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Syphilis

Disease Name : Syphilis, Symptoms : ulcer : Typically, a solitary, small firm red painless papule on the genital area quickly becomes a painless ulcer with a well-defined margin and an indurated base., systemic symptoms : In secondary syphilis, there are systemic symptoms which includes fever, headache, malaise, myalgia, arthralgia, and lymphadenopathy., cutaneous symptoms : A non-itchy rash is present in 90% of patients with secondary syphilis The rash might be subtle or might appear as rough, red or reddish-brown papules or plaques The rash occurs typically on the trunk and frequently affects palms and soles Rarely, the rash presents as a cluster of erythematous papules around a central scaly plaque, resembling a flower; this floral morphology is described as ‘corymbose’ syphilis Patchy hair loss (alopecia) can occur Mucosal surfaces — such as inside the mouth, throat, genital area, vagina, and anus — can become raw and red (mucous patches) Greyish-white, moist plaques called condyloma lata occur in the groin, inner thighs, armpits, umbilicus, or under the breasts, Signs : Generalized lymphadenopathy : Generalized lymphadenopathy with firm, nontender nodes is a common physical finding in secondary syphilis., Macular syphilide (roseolar rash) : The classic rash of secondary syphilis are painless, macular, reddish or copper colored lesions on the palms or soles of the feet and is the most commonly recognized form of syphilis., Papulosquamous palmar rash : The rash is pink or dusky red and typically involves the palms and soles., Condylomata lata : Condylomata lata refers to a benign and painless cutaneous manifestation of secondary syphilis. They are skin-colored or hypopigmented growths characterized by gray to white lesions, typically located in the genital area or around the mouth., Condylomata lata : Sign of secondary syphilis is mucous patch on upper lip and “split papules” at angles of mouth., "chancre : The first sign of syphilis is a small sore, called a chancre (SHANG-kur). The sore appears at the spot where the bacteria entered your body. While most people infected with syphilis develop only one chancre, some people develop several of them. The chancre usually develops about three weeks after exposure. Many people who have syphilis dont notice the chancre because its usually painless, and it may be hidden within the vagina or rectum. The chancre will heal on its own within three to six weeks.", Gummata : Gummata are growths of pink, fleshy tissue that contain syphilis bacteria. They may appear as nodules or ulcers or become masses that are like tumors. Gummata are rare and may be up to 0.5 in., Treatment : Follow up : Serological test is to be performed 1, 3, ,6, and 12 months after treatment of early syphilis. In late ,symptomatic cases, surveillance is for life; the serological test ,is to be done annually. All women with simultaneous syphilis ,and HIV infection may have high rate of treatment failure, Early syphilis (primary, secondary, and early latent ,syphilis of less than 1 year duration),Benzathine penicillin G 2.4 million units is given ,intramuscularly in a single dose, half to each buttock.,In penicillin allergic cases, tetracycline 500 mg, ,4 times a day or doxycycline 100 mg BID PO for 14 days is ,effective.,Late syphilis : Benzathine penicillin G 2.4 million units is ,given IM weekly for 3 weeks (7.2 million units total).,Alternative regimen : Doxycycline 100 mg orally twice ,daily or tetracycline 500 mg orally 4 times a day for 4 weeks., Pathophysiology : Treponema is a very tiny organism that is invisible on light microscopy. Thus, it is identified by its distinct spiral movements on darkfield microscopy. Outside the body, it does not survive for long.The classic primary syphilis presentation is a solitary non-tender genital chancre in response to invasion by the T. pallidum. However, patients can have multiple non-genital chancres, such as digits, nipples, tonsils, and oral mucosa. These lesions can occur at any site of direct contact with the infected lesion and are accompanied by tender or non-tender lymphadenopathy. Even without treatment, these primary lesions will go away without scarring. If untreated, primary syphilis can progress to secondary syphilis, with many clinical and histopathological findings.The clinical manifestations of secondary syphilis result from hematogenous dissemination of the infection and are protean :  condyloma lata (papulosquamous eruption), hands and feet lesions, macular rash, diffuse lymphadenopathy, headache, myalgia, arthralgia, pharyngitis, hepatosplenomegaly, alopecia, and malaise. As a result, syphilis has been named the great imitator.Both primary and secondary lesions resolve without treatment, and the patient enters either an early or latent phase in which no clinical manifestations are present. The infection can only be detected at this stage with serological testing. Some patients in this stage will progress to the tertiary stage, characterized by cardiovascular syphilis, neurosyphilis, and late benign syphilis., Epidemiology : From 2008 to 2012, rates of congenital syphilis declined, but the incidence in adults increased by 38%. In 2016, 628 cases of congenital syphilis were reported, with rates 8.0-times and 3.9-times higher among infants born to Black and Hispanic mothers, respectively, compared to White-race mothers., variable, The only way to prevent syphilis (and other STIs) is to abstain from sex. If you’re sexually active, you can reduce your risk of infection by always using a condom or dental dam during sex. It’s important to use a condom properly to lower your chance of getting the infection.,,Ask your sexual partners about their history and if they’ve been tested for STIs. If your partner has syphilis, they can reinfect you. It’s important that they get treatment, too., Complications : Aortic Aneurysm, Meningitis, Dementia, Diagnostics : TREPONEMA PALLIDIUM HEMAGGLUTINATIONASSAY TPHA, VDRL, FTA-ABS TEST, enzyme immunoassays (EIAs), Differential diagnosis : nan, disease description : Syphilis is a systemic bacterial infection caused by the spirochete Treponema pallidum. Due to its many protean clinical manifestations,  it has been named the “great imitator and mimicker.” The origin of syphilis has been controversial and under great debate, and many theories have been postulated regarding this.The pre-Columbian theory looked at findings on skeletal markers of syphilis before 1490. However, there is insufficient proof, as evidenced by the DNA and paleopathology findings, to support the existence of syphilis before 1492.The Columbian and most accepted theory postulates that syphilis came from Europe in the 1490s when Columbus arrived in the New World (America). Syphilis spread when Christopher Columbus arrived in Naples (Italy). After Naples lost the battle to the French troops, this new disease spread across Europe.

Syphilitic Interstitial Keratitis

Disease Name : Syphilitic Interstitial Keratitis, Symptoms : eye pain : Syphilitic Interstitial Keratitis is a painful condition., Lacrimation : Syphilitic Interstitial Keratitis causes excessive tearing., Loss of vision : Interstitial keratitis is inflammation of the tissue of the cornea, the clear window on the front of the eye. This condition can lead to vision loss., photophobia : Syphilitic interstitial keratitis causes patients to become sensitive to light., Signs : blepharospasm : Blepharospasm is a rare neurological disorder affecting the muscles that control your eyelids. It starts with constant blinking that progresses to not being able to keep your eyes open., CORNEAL EDEMA : The deep stroma of the cornea is primarily involved in syphilitic keratitis and manifests clinically as a stromal haze or focal infiltrate. The inflammation appears most commonly in the superior cornea and can lead to corneal thickening., Salmon patch appearance in cornea : New blood vessels grow in from the limbus (neovascularization) and cause orange-red areas (salmon patches)., Treatment : medication : Dexamethasone , Atropine/ Atropine methonitrate, Penicillin, • Topical corticosteroid drops e.g., dexamethasone,0.1% drops every 2–3 hours. • Atropine eye ointment 1% 2–3 times a day. Systemic treatment includes : • Penicillin in high doses should be started to,prevent development of further syphilitic lesions. • Systemic steroids may be added in refractory cases,of keratitis., Keratoplasty is required in cases where dense,corneal opacities are left., Pathophysiology : It is now generally accepted that the disease is a manifestation of local antigen-antibody reaction. It is presumed that Treponema pallidum invades the cornea and sensitizes it during the period of its general diffusion throughout the body in the foetal stage. Later a small scale fresh invasion by Treponema or toxins excite the inflammation in the sensitized cornea. The inflammation is usually triggered by an injury or an operation on the eye. Interstitial keratitis characteristically forms one of the late manifestations of congenital syphilis. Many times it may be a part of Hutchinson’s triad, which includes interstitial keratitis, Hutchinson’s teeth and vestibular deafness. The clinical features of interstitial keratitis can be divided into three stages : initial progressive stage, florid stage and stage of regression. 1. Initial progressive stage. The disease begins with oedema of the endothelium and deeper stroma, secondary to anterior uveitis, as evidenced by the presence of keratic precipitates (KPs). There is associated pain, lacrimation, photophobia, blepharospasm and circumcorneal injection followed by a diffuse corneal haze giving it a ground glass appearance. This stage lasts for about 2 weeks. 2. Florid stage. In this stage, eye remains acutely inflamed. Deep vascularization of cornea, consisting of radial bundle of brush-like vessels develops. Since, these vessels are covered by hazy cornea, they look dull reddish pink which is called ‘Salmon patch appearance’. There is often a moderate degree of superficial vascularization. These vessels arising from the terminal arches of conjunctival vessels, run a short distance over the cornea. These vessels and conjunctiva heap at the limbus in the form of epulit. This stage lasts for about 2 months. 3. Stage of regression. The acute inflammation resolves with the progressive appearance of vascular invasion. Clearing of cornea is slow and begins from periphery and advances centrally. Resolution of the lesion leaves behind some opacities and ghost vessels. This stage may last for about 1 to 2 years., Epidemiology : The overall incidence of interstitial keratitis is rare, responsible for only 3% of all keratoplasties performed in the United States, variable, Prevention consists of avoiding the infection that causes interstitial keratitis. If you do get infected, get prompt and thorough treatment and follow-up., Complications : corneal vascularisation, Diagnostics : VDRL, Microscopic Examination of SCRAPINGS, ophthalmoscopy, Culture on blood agar, Differential diagnosis : EPISCLERITIS, KERATITIS, Sarcoidosis, SCLERITIS, TUBERCULOSIS, disease description : Syphilitic keratitis is a non-ulcerative interstitial keratitis that typically manifests as a late sequela of congenital or acquired syphilis. Syphilitic keratitis is seen more commonly in patients with congenital syphilis than in those who acquire syphilis later in life. In congenital syphilis, keratitis is typically bilateral in up to 80% of cases and presents as late congenital syphilis in children or adolescents most often between ages 5 and 15. Involvement of the second eye is typically seen within a few weeks following onset of disease in the first eye, but may also occur simultaneously. Syphilitic keratitis can be the only manifestation of late congenital syphilis, but oral pathology (misshapen teeth) is seen in 50% of cases as well.1 The deep stroma of the cornea is primarily involved in syphilitic keratitis and manifests clinically as a stromal haze or focal infiltrate. The inflammation appears most commonly in the superior cornea and can lead to corneal thickening. Neovascularization of the cornea often occurs after the onset of stromal haze and edema. Neovascularization occurs as extensions of both the limbal and anterior ciliary vessels often coinciding with increased lymphatic extension into the peripheral cornea.The combination of neovascularization and lymphatic extension leads to the classic salmon-colored patch seen in the disease. Treatment is important in the active stage of the disease to limit the neovascularization and lymphatic extension by inhibiting the inflammatory response. After appropriate treatment, recurrence occurs in 5-15% of patients

Syphilitic Otitis Media

Disease Name : Syphilitic Otitis Media, Symptoms : ear discharge, tinnitus, vertigo, SENSORINEURAL HEARING LOSS, Signs : nan, Treatment : Treatment consists of antisyphilitic therapy with attention ,to aural toilet and control of secondary infection., Surgery ,may be required for removal of sequestra., Pathophysiology : It is a rare condition. Spirochaetes reach middle ear through eustachian tube when syphilitic lesions are present in the nose or nasopharynx. Infection may also be blood-borne. Sensory end organs of the inner ear and their nerves are soon invaded by spirochaetes leading to profound sensorineural hearing loss, tinnitus and vertigo. Bone necrosis and sequestrum formation are common and they lead to foetid ear discharge. Secondary pyogenic infection may occur, giving a clinical picture very much like chronic suppurative otitis media. Definite diagnosis of syphilitic otitis media can only be made by specific treponemal antigen tests such as treponemal pallidum immobilization (TPI) test and fluorescent treponemal antibody absorption test (FTA-ABS). VDRL and RPR (reactive plasma reagin) tests are nonspecific but useful to monitor disease, however false positive tests may occur. Treatment consists of antisyphilitic therapy with attention to aural toilet and control of secondary infection. Surgery may be required for removal of sequestra., Epidemiology : GOOD, To Do : aural toilet and control of secondary infection.,Surgery may be required for removal of sequestra, Complications : bone necrosis, Diagnostics : RPR Rapid Plasma Reagin, TREPONEMA PALLIDIUM HEMAGGLUTINATIONASSAY TPHA, VDRL, Differential diagnosis : chronic suppurative otitis media, disease description : It is a rare condition. Spirochaetes reach middle ear through eustachian tube when syphilitic lesions are present in the nose or nasopharynx. Infection may also be blood-borne. Sensory end organs of the inner ear and their nerves are soon invaded by spirochaetes leading to profound sensorineural hearing loss, tinnitus and vertigo. Bone necrosis and sequestrum formation are common and they lead to foetid ear discharge. Secondary pyogenic infection may occur, giving a clinical picture very much like chronic suppurative otitis media....

Syringocystadenoma Papilliferum

Disease Name : Syringocystadenoma Papilliferum, Symptoms : NODULES : SCAP typically presents as slow developing, non-specific, smooth, skin-colored to pink papule, verruca or nodule, which may be exudative., Signs : nan, Treatment : Surgical excision., Pathophysiology : Embryonic Rest Theory : This theory suggests that syringocystadenoma papilliferum arises from remnants of embryonic structures. It is believed that cells with sweat gland differentiation potential may persist in the skin after embryonic development and later give rise to the tumor.Ductal Differentiation Theory : According to this theory, syringocystadenoma papilliferum originates from the eccrine sweat gland ducts or their precursors. The tumor cells may undergo abnormal differentiation and form papillary projections and cystic structures within the skin.Neoplastic Transformation : Some researchers propose that syringocystadenoma papilliferum results from neoplastic transformation of cells within the eccrine sweat gland ducts. Mutations or genetic alterations could trigger uncontrolled cell growth and the formation of the characteristic papillomatous structures.Hormonal Influence : Hormonal factors may also play a role in the development of syringocystadenoma papilliferum. The tumor has been reported to occur more frequently during puberty and pregnancy, suggesting a potential hormonal influence on its growth.Genetic Factors : While specific genetic mutations associated with syringocystadenoma papilliferum have not been clearly identified, genetic factors could contribute to the development of the tumor. Research into the genetic basis of this condition may provide further insights into its pathophysiology., Epidemiology : Syringocystadenoma papilliferum (SCAP) may be present at birth (50% of cases) or develop around puberty (15-30% of cases)., variable, NA, Complications : Metastasis, Diagnostics : Cytogenetics, BIOPSY FROM SKIN LESION, Immunostaining, Differential diagnosis : Hidradenoma papilliferum, Syringocystadenoma papilliferum, disease description : Syringocystadenoma papilliferum is a benign adnexal skin tumour of the apocrine or the eccrine type with characteristic histological features and varied and non-distinct clinical findings. It is relatively a rare neoplasm, which is called as a childhood tumour, since it usually appears at birth or during puberty.

Syringofibroadenoma

Disease Name : Syringofibroadenoma, Symptoms : papules, NODULES, plaques, Signs : Solitary nodule, Treatment : Benign condition,Single lesions are treated by surgical excision.,Therapy for cases with multiple lesions depends on size and location.,Laser therapy with dual pulse width flashlamp has been used successfully.,Etretinate topical therapy has been used successfully for diffuse lesions., Pathophysiology : Eccrine Duct Obstruction and Dilatation : One prevailing theory suggests that syringofibroadenoma arises due to the obstruction and dilatation of the eccrine sweat gland ducts. This obstruction could result from factors such as inflammation, trauma, or other unknown triggers. The accumulation of sweat and other substances within the ducts may lead to the formation of cystic structures and subsequent tumor growth.Proliferation of Basal Cells : Another theory proposes that the tumor develops from the proliferation of basal cells within the eccrine sweat gland ducts. Basal cells are responsible for regenerating and maintaining the sweat gland tissue. In syringofibroadenoma, an overgrowth of these basal cells could contribute to the formation of the tumor.Genetic and Molecular Factors : While specific genetic mutations associated with syringofibroadenoma have not been definitively identified, genetic and molecular factors likely play a role in its development. Abnormalities in cell signaling pathways, growth factors, and other molecular mechanisms may contribute to the uncontrolled growth of sweat gland cells.Immune and Inflammatory Factors : Inflammation and immune responses within the skin could also contribute to the development of syringofibroadenoma. Inflammatory processes may disrupt the normal function of eccrine sweat glands and contribute to the formation of the tumor.Trauma or Injury : Some cases of syringofibroadenoma have been associated with preceding trauma or injury to the skin. It is possible that such trauma could trigger abnormal cellular responses and lead to the development of the tumor., Epidemiology : Rare only 75 cases reported Wide age range (16-80), variable, NA, Complications : Syringofibroadenoma, squamous cell carcinoma., Diagnostics : ELECTRON MICROSCOPY, Immunostaining, Differential diagnosis : Basal cell carcinoma, Porocarcinoma, Poroma, disease description : Syringofibroadenoma is a benign adnexal tumour thought to be of eccrine origin, also named syringofibroadenoma of Mascaro, after the man who first described this tumour. It typically occurs on the extremities.Eccrine syringofibroadenoma (ESFA) is a rare neoplasm that usually presents as a solitary, often large, hyperkeratotic nodular lesion with predilection for the extremities. Histologically, there are thin anastomosing epithelial cords and strands forming a lattice and connected to the undersurface of the epidermis.

