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Distichiasis

Disease Name : Distichiasis, Treatment : Management is by lid splitting with,cryotherapy to the base of the hair follicles., "Epilation. The extra eyelashes are plucked. This is a temporary treatment because the lashes will grow back.,,Lid splitting. In this surgical procedure, your doctor will split your eyelid open so the follicles of your eyelashes are exposed. Then, theyll remove the extra eyelashes. In many cases, youd get this along with cryotherapy or electrolysis", Pathophysiology : Congenital distichiasis is a rare anomaly in which an extra row of cilia occupies the position of Meibomian glands which open into their follicles as ordinary sebaceous glands. These cilia are usually directed backwards and when rubbing the cornea, should be electroepilated or cryoepilated. Acquired distichiasis (metaplastic lashes) occurs when due to metaplasia and differentiation, the meibomian glands are transformed into hair follicles. The most important cause is late stage of cicatrizing conjunctivitis associated with chemical injury, Stevens-Johnson syndrome and ocular cicatricial pemphigoid.Distichiasis can affect the lower and upper lids. When these abnormal lashes come in contact with the cornea, they may cause severe irritation, epiphora, corneal abrasion, or even corneal ulcers., Epidemiology : 1 in 10, 000 people., Fine lashes are usually well tolerated., You can’t prevent congenital distichiasis. You may want to consult a genetic counselor if you have lymphedema distichiasis syndrome.,,You may be able to prevent getting distichiasis as a result of chemical burns or other injuries to your eye if you wear proper protective equipment when working with chemicals or with equipment related to fires., Complications : Lid margin is outrolled, Diagnostics : Slit lamp examination, PHYSICAL EXAMINATION, fluorescein staining, Differential diagnosis : ENTROPION, trichiasis, disease description : This is a rare condition in which there is an extra posterior row of cilia, occasionally in all four lids. The posterior row occupies the position of the meibomian glands which are reduced to ordinary sebaceous glands performing the normal function of lubricating the hair; these lashes may irritate the cornea.

Disturbances Of Oculo-motor Function

Disease Name : Disturbances Of Oculo-motor Function, Treatment : Includes a form of vision therapy involving specific neuro-optometry activities designed to improve fixation, strengthen your visual muscles, saccadic and pursuit eye movements, as well as improve information processing skills., Treatment may also include lenses, prisms, and special tints to prescription eyewear for symptomatic relief during and after treatment., Pathophysiology : Oculomotor Dysfunction is a relatively common visual condition that can affect individuals of all ages, usually due to a developmental delay or a result of a concussion (mTBI) or more serious traumatic brain injury (TBI). Without treatment, those with this condition typically develop or rely on compensatory techniques, such as using a finger as a marker while reading.Oculomotor Dysfunction (OMD) is also known as Ocular Motility Dysfunction and is characterized by a deficiency in one or more of the following visual skills : Fixation : the ability to “hold” the eyes steady without moving off the targetSaccadic eye movements : the ability of the eyes to accurately “jump” from one target to anotherPursuit eye movements : the ability of the eyes to accurately “follow” a moving target, Epidemiology : 4.0 per 100 000., good, exercising them can help them perform better. As a result, vision therapy is one of the best treatments for ocular motor dysfunction. Vision therapy allows you to practice new skills to strengthen eye muscles’ ability to work together effectively., Complications : severe headache, blurred or unstable vision, Diagnostics : MRI, ophthalmoscopy, Cover-uncover test, Extra Ocular muscle function test, Field of binocular fixation, Differential diagnosis : injury, stroke, disease description : It is a common vision problem that occurs when there is a developmental delay, trauma to the brain, or disease that affects the central nervous system and interferes with the brain’s ability to coordinate the eyes to move with accuracy and control. This condition can affect reading, balance, depth perception, and most visually related tasks. Oculomotor Dysfunction affects patients of all ages, both children and adults.It is not a condition that can be outgrown. If left untreated, Oculomotor Dysfunction patients will rely on compensatory techniques such as using a finger as a marker for reading or tilting the head to direct the eyes. It is important to note that many children are misdiagnosed with Dyslexia as Oculomotor Dysfunction and Dyslexia share many of the same symptoms. However, Oculomotor Dysfunction is a result of an anomaly within the vision system.

Divergent Squint

Disease Name : Divergent Squint, Treatment : 1. Spectacles with full correction of refractive error,should be prescribed in every case. 2. Occlusion therapy, Squint surgery. It is required in most of the cases,to correct the deviation., Pathophysiology : The exact pathophysiology of congenital exotropia is not well known. But strabismus is very commonly seen to run in families, which points towards an autosomal dominant inheritance pattern. The exodeviations are related to the excessive divergence tone that may exceed the convergence tone, leading to drifting of eyes outwards. The deviations often start as an exophoria. In this stage, the eyes are well aligned most of the time, and an exodeviation is noted only on breaking the fusion with a cover test. Patients have good bifoveal fixation in this stage.In due course of time, these patients often progress to intermittent exotropia. In the stage of intermittent exotropia, eyes are well aligned most of the time and dissociate spontaneously, especially when the patient is daydreaming or physically or mentally exhausted. The next stage is of constant exotropia, in which the patient is not able to fuse at a single object with both his eyes at one point., Epidemiology : prevalence of exotropia as 1.23%., incidence of 64.1/100, 000 patients younger than 19 years., Variable, You can’t prevent exotropia., Complications : blurred vision, Diagnostics : FUNDOSCOPY, VISUAL ACUITY TEST, Perimetry, Extra Ocular muscle function test, Pupillary reactions, Cover tests, Hirschberg corneal reflex test, The prism and cover test, Krimsky corneal reflex test, Measurement of deviation with synoptophore, Worth’s four-dot test, Tests for fixation, Differential diagnosis : MYASTHENIA GRAVIS, myositis, Paralysis, Third nerve palsy, THYROID EYE DISEASE, disease description : Exotropia is the outward deviation of eyes, i.e., away from the nose. Exodeviations can be congenital or acquired. These can be concomitant or incomitant. Concomitant deviation means that the divergent deviation of the visual axis remains the same in all positions of gaze. Incomitant deviation implies that the divergent deviation of the visual axis is variable in different gazes. These are often associated with the limitation of extraocular movements resulting either from paralytic or a restrictive etiology. The concomitant exotropia is further divided into congenital, primary, sensory, or consecutive exotropia.

Diverticulitis

Disease Name : Diverticulitis, Treatment : Taking over-the-counter medications for pain and following a low-fiber diet or a liquid diet may be recommended until your symptoms improve. Once your symptoms improve, you can slowly return to soft foods, then a more normal diet, which should be one that includes many high-fiber foods. You and your healthcare provider will discuss the specifics of your treatment plan., Mild diverticulitis : oral antibiotic, such as metronidazole (Flagyl®), trimethoprim-sulfamethoxazole (Bactrim®), ciprofloxacin (Cipro®) or amoxicillin and clavulanic acid (Augmentin®)., If your diverticulitis is SEVERE , you have rectal bleeding or are having a repeat bout of diverticulitis, you may be admitted to the hospital to receive intravenous (IV) antibiotics, IV fluids or possibly be considered for surgery., Pathophysiology : Diverticulitis is the result of microscopic and macroscopic perforations of the diverticular wall. Previously, practitioners thought that obstruction of colonic diverticulum with fecaliths led to increased pressure within the diverticulum and subsequent perforation. They now theorized that increased luminal pressure is due to food particles that lead to erosion of the diverticular wall. This causes focal inflammation and necrosis of the region, causing perforation. Surrounding mesenteric fat may easily contain micro-perforations. This can result in local abscess formation, fistulization of adjacent organs, or intestinal obstruction. Ultimately, frank bowel wall perforations can lead to peritonitis and death without rapid diagnosis and treatment., Epidemiology : 10% to 25%., Depends on age at presentation, the presence of co, Healthcare providers don’t know enough about why diverticulitis happens or why it returns to know definitively how to prevent it. But they suspect that general bowel wellness can help. Eating more plants and fewer animal fats, drinking enough water and getting some regular exercise can help keep your bowel movements healthy. For some people, they might recommend fiber supplements or probiotics.,,In the past, people with diverticulosis were told to avoid seeds and nuts, in case one might get stuck in a diverticulum and cause diverticulitis. This risk is considered mostly a myth today. Seeds and nuts are great sources of fiber and plant-based protein, and they tend to appear in healthy meals. It’s much better for your bowels to maintain a healthy diet overall than to worry about the rare chance of a seed going awry., Complications : Bowel obstruction, intestinal perforation, peritonitis, sepsis, pelvic abscess, Diagnostics : Total Leucocyte Count (TLC), colonoscopy, X-RAY Abdomen, MRI, CT SCAN, USG, Differential diagnosis : Acute Appendicitis, acute cholecystitis, Acute Pancreatitis, cholangitis, constipation, Crohns Disease, disease description : An inflammation due to micro-perforation of a diverticulum. The diverticulum is a sac-like protrusion of the colon wall. Diverticulitis can present in about 10% to 25% of patients with diverticulosis. Diverticulitis can be simple or uncomplicated and complicated. Uncomplicated diverticulitis is without any associated complications. Complicated diverticulitis is associated with the formation of abscess, fistula, bowel obstruction, or frank perforation. Diverticulitis has conventionally been known and treated as a primarily surgical illness, but this has transitioned to be a medically managed entity even in its most acute phase.

Diverticulosis

Disease Name : Diverticulosis, Treatment : medication : Methotrexate, Administration of intramuscular methotrexate or performance of laparoscopic surgery is safe and effective treatment modalities in hemodynamically stable women with a non-ruptured ectopic pregnancy. The decision of which modality to pursue is guided by the patient’s clinical picture, their laboratory findings, and radiologic imaging as well as the patient’s well-informed choice after having reviewed the risks and benefits with each procedure. Patients with relatively low hCG levels would benefit from the single-dose methotrexate protocol. Patients with higher hCG levels may necessitate two-dose regimens. There is literature suggestive that methotrexate treatment does not have adverse effects on ovarian reserve or fertility. hCG levels should be trended until a non-pregnancy level exists post-methotrexate administration. Surgical management is necessary when the patients demonstrate any of the following : an indication of intraperitoneal bleeding, symptoms suggestive of ongoing ruptured ectopic mass, or hemodynamically instability., Surgical management including salpingostomy or salpingectomy should be guided by clinical status, the extent of fallopian tube compromise, and desire for future fertility. In simplest form salpingectomy involves removing the fallopian tube partially or in full. Salpingostomy, or salpingotomy, involves removal of the ectopic pregnancy via tubal incision while leaving the fallopian tube in situ., Pathophysiology : Heres an overview of the pathophysiology : Structural Changes : Diverticula develop due to structural changes in the colonic wall. The outer layer of the colon weakens, causing the inner layer to bulge out through the weak points, forming diverticula. These weak points are often located where blood vessels penetrate the colon wall.Increased Pressure : Increased pressure within the colon is considered a key factor in the development of diverticula. The pressure can be attributed to factors such as low-fiber diets and decreased motility of the colon. A low-fiber diet can result in smaller and harder stools, leading to increased pressure during bowel movements. Decreased motility or sluggish movement of the colon can also contribute to increased pressure and facilitate the formation of diverticula., Epidemiology : 20%, 10% in those younger than 40 years up to 50 to 70% in those older than 80 years., variable, Eating more plants and whole foods, getting regular exercise and drinking enough water each day will help keep your bowel movements healthy and regular. This may prevent diverticulosis. If you already have diverticulosis, it may prevent further diverticula from occurring. While it’s not guaranteed, these healthy lifestyle factors help to prevent most types of lower bowel disease., Complications : Abortion, vaginal bleeding, hemorrhage, Diagnostics : Complete Blood Count CBC, colonoscopy, USG, HISTORY TAKING, PHYSICAL EXAMINATION, Differential diagnosis : Acute Appendicitis, corpus luteal melanoma, FIBROID UTERUS, Pelvic Inflamatory Disease, Septic Abortion, Torsion or rupture of ovarian cyst, TUBO OVARIAN ABSCESS, URETERIC CALCULI, disease description : Diverticulosis occurs when small defects in the muscle of the wall of the large intestine or colon allow small pockets or pouches (diverticula) to form. Diverticulitis is infection or inflammation of these abnormal pouches. Together, these conditions are called diverticular disease.Diverticulosis is usually asymptomatic (has no symptoms). However, when many diverticula (pouches) are present, the normal smooth working of the bowel can be affected. This may cause a range of symptoms.

Donovanosis

Disease Name : Donovanosis, Treatment : medication : Azithromycin , Doxycycline , Erythromycin , Tetracycline , Sulfamethoxazole + Trimethoprim Co-trimoxazole , Azithromycin : Tablet\t1.00 - 0.00gm\tDaily 1 Days ON DAY 1.,Azithromycin : Tablet\t500.00 - 0.00mg\tDaily 7 Days\tAFTER DAY 1.,Sulfamethoxazole + Trimethoprim Co-trimoxazole : Tablet\t960.00 -0.00mg BD\t14 Days.,Doxycycline\t : Tablet 100.00 - 0.00\tmg\tBD 14 Days.,Erythromycin : Tablet 500.00 - 0.00\tmg\tQID\t14 Days IN PREGNENT WOMEN.,Tetracycline\t : Tablet 500.00 - 0.00mg\tQID\t14 Days., Pathophysiology : Donovanosis is a sexually transmitted infection that can rarely have non-sexual modes of transmission. It is classically associated with genital ulcers that demonstrate Donovan bodies on tissue smear samples The causative organism has been reclassified as Klebsiella granulomatis A lesion starts as a papule or subcutaneous nodule that later ulcerates after trauma. The incubation period is uncertain, but experimental infections in humans indicate a duration of ~50 days. Four types of lesions have been described : (1) the classic ulcerogranulomatous lesion, a beefy red ulcer that bleeds readily when touched; (2) a hypertrophic or verrucous ulcer with a raised irregular edge; (3) a necrotic, offensive-smelling ulcer causing tissue destruction; and (4) a sclerotic or cicatricial lesion with fibrous and scar tissue. The genitals are affected in 90% of patients and the inguinal region in 10%. The most common sites of infection are the prepuce, coronal sulcus, frenum, and glans in men and the labia minora and fourchette in women. Cervical lesions may mimic cervical carcinoma. In men, lesions are associated with lack of circumcision. Lymphadenitis is uncommon. Extragenital lesions occur in 6% of cases and may involve the lip, gums, cheek, palate, pharynx, larynx, and chest. Hematogenous spread with involvement of liver and bone has been reported., Epidemiology : There are about 100 cases reported per year in the United States., The present study showed an incidence of 1.53%, , NOT SPECIFIC, You can reduce your risk of donovanosis by : ,,Avoiding unprotected sex and multiple partners.,Making sure you get diagnosed and treated quickly for any STIs to stop the spread to others.,Using barrier protection like condoms or dental dams during any kind of sexual intercourse., Complications : polyarthritis, URETHRAL STRICTURE, Diagnostics : PAP SMEAR, PCR, INDIRECT IMMUNOFLORESCENCE ASSAY, TISSUE SMEAR, direct microscopy, Differential diagnosis : CANCER CERVIX, disease description : Donovanosis is a chronic, progressive bacterial infection that usually involves the genital region. The condition is generally regarded as a sexually transmitted infection of low infectivity. This infection has been known by many other names, the most common being granuloma inguinale.

Down Syndrome

Disease Name : Down Syndrome, Treatment : The parents of a child with Down syndrome should be,counseled with tact, compassion and truthfulness. Briefly,one should : (i) inform about the disorder as early as possible,after diagnosis is confirmed; (ii) counsel in presence of,both the parents in privacy; (iii) talk in simple and positive,language giving hope and allow sufficient time to the,parents to ask questions; (iv) discuss known problems and,associated disorders; (v) highlight the importance of early,stimulation; (vi) not discuss institutionalization and,adoption, wuess asked, and discourage both the options;,(vii) ask the parents to contact the local Down syndrome,association, if one exists; (viii) talk about genetics only after,chromosomal analysis; (ix) inform about recurrence risks,and possibilities of prenatal diagnosis; and (x) schedule,future appointments., There is no cure for Down syndrome, but treatment is available to help your child. Your child may need physical, occupational, and speech therapy to help with their development. Many children are helped with early intervention and special education., Pathophysiology : An extra copy of chromosome 21 is associated with Down syndrome, which occurs due to the failure of chromosome 21 to separate during gametogenesis resulting in an extra chromosome in all the body cells. Robertsonian translocation and isochromosome or ring chromosome are the other 2 possible causes of trisomy 21. Isochromosome is a condition when 2 long arms separate together instead of the long and short arm while in Robertsonian translocation. This occurs in 2% to 4% of the patients. The long arm of chromosome 21 is attached to another chromosome, mostly chromosome 14. In mosaicism, there are 2 different cell lines because of error of division after fertilization., Epidemiology : 1 in every 700 babies born., DEPENDS ON SEVERITY OF ASSOCIATED ABNORMALITIES, You can’t prevent Down syndrome since it’s a genetic condition. To learn more about your risk of having a child with a genetic condition, talk to your healthcare provider about genetic testing., Complications : Alzheimers Disease, conjunctivitis, infections, otitis media, rhinitis, Cardiovascular mortality, MALIGNANCY, Diagnostics : Karyotype, USG Obstetrics, X RAY, AMNIOTIC FLUID EXAMINATION, PHYSICAL EXAMINATION, chorionic villus sampling (CVS), blood test, Nuchal translucency test, Differential diagnosis : Congenital HYPOTHYROIDISM, trisomy 13/patau syndrome, trisomy 18/edward syndrome, Zellweger Syndrome, disease description : Down syndrome is a genetic disorder caused when abnormal cell division results in an extra full or partial copy of chromosome 21. This extra genetic material causes the developmental changes and physical features of Down syndrome.Down syndrome varies in severity among individuals, causing lifelong intellectual disability and developmental delays. Its the most common genetic chromosomal disorder and cause of learning disabilities in children. It also commonly causes other medical abnormalities, including heart and gastrointestinal disorders.

Dracunculiasis Dermatology

Disease Name : Dracunculiasis Dermatology, Treatment : medication : Metronidazole , The object of treatment is the removal of the worm. This is now facilitated by oral treatment with an oral benzimidazole, such as metronidazole. After a few days, the inflammation lessens and it may be ,possible to extract the worm gently. It may be difficult to extract the ,worm if mebendazole is used. The more traditional approach is ,to induce the worm to discharge larvae by applying water or ethyl ,chloride and to wind the free end around a matchstick or other small ,stick. By gradually winding more and more of the worm onto the ,spool, the whole nematode can be recovered., Pathophysiology : The adult female worm matures over a 1-year period in humans and discharges larvae through an ulcerated skin lesion. Millions of these larvae are produced, particularly on contact with water; these survive for 3–4 days and can develop further in copepods or water fleas (Cyclops spp. such as C. leukarti). After ingestion by the Cyclops, they pass through two developmental stages before reaching the infective third stage (L3) after 2 weeks. Humans are infected via drinking water containing infected Cyclops spp.; the larvae are released and penetrate the intestine. Further maturation occurs in the retroperitoneal space or other sites; mating occurs after about 3 months, and the males subsequently die. The females grow and migrate downwards, usually to the lower limbs. Aberrant migration can, however, occur. The female penetrates the skin of the leg and can then discharge larvae after exposure to water. Each female contains 2–3 million larvae. Migration of the worm and larval forms is largely subclinical. Disease is associated with the presence of the adult female in subcutaneous tissue in the lower limbs., Epidemiology : The disease is most prevalent in Sudan with over 5, Complications : secondary infection, Diagnostics : light microscopy, Differential diagnosis : CELLULITIS, FILARIASIS, disease description : Dracunculiasis is a chronic infection of humans due to the nematode, Dracunculus medinensis, which is among the longest nematodes infecting humans. Mature female worms migrate along subcutaneous tissue, forming a painful ulcerating blister.

Dracunculiasis

Disease Name : Dracunculiasis, Treatment : medication : Ibuprofen , Aspirin/Acetylsalicylic acid, Steps for worm extraction include : Exposing the affected body area to water facilitating the worm migration to the skin. The wound should then be cleaned. The worm should be slowly pulled out by applying gentle traction to the worm and should make sure to avoid breaking it. The worm is wrapped around a stick like a match stick or a gauze to apply tension and prevent it from going back inside. Topic antibiotics are used to avoid the development of secondary bacterial infections. Gauze and bandage are applied to the affected site., Pathophysiology : After ingestion of cyclops contaminated water, infected larvae released in the stomach penetrate the mucosa of the stomach and intestinal wall and migrate into the connective tissue. The larvae then mature into adult worms. After maturation and impregnation of the female worms, the male worms die. Female worms fully mature after 9 to 14 months and can measure up to 1 meter in length. Worms migrate through the subcutaneous tissue. Approximately after one year of infection, the female worms are attracted to the cooler surface of the skin and emerge from the skin, usually the feet. Before emerging, they form a painful blister at the skin site. Patients usually place or soak their legs in cold water to get relief from the symptoms, and this causes the worm to break from the blister and emerge from the skin., Epidemiology : 15% to 70%, 27 human cases reported in 2020, variable, The following can help prevent dracunculiasis : ,,Filtering drinking water through a piece of fine-mesh cheesecloth,Boiling water,Drinking only chlorinated water,Infected people are instructed not to enter sources of drinking water, such as open wells or reservoirs, so that these sources do not become contaminated., Complications : abscess, sepsis, Diagnostics : PHYSICAL EXAMINATION, MICROSCOPIC EXAMINATION, Differential diagnosis : nan, disease description : Dracunculiasis is an infection caused by a parasite called the Guinea worm. A person becomes infected when they drink contaminated water. This disease has been eliminated in most parts of the world, but still exists in Chad, Ethiopia, Mali and South Sudan. Usually the disease has no initial symptoms.

Drowning

Disease Name : Drowning, Treatment : medication : Phenobarbital/Phenobarbitone, Fosphenytoin , "Current recommendations state that rescue breaths should begin as soon as possible, and the breaths should be given with the patients their chin and airway extended when safe to do so. One recommendation is to start resuscitation with five rescue breaths instead of the usual two and to perform the rescue breaths before performing chest compressions.", Initial management of the patient includes delivering oxygen via nasal cannula, non-rebreather, non-invasive positive pressure ventilation, or endotracheal tube. Oxygen should be titrated to maintain oxygen saturation between 92% - 96% and to avoid over oxygenation. Nebulized albuterol may be given for bronchospasm. Cardiac support should be employed. Advanced cardiac life support (ACLS) protocol should be followed if needed. Infusion of crystalloids, and at times vasopressors, may be needed for refractory hypotension., Pathophysiology : When a person suffers from submersion or immersion in a liquid medium, vital tissues may become hypoxic and acidotic which may result in cardiac dysrhythmias (progressing from tachycardia, bradycardia, pulseless electrical activity, and asystole). Aspirated fluid can lead to surfactant washout and dysfunction, increased permeability of the alveolar-capillary membrane, decreased lung compliance, and ventilation/perfusion ratio mismatching. This can result from minor to no respiratory complaints to fulminant non-cardiogenic pulmonary edema, with a clinical picture similar to adult or acute respiratory distress syndrome (ARDS). The highest morbidity and mortality are related to cerebral hypoxia, and management is aimed at reversing hypoxia as quickly as possible. Interestingly, hypothermic exposure with the incident may be tissue-protective, although may result in an increased occurrence of cardiac dysrhythmias.Determination of the toxicity of the water that the victim was immersed in (eg saltwater versus freshwater) is of little importance in non-fatal drowning. Volume or serum (electrolyte) changes only occur when a significant volume of fluid is aspirated. It is more important to note if the fluid was obviously contaminated (sewage), as those patients are highly prone to pulmonary infection and prophylactic antibiotics may be warranted at presentation. Additionally, current recommendations state that routine use of cervical spine immobilization and imaging is not warranted unless the history or exam suggests that the patient suffered from a traumatic injury.At least 20% of individuals develop tight laryngospasm that lasts even after cardiac arrest. These victims seldom aspirate any fluid and are said to have dry drowning.The two major sequelae of drowning are to the CNS and cardiac system. Within 2 minutes most victims lose consciousness and within 4-6 minutes will develop irreversible brain injury. Global CNS hypoperfusion induces releases of excitotoxic neurotransmitters, free radicals, and lipid peroxidation. Cerebral edema followed by autonomic instability often results followed by ST-segment changes, indicating stress-related myocardial damage. The hypoxemia also induces ventricular arrhythmias and severe pulmonary hypertension., Epidemiology : 3, 500 to 4, 000 people drown per year., variable, 1. Learn basic swimming and water safety skills - ,Formal swimming lessons can reduce the risk of drowning. Children who have had swimming lessons still need close and constant supervision when in or around water.,,2. Build fences that fully enclose pools -,Construct and use a four-sided fence that is at least four feet in height and fully encloses the pool and separates it from the house, with self-closing and self-latching gates. Remove all toys from the pool area that might attract children to the pool when the pool is not in use.,,3. Supervise closely - ,Designate a responsible adult to supervise closely and constantly when children are in or near water (including bathtubs). You can assign a specific adult to supervise each child when they have access to water. Adults watching kids in or near water should avoid distracting activities like reading, using the phone, and consuming alcohol or drugs, because drowning happens quickly and quietly. After swim time is over, shut and lock doors that give access to water. Be proactive and learn about any risks when visiting another home or unfamiliar location. Adults should supervise children closely even when lifeguards are present.,,4. Wear a life jacket -,Life jackets reduce the risk of drowning while boating for people of all ages and swimming abilities. Life jackets should be used by children for all activities while in and around natural water. Life jackets can also be used by weaker swimmers of all ages in and around natural water and swimming pools. Do not rely on air-filled or foam toys, as these are not safety devices.,,5. Learn CPR - ,Your CPR skills could save someone’s life in the time it takes for paramedics to arrive. Many organizations such as American Red Cross and American Heart Association offer CPR training courses, both online and in-person.,,6. Know the risks of natural waters - ,Lakes, rivers, and oceans have hidden hazards such as dangerous currents or waves, rocks or vegetation, and limited visibility. Check the forecast before activities in, on, or near water. Local weather conditions can change quickly and cause dangerous flash floods, strong winds, and thunderstorms with lightning strikes.,,7. Avoid alcohol -,Avoid drinking alcohol before or during swimming, boating, or other water activities. Alcohol impairs judgment, balance, and coordination.9 Do not drink alcohol while supervising children.,,8. Use the buddy system - ,Always swim with a buddy. Choose swimming sites that have lifeguards when possible. The buddy system is especially beneficial for people with seizure disorders or other medical conditions that increase their risk of drowning.,,9. Take additional precautions for medical conditions - ,Know if your medical condition might increase your risk for drowning and take extra care. For example, if you or a family member have a seizure disorder like epilepsy, have one-on-one supervision around water. People with seizure disorders can also consider taking a shower rather than a bath. Take extra precaution around water if you or a family member has other conditions that can increase drowning risk, like heart conditions or autism.,,10. Consider the effects of medications -,Avoid swimming if you take medications that impair your balance, coordination, or judgement. These side effects increase the risk of drowning. Several medications can produce these side effects, such as those used for anxiety and other mental health conditions.,,11. Don’t hyperventilate or hold your breath for a long time -,Do not hyperventilate before swimming underwater or try to hold your breath underwater for long periods of time. This can cause you to pass out and drown. This is sometimes called “hypoxic blackout” or “shallow water blackout”., Complications : Cardiac arrest, Hypoxia, Respiratory arrest, Diagnostics : ABG PO2, PHYSICAL EXAMINATION, Diatom test, Electrolyte study, Differential diagnosis : abuse potential, Arrhythmias, Suicide attempt, disease description : Drowning is defined as a process of experiencing respiratory impairment from submersion/immersion in a liquid medium. To delineate the incidents outcome, this is further divided into descriptive terms such as death, morbidity, and no morbidity. Wet drowning, dry drowning, and near-drowning are no longer accepted terms, although they may still be used when discussing drowning.Drowning is a major public health problem, especially in children. Drowning usually occurs in a rapid fashion and is most often silent. Individuals who thrash wildy in water while drowning are rare. In most cases, a motionless individual floating in water who rapidly disappears beneath the surface is the classic scenario. Drowning can occur in both warm and cold water. In many cases, cold water can be protective especially in children. The most immediate threat in drowning is dysfunction of the cardiac and CNS systems. Hypoxemia and acidosis need to be corrected immediately if mortality is to be avoided. Even those who survive may develop a vegetative state due to the prolonged cerebral hypoxia.

Drug-induced Acneform Eruptions

Disease Name : Drug-induced Acneform Eruptions, Treatment : Drug withdrawal usually improves acneform eruptions, however ,such a decision needs to be balanced against the drug indication ,and/or if alternative agents are available. Topical and systemic ,medications used for acne vulgaris may be useful., Pathophysiology : Acneform eruptions are not hypersensitivity reactions. Pathological mechanisms vary according to the implicated agent. In acne vulgaris, Propionibacterium acnes facilitates inflammation through the binding of toll-like receptor 2 (TLR-2). Up-regulation of TLR-2 has been reported in human keratinocytes treated with glucocorticoids and this may explain why corticosteroid-associated acne consists of predominantly inflammatory lesions of papules and pustules . Androgenic hormones stimulate follicular keratinocyte proliferation, promote sebaceous gland hyperplasia and increase sebum production. Sirolimus may induce acneform lesions via direct toxicity, chemical modification of sebum or its effects on epidermal growth factor receptors (EGFR) and testosterone synthesis. Pathology There is variation in the histopathology of drug-induced acneform eruptions dependent on the underlying drug. In steroid-induced acne initial lesions show features of focal necrosis in the infundibulum of the follicular epithelium with a localized intrafollicular and perifollicular neutrophilic inflammatory reaction . EGFR- associated acneform eruptions are characterized by ectatic follicular infundibula with rupture of the epithelial lining associated with superficial neutrophilic folliculitis. History A drug-induced acneform eruption is to be suspected if the onset of acne is sudden and abrupt in the absence of past history of acne vulgaris. Other presentations include an unusually severe acne flare in a patient with a past history of mild acne vulgaris, or acne developing at an unusual age of onset . The latency between drug initiation and onset of acne varies between various types of drugs. Shorter latencies of 1 month or less have been reported with systemic corticosteroids , androgens and vitamin b; latencies of greater than 1 month are usually observed with ciclosporin 176, amineptine , lithium , anti-epileptics and anti-tuberculosis treatment . A characteristic papulopustular eruption may occur with EGFR inhibitors. The incidence ranges from 24 to 91%, being more common in monoclonal antibodies, such as cetuximab and panitumumab, compared to oral tyrosine kinase inhibitors such as erlotinib, gefitinib and lapatinib. Median latency from drug initiation to onset of acneform eruptions is 7–10 days, with the maximum severity being reached in the second week., Epidemiology : Acneform eruptions represent 1% of all drug-induce, Improves on withdrawal of the offending drug, Simply removing the offending agent or limiting exposure., Complications : blurred or unstable vision, KELOID, Diagnostics : biopsy, PHYSICAL EXAMINATION, Differential diagnosis : Acne vulgaris, folliculitis, disease description : Drug-induced acneform eruptions are inflammatory follicular reactions which resembles acne vulgaris. Clinically, monomorphic papules and pustules are seen and a variety of drugs have been implicated, including hormones, vitamins, halogens, neuropsychotherapeutic drugs, anti-tubercular treatments, immunomodulating agents, cytotoxic agents and newer targeted therapies.

Drug-induced Eczema

Disease Name : Drug-induced Eczema, Treatment : Antibiotics to treat bacterial infections,Topical corticosteroids, Lukewarm baths or showers using a non-soap cleanser,Emollients,Antibiotics to treat bacterial infections,Topical corticosteroids,Phototherapy,Immune-modulating medications, such as methotrexate., Phototherapy, Pathophysiology : The eczematous response is mediated by drug-specific T-cell induced inflammation in the skin. The principal histological features are dermatitic changes with spongiosis and a superficial perivascular infiltrate, primarily composed of mononuclear cells. Three primary pathophysiologic etiologies : (1) cutaneous immunomodulation, (2) skin dehydration, and (3) delayed hypersensitivity., Epidemiology : about 20% of children and up to 10% of adults, two cases per 1000 people, GOOD, Avoid irritants and allergens., Complications : recurrence, Diagnostics : Skin Biopsy With Immunofluorescence, HISTOLOGIC EXAMINATION, blood test, Differential diagnosis : allergic contact dermatitis, Idiopathic eczematous reactions, Irritant eczema, disease description : Eczematous drug eruptions are a heterogenous group of pruritic, eczematous reactions that occur after exposure to a variety of medications, even in patients without prior eczematous dermatitis. Some medications frequently implicated include calcium channel blockers, thiazides, anti-tumor necrosis factor (TNF)-alpha agents, the IL-23 inhibitors guselkumab and ustekinumab, antiviral medications (such as peginterferon / ribavirin and telaprevir), immunomodulatory agents (including everolimus, temsirolimus, and tacrolimus), chemotherapies (including the multikinase inhibitors sorafenib, regorafenib, and imatinib; the epidermal growth factor receptor EGFR inhibitors gefitinib, erlotinib, cetuximab, and panitumumab; and anti-PD-1 checkpoint inhibitors nivolumab and pembrolizumab), and intravenous immunoglobulin (IVIG).

