in Pendred, Waardenburg, branchio-oto-renal, Treacher-Collins and Wildervanck syndromes. (f) Enlarged vestibular aqueduct. Vestibular aqueduct is enlarged (>2 mm), endolymphatic sac is also enlarged and can be seen on T 2 MRI. It causes early onset sensorineural hearing loss which is progressive. Vertigo may be present. Perilymphatic fistula may occur. (g) Semicircular canal malformations. Both superior and lateral or only lateral semicircular canal malformations may be seen. They can be identified on imaging techniques. 2.MATERNALFACTORS (a) Infections during pregnancy. (b) Drugs during pregnancy. (c) Radiation to mother in the first trimester. (d) Other factors. Syndromes commonly associated with hearing loss are given below. 1. Waardenburg syndrome 2. Usher syndrome 3. Jervell and LangeNielson syndrome 4. Pendred syndrome 5. Alport syndrome 6. Treacher-Collins syndrome (mandibulofacial dysostosis) (a) Infections during pregnancy. Infections which affect the developing fetus are toxoplasmosis, rubella, cytomegaloviruses, herpes type 1 and 2 and syphilis. Remember mnemonic, TORCHES. (b) Drugs during pregnancy. Streptomycin, gentamicin, tobramycin, amikacin, quinine or chloroquine, when given to the pregnant mother, cross the placental barrier and damage the cochlea. Thalidomide not only affects ear but also causes abnormalities of limbs, heart, face, lip and palate. (c) Radiation to mother in the first trimester. (d) Other factors. Nutritional deficiency, diabetes, toxaemia and thyroid deficiency. Maternal alcoholism is also teratogenic to the developing auditory system. B. PERINATAL CAUSES They relate to causes during birth or in early neonatal period. They are as follows. 1. ANOXIA. It damages the cochlear nuclei and causes haemorrhage into the ear. Placenta praevia, prolonged labour, cord round the neck and prolapsed cord can all cause fetal anoxia. 2. PREMATURITY AND Low BIRTH WEIGHT. Born before term or with birth weight less than 1500 g (3.3 lb). 3. BIRTH INJURIES. e.g. forceps delivery. They may cause intracranial haemorrhage with extravasation of blood into the inner ear. 4. Neonatal Jaundice. Bilirubin level greater than 20 mg% damages the cochlear nuclei. 5. Neonatal Meningitis 6. Sepsis 7. Time Spent in Neonatal ICU 8. Ototoxic Drugs. used for neonatal meningitis or septicaemia.C. POSTNATAL CAUSES 1. Genetic. Though deafness is genetic, it manifests later in childhood or adult life. Deafness may occur alone as in familial progressive sensorineural deafness or in association with certain syndromes, e.g. Alport, Klippel-Feil, Hurler, etc. 2. Nongenetic. They are essentially same as in adults and include : (a) Viral infections (measles, mumps, varicella, influenza), meningitis and encephalitis. (b) Secretory otitis media. (c) Ototoxic drugs. (d) Trauma, e.g. fractures of temporal bone, middle ear surgery or perilymph leak. (e) Noise-induced deafness, Epidemiology : POOR, Following are tips for parents to help prevent hearing loss in their children : ,,1. Have a healthy pregnancy.,2. Make sure your child gets all the regular childhood vaccines.,3. Keep your child away from high noise levels, such as from very loud toys., Complications : nan, Diagnostics : EVOKED POTENTIAL, Impedance Audiometry, HISTORY TAKING, Differential diagnosis : Acute Otitis Media, Alport Syndrome, CHOLESTEATOMA, Down syndrome, Keratosis Obturans, middle ear tumours, OTITIS EXTERNA, disease description : Children with profound (>90 dB loss) or total deafness fail to develop speech and have often been termed deaf-mute or deaf and dumb. However, these children have no defect in their speech producing apparatus. The main defect is deafness. They have never heard speech and therefore do not develop it. In lesser degrees of hearing loss, speech does develop but is defective. The period from birth to 5 years of life is critical for the development of speech and language, therefore, there is need for early identification and assessment of hearing loss and early rehabilitation in infants and children. It was observed that children whose hearing loss was observed and managed before 6 months of age had higher scores of vocabulary, better expressive and comprehensive language skills than those diagnosed and managed after 6 months of age emphasizing the importance of early identification and treatment.

Dedifferentiated Liposarcoma

Disease Name : Dedifferentiated Liposarcoma, Treatment : systemic therapy options have been limited to cytotoxic chemotherapy agents, including doxorubicin, ifosfamide, gemcitabine, and docetaxel, that were shown to have efficacy in unselected populations of patients with soft tissue sarcomas., The management of dedifferentiated liposarcomas includes resection., Pathophysiology : The pathophysiology of DDLPS involves complex genetic and molecular alterations that contribute to the development and progression of the tumor.Chromosomal Aberrations : DDLPS is characterized by chromosomal abnormalities, most commonly involving the amplification of the 12q13-15 region. This amplification leads to the overexpression of several genes, including MDM2 and CDK4, which play crucial roles in cell cycle regulation and cell growth.Loss of Well-Differentiated Liposarcoma Features : DDLPS typically arises from a pre-existing well-differentiated liposarcoma (WDLPS). In DDLPS, there is a loss of the adipocytic differentiation seen in WDLPS, with the development of non-lipogenic, dedifferentiated components. This loss of differentiation is associated with the acquisition of aggressive behavior and metastatic potential.p53 Pathway Alterations : DDLPS often exhibits alterations in the p53 pathway, such as mutations or inactivation of the tumor suppressor gene TP53. Loss of p53 function leads to dysregulation of cell cycle control, impaired DNA repair mechanisms, and resistance to apoptosis, promoting tumor growth and progression., Epidemiology : 2% to 4% of soft-tissue sarcomas, approximately 2000 individuals each year in the United States., VARIABLE, There are no known preventive strategies to limit the incidence of this disease thus far., Complications : MALIGNANCY, Diagnostics : Cytogenetics, Immunostaining, Differential diagnosis : ANGIOMYOLIPOMA, malignant peripheral nerve sheath tumour, melanoma, Myxoid liposarcoma, Pleomorphic liposarcoma, rhabdomyosarcoma, Teratoma, disease description : ?Dedifferentiated liposarcomas (DDLPS) are malignant adipocytic soft tissue neoplasms that have progressed from primary or recurrent atypical lipomatous tumors/well-differentiated liposarcomas and are characterized by a much higher rate of recurrence, metastasis in about one-fourth of the cases and a much higher overall mortality. Well differentiated liposarcoma (WDL) with transition, either in the primary tumor or as a recurrence, to a sarcoma that is typically nonlipogenic.Although historically considered to only be high grade, variable grading is now recognized in dedifferentiated liposarcoma (DDL).

Deep Benign Fibrous Histiocytoma, symptoms

Disease Name : Deep Benign Fibrous Histiocytoma, symptoms : nan, Treatment : Surgical excision, The treatment of deep fibrous histiocytomas usually is surgical excision. Local recurrence is observed in about one-fifth of the cases. There are occasional metastases reported in up to 5%, Pathophysiology : Deep fibrous histiocytomas are well-defined proliferations with a mixed fascicular and storiform cell pattern characterized by monomorphic histiocytoid or spindled cells with interposed branching vessels., Epidemiology : Deep fibrous histiocytomas are rare tumors. They make up for less than 1% of all fibrohistiocytic tumors and occur over a wide age range., Men are slightly more often affected than women, VARIABLE, Because exact causes are unclear, it may not be possible to fully prevent it from occurring. However, you can reduce the risk of by making healthy lifestyle choices, like eating a balanced diet, exercising regularly and avoiding tobacco products., Complications : nan, Diagnostics : MRI, MRI, CT SCAN, CT SCAN, USG, Immunostaining, Differential diagnosis : dermatofibroma, dermatofibrosarcoma protuberans, Pleomorphic ‘MFH’ / Undifferentiated pleomorphic sarcoma, disease description : Benign fibrous histiocytoma (FH) is one of the most common mesenchymal neoplasms of the skin. Several histologic variants of cutaneous FH have been described, some of which also have distinct clinical features including a propensity for local recurrence. Deep benign FH is an uncommon and poorly recognized clinical subtype that arises in subcutaneous or deep soft tissue.

Deep Coma

Disease Name : Deep Coma, Treatment : Once an individual is out of immediate danger, the medical care team focuses on preventing infections and maintaining a healthy physical state. This will often include preventing pneumonia and bedsores and providing balanced nutrition, Physical therapy may also be used to prevent contractures (permanent muscular contractions) and deformities of the bones, joints, and muscles that would limit recovery for those who emerge from coma., Pathophysiology : A coma is a state of unconsciousness where a person is unresponsive and cannot be woken.It can result from injury to the brain, such as a severe head injury or stroke. A coma can also be caused by severe alcohol poisoning or a brain infection (encephalitis).People with diabetes could fall into a coma if their blood glucose levels suddenly became very low (hypoglycaemia) or very high (hyperglycaemia).Someone who is in a coma is unconscious and has minimal brain activity. Theyre alive but cant be woken up and show no signs of awareness.The persons eyes will be closed and theyll appear to be unresponsive to their environment. They wont normally respond to sound or pain, or be able to communicate or move voluntarily, and basic reflexes, such as coughing and swallowing, will be greatly reduced.They may be able to breathe on their own, although some people require a machine to help them breathe.Over time, the person may start to gradually regain consciousness and become more aware. Some people will wake up after a few weeks, while others may go into a vegetative or minimally conscious state. Read more about disorders of consciousness., Epidemiology : prevalence was 20 coma cases per 100 000 population., 2 in 1, 000 people per year, poor, It’s possible to prevent — or reduce your risk of having — many of the conditions that cause comas. Some of the most important ways you can prevent or reduce your risk of being in a coma include : ,,1. Managing your chronic conditions. Following your healthcare provider’s guidance on managing chronic conditions like diabetes and epilepsy can lower your odds of being in a coma in the future.,2. Wearing safety equipment as needed. Head injuries, especially concussions and traumatic brain injuries, are very common causes of comas. When applicable, wear safety equipment like helmets and seat belts to protect yourself.,3. Eating a balanced diet. Many of the most common causes of coma are related to diet, like electrolyte imbalances and nutrient deficiencies. Your diet also affects your circulatory health, which can help you avoid comas related to conditions like stroke.,4. Staying physically active and maintaining a weight that’s healthy for you. Your weight and activity level can prevent or delay conditions that affect your brain, especially conditions that can lead to comas.,5. Avoiding substance and nonmedical drug use, and using alcohol in moderation. Substance use disorders greatly increase the risk of a coma. You should also take prescription medications as directed, as this reduces the risk of complications and side effects like a coma., Complications : BEDSORES, PNEUMONIA, Urinary Tract Infection, blood clot formation, contractures of tissue, Diagnostics : X Ray skull, Differential diagnosis : Alcoholism, hyperglycemia, Seizure disorders, disease description : Coma is a state of prolonged loss of consciousness. It can have a variety of causes, including traumatic head injury, stroke, brain tumor, or drug or alcohol intoxication. A coma may even be caused by an underlying illness, such as diabetes or an infection.Coma is a medical emergency. Quick action is needed to preserve life and brain function..A coma doesnt usually last longer than several weeks. People who are unconscious for a longer time might transition to a lasting vegetative state, known as a persistent vegetative state, or brain death.

Deep Leiomyoma, symptoms

Disease Name : Deep Leiomyoma, symptoms : nan, Treatment : Excision; rarely recurs., Hysterectomy is the definitive surgical operation, but myomectomy is still commonly performed especially in women who desire future fertility. More recently developed techniques, which include uterine artery embolization (UAE), magnetic resonance-guided focused-ultrasound surgery (MRgFUS), and myolysis, are emerging as minimally invasive alternative procedures., Pathophysiology : These slow-growing, solitary tumors are extremely infrequent and have a tendency to grow to enormous sizes.Leiomyoma of deep soft tissue usually affects the thigh; the other tumor areas include the abdomen and pelvic region. Both, men and women in their mid-adult phase of life, are commonly affected.In summary, the pathophysiology of deep leiomyomas involves a complex interplay of genetic, hormonal, ECM-related, angiogenic, inflammatory, and mechanical factors. These factors collectively contribute to abnormal cell growth, increased ECM deposition, angiogenesis, and inflammation within the myometrium, leading to the development and growth of deep leiomyomas., Epidemiology : 20-25% of women of reproductive age, and 30-40% of women older than 40 years, The prognosis is excellent with appropriate treatm, Current medical research has not established a method of preventing Leiomyoma of Deep Soft Tissue., Complications : nan, Diagnostics : CT SCAN, Immunostaining, Differential diagnosis : Epithelioid leiomyosarcoma, myolipoma, disease description : Leiomyomas are benign tumours of smooth-muscle origin representing 4.4% of all benign soft-tissue neoplasms. They are classified as cutaneous, vascular and leiomyomas of deep soft tissues. Leiomyomas rarely occur in extremities and are more common in the lower limb than in the upper extremity.

Deep Palmar Abscess

Disease Name : Deep Palmar Abscess, Treatment : immobilization with hand elevation, antibiotic coverage, A strong suspicion and a,throbbing pain are indications of deep seated pus,requiring drainage. A needle aspiration may be,helpful in confirming the presence of pus.,A central transverse incision is made in the line of,the flexor crease, passing across the middle of the,palm at the site of maximum tenderness. If pus is,encountered beneath the aponeurosis, the floor of,the abscess must be probed systematically for a,sinus leading to a deeper plane. In order to ensure,free drainage of the pus, the skin edges as well as,those of the palmar fascia are trimmed., Pathophysiology : In all closed spaces of the hand, accumulation of purulent material is raising the pressure, compromising the blood flow, and causing ischemia and necrosis. These conditions are further aggravating the infection, establishing a vicious circle. Direct inoculation (epithelium lysis), spread from the adjacent necrotic tissues or through the lymphatic pathway, could result in the establishment of hand infections., Epidemiology : 24.6 per 1000 people per year, These have a fair prognosis, Instruct patients to avoid predisposing factors, such as repeated exposure to water and/or irritants., Complications : stiffness, DISCHARGE, Diagnostics : X RAY, Differential diagnosis : CELLULITIS, pyoderma gangrenosum, disease description : ?An abscess beneath the palmar fascia is a serious but rare infection of the hand. It may be an infection in the the mid-palmar space. The accumulation of purulent material subsequently raises the pressure within the closed-space, leading to ischemia and necrosis. These infections are usually attributed to gram-positive cocci. ?

Deep Venous Thrombosis

Disease Name : Deep Venous Thrombosis, Treatment : medication : Warfarin , Low-molecular-weight Heparins, Compression hosiery : Below-knee graduated compression stockings with an ankle pressure greater than 23 mm Hg for two years if there are no contraindications, Pathophysiology : According to Virchows triad, the following are the main pathophysiological mechanisms involved in DVT : Damage to the vessel wallBlood flow turbulenceHypercoagulabilityThrombosis is a protective mechanism that prevents the loss of blood and seals off damaged blood vessels. Fibrinolysis counteracts or stabilizes thrombosis. The triggers of venous thrombosis are frequently multifactorial, with the different parts of the triad of Virchow contributing in varying degrees in each patient, but all result in early thrombus interaction with the endothelium. This stimulates local cytokine production and causes leukocyte adhesion to the endothelium, promoting venous thrombosis. Depending on the relative balance between the coagulation and thrombolytic pathways, thrombus propagation occurs. DVT is commonest in the lower limb below the knee and starts at low-flow sites, such as the soleal sinuses, behind venous valve pockets.A potential correlation between DVT and atherosclerosis (AS) has been proposed. The endothelial dysfunction involved in the pathophysiological mechanism of DVT would potentially result in AS. Accordingly, a greater risk of subsequent AS in patients with DVT is predicted., Epidemiology : prevalence of lower limb DVT of 1 case per 1000 population, It is thought the annual incidence of DVT is 80 cases per 100, 000, GOOD, If you’ve never had a DVT, but have an increased risk of developing one, be sure to : ,,Exercise your calf muscles if you need to sit still for a long time. Stand up and walk at least every half hour if you’re on a long flight. Or get out of the car every hour if you’re on a long road trip.,Get out of bed and move around as soon as you can after you’re sick or have surgery. The sooner you move around, the less chance you have of developing a DVT.,Take medications or use compression stockings after surgery (if your provider prescribes them) to reduce your risk of a clot.,Follow up with your provider as directed and follow their recommendations to reduce your risk of a clot., Complications : Pulmonary Embolism, Chronic venous insufficiency, Post-thrombotic syndrome, Diagnostics : 2-D Echo, Color Doppler, contrast venography, compression USG, PLASMA D DIMER ELISA, ABG PO2, VENOUS COLOUR DOPPLER, CHEST ROENTGENOGRAPHY, LUNG SCAN, VENOUS MRI, CONTRAST PHLEBOGRAPHY, Differential diagnosis : CELLULITIS, Chronic venous insufficiency, disease description : Lower extremity DVT usually begins in the calf and propagates proximally to the popliteal vein, femoral vein, and iliac veins. Leg DVT is about 10 times more common than upper extremity DVT, which is often precipitated by placement of pacemakers, internal cardiac defibrillators, or indwelling central venous catheters. The likelihood of upper extremity DVT increases as the catheter diameter and number of lumens increase. Superficial venous thrombosis usually presents with erythema, tenderness, and a “palpable cord.” Patients are at risk for extension of the thrombosis to the deep-venous system.

Deep-vein Thrombosis

Disease Name : Deep-vein Thrombosis, Treatment : "Blood thinners. These medicines, also called anticoagulants, help prevent blood clots from getting bigger. Blood thinners reduce the risk of developing more clots.,,Blood thinners may be taken by mouth or given by IV or an injection under the skin. ,Clot busters (thrombolytics). These drugs are used for more-serious types of DVT or PE, or if other medications arent working.,,Clot busters are given by IV or through a tube (catheter) placed directly into the clot. ,Filters. If you cant take medicines to thin your blood, a filter may be placed into a large vein — the vena cava — in your belly (abdomen).,Support stockings (compression stockings). These special knee socks help prevent blood from pooling in the legs. They help reduce leg swelling.", The cornerstone of treatment is anticoagulation.Below-knee graduated compression stockings with an ankle pressure greater than 23 mmHg for 2 years, Pathophysiology : In 1856, Virchow postulated that the main causes of thrombus formation were damage to the vessel wall, alterations in blood flow and hypercoagulability. This is called ‘Virchow’s triad’ and is still valid today. All results in early thrombus interaction with the endothelium This then stimulates local cytokine production and causes leukocyte adhesion to endothelium, both of which promote venous thrombosis. DVT is commonest in the lower limb below the knee and starts at low-flow sites, such as the soleal sinuses, behind venous valve pockets., Epidemiology : prevalence of lower limb DVT of 1 case per 1000 p, 80 cases per 100, 000., Risk of recurrence of DVT is high (up to 25%) Deat, After you have a DVT, you’ll need to reduce your risk of future DVT/PE clots by : ,,Taking your medications exactly as your healthcare provider tells you to.,Keeping your follow-up appointments with your doctor and the laboratory. These tell your provider how well your treatment is working.,Making lifestyle changes, such as eating healthier foods, being more active and avoiding tobacco products.,If you’ve never had a DVT, but have an increased risk of developing one, be sure to : ,,Exercise your calf muscles if you need to sit still for a long time. Stand up and walk at least every half hour if you’re on a long flight. Or get out of the car every hour if you’re on a long road trip.,Get out of bed and move around as soon as you can after you’re sick or have surgery. The sooner you move around, the less chance you have of developing a DVT.,Take medications or use compression stockings after surgery (if your provider prescribes them) to reduce your risk of a clot.,Follow up with your provider as directed and follow their recommendations to reduce your risk of a clot., Complications : Pulmonary Embolism, Post-thrombotic syndrome, Diagnostics : BLOOD UREA NITROGEN ( BUN ), Complete Blood Count CBC, LIVER FUNCTION TEST LFT, SERUM ELECTROLYTE, contrast venography, DUPLEX ULTRASONOGRAPHY, CHEST X RAY, MR VENOGRAPHY, Differential diagnosis : Arteriovenous fistula and congenital vascular abnormalities, CELLULITIS, CIRRHOSIS, heart failure, nephrotic syndrome, Post-thrombotic syndrome, Ruptured Baker’s cyst, Superficial thrombophlebitis, Trauma, vasculitis, Venous or lymphatic obstruction, disease description : Deep vein thrombosis (DVT, also called venous thrombosis) occurs when a thrombus (blood clot) develops in veins deep in the  body because  veins are injured or the blood flowing through them is too sluggish. The blood clots may partially or completely block blood flow through  vein. Most DVTs happen in y lower leg, thigh or pelvis, but they also can occur in other parts of  body including your arm, brain, intestines, liver or kidney.

Defective Expression Of Major Histocompatibility C

Disease Name : Defective Expression Of Major Histocompatibility C, Treatment : Treatment with interferon-? did not result in expression of class I by the cells, although the cells were responsive to interferon-? because they upregulated class II expression after exposure to the cytokine in vitro., Pathophysiology : The pathophysiology of defective MHC-I expression can be understood in the context of two main mechanisms : loss of MHC-I expression and aberrant MHC-I expression.Loss of MHC-I Expression : Downregulation of MHC-I Genes : Some viruses and tumor cells have developed mechanisms to downregulate the expression of MHC-I genes. Viruses, such as human immunodeficiency virus (HIV), human cytomegalovirus (HCMV), and hepatitis C virus (HCV), can interfere with the expression or transportation of MHC-I molecules, evading immune recognition.Genetic Mutations : In certain genetic disorders, mutations in genes encoding components of the MHC-I pathway, such as ß2-microglobulin (ß2M) or transporter associated with antigen processing (TAP), can lead to loss of MHC-I expression. This can result in impaired immune surveillance and an increased susceptibility to viral infections and tumor development.Autoimmune Disorders : Autoimmune diseases, like systemic lupus erythematosus (SLE) and rheumatoid arthritis, may be associated with reduced MHC-I expression on target cells due to autoantibodies targeting MHC-I molecules. This abnormality can impact the immune response and contribute to the development and progression of these diseases.Aberrant MHC-I Expression : Altered Peptide Presentation : Some diseases, including cancer, can exhibit aberrant MHC-I expression with alterations in the peptide repertoire presented on MHC-I molecules. This can result in the presentation of aberrant or modified peptides, which can potentially trigger inappropriate immune responses or escape immune recognition.Tumor Immune Evasion : Tumor cells may exhibit defects in MHC-I expression or presentation, allowing them to evade recognition and destruction by cytotoxic T cells. This immune evasion mechanism is associated with tumor immune escape and can contribute to tumor progression and metastasis., Epidemiology : unknown, variable, Complications : nan, Diagnostics : immunohistology, SERUM IMMUNOGLOBULINS, Differential diagnosis : nan, disease description : MHC class I presents endogenous antigens to CD8+ T cells. These endogenous antigens are derived from proteins manufactured by the cells. In contrast, CD4+ T cells recognize exogenous antigen, taken up from outside the cell by antigen-presenting cells and presented as part of the MHC class II complex. If intact tumor cells are to be directly recognized by T cells, they must express class I or class II MHC and be able to process and present antigen to the T-cell receptor. Human T-cell recognition of tumors in an antigen-specific MHC-restricted fashion has been described in patients with melanoma

Defects Of Heart Conduction

Disease Name : Defects Of Heart Conduction, Treatment : Vagal maneuvers, which are techniques to slow down your heart rate, Medicines to make your heart beat faster or slower, depending on the problem with your heart, Surgery or implantable devices such as defibrillators or pacemakers, Pathophysiology : The signal starts with cells in the sinoatrial (SA) node that cause the heart to beat. These are called pacemaker cells. The signal causes your right and left atria to contract. The signal then travels down to your atrioventricular (AV) node and bundle branches, causing your right and left ventricles to contract.There are many types of conduction disorders that can happen anywhere along the cardiac conduction system : at the SA node, the AV node, or the bundle branches.Sick sinus syndrome (SSS), also known as sinus node disease : The SA node controls the rate and rhythm of your heartbeat. SSS can cause a slow or fast heart rate. It can also cause problems with increasing your heart rate when needed, such as when you exercise.Atrioventricular (AV) block : There are three degrees of AV block, depending on how serious your condition is. The third degree is called complete heart block. This happens when no signals reach your ventricles, the lower chambers of the heart. This can cause serious symptoms such as a very slow heart rate, fainting, and chest pain.Bundle branch blocks : These happen when the electrical signals travel more slowly in one side of your heart than in the other. This causes your ventricles to contract at different times than normal. You may have a left bundle branch block or a right bundle branch block, depending on which side is delayed.Ion channel disorders : On the surface of each heart muscle cell are tiny pores called ion channels. These channels help produce your heart’s electrical activity. The most common type of ion channel disorder is long QT syndrome. Other types include Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia, and short QT syndrome., Epidemiology : the prevalence of third-degree atrioventricular (AV) block (complete heart block) is 0.02%, incidence of AV block in surviving bifascicular block patients is 11% at 5 years, with 7% reflect- ing spontaneous block, variable, Some cases of heart block may be congenital (present at birth). But most heart block develops after birth. Some causes can’t be prevented. We also know that the risk of heart block increases with age and so does heart disease. Some causes of heart disease are preventable.,,Steps you can take to keep your heart and body as healthy as possible include : ,,Lead a heart-healthy lifestyle, which includes eating a heart healthy diet, exercising regularly, getting an adequate amount of sleep each night, reducing stress, limiting alcohol and stopping smoking and use of illicit drugs.,Talk with your healthcare provider about reviewing medications and other supplements you are taking to determine if any change the normal levels of potassium, calcium and magnesium – substances in your body that play a role with your heart’s electrical system. Your provider can change your medication to a different drug class if needed., Complications : Cardiac arrest, heart failure, Diagnostics : STRESS TEST (TREADMILL TEST TMT), GENETIC TESTING, Electrocardiography (EKG), Electrophysiological (EP) study, Differential diagnosis : Arrhythmias, Wolff-Parkinson-White syndrome, disease description : A conduction disorder, also known as heart block, is a problem with the electrical system that controls your heart’s rate and rhythm. This system is called the cardiac conduction system.Normally, the electrical signal that makes your heart beat travels from the top of your heart to the bottom. The signal causes your heart muscle to beat and pump blood to your lungs and the rest of your body. In conduction disorders, this electrical signal either does not get produced properly, does not travel the way it should through the heart, or both.

Deficiency Glossitis

Disease Name : Deficiency Glossitis, Treatment : medication : Vitamin B12 / cyanocobalamin/mecobalamin/methylcobalamin, . The cause of the defi ciency should be sought before ,replacement treatment is given., Intramuscular injections of Vitamin B12 /cyanocobalamin/mecobalamin/methylcobalamin., Pathophysiology : The precise pathogenesis of geographic tongue is poorly understood. Stress is a well-documented exacerbating factor, and patients may report worsening of symptoms with exposure to particular foods (acidic and spicy foods, classically), Epidemiology : 0.2%, up to 3% of the general population, Good, It may not always be possible to prevent glossitis. However, a person can lower their risk of developing the condition by : ,,maintaining a healthful diet,practicing good oral hygiene with regular brushing, flossing, and mouthwashes,avoiding irritants, such as spicy foods, cigarettes, and acidic foods,,,You can also reduce your risk for glossitis by avoiding the triggers that cause it. Possible triggers include smoking, drinking alcohol and eating hot and spicy foods., Complications : nan, Diagnostics : Hb, SERUM IRON, serum Vitamin B12 level, biopsy, THYROID PROFILE, PHYSICAL EXAMINATION, Differential diagnosis : Burning mouth syndrome, candidiasis, Vitamin B12 deficiency, Xerostomia, disease description : Deficiency glossitis may be related particularly to deficiency of iron, folate or vitamin B 12 , and may then be associated with angular stomatitis and/or mouth ulcers. Deficiencies of other B-group vitamins occasionally cause glossitis, usually in chronic alcoholics or in those with malabsorption.