Syringoma

Disease Name : Syringoma, Symptoms : papules : A round bump (papule) that’s 1 to 3 millimeters in diameter. The papule is firm. The papule is yellow, translucent or the same color as your natural skin tone. The papule is part of a group or cluster of papules of a similar size, shape and color., Signs : nan, Treatment : Treatment necessary only for cosmetic reasons or quality of life.,Excision or cryotherapy / laser therapy is most common.,Does not respond to topical steroids.,Microinsulated needle radiofrequency for better cosmetic results., Carbon dioxide laser ablation may leave a scar and hyperpigmentation. Topical atropine to alleviate pruritus and reduce size of lesion., The main reason for treatment is cosmetic. Careful destruction ,with diathermy can produce good cosmetic results. Lesions treated ,with carbon dioxide laser may recur., Pathophysiology : The lesion has a characteristic architectural pattern on light microscope scanning power. Collections of convoluted and cystic ducts are seen in the upper half of the dermis. Most are lined by a double layer of cells similar to, but flatter than, those that line normal eccrine ducts. The lumina contain amorphous debris. A characteristic feature is the tail-like strand of cells projecting from one side of the duct into the stroma, giving a resemblance to a tadpole or comma. Occasional cases show cells with prominent clear-cell change. The ducts may be enclosed in a fibrous stroma similar to the hair follicle hamartomas, but in most cases it is narrower and less cellular., Epidemiology : approximately 1% of the population., benign, While it’s not easy to simply prevent all types of syringomas from forming on your skin, you can reduce your risk by : ,,Reducing stress on your body.,Protecting your skin from the sun by wearing sunscreen.,Using a cleanser or exfoliating product to clean your skin at the end of each day.,Talking to your provider about treatment options for your overworking sweat glands., Complications : dyspigmentation at wound, Diagnostics : HISTOPATHLOGY, Cytogenetics, Optical coherence tomography (OCT), ELECTRON MICROSCOPY, Dermoscopy, Differential diagnosis : Acne vulgaris, Basal cell carcinoma, Lichen Planus, disease description : A syringoma is a firm bump that resembles a pimple (papule) on your skin that usually forms in small clusters or groups on your skin, most often on your face. Syringomas are the result of your overgrowth of your sweat glands. These bumps are harmless to your body.Syringoma is a non-cancerous (benign) bump, usually found on the upper cheeks and lower eyelids of young adults. Syringomas are completely harmless and are caused by the overgrowth of cells from sweat glands (eccrine glands).

Syringomyelia

Disease Name : Syringomyelia, Symptoms : headache : Straining or coughing can increase the pressure within your head and brain, causing you to develop a headache., muscle spasm : Muscle spasms or tightness in your back, shoulders, neck, arms or legs., muscle weakness : Muscle weakness and wasting, especially of the hands, arms, and eventually the shoulders, may also develop., Numbness : Numbness or tingling in your arms and/or legs., Radiculopathy : Pain down your arms, neck, into the middle of your back or your legs., temperature instability : Loss of sensitivity to pain or temperature, especially in your hands., Signs : absence of superficial abdomonal reflexes : An abnormal or absent superficial abdominal reflex (SAR) may be associated with an underlying spinal cord syrinx., nystagmus : Ophthalmic features such as nystagmus or oscillopsia should alert one to the potential diagnosis of hindbrain-related syringomyelia., vocal cord paralysis : Syringomyelia causes bilateral vocal cord palsy., sensory disturbances : The most common sensory symptom is paresthesia/hyperesthesia followed by non-radicular segmental pain., vertigo : Syringobulbia is a slowly progressive disorder that may cause dizziness., Treatment : A neurosurgical and orthopaedic evaluation is warranted for all ,patients with a syrinx. Surgical indications have been stated as : nan,progression of motor/sensory loss, scoliosis, associated pain and ,size of the syrinx, Pathophysiology : The exact pathogenesis of syringomyelia is uncertain. The condition has several distinct cavitary patterns, which probably determine the pathogenesis and the clinical features of the condition . The majority of lesions occur in association with type 1 Chiari syndrome. It is proposed that syrinx development, particularly in CM-1 patients, follows a differential between intracranial pressure and spinal pressure caused by a valve-like action at the foramen magnum. Other causes include trauma and tumours., Epidemiology : 8.4 cases per 100 000 population, variable, While syringomyelia generally can’t be prevented, early diagnosis and treatment may help prevent the worsening of symptoms., Complications : Guillain-Barre Syndrome, scoliosis, Diagnostics : HISTOPATHLOGY, MRI Brain, CT SCAN, PHYSICAL EXAMINATION, Differential diagnosis : diabetic neuropathy, Down syndrome, Glioma, Horner’s syndrome, , Hydrocephalus, nystagmus, vertigo, disease description : Syringomyelia describes conditions involving abnormal fluid cavities within the spinal cord. A ‘syrinx’ is a fluid-filled cavity within the spinal cord parenchyma.

Systemic Anaplastic Large Cell Lymphoma

Disease Name : Systemic Anaplastic Large Cell Lymphoma, Symptoms : "fatigue : Fatigue is a feeling of extreme tiredness and weakness that isnt improved after rest or sleep.", lymphadenopathy : The fever caused by systemic anaplastic large cell lymphoma is unexplained., night sweats : This occurs because the lymphoma cells produce certain chemicals that can increase a person’s body temperature. As a result, it’s common for individuals with lymphoma to experience severe night sweats that leave their pajamas, sheets and blankets soaking wet. Night sweats may also occur as a response to certain chemicals produced by the lymphoma cells in the body., weight loss : Unexplained weight loss., Signs : lymphadenopathy : Both ALK-positive and ALK-negative ALCL often cause swollen lymph nodes at the site where the cancer’s growing. The most common areas are your neck, underarm and groin., Treatment : nan, Pathophysiology : Genetic Alterations and ALK Protein Expression : The hallmark of sALCL is the presence of the ALK gene rearrangement, leading to the expression of the abnormal ALK protein. This fusion protein, often referred to as NPM-ALK due to the fusion partner, plays a critical role in the development and progression of sALCL. The abnormal ALK protein functions as a constitutively active tyrosine kinase, leading to uncontrolled signaling pathways that promote cell survival, proliferation, and resistance to apoptosis (programmed cell death).Tumor Formation and Growth : The ALK protein, along with other genetic alterations and molecular changes, contributes to the transformation of normal lymphocytes into malignant anaplastic cells. These cells grow and accumulate, forming tumors primarily in lymph nodes but also potentially in other tissues and organs.Cell Signaling Pathways : The aberrant ALK protein activates several signaling pathways, including the JAK/STAT, PI3K/Akt, and Ras/MAPK pathways, which are involved in cell growth, survival, and proliferation. Dysregulation of these pathways contributes to the aggressive behavior of sALCL cells.Microenvironment and Immune System Interaction : The tumor microenvironment, composed of various cell types and extracellular components, plays a crucial role in sALCL pathophysiology. The interaction between sALCL cells and immune cells within the microenvironment can influence disease progression. sALCL cells may evade immune surveillance and immune-mediated cell death mechanisms., Epidemiology : 3% of adult non-Hodgkin lymphomas and 10% to 20% of childhood lymphomas., 2-8% of adult non-Hodgkin lymphoma cases and as many as 30% of childhood non-Hodgkin lymphoma cases., variable, Complications : nan, Diagnostics : Complete Blood Count CBC, biopsy, Differential diagnosis : Carcinomas, Hodgkin lymphoma, inflammatory myofibroblastic tumor, rhabdomyosarcoma, sarcoma, disease description : Anaplastic large cell lymphoma (ALCL) is a rare form of non-Hodgkin lymphoma. Like all non-Hodgkin lymphoma, ALCL is a type of cancer. With non-Hodgkin lymphoma, white blood cells called lymphocytes grow out of control. Lymphocytes are part of your immune system. They help protect your body from germs and diseases.Lymphocytes include two main types of cells : B-cells (B lymphocytes) and T-cells (T lymphocytes). In ALCL, your T lymphocytes grow abnormally. The conditions name — anaplastic large cell lymphoma — describes how the abnormal T lymphocytes look when viewed under a microscope.Anaplastic : “Anaplastic” is a word used to describe odd-looking cancer cells. The cancer cells in ALCL look abnormal when compared to healthy T lymphocytes.Large cell : The abnormal T lymphocytes appear larger than normal T lymphocytes when viewed under a microscope.Lymphoma : Lymphoma is cancer that involves the out-of-control growth of white blood cells called lymphocytes. ALCL forms from T lymphocytes.

Systemic Primary Carnitine Deficiency

Disease Name : Systemic Primary Carnitine Deficiency, Symptoms : Cardiomyopathy : Cardiomyopathyis a disease of the heart muscle that makes it harder for the heart to pump blood to the rest of the body., Confusion : Primary carnitine deficiency leads to confusions among the patients., muscle weakness : Primary carnitine deficiency causes muscle weakness in the patients., Signs : encephalopathy : Signs of primary carnitine deficiency typically appear during infancy or early childhood and can include severe brain dysfunction (encephalopathy), Treatment : medication : L-Carnitine , Glucose/Dextrose, Carrier testing for at-risk family members and prenatal diagnosis for pregnancies at increased risk are possible if the SLC22A5 pathogenic variants in the family are known., SURVEILLANCE - Echocardiogram and electrocardiogram : annually during childhood and less frequently in adulthood; monitor plasma carnitine concentration frequently until levels reach the normal range, then, measure three times a year during infancy and early childhood, twice a year in older children, and annually in adults; evaluate serum creatine kinase concentration and liver transaminases during acute illnesses, Pathophysiology : Mutations in the SLC22A5 gene cause primary carnitine deficiency. This gene provides instructions for making a protein called OCTN2 that transports carnitine into cells. Cells need carnitine to bring certain types of fats (fatty acids) into mitochondria, which are the energy-producing centers within cells. Fatty acids are a major source of energy for the heart and muscles. During periods of fasting, fatty acids are also an important energy source for the liver and other tissues. Mutations in the SLC22A5 gene result in an absent or dysfunctional OCTN2 protein. As a result, there is a shortage (deficiency) of carnitine within cells. Without carnitine, fatty acids cannot enter mitochondria and be used to make energy. Reduced energy production can lead to some of the features of primary carnitine deficiency, such as muscle weakness and hypoglycemia. Fatty acids may also build up in cells and damage the liver, heart, and muscles. This abnormal buildup causes the other signs and symptoms of the disorder., Epidemiology : Exact prevalence is unknown and varies depending on ethnicity., The incidence of primary carnitine deficiency in the general population is approximately 1 in 100, 000 newborns, variable, Primary carnitine deficiency is inherited in an autosomal recessive pattern. It occurs because of a genetic mutation in the SLC22A5 gene. You can’t prevent it from happening.,,Talk with your healthcare provider about genetic testing if you plan on becoming pregnant to see if you’re at risk of having a child with a genetic condition., Complications : Cardiomyopathy, encephalopathy, Hypoglycaemia, Diagnostics : SERUM CK LEVEL, GENETIC TESTING, SERUM LACTATE, plasma creatinine, ammonia level, Differential diagnosis : HEMODIALYSIS, Malnutrition, Metabolic disorders, Renal tubular dysfunction, REYE SYNDROME, disease description : Primary carnitine deficiency is a condition that prevents the body from using certain fats for energy, particularly during periods without food (fasting). Carnitine, a natural substance acquired mostly through the diet, is used by cells to process fats and produce energy.

Taenia Solium And Saginata Infestation

Disease Name : Taenia Solium And Saginata Infestation, Symptoms : ENCEPHALITIS : Symptoms of cysticercal encephalitis includes nausea, vomiting & confusion., Gastrointestinal symptoms : With T saginata infection, usually, the patient becomes aware of infection when worm segments are passed in the stool. Some patients complain of epigastric pain, diarrhea, and weight loss. Similar to T solium infection, the presence of cysticerci in T saginata infection can result in symptoms of obstruction of the appendix, biliary duct, and pancreatic duct., headache : It occurs due to the presence of larvae in the brain., systemic symptoms : T solium infections are usually asymptomatic; however, infected patients may have generalized complaints include epigastric or periumbilical discomfort; nausea; hunger; and weight loss, anorexia, or increased appetite., cutaneous symptoms : Includes lumps under the skin., Ocular symptoms : Symptoms of cysticercosis of the eye includes eye pain, diplopia, uveitis, limited eye movement, proptosis & vision loss., Ocular symptoms : Symptoms of cysticercosis of the eye includes eye pain., Signs : seizures : When they enter the central nervous system, they can cause neurological symptoms (neurocysticercosis), including epileptic seizures., Treatment : medication : Albendazole , Niclosamide , Praziquantel , Prednisolone, Treatment of taeniasis is similar for both infestations.,Niclosamide or praziquantel are effective drugs. FOR CYSTICERCOSIS : Albendazole- 7.5 mg/kg (max 400 mg) q 12 hr for 8-30 day; Praziquantel-33.3 mg/kg q 8 hr on day 1; then 16.7 mg/kg; Anticonvulsants; q 8 hr for 29 days, Pathophysiology : Infection with the intermediate stage (larvae) of T. solium results in cysticercosis. Neurocysticercosis is the most common parasitic infection of the CNS and may account for as high as 20-50% cases of seizures. Following ingestion, eggs develop into larvae in the small intestine. Larvae migrate across the intestinal wall and are carried to the target organs by bloodstream. The common target organs for cysticerci are brain, muscle and subcutaneous tissue. The larvae mature into cysticerci in about two months time. The size of cysticerci varies from 2 mm to 2 cm. Clinical manifestations depend on the location, number and size of cysts in the brain and host inflammatory response. Viable cysts generally do not elicit a strong response. On the other hand, degenerating cysts provoke a vigorous host response. Most cysts remain viable for 5-10 yr. Neurocysticercosis may manifest as partial or generalized seizure, raised intracranial tension, focal neurological deficits, or disturbances unconsciousness or behavior., Epidemiology : 10·4%, 7.7 cases/100, 000 people, GOOD, To prevent, control and possibly eliminate T. solium, public health interventions including veterinary, human health and environmental sectors are required. ,There are several interventions for the control of T. solium that can be used in different combinations. In a meeting of experts in 2009, they were identified as : ,,Core “rapid impact” interventions : ,,treatment of human taeniasis;,intervention in pigs (vaccination plus anthelmintic treatment);,,Supporting measures : ,,community health education, including hygiene and food safety;,improved sanitation - ending open defecation;,,Measures requiring more fundamental societal changes : ,,improved pig husbandry - no free-roaming pigs; and,improved meat inspection and processing of meat products.,,Mathematical models have been used to determine the probability of success of the different strategies’ combinations and the implementation period required to achieved sustained control, but they are still based in many assumptions and unknowns. However, they usually coincide in that integrated One-Health interventions, are the ones more likely to achieve a faster sustainable control., Complications : FOCAL NEUROLOGICAL SIGNS, raised intracranial tension, seizures, neurocysticercosis, Diagnostics : Complete Blood Count CBC, serum IgE level, PCR, CT SCAN, ANTIGEN DETECTION, Differential diagnosis : Amebic Meningoencephalitis, ASEPTIC MENINGITIS, BACTERIAL MENINGITIS, Gnathostomiasis, INFLAMMATORY BOWEL DISEASES, disease description : These worms are also known as the pork tapeworm (T. solium) and beef tapeworm (T. saginata), reflecting the principal intermediate hosts for each of them. Man is the only definitive host for both the parasites. Pork tapeworm consists of a scolex with suckers and hooks by means of which it attaches to the intestinal wall. Hooks are absent in T. saginata. Usually, only one adult worm is found in the intestine which may live for up to 25 yr.

Takayasu Arteritis

Disease Name : Takayasu Arteritis, Symptoms : chest pain : Reduced blood flow to arms, legs and major organs may cause symptoms of chest pain., Dizziness : When the aorta and the major arteries in the neck (carotid arteries) are affected by Takayasu arteritis, the patient usually experiences lightheadedness, dizziness, and brief moments of unconsciousness (syncope). These symptoms are the result of a decrease in blood supply to the brain (cerebral ischemia)., "Flu-like illness : Early-stage or first-stage symptoms of Takayasus arteritis include : Fever. Fatigue. Pain in your muscles or joints.", headache : Headaches occur due to possibly due to reduced cerebral blood flow., myalgia : The arms ache and tire easily when repetitive arm movements are done or the arms are elevated for a long period of time., Abdominal Pain : Intestinal involvement usually presents with abdominal pain., Signs : asymmetric blood pressures : Arterial pulses in arms and legs may be diminished and asymmetric., diminished pulses : Absent or diminished pulses are the clinical hallmark of Takayasu arteritis., hypertension : Renovascular hypertension is the major renal problem., Treatment : medication : Prednisolone, Steroids have formed the mainstay of treatment for Takayasu arteritis and reports of efficacy vary. This may relate to the stage of disease at which treatment is introduced in addition to disease extent., Immunosuppressive agents including cyclophosphamide, azathioprine, and methotrexate have all been tried., "Surgical options are best performed when inflammation of the arteries has been reduced. They include : ,,Bypass surgery. In this procedure, an artery or a vein is removed from a different part of your body and attached to the blocked artery, providing a bypass for blood to flow through. Bypass surgery is usually performed when the narrowing of the arteries is irreversible or when there is significant obstruction to blood flow.,Blood vessel widening (percutaneous angioplasty). This procedure may be indicated if the arteries are severely blocked. During percutaneous angioplasty, a tiny balloon is threaded through a blood vessel and into the affected artery. Once in place, the balloon is expanded to widen the blocked area, then its deflated and removed.,Aortic valve surgery. Surgical repair or replacement of the aortic valve may be needed if the valve is leaking significantly.", Pathophysiology : Immune-Mediated Inflammation : Takayasu arteritis is characterized by chronic inflammation of the arterial walls, leading to vessel thickening, narrowing, and potentially occlusion. It is believed that an immune-mediated process triggers an abnormal immune response against components of the arterial wall, especially the endothelial cells that line the inner surface of blood vessels.Genetic Predisposition : There is evidence to suggest a genetic predisposition to Takayasu arteritis. Certain genetic markers and variations have been associated with an increased risk of developing the disease. However, no single gene or genetic mutation has been definitively linked to its development.Autoimmunity and Immune Dysregulation : The immune system appears to play a central role in the development of Takayasu arteritis. In individuals predisposed to the disease, an autoimmune reaction may be triggered by unknown factors. Immune cells, such as T cells and macrophages, infiltrate the arterial wall, release inflammatory cytokines, and contribute to tissue damage.Endothelial Dysfunction : Endothelial dysfunction, characterized by impaired function of the endothelial cells that line blood vessels, is thought to be a key early event in Takayasu arteritis. Dysfunction of the endothelium can lead to abnormal immune responses, increased adhesion of immune cells, and the release of molecules that promote inflammation and vessel damage.Granulomatous Inflammation : Histopathological examination of affected arteries often reveals granulomatous inflammation. Granulomas are clusters of immune cells that form in response to chronic inflammation. These structures can further contribute to vessel thickening and narrowing.Vascular Remodeling and Fibrosis : Over time, the chronic inflammation and immune response lead to changes in the structure of affected blood vessels. There may be remodeling of the vessel wall, including fibrosis (excessive formation of connective tissue) and scarring. These changes contribute to the narrowing of arteries and can lead to reduced blood flow to various organs and tissues., Epidemiology : 2.6-6.4 persons per million population., 2.6 persons per million annually., variable, Eat a healthy diet.,Exercise regularly.,Avoid all tobacco products, Complications : ANEURYSM, heart failure, Stroke, Diagnostics : HISTOPATHLOGY, PET SCAN, biopsy, MR ANGIOGRAPHY, DOPPLER USG, ANGIOGRAPHY, Differential diagnosis : Atherosclerosis, "Behcets syndrome/disease", COARCTATION OF AORTA, Giant cell arteritis, Kawasaki Disease, Rheumatoid arthritis, Sarcoidosis, disease description : Takayasu arteritis (pulseless disease) is a systemic inflammatory condition characterized by damage to the large and medium arteries and their branches. It presents at first with nonspecific constitutional symptoms such as fever, malaise, weight loss, and anorexia. 