Drug-induced Erythema Nodosum

Disease Name : Drug-induced Erythema Nodosum, Treatment : Pain management may include extended rest, colchicine (1–2 mg/day), NSAIDs (non-steroidal anti-inflammatory drugs), and venous compression therapy .,Systemic corticosteroids (1 mg/kg daily until resolution of erythema nodosum) may be prescribed if infection, sepsis, and malignancy have been ruled out .,Oral potassium iodide as a supersaturated solution (400–900 mg/day) may be prescribed for one month if available ., The offending drug should be withdrawn and treatment is otherwise symptomatic. NSAIDs and compression hosiery may reduce ,pain and inflammation. Systemic corticosteroids are rarely indicated, Pathophysiology : EN is the result of a nonspecific cutaneous reaction to various antigens. The mechanism involved would be immunologically mediated. Numerous direct and indirect evidence supports the notion of type IV delayed hypersensitivity response to many antigens. It is postulated that the pathogenesis may be due to the deposition of immune complexes in the venules of subcutaneous fat, the production of oxygen free radicals, TNF-alpha, and granuloma formation. However, this hypothesis is not accepted by all authors., Epidemiology : The incidence of EN is estimated to be 1–5 cases, The clinical course is self-limiting following dru, Current medical research has not established a method of preventing Drug-Induced Erythema Nodosum. However, the following may be observed : ,,Drugs that cause erythema nodosum may be discontinued or alternative medications used,Inform your physician if you are allergic to certain drugs,Periodic monitoring or follow-up of the condition with the healthcare provider is recommended, Complications : osteomyelitis, Diagnostics : TISSUE BIOPSY, X RAY CHEST, fluid microbiological culture, SEROLOGIC TEST, PHYSICAL EXAMINATION, Fluorescence with Wood’s light, Dermoscopy, Differential diagnosis : Panniculitis, Polyarteritis Nodosa, disease description : Erythema nodosum is a skin condition that causes painful red subcutaneous nodules. It may be caused by numerous factors including certain infectious diseases, pregnancy, inflammatory bowel disease, blood cancer, and many other disordersDrug-Induced Erythema Nodosum is caused by the use of certain medications, such as oral contraceptives, antibiotics, or certain anticonvulsants, among others. It may be considered as a reactive condition of the body to the specific medicationThe nodules in Drug-Induced Erythema Nodosum may occur on the legs and arms. Apart from cosmetic concerns in some individuals, no significant complications are noted in many casesStopping or discontinuing the use of such medications may decrease progression of Drug-Induced Erythema Nodosum, or may result in a cure. The prognosis is good in a majority of cases with adequate treatment

Drug-induced Exanthem

Disease Name : Drug-induced Exanthem, Treatment : Cessation of the culprit drug is essential. On withdrawal of the ,drug, maculopapular drug eruptions usually fade with desquamation, sometimes with post-inflammatory hyperpigmentation, Generally, symptomatic treatment only is required; most cases benefit ,from emollients. Approximately 50% of exanthematous eruptions ,are pruritic and intermediate potency topical corticosteroids may ,be useful for these cases, Pathophysiology : The mechanism of cutaneous inflammation in drug-induced exanthems is mediated by drug-specific T cells. Pathology Histology is generally non-specific. However, some histological features are used to discriminate drug-induced exanthems from non-drug exanthems including : apoptotic keratinocytes, eosinophils within the inflammatory infiltrate, papillary oedema and vascular changes., Epidemiology : French study identified 3.6 cutaneous allergic rea, The illness follows a benign course, and resolves , The condition usually clears up if you stop taking the medicine that is causing the reaction., Complications : exfoliative dermatitis, Diagnostics : GENRAL BLOOD PICTURE, PCR, Viral cultures, Differential diagnosis : chickenpox, MEASLES, viral infections, disease description : An exanthem is the most frequent of all cutaneous reactions to medicines, and can occur after almost any drug at any time up to 3 weeks, but usually 1–2 weeks after administration. A variety of drugs can cause drug-induced exanthems, the commonest being penicillins, aromatic anticonvulsants, sulphonamides, non-steroidal anti-inflammatory drugs (NSAIDs) and allopurinol . It is not possible to identify the offending drug by the nature of the eruption.

Drug-induced Generalized Exfoliative Dermatitis

Disease Name : Drug-induced Generalized Exfoliative Dermatitis, Treatment : Identification and withdrawal of the offending drug is key. Topical ,and systemic corticosteroids are often indicated., Pathophysiology : GED is characterized by increased epidermal turnover, decreased transit time and increased mitotic activity. It is unclear how medications drive these immunological pathways but a complex interaction of cytokines, chemokines and adhesion molecules is believed to be involved. Cases of benign exfoliative dermatitis (including drug-induced cases) were found to have an overexpression of both Th1- and Th2-related chemokine receptors and respective ligands as opposed to a Th2 cytokine profile in Sézary syndrome. Upregulation of adhesion molecules such as CD62L on keratinocytes may also facilitate the hypersensitivity reaction through the recruitment of epidermal T cells and Langerhans cells . Genetics There are no genetic markers specifically for drug-induced GED. However, in certain ethnic populations, there are strong drug- specific human leukocyte antigen (HLA) associations for DRESS (e.g. HLA-B*5801 for allopurinol DRESS in Han Chinese, and HLA-A*3101 in white people). Pathology The utility of histology in diagnosing drug-induced GED remains limited. Correlation between pathological and clinical diagnosis of drug-induced GED occurs in only 35% of cases. Traditionally thought to be a discriminant, tissue eosinophils are not specific to drug-related cases and are present in cases of GED attributed to other inflammatory skin diseases, Epidemiology : GED accounts for between 2 and 8% of all cutaneous, Drug-associated erythroderma tends to resolve quic, Discontinuation of the offending agent, Complications : cardiac failure, hypothermia, Electrolyte imbalance, Diagnostics : DIRECT IMMUNOFLORESCENCE ASSAY, Patch Test, Differential diagnosis : Cutaneous T-cell lymphoma, ECZEMA, psoriasis, disease description : Generalized exfoliative dermatitis (GED) is an adverse drug reaction characterized by erythema and scaling affecting more than 90% of the body surface area.Drugs are a known trigger for generalized exfoliative dermatitis, which is a reaction pattern characterized by erythema, pruritus and scaling affecting more than 90% of the body. Although GED usually occurs on its own, it may evolve from exanthematous drug reactions or DRESS

Drug-induced Pityriasis Rosea

Disease Name : Drug-induced Pityriasis Rosea, Treatment : The cutaneous reaction often resolves without treatment on discontinuation of the culprit drug. Topical corticosteroids may ,be useful in cases that are slow to respond, Pathophysiology : The exact pathomechanism is unclear. However, some reports have shown that these reactions are dose dependent, suggesting that they may be due to the pharmacological effect of the medication (e.g. induction of increased levels of kinins by ACE inhibitors; inhibition of cyclo-oxygenase by NSAIDs) rather than a true hypersensitivity reaction . The histological features of such reactions are similar to classical PR, demonstrating parakeratosis and focal spongiosis with papillary dermal oedema and superficial perivascular infiltrate of lymphocytes. In contrast to classical PR eosinophils., Epidemiology : Drug-induced PR-like reactions made up 2% of all c, variable, withdrawal of the offending drug., Complications : DRY SCALY SKIN, Diagnostics : biopsy, Provocative tests, Differential diagnosis : ECZEMA, pityriasis rosea, syphilis, disease description : A drug-induced dermatosis which clinically resembles pityriasis rosea (PR). Drug-induced PR-like eruption is an uncommon cutaneous adverse reaction characterized by erythematous scaly papules and plaques that are typically located on the trunk

Drug-induced Pruritus

Disease Name : Drug-induced Pruritus, Treatment : Cooling emollients ,such as 0.5% menthol in aqueous cream may be of benefit., introduction of naloxone, naltrexone (µ-receptor antagonists) or ,nalbuphine (partial µ-receptor agonist, µ-receptor antagonist) ,may be tried, but all of these approaches are likely to lead to loss ,of pain control. Other approaches include adding D2 receptor ,antagonists, serotonin (5-HT3) receptor antagonists (ondanse\x02tron, dolasetron), antihistamines and gabapentin 19. Interest\x02ingly, µ-receptor antagonists have also been utilized in other ,forms of pruritus especially where endogenous endorphins are ,thought to be pathogenic, such as in cholestatic pruritus, Pathophysiology : Drug-induced pruritus may be primary, via neuronal/central nervous system interaction, or through secondary mechanisms. Secondary pruritus includes : (i) direct skin effects, e.g. induction of a hypersensitivity drug rash, other inflammatory skin disease or xerosis; (ii) alteration of biochemical profiles (e.g. renal or hepatic dysfunction); and (iii) other unexplained mechanisms. Opioids can induce mast cell degranulation and histamine release causing an itchy urticarial rash, however most opioid pruritus appears to involve binding of the drug to central µ-opioid pain receptors in the medullary dorsal horn. Serotonin and dopamine D(2) receptors, spinal inhibitory pathways and prostaglandins have also been implicated in opioid-induced pruritus. Chloroquine can cause mast cell induced histamine pruritus. However, the precise cause of generalized pruritus seen in 60–70% of black Africans treated with antimalarials is unclear and likely to be multifactorial including µ-opioid receptor signalling as well as genetic (it is less common in white people) . Selective serotonin reuptake inhibitor (SSRI) induced pruritus is also well recognized and these drugs can induce itching when injected into the skin . Interestingly, SSRIs can also be used to treat psychogenic itching . Hydroxyethyl starch (HES) is used for colloid fluid replacement in some settings and has been associated with chronic pruritus in approximately one third of patients. HES-induced itch can arise with the administration of small volumes but the complication is more common with greater exposure. The symptoms typically arise after 1–6 weeks of HES infusion , can persist for 12–24 months and are generally refractory to treatment., Epidemiology : Pruritus has been reported to arise in 13.3% of ad, variable, WITHDRAWAL OF OFFENDING AGENT.,,you can take steps to reduce your risk of getting itchy skin by : ,,Wearing sunscreen when you go outside or wearing UV-protective clothing and accessories.,Drinking plenty of water.,Moisturizing your skin daily or multiple times per day.,Using warm (not hot) water when taking a shower or bath or washing your hands.,Managing any chronic conditions you have.,Using a humidifier in your home.,Avoiding allergens., Complications : DRY SCALY SKIN, Diagnostics : ABG, Differential Leucocyte Count DLC, Erythrocyte Sedimentation Rate (ESR), X RAY CHEST, Differential diagnosis : scabies, disease description : Itch caused by a drug. Drug-induced pruritus may be localized or generalized.Pruritus is generally a complication of systemic drugs but is also associated following the application of some topical agents, such as calcineurin inhibitors and ß-adrenergic blockers.

Drug-induced Serum Sickness-like Reaction

Disease Name : Drug-induced Serum Sickness-like Reaction, Treatment : Serum sickness is a self-limited entity that will usually resolve upon discontinuation of the offending agent, with or without additional treatment., Pathophysiology : The pathophysiology of SSLR is not well studied. Prior in vitro studies on cefaclor suggest that drug metabolism and biotransformation of the parent drug to reactive metabolites is essential and inherited defects in the metabolism of these reactive intermediates may be a predisposing factor. The downstream mechanism is unclear. However, the absence of circulating immune complexes and the lack of cross-reactivity between cases of cefaclor-induced SSLR and other cephalosporins suggest that a true hypersensitivity reaction is unlikely. The histological features of SSLR are consistent with an urticarial reaction pattern. Findings include dermal oedema with a superficial and deep perivascular infiltrate of lymphocytes, neutrophils and eosinophils. Vasculitis is usually absent., Epidemiology : SSLR accounts for about 2% of all cutaneous reaction, good, People who have had serum sickness or drug allergy should avoid future use of the antiserum or drug., Complications : recurrence, Diagnostics : CRP, Patch Test, Provocative tests, blood test, Differential diagnosis : Kawasaki Disease, meningococcemia, Schnitlzer syndrome, Still disease, , Urticarial vasculitis, disease description : SSLR is a drug reaction pattern, so named because of its similarity in clinical presentation to serum sickness. Classical serum sickness is a type III hypersensitivity reaction to foreign proteins resulting in the deposition of immune complexes in small blood vessels of various organs such as the skin, joints and other systems. In distinction, SSLR is typically due to medications and despite the clinical similarity, circulating immune complexes are not usually found. SSLR is more commonly reported in children and this may reflect the relatively frequent use of high-risk medications such as cefaclor in the young.

Drug-induced Urticaria, Angio-oedema And Anaphylax

Disease Name : Drug-induced Urticaria, Angio-oedema And Anaphylax, Treatment : Oral/IV antihistamines, oral/IV corticosteroids and s/c ,epinephrine/adrenaline may be required as per local guidelines . Although cross-reactivity occurs throughout the NSAID ,class, selective COX-2 inhibitors are recommended in low-risk ,NSAID sensitive patients where anti-inflammatory therapy is required, Pathophysiology : The mechanisms underlying drug-induced vasodilation, oedema and itch in urticaria are identical to those seen in angio-oedema (deeper in skin) and anaphylaxis (systemic circulation). Classically, these reactions are mediated by the presence of drug-specific IgE. On exposure to the drug, cross-linking of IgE on the surface of mast cells (and possibly basophils) is followed by inflammatory mediator release (including histamine), which induces vasodilation, neuronal activation and smooth muscle contraction. Cyclo-oxygenase inhibitors, such as aspirin and indometacin, may also cause urticaria or angio-oedema by pharmacological mechanisms. Other drugs, such as radiocontrast media, local anaesthetics and dextrans (in plasma expanders) may release mast cell mediators directly. Angiotensin-converting enzyme (ACE) inhibitors can cause angio-oedema which is bradykinin mediated rather than histamine dependent and will therefore not respond to antihistamines., Epidemiology : Drug-induced urticaria is seen in 0.16% of medica, variable, Avoiding the medication or other triggers that cause allergic reactions., Complications : death, recurrence, Diagnostics : Complete Blood Count CBC, CRP, Erythrocyte Sedimentation Rate (ESR), Skin test, Skin Prick test, SERUM IMMUNOGLOBULINS, Differential diagnosis : infection, disease description : Urticaria and angio-oedema are physical signs which involve circumscribed skin oedema and erythema. Anaphylaxis is a constellation of clinical findings which describes respiratory and cardiovascular compromise (bronchoconstriction and hypotension) in a life-threatening manner. This section is concerned with drug-induced causes of these reaction patterns. Pseudoallergy (non-immune mediated) describes a presentation which is clinically indistinguishable from true allergy (IgE mediated). Pseudoallergic urticaria, angio-oedema and anaphylaxis are commonly mediated by drugs. Introduction and general description Drug-induced urticaria can be seen in isolation or in association with anaphylaxis and angio-oedema. Aspirin and NSAIDs are the most frequently implicated drugs in allergic reactions, most frequently causing urticaria as well as exacerbating idiopathic urticaria

Dry Gangrene

Disease Name : Dry Gangrene, Treatment : medication : Clopidogrel , Amoxicillin and Clavulanic acid , Aspirin/Acetylsalicylic acid, Medical treatment of ischemic gangrene includes the use of antiplatelet therapy with aspirin or clopidogrel and treatment of hypertension with beta-blockers and angiotensin-converting enzyme inhibitors., Surgical treatment of limb ischemia is focused on revascularization to improve pain and prevent limb loss. In the setting of acute ischemia, catheter-based intravascular thrombolysis can be used. Otherwise, revascularization can be pursued with endovascular intervention with balloon angioplasty (with or without stent), and surgical therapy can bypass a stenotic area or directly remove a blockage.,Primary amputation (amputation before an attempt at revascularization) is recommended if there is significant necrosis of the weight-bearing portion of the foot, refractory pain, sepsis/uncontrolled infection, paresis of the extremity, or limited life expectancy.,Treatment with hyperbaric oxygen therapy has been proposed as a method to increase oxygen tension in ischemic tissue., 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. In gas gangrene, bacteria such as C.perfringens and group A streptococcus can produce multiple exotoxins, resulting in local tissue destruction and subsequent systemic infection.Alpha-toxin, a C-lecithinase, can result in extensive tissue necrosis and promote systemic hemolysis., Epidemiology : 1.6 cases per 100, 000, poor, 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 : X RAY, WOUND TISSUE CULTURE, CT SCAN, blood test, Differential diagnosis : compartment syndrome, diabetic neuropathy, disease description : Dry gangrene is dehydrated ischemic tissue caused by progressive ischemia distal to arterial occlusion, often a progression of peripheral artery disease. Wet gangrene, which may be dry, complicated by a secondary infection, has associated edema and erythema but no crepitus. Gas gangrene is a specific type of necrotizing infection with edema, crepitus, and gas on radiographs. Necrotizing soft tissue infections overlap with the infectious causes of gangrene and involve necrotic skin lesions that may extend into subcutaneous, fascial, and muscle compartments.

Dubin Johnson Syndrome

Disease Name : Dubin Johnson Syndrome, Treatment : No treatment is indicated for disease which presents outside of the neonatal,period., Phenobarbital and ursodeoxycholic acid are therapeutic for significant cholestasis that occurs in neonatal DJS., Pathophysiology : Disease results from absent function of multiple drug-resistant protein 2 (MRP2, encoded by the gene ABCC2 ), an adenosine triphosphate–dependent canalicular transporter. More than 10 different mutations, including compound heterozygous mutation in the CMOAT gene, have been identified and either affect localization of MRP2 with resultant increased degradation or impair MRP2 transporter activity in the canalicular membrane. Bile acid excretion and serum bile acid levels are normal. Total urinary coproporphyrin excretion is normal in quantity but coproporphyrin I excretion increases to approximately 80% with a concomitant decrease in coproporphyrin III excretion. Normally, coproporphyrin III is >75% of the total. Cholangiography fails to visualize the biliary tract and x-ray of the gallbladder is also abnormal. Liver histology demonstrates normal architecture, but hepatocytes contain black pigment similar to melanin. Liver function is normal and prognosis is excellent., Epidemiology : Dubin-Johnson syndrome has a high prevalence among people living in Iran, Iraq, Morocco and Japan, where an estimated 1 in 1, 300 people have the condition., GOOD, You can’t prevent Dubin-Johnson syndrome since it’s a genetic condition. If you plan on becoming pregnant and want to understand your risk of having a child with a genetic condition, talk to your provider about genetic testing or genetic counseling., Complications : jaundice, HEPATOMEGALY, Diagnostics : HISTOPATHLOGY, Serum Bilirubin (Total ), ELECTRON MICROSCOPY, Differential diagnosis : Crigler-Najjar Syndrome/Hyperbilirubinemia, Gilbert syndrome/ Hyperbilirubinemia, intrahepatic cholestasis, Rotor Syndrome, disease description : Dubin-Johnson syndrome is an autosomal recessive inherited defect in hepatocyte secretion of bilirubin glucuronide. The defect in hepatic excretory function is not limited to conjugated bilirubin excretion but also involves several organic anions normally excreted from the liver cell into bile. DJS is rare, occurs equally among men and women, and typically manifests in adolescence or young adulthood.

Duchenne And Becker Muscular Dystrophies

Disease Name : Duchenne And Becker Muscular Dystrophies, Treatment : medication : Prednisolone, Deflazacort, The,mainstays of management are maintenance of strength and,joint range of motion by exercise, physiotherapy and,avoidance of prolonged immobility. Corticosteroids,(prednisone and deflazacort) are the only therapies proven to improve strength and prolong ambulation in children with,Duchenne muscular dystrophy. Low dose prednisolone may,be started with aim of preserving upper limb strength, ,reducing progression of scoliosis and delaying the decline,in respiratory and cardiac function. Other supportive,management includes pulmonary and cardiac care, nutrition, ,calcium homeostasis, appropriate immunization and,orthopedic care., ACE inhibitors are used with or without beta blockers for cardiomyopathy in both DMD and BMD phenotypes.,Corticosteroid therapy improves muscle strength and function for individuals with DMD between ages five and 15 years, Pathophysiology : Dystrophinopathies are a group of disorders resulting from mutations in the dystrophin gene (located on the short arm of X chromosome in the Xp21 region). Duchenne muscular dystrophy is the most common dystrophinopathy with an incidence of 1 in 3500 live male births. Its allelic variant, Becker muscular dystrophy, differs from Duchenne muscular dystrophy by its later age of onset (usually >6 yr of age), later age of wheelchair confinement(> 15 yr), more i ncidence of myalgias, occasional rhabdomyolysis following exercise and early cardiomyopathy. Over 4700 mutations have been reported in the Leiden Duchenne muscular dystrophy mutation database. Deletion of > : 1 exons is the most common mutation seen (-65%). In dystrophinopathies, 65% of the pathogenic changes are large partial deletions. Mutations in the dystrophin gene can cause Duchenne muscular dystrophy or Becker muscular dystrophy. This is explained by the reading frame hypothesis, which states that mutations that disrupt the reading frame (frame-shift) eventually leads to dystrophin deficiency and usually cause Duchenne muscular dystrophy. In Becker muscular dystrophy, however, mutations maintain the reading frame (inframe mutations) and generally result in abnormal but partly functional dystrophin. The reading frame rule holds true for over 92% of all dystrophinopathies. Children with Duchenne muscular dystrophy usually become symptomatic before age of 5 yr and may even have history of delayed walking. Gait disturbances often become apparent at 3-4 yr of age. Waddling gait, Gower sign and calf muscle pseudohypertrophy are classical findings at this stage. Neck flex or muscle weakness is early. Other muscles to show hypertrophy may be vastus lateralis, infraspinatus, deltoid, gluteus maximus, triceps and masseter. The progression of weakness may plateau between 3 and 6 yr of age. Subsequently there is increasing gait difficulty, development of contractures (initially dynamic and then fixed) and increased lumbar lordosis. Natural history studies have shown the age at loss of independent ambulation in untreated Duchenne muscular dystrophy to be between 8.8 and 10.5 yr. After loss of ambulation, there is worsening kyphoscoliosis, , Epidemiology : 1 in 3500 live male births, variable, Unfortunately, there isn’t anything you can do to prevent getting muscular dystrophy. If you have the disease, these steps can help you enjoy a better quality of life : ,,Eat a healthy diet to prevent malnutrition.,Drink lots of water to avoid dehydration and constipation.,Exercise as much as possible.,Maintain a healthy weight to prevent obesity.,Quit smoking to protect your lungs and heart.,Get flu and pneumonia vaccines., Complications : Cardiac arrhythmias, Cardiomyopathies, respiratory difficulties, Diagnostics : CK (Creatine Kinase) test, Muscle Biopsy, ECG, ELECTROMYOGRAPHY, PLASMA CREATINE KINASE, Differential diagnosis : DILATED CARDIOMYOPATHY, EMERY-DREIFUSS MUSCULAR DYSTROPHY, Spinal Muscular Atrophies, disease description : The dystrophinopathies cover a spectrum of X-linked muscle disease ranging from mild to severe that includes Duchenne muscular dystrophy, Becker muscular dystrophy, and DMD-associated dilated cardiomyopathy (DCM) The muscular dystrophies are diseases of muscle membrane or supporting proteins which are generally characterized by pathological evidence of ongoing muscle degeneration and regeneration. Diagnosis of these disorders is based on clinical presentation, genetic testing, muscle biopsy and muscle imaging. they occur more commonly in males but can occur in females also in rare instances.

Duct Ectasia/periductal Mastitis

Disease Name : Duct Ectasia/periductal Mastitis, Treatment : medication : Levofloxacin , Cone excision of involved major ducts (Adair-Hadfield ,operation). ,Antibiotics. , Me/hem Novel modified breast ductal system excision., Pathophysiology : The presumed pathogenesis is that the affected duct becomes dilated and tortuous, either due to breast involution or other factors, and accumulates granular debris with numerous lipid-laden macrophages. A significant histological difference hinting these may be separate processes is that in MDE, there will be no epithelial proliferation near the opening of the duct, as opposed to PDM, where this is a cardinal feature. Periductal collagenization and fibrosis may eventually produce skin and nipple retraction, which may predispose to one or both conditions., Epidemiology : prevalence is unknown., incidence is between 7% to 10%, will recover with appropriate treatment., Breastfeeding moms can take these steps to lower their chances of getting mastitis : ,,Air out your nipples after nursing.,Don’t wear nursing pads or tight-fitting bras that keep nipples moist.,Nurse your baby on one side, allowing the breast to empty, before switching to the other breast.,Switch up breastfeeding positions to fully empty all areas of the breast.,Use your finger to break your baby’s suction on a nipple if you need to stop a feeding., Complications : status epilepticus, Diagnostics : mammography, Differential diagnosis : BREAST ABSCESS, breast cancer., GALACTOCOELE, disease description : It is dilatation of lactiferous ducts due to muscular relaxation (myoepithelial relaxation) of duct wall with periductal mastitis.It is also called plasma cell mastitis as periductal inflammation contains plasma cells. Commonly many ducts are involved. Common in multiple pregnancies, perimenopausa/ age, hyperprolactin status.

Ductal Adenocarcinoma

Disease Name : Ductal Adenocarcinoma, Treatment : medication : Cisplatin , Oxaliplatin, Irinotecan, Paclitaxel, Gemcitabine hydrochloride, Capecitabine, Docetaxel, Fluorouracil , Systemic chemotherapy is commonly employed as first-line treatment in patients with non-resectable or borderline-resectable tumors. This encompasses nucleoside analogues, including gemcitabine and capecitabine, or the pyrimidine analogue 5-fluorouracil (5-FU) in monotherapy settings or in combination with other treatment modalities, such as radiotherapy, respectively., Radio(chemo)therapy has been rather infrequently adopted for the treatment of PDAC, since the majority of patients suffer from disseminated stages in which local treatment procedures are of secondary importance., Surgical resection followed by adjuvant chemotherapy is the only possibly curative therapy available, Pathophysiology : The genetic events found in ductal adenocarcinoma have been well characterized, and complete exome sequencing has been done for the common types of tumor. Four genes have each been found to be mutated in the majority of adenocarcinomas : KRAS (in 95% of cases), CDKN2A (also in 95%), TP53 (75%), and SMAD4 (55%). The last of these is especially associated with a poor prognosis. SWI/SNF mutations/deletions occur in about 10–15% of the adenocarcinomas. The genetic alterations in several other types of pancreatic cancer and precancerous lesions have also been researched. Transcriptomics analyses and mRNA sequencing for the common forms of pancreatic cancer have found that 75% of human genes are expressed in the tumors, with some 200 genes more specifically expressed in pancreatic cancer as compared to other tumor types.The genetic events found in ductal adenocarcinoma have been well characterized, and complete exome sequencing has been done for the common types of tumor. Four genes have each been found to be mutated in the majority of adenocarcinomas : KRAS (in 95% of cases), CDKN2A (also in 95%), TP53 (75%), and SMAD4 (55%). The last of these is especially associated with a poor prognosis. SWI/SNF mutations/deletions occur in about 10–15% of the adenocarcinomas. The genetic alterations in several other types of pancreatic cancer and precancerous lesions have also been researched. Transcriptomics analyses and mRNA sequencing for the common forms of pancreatic cancer have found that 75% of human genes are expressed in the tumors, with some 200 genes more specifically expressed in pancreatic cancer as compared to other tumor types., Epidemiology : incidence rates of 7.2 and 2.8 per 100, 000 populations., Prognosis Depends on Stage at Diagnosis, Even though you can’t prevent cancer altogether, there are some things you can do to significantly lower your risk. Making healthy lifestyle choices is the best way to prevent adenocarcinoma and other types of cancer : ,,Avoid tobacco products.,Be physically active.,Maintain a healthy weight.,Eat a well-balanced diet.,Visit your healthcare provider regularly., Complications : delirium, insomnia, anemia, Diagnostics : ERCP, MRCP, PET SCAN, Differential diagnosis : Chronic Pancreatitis, disease description : Pancreatic ductal adenocarcinoma (PDAC) is a highly devastating disease with poor prognosis and rising incidence. Late detection and a particularly aggressive biology are the major challenges which determine therapeutic failure.Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal diseases, with an average 5-year survival rate of less than 10%. Unfortunately, the majority of patients have unresectable, locally advanced, or metastatic disease at the time of diagnosis. Moreover, traditional treatments such as chemotherapy, surgery, and radiation have not been shown to significantly improve survival.

Duodenal Ulcer

Disease Name : Duodenal Ulcer, Treatment : Antisecretory agents include H2 receptor antagonists as well as proton pump inhibitors. The duration of therapy varies highly depending on the presenting symptoms, level of compliance suspected, as well as the risk of recurrence.,Patients diagnosed with H. pylori must receive triple therapy (two antibiotics and a proton pump inhibitors), and elimination must be confirmed., Pathophysiology : Duodenal ulcers are the result of the corrosive action of gastric secretions on the surface epithelium of the small intestine that has undergone prior injury. In duodenal ulcers, there are multiple underlying comorbidities to consider when establishing the diagnosis and underlying cause. H. pylori and NSAID use are the two main underlying etiologies to consider and discussed here. The mechanism by which H. pylori predisposes individuals is unclear. However, the thinking is that H. pylori colonization and persistent inflammation lead to the weakening of the mucosal surface layer causing it to be vulnerable to exposure to gastric acid. A secondary running theory considers the possibility that H. pylori also can increase acid production via inflammatory mechanisms, further exacerbating the initial injury caused by the infection and initial acid-driven injury. Prostaglandins play a crucial role in developing the protective mucosa in the gastrointestinal tract, including gastric and small intestine mucosa. Their biosynthesis is catalyzed by the enzyme cyclooxygenase (COX), which exists in two isoforms, COX-1 and COX-2. NSAIDs exhibit their therapeutic effect by inhibiting the COX-1 and COX-2 pathways. Recurrent use of NSAIDs causes a significant and persistent decrease in prostaglandins leading to susceptibility to mucosal injury. It is thought to be one of the primary predisposing pathophysiologic factors for the development of duodenal ulcers. Other secondary causes for duodenal ulcers may work through different underlying mechanisms. However, the ultimate result is generally recurrent mucosal injury that predisposes the tissue to ulceration or an elevation in the amount of acid the mucosa is exposed to, which in turn causes tissue damage., Epidemiology : 5 to 15% of western popoulation, Variable, You may be able to prevent ulcers from forming if you : ,,Talk to your doctor about alternatives to NSAID medications (like acetaminophen) to relieve pain.,Discuss protective measures with your doctor, if you can’t stop taking an NSAID.,Opt for the lowest effective dose of NSAID and take it with a meal.,Quit smoking.,Drink alcohol in moderation, if at all., Complications : bleeding, obstruction, perforation, Diagnostics : Total Leucocyte Count (TLC), Barium Imaging, Upper GI Endoscopy, X RAY CHEST, CT SCAN, Differential diagnosis : GASTRITIS, Gastroesophageal reflux disease (GERD), Pancreatitis, disease description : Duodenal ulcers occur when there is a disruption to the surface of the mucosa of the duodenum. These ulcers are part of peptic ulcer disease, which involves the stomach and first part of the duodenum. Anatomically, both the gastric and duodenal surfaces contain a defense system that includes pre-epithelial, epithelial, and subepithelial elements. Ulceration occurs from damage to the mucosal surface that extends beyond the superficial layer.The two primary causes for duodenal ulcers are a history of recurrent or heavy NSAID use and a diagnosis of H. pylori.

Duplication Of Ureter

Disease Name : Duplication Of Ureter, Treatment : Ureteric meatotomy is done if there is narrowing of the ,orifice.,Often heminephrectomy including removal of corresponding ureter may be essential as treatment. ,, In females with complete duplication, lower ureteric ,orifice is ectopic, causing urinary incontinence which ,needs partial nephrectomy or ureteric reimplantation, Pathophysiology : Duplex kidney, also known as duplicated ureters or duplicated collecting system, is the most common birth defect related to the urinary tract. This occurs due to an incomplete fusion of the upper and lower pole of the kidney which creates two separate drainage systems from the kidney.Duplex kidney can take on one of two forms : Incomplete : Two separate ureters are attached to the same kidney but join together at some distance away from the kidney to form a single ureter that enters the bladder.Complete : Two separate ureters lead away from the same kidney and enter the bladder separately., Epidemiology : OCCURS IN approximately 1% of the population. It occurs in about 0.7% of healthy adults and in 2% to 4% of people with urinary tract issues., GOOD, There is no known way to prevent a duplex kidney, as it results from a birth defect. However, the previously discussed surgeries can be performed to relieve symptoms and protect the kidneys from damage., Complications : HYDRONEPHROSIS, INCONTINENCE OF URINE, urinary tract infections, Diagnostics : IVP, USG ABDOMEN(W/A), MRI, CT SCAN, CYSTOSCOPY, USG, Differential diagnosis : HYDRONEPHROSIS, disease description : It is most common congenital anomaly of the upper urinary tract (4%). Usually unilateral. Common on the left side. In 3% of cases, it is associated with duplication of ureter. Upper renal pelvis is small, drains the upper calyces. Lower renal pelvis is larger, drains the middle and lower calyces. Double ureter when associated, may be partial where two ureters join in lower third or complete where upper ureter opens into the bladder at a lower level and lower ureter opens into the bladder at the upper, normal ureteric orifice. This is called as "Weigert Meyer Law".

Dupuytrens Contracture

Disease Name : Dupuytrens Contracture, Treatment : medication : Imiquimod , Tamoxifen citrate , * Needle Aponeurectomy is typically reserved for mild contractures,* Collagenase Injection - The injected enzyme is a metalloprotease that lyses collagen, Surgical fasciectomy can be either partial or total. Partial palmar fasciectomy entails the limited resection of diseased tissue within a ray. Dissection generally is performed from proximal to distal as this usually allows for the identification of neurovascular structures before encountering the spiral cord. Incisions are customized to each patient in a Brunner zigzag pattern. A V-Y incision and Z-plasty can also be used to lengthen contracted skin., Pathophysiology : The pathophysiology of Dupuytren disease involves abnormal myofibroblastic growth in the hand, predominantly composed of type III collagen. Numerous cytokines are involved including interleukin-1, transforming growth factor beta-1, transforming growth factor beta-2, epidermal growth factor, platelet-derived growth factor, and connective tissue growth factor. Dupuytren contracture progresses through three phases : (1) proliferative, (2) involution, and (3) residual. The proliferative phase has a characteristically high concentration of immature myofibroblasts and fibroblasts arranged in a whorled pattern. In the involution phase, fibroblasts become aligned in the longitudinal axis of the hand following lines of tension. In the residual phase, relatively acellular collagen-rich chords remain causing contracture deformity. , Epidemiology : 8.2%, GOOD, There’s nothing you can do to prevent Dupuytren contracture. In the same way that there’s no cure, it develops without warning. Talk to your provider if someone in your family has been diagnosed with Dupuytren contracture., Complications : hematomas, INCONTINENCE OF URINE, infection, Redness, stiffness, swelling, NERVE INJURY, recurrence, Diagnostics : ultrasound, MRI, X RAY, Differential diagnosis : Peripheral neuropathy, Tendonitis, disease description : Dupuytren disease is predominantly a myofibroblastic disease that affects the palmar and digital fascia of the hand and results in contracture deformities. The most commonly affected digits are the fourth (ring) and fifth (small or pinky) digits. The disease begins in the palm as painless nodules that form along longitudinal lines of tension. The nodules form cords that produce contracture deformities within fascial bands and tissues of the hand. This is a condition characterised by a flexion deformity of one or more fingers due to a thickening and shortening of the palmar aponeurosis. The cause is unknown, but a hereditary predisposition has been established. There is an increased incidence of the disorder among cirrhotic patients and in epileptics on sodium hydantoin...