Degloving Injury

Disease Name : Degloving Injury, Treatment : Management can consist of compressive therapy, needle aspiration, sclerodesis, limited or radical surgical irrigation, and debridement., Most surgeons therefore rely upon serial excision,until punctate dermal bleeding is obvious. Split-skin grafts can,be harvested from the degloved non-viable skin and meshed to cover the raw areas resulting from debridement., Pathophysiology : Normal skin and musculoskeletal anatomy include the following general layers from superficial to deep : skin, subcutaneous fat, superficial fascia, deep fat, deep fascia, muscle, bone. When a mechanism occurs that causes a tangential shearing of these layers, an internal degloving may take place. Essentially, the bone, muscle, and deep fascia shear one way, and the more superficial layers slide in the opposite direction. This event transects the perforating arteries and lymphatics that are traversing the fascial layers and leads to a collection of blood, lymphatic fluid, and necrotic fat in the newly created potential space. In addition, local inflammation and increased cellular permeability of nearby viable cells can add to the expansion. Over time, the body tries to sequester the lesion leading to either resorption of the fluid by nearby cells or a pseudocapsule formation and maturation of the fluid collection. As with any subdermal fluid collection, especially with necrotic tissue present, there is the possibility of infection. Another concern is the viability of the skin overlying the zone of injury. Two mechanisms are considered at fault for the cutaneous injury. First, the destruction of the skin and subcutaneous layers directly from the trauma leading to necrosis. Second, the blood flow from the rich vascular plexus in the dermis is interrupted, which allows the skin to become ischemic and eventually die., Epidemiology : The prevalence of overall degloving injuries among trauma patients was 1.56%, 4 % among trauma admissions, Variable, Complications : necrosis, skin necrosis, Diagnostics : MRI, CT, aspiration, EXAMINATION UNDER ANESTHESIA, Differential diagnosis : abscess, disease description : Degloving, also called avulsion, is a type of severe injury that happens when the top layers of your skin and tissue are ripped from the underlying muscle, connective tissue, or bone. It can affect any body part, but it’s more common in the legs. Degloving injuries are often life-threatening. This is because they involve large amounts of blood loss and tissue death.

Delayed Premature Labour

Disease Name : Delayed Premature Labour, Treatment : Bed rest. This can be done either at home or in the hospital, Antibiotics. These are used to treat infection, Corticosteroids. These may help the lungs of your baby grow and mature. Preterm babies’ lungs may not be able to work on their own., Tocolytic medicines. These help slow or stop contractions. They may be given as a shot (injection) or into the vein (intravenously)., Cervical cerclage. This procedure is used to stitch the cervix closed. It may be done when the cervix is weak and not able to stay closed., Pathophysiology : One of the key events to occur in preterm labor that is pathological is the fetal inflammatory response syndrome (FIRS) which involves systemic inflammation and elevation of fetal plasma interleukin-6, typically in response to a trigger such as chorioamnionitis. A signal is sent by the fetal hypothalamus leading to secretion of CRH, stimulating the release of ACTH and therefore cortisol production by the fetal adrenal glands, which triggers the parturition pathway to activate. An influx of inflammatory cells into the cervical stroma leads to the release of cytokines and prostaglandins which stimulate cervical ripening. These changes influence the structures of the collagen and glycosaminoglycans that make up cervical tissue. Estrogen stimulates collagen degradation whereas progesterone inhibits it. Therefore, progesterone is used to prevent or delay ripening. Both hormones are implicated in regulating the gap-junction formation and the upregulation of connexin 43 proteins which contribute to parturition.Additionally, contractions are an integral contributor to labor. The change from uncoordinated myometrial contractions to coordinated uterine contractions is attributed to neural control. Oxytocin plays an essential role in the circadian rhythm of these contractions.The degradation of the extracellular matrix is assessed by fetal fibronectin detection in cervicovaginal secretions and is also part of the parturition process. When detected between 22 and 37 weeks gestational age, it indicates the disruption of the decidual-chorionic interface and increased risk of preterm labor. Evidence implicates apoptosis as a critical factor leading in the above process., Epidemiology : Incidence 7-10% of deliveries are preterm (3% are early preterm), variable, It’s hard to prevent going into labor early, but there are some ways to lower your risk for preterm labor. Some things you can do are : ,,Don’t smoke cigarettes, drink alcohol, use recreational drugs or improperly use prescription drugs.,Get to a healthy weight before pregnancy and gain an appropriate amount of weight during pregnancy.,Eat healthy foods and take a prenatal vitamin. Find ways to reduce or manage your stress levels. Stay active, go for walks, read books or take time to relax every day.,Go to all prenatal appointments and schedule a cleaning with your dentist. There’s a link between your gum health and preterm labor.,Get treated for or manage any medical conditions you have like hypertension, gestational diabetes, depression or vaginal infections.,Space your pregnancies by at least 12 to 18 months., Complications : intraventricular hemorrhage, Neonatal necrotising enterocolitis, Diagnostics : USG, AMNIOTIC FLUID EXAMINATION, Differential diagnosis : appendicitis, nephrolithiasis, placenta abruptio, Pyelonephritis, Uterine fibroids, disease description : ? A pregnancy is “at term” at 37 weeks — anything before 37 weeks is called preterm. Preterm labor may result in premature birth (being born early).It further categorizes into early and late preterm. Early preterm is when the baby is born before 33 weeks, and late preterm is when a baby is born between 34 and 36 weeks.

Delayed Puberty

Disease Name : Delayed Puberty, Treatment : medication : TESTOSTERONE UNDECANOATE, 25–50 mg testosterone enanthate or testosterone cypionate every 2 weeks, or by ,using a 2.5-mg testosterone patch or 25-mg testosterone gel.Because ,aromatization of testosterone to estrogen is obligatory for mediating ,androgen effects on epiphyseal fusion, concomitant treatment with ,aromatase inhibitors may allow attainment of greater final adult ,height. Testosterone treatment should be interrupted after 6 months ,to determine if endogenous LH and FSH secretion have ensued., Pathophysiology : There are four main categories of delayed puberty : (1) constitutional delay of growth and puberty (~60% of cases); (2) functional hypogonadotropic hypogonadism caused by systemic illness or malnutrition (~20% of cases);(3) hypogonadotropic hypogonadism caused by genetic or acquired defects in the hypothalamic-pituitary region (~10% of cases); and (4) hypergonadotropic hypogonadism secondary to primary gonadal failure (~15% of cases). The constitutional delay of growth and puberty clusters in families displays an autosomal dominant pattern of inheritance, and has been linked in some families with a locus on pericentromeric region of chromosome 2. Functional hypogonadotropic hypogonadism is more common in girls than in boys. Permanent causes of hypogonadotropic or hypergonadotropic hypogonadism are identified in <25% of boys with delayed puberty. Between 25 and 40% of delayed puberty in girls is of ovarian origin, with Turner’s syndrome accounting for the majority of such patients. Delayed puberty may occur in the setting of systemic illnesses, including celiac disease and chronic renal disease, and endocrinopathies such as diabetes and hypothyroidism. In addition, girls appear to be particularly susceptible to the adverse effects of decreased energy balance resulting from exercise, dieting, and/or eating disorders and thus, functional hypothalamic amenorrhea (HA) can present with primary amenorrhea. Together these reversible conditions account for ~25% of delayed puberty in girls. Congenital hypogonadotropic hypogonadism in girls or boys can be caused by mutations in several different genes or combinations of genes. Approximately 50% of girls with congenital hypogonadotropic hypogonadism, with or without anosmia, have a history of some degree of breast development, and 10% report one to two episodes of vaginal bleeding. Family studies suggest that genes identified in association with absent puberty may also cause delayed puberty, and recent reports have further suggested that a genetic susceptibility to environmental stresses such as diet and exercise may account for at least some cases of functional HA, including in girls who present with primary amenorrhea. Although neuroanatomic causes of delayed puberty are considerably less common in girls than in boys, it is always important to rule these out in the setting of hypogonadotropic hypogonadism., Epidemiology : The prevalence of delayed puberty was 8.7% (10.4% females, 6.7% males)., 1-10 cases per 100, 000 individuals worldwide., variable, Genetic disorders cannot be cured, but hormone therapy may help sex characteristics develop.,,Patients and families should receive education about what the first signs of puberty consist of in males and females. Counselling is also necessary about the normal timing of puberty, which is between 8 to 13 years in females and 9 to 14 years in males. When there is concern about early or delayed puberty, patients and caregivers should seek help from a medical provider for a prompt and accurate diagnosis. The primary provider may also choose to consult a pediatric endocrinologist, who may further evaluate and manage the patient., Complications : nan, Diagnostics : SERUM TESTOSTERONE LEVEL, MRI Head, USG ABDOMEN(W/A), Serum LH Level Test, Serum FSH Level Test, X RAY, Gonadotropin-Releasing Hormone Stimulation Test, Differential diagnosis : Galactosemia, KALLMAN SYNDROME, Klinefelter syndrome., Malnutrition, Turners syndrome, disease description : Puberty that happens late is called delayed puberty. This means a childs physical signs of sexual maturity don’t appear by age 12 in girls or age 14 in boys. This includes breast or testicle growth, pubic hair, and voice changes. These are known as secondary sexual characteristics. Puberty is delayed in boys if it has not ensued by age 14, an age that is 2–2.5 standard deviations above the mean for healthy children. Delayed puberty is more common in boys than in girls Delayed puberty in girls is defined as the absence of secondary sexual characteristics by age 13 in girls. The diagnostic considerations are very similar to those for primary amenorrhea.

Dementia With Lewy Bodies

Disease Name : Dementia With Lewy Bodies, Treatment : Palliative care., People with LBD can take part in different therapies to improve their quality of life, including : ,,Physiotherapy.,Occupational therapy.,Speech therapy.,Support groups.,Individual and family psychotherapies (talk therapies).,Exercise., Cholinesterase inhibitors : This type of medication, which includes rivastigmine, galantamine and donepezil, helps manage the cognitive symptoms of LBD.,Carbidopa-levodopa : Symptoms of parkinsonism, like tremors, are usually treated with levodopa, a drug commonly used to treat Parkinson’s disease. However, it has serious side effects and can lead to delusions, hallucinations and confusion.,Pimavanserin : This medication can be used to treat psychosis (hallucinations, delusions) in people with Parkinson’s disease dementia.,Clonazepam and melatonin : These medications can help treat REM sleep behavior disorder.,Antidepressants : Depression is common in people with LBD and often requires antidepressant therapy with selective serotonin reuptake inhibitors (SSRIs).,Memantine : This drug is typically used to treat dementia caused by Alzheimer’s disease, but it’s been investigated in clinical trials and may work in people with LBD who are in the early phases of the condition., Pathophysiology : A buildup of Lewy bodies (proteins called alpha-synuclein) causes both dementia with Lewy bodies and Parkinson’s disease dementia. When Lewy bodies build up in neurons, they cause damage to certain areas of your brain.Researchers don’t know why some people develop LBD while others don’t. There’s some thought that the combination of mutations in a person’s genes, environmental risk factors and natural aging might lead to the development of LBD in some people. Research into specific causes is ongoing.One of the more recent discoveries toward identifying a cause of Lewy body dementia is the finding of an increasing number of gene mutations. Two genetic risk factors recently discovered are variants in the APOE and GBA genes.APOE is already known to increase the risk of developing Alzheimer’s disease. There’s growing evidence that it also increases the risk for dementia with Lewy bodies. Similarly, the GBA gene increases the risk for both Parkinson’s disease and dementia with Lewy bodies. Despite these findings, genetic changes as a cause of LBD are still considered rare by scientists. Most cases of Lewy body dementia aren’t thought to be inherited (passed down from parent to child)., Epidemiology : 3.6%, 3.5 per 100, 000 person-years overall, , variable, "While theres no guaranteed way to completely prevent dementia with Lewy bodies, evidence suggests that looking after our brain health may reduce our risk of dementia.,,To keep our brains healthy : ,,Keep physically and mentally active.,Don’t smoke.,Have your blood pressure, cholesterol and hearing checked regularly.,Maintain a healthy weight.,Eat a healthy balanced diet.,Drink alcohol in line with government recommendations.,Keep blood glucose in check if you have diabetes type 2.,Stay connected and do hobbies you enjoy.", Complications : Depressive symptoms, intraventricular hemorrhage, PNEUMONIA, heart problem, IMMOBILITY, Diagnostics : CT SCAN, HISTORY TAKING, NEUROLOGICAL EXAMINATION, blood test, Differential diagnosis : Alcoholism, Alzheimer’s disease, Pellagra, subacute combined degeneration, Wernicke’s encephalopathy, disease description : ?Lewy body dementia (LBD) is a type of dementia in which Lewy bodies are present in your brain. Lewy bodies are clumps of proteins that build up inside certain neurons (brain cells). They cause damage to neurons in the areas of your brain that affect mental capabilities, behavior, movement and sleep. Lewy body dementia is a progressive disease, meaning symptoms start slowly and get worse over time. In people over the age of 65, LBD is one of the most common causes of dementia. The symptoms of LBD may closely resemble those of other neurological conditions, including Alzheimer’s disease and Parkinson’s disease. There’s no cure for LBD, but the symptoms can be managed with certain medications.

Dementia

Disease Name : Dementia, Treatment : Unfortunately, there isn’t a cure for the most common types of dementia. Currently, approved medications can, at best, slow the decline., Drugs approved for the most common form of dementia, Alzheimer’s disease, include : ,,Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon) and galantamine (Razadyne).,NMDA receptor antagonist memantine (Namenda).,Anti-amyloid antibody aducanumab (Aduhelm)., Pathophysiology : Dementia is a symptom of a variety of specific structural brain diseases as well as several system degenerations. Alzheimers disease presently is the commonest cause in the developed world, causing a cortical-subcortical degeneration of ascending cholinergic neurons and large pyramidal cells in the cerebral cortex. Clinically, the disease reflects predominantly deterioration of function in the association cortex. Pharmacologically and pathologically, abnormalities are more diffuse and extend into sensorimotor cortical areas as well., Epidemiology : more than 55 million people have dementia worldwide, over 60% of whom live in low-and middle-income countries. Every year, there are nearly 10 million new cases., 3% of people age 65-74, 17% of people age 75-84 and 32% of people age 85 or older, Poor, Although dementia can’t be prevented, living a health-focused life might reduce risk factors for certain types of dementia.,,Keeping blood vessels clear of cholesterol buildup, maintaining normal blood pressure, maintaining healthy blood sugar levels, staying at a healthy weight — basically, staying as healthy as you can — can keep your brain fueled with the oxygen and nutrients it needs to function at its highest possible level. Specific healthful steps you can take include : ,,Stop smoking.,Follow a Mediterranean diet, which is one filled with whole grains, vegetables, fruits, fish and shellfish, nuts, beans, olive oil and only limited amounts of red meats.,Exercise. Get at least 30 minutes of exercise most days of the week.,Keep your brain engaged. Solve puzzles, play word games and try other mentally stimulating activities. These activities may delay the start of dementia.,Stay socially active. Interact with people, discuss current events, and keep your mind, heart and soul engaged., Complications : BEDSORES, kidney damage, sepsis, stroke, heart problem, Bedwetting, Malnutrition, Dehydration, Diagnostics : MRI Brain, PET SCAN, HISTORY TAKING, PHYSICAL EXAMINATION, Nuclear Imaging (including 18F-fluorodeoxyglucose positron emission tomography FDG-PET), blood test, Differential diagnosis : Parkinson’s Disease, disease description : Dementia is a general term that represents a group of diseases and illnesses that affect your thinking, memory, reasoning, personality, mood and behavior. The decline in mental function interferes with your daily life and activities. It’s estimated that about 50% of people age 85 and older have dementia. Current medications may help slow the mental decline.

Dengue Without Warning Signs

Disease Name : Dengue Without Warning Signs, Treatment : "BLOOD TRANSFUSION IS INITIATED AT THE EARLIEST WARNING SIGNS OF CRITICAL PHASE, PACKED CELLS & RBCS ARE RECOMMENDED.", THERE IS NO SPECIFIC TREATMENT FOR DENGUE FEVER, SYMPTOMATIC TREATMENT IS GIVEN IN INITIAL PHASES WITH ACETAMINOPHEN, AVOID ASPIRIN(CAUSES BLEEDING), Pathophysiology : When a mosquito carrying dengue virus bites a person, the virus enters the skin together with the mosquitos saliva. It binds to and enters white blood cells, and reproduces inside the cells while they move throughout the body. The white blood cells respond by producing a number of signaling proteins, such as cytokines and interferons, which are responsible for many of the symptoms, such as the fever, the flu-like symptoms, and the severe pains. In severe infection, the virus production inside the body is greatly increased, and many more organs (such as the liver and the bone marrow) can be affected. Fluid from the bloodstream leaks through the wall of small blood vessels into body cavities due to capillary permeability. As a result, less blood circulates in the blood vessels, and the blood pressure becomes so low that it cannot supply sufficient blood to vital organs. Furthermore, dysfunction of the bone marrow due to infection of the stromal cells leads to reduced numbers of platelets, which are necessary for effective blood clotting; this increases the risk of bleeding, the other major complication of dengue fever., Epidemiology : VERY COMMON, 400 million infections per year worldwide, GOOD, The two main ways to protect yourself from dengue are through avoiding mosquito bites and vaccination.,,Mosquito protection,The best way to reduce your risk of dengue fever is to protect yourself from mosquito bites : ,,Use EPA-registered insect repellents that contain 20% to 30% DEET or other ingredients known to help keep Aedes mosquitos away.,Cover exposed skin outdoors, especially at night when mosquitos are more likely to be around.,Remove standing water (buckets or barrels, bird baths, old tires that may hold rainwater) and fill low spots where water can pool.,Keep mosquitos outside of your home by repairing holes in screens and keeping windows and doors closed if possible.,Use mosquito netting at night in areas where dengue is common.,If you’re pregnant, avoid traveling to areas where dengue is common if possible.,When traveling, be sure to check with the CDC to understand if there are any outbreaks of illness in your destination before you leave.,Dengue vaccine,The dengue vaccine (Dengvaxia™) is recommended only if you’ve already had dengue before. It can reduce your risk of severe dengue (dengue hemorrhagic fever) if you get a different version of the dengue virus in the future.,,Getting the vaccine isn’t recommended if you’ve never had dengue before. Because getting infected once with dengue makes you more likely to get sicker if you get another version of the virus (antibody-dependent enhancement), getting vaccinated before having dengue for the first time can increase your risk of severe dengue. Your healthcare provider will do a blood test to check for signs of a previous dengue infection to confirm that you’ve had dengue before getting the vaccine.,,Vaccination isn’t available to everyone. For instance, travelers from the U.S. aren’t yet eligible., Complications : nan, Diagnostics : Dengue IGG IGM NS 1, Hb, PLATELET COUNT, Total Leucocyte Count (TLC), IgM ELISA, ANTIGEN DETECTION ELISA, Differential diagnosis : Chikungunya fever, Leptospirosis, Malaria, MEASLES, TYPHOID FEVER, disease description : Dengue fever is a mosquito-borne disease that occurs in tropical and subtropical areas of the world. Mild dengue fever causes a high fever, rash, and muscle and joint pain. A severe form of dengue fever, also called dengue hemorrhagic fever, can cause severe bleeding, a sudden drop in blood pressure (shock) and death. Millions of cases of dengue infection occur worldwide each year. Dengue fever is most common in Southeast Asia and the western Pacific islands, but the disease has been increasing.

Dental Caries

Disease Name : Dental Caries, Treatment : Fluoride : When decay is caught early, fluoride treatments can repair tooth enamel. This process is called remineralization. You may need prescription toothpaste and mouthwash, as well as fluoride treatments at the dental office., Fillings : Once a hole forms in the tooth, dentists drill out the decayed material and fill the hole. Dental fillings are made of silver amalgam, composite resin or gold, Root canal : A root canal treats pain from root decay. Endodontists are dental specialists who treat problems that affect a tooth’s root. During a root canal, this healthcare provider removes the pulp that contains nerve endings that cause pain., Tooth extraction : If a root canal isn’t possible, your healthcare provider may extract (pull) the tooth. You may need a dental implant to replace a pulled permanent tooth. Implants keep teeth from shifting and changing your appearance and bite., Pathophysiology : The pathophysiology of dental caries can be understood through the following processes : Dental Plaque Formation : Dental plaque is a biofilm composed of bacteria, salivary proteins, and extracellular polysaccharides. It forms on tooth surfaces and along the gumline. Plaque provides an environment for bacterial colonization and serves as a reservoir for nutrients.Acid Production by Bacteria : Certain species of bacteria, particularly Streptococcus mutans and Lactobacillus spp., play a significant role in dental caries. These bacteria metabolize dietary carbohydrates, particularly fermentable sugars, and produce organic acids, mainly lactic acid. The acid production lowers the pH of the plaque, leading to demineralization of the tooth enamel.Demineralization and Enamel Breakdown : The acidic environment created by the bacteria leads to the demineralization of the tooth enamel. The minerals, such as calcium and phosphate, are dissolved from the enamel structure, causing it to weaken and lose its protective function. Over time, if left untreated, this demineralization progresses, resulting in the breakdown of the enamel and the formation of cavities.Remineralization and Saliva Protection : Saliva plays a crucial role in maintaining oral health. It contains minerals, such as calcium and phosphate, which can help in the remineralization process. Saliva also acts as a buffer, neutralizing acids and maintaining a more favorable pH in the oral cavity. However, if the demineralization exceeds the remineralization capacity, cavities can develop.Secondary Factors : Several additional factors can influence the pathophysiology of dental caries. These include poor oral hygiene, inadequate fluoride exposure, dry mouth (xerostomia), frequent snacking on sugary or acidic foods and beverages, and certain systemic conditions or medications that affect saliva production or composition., Epidemiology : 54.16%, 2 billion people suffer from caries of permanent teeth and 514 million children suffer from caries of primary teeth., Variable, Proper oral hygiene, including regular brushing and flossing, can get rid of plaque, acids and cavity-causing bacteria. Good teeth and gum care includes : ,,Brushing your teeth with a soft-bristled brush and fluoride toothpaste at least twice a day, and preferably after every meal.,Cutting back on sugary, starchy foods and drinks.,Daily flossing to get rid of food and plaque stuck between your teeth.,Dental checkups at least twice a year. (You might need more frequent visits if you’re prone to tooth decay, gum disease or other oral health issues.),Dental sealants to protect the top chewing surfaces of your teeth., Complications : abscess, CELLULITIS, sepsis, PERIOSTITIS, osteomyelitis, Diagnostics : X RAY, PHYSICAL EXAMINATION, Fibre Optic Transilumination, Differential diagnosis : Dental fluorosis, hypoplasia, disease description : Dental caries is a common chronic infectious resulting from tooth-adherent cariogenic bacteria, primarily Streptococcus Mutans, which metabolize sugars to produce acid, demineralizing the tooth structure over time. Dental caries is reported to be one of the oldest and most common diseases found in humans. Dental caries is a prevalent chronic infectious disease resulting from tooth-adherent cariogenic bacteria that metabolize sugars to produce acid, which over time demineralizes tooth structure.

Dentinal Hypersensitivity

Disease Name : Dentinal Hypersensitivity, Treatment : use of tooth pastes containing potassium salts and fluoride, Pathophysiology : Based on the studies, DH is developed in two phases : Lesion localizationLesion initiationIn the first phase, dentinal tubules, due to loss of enamels, are exposed by attrition, abrasion, erosion, and abfraction. However, dentinal exposure mostly occurs due to gingival recession along with the loss of cementum on the root surface of canines and premolars in the buccal surface. It is worth noticing that not all the exposed dentins are sensitive. However, their calcified smear layer, as compared to non sensitive dentin, is thin and this leads to an increase in the fluid movement and consequently the pain response. In the second phase, for the exposed dentin to be sensitized, the tubular plugs and the smear layer are removed and consequently, dentinal tubular and pulp are exposed to the external environment. Plug and smear layer on the surface of exposed dentine are composed of elements of protein and sediments which are derived from salivary calcium phosphates and seal the dentinal tubules inconsistently and transiently.The findings of laboratory research indicate that both mechanical and chemical factors are effective in removing the smear layer from the dentinal tubules. However, the results of clinical investigations, the mechanical factors are not the only key factors in removal of the smear layer and when they are accompanied with acidic foods or drinks they lead to the removal of smear layer. It seems that microbial plaque is not a significant factor in triggering DH. First, as mentioned previously, the canines and first premolars have the greatest recession and sensitivity. The same teeth also reveal the lowest buccal plaque scores. Secondly, teeth with DH are cleaned extremely by patients suffering from the condition. This would suggest that plaque does not produce dentin hypersensitivity itself nor does it act as a stimulus for pain. However, the effect of plaque on DH is a controversial issue. , Epidemiology : 2-8% to 74%, incidence ranges from 4-74%., good, 1. Healthy dietary and oral hygiene practices. Using a non-traumatic toothbrushing technique will help prevent receding gums and tooth wear around the cervical margin of teeth.,2. Non-abrasive fluoride-containing toothpastes should be used, at least twice daily for two minutes at a time. ,3. The consumption of acidic foods and drinks should be avoided if possible., Complications : Dental Caries, Diagnostics : PHYSICAL EXAMINATION, PALPATION, Differential diagnosis : Dental Caries, disease description : Dentin hypersensitivity (DH), more commonly known as sensitive teeth, refers to a type of dental pain. Discomfort typically arises from exposed dentin responding to heat, cold, touch, pressure, or acidic foods. DH can have many causes and is often treatable with changes to a person’s oral hygiene regimen.