Tanapox

Disease Name : Tanapox, Symptoms : fever : Tanapox infection begins with a short febrile (38° to 39° C) illness that persists for 2 to 4 days and is sometimes accompanied by headache, backache, or prostration., LESIONS : In humans, tanapox typically manifests with 1 or 2 characteristic, nodular skin lesions that are large, raised, umbilicated, and painful and generally ulcerate without becoming pustular. The eruption of a lesion is frequently heralded by pruritus at the site of the outbreak., Signs : nan, Treatment : The disease is self-limiting., Pathophysiology : The epidermis shows degeneration and the keratinocytes have vacuolated cytoplasm with eosinophilic inclusions. Papillary dermal oedema and a mild inflammatory infiltrate are seen. Presentation A mild fever with myalgia and headache at presentation is followed within 2 days by the appearance of a skin papule, most commonly on the limbs. The general symptoms quickly abate, but the lesion grows to reach a maximum size of 1–2 cm within 2 weeks. It is usually tender, occasionally itchy and may ulcerate. There may be regional lymphadenopathy. The nodule clears within 6 weeks leaving a small scar., Epidemiology : 16.3%, SELF LIMITING, Tanapox is most likely transmitted through arthropod vectors or through direct contact with a lesion; lesions should therefore be bandaged to prevent possible spread of the disease., Complications : secondary infection, Diagnostics : PCR, ELECTRON MICROSCOPY, Differential diagnosis : Molluscum Contagiosum, MONKEYPOX, Rickettsialpox dermatology, VACCINIA, Varicella, disease description : This is an acute febrile illness associated with a localized nodular skin lesion. Incidence and prevalence sporadic cases and occasional outbreaks occur in central Africa, especially in the Congo Basin The tanapox virus is known to infect both monkeys and humans, but no other natural reservoir has been identified.

Teitz Syndrome

Disease Name : Teitz Syndrome, Symptoms : Pain in the chest : Tietze syndrome happens when the cartilage in the joint where your ribs connect to your breastbone — your costochondral joint — is irritated. This irritation leads to inflammation around the joint and causes chest pain., swelling : Tietze syndrome happens when the cartilage in the joint where your ribs connect to your breastbone — your costochondral joint — is irritated. This irritation leads to inflammation around the joint and causes swelling., localized pain : Tietze syndrome is characterized by mild to severe localized pain and tenderness in one or more of the upper four ribs. The second or third ribs are most often affected. In most people, the cartilage of only one rib is affected. A firm, spindle-shaped swelling occurs in the cartilage of the affected rib. An aching, gripping, sharp, dull, or neuralgic pain occurs in this area. Sometimes, the pain may spread to affect the neck, arms and shoulders. Redness (erythema) and warmth of the affected area may be present. The onset of pain may be gradual or sudden, and can vary in intensity. The pain associated with Tietze syndrome may worsen due to sneezing, coughing, or strenuous activity or exercise. The pain usually subsides after several weeks or months, but the swelling may persist., Signs : nan, Treatment : The keystone of Tietze syndrome treatment is conservative therapy and reassurance that this disease process will often resolve on its own with no permanent sequelae, many times within a few weeks. There is, however, the potential for it to last months, or even up to a year. First-line medical management is oral or topical anti-inflammatory and analgesic agents.,,If those do not provide significant relief, patients may benefit from a focused injection of local anesthetic, steroid, or both at the site of maximum swelling, which should be visualized via sonogram. Some patients have reported benefits with warming pads applied to the affected area. There are reports in which cartilage has been resected as a treatment option in persistent, severe cases. However, this is not generally recommended and should only be considered on a case by case basis., Pathophysiology : Tietze syndrome is described as a localized, painful, swollen, non-pustular mass commonly without rubor or erythema. It is most often associated with the cartilage of ribs two or three and contained to one side in approximately 70% of patients, though it has been identified at the sternoclavicular and xiphisternal joints.There have been discussions regarding the possibility that this disease process is inflammatory and may be part of a more comprehensive seronegative pathology. The symptoms are often self-limiting, but Tietze syndrome recurrences are possible. , Epidemiology : Tietze syndrome can affect anyone, but it’s more common in people under 40., Because experts aren’t sure what causes Tietze syndrome, it’s hard to say for sure how you can prevent it.,,In general, avoid putting too much stress on your chest and ribs. Make sure to rest after intense physical activity to give your body time to recover., Complications : Restricted mobility, Diagnostics : ECG, ultrasound, MRI, CT SCAN, PHYSICAL EXAMINATION, Differential diagnosis : Acute coronary syndromes, Fibromyalgia, Gastroesophageal reflux disease (GERD), hypertensive crisis, inflammatory disease, Rheumatoid arthritis, signs of inflammation, disease description : Tietze syndrome happens when the cartilage in the joint where your ribs connect to your breastbone — your costochondral joint — is irritated. This irritation leads to inflammation around the joint and causes chest pain and swelling.

Telangiectases

Disease Name : Telangiectases, Symptoms : nose bleeding, Signs : erythema, spider telangiectasias, port-wine birthmark involving the forehead and upper eyelid, Treatment : Sclerotherapy, the treatment most often used for telangiectasias, is low cost but is not free from complications. Laser therapy is a safe and efficacious treatment of telangiectasias and can be achieved with multiple lasers, Pathophysiology : The telangiectases are a heterogeneous group of disorders. They can be broadly divided into primary and secondary according to their aetiology though one of the commonest naevi (spider naevi) can be both, Epidemiology : nan, Complications : double vision in eyes, Hemorrhagic Stroke (HS), seizures, Stroke, Diagnostics : HISTORY TAKING, Differential diagnosis : angioma serpiginosum, arterio venous malformation, infantile haemangioma, disease description : Telangiectases (Latin : tel = end + Greek : angos = vessel + ectasis from Greek : ektasis = expansion) are chronically dilated capillaries or venules. Telangiectases appear on the skin and mucous membranes as small, dull red, linear, stellate or punctate markings. They represent dilatations (expansion, stretching) of pre-existing vessels without any apparently new vessel growth (angiogenesis) occurring.

Tendon Xanthoma

Disease Name : Tendon Xanthoma, Symptoms : papules : Tendon xanthomas are cholesterol deposits in tendons. They appear as slowly enlarging papules or subcutaneous nodules attached to tendons, ligaments, fascia and periosteum and commonly affect the tendons of the dorsal surface of the hands and the achilles tendon., Signs : nan, Treatment : Tendon xanthomas sometimes improve with cholesterol reduction, but do not tend to resolve completely, Pathophysiology : All xanthomas contain macrophages loaded with cholesterol and cholesterol esters (‘foam cells’). Tendon xanthomas are most frequently seen in familial hypercholesterolaemia (FH) (see section later in this chapter), but are also a feature of the secondary hypercholesterolaemia seen in prolonged cholestasis. They also occur in the rare lipid disorders cerebrotendinous xanthomatosis and sitosterolaemia in which the tendon xanthomas are not associated with raised serum cholesterol levels., Epidemiology : one in 250–500 and one in 1 million respectively, variable, Maintain normal lipid profile, Complications : post-surgical complications, Diagnostics : LIPID PROFILE, MRI, Differential diagnosis : amyloidosis, Cerebrotendinous Xanthomatosis, Lipoid proteinosis, Necrobiosis lipoidica, Necrobiotic xanthogranuloma, disease description : Tendon xanthomas are cholesterol deposits in tendons. They appear as slowly enlarging papules or subcutaneous nodules attached to tendons, ligaments, fascia and periosteum and commonly affect the tendons of the dorsal surface of the hands and the achilles tendon.

Tennis Elbow

Disease Name : Tennis Elbow, Symptoms : pain in elbow : Pain when twisting or bending your arm (for instance, to turn a doorknob or open a jar)., stiffness in elbow : Stiffness when extending your arm., swelling : Swollen elbow joint that’s tender to touch., Burning : Burning or pain on your outer elbow that may travel to your wrist (these sensations may get worse at night)., Signs : nan, Treatment : A physical therapist can teach you exercises to gradually stretch and strengthen your muscles, especially the muscles of your forearm. Eccentric exercises, which involve lowering your wrist very slowly after raising it, are particularly helpful. A forearm strap or brace may reduce stress on the injured tissue., "Surgical or other procedures,Injections. Your doctor might suggest injecting platelet-rich plasma, Botox or some form of irritant (prolotherapy) into the painful tendon. Dry needling — in which a needle pierces the damaged tendon in many places — can also be helpful.,Ultrasonic tenotomy (TENEX procedure). In this procedure, under ultrasound guidance, a doctor inserts a special needle through your skin and into the damaged portion of the tendon. Ultrasonic energy vibrates the needle so swiftly that the damaged tissue liquefies and can be suctioned out.,Surgery. If your symptoms havent improved after six to 12 months of extensive non-operative treatment, you may be a candidate for surgery to remove damaged tissue. These types of procedures can be performed through a large incision or through several small incisions. Rehabilitation exercises are crucial to recovery.", Pathophysiology : Tennis elbow is an overuse and muscle strain injury. The cause is repeated contraction of the forearm muscles that you use to straighten and raise your hand and wrist. The repeated motions and stress to the tissue may result in a series of tiny tears in the tendons that attach the forearm muscles to the bony prominence at the outside of your elbow., Epidemiology : 1–3% of the adult population each year, 4–7 per 1000 individuals., good, "These steps can help you avoid tennis elbow : ,,Dont push through pain. Pain is your body’s way of talking to you, and you need to listen. Pushing through pain can lead to damage to your tendon and potential tearing.,Check equipment for proper fit. For example, stiff or loose-strung racquets may reduce stress on your forearm.,Lift weights to strengthen forearms and wrist muscles.,Stretch wrists and arms before starting work or an activity.,Wear an elbow brace to keep symptoms from worsening.", Complications : infection, tendon damage, NERVE INJURY, Diagnostics : EMG/NCS, MRI, HISTORY TAKING, PHYSICAL EXAMINATION, Differential diagnosis : BURSITIS, fracture, "GOLFERS ELBOW", Osteoarthritis, Radiculopathy, tendinitis, disease description : Tennis elbow (lateral epicondylitis) is a painful condition that occurs when tendons in your elbow are overloaded, usually by repetitive motions of the wrist and arm.The pain of tennis elbow occurs primarily where the tendons of your forearm muscles attach to a bony bump on the outside of your elbow. Pain can also spread into your forearm and wrist.Rest and over-the-counter pain relievers often help relieve tennis elbow. If conservative treatments dont help or if symptoms are disabling, your doctor might suggest surgery.

Tenosynovitis

Disease Name : Tenosynovitis, Symptoms : joint pain, joint stiffness, Joint swelling, inability to move his limb, Signs : swelling in elbow, pain in elbow, Treatment : rest, analgesics and ultrasonic,therapy., in addition to antibiotics, may require surgical debridement and washout and sometimes necessitate amputation. Treatment of non-infectious tenosynovitis revolves around the underlying etiology but may result in long-term pain and disability if untreated., Pathophysiology : Irritative tenosynovitis is commonly seen in the tendons of the hand and results in pain and swelling. Treatment is by rest, analgesics and ultrasonic therapy. Some cases need local hydrocortisone infiltration. Infective tenosynovitis is an infection of the synovial lining of the tendon by pyogenic or tubercular bacteria. Pyogenic infection is common Irritative tenosynovitis is commonly seen in the tendons of the hand and results in pain and swelling. Treatment is by rest, analgesics and ultrasonic therapy. Some cases need local hydrocortisone infiltration. Infective tenosynovitis is an infection of the synovial lining of the tendon by pyogenic or tubercular bacteria. Pyogenic infection is commonIrritative tenosynovitis is commonly seen in the tendons of the hand and results in pain and swelling. Treatment is by rest, analgesics and ultrasonic therapy. Some cases need local hydrocortisone infiltration. Infective tenosynovitis is an infection of the synovial lining of the tendon by pyogenic or tubercular bacteria. Pyogenic infection is commonin the flexor tendons of the hand. Tubercular tenosynovitis of the sheaths of the flexor tendons of the forearm at the level of the wrist occurs commonly (compound palmar ganglion., Epidemiology : nan, the incidence is between 1.7 to 2.6%, GOOD, To Do : REST, Complications : infection, stiffness, Diagnostics : ultrasound, plain radiograph, Differential diagnosis : CELLULITIS, Gout, Osteoarthritis, pseudogout, PSORIATIC ARTHRITIS, Rheumatoid arthritis, disease description : Tenosynovitis is a broad term describing the inflammation of the fluid-filled synovium within the tendon sheath. It commonly manifests as pain, swelling, and contractures, depending on the etiology. The condition can affect any tendon in the body surrounded by a sheath but has a predilection for the hand, wrist, and foot. A basic understanding of the tendon anatomy allows the clinician to appreciate the pathophysiology, treatment, and complications. The tendon anatomy and relationship to the tendon sheath are well illustrated in the hand. The tendons intricate arrangement in the hand permits the gripping, grasping, and precise motor function of the hand. Shortly after exiting the carpal tunnel at the wrist, the tendons of flexor digitorium superficialis and profundus muscles cross the palm and enter tunnels formed by the fibrous sheaths on the palmar aspect of each digit. Within each tunnel, the tendons are surrounded by a synovial sheath or bursa. Together, the fibrous tunnel and synovial covering form the tendon sheath.

Tension-type Headaches

Disease Name : Tension-type Headaches, Symptoms : headache : Dull, aching head pain., photophobia : Patients describe low intensity light as “glaring” or “painful” during an attack, making photophobia one of the cardinal diagnostic criteria., Tenderness : Tenderness in the scalp, neck and shoulder muscles., Blurring of vision : The pressure causes headaches that are usually felt at the back of the head and are worse at night or upon waking. It can also cause vision problems, such as blurred or double vision., Signs : nan, Treatment : medication : Amitriptyline , flupirtine maleate, Talk to a counselor or therapist. Talk therapy may help you cope with the effects of chronic pain.,Join a support group. Support groups can be good sources of information. Group members often know about the latest treatments. Your doctor may be able to recommend a group in your area., Acute medications,Pain relievers, Triptans and narcotics,Preventive medications,Tricyclic antidepressants, Anticonvulsants and muscle relaxants, Pathophysiology : Unlike some forms of migraine, tension-type headaches usually arent associated with visual disturbances, nausea or vomiting. Although physical activity typically aggravates migraine pain, it doesnt make tension-type headache pain worse. An increased sensitivity to either light or sound can occur with a tension-type headache, but this symptom isnt common.The cause of tension-type headaches is not known. Experts used to think tension-type headaches stemmed from muscle contractions in the face, neck and scalp, perhaps as a result of heightened emotions, tension or stress. But research suggests that muscle contraction isnt the cause., Epidemiology : 35.1 %, variable, Researchers have yet to uncover how to prevent all headaches. If you experience chronic tension-type headaches or frequent tension-type headaches certain medications may stop some headaches before they start. These are antidepressants such as amitriptyline or venlafaxine or duloxetine. These work on the pain centers in the brain.,,Overall, lifestyle changes and reducing your response to stress is the best way to prevent tension headaches. The most effective stress management tool is the one that fits into your life and you feel good using. You may want to try : ,,Massage therapy.,Exercising regularly.,Staying hydrated.,Getting regular, restful sleep., Complications : visual disturbances, brain damage, anxiety, DEPRESSION, Diagnostics : MRI, CT SCAN, PHYSICAL EXAMINATION, Differential diagnosis : cluster headache, Meningioma, migraine, disease description : A tension-type headache (TTH) is generally a mild to moderate pain thats often described as feeling like a tight band around the head. A tension-type headache is the most common type of headache, yet its causes arent well understood.Tension-type headaches are a common headache often causing mild-to-moderate pain, which some describe as feeling like a tight band around their head. Tension headaches can be treated with over-the-counter pain relievers or antidepressants if a prescription is needed. Other treatments include lifestyle changes and learning to ways to respond to stresses

Teratoma

Disease Name : Teratoma, Symptoms : palpable abdominal mass : Gastric teratoma presents as a palpable mass in 75%., vaginal bleeding : Uterine teratomas usually present with abnormal per vaginal (p.v.) bleeding., Abdominal Pain : In about 6–65% of cases, mature cystic teratomas do not cause symptoms. If symptoms occur, they may include : pain, which occurs in 44–47% of cases. noticeable abdominal growth or tumor., Signs : nan, Treatment : First, your healthcare provider will determine if the teratoma is cancerous or noncancerous. Nearly all teratomas should be removed when discovered. Even if they aren’t cancerous, they can still grow rapidly or rupture, leading to other problems. If your teratoma is cancerous, your healthcare provider may recommend chemotherapy, radiation therapy or a combination of the two in addition to surgical removal., In premenopausal women, symptomatic dermoid lesions less than 5 cm are preferably removed by simple laparoscopic cystectomy, rather than removing the entire ovary. Cysts larger than 5 to 6 cm and have involved the entire ovary with distortion of its structure should be removed by oophorectomy. Oophorectomy should be considered in postmenopausal women with multiple cysts. Histological examination of the surgical specimen confirms the diagnosis, including staging in case of carcinoma. In such cases, complete resection with bilateral salpingo-oophorectomy, hysterectomy, and even platinum-based chemotherapy is the mainstay of treatment. Laparoscopy is the gold standard technique for surgical management., Pathophysiology : Since the discovery of grotesque teratoma lesions which resembled deformed fetus, several theories emerged based on concepts from religious to scientific assumptions. Some of the interesting ideas involved the likely cause of witchcraft, perverted gestation, immoral acts, and ingestion of hair and bones embedded in the ovaries. It was later believed that these tumors originated from degenerated ova, in situ impregnation of ovum within the ovary (fetus in the fetus). Evidence of dermoid cyst in virgins, post-menopausal women, males, and extra ovarian sites (stomach, mediastinum) convinced the biologists that structures like bone, teeth could develop within a tumor instead of its origin as a result of aberrant fertilization.Analysis of biochemical and cytogenetic data showed that cystic teratomas of the ovary are parthenogenetic tumors formed by spontaneous asexual development of an unfertilized ovum after the first meiotic division. Another explanation is the alteration of blastodermal elements in a fertilized ovum. Despite all these theories, the pathophysiology of teratoma formation is still obscure and the focus of many experimental studies. An extraordinary feature of the teratoma is its ability to not only differentiate into tissue cells but also develop into organ systems. For example, respiratory epithelium with blocks of cartilage and bone fragments developing into digits or partial limb at rare instances., Epidemiology : Cystic teratomas are the most common ovarian germ cell tumors comprising 20% of all the ovarian tumors in adults, annual incidence rate of CT was 1.2 to 14.2 cases per 100, 000, Prognosis largely depends upon the extent of the d, NA, Complications : infection, TORSION, Diagnostics : HISTOPATHLOGY, LDH, Color Doppler, ECG, HCG, MRI, CT SCAN, USG, Differential diagnosis : ectopic pregnancy, endometrial carcinoma, Peritoneal cyst, Renal cysts, disease description : A type of germ cell tumor that may contain several different types of tissue, such as hair, muscle, and bone. Teratomas may be mature or immature, based on how normal the cells look under a microscope. Sometimes teratomas are a mix of mature and immature cells. Teratomas usually occur in the ovaries in women, the testicles in men, and the tailbone in children. They may also occur in the central nervous system (brain and spinal cord), chest, or abdomen. Teratomas may be benign (not cancer) or malignant (cancer).