Dysembryoplastic Neuroepithelial Tumour (who Grade

Disease Name : Dysembryoplastic Neuroepithelial Tumour (who Grade, Treatment : Gross total resection or even subtotal resection usually achieves stabilization and seizure control., Pathophysiology : Dysembryoplastic neuroepithelial tumours are largely glioneuronal tumours, meaning they are composed of both glial cells and neurons.Three subunits of DNTs have been commonly identified : Simple : Specific glioneuronal elements are the sole components of simple DNTs.Complex : Glial nodules and/or type 3b focal cortical dysplasia (FCD), in addition to the glioneuronal elements are present in complex DNTs. Both the nodules and FCD can be present within the same tumour, though only 47% of complex DNTs are linked to FCD.Nonspecific : Nonspecific DNTs are lacking the glioneuronal elements common to DNTs but will show glial nodules and/or type 3b FCD. Eighty-five percent of nonspecific case of DNTs show this FCD.There currently exists some debate over where to make the proper division for the subunits of DNTs. A fourth subunit is sometimes noted as a mixed subunit. This mixed subunit expresses the glial nodules and components of ganglioglioma. Other findings suggest that DNTs require a reclassification to associate them with oligodendrogliomas, tumours that arise from solely glial cells. These reports suggest that the neurons found within DNTs are much rarer than previously reported. For the neurons that are seen in the tumours, it is suggested that they had been trapped within the tumor upon formation, and are not a part of the tumour itself., Epidemiology : 2%, Incidence : ,1.2% of all neuroepithelial tumors diagnosed in patients younger than 20 years,1 - 19% of surgical resections for epilepsy, Prognosis is excellent, Primary Prevention -,There are no known primary preventive measures for dysembryoplastic neuroepithelial tumor.,,Secondary Prevention -,Secondary prevention strategies following diagnosis and treatment of dysembryoplastic neuroepithelial tumor include regular follow-up MRI evaluation, EEG, and neurological exam., Complications : status epilepticus, Diagnostics : MRI, CT SCAN, ELECTRON MICROSCOPY, immunohistochemistry, Differential diagnosis : oligodendroglioma (who grade 2), disease description : ?Dysembryoplastic neuroepithelial tumour (DNT, DNET) is a type of brain tumor. Most commonly found in the temporal lobe, DNTs have been classified as benign tumours.  These are glioneuronal tumours comprising both glial and neuron cells and often have ties to focal cortical dysplasia. Varying subclasses of DNTs have been presently identified, with dispute existing in the field on how to properly group these classes. The identification of possible genetic markers to these tumours is currently underway. With DNTs often causing epileptic seizures, surgical removal is a common treatment, providing high rates of success. 

Dysfunctional Uterine Bleeding

Disease Name : Dysfunctional Uterine Bleeding, Treatment : medication : Oestradiol/Oestrogen, Progesterone , Tranexamic acid , Mefenamic acid , Danazol, Ethamsylate, MIRENA IUCD, ORMELOXIFENE, GESTRINONE, Ablative technique,1st generation,• Hysteroscopic ablation endometrium resectoscope, roller,ball laser (TCRE),2nd generation,• Radiofrequency-induced thermal ablation, balloon therapy, ,microwave ablation,• Uterine tamponade in acute bleeding,• Bilateral uterine artery embolization,• Hysterectomy—vaginal, abdominal, laparoscopy, Pathophysiology : Endometrium normally produces prostaglandins from arachidonic acid, which is a fatty acid. Of these, PGE2 and PGI2 are vasodilators and antiplatelet aggregates. PGF2a and thromboxane A2 cause vasoconstriction and platelet aggregates. Progesterone is responsible for secretion of PGF2a. In anovulatory cycles, the absence of progesterone and thereby of PGF2a causes menorrhagia. In some cases, tissue plasminogen activator (TPA) which is a fibrinolytic enzyme is increased, thereby causing menorrhagia. Endothelin present in the endothelial wall is also a vasoconstrictor, which may be lacking or low when there is abnormal menstruation., Epidemiology : 3%–30% of women, GOOD, You can’t prevent many causes of abnormal uterine bleeding. But you can reduce your risk of certain conditions that lead to abnormal bleeding. For instance, maintaining a healthy weight plays a potential role in keeping your hormones balanced. Avoiding diets that contain a high amount of animal fat can reduce your risk of some cancers. Practicing safer sex can reduce your risk of certain sexually transmitted infections (STIs) that can cause abnormal uterine bleeding., Complications : Endometrial cancer, infertility, Diagnostics : USG, HYSTEROSCOPY, ENDOMETRIAL BIOPSY, blood test, Differential diagnosis : CANCER CERVIX, ectopic gestation, Endometrial cancer, Microcystic adnexal carcinoma, Polycystic Ovarian Disease, uterine cancer, disease description : Abnormal uterine bleeding is a broad term that describes irregularities in the menstrual cycle involving frequency, regularity, duration, and volume of flow outside of pregnancy. Abnormal uterine bleeding is common during the extremes of reproductive life, following pregnancy and during lactation. It has been shown that 55.7% of adolescents experience abnormal menstrual bleeding in the first year or so after the onset of menarche because of the immaturity of the hypothalamic–pituitary–ovarian axis leading to anovulatory cycles. Dysfunctional uterine bleeding’ (DUB) was coined to describe abnormal heavy menstrual bleeding when no structural genital tract abnormality or general cause was detected, in a woman of reproductive age in the absence of pregnancy.

Dyslipidemia

Disease Name : Dyslipidemia, Treatment : medication : Rosuvastatin , Atorvastatin , Ezetimibe , lifestyle modifications., Lifestyle changes (eg, exercise, dietary modification),For high LDL-C, statins, bile acid sequestrants, ezetimibe, bempedoic acid, and PCSK9 (proprotein convertase subtilisin/kexin type 9) inhibitors,For high TG, fibrates, omega-3 fatty acids., Pathophysiology : types of hyperlipdimia Phenotype I is an abnormality of chylomicrons and triglycerides. Phenotype IIa consists mainly of LDL cholesterol abnormality Phenotype IIb consists of abnormality in LDL and very-low-density lipoprotein (VLDL) cholesterol. Phenotype III is an abnormality in VLDL remnants and chylomicrons, which results in elevated total cholesterol and triglycerides., Epidemiology : The prevalence of dyslipidemia was 81.6%, high cholesterol is present in 25–30% of urban and 15–20% rural subjects., variable, Changes you make in your life can keep you from getting hyperlipidemia. Things you can do include : ,,Stop smoking.,Stay active instead of sitting too much.,Keep your stress level down.,Get the right amount of sleep.,Eat healthy foods.,Cut back on eating fatty meats.,Don’t buy snacks that have “trans fat” on the label.,Stay at a healthy weight., Complications : Cardiovascular Disease, Diagnostics : random blood sugar RBS, Complete Blood Count CBC, LIPID PROFILE, Differential diagnosis : biliary obstruction, Hypothyroidism, nephrotic syndrome, disease description : Dyslipidemia is the imbalance of lipids such as cholesterol, low-density lipoprotein cholesterol, (LDL-C), triglycerides, and high-density lipoprotein (HDL). Lipids, such as cholesterol or triglycerides, are absorbed from the intestines and are carried throughout the body via lipoproteins for energy, steroid production, or bile acid formation. Major contributors to these pathways are cholesterol, low-density lipoprotein cholesterol (LDL-C), triglycerides, and high-density lipoprotein (HDL). An imbalance of any of these factors, either from organic or nonorganic causes, can lead to dyslipidemia.

Dysmenorrhoea

Disease Name : Dysmenorrhoea, Treatment : medication : Mefenamic acid , Pathophysiology : nan, Epidemiology : nan, Complications : nan, Diagnostics : nan, Differential diagnosis : nan, disease description : nan

Dyspareunia

Disease Name : Dyspareunia, Treatment : medication : Lidocaine/Lignocaine, Local abnormalities,at the vulva can usually be cured by appropriate,treatment, but when dyspareunia is caused by abnormalities,in the pouch of Douglas, an abdominal operation is necessary.,The ovaries may be freed from adhesions, endometriosis and,chocolate cysts can be excised and the uterus can be fixed in a,position of anteversion by an operation of ventrosuspension., K-Y Jelly (lubricant) and Rejois vaginal moisturizer two,to three times a week relieves dyspareunia due to lower,genital tract. Postural change may help.,n Lignocaine ointment is an anaesthetic drug that relieves pain., Pathophysiology : Due to the Male Partner -Gross congenital abnormality of the penis. - Impotence, usually partial, e.g. failure to maintain an erection long enough for penetration. - Premature ejaculation. - Complete and surprising ignorance in the technique of coitus. Due to the Female Partner 1. Painful lesions in the region of the introitus, such as vulvitis (acute and chronic), urethral caruncle, Bartholin’s cyst or abscess, tender scar from obstetric trauma or operation and painful lesions of the anal canal, notably fissures. 2. Obstructive conditions at the vaginal introitus : -Rigid or imperforate hymen and painful carunculae myrtiformes giving rise to spasm. - Narrow introitus due to congenital hypoplasia, kraurosis or lichen sclerosis : poor lubrication in a menopausal woman. -Traumatic stenosis due to obstetric injury followed by scarring, such as painful episiotomy scar, tightly sewn perineal tear or perineorrhaphy operation, mutilation, vulvodynia and vulvar vestibulitis. - Cicatrization due to chemical burns. - The functional spasm of vaginismus. A large tender Bartholin’s cyst is occasionally obstructive to entry. 3. Obstructive conditions above the vaginal introitus : - Congenital stenosis and the various maldevelopment : partial noncanalization of the vagina. - Acquired stenosis—chemical burns are rare but the important causes here are the result of surgical operation. Vaginal hysterectomy and prolapse repairs, Wertheim’s operation, radium insertion and radiation therapy result in narrowing and shortening of the vagina. Sometimes, the anterior and posterior suture lines of a colporrhaphy become densely adherent and fuse to form a stout septum which allows only partial penetration. Uterine conditions which are not obstructive but because they are painful give rise to collision dyspareunia : -Cervicitis. Chronic inflammatory lesions of the cervix associated with parametritis can cause pain. Deep dyspareunia is due to : - Chronic parametritis and parametrial scars. - Adenomyosis uterus. - A fixed retroversion associated with chronic pelvic inflammatory disease (PID). 5. Lesions of the uterine appendages : - Prolapsed ovaries associated with retroversion cause deep dyspareunia. - Acute and chronic salpingo-oophoritis. Ovarian residual syndrome. - Endometriosis of the pouch of Douglas, rectovaginal septum and uterosacral ligaments. 6. Extragenital lesions in the bowel, such as diverticulitis of the sigmoid colon usually adherent to the left appendages and uterus, and cystitis. Difficult coitus. Difficult coitus may be caused by many of the same factors that are responsible for painful coitus. If the cause is insuperable, such as bony ankylosis of the hip in extreme adduction, consummation may be impossible and the correct term is not dyspareunia but apareunia. The latter naturally occurs with severe developmental defects of the vagina such as failure of canalization (vaginal aplasia)., Epidemiology : GOOD, To Do : POSTURE CHANGE DURING COITUS, Complications : nan, Diagnostics : Complete Blood Count CBC, USG, Differential diagnosis : nan, disease description : The term dyspareunia is loosely used for difficult as well as painful coitus.

Dysphonia Plica Ventricularis

Disease Name : Dysphonia Plica Ventricularis, Treatment : Functional type- voice therapy ,and psychological counselling., Conservative phoniatric therapy has been the primary modality of treatment for dysphonias resulting from ventricular fold hypertrophy., surgical intervention being reserved for those patients not responding to speech therapy., Pathophysiology : Here voice is produced by ventricular folds (false cords) which have taken over the function of true cords. Voice is rough, low-pitched and unpleasant. Ventricular voice may be secondary to impaired function of the true cord such as paralysis, fixation, surgical excision or tumours. Ventricular bands in these situations try to compensate or assume phonatory function of true cords. Functional type of ventricular dysphonia occurs in normal larynx. Here cause is psychogenic. In this type, voice begins normally but soon becomes rough when false cords usurp the function of true cords. Diagnosis is made on indirect laryngoscopy; the false cords are seen to approximate partially or completely and obscure the view of true cords on phonation. Ventricular dysphonia secondary to laryngeal disorders is difficult to treat but the functional type can be helped through voice therapy and psychological counselling., Epidemiology : 0.98%, GOOD, There are some easy ways to prevent a hoarse voice. You should practice them especially if you use your voice for professional reasons, particularly if that’s every day. Try the following to help prevent hoarseness : ,,Quit smoking. Stay away from second-hand smoke.,Avoid alcohol and caffeine and other fluids that dehydrate your body.,Drink plenty of water.,Use a humidifier.,Avoid spicy foods.,Keep yourself from using your voice for too long.,Keep yourself from using your voice too loudly., Complications : DRY SCALY SKIN, edema, Diagnostics : Indirect Laryngoscopy, Differential diagnosis : lymphoma, Multiple Sclerosis, Sarcoidosis, disease description : The voice is produced by ventricular folds (false cords) which have taken over the function of true cords. Voice is rough, low-pitched and unpleasant. Ventricular voice may be secondary to impaired function of the true cord such as paralysis, fixation, surgical excision or tumours. Ventricular bands in these situations try to compensate or assume phonatory function of true cords.

Dysplasia Epiphysealis Hemimelica (trevor’s Diseas

Disease Name : Dysplasia Epiphysealis Hemimelica (trevor’s Diseas, Treatment : Supportive joint care, consisting of short-term splinting of the joint, may be beneficial in management., The treatment of DEH is essentially surgical removal of the osteocartilaginous lesion, usually by a pediatric orthopedic surgeon,,,Treatment is therefore based on the level of,symptoms and involves excision, avoiding damaging,the uninvolved articular cartilage. In patients with,large lesions, with secondary deformities, corrective,osteotomies may be undertaken without excision., Pathophysiology : Many theories exist regarding the pathophysiology of DEH. Connor et al suggested that the fundamental defect was an abnormality of the regulation of cartilage proliferation in the affected epiphysis, resulting in cartilaginous exostosis. Trevor considered DEH to be a congenital error in epiphyseal development that affects the limb buds during early fetal life; it was thought to involve an altered process of cell proliferation at the superficial zone of articular cartilage, allowing for persistent proliferation and production of a large cartilaginous mass. Fairbank suggested that the disorder derived from a localized disturbance of the preaxial or postaxial apical cap of the limb bud in early fetal development. The etiology of DEH is unknown; the disease does not appear to be genetically transmitted., Epidemiology : DEH usually affects children between the ages of 1 and 15. Males are affected more often than females. The incidence of DEH has been estimated at 1 in 1, 000, 000 individuals in the general population, Incidence,extremely rare,estimated at ~ 1 : 1, 000, 000, May lead to early osteoarthritis of affected joint, Complications : leg-length discrepancy, Diagnostics : MRI, X RAY, CT SCAN, Differential diagnosis : Chondroblastoma, Chondroma : Enchondroma, Periosteal chondroma, Mul, disease description : Dysplasia epiphysealis hemimelica (DEH), also known as Trevor’s disease, is a developmental bone disease of childhood. It is rare and clinical experience with this condition is limited. Most cases are diagnosed before 8 years of age. It is characterized by an abnormal growth of cartilage arising from the cartilage of the terminal ends (epiphysis) of the long bones, particularly of the lower limbs. The bones of the knee and ankle joints are most commonly affected, as well as part of the foot (tarsal bones). The upper limbs and spine are rarely involved. The abnormal cartilage produces an irregular nodular mass located either in the medial or lateral part of the bone (hemimelic), usually medial. DEH may affect a single bone (localized form), multiple bones in a single limb (classical form) or an entire limb (generalized) usually involving a leg from the pelvis to the foot.

Dysthyroid Orbitopathy

Disease Name : Dysthyroid Orbitopathy, Treatment : medication : Propranolol , Propylthiouracil , Carbimazole , The treatment options include medical decompression using corticosteroids, , surgical decompression, Pathophysiology : Although the underlying mechanisms of action of these processes are not completely understood, the presumed mechanism is activation of orbital fibroblasts by Graves disease-related autoantibodies, which lead to the release of T cell chemoattractants, initiating an interaction which ultimately results in fibroblasts expressing extracellular matrix molecules, biologic materials proliferating and differentiating into myofibroblasts or lipofibroblasts and deposition of glycosaminoglycans which bind water that lead to swelling, congestion in addition to connective tissue remodeling. This results in extraocular muscle enlargement and orbital fat expansion., Epidemiology : Approximately every 5 in 100 patients with TED progress to sight-threatening optic neuropathy., Patients diagnosed over 50 -year have worse progno, There are no effective means of preventing the disease or reliably altering its course., Complications : blindness, Diagnostics : THYROID PROFILE, Differential diagnosis : Arteriovenous malformation, Erdheim-Chester disease, LYMPHOEDEMA DISEASE, metastatic disease, Sarcoidosis, disease description : Dysthyroid optic neuropathy (DON) is a sight-threatening complication of thyroid eye disease (TED), characterized by thyroid-related impairment of visual function, leading to permanent sight loss. To avoid blindness, prompt diagnosis and timely intervention are required. This activity reviews the evaluation and treatment of DON and highlights the role of the interprofessional team in managing patients with this condition. Dysthyroid optic neuropathy (DON) represents the most dreaded manifestation of Thyroid Eye Disease (TED), one of the most common autoimmune diseases of the orbit. DON, previously termed as the crowded orbital apex syndrome, is characterized by thyroid-related impairment of optic nerve function that may lead to a profound loss of vision

Eales’ Disease

Disease Name : Eales’ Disease, Treatment : Course of oral corticosteroids,for extended periods is the mainstay of treatment during stage of active inflammation. A course of,antitubercular therapy has also been recommended,in selective cases., 1.Laser photocoagulation, 2.Vitreoretinal surgery, Pathophysiology : The pathophysiology of Eales disease involves retinal periphlebitis, retinal ischemia, and neovascularization. Initially, the blood vessels of the retinal periphery get inflamed. This vasculitis manifests as sheathing of blood vessels. This vasculitis leads to obliteration of the lumen of the blood vessel. This obliteration leads to ischemia of that part of the retina perfused by the affected blood vessel. Vascular endothelial growth factor (VEGF) production is increased by persistent ischemia. Increased levels of VEGF lead to neovascularization. This neovascularization could be at or within one disc diameter of the optic disc, or it could be present anywhere else in the retina. Rubeosis of the iris may rarely develop, which may eventually give rise to neovascular glaucoma. New vessels are fragile and bleed easily. The fragility of these new blood vessels leads to recurrent vitreous hemorrhages. Vitreous hemorrhages generally resolve in 3 to 6 months. If they happen to persist beyond this duration, the probability of membrane formation in the vitreous increases with increased chances of tractional retinal detachment. Eales disease follows a very variable course of progression. Some patients may show spontaneous regression of new blood vessels, and others may have relentless vitreous hemorrhages., Epidemiology : It more commonly affects males than females. Males are generally afflicted by the disease at 20-40 years of age. In 90% of the patients, Eale disease is bilateral, with the rest 10% being unilateral. Asymmetric bilateral presentation is not very uncommon., 1 of every 135 to 250 patients evaluated at tertiary eye care centers in India, good, There are no preventive measures for Eales disease. Patients are advised to report to a retina specialist on an urgent basis in case of complaints of floaters, flashes of light, or sudden diminution of vision., Complications : epiretinal membrane, Macular edema, RETINAL DETACHMENT, VITREOUS HAEMORRHAGE, neovascular glaucoma, Choroidal neovascularization, Diagnostics : RETINOSCOPY, ultrasound, Fluorescein angiography, Fundus fluorescein angiography (FFA), Differential diagnosis : coats disease, Cytomegalovirus (CMV), diabetic neuropathy, Lyme disease, Syphilis, disease description : Eales disease classically presents with repeated vitreous hemorrhage in young adults. It is most commonly found in the Indian subcontinent. It commonly affects the peripheral fundus and is characterized by retinal vasculitis. In the year 1880, it was Sir Henry Eales, who first described the Eales disease in a cluster of young males, as idiopathic obliterative vasculopathy, which presented with recurrent vitreous hemorrhage in association with headache, constipation, and epistaxis.

Early Invasive (microinvasive) Squamous Cell Carci

Disease Name : Early Invasive (microinvasive) Squamous Cell Carci, Treatment : medication : Bevacizumab , Cisplatin , Paclitaxel, The treatment of squamous cervical cancer may be surgical and/or radiotherapeutic. Radiotherapy may be used for all stages of squamous cervical cancer, although in practice few centres would treat stage IA1 disease other than by surgical excision. Surgery is usually reserved for disease confined to the cervix. Radiotherapy regimes vary and may be used exclusively or to shrink the tumour in preparation for surgical excision., Pathophysiology : The pathophysiology of early invasive SCC involves a progression of genetic and cellular changes that lead to uncontrolled growth and invasion of squamous cells.Genetic Alterations : Early invasive SCC is associated with genetic mutations and alterations in the affected squamous cells. These mutations can be acquired or inherited and affect key genes involved in cell growth regulation, DNA repair, and apoptosis (programmed cell death). Specific genes that are commonly affected in SCC include TP53, NOTCH1, and CDKN2A, among others. These genetic alterations disrupt the normal cellular processes and allow the affected cells to proliferate uncontrollably.Dysregulation of Cell Proliferation : The genetic alterations in early invasive SCC lead to dysregulation of cell proliferation and cell cycle control. Normal mechanisms that ensure proper cell division and growth are disrupted, resulting in the uncontrolled proliferation of squamous cells within the epithelial layer. The rapid proliferation of these abnormal cells contributes to the growth and expansion of the tumor.Invasion of Tumor Cells : As the tumor progresses from carcinoma in situ (non-invasive) to early invasive SCC, the malignant squamous cells acquire the ability to invade surrounding tissues. This invasion involves the degradation of the basement membrane and extracellular matrix, allowing the tumor cells to penetrate into deeper layers of tissue. Various proteolytic enzymes, such as matrix metalloproteinases (MMPs), are involved in this process by breaking down the extracellular matrix components.Angiogenesis : Tumor cells need a blood supply to sustain their growth and invasion. To promote angiogenesis (formation of new blood vessels), tumor cells secrete various angiogenic factors, such as vascular endothelial growth factor (VEGF). The newly formed blood vessels provide oxygen and nutrients to the growing tumor, enabling its further progression., Epidemiology : 90–95% of cases of invasive cervical disease are squamous cell carcinomas, 5 - 499 per 1, 000 individuals, variable, Complications : nan, Diagnostics : Colposcopy, Differential diagnosis : nan, disease description : “Microinvasive disease” is a widely used term, which refers to very early disease that has breached the basement membrane but has not spread beyond the superficial stroma. Currently, the term is reserved for lesions with a depth of less than 3 mmthese very early lesions are usually asymptomatic and are recognized either colposcopically or, more usually, at histological examination of colposcopically directed biopsies. A screening test may have been positive. Symptoms, when present, would usually be confined to intermenstrual or postcoital bleeding. 

Eastern Equine Encephalitis

Disease Name : Eastern Equine Encephalitis, Treatment : symptomatic treatment, There is no specific treatment for eastern equine encephalitis (EEE); clinical management is supportive. Patients with severe meningeal symptoms often require pain control for headaches and antiemetic therapy and rehydration for associated nausea and vomiting., Pathophysiology : The pathophysiology of EEE involves several key steps in the progression of the disease : Transmission : The primary transmission cycle of EEE involves mosquitoes as the vectors. Mosquitoes become infected with EEEV by feeding on infected birds, which serve as the natural reservoir hosts. Once infected, mosquitoes can transmit the virus to humans and other mammals through their bites.Entry and replication : When an infected mosquito bites a human, the EEEV is introduced into the bloodstream. The virus primarily targets cells of the central nervous system (CNS), including neurons and glial cells. The virus enters these cells and begins to replicate, leading to the spread and multiplication of the virus within the CNS.Inflammatory response : As the virus replicates in the CNS, it triggers an immune response. This immune response involves the activation of immune cells, such as microglia and astrocytes, which release inflammatory molecules called cytokines. The inflammatory response is an essential defense mechanism against the virus, but it can also contribute to the pathogenesis of EEE by causing damage to the surrounding healthy brain tissue.Neuronal injury and cell death : The replication of EEEV and the associated inflammatory response can lead to direct injury to neurons in the brain. The virus can disrupt normal cellular processes, damage neuronal membranes, and induce apoptosis (programmed cell death). This neuronal injury and cell death contribute to the clinical manifestations of EEE, including neurological symptoms.Blood-brain barrier disruption : The blood-brain barrier (BBB) is a protective barrier that separates the bloodstream from the brain. In EEE, the inflammatory response can lead to the disruption of the BBB, allowing immune cells and other molecules to enter the brain more easily. This disruption further amplifies the inflammatory response and can contribute to the worsening of neurological symptoms.Severe brain inflammation : In some cases of EEE, the inflammatory response becomes dysregulated and excessive, leading to severe brain inflammation, also known as encephalitis. This can result in swelling of the brain, increased intracranial pressure, and further neurological damage., Epidemiology : an average of 11 human cases of EEE are reported annually., 1 case per 200, 000 population in the United States, , variable, mosquito replaint ,mosquito net ,full cover clothes, Complications : nan, Diagnostics : CSF EXAMINATION, PCR, Differential diagnosis : nan, disease description : Eastern equine encephalitis (EEE) virus is spread to people by the bite of an infected mosquito. Only a few cases are reported in the United States each year. Most cases occur in eastern or Gulf Coast states. Although rare, EEE is very serious. Approximately 30% of people with EEE die and many survivors have ongoing neurologic problems.

Ebolavirus And Marburgvirus Infections

Disease Name : Ebolavirus And Marburgvirus Infections, Treatment : Treatment of EVD,and MVD is entirely supportive because no accepted/approved, ,efficacious, specific antiviral agents or vaccines are yet licensed.,Exceptions are hyperimmune equine immunoglobulin, which has,been approved in Russia for emergency treatment of laboratory,infections, and the anti–Ebola virus monoclonal antibody cocktail,ZMapp, which is on its way to becoming available under U.S., Pathophysiology : Human infections typically occur through direct exposure of skin lesions or mucosal surfaces to contaminated bodily fluids or material or by parenteral inoculation (e.g., via accidental needlesticks or reuse of needles in poorly equipped hospitals). Numerous studies, both in vitro and in vivo (in several animal models of human disease), have shed light on key pathogenetic events that evolve subsequent to filovirion exposure. The GP1, 2 spikes on the surface of filovirions determine their cell and tissue tropism by engaging yet-unidentified cell-surface molecules and the intracellular receptor Niemann-Pick C1. One of the pathogenetic hallmarks of filovirus infection is a pronounced modulation of the immune system. The first targets of filovirions are local macrophages, monocytes, and dendritic cells. Several structural proteins of filovirions (i.e., VP35, VP40, and/or VP24) then suppress intrinsic and innate immune responses by, for instance, inhibiting the interferon pathways and enabling a productive filovirus infection. The result is the secretion of copious numbers of progeny virions, as evidenced by high titers in the bloodstream (>106 plaque-forming units pfu/mL of serum in humans) and the lymphatics, and dissemination to most tissues. Filovirions then infect additional phagocytic cells, including other macrophages (alveolar, peritoneal, and pleural macrophages; Kupffer cells in the liver; and microglia). Other targets, such as adrenal cortical cells, fibroblasts, hepatocytes, endothelial cells, and a variety of epithelial cells, are also infected. Infection leads to the secretion of soluble signaling molecules (varying with the cell type) that most likely are crucial factors in immune response modulation and development of multiorgan dysfunction syndrome. For instance, infected macrophages react by secreting proinflammatory cytokines, a response that leads to further recruitment of macrophages to the site of infection. In contrast, infected dendritic cells are not activated to secrete cytokines, and expression of major histocompatibility class II antigens is partially suppressed. Immunosuppression occurs in part by massive lymphoid depletion in lymph nodes, spleen, and thymus in the absence of reactive inflammatory cellular responses. Other pathogenetic hallmarks of filovirus infections are a severe disturbance of the clotting system and the impairment of vascular integrity. Disseminated intravascular coagulation is the cause of the severe imbalance in the clotting system of filovirus-infected patients. Thrombocytopenia, increased concentrations of tissue factor, consumption of clotting factors, increased concentrations of fibrin degradation products (d-dimers), and declining concentrations of protein C are typical features of infection. Consequently, the occlusion of small vessels by widely distributed microthrombi leads to extensive necroses/hypoxic infarcts in target tissues (particularly the gonads, kidneys, liver, and spleen) in the absence of marked inflammatory responses. In addition, petechiae, ecchymoses, extensive visceral effusions, and other hemorrhagic signs are observed in internal organs, mucous membranes, and skin. Actual severe blood loss, however, is a rare event (although it frequently occurs during or after childbirth). Aberrance in cytokines 1513 or other factors such as nitric oxide and direct infection and activation of endothelial cells most likely are responsible for upregulated permeability of blood-vessel endothelia. This upregulation leads to fluid redistribution (third spacing); interstitial and myocardial edema and hypovolemic shock are common developments. Clinical improvement is possible and is usually characterized by falling viral titers during the development of a virus-specific immune response., Epidemiology : POOR, Currently, filovirus vaccines are not available. Prevention of filovirus infection in nature is difficult because the ecology of the viruses is not completely understood.To prevent spread, symptomatic patients with possible Ebola or Marburg virus infection must be isolated in dedicated containment facilities. Standard intensive care units (ICUs) in public hospitals are not suitable. Special containment facilities provide for total control of fluid effluent and respiratory products., Complications : coma, death, delirium, jaundice, seizures, shock, organ failure, severe bleeding, Diagnostics : ABG, SERUM Creatinine, MRI Brain, LIVER FUNCTION TEST LFT, SERUM ELECTROLYTE, ELISA, RT PCR, Differential diagnosis : Chikungunya, Dengue without warning signs, TYPHOID FEVER, disease description : Several viruses of the family Filoviridae cause severe and frequently fatal infections in humans. Introduction of filoviruses into human populations is an extremely rare event that most likely occurs by direct or indirect contact with healthy filovirus hosts or by contact with infected, sick, or deceased mammals. Filoviruses are highly infectious but not especially contagious. Human-to-human transmission takes place through direct person-to-person (usually skin-to-skin) contact or exposure to infected bodily fluids and tissues; no evidence of such transmission by aerosol or respiratory droplets in natural outbreak settings is available. Infections progress rapidly from influenza-like to gastrointestinal manifestations and coagulopathy, typically culminating in multiple-organ dysfunction syndrome and shock. The occurrence of primary subclinical infections is controversial, but a small percentage of survivors may be subclinically and persistently infected. Treatment of filovirus infections is entirely supportive in nature because no specific efficacious antiviral agents or vaccines are yet licensed. Filoviruses are categorized as World Health Organization (WHO) Risk Group 4 Pathogens. Consequently, all work with material suspected of containing replicating filoviruses should be conducted only in maximal containment (biosafety level 4) laboratories, or the viruses should be properly inactivated prior to further analysis in biosafety level 2 laboratories. Experienced personnel handling these viruses must wear appropriate personal protective equipment (see “Control and Prevention, ” below) and follow rigorous standard operating procedures. The proper national authorities and WHO reference laboratories should be contacted immediately when filovirus infections are suspected.

Ebstein Anomaly

Disease Name : Ebstein Anomaly, Treatment : In infants, the mainstay of treatment is supportive to help reduce pulmonary vascular resistance and hypoxemia. In symptomatic infants with either heart failure or cyanosis, inhaled nitric oxide can help reduce pulmonary vascular resistance. In cases of extreme cyanosis, prostaglandin E1 infusion can be used to keep the patent ductus arteriosus open and lower pulmonary vascular resistance by increasing pulmonary vasodilation. Newborns with heart failure and cardiogenic shock may need to be treated with inotropes, of which Milrinone is the drug of choice since it also helps with pulmonary vasodilation. Catecholamines like epinephrine and norepinephrine are avoided as they carry a high risk of tachyarrhythmias in these patients ., Due to high periprocedural mortality, surgery is usually delayed till age four and avoided in newborns unless they meet specific indications. Indications for surgery in a neonate include : ,,Right heart failure due to severe tricuspid regurgitation,A cardiothoracic ratio of greater than 80 percent,Severe cyanosis,In children and adults, indications for surgery are : ,,Heart failure symptoms,Evidence of right ventricular dysfunction or progressive dilation,Evidence of paradoxical emboli,Intractable atrial arrhythmia,Cyanosis,Severe tricuspid regurgitation ., Pathophysiology : The tricuspid valve anomaly results in obstruction to forward flow of blood as well as regurgitation of blood from the right ventricle into the right atrium. In addition, there is a large part of the right ventricle that is atrialized as a result of downward displacement of the tricuspid valve attachment. This atrialized right ventricle contracts with the rest of the ventricle and does not allow effective forward flow into the pulmonary circulation. The right atrium progressively dilates, to accommodate the extra volume. The foramen ovale may be patent or there is an atrial septal defect allowing a right to left shunt to occur. This results in cyanosis. The greater the tricuspid valve displacement, the more the cyanosis., Epidemiology : unknown, 1 per 200 000 live births and accounting for <1% of all cases of congenital, variable, Since healthcare providers don’t know how Ebstein’s anomaly develops, you can’t prevent it., Complications : cardiac failure, Infective endocarditis, neurological disturbances, PULMONARY ARTERIAL HYPERTENSION, Diagnostics : 2-D Echo, ECG, X RAY CHEST, CHEST X RAY, Differential diagnosis : Congenital tricuspid atresia, hypoplastic left heart syndrome, pulmonary atresia, tetralogy of fallot, "Uhls anomaly", disease description : An unusual and rare cyanotic congenital heart disease with diminished pulmonary blood flow results from an abnormality of the tricuspid valve. The posterior as well as the septal leaflet of the tricuspid valve is displaced downwards to a variable extent. The result is an attachment to the posterior wall of the right ventricle. In addition, the leaflets are malformed and fused resulting in obstruction to flow of blood into the right ventricle. The portion of the right ventricle above the leaflet attachment thins out and is called atrialized right ventricle. The right ventricular contraction is also abnormal.