Depersonalization Disorder

Disease Name : Depersonalization Disorder, Treatment : Psychotherapy,Treatment of depersonalization/derealization disorder must address all stresses associated with onset of the disorder as well as earlier stresses (eg, childhood abuse or neglect), which may have predisposed patients to late onset of depersonalization and/or derealization.,,Various psychotherapies (eg, psychodynamic psychotherapy, cognitive-behavioral therapy) are successful for some patients : ,,Cognitive techniques can help block obsessive thinking about the unreal state of being.,Behavioral techniques can help patients engage in tasks that distract them from the depersonalization and derealization.,Grounding techniques use the 5 senses (eg, by playing loud music or placing a piece of ice in the hand) to help patients feel more connected to themselves and the world and feel more real in the moment.,Psychodynamic therapy helps patients deal with negative feelings, underlying conflicts, or experiences that make certain affects intolerable to the self and thus dissociated.,Moment-to-moment tracking and labeling of affect and dissociation in therapy sessions works well for some patients., Pathophysiology : he exact pathophysiology of DPD is not fully understood, but several factors have been proposed to contribute to its development : Neurobiological Factors : Abnormalities in Temporal Lobe Function : Some studies suggest that temporal lobe dysfunction may be involved in the pathophysiology of DPD. The temporal lobes are responsible for processing sensory information and emotions, and disruptions in their functioning could contribute to the altered perception and emotional numbing seen in depersonalization.Dysregulation of Serotonin and Glutamate : Imbalances in neurotransmitters, particularly serotonin and glutamate, have been implicated in DPD. Serotonin is involved in regulating mood, emotions, and perception, while glutamate is an excitatory neurotransmitter important for information processing. Dysregulation of these neurotransmitters may contribute to the dissociative symptoms observed in DPD.Stress and Trauma : Psychological Trauma : Experiencing trauma, particularly in early childhood, has been associated with the development of DPD. Traumatic experiences may disrupt the normal development of self-identity and lead to the dissociative symptoms seen in DPD.Coping Mechanisms : Dissociation, including depersonalization, can be a coping mechanism in response to overwhelming stress or traumatic experiences. The dissociative symptoms may serve as a defense mechanism to protect the individual from the emotional impact of the traumatic event.Cognitive and Emotional Factors : Attentional Bias : Individuals with DPD often exhibit an attentional bias towards internal stimuli (e.g., bodily sensations, thoughts, or emotions) rather than external stimuli. This excessive focus on internal experiences may contribute to the feeling of detachment and self-alienation.Emotional Regulation : Difficulties in emotional regulation, such as alexithymia (difficulty identifying and expressing emotions), have been associated with DPD. Emotional dysregulation may contribute to the dissociative symptoms and the inability to fully connect with ones emotions or experiences., Epidemiology : less than 2% of the population., . About half of all Americans are thought to experience at least one or two depersonalization episodes during their lifetime. Roughly 200, 000 people in the United States each day experience a depersonalization event., variable, It may not be possible to prevent depersonalization/derealization disorder. But it’s helpful to recognize the symptoms so you can get treatment.,,If you have experienced a traumatic event, seek help. Quick intervention can reduce the risk of developing a dissociative disorder., Complications : panic attacks, Diagnostics : HISTORY TAKING, Differential diagnosis : Obsessive-compulsive disorder (OCD), Panic disorder, disease description : Depersonalisation disorder is characterised by prominent depersonalisation and often derealisation, without clinically notable memory or identity disturbances. The disorder has an approximately 1 : 1 gender ratio with onset at around 16 years of age. The course of the disorder is typically long term and often continuous. Mood, anxiety and personality disorders are often comorbid with depersonalisation disorder but none predict symptom severity.

Dercum Disease

Disease Name : Dercum Disease, Treatment : medication : Paracetamol/Acetaminophen, FOR PAIN- NSAIDS, Topical lidocaine with or without prilocaine , intralesional ,lidocaine and intravenous lidocaine. Systemic corticosteroids have been reported to improve pain ,in some, while worsening it in other patients. Methotrexate alone and in combination with infliximab, pregabalin or oxacarbazepine has also been ,used., Pathophysiology : While the exact aetiology of Dercum disease is not known, many theories have been proposed. A local defect in lipid metabolism has been considered. One study showed a difference in the formation of long-chain mono-unsaturated fatty acids between the painful adipose tissue and the unaffected adipose tissue in the same patient. Another study showed that the proportion of mono- saturated fatty acids was significantly higher in Dercum disease patients than in healthy controls. Painful adipose tissue from a Dercum disease subject was found to have significantly lower conversion rate of glucose to neutral glycerides than non-painful adipose tissue from the same subject. In vitro analysis demonstrated that painful adipose tissue had reduced responsiveness to norepinephrine and lack of response to the antilipolytic effect of insulin compared with non-painful adipose tissue. Genetics The majority of cases occur sporadically. An autosomal dominant inheritance with variable expression has also been reported. HLA typing has not been revealing. A to G mutation at position A8344 of mitochondrial DNA, which is sometimes associated with familial multiple lipomas, is not detected., Epidemiology : The prevalence of Dercum’s disease has not yet been exactly established., Five to thirty times more common in women than in men, variable, "Most cases of adiposis dolorosa are sporadic, which means they occur in people with no history of the disorder in their family.,,A small number of familial cases of adiposis dolorosa have been reported. When the condition runs in families, it appears to have an autosomal dominant pattern and therefore it cant be prevented. ,,Counselling is advisable.", Complications : Psychiatric disturbances, Diagnostics : biopsy, CT SCAN, HISTORY TAKING, Differential diagnosis : Fibromyalgia, lipomatosis, disease description : Dercum’s disease, also known as adiposis dolorosa, is a rare disease typically characterized by development of painful subcutaneous adipose tissue deposits of different size, multiplicity and localization. Dercum disease is a rare disease characterized by generalized overweight status or obesity and pronounced pain in the adipose tissue with or without the presence of lipomas.The disease is characterized by diffuse or localized pain involving adipose tissue, usually affecting those who are overweight or obese. Patients experience a number of other somatoform symptoms, and management of the condition is a challenge. Dercum’s disease affects females more often than males with medical publications citing the disease as 5-30 times more common in women.

Dermal Melanocytic Lesions

Disease Name : Dermal Melanocytic Lesions : Mongolian Spot, Naevus, Treatment : Congenital dermal melanocytosis will commonly fade within 1 year, rarely persisting after 6 years old. However, for extra-sacral lesions can be treated for cosmetic purposes. A previous case of congenital dermal melanocytosis involving the mandibular area reported significant improvement after four treatments with a 755-nm Q-switched alexandrite laser., Pathophysiology : In normal fetal development, melanocytes (derived from neural crest cells) are present in the dermis of the embryo by ten weeks gestational age and migrate to the epidermis between weeks 11 to 14 of gestation. No melanocytes should remain in the dermal layer by week 20 of gestation via migration or macrophage clearance. In congenital dermal melanocytosis, melanocytes remain in the dermis and actively produce melanin. The blue-gray color of affected skin can be explained by the Tyndall effect, where dermal melanin scatters the shorter wavelengths of light (blue light), which reflect to the skin surface. An extracellular fibrous sheath protects the dermal melanocytes. However, this sheath becomes gradually lost and destroyed during fetal life and early childhood., Epidemiology : was 20% and 31% in boys and girls, , More than 90% of Native Americans, 80% of Asians, and 70% of Hispanics have Mongolian spots; less than 10% of whites have Mongolian spots., variable, Pediatricians and primary care providers that work with newborns and infants will frequently encounter congenital dermal melanocytosis in their practice.,,Parents should be informed of the benign nature of congenital dermal melanocytosis; it requires no further treatment or evaluation. Parents are educated that this condition should fade by 1 year old and rarely persist past 6 years old. Should extra-sacral lesions persist, laser therapy is a potential option for cosmetic treatment., Complications : nan, Diagnostics : HISTOPATHLOGY, PHYSICAL EXAMINATION, Differential diagnosis : bruises in body, disease description : Congenital dermal melanocytosis, also known as Mongolian spot or slate gray nevus, is one of many frequently encountered newborn pigmented lesions. It is a type of dermal melanocytosis, which presents as gray-blue areas of discoloration from birth or shortly thereafter.

Dermatitis And Eczema Of The Hands

Disease Name : Dermatitis And Eczema Of The Hands, Treatment : medication : Cyclosporine/Ciclosporine, Tacrolimus , Methotrexate, Azathioprine , Mometasone, First line ,• Hand care advice ,• Irritant and allergen avoidance,• Emollients,• Soap substitute, Second line ,• Potent or very potent topical corticosteroids, Third line ,• Alitretinoin/PUVA/azathioprine/ciclosporin/methotrexate, Pathophysiology : Predisposing factors , a naturally dry skin, or a superadded contact allergic or irritant dermatitis, are all predisposing factors. The common link is now known to be filaggrin gene mutations, as discussed in the Genetics section below. The role of stress in aggravating hand eczema is difficult to evaluate, and the disease itself is very stressful. Many patients give a convincing account of exacerbations at times of acute anxiety, frustration or grief. The role of hormonal factors is also difficult to assess. Occasionally, there is a history of premenstrual exacerbation, or deterioration during pregnancy. In general, the differences between the various forms of hand eczema are clinical rather than histological, but the considerably thickened horny layer and the presence of numerous sweat glands modify the histological features of eczema on the hands. Environmental factors Contact irritants are the commonest exogenous cause of hand eczema, but contact allergens including chromate, epoxy glues and rubber are also important. All patterns of hand eczema are possible in contact allergy. Rubber dermatitis usually affects the dorsa of the hands, but so can contact irritant and atopic eczema . Certain occupations are particularly likely to provoke hand eczema. The problem of occupational eczema in hairdressers, fish industry workers, farmers, construction workers, dental and medical personnel, metal workers and caterers has provoked many studies to determine its prevalence and to develop programmes for the prevention of hand dermatitis., Epidemiology : hand eczema point prevalence of about 4%, a one-year, 5.5 cases per 1000 person-years, variable, The best way to prevent contact dermatitis is to avoid contact with the allergens or irritants that cause your symptoms.,,If you cannot avoid contact, you can take steps to reduce the risk of the allergens or irritants causing symptoms, including : ,,cleaning your skin – if you come into contact with an allergen or irritant, rinse the affected skin with warm water and an emollient as soon as possible,using gloves to protect your hands – but take them off every now and again, as sweating can make any symptoms worse; you may find it useful to wear cotton gloves underneath rubber gloves if the rubber also irritates you,changing products that irritate your skin – check the ingredients on make-up or soap to make sure it does not contain any irritants or allergens; in some cases, you may need to contact the manufacturer or check online to get this information,applying emollients frequently and in large amounts – these keep your skin hydrated and help protect it from allergens and irritants; you could also use emollient soap substitutes rather than regular bar or liquid soaps, which can dry out your skin, Complications : secondary infection, Diagnostics : Patch Test, full thickness skin biopsy, blood test, Differential diagnosis : Lichen Planus, pityriasis rubra pilaris, psoriasis, Tinea manuum, disease description : It is one of the most common types of eczema (also referred to as ‘dermatitis’). It mainly affects the palms but can also affect other parts of the hand. The main symptoms are dry, itchy and red skin affecting the whole hand, including the fingers. Other symptoms may include cracking, soreness and bleeding. In some cases, blisters may develop. The skin is generally dry, scaly and thickened, and the fingers can become quite swollen when the eczema is flaring. If the eczema is severe over a long time, the hands can become very painful, making it difficult to carry out day-to-day tasks such as doing up buttons, holding a pen or using a computer.

Dermatitis And Eczema Of The Lower Legs

Disease Name : Dermatitis And Eczema Of The Lower Legs, Treatment : medication : Tacrolimus , Obese patients should be urged to lose,weight. Well-fitted support stockings or firm bandages can be helpful if worn regularly and care is taken to avoid the formation of a band at the top of the leg. The legs should be elevated as effectively as possible., First line ,• Skin care, including leg elevation, emollients and topical,corticosteroids, Referral to vascular surgeon to consider surgical intervention, Pathophysiology : Venous eczema is more likely after a previous DVT and in the presence of venous stasis, which is itself linked to obesity, immobility, and previous cellulitis. Pathology : In venous eczema, the oxygen content in the femoral venous blood of the leg affected by venous hypertension is increased, and the venous blood in such limbs has a faster circulation time than normal These observations could be explained by the development of arteriovenous shunts in the affected areas, but the use of radioactively labelled macroaggregates or microspheres has failed to provide any evidence for such shunts. An alternative explanation for these findings has been provided by Browse and Burnand, who suggested that the high ambulatory venous pressure within the calf muscle pump is transmitted to the capillary circulation in the skin and subcutaneous tissues of the calf. This distends the local capillary bed and widens the endothelial pores, thus allowing fibrinogen molecules to escape into the interstitial fluid, where they form a fibrin sheath around the capillaries. This layer of fibrin presumably forms a pericapillary barrier to the diffusion of oxygen and other nutrients that are essential for the normal vitality of the skin. The hypothesis that pericapillary fibrin impedes oxygen diffusion has been supported by a study using positron emission tomography. It has also been suggested that cutaneous inflammation in venous hypertension may result from increased sequestration of white cells in the venules, with a consequent release of proteolytic enzymes and free radicals which produce tissue damage. In normal subjects, white cells are sequestered in the limb when venous pressure is elevated, and in patients with venous insufficiency the effect is enhanced, with increased endothelial contact and adhesion of white cells. This effect may be related to an increase in expression of adhesion molecules intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) on the vascular endothelium in affected skin., Epidemiology : 15-20% of children and 1-3% of adults worldwide, Relapse, The American Academy of Dermatology Association (AADA) makes these suggestions that may help lower your risk and reduce symptoms : ,,Take breaks from sitting or standing,If you sit or stand for more than an hour, take breaks from doing so by walking briskly for at least 10 minutes to boost blood flow.,,Work out,Working out helps enhance blood flow and strengthen your leg muscles.,,Avoid injury at or near varicose veins,Try to protect affected areas of your skin from getting injured as these can lead to open sores.,,Do not scratch these areas or touch things that can further inflame your skin such as : ,,harsh cleaning products,grass,pet hair,perfumes,skin care products with fragrance,Wear cotton clothing that fits loosely,Rough fabrics such as wool and rayon can chafe your skin while tight clothes can hamper blood flow and rub against your skin.,,Maintain a moderate weight,Try to get to and stay at a moderate weight. This helps ease swelling and pressure on your veins. It also helps support your total health and lower your risk of other health conditions related to varicose eczema.,,Hydrate well,Make sure you get enough fluids each day by drinking healthy fluids such as water or eating water-rich fruits and vegetables. This can improve blood flow and ease swelling.,,Watch your salt intake,Try to limit your daily salt intake as having too much of it can hamper blood flow., Complications : allergic contact dermatitis, venous complications, secondary infection, Diagnostics : Patch Test, full thickness skin biopsy, blood test, Differential diagnosis : kaposi sarcoma, nummular dermatitis, psoriasis, disease description : Dermatitis and eczema of the lower legs is subclassified by ICD-11 as venous eczema, stasis dermatitis and allergic contact dermatitis. Lower limb venous eczema encompasses the skin changes that result from venous hypertension. Stasis dermatitis relates to the skin changes that result from reduced lower leg venous flow. Venous eczema and stasis dermatitis both result from dysfunctional venous drainage of the lower legs. There is a great deal of overlap between the two skin conditions, which share the same clinical features, and they are distinguished by the presence or absence of venous hypertension. Allergic contact dermatitis of the lower legs is a common complication of both skin conditions.

Dermatophytide

Disease Name : Dermatophytide, Treatment : The dermatophytid reaction goes away once the dermatophyte infection has been cured. To relieve symptoms of dermatophytid reactions, doctors give corticosteroid creams, anti-itch drugs taken by mouth (such as hydroxyzine), or both., Treatment consists of topical or systemic antifungal drugs with antidermatophyte activity., Although combination antifungal and low-potency corticosteroid products can be effective and may accelerate resolution of the clinical manifestations of superficial dermatophyte infections., Pathophysiology : The pathophysiology of dermatophytide involves an allergic or hypersensitivity reaction to the fungal infection, even in areas of the body distant from the primary infection site.Here are the key aspects of the pathophysiology of dermatophytide : Sensitization : The initial step in the pathophysiology is the sensitization of the immune system to the dermatophyte infection. During the infection, the bodys immune response is triggered by the presence of the fungal antigens. Antigen-presenting cells, such as dendritic cells, present these antigens to T lymphocytes, initiating an immune response.Immune Response : In individuals who develop dermatophytide, the immune response to the fungal infection is characterized by a delayed-type hypersensitivity reaction (Type IV hypersensitivity). This immune reaction involves the activation of T cells, primarily CD4+ T cells, which release pro-inflammatory cytokines, such as interferon-gamma (IFN-?) and interleukin-2 (IL-2). These cytokines recruit and activate other immune cells, including macrophages, neutrophils, and eosinophils., Epidemiology : 20000-25000 per 100, 000 persons., variuable, 1. Application of antifungal agents.,2. Humid areas such as the floor and carpet of a bathroom should be cleaned or washed regularly. ,3. Cleaning the feet by wiping with a towel or washing with soap seemed to be an effective prophylactic measure after stepping into public spaces where people enter without shoes., Complications : secondary infection, Diagnostics : PHYSICAL EXAMINATION, Microbiological skin swabs, Differential diagnosis : bacterial infection (sepsis), pityriasis rosea, disease description : A dermatophytid reaction is the bodys reaction to a dermatophyte (fungal) infection and is a skin eruption that appears on an area of the A dermatophytide is an allergic rash caused by an inflammatory fungal infection (tinea) at a distant site. The rash is usually itchy like dermatitis, with bumps or blisters scattered on face, trunk and/or limbs. Fungus cannot be cultured from an ide. The ide can be treated with topical steroid and will resolve once the original infection has been controlled.body that is not the area where the infection first began.

Dermatophytoses

Disease Name : Dermatophytoses, Treatment : medication : Griseofulvin , Terbinafine , The therapy of tinea capitis comprises griseofulvin,(15 mg/kg/ day of ultramicrosized formulation) for a,duration of 8weeks. Terbinafine (5 mg/kg/day for 4 weeks),is effective in noninflammatory tinea capitis. Longer,treatment (8 weeks) is needed for kerion. Use of terbinafine,in children is hindered by absence of liquid formulation,and an unpleasant aftertaste of the tablet. Washing with,ketoconazole shampoo helps to reduce transmission.,Sharing of combs and head wear should be avoided.,Localized lesions of tinea corporis are managed by,topical therapy (azoles available as clotrimazole, miconazole or ketoconazole in lotion, gel and cream,formulations). Widespread lesions require systemic,antifungal therapy with terbinafine (2 weeks) or,griseofulvin (for 4 weeks)., Pathophysiology : A simplified explanation of the complex and not well-understood pathophysiology of dermatophytes includes the organisms use of proteinases to digest keratin found in the skins stratum corneum.Tinea Capitis- Three patterns are commonly seen : Noninflammatory or epidemic type. Caused by anthropophilic organisms and so is responsible for epidemics. It presents as a patch of alopecia with marked scaling at periphery. Hairs break off easily and inflammation is minimal. Inflammatory or kerion. Caused by zoophilic organisms and so does not cause epidemics. It presents as a boggy swelling which drains pus from multiple openings . Hair is easily pluckable without pain. Usually associated with occipital lymphadenopathy. Favus. Caused by T. schoenleinii, presents as yellowish, foul smelling cup-shaped crusts with matting of hair. Tineo Corporis Shows classical features of tinea and is most frequent on exposed parts. Infection of face is common in children. The diagnosis is confirmed by the KOH test that shows fungal hyphae. Culture helps in identification of species and this is important in patients with tinea capitis., Epidemiology : prevalence of dermatophytosis in India ranges from 36.6–78.4%, 20000-25000 per 100, 000 persons., GOOD, Better surveillance, improved living conditions and,improved treatments can decrease the overall prevalence. Hygiene, and,prevention of contact are helpful in individual cases. Measures such as moisture control (e.g., in tinea pedis) are,important in reducing susceptibility., Complications : skin atrophy, telangiectasias, secondary bacterial infections, recurrence, Diagnostics : MICROSCOPIC EXAMINATION with KOH, Differential diagnosis : candidiasis, nummular dermatitis, pityriasis rosea, psoriasis, seborrhoeic dermatitis, Tinea Versicolor, disease description : Three genera of fungi cause dermatophytoses Trichophyton, Epidermophyton and Microsporum. The infection is given different names depending on the site affected. Dermatophyte infection of skin is known as tinea corporis, of groin as tinea cruris, of hands as tinea manuum, of feet as tinea pedis and of nails as tinea unguium. The classical lesion is an annular or arcuate plaque with a clear center and an active edge showing papulovesiculation and scaling. Tinea cruris, also known as jock itch, is an infection involving the genital, pubic, perineal, and perianal skin caused by pathogenic fungi known as dermatophytes

Dermoid Cyst

Disease Name : Dermoid Cyst, Treatment : Making a skin incision,Extending the incision down to access the bone,Drilling or scraping the dermoid cyst cells out of the bone, Surgical removal is the only effective treatment for any type of dermoid cyst., Pathophysiology : Dermoid cysts result from an abnormal alteration in fetal development. They occur due to the abnormal sequestration and inclusion of the surface ectoderm along the lines of skin fusion during embryologic development.  Due to this abnormality, a dermoid cyst can usually be found along cranial sutures or the anterior fontanelle.Simple dermoid. It occurs as a midline swelling under the skin but in front of the nasal bones. It does not have any external opening. • Dermoid with a sinus. It is seen in infants and children and is represented by a pit or a sinus in the midline of the dorsum of nose. Hair may be seen protruding through the sinus opening. In these cases, the sinus track may lead to a dermoid cyst lying under the nasal bone in front of upper part of nasal septum or may have an intracranial dural connection. In those with intracranial extension, sinus tract passes through the cribriform plate or foramen caecum and is attached to dura or has other intracranial connection. Meningitis occurs if infection travels along this path. Treatment of such cysts may necessitate splitting of the nasal bones to remove any extension in the upper part of the nasal septum. A combined neurosurgical–otolaryngologic approach is required in those extending intracranially so as to close simultaneously any bony defect through which the fistulous tract passed., Epidemiology : prevalence of up to 20%, approximately 15-25% of ovarian neoplasms. Almost 10-15% is bilateral., GOOD, Dermoid cysts are congenital (present at birth). You can’t reduce the chances of a dermoid cyst., Complications : osteomyelitis, BACTERIAL MENINGITIS, Diagnostics : ultrasound, PHYSICAL EXAMINATION, Differential diagnosis : juvenile xanthogranuloma (JXG), lipoma, maxillofacial trauma, neurofibroma, rhabdomyosarcoma, Teratoma, disease description : A dermoid cyst is a benign cutaneous developmental anomaly that arises from the entrapment of ectodermal elements along the lines of embryonic closure.These benign tumors are lined by stratified squamous epithelium with mature skin appendages found on their wall and their lumens filled with keratin and hair. Dermoid cysts are considered to be congenital, but not all of them are diagnosed at birth. Dermoid cysts are usually congenital, with about 70% of cases discovered in children five years old or younger.

Dermoids

Disease Name : Dermoids, Treatment : surgical excision, Pathophysiology : These are common developmental tumours which arise from an embryonic displacement of the epidermis to a subcutaneous location. The cystic component is lined with keratinizing epithelium and may contain one or more dermal adnexal structures such as hair follicles and sebaceous glands. Dermoids are of two types : a. Superficial dermoid. It is seen in infancy. Appears as a firm, round, localised lesion in the upper temporal or upper nasal aspect of the orbit. These do not extend deep into the orbit and are not associated with bony defects. Displacement of globe is also not seen as these are located anterior to the orbital septum. b. Deep dermoids. These are present in adolescence with proptosis or a mass lesion having indistinct posterior margins (as they arise from deeper sites). They may be associated with bony defects., Epidemiology : 15.4%-58.5% of all scalp and skull masses in pediatric patients., 10% to 15% of cases., good, Complications : nan, Diagnostics : nan, Differential diagnosis : nan, disease description : These are common developmental tumours which arise from an embryonic displacement of the epidermis to a subcutaneous location. The cystic component is lined with keratinizing epithelium and may contain one or more dermal adnexal structures such as hair follicles and sebaceous glands. Dermoids are of two types : a. Superficial dermoid b. Deep dermoids

Desbuquois Syndrome

Disease Name : Desbuquois Syndrome, Treatment : Treatment for the condition is geared towards the signs and symptoms present in each individual, Pathophysiology : The pathophysiology of Desbuquois syndrome involves mutations in genes that play a crucial role in skeletal development and growth. Two genes have been primarily associated with the syndrome : CANT1 (calcium-activated nucleotidase 1) and XYLT1 (xylosyltransferase 1)., Epidemiology : less than 50 cases have been described in the literature., Fewer than 1, 000 people in the U.S. have this disease., variable, Genetic counseling - ,Transmission is autosomal recessive and genetic counseling is recommended., Complications : scoliosis, Growth retardation, Diagnostics : GENETIC TESTING, PHYSICAL EXAMINATION, Differential diagnosis : Chondrodysplasia punctata 1, X-linked (CDPX1), LARSEN’S SYNDROME, disease description : Desbuquois syndrome (DBQD) is a rare type of osteochondrodysplasia (a disorder of the development of bones and cartilage). Characteristics may vary in severity and can include short stature with short extremities, severe joint laxity with dislocation, osteopenia, kyphoscoliosis, distinctive facial characteristics and other abnormalities.Two forms have been distinguished on the basis of the presence (type 1) or the absence (type 2) of characteristic hand anomalies. 

Desmodesmus Infection

Disease Name : Desmodesmus Infection, Treatment : nan, Pathophysiology : Entry and colonization : Algae, including Desmodesmus, can enter the body through various routes, such as inhalation, ingestion, or direct contact with contaminated water. Once inside the body, the algae may attempt to colonize specific tissues or organs, depending on their tropism.Inflammatory response : The presence of algae in tissues can trigger an inflammatory response from the immune system. Immune cells, such as macrophages and neutrophils, are recruited to the site of infection to eliminate the algae. Inflammatory cytokines and chemokines are released, leading to localized inflammation.Tissue damage and dysfunction : In some cases, the immune response may cause collateral damage to surrounding tissues. The release of inflammatory mediators and the activity of immune cells can lead to tissue damage and dysfunction. The severity of tissue damage depends on the type and extent of the immune response and the virulence factors produced by the algae., Epidemiology : prevalence of 1–2% worldwide., variable, Complications : nan, Diagnostics : FUNGAL CULTURE, Differential diagnosis : nan, disease description : Desmodesmus is a genus of green algae in the family Scenedesmaceae. It is the only chlorophyll-containing organism known to have caused human infections in immunocompetent individuals. All known cases involved open injuries occurring in fresh water.

Desmoid-type Fibromatoses

Disease Name : Desmoid-type Fibromatoses, Treatment : Tyrosine Kinase Inhibitors,,Tyrosine Kinase Inhibitors (TKIs) are a newer type of treatment called a targeted therapy. They work by blocking growth signals inside the tumour cells. The main drugs used to treat DF this way are called sorafenib, pazopanib and imatinib., Hormones are substances produced naturally in the body that control the activity of cells and organs. Hormonal therapies use drugs to interfere with the way hormones are made or how they work in the body. Tamoxifen is an anti-estrogen drug used to treat breast cancer. It has been found to work in treated DF either using this drug alone or alongside nonsteroidal anti-inflammatory drugs. It is commonly used as the first medical treatment for DF, particularly if the DF is in the abdominal wall, Anti-inflammatory drugs,,Nonsteroidal anti-inflammatory drugs (NSAIDs) can be used to treat DF. They have an impact on the nature of the tumour and can reduce any pain or swelling you may be experiencing., Radiotherapy uses high-energy radiation beams to destroy tumour cells. It can be used after surgery or as a treatment on its own. It is used to improve symptoms and to try and get the tumour to switch itself off and get smaller. DF patients are usually fit and healthy and radiotherapy can have significant long term side effects, so the decision to use radiotherapy needs to be balanced with how significant the symptoms are. It is rarely used to treat children and younger adults., It is sometimes possible for your surgeon to remove the tumour. Sometimes after surgery for DF, the part of the body where the tumour was removed does not work properly or you are left with cosmetic changes to your physical appearance. Surgery also does not guarantee the tumour will not return. This is why, for most DF patients, surgery is not routinely offered or will only be offered after a period of active surveillance and after their case has been reviewed by an MDT., Pathophysiology : Scientists are always working to understand how tumors form but it can be hard to prove. We know that some people with a family history of desmoid tumors have a change in a gene called adenomatous polyposis coli, or APC. This change causes too much of a protein called beta-catenin in parts of your cells. Too much beta-catenin can cause cells to grow when they shouldn’t. In some desmoid tumors, there is too much beta-catenin, even though APC is normal.APC and beta-catenin are important in many common cancers, such as colon cancer, and scientists are trying to use this information to develop better cancer treatments, which will help people with desmoid tumors., Epidemiology : For every one million people worldwide, two to four are diagnosed with a desmoid tumor per year., Each year, approximately 900 to 1, 500 people in the United States will be diagnosed with a desmoid tumor., Fair, Because desmoid tumors are usually associated with genetic conditions, there isn’t anything you can do to prevent them., Complications : fatigue, loss of appetite, anemia, recurrence, Diagnostics : biopsy, MRI, PHYSICAL EXAMINATION, Differential diagnosis : Leiomyosarcoma, Liposarcoma, lymphoma, Nodular fasciitis, rhabdomyosarcoma, disease description : A type of soft tissue tumor that forms in fibrous (connective) tissue, usually in the arms, legs, or abdomen. It may also occur in the head and neck. Desmoid-type fibromatoses are usually benign (not cancer). They often recur (come back) after treatment and spread to nearby tissue, but they rarely spread to other parts of the body. They may occur in adults or children. Also called aggressive fibromatosis and desmoid tumor.