Terrien’s Marginal Degeneration

Disease Name : Terrien’s Marginal Degeneration, Symptoms : corneal damage : In severe cases, the cornea may puncture or tear due to injury or trauma. This is a medical emergency that can cause serious vision issues., Eye irritation : Mild eye irritation due to an uneven cornea surface., Defective vision : Gradual vision changes due to astigmatism., Signs : "Dense yellowish white deposits may be seen at the sharp leading edge in cornea : Terriens marginal degeneration is an uncommon but distinct variety of marginal thinning of the cornea. It causes a slowly progressive non-inflammatory, unilateral or asymmetrically bilateral peripheral corneal thinning and is associated with corneal neovascularization, opacification and lipid deposition.", Treatment : Most common medical therapy is contact lenses to address the corneal astigmatism., In severe thinning, a patch,of corneal graft may be required, Surgical correction is indicated when perforation is imminent due to progressive thinning or when astigmatism significantly limits visual acuity. Crescent-shaped lamellar or full-thickness corneoscleral patch grafts may be used. These grafts have been reported to arrest progression of severe against-the-rule astigmatism for up to 20 years. Annular lamellar keratoplasty grafts may be required in severe cases of 360° marginal degeneration., Pathophysiology : The epithelium may be normal, thickened or thinned. Bowman’s membrane is typically absent or degenerated. Thinning and occasional breaks may be seen in Descemet’s membrane. Subepithelia fibrillar collagen degeneration has been seen with light microscopy. Electron microscopy demonstrates collagen precursors, stromal ground substance, and possibly lipid phagocytized by histiocytic cells with high lysosomal activity. Histocytes with a high degree of lysosomal activity are responsible for the destruction of collagen fibrils., Epidemiology : Terrien’s marginal degeneration is typically seen in patients 20-40 years of age, although it may present in childhood. It is more common in men than women (3 : 1), variable, NA, Complications : Corneal perforation, Corneal neovascularization, pseudopterygia, Diagnostics : Slit lamp examination, PHYSICAL EXAMINATION, Corneal topography, Differential diagnosis : Collagen vascular disease, Dellen (thinning of the corneal stroma), Keratoconjunctivits sicca, Staphylococcal marginal keratitis, disease description : Terrien’s marginal degeneration is an uncommon but distinct variety of marginal thinning of the cornea. It causes a slowly progressive non-inflammatory, unilateral or asymmetrically bilateral peripheral corneal thinning and is associated with corneal neovascularization, opacification and lipid deposition. Degeneration may lead to a high degree of against-the-rule or oblique astigmatism.

Tetanus

Disease Name : Tetanus, Symptoms : Breathing difficulty : Sometimes, the spasms affect muscles that help with breathing, which can lead to breathing problems., seizures : Progression of tetanus results in repeated painful, seizure-like spasms that last for several minutes., fever : Tetanus causes low-grade fever., DROOLING OF SALIVA : Generalized muscle spasm is associated with drooling., muscular spasm : Tension of muscles around your lips, sometimes producing a persistent grin., "lockjaw : It often causes a persons neck and jaw muscles to lock, making it hard to open the mouth or swallow.", Tachycardia : In severe cases of tetanus an overactivity of the sympathetic nervous system has been postulated because of the clinical symptoms including tachycardia., Signs : nan, Treatment : medication : Magnesium/Magnesium Sulphate, Phenobarbital/Phenobarbitone, Chlorpromazine , Metronidazole , Human normal immunoglobulin , Tetanus vaccine , Penicillin, Metronidazole (400 mg rectally or ,500 mg IV every 6 h for 7 days) is preferred for antibiotic therapy. An ,alternative is penicillin (100, 000–200, 000 IU/kg per day), although ,this drug theoretically may exacerbate spasms and in one study ,was associated with increased mortality. Human tetanus immune globulin ,(TIG). A single ,IM dose (3000–5000 IU) is given, with a portion injected around the ,wound. Equine-derived antitoxin is available widely and is used in ,low-income countries; after hypersensitivity testing, 10, 000–20, 000 U is ,administered IM as a single dose or as divided doses.Spasms are controlled by heavy sedation with benzodiazepines. ,Chlorpromazine and phenobarbital are commonly used worldwide and IV magnesium sulfate has been used as a muscle relaxant., Pathophysiology : Clostridium tetani is the name of the bacteria that causes tetanus. The bacterium can live in soil and animal excrement in a latent form. Its basically shut down until it finds a place to thrive. When dormant bacteria enter a wound, which promotes growth, the cells become "awakened." They produce a poison called tetanospasmin as they grow and divide. The poison damages the nerves that control the body muscles., Epidemiology : about 41, 951 incident cases of tetanus occurred among men in 2019, resulting in 19, 416 deaths worldwide, poor, Tetanus can be prevented through immunization with tetanus-toxoid-containing vaccines (TTCV), which are included in routine immunization programmes globally and administered during antenatal care contacts.,,To be protected throughout life, WHO recommends that an individual receives 6 doses (3 primary plus 3 booster doses) of TTCV., Complications : heart block, PNEUMONIA, Pulmonary Embolism, respiratory failure, Diagnostics : EMG/NCS, lumbar puncture, PCR, WOUND TISSUE CULTURE, ANTI TETANUS IgG BY ELISA, SERUM TETANUS TOXIN BIOASSAY, PHYSICAL EXAMINATION, Differential diagnosis : acute abdomen, infections, Malignant hyperthermia, serotonin syndrome, Stiff person syndrome, disease description : Tetanus is an acute disease manifested by skeletal muscle spasm and autonomic nervous system disturbance. It is caused by a powerful neurotoxin produced by the bacterium Clostridium tetani and is completely preventable by vaccination. C. tetani is found throughout the world, and tetanus commonly occurs where the vaccination coverage rate is low. In developed countries, the disease is seen occasionally in individuals who are incompletely vaccinated. In any setting, established tetanus is a severe disease with a high mortality rate.

Tethered Cord

Disease Name : Tethered Cord, Symptoms : asymmetry of the feet, back pain, HEMANGIOMA, hair patch, lipoma, Signs : calf is atrophied, high arch and clawing of the toes, Numbness, Skin discoloration, Tingling of the skin, Treatment : In children, early surgery is recommended to prevent further neurological deterioration. Regular follow-up is important : retethering may occur in some individuals during periods of rapid growth and may be seen between five to nine years of age. If surgery is not advisable, spinal cord nerve roots may be cut to relieve pain. In adults, surgery to free (detether) the spinal cord can reduce the size and further development of cysts in the cord and may restore some function or alleviate other symptoms. Other treatment is symptomatic and supportive., Pathophysiology : Attachments may occur congenitally at the base of the spinal cord (conus medullaris) or they may develop near the site of an injury to the spinal cord.  These attachments cause an abnormal stretching of the spinal cord.  The course of the disorder is progressive.  In children, symptoms may include lesions, hairy patches, dimples, or fatty tumors on the lower back; foot and spinal deformities; weakness in the legs; low back pain; scoliosis; and incontinence.  This type of tethered spinal cord syndrome appears to be the result of improper growth of the neural tube during fetal development, and is closely linked to spina bifida., Epidemiology : 0.25 per 1, 000 births, Complications : bleeding, infection, MENINGOCOELE, Diagnostics : MRI Spine, Differential diagnosis : HERNIATION SYNDROMES, SPONDYLOLISTHESIS, THORACIC SPINE DISEASES, disease description : Tethered spinal cord syndrome is a neurological disorder caused by tissue attachments that limit the movement of the spinal cord within the spinal column.  Attachments may occur congenitally at the base of the spinal cord (conus medullaris) or they may develop near the site of an injury to the spinal cord.  

Tetralogy Of Fallot

Disease Name : Tetralogy Of Fallot, Symptoms : "Arrhythmias : It might mean their brains dont get enough oxygen, so they may shake or seem to have seizures.", heart murmur : Tetralogy of Fallot causes a a “whooshing” sound caused by blood not flowing properly through the heart., Restlessness : Tetralogy of Fallot makes the infants irritable, easily tired., "tetralogy of fallot : Sometimes, babies who have tetralogy of Fallot will suddenly develop deep blue skin, nails and lips after crying or feeding, or when agitated. These episodes are called tet spells. Tet spells are caused by a rapid drop in the amount of oxygen in the blood. Tet spells are most common in young infants, around 2 to 4 months old. Toddlers or older children might instinctively squat when theyre short of breath. Squatting increases blood flow to the lungs.", poor weight gain : Neonates with severe tetralogy of fallot have severe cyanosis and dyspnea during feeding, leading to poor weight gain., Breathing difficulty : Shortness of breath and rapid breathing, especially during feeding or exercise., Signs : "cyanosis : Infants with tetralogy of Fallot can have a bluish-looking skin color?called cyanosis?because their blood doesnt carry enough oxygen.", clubbing : An abnormal, rounded shape of the nail bed in the fingers and toes., Treatment : medication : Sodium bicarbonate , Propranolol , Morphine, The medical management of TOF is limited to prevention,and management of complications and correction of,anemia. Oral beta-blockers help prevent cyanotic spells.,Maximally tolerated doses of propranolol ranging from,0.5-1.5 mg/kg/ dose should be administered. Iron supplementation,is recommended for all infants and young,children with TOF., Definitive surgery for TOF involves closure of the VSD,and relief of the RVOT obstruction. Although definitive operation is feasible in young,infants, some centers opt for palliative options initially.,This is typically done through the Blalock-Taussig shunt, ,which consists of subclavian artery-pulmonary artery,anastomosis using a Goretex graft. Alternatives include,balloon dilation of the pulmonary valve or stenting of the,patent arterial duct (if present)., Pathophysiology : Normally the left side of the heart only pumps blood to the body, and the hearts right side only pumps blood to the lungs. In a child with tetralogy of Fallot, blood can travel across the hole (VSD) from the right pumping chamber (right ventricle) to the left pumping chamber (left ventricle) and out into the body artery (aorta). Obstruction in the pulmonary valve leading from the right ventricle to the lung artery prevents the normal amount of blood from being pumped to the lungs. Sometimes the pulmonary valve is completely obstructed (pulmonary atresia)., Epidemiology : 1 in 3, 000 live births, DEPENDS ON SEVERITY OF SYMPTOMS, Although healthcare providers don’t know the cause of tetralogy of Fallot, you may be able to reduce a fetus’s risk of tetralogy of Fallot in these ways : ,,Don’t use tobacco products or drink alcohol while pregnant.,Avoid certain medicines. Ask your provider for substitute medicines you can take during pregnancy.,If you have phenylketonuria, eat less protein.,Make sure your rubella vaccine is still working to keep you from getting rubella during pregnancy.,Keep your diabetes well managed., Complications : congestive heart failure (CHF), Infective endocarditis, PULMONIC STENOSIS, Diagnostics : ABG, Complete Blood Count CBC, ECG, CARDIAC CATHETERIZATION, CT CHEST, CHEST X RAY, Differential diagnosis : cyanosis, Ebstein Anomaly, failure to thrive, pulmonary atresia, respiratory distress, disease description : A heart defect that features four problems :  a hole between the lower chambers of the heartan obstruction from the heart to the lungsThe aorta (blood vessel) lies over the hole in the lower chambersThe muscle surrounding the lower right chamber becomes overly thickened

Thalassemia

Disease Name : Thalassemia, Symptoms : abdominal swelling : Splenomegaly may cause abdominal enlargement or swelling., EXERCISE INTOLERANCE : Exercise performance is lower among patients with beta-thalassemia compared with healthy people., fever : Fever is the most common presenting feature, often associated with abdominal pain and diarrhoea or vomiting., DARK URINE : This happens because the breakdown of red blood cells produces bilirubin, which causes the urine to appear dark brown or even black., Facial abnormalities : When facial bones are affected it can result in distinctive facial features including an abnormally prominent forehead (frontal bossing), full cheek bones (prominent malar eminence), a depressed bridge of the nose, and overgrowth (hypertrophy) of the upper jaw (maxillae), exposing the upper teeth., short stature : If the production of growth hormone is disrupted by iron deposition, the affected children may not grow very tall. Short stature is very common amongst people with thalassaemia., DEPRESSION : Depression is the most common psychological complication for individuals with thalassemia., Signs : heart murmur : The increased cardiac output may lead to flow murmurs on cardiac auscultation., hepatosplenomegaly : An enlarged spleen in a child with beta-thalassemia can be caused by increased red blood cell destruction, the formation of blood cells outside of the bone marrow, repeated blood transfusions, or iron overload., Severe Pallor : Individuals with ß-thalassemia major present between ages six and 24 months with pallor due to severe anemia., Treatment : medication : deferoxamine / desferrioxamine, Hydroxycarbamide (Hydroxyurea), Deferiprone , Patients with thalassemia intermedia require monitoring,to assess the need for transfusion, as persistently low,hemoglobin may retard growth. Hydroxyurea at a dose,of 15-20 mg/kg/ day may be used to increase HbF production,and reduce the need for transfusion support. This,therapy is most effective in children with XLM1 mutation.,Patients with thalassemia trait do not require medical,followup after the initial diagnosis. Iron therapy should,not be used unless a definite deficiency is confirmed.,Genetic counseling is indicated to create awareness and,prevent thalassemia major in subsequent offspring., Hematopoietic Stem Cell Transplantation and ,,Splenectomy, Pathophysiology : Two related features contribute to the sequelae of ß-thalassemia syndromes : inadequate ß-globin gene production leading to decreased levels of normal hemoglobin (HbA) and unbalanced a- and ß-globin chain production leading to ineffective erythropoiesis. In ß-thalassemia a-globin chains are in excess to non– a-globin chains, and a-globin tetramers (a4 ) are formed and appear as RBC inclusions. The free a-globin chains and inclusions are very unstable, precipitate in RBC precursors, damage the RBC membrane, and shorten RBC survival, leading to anemia and increased erythroid production. This results in a marked increase in erythropoiesis, with early erythroid precursor death in the bone marrow. Clinically, this is characterized by a lack of maturation of erythrocytes and an inappropriately low reticulocyte count. This ineffective erythropoiesis and the compensatory massive marrow expansion with erythroid hyperactivity characterize ß-thalassemia. Due to the low or absent production of ß-globin, the a-chains combine with gamma-chains, resulting in HbF being the dominant hemoglobin.  The d-chain synthesis is not usually affected in ß-thalassemia or ß-thalassemia trait, and therefore patients have a relative or absolute increase in HbA2 production (a2 d2 ). In the a-thalassemia syndromes , there is a reduction in a-globin production. Normally, there are 4 a-globin genes (2 from each parent) that control a-globin production. a-thalassemia syndromes vary from complete absence (hydrops fetalis) to only slightly reduced (a-thalassemia silent carrier) a-globin production. , Epidemiology : 1 in 100, 000 individuals in the general population., DEPENDS ON SEVERITY OF SYMPTOMS, You can’t prevent thalassemia, but genetic testing can reveal whether you or your partner carry the gene. Knowing this information can help you plan your pregnancy if you plan to conceive.,,Speak to a genetic counselor for guidance on family planning if you suspect you or your partner may carry gene mutations for thalassemia., Complications : failure to thrive, hepatosplenomegaly, pulmonary hypertension, SIGN OF SEVERE ANEMIA, Endocrine disorders, Diagnostics : Complete Blood Count CBC, Peripheral Blood Smear, Reticulocyte Count, Reticulocyte Count, hemoglobin HB, White Blood Cell count WBC, MEAN CORPUSCULAR VOLUME(MCV, MEAN CORPUSCULAR HEMOGLOBIN(MCH), HISTORY TAKING, Hemoglobin A1C TEST, HbF, Differential diagnosis : anemia, iron deficiency anemia, Lead Poisoning, disease description : Thalassemia is an inherited (i.e., passed from parents to children through genes) blood disorder caused when the body doesn’t make enough of a protein called hemoglobin, an important part of red blood cells. When there isn’t enough hemoglobin, the body’s red blood cells don’t function properly and they last shorter periods of time, so there are fewer healthy red blood cells traveling in the bloodstream.Red blood cells carry oxygen to all the cells of the body. Oxygen is a sort of food that cells use to function. When there are not enough healthy red blood cells, there is also not enough oxygen delivered to all the other cells of the body, which may cause a person to feel tired, weak or short of breath. This is a condition called anemia. People with thalassemia may have mild or severe anemia. Severe anemia can damage organs and lead to death.