Ecchymosis Of Conjunctiva

Disease Name : Ecchymosis Of Conjunctiva, Treatment : • Treat the cause when discovered.,• Placebo therapy with astringent eye drops.,• Psychotherapy and assurance to the patient is most,important part of treatment.,• Cold compresses to check the bleeding in the,initial stage and hot compresses may help in,absorption of blood in late stages., Pathophysiology : Subconjunctival haemorrhage may be associated with following conditions : 1. Trauma. It is the most common cause of subconjunctival haemorrhage. It may be in the form of (i) local trauma to the conjunctiva including that due to surgery and subconjunctival injections, (ii) retrobulbar haemorrhage which almost immediately spreads below the bulbar conjunctiva. Mostly, it results from a retrobulbar injection and from trauma involving various walls of the orbit. 2. Inflammations of the conjunctiva. Petechial subconjunctival haemorrhages are usually associated with acute haemorrhagic conjunctivitis caused by picorna viruses, pneumococcal conjunctivitis and leptospirosis, icterohaemorrhagica conjunctivitis. 3. Sudden venous congestion of head. The subconjunctival haemorrhages may occur owing to rupture of conjunctival capillaries due to sudden rise in pressure. Common conditions are whooping cough, epileptic fits, strangulation or compression of jugular veins and violent compression of thorax and abdomen as seen in crush injuries. 4. Spontaneous rupture of fragile capillaries may occur in vascular diseases such as arteriosclerosis, hypertension and diabetes mellitus. 5. Local vascular anomalies like telangiectasia, varicosities, aneurysm or angiomatous tumour. 6. Blood dyscrasias like anaemias, leukaemias and dysproteinaemias. 7. Bleeding disorders like purpura, haemophilia and scurvy. 8. Acute febrile systemic infections such as malaria, typhoid, diphtheria, meningococcal septicaemia, measles and scarlet fever. 9. Vicarious bleeding associated with menstruation is an extremely rare cause of subconjunctival haemorrhage. Subconjunctival haemorrhage per se is symptomless. However, there may be symptoms of associated causative disease. • On examination, subconjunctival haemorrhage looks as a flat sheet of homogeneous bright red colour with well-defined limits . • In traumatic subconjunctival haemorrhage, posterior limit is visible when it is due to local trauma to eyeball, and not visible when it is due to head injury or injury to the orbit. • Most of the time it is absorbed completely within 7 to 21 days. During absorption colour changes are noted from bright red to orange and then yellow. In severe cases, some pigmentation may be left behind after absorption., Epidemiology : prevalence under 0.5%, GOOD, There is no known prevention., Complications : infection, Coagulopathy, Diagnostics : PHYSICAL EXAMINATION, Differential diagnosis : corneal abrasions, CORNEAL ULCER, ENDOPHTHALMITIS, EPISCLERITIS, Hyphema, Intraocular foreign body, iritis, disease description : Ecchymosis or subconjunctival haemorrhage is of very common occurrence. It may vary in extent from small petechial haemorrhage to an extensive one spreading under the whole of the bulbar conjunctiva and thus making the white sclera of the eye invisible. The condition though draws the attention of the patients immediately as an emergency but is most of the time trivial.

Eccrine Syringosquamous Metaplasia

Disease Name : Eccrine Syringosquamous Metaplasia, Treatment : The condition resolves spontaneously but symptom control may be required., treatment with busulfan, fludarabine, and antithymocyte globulin in preparation for bone marrow transplantation., Pathophysiology : Eccrine syringosquamous metaplasia is characterized by the transformation of cuboidal ductal epithelial cells into areas of squamous differentiation. This process has been reported in a wide variety of different settings including pyoderma gangrenosum, panniculitis and infection . It is considered a non-specific marker of eccrine duct damage and may be confused histologically with squamous cell carcinoma. Similar histological changes are seen in patients undergoing chemotherapy, presumably forming part of a spectrum of cytotoxic eccrine damage, which includes neutrophilic eccrine hidradenitis, Epidemiology : three cases of eccrine squamous syringometaplasia secondary to extravasation of docetaxel., variable, Complications : nan, Diagnostics : PHYSICAL EXAMINATION, full thickness skin biopsy, Differential diagnosis : nan, disease description : Eccrine squamous syringometaplasia (ESS) is a histologically distinctive skin eruption occurring predominantly in acral or intertriginou ESS is histologically defined as metaplasia of the normal eccrine duct epithelium into two or more layers of squamous epithelial cells2. It has been described in patients receiving chemotherapeutic agents for various malignant neoplasms, however, several infectious, neoplastic and inflammatory skin diseases have been found to induce ESS as wells areas presenting as erythematous macules, papules or patches.

Echinococcosis

Disease Name : Echinococcosis, Treatment : Small CL, CE1, and CE3 lesions,may respond to chemotherapy with albendazole, For CE1 lesions,and uncomplicated CE3 lesions, PAIR (percutaneous aspiration, ,infusion of scolicidal agents, and reaspiration) is now recommended,instead of surgery. PAIR is contraindicated for superficially located,cysts (because of the risk of rupture), for cysts with multiple thick,internal septal divisions (honeycombing pattern), and for cysts,communicating with the biliary tree, For prophylaxis of secondary peritoneal echinococcosis due to inadvertent spillage of fluid during PAIR, the administration of albendazole (15 mg/kg daily in two divided doses) should be initiated at least 2 days before the procedure and continued for at least 4 weeks afterward. Ultrasoundor CT-guided aspiration allows confirmation of the diagnosis by demonstration of protoscolices in the aspirate., Surgery remains the treatment of choice for complicated cystic,echinococcosis (e.g., cysts communicating with the biliary tract), for,most thoracic and intracranial cysts, and for areas where PAIR is,not possible, Pathophysiology : The pathophysiology of echinococcosis involves several key steps : Infection : The life cycle of Echinococcus involves two hosts. The adult tapeworm resides in the intestines of definitive hosts, typically dogs or other canids. Eggs are released in the feces of the definitive hosts and can contaminate the environment. Intermediate hosts, such as livestock or humans, become infected by ingesting the eggs through contaminated food, water, or direct contact with infected animals.Larval stage formation : Once the eggs are ingested by an intermediate host, they hatch in the intestine and release oncospheres. These oncospheres penetrate the intestinal wall, enter the bloodstream or lymphatic system, and are carried to various organs, primarily the liver and lungs.Hydatid cyst formation : Within the liver or lungs, the oncospheres develop into hydatid cysts, which are the characteristic lesions of echinococcosis. The hydatid cyst is composed of an outer fibrous layer (pericyst) and an inner germinal layer (endocyst) that produces daughter cysts (protoscolices). The cysts grow slowly over time and can reach a considerable size, exerting pressure on the surrounding tissues.Immune response and cyst growth containment : The hosts immune system recognizes the presence of the hydatid cyst and mounts an immune response. However, the cyst is equipped with various mechanisms to evade the host immune system, such as the production of immunomodulatory molecules. The immune response typically leads to the formation of a fibrous capsule around the cyst, attempting to contain its growth and prevent systemic dissemination., Epidemiology : More than 1 million people are affected with echinococcosis at any one time, 50 per 100 000 person-years, variable, To Do : Prevention In endemic areas, echinococcosis can be prevented by administering praziquantel to infected dogs, by,denying dogs access to viscera from infected animals, or by,vaccinating sheep. Limiting the number of stray dogs is helpful in reducing the prevalence of infection among humans. In Europe, E. multilocularis infection has been associated with gardening; gloves should be used when working with soil., Complications : RUPTURE OF CYST, Compression of a bile duct or leakage of cyst fluid into the biliary tree, Diagnostics : LIVER FUNCTION TEST LFT, ELISA, CT SCAN, USG, Differential diagnosis : AMOEBIC LIVER ABSCESS, Cardiac myxoma, hepatocellular carcinoma, PYOGENIC LIVER ABSCESSS, disease description : Echinococcosis is a parasitic disease that occurs in two main forms in humans : cystic echinococcosis (also known as hydatidosis) and alveolar echinococcosis, caused by the tapeworms Echinococcus granulosus and Echinococcus multilocularis, respectively.Dogs, foxes and other carnivores harbour the adult worms in their intestine and evacuate the parasite eggs in their faeces. If the eggs are ingested by humans, they develop into larvae in several organs, mainly the liver and lungs.Both cystic and alveolar echinococcosis are characterized by asymptomatic incubation periods that can last many years until the parasite larvae evolve and trigger clinical signs.Both diseases can cause serious morbidity and death.

Eclampsia

Disease Name : Eclampsia, Treatment : medication : Magnesium/Magnesium Sulphate, "Magnesium sulfate should be given to control convulsions and is the first-line treatment for eclamptic seizures. A loading dose of 4 to 6 grams should be given intravenously over 15 to 20 minutes. A maintenance dose of 2 g per hour should subsequently be administered. Magnesium treatment should be continued for at least 24 hours after a patients last seizure.,Other antiepileptic medications include diazepam or phenytoin. Benzodiazepines and barbiturates are used for refractory seizures that are unresponsive to magnesium.Corticosteroids should be given to women with fetal gestation less than 34 weeks if time and circumstances permit to help aid in lung maturation. Delivery should not be delayed for steroid administration.", CAESEREAN SECTION, Pathophysiology : Since eclampsia is a severe form of preeclampsia, the histopathological and biochemical changes are similar; although, intensified than those of preeclampsia as already described. The cause of cerebral irritation leading to convulsion is not clear. The irritation may be provoked by : (1) Anoxia — spasm of the cerebral vessels increased cerebral vascular resistance, fall in cerebral oxygen consumption anoxia, (2) Cerebral edema — may contribute to irritation, (3) Cerebral dysrhythmia — increases following anoxia or edema. There is excessive release of excitatory neurotransmitters (glutamate). Fits occur more commonly in the third trimester (> 50%). On rare occasions, convulsion may occur in early months as in hydatidiform mole. — Antepartum (50%) : Fits occur before the onset of labor. More often, labor starts soon after and at times, it is impossible to diff erentiate it from intrapartum ones. — Intrapartum (30%) : Fits occur for the fi rst time during labor., Epidemiology : 1 in 500 to 1 in 30.(INDIA), POOR, Getting treatment for preeclampsia can reduce your risk of developing eclampsia. Getting prompt medical care, attending all your prenatal appointments and following a healthy lifestyle can also help reduce your risk. Certain conditions (some beyond your control) can put you at higher risk for preeclampsia and eclampsia. Starting low-dose aspirin in the first trimester might decrease your risk of getting preeclampsia if you’re at increased risk., Complications : cardiac failure, Psychosis, renal failure, sepsis, shock, thrombocytopenia, Coagulopathy, edema, Maternal death, TONGUE BITE, Diagnostics : SERUM Creatinine, MRI Brain, URINARY PROTEIN, ABG PO2, CT SCAN, SERUM LACTIC ACID LEVEL, URINE OUTPUT, blood test, Differential diagnosis : cerebral malaria, Epilepsy, Meningitis., Poisoning, disease description : Preeclampsia when complicated with grandmal seizures (generalized tonic-clonic convulsions) and/or coma is called eclampsia. Thus, it may occur in patients with preeclampsia or in patients who have preeclampsia superimposed on essential hypertension or chronic nephritis.

Ecthyma

Disease Name : Ecthyma, Treatment : medication : Doxycycline , Erythromycin , Clindamycin , Sulconazole nitrate , Fusidic acid /Sodium Fusidate, Mupirocin , Miconazole, Flucloxacillin, Necrotic infected adherent crust should ,be gently removed after soaking with a disinfectant and softening with an oily cream. Topical antibiotics such as fusidic acid and ,mupirocin can be applied twice daily to localized lesions. Topical ,therapy either with sulconazole or miconazole cleared lesions ,satisfactorily over 1 week . Oral antibiotics for 1–2 weeks may ,be required in the context of multiple lesions or immunocompromised vulnerable patients. ,,,First line,•\tTopical fusidic acid,•\tTopical mupirocin,•\tOral flucloxacillin,Second line,•\tTopical sulconazole,•\tTopical miconazole,•\tOral erythromycin,•\tOral doxycycline,Third line,•\tOral clindamycin,•\tPiperacillin iv,•\tGentamicin iv,•\tAmikacin iv,•\tCiprofloxacin iv,•\tOfloxacin iv, Pathophysiology : The GAS may lead to ecthyma on normal skin or may opportunistically penetrate through damaged skin (trauma or underlying dermatitis) and more commonly affects vulnerable patients with immunocompromise (HIV, neutropenia), diabetes and outbreaks in the military are reported. It also more frequently occurs in high humidity environments and in the context of poor hygiene. Pharyngeal carriers of S. pyogenes are also more susceptible to recurrent disease. The infection and resultant inflammation is much deeper in ecthyma than in impetigo and thus there is loss of the epidermis and dermis leading to ulceration and the lesions heal with scarring. Presentation Small bullae or pustules on an erythematous base are soon surmounted by a hard crust of dried exudate, which increases in size by peripheral accretion, with an indurated base. The crust is thicker than that formed in impetigo and is only removed with difficulty, to reveal a purulent, irregular ulcer. The lesions are usually few but new lesions may develop by autoinoculation over a long period. The buttocks, thighs and legs are most commonly affected., Epidemiology : prevalence of > 10% or 15%, Healing usually occurs after a few weeks with scar, Carefully clean the skin after an injury, such as a bite or scratch. Do not scratch or pick at scabs and sores., Complications : CELLULITIS, gangrene, infection, lymphangitis, skin disorders, Diagnostics : Microbiological skin swabs, Differential diagnosis : pyoderma gangrenosum, disease description : Ecthyma is a pyogenic infection of the skin characterized by the formation of adherent crusts, beneath which ulceration occurs. Ecthyma most commonly results from GAS and causes a deeper infection than in impetigo. Extremes of age are most commonly affected.

Ectopic Gestation

Disease Name : Ectopic Gestation, Treatment : medication : Methotrexate, Administration of intramuscular methotrexate or performance of laparoscopic surgery is safe and effective treatment modalities in hemodynamically stable women with a non-ruptured ectopic pregnancy. The decision of which modality to pursue is guided by the patient’s clinical picture, their laboratory findings, and radiologic imaging as well as the patient’s well-informed choice after having reviewed the risks and benefits with each procedure. Patients with relatively low hCG levels would benefit from the single-dose methotrexate protocol. Patients with higher hCG levels may necessitate two-dose regimens. There is literature suggestive that methotrexate treatment does not have adverse effects on ovarian reserve or fertility. hCG levels should be trended until a non-pregnancy level exists post-methotrexate administration. Surgical management is necessary when the patients demonstrate any of the following : an indication of intraperitoneal bleeding, symptoms suggestive of ongoing ruptured ectopic mass, or hemodynamically instability., Surgical management including salpingostomy or salpingectomy should be guided by clinical status, the extent of fallopian tube compromise, and desire for future fertility. In simplest form salpingectomy involves removing the fallopian tube partially or in full. Salpingostomy, or salpingotomy, involves removal of the ectopic pregnancy via tubal incision while leaving the fallopian tube in situ., Pathophysiology : The mechanisms responsible for ectopic implantation are unknown. The four main possibilities are an anatomic obstruction to the passage of the zygote, an abnormal conceptus, abnormalities in the mechanisms responsible for tubal motility, and transperitoneal migration of the zygote.Anatomic distortion and obstruction of the fallopian tube are widely believed to be responsible for most ectopic implantations. Obstruction could result from PID, salpingitis isthmica nodosa, tubal endometriosis, or postsurgical fibrosis. Scarring of the endosalpinx could lead to diverticuli formation, in which the zygote could be trapped, or to simple obstruction of the tubal passage. Support for the contribution of an anatomic cause is the demonstration of histologic and gross evidence of past infection in 30–50% of cases of ectopic gestation. Other researchers studying the isthmic portion of the fallopian tube, however, have failed to demonstrate significant pathology (e.g., fibrosis, chronic inflammation of endometriosis) associated with ectopic pregnancy. This observation suggests the contribution of nonanatomic factors to the etiology of ectopic pregnancy. Functional causes could include a defective conceptus, abnormalities in the motility of the fallopian tube, or transperitoneal migration.An abnormal conceptus could theoretically result in defective migration of premature implantation in an ectopic site. This possibility has been investigated by examining the chromosomal constitution of ectopic gestations. Elias and co-workers found that the incidence of chromosomal abnormalities in ectopic pregnancies is no different from that in intrauterine pregnancies. The bias with this type of study, however, is that a significant proportion of ectopic pregnancies cannot be adequately karyotyped because of the nonviability of their cells in culture. Similarly, Fedele and colleagues, in a case-control study, reported the risk of ectopic pregnancy (after adjustment for maternal age and parity) to be fourfold greater in women with a history of recurrent spontaneous abortion., Epidemiology : The estimated rate of ectopic pregnancy in the general population is 1 to 2% and 2 to 5% among patients who utilized assisted reproductive technology., The reported incidence of ectopic gestation increased from a total of 17, 800 cases in 1970 to 108, 800 cases in 1992 (19.7/1000 reported pregnancies., POOR, You can’t prevent an ectopic pregnancy. However, you can try to reduce your risk by following good lifestyle habits. These can include not smoking, reaching and maintaining a healthy weight and preventing any sexually transmitted infections (STIs). Talk to your healthcare provider about any risk factors you may have before trying to become pregnant., Complications : Abortion, death, vaginal bleeding, hemorrhage, Diagnostics : PREGNACY TEST, TVS (Transvaginal ultrasound), USG, MRI PELVIS, Differential diagnosis : FIBROID UTERUS, Pelvic Inflamatory Disease, Septic Abortion, Torsion or rupture of ovarian cyst, TUBO OVARIAN ABSCESS, disease description : Ectopic pregnancy is a known complication of pregnancy that can carry a high rate of morbidity and mortality when not recognized and treated promptly.  It is essential that providers maintain a high index of suspicion for an ectopic in their pregnant patients as they may present with pain, vaginal bleeding, or more vague complaints such as nausea and vomiting. Fertilization and embryo implantation involve an interplay of chemical, hormonal, and anatomical interactions and conditions to allow for a viable intrauterine pregnancy.  Much of this system is outside the scope of this article but the most relevant anatomical components to our discussion on the ovaries, fallopian tubes, uterus, egg, and sperm.  Ovaries are the female reproductive organs located to both lateral aspects of the uterus in the lower pelvic region. Ovaries serve multiple functions, one of which is to release an egg each month for potential fertilization. The fallopian tubes are tubular structures that serve as a conduit to allow transport of the female egg from the ovaries to the uterus. When sperm is introduced, it will fertilize the egg forming an embryo. The embryo will then implant into endometrial tissue within the uterus. An ectopic pregnancy occurs when this fetal tissue implants somewhere outside of the uterus or attaching to an abnormal or scarred portion of the uterus.

Ectopic Hamartomatous Thymoma

Disease Name : Ectopic Hamartomatous Thymoma, Treatment : Local mass resection is the recommended treatment method., Pathophysiology : Pathogenesis involves-Sheets of spindled epithelial cells resembling neurogenic or fibroblastic tumorsAlso epithelial nests, thin anastomosing cords and epithelial lined cystsMay have focal adipose tissue, small lymphocytesNo atypia, no necrosis, no mitotic figures, Epidemiology : There are 80 cases of the disease reported i, variable, Complications : nan, Diagnostics : CT SCAN, ELECTRON MICROSCOPY, Immunostaining, Differential diagnosis : ANGIOMYOLIPOMA, Fibrosarcoma, Mixed tumour (chondroid syringoma), disease description : Ectopic hamartomatous thymoma (EHT) is a rare benign neoplasm that almost exclusively occurs in the lower neck area of adult patients with a remarkable male predominance 1. Histologically, EHT is characterized by an admixture of spindle cells, epithelial islands, and adipocytes

Ectropion

Disease Name : Ectropion, Treatment : 1.Involutional ectropion : Medial conjunctivoplasty, Horizontal lid shortening, Byron Smith’s modified Kuhnt-Szymanowski,operation, Lateral tarsal strip technique. 2. Paralytic ectropion : Horizontal lid tightening with or without middle,lamellar buttress such as ear cartilage, Palpebral sling operation.3. Cicatricial ectropion : V-Y operation, Z-plasty (Elschnig’s operation), Excision of scar tissue and full thickness skin,grafting, 4.Mechanical ectropion. It is corrected by treating,underlying mechanical force causing ectropion, 5. Congenital ectropion : Moderate or severe ectropion is,treated like cicatricial ectropion with horizontal lid,tightening and full thickness skin graft to vertically,lengthen anterior lamella., Pathophysiology : Senile Ectropion Involutional ectropion usually develops as a result of laxity of the suspensory system of the lower eyelid, and the medial and lateral canthal ligaments, allowing the lid to fall away from the globe. This laxity is accompanied by a horizontal lengthening of the lid. Paralytic Ectropion Paralytic ectropion is commonly caused by a paralysis of the facial nerve, in Bell palsy, parotid surgeries, trauma and tumours such as an acoustic neuroma. Initial conservative therapy with taping of the lids and the use of lubricants allows time for recovery of the palsy. As a more permanent solution, lateral tarsorrhaphy may be indicated. In this operation the palpebral aperture is shortened by uniting the lids at the outer canthus. Cicatricial Ectropion Cicatricial ectropion is commonly the result of burns, trauma and chronic inflammations of the skin which shorten the anterior lamina of the eyelid, i.e. the skin–muscle layers. This pulls the eyelid away from the globe., Epidemiology : The prevalence of involutional lower lid ectropion in elderly patients has been reported as high as 2%. It may be associated with trauma., GOOD, Most of the time, you really can’t prevent ectropion. However, you can take some steps to protect your eyes and eyelids. For instance, you can be careful about how often and how firmly you rub your eyes, taking care not to stretch your skin there.,,You can also protect your skin and eyes from harsh sunlight and wear sunglasses. Always wear safety glasses when you need them for work.,,If you do wear contact lenses, make sure you clean them properly and dispose of them when you should. Always make sure your hands are clean when you’re putting lenses in and taking them out. Try to be gentle with your lids., Complications : corneal ulcers, dermatitis, ECZEMA, Dryness and thickening of conjunctiva, Diagnostics : PHYSICAL EXAMINATION, Differential diagnosis : Basal cell carcinoma, Bell’s palsy, ichthyosis, Squamous cell carcinoma, disease description : Ectropion is an outward turning of the eyelid margin. This typically occurs on the lower eyelids. When the globe is not protected properly, the eye can become very dry. This dryness may lead to symptoms of redness, tearing, and foreign body sensation secondary to exposure of the ocular surface and an inadequate tear film. In extreme cases, the cornea can develop punctate epithelial erosions, ulceration, and permanent vision loss. Management almost always begins with lubrication with artificial tears, gels, and ointments. Surgical repair is commonly needed to improve the function of the eyelid and to protect the globe permanently .

Eczema Herpeticum

Disease Name : Eczema Herpeticum, Treatment : medication : Valaciclovir , Famciclovir , Aciclovir , First line,Less ill patients respond well to oral aciclovir, valaciclovir or ,famciclovir.,,Second line,Severe cases should receive intravenous aciclovir as early as ,possible. Infection in pregnancy has been treated with aciclovir ,without adverse effect to the baby.,,Third line,Frequently recurrent disease may benefit from low-dose prophylactic aciclovir or valaciclovir., Pathophysiology : Localized eczema herpeticum is not rare among patients with atopic eczema. Eczema herpeticum may be worse in patients with severe, especially erythrodermic, atopic eczema, but frequently occurs in mild or quiescent case. In localized cases, local spread seems likely, but widespread dissemination is haematogenous. Patients who develop eczema herpeticum are usually immunocompetent and have, or can develop, antibodies against the virus. Recent studies have identified possible risk factors for the development of eczema herpeticum in individuals with atopic eczema. An early age of onset of atopic eczema, high IgE level , antibodies against Malassezia sympodialis, a poor in vitro response of peripheral blood mononuclear cells to HSV particles and a low NK cell count have all been found in eczema herpeticum patients. A further possible predisposing factor is a defect in the innate immune response as shown by a low skin level of the antimicrobial peptide cathelicidin, LL-37 , human ß-defensin 452 and abnormalities in the interferon pathway . An association with systemic or topical steroid treatment has not been consistently found. Other topical and systemic immunosuppression has also been associated with eczema herpeticum, namely topical tacrolimus or pimecrolimus. One study from Japan has suggested that genetic variation in the IL-18 gene in individuals with atopic eczema may cause an increased propensity to develop eczema herpeticum. It is possible that the predisposition to develop widespread herpes simplex is linked more with the severity of the eczema or a limited immune defect rather than with the type or quantity of treatment used., Epidemiology : 15-20% of children 1 and 1-3% of adults worldwide, FAIR, To Do : should avoid close contact with relatives and ,friends with active herpes simplex, Complications : Bone marrow suppression, infection, meningoencephalitis, herpetic keratitis, , Disseminated intravascular coagulation, Diagnostics : BLOOD CULTURE test, Erythrocyte Sedimentation Rate (ESR), SEROLOGIC TEST, PCR, LYMPHOCYTES - ABSOLUTE COUNT, Tzanck smear, Differential diagnosis : allergic dermatitis, Irritant contact dermatitis, Lichen simplex, psoriasis, scabies, disease description : Eczema herpeticum (EH) is a disseminated cutaneous infection with herpes simplex virus that develops in a patient with atopic dermatitis. EH typically presents as a sudden onset eruption of monomorphic vesicles and "punched-out" erosions with hemorrhagic crusts over eczematous areas.

Eczematous Otitis Externa.

Disease Name : Eczematous Otitis Externa., Treatment : medication : Prednisolone, chloromycetin, Treatment is withdrawal of topical antibiotic ,causing sensitivity, 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 : The external auditory canal is covered by hair follicles and cerumen-producing glands. Cerumen provides a protective barrier and an acidic environment that inhibits bacterial and fungal growth. The inflammatory response in otitis externa is believed to be caused by a disruption of the normal pH and protective factors within the auditory canal. This includes a sequential process of damage to the epithelium, loss of protective wax, and accumulation of moisture that leads to a higher pH and bacterial growth ., Epidemiology : Otitis externa is a common condition and can occur in all age groups. It is uncommon in patients younger than 2 years old .. Approximately 10% of people will develop otitis externa during their lifetime, and the majority of cases (95%) are acute., Its incidence is unknown, but it peaks around the age of 7-14, good, "To help reduce your chances of developing otitis externa, you should avoid inserting cotton wool buds and other things into your ears (including your fingers), as this can damage the sensitive skin in your ear canal.,,If youre a regular swimmer, consider using ear plugs when swimming or wearing a swimming cap to cover your ears and protect them from water.,,You should also try to avoid getting water, soap or shampoo into your ears when you have a shower or bath.", Complications : osteomyelitis, PERICHONDRITIS, Myringitis Bullosa, Facial cellulitis and acute ethmoiditis, necrotizing otitis externa, Diagnostics : Skin Prick test, Patch Test, PHYSICAL EXAMINATION, PHYSICAL EXAMINATION, allergy skin test, Differential diagnosis : Bullous impetigo, Dermatitis herpetiformis, disseminated infection, ECZEMA, HAND FOOT MOUTH DISEASE, Varicella, disease description : Otitis externa is an inflammatory condition of the external auditory canal (the ear canal). It is characterised by redness, swelling, scaling and thickening of the canal skin lining and is accompanied by varying degrees of discomfort, itch, deafness and discharge.Otitis externa (OE) is an inflammation, that can be either infectious or non-infectious, of the external auditory canal. In some cases, inflammation can extend to the outer ear, such as the pinna or tragus. OE can be classified as acute (lasts less than 6 weeks) or chronic (lasts more than 3 months). It is also known as swimmers ear as it often occurs during the summer and in tropical climates and having retained water in the ears increases the risk for it.

Eczema

Disease Name : Eczema, Treatment : medication : Mycophenolate mofetil/ Mycophenolate sodium, Cyclosporine/Ciclosporine, Tacrolimus , Methotrexate, Azathioprine , Hydroxyzine, First line ,• Avoidance of irritants and allergens, emollients and soap,substitutes , Second line ,• Topical corticosteroids and topical calcineurin inhibitors, Phototherapy, Pathophysiology : Certain irritants may provoke a chronic reaction in which an effect on epidermal cell turnover predominates, leading to lichenification; whereas in acute irritant reactions inflammatory mediator and cytokine release is similar to that seen in acute allergic contact dermatitis. There is debate whether the cytokine profiles of the two reactions differ. Indeed, it has been proposed that irritant reactions to haptens may be required to facilitate contact sensitization. After activation of the immune pathway by cytokine release, the accumulation of inflammatory cells progresses, leading to the morphological changes that are apparent histologically and clinically. The histological changes of primary irritant dermatitis are similar to those seen in allergic contact dermatitis , but they appear to proceed more quickly, depending on the concentration of the irritant used. Both intracellular and intercellular oedema are visible throughout the epidermis at 3–6 h, and within 24 h there may be epidermal necrosis, with cellular vacuolation and nuclear pyknosis. In severe forms, the primary epidermal damage may progress to subepidermal blister formation., Epidemiology : 10.1%, Nearly 10% of Indian adults suffer from eczema., variable, There are steps you can take that may prevent eczema flare-ups and outbreaks, including : ,,Moisturize your skin regularly or when your skin becomes dry. Seal in moisture after a bath or shower by immediately applying moisturizer to your skin.,Take baths or showers with warm, not hot, water.,Stay hydrated and drink at least eight glasses of water each day. Water helps keep your skin moist.,Wear loose clothes made of cotton and other natural materials. Wash new clothing before wearing it. Avoid wool or synthetic fibers.,Manage your stress and emotional triggers. See a psychiatrist for medication and a therapist for counseling if you’re experiencing symptoms of poor mental/emotional health.,Use a humidifier if dry air makes your skin dry.,Avoid irritants and allergens., Complications : fever with chills, WEEPING ECZEMA, INFECTED ECZEMA, Diagnostics : serum IgE level, Bacteria Culture Test, Patch Test, skin biopsy with immunohistochemistry, direct microscopy, Dermoscopy, Differential diagnosis : Acute Otitis Media, Atopic dermatitis, Folliculitis and furunculosis, psoriasis, ramsay hunt syndrome, Subacute cutaneous lupus erythematosus, disease description : Eczema, a term derived from the Greek word ‘e??eµa’ meaning ‘to boil’, is a clinical and histological pattern of inflammation of the skin seen in a variety of dermatoses with widely diverse aetiologies. Clinically, eczematous dermatoses are characterized by variable intensity of itching and soreness, and, in variable degrees, a range of signs including dryness, erythema, excoriation, exudation, fissuring, hyperkeratosis, lichenification, papulation, scaling and vesiculation.

Edema Of Larynx (post Intubation Laryngeal Edema)

Disease Name : Edema Of Larynx (post Intubation Laryngeal Edema), Treatment : medication : Adrenaline (Epinephrine), If there is airway obstruction, intubation of larynx or tracheostomy will be immediately required., Less severe cases ,are treated conservatively and treatment will depend on ,the cause. Steroids are useful in epiglottitis, laryngo-tracheo-bronchitis or oedema due to traumatic allergic or postradiation causes, Pathophysiology : Post-intubation laryngeal edema, also known as edema of the larynx, is a condition characterized by swelling and inflammation of the laryngeal structures following intubation or airway manipulation. The pathophysiology of post-intubation laryngeal edema involves several factors and mechanisms : Mechanical Injury : The placement of an endotracheal tube or other airway devices can cause direct mechanical trauma to the laryngeal tissues. The pressure exerted by the tube, along with friction and movement during intubation or extubation, can damage the delicate mucosal lining of the larynx and disrupt blood vessels, leading to tissue injury and subsequent edema.Ischemia and Reperfusion Injury : During intubation, there may be temporary interruption of blood flow to the laryngeal tissues, leading to ischemia (lack of oxygen and nutrients). When blood flow is restored after tube placement or removal, reperfusion injury can occur. Reperfusion injury involves the generation of reactive oxygen species and the release of inflammatory mediators, causing tissue damage and edema.Inflammatory Response : The mechanical trauma and ischemia-reperfusion injury trigger an inflammatory response within the laryngeal tissues. This response involves the release of various inflammatory mediators, such as cytokines, leukotrienes, and prostaglandins. These mediators cause blood vessel dilation, increased vascular permeability, and recruitment of immune cells, leading to tissue swelling and edema.Increased Capillary Permeability : Inflammation and the release of inflammatory mediators disrupt the integrity of the blood vessel walls, leading to increased capillary permeability. This allows fluid, proteins, and immune cells to leak into the interstitial spaces of the laryngeal tissues, resulting in localized edema., Epidemiology : between 5% to 54 %, GOOD, avoidance of cold fluid, cold air , smoking & alcohol consumption.,Absolute voice rest, Complications : infections, respiratory failure, Diagnostics : Laryngoscopy, USG, Indirect Laryngoscopy, Differential diagnosis : angioedema, foreign body, laryngospasm, post-surgical complications, vocal cord palsy, disease description : Laryngeal injuries are common after endotracheal intubation, which could manifest as varying degrees of edema, ulceration, granulation, and restricted vocal cord mobility, often resulting in luminal narrowing. Among these conditions, laryngeal edema is a common complication following intubation and usually results from the direct pressure and the inflammatory reaction triggered by the endotracheal tube on surfaces of contact.Post-intubation laryngeal edema (rather than the term post-extubation laryngeal edema) might be a more appropriate term to denote laryngeal edema, which has got the potential to cause respiratory difficulty and/or stridor following extubation. The pathologic process, which results in edema, indeed, starts soon after intubation though it becomes clinically evident only after removal of the endotracheal tube. The prompt recognition and management of post-intubation laryngeal edema before extubating a patient is extremely important, given the fact that any reintubation event could increase the morbidity and mortality of the patients .