Desmoplastic Fibroblastoma

Disease Name : Desmoplastic Fibroblastoma, Treatment : Conservative excision, does not recur or metastasize, The treatment of bone desmoid-type fibromatosis includes marginal or wide resection with or without replacement by allograft, or amputation in certain cases. However, complete surgical excision is a recommended treatment for desmoplastic fibroblastoma due to the benign nature of this neoplasm., Pathophysiology : Pathogenesis involves-GeneticsIn desmoplastic fibroblastomas, recurrent 11q12 rearrangements with deregulated FOSL1 gene expression have been observed.ImmunophenotypeImmunohistochemistry stains might express vimentin or desmin and be focally positive for smooth muscle actin (SMA). , Epidemiology : This tumor occurs predominantly in males, with a male-female ratio of 2.5 : 1, Good, Complications : nan, Diagnostics : MRI, CT SCAN, Differential diagnosis : fibromatosis, Palmar fascial fibromatosis, disease description : Desmoplastic fibroblastoma (collagenous fibroma) is an uncommon benign soft-tissue tumor, rarely involving bone. It shares some overlapping features with other infiltrate tumors, such as desmoid-type fibromatosis, neurofibroma, and low-grade fibromyxoid sarcoma. 

Desmoplastic Fibroma

Disease Name : Desmoplastic Fibroma, Treatment : DF of maxilla or mandible with extra-osseous extensions is treated with complete excision including a margin of uninvolved soft tissue. These tumors are locally aggressive and can recur with a subtotal resection. The recurrence rate of about 40-47% is seen in lesions treated by curettage or intra-lesional resection making follow-up a necessity., Pathophysiology : The pathophysiology of desmoplastic fibroma involves several key processes : Cellular proliferation : The tumor originates from the uncontrolled proliferation of mesenchymal cells, which are the precursor cells that give rise to various connective tissues. The exact triggers for this abnormal cell growth are not well understood, but genetic and molecular factors likely play a role.Dysregulation of cellular differentiation : As the mesenchymal cells proliferate, they also undergo abnormal differentiation, leading to the formation of fibrous tissue. The fibrous tissue infiltrates the bone, replacing the normal bone matrix and causing bone destruction.Extracellular matrix remodeling : Desmoplastic fibroma is characterized by the production and deposition of an excessive amount of collagen, a major component of the extracellular matrix. The collagen-rich fibrous tissue infiltrates the bone, resulting in the characteristic desmoplastic appearance of the tumor., Epidemiology : Represents 0. 06% of all osseous tumours and 0.3% , Desmoplastic fibroma (DF) is an extremely rare, Prognosis is difficult, Complications : pathological fracture, Diagnostics : biopsy, MRI, CT SCAN, Differential diagnosis : Aneurysmal bone cyst, Chondromyxoid fibroma, fibrous dysplasia, Giant cell tumour, NON-OSSIFYING FIBROMA, Osteoblastoma, osteosarcoma, disease description : Desmoplastic fibroma (DF) is a benign intra-osseous neoplasm, that is, recognized as the intra-osseous counterpart of soft tissue fibromatosis in both gnathic and extra-gnathic sites. It has a propensity for locally aggressive behavior and local recurrence. An occurrence of intra-osseous lesion other than that of odontogenic origin is rare in the jaws.Desmoplastic fibroma (DF), a benign locally aggressive lesion of the bone is recognized as an intra-osseous counterpart of soft tissue fibromatosis and is usually seen affecting the long bones, pelvis and only occasionally presents itself as a jaw lesion

Desmoplastic Infantile Astrocytoma And Ganglioglio

Disease Name : Desmoplastic Infantile Astrocytoma And Ganglioglio, Treatment : Chemotherapy if infiltrative or progressive, Gross total reseGross total resectionction, Pathophysiology : The pathophysiology of these tumors is not fully understood, but there are some known characteristics and hypotheses regarding their development.Cellular origin : Both DIA and DIG are believed to originate from glial cells in the brain. DIA is thought to arise from astrocytes, which are a type of supportive cell in the central nervous system. DIG is believed to arise from a mixed population of both astrocytes and neuronal cells called ganglion cells.Genetic alterations : Studies have identified specific genetic alterations that are commonly associated with DIA and DIG. These tumors frequently exhibit a loss of genetic material from a region of chromosome 11 known as 11q23. Additionally, alterations in the BRAF gene, specifically a fusion protein called KIAA1549-BRAF, have been detected in a subset of cases. These genetic alterations may play a role in the development and progression of DIA and DIG, but their precise contribution to tumor formation is still under investigation.Abnormal cell proliferation and growth : In DIA and DIG, there is an abnormal proliferation of glial cells or a mixed population of glial and neuronal cells. This uncontrolled cell growth leads to the formation of a mass or tumor within the brain. The mechanisms that drive this abnormal cell proliferation are not yet fully understood, but they may involve dysregulation of signaling pathways involved in cell cycle control and cell growth.Desmoplastic stromal reaction : One distinguishing feature of DIA and DIG is the presence of a desmoplastic stromal reaction. This reaction refers to the growth of fibrous tissue within the tumor mass. The fibrous tissue creates a dense, collagen-rich stroma that surrounds and supports the tumor cells. The exact cause of this stromal reaction is unknown, but it may be a response to the tumor cells or a result of altered cellular interactions within the tumor microenvironment., Epidemiology : Incidence : rare ( < 0.1% of CNS tumors), good, Complications : nan, Diagnostics : nan, Differential diagnosis : ependymoma, pleomorphic xanthoastrocytoma (who grade 2), disease description : Desmoplastic infantile ganglioglioma/astrocytoma is a rare intracranial tumor, which despite its aggressive appearances tend to have a good prognosis and are considered WHO grade 1 tumor. Previously considered separate entities, desmoplastic infantile astrocytoma and desmoplastic infantile ganglioglioma are now grouped together in the current (2021) WHO classification of CNS tumor, recognizing the clinical, radiological and pathological similarities of the two entitie. 

Desmoplastic Small Round Cell Tumour

Disease Name : Desmoplastic Small Round Cell Tumour, Treatment : When the tumors are large, or the cancer cells have spread to other parts of the body, chemotherapy is used along with surgery., Radiation therapy uses radiation to kill the cancer cells. External radiation therapy comes from a machine that aims radiation at the tumors. For internal radiation therapy, seeds, ribbons, or capsules that contain a radiation source are placed in your body, in or near the tumor., Surgery is used to remove as much of the DSRCT as possible. If some cancer cells are left behind, the cancer can come back in the same spot or a different part of the body., Pathophysiology : We know that in DSRCT, chromosomes (the parts of your cells that contain all of your genes) break apart and get put back together in the wrong way. This can cause cells to not function like they should. In DSRCT, a gene called EWS wrongly joins with a region called WT1. Doctors will look for this change in chromosomes to confirm that your cancer is DSRCT. , Epidemiology : 0.2/1, 000, 000/year, Variable, Complications : lymph nodes, Diagnostics : PET SCAN, biopsy, GENETIC TESTING, MRI, CT SCAN, Differential diagnosis : "Ewings sarcoma", lymphoma, rhabdomyosarcoma, small cell carcinoma, "Wilms tumour", disease description : Desmoplastic small round cell tumors, or DSRCT, are tumors that grow in the abdomen and pelvic area of the body. Desmoplastic small round cell tumors are a type of soft tissue sarcoma, which is a type of cancer that forms in the connective tissue of the body.?Desmoplastic small round cell tumor (DSRCT) is a malignant mesenchymal neoplasm composed of small round tumor cells associated with prominent stromal desmoplasia, polyphenotypic differentiation and EWSR1-WT1 gene fusion

Desmosterolosis

Disease Name : Desmosterolosis, Treatment : nan, Pathophysiology : People with desmosterolosis commonly have muscle stiffness (spasticity) and stiff, rigid joints (arthrogryposis) affecting their hands and feet. Other features seen in some affected individuals include short stature, abnormal head size (either larger or smaller than normal), a small lower jaw (micrognathia), an opening in the roof of the mouth (cleft palate), involuntary eye movements (nystagmus) or eyes that do not look in the same direction (strabismus), heart defects, and seizures., Epidemiology : prevalence of ~1 : 20, 000 births, with males and females equally., <1 : 10, 000, 000, variable, "This condition is inherited in an autosomal recessive pattern and therefore it cant be prevented. ,Although Genetic counselling is advisable.", Complications : developmental delay, delayed motor skills, Diagnostics : MRI, PHYSICAL EXAMINATION, Differential diagnosis : nan, disease description : Desmosterolosis, a rare disorder of cholesterol biosynthesis, is caused by mutations in DHCR24, the gene encoding the enzyme 24-dehydrocholesterol reductase (DHCR24). To date, desmosterolosis has been described in only two patients. Desmosterolosis is a condition that is characterized by neurological problems, such as brain abnormalities and developmental delay, and can also include other signs and symptoms. Children with desmosterolosis have delayed speech and motor skills (such as sitting and walking). Later in childhood, some affected individuals are able to walk with support; verbal communication is often limited to a few words or phrases. Common brain abnormalities in desmosterolosis include malformation of the tissue that connects the left and right halves of the brain (the corpus callosum) and loss of white matter, which consists of nerve fibers covered by a fatty substance called myelin

Deviated Nasal Septum

Disease Name : Deviated Nasal Septum, Treatment : Submucous Resection (SMR) Operation, Septoplasty, Pathophysiology : Deviation may involve only the cartilage, bone or both the cartilage and bone. 1. Anterior Dislocation. Septal cartilage may be dislocated into one of the nasal chambers. This is better appreciated by looking at the base of nose when patient’s head is tilted backwards. 2. C-shaped Deformity. Septum is deviated in a simple curve to one side. Nasal chamber on the concave side of the nasal septum will be wider and may show compensatory hypertrophy of turbinates. 3. S-shaped Deformity. Either in vertical or anteroposterior plane. Such a deformity may cause bilateral nasal obstruction. 4. Spurs. A spur is a shelf-like projection often found at the junction of bone and cartilage. A spur may press on the lateral wall and gives rise to headache. It may also predispose to repeated epistaxis from the vessels stretched on its convex surface. 5. Thickening. It may be due to organized haematoma or overriding of dislocated septal fragments., Epidemiology : 80% of people have a deviated septum., GOOD, Some people are born with a deviated septum. It can’t be prevented.,,If you don’t have a deviated septum at birth, you can take steps to reduce your risk of injury. You can protect your nose by : ,,Using a face mask or helmet during sports.,Wearing your seat belt.,Avoiding high-contact sports., Complications : nasal congestion, Sleep disturbances, Diagnostics : Diagnostic nasal Examination(DNE), X RAY PNS(OF/OM), CT SCAN, Nasal endoscopy, acoustic rhinometry (AR), Differential diagnosis : nasal foreign bodies, nasal polyps, disease description : A deviated septum occurs when the thin wall (nasal septum) between your nasal passages is displaced to one side. In many people, the nasal septum is off-center — or deviated — making one nasal passage smaller.When a deviated septum is severe, it can block one side of the nose and reduce airflow, causing difficulty breathing. The exposure of a deviated septum to the drying effect of airflow through the nose may sometimes contribute to crusting or bleeding in certain people. A nasal blockage or congestion (obstruction) can occur from a deviated nasal septum, from swelling of the tissues lining the nose or from both.?

Dhatura Poisoning

Disease Name : Dhatura Poisoning, Treatment : Management is mainly supportive. It consists of gastric decontamination with activated charcoal administered by mouth or tube, sedation with benzodiazepines to control agitation, and the hyperpyrexia control (fluids administration and internal and external cooling methods) . Gastric emptying and decontamination are necessary managing tools if they are initiated early., physostigmine at a dose 0.1 mg/kg (max 2 mg) IV slowly., Pathophysiology : The classic anticholinergic poisoning occurs by consumption of the tropane alkaloid-containing plant. Tropane alkaloids include hyoscyamine contained in leaves, roots, seeds; hyoscine, atropine (dl-hyoscyamine) and scopolamine (l-hyoscine) found in roots. They act as competitive antagonists to peripheral and central muscarinic acetylcholine receptors leading to a general paralysis of the parasympathetic innervated organs. Acute psychosis or delirium can occur due to its effect on the central nervous system as tertiary amines can inhibit CNS receptors.  Coma and seizures are rare findings but raise concerns of extreme gravity.  Teenagers with intentional ingestion of the plant represent most cases of Datura stramonium poisoning reported in the literature, as they seek for its hallucinogenic and euphoric effects., Epidemiology : prevalence for use of Datura was 2.6%, Good, Inhibit the abuse with overloading., Complications : Acute Renal Failure, cardiac dysfunction, hallucinations, panic attacks, respiratory difficulties, Diagnostics : ECG, alanine transaminase (ALT), USG, PHYSICAL EXAMINATION, Differential diagnosis : Intense poisoning, disease description : Datura stramonium (DS), also known as Jimson Weed, Locoweed, Angel’s Trumpet, Thorn Apple, Devil’s Trumpet is a hallucinogenic plant found in the urban and rural areas, along roadsides, in cornfields and pastures . The range of toxicity of Datura stramonium is highly variable and unpredictable. It occurs when ingested, smoked and absorbed topically, in particular through mucous membranes. Toxicity may vary between leaves, plants and from one season to another. The highest levels of toxins are found in the seeds approximating 0.1 mg of atropine per seed or 3–6 mg

Diabetes Insipidus

Disease Name : Diabetes Insipidus, Treatment : medication : Hydrochlorothiazide , Amiloride , Indomethacin , Desmopressin , Treatment of NDI includes maintenance of adequate fluid intake and access to,free water, minimizing the urine output by limiting the solute load with a lowosmolar, ,low-sodium diet, and administering medications directed at decreasing,the urine output., Pathophysiology : The ability to concentrate urine (and thus absorb water) requires the delivery of urine to the collecting tubule; an intact concentrating gradient in the renal medulla; and the ability to modulate water permeability in the collecting tubule by ADH. ADH (also called arginine vasopressin AVP), is synthesized in the hypothalamus and stored in the posterior pituitary. Under basal situations, the collecting tubule is impermeable to water. However, in response to increased serum osmolality (as detected by osmoreceptors in the hypothalamus) and/or severe volume depletion, ADH is released into the systemic circulation. It then binds to its receptor, vasopressin V2 R (AVPR2), on the basolateral membrane of the collecting tubule cell. Binding of the hormone to its receptor activates a cyclic adenosine monophosphate–dependent cascade that results in movement of preformed water channels (aquaporin 2 AQP2) to the luminal membrane of the collecting duct, rendering it permeable to water. Defects in the AVPR2 gene cause the more common X-linked form of NDI. Mutations in the AQP2 gene have been identified in patients with the rarer autosomal dominant and recessive forms. Prenatal testing is available for families at risk for X-linked NDI. Patients with secondary forms of NDI can have ADH resistance owing to defective aquaporin expression (as seen in lithium intoxication). Secondary ADH resistance usually occurs as the result of loss of the hypertonic medullary gradient as a result of solute diuresis or tubular damage, resulting in the inability to absorb sodium or urea., Epidemiology : It affects about 1 in 25, 000 people worldwide., depends upon underlying causes, You’re more likely to develop diabetes insipidus if you : ,,Have a family history of diabetes insipidus.,Had brain surgery or a major head injury.,Take medications that can cause kidney problems.,Have certain metabolic disorders, such as high blood calcium levels or low blood potassium levels.,If you’re pregnant, you’re at a higher risk of developing gestational diabetes insipidus if you : ,,Are pregnant with more than one baby.,Have a condition, Complications : developmental delay, hypernatremia, weight loss, Diagnostics : SERUM Osmolality, SERUM Sodium Na+, URINE OSMOLALITY, URINARY SODIUM Na+, MRI Brain, URINE OUTPUT, water deprivation test, Differential diagnosis : Diabetes mellitus type 1, hypokalemia, sickle cell anemia, disease description : Nephrogenic diabetes insipidus (NDI) is a rare congenital or, more commonly, acquired, disorder of water metabolism characterized by an inability to concentrate urine, even in the presence of antidiuretic hormone (ADH). The most common pattern of inheritance in congenital NDI is as an X-linked recessive disorder. Rarely, affected females are seen, presumably secondary to nonrandom X-chromosome inactivation. Approximately 10% of cases of congenital NDI are inherited as autosomal dominant or recessive disorders, with males and females affected equally. The clinical phenotype of autosomal recessive forms is similar to that of the X-linked form. Secondary (acquired), either partial or complete, forms of NDI are not uncommon. They may be seen in many disorders affecting renal tubular function, including obstructive uropathies, acute or chronic renal failure, renal cystic diseases, interstitial nephritis, nephrocalcinosis, or toxic nephropathy caused by hypokalemia, hypercalcemia, lithium, or amphotericin B.

Diabetes Mellitus Type 1

Disease Name : Diabetes Mellitus Type 1, Treatment : medication : Insulin , All patients with T1DM require insulin therapy. Multiple daily insulin injections (MDI) using a basal/bolus insulin regimen or continuous subcutaneous insulin infusion through an insulin pump are the preferred treatment. The patient’s weight in kilograms is multiplied by 0.5 to 0.6 units to calculate the initial total daily insulin dose (TDD) in an adult., Pathophysiology : Genetic predisposition : Type 1 diabetes has a strong genetic component. Certain human leukocyte antigen (HLA) genes, particularly those within the HLA complex on chromosome 6, are associated with an increased risk of developing the condition. However, having these genes alone is not sufficient to cause type 1 diabetes. Other factors, such as environmental triggers, are also required.Autoimmune response : In individuals with a genetic predisposition, an environmental trigger, such as a viral infection or exposure to certain dietary factors, can trigger an autoimmune response. The exact trigger is not fully understood. This autoimmune response involves the activation of immune cells, primarily T lymphocytes, which mistakenly recognize the beta cells as foreign or harmful and mount an immune attack against them.Destruction of beta cells : The activated T lymphocytes release cytokines and other mediators that recruit other immune cells, including macrophages and B lymphocytes, to the pancreatic islets, where the beta cells reside. These immune cells further contribute to the destruction of beta cells through various mechanisms, such as direct cell-to-cell contact, secretion of cytotoxic substances, and production of antibodies targeting beta cell antigens.Insulin deficiency : As the destruction of beta cells progresses, the production and secretion of insulin decrease. Insulin is crucial for the regulation of blood glucose levels as it facilitates the uptake of glucose from the bloodstream into cells, particularly in muscle and adipose tissue. The reduction in insulin levels leads to impaired glucose uptake and utilization, resulting in elevated blood glucose levels (hyperglycemia).Metabolic dysregulation : In the absence of sufficient insulin, the bodys cells are unable to take up glucose effectively, leading to a state of cellular starvation despite high blood glucose levels. This triggers a cascade of metabolic alterations, including increased breakdown of fats (lipolysis) and proteins, leading to the release of ketone bodies. The accumulation of ketone bodies can result in a potentially life-threatening condition called diabetic ketoacidosis (DKA)., Epidemiology : India has three new cases of T1DM/100, 000 children of 0–14 years. Three sets of prevalence data shows 17.93 cases/100, 000 children in Karnataka, 3.2 cases/100, 000 children in Chennai, and 10.2 cases/100, 000 children in Karnal (Haryana)., About 1 in every 400-600 children and adolescents has type 1 DM. In adults, type 1 DM constitutes approximately 5% of all diagnosed cases of diabetes., variable, Unfortunately, there’s nothing you can do to prevent developing Type 1 diabetes.,,Since Type 1 diabetes can run in families, your healthcare provider can test your family members for the autoantibodies that cause the disease. Type 1 Diabetes TrialNet, an international research network, also offers autoantibody testing to family members of people with Type 1 diabetes.,,The presence of autoantibodies, even without diabetes symptoms, means you’re more likely to develop Type 1 diabetes. If you have a sibling, child or parent with Type 1 diabetes, you may want to get an autoantibody test. These tests can help catch Type 1 diabetes in its earliest phases., Complications : cardiomyopathy, Diabetic Ketoacidosis, Nephropathy, retinopathy, Diagnostics : Blood Glucose test, random blood sugar RBS, HbA1c, Oral Glucose Tolerance Test, fasting glucose, Differential diagnosis : Diabetic Foot Ulcers, Diabetic Ketoacidosis, Diabetic Nephropathy, Lead Nephropathy, disease description : Type 1 diabetes mellitus (T1DM) is an autoimmune disease that leads to the destruction of insulin-producing pancreatic beta cells. Insulin is an essential anabolic hormone that exerts multiple effects on glucose, lipid, protein, and mineral metabolism, as well as growth. in T1DM, there is the immune destruction of the beta cells in the pancreatic islets over months or years, causing an absolute deficiency of insulin. Although the exact etiology of T1DM is still unknown, researchers believe there is a genetic predisposition, with a strong link with specific HLA (DR and DQ) alleles, especially DRB103-DQB10201 and DRB 10401-DQB10302H. Multiple other genes contribute to heritability, as well. 

Diabetes Mellitus Type 2

Disease Name : Diabetes Mellitus Type 2, Treatment : medication : Insulin , Metformin , pioglitazone, For both T1DM and T2DM, the cornerstone of therapy is diet and exercise.,,A diet low in saturated fat, refined carbohydrates, high fructose corn syrup, and high in fiber and monounsaturated fats needs to be encouraged. Aerobic exercise for a duration of 90 to 150 minutes per week is also beneficial. The major target in T2DM patients, who are obese, is weight loss., Pathophysiology : T2DM is an insulin-resistance condition with associated beta-cell dysfunction. Initially, there is a compensatory increase in insulin secretion, which maintains glucose levels in the normal range. As the disease progresses, beta cells change, and insulin secretion is unable to maintain glucose homeostasis, producing hyperglycemia., Epidemiology : The global prevalence of DM was 425 million in 2017., variable, You can prevent or delay Type 2 diabetes by : ,,Eating a healthy diet.,Exercising.,Losing weight.,Regular checkups and screenings with your healthcare provider can also help you keep your blood sugar in check., Complications : blindness, Cardiovascular Disease, kidney damage, retinal changes, Diagnostics : random blood sugar RBS, HbA1c, Oral Glucose Tolerance Test, fasting glucose, Differential diagnosis : Diabetes insipidus, glycosuria, hyperthyroidism, disease description : Type 2 diabetes mellitus (T2DM) accounts for around 90% of all cases of diabetes. In T2DM, the response to insulin is diminished, and this is defined as insulin resistance. During this state, insulin is ineffective and is initially countered by an increase in insulin production to maintain glucose homeostasis, but over time, insulin production decreases, resulting in T2DM. T2DM is most commonly seen in persons older than 45 years. Still, it is increasingly seen in children, adolescents, and younger adults due to rising levels of obesity, physical inactivity, and energy-dense diets.

Diabetes Mellitus

Disease Name : Diabetes Mellitus, Treatment : medication : Insulin , Pramlintide , Metformin , Glimepiride , liraglutide , Acarbose , Pioglitazone Hydrochloride , Repaglinide , Dapagliflozin, Linagliptin, INSULIN AND ORAL HYPOGLYCEMIC DRUGS., Pathophysiology : A patient with DM has the potential for hyperglycemia. The pathology of DM can be unclear since several factors can often contribute to the disease. Hyperglycemia alone can impair pancreatic beta-cell function and contributes to impaired insulin secretion. Consequentially, there is a vicious cycle of hyperglycemia leading to an impaired metabolic state. Blood glucose levels above 180 mg/dL are often considered hyperglycemic in this context, though because of the variety of mechanisms, there is no clear cutoff point. Patients experience osmotic diuresis due to saturation of the glucose transporters in the nephron at higher blood glucose levels. Although the effect is variable, serum glucose levels above 250 mg/dL are likely to cause symptoms of polyuria and polydipsia.Insulin resistance is attributable to excess fatty acids and proinflammatory cytokines, which leads to impaired glucose transport and increases fat breakdown. Since there is an inadequate response or production of insulin, the body responds by inappropriately increasing glucagon, thus further contributing to hyperglycemia. While insulin resistance is a component of T2DM, the full extent of the disease results when the patient has inadequate production of insulin to compensate for their insulin resistance. Chronic hyperglycemia also causes nonenzymatic glycation of proteins and lipids. The extent of this is measurable via the glycation hemoglobin (HbA1c) test. Glycation leads to damage in small blood vessels in the retina, kidney, and peripheral nerves. Higher glucose levels hasten the process. This damage leads to the classic diabetic complications of diabetic retinopathy, nephropathy, and neuropathy and the preventable outcomes of blindness, dialysis, and amputation, respectively., Epidemiology : 415 million cases, The incidence of T1DM has been increasing worldwide. In Europe, Australia, and the Middle East, rates are rising by 2% to 5% annually, significantly influenced by the degree of glucose , Although diabetes risk factors like family history and race can’t be changed, there are other risk factors that you can manage, to an extent. Adopting some of the healthy lifestyle habits listed below can improve these modifiable risk factors and help to decrease your chances of getting diabetes : ,,1. Eat a healthy diet, such as the Mediterranean or Dash diet. ,2. Get physically active.,3. Get physically active.,4. Lower your stress. ,5. Limit alcohol intake,6. Get an adequate amount of sleep. ,7. Quit smoking., Complications : Cardiovascular Disease, Nephropathy, neuropathy, retinopathy, Diagnostics : Blood Glucose test, random blood sugar RBS, HbA1c, Oral Glucose Tolerance Test, Differential diagnosis : CUSHING DISEASE, genetic disorders, Metabolic syndrome, disease description : Diabetes mellitus (DM) refers to a group of common metabolic disorders that share the phenotype of hyperglycemia. Several distinct types of DM are caused by a complex interaction of genetics and environmental factors. Depending on the etiology of the DM, factors contributing to hyperglycemia include reduced insulin secretion, decreased glucose utilization, and increased glucose production. The metabolic dysregulation associated with DM causes secondary pathophysiologic changes in multiple organ systems that impose a tremendous burden on the individual with diabetes and on the health care system.