Thecoma

Disease Name : Thecoma, Symptoms : vaginal bleeding : These tumors are commonly estrogenic and most women present with abnormal vaginal bleeding., Signs : nan, Treatment : Oophorectomy if fertility sparing is desired.,Total hysterectomy with bilateral salpingo-oophorectomy is indicated in postmenopausal patients., Pathophysiology : Pathogenesis includes-Molecular alterations, such as trisomy 12 and loss of heterozygosity (LOH) at the PTCH gene., Epidemiology : Account for approximately 0.5-1% of all ovarian tumors, variable, NA, Complications : post-surgical complications, Diagnostics : Cytogenetics, PET SCAN, MRI, USG, ELECTRON MICROSCOPY, Immunostaining, Differential diagnosis : Adult granulosa cell tumour, Fibroma, Sclerosing stromal tumour, disease description : Thecomas are defined as stromal tumors that resemble thecal cells of the developing follicle and that are composed of a minimum (less than 10%) of cells with granulosa cell differentiation.Thecomas or theca cell tumors are benign ovarian neoplasms composed only of theca cells. Histogenetically they are classified as sex cord-stromal tumours.They are typically estrogen-producing and they occur in older women (mean age 59; 84% after menopause). (They can, however, appear before menopause.1)60% of patients present with abnormal uterine bleeding, and 20% have endometrial carcinoma.

Thiel-behnke Corneal Dystrophy

Disease Name : Thiel-behnke Corneal Dystrophy, Symptoms : ocular discomfort, ocular pain, Visual impairment, Signs : corneal opacification, (honeycomb) opacities of cornea, Blurring of vision, Treatment : nan, Pathophysiology : Signs include : symmetrical subepithelial reticular (honeycomb) opacities with peripheral cornea typically uninvolved, which can progress to deep stromal layers and corneal periphery. Symptoms : Recurrent corneal erosions cause ocular discomfort and pain in the first and second decade. Gradual visual impairment develops later, Epidemiology : nan, Complications : CORNEAL OPACITIES, Visual impairment, Diagnostics : ophthalmoscopy, Differential diagnosis : Congenital Stromal Corneal Dystrophy, Gelatinous Drop-Like Corneal Dystrophy (GDLD), Grayson-Wilbrandt Corneal Dystrophy, herpetic keratitis, , Lattice corneal dystrophy, Lisch Corneal Dystrophy, Meesmann Corneal Dystrophy, Reis-Bucklers Corneal Dystrophy, disease description : Thiel-Behnke corneal dystrophy (TBCD) also known as corneal dystrophy of Bowman layer, type II (CDB2) or honeycomb-shaped corneal dystrophy occurs in childhood and causes slowly progressive deterioration of vision. Genetic locus is 5q31 and the gene involved is TGFB1. Inheritance is autosomal dominant. Onset and course. Occurs in childhood and there occurs slowly progressive deterioration of vision from increasing corneal opacification.

Threatened Miscarriage

Disease Name : Threatened Miscarriage, Symptoms : Pain : Abdominal cramps. The pain is typically dull, not sharp or intense. However, it can progress to constant, severe pain., Signs : nan, Treatment : medication : Diazepam , Rest : The patient should be in bed for few days until bleeding stops. Prolonged restriction of activity,has got no therapeutic value. Drugs : Relief of pain may be ensured by diazepam 5 mg tablet twice daily, Drugs : Relief of pain may be ensured by diazepam 5 mg tablet twice daily. ,There is some evidence that treatment with progesterone improves the outcome. Progesterone induces ,immunomodulation to shift the Th-1 (proinflammatory response) to Th-2 (antiinflammatory response). Use of ,hCG is not prefered, Pathophysiology : Miscarriage is common. Small falls, injuries or stress during the first trimester of pregnancy can cause threatened miscarriage. It occurs in almost one half of all pregnancies. The chance of miscarriage is higher in older women. About one half of women who have bleeding in the first trimester will have a miscarriage., Epidemiology : approximately 20% of all pregnancies, It occurs in 20-25% of pregnancies and is associated with an increased rate of fetal loss, variable, There’s rarely anything you or your provider can do to prevent a threatening miscarriage. Follow the advice of your pregnancy care provider if they believe your pregnancy is at risk for a miscarriage. Attending all of your prenatal appointments and listening to your pregnancy care provider are things you can control.,,Other things you can do to support a healthy pregnancy include : ,,Avoiding drinking alcohol, smoking cigarettes or using recreational drugs.,Avoiding exposure to chemicals, toxins or other substances known to harm a fetus.,Taking a prenatal vitamin containing folic acid.,Eating a healthy diet full of vegetables and fruits.,Exercising around 20 to 30 minutes per day.,Getting treatment for or managing any diseases, infections or chronic health conditions., Complications : Septic Abortion, vaginal bleeding, ENDOMETRITIS, Diagnostics : Complete Blood Count CBC, Hb, USG Obstetrics, URINE ANALYSIS (Volume), HISTORY TAKING, Differential diagnosis : cervical trauma, Cervicitis, vaginal trauma, disease description : A threatened miscarriage (threatened abortion) describes a pregnancy that could possibly end in miscarriage due to mild vaginal bleeding with or without abdominal pain or cramping. The bleeding tends to stay light and cramping remains mild, sometimes lasting several days or weeks. Threatened miscarriages occur in the first half (up to 20 weeks) of pregnancy, but most commonly in the first trimester (13 weeks) of pregnancy.

Thromboangiitis Obliterans

Disease Name : Thromboangiitis Obliterans, Symptoms : "inflammation : Inflammation of a vein just below the skins surface, due to a blood clot in the vein.", muscle cramps : Cramps occur in the calf muscles or feet if the legs are affected and in the hands or forearms if the arms are affected., Numbness : Tingling or numbness in the fingers or toes., "Raynaud’s syndrome : Fingers and toes that turn white then blue when exposed to cold, known as Raynauds disease", Pain : Pain in the feet that occurs with walking. The pain may make it difficult to walk long distances. Painful open sores on fingers and toes. Pain in the fingers and toes may become severe and occur at rest., "Skin ulcers : Thromboangiitis obliterans (TAO) or Buergers disease is associated with both distal ulcers in the extremities and the possibility of amputation.", blood clot formation : Thromboangiitis obliterans (Buerger disease) is caused by small blood vessels that become inflamed and swollen. The blood vessels then narrow or get blocked by blood clots (thrombosis)., Skin color changes. : Changes in skin color in the hands and feet. The skin may look pale gray, red or blue., Signs : nan, Treatment : First line Cessation of smoking. This is the only intervention of proven value,and is most beneficial if undertaken before the onset of gangrene ,or tissue loss, Medical : prostacyclin analogue infusions, calcium-channel blockers, ,thrombolytics, anticoagulants,Sympathectomy : spinal cord stimulators,Stimulating angiogenesis through autologous bone marrow cells,rich in endothelial progenitor cells, Second line Surgical : ,• revascularization if possible (most occlusions are not amenable ,because they are too distal or diffuse and segmental),• amputation for gangrene, Pathophysiology : General pathophysiology is not well known : An inflammatory and immunologic pathogenesis is postulated.Tobacco use could be a toxic trigger, or cause a delayed hypersensitivity reaction, Epidemiology : 0.5-5.6% in Western Europe, 15-66% in Korean and Japan, and 45-63% in India, variable, To avoid getting Buerger’s disease, don’t smoke or use tobacco of any kind. You should avoid nicotine patches and marijuana as well., Complications : gangrene, Ulcers, Diagnostics : Complete Blood Count CBC, Erythrocyte Sedimentation Rate (ESR), HISTOPATHLOGY, ANGIOGRAM, ARTERIOGRAPHY, Differential diagnosis : Scleroderma crisis, Trauma, vasculitis, disease description : This is a non-atherosclerotic segmental inflammatory disease of the small and medium sized arteries of the distal extremities of predominantly young male smokers. These patients are normally seen by vascular surgeons but may present to dermatologists with erythema and or ulceration of the skin of the fingers and toes

Thrombophlebitis

Disease Name : Thrombophlebitis, Symptoms : painful swelling, edema, Warm Skin, Pruritis, Tenderness on palpation, severe pain, Signs : signs of inflammation, Treatment : Elevation and Anti-inflammatory drugs, antibiotics. Application of crepe bandage-compression therapy. heparin is the recommended treatment given that multiple pathways contribute to the development of the thrombus, Pathophysiology : a. Acute : Due to IV cannulation, trauma, minor infections, hypercoagulability. b. Recurrent. c. Spontaneous : Polycythaemia vera, polyarteritis, Buergers disease. d. Thrombophlebitis migrans (Trousseaus sign, 1876) : It is spontaneous migrating thrombophlebitis seen in visceral malignancy like pancreas, stomach. e. Mondors disease. It can be-SVT with varicose veins (V-SVT) or SVT without varicose veins (NV-SVT). It can also be- primary or secondary. Duplex ultrasound Doppler of both limbs is a must., Epidemiology : nan, Complications : deep vein thrombosis, VARICOSE VEINS, Embolic events, Diagnostics : Complete Blood Count CBC, CT Abdomen, compression USG, DUPLEX ULTRASONOGRAPHY, COAGULATION PROFILE, Differential diagnosis : ANAPLASTIC CARCINOMA OF THYROID, CARCINOID TUMORS, CARCINOMA OF THE PANCREAS, CARCINOMA ANAL CANAL, CARCINOMA BLADDER, CARCINOMA COLON, CARCINOMA GALL BLADDER, CARCINOMA OF BREAST, CARCINOMA OF THE OESOPHAGUS, CARCINOMA PENIS, CARCINOMA PROSTATE, CARCINOMA RECTUM, CHOLANGIOCARCINOMA, FOLLICULAR CARCINOMA, Hepatocellular carcinoma, medullary carcinoma, PAPILLARY CARCINOMA, PARATHYROID CARCINOMA, disease description :  thrombophlebitis is an inflammatory disorder  veins with coexistent venous thrombosis. It usually affects lower limbs, particularly the great saphenous vein (60% to 80%) or the small/short saphenous vein (10% to 20%). However, it can occur at other sites (10% to 20%) and may occur bilaterally (5% to 10%).Traditionally, this relatively common process was considered benign and self-limited. More recently, superficial thrombophlebitis, also called superficial venous thrombosis (SVT), has been associated with other venous thromboembolic disorders, primarily deep venous thrombosis (DVT) and pulmonary embolism (PE). 

Thygeson’s Superficial Punctate Keratitis

Disease Name : Thygeson’s Superficial Punctate Keratitis, Symptoms : Ocular symptoms : Patients with Thygeson superficial punctate keratitis (TSPK) often report bilateral tearing, burning, photophobia, foreign body sensation, and ocular irritation during exacerbations. Patients also may experience mild blurring of vision. There usually is minimal or no conjunctival hyperemia and no discharge., Signs : corneal lesions : The typical TSPK is an elevated or flat round-oval shaped, gray-whitish lesion, occupying the central intraepithelial corneal area with minimal underlying stromal edema or inflammation. The acute lesion may stain minimally with fluorescein, and may or may not stain with vital dyes (rose bengal or lissamine green). On occasions, the lesion is described as starry, and in the late stages, subepithelial fibrosis or an anterior stromal scar can be noticed. Around 20 of them are present in each eye, but up to 50 lesions have been reported. The lesions tend to disappear without leaving a trace in the course of 4 to 6 weeks. Corneal sensitivity is usually preserved or slightly diminished. The conjunctiva remains quiet but in a few cases, redness and filament formation may also be found., Treatment : Therapeutic soft contact lenses may be required in,steroid-resistant cases., • Disease is self-limiting with remissions and may,permanently disappear in a period of 5–6 years.,• Topical steroids during exacerbations the lesions,and associated symptoms usually respond,quickly to topical steroids (so, should be tapered,rapidly)., Due to its therapeutic success and security profile compared to corticosteroids, topical cyclosporine (CsA) has been proposed as first-line treatment for patients with TSPK., Multiple therapeutic strategies have been tried over the years for the management of TSPK, but none of them have resulted to be entirely successful. Antibiotics have not been effective so far. On the other hand, antivirals have shown mixed results. While mild improvements have been reported with trifluridine therapy, idoxuridine has been shown to cause persistent anterior stromal ghost opacities and scarring, and is therefore contraindicated for TSPK., Pathophysiology : The pathophysiology of TSPK remains unknown. Both, viral and immunologic mechanisms have been implicated. Adenovirus,  herpes simplex virus, and varicella zoster virus, have all been implicated as a possible causes of the disease. However, Braley and Alexander provided questionable results suggesting a virus may be responsible for TSPK, and in 1974, Lemp, et al isolated varicella zoster virus from the corneal surface of a 10 years old boy with TSPK. More recent studies using polymerase chain reaction (PCR), were not able to detect varicella zoster virus from eyes with TSPK, providing doubts this virus is a causative agent. On the other hand, an immune based etiology has also been proposed, since the presence of the HLA-DR3, a class-II MHC molecule associated with immune response genes and multiple autoimmune disorders (Gluten enteropathy, Addisons and Sjögrens syndromes, systemic lupus erythematosus, diabetes mellitus) has been positively implicated to patients with TSPK., Epidemiology : TSPK may affect both sexes, but a higher incidence has been reported in females.The incidence of TSPK is lower in children (4.1%) than adults (32.0%), variable, NA, Complications : visual blurring, corneal damage, Visual impairment, Diagnostics : Slit lamp examination, Differential diagnosis : ACANTHAMOEBA KERATITIS, HERPES SIMPLEX KERATITIS, herpetic keratitis, Pneumococcal conjunctivitis, Staphylococcal blepharitis, Staphylococcal epithelial keratitis, disease description : Thygesons superficial punctate keratitis (TSPK) is an insidious, chronic and recurrent disorder, characterized by small and elevated oval corneal intraepithelial, whitish-gray opacities, extending to the entire anterior surface of the cornea of both eyes. Corneal lesions show a tendency for the central pupillary area distribution with mild or absent conjunctival inflammation and no association to systemic disease.

Thymic Hypoplasia

Disease Name : Thymic Hypoplasia, Symptoms : muscle spasm, twitching of the face or limbs, Respiratory infections, Signs : an antimongoloid slant to the eyes, bifid uvula, hypertelorism, hypocalcemic seizures during the neonatal period, Treatment : An effective clinical treatment option for such a patient is an allogeneic thymic tissue transplant, first depleted of thymocytes prior to the placement of small fragments of this tissue within the quadricep muscles (67–70). The thymic stromal tissue consists of TECs, mesenchymal cells, and endothelial cells, Pathophysiology : Chaoui et?al.22 and Barrea et?al.23 investigated the fetal thymus and found that absent or hypoplastic thymus on US is a marker for deletion 22q11.2 in fetal cardiac defects, with a sensitivity of at least 90% and specificity of 98.5% in a group of fetuses with prenatally diagnosed cardiac defects. A larger study of 74 fetuses with confirmed 22q11.2 deletion by fluorescence in situ hybridization (FISH) analysis found that 86% of these fetuses had a thymic abnormality at autopsy, with 53.3% having complete thymic agenesis and 46.7% demonstrating thymic hypoplasia.24 Taken together, these studies suggest that thymic evaluation by ultrasound can be useful to identify patients at risk for 22q11.2 deletion in the presence of small or absent thymus.Cromi et?al.25 assessed fetal thymus size in growth-restricted fetuses and found that the vast majority of growth-restricted fetuses (58/60, 97%) demonstrated thymic size smaller than fifth percentile, compared with only 7/60 (11%) controls having small thymus. The authors postulated that a small fetal thymus is a marker of the fetal immune-endocrine response to malnutrition. A clinically relevant study by Ekin et?al.26 assessed the implication of small thymus in cases of growth-restricted fetuses and confirmed significantly smaller thymuses than in normally grown controls. Importantly, they also found that smaller thymus size within the growth-restricted fetuses was associated with significantly higher risk of perinatal morbidity including preterm delivery,  respiratory distress syndrome, early neonatal sepsis, and longer intensive care unit stays., Epidemiology : nan, Complications : Respiratory Distress Syndrome, PERINATAL LOSS, FETAL GROWTH RESTRICTION, Neonatal sepsis, Diagnostics : molecular genetic testing, Differential diagnosis : congenital malformation (a birth defect), DiGeorge syndrome, HIV, disease description : hymic hypoplasia is a condition in which the thymus is underdeveloped or involuted. Thymic aplasia is congenital absence of the thymus. Thymic hypoplasia and thymic aplasia have been reported as an associated finding in various diseases, such as 22q11.