Ehlers-danlos Syndrome

Disease Name : Ehlers-danlos Syndrome, Treatment : Any provider caring for a patient with Ehlers-Danlos syndrome should be aware of the multitude of complications of the disease and potential preventative measures. Treatment and management of patients with EDS should use a multidisciplinary approach that focuses on preventing disease progression and subsequent complications as there is no cure for the disease. Specialists generally manage specific care within the field of which the patient has concerning pathology. For example, cardiovascular concerns will be monitored by a cardiologist; likewise, musculoskeletal pathology is monitored and treated by an orthopedist. Often, a geneticist or family medicine provider acts as the primary provider referring the patient to these specialists., Specific orthopaedic management is directed at,addressing painful or unstable joints, and physiotherapy,is a central component of treatment. Persistent,instability and severe and deteriorating joint pain, ,refractory to non-operative treatment, may require a,surgical solution, Pathophysiology : The pathophysiology of most Ehlers Danlos syndrome subtypes involves heritable mutations in collagen synthesis and/or processing. The inheritance pattern of these mutations is variable, including autosomal dominant and recessive inheritance involving different mutations; however, it is worth noting that there are reports of spontaneous mutations causing identical genotypes and phenotypes. The collagen affected by these mutations is integral to every body system, from the skin to the integrity of the vasculature, and as such, the symptoms of the disease can be variable and widespread, as discussed throughout this manuscript.The collagen defect is identified in at least six of the variants of EDS. The vascular type, sometimes referred to as type IV, is secondary to a decreased amount of type III collagen. It is caused by genetic mutations in the COL3A1 gene resulting in excessive connective tissue fragility causing arterial, uterine, and intestinal ruptures and premature death.  Types V and VI are caused by deficiencies in hydroxylase and lysyl oxidase, important posttranslational modifying enzymes in collagen synthesis. The deficiency of amino-terminal procollagen peptidase characterizes type VII. Type IX is caused by abnormal copper metabolism, and nonfunctioning plasma fibronectin is found in type X.In Ehlers-Danlos syndrome types I and II, causative mutations may include the COL5A1, COL5A2,  and tenascin-X genes and are suggested to be in the COL1A2 gene. Nevertheless, in most families with autosomal dominant EDS, the disease seems to be associated with loci that bear the COL5A1 or COL5A2 genes. A significant number of the mutations cause low levels of mRNA due to the mutant allele as a result of nonsense-mediated mRNA decay.Wenstrup et al. observed haploinsufficiency of the COL5A1 that encodes type V collagen in the classic type of EDS. 8 of 28 probands with classic EDS had complete or almost complete loss of expression of 1 COL5A1 allele. One-third of patients with classic EDS were observed to have mutations of COL5A1,  resulting in haploinsufficiency. These findings indicate that the normal synthesis of the heterotypic collagen fibrils containing types I, III, and V collagen needs the expression of both COL5A1 alleles. In classic Ehlers-Danlos syndrome, type V collagen mutations are pivotal.Autosomal recessive–type VI EDS, also referred to as the kyphoscoliotic type, manifests as neonatal kyphoscoliosis, widespread joint laxity, severe muscle hypotonia, and skin fragility at birth. Biochemically, the deficiency of lysyl hydroxylase (LH) is responsible for this type. More than 20 mutations have been identified in the LH1 gene causing LH deficiency and clinical EDS type VI ., Epidemiology : The prevalence of Ehlers-Danlos syndrome is estimated to be between 1 in 5000 and 1 in 100, 000, based on the EDS subtype, but this could be an underestimation. The accurate prevalence of the different EDS subtypes is still not known, an incidence between 1 in 10000 and 1 in 15000, poor, No, you can’t prevent Ehlers-Danlos syndrome. Because you can’t control the genetic mutations that cause it, there’s no way to prevent EDS. Talk to your healthcare provider about genetic counseling if you’re worried about passing EDS (or any other genetic condition) on to your biological children., Complications : MITRAL VALVE PROLAPSE, Cardiac abnormalities, VASCULAR DISORDER, Diagnostics : 2-D Echo, GENETIC TESTING, X RAY, Differential diagnosis : Chronic fatigue syndrome, Fibromyalgia, Marfan syndrome, osteogenesis imperfecta, disease description : Ehlers Danlos syndrome (EDS) is a group of hereditary connective tissue disorders that manifests clinically with skin hyperelasticity, hypermobility of joints, atrophic scarring, and fragility of blood vessels. It is largely diagnosed clinically, although identifying the gene encoding the collagen or proteins interacting with it is necessary to identify the type of EDS. Identifying the type of EDS to guide management and counseling is important. In 2017, a new international classification of EDS was proposed with 13 different variants. This syndrome is heterogeneous and has been classified into six types (classical, vascular, hypermobile, arthrochalasis, kyphoscoliotic, and dermatosparaxis), with the causative collagen pathology being different for each type.Asymptomatic, nonsyndromic joint hypermobility, Ehlers-Danlos syndrome, and hypermobility spectrum disorders (particularly the hypermobile type) are the commonest phenotypes associated with joint hypermobility. Compilations of these syndromes can be chronic pain, dysautonomia, gastrointestinal dysmotility, mast cell activation, and anxiety and phobic states. Many new variants have been identified with the advancements, which tend to be more complex and clinically overlapping.  Clinical recognition of EDS variants is important. For instance, it is important to know that the patient has the vascular type, which is associated with arterial rupture and organ perforation, with potentially life-threatening consequences .

Ehrlichiosis

Disease Name : Ehrlichiosis, Treatment : medication : Doxycycline , Tetracycline , Doxycycline is the treatment of choice for ehrlichiosis and all other tickborne rickettsial diseases. Presumptive treatment with doxycycline is recommended in patients of all ages, including children <8 years., Treatment depends on the use of tetracycline or doxycycline., Pathophysiology : Infection with Ehrlichia species begins with the intracellular uptake of the infectious extracellular form of the organism, the elementary body (EB), or dense core (DC). The elementary body/dense core is then taken up by endocytosis, where the organism replicates and matures to form a reticulate body or reticulate core (RB/RC) and then morula before redifferentiating into an elementary body/dense core that leaves the infected host cell to spread infection. During this process,  Ehrlichia utilizes many immune evasion mechanisms, including suppressing apoptosis of host cells, modulation of chemokine and cytokine responses, and down-regulation of host pattern recognition receptors that might enable clearance of the infection. Ehrlichia preferentially infect peripheral blood leukocytes, with E. chaffeensis associated with human monocytic cells, including monocytes and macrophages, and neutrophil infections reported in E. ewingii. Multiorgan involvement can occur, with organisms detected in the spleen, lymph nodes, bone marrow, and peripheral blood. The clinical manifestations of Ehrlichia infections appear to be due to the host inflammatory response to the infection rather than direct damage from the bacteria., Epidemiology : 0.7 cases per million inhabitants, , variable, Avoiding tick bites is the best way to reduce your risk of ehrlichiosis.,,Keep grass cut shorter than 5 inches.,Stay on cleared paths while in wooded areas.,Use bug sprays with DEET or other ingredients approved to keep ticks away.,Use clothing to cover as much of your skin as possible when you’re in the woods or areas with long grass. You can buy special tick-repellant clothing if you’re often in areas with ticks.,Check yourself for ticks after you’ve been outside. If possible, have someone else check you in places you can’t see yourself (like your back and scalp).,Ask your veterinarian about the best way to protect your pets from ticks. Check your pets for ticks often, especially after they’ve been outside.,Follow directions for safely removing a tick if you find one on you., Complications : heart failure, respiratory failure, septic shock, brain problem, kidney dysfunction, hemorrhage, Diagnostics : SEROLOGIC TEST, LYMPHOCYTES - ABSOLUTE COUNT, THROMBOCYTE COUNT, USG, Differential diagnosis : Bacterial infection, Endocarditis, hepatitis, Influenza, Kawasaki Disease, Leptospirosis, Murine typhus, Q Fever, rocky mountain spotted fever, toxic shock syndrome, TYPHOID FEVER, disease description : The genus Ehrlichia consists of several species of obligate intracellular gram-negative bacteria that infect humans and various other mammals via tick bite. Clinically, Ehrlichia infections share many symptoms and geographic distribution with rickettsial infections, and thus, one must also consider Ehrlichia infections when evaluating patients with flu-like illnesses in endemic areas.

Eisenmenger Syndrome

Disease Name : Eisenmenger Syndrome, Treatment : medication : Warfarin , Cardiopulmonary transplantation is curative for Eisenmenger syndrome. However, this is impractical in most settings. Pharmacology has improved symptoms but not mortality. Potential pharmaceuticals for the treatment of Eisenmenger syndrome include diuretics, antiarrhythmics, and anticoagulation in some patients. ,,Supplemental oxygen has not definitively shown to have a mortality benefit., Vasodilator therapies may provide an opportunity for clinical research, and studies have shown some symptomatic improvement. The Bosentan Randomized Trial of Endothelin Antagonist Therapy-5 (BREATHE-5) trial showed improved exercise capacity and symptomatic improvement with endothelin antagonists in patients with ASD, VSD, and PDA with Eisenmenger syndrome . Warfarin has been classically used for anticoagulation in Eisenmenger syndrome ., Surgical correction of the causative heart defect in adult patients is generally contraindicated . In patients who have developed PAH as a consequence of unrepaired CHD, the defect itself may be acting as a protective measure, preventing worsening of the pulmonary vascular resistance in the face of increasing right ventricular pressure. In children, the development of pulmonary vascular disease (greater than 6 Woods units/m2) with poor vasodilator response is likely to face post-surgical complications, including right heart failure, increased pulmonary hypertension, and hypertensive crises., Pathophysiology : The most common defects leading to Eisenmenger syndrome are ASD, VSD, and PDA defects. The following three main processes result in the ultimate reversal of a left-to-right into a right-to-left shunt :  Vasoconstriction due to imbalances in pulmonary vascular tone,  followed by  Vascular remodeling due to the proliferation of pulmonary vascular smooth muscle,  and finally  Thrombosis caused by the increased resistance of blood flow. , Epidemiology : Eisenmenger syndrome is a relatively rare disorder that is usually seen in persons with poor healthcare access (i.e., rural/underserved areas), in whom large anatomical defects may go undetected for many years., DEPENDS ON SEVERITY OF SYMPTOMS, The only way to prevent Eisenmenger syndrome is to have congenital heart defects repaired as early in life as possible., Complications : bleeding diathesis, paradoxical excitation, pulmonary hypertension, stroke, sudden death, Diagnostics : 2-D Echo, ECG, CARDIAC CATHETERIZATION, MRI, X RAY, CT SCAN, blood test, Differential diagnosis : Chronic Hepatitis B, Hepatitis C, HIV, Mixed Connective Tissue Disease, scleroderma, SYSTEMIC LUPUS ERYTHEMATOSUS, disease description : Eisenmenger syndrome (ES) is a constellation of symptoms that arise from a congenital heart defect and result in large anatomic shunts. Due to anatomic variations present at birth, hemodynamic forces initially result in a left-right shunt,  which develops into severe pulmonary arterial hypertension (PAH) and elevated vascular resistance. Ultimately,  due to increased pulmonary vascular resistance,  the left-to-right shunt will become a right-to-left shunt, resulting in significant hypoxemia and cyanosis. PAH is a mean pulmonary arterial pressure greater than 25 mmHg while resting or 30 mmHg when exercising. This may occur in large shunts or complex, unrepaired congenital heart disease as early as the first decade of life. 

Elastofibroma

Disease Name : Elastofibroma, Treatment : Complete surgical excision in symptomatic patients remains the treatment of choice. postoperative suction is recommended, Pathophysiology : Although elastofibroma has been regarded as the result of a degenerative process involving elastic fibres and in association with trauma, the presence of cytogenetic abnormalities in some tumours suggest that it is more likely to be neoplastic . Comparative genomic hybridization in a series of elastofibromas has found chromosomal alterations in a percentage of cases. The most common alteration consists of gains at chromosome Xq12- q22. The mass is poorly circumscribed, and the appearances are characteristic. Abundant hypocellular hyalinized collagen containing numerous large thick eosinophilic elastic fibres is the most distinctive feature. Sometimes the fibres are beaded and fragmented. Staining for elastic tissue nicely highlights the changes., Epidemiology : incidental lesions in 2%, good, prevention not known ., Complications : hematomas, Diagnostics : MRI, USG, Immunostaining, Immunostaining, Differential diagnosis : Fibroma, sarcoma, spindle cell/pleomorphic lipoma, disease description : Eastofibroma is a rare benign soft-tissue tumor. It is a slow-growing tumor, predominantly seen in elderly females. It often has bilateral location in the thoracic wall. The most common site is in the infrascapular region beneath the muscular tissue.

Elastosis Perforans Serpiginosa

Disease Name : Elastosis Perforans Serpiginosa, Treatment : First line,•\t Conservatism, Second line,•\tTrial of cryotherapy initially to test site, Third line,•\t Curettage, Pathophysiology : Pathogenesis includes the earliest detectable change is the focal development of elastotic-staining tissue and basophilic debris in the dermis. This is followed by a reaction of the overlying epidermis, which grows down to engulf the elastotic material., Epidemiology : approximately 1% of patients treated with the drug., good, Most Of The Time, It’s Not Possible To Prevent The Conditions That Lead To Elastosis perforans . However, Seeking Treatment Early Can Help Minimize Damage And Avoid Serious Complications., Complications : connective tissue disease, Diagnostics : PHYSICAL EXAMINATION, full thickness skin biopsy, Differential diagnosis : Acquired perforating dermatosis, familial reactive perforating collagenosis, perforating granuloma annulare, porokeratosis of Mibelli, disease description : Elastosis perforans serpiginosa is a rare skin disease characterized by transepidermal elimination of abnormal elastic fibers. This condition classically presents as small papules arranged in serpiginous or annular patterns on the neck, face, arms, or other flexural areas. While these lesions may spontaneously resolve, they often persist for longer periods of time.

Embryonal Carcinoma

Disease Name : Embryonal Carcinoma, Treatment : Non-seminomatous germ cell tumors are the most sensitive testicular cancers to cisplatin-based chemotherapy. Patients with elevated markers are typically given 3-4 cycles of bleomycin, etoposide, and cisplatin (BEP) chemotherapy. After completion of chemotherapy, tumor markers are repeated to see the decline in values, along with a contrast-enhanced CT scan to evaluate for any residual mass. If a mass is present with normal tumor markers, this is considered an indication for RPLND. In patients who developed pulmonary fibrosis or with a history of significant pre-existing pulmonary disease, bleomycin would be contraindicated. If the patient still has elevated markers, second-line chemotherapy, including vincristine, ifosfamide, and cisplatin (VIP), should be considered. Other second and third-line agents include gemcitabine, etoposide, paclitaxel, and oxaliplatin. Chemotherapy causes azoospermia in most patients for at least 2 to 3 years after treatment. Cisplatin and similar alkylating agents are the most injurious to spermatogenesis, with Sertoli cells being relatively sensitive but Leydig cells being relatively resistant. Sertoli cells are also very radiosensitive. Overall, fertility is reduced by an average of 30% after chemotherapy treatment for NSGCT, Initial management is radical inguinal orchiectomy., Pathophysiology : The tumor pathogenesis of testicular germ cell tumors is only vaguely understood. It arises from a precursor lesion, germ cell neoplasia in situ (GCNIS), which develops from arrested spermatocytes that failed to differentiate. In mothers during pregnancy, higher estrogen exposure, increased serum levels of polychlorinated biphenyls (other organic pollutants), exposure to organochloride pesticides, firefighting, and aircraft maintenance occupations are hypothesized as risk factors, but this remains controversial. An increased number of genetic material copies from the short arm of chromosome 12 is a universal finding in postpubertal testicular and extragonadal germ cell tumors except for spermatocytic cancers.Non-seminomatous germ cell tumors tend to spread lymphatically, with the exception of choriocarcinoma, which metastasizes hematogenously. Right and left-sided tumors tend to stay on their respective sides initially but may overlap when they become bulky. Right-sided tumors are more likely to develop contralateral nodal metastases due to the higher right-to-left lymphatic flow. Lymphatic drainage from the right testicle is directly into the interaortocaval node at the L2 level, while the lymph drainage from the left testicle empties into the left paraaortic lymph nodes., Epidemiology : Embryonal carcinoma is the most frequent tumor component of testicular mixed GCT, present in ~80 - 90% of cases, Testicular cancer is the most common solid malignancy among young men. The incidence is highest among White race individuals, lowest among African-Americans, and most rapidly increasing in Hispanic populations.25 The incidence in the White race is roughly 4 times higher than in African-Americans ., VARIABLE, "Prevention. Theres no way to prevent testicular cancer. If you get testicular cancer, theres nothing you could have done to prevent it.", Complications : infertility, Retrograde ejaculation, bladder neck incontinence, , Diagnostics : Cytogenetics, MRI, CT SCAN, USG, ELECTRON MICROSCOPY, Immunostaining, Immunostaining, Differential diagnosis : Choriocarcinoma, EPIDIDYMOORCHITIS, Orchitis(Painful and tender testis), SEMINOMA, TORSION OF TESTIS, VARICOCELE, Yolk sac tumor, disease description : Embryonal carcinoma is a type of testicular cancer, which is cancer that starts in the testicles, the male reproductive glands located in the scrotum. It most often develops in young and middle-aged men. It tends to grow rapidly and spread outside the testicle.Testicular neoplasms constitute the most common solid organ malignancy in males between the ages of 15 and 35. They represent only 0.5% to 1% of all solid male cancers (or about 10, 000 cancer cases yearly) in the US and have an excellent five-year survival rate .There are three main types of primary testicular neoplasm : germ cell tumors, sex cord-stroma tumors, and extragonadal tumors. The germ cell tumors are classified histologically into two broad classes : seminomas and non-seminomas. Seminomas are the most common of these germ cell tumors. Still, the non-seminomatous germ cell tumor (NSGCT) is found almost as frequently. It is the most likely testicular cancer to cause metastases which typically affect the lungs, liver, central nervous system, and bone in order of frequency.

Emery-dreifuss Muscular Dystrophy

Disease Name : Emery-dreifuss Muscular Dystrophy, Treatment : Treatment should be supportive, with special attention to cardiac conduction,defects, and can require medications or a pacemaker. Implantable cardioverterdefibrillators are now available and have prevented sudden death in some,patients with Emery-Dreifuss muscular dystrophy, Orthopedic management, use of orthotic devices, or physical therapy,to try to minimize or slow down the rate of progression of contractures may be,beneficial., Pathophysiology : The defective gene in the X-linked form is called EMD or EDMD and encodes a protein, emerin. Unlike other dystrophies in which the defective gene is expressed at the sarcolemmal membrane, emerin is expressed at the inner nuclear membrane; this protein stabilizes the nuclear membrane against the mechanical stresses that occur during muscular contraction. It interacts with Nesprin-1 and Nesprin-2 genes, also critical for nuclear membrane integrity. Complete deletion of EDMD occurs in approximately 25% of cases and results from an inversion in the Xq28 region; total absence of emerin is demonstrated by both Western blotting and immunoreactivity in tissue sections. Another gene, LMNA, at the 1q21 locus, is linked to the nuclear envelope and encodes lamins A and C, sometimes termed laminopathy. This genetic mutation causes a similar clinical phenotype to EMD defects, except that both sexes are affected and it is transmitted as either an autosomal dominant or recessive trait. Most EMD deletions are null mutations, whereas more than 80% of LMNA alterations are caused by missense mutations, and with a minority of mutations being nonsense or out-of-frame mutations. Desmin protein also may be mutated and seen to be abnormally expressed in the muscle biopsy. Homozygous nonsense mutations in these lamin A/C genes are lethal due to cardiomyopathy and conduction disturbances. There are still many patients with an EDMD phenotype clinically, where the underlying genetic defect remains unknown., Epidemiology : EDMD is an uncommon if not rare disorder, although its overall incidence and prevalence are not known . In a meta-analysis, the pooled prevalence of EDMD in all age groups was 0.39 per 100, 000 ., EDMD is an uncommon if not rare disorder, although its overall incidence and prevalence are not known, , VARIABLE, You can’t prevent Emery-Dreifuss muscular dystrophy since it’s a genetic condition. If you plan on becoming pregnant and want to understand your risk of having a child with a genetic condition, talk to your provider about genetic testing or genetic counseling., Complications : cardiomyopathy, irregular heart beat, muscle damage, sudden cardiac death, heart disease, Diagnostics : Muscle Biopsy, ECG, MRI Brain, doppler echocardiography, WESTERN BLOT TEST, Differential diagnosis : Ankylosing spondylitis, FACIOSCAPULOHUMERAL MUSCULAR DYSTROPHY, myopathy, Myotonic Muscular Dystrophy, disease description : Emery-Dreifuss muscular dystrophy (EDMD) is characterized by the clinical triad of : joint contractures that begin in early childhood; slowly progressive muscle weakness and wasting initially in a humero-peroneal distribution that later extends to the scapular and pelvic girdle muscles; and cardiac involvement that may manifest as palpitations, presyncope and syncope, poor exercise tolerance, and congestive heart failure along with variable cardiac rhythm disturbances. 

Empyema Of Gall Bladder

Disease Name : Empyema Of Gall Bladder, Treatment : medication : Ceftriaxone , Cefotaxime , Hydroquinone, "1-Cholecystectomy-an emergency procedure,2-Often initially cholecystostomy is done, with either Foleys or ,Malecots catheter kept in situ. ,Later after 3- 6 weeks, cholecystectomy is done. ,Laparoscopic cholecystectomy can be tried.", Pathophysiology : The stagnant bile due to cystic duct obstruction in the background of gallstone disease can become infected. Severe infection is caused by pathogenic Escherichia coli,  Klebsiella,  Streptococcus faecalis,  and anaerobes such as Bacteroids and Clostridia. Pus formation follows this infection, tightly filling the lumen of the gallbladder. In a tense and edematous gallbladder, necrosis of the wall and perforation may ensue if drainage or removal of the gallbladder is not performed promptly. If not treated rapidly, patients can develop generalized sepsis or gangrene of the gallbladder resulting in perforation of the gallbladder. Rarely a fistula between the gallbladder and duodenum can occur as a sequela of inadequately treated empyema of the gallbladder. Untreated cases develop symptoms of localized sepsis due to micro-perforation or generalized sepsis due to macro perforation., Epidemiology : Empyema of the gallbladder is estimated to occur in 5 to 15% of cases diagnosed to have acute cholecystitis. It is noted to be the more morbid condition when occurring in the older age group., 5-15%, high mortality., avoid fatty foods like fried foods or cheese for a while. They can cause symptoms, such as diarrhea or bloating. Drink plenty of fluids (unless your doctor tells you not to). You may notice that your bowel movements are not regular right after your surgery., Complications : bleeding, infection, peritonitis, septicaemia, Subphrenic Abscess, Diagnostics : Differential Leucocyte Count DLC, Total Leucocyte Count (TLC), ERCP, MRCP, USG ABDOMEN(W/A), X RAY ABDOMEN, PERCUTANEOUS TRANSHEPATIC CHOLANGIOGRAPHY(PTC), MR CHOLENGIOGRAPHY MRC, CHOLEDOCHOSCOPY, DIRECT CHOLENGIOGRAPHY, Differential diagnosis : cholecystitis, Gallstones, disease description : Empyema of the gallbladder is the most severe form of acute cholecystitis. Empyema of the gallbladder is usually the result of a progression of acute cholecystitis in a background of bile stasis and cystic duct obstruction. This is a surgical emergency that requires prompt treatment with antibiotics and urgent aspiration/removal of the gallbladder to reduce the risk of septic shock.

Encephalitis

Disease Name : Encephalitis, Treatment : medication : Ganciclovir , Foscarnet , Cidofovir , Aciclovir , SUPPORTIVE TREATMENT & BASIC MANAGEMENT OF ICP, FLUID RESTRICTION, AVOIDANCE OFF HYPOTONIC IV SOLUTIONS., ANTI VIRAL THERAPY, Pathophysiology : In addition to the acute febrile illness with evidence of meningeal involvement characteristic of meningitis, the patient with encephalitis commonly has an altered level of consciousness (confusion, behavioral abnormalities), or a depressed level of consciousness ranging from mild lethargy to coma, and evidence of either focal or diffuse neurologic signs and symptoms. Patients with encephalitis may have hallucinations, agitation, personality change, behavioral disorders, and, at times, a frankly psychotic state. Focal or generalized seizures occur in many patients with encephalitis. Virtually every possible type of focal neurologic disturbance has been reported in viral encephalitis; the signs and symptoms reflect the sites of infection and inflammation. The most commonly encountered focal findings are aphasia, ataxia, upper or lower motor neuron patterns of weakness, involuntary movements (e.g., myoclonic jerks, tremor), and cranial nerve deficits (e.g., ocular palsies, facial weakness). Involvement of the hypothalamic-pituitary axis may result in temperature dysregulation, diabetes insipidus, or the development of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Even though neurotropic viruses typically cause pathologic injury in distinct regions of the central nervous system (CNS), variations in clinical presentations make it impossible to reliably establish the etiology of a specific case, Epidemiology : 6.34 per 100, 000 people per year., POOR, You can stay current with vaccines for diseases that cause encephalitis, such as the measles, mumps and rubella (MMR) injection.,,Traveling to certain countries can expose you to germs and diseases that are not common in the U.S. Some of these diseases can cause brain infections.,,You may benefit from vaccines for : ,,1. Japanese encephalitis.,2. Rabies.,3. Tick-borne encephalitis., Complications : Epilepsy, Memory loss, Personality change, Impaired vision, Diagnostics : CSF EXAMINATION, BRAIN BIOPSY, EEG, MRI, Differential diagnosis : Chronic renal disease, encephalopathy, Japanese Encephalitis, Malaria, disease description : Encephalitis (en-sef-uh-LIE-tis) is inflammation of the brain. There are several causes, including viral infection, autoimmune inflammation, bacterial infection, insect bites and others. When inflammation is caused by an infection in the brain, its known as infectious encephalitis. And when its caused by your own immune system attacking the brain, its known as autoimmune encephalitis.

Encephalocele

Disease Name : Encephalocele, Treatment : Treatment is neurosurgical; severing the tumour stalk from the brain and repairing the bony defect through which herniation has taken place., Pathophysiology : Here are the key steps in the pathophysiology of encephalocele : Neural tube development : During embryogenesis, the neural tube forms early in the development of the central nervous system. The neural tube normally closes and fuses completely by the fourth week of gestation to form the brain and spinal cord. However, in cases of encephalocele, there is a failure of complete closure of the neural tube, leading to a defect in the skull and meninges.Neural tube closure defects : The incomplete closure of the neural tube results in an opening or defect in the skull bones, typically in the midline region. This defect allows brain tissue to herniate or protrude through the opening, forming a sac-like structure covered by a layer of meninges.Herniation of brain tissue : The herniated brain tissue, typically containing both gray and white matter, protrudes through the defect in the skull. The size and location of the encephalocele can vary, and it may involve different regions of the brain, such as the occipital, frontal, or nasal regions.Meningeal involvement : Along with the herniated brain tissue, the encephalocele sac also contains meninges, which are the protective membranes that cover the brain and spinal cord. These meninges are derived from the same embryonic tissue as the neural tube. The meninges contribute to the covering of the protruded brain tissue, encapsulating it within the encephalocele sac., Epidemiology : 15%-20% of all NTDs, 1 in 3000 to 1 in 10, 000 live births, VARIABLE, Complications : Meningitis, developmental delay, Hydrocephalus, seizures, Diagnostics : MRI, Differential diagnosis : Congenital dacryocystitis, HEMANGIOMA, NASAL DERMOID, nasal polyps, disease description : Encephalocele (pronounced en-sef-a-lo-seal) is a rare condition that happens before birth (congenital). Normally, the brain and spinal cord form during the third and fourth weeks of pregnancy. They are formed out of the neural tube. Most encephaloceles happen when the neural tube does not fully close. This should happen when the baby’s brain, nervous system and skull are first starting to form. When the neural tube does not close, it can cause a sac-like bulge with brain tissue and spinal fluid that pokes through the skull.

Encephalocraniocutaneous Lipomatosis

Disease Name : Encephalocraniocutaneous Lipomatosis, Treatment : ECCL is not known to be inherited. No confirmed vertical transmission or sib recurrence has been reported. Given the postzygotic mutational mechanism of ECCL, the risk for an affected sib would be expected to be the same as in the general population., .,Treatment of manifestations : Standard treatment for skin manifestations (when appropriate; most of the skin findings do not require active management), choristomas / eye anomalies (including community vision services, as needed), low-grade gliomas, DD/ID, and jaw/dental anomalies; standard treatment with anti-seizure medication for those with epilepsy; standard treatment of Wilms tumor per oncologist., Pathophysiology : The pathogenesis of ECCL is unknown. Most tissues affected in ECCL are of neural crest origin. In addition, because all the CNS anomalies are caused by a mesenchymal defect affecting tissues surrounding the brain or the vessels, and since no primary structural brain malformation is observed, it is postulated that a gene involved in vasculogenesis and the development of multiple mesenchymal tumours may be involved. Pathology The histopathology of naevus psiloliparus shows focal dermal fibrosis with subcutaneous fat in the reticular dermis., Epidemiology : The prevalence of ECCL is unknown. At least 85 individuals who meet the clinical diagnostic criteria or who have a molecular diagnosis of ECCL have been reported., 60 cases reported in the English literature, VARIABLE, The optimal time for determination of genetic risk and discussion of the availability of prenatal/preimplantation genetic testing is before pregnancy.,It is appropriate to offer genetic counseling (including discussion of potential risks to offspring and reproductive options) to young adults who are affected., Complications : mental retardation, scoliosis, contractures of tissue, csf malformation, Diagnostics : CT Orbit, ECG, MRI Brain, Transthoracic echocardiography (TTE), skin lesion biopsy, Differential diagnosis : Neurocutaneous melanosis, NRAS., Oculocerebrocutaneous syndrome (OCCS), Schimmelpenning-Feuerstein-Mims syndrome, Sturge-Weber Syndrome, disease description : Encephalocraniocutaneous lipomatosis (ECCL) comprises a spectrum of predominantly congenital anomalies. In its typical form, ECCL is characterized by congenital anomalies of the skin (nevus psiloliparus, patchy or streaky non-scarring alopecia, subcutaneous lipomas in the frontotemporal region, focal skin aplasia or hypoplasia on the scalp, and/or small nodular skin tags on the eyelids or between the outer canthus and tragus), eye (choristoma), and brain (in particular intracranial and spinal lipomas). To a much lesser degree, the bones and the heart can be affected. About 40% of affected individuals have bilateral abnormalities of the skin or the eyes. About one third of affected individuals have normal cognitive development, another one third have mild developmental delay (DD) or intellectual disability (ID), and the final one third have severe or unspecified DD/ID. Half of individuals have seizures. Affected individuals are at an increased (i.e., above the general population) risk of developing brain tumors, particularly low-grade gliomas such as pilocytic astrocytomas. There is evidence that oculoectodermal syndrome (OES) may constitute a clinical spectrum with ECCL, with OES on the mild end and ECCL on the more severe end of the spectrum.

Enchondroma

Disease Name : Enchondroma, Treatment : Treatment,is usually not required although, occasionally in the,hand, the lesion may be removed through curettage, ,particularly if there is pain or pathological fracture.,Serial X-rays may be helpful if there is a suspicion of a,grade 1 chondrosarcoma, as enchondromas in skeletal,maturity do not grow., Pathophysiology : Enchondromatosis possesses associations with somatic mutations in isocitrate dehydrogenase-1 (IDH1) and 2 (IDH2) genes. The mutations are rare and often sporadic. Isocitrate dehydrogenase is an enzymatic component of the tricarboxylic acid (TCA) cycle functioning to convert isocitrate to alpha-ketoglutarate.Mutations in IDH1 and IDH2 cause malfunction of this enzyme resulting in increased levels of the oncometabolite D-2-hydroxyglutarate (D-2-HG.) D-2-HG competitively inhibits alpha-ketoglutarate-dependent enzymes. DNA hypermethylation and histone modification ensue, affecting differentiation.  Inhibition of the osteogenic differentiation of mesenchymal stem cells occurs via elevations in D-2-HG resulting from IDH1 and IDH2 mutations. All-in-all, blocking osteogenic differentiation during the formation of the skeleton results in cartilaginous tumor formation ., Epidemiology : prevalence estimated to be about 1 in 100, 000, Ollier disease characteristically demonstrates multiple enchondromas in the appendicular skeleton in an asymmetric manner ., POOR, there is no such prevention ., enchondromas do not require treatment. In rare cases, however, multiple tumors may weaken the bone, causing it to fracture. When this occurs, surgery may be needed to remove the tumor and prevent additional fractures., Complications : joint disorders, stiffness, Maffucci syndrome, contractures of tissue, Diagnostics : TUMOUR TISSUE BIOPSY, LESION TISSUE HISTOLOGY, MRI, X RAY, X RAY, CT SCAN, Differential diagnosis : Chondroblastoma, granuloma, Tuberculous dactylitis, disease description : Enchondromas are cartilaginous tumors of the benign bone tumor family. Common benign bone tumors include enchondroma, osteochondroma, chondroblastoma, and chondromyxoid fibroma, all hail from a cartilage origin. Enchondromas are medullary cavity tumors classified in an overarching category of chondromas : benign tumors of hyaline cartilage occurring in bones of endochondral origin.These tumors are usually solitary, central, metaphyseal lesions of tubular bones, favoring the small bones of the hand and feet, followed by the femur and humerus. These are also the most common primary bone tumors of the hand.  In the hands, they most commonly involve the proximal phalanges, followed by the middle phalanges, metacarpals, and then distal phalanges. The hand enchondromas are unique as they may also demonstrate cellular atypia, confusing the histopathological picture with that of chondrosarcoma.  Enchondromatous tumors typically begin and grow in childhood arising from rests of growth plate cartilage or chondrocytes that proliferate and enlarge, then stop growing but remain present throughout adulthood.