Diabetic Gangrene

Disease Name : Diabetic Gangrene, Treatment : medication : Amoxicillin and Clavulanic acid , Antibiotics-decided by pus C/S. , : .- Regular dressing. , : .- Drugs : Vasodilators, pentoxiphylline, dipyridamole, low ,dose aspirin. ,, , Diabetes is controlled by insulin only. , : .- Diet control, control of obesity. ,Surgical debridement of wound. ,, , Amputations of the gangrenous area. Level of amputa\x02tion has to be decided by skin changes and temperature ,changes or Doppler study. ,, Care of feet in diabetic : nan,- Any injury has to be avoided. ,- MCR footwears must be used (microcellular rubber). ,- Feet has to be kept clean and dry, especially the toes ,and clefts; Hyperkeratosis has to be avoided., Pathophysiology : In ischemic gangrene, reduced arterial perfusion leads to arteriole dilation as compensation, resulting in distal edema and endothelial damage. This can trigger a cycle of micro thrombosis resulting in worsening tissue damage. Due to the ischemic environment, localized cellular dysregulation limits the ability to have adequate wound healing and set the tissue up for continued damage and infection. High glucose level in tissues is a good culture media for bacteria. So infection is common. Diabetic microangiopathy causes blockade of microcirculation leading to hypoxia. Diabetic neuropathy Due to sensory neuropathy, minor injuries are not noticed and so infection occurs. Due to motor neuropathy, dysfunction of muscles, arches of foot and joints occurs. And loss of reflexes of foot occurs causing more prone for trauma and abscess. Due to autonomic neuropathy, skin will be dry, causing defective skin barrier and so more prone for infection. Diabetic atherosclerosis itself reduces the blood supply and causes gangrene. Thrombosis can be precipitated by infection causing infective gangrene. Blockage occurs at plantar, tibial, and dorsalis pedis vessels. Increased glycosylated haemoglobin in blood causes defective oxygen dissociation leading to more hypoxia. At tissue level there will be increased glycosylated tissue proteins, which prevents proper oxygen utilisation and so aggravates hypoxia., Epidemiology : 6.3%, between 9.1 to 26.1 million., variable, You can do many things to improve your blood flow and prevent gangrene. If you have risk factors like peripheral artery disease or diabetes, it’s especially important to : ,,Eat a heart-healthy diet low in saturated fat and cholesterol.,Exercise regularly, following your provider’s guidance.,Keep your blood glucose levels within the normal range.,Learn about complications from diabetes that can affect your legs and feet.,Quit smoking, and avoid all tobacco products.,Regularly check your feet and legs for signs of injury or skin breakdown.,It’s also important to practice good foot hygiene and take special care of your feet. Tips include : ,,Ask your provider to check your feet every time you have an appointment.,Never go barefoot, especially outdoors.,Trim your toenails in a straight line, all the way across. Use a nail file to smooth the corners rather than using clippers to cut them.,Wash and dry your feet daily. Moisturize any dry spots.,Wear socks and shoes that fit you well. It’s a good idea to shop for shoes near the end of the day when your feet are at their largest. This ensures you buy shoes that won’t squeeze your feet too tightly., Complications : AMPUTATION, Diagnostics : random blood sugar RBS, HbA1c, PUS CULTURE, Urine Ketone, CT SCAN, Differential diagnosis : diabetic neuropathy, disease description : Dry/ischemic gangrene is most commonly secondary to atherosclerosis and progressive occlusion of the peripheral arterial blood supply to distal tissue. The risk factors of peripheral atherosclerosis overlap with the risk factors for coronary artery disease : diabetes, smoking, hypertension, and hyperlipidemia. Foot is a complex structure with many layers of muscles, ligaments, joints, arches, fat, thick plantar fascia, vascular arches, neurological system which maintains weight-bearing, gravity, normal walk, stability and gait (swing and stance phases). Problems in diabetic foot : Callosities, ulceration, Abscess and cellulitis of foot, Osteomyelitis of different bones of foot like metatarsals, cuneiforms, calcaneum, Diabetic gangrene, Arthritis of the joints.

Diabetic Ketoacidosis

Disease Name : Diabetic Ketoacidosis, Treatment : medication : Insulin , fluid-,Infusion of 15-20 ml per Kg body weight in the first 1 hour is typically appropriate. Aggressive hydration with 1 liter/hour for 4 hours has been compared in a study to a slower rate of hydration at half the rate. Slower hydration was found to be equally effective.,Maintainance : ,,The subsequent choice for fluid replacement depends on hemodynamics, the state of hydration, serum electrolyte levels, and urinary output., Insulin treatment has evolved from the use of high-dose insulin, with doses up to 100 U/h by various routes of administration, to lower doses in the range of 5–10 U/h.14 We recommend an initial bolus of regular insulin of 0.1 U/kg followed by continuous insulin infusion., Pathophysiology : The pathophysiology of DKA involves a series of complex metabolic changes. Heres an overview of the key processes involved : Insulin deficiency : DKA typically occurs when there is a relative or absolute deficiency of insulin in the body. In individuals with type 1 diabetes, this can result from a lack of insulin production by the pancreas due to autoimmune destruction of beta cells. Insulin is necessary for the uptake and utilization of glucose by cells. In its absence, glucose cannot enter cells, leading to increased blood glucose levels (hyperglycemia).Lipolysis and ketogenesis : Insulin deficiency promotes the breakdown of stored fats (lipolysis) in adipose tissue. Fatty acids are released into the bloodstream and transported to the liver. In the liver, these fatty acids are converted to ketone bodies, including acetoacetate and beta-hydroxybutyrate. Ketone bodies are acidic molecules.Increased ketone body production : In the absence of insulin, the livers regulation of ketone body production is impaired. This leads to an excessive production and release of ketone bodies into the bloodstream. The increased levels of circulating ketone bodies contribute to the development of metabolic acidosis., Epidemiology : 0–128 per 1000 people, 10·8%., variable, "If you dont have diabetes but are experiencing symptoms of diabetes-related ketoacidosis, call your healthcare provider immediately or go to the nearest emergency room. The only way to prevent more severe symptoms and side effects of DKA, in this case, is to seek medical attention and treatment.,,If you already have diabetes, there are many things you can do to prevent diabetes-related ketoacidosis, including : ,,Check your blood sugar often : Checking your blood sugar with a glucometer and/or using a continuous glucose monitor (CGM) is crucial to managing diabetes and preventing complications. Try to at least check your blood sugar before and after meals and before you go to sleep. It’s important to treat high blood sugar as soon as possible in order to prevent DKA.,Take your insulin and/or medication regularly : Follow your healthcare provider’s instructions for taking your insulin and/or medication. Missed doses can lead to DKA.,Check for ketones : If you are experiencing sustained high blood sugar, check for ketones using a urine or blood test to be sure you are not close to developing DKA.,Check your insulin pump : If you use an insulin pump to manage your diabetes and are experiencing high blood sugar, be sure to check your pump for issues such as a kinked cannula or a disconnected site/tubing. These issues could be preventing you from receiving insulin.,Have a sick day plan : Talk with your healthcare provider about how to take care of yourself and manage your diabetes when you are sick. Since illness can trigger DKA, it’s important to know what to do if you get sick before it happens so that you are prepared.,See your healthcare provider regularly : It’s important to see your healthcare provider regularly to be sure that your diabetes management plan is working. If your management plan isn’t working for you, reach out to your healthcare provider or schedule an appointment to make improvements to your management.,Stay educated : Don’t be afraid to ask your healthcare team about DKA. The more you know about DKA and your diabetes management, the more likely you will be able to prevent DKA or catch it in its early stage.,Ask for help : Diabetes management can be confusing and difficult. If youre struggling to manage your diabetes, contact your healthcare provider and reach out to family and friends for support.", Complications : nan, Diagnostics : random blood sugar RBS, ABG, SERUM Sodium Na+, Urine Ketone, Differential diagnosis : Acute Pancreatitis, Lactic acidosis, Rhabdomyolysis, disease description : This condition is caused by increased fatty acid metabolism and the accumulation of ketoacids (acetoacetate and ß-hydroxybutyrate). DKA usually occurs in insulin-dependent diabetes mellitus in association with cessation of insulin or an intercurrent illness such as an infection, gastroenteritis, pancreatitis, or myocardial infarction, which increases insulin requirements temporarily and acutely. The accumulation of ketoacids accounts for the increment in the AG and is accompanied most often by hyperglycemia (glucose >17 mmol/L 300 mg/dL)

Diabetic Maculopathy

Disease Name : Diabetic Maculopathy, Treatment : Treatment is by photo-coagulation,using argon, diode, frequency doubled YAG laser, Pathophysiology : Pathogenesis includes clinico-angiographic classification of diabetic maculopathy-1. Focal exudative maculopathy. It is characterised by microaneurysms, haemorrhages, well-circumscribed macular oedema and hard exudates which are usually arranged in a circinate pattern. Fluorescein angiography reveals focal leakage with adequate macular perfusion. 2. Diffuse exudative maculopathy. It is characterised by diffuse retinal oedema and thickening throughout the posterior pole, with relatively few hard exudates. Fluorescein angiography reveals diffuse leakage at the posterior pole. 3. Ischaemic maculopathy. It occurs due to microvascular blockage. Clinically, it is characterised by marked visual loss with microaneurysms, haemorrhages, mild or no macular oedema and a few hard exudates. Fluorescein angiography shows areas of non-perfusion which in early cases are in the form of enlargement of foveal avascular zone (FAZ), later on areas of capillary dropouts are seen and in advanced cases precapillary arterioles are blocked. 4. Mixed maculopathy. In it combined features of ischaemic and exudative maculopathy are present. OCT classification of diabetic macular oedema. On the basis of OCT examination the diabetic macular oedema (DME) has been classified as below : 1. Non-tractional DME. It may be of following types : a. Spongy thickness of macula (>250 µ), b. Cystoid macular oedema (CME), and c. Neurosensory detachment with or without (a) or (b) above. 2. Tractional DME. It may be of following types : a. Vitreo-foveal traction (VFT), and b. Taut/thickened posterior hyaloid membrane. Note. The OCT classification has a bearing on the management since non-tractional DME is treated conservatively whereas tractional DME is purely treated by pars-plana vitrectomy (PPV) with removal of posterior hyaloid., Epidemiology : between 4.2 and 7.9 %, 4.2% to 14.3% in people with type 1 diabetes and 1.4% to 5.57% in people with type 2 diabetes., variable, "Keeping your blood sugar levels, blood pressure and cholesterol levels under control.,,This can often be done by making healthy lifestyle choices, although some people will also need to take medication.,,HEALTHY LIFESTYLE -,Adopting a few lifestyle changes can improve your general health and reduce your risk of developing retinopathy.,,These include : ,,eating a healthy, balanced diet – in particular, try to cut down on salt, fat and sugar,losing weight if youre overweight – you should aim for a BMI of 18.5-24.9; use the BMI calculator to work out your BMI,exercising regularly – aim to do at least 150 minutes of moderate-intensity activity, such as walking or cycling, a week; doing 10, 000 steps a day can be a good way to reach this target,stopping smoking if you smoke,not exceeding the recommended alcohol limits – men and women are advised not to regularly drink more than 14 alcohol units a week,You may also be prescribed medication to help control your blood sugar level (such as insulin or metformin), blood pressure (such as ACE inhibitors) and cholesterol level (such as statins).,,,KNOW YOUR BLOOD SUGAR, BLOOD PRESSURE and CHOLESTEROL LEVELS - ,It can be easier to keep your blood sugar levels, blood pressure and cholesterol levels under control if you monitor them regularly and know what level they are.,,The lower you can keep them, the lower your chances of developing retinopathy are.,,,REGULAR SCREENING - ,Even if you think your diabetes is well controlled, its still important to attend your annual diabetic eye screening appointment, as this can detect signs of a problem before you notice anything is wrong.,,Early detection of retinopathy increases the chances of treatment being effective and stopping it getting worse.,,You should also contact your GP or diabetes care team immediately if you develop any problems with your eyes or vision, such as : ,,gradually worsening vision,sudden vision loss,shapes floating in your field of vision (floaters),blurred vision,eye pain or redness,difficulty seeing in the dark,These symptoms do not necessarily mean you have diabetic retinopathy, but its important to get them checked out straight away.", Complications : blurred vision, Diagnostics : slit-lamp biomicroscopic examination, Fluorescein angiography, Differential diagnosis : Diabetic Retinopathy, disease description : Macular oedema occurs in a large number of eyes and, with central hard exudates, is the commonest cause of diminution of vision in diabetic retinopathy. Both are caused by leakage from dilated capillaries. Clinically significant macular oedema (CSME) is defined as oedema or hard exudates present within 500 µm of the foveal centre, or oedema of more than one disc area in extent, any part of which is within 1 DD of the foveal centre. The leakage can be focal or diffuse, resulting in focal or diffuse maculopathy. Ischaemic maculopathy is the result of ischaemic changes at the macula. histological picture of oedema and ischaemia at the macular area is fairly common.

Diabetic Nephropathy

Disease Name : Diabetic Nephropathy, Treatment : medication : Insulin , Treatment to delay DN progression involves adequate control of metabolic and hemodynamic abnormalities. In practical terms, this means adequate blood glucose lowering and control of hypertension. A description of all glucose lowering agents is beyond the scope of this review but certain agents have theoretical benefits beyond glucose lowering. Certain antihypertensives are also preferred based on studies which have demonstrated reductions in proteinuria or preservation of GFR, or both., Pathophysiology : ?Hyperglycemia leads to the production of reactive oxygen species and activation of pathways, including protein kinase C, polyol, hexosamine, and advanced glycation end products (AGE). A significant feature is marked inflammation manifested by an increase in cytokines and chemokines, including IL-6, MCP-1, TGF-beta (transforming growth factor-beta), and VEGF (vascular endothelial growth factor), causing inflammation fibrosis and increased vascular permeability. A podocytopathy ensues, resulting in albuminuria. The resulting systemic and intraglomerular hypertension results in proteinuria. Proteinuria causes epithelial-mesenchymal cell transformation leading to fibroblasts and chronic tubular injury., Epidemiology : 34.4%, 20% to 30% of all diabetics will progress to evident nephropathy, although a greater percentage of type 1 patients progress to ESKD., Poor, The best way to prevent diabetes-related nephropathy is to manage your diabetes and lower your blood pressure. Be sure to follow your treatment plan as prescribed by your healthcare provider., Complications : Diabetic Retinopathy, fluid retention, hyperkalemia, pulmonary edema, anemia, Diagnostics : random blood sugar RBS, URINE CULTURE, USG KUB, RENAL USG IMAGING, plasma creatinine, ESTIMATED GLOMERULAR FILTRATION RATE (eGFR), Differential diagnosis : nephrotic syndrome, RENAL ARTERY STENOSIS, Tubulointerstitial Nephritis, disease description : Diabetic kidney disease (DKD) is the leading cause of end-stage kidney disease (ESKD) in developed countries, including the United States.  It is considered a microvascular complication and occurs in both diabetes mellitus type 1 (T1DM) and diabetes mellitus type 2 (T2DM). The disorder presents with persistent albuminuria and a progressive decline in the glomerular filtration rate. There is substantial evidence that early treatment can delay or prevent the progression of the disorder.Reliable tests for diagnosis and monitoring include urine albuminuria and the estimated GFR (eGFR). Optimizing glycemia and reasonable blood pressure control are pivotal in halting the progression of DKD. Diabetic nephropathy (DN) or diabetic kidney disease is a syndrome characterized by the presence of pathological quantities of urine albumin excretion, diabetic glomerular lesions, and loss of glomerular filtration rate (GFR) in diabetics. Diabetes may be classified as type 1 (autoimmune ß-cell destruction and absolute insulin deficiency), type 2 (relative insulin deficiency and resistance), and other types (eg, pancreatic disease).

Diabetic Neuropathy

Disease Name : Diabetic Neuropathy, Treatment : medication : Pregabalin , Duloxetine , Lifestyle modifications (exercise, diet) has some efficacy ,in DSPN in type 2 DM and hypertension and hypertriglyceridemia ,should be treated. Efforts to improve glycemic control in long-standing diabetes may be confounded by hypoglycemia unawareness. ,Avoidance of neurotoxins (alcohol) and smoking, supplementation ,with vitamins for possible deficiencies (B12, folate, Pathophysiology : Most characteristic findings of the peripheral nervous system in diabetic patients are distal and sensory predominant nerve fiber degeneration, axonal loss and endoneurial microangiopathy. Both large and small caliber sizes of nerve fibers are affected. Based on this anatomical condition, Dyck et al. proposed that microvascular injury is the most probable factor for focal fiber loss and its summation appears to be the cause of diffuse fiber loss of distal predominant axonal neuropathy in diabetes. However, this explanation is too simplistic and does not explain why hyperglycemia and duration of diabetes are crucial for its occurrence. There also emerges a controversy as to whether there is any predominance for the involvement of small fibers in early diabetic neuropathy. Questions on this issue were further raised by the report that the focality of nerve fiber loss was not universally demonstrated, indicating that microangiopathy does not always account for the fiber loss. Nevertheless, vascular influence on the development of neuropathy was further supported by subsequent studies on humans. Malik et al. showed that patients who did not have clinically evident neuropathy at the time of nerve biopsy, but who showed high-grade microangiopathic changes of endoneurial microvessels later, developed overt neuropathy, whereas the patients without microvessel changes did not develop neuropathy. The extent of microangiopathic changes correlated well with subsequent nerve fiber loss in diabetic nerves. We ourselves found a correlation between the thickness of the basement membrane of endoneurial microvessels and reduced myelinated fiber density. The most distal axons of small fibers distribute in the epidermis of the skin, sensing pain or pricking. Currently, punched skin biopsy immunostained with protein gene product (PGP)-9.5 is widely used for the evaluation of peripheral neuropathy. The method is simple and minimally invasive, but requires the equipment of confocal laser scan microscopy and skills for the staining and measurement. Usually, skin over the calf muscle is used, but other sites might also be added. In diabetes, the nerve fibers in the epidermis of the skin are significantly affected, resulting in distortion, twisting, focal swelling or beading, and finally, disappearance of nerve fibers. The reduction was found even in subjects of impaired glucose tolerance (IGT) and the extent of fiber loss was marked in established diabetic patients. The nerve fiber loss in the skin was associated with fiber loss in the nerve trunk of the sural nerve, thus in keeping with the presence of clinically evident neuropathy. In relation to the alteration of epidermal innervation, a non-invasive method using corneal confocal microscopy has now been developed for the evaluation of neuropathy. With this method, small nerve fibers distributed in the cornea can be observed without tissue sampling in live conditions. Diabetic patients showed significant loss of nerve fibers, twisting and increased branching on the cornea. Taking advantage of non-invasiveness, it is easy to follow by repeated observations and to evaluate the treatment effects on neuropathy by this method. In fact, the recovery of nerve fibers by regeneration was detected in long-standing type 1 diabetic patients 6 months after pancreas transplantation. To understand the cause and the development of neuropathy, spatial and temporal changes of nerve pathology and their clinical significance should be explored in more detail.To compensate for the paucity of information on human materials, animal models have served the basis of functional and biochemical changes that might be translated into human diabetic neuropathy. Unfortunately, diabetic animal models did not show the pathological features in the peripheral nerves trunk observed in human diabetic patients. However, recent studies have overcome this discrepancy by showing significant nerve fiber loss in the skin of diabetic animal models. It is therefore now possible to search in more detail for the contribution of possible factors to the loss of nerve fibers of the skin by studying animal models. More importantly, it provides us a great tool for the exploration of effective compounds to inhibit nerve fiber loss and promote nerve fiber regeneration. Unlike human diabetic subjects, distinct pathological changes of endoneurial microvessels are not consistently shown in animal models, although reduced nerve blood flow is reproducibly shown. In streptozotocin (STZ)-induced diabetic rats, there was only a modest dilatation of vascular lumina, but no reduction of microvessel density or thickening of basement membranes in the peripheral nerve. Although some studies reported reduced microvessel density in diabetic animals that reverted to normal by intervention with vascular endothelial growth factor (VEGF) or other angiotrophic factors, the recovery of nerve blood flow by these agents might be explained by functional improvement of endoneurial vessels rather than robust angiogenesis in the endoneurium., Epidemiology : prevalence ranging from 18.8 to 61.9% in India, approximately 50 percent of patients with diabetes will eventually develop neuropathy, bad, If you have diabetes, it’s important to manage your : ,,Blood glucose (sugar).,Blood pressure.,Cholesterol.,You can decrease your risk of diabetes complications and diabetes-related nerve pain by : ,,Following a healthy meal and exercise plan.,Limiting your alcohol intake to no more than one to two drinks per day.,Quitting smoking.,Visiting your healthcare provider for a checkup and foot exam at least once per year., Complications : Urinary Tract Infection, heart problem, NERVE INJURY, Digestive problems, Diagnostics : Complete Blood Count CBC, CRP, serum Vitamin B12 level, fasting glucose, Differential diagnosis : Acute Appendicitis, acute cholecystitis, ANEURYSM, DIVERTICULITIS, Uremia, disease description : Diabetic neuropathy is a type of nerve damage that can occur if you have diabetes. High blood sugar (glucose) can injure nerves throughout the body. Diabetic neuropathy most often damages nerves in the legs and feet.Depending on the affected nerves, diabetic neuropathy symptoms include pain and numbness in the legs, feet and hands. It can also cause problems with the digestive system, urinary tract, blood vessels and heart. Some people have mild symptoms. But for others, diabetic neuropathy can be quite painful and disabling.Diabetic neuropathy is a serious diabetes complication that may affect as many as 50% of people with diabetes. But you can often prevent diabetic neuropathy or slow its progress with consistent blood sugar management and a healthy lifestyle.

Diabetic Retinopathy

Disease Name : Diabetic Retinopathy, Treatment : medication : Ranibizumab , Triamcinolone , Bevacizumab , I. Metabolic control of diabetes mellitus and associated,risk factors.The,normal values as under should be targeted : • Control of glycaemia. Target blood glucose level : ,fasting <120 mg%, post-prandial <180 mg%, and,HbA1c (glycosylated haemoglobin) <7%.,• Control of dyslipidaemia. Target lipid profile,(fasting) : Cholesterol <200 mg%, Triglycerides,<150 mg%, HDL >50 mg%, and LDL <150 mg%.,• Renal function tests. Target level are serum,creatinine 1.0 mg%, blood urea 20–40 mg%, and,24-hour urinary protein <200 mg%.,• Control of associated anaemia. Target hemoglobin,>10 mg%.,• Control of associated hypertension. Target blood,pressure levels : 130/80 mm Hg.,• Life style changes. Patients should be counselled,to prohibit smoking and alcohol consumption, and,take regular exercises. II. Intravitreal anti-VEGF drugs. Vascular endothelial,growth factor (VEGF) plays a pivotal role in the,etiopathogenesis of diabetic maculopathy and,retinopathy. Anti-VEGFs, e.g., Bevacizumab (1.25 mg),and Ranibizumab (0.5 mg) when given intravitrealy,in 0.1 ml vehicle lead to improvement in vision in,>40% cases and stabilize vision in another >40%,cases. III. Intravitreal steroids. Intravitreal triamcinolone,acetonide (IVTA) (20 mg) is another drug which is,being tried. It restores inner retinal barrier and has,some anti-VEGF effects as well. However, risk of,glaucoma, steroid induced cataract, and increased,vulnerability to endophthalmitis restrict its use.,Hence, anti-VEGFs are preferred over IVTA these,days. However, in recalcitrant cases IVTA may be,given along with anti-VEGFs., Laser therapy : i. Macular photocoagulation. It is of two types : ,• Focal photocoagulation. It is the,treatment of choice for focal DME not involving,the centre of fovea.,• Grid photocoagulation. It is no more,the treatment of choice for diffuse DME. It may,be considered only for recalcitrant cases not,responding to anti-VEGFs and intravitreal steroids. ii. Panretinal photocoagulation (PRP) or scatter laser,consists of 1200–1600 spots, each 500 mm in size and,0.1 sec duration. Laser burns are applied outside,the temporal arcades and on nasal side one disc,diameter from the disc upto the equator., • Tractional DME with NPDR. Treatment of choice,is pars plana vitrectomy (PPV) with removal of,posterior hyaloid.,• Advanced PDR with dense vitreous haemorrhage.,PPV along with removal of opaque vitreous gel,and endophotocoagulation should be done at an,early stage.,• Advanced PDR with extensive fibrovascular,epiretinal membrane should be treated by PPV along with removal of fibrovascular epiretinal,membrane and endophotocoagulation.,• Advanced PDR with tractional retinal detachment,should be treated by PPV with endophotocoagulation,and reattachment of detached retina,along with other methods like scleral buckling,and internal tamponade using intravitreal silicone,oil or gases like sulphur hexafluoride (SF6) or,perfluoropropane (C3F8)., Pathophysiology : Hypergylcemia, in uncontrolled diabetes mellitus, is the starting point for development of DR. Microangiopathy, affecting retinal pre-capillary arterioles, capillaries and venules, produced by hyperglycaemia is the basic pathology in diabetic retinopathy. Mechanisms by which hyperglycemia produces microangiopathy include : i. Cellular damage. Hyperglycaemia produces damage to the cells of retina, endothelial cells, loss of pericytes and thickening of basement membrane of capillaries by following effects : • Sorbitol accumulation in the cells due to aldose reductase mediated glycolysis, • Advanced glycation end (AGE) product accumulates in the cells due to non-enzymatic binding of several sugars to proteins, • Activation of several protein kinase C isoforms, and • Excessive oxidative stress to the cells due to excess of free radicals. ii. Hematological and biochemical changes induced by hyperglycaemia which play role in the development of microangiopathy include : • Platelet adhesiveness increase, • Blood viscosity increase, • Red blood cells deformation and Rouleaux formation, • Serum lipids altered abnormally, • Leukostasis increase due to increased intracameral adhesion molecule-1-(ICAM-1) level expression, and • Fibrinolysis increase. Effects of microangiopathy producing DR include : • Breakdown of blood-retinal barrier leads to retinal oedema, haemorrhages, and leakage of lipids (hard exudates). • Weakened capillary wall produces microaneurysms, and haemorrhages. • Microvascular occlusions produce ischaemia and its effects, and arteriovenous shunts, i.e., intraretinal microvascular abnormalities (IRMAs). Neovascularization of retina is induced by : • Proangiogenic factors such as vasculoendothelial growth factors (VEGFs), platelet derived growth factor (PDGF), and hepatocyte growth factor (HGF) which are released as a result of ischaemia produced by microvascular occlusions. Release of angiogenic factors is also mediated by hyperglycemia-induced oxidative stress, activation of protein kinase C and cytokines. • Deletion of anti–angiogenic factors such as endostatin, angiostatin, pigment epithelial derived factor (PEDF), thrombospondin-1 and platelet factor 4, also play role in causing neovascularization. Classification of Diabetic Retinopathy Diabetic retinopathy has been variously classified. Presently followed classification is as follows : I. Non-proliferative diabetic retinopathy (NPDR) • Mild NPDR • Moderate NPDR • Severe NPDR • Very severe NPDR II. Proliferative diabetic retinopathy (PDR) III. Diabetic maculopathy IV. Advanced diabetic eye disease (ADED) I. Non-proliferative diabetic retinopathy (NPDR) Ophthalmoscopic features of NPDR include : • Microaneurysms are seen in the macular area (the earliest detectable lesion) and elsewhere in relation to area of capillary nonperfusion. These are formed due to focal dilation (out pouching) of capillary wall following loss of pericytes. These appear as red dots and leak fluid, proteins, lipids and also fluorescein dye on FFA. , Epidemiology : 27.0%, estimated 285 million people with diabetes mellitus worldwide, , bad, If you have diabetes, you can lower your risk of developing diabetes-related retinopathy by : ,,Avoiding smoking.,Controlling your blood sugar.,Exercising regularly.,Having annual eye exams.,Keeping your blood pressure within a healthy range.,Taking any medications exactly as prescribed., Complications : blindness, Diagnostics : HbA1c, Optical coherence tomography (OCT), LIPID PROFILE, Urine analysis, Fundus fluorescein angiography (FFA), Fundus examination, Differential diagnosis : hypertension with diabetes, OCULAR ISCHAEMIC SYNDROME, disease description : Diabetic retinopathy (DR) refers to retinal changes seen in patients with diabetes mellitus. With increase in the life expectancy of diabetics, the incidence of diabetic retinopathy (DR) has increased. Diabetic retinopathy is a leading cause of blindness. Etiopathogenesis Risk factors 1. Duration of diabetes is the most important determining factor. • After 10 years, 20% of type I and 25% of type II diabetics develop retinopathy. • After 20 years, 90% of type I and 60% of type II diabetics develop retinopathy. • After 30 years, 95% of both type I and type II diabetics develop retinopathy. Note. It is important to note that it is the duration of disease after the onset of puberty which acts as a risk factor