Thyroid Disorder In Pregnancy

Disease Name : Thyroid Disorder In Pregnancy, Symptoms : constipation : Constipation is a common symptom of hypothyroidism., muscle cramps : Some people also experience muscle stiffness and painful muscle cramps., puffy face : Thyroid disorder in pregnancy leads to swelling of the face., skin problem : Skin and hair changes, including dry skin and loss of eyebrows., Carpal tunnel syndrome : Carpal Tunnel Syndrome (CTS) is an entrapment neuropathy that occurs due to compression of median nerve in the carpal tunnel and hypothyroidism is one of the important causes of CTS., Hoarse voice : Low thyroid hormone levels cause fluid to accumulate in the vocal folds, and when the thyroid gland enlarges due to disease, the vocal chords can become pinched or partially paralyzed due to their snug proximity., Signs : nan, Treatment : If you have mild hyperthyroidism during pregnancy, you probably won’t need treatment. If your hyperthyroidism is linked to hyperemesis gravidarum, you only need treatment for vomiting and dehydration., antithyroid medicine propylthiouracil NIH external link (PTU) during the first 3 months of pregnancy., If your hyperthyroidism is more severe, your doctor may prescribe antithyroid medicines, which cause your thyroid to make less thyroid hormone. This treatment prevents too much of your thyroid hormone from getting into your baby’s bloodstream., Pathophysiology : Pregnancy is a time of complex hormonal changes. In women with normal thyroid function, there is an increase in thyroxine (T4) and triiodothyronine (T3) production, which results in inhibition of thyroid-stimulating hormone (TSH) in the first trimester of pregnancy, due to a high human chorionic gonadotropin (hCG) level that stimulates the TSH receptor because of partial structural similarity. A large plasma volume and thus an altered distribution of thyroid hormone, increased thyroid hormone metabolism, increased renal clearance of iodide, and higher levels of hepatic production of thyroxine-binding globulin (TBG) in the hyperestrogenic state of pregnancy are responsible for higher thyroxine requirements in pregnancy. It is very important to remember that biochemical thyroid function should be free thyroid hormone, as total hormone will mislead showing more than normal value when the patient is euthyroid., Epidemiology : The prevalence of thyroid dysfunction was 13.2% in our population., The incidence of hypothyroidism in pregnancy is between 0.5%–3.5%., Good with an effective treatment plan., "Cant be prevented since Pregnancy is a time of complex hormonal changes. However, with correct diagnosis at the start of pregnancy and with adequate treatment plan, it can be effectively managed.", Complications : low birth weight, anxiety, Diagnostics : Complete Blood Count CBC, HISTOPATHLOGY, Triiodothyronine (T3) Tests, Thyroid Stimulating Hormone TSH, biopsy, TOTAL THYROXINE (T4), Differential diagnosis : factitious hyperthyroidism, Familial Hypercholesterolemia, Goiter, Graves Disease or Hyperthyroidism, infertility, IODINE DEFICIENCY, disease description : Thyroid disorders are common in pregnancy and the most common disorder is subclinical hypothyroidism. Due to the complex hormonal changes during pregnancy, it is important to remember that thyroxine requirements are higher in pregnancy. Maternal hypothyroidism is an easily treatable condition that has been associated with increased risk of low birth weight, fetal distress, and impaired neuropsychological development. Hyperthyroidism in pregnancy is less common as conception is a problem. Majority of them are due to Graves’ disease, though gestational hyperthyroidism is to be excluded. 

Thyroid Eye Disease

Disease Name : Thyroid Eye Disease, Symptoms : Ocular symptoms : Includes dry eyes, grittiness, watery, red eyes, proptosis, diplopia, difficulty closing your eyes completely, pain behind your eyes and pain with eye movements.., Signs : Chemosis of conjunctiva : Thyroid eye disease (TED) causes inflammation of the eyes and the tissues around the eyes, often resulting in chemosis., "Retraction of the upper lids (Dalrymple’s sign) : Dalrymples sign is a widened palpebral (eyelid) opening, or eyelid spasm, seen in thyrotoxicosis (as seen in Graves disease, exophthalmic goitre and other hyperthyroid conditions), causing abnormal wideness of the palpebral fissure. As a result of the retraction of the upper eyelid, the white of the sclera is visible at the upper margin of the cornea in direct outward stare.", "Lid lag (von Graefe’s sign) : Von Graefes sign is the lagging of the upper eyelid on downward rotation of the eye, indicating exophthalmic goiter (Graves disease). It is a dynamic sign, whereas lid lag is a static sign which may also be present in cicatricial eyelid retraction or congenital ptosis.", Fullness of eyelids (Enroth’s sign) : Edema esp. of the upper eyelid., Difficulty in eversion of upper lid (Gifford’s sign) : Difficulty in eversion of upper lid., "Infrequent blinking (Stellwag’s sign) : Stellwags sign is a sign of infrequent or incomplete blinking associated with exophthalmos or Graves orbitopathy. It is accompanied by Dalrymples sign, which is a retraction of the upper eyelids resulting in an apparent widening of the palpebral opening.", Treatment : 1. Smoking cessation should be insisted with the,patients as it may markedly influence the course,of disease.,2. Head elevation at night and cold compresses in the,morning help in reducing periorbital oedema., 1. Lubricating artificial tear drops, 2. Guanethidine 5% eyedrops may decrease the,lid retraction caused by overaction of Muller’s,muscle, 3. Systemic steroids, Combined therapy with low dose steroids, ,azathioprine and irradiation is reported to be,more effective than steroids or radiotherapy alone., Radiotherapy. 2000 rads given over 10 days,period may help in reducing orbital oedema,in patients where steroids are contraindicated., 1. Orbital decompression, 2. Extraocular muscle surgery(Inferior rectus recession is the most,commonly performed surgery.), 3. Eyelid surgery(Mullerotomy, Levator recession/disinsertion, Scleral grafts with LPS recession, Recession of lower eyelid retractors and Blepharoplasty), Pathophysiology : Thyroid eye disease is being considered an autoimmune disease with orbital fibroblasts as the primary target of inflammatory attack and extraocular muscles being secondarily involved. It is probable that the target antigen is shared between the thyroid follicular cells and orbital fibroblasts. The activated T-cells probably act on the fibroblast-adipocyte lineage within the orbit and stimulate adipogenesis, fibroblast proliferation, and glycosaminoglycan synthesis. As a consequence, the extraocular muscles are enlarged due to edema and infiltration with round cells. The orbital soft tissue shows increased amounts of acid mucopolysaccharide and infiltration with lymphocytes, plasma cells, macrophages and mast cells. Thyroid eye disease (TED) is a self-limiting disease that lasts from 1–5 years (longer in smokers as compared to non-smokers). Its clinical course is divided into two phases : 1. Congestive or Active phase of increasing severity is characterized by active inflammation with marked lid oedema, conjunctival chemosis and congestion and increasing exophthalmos. Within 2 to 3 years, in majority of cases, there starts regression and most of the signs slowly settle down. 2. Fibrotic or Inactive phase, also known as quiescent burnt-out phase, ensues after the regression phase. In this phase eyes are white, however, a painless motility defect may be present., Epidemiology : Incidence of clinically apparent Graves orbitopathy was 16 per 100000 in females and 2.9 per 100000 in males, GOOD, You can’t prevent thyroid eye disease., Complications : impair vision, KERATITIS, Exophthalmos, Diagnostics : MRI Head, CT SCAN, THYROID PROFILE, PHYSICAL EXAMINATION, Orbital ultrasonography, Differential diagnosis : amyloidosis, Blow-out fracture of the orbit, Hashimotos Disease or Hypothyroidism, lymphoma, orbital cellulitis, POLYMYOSITIS, disease description : The term thyroid eye disease denotes typical ocular changes which include lid retraction, lid lag, and proptosis. These changes have also been labelled as : endocrine exophthalmos, malignant exophthalmos, dysthyroid ophthalmopathy, ocular Graves’ disease (OGD), Graves’ ophthalmopathy, and thyroid associated ophthalmopathy (TAO).

Thyroid Hormone Dysfunction

Disease Name : Thyroid Hormone Dysfunction, Symptoms : dry skin, Hair Thinning, menorrhagia, muscle pain, muscle weakness, tremor, weight gain, hoarseness of voice, dyspnea, Signs : Bradycardia, peripheral edema, Treatment : medication : Levothyroxine/Tetra idothyronine, Anti-thyroid drugs (methimazole and propylthioracil) : These are medications that stop your thyroid from making hormones., Beta blockers : These medications don’t change the amount of hormones in your body, but they help manage your symptoms., If you have low levels of thyroid hormones (hypothyroidism), the main treatment option is : ,,Thyroid replacement medication : This drug is a synthetic (man-made) way to add thyroid hormones back into your body. One drug that’s commonly used is called levothyroxine. By using a medication, you can manage thyroid disease and live a normal life., Radioactive iodine : This treatment damages the cells of your thyroid, preventing it from making high levels of thyroid hormones., Surgery : A more permanent form of treatment, your healthcare provider may surgically remove your thyroid (thyroidectomy). This will stop it from creating hormones. However, you will need to take thyroid replacement hormones for the rest of your life., Pathophysiology : The understanding of thyroid disease and the interpretation of thyroid function tests requires an understanding hypothalamic–pituitary–thyroid feedback control. It also demands an appreciation of thyroid hormone transport and the response of cells to non-protein-bound thyroid hormone. The hypothalamic hormone, thyrotropin releasing hormone (TRH), modulates the release of pituitary thyroid stimulating hormone (TSH). TSH interacts with specific receptors on thyroid follicular cells to stimulate thyroid hormone production approximately 80% thyroxine (T4) and 20% triiodothyronine (T3). T4 and T3 are transported in blood bound to serum proteins. The remainder of T3 production (80%) comes from the conversion of T4 in peripheral tissues. T3 is the most active form of thyroid hormone. Non-protein-bound thyroid hormones, representing a minor fraction of the total circulating thyroid hormones, enter peripheral cells and interact with a specific nuclear binding protein. This interaction leads to induction of many enzymes to finally express the effect of the thyroid hormones. Circulating levels of T4 and T3 are sensed by the pituitary gland and perhaps by the hypothalamus to control the secretion of TSH and thereby maintain blood levels of thyroid hormones within normal limits. Disturbances in many aspects of this complex system can present the physician with clinical and laboratory findings of hyper- or hypothyroidism, goiter, or apparent abnormalities of thyroid function testing without definite clinical correlates. Often, the discordance between clinical Findings arid laboratory testing makes the diagnosis of thyroid disorders challenging and stimulating.Thyroid problems may also directly result from medical or surgical therapies of the thyroid gland or indirectly from treatment of nonthyroid conditions. Examples include hypothyroidism after radioactive iodine or surgery for Graves disease, and thyroid cancer after x-ray therapy to the head or neck. Hypothyroidism and hyperthyroidism have been reported after treatment of arrhythmias with Amiodarone, which contains iodine., Epidemiology : The mean annual incidence rate of autoimmune hypothyroidism is up to 4 per 1000 women and 1 per 1000 men, variable, Here are the things that you can do to prevent thyroid disease : ,,If you are a smoker, quit smoking. This not only lowers your chance of developing thyroid disease but also many other health issues, including those of a cardiovascular nature.,Eat less soy. The popular ingredient is not necessarily unhealthy, but it is controversial, especially when we consider thyroid health.,Ask for a thyroid collar during x-rays to protect your thyroid gland from radiation exposure.,Consider selenium supplements. Selenium is a nutrient found in specific proteins, and it has a vital role in keeping your thyroid gland healthy. If your diet is healthy, you’re already taking enough selenium. Still, you may consider increasing your selenium intake to boost your immune system and decrease symptoms of hypothyroidism.,Visit your doctor regularly. Regular checkups are not only good for your overall health but also your thyroid health., Complications : heart failure, Mental disturbances including depression, Thyroid storm, infertility, Exophthalmos, Goiter, Myxedema, Diagnostics : Free T3, Free T4, Triiodothyronine (T3) Tests, Thyroxine (T4) Test, Thyroid Stimulating Hormone TSH, USG Thyroid, thyroid antibodies, Differential diagnosis : "Addisons Disease", anemia, DEPRESSION, goitre, disease description : Thyroid disease is a general term for a medical condition that keeps your thyroid from making the right amount of hormones. Your thyroid typically makes hormones that keep your body functioning normally. When the thyroid makes too much thyroid hormone, your body uses energy too quickly. This is called hyperthyroidism. Using energy too quickly will do more than make you tired — it can make your heart beat faster, cause you to lose weight without trying and even make you feel nervous. On the flip-side of this, your thyroid can make too little thyroid hormone. This is called hypothyroidism. When you have too little thyroid hormone in your body, it can make you feel tired, you might gain weight and you may even be unable to tolerate cold temperatures.These two main disorders can be caused by a variety of conditions. They can also be passed down through families (inherited).

Thyroid Incidentaloma

Disease Name : Thyroid Incidentaloma , Symptoms : Nodule in thyroid, often asymptomatic., Signs : Nodule formation : Thyroid incidentalomas (TIs) are asymptomatic nodules discovered accidentally during imaging studies indicated for other reasons., Treatment : Percutaneous Ethanol Injection Therapy,When used in solid nodules, whether functioning or not, volume is usually reduced by approximately 50-70%, depending on the number of sessions, with a concomitant improvement in symptomatology.,Interstitial Laser Photocoagulation,Increasingly used, and based on long-term follow-up studies, interstitial laser photocoagulation can achieve approximately the same results as percutaneous ethanol injection therapy, but with a more benign side-effect profile due to the ability to contain the energy intranodularly., In case of large symptomatic multinodular goiters, the reference treatment remains surgery, total or near-total thyroidectomy, or radioiodine therapy, Pathophysiology : Certain clinical features are regarded as highly suspicious of thyroid carcinoma in a patient with an incidentally discovered thyroid nodule or thyroid incidentaloma. These include (1) a nodule discovered in childhood or adolescence (2) nodule being discovered in a male patient, or (3) a nodule found in those with a history of exposure to radiation or (4) a nodule in a patient having a family history of medullary carcinoma of thyroid. The patients from an iodine-deficient areas are also at higher risk of thyroid malignancy., Epidemiology : There is a female preponderance and an increase in prevalence with age, reaching 30-40%, variable, NA, Complications : Thyroid cancer, Diagnostics : FNAC, MRI, CT, Differential diagnosis : ANAPLASTIC CARCINOMA OF THYROID, CHRONIC LYMPHOCYTIC(AUTOIMMUNE) THYROIDITIS, THYROID NODULE, disease description : A thyroid incidentaloma is defined as an unexpected, asymptomatic thyroid tumor discovered during the investigation of an unrelated condition. Palpable thyroid nodules are known to be frequent, with a 5% prevalence rate in the general population . Over the latest two decades the use of imaging procedures, especially ultrasonography (US) has been the culprit of an epidemic of thyroid incidentalomas . Thus, the clinician is confronted with a situation that necessitates managing a condition that the patient did not complain of. In the first part, this paper outlines the magnitude of the problem and updates the concept of US risk stratification of thyroid nodules based on the TIRADS (thyroid imaging reporting and data system) classification. The second part deals with the indications for US fine-needle aspiration biopsy (FNA), addresses specifically the problem of subcentimetric incidentalomas and microcarcinomas, and finally discusses the potential of nonsurgical therapeutic alternatives

Thyroid Nodule

Disease Name : Thyroid Nodule, Symptoms : hyperthyroidism : In some cases, thyroid nodules produce additional thyroxine, a hormone secreted by your thyroid gland. The extra thyroxine can cause symptoms of an overproduction of thyroid hormones (hyperthyroidism), such as palpitations, nervous, weight loss, diarrhea, difficulty sleeping & missed menstrual periods., Hypothyroidism : Thyroid nodules may also be associated with low thyroid hormone levels (hypothyroidism). Symptoms of hypothyroidism include fatigue, numbness and tingling in your hands, weight gain, dry, coarse skin and hair, constipation, depression & h heavy menstrual periods., NODULES : Most thyroid nodules don’t cause symptoms. In rare cases, nodules can grow big enough to cause symptoms such as trouble with swallowing or breathing, hoarseness, pain in the front of your neck & oitre., Signs : nan, Treatment : Non-diagnostic biopsies (Bethesda I) are considered cytologically inadequate. The absence of malignant cells should not be interpreted as a negative biopsy if scant follicular tissue is obtained. FNA is usually repeated in 4 to 6 weeks.,,Patients with benign nodules (Bethesda II), such as macrofollicular, colloid adenomas, nodular goiter, and Hashimoto thyroiditis, are usually followed without surgery. Periodic US monitoring initially at 12 to 24 months, with increasing intervals, is preferred. If the US shows highly suspicious findings, then FNA should be repeated within 12 months despite a benign initial biopsy.,,For nodules with indeterminate cytology (Bethesda III and IV), the approach varies with institutional practices. Some institutions obtain an additional FNA sample for molecular testing, while other centers repeat the FNA after 6 to 12 weeks. A radionuclide scan may also be obtained if repeat aspirates show only architectural atypia.For nodules that fall within the category of Bethesda V, suspicious for malignancy, treatment should include surgery. Molecular markers should not be used. Bethesda VI includes papillary cancer, MTC, thyroid lymphoma, anaplastic cancer, and cancer metastatic to the thyroid. These patients should also be referred for surgery, Pathophysiology : The pathophysiology of a thyroid nodule will vary depending on the lesion. Several disorders may cause thyroid nodules. The most common type is benign macrofollicular nodules, representing either monoclonal adenomas or colloid nodules in multinodular goiter. The latter represents the expansion of relatively monoclonal cells replicating in a nodular fashion.Follicular neoplasms may represent a diagnostic problem as these only differ from follicular carcinomas by lack of vascular or capsular invasion.The association between thyroid irradiation and tumorigenesis is well-known. Radiation may cause a wide range of somatic mutations that increase the risk of cancer, particularly in radiation-sensitive organs such as the thyroid. Compared to adults, children have a higher risk of thyroid cancer after irradiation; this is most likely due to the higher proliferative activity of the thyroid tissue in younger individuals.RET proto-oncogene translocations have been found in thyroid malignancies associated with ionizing irradiation. The presence of RET/PCT translocations has been described in follicular adenomas presenting after irradiation., Epidemiology : 4–7% to 67%., variable, Since researchers don’t know what causes the majority of thyroid nodules, you can’t prevent them in most cases.,,You can, however, try to decrease your risk of developing them by managing certain risk factors. For example, if you have obesity, talk to your healthcare provider about attaining a healthy weight for you. If you smoke cigarettes, try to quit. It’s also important to make sure you get enough iodine in your diet. If you use iodized table salt, you’re likely consuming enough.,,Studies have shown that people who take oral birth control and/or statins may have a reduced risk of developing thyroid nodules., Complications : hyperthyroidism, inflammation, NODULES, Diagnostics : FNAC, Thyroid Stimulating Hormone TSH, USG Thyroid, THYROID SCAN, PHYSICAL EXAMINATION, Differential diagnosis : Inflammatory neck masses, Thyroid cancer, tonsillar malignancy, disease description : The American Thyroid Association (ATA) defines the thyroid nodule as a discrete lesion within the thyroid gland. It is radiologically distinct from the surrounding thyroid parenchyma. Nodules may be solitary, multiple, cystic, or solid.Nodules in the thyroid gland are a common entity and are detected in approximately 5% to 7% of the adult population by physical examination alone. However, autopsy data have shown a 50% prevalence of thyroid nodules larger than one centimeter in patients without previously diagnosed thyroid disease.Nodules are found with increasing frequency, likely due to the widespread use of modern imaging modalities, particularly ultrasound (US), but also computed tomography (CT), magnetic resonance imaging (MRI), and positron emission tomography (PET).Although more than 90% of detected nodules are clinically insignificant benign lesions,  thyroid nodules are clinically important as they may represent thyroid cancer in approximately 4.0% to 6.5% of cases.