Endemic Goitre And Cretinism

Disease Name : Endemic Goitre And Cretinism, Treatment : medication : Levothyroxine/Tetra idothyronine, Treatment of endemic goiter can be carried out by oral administration of L-thyroxine (100 to 200 mcg/day) for a prolonged period., Pathophysiology : Endemic goiter and cretinism are both conditions associated with iodine deficiency, which affects thyroid gland function and can lead to significant health consequences. Heres the pathophysiology of these conditions : Iodine deficiency : Endemic goiter and cretinism primarily occur in regions where iodine intake is chronically low. Iodine is an essential nutrient required for the synthesis of thyroid hormones, namely thyroxine (T4) and triiodothyronine (T3). Inadequate iodine intake disrupts the normal production and release of thyroid hormones.Thyroid hormone synthesis : The thyroid gland takes up iodine from the bloodstream and incorporates it into the synthesis of thyroid hormones. The process begins with the uptake of iodine by the sodium-iodide symporter (NIS) located on the surface of thyroid follicular cells. Within the follicular cells, iodine is oxidized and attached to the amino acid tyrosine, forming iodotyrosines.Thyroid hormone production : The iodotyrosines are then combined to form either T4 (containing four iodine atoms) or T3 (containing three iodine atoms). The synthesis of thyroid hormones is regulated by thyroid-stimulating hormone (TSH) released from the pituitary gland. TSH stimulates the thyroid gland to produce and release thyroid hormones into the bloodstream.Goitrogenesis : In the absence of sufficient iodine, the thyroid gland becomes unable to synthesize an adequate amount of thyroid hormones. As a compensatory mechanism, the pituitary gland produces and releases more TSH in an attempt to stimulate the thyroid gland. This increased TSH stimulates the growth and proliferation of thyroid cells, resulting in the enlargement of the thyroid gland, a condition known as goiter.Goiter development : The enlargement of the thyroid gland in response to increased TSH levels is an adaptive mechanism to enhance iodine uptake. However, despite the goiter formation, the thyroid gland cannot produce adequate amounts of T4 and T3 due to iodine deficiency, leading to low circulating thyroid hormone levels. The goiter is characterized by a visibly enlarged thyroid gland in the neck region., Epidemiology : 3.46%, 1 : 3000 to 1 : 4000 in an iodine-deficient endemic area., VARIABLE, Complications : nan, Diagnostics : Triiodothyronine (T3) Tests, Thyroxine (T4) Test, Thyroid Stimulating Hormone TSH, URINARY IODINE LEVEL, Differential diagnosis : nan, disease description : Disorder associated with endemic goiter and severe iodine deficiency with characteristic clinical features, which include deaf-mutism, squint, mental retardation and characteristic spastic or rigid neuromotor disorder. Two types of endemic cretinism are described. Neurological cretinism is characterized by deafmutism, squint, proximal spasticity and rigidity more in the lower extremities, disorders of stance and gait with preservation of vegetative functions, occasional signs of cerebellar or oculomotor disturbance and severe mental deficiency. 

Endemic Treponematoses

Disease Name : Endemic Treponematoses, Treatment : medication : Benzathine benzylpenicillin , Azithromycin , Treatment of treponematosis is based on single-dose antibiotic therapy with benzathine penicillin or azithromycin.,,Treponemes are highly sensitive to azithromycin and penicillin, which are the drugs of choice., Pathophysiology : Treponematosis ordinarily involves only the skin and mucous membranes. Occasionally, regional lymph nodes are involved, but systemic infections have not been described. Gross lesions of treponematosis are described above. Microscopic lesions consist of ulceration, hyperkeratosis, hyperplasia, and acanthosis of the epidermis. Ulcers are frequently overlaid by crusts composed of exudate, necrotic epithelial cells, and inflammatory cells. The dermis contains a prominent inflammatory cell infiltrate, consisting mainly of macrophages and plasma cells., Epidemiology : 2.5 million infected persons, 460, 000 new cases per year (mostly yaws), NOT SPECIFIC, no vaccination for the disease is available. the principal of prevention are based on the interruption of transmission by early diagnosis and treatment of affected individuals and their contact., Complications : deformity of face, Diagnostics : Antibody Serology Tests, PCR, DARK FIELD MICROSCOPY, Differential diagnosis : ECZEMA, Leishmaniasis, psoriasis, pyoderma gangrenosum, scabies, disease description : The endemic treponematoses are chronic diseases that are transmitted by direct contact, usually during childhood, and, like syphilis, can cause severe late manifestations years after initial infection. These diseases are caused by very close relatives of Treponema pallidum subspecies pallidum, the etiologic agent of venereal syphilis.. Yaws, pinta, and endemic syphilis (bejel) are traditionally distinguished from venereal syphilis by mode of transmission, age of acquisition, geographic distribution, and clinical features; however, there is some overlap for each of these factors. Our “knowledge” about these infections is based on observations by health care workers who have visited endemic areas. Except for recent pilot programs of mass drug administration (MDA) for yaws, virtually no well-designed studies of the natural history, diagnosis, or treatment of these infections have been conducted.

Endocardial Cushion Defect

Disease Name : Endocardial Cushion Defect, Treatment : medication : Furosemide , Digoxin , Enalapril Maleate, The medicines will help your child gain weight and strength before surgery. Medicines often used include : ,,Diuretics (water pills),Drugs that make the heart contract more forcefully (inotropic agents) ., "Surgery is needed to close the holes between the heart chambers, and to create distinct tricuspid and mitral valves. The timing of the surgery depends on the childs condition and the severity of the ECD. It can often be done when the baby is 3 to 6 months old. Correcting an ECD may require more than one surgery.,,Your child’s doctor may prescribe medicine : ,,To treat the symptoms of heart failure,Before surgery if ECD has made your baby very sick", Pathophysiology : The endocardial cushion defect, or complete common AV canal, consists of defects in the atrial and ventricular septa and the AV valvular tissue. All four chambers communicate and share a single common AV valve. The atrial and ventricular shunts communicate volume and systemic pressures to the right ventricle and pulmonary artery. The ventricular shunt orifice usually is nonrestrictive (simple shunt); therefore PVR governs the degree of excess pulmonary blood flow. Mitral regurgitation and direct left-ventricular-to-right-atrial shunting may further contribute to atrial hypertension and total left-to-right shunting., Epidemiology : The frequency rate of endocardial cushion defect (atrioventricular AV canal or septal defects) is about 3% of children with congenital heart disease ., affects around 126 million individuals, VARIABLE, If you have a history of endocardial cushion defect in your family, you may want to consider genetic counseling before pregnancy. There’s a connection between ECD and some genetic issues., Complications : congestive heart failure (CHF), death, Eisenmenger Syndrome, High blood pressure in the lungs, Irreversible damage to the lungs, Diagnostics : ECG, X RAY CHEST, CARDIAC CATHETERIZATION, X RAY, Electrocardiography (EKG), Differential diagnosis : ATRIAL SEPTAL DEFECTS, Atrioventricular block (AV block), VENTRICULAR SEPTAL DEFECTS, disease description : Endocardial cushion defect (ECD) is an abnormal heart condition. The walls separating all four chambers of the heart are poorly formed or absent. Also, the valves separating the upper and lower chambers of the heart have defects during formation. ECD is a congenital heart disease, which means it is present from birth.

Endocarditis-associated Glomerulonephritis

Disease Name : Endocarditis-associated Glomerulonephritis, Treatment : medication : Cefoperazone , Pathophysiology : The pathophysiology of EAG involves immune complex deposition and inflammation in the glomeruli of the kidneys. Heres a breakdown of the key steps : Infective endocarditis : The pathophysiology of EAG starts with the presence of infective endocarditis. This condition occurs when bacteria or other microorganisms infect the heart valves, leading to the formation of vegetations composed of fibrin, platelets, and microorganisms. These vegetations can release fragments into the bloodstream.Immune complex formation : As the microorganisms circulate in the bloodstream, they can interact with antibodies produced by the immune system, leading to the formation of immune complexes. These immune complexes consist of antigens from the microorganisms and antibodies.Deposition in the glomeruli : The immune complexes can be deposited within the glomeruli, which are the filtering units of the kidneys. The glomeruli have a complex structure consisting of capillaries and specialized cells called podocytes. The immune complexes become trapped within the glomerular capillaries or in the mesangium, the region between the capillaries.Activation of complement system : The deposition of immune complexes in the glomeruli activates the complement system, which is a part of the immune response. The complement system consists of a cascade of proteins that can trigger inflammation and recruit immune cells to the site of immune complex deposition.Inflammatory response : The activation of the complement system and the subsequent release of inflammatory mediators, such as cytokines and chemokines, lead to an inflammatory response within the glomeruli. This response attracts immune cells, such as neutrophils and monocytes, to the affected area.Glomerular injury : The presence of immune complexes and the inflammatory response in the glomeruli can cause damage to the glomerular structures. The immune complexes can activate immune cells, leading to the release of enzymes and reactive oxygen species that can injure the glomerular cells and disrupt the filtration function., Epidemiology : 18–33%, 2.6 to 7 cases per 100, 000 population per year., VARIABLE, Complications : nan, Diagnostics : ECG, trans thoracic 2D ECHO, 24 Hr URINARY ALBUMIN, 24 Hr URINARY ALBUMIN-CREATNINE LEVEL, Differential diagnosis : nan, disease description : Infective endocarditis (IE) is a serious disease with a high associated mortality rate, particularly when complicated by acute renal failure (ARF). Although valve surgery and treatment with antibiotic agents are recommended, surgical options and the optimal thDespite improvements in diagnostic methods and antimicrobial agents, the incidence of infective endocarditis (IE) remains high in specific populations of individuals, such as hemodialysis patients and drug abusers erapy are not as yet well documented.

Endocervical Adenocarcinoma

Disease Name : Endocervical Adenocarcinoma, Treatment : The length of the cycle and the schedule or frequency of chemotherapy varies depending on the drug used and where cancer is located., o kill cancer cells on your cervix, "Laser surgery : This surgery uses a laser beam to burn off cancer cells.,Cryosurgery : This surgery freezes cancer cells.,Cone biopsy : A surgery in which a cone-shaped piece of tissue is removed from your cervix.,Simple hysterectomy : This surgery involves the removal of your uterus but not the tissue next to your uterus. Your vagina and pelvic lymph nodes arent removed.,Radical hysterectomy with pelvic lymph node dissection : With this surgery, your uterus, surrounding tissue called the parametrium, your cervix, a small portion of the upper part of your vagina and lymph nodes from your pelvis are removed.,Trachelectomy : This procedure removes your cervix and the upper part of your vagina but not your uterus.,Pelvic exenteration : This is the same as a radical hysterectomy but includes your bladder, vagina, rectum and part of your colon, depending on where cancer has spread", Pathophysiology : Pathogenesis involves-A periglandular stromal reaction, which may be rather subtle.A more extensive, crowded proliferation than the normal/background endocervical glandular pattern, with tight clustering of small glands, early interglandular cribriform growth, and/or early gland fusion.Surface exophytic villoglandular growth beyond what is within the spectrum allowed for superficial AIS.An extensive proliferation that may not be excessively crowded but extends into deeper cervical stroma in a haphazard pattern (appearing as if the glands had been strewn across the slide), even if desmoplasia is lacking., Epidemiology : 67%, 10–20% of all cervical cancers, VARIABLE, "To reduce your risk of cervical cancer : ,,Ask your doctor about the HPV vaccine. Receiving a vaccination to prevent HPV infection may reduce your risk of cervical cancer and other HPV-related cancers. Ask your doctor whether an HPV vaccine is appropriate for you.,Have routine Pap tests. Pap tests can detect precancerous conditions of the cervix, so they can be monitored or treated in order to prevent cervical cancer. Most medical organizations suggest beginning routine Pap tests at age 21 and repeating them every few years.,Practice safe sex. Reduce your risk of cervical cancer by taking measures to prevent sexually transmitted infections, such as using a condom every time you have sex and limiting the number of sexual partners you have.,Dont smoke. If you dont smoke, dont start. If you do smoke, talk to your doctor about strategies to help you quit.", Complications : Bleeding complications, kidney damage, blood clot formation, Diagnostics : PAP SMEAR, USG Pelvis, biopsy, HUMAN PAPPILOMA VIRUS(HPV) LEVEL, MRI PELVIS, Differential diagnosis : cervical fibroid, endocervical polyp, Endometriosis, disease description : Endocervical adenocarcinomas can be classified into two main types of tumors, namely, those related to high-risk human papillomavirus and those unrelated to high-risk human papillomavirus. The former, representing the vast majority, are referred to as endocervical adenocarcinomas of usual type and the latter are dominated by the gastric-type mucinous adenocarcinomas. Commonly encountered diagnostic problems concerning these endocervical adenocarcinomas include : (1) diagnosing invasion for endocervical adenocarcinomas of usual type, particularly superficial forms which must be distinguished from extensive endocervical adenocarcinoma in situ; (2) distinguishing high-risk human papillomavirus-related endocervical adenocarcinomas from endometrial endometrioid carcinomas; and (3) distinguishing benign/hyperplastic mucinous endocervical glandular proliferations from gastric-type mucinous endocervical adenocarcinomas, particularly minimal deviation adenocarcinoma. 

Endocervical Polyp

Disease Name : Endocervical Polyp, Treatment : Symptomatic, large, or atypical polyps usually warrant removal. Some techniques for polyp management include polypectomy for polyps with slender pedicles, which consists in grasping the base of the polyp with a ring forceps and twisting and rotating it until it comes of off; for smaller polyps, punch biopsy forceps are used, and polyps with a thick stalk usually require electrosurgical excision or hysteroscopic removal., Pathophysiology : Endocervical polyps, which are the most common type, microscopically show a loose, edematous stroma with variably sized vasculature, large dilated or small thick-walled. The stromal cells often present with mixed acute or chronic inflammation, erosion, as well as benign microglandular hyperplasia. These manifestations are usually visible on the surface of larger polyps protruding through the cervical os, depending on the extent of irritation ., Epidemiology : In the general population, the estimated prevalence of cervical polyps is between 2 to 5 % of women., Multigravida women have an increased risk of developing cervical polyps compared to the nulliparous., variable, Cervical polyps are hard to prevent, but you can take certain steps to reduce your risk of infection like practicing safe sex (using a condom). Other causes of cervical polyps are out of your control. Getting regular pelvic exams and Pap tests is the best way to find and treat polyps before symptoms start., Complications : infection, hemorrhage, uterine perforation, Diagnostics : PAP SMEAR, biopsy, USG, CERVICAL CYTOLOGY, Differential diagnosis : adenomyosis, Ectopic pregnency, Endometriosis, Uterine fibroids, disease description : Endocervical polyps, which are the most common type, microscopically show a loose, edematous stroma with variably sized vasculature, large dilated or small thick-walled. The stromal cells often present with mixed acute or chronic inflammation, erosion, as well as benign microglandular hyperplasia. These manifestations are usually visible on the surface of larger polyps protruding through the cervical os, depending on the extent of irritation.

Endometrial Cancer

Disease Name : Endometrial Cancer, Treatment : "Chemotherapy uses chemicals to kill cancer cells. You may receive one chemotherapy drug, or two or more drugs can be used in combination. You may receive chemotherapy drugs by pill (orally) or through your veins (intravenously). These drugs enter your bloodstream and then travel through your body, killing cancer cells.,,Chemotherapy is sometimes recommended after surgery if theres an increased risk that the cancer might return. It can also be used before surgery to shrink the cancer so that its more likely to be removed completely during surgery.,,Chemotherapy may be recommended for treating advanced or recurrent endometrial cancer that has spread beyond the uterus.", Hormone therapy involves taking medications to lower the hormone levels in the body. In response, cancer cells that rely on hormones to help them grow might die. Hormone therapy may be an option if you have advanced endometrial cancer that has spread beyond the uterus., "Radiation therapy uses powerful energy beams, such as X-rays and protons, to kill cancer cells. In some instances, your doctor may recommend radiation to reduce your risk of a cancer recurrence after surgery. In certain situations, radiation therapy may also be recommended before surgery, to shrink a tumor and make it easier to remove.,,If you arent healthy enough to undergo surgery, you may opt for radiation therapy only.,,Radiation therapy can involve : ,,Radiation from a machine outside your body. During external beam radiation, you lie on a table while a machine directs radiation to specific points on your body.,Radiation placed inside your body. Internal radiation (brachytherapy) involves placing a radiation-filled device, such as small seeds, wires or a cylinder, inside your vagina for a short period of time.", "Treatment for endometrial cancer usually involves an operation to remove the uterus (hysterectomy), as well as to remove the fallopian tubes and ovaries (salpingo-oophorectomy). A hysterectomy makes it impossible for you to become pregnant in the future. Also, once your ovaries are removed, youll experience menopause, if you havent already.,,During surgery, your surgeon will also inspect the areas around your uterus to look for signs that cancer has spread. Your surgeon may also remove lymph nodes for testing. This helps determine your cancers stage.", Pathophysiology : Uninterrupted by intervention, the natural history of endometrial carcinomas begin as preinvasive intraepithelial lesions, which progress to full-blown invasive cancers (see above : Etiology and Epidemiology) involving endometrial stroma, then penetrating ever more deeply into the myometrium to engage lymphatic capillaries that carry the malignancy to regional lymph nodes, whence metastases may occur through vascular channels. Tumorous involvement of the uterine cervix and stroma probably is mostly through lymphatic channels, particularly by dedifferentiated carcinomas; although surface spread can occur from endometrial cancers in the lower uterine segment (LUS).Lymphatic capillaries also may carry endometrial carcinoma cells to the adnexa, in other words, fallopian tubes and ovaries. Anatomically, lymphatic channels usually follow the corresponding veins; thus a regional extension of cancers confined to the uterine corpus or extended only to adnexal organs is considered to be the para-aorta and para-cava nodes; whereas, a regional extension of invasive endometrial cancers involving the uterine cervix and LUS is to para-ureteral and pelvic lymph nodes. Locally advancing endometrial cancers may penetrate fully through the myometrium and uterine serosa to involve surrounding peritoneum, supporting tissues and other pelvic organs. Low-grade, type 1 endometrioid carcinomas tend to remain confined to the uterus and are characterized by rather a favorable prognosis; whereas, high-grade, type 2 endometrioid and non-endometrioid carcinomas with TP53 mutations often metastasize via the lymphatic system or transit through the fallopian lumens to disseminate throughout the pelvis and abdomen, manifesting at advanced stage and portending grave prognoses., Epidemiology : The prevalence of endometrial cancer in the United States is 25.7/100, 000 women per year. The lifetime risk for developing this disease is approximately 2.8% in American women., 4.3 per 100, 000 women., variable, - Avoiding risk factors and increasing protective factors may help prevent cancer.,,- The following protective factors decrease the risk of endometrial cancer : ,Pregnancy and breast-feeding,Hormonal contraceptives,Weight loss,Physical activity, Complications : perforation, anemia, Diagnostics : TVS (Transvaginal ultrasound), MRI, CT, DILATATION & CURETTAGE, HYSTEROSCOPY, ENDOMETRIAL BIOPSY, PHYSICAL EXAMINATION, Differential diagnosis : abnormal vaginal bleeding, adenomyosis, FALLOPIAN TUBE CANCER, leiomyoma, MALIGNANCY, pelvic mass, Polyps, symptomatic uterine leiomyomas, disease description : Uterine corpus cancer is the most prevalent gynecologic malignancy in American women with over 60, 000 new cases expected during the next year and accounting for nearly 11, 000 deaths. Endometrial carcinomas account for the greatest number of these cases, as fewer than 10% of uterine corpus cancers are sarcomas. Endometrioid carcinomas compose more than 83% of uterine corpus cancers. More virulent serous and papillary serous carcinomas make up some 4% to 6% of endometrial carcinomas, and 1% to 2% are clear cell carcinomas.1 It is essential to differentiate type 1 endometrioid from type 2 serous endometrial carcinomas and other highly aggressive non-endometrioid carcinoma histotypes to understand, manage and possibly prevent these diseases.

Endometrial Polyp

Disease Name : Endometrial Polyp, Treatment : . Certain hormonal medications, including progestins and gonadotropin-releasing hormone agonists, may lessen symptoms of the polyp. But taking such medications is usually a short-term solution at best — symptoms typically recur once the medicine is stopped., Premenopausal : polypectomy for symptomatic polyps, multiple polyps, polyps > 1.5 cm, prolapsed polyps or those associated with infertility.,Postmenopausal : polypectomy or hysterectomy.,Hysteroscopic removal or morcellation.,Excision is curative if the circumscribed foci of endometrial hyperplasia are in polyp with no background hyperplasia., Pathophysiology : Polyps are endometrial epithelial proliferations comprised of vascular, glandular, fibromuscular, and connective tissues. Endometrial polyps are primarily covered by epithelial tissue superficially and contain a largely vascular core. Polyps may be classified as sessile, pedunculated, or prolapsing. A prolapsed polyp may contain areas of squamous metaplasia, infection, or ulceration. A majority of polyps will be composed of the endometrium that differs from the surrounding endometrium and does not respond to cyclic hormonal changes. Other histological findings include carcinomatous, atrophic, or hyperplastic. , Epidemiology : Endometrial polyps occur in all age groups, with a peak incidence between the age of 40 to 49. The prevalence of endometrial polyps in reproductive-aged women with abnormal uterine bleeding is estimated between 20 to 40 percent., Incidence in asymptomatic females with infertility : 10 - 32%, variable, You can’t prevent uterine polyps. You can take steps to catch them early so that they don’t cause complications or unpleasant symptoms. Getting regular gynecological checkups can allow your provider to catch polyps early., Complications : infertility, Diagnostics : Cytogenetics, TVS (Transvaginal ultrasound), USG, DILATATION & CURETTAGE, HYSTEROSCOPY, Sonosalpingography, ENDOMETRIAL BIOPSY, Immunostaining, Differential diagnosis : adenomyoma, adenosarcoma, endocervical polyp, ENDOMETRIAL HYPERPLASIA, endometrial stromal sarcoma, ENDOMETRITIS, leiomyoma, disease description : Endometrial polyps refer to overgrowths of endometrial glands and stroma within the uterine cavity. Endometrial polyps vary in size from a few millimeters to several centimeters in diameter. Polyps may be found as a single lesion or multiple lesions filling the entire endometrial cavity. Endometrial polyps may be diagnosed at all ages; however, peak incidence occurs between the age of 40 to 49 years old. Although these polyps are considered benign, there is a small risk of malignant transformation.

Endometrial Stromal Nodule

Disease Name : Endometrial Stromal Nodule, Treatment : Hysterectomy if fertility is complete or not desired,If fertility preservation is desired, conservative excision followed by hysteroscopy to monitor for regrowth,Conservative excision may be adequate but usually limits ability to sample margins, Pathophysiology : Endometrial stromal tumors are very rare, accounting for 3% of all uterine neoplasms . These tumors are characterized primarily by the tumor invasiveness and degree of stromal differentiation. However, both ESS and ESN can appear histologically similar with distinction made only after evaluation of the full hysterectomy specimen; findings of myometrial or vascular invasion less than 3?mm readily make the diagnosis of ESN. ESNs show focal smooth muscle differentiation and express CD10 and hormone receptors 8. Pathological examination of the removed uterus in the present case revealed an ESN measuring 19?mm with an invasion of two mm. Cellular atypia was present with slightly elevated mitotic count (six per ten high-power fields). The tumor was well defined against the underlying myometrium in the part of the fundus, but, in other places, it was more irregular with finger-like projections into the myometrium, however not exceeding three mm. Immunohistochemical analysis showed high positivity for CD10 but showed in a lesser extent positivity for smooth muscle myosin.Pathological examination of the removed uterus in the present case revealed an ESN measuring 19?mm with an invasion of two mm. Cellular atypia was present with slightly elevated mitotic count (six per ten high-power fields). The tumor was well defined against the underlying myometrium  in the part of the fundus, but, in other places, it was more irregular with finger-like projections into the myometrium, however not exceeding three mm. Immunohistochemical analysis showed high positivity for CD10 but showed in a lesser extent positivity for smooth muscle myosin., Epidemiology : 2 per million women, variable, Current medical research has not established a method of preventing Endometrial Stromal Nodule. However, the following general factors may be considered to reduce the risk for tumor development : ,,Address any condition causing hormonal imbalance in the body,Maintain weight through proper diet modification and physical exercises, if you are overweight/obese,Avoid alcohol consumption or limit its intake,Have a balanced diet that is not high in meat and low in vegetables; a balanced diet can also help avoid any mineral or vitamin deficiencies in the body,Regular medical screening at periodic intervals with blood tests, radiological scans, and physical examinations are mandatory, due to risk of recurrence of the tumor. Often several years of active vigilance may be necessary, Complications : infertility, anemia, excruciating pain, Diagnostics : Cytogenetics, MRI, Immunostaining, Immunostaining, Differential diagnosis : cns primitive neuroectodermal tumour (pnet) (who g, Embryonal rhabdomyosarcoma (incl. spindle cell, b, Endometrial polyp, disease description : Benign tumor composed of cells reminiscent of proliferative phase endometrial stroma with absent or minimal myometrial invasion (< 3 mm and < 3 protrusions) and lacking vascular invasion.The stromal nodules have expansile, noninfiltrative margins that compress the surrounding endometrium and myometrium. Minor irregularities of the margin are common, but invasion of the surrounding myometrium indicates that the tumor is a stromal sarcoma, not a stromal nodule

Endometrial Stromal Sarcoma

Disease Name : Endometrial Stromal Sarcoma, Treatment : Low grade and high grade, stage I : hysterectomy and bilateral salpingo-oophorectomy ; may also receive adjuvant radiation or hormonal treatment with progestational agents or aromatase inhibitors,Undifferentiated : should be treated by hysterectomy and bilateral salpingo-oophorectomy and adjuvant radiation or chemotherapy, Pathophysiology : Pathogenesis involves-Polypoid mass extending into broad ligament, ovaries and fallopian tubes.Lymphatic tumor plugs as yellow, ropy or ball-like masses.Monotonous ovoid cells to spindly cells with minimal cytoplasm.Prominent arterioles. Angiolymphatic invasion common.Up to 10-15 mitotic figures per 10 HPF in most active areas.Tongue-like infiltration between muscle bundles of myometrium.May exhibit myxoid, epithelioid and fibrous change.May have foam cells or hyalinization in the stroma., Epidemiology : Half occur in premenopausal women, with most patients presenting in the 5th decade., two cases per 100, 000 women, Tumor stage is the most important prognostic facto, "We dont know how to prevent uterine sarcoma yet, but we know about certain risk factors, such as receiving pelvic area radiation and taking tamoxifen for breast cancer. Treatment benefits often outweigh the risks associated with developing uterine sarcoma, especially since its so rare.", Complications : infertility, anemia, Diagnostics : MRI, USG, immunohistochemistry, Histopathological examination, Differential diagnosis : adenomyosis, Endometrial polyp, Endometrial stromal nodule, Epithelioid leiomyosarcoma, Highly cellular leiomyoma, disease description : Endometrial stromal sarcoma (ESS) is a rare malignant tumor of the endometrium, occurring in the age group of 40–50 years. This is a case of low-grade ESS presenting as rapid enlargement of a fibroid uterus. Cancers arising from mesodermal structures like muscles and connective tissue are called sarcomas. Sarcomas of the uterus are uncommon, and may arise from connective tissue, smooth muscle or the endometrial stroma

Endometrioid Adenocarcinoma

Disease Name : Endometrioid Adenocarcinoma : Variant With Squamous, Treatment : Adjuvant chemo / radiotherapy largely dependent on postoperative surgical stage and histologic grade but incorporates other factors (lymphovascular invasion, age, tumor size and involvement of lower uterine segment / surface cervical glands), Hormonal therapy (progesterone, leuprolide) alone can lead to complete remission in early stage, low grade tumor for women who want to preserve fertility but long term follow up studies not available, Primary treatment is surgical (hysterectomy and bilateral salpingo-oophorectomy with staging), unless patient desires fertility, Pathophysiology : Pathogenesis includes Increased endogenous or exogenous estrogen, unopposed by progesterone : Initially, estrogen has mitogenic effect on both endometrial glands and stromaChronic estrogenic stimulation without progesterone affects glands to a greater extent ? glandular overgrowth (hyperplasia) adenocarcinoma, Epidemiology : Reproductive age as well as postmenopausal women, 25.1 per 100, 000 women per year., variable, Complications : nan, Diagnostics : CA 125, TVS (Transvaginal ultrasound), MRI, CT SCAN, Immunostaining, Differential diagnosis : endometrial hyperplasia., Endometrial polyp, disease description : Adenocarcinoma with squamous differentiation represents a continuum of lesions, ranging from adenoacanthoma, which is exceptionally well differentiated and has a benign-looking squamous component, to adenosquamous carcinoma, which is poorly differentiated and has a malignant squamous component?

Endometrioid Adenocarcinoma

Disease Name : Endometrioid Adenocarcinoma, Treatment : Systemic chemotherapy is reserved for women with disseminated disease or extrapelvic recurrence. Although the combination of cisplatin plus doxorubicin is commonly used, carboplatin plus paclitaxel represents an efficacious, low-toxicity regimen for advanced or recurrent cases., Surgery and radiation therapy form the main treatment. Total abdominal hysterectomy and bilateral salpingo-oophorectomy with lymph node dissection remains the cornerstone of treatment., Pathophysiology : Endometrioid carcinoma is arising from precursor endometrial hyperplasia and associated with PTEN gene mutation in 30-90% of cases. They demonstrate a well-defined glandular pattern resembling normal endometrial glands lined by malignant stratified columnar epithelial cells. Higher-grade endometrioid adenocarcinomas have undifferentiated cells with more solid sheets of tumor cells, which are not organized into well-defined glands and are associated with an atrophied endometrium., Epidemiology : 25.7/100, 000 women per year, poor, "Talk to your doctor about the risks of hormone therapy after menopause. If youre considering hormone replacement therapy to help control menopause symptoms, talk to your doctor about the risks and benefits. Unless youve undergone a hysterectomy, replacing estrogen alone after menopause may increase your risk of endometrial cancer. Taking a combination of estrogen and progestin can reduce this risk. Hormone therapy carries other risks, so weigh the benefits and risks with your doctor.,Consider taking birth control pills. Using oral contraceptives for at least one year may reduce endometrial cancer risk. The risk reduction is thought to last for several years after you stop taking oral contraceptives. Oral contraceptives have side effects, though, so discuss the benefits and risks with your doctor.,Maintain a healthy weight. Obesity increases the risk of endometrial cancer, so work to achieve and maintain a healthy weight. If you need to lose weight, increase your physical activity and reduce the number of calories you eat each day.", Complications : anemia, Diagnostics : USG Pelvis, CT, MRI PELVIS, CERVICAL CYTOLOGY, ENDOMETRIAL BIOPSY, Differential diagnosis : nan, disease description : Endometrial adenocarcinoma is the third common malignancy of the female genital tract occurring most often in the postmenopausal age group. High tumor grade, advanced surgical stage, and lymphovascular space invasion are implicated as poor prognostic factors for dissemination of disease.

Endometriosis

Disease Name : Endometriosis, Treatment : medication : Norethisterone , Anastrozole , Medroxy Progesterone Acetate , Progesterone , Goserelin , Danazol, GESTRINONE, combined oral contraceptives, dihydrogesterone, Aspiration of peritoneal fluid in cul-de-sac, Destruction of endometriotic implants less than 3 cm by,diathermy cauterization, or vaporization by CO2 or,Nd : YAG laser, Laparoscopic breaking of adhesions in the pelvis relieves,dysmenorrhoea and pelvic pain, LUNA (Laser uterosacral nerve ablation, , Pathophysiology : The understanding of the pathophysiology of endometriosis remains incomplete in many aspects, and there is not a coherent suggested theory to explain all different types of endometriosis, integrating the epigenetic, genetic, immunological, and environmental data. From the proposed pathogenic theories, the most plausible is Sampson’s theory, suggesting that with retrograde menstruation, viable cells and menstrual fragments can migrate through the Fallopian tubes, infiltrate into the peritoneal cavity, and then proliferate and cause chronic inflammation. The fact that retrograde menstruation is a phenomenon caused in a large proportion of women of reproductive age, but not all of them suffer from endometriosis, indicates that retrograde menstruation is not enough by itself to cause endometriosis, indicates that there are also other factors contributing to the generation of disease. Other theories, such as the coelomic metaplastic theory, the vascular and lymphatic metastatic theory, are necessary to explain some forms of endometriosis. The role of oxidative stress and ROS, together with genetic, epigenetic, and environmental factors are necessary to be integrated for a more complete picture of the pathogenesis of endometriosis., Epidemiology : The exact prevalence cannot be easily defined since the definitive diagnosis of the disease; a laparoscopic examination needs to be conducted. It is estimated that endometriosis affects approximately 10% to 15% of women of reproductive age, whereas this prevalence increases by up to 70% in women with chronic pelvic pain., 10% WOMEN incidence is 20% and is 15% in women wit, GOOD, "Endometriosis isn’t a condition you can necessarily prevent. There are certain factors that can reduce your risk of developing the condition, but in some cases, you may still have endometriosis. There could be a genetic reason that some people develop endometriosis. If other people in your family (mother or grandmother) have been diagnosed with endometriosis, talk to your provider about your risk of also developing the condition.,,A few factors that can reduce your risk of endometriosis include : ,,Pregnancy.,Breastfeeding.,Maintaining a weight thats healthy for you.,Starting your menstrual period at a later age.", Complications : Dysmenorrhoea, infertility, DYSPAREUNIA, CHRONIC PAIN, bowel\\/bladder dysfunction, Diagnostics : CA 125, TVS (Transvaginal ultrasound), biopsy, MRI, USG, LAPAROSCOPY, Cytopathology, HISTOLOGIC EXAMINATION, PHYSICAL EXAMINATION, Differential diagnosis : adenomyosis, ADHESIONS, Dysmenorrhoea, Endometriosis, Pelvic Inflamatory Disease, disease description : Endometriosis is a chronic gynecologic disease characterized by the development and presence of histological elements like endometrial glands and stroma in anatomical positions and organs outside of the uterine cavity. The main clinical manifestations of the disease are chronic pelvic pain and impaired fertility. The localization of endometriosis lesions can vary, with the most commonly involved focus of the disease the ovaries followed by the posterior broad ligament, the anterior cul-de-sac, the posterior cul-de-sac, and the uterosacral ligament. Endometriotic nodules also affect the intestinal tract and the urinary system like the ureter, the bladder, and the urethra. Nevertheless, endometriosis is not limited to the pelvis but can damage extra pelvic structures like the pleura, the pericardium, or the central nervous system. The main theories utilized to explain the pathogenesis of endometriosis are Sampson’s theory, the coelomic metaplastic theory, the stem cell theory, the Müllerian remnant theory, and the vascular and lymphatic metastasis theory.