Diastematomyelia

Disease Name : Diastematomyelia, Treatment : The treatment of split-cord malformations is surgical. This abnormality is a form,of tethered cord syndrome, and its treatment is to release the spinal cord to move,freely with movement of the spine. In type 1 split-cord malformations, the two,half cords are in separate dural sacs with medial attachment to the dura and bony,septum. In this case, the dura needs to be opened, the bony septum removed, the,medial attachments to the dura lysed, and a single dural tube created., Pathophysiology : Diastematomyelia is a "dysraphic state" of unknown embryonic origin, but is probably initiated by an accessory neurenteric canal (an additional embryonic spinal canal.) This condition may be an isolated phenomenon or may be associated with other segmental anomalies of the vertebral bodies such as spina bifida, kyphoscoliosis, butterfly vertebra, hemivertebra and block vertebrae which are observed in most of the cases. Scoliosis is identified in more than half of these patients. In most of the symptomatic patients, the spinal cord is split into halves by a bony spicule or fibrous band, each half being surrounded by a dural sac. Other conditions, such as intramedullary tumors, tethered cord, dermoids, lipoma, syringomyelia, hydromyelia and Arnold–Chiari malformations have been described in medical literature, but they are exceptionally rare.Diastematomyelia usually occurs between 9th thoracic and 1st sacral levels of the spinal column with most being at the level of the upper lumbar vertebra. Cervical diastematomyelia is a very rare entity. The extent (or length of spinal cord involved) varies from one affected individual to another. In approximately 60% of patients with diastematomyelia, the two hemicords, each covered by an intact layer of pia arachnoid, travel through a single subarachnoid space surrounded by a single dural sac. Each hemicord has its own anterior spinal artery. This form of diastematomyelia is not accompanied by any bony spur or fibrous band and is rarely symptomatic unless hydromyelia or tethering is present. The other 40% of patients have a bony spur or a fibrous band that passes through the two hemicords. In these cases, the dura and arachnoid are split into two separate dural and arachnoidal sacs, each surrounding the corresponding hemicord which are not necessarily symmetric. Each hemicord contains a central canal, one dorsal horn (giving rise to a dorsal nerve root), and one ventral horn (giving rise to a ventral nerve root.) One study showed the bony spur typically situated at the most inferior aspect of the dural cleft. They advised that if the imaging appears to show otherwise, a second spur (present in about 5% of patients with diastematomyelia) is likely to be present.The conus medullaris is situated below the L2 level in more than 75% of these diastematomyelia patients. Thickening of the filum terminale is seen in over half of the cases. While the level of the cleft is variable, it is most commonly found in the lumbar region. The two hemicords usually reunite caudally to the cleft. Occasionally, however, the cleft will extend unusually low and the cord will end with two separate coni medullarae and two fila terminale ("Diplomyelia")., Epidemiology : The prevalence is estimated to be 1 in 5499 live births (0.02%), with a slight female predominance (1.3 : 1), 300, 000 newborns per year., variable, Folic acid supplements may help reduce the risk of neural tube defects. ,It is recommended that any woman considering becoming pregnant take 0.4 mg of folic acid a day. Pregnant women with high risk need higher dosage.,,It is important to remember that folic acid deficiencies must be corrected before becoming pregnant, because the defects develop very early.,,Women who plan to become pregnant may be screened to determine the amount of folic acid in their blood., Complications : FREQUENT INFECTIONS, lymph nodes, Diagnostics : MRI Spine, Differential diagnosis : scoliosis, Syringomyelia, disease description : Diastematomyelia is a relatively rare form of occult dysraphism in which the spinal cord is divided into two halves and can present as tethered spinal cord. In type 1 split-cord malformation, there are two spinal cords, each in its own dural tube and separated by a spicule of bone and cartilage. In a type 2 split-cord malformation, the two spinal cords are enclosed in a single dural sac with a fibrous septum between the two spinal segments

Diastrophic Dysplasia

Disease Name : Diastrophic Dysplasia, Treatment : Treatment of diastrophic dysplasia is directed at,early correction of joint contractures, initially with,physical therapy, but surgical release of contractures,at the hip, knee and elbow may be necessary. Foot,deformities are often severe and rigid and require,extensive open releases to produce a plantigrade foot.,Patients with atlantoaxial instability with neurological,symptoms require occipital–cervical fusion. Cervical,kyphosis usually resolves spontaneously, but in refractory,cases it may require corrective fusion. Patients,with progressive kyphoscoliosis may also require posterior,spinal fusion., Pathophysiology : The specific gene mutation that causes DTD occurs in the SLC26A2 gene. It’s also called DTDST (diastrophic dysplasia sulfate transporter). The gene is responsible for making a protein important in making cartilage, as well as changing cartilage to bone.A person can be a carrier of the genetic mutation but not have the disorder. If a baby’s mother and father are both carriers, a baby has a 25% chance of developing the disorder., Epidemiology : estimated incidence of 1 : 1 000 000., POOR, "This condition is inherited in an autosomal recessive pattern and therefore theres no way to prevent diastrophic dwarfism. If someone in your family has the disorder, consider talking to your healthcare provider about genetic testing before pregnancy. Testing and counseling can help determine whether you are a carrier and what it means for your family.", Complications : nan, Diagnostics : X RAY, Soft Tissue Lateral View Neck Radiographs, Differential diagnosis : Desbuquois syndrome, LARSEN’S SYNDROME, disease description : Diastrophic dysplasia is an autosomal recessive disorder, occurring secondary to a mutation in the SLC26A2 gene. This results in defective production of a sulphate transporter protein, resulting in abnormalities of cartilage proteoglycan.

Dicarboxylic Aminoaciduria

Disease Name : Dicarboxylic Aminoaciduria, Treatment : Aminoaciduria is often treated with a restrictive diet, to minimize or eliminate exposure to a particular amino acid., Pathophysiology : The pathophysiology of dicarboxylic aminoaciduria can vary depending on the underlying cause, but here are some general mechanisms involved : Genetic defects : In some cases, dicarboxylic aminoaciduria is caused by genetic mutations affecting specific transporters or enzymes involved in amino acid metabolism. For example, defects in the SLC3A1 and SLC7A9 genes, which encode the cystine/glutamate transporter system, can result in cystinuria, a type of dicarboxylic aminoaciduria. These genetic defects impair the reabsorption of certain dicarboxylic amino acids in the kidneys, leading to their increased excretion in the urine.Disrupted amino acid transport : Dicarboxylic aminoaciduria can also arise due to acquired conditions or factors that disrupt the normal functioning of amino acid transporters in the kidneys. These transporters are responsible for the reabsorption of amino acids from the urine back into the bloodstream. Disruptions in these transporters can lead to impaired reabsorption and increased excretion of dicarboxylic amino acids.Metabolic abnormalities : Dicarboxylic aminoaciduria can be associated with metabolic disorders that affect amino acid metabolism. For instance, certain inborn errors of metabolism, such as glutaric acidemia type II, can result in the accumulation of dicarboxylic acids, including glutaric acid and adipic acid. These dicarboxylic acids are then excreted in the urine, leading to dicarboxylic aminoaciduria., Epidemiology : 1 : 35 000 births, variable, there are no known prevention methods, Complications : liver disease, kidney disease, Diagnostics : Urine analysis, Differential diagnosis : chronic liver disease, Hemolytic Uremic Syndrome, thrombotic thrombocytopenic purpura, disease description : Dicarboxylic aminoaciduria is caused by mutations in the SLC1A1 gene. It is inherited in an autosomal recessive fashion.Less than 10 cases have been reported to date. Defects in renal and intestinal glutamate and aspartate transport were also reported, suggesting that anomalies of the EAAC1 transporter, involved in the transport of these two amino acids, are the underlying cause of this syndrome. Dicarboxylic aminoaciduria is a rare metabolic disorder characterized by the excessive loss of aspartate and glutamate in urine. Symptoms have varied greatly among the few reported cases. 

Dic

Disease Name : Dic, Treatment : medication : Heparin , Administration of FFP and/or platelet concentrates is indicated for ,patients with active bleeding or at high risk of bleeding,Drugs to control coagulation such as heparin, antithrombin III ,(ATIII) concentrates, or antifibrinolytic drugs have all been tried ,in the treatment of DIC, Pathophysiology : Also referred to as consumptive coagulopathy, DIC involves the homeostatic imbalance between coagulation and bleeding. Tissue factor (TF), which may be released into the circulation from vascular endothelial damage from trauma or certain cancer treatments, bacterial endotoxins,  or cytokine exposure, activates coagulation factor VII to VIIa in the coagulation pathway. Via the extrinsic pathway, thrombin and fibrin are formed and result in the formation of clots in the circulation. As this process continues, thrombin and fibrin further impair the coagulation cascade through positive feedback loop stimulation and coagulation inhibitor consumption. Clotting factors, as a result, are consumed due to clotting, which can lead to excessive bleeding. Platelets also may become trapped and consumed in this process. Additionally, pathways including the protein C system and antithrombin III appear to be dysregulated in DIC. Furthermore, an increase in plasma activator inhibitor-1 (PAI-1) can prevent the inhibition of fibrinolysis., Epidemiology : as many as 1% of hospitalized patients., incidence of COVID-19 patients developing DIC was 3%, depends on severity, DIC is linked to medical conditions such as cancer, pancreatitis and liver disorders. Unfortunately, that means there’s very little you can do to prevent DIC. What you can do is to talk to your healthcare provider about DIC so you know what changes in your body might be a sign of it., Complications : acute kidney injury, cardiac tamponade, Hemothorax, hepatic dysfunction, respiratory depression, shock, INTRACEREBRAL HEMORRHAGE, Diagnostics : APTT, FDP(Fibrin degradation products) BLOOD TEST, PLATELET COUNT, PROTHROMBIN TIME(PT), Blood smear, Differential diagnosis : nan, disease description : Disseminated intravascular coagulation (DIC) can be defined as a widespread hypercoagulable state that can lead to both microvascular and macrovascular clotting and compromised blood flow, ultimately resulting in multiple organ dysfunction syndrome or MODS. As this process begins consuming clotting factors and platelets in a positive feedback loop, hemorrhage can ensue, which may be the presenting symptom of a patient with DIC. Disseminated intravascular coagulation typically occurs as an acute complication in patients with underlying life-threatening illnesses such as severe sepsis, hematologic malignancies, severe trauma, or placental abruption. Determining the consequences of DIC and the overall mortality rate of DIC remains difficult as patients with this condition also have additional diagnoses that can cause many of the signs and symptoms consistent with DIC, particularly if they are also suffering from acute or chronic liver failure. While concomitant disease states can obscure a patient’s prognosis, mortality rates have been shown to double in septic patients or those with severe trauma if they are also suffering from DIC

Dientaamoebiasis

Disease Name : Dientaamoebiasis, Treatment : diiodohydroxyquin or tetracycline, iodoquinol, doxycycline, metronidazole, paromomycin, and secnidazole, Pathophysiology : The pathophysiology of dientamoebiasis involves several stages, including transmission, colonization, invasion, and tissue damage. Heres an overview of the pathophysiology : Transmission : The primary mode of transmission is the ingestion of water or food contaminated with fecal matter containing the cysts of Entamoeba histolytica. This typically occurs through the ingestion of contaminated water or food, poor hygiene practices, or direct contact with infected individuals.Colonization : Once the cysts are ingested, they reach the small intestine, where they excyst and release trophozoites. These trophozoites colonize the intestinal lumen and multiply, leading to the establishment of the infection.Invasion : Some trophozoites have the ability to invade the intestinal mucosa and gain access to the bloodstream. They can penetrate the mucosal layer and invade the epithelial cells, causing tissue damage and inflammation. The trophozoites can then disseminate to other organs, most commonly the liver, through the bloodstream.Tissue damage : The trophozoites, particularly those that have invaded the intestinal mucosa and other organs, cause tissue destruction through several mechanisms. They produce enzymes, such as cysteine proteases, that degrade host tissues, leading to ulceration and necrosis. Trophozoites can also induce an inflammatory response, attracting immune cells and contributing to tissue damage., Epidemiology : 12.04%., as high as 42% in some regions., variable, Complications : nan, Diagnostics : STOOL CULTURE, Differential diagnosis : nan, disease description : Dientamoebiasis is a medical condition caused by infection with Dientamoeba fragilis, a single-cell parasite that infects the lower gastrointestinal tract of humans. It is an important cause of travelers diarrhea, chronic abdominal pain, chronic fatigue, citation needed and failure to thrive in children.

Diffuse Large B Cell Lymphoma

Disease Name : Diffuse Large B Cell Lymphoma, Treatment : The treatment of B cell lymphomas depends not only on their staging but also on the type of the disease (indolent or aggressive) and the molecular subtype. Though DLBCL is aggressive, with appropriate chemotherapy, the survival can be long, but with a limited cure rate. Patients with GCB DLBCL respond well to 6 cycles of rituximab along with cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) regimen given every 21 days., Pathophysiology : To better understand the molecular diversity among morphologically similar variants of DLBCL, high throughput technology such as gene expression profiling (GEP) could classify DLBCL into germinal center B-cells (GCB) and activated B-cells (ABC). Most of the patients with DLBCL show gene rearrangements in the heavy and light chains of the immunoglobulin. About 80% of DLBCL expresses B cell leukemia or lymphoma 2 (BCL2) protein, and 70% expresses B cell lymphoma 6 (BCL6) protein. Some of them also express abnormalities in the gene MYC. The flow cytometry reveals CD19, CD20, CD22, CD45 and CD79a. CD30 can be seen in 25% and carries a favorable prognosis. Very rarely, they can express CD5, which has a poor prognosis.More than 50% of the DLBCL expresses surface or cytoplasmic immunoglobulin IgM. Double hit lymphoma presents like DLBCL but has MYC along with BCL2 and/or BCL6. A triple hit lymphoma has rearrangements in BCL2, BCL6, and MYC. The (14;18) translocation is related to disseminated and nodal disease and does not imply a poor prognosis. The t(14 : 18) is seen in more than 90% of FL and about 30% of DLBCL patients. DLBCL commonly involves extranodal sites, which include the brain, bones, kidneys, adrenal glands, and other soft tissues.Pathophysiology of non-Hodgkin B cell lymphomas is dependent on the type of lymphoma. B cell lymphomas are categorized based on the stage of B cell development that has resulted in malignancy (i.e., mantle cell vs. marginal cell lymphoma). Lymphadenopathy occurs due to the proliferation of B cells in or around the germinal center. Systemic symptoms (B-symptoms) are due to increased cytokine production. Elevated levels of LDH and uric acid suggest high cell turnover and release of degradation products into the bloodstream., Epidemiology : DLBCL accounts for about 25% of all NHL cases worldwide, 7 cases per 100, 000 per year, Variable, A risk factor is an activity or condition that increases your risk of developing a condition. There are DLBCL risk factors you can’t control, like having an autoimmune disease or immunodeficiency. And there are risk factors you may be able to avoid, like developing certain infections.,,Avoiding risk factors may help, but there’s no guarantee you won’t develop DLBCL. That’s because this condition happens when certain genes mutate and create cancerous cells. These are acquired genetic mutations, meaning you develop them during your lifetime instead of being born with them. Medical researchers aren’t sure why these mutations happen or the specific role that risk factors may play. Additional risk factors for diffuse large B-cell lymphoma include : ,,Immunosuppressant drugs taken after organ transplants.,Exposure to agricultural pesticides.,Exposure to ionizing radiation., Complications : renal failure, CNS manifestation, Diagnostics : BONE MARROW BIOPSY, Complete Blood Count CBC, LYMPH NODE BIOPSY, lumbar puncture, CT, Differential diagnosis : "Hodgkins lymphoma", infectious mononucleosis, melanoma, disease description : The B cell lymphomas result from the malignant proliferation of B cells during their various stages of development. Depending on the morphology, genetics, and immunophenotype of the neoplastic cells, a cell of origin (COO) is proposed. The development of B cells can be categorized into 3 stages- pre-germinal, germinal, and post-germinal center. Most of the B- cell lymphomas are derived from the germinal center. Likewise, an immunosuppressive medication used in transplant patients is a risk factor for the development of B-cell lymphomas. Also, the transformation from different kinds of lymphomas, including splenic marginal zone lymphoma, marginal zone (MALT) lymphoma, chronic lymphocytic leukemia (Ritcher transformation), can result in DLBCL. Other risk factors for the development of B-cell lymphomas include family or personal history of lymphoma, history of radiation, and chemotherapy. Chemical agents such as dyes and pesticides can also increase the risk for lymphoma. Non-Hodgkin lymphoma (NHL) is more common in obese and patients with an underlying history of autoimmune diseases.

Diffuse Otitis Externa

Disease Name : Diffuse Otitis Externa, Treatment : Ear toilet, Medicated wicks, Antibiotics and Analgesics., Polymyxin B, neomycin, and hydrocortisone 3 to 4 drops to the affected ear four times a day,Ofloxacin 5 drops to the affected ear twice daily,Ciprofloxacin with hydrocortisone 3 drops to the affected ear twice daily, Pathophysiology : Acute phase is characterized by hot burning sensation in the ear, followed by pain which is aggravated by movements of jaw. Ear starts oozing thin serous discharge which later becomes thick and purulent. Meatal lining becomes inflamed and swollen. Collection of debris and discharge accompanied with meatal swelling gives rise to conductive hearing loss. In severe cases, regional lymph nodes become enlarged and tender with cellulitis of the surrounding tissues. Chronic phase is characterized by irritation and strong desire to itch. This is responsible for acute exacerbations and reinfection. Discharge is scanty and may dry up to form crusts. Meatal skin which is thick and swollen may also show scaling and fissuring. Rarely, the skin becomes hypertrophic leading to meatal stenosis (chronic stenotic otitis externa)., Epidemiology : prevalence of 10%, 12–14 per 1000 population per year, Good, Yes, there are things you can do to prevent swimmer’s ear. Keeping your ears dry is the most effective way to prevent swimmer’s ear.,,Dry your ears,Swimmer’s ear happens when there’s water trapped in your ear canal, creating a place for bacteria and fungi to multiply. Ways to dry your ears include : ,,Wear clean earplugs when you swim or spend time in the water.,Wear a shower cap when you shower.,When you wash your hair, put cotton balls in your ears to reduce the amount of water in your ears.,Use a dry towel to dry your ears after bathing, swimming or being in the water.,Drain water from your ears by tipping your head from side to side and pulling your earlobe in different directions. The combination of tilting and pulling will help water drain from your ear canal.,Use a hairdryer to dry out water in your ears. Use the lowest possible settings for the fan speed and heat level and hold the nozzle of the dryer several inches from your ears. That way, you won’t run the risk of burning your ear.,Protect your ears,Ask a provider about drops to dry your ear canal after swimming or bathing. Ask if they recommend a homemade solution of vinegar and rubbing alcohol.,Don’t stick anything into your ear canal.,Don’t swim in polluted water.,If you use earbuds or wear hearing aids, be sure to clean them before you put them in your ears. If you use hearing aids, ask your audiologist how to keep your hearing aids clean., Complications : MASTOIDITIS (LATENT), Diagnostics : Gram Staining, Otoscopy, CT, Differential diagnosis : otitis media, disease description : It is diffuse inflammation of meatal skin which may spread to involve the pinna and epidermal layer of tympanic membrane. Disease is commonly seen in hot and humid climate and in swimmers. Excessive sweating changes the pH of meatal skin from that of acid to alkaline which favours growth of pathogens. Two factors commonly responsible for this condition are : (i) trauma to the meatal skin and (ii) invasion by pathogenic organisms.

Diffuse Serous Labyrinthitis

Disease Name : Diffuse Serous Labyrinthitis, Treatment : medication : Dimenhydrinate , Prochlorperazine , Medical,1. Patient is put to bed, his head immobilized with affected ear above.,2. Antibacterial therapy is given in full doses to control infection.,3. Labyrinthine sedatives, e.g. prochlorperazine ,(Stemetil) or dimenhydrinate (Dramamine), are given for symptomatic relief of vertigo, Myringotomy is done if labyrinthitis has followed,acute otitis media and the drum is bulging. Pus is,cultured for specific antibacterial therapyCortical mastoidectomy (in acute mastoiditis),or modified radical mastoidectomy (in chronic middle,ear infection or cholesteatoma) will often be required,to treat the source of infection., Pathophysiology : Most often it arises from pre-existing circumscribed labyrinthitis associated with chronic middle ear suppuration or cholesteatoma. In acute infections of middle ear cleft, inflammation spreads through annular ligament or the round window. It can follow stapedectomy or fenestration operation.Mild cases complain of vertigo and nausea but in severe cases, vertigo is worse with marked nausea, vomiting and even spontaneous nystagmus. Quick component of nystagmus is towards the affected ear. As the inflammation is diffuse, cochlea is also affected with some degree of sensorineural hearing loss. Serous labyrinthitis, if not checked, may pass onto suppurative labyrinthitis with total loss of vestibular and cochlear function., Epidemiology : GOOD, Because labyrinthitis is usually an underlying symptom of other conditions, the best way to avoid it is to wash your hands regularly and take proper precautions during cold and flu season., Complications : MASTOIDITIS (LATENT), Diagnostics : FUNDOSCOPY, MRI, CT SCAN, Audiometry, Differential diagnosis : acoustic neuroma, "menieres disease", vestibular neuronitis, disease description : It is diffuse intralabyrinthine inflammation without pus formation and is a reversible condition if treated early... Labyrinthitis is an inner ear infection that can affect a person’s balance and hearing. It may occur when a cold, the flu, or a middle ear infection spreads to the inner ear.

Diffuse Simple(nontoxic) Goiter

Disease Name : Diffuse Simple(nontoxic) Goiter, Treatment : medication : Levothyroxine/Tetra idothyronine, Iodine (Sodium iodide, potassium iodide) , Nontoxic goiter usually evolves slowly and asymptomatic, so it needs no treatment and left for follow up., Non-emergent surgical treatment is indicated in patients with compressive symptoms or complications. Thyroidectomy is indicated in retrosternal goiter even if asymptomatic because delaying treatment to symptoms appearance may need more complicated surgical procedures., Pathophysiology : The deficiency of iodine or increasing demands for thyroid hormones leads to pituitary gland stimulation that increases TSH secretion. TSH stimulates thyroid follicular cells and with continuous long-term stimulation leads to follicular hyperplasia and thyroid enlargement. When iodine is supplied again or when thyroid hormone deficiency is corrected thyroid gland may decrease in size due to decreased TSH levels and the thyroid gland is not more stimulated. , Epidemiology : In the case of moderate deficiency, the prevalence is 20% to 30%., When there is a mild deficiency of iodine, the incidence of goiters is 5% to 20%, good, A goiter caused by iodine deficiency (simple goiter) is generally the only type of goiter you can prevent. Consuming a diet that includes fish, dairy and a healthy amount of iodized table salt prevents these types of goiters. Iodine supplements and other supplements are generally not recommended and may do more harm than good., Complications : MASTOIDITIS (LATENT), Diagnostics : FNAC, Triiodothyronine (T3) Tests, Thyroxine (T4) Test, Thyroid Stimulating Hormone TSH, TPOAb (Thyroid peroxidase antibodies), URINARY IODINE LEVEL, USG, Differential diagnosis : Thyroid cancer, disease description : Goiter is the enlargement of the thyroid gland. Nontoxic goiter is thyroid gland enlargement with no disturbance in the thyroid function. It is not due to inflammation or neoplasia. The goiter may be diffuse or a localized growth. If the goiter is large, it may extend into the retrosternal space. Because of the limited space in the mediastinum, the goiter can cause compression of the upper trachea, laryngeal nerves, and esophagus. 

Diffuse Superficial Keratitis

Disease Name : Diffuse Superficial Keratitis, Treatment : medication : Gentamicin , It consists of frequent instillation,of antibiotic eyedrops such as tobramycin or,gentamycin 2–4 hourly., Pathophysiology : Corneal infections often start as epithelial ulceration. This is followed by stromal infiltration by polymorphonuclear (PMN) and lymphomononuclear cells, which in turn causes the destruction of Bowmans layer and then stromal necrosis. In severe cases, there can be perforation of the Descemets membrane. Suppurative infections lead to infiltrates in the anterior two-thirds of the stroma and abscess formation. Epithelial regeneration, vascularization, edema, giant cell reaction, myofibroblatic transformation and stromal remodeling (scarring), and round cell infiltration can occur with chronic infections., Epidemiology : 2.0–3.5 million cases of bacterial keratitis are reported annually., 3.3–52.1 per 100, 000, , VARIABLE, The best way to prevent keratitis is to look out for symptoms such as eye redness, pain, discomfort and change in vision. Contact lens hygiene is also essential to prevention. “If you wear contacts, it’s so important to follow the proper steps to clean and disinfect your lenses and change them out when needed, " says Liu. "This prevents bacteria and other unsanitary bodies from infecting your eyes.”, Complications : ulcerative keratitis, Toxic iridocyclitis, Descemetocele, Diagnostics : Slit lamp examination, Differential diagnosis : conjunctivitis, Infectious keratitis, Sjogren’s Syndrome, viral keratitis, disease description : Superficial punctate keratitis (SPK) is damage to the cells of the cornea’s outer layer. SPK can be visualized by staining the eye with a dye and looking under high magnification and a bright light. It is caused by many conditions and results in discomfort, redness and watery eyes. 

Diffuse Suppurative Labyrinthitis

Disease Name : Diffuse Suppurative Labyrinthitis, Treatment : medication : Dimenhydrinate , Prochlorperazine , Medical,1. Patient is put to bed, his head immobilized with affected ,ear above.,2. Antibacterial therapy is given in full doses to control ,infection.,3. Labyrinthine sedatives, e.g. prochlorperazine (Stemetil) ,or dimenhydrinate (Dramamine), are given for symp\x02tomatic relief of vertigo, Cortical mastoidectomy (in acute mastoiditis) or ,modified radical mastoidectomy (in chronic middle ear ,infection or cholesteatoma) will often be required to treat ,the source of infection., Pathophysiology : It usually follows serous labyrinthitis, pyogenic organisms entering through a pathological or surgical fistula. Clinical Features. There is severe vertigo with nausea and vomiting due to acute vestibular failure. Spontaneous nystagmus will be observed with its quick component towards the healthy side. Patient is markedly toxic. There is total loss of hearing. Relief from vertigo is seen after 3-6 weeks due to adaptation., Epidemiology : 1–2% were considered low and 3–6% were high;, 3.5 cases per 100, 000, GOOD, Complications : Brain Abscess, Chronic and Recurrent Meningitis, Diagnostics : MRI, CT SCAN, Differential diagnosis : acoustic neuroma, vestibular neuronitis, disease description : This is diffuse pyogenic infection of the labyrinth with permanent loss of vestibular and cochlear functions.. Suppurative labyrinthitis, is inflammation caused directly by the bacteria. This will have entered the inner ear through the aforementioned oval window or round window, connecting the inner ear to the middle ear or via the central nervous system through the cochlear aqueduct or auditory canal. The round window is the most common entry point. They may also arise from acquired and congenital defects in the bony labyrinth.