Thyroid Storm

Disease Name : Thyroid Storm, Symptoms : coma : If untreated, the affected person may fall into a coma., congestive heart failure (CHF) : Congestive heart failure may occur and lead to hypotension and shock, delirium mania : Hyperthyroidism is frequently associated with : irritability, insomnia, anxiety, restlessness, fatigue, impairment in concentrating and memory, these symptoms can be episodic or may develop into mania, depression and delirium., Tachycardia : Rapid heart rate that can exceed 140 beats per minute., fever : A temperature between 104 degrees to 106 degrees Fahrenheit is common., Signs : nan, Treatment : Therapy to control increased adrenergic tone : Beta-blocker,Therapy to reduce thyroid hormone synthesis : Thionamide,Therapy to reduce the release of thyroid hormone : Iodine solution,Therapy to block peripheral conversion of T4 to T3 : Iodinated radiocontrast agent, glucocorticoid, PTU, propranolol,Therapy to reduce enterohepatic recycling of thyroid hormone : Bile acid sequestrant, Surgery may be required in patients with Graves disease to treat hyperthyroidism. These patients must be pretreated with beta-blockers, glucocorticoids, and iodine formulas. Surgery is usually done after 5 to 7 days., Pathophysiology : Thyroid storm is rare. It develops in people who have hyperthyroidism but aren’t receiving appropriate treatment. This condition is marked by the extreme overproduction of the two hormones produced by the thyroid gland. Not all people with hyperthyroidism will develop thyroid storm., Epidemiology : between 0.57 and 0.76 cases/100, 000 persons per year., variable, Not all cases of thyroid storm are preventable, but if you have hyperthyroidism, there are things you can do to try to prevent thyroid storm, including : ,,Always taking your medication as prescribed by your healthcare provider.,Seeing your healthcare provider regularly to make sure your treatment is working.,Managing your stress.,Thyroid storm can be caused by your body’s stress response to surgery or anesthesia. Because of this, your healthcare provider may give you antithyroid medication before you have surgery to try to prevent thyroid storm.,,If you have hyperthyroidism and are having thyroid surgery (thyroidectomy), your provider will most likely give you certain medication before the surgery to try to prevent thyroid storm., Complications : Arrhythmias, coma, delirium, seizures, Diagnostics : Free T3, Free T4, Thyroid Stimulating Hormone TSH, ECG, LIVER FUNCTION TEST LFT, CT HEAD, CHEST X RAY, Differential diagnosis : infection, Neuroleptic malignant syndrome, PHEOCHROMOCYTOMA, Psychosis, sepsis, disease description : Thyroid storm, also known as thyrotoxic crisis, is an acute, life-threatening complication of hyperthyroidism that presents with multi-system involvement. The mortality associated with thyroid storm is estimated to be 8 to 25% despite modern advancements in its treatment and supportive measures. Thus, it is very important to recognize it early and start aggressive treatment to reduce mortality. This activity reviews the tools available to assist with the diagnosis and management of thyroid storms and highlights the role of the interprofessional team in caring for affected patients

Thyroiditis

Disease Name : Thyroiditis, Symptoms : hyperthyroidism : The hypothyroid phase of thyroiditis can be long-lasting and may become permanent. If your thyroid cells are damaged and thyroid hormone levels fall, you might experience the symptoms of hypothyroidism, which include fatigue, constipation, depression, unexplained weight loss, dry skin, increased sensitivity to cold, & muscle weakness., THYROTOXICOSIS : The thyrotoxic phase of thyroiditis is usually short, lasting one to three months. If your thyroid cells are damaged quickly and there’s a leak of excess thyroid hormone, you might experience symptoms of hyperthyroidism (overactive thyroid), which include fast heart rate, increased appetite, unexplained weight loss, anxiety, irritability, trouble sleeping, increased sweating and sensitivity to heat & tremors., Signs : goitre : A goiter may be an overall enlargement of the thyroid, or it may be the result of irregular cell growth that forms one or more lumps (nodules) in the thyroid., Treatment : medication : Ibuprofen , Propranolol , Levothyroxine/Tetra idothyronine, Prednisolone, Atenolol , Treatment for patients with thyroiditis is typically aimed at alleviating the pain,and addressing the symptoms of the thyrotoxicosis such as tachycardia, ,palpations, and tremors. Non-steroidal anti-inflammatory drugs (NSAIDs) are,usually effective in alleviating thyroid tenderness. If pain is severe, a short,course of steroids (prednisone) can be considered. Given that the thyrotoxicosis,is due to release of preformed thyroid hormone, antithyroid drugs are usually not,effective. Rather, treatment with ß-blockers (atenolol or propranolol) to help,control the cardiovascular symptoms is useful. If there is evidence of overt hypothyroidism (elevated TSH with low free T4 ), ,treatment with levothyroxine is indicated at doses specific for size and age. The,goiter usually shows some decrease in size but can persist for years. In a,euthyroid patient, treatment with suppressive doses of levothyroxine is unlikely,to lead to a significant decrease in size of the goiter. Antibody levels fluctuate in,both treated and untreated patients and persist for years., Pathophysiology : Thyrotoxic phase : During this phase, your thyroid is inflamed and releases too many hormones, causing temporary thyrotoxicosis.Hypothyroid phase : Following the excessive release of thyroid hormones for a few weeks or months, your thyroid won’t have enough thyroid hormones to release. This leads to a lack of thyroid hormones or hypothyroidism. Hashimoto’s thyroiditis and radiation-induced thyroiditis usually permanently stay in the hypothyroid phase.Euthyroid phase : During the euthyroid phase, your thyroid hormone levels are normal. This phase may come temporarily after the thyrotoxic phase before going to the hypothyroid phase, or it may come at the end after your thyroid gland has recovered from the inflammation and can maintain a normal hormone level., Epidemiology : The most common form of thyroiditis is Hashimoto’s thyroiditis, which affects approximately 1% to 2% of people in the United States., variable, Unfortunately, most cases of thyroiditis can’t be prevented.,,If you have a condition that requires treatment using radioactive iodine or radiation therapy, talk to your healthcare provider about your risk of thyroiditis. You may be able to start with other treatments to avoid developing thyroiditis.,,If you take prescription drugs that can cause thyroiditis, talk to your provider about your risk and if you can stop taking them. You still may not be able to avoid thyroiditis., Complications : Sexual dysfunction, mental retardation, Goiter, Diagnostics : CRP, Erythrocyte Sedimentation Rate (ESR), Free T4, Triiodothyronine (T3) Tests, Thyroid Stimulating Hormone TSH, Total Leucocyte Count (TLC), ultrasound, Rbc antibody screen, THYROID PROFILE, thyroid antibodies, Differential diagnosis : acute pharyngitis, Thyroid cancer, THYROID NODULE, Tonsillitis, disease description : The term thyroiditis reflects inflammation of the thyroid gland. Thyroiditis can be classified based on the onset of symptoms, underlying etiology, and clinical symptoms. The most common cause of thyroiditis is an autoimmune disease. In the United States, Hashimoto thyroiditis is the most common cause of hypothyroidism.1 Thyroiditis can cause transient or permanent hypo and hyperthyroidism.

Thyrotoxicosis

Disease Name : Thyrotoxicosis, Symptoms : Tachycardia, high fever, Signs : Arrhythmias, Tachycardia, high fever, Treatment : Anti-thyroid drugs : Anti-thyroid drugs such as methimazole (Tapazole) and propylthiouracil (PTU) block your thyroid from making hormones. People who have hyperthyroidism may take this medication., Beta blockers : These drugs block the action of thyroid hormones on your body. They don’t change the level of hormones in your blood, but they can help control symptoms, such as rapid heartbeat and shakiness, that are caused by thyrotoxicosis., Glucocorticoids : Glucocorticoids are a type of corticosteroid. If you have thyroiditis that’s causing you pain, your provider may prescribe you glucocorticoids., Surgery : Your healthcare provider may recommend removing your thyroid gland through surgery (thyroidectomy). This will correct your hyperthyroidism, but it will usually cause hypothyroidism. People who have a thyroidectomy have to take thyroid hormone drugs for the rest of their lives to maintain appropriate hormone levels., Pathophysiology : Thyrotoxicosis results from thyroid hormone excess either from endogenous over-secretion of T3 and T4 or from exogenous ingestion of synthetic thyroid hormone. Thyroid hormone affects almost every tissue and organ system in the body by increasing basal metabolic rate and tissue thermogenesis by upregulating alpha-adrenergic receptors leading to an increase in sympathetic activity. Thyroid hormone causes increased expression of myocardial sarcoplasmic reticulum calcium-dependent ATP, increasing heart rate and myocardial contractility with the net effect of increased cardiac output. Decreased systemic vascular resistance (SVR) and decreased afterload results from arterial smooth muscle relaxation by metabolic end products, such as lactic acid, produced with increased consumption of oxygen. Decreased SVR leads to activation of the renin-angiotensin system, increasing reabsorption of sodium and expanding blood volume to increase preload. If left untreated, this may lead to left ventricular hypertrophy and congestive heart failure.Graves’ disease is an autoimmune disease comprised of antibodies that stimulate TSH receptors to cause excess secretion of thyroid hormones via a type II hypersensitivity reaction. In toxic multinodular goiter and toxic adenoma, autonomously functioning nodules over-secrete thyroid hormone independently without stimulation from TSH.In thyroiditis, thyrotoxicosis is caused by the release of preformed thyroid hormone into the circulation as inflammation destroys thyroid follicles. Gestational hyperthyroidism generally occurs in the first trimester of pregnancy, due to increased stimulation of the thyroid gland by excess human chorionic gonadotropin (HCG), which is similar in structure to TSH and binds the TSH receptor., Epidemiology : United States - 1.2%, including 0.5% overt thyrotoxicosis and 0.7% subclinical., Graves’ disease is the most common cause with an incidence of 20 to 50 cases per 100, 000 persons, variable, Most cases of thyrotoxicosis aren’t preventable. If you’re taking thyroid medication, you can prevent thyrotoxicosis by never taking more medication than your healthcare provider has prescribed you. Taking too much thyroid medication can lead to thyrotoxicosis., Complications : Thyroid storm, anxiety, Diagnostics : CRP, HISTOPATHLOGY, Thyroid Stimulating Hormone TSH, THYROID SCAN, USG, PHYSICAL EXAMINATION, Differential diagnosis : gestational thyrotoxicosis, Graves Disease or Hyperthyroidism, TOXIC ADENOMA, disease description : Thyrotoxicosis is a clinical state of inappropriately high levels of circulating thyroid hormones (T3 and/or T4) in the body from any cause.  It is often incorrectly used interchangeably with hyperthyroidism, which is a form of thyrotoxicosis caused by excessive endogenous thyroid hormone production. 

Tibial Plateau Fracture

Disease Name : Tibial Plateau Fracture, Symptoms : localized pain, localized swelling, DEFORMITY, Walking impairment, Signs : Tenderness, Treatment : (A)Conservative methods : are used for minimally displaced fractures, and those in elderly people. There is more and more trend towards accurate reduction and early mobilisation of these fractures.,(B) Surgical treatment : nan,of these fractures is a technically demanding,procedure, and needs variety of equipment and lot,of experience., Pathophysiology : Fractures of the tibial plateau are caused by a varus (inwardly angulating) or valgus (outwardly angulating) force combined with axial loading or weight bearing on knee. The classically described situation in which this occurs is from a car striking a pedestrians fixed knee ("bumper fracture"). However, most of these fractures occur from motor vehicle accidents or falls. Injury can be due to a fall from height in which knee forced into valgus or varus. The tibial condyle is crushed or split by the opposing femoral condyle, which remains intact. The knee anatomy provides insight into predicting why certain fracture patterns occur more often than others. The medial plateau is larger and significantly stronger than the lateral plateau. Also, there is a natural valgus or outward angulation alignment to the limb which coupled with the often valgus or outwardly angulating force on impact will injure the lateral side. This explains how 60% of plateau fractures involve the lateral plateau, 15% medial plateau, 25% bicondylar lesions. Partial or complete ligamentous ruptures occur in 15-45%, meniscal lesions in about 5-37% of all tibial plateau fractures., Epidemiology : Peak age is 30–40 years old in men and 60–70 in women., Tibial plateau fractures constitute 1% of all fractures., GOOD, Avoid trauma, Complications : deep vein thrombosis, compartment syndrome, Diagnostics : MRI, X RAY, CT SCAN, PHYSICAL EXAMINATION, Differential diagnosis : distal femur fractures, soft tissue injuries to anterior cruciate ligament, soft tissue injuries to the medial and lateral meniscus, tibial spine fractures, disease description : These are common fractures sustained in two wheeler accidents when one lands on the knee. Either or both condyles of tibia are fractured. The mechanism of injury is : (a) an indirect force causing varus or valgus force on the knee or (b) a direct hit on the knee. Types of fracture : These fractures commonly occur in six patterns (Schatzker types). Type I-IV involve only one condyle, lateral or medial. Type V and VI are more complex intercondylar fractures.

Tick Typhus Dermatology

Disease Name : Tick Typhus Dermatology, Symptoms : headache, Malaise, Rashes, fever, joint pain, regional lymphadenopathy, fever with chills, Signs : maculopapular rash, maculopapular eruption, Treatment : medication : Chloramphenicol , 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) ,•\tAlternative treatments : chloramphenicol is also effective and,has been recommended for Rocky Mountain spotted fever in ,pregnant women and children aged 8 years and under. ,General supportive measures are necessary in severe cases., Pathophysiology : The essential pathological lesion is produced by the multiplication of rickettsiae in the endothelial cells of small blood vessels, leading to obstruction, thrombosis, haemorrhage and perivascular inflammatory infiltration. The lesions are widely distributed but are often numerous in the skin, brain and heart. After an incubation period, which is usually between 5 and 7 days, the onset of fever is accompanied by headache, malaise, joint and stomach pains and, sometimes, mental confusion. Fever of 39–40°C lasts for 7–14 days. In some 80% of cases, the onset of fever coincides with the development of a small ulcer (the tache noire) at the site of the tick bite. The ulcer, which is 2–5 mm in diameter, has a black necrotic centre and a red areola. The regional lymph nodes are enlarged and tender. Three or four days later, a pink maculopapular eruption develops first on the forearms and then rapidly generalizes, involving the face, palms and soles. It increases in density for a few days and in severe cases may be haemorrhagic; rarely more severe reactions such as digital necrosis and pneumonia have been described., Epidemiology : nan, Complications : necrosis, PNEUMONIA, Diagnostics : SEROLOGIC TEST, PCR, complement fixation (CF) test, Differential diagnosis : fever, Rickettsial Infection, septicaemia, disease description : An acute febrile illness accompanied by an exanthema often preceded by a primary site of inoculation from a tick bite. In many countries, tick typhus is caused by Rickettsia conori, which is transmitted by the bites of a variety of ixodid ticks. Different genetic clades (strains) are endemic in the countries around the Mediterranean and in many parts of Africa, Asia and India.

Ticks (acari) Bite

Disease Name : Ticks (acari) Bite, Symptoms : muscle pain : Tickborne diseases can cause headache, fatigue, and muscle aches., Skin rashes : A small bump may appear at the site of the tick bite. But if it develops into a rash, that may indicate illness. A rash usually appears 3-14 days after the tick bite but it can look different depending on the type of tick. Watch for small reddish or purplish spots, or expanded rashes that look like a bullseye., petechiae : Small reddish or purplish spots (called petechiae) happen in Rocky Mountain spotted fever., fever with chills : Tick-borne relapsing fever (TBRF) is an infection caused by certain species of Borrelia bacteria, which can be transmitted by tick bite. The main symptoms of TBRF are high fever, headaches, and muscle and joint aches., Signs : nan, Treatment : medication : Doxycycline , Tick removal, Except for viral fevers and babesiosis, tetracycline is the antibiotic ,of choice for most tick-borne diseases. Delayed antibiotherapy can ,be fatal especially in Rocky Mountain spotted fever, so therapy ,should be started quickly in case of fever and headache in an ,endeminc area, without awaiting laboratory confirmation., Pathophysiology : The pathophysiology of acute tick bite lesions remains unclear. Tick biting parts can reach into the deep dermis, exposing these tissue layers to mouthpart and salivary antigens. Reactions may vary, depending on the interaction between host and a particular tick species. At the point of penetration of the tick mouthparts there is coagulation necrosis of the epidermis and papillary dermis. Surrounding the hypostome is the homogeneous cement. The punctured epidermis shows parakeratosis, spongiosis and frequently pseudoepitheliomatous hyperplasia. There is marked dilatation of upper dermal blood vessels, and a dense perivascular infiltrate of neutrophils and lymphocytes. Histology of the bite site several weeks after removal of the tick shows a perivascular and periadnexal infiltrate of lymphocytes, plasma cells and histiocytes. Foreign-body giant cells may also be present in the infiltrate. If the hypostome has been damaged during removal of the tick, fragments of the mouthparts may be seen., Epidemiology : The overall prevalence of ticks was found to be 73.4%, Ticks are responsible for approximately 95% of all locally acquired vectorborne diseases, variable, To Do : Avoidance of tick-infested areas, use of repellents and rapid tick ,removal are the key points of primary prevention., Complications : Anaphylaxis, secondary infection, Diagnostics : Antibody Serology Tests, PHYSICAL EXAMINATION, PCR tests, Differential diagnosis : erythema migrans, Influenza, Leptospirosis, MEASLES, meningococcemia, disease description : Ticks are large acarines, which are blood-sucking ectoparasites of vertebrates. They are important vectors of diseases such as tick- borne relapsing fever, and in a number of viral, rickettsial. Ixodid ticks have four stages in their life cycle : egg, larva, nymph and adult. 