Entercoccal Infection

Disease Name : Entercoccal Infection, Treatment : 1 Linezolid with gentamicin, doxycycline, or rifampicin,2Daptomycin with ceftaroline, ampicillin, ertapenem, tigecycline, and fosfomycin.,3 Oritavancin,4Tigecycline, Pathophysiology : Enterococci do not produce toxins like staphylococci and streptococci, but their virulence comes from other properties like durability, structure, and antibiotic resistance.Enterococcal surface components include the polysaccharide capsule, adhesins, pili, and the aggregation substance.Their ability to form biofilms promotes adherence to catheters, dental prostheses, and heart valves and limits antibiotic penetration, causing persistent infections that are often even polymicrobial.Enterococci secrete virulence factors like bacteriocins, hemolysin/cytolysin, gelatinase, and serine protease. Moreover, they are also capable of producing toxic oxygen metabolites, leading to cell injury.Enterococci are intrinsically resistant to cephalosporins, clindamycin, aminoglycosides, and trimethoprim-sulfamethoxazole.They also gain antibiotic resistance through their ability to acquire and transfer resistance-related mobile genetic elements (MGE) via various mechanisms like plasmids, conjugation, and transposons. This latter property is believed to be due to the absence of CRISPR-Cas gene loci, which usually limits invading harmful DNA., Epidemiology : approximately 10 percent of all UTIs., between 5 to 15% of cases of infectious endocarditis, , variable, Complications : infection, Diagnostics : BLOOD CULTURE test, STOOL CULTURE, colonoscopy, CT Abdomen, USG, Transthoracic echocardiography (TTE), Differential diagnosis : infection, infection, infection, infection, disease description : Enterococci are Gram-positive facultative anaerobic cocci in short and medium chains, which cause difficult to treat infections in the nosocomial setting. They are a common cause of UTI, bacteremia, and infective endocarditis and rarely cause intra-abdominal infections and meningitis. Enterococci are found in the soil, water, food, sewage, plants, human skin, the oral cavity, and the large intestine, constituting less than 1% of the total microbiota.

Enteric Fever

Disease Name : Enteric Fever, Treatment : medication : Amoxicillin and Clavulanic acid , Cefixime , Ceftriaxone , Azithromycin , Chloramphenicol , Ciprofloxacin , Currently, third-generation cephalosporins such as,ceftriaxone and cefixime are the first-line agents for,therapy of enteric fever. Azithromycin is a new drug that,is being used as an alternative agent., Pathophysiology : S. enterica serotype typhi/paratyphi is a gram-negative, nonlactose fermenting, flagellate bacterium. The somatic or 0 antigen is shared among various salmonellae; the flagellar or H antigen is specific to the serovar. S. enterica var typhi also possesses a Vi polysaccharide capsule. The infective dose of typhoid/paratyphoid bacillus varies from 103 to 106 organisms. The organism must survive the gastric barrier to reach the small intestine; hence, conditions which reduce gastric acidity, such as use of antacids, H2 receptor blockers and proton pump inhibitors, reduce the infective dose. On reaching the small intestine, the organism penetrates the mucosa and infects the lymphoid follicles and subsequently the draining mesenteric lymph nodes and the liver and spleen. It multiplies in the reticuloendothelial system and after incubation period varying from 7 to 14 days spills into the bloodstream and is widely disseminated, especially to liver, spleen, bone marrow, gallbladder and the Peyers patches of the terminal ileum. This spill marks the onset of clinical manifestations of enteric fever. Infection leads to both local and systemic immune responses, which are, however, inadequate to prevent relapse or reinfection. There is no appreciable difference between the manifestations of typhoid and paratyphoid fever. The hallmark of enteric fever is fever which starts as a low grade fever and then shows stepwise increase peaking to as high as 103-104 °C by the end of the first week. This pattern differentiates it from viral fever where the peak is usually at the onset of fever. With fever, there is associated malaise, dull headache, anorexia, nausea, poorly localized abdominal discomfort, mild cough and malaise. There may be diarrhea; constipation in children is rare. Relapse Relapse may occur in 5-15% of treated cases, usually due to the organism with the same susceptibility as the original attack and is relatively a milder illness. Rate of relapse is dependent on choice of drug therapy. It is higher with beta lactams such as cefixime or ceftriaxone as compared to quinolones and azithromycin. Carrier state Although 5-10% adult patients may shed salmonella in stool following an acute attack for up to 3 months, only 1-4% excrete bacilli for more than 1 yr., Epidemiology : 12 to 1622 cases per 100, 000 child-years among children between the ages of 6 months and 14 years and from 108 to 970 cases per 100, 000 person-years among those who were 15 years of age or older, An estimated 14.3 million cases of enteric fever caused by Salmonella enterica serovar Typhi and Paratyphi, GOOD, The best way to reduce your risk of typhoid fever is to get vaccinated if you live in or are traveling to an area where it’s common. Hand washing and safe food handling are also important for limiting the spread of typhoid., Complications : bleeding, coma, delirium, hepatitis, intestinal perforation, perforation, PNEUMONIA, Disseminated lntravascular Coagulopathy, Diagnostics : CRP, EOSINOPHILS - ABSOLUTE COUNT, Hb, PLATELET COUNT, STOOL CULTURE, TYPHIDOT IgG, WIDAL TEST, BLOOD CULTURE, PCR, BODY FLUID CULTURE, ELISA, CHEST X RAY, BONE MARROW CULTURE, NEUTROPHILS, ASPARTATE AMINOTRANSFERASE (SGOT ), ALANINE TRANSAMINASE (SGPT), PHYSICAL EXAMINATION, Differential diagnosis : AMOEBIC LIVER ABSCESS, Dengue without warning signs, Malaria, Rickettsial Infection, disease description : The term enteric fever includes typhoid fever caused by Salmonella enterica var typhi and paratyphoid fever caused by S. enterica var paratyphi A, B or C. Paratyphoid infections constitute about 20% of all cases of enteric fever worldwide. As enteric fever is a disease transmitted by the feco-oral route, its greatest burden is in resource limited countries where water supply and sanitary conditions are poor. In a community-based study in urban slums of Delhi the incidence was estimated to be 980/ 100, 000 population. Enteric fever is the most common cause of fever lasting for more than 7 days in clinical practice in India.

Enterobiasis

Disease Name : Enterobiasis, Treatment : medication : Albendazole , Ivermectin , Mebendazole , Pyrantel Pamoate, First line,•\tAlbendazole, 400 mg orally for 1 day, then repeat dose in ,2 weeks,•\tMebendazole 100 mg orally for 1 day, then repeat dose in ,2 weeks,Second line,•\tPyrantel pamoate : dose varies per weight (11 mg/kg; ,maximum 1 g); one time, then repeat dose in 2 weeks,Third line,•\tIvermectin 0.2 mg/kg twice a day for 10 days, Pathophysiology : Male and female worms develop in the caecum, becoming mature 2–8 weeks after ingestion of fertile eggs. Gravid female worms migrate to the anus, and at night crawl on the perianal skin where they lay up to 16 000 eggs and expire. The eggs mature within a few hours. Transmission is by ingestion of eggs, most commonly carried by fingernails, because of the itching during sleep. Hands may also become contaminated through sharing a bed or bedroom. Occasionally, transmission is airborne from infected dust, in which eggs may survive for up to 13 days. Adult worms live for 6–12 weeks. Gravid female worms migrating on the skin cause intense itching, although not in all infected people. It is not known whether an allergic reaction is involved. Adult worms may burrow into the submucosa of the appendix or bowel and be associated with inflammation, although causation has not been clearly established. Female worms may migrate from the anus to the vagina, causing irritation and inflammation, and from there to the fallopian tubes or even peritoneal cavity, causing salpingitis and occasionally peritoneal nodules., Epidemiology : about 200 million people worldwide are supposedly infected, with children aged 5~10 years old accounting for over 30% of cases, incidence rate of 11.4% among people of all ages, variable, The most effective way to prevent a pinworm infection is by practicing cleanliness in the following ways : ,,1. Wash your hands often.,2. Keep surfaces clean.,3. Shower often.,4. Trim your fingernails.,5. Avoid touching the anal area.,6. Wash sheets, towels and underclothes frequently., Complications : nan, Diagnostics : STOOL EXAMINATION, PHYSICAL EXAMINATION, light microscopy, Differential diagnosis : nan, disease description : Enterobiasis, colloquially known as pinworm, is one of the most common parasitic worm infections in the world. Its cause is infection by the roundworm Enterobius vermicularis. Usually a childhood disease, it can range from asymptomatic to causing severe anal and perianal itching. It is considered more a nuisance rather than a serious infection. Enterobius vermicularis is the commonest human intestinal worm, with a worldwide distribution. It is prevalent in both temperate and tropical climates, and is associated with crowding and poverty. Children are most commonly affected, and females more than males. Whole families and communities, notably schools, may be infected.

Enterocutaneous Fistula

Disease Name : Enterocutaneous Fistula, Treatment : "Resuscitation and restoration of volume with crystalloids ,and colloids, blood transfusion to achieve haematocrit of ,30%, maintenance of albumin level at 3.0 gm/di with albumin ,infusion. ,Sepsis control with antibiotics, percutaneous drainage of ,abscess under guidance or open drainage. ,Skin care to prevent excoriation using Karya powder, zinc ,oxide cream/powder, ion exchange resins, stoma adhesive and ,controlled fistula drainage using sump constructed suction ,catheter drain system or vacuum assisted closure (VAC) ,system or silicone barrier or created inverted cone system. ,Reduction of output of fistula-proton-pump inhibitors, ,histamine antagonists, sucralfate, octreotide, infliximab (in ,fistula in Crohns patients). Long-term nasogastric aspiration ,should be avoided.", It is resection of fistula tract ,with adjacent bowel and anastomosis or creation of stomas ,like ileostomy, gastrostomy, colostomy, depending on ,anatomical location of the fistula. In small bowel fistula, after ,excising the fistula track with its adjacent skin, entire small ,bowel along its length should be mobilized after adhesiolysis., Pathophysiology : The pathophysiology of an enterocutaneous fistula is simple since it is nothing more than an aberrant connection between intestine and skin. Anything that causes a potential communication between the intestine and the epidermis can lead to the development of an enterocutaneous fistula. A constant stream of fluid traveling through this connection will keep the tract patent, and it will provide time for epithelial tissue to migrate into and cover the inner surface of the tract. Epithelialization of the tract will further stabilize the patency of the fistula. These factors contribute to the reasons why short, wide, high output fistulas are more prone to stabilize than long, narrow, low-output fistulas ., Epidemiology : Enterocutaneous fistula mortality rates vary from 6% to 33%., Incidence is dependent on etiology. Infected pancreatic necrosis has an extremely high incidence of 50%. Trauma patients have a 2% to 25% incidence, and abdominal sepsis has a 20% to 25% incidence ., variable, factors that prevent enterocutaneous fistula .Rehydration.,Administration of antibiotics.,Correction of anemia.,Electrolyte repletion.,Drainage of obvious abscess.,Nutritional support.,Control of fistula drainage.,Skin protection., Complications : sepsis, Malnutrition, Intestinal failure, fluid or electrolyte abnormalities, Diagnostics : Complete Blood Count CBC, CRP, CECT Abdomen, MRI, CT, FISTULOGRAPHY, USG, METHYLENE BLUE TEST, Differential diagnosis : Abdominal Abscess, Abdominal aortic aneurysm, ABDOMINAL TRAUMA, colon cancer, INFLAMMATORY BOWEL DISEASES, local wound infection, obstruction, PEPTIC ULCER DISEASE, Urinary Tract Infection, disease description : A fistula is an abnormal connection between two epithelized surfaces. Fistulas can form between any two hollow spaces including blood vessels, intestine, vagina, bladder, and skin. There are three different categories used to define a fistula, anatomic, physiologic, and etiologic. Anatomically, fistulas are subdivided into two categories, internal and external. Internal fistulas are connections between two internal structures. A few examples of an internal fistula would be enterocolic, ileosigmoid, and aortoenteric. Alternatively, external fistulas form connections between an internal structure and external structure. Examples of this would be enterocutaneous, enteroatmospheric, and rectovaginal fistulas. When categorized physiologically, the fistula is differentiated based on fluid output. Low-output fistulas drain less than 200 ml of fluid per day, high-output fistulas drain greater than 500 ml of fluid per day, and medium-output fistulas fall between the two. Etiology is the last way in which fistulas are categorized. Common etiologic categories are traumatic fistulas, surgical site fistulas, and fistulas associated with Crohns disease. This article will specifically cover fistulas that fall under the anatomical category of enterocutaneous fistulas .

Entropion

Disease Name : Entropion, Treatment : medication : Moxifloxacin , Congenital entropion : excision of a,strip of skin and muscle with plastic reconstruction,of the lid crease (Hotz procedure).,,Cicatricial entropion : i. Anterior lamellar resection, ii. Tarsal wedge resection, iii. Transposition of tarsoconjunctival wedge, iv. Posterior lamellar graft, Senile entropion : i. Transverse everting suture, ii. Wies operation, iii. Plication of lower lid retractors (Jones operation)., Pathophysiology : Pathophysiology is dependent on the type of entropion seen. In general, the lower lid is stabilized from, the lower lid retractors, orbicularis, tarsus, and canthal tendons. The canthal tendons and tarsal plate horizontally stabilize the lid. The weakening of these structures, permits the inversion of the lid. The lower lid retractors stabilize vertically. In the upper lid, the levator aponeurosis and Muellers muscle provide this role. The lower lid retractors connect to the orbicularis muscle and overlying skin. As these extensions weaken, the preseptal orbicularis can travel superior and override the pretarsal muscle causing the eyelid margin to rotate against the eye. Inversion of the lid margin is also thought to be due to tarsal atrophy with the loss of support from the verticle lid and orbital fat atrophy.Involutional entropion is caused by horizontal laxity of the eyelid, attenuation or disinsertion of eyelid retractors, and overriding by the preseptal orbicularis oculi muscle. Acute spastic entropion is a condition that arises following ocular irritation or inflammation.  Sustained orbicularis oculi muscle overwhelms the oppositional action of the lower eyelid retractors causing inward rotation of the eyelid margin. A cycle of increasing frequency of spasm caused by corneal irritation perpetuates the problem, often only interrupted by intervention. Cicatricial entropion is caused by vertical tasoconjunctival contracture and internal rotation of the eyelid margin., Epidemiology : 2.4%, compared to 1.9% in men. Involutional entropion has a reported prevalence of 2.4% in whites and 0.8% in blacks., good, Because entropion often occurs naturally with aging or after scarring, it’s difficult to prevent. To reduce your risk of developing entropion caused by injury, wear protective eyewear during activities that could injure your eye., Complications : CORNEAL OPACITIES, corneal vascularization, corneal ulceration, Diagnostics : PHYSICAL EXAMINATION, Differential diagnosis : Distichiasis, Trachoma, trichiasis, disease description : Entropion is an inversion or inward turning of the eyelid margin. This can result in trichiasis, where the eyelashes are directed posteriorly toward the globe. It is one of the most common eyelid malpositions. This malposition can cause corneal and conjunctival damage leading to corneal abrasions, scarring, corneal thinning, or corneal neovascularization.  Entropion may be unilateral or bilateral. There are four types of entropion : congenital, involutional, acute spastic, and cicatricial. Lower eyelids are often involutional while the upper eyelid is cicatricial. Lower eyelid entropion is much more common than upper eyelid entropion.

Eosinophilic Esophagitis

Disease Name : Eosinophilic Esophagitis, Treatment : medication : Fluticasone , Montelukast , Pantoprazole , Depending on your response to tests for food allergies, your health care provider may recommend that you stop eating certain foods. Cutting out some foods, such as dairy or wheat products, may help to relieve symptoms and reduce inflammation. Sometimes, it may be recommended to limit your diet even more., "Proton pump inhibitor (PPI). Your provider will likely first prescribe an acid blocker such as a PPI. This treatment is the easiest to use, but most peoples symptoms dont improve.,Topical steroid. If you do not respond to the PPI, your provider will then likely prescribe a steroid, such as fluticasone or budesonide. This steroid is in a liquid form that is swallowed to treat eosinophilic esophagitis. This type of steroid is not absorbed into the bloodstream, so you are unlikely to have the typical side effects often associated with steroids.,Monoclonal antibodies. The Food and Drug Administration (FDA) recently approved dupilumab (Dupixent) for treatment of adults and children 12 years and older with eosinophilic esophagitis. Dupilumab is a type of medicine known as a monoclonal antibody. It works to block the action of certain proteins in the body that cause inflammation. Dupilumab is given weekly via injection.", Pathophysiology : Eosinophils are inflammatory cells that release a variety of chemical signals which inflame the surrounding esophageal tissue. This results in the signs and symptoms of pain, visible redness on endoscopy, and a natural history that may include stricturing. Eosinophils are normally present in other parts of a healthy gastrointestinal tract, these white blood cells are not normally found in the esophagus of a healthy individual. The reason for the migration of eosinophils to the tissue of the esophagus is not fully understood but is being studied extensively. It is thought the migration of eosinophils to the esophagus may be due to genetic, environmental, and host immune system factors.At a tissue level, EoE is characterized by a dense infiltrate with white blood cells of the eosinophil type into the epithelial lining of the esophagus. This is thought to be an allergic reaction against ingested food, based on the important role eosinophils play in allergic reactions. The eosinophils are recruited into the tissue in response to local production of eotaxin-3 by IL-13 stimulated esophageal epithelial cells ., Epidemiology : The prevalence of eosinophilic esophagitis has increased over time and currently ranges from 1 to 6 per 10, 000 persons., varIABLE, You cannot prevent or avoid EoE. It may run in families., Complications : esophageal stricture, narrowing of the esophagus., Damage to the esophagus, Diagnostics : Complete Blood Count CBC, EOSINOPHILS - ABSOLUTE COUNT, Endoscopic USG, Upper GI Endoscopy, biopsy, BARIUM ESOPHAGOGRAM, ESOPHAGOSCOPY, ESOPHAGEAL MUCOUS BIOPSY, BARIUM SWALLOW, Differential diagnosis : gastroenteritis, Gastroesophageal reflux disease (GERD), disease description : Eosinophilic esophagitis (EoE) is a chronic disease of the esophagus. Your esophagus is the muscular tube that carries food and liquids from your mouth to the stomach. If you have EoE, white blood cells called eosinophils build up in your esophagus. This causes damage and inflammation, which can cause pain and may lead to trouble swallowing and food getting stuck in your throat.EoE is rare. But because it is a newly recognized disease, more people are now getting diagnosed with it. Some people who think that they have reflux (GERD) may actually have EoE.

Eosinophilic Granulomatosis With Polyangiitis

Disease Name : Eosinophilic Granulomatosis With Polyangiitis, Treatment : • Localized disease . Prednisolone 1 mg/kg/day,Patients without organ- or life-threatening involvement the addition of methotrexate 20–25 mg/week , Systemic disease . Intravenous pulsed cyclophosphamide 15 mg/kg/pulse at 2–3-weekly intervals.,prednisolone 1 mg/kg/day (maximum 60 mg) is the currently preferred regimen ,Refractory disease . Rituximab, Pathophysiology : Allergy probably plays a central role, but the disease the inflammatory response is primarily Th2 in nature, although Th1 and Th17 responses are seen is almost certainly multifactorial. The Th2 response has been thought to be responsible for eosinophilic activation, and prolonged eosinophil survival. The products of eosinophilic and neutrophilic degradation have been observed in inflamed tissues and are probably responsible for tissue injury HLA-DRB4 may be a risk factor for the development of EGPA., Epidemiology : prevalence of 10–15 per million, The incidence is 1–2.5 per million, good, At this time there are no known ways to prevent this disease., Complications : kidney damage, heart disease, Peripheral nerve damage, Diagnostics : Differential Leucocyte Count DLC, serum IgE level, CT PNS, ANCA, biopsy, URINE MICROSCOPY, CT SCAN, CHEST RADIOGRAPH, Differential diagnosis : Acute Eosinophilic Pneumonia, Chronic Eosinophilic Pneumonia, EOSINOPHILIC ESOPHAGITIS, parasitic infections, vasculitis, disease description : Eosinophilic granulomatosis with polyangiitis (EGPA)—or, as it was traditionally termed, Churg-Strauss syndrome—is a rare systemic necrotizing vasculitis that affects small-to-medium-sized vessels and is associated with severe asthma and blood and tissue eosinophilia.  Like granulomatosis with polyangiitis (Wegener granulomatosis), and the microscopic form of periarteritis (ie, microscopic polyangiitis), EGPA is an antineutrophil cytoplasmic antibody (ANCA)–associated vasculitide.

Eosinophilic Pleuropericarditis

Disease Name : Eosinophilic Pleuropericarditis, Treatment : nan, Pathophysiology : The exact pathophysiology of eosinophilic pleuropericarditis is not fully understood, but it is believed to be related to an abnormal immune response. Heres a general overview of the possible pathophysiological mechanisms : Immune dysregulation : Eosinophilic pleuropericarditis may result from an abnormal immune response, where the immune system overreacts to an unknown trigger. This exaggerated immune response can lead to the recruitment and activation of eosinophils in the pleura and pericardium.Eosinophil activation : Eosinophils are activated and release various substances that contribute to tissue inflammation. These include cytokines, chemokines, and granule proteins like major basic protein, eosinophil cationic protein, and eosinophil peroxidase. These substances can damage the tissues and attract other immune cells, perpetuating the inflammatory response.Mast cell involvement : Mast cells, another type of immune cell, may also play a role in eosinophilic pleuropericarditis. Activation of mast cells can lead to the release of mediators like histamine, leukotrienes, and prostaglandins, which further promote eosinophil recruitment and inflammation., Epidemiology : nan, Complications : nan, Diagnostics : Complete Blood Count CBC, X RAY, Differential diagnosis : nan, disease description : nan

Ependymoma (who Grade 2)

Disease Name : Ependymoma (who Grade 2), Treatment : No established guidelines use the molecular subgroups to guide the treatment of ependymoma. The current consensus, however, recommends that patients with PF-EPN-A positive ependymoma, who are older than 12 months of age, undergo maximal safe micro-neurosurgical removal in addition to local radiotherapy., For intracranial ependymomas, surgery is typically the mainstay treatment. Complete resection without residual disease has presented better clinical outcomes and overall survival than partial resection. As discussed previously, there is insufficient evidence to support the use of chemotherapy., Pathophysiology : The exact pathophysiology of ependymomas is not fully understood, but here is an overview of the potential underlying mechanisms : Cellular origin : Ependymomas arise from ependymal cells, which are specialized cells that line the ventricles and central canal of the spinal cord. These cells play a role in the production and circulation of cerebrospinal fluid (CSF). Genetic mutations or alterations in these cells can lead to their transformation into tumor cells.Genetic alterations : Various genetic alterations have been associated with ependymoma development. The most common genetic alteration observed in ependymomas is the loss of a specific region on chromosome 22, known as 22q. This region contains tumor suppressor genes that help regulate cell growth and prevent tumor formation. Loss of this region can disrupt normal cellular processes and contribute to tumor development.Abnormal cellular proliferation : Ependymomas are characterized by uncontrolled cellular proliferation. Genetic alterations, such as mutations in tumor suppressor genes like TP53 and PTEN, can disrupt the normal regulation of cell growth and division. This leads to the accumulation of abnormal cells and the formation of a tumor.Disruption of CSF flow : Ependymomas can obstruct the flow of cerebrospinal fluid within the ventricles and central canal of the spinal cord. This obstruction can result in the buildup of fluid, leading to hydrocephalus (enlargement of the ventricles) and increased intracranial pressure. The exact contribution of CSF flow disruption to the pathophysiology of ependymomas is still under investigation., Epidemiology : ependymal tumors represent 1.7% of all brain and CNS tumors, variable, There is no way to prevent ependymoma because there are no known risk factors besides NF2., Complications : neurological deficit, Secondary malignancies, SENSORINEURAL HEARING LOSS, Diagnostics : biopsy, lumbar puncture, MRI, CT SCAN, Differential diagnosis : medulloblastoma, disease description : Ependymomas are glial cell tumors that commonly arise in the lining cells of the ventricular system, and less commonly outside the central nervous system (CNS), or within the brain parenchyma. They are comprised of genetically distinct subgroups of tumors and affect children more commonly than adults.

Epidemic Typhus

Disease Name : Epidemic Typhus, Treatment : medication : Doxycycline , •\tFirst line of treatment : doxycycline is the drug of choice and,treatment should be started as soon as the clinical diagnosis ,is made. The drug is given in full dose as a course of 7 days, ,except that epidemic typhus and scrub typhus respond to a ,single 200-mg dose of doxycycline (100 mg for children), Pathophysiology : The human body louse is only a vector and not a reservoir because infected lice die five to seven days after they become infected with R. prowazekii. R. prowazekii multiplies in the gut epithelium of the louse which then detaches, ruptures, and releases rickettsiae into the feces. Rickettsiae from the infected feces enter the skin via abrasions or bite site and access the human host.After entering the host,  R. prowazekii enters the microcirculation and the endothelial cells like R. rickettsii. Once inside the cell,  R. prowazekii escapes the phagosome and multiplies in the cytoplasm. R. prowazekii seldom gets into the nucleus as it lacks the actin-based directed mobility. R. prowazekii can multiply inside the endothelial cell until the cell bursts, releasing the contents into the extracellular space. The injury to the endothelial cells occurs due to the multiplication of the rickettsiae which causes the cells to burst. There is no evidence of endotoxin or exotoxin production by R. prowazekii. Thus, a network of endothelial cells is infected, inviting host cell response. R. prowazekii infection seldom disables the host machinery completely. The host mechanisms to contain Rickettsia prowazekii are like other rickettsial infections. Cytotoxic T-cell lymphocytes, particularly the CD8 group, are essential for the clearance of the rickettsiae. Interferon-gamma and tumor necrosis factor alpha activate the endothelial cells to kill the intracellular rickettsiae. However, despite adequate treatment R. prowazekii is known to cause latent infection (BZD).Endothelial cell injury leads to increased permeability of vascular endothelium and vasodilation. In severe cases, increased vascular permeability leads to interstitial edema, hypovolemia, hypotension, and hypoalbuminemia. In response to hypovolemia, secretion of antidiuretic hormone causes hyponatremia. Increased vascular permeability in the pulmonary circulation causes noncardiogenic pulmonary edema.  Thus, a picture of severe multi-organ system failure unfolds., Epidemiology : more than 1 million cases occur annually, Untreated, up to 40% of cases are fatal, - There is no vaccine to prevent epidemic typhus.,- Reduce your risk of getting epidemic typhus by avoiding overcrowded areas.,- Body lice thrive in areas that are overcrowded and where people aren’t able to bathe or change clothes regularly. ,- To avoid body louse infestations : Bathe regularly and change into clean clothes at least once a week, Wash louse-infested clothing at least once a week, Do not share clothing, beds, bedding, or towels used by a person who has body lice or is infected with typhus, Treat bedding, uniforms, and other clothing with 0.5% permethrin, People should avoid contact with flying squirrels and their nests., Complications : Gangrene of digits, kidney damage, liver damage, PNEUMONIA, septic shock, internal bleeding, low blood pressure, SPLEEN ENLARGED, Diagnostics : Immunofluorescence, biopsy, SEROLOGIC TEST, PCR, X RAY, Differential diagnosis : Epstein-Barr Virus, fever, Kawasaki Disease, Leptospirosis, Malaria, Meningitis, meningococcemia, relapsing fever, Rocky Mountain spotted fever, septicaemia, Syphilis, toxic shock syndrome, disease description : Rickettsia prowazekii is an intracellular, gram-negative coccobacillus. It is an obligate parasite. R. prowazekii belongs to the genus Rickettsia and is the causative agent of epidemic typhus. The genus Rickettsia is composed of gram-negative bacteria. Rickettsiae are the closest known relatives of mitochondria in eukaryotic cells .

Epidermodysplasia Verruciformis

Disease Name : Epidermodysplasia Verruciformis, Treatment : First line,•\tImiquimod,•\tPhotodynamic therapy,•\t Cryotherapy,Second line,•\tAcitretinoin,•\tIsotretinoin, Pathophysiology : The majority of HPV infection within cutaneous keratinocytes is cleared in the general population without progression to malignancy. In the general population, infection with HPV types 3 and 10 are mainly associated with development of verruca vulgaris. In persons with Epidermodysplasia verruciformis (EV), a decreased innate ability to clear HPV infection leads to persistent infection and progression to dysplasia and malignancy in the form of widespread pityriasis versicolor-like lesions and verruca plana like lesion formation as well as increased risk of persistent infection with beta-HPV leading to development of non-melanoma skin cancer. Mutations of TMC6/EVER1 or TMC8/EVER2 account for over 50% of the mutations which are responsible for the inherited form of EV. The exact mechanisms on cellular and/or molecular levels which lead to increased susceptibility to HPV infection and persistence within keratinocytes are not known, but some hypotheses suggest that the TMC6/EVER1 or TMC8/EVER2 are transmembrane channel proteins that serve to limit and restrict viral replication and gene expression of beta-HPV within keratinocytes.  These proteins may also influence zinc transporters which affect the intracellular zinc concentration. Zinc plays a pivotal role in transcription factors which activate steps in the HPV life cycle. AP-1 is one such factor affected by the zinc concentration and involved in HPV cellular proliferation. Merkel cell polyomavirus has also been identified in EV lesions ., Epidemiology : more than 200 cases have been reported, variable, Because EV is an inherited condition, there is little anyone with the abnormal genes can do to prevent the disorder.,,If you have a family member with the disease or know that your parents carry the abnormal EV gene, talk with your doctor. They can test your genes and determine your next steps., Complications : Skin cancer lesions, MALIGNANCY, Diagnostics : PCR For HPV, CT SCAN, full thickness skin biopsy, Differential diagnosis : Lichen Planus, Pityriasis versicolor, disease description : Epidermodysplasia verruciformis is an inherited disorder in which there is widespread and persistent infection with HPV, giving rise to a characteristic combination of plane warts, pityriasis versicolor-like lesions and reddish plaques. Malignant change is very common in adult life but metastasis is rare. Human papillomaviruses can be detected in a number of conditions in which widespread plane warts, thin keratosis and areas of flaking are seen and the risk of squamous cell carcinoma is increased. EV was described first and EV-like syndromes are seen in immunosuppressed states. Epidermodysplasia verruciformis comprises flaking or hyperkeratotic skin lesions predominantly in sun-exposed sites presenting in childhood, a mild cell-mediated immune deficiency and a high risk of development of cutaneous squamous cell carcinomas in early adult life. The susceptibility to the virus is inherited, usually autosomal recessive, though autosomal dominant and probable X- linked dominant patterns have been reported. Two loci on chromosome 17 are associated with the disease within some studied families. Mutations in two genes EVER1 and EVER2 are linked with the disease in many but not all cases. The EVER1 and EVER2 genes code for zinc-containing transmembrane proteins (TMC6 and TMC8, respectively)

Epidermoid Carcinoma

Disease Name : Epidermoid Carcinoma, Treatment : Excisional surgery,Mohs surgery,Cryosurgery,Curettage and electrodesiccation (electrosurgery),Laser surgery,Radiation,Photodynamic therapy (PDT),Topical medications, Pathophysiology : The pathophysiology of epidermoid carcinoma involves a series of genetic and cellular changes that lead to the uncontrolled growth and spread of malignant squamous cells. Here is an overview of the potential underlying mechanisms : Genetic mutations : Epidermoid carcinoma is often associated with genetic mutations or alterations that disrupt the normal regulation of cell growth and division. These mutations can occur spontaneously or be acquired due to exposure to carcinogens, such as tobacco smoke, ultraviolet (UV) radiation, or certain viruses (e.g., human papillomavirus). Common mutations observed in epidermoid carcinoma include alterations in tumor suppressor genes (e.g., TP53, PTEN) and oncogenes (e.g., EGFR, KRAS).Abnormal cellular proliferation : Genetic mutations in epidermoid carcinoma can result in the dysregulation of cellular proliferation. Normal cells have tightly controlled mechanisms to ensure that cell division occurs in a controlled and orderly manner. However, in epidermoid carcinoma, these mechanisms are disrupted, leading to uncontrolled and excessive cell division. The accumulated malignant squamous cells form a tumor mass.Invasion and metastasis : Epidermoid carcinoma can invade nearby tissues and structures as the tumor grows. The malignant cells can penetrate the basement membrane that separates the epithelial tissue from underlying tissues, allowing them to invade surrounding tissues and potentially spread to nearby lymph nodes. Additionally, cancer cells may enter blood vessels or lymphatic vessels, facilitating metastasis (the spread of cancer to distant organs or tissues)., Epidemiology : About 2, 000 cases of MCC are diagnosed in the United States each year, 1% and 2% of all, variable, Complications : nan, Diagnostics : MRI, CT SCAN, PHYSICAL EXAMINATION, full thickness skin biopsy, Differential diagnosis : nan, disease description : Epidermoid tumors are congenital lesions that arise from ectodermal cells misplaced during the closure of the neural tube in the process of embryogenesis. They start to form during the very early stages of the development of the embryo during the closure of the neural tube where epithelial cells are trapped. They have a benign nature and slow growth rate. Epidermoids consist only of ectodermal germ cells, while dermoids contain both ectodermal and mesodermal germ cells. They can also be called central nervous system epidermoid cyst, intracranial epidermoid cyst, and epidermoid brain cyst. 