Diffuse-type Giant Cell Tumour

Disease Name : Diffuse-type Giant Cell Tumour, Treatment : Embolization blocks the blood vessels that send blood to the tumor so the tumor starts to die., Medication may target certain parts of the cells in a bone GCT to slow down tumor growth and prevent your bones from breaking down., To treat bone GCTs, your healthcare provider scrapes the tumor away from your bone (curettage). Then, they fill the bone in with another piece of bone or a bone cement mixture (bone graft). When tumors are very big, your doctor may prescribe medications, followed by resection (removal) of the bone segment and reconstruction with a prosthesis., To treat TGCTs, your healthcare provider removes the tissue lining in your joint where the TGCT is., Pathophysiology : PathophysiologyGCTB related clonal aberrations occur in a background of epigenetic histone modifications (especially the G34W mutation of H3F3A gene) Neoplastic mononuclear stromal cells in GCTB express receptor activator of NF?ß ligands (RANKLs) and various chemokines and cytokines associated with monocyte recruitment and reactive multinucleated giant cells (osteoclastogenesis) Activation of Wnt / beta catenin pathway in GCTB tumorigenesis Clonal telomeric associations (tas) were found in GCTB Transformation to malignancy may occur after therapeutic irradiation TP53 and HRAS mutations have been identified in malignant GCTB not associated with prior radiation, Epidemiology : Incidence,1.7 per million people, Variable, Experts don’t know what causes giant cell tumors, so there’s no way to prevent them. If you notice pain, swelling or a lump around one of your bones or joints, see your healthcare provider. GCTs are often easier to treat when they’re found early., Complications : recurrance, Diagnostics : BONE SCAN, biopsy, MRI, USG, Differential diagnosis : Chondroblastoma, Chordoma, osteosarcoma, disease description : ?A giant cell tumor (GCT) is a type of noncancerous (benign) growth (tumor). GCTs aren’t cancer, so they don’t usually spread to other parts of your body; although very rarely, they can spread to  lungs. But they may grow quickly and damage surrounding tissues, as they’re considered a locally aggressive tumor.Giant cell tumo are present  at the end of one of your bones. These tumors often grow near your knee, either at the bottom of your thigh (femur) or the top of your shin (tibia). GCTs that grow in the soft tissues are called tenosynovial giant cell tumor (TGCT). TGCTs are also locally aggressive, but they’re even less likely to spread than GCTs.

Digeorge Syndrome

Disease Name : Digeorge Syndrome, Treatment : medication : Vitamin D3/Tacalcitol, PTH HORMONE, "Fortunately, many patients with DGS have minor immunodeficiency, with preservation of T cell function despite decreased T cell production. Frequent follow-up with an immunologist experienced in treating primary immunodeficiencies is advisable. ,Immunization, boosters, intravenous immunoglobulin, and antibiotic prophylaxis regimens should revolve around the individual patients laboratory values. Antibody titer to administered vaccines should be re-evaluated every six to twelve months to determine the necessity of re-vaccination.,Hypocalcemia is manageable with calcium and vitamin D supplementation.", Pathophysiology : DGS results from microdeletion of 22q11.2, which encodes over 90 genes. Patients with DGS display a broad array of phenotypes, and the most common findings include cardiac anomalies, hypocalcemia, and hypoplastic thymus. Failure in embryologic development of the pharyngeal pouches, which is driven by TBX1, leads to absence or hypoplasia of the thymus and parathyroid glands., Epidemiology : 22q11.2 microdeletion in live births occurs at an estimated rate of 1 in 4000 to 6000, About 1 in 4, 000 people in the U.S. receive a 22q11. 2 deletion syndrome diagnosis annually., variable, You can’t prevent DiGeorge syndrome since it’s a genetic condition. If you plan on becoming pregnant and want to learn about your risk of having a child with a genetic condition, talk to your provider about genetic testing.,,If you’re pregnant and have a family member with 22q11.2 deletion syndrome, ask your provider about prenatal and newborn screenings. These tests can reveal signs of the condition, such as heart and kidney abnormalities, before your baby is born. Detecting the condition early can help you and your provider prepare for your baby’s care after they’re born., Complications : nan, Diagnostics : X RAY CHEST, CT SCAN, Differential diagnosis : ALAGILLE SYNDROME, CHARGE Syndrome, Smith-Lemli-Opitz syndrome, disease description : DiGeorge syndrome (DGS) is a congenital disorder with a broad phenotypic presentation, which results predominantly from the microdeletion of chromosome 22 at a location known as 22q11.2. This mutation results in the failure of appropriate development of the pharyngeal pouches, which are responsible for the embryologic development of the middle and external ear, maxilla, mandible, palatine tonsils, thyroid, parathyroids, thymus, aortic arch, and cardiac outflow tract. Features of DGS include cardiac anomalies, recurrent infections, abnormal facies, thymic hypoplasia or aplasia, cleft palate, developmental delay, and hypocalcemia. This activity outlines the diagnosis, evaluation, treatment, and management of patients with DGS, and highlights the role of the interprofessional team in managing patients with this condition

Digital Myxoid Cyst

Disease Name : Digital Myxoid Cyst, Treatment : conservative treatments ,such as multiple needling or aspiration followed by steroid injection, sclerosant injection, cryotherapy, infrared coagulation or CO 2,laser, excision, Pathophysiology : It has been proposed that mucous cysts could be an outpouching of the synovial lining of a joint. Studies have been performed where dye is injected into the joint and has shown communication between the joint and the cyst. However, when the dye is injected into the cyst, there does not appear to be a communication of the cyst to the joint. This could indicate that there is a one-way valve, where the fluid is originating from the joint but it is unable to go back into the joint. Others have proposed that there could be a rent in the tendon sheath or the capsule surrounding the joint, causing irritation and a local reaction and thus the formation of the cyst. Another theory is that the connective tissue surrounding the joint is undergoing mucoid degeneration, with byproducts of collagen breakdown collecting in the cyst.  In a study by Eaton, all mucous cysts excised with marginal osteophyte resection were observed to communicate with the DIP joint., Epidemiology : the cited prevalence of mucous cysts in OA varies widely, ranging from 64 to 93%., Variable, Complications : joint stiffness, osteomyelitis, Soft tissue infection, recurrence, Diagnostics : X RAY, Transillumination test, Histopathological examination, Differential diagnosis : Giant cell tumor of bone, Gout, "HEBERDENS NODES", disease description : Digital mucous cysts are a type of ganglion commonly found on the hand. A ganglion is a soft tissue tumor that is found next to a joint or tendon. A digital mucous cyst is a ganglion that arises from the dorsum of the distal interphalangeal joint (DIP joint). Digital mucous cysts commonly have an association with underlying DIP joint osteoarthritis.

Digital Myxoid Pseudocyst

Disease Name : Digital Myxoid Pseudocyst, Treatment : *Repeatedly pressing firmly on the cyst,*Squeezing out its contents (make a hole with a sterile needle),*Cryotherapy (freezing),*Steroid injection,*Sclerosant injection,*Surgical removal., Second line,•\tMethylene-blue guided surgery, Pathophysiology : It is now believed that digital myxoid pseudocysts result from leakage of synovial fluid through a breach in the joint capsule of the distal interphalangeal joint , as could be demonstrated in more than 85% of cases in a study using MRI Pathology Digital myxoid pseudocysts manifest as well-circumscribed but unencapsulated cyst-like dermal swellings, devoid of any lining. They consist of large mucin-filled spaces containing spindle- shaped and stellate fibroblasts without atypia., Epidemiology : 64 percent to 93 percent of people with osteoarthritis have myxoid cysts., Variable, Complications : joint stiffness, osteomyelitis, recurrence, Diagnostics : MRI, X RAY, Differential diagnosis : fibrokeratoma in subtype B, Giant cell tumour, Gout, "HEBERDENS NODES", disease description : Digital myxoid pseudocysts are the second most common benign tumours of the digits A digital myxoid pseudocyst is a shiny papule found at the end of a finger or toe, close to the nail. It is called a pseudocyst because it is not surrounded by a capsule, unlike a true cyst. It is also called a myxoid cyst, a mucous cyst, a digital ganglion cyst, and a digital synovial cyst.

Digital Papillary Carcinoma

Disease Name : Digital Papillary Carcinoma, Treatment : Complete excision or amputation of the affected digit. ,Sentinel lymph node biopsy may translate into decreased local recurrence and metastasis. ,The role of chemotherapy remains unclear. ,Radiation can be used effectively at conventional palliative doses. ,FGFR or BRAF targeted therapy may be useful., Pathophysiology : Pathogenesis includes-Ultrastructural studies demonstrated three types of neoplastic cells : clear cells, dark cells and myoepithelial cellsSome dark cells have dense granulesMolecular / cytogenetics descriptionBRAFV600E (1/9)Tumor overexpression of FGFR2 (6/6)Histopathological findings include a well-circumscribed or infiltrative growth pattern and tubuloalveolar ductal structures with areas of papillary projection that protrude into the cystic lumen. The papillary projections are associated with fibrovascular cores in some foci. Lesions have solid and cystic components with closely aggregated back-to-back glandular architectures lined by cuboidal or columnar epithelia that are surrounded by a basal myoepithelial cell layer. Cytologic atypia or mitotic counts have been observed but are variable. Cysts contain either necrotic debris or eosinophilic secretory material., Epidemiology : 0.08 cases/1, 000, 000, variable, you can take steps to reduce your risk by : ,,Avoiding excessive sun exposure.,Avoid using tanning beds.,Using sunscreen when you’re outdoors.,Wearing protective clothing and accessories from the sun, including sunglasses, hats and clothing with UPF protection.,Stopping smoking.,Avoid exposing yourself to chemicals without wearing personal protective equipment., Complications : recurrence, Diagnostics : MRI, Immunostaining, Differential diagnosis : Hidradenocarcinoma, Hidradenoma, metastatic adenocarcinoma, Microcystic adnexal carcinoma, disease description : Digital papillary carcinoma (DPC) is a rare, slow growing, malignant tumor with eccrine differentiation that occurs predominantly in digits.  DPC presents as solitary non-tender masses that arise from fingers and toes and/or adjacent skin of the palms and soles. The distal portion of a finger or thumb is frequently documented as a DPC location. Clinical diagnoses included cysts, vascular lesions, and giant cell tumors. Lesions may range in size from 10 to 40 mm (mean, 20 mm), with variable duration 

Dihydrofolate Reductase (dhfr) Deficiency

Disease Name : Dihydrofolate Reductase (dhfr) Deficiency, Treatment : . Transfusions are indicated only when the anemia is severe or the child is,very ill., folic acid may be administered orally or parenterally at 0.5-1.0 mg/day.Folic acid therapy (0.5-1.0,mg/day) should be continued for 3-4 wk until a definite hematologic response,has occurred. Maintenance therapy with a multivitamin (containing 0.2 mg of,folate) is adequate. Very high doses of folate may be required in the setting of,HFM, Pathophysiology : Hereditary folate malabsorption (HFM) is an autosomal recessive disorder that is linked to several loss-of-function mutations in the SLC46A1 gene encoding the protein-coupled folate transporter. HFM is associated with an inability to absorb folic acid, 5-tetrahydrofolate, 5-methyltetrahydrofolate, or 5- formyltetrahydrofolate (folinic acid). It can become apparent at 2-6 mo of age with megaloblastic anemia and other deficits, including infections and diarrhea. Neurologic abnormalities attributable to folate deficiency in the central nervous system (CNS) include seizures, developmental delay, and intellectual disability. Folate transport is impaired both in the intestine and at the brains choroid plexus. Serum and cerebrospinal fluid (CSF) folate levels are very low, with a loss of the normal 3 : 1 ratio of CSF to serum folate. Treatment, specifically in the context of HFM, usually involves parenteral folate, although oral administration has been useful in some cases. Reduced folates are more effective than folic acid. Folate sufficiency should be maintained in both blood and CSF to avoid important complications. The megaloblastic anemia in HFM can be reversed with relatively low levels of serum folate, but adequate CSF levels may be quite difficult to achieve, and very large folate doses may be needed. Functional methionine synthase deficiency may result from mutations affecting the function of methionine synthase reductase or methionine synthase. These disorders are autosomal recessive and are characterized not only by megaloblastic anemia, but also by cerebral atrophy, nystagmus, blindness, and altered muscle tone. Both respond to hydroxocobalamin plus betaine with variable clinical success. Dihydrofolate reductase (DHFR) deficiency is extremely rare and is associated with homozygous mutations in the DHFR gene. Clinical symptoms include megaloblastic anemia and neurologic manifestations. Although methylenetetrahydrofolate reductase (MTHFR) deficiency is the most common inborn error of folate metabolism, and severe cases can produce a number of neurologic and vascular complications, there is no associated megaloblastic anemia., Epidemiology : 23%, rare, variable, there are no known prevention methods, Complications : MEGALOBLASTIC ANAEMIA, neurological problem, Diagnostics : serum Folic Acid, GENRAL BLOOD PICTURE, RBC folate, BONE MARROW IRON STORES, Differential diagnosis : B12 Deficiency, disease description : Dihydrofolate reductase (DHFR) deficiency is extremely rare and is associated with homozygous mutations in the DHFR gene. Clinical symptoms include megaloblastic anemia and neurologic manifestations. Folic acid deficiency can result from inadequate folate intake, decreased folate absorption, or acquired and congenital disorders of folate metabolism or transport. 

Dihydropyrimidinase Deficiency

Disease Name : Dihydropyrimidinase Deficiency, Treatment : In symptomatic cases, ,treatment with ß-alanine has been attempted with equivocal results. A single case,of increased sensitivity to 5-FU has been reported., Pathophysiology : DPH is the 2nd enzyme in the 3-step degradation pathway of uracil and thymine. DPH deficiency is characterized by increased urinary excretion of dihydrouracil and dihydrothymine (dihydropyrimidinuria ), as well as uracil and thymine. Similar to DPD deficiency, there is a variable clinical phenotype. Genetics This is an autosomal recessive disorder, with the DPYS gene mapped to chromosome 8q22. One study found no significant difference in residual activity between mutations observed in symptomatic and asymptomatic individuals, again similar to DPD deficiency. Population prevalence in a Japanese sample was 0.1%..The neurological abnormalities that occur most often in people with dihydropyrimidinase deficiency are intellectual disability, seizures, and weak muscle tone (hypotonia). An abnormally small head size (microcephaly) and autistic behaviors that affect communication and social interaction also occur in some individuals with this condition.Gastrointestinal problems that occur in dihydropyrimidinase deficiency include backflow of acidic stomach contents into the esophagus (gastroesophageal reflux) and recurrent episodes of vomiting (cyclic vomiting). Affected individuals can also have deterioration (atrophy) of the small, finger-like projections (villi) that line the small intestine and provide a large surface area with which to absorb nutrients. This condition, called villous atrophy, can lead to difficulty absorbing nutrients from foods (malabsorption), resulting in a failure to grow and gain weight at the expected rate (failure to thrive)., Epidemiology : Population prevalence in a Japanese sample,was 0.1%., variable, "This condition is inherited in an autosomal recessive pattern and therefore, it cant be prevented. ,Although Genetic counselling is advisable.", Complications : seizures, hypotonia, intellectual disability, Diagnostics : Urine analysis, Differential diagnosis : nan, disease description : DPH is the 2nd enzyme in the 3-step degradation pathway of uracil and thymine. DPH deficiency is characterized by increased urinary excretion of dihydrouracil and dihydrothymine (dihydropyrimidinuria ), as well as uracil and thymine. Similar to DPD deficiency, there is a variable clinical phenotype.Dihydropyrimidinase deficiency is a disorder that can cause neurological and gastrointestinal problems in some affected individuals. Other people with dihydropyrimidinase deficiency have no signs or symptoms related to the disorder, and in these individuals the condition can be diagnosed only by laboratory testing.

Dihydropyrimidine Dehydrogenase Deficiency

Disease Name : Dihydropyrimidine Dehydrogenase Deficiency, Treatment : patients with,seizures do respond to anticonvulsant medications. DPYD genetic variants,associated with partial or complete DPD activity and occurring with relatively,high frequency in populations are potentially useful predictive markers of patient,response to 5-FU chemotherapy., Pathophysiology : DPD deficiency is an autosomal recessive disorder, with the DPYD gene mapping to chromosome 1p22, with at least 32 polymorphisms detected. It is estimated that the frequency of heterozygosity may be as high as 3%. Symptoms may be linked to altered uracil, thymine, or ß-alanine homeostasis. Because ß-alanine is a structural analog of -aminobutyric acid and glycine, it has been proposed that it may affect inhibitory neurotransmission. DPD is the initial and rate-limiting enzyme in the inactivation of the antineoplastic drug 5- fluorouracil (5-FU), being responsible for 80% of its catabolism. Patients with partial DPD deficiency are at risk for developing a severe 5-FU–associated toxicity. In adult patients, neurotoxicity (headache, somnolence, visual illusions, memory impairment) linked to pyrimidinemia after 5-FU treatment for cancer is reported in previously healthy individuals., Epidemiology : 2 and 8 percent of the general population may be vulnerable to toxic reactions to fluoropyrimidine drugs caused by otherwise asymptomatic dihydropyrimidine dehydrogenase deficiency., variable, "Dihydropyrimidine dehydrogenase deficiency is inherited in an autosomal recessive pattern and therefore, it cant be prevented. ,,Although Genetic counselling is advisable.", Complications : seizures, intellectual disability, Diagnostics : SERUM URIC ACID, Urine analysis, Differential diagnosis : Metabolic disorders, disease description : Dihydropyrimidine dehydrogenase deficiency is an autosomal recessive metabolic disorder in which there is absent or significantly decreased activity of dihydropyrimidine dehydrogenase, an enzyme involved in the metabolism of uracil and thymine.Individuals with this condition may develop life-threatening toxicity following exposure to 5-fluorouracil (5-FU), a chemotherapy drug that is used in the treatment of cancer. Beside 5-FU, widely prescribed oral fluoropyrimidine capecitabine (Xeloda) could put DPD-deficient patients at risk of experiencing severe or lethal toxicities as well.

Dilated Cardiomyopathy

Disease Name : Dilated Cardiomyopathy, Treatment : medication : Carvedilol , Digoxin , Metoprolol , ventricular,assist device (VAD), total artificial heart, extracorporeal membrane oxygenation,(ECMO), and ultimately cardiac transplantation., PACEMAKERS(dual-chamber,and biventricular pacing therapy), Pathophysiology : The pathogenesis of the ventricular dilation and altered contractility seen in DCM varies depending on the underlying etiology; systolic dysfunction and myocyte injury are common. Genetic abnormalities of several components of the cardiac muscle, including sarcomere proteins, the cytoskeleton, and the proteins that bridge the contractile apparatus to the cytoskeleton, have been identified in autosomal dominant and X-linked inherited disorders. DCM can occur following viral myocarditis. Although the primary pathogenesis varies from direct myocardial injury to viral-induced inflammatory injury, the resulting myocardial damage, ventricular enlargement, and poor function likely occur by a final common pathway similar to that in genetic disorders. In 20–50% of cases, the DCM is familial with autosomal dominant inheritance most common. Duchenne and Becker muscular dystrophies are X-linked cardiomyopathies that account for 5–10% of DCM cases. These dystrophinopathies result in an abnormal sarcomere cytoskeleton connection, causing impaired myocardial force generation, myocyte damage/scarring, chamber enlargement, and altered function. Female carriers of dystrophinopathies may also manifest DCM. Mitochondrial myopathies , as with the muscular dystrophies, may present clinically with a predominance of extracardiac findings and are inherited in a recessive or mitochondrial pattern. Disorders of fatty acid oxidation present with systemic derangements of metabolism (hypoketotic hypoglycemia, acidosis, and hepatic dysfunction), some with peripheral myopathy and neuropathy, and others with sudden death or life threatening cardiac arrhythmias. Anthracycline cardiotoxicity (doxorubicin Adriamycin) on rare occasion causes acute inflammatory myocardial injury, but more classically results in DCM and occurs in up to 30% of patients given a cumulative dose of doxorubicin exceeding 550 mg/m2 . The risk of toxicity appears to be exacerbated by concomitant radiation therapy. Identifying methods to reduce toxicity and developing precision medicine approaches to identify and treat individuals at high risk are active areas of research., Epidemiology : younger than 18 yr is 0.57 cases per 100, 000 per year, AFTER SURGERY-5 YEAR SURVIVAL RATE=70-80%, It’s not always possible to prevent this condition, especially if it runs in your family or is a side effect of lifesaving care, like chemotherapy.,,However, certain causes are manageable. You may be able to prevent dilated cardiomyopathy by : ,,Avoiding cocaine.,Consuming alcohol in moderation.,Managing conditions like diabetes and high blood pressure.,Taking good care of your heart to prevent a heart attack., Complications : Cerebrovascular accident, sudden cardiac death, VALVULAR HEART DISEASE, Congestive heart failure, thromboembolism, Diagnostics : Complete Blood Count CBC, 2-D Echo, ECG, Radionuclide Imaging technique, X RAY CHEST, CARDIAC CATHETERIZATION, doppler echocardiography, X RAY, Differential diagnosis : Acute coronary syndromes, Acute Pericarditis, cardiac temponade, HYPERTENSIVE CARDIOMYOPATHY, restrictive cardiomyopathy, disease description : Dilated cardiomyopathy (DCM ), the most common form of cardiomyopathy in children, is the cause of significant morbidity and mortality as well as a common indication for cardiac transplantation. The etiologies are diverse. Unlike adult patients with DCM, ischemic etiologies are rare in children, although these include anomalous origin of the left coronary artery from the pulmonary artery, premature coronary atherosclerosis (homozygous familial hypercholesterolemia, rare genetic syndromic disease such as progeria), and coronary inflammatory diseases, such as Kawasaki disease. It is estimated that up to 50% of cases are genetic (usually autosomal dominant; some are autosomal recessive or Xlinked), including some with metabolic causes. Although the most common etiology of DCM remains idiopathic , it is likely that undiagnosed familial/genetic conditions and myocarditis predominate. The annual incidence of DCM in children younger than 18 yr is 0.57 cases per 100, 000 per year. Incidence is higher in males, blacks, and infants <1 yr old

Dimethylglycine Dehydrogenase Deficiency (dmgdhd)

Disease Name : Dimethylglycine Dehydrogenase Deficiency (dmgdhd), Treatment : nan, Pathophysiology : The exact pathophysiology of DMGDHD is not fully understood, but here is a general overview : Enzyme Deficiency : DMGDHD is caused by mutations in the DMGDH gene, which encodes the enzyme dimethylglycine dehydrogenase. This enzyme is responsible for the conversion of DMG to sarcosine in a step of the glycine degradation pathway. Mutations in the DMGDH gene lead to a deficiency or dysfunction of this enzyme, resulting in impaired DMG metabolism.DMG Accumulation : In individuals with DMGDHD, the impaired activity of dimethylglycine dehydrogenase leads to the accumulation of DMG and its derivatives, such as sarcosine and betaine, in various tissues and body fluids. The exact mechanisms of DMG accumulation and its impact on cellular processes are not fully understood.Disrupted Cellular Processes : Elevated levels of DMG and its derivatives can disrupt various cellular processes. DMG is known to act as a competitive inhibitor of certain enzymes involved in folate metabolism, which can affect the production of essential molecules like methionine and S-adenosylmethionine (SAM). SAM is a crucial methyl donor involved in numerous biochemical reactions, including DNA and protein methylation. Disruptions in these processes can have wide-ranging effects on cellular function and metabolism., Epidemiology : Prevalence : <1 / 1 000 000;, variable, there are no known prevention methods, Complications : nan, Diagnostics : GENETIC TESTING, PLASMA CREATINE KINASE, Gas chromatography Mass spectrometry (GC-MS), Urine analysis, Differential diagnosis : nan, disease description : Dimethylglycine dehydrogenase deficiency (DMGDHD) is a rare autosomal recessive disorder characterized by fish odor, and unusual muscle fatigue with increased serum creatine kinase. Dimethylglycine dehydrogenase (DMGDH) is a mitochondrial matrix enzyme involved in the metabolism of choline.

Diphtheria

Disease Name : Diphtheria, Treatment : medication : Azithromycin , Erythromycin , DPT, DIPHTHERIA ANTITOXIN, 1- Procaine penicillin G, 600, 000 U IM q12hr until the patient can swallow comfortably;then oral penicillin V, 125–250 mg qid to complete a 14-day course.,2- Erythromycin, 500 mg IV q6h (for children : 40–50 mg/kg per day IV in two or four divided doses) until the patient can swallow comfortably; then 500 mg PO qid to complete a 14-day course, Pathophysiology : Exotoxin production is the primary mechanism by which the organism shows its typical clinical characteristics. Exotoxin is a single polypeptide consisting of two subunits; A and B. B subunit mediates the binding of the toxin to the receptor on the cell membrane. A subunit has an enzymatic property that cleaves nicotinamide from nicotinamide adenine dinucleotide (NAD), thus inhibiting protein synthesis by ADP-ribosylation of elongation factor 2 (EF-2). The host response to the bacteria results in the local inflammation in the throat and pharynx, forming a tough, gray pseudomembrane, which is the characteristic physical finding of the diseases., Epidemiology : 7321 diphtheria cases were reported in 2014, Variable, Yes. There are many different vaccines in the U.S. that are designed to stop diphtheria. Several of them protect you against multiple infections at once, such as pertussis (whooping cough) and tetanus as well as diphtheria. There are different immunization schedules for getting the series of shots, including booster shots after the first ones are given.,,In general, vaccine side effects might include fever, pain or redness at the needle site, and rarely, an allergic reaction to the vaccine itself., Complications : ENCEPHALITIS, myocarditis, PNEUMONIA, polyneuropathy, Pulmonary Embolism, renal failure, respiratory difficulties, Diagnostics : Complete Blood Count CBC, Bacteria Culture Test, SERUM ANTIBODY/TOXIN, THROAT SWAB CULTURE, PCR, Differential diagnosis : acute tonsillitis, agranulocytosis, infectious mononucleosis, tonsillitis, disease description : Diphtheria is a nasopharyngeal and skin infection caused by Corynebacterium diphtheriae. Toxigenic strains of C. diphtheriae produce a protein toxin that causes systemic toxicity, myocarditis, and polyneuropathy. The toxin is associated with the formation of pseudomembranes in the pharynx during respiratory diphtheria. While toxigenic strains most frequently cause pharyngeal diphtheria, nontoxigenic strains commonly cause cutaneous disease.

Diphyllobothriasis

Disease Name : Diphyllobothriasis, Treatment : medication : Praziquantel , Vitamin B12 / cyanocobalamin/mecobalamin/methylcobalamin, Pathophysiology : The life cycle of D. latum, as it relates to humans, begins when un-embryonated eggs are released into the feces of humans that were infected with the intestinal parasite. These eggs will become embryonated in water under appropriate conditions, with the process usually lasting 18 to 20 days. During this maturation process, oncospheres, which are the first larval forms of the tapeworm, materialize within the egg. The oncosphere is then covered by an outer envelope that contains cilia and is called a coracidium. This coracidium hatches from the egg in the surrounding water and becomes a free-swimming larval stage that subsequently goes on to attract the first intermediate host. The free-swimming coracidium is consumed by the first intermediate host. This is usually an aquatic arthropod, such as crustaceans from the subclass Copepoda.Next, within these copepods, the second larval stage of D. latum develops, called the procercoid. This occurs through a complex host of interactions where the coracidium penetrates the intestinal wall of the first intermediate host. This procercoid stage contains six embryonic hooks on its posterior appendage, which helps to anchor it. When the infected crustacean is ingested, usually by freshwater or marine fish, this second intermediate host now takes over as the site of further larval maturation. The ingestion of the copepod allows the procercoid larvae to be released, and they migrate to enter the tissues of the second intermediate host in order to develop into the third larval stage called the plerocercoid. This is the infective stage of the larvae, and when these smaller second intermediate hosts are consumed by larger fish, the plerocercoid will migrate to the musculature of these larger fishes. Human transmission occurs when humans consume these raw or undercooked fish that are infected with D. latum.In humans, the plerocercoid develops into mature tapeworms, which attach and reside in the intestine. The fecundity, which is the reproductive potential of these tapeworms, is extremely high, and one tapeworm is estimated to produce up to 1 million eggs per day. Once established, the tapeworm infection is postulated to induce changes in the concentration of several neuromodulators in the host tissue and serum. Additionally,  D. latum infection has been shown to cause structural changes locally, leading to altered gastrointestinal tract functioning by modulating the neuroendocrine response and causing enhanced secretion as well as changing gut motility. Additionally, studies have shown that damage caused by these infections is also mediated through induction of mast cell and eosinophilic granule cell degranulation, leading to the release of inflammatory cytokines. Infection with D. latum has also been shown to lead to anemia secondary to the dissociation of vitamin B12 from its intrinsic factor complex in the gut, which is due to the faster absorption rate of vitamin B12 by the tapeworm relative to the human gut.  , Epidemiology : 20 million people are thought to be infected worldwide.,Diphyllobothrium species are found worldwide, including foci in Europe, North and South America, and Asia., GOOD, To Do : infection can be prevented by heating fish to 54°C for 5 min or by freezing it at –18°C for 24 h. Placing fish in brine with a high salt concentration for long periods kills the eggs., Complications : cholangitis, cholecystitis, intestinal obstruction , MEGALOBLASTIC ANAEMIA, Diagnostics : Complete Blood Count CBC, EOSINOPHILS - ABSOLUTE COUNT, Peripheral Blood Smear, stool microscopy, HEMOGLOBIN, Differential diagnosis : Influenza, iron deficiency anemia, disease description : Diphyllobothriasis is the infection caused by tapeworms of the genus Diphyllobothrium (commonly D. latum and D. nihonkaiense).Diphyllobothriasis mostly occurs in regions where raw fish is regularly consumed; those who consume raw fish are at risk of infection. The infection is often asymptomatic and usually presents only with mild symptoms, which may include gastrointestinal complaints, weight loss, and fatigue. Rarely, vitamin B12 deficiency (possibly leading to anaemia) and gastrointestinal obstructions may occur. Infection may be long-lasting in absence of treatment. Diphyllobothriasis is generally diagnosed by looking for eggs or tapeworm segments in passed stool. Treatment with antiparasitic medications is straightforward, effective, and safe.

Dirofilariasis

Disease Name : Dirofilariasis, Treatment : Treatment is by surgical removal of the nodule, Pathophysiology : The dirofilarial life cycle, like that of all filarial and helminthic nematodes, consists of 5 developmental or larval stages in a vertebral host, an arthropod (mosquito) intermediate host, and a vector. Adult female worms produce thousands of first-stage larvae (microfilariae), which are ingested by a feeding insect vector. After ingestion, microfilariae eventually transform into third-stage larvae within the mosquito and migrate from the abdomen to the thorax and finally to the salivary glands, allowing transmission of infection to a new host upon a subsequent blood meal., Epidemiology : prevalence ranges from 4.7%-29.5%, Good, Dirofilariasis can be prevented by avoiding mosquito bites in areas where mosquitoes may be infected with Dirofilaria larvae. The risk of such mosquito bites can be reduced by leaving as little skin exposed as possible, by the use of insect repellent when exposed to mosquitoes, and by sleeping under an insecticide-treated bednet in areas where Dirofilaria-infected mosquitoes bite at night and have access to sleeping areas., Complications : MEGALOBLASTIC ANAEMIA, Diagnostics : Complete Blood Count CBC, X RAY CHEST, PCR, SPUTUM CYTOLOGY, Differential diagnosis : Ascariasis, mycotic infection, disease description : Dirofilariasis is the disease caused by Dirofilaria worm infections. In dogs, one form is called “heartworm disease” and is caused by D. immitis.  humans become infected with Dirofilaria through mosquito bites. In persons infected with D. immitis, dying worms in pulmonary artery branches can produce granulomas (small nodules formed by an inflammatory reaction), a condition called “pulmonary dirofilariasis.” The granulomas appear as coin lesions (small, round abnormalities) on chest x-rays. Most persons with pulmonary dirofilariasis have no symptoms.

Discoid Lupus Erythematosus.

Disease Name : Discoid Lupus Erythematosus., Treatment : Current first-line treatment for DLE consists of photoprotection in conjunction with topical or intralesional corticosteroids and topical calcineurin inhibitors.Chronic DLE lesions that are not responsive to topical therapy or have a widespread disease involvement are candidates for systemic therapy. When DLE is refractory to these measures, other agents with varying degrees of proven efficacy are used. Currently, no medications have been approved specifically, and many of the drugs described in the literature were developed for use in other autoimmune disorders., Pathophysiology : The pathogenesis of cutaneous lupus erythematosus is multifactorial, with an interplay between genetic and environmental factors. Some contributing environmental factors include ultraviolet radiation (UVR), medications, cigarette smoking, and possibly, viruses. The interaction between these multiple factors triggers an inflammatory cascade of cytokine, chemokine, and inflammatory cell responses. Genes previously associated with SLE are TYK2,  IRF5,  and CTLA4 and confer an increased risk of developing DLE.A recent study found a significantly higher level of anti-annexin 1 antibodies in DLE patients, suggesting that anti-annexin 1 antibodies might be a new diagnostic marker for DLE. Anti-annexin 1 antibodies level in the serum did not correlate with DLE activity , Epidemiology : SLE prevalence is four-fold higher in African-American women than White-race American women (4 in 1000 versus 1 in 1000). In addition, African-Americans tend to develop the disease at an earlier age and have a higher mortality rate, GOOD, Complications : nan, Diagnostics : HISTOPATHLOGY, DIRECT IMMUNOFLORESCENCE ASSAY, Differential diagnosis : Cutaneous Leishmaniasis, LUPUS VULGARIS, psoriasis, Sarcoidosis, TUBERCULOSIS, disease description : Lupus erythematosus is a multisystem disorder that predominantly affects the skin. There are several types of cutaneous lupus. The most common types are acute cutaneous lupus (ACLE), subacute cutaneous lupus (SCLE), and discoid lupus (DLE). The most common subset of chronic cutaneous lupus erythematosus is DLE. These patients may or may not report photosensitivity, but lesions are frequently photo distributed and tend to have secondary atrophy or scarring. Most patients with DLE do not have significant systemic disease. DLE can also occur as a manifestation of SLE in approximately 20% of patients.

Discoid Lupus Erythematosus

Disease Name : Discoid Lupus Erythematosus, Treatment : medication : Hydroxychloroquine , Chloroquine , Dapsone , Methotrexate, Acitretin, Auranofin, First line : , Topical therapy can frequently control and sometimes clear,lesions without the need for systemic treatment; 0.025% fluocinolone cream or 0.1% betamethasone 17-valerate cream alone,can be effective without inducing epidermal atrophy. Topical calcineurin inhibitors, such as,tacrolimus, provide a useful alternative to corticosteroids in those,with localized disease.,,Second line : , For patients with severe, extensive or scarring disease, particularly,affecting the scalp, oral prednisolone is often the most helpful initial treatment. A dosage of 0.5 mg/kg, rapidly tapered over 6 weeks,is quickly effective, minimizes scarring and allows the slower acting agents such as antimalarials to work. Methylprednisolone 500–1000 mg/day for 2,or 3 days, given as an intravenous pulse therapy, may help resistant lesions.Most would start therapy with hydroxychloroquine, initially at 200 mg twice daily, reducing to 200 mg/day,once a response is achieved.,,Third line : , For cases not responding to topical steroids, antimalarials and,sunscreens, oral thalidomide, methotrexate and mycophenolate,are the most effective third line agents., Pathophysiology : The pathogenesis of cutaneous lupus erythematosus is multifactorial, with an interplay between genetic and environmental factors. Some contributing environmental factors include ultraviolet radiation (UVR), medications, cigarette smoking, and possibly, viruses. The interaction between these multiple factors triggers an inflammatory cascade of cytokine, chemokine, and inflammatory cell responses. Genes previously associated with SLE are TYK2,  IRF5,  and CTLA4 and confer an increased risk of developing DLE.An analysis of 405 patients by Bockle et al. found that smoking is highly associated with discoid lupus erythematosus. Bockle et al. hypothesized that smoking might play a pathogenic role in cutaneous lupus erythematosus variants (DLE, tumid lupus) by inducing apoptosis, stimulating T-cell proliferation, and increasing photosensitivity. Another explanation might be that smoking provokes DNA damage, resulting in the formation of DNA adducts and the production of ds-DNA antibodies. Keratinocytes may also participate in lupus skin damage by increasing the apoptotic rate and the production of proinflammatory cytokines such as IFN-alpha and IL-6 for SLE and IFN-lambda for DLE., Epidemiology : 17-48 cases per 100, 000 population. T, the incidence of cutaneous lupus was 4/100 000, , variable, There is no way to prevent lupus. If you have discoid lupus, you can manage symptoms by avoiding sun exposure. To reduce chances of infection and scarring, you should avoid scratching or picking at sores., Complications : arthritis, myositis, pancytopenia, thromboembolism, Diagnostics : ANA, Complete Blood Count CBC, URINE R/M, full thickness skin biopsy, Differential diagnosis : nan, disease description : DLE is a benign inflammatory disorder of the skin, most frequently involving the face and scalp, and characterized by well-defined red, scaly patches of variable size, which heal with atrophy, scarring and pigmentary changes. The disease may also be more generalized, affecting areas away from the face and scalp. The histology is characteristic. There are haematological and serological changes in approximately half of patients, and these changes, with other evidence, suggest an autoimmune aetiology. The condition forms one end of a spectrum of skin and internal organ disease, ending with SLE.

Dislocation Of The Metacarpo-phalangeal Joints

Disease Name : Dislocation Of The Metacarpo-phalangeal Joints, Treatment : Nonoperative,closed reduction,indications,simple dislocations, Operative,open reduction ,indications,complex dislocations/delayed presentation, Pathophysiology : Pathophysiology  - Mechanism of injury : usually a fall on outstretched hand leading to hyperextension of MCP joint leads to avulsion of the volar plate from metacarpal neck.Associated conditions- metacarpal and phalanx fractures.Fractures of the base of proximal phalanx or metacarpal head seen in up to 50%., Epidemiology : Incidence,rare,< 1 per 100, 000 annually, good, Although no studies exist with regard to efficacy, most practitioners recommend appropriate buddy taping of the injured finger to an uninjured digit during forceful activities, especially contact sports, to help prevent reinjury., Complications : joint stiffness, Diagnostics : X RAY, PHYSICAL EXAMINATION, Differential diagnosis : bone fractures, Contusion, injury, disease description : These are uncommon injuries, resulting from hyperextension of the metacarpo-phalangeal (MP) joint, so that the head of the metacarpal button-holes through the volar capsule. The MP joint of the index finger is affected most commonly. MCP Dislocations are a dislocation of the metacarpophalangeal joint, usually dorsal, caused by a fall and hyperextension of the MCP joint.

Dislocation Of The Patella

Disease Name : Dislocation Of The Patella, Treatment : reduction,and immobilisation in a cylinder cast or knee,immobiliser for 3 weeks. A piece of bone covered,with articular cartilage (osteochondral fragment), ,may be shaved off from the patella or the femoral,condyle at the time of dislocation, Pathophysiology : Patellar dislocations tend to occur in a lateral direction, partly because the direction of pull of the quadriceps muscle is slightly lateral to the mechanical axis of the limb. Medial instability is rare and more likely to result from congenital conditions, quadriceps atrophy, or iatrogenically. Intra-articular dislocation is also uncommon, but can occur following trauma where the patella is avulsed from the quadriceps tendon and is then rotated. Superior dislocations can occur in elderly patients where forced hyperextension causes the patella to lock on an anterior femoral osteophyte., Epidemiology : Incidence is reported as 5.8 per 100, 000 but could be as high as 29 per 100, 000 in the adolescent population, good, All dislocations stretch the ligaments and deteriorate the cartilage of the joint to some extent. Once your patella has dislocated, it’s more likely to happen again if it’s similarly injured. Accidents are hard to prevent, but sometimes there are contributing factors that we can try to reduce. Depending on what made your patella dislocate in the first place, you may want to take one or several of these preventative measures : ,,Diligent rehabilitation. The most important thing you can do to avoid a recurrent patella dislocation is to recover fully from your first one. That means following through with physical therapy as prescribed and making sure not to try and use the leg too much too soon. Give it the time and attention it needs to heal as well as it can.,Leg muscle conditioning. Systematically strengthening each of the different muscle groups that stabilize the knee can help ensure that no one muscle group is carrying too much stress. Stretching is also important, to ensure that each muscle group is offering the full range of mobility that it should. A physical therapist or personal trainer can help set you on the right course for a lifelong practice.,Proper athletic form. If you’re an athlete, you might want to have a specialist analyze the way you practice certain movements and exercises and make sure that your form is correct. Practicing with incorrect form can put repetitive stress on your muscles and joints.,Surgery. If you have anatomical factors contributing to patellar instability, it might be worth considering surgery to help fortify the knee. Consult your healthcare provider to find out if you are a good candidate for reconstructive surgery., Complications : infection, joint stiffness, recurrence, Diagnostics : MRI, X RAY, CT SCAN, Differential diagnosis : injury, injury, MENISCAL INJURIES OF THE KNEE, disease description : Acute patellar dislocations typically occur as a result of trauma, usually a non-contact twisting injury to the knee, or from a direct blow to the medial aspect of the knee. A common mechanism is external tibial rotation with the foot fixed on the ground. Patellar dislocations can also occur in patients with generalized ligamentous laxity. However, those patients mostly tend to have recurrent subluxations of their patella as opposed to a frank dislocation The patella usually dislocates laterally. It can be one of three types : (i) acute dislocation; (ii) recurrent dislocation; and (iii) habitual dislocation. Acute dislocation of the patella results from a sudden contraction of the quadriceps while the knee is flexed or semi-flexed. The patella dislocates laterally and lies on the outer side of the knee.

Dislocation Of The Shoulder

Disease Name : Dislocation Of The Shoulder, Treatment : "reduction under,sedation or general anaesthesia, followed by,immobilisation of the shoulder in a chest-arm,bandage for three weeks. After the bandage is,removed, shoulder exercises are begun.,TECHNIQUES OF REDUCTION OF SHOULDER DISLOCATION,1- Kochers manoeuvre,2- Hippocrates manoeuvre", Pathophysiology : A fall on an out-stretched hand with the shoulder abducted and externally rotated, is the common mechanism of injury. Occasionally, it results from a direct force pushing the humerus head out of the glenoid cavity. A posterior dislocation may result from a direct blow on the front of the shoulder, driving the head backwards. More often, however, posterior dislocation is the consequence of an electric shock or an epileptiform convulsion. Pathological changes : The following pathological changes occur in the commoner, anterior dislocation : a) Bankarts lesion : Dislocation causes stripping of the glenoidal labrum along with the periosteum from the antero-inferior surface of the glenoid and scapular neck. The head thus comes to lie in front of the scapular neck, in the pouch thereby created. In severe injuries, it may be avulsion of a piece of bone from antero-inferior glenoid rim, called bony Bankart lesion. b) Hill-Sachs lesion : This is a depression on the humeral head in its postero-lateral quadrant, caused by impingement by the anterior edge of the glenoid on the head as it dislocates. c) Rounding off of the anterior glenoid rim occurs in chronic cases as the head dislocates repeatedly over it. d) There may be associated injuries : like fracture of greater tuberosity, rotator-cuff tear, chondral damage etc., Epidemiology : more common in teens than younger children., 23.9 per 100, 000 person years, and approximately 85-98% of shoulder dislocations are anterior dislocations., Fair, You can’t always prevent a dislocated shoulder. It usually happens because of unexpected accidents and trauma.,,During sports or other physical activities : ,,Wear the right protective equipment.,Don’t “play through the pain” if your shoulder hurts during or after physical activity.,Give your body time to rest and recover after intense activity.,Stretch and warm up before playing sports or working out.,Cool down and stretch after physical activity.,Follow these general safety tips to reduce your risk of an injury : ,,Make sure your home and workspace are free from clutter that could trip you or others.,Always use the proper tools or equipment at home to reach things. Never stand on chairs, tables or countertops.,Use a cane or walker if you have difficulty walking or have an increased risk of falls., Complications : JOINT DISLOCATION, NERVE INJURY, Diagnostics : MRI, X RAY, CT SCAN, Differential diagnosis : CLAVICLE FRACTURE, Tendonitis, disease description : A dislocated shoulder is an injury in which the upper arm bone pops out of the cup-shaped socket thats part of the shoulder blade. The shoulder is the bodys most flexible joint, which makes it more likely to dislocate.Shoulder dislocation can also cause numbness, weakness or tingling near the injury, such as in the neck or down the arm. The muscles in the shoulder might spasm, which can increase the pain.

Disorders Of Purine Metabolism

Disease Name : Disorders Of Purine Metabolism, Treatment : medication : Allopurinol , The treatment for a disorder of purine or pyrimidine metabolism depends on the specific enzyme deficiency or superactivity. ,,1. ADA : bone marrow transplantation and enzyme replacement with PEG-ADA. There are current gene therapies for patients with ADA. Results to this point have been encouraging.,2. Adenosine monophosphate deaminase deficiency is treated with ribose and xylitol., Pathophysiology : Mutations in a large number of genes can lead to disorders of purine and pyrimidine metabolism by causing a loss of function of necessary enzymatic activity., Epidemiology : 3.9%, roughly 1–2% of the population, Variable, Prenatal counseling and testing of known carrier parents.,,Avoidance of foods and medications containing offending substrates, Complications : recurrence, Diagnostics : Complete Blood Count CBC, SERUM URIC ACID, GENETIC TESTING, ammonia level, Differential diagnosis : genetic disorders, hematologic abnormalities, Metabolic disturbances, nephrolithiasis, disease description : The purines are a group of molecules used by all cells of the body for many essential biochemical processes. They are synthesized by a multistep pathway known as the de novo synthetic pathway, they pass through several steps where they may be interconverted, and ultimately they are degraded and excreted as uric acid (Fig. 187.1). An example purine is adenosine triphosphate (ATP), which is required for many energy-requiring enzymatic reactions. ATP and guanosine triphosphate (GTP) also serve as building blocks for the synthesis of DNA and RNA. Some purine molecules, such as nicotinamide adenine dinucleotide (NAD) and flavin adenine dinucleotide (FAD), serve as cofactors that are used in other reactions. The cyclic nucleotides, cAMP and cGMP, play a key role in many intracellular signaling pathways.

Disseminated Lntravascular Coagulopathy

Disease Name : Disseminated Lntravascular Coagulopathy, Treatment : In snake bites anti-snake venom should be administered. In,patients who have low levels of platelets, fibrinogen and,other clotting factors as revealed by deranged coagulation,tests, replacement of deficient components is useful.,Replacement therapy is not indicated if there is no clinical,bleeding and if no invasive procedures are planned., The different blood components available and commonly,used in DIC are : fresh frozen plasma, cryoprecipitate, ,platelet concentrates and packed red cells, Pathophysiology : There are three main pathologic processes involved. Initiation of fibrin deposition Thrombin generation in DIC is mediated by the extrinsic (tissue factor) pathway. The tissue factor accumulates on activated platelets by binding to platelet P-selectin which results in thrombin generation. Amplification role of thrombin Thrombin generated amplifies inflammation and clotting by activating platelets and factors V, VIII and IX, which lead to more thrombin production. Activated factor XIII leads to it cross-linking with fibrin clots making them insoluble, while thrombin activates the fibrinolysis inhibitor, making the clot resistant to fibrinolysis. Propagation of fibrin deposition There is suppression of fibrinolysis secondary to sustained increase in plasma levels of plasminogen-activator inhibitor. Following injury, infection or other precipitating factors, there is release of cytokines (tumor necrosis factor alpha, IL-1 and IL-6) which change the endothelium from an anticoagulant to a procoagulant surface and interfere with fibrinolysis. As DIC continues, fibrinogen, prothrombin, platelets and other clotting factors are consumed beyond the capacity of the body to compensate and bleeding ensues. Activated protein C has an anti-inflammatory effect; it downregulates the tissue factor and decreases calcium ion flux., Epidemiology : DEPENDS ON SEVERITY OF SYMPTOMS, Complications : Bleeding complications, Infarction, Diagnostics : APTT, Peripheral Blood Smear, PLASMA FIBRINOGEN, PLATELET COUNT, PLASMA D DIMER ELISA, PROTHROMBIN TIME(PT), Differential diagnosis : Hemolytic anemia, hemophilia A and B, thrombocytopenia, disease description : Disseminated intravascular coagulation (DIC) is an acquired dysregulation of hemostasis. The presentation ranges from an isolated derangement of laboratory parameters to severe bleeding from multiple sites, associated with high mortality. DIC may be triggered by a variety of conditions that result in activation of the clotting cascade, deposition of fibrin in the microcirculation and consumption of platelets and clotting factors. The diagnosis of DIC is clinical laboratory tests provide confirmatory evidence.

Dissociation

Disease Name : Dissociation, Treatment : EMDR therapy : Eye movement desensitization and reprocessing (EMDR) therapy involves moving your eyes a specific way while you process traumatic memories. EMDR’s goal is to help you heal from trauma or other distressing life experiences. Compared to other therapy methods, EMDR is relatively new., Hypnosis : Hypnosis (hypnotherapy) is a state of deep relaxation and focused concentration. When you’re under hypnosis, this intense level of concentration and focus allows you to ignore ordinary distractions and be more open to guided suggestions to make changes to improve your health., Treatment of dissociative disorders usually consists of psychotherapy (talk therapy) to help you gain control over the dissociative process and symptoms.,,Specific types of psychotherapy commonly used for dissociative disorders include : ,1. Cognitive behavioral therapy (CBT),2. Dialectical behavior therapy (DBT), No specific medications treat dissociative disorders. But your provider may recommend certain medications, such as antidepressants, to treat co-occurring mental health conditions., Pathophysiology : The DID person, per the International Society for the Study of Trauma and Dissociation,  is described as a person who experiences separate identities that function independently of each other and are autonomous of each other. The International Society describes alternate identities or alters as independent identities which have their own distinct behaviors, have memories that are distinct from others, and even may differ in language and expressions used. Signs of a switch to an altered state include trance-like behavior, eye blinking, eye-rolling, and changes in posture. The major hypothesis by Putnam et al. is that “alternate identities result from the inability of many traumatized children to develop a unified sense of self that is maintained across various behavioral states, particularly if the traumatic exposure first occurs before the age of 5 “. The theories have been studied by groups in the inpatient unit services in the 1990s., Epidemiology : prevalence ranged from 4.6% to 46%, 1.5% of the global population., Variable, This page offers some practical suggestions for helping you cope with dissociation, such as : ,,1. Keep a journal,2. Try visualisation,3. Try grounding techniques,4. Think about practical strategies,5. Make a personal crisis plan,6. Talk to people with similar experiences ,7. Look after your wellbeing,8. Dealing with stigma,,Having a psychologist or counselling professional is pinnacle to increase the chances of recovery from trauma-induced dissociation., Complications : recurrence, Diagnostics : CT HEAD, PHYSICAL EXAMINATION, Differential diagnosis : Borderline Personality Disorder, Schizophrenia, disease description : Dissociative disorders are a range of conditions that can cause physical and psychological problems.Some dissociative disorders are very shortlived, perhaps following a traumatic life event, and resolve on their own over a matter of weeks or months. Others can last much longer. Dissociative disorders are mental health conditions that involve feelings of being detached from reality, being outside of your own body or experiencing memory loss (amnesia).The word “dissociation” means to be disconnected from others, from the world around you or from yourself.Dissociative disorders typically develop after short-term or long-term trauma.

Distal Renal Tubular Acidosis

Disease Name : Distal Renal Tubular Acidosis, Treatment : medication : Hydrochlorothiazide , Sodium bicarbonate , Vitamin D Substances, The base requirement for distal RTAs is generally in the range of 2-4,mEq/kg/24 hr, although individual patients’ requirements can vary, Pathophysiology : Distal RTA can be sporadic or inherited. It can also occur as a complication of inherited or acquired diseases of the distal tubules. Primary or secondary causes of distal RTA can result from damaged or impaired functioning of one or more transporters or proteins involved in the acidification process, including the H+ /ATPase, the HCO3 - /Cl- anion exchangers, or the components of the aldosterone pathway. Because of impaired hydrogen ion excretion, the urine pH cannot be reduced to < 5.5, despite the presence of severe metabolic acidosis. Loss of sodium bicarbonate distally, owing to lack of H+ to bind to in the tubularlumen , results in increased chloride absorption and hyperchloremia. Inability to secrete H+ is compensated for by increased K+ secretion distally, leading to hypokalemia. Hypercalciuria is usually present and can lead to nephrocalcinosis or nephrolithiasis. Chronic metabolic acidosis also impairs urinary citrate excretion. Hypocitraturia further increases the risk of calcium deposition in the tubules. Bone disease is common, resulting from mobilization of organic components from bone to serve as buffers to chronic acidosis., Epidemiology : 0.46/10, 000 inhabitants., 10 in 100, 000 population., GOOD, There is no prevention for this disorder., Complications : nephrolithiasis, Pyelonephritis, MEDULLARY SPONGE KIDNEY, Diagnostics : serum potassium K+, GENETIC TESTING, URINARY CALCIUM CA++, URINE pH Level, URINARY CITRATE LEVEL, X RAY, USG, Urine analysis, Differential diagnosis : cystinosis, multiple myeloma, Sjogren syndrome, Tyrosinemia I, II, III, WILSONS DISEASE, disease description : Renal tubular acidosis (RTA) is a disease state characterized by a non–anion gap (hyperchloremic) metabolic acidosis in the setting of a normal or near-normal glomerular filtration rate. There are four main types : proximal (type II) RTA, classic distal (type I) RTA, hyperkalemic (type IV) RTA, and a combined proximal and distal (type III). Proximal RTA results from impaired bicarbonate reabsorption and distal RTA from failure to secrete acid. Either of these defects may be inherited and persistent from birth or acquired, as is seen more commonly in clinical practice.