Epidermolysis Bullosa Acquisita

Disease Name : Epidermolysis Bullosa Acquisita, Treatment : medication : Mycophenolate mofetil/ Mycophenolate sodium, Cyclosporine/Ciclosporine, Prednisolone, First line,•\tPrednisolone 0.5–2.0 mg/kg/day (depending on disease ,severity) + colchicine 0.5–3.0 mg/day (the highest dose that ,does not lead to diarrhoea) ± dapsone 1.5 mg/kg/day,Second line,•\t+ Mycophenolates (2 g/day; 1.440 mg/day) or,•\t+ Ciclosporin 3–6 mg/kg/day,Third line,•\tImmunoadsorption ±,•\tIVIG 2 g/kg/month or,•\tRituximab 2 × 1 g, Pathophysiology : The autoantigen of EBA is homotrimeric type VII collagen, a constituent of the anchoring fibrils. Its N terminal 145 kDa NC1 domain has been identified as the immunodominant region with epitopes spreading across all of this region. Only rare cases with reactivity against the C terminal NC2 or the central collagenous domain are reported. Patients with intermolecular epitope spreading and reactivity with other DEJ antigens, i.e. BP180, BP230, laminin 332 and the p200 antigen in addition to type VII collagen-specific antibodies, may occasionally been found. The pathogenic relevance of autoantibodies in EBA has been shown unequivocally. Serum levels of anti-type VII collagen antibodies correlate with the disease activity in patients and transient neonatal disease was observed following placental transfer of autoantibodies from an affected mother., Epidemiology : The prevalence may be higher in Korean and African-American populations ., Epidermolysis bullosa acquisita is one of the rarest subepidermal bullous diseases in Western Europe, with an estimated annual incidence of 0.2 to 0.5 per million people ., EBA is a chronic relapsing disease, "Its not possible to prevent epidermolysis bullosa. But these steps may help prevent blisters and infection.,,Handle your child gently. Your infant or child needs cuddling, but be very gentle. To pick up a child with epidermolysis bullosa, place the child on soft material and give support under the buttocks and behind the neck. Dont lift the child from under the arms.,Take special care with the diaper area. If your child wears diapers, remove the elastic bands and avoid cleansing wipes. Line the diaper with a nonstick dressing or spread it with a thick layer of zinc oxide paste.,Keep the home environment cool. Try to keep your home cool and the temperature steady.,Keep the skin moist. Gently apply moisturizer as needed throughout the day.,Dress your child in soft clothes. Use soft clothing thats simple to get on and off. It may help to remove labels and put on clothing seam-side out to reduce scratching. Try sewing foam pads into the lining of clothing by elbows, knees and other pressure points. Use soft special shoes, if possible.,Prevent scratching. Trim your childs fingernails regularly.,Encourage your child to be active. As your child grows, encourage activities that reduce the risk of skin injury. Swimming is a good option. For children with mild forms of epidermolysis bullosa, they can protect the skin by wearing long pants and sleeves for outdoor activities.,Cover hard surfaces. Consider padding a car seat or bathing tub with sheepskin, foam or a thick towel. Soft cotton or silk can be used as a top layer over the padding.", Complications : Syndactyly, JOINT CONTRACTURES, NASAL SYNECHIA, loss of nails, Diagnostics : ELISA, DIRECT IMMUNOFLORESCENCE ASSAY, INDIRECT IMMUNOFLORESCENCE ASSAY, skin lesion biopsy, Differential diagnosis : Bullous pemphigoid, Epidermolysis bullosa acquisita, Friction blisters, insect bites, Pemphigus Vulgaris, disease description : Epidermolysis bullosa acquisita (EBA) is a rare chronic autoimmune blistering disease of the skin and mucous membranes. EBA is caused by autoantibodies to type VII collagen, a major component of anchoring fibrils in the dermal-epidermal junction (DEJ). These anchoring fibrils are responsible for attaching the epidermis to the underlying dermis, and binding of autoantibodies to type VII collagen subsequently leads to detachment of the epidermis, resulting in skin fragility, blisters, erosions, scars, milia, and nail loss. Clinically, patients can present with various phenotypes. The mechanobullous and bullous pemphigoid-like forms of EBA are the two most common presentations. The classic mechanobullous EBA resembles dystrophic epidermolysis bullosa (EB) with bullae and erosions occurring at sites of trauma. The inflammatory forms of EBA present with clinical manifestations similar to other autoimmune blistering disorders, including bullous pemphigoid (BP) and mucous membrane pemphigoid (MMP). EBA has been reported in association with several systemic diseases, including inflammatory bowel disease, thyroiditis, rheumatoid arthritis, hepatitis C infection, and diabetes mellitus .

Epidermolysis Bullosa

Disease Name : Epidermolysis Bullosa, Treatment : The management depends on expert nursing care and follows the,principles used for other sites., Medications can help control pain and itching. Your health care provider may also prescribe pills to fight infection (oral antibiotics) if there are signs of widespread infection, such as fever and weakness., Surgical treatment may be needed. Options sometimes used for this condition include : ,,Widening the esophagus. Blistering and scarring of the long, hollow tube that runs from the throat to the stomach (esophagus) may lead to narrowing of the tube. This makes it hard to eat. Making the tube wider with surgery can make it easier for food to travel to the stomach.,Placing a feeding tube. To improve nutrition and help with weight gain, a feeding tube (gastrostomy tube) may be needed to deliver food directly to the stomach.,Grafting skin. If scarring has affected the function of a hand, the surgeon may suggest a skin graft.,Restoring movement. Repeated blistering and scarring can cause fusing of the fingers or toes or unusual bends in the joints (contractures). A surgeon might recommend surgery to correct these conditions if they restrict movement., Pathophysiology : The human skin consists of two layers : an outermost layer called the epidermis and a layer underneath called the dermis. In individuals with healthy skin, there are protein anchors between these two layers (Dermo epidermal junction) that prevent them from moving independently from one another (shearing). In people born with EB, the two skin layers lack the protein anchors that hold them together, resulting in extremely fragile skin—even minor mechanical friction (like rubbing or pressure) or trauma will separate the layers of the skin and form blisters and painful sores. EB  individuals manifest unremitting skin blistering that evolves into chronic wounds, inflammation, and fibrosis. People with EB have compared the sores with third-degree burns. Furthermore, as a complication of the chronic skin damage, people with EB have an increased risk of malignancies (cancers) of the skin. Virtually any organ lined or covered by epithelium may be injured in inherited EB. External eye, esophagus, upper airway, and genitourinary tract are the epithelial surfaced tissues that are at particular risk., Epidemiology : 19.6 per one million of live-born infants, 1 out of every 50, 000 live births., variable, Because it’s genetic, you can’t prevent EB. People with a family history of EB who are thinking about becoming parents may benefit from genetic counseling to decide how to grow their families.,,In addition, experts don’t currently know what causes EB acquisita. Therefore, healthcare providers don’t know how to prevent it., Complications : constipation, death, infection, dental problem, Skin cancer lesions, VULVA CARCINOMA, Diagnostics : Immunofluorescence, DNA analysis for mutation, biopsy, GENETIC TESTING, X RAY, Differential diagnosis : Bullous pemphigoid, Mucous membrane pemphigoid, Porphyria Cutanea Tarda, disease description : Epidermolysis bullosa (ep-ih-dur-MOL-uh-sis buhl-LOE-sah) is a rare condition that causes fragile, blistering skin. The blisters may appear in response to minor injury, even from heat, rubbing or scratching. In severe cases, the blisters may occur inside the body, such as the lining of the mouth or stomach.Epidermolysis bullosa is inherited, and it usually shows up in infants or young children. 

Epidermolytic Palmoplantar Keratoderma

Disease Name : Epidermolytic Palmoplantar Keratoderma, Treatment : The mainstay is mechanical debridement, followed by mild keratolytic re-lubrication to help avoid fissures., The following treatments soften the thickened skin and makes it less noticeable.,,Emollients,Keratolytic agents (eg, 6% salicylic acid, 70% propylene glycol, 30% water),Topical retinoids,Topical vitamin D ointment (calcipotriol),Oral retinoids (acitretin), Pathophysiology : Epidermolytic palmoplantar keratoderma was initially found to map to the type I keratin gene cluster on chromosome 17 and subsequently shown to result from rare mutations in KRT1 and more common mutations in KRT9, which is preferentially expressed in palmoplantar skin. Disruption of intermediate filament integrity due to these mutations is predicted to reduce the resilience of the cytoskeleton to minor external trauma, leading to blistering and hyperkeratosis as well as epidermolysis with tonofilament clumping. Most mutations identified to date affect the helix initiation peptide, but a 3-bp insertion in the helix termination motif has also been identified. Infrequently, keratin 1 is involved : KRT1 gene mutations affecting the 2B domain, in the helix termination peptide and splice site mutations have been described. EPPK with unusual ‘tonotubular’ filaments on electron microscopy is due to mutations altering the 1B rod domain of keratin 1., Epidemiology : 4.4/100 000, variable, Complications : nan, Diagnostics : GENETIC TESTING, CT SCAN, HISTOLOGIC EXAMINATION, full thickness skin biopsy, Differential diagnosis : nan, disease description : Palmoplantar keratoderma is associated with epidermolytic changes on histology and is due to mutations localized to a hotspot region of KRT9 or infrequently to specific domains of KRT1. Voerner described diffuse PPK with autosomal dominant inheritance, clinically indistinguishable from that described by Thost and Unna but with histological features of EHK in affected palms and soles. Thost’s original family in fact was apparently also affected with EPPK.

Epididymoorchitis

Disease Name : Epididymoorchitis, Treatment : medication : Doxycycline , If a sexually transmitted infection is the cause then you should not have sex until treatment and follow-up have been completed. Sexual partners of men with epididymo-orchitis caused by a sexually transmitted infection may also need antibiotic treatment.,,Antibiotics do not kill viruses and they are not needed if a viral infection is the cause - for example, mumps.,,You may find that supporting underwear helps to ease the pain. Painkillers and ice packs (never apply ice directly to your skin) will also ease the pain., A course of antibiotic medicines is usually advised as soon as epididymo-orchitis is diagnosed. These normally work well. Pain usually eases within a few days but swelling may take a week or so to go down, sometimes longer. The choice of the antibiotic depends on the underlying cause of the infection., Pathophysiology : Infection reaches the epididymis via the vas from a primary infection of the urethra, prostate or seminal vesicles. A general rule is that epididymitis arises in sexually active young men from a sexually transmitted genital infection, while in older men it more usually arises from a urinary infection or may be secondary to an indwelling urethral catheter. In young sexually active men, the most common cause of epididymitis is now Chlamydia trachomatis, but gonococcal epididymitis is still occasionally seen. In older men with bladder outflow obstruction, epididymitis may result from a urinary infection – it is proposed that a high pressure in the prostatic urethra might cause reflux of infected urine up the vasa. Blood-borne infections of the epididymis are less common but may be suspected when there is epididymal infection without evidence of urinary infection; it is presumably the only possible mechanism in men who have previously undergone a vasectomy. Acute epididymo-orchitis can follow any form of urethral instrumentation and it is particularly common when an indwelling catheter is associated with infection of the prostate. Infection usually starts in the tail of the epididymis and spreads to the rest of the epididymis and occasionally to the testis. Complications include abscess formation, testicular infarction, testicular atrophy, chronic induration and inflammation and infertility., Epidemiology : (0.69 percent), 9.09 per 100, 000 population., variable, To Do : drink plenty of fluid. Local measures,including scrotal support and analgesia are helpful.., Complications : abscess, atrophy, induration, Infarction, MALE INFERTILITY, Diagnostics : URINE CULTURE, Color Doppler, urethral swab, nucleic acid amplification testing, USG, NAAT TEST, Differential diagnosis : HYDROCELE, Scrotal trauma, Spermatocele, Testicular trauma, Urinary Tract Infection, disease description : Epididymo-orchitis is an inflammation of the epididymis and/or testicle (testis). In adults, epididymo-orchitis is usually due to infection, most commonly from a urine infection or a sexually transmitted infection.As the epididymis and testis lie next to each other, it is often difficult to tell if the epididymis, the testis, or both are inflamed. Therefore, the term epididymo-orchitis is often used.

Epilepsy

Disease Name : Epilepsy, Treatment : medication : Phenobarbital/Phenobarbitone, Phenytoin , Ethosuximide , Levetiracetam , Lamotrigine , Carbamazepine, Clonazepam, Clobazam, Antiepileptic drug ,therapy should be started in any patient with recurrent seizures ,of unknown etiology or a known cause that cannot be reversed. ,Whether to initiate therapy in a patient with a single seizure is controversial. Patients with a single seizure due to an identified lesion ,such as a CNS tumor, infection, or trauma, in which there is strong ,evidence that the lesion is epileptogenic, should be treated., Pathophysiology : Seizures (convulsions, fits) are caused by abnormal electrical discharges from the brain resulting in abnormal involuntary, paroxysmal, motor, sensory, autonomic or sensorial activity. About 5 percent children experience convulsions during the first five years of life. Motor movements consisting of tonic and clonic components are the most commonly observed phenomenon, except in the newborn period. Focal seizure activity can begin in a very discrete region of cortex and then slowly invade the surrounding regions. The hallmark of an established seizure is typically an electrographic “spike” due to intense near-simultaneous firing of a large number of local excitatory neurons, resulting in an apparent hypersynchronization of the excitatory bursts across a relatively large cortical region. The bursting activity in individual neurons (the “paroxysmal depolarization shift”) is caused by a relatively long-lasting depolarization of the neuronal membrane due to influx of extracellular calcium (Ca2+), which leads to the opening of voltage-dependent sodium (Na+) channels, influx of Na+, and generation of repetitive action potentials. This is followed by a hyperpolarizing afterpotential mediated by gamma-aminobutyric acid (GABA) receptors or potassium (K+) channels, depending on the cell type. The synchronized bursts from a sufficient number of neurons result in a so-called spike discharge on the EEG. The spreading seizure wavefront is thought to slow and ultimately halt by intact hyperpolarization and a “surround” inhibition created by feedforward activation of inhibitory neurons. With sufficient activation, there is a recruitment of surrounding neurons via a number of synaptic and nonsynaptic mechanisms, including : (1) an increase in extracellular K+, which blunts hyperpolarization and depolarizes neighboring neurons; (2) accumulation of Ca2+ in presynaptic terminals, leading to enhanced neurotransmitter release; (3) depolarization-induced activation of the N-methyl-d-aspartate (NMDA) subtype of the excitatory amino acid receptor, which causes additional Ca2+ influx and neuronal activation; and (4) ephaptic interactions related to changes in tissue osmolarity and cell swelling. The recruitment of a sufficient number of neurons leads to the propagation of excitatory currents into contiguous areas via local cortical connections and to more distant areas via long commissural pathways such as the corpus callosum., Epidemiology : 5–30 persons per 1000, ~0.3–0.5%, GOOD, Although many causes of epilepsy are out of your control and unpreventable, you can reduce your chance of developing a few conditions that might lead to epilepsy, such as : ,1. To lower your risk of traumatic brain injury (from blows to your head), always wear your seatbelt when driving and drive “defensively”; wear a helmet when biking; clear your floors of clutter and power cords to prevent falls; and stay off ladders.,2. To lower your risk of stroke, eat a healthy diet (such as the Mediterranean diet), maintain a healthy weight and exercise regularly.,3. Seek therapy for substance abuse. Alcohol and other illegal drugs can damage your brain, which can then lead to epilepsy., Complications : seizures, Behavioural DIsorder, Diagnostics : EEG, PET SCAN, SINGLE-PHOTON EMISSION COMPUTED TOMOGRAPHY (SPECT), lumbar puncture, SERUM ELECTROLYTE, serum calcium Ca++, CT HEAD, GENETIC TESTING, MRI, BLOOD GLUCOSE, NEUROLOGICAL EXAMINATION, Differential diagnosis : Confusional state, Metabolic disturbances, panic attacks, syncope, transient ischaemic attacks, disease description : Epilepsy describes a condition in which a person has a risk of recurrent seizures due to a chronic, underlying process. This definition implies that a person with a single seizure, or recurrent seizures due to correctable or avoidable circumstances, does not necessarily have epilepsy (although a single seizure associated with particular clinical or electroencephalographic features may establish the diagnosis of epilepsy). Using the definition of epilepsy as two or more unprovoked seizures, the incidence of epilepsy is ~0.3–0.5% in different populations throughout the world, and the prevalence of epilepsy has been estimated at 5–30 persons per 1000.

Epiretinal Membrane

Disease Name : Epiretinal Membrane, Treatment : There are no eye drops, medications or nutritional supplements to treat ERMs. A surgical procedure called vitrectomy is the only option in eyes that require treatment., Surgical management involves pars-plana vitrectomy (PPV) with ERM and ILM peeling. PPV with membrane peeling has been used successfully for many decades, with an excellent visual outcome and a reduced recurrence rate. ILM is thought to provide a platform for the proliferation of fibroblasts, glial cells, and astrocytes for the retina to form ERM. ILM peeling along with membrane peeling has become a standard procedure following the advent of staining dyes like trypan blue, indocyanine green (ICG), and brilliant blue G (BBG). Triamcinolone is used to stain the vitreous and the membrane. Triamcinolone staining helps to induce posterior vitreous detachment and to ensure an excellent subtotal vitrectomy. Accelerated nuclear sclerosis or a worsening of cataract is the most common complication of vitrectomy. If a cataract is present, the procedure should be combined with a cataract removal to ensure better visualization of the surgical procedure and also to prevent a subsequent second surgery., Pathophysiology : A fibrocellular proliferation over the internal limiting membrane (ILM) characterizes the epiretinal membrane (ERM). The initiating event in an idiopathic ERM is the posterior vitreous detachment (PVD). Aging vitreous liquefies and detaches from its posterior attachments leading to posterior vitreous detachment. PVD causes dehiscence in the internal limiting membrane, which allows the microglial cells to migrate to the preretinal surface where they interact with the hyalocytes and laminocytes of the vitreous cellular membrane. These cells later transdifferentiate into fibroblast-like cells to form a cellophane thin epiretinal membrane. PVD causes 95% of cases of idiopathic ERM. Retinal folds from ERM contracts to create a macular pucker. Retinal glial cells, hyalocytes, fibroblasts, and myofibroblasts are predominantly seen in idiopathic ERM. Retinal pigment epithelial cells, macrophages, T, and B cells are seen in secondary ERM as inflammation is the triggering event. A prerequisite for the formation of ERM is dehiscence in the ILM most commonly caused by posterior vitreous detachment. The following are the theories hypothesized for the ERM formation : Microglial cells migrate to the retinal surface over micro leaks produced by PVD. These cells later differentiate to form the fibroblasts.Following PVD, segments of cellular vitreous remain on the surface. These segments contain hyalocytes that transdifferentiate into myofibroblasts from ERM.PVD induced ILM avulsion in the posterior paravascular retina upregulates the cytokines to form the ERM., Epidemiology : up to 7% of the population, variable, ILM peeling at the time of rhegmatogenous retinal detachment repair may decrease the likelihood of symptomatic ERM development and the need for subsequent surgery., Complications : endophthalmitis, macular hole, VITREOUS HAEMORRHAGE, Retinal breaks or detachment, Accelerated nuclear sclerosis or cataract formation, Macular toxicity (trauma\\/light), Diagnostics : Optical coherence tomography (OCT), Slit lamp examination, Fluorescein angiography, Differential diagnosis : Fine vessel tortuosity : Combined hamartoma of retina and RPE, Membrane over the retina : Proliferative vitreoretinopathy and tractional retinal detachment., disease description : Epiretinal membrane is a commonly occurring condition affecting the posterior pole of the retina over the macula. It appears as a greyish semi-translucent avascular membrane over the internal limiting membrane (ILM) on the surface of the retina. It appears as a greyish semi-translucent avascular membrane over the internal limiting membrane (ILM) on the surface of the retina. The other synonyms for ERM are macular pucker, preretinal macular fibrosis, surface wrinkling retinopathy, epimacular proliferations, epiretinal fibrosis or gliosis, and cellophane maculopathy.

Episcleritis

Disease Name : Episcleritis, Treatment : medication : Indomethacin , Carboxymethyl cellulose , Fluorometholone , Flurbiprofen , Ketorolac trometamol, 1. Topical NSAIDs, e.g., ketorolac 0.3% may be useful.,2. Topical mild corticosteroid eyedrops e.g., ,fluorometholone or loteprednol instilled 2–3,hourly, render the eye more comfortable and,resolve the episcleritis within a few days.,3. Topical artificial tears e.g., 0.5% carboxy methyl,cellulose have soothing effect. 4. Cold compresses applied to the closed lids may,offer symptomatic relief from ocular discomfort.,5. Systemic nonsteroidal anti-inflammatory drugs,(NSAIDs) such as flurbiprofen (300 mg OD), ,indomethacin (25 mg three times a day), or,oxyphenbutazone may be required in recurrent,cases., Pathophysiology : The pathophysiology of episcleritis is a non-granulomatous inflammation of the episcleral vascular network.1 This acute inflammatory process involves the activation of resident immune cells, including lymphocytes and macrophages. Once activated, they release inflammatory mediators causing vasodilation, increased vascular permeability, and the migration of more white blood cells and macrophages. The process is self-limited and generally lasts between 2 and 21 days ., Epidemiology : 5.54 per 100, 000 per year, good, Since there’s often no way of telling what’s causing episcleritis, there’s no real way to prevent it from happening., Complications : Glaucoma, ANTERIOR UVEITIS (IRIDOCYCLITIS), INTERMEDIATE UVEITIS, corneal dellen, peripheral corneal infiltrates, Declining vision, Diagnostics : Complete Blood Count CBC, SERUM URIC ACID, VDRL, Slit lamp examination, biopsy, ophthalmoscopy, Differential diagnosis : ACUTE BACTERIAL CONJUNCTIVITIS, Contact lens-associated red eye (CLARE), PINGUECULA, SCLERITIS, disease description : Episcleritis is an acute unilateral or bilateral inflammation of the episclera, the thin layer of tissue between the conjunctiva and sclera. The episclera is composed of loose connective tissue with its vascular supply coming from the anterior ciliary arteries, which are branches of the ophthalmic artery. Episcleritis can be diffuse, sectoral or nodular, and is most often idiopathic but is also often associated with systemic collagen vascular diseases, autoimmune diseases, and even some infections. Patient symptoms include redness, mild ocular discomfort or pain, and normal visual acuity. They rarely experience discharge or photophobia.

Epithelial Basement Membrane Dystrophy Of Cornea

Disease Name : Epithelial Basement Membrane Dystrophy Of Cornea, Treatment : The first course of action is to augment the natural lubrication of the eye, using artificial tears during the day and ointments or gel lubricants at night. (This is because thicker lubrication modalities blur vision.) Hypertonic saline solutions, which contain more salt than normal tears, are also useful; lubricants are usually recommended on a regular schedule throughout the day as well.,,In more severe cases, patients may need to use a soft contact lens as a bandage to protect the epithelium. Increasing humidity in the home using vaporizers or similar equipment may be recommended.,,More permanent treatments include puncturing the corneal epithelium to allow better adherence of the epithelial cells, corneal scraping to remove eroded areas and allow regeneration of healthy epithelial tissue. Sometimes, the excimer laser may be used to remove surface irregularities., simple epithelial debridement, Pathophysiology : Corneal dystrophies are inherited disorders in which the cells have some inborn defects due to which pathological changes may occur with passage of time leading to development of corneal haze in otherwise normal eyes that are free from inflammation or vascularization. There is no associated systemic disease. Dystrophies occur bilaterally, manifesting occasionally at birth, but more usually during first or second decade and sometimes even later in life. Presents in adult life, rarely seen in children. Asymptomatic or recurrent erosions with pain, lacrimation and blurred vision are observed. Except for the bleb pattern, on-axis lesions may also cause blurred vision due to irregular astigmatism. Location and degree of pathology can fluctuate with time.  Typical lesions include : • Maps. Irregular islands of thickened, gray, hazy epithelium with scalloped, circumscribed borders, particularly affecting the central or paracentral cornea. Isolated or combined with other signs. • Dots (Cogan). Irregular round, oval or commashaped, non-staining, putty-gray opacities. Clustered like an archipelago in the central cornea. Typically combined with other signs, especially with maps. • Fingerprint lines. Parallel, curvilinear lines, usually paracentral, best seen in retroillumination. They may be isolated or combined with other signs, especially maps. • Bleb pattern (Bron). A subepithelial pattern like pebbled glass, best seen by retroillumination. Isolated or combined with other signs. Note. Poor adhesion of basal epithelial cells to abnormal basal laminar material is thought predisposition to recurrent erosions., Epidemiology : Epithelial basement membrane dystrophy (EBMD) is the most common of the anterior corneal dystrophies. Its prevalence varies between 2% and 6% of the general population ., approximately 2 percent of the population, variable, There is no real prevention for EBMD. If recurrent corneal erosions are present with the EBMD, they may be prevented with nighttime lubricating or hypertonic saline ointments or with various surgical procedures described below and in the eyewiki article "Anterior Stromal Puncture.", Complications : visual acuity, Diagnostics : Optical coherence tomography (OCT), ophthalmoscopy, retroillumination, Differential diagnosis : corneal abrasions, "Meesmans Juvenile Epithelial Dystrophy", recurrent corneal erosions, "Reis-Bucklers Dystrophy", disease description : Epithelial basement membrane dystrophy (EBMD) is also known as map-dot-fingerprint dystrophy or Cogan microcystic epithelial dystrophy or anterior basement membrane dystrophy. Inheritance. Most cases have no inheritance documented. Genetic locus and gene are 5q31 and TGFb1, respectively.

Epithelial Recurrent Erosion Dystrophy

Disease Name : Epithelial Recurrent Erosion Dystrophy, Treatment : CORNEAL GRAFTS : About 25% of the patients may eventually,need corneal grafts at the mean age of 45 years., Pathophysiology : Epithelial recurrent erosion dystrophy (ERED), also known as corneal erosions or recurring hereditary dystrophy, usually occurs in first decade of life. • Corneal erosions are seen during the attack recurrent corneal erosions appear typically at 4–6 years of age but occasionally as early as 8 months of age. Attacks generally decline in frequency and intensity and cease by the age of 50 years. • Subepithelial haze or blebs may be seen between the attacks. • Central subepithelial corneal opacities, may appear as early as 7 years of age. These vary from subepithelial fibrosis to protruding keloid-like nodules. Symptoms are precipitated by minimal trauma or occur spontaneously and are in the form of attacks of redness, photophobia, epiphora and ocular pain., Epidemiology : approximately 2 percent of the population, , unknown, variable, Complications : nan, Diagnostics : Slit lamp examination, ophthalmoscopy, fluorescein staining, Corneal topography, Differential diagnosis : nan, disease description : Epithelial recurrent erosion dystrophy (ERED) is characterized by frequent painful recurrent corneal erosions, with onset in the first decade of life and subsequent gradual decrease in frequency, with cessation in the third or fourth decade. Small gray anterior stromal flecks associated with larger focal gray-white disc-shaped, circular, or wreath-like lesions with central clarity, in the Bowman layer and immediately subjacent anterior stroma, varying from 0.2 to 1.5 mm in diameter, appear to be clinically diagnostic of ERED

Epithelial-myoepithelial Carcinoma

Disease Name : Epithelial-myoepithelial Carcinoma, Treatment : EMC is considered to be a low-grade malignant tumor, adequate resection with negative soft-tissue margins is the minimum recommended and necessary therapy. Neck node dissection should be considered in cases of lymph node positivity along with chemotherapy and radiotherapy in patients with highly advanced disease, positive surgical margins, or surgically unresectable disease, although there have been almost no studies of these therapies., Pathophysiology : A nodular, well-circumscribed mass was surgically excised with a surrounding portion of normal parotid gland. The specimen comprised a 4 cm × 3.5 cm × 1 cm lobulated portion of tissue. Grossly, the lesion was apparently well circumscribed, multilobated and grey-white in appearance; the cut surface revealed many small cysts with hemorrhagic content . Histological examination showed a multilobular appearance with well-circumscribed multiple nodules surrounded by a dense fibrous stroma. The tumor was not encapsulated and had an incomplete, dense fibrous pseudocapsule partially surrounding the neoplastic tissue : The tumor showed expansive edges. The tumor comprised mainly a population of large, polygonal clear cells, only focally spindled and with large nuclei that were often nucleolated. The cells had indistinct cytoplasmic borders and were of the myoepithelial type. These cells were arranged in sheets, nests and tubules surrounded by an abundant homogeneous, eosinophilic, hyalinized stroma with small inconspicuous vessels in its context . In some areas, another population of cells was evident, arranged in ductal structures and surrounded by the above-described population of cells; this population comprised small cuboidal, eosinophilic cells with uniform round nuclei surrounding luminal spaces occupied by eosinophilic proteinaceous material. There was no mitotic activity, atypia, or necrosis. Occasional microscopic tumor foci were present in adjacent areas; the salivary gland tissue was otherwise unremarkable. The tumor approached the surgical margins but appeared to be completely excised. Immunohistochemical evaluation revealed positivity for CKAE1/AE3 and CK7 in the small cuboidal, epithelial eosinophilic cells surrounding luminal spaces, arranged in ductal structures; the myoepithelial cells were strongly reactive for p63 , smooth muscle actin , vimentin and S-100 protein. There was scattered, weak staining for glial fibrillary acidic protein among the neoplastic myoepithelial cells. CD117 was negative. Ki67 was positive about in 5% of the neoplastic cells., Epidemiology : There is a female predominance, with a peak occurrence in the seventh decade of life., EMC represents <1% of all salivary gland tumors and arises most commonly in the parotid gland, but it has also been described in the submandibular gland, minor salivary glands and palate., good, Complications : nan, Diagnostics : ultrasound, biopsy, CT SCAN, Fine-needle aspiration biopsy, Immunostaining, Differential diagnosis : Acinic cell carcinoma, adenoid cystic carcinoma, Metastatic renal cell carcinoma, Pleomorphic adenoma, disease description : Epithelial-myoepithelial carcinoma (EMC) is a rare biphasic tumor of the salivary gland. It is generally composed of variable proportions of two cell types : An inner layer of duct lining cells and an outer layer of clear cells, which typically form double-layered duct-like structures.

Epithelioid Haemangioendothelioma

Disease Name : Epithelioid Haemangioendothelioma, Treatment : .Doctors may use chemotherapy with other treatments. It is important to discuss the side effects with your doctor., Immunotherapy uses different treatments to help the body’s immune system kill tumor cells., Bevacizumab , Carboplatin, Interferon Alpha, Paclitaxel, Thalidomide, Doctors sometimes use radiation therapy to treat EHE, with or without surgery. Radiation therapy is most often used to treat EHE that grows in the bones. Because radiation therapy can cause other cancers in the future, it is important to discuss this option with your doctor., Complete excision with clear margins is essential, Pathophysiology : The neoplasm is infiltrative and is composed of strands, cords and nests of endothelial cells in a hyaline or myxoid stroma. Dermal lesions often consist of a fairly well-defined nodule. The tumour cells have epithelioid morphology and consist of pink cytoplasm, vesicular nuclei and inconspicuous nucleoli. Angiocentricity is commonly seen and tumours often arise from a medium-sized vein or even an artery. Formation of vascular channels is not readily apparent but a common finding is the presence of intracytoplasmic vacuoles with or without red blood cells. A small number of cases display cytological atypia, which may be prominent, and a high mitotic count. There is no clear correlation between cytological grade and behaviour. Occasional tumours overlap with epithelioid angiosarcoma. Staining for endothelial cell markers, including ERG and CD31, is usually positive, and 20–30% of cases are focally positive for keratin . Podoplanin (D2-40) is also frequently positive in tumour cells. Most tumours show a translocation t(1;3) (p36.3;q25) that results in fusion of the WWTR1 and CAMTA1 genes. In a group of tumours, a novel fusion, involving genes YAP1 and TFE3 on chromosomes 11 and X, respectively, has been demonstrated., Epidemiology : It is so rare that only 0.01 percent of the cancer population has it and it affects about 1 person in every 1, 000, 000 worldwide ., recurrence occur, Complications : nan, Diagnostics : biopsy, MRI, X RAY, CT SCAN, Differential diagnosis : granulomatous infections, pulmonary arteriovenous malformations, pulmonary hyalinizing granuloma, "relapsed follicular beta cell non-Hodgkins lymphoma", Sarcoidosis, "wegeners granulomatosis", disease description : Epithelioid haemangioendothelioma is a distinctive tumour characterized by epithelioid endothelial cells arranged in strands or as individual units, in a myxoid or hyalinized stroma. It was initially described as a low-grade malignant tumour, but it has recently been proposed that it should be classified as a fully malignant neoplasm, in view of the associated morbidity and mortality . However, small primary cutaneous lesions appear to have an indolent behaviour. There is predilection for middle-aged adults. Sex Males are equally affected than females.