Tinea Capitis Dermatology

Disease Name : Tinea Capitis Dermatology, Symptoms : hair loss, itching, Signs : Scaling, papules, alopecia, appearance varies from a few dull grey, broken-off hairs with a little scaling, Treatment : medication : Griseofulvin , Terbinafine , Itraconazole , First line ,• Terbinafi ne : <10 kg, 62.5 mg; 10–20 kg, 125 mg; >20 kg, ,250 mg. All given daily for 4 weeks ,• Itraconazole 2–4 mg/kg/day for 4–6 weeks ,• Griseofulvin 10 mg/kg for 6 weeks (20 mg/kg considered ,in some T. tonsurans and T. schoenleinii infections) , Second line ,• Itraconazole 5 mg/kg in weekly pulses for 2–3 rounds, Pathophysiology : The principles of hair invasion and the distinctions between in vitro and in vivo activity have been already outlined (see section on the basic biology of dermatophytosis). The spores of ringworm fungi causing tinea capitis can be demonstrated in the air in close proximity to patients with the condition. It is highly likely that scalp hair acts as a trapping device, and it is known that contamination of hair without demonstrable clinical findings may occur among classmates of children with tinea capitis. From experimental work on M. audouinii , it is clear that if actual hair infection is to occur, invasion of the stratum corneum of the scalp skin must first develop. Trauma assists inoculation, which is followed, after approximately 3 weeks, by clinical evidence of hair shaft infection. Infection spread to other follicles, then for a period of variable duration the infection persists but does not spread further. Finally, there is a period of regression with or without an infl ammatory phase. Ectothrix type. This may be a small-spored ectothrix caused by M. audouinii (including variants previously called M. audouinii var. rivalieri ), M. canis (including variants previously called M. canis var. distortum ), M. equinum or M. ferrugineum . In this type, the hair shaft is invaded mid-follicle. The intrapilary hyphae continue to grow inwards towards the bulb of the hair. Secondary, extrapilary hyphae burst out and grow in a tortuous manner over the surface of the hair shaft, which is growing outwards continuously. Endothrix type. The endothrix type may be caused by T. tonsurans , T. soudanense , T. violaceum, T. yaoundei , T. gourvilii or T. rubrum (rare). Intrapilary hyphae fragment into arthroconidia up to 8 µm in diameter, which are entirely contained within and completely fi ll the hair shaft. Hair thus affected is especially fragile, and breaks off close to the scalp surface. This type is non-fl uorescent. Favus. Favic type is caused by T. schoenleinii. Broad, regularly septate hyphae and air spaces are seen in the hair shaft, but disarticulated arthroconidia are absent. The affected hair is less damaged than in other types, and may continue to grow to considerable lengths. Greenish grey fl uorescence is present. Air spaces are characteristic and fungal hyphae form large clusters in the vicinity of hair follicles., Epidemiology : the incidence of tinea capitis is 8.7% among children aged 4-14 years, "To Do : .Frequent hand-washing and disinfecting surfaces help, but nothing is a guarantee.,.Two rotavirus vaccines were authorised for prevention of rotavirus .,.Hygiene improvements and disease tracking.,.Vaccination,.To reduce the spread of rotavirus, wash your hands thoroughly and often — especially after you use the toilet, change your childs diaper or help your child use the toilet. But even strict hand-washing doesnt offer any guarantees.,. And commonly used alcohol-based hand sanitizers have little effect on rotavirus..,.", Complications : nan, Diagnostics : MICROSCOPIC EXAMINATION with KOH, Differential diagnosis : ECZEMA, psoriasis, seborrhoeic dermatitis, disease description : This is ringworm of the scalp in which the essential feature is invasion of the hair shafts by a dermatophyte fungus. Ringworm of the beard area, although essentially similar, is discussed separately. Those species of dermatophyte fungi most likely to cause tinea capitis vary from region to region. Moreover, in any given location, the species may change with time, particularly as new organisms are introduced by immigration. In tinea capitis, anthropophilic species predominate. The principal feature of tinea capitis in recent years has been the rise of M. canis as the dominant organism in infections in some parts of Europe , and the spread of T. tonsurans in urban communities in the USA and western Europe, particularly the UK, and in some other European countries. Tinea capitis is predominantly an infection of children, although adult cases are seen, particularly with T. tonsurans infections.

Tinea Corporis Dermatology

Disease Name : Tinea Corporis Dermatology, Symptoms : pruritus, Signs : hypopigmentation, scaling of skin, Characteristic lesions are circular, usually sharply marginated with a raised edge, pruritus of the skin, Treatment : medication : Griseofulvin , Terbinafine , Itraconazole , Localized disease, recent onset ,• Topical terbinafi ne twice daily for 2 weeks , Or ,• Topical azole once or twice daily for 2–4 weeks , Widespread disease , First line ,• Oral terbinafi ne 250 mg/day 2–3 weeks , Or ,• Itraconazole 100 mg/day 2–4 weeks , Second line ,• Griseofulvin 1 g/day for 4 weeks, Pathophysiology : The source of infection is usually an active lesion on an animal or on another human, although fomite transmission is known to occur, and infection from soil is a well-established if unusual occurrence. In young children infected with Trichophyton rubrum and Epidermophyton fl occosum , half of the infections may come from their parents. In geriatric wards, epidemics may occur. Spread from existing localized infection (e.g. feet, groins, scalp and nails) is not uncommon. Invasion of the skin at the site of infection is followed by centrifugal spread through the horny layer of the epidermis. After this period of establishment (incubation), which lasts 1–3 weeks, the tissue responses to infection become evident. The characteristic annular appearance of many ringworm infections results from the elimination of the fungus from the centre of the lesion, and the subsequent resolution of the infl ammatory host response at that site. This area usually becomes resistant to reinfection, although a second wave of centrifugal spread from the original site may occur with the formation of concentric erythematous infl ammatory rings. The site of infection is typically on exposed skin, unless the infection represents an extension from a pre-existing infection. In such cases, infection may spread from the scalp, down the neck on to the upper trunk, or from the groins on to the buttocks and lower trunk., Epidemiology : nan, Complications : abscess, Diagnostics : MICROSCOPIC EXAMINATION with KOH, Differential diagnosis : Alopecia Areata, Discoid Lupus Erythematosus., Lichen Planus, disease description : Tinea corporis is ringworm of the glabrous skin. The clinical manifestations result from invasion and proliferation of the causal fungi in the stratum corneum. Terminal hair in the affected parts may be invaded. By defi nition, it includes lesions of the trunk and limbs, excluding ringworm of specialized sites such as the scalp, feet and groins, which are considered later.

Tinea

Disease Name : Tinea, Symptoms : nail changes : Tinea unguium is increasingly prevalent with increased age. It can present as several different patterns : Lateral onychomycosis. A white or yellow opaque streak appears at one side of the nail. Subungual hyperkeratosis. Scaling occurs under the nail. Distal onycholysis. The end of the nail lifts up. The free edge often crumbles. Superficial white onychomycosis. Flaky white patches and pits appear on the top of the nail plate. Proximal onychomycosis. Yellow spots appear in the half-moon (lunula). Complete destruction of the nail. Onychomycosis may look similar to nail dystrophy due to trauma, psoriasis, lichen planus, aging changes and even melanoma. Fungal infection is quite common in damaged nails, so antifungal therapy does not always return the nail to normal even when culture is positive., Tinea Versicolor : For most people, tinea versicolor causes mild symptoms. These may include : Skin discoloration, usually on your back, chest and abdomen. Discolored patches can appear anywhere on your body and be shades of pink, yellow, brown, tan or white. Itching at or around areas of skin affected by tinea versicolor. Excessive sweating. Patches of skin that may dry out and form scales. Patches of skin that don’t darken or tan in the sun., Tinea capitis : Tinea capitis may affect all or part of your child’s scalp. Symptoms may include : Swollen red patches, dry, scaly rashes, severe itchiness, patches of hair loss (alopecia), flaking scalp that resembles dandruff, low fever, swollen lymph nodes., Jock itch : Symptoms of jock itch are a spreading rash that begins in the crease of the groin and moves down the upper thigh and buttocks. A rash whose center tends to clear as the rash spreads. A rash that may be full or partially ring shaped. A rash bordered with small blisters. Itchiness. Scaly skin. A rash that might be red, brown, purple or gray depending on your skin color., Tinea nigra : Tinea nigra is clinically characterized by a sharply marginated, light-brown to black, nonscaly, oval-shaped macule. In some patients, this macule is mottled and might be irregular in shape. Although lesions present usually as single and asymptomatic and they are mainly observed on the palmar surface., Tinea barbae : Tinea barbae causes red, ring-shaped rashes on the outer layer of your skin (epidermis). The rash may be itchy, but it isn’t painful., Tinea faciei : Tinea faciei resembles tinea corporis (ringworm). It may be acute (sudden onset and rapid spread) or chronic (slow extension of a mild, barely inflamed, rash). There are round or oval red scaly patches, often less red and scaly in the middle or healed in the middle. It is frequently aggravated by sun exposure. It may also present as a kerion (fungal abscess)., Tinea pedis : Tinea pedis tends to be asymmetrical, and may be unilateral. It usually presents in one of three ways : Itchy erosions and/or scales between the toes, especially between 4th and 5th toes Scale covering the sole and sides of the feet (hyperkeratotic/moccasin type, usually caused by T. rubrum) Small to medium-sized blisters, usually affecting the inner aspect of the foot (vesiculobullous type). It can also uncommonly cause oozing and ulceration between the toes (ulcerative type), or pustules (these are more common in tinea pedis due to T. interdigitale than that due to T. rubrum)., Tinea manuum : The most common symptoms of tinea manuum are itchy, round patches on the back of your hands. On lighter skin, the patches may appear red or pink. On darker skin, the patches may look brown or gray. The patches may develop into a series of rings or circles with central clearings. The rings may have raised, scaly borders., Signs : nan, Treatment : Ketoconazole (Ketoconazole, Nizoral, others) cream, gel or shampoo,Ciclopirox (Loprox, Penlac) cream, gel or shampoo,Fluconazole (Diflucan) tablets or oral solution,Itraconazole (Onmel, Sporanox) tablets, capsules or oral solution,Selenium sulfide (Selsun) 2.5 percent lotion or shampoo, Pathophysiology : Fungal Invasion : Dermatophyte fungi, including species like Trichophyton, Microsporum, and Epidermophyton, are the primary causative agents of tinea. These fungi have the ability to invade and thrive on keratinized tissues such as the skin, hair, and nails. They secrete enzymes like keratinases that break down the protein keratin, which is a major component of these tissues.Transmission and Entry : Tinea is highly contagious and can be transmitted through direct contact with an infected person, animal, or contaminated surfaces like towels, combs, and clothing. Once the fungal spores come into contact with the susceptible hosts skin, they can find their way into the outermost layers of the skin.Inflammatory Response : The presence of the fungi triggers an inflammatory response from the hosts immune system. This immune response involves the activation of various immune cells and the release of inflammatory mediators, such as cytokines and chemokines. These molecules attract immune cells to the infected area, leading to redness, itching, and swelling.Hyphae Formation : Once the dermatophyte fungi penetrate the skin, they grow hyphae (thread-like structures) that invade the keratinized layers. These hyphae secrete enzymes that help the fungi break down and digest keratin, which provides the fungi with a source of nutrition. This process weakens the structural integrity of the skin, hair, or nails, leading to the characteristic symptoms of tinea., Epidemiology : 26.9%, variable, It is important to remember that tinea is contagious. Suggestions on how to prevent the spread of infection to others include : ,,Treat tinea infections with antifungal cream.,Wash your hands after touching infected areas.,Do not share towels.,Do not walk around barefoot if you have tinea pedis (tinea of the feet).,Clean the shower, bath and bathroom floor after use., Complications : secondary infection, Diagnostics : Protein, FUNGAL CULTURE, TISSUE MICROSCOPY, Differential diagnosis : Candidosis, nummular dermatitis, pityriasis rosea, psoriasis, seborrhoeic dermatitis, seborrhoeic dermatitis, disease description : Tinea is a contagious fungal skin infection. The most commonly affected areas include the feet, groin, scalp and beneath the breasts. Tinea can be spread by skin-to-skin contact or indirectly through towels, clothes or floors. Tinea is also known as ringworm, which is a misleading name as no worm is involved.Tinea variants-Tinea pedis (foot)-Athletes foot (also known as "ringworm of the foot", tinea pedum, and "moccasin foot")Tinea unguium (nails) Tinea manuum (hand)-(or tinea manus) Tinea cruris (groin)Tinea unguium (nails)Tinea manuum (hand)-(or tinea manus)Tinea corporis (body)Tinea capitis (scalp)Tinea cruris (groin)Tinea faciei (face)Tinea barbae (beard)Tinea imbricata (overlapping pattern)Tinea nigra (black)Tinea versicolor (various colors)Tinea incognito (disguised)

Tolosa–hunt Syndrome

Disease Name : Tolosa–hunt Syndrome, Symptoms : headache : Many individuals with Tolosa-Hunt syndrome experience the sudden onset of severe periorbital headache., ptosis : Drooping of the upper eyelid is seen in Tolosa-Hunt syndrome., proptosis : Affected individuals may also exhibit protrusion of the eye., OPHTHALMOPLEGIA : Headache is followed by decreased eye movements., paralysis : Paralysis (palsy) of certain cranial nerves., Signs : nan, Treatment : Corticosteroids are the treatment of choice for Tolosa-Hunt syndrome (THS), usually providing significant pain relief within 24–72 hours of therapy initiation. Ophthalmoparesis usually requires weeks to months for resolution; indeed, ophthalmoparesis may not completely resolve in some cases depending on the degree of inflammation and the aggressiveness of therapy. For refractory cases, azathioprine (Imuran), methotrexate, or radiation therapy has been employed., Neuro-ophthalmology evaluation is helpful to confirm the diagnosis of Tolosa-Hunt syndrome and to exclude other etiologies of presenting symptoms. Consultation with a neurosurgeon may be useful in cases requiring biopsy., Pathophysiology : Nonspecific inflammation (noncaseating granulomatous or nongranulomatous) within the cavernous sinus or superior orbital fissure is the cause of the constant pain, which characterizes the onset of this disorder. Ophthalmoparesis or disordered eye movements occur when cranial nerves III, IV, and VI are damaged by granulomatous inflammation. Pupillary dysfunction may be present and is related to injury to the sympathetic fibers in the cavernous portion of ICA or parasympathetic fibers that surround the oculomotor nerve. Trigeminal nerve involvement (primarily V1) may cause paresthesias of the forehead. Pathological involvement beyond the cavernous sinus, superior orbital fissure, or apex of the orbit occurs rarely, and the disorder is part of a continuum with idiopathic orbital pseudotumor, with which it shares histopathologic features. Spontaneous remissions can occur; relapses may occur in up to 40% of the patients., Epidemiology : THS affects males and females equally., one case per million per year, Tvariable, Patients should understand that this is an idiopathic condition that is usually self-limited. Relapses may occur (30-40% of patients may experience relapse), and patients should know that the course of any relapse often follows the original event but may require additional testing., Complications : visual defects, Diagnostics : Complete Blood Count CBC, Erythrocyte Sedimentation Rate (ESR) test, VISUAL ACUITY TEST, MRI, fluorescent treponemal antibody absorption (FTA-ABS) tests, Differential diagnosis : Meningitis, NEUROSARCOIDOSIS, Polyarteritis Nodosa, systemic lupus erythematosus (SLE), Varicella zoster, disease description : Tolosa Hunt syndrome (THS) is described as severe and unilateral periorbital headache associated with painful and restricted eye movements. Synonyms for Tolosa Hunt syndrome include painful ophthalmoplegia, recurrent ophthalmoplegia, ophthalmoplegia syndrome.

Tornwaldt’s Disease (pharyngeal Bursitis)

Disease Name : Tornwaldt’s Disease (pharyngeal Bursitis), Symptoms : nasal symptoms : When there is an enlargement of the cyst, it causes symptoms like nasal obstruction, post-nasal discharge with foul-smelling odour., "ear problem : Tornwaldts disease causes ear problems such as blockage of the Eustachian tube causing otalgia and secretory otitis media, retro-orbital pain.", systemic symptoms : The symptoms are occipital headache, cough, middle ear effusion, cervical myalgia, and halitosis, i.e. bad breath., Signs : nan, Treatment : Antibiotics are given to treat infection and marsupialization,of the cystic swelling and adequate removal of its,lining membrane, Pathophysiology : Anatomical Features : Tornwaldts cyst is a remnant of the embryonic notochord and is lined with epithelial cells. It is located close to the pharyngeal tonsil (adenoid) and is covered by the mucous membrane of the nasopharynx. The proximity to the adenoid tissue makes the cyst susceptible to irritation, inflammation, and infection.Obstruction and Stagnation : It is thought that the Tornwaldts cyst may become obstructed or blocked, preventing proper drainage of its contents. This obstruction could be due to various factors, such as mucus accumulation, infection, or anatomical variations. Stagnation of fluid within the cyst may contribute to the development of inflammation and secondary infection.Infection and Inflammation : Infection is believed to play a significant role in the development of Tornwaldts disease. The obstruction of the cyst can create an environment conducive to bacterial or viral growth. Over time, this can lead to localized infection and inflammation within the cyst and the surrounding nasopharyngeal tissues., Epidemiology : It has an incidence of 3% in the adult population, GOOD, NA, Complications : Halitosis, occipital headache, Diagnostics : MRI, MRI, CT, Nasal endoscopy, Differential diagnosis : Cysts, MENINGOCOELE, mucous retention cyst, tumors, disease description : It is infection of the pharyngeal bursa which is a median recess representing attachment of notochord to endoderm of the primitive pharynx. Pharyngeal bursa is located in the midline of posterior wall of the nasopharynx in the adenoid mass.?

Torsade De Pointes

Disease Name : Torsade De Pointes, Symptoms : Dizziness : Affected patients experience diziness., palpitations : Torsade de pointes causes hearts to race., Signs : syncope : In more serious cases, torsades de pointes can cause a lack of consciousness, known as syncope, or even a cardiac arrest, which can lead to death., Treatment : Temporary or permanent cardiac pacemaker.,Implantable cardioverter defibrillator (ICD).,Electrical cardioversion.,Defibrillation., Magnesium and/or potassium.,Isoproterenol.,Beta blockers like Nadolol (Corgard®)., Pathophysiology : The proposed mechanism for Torsades de Pointes involves inhibition of the delayed rectifier potassium current. This leads to an excess of positive ions within the cellular membrane causing a prolonged repolarization phase. If an ectopic beat is generated during this prolonged repolarization phase, known as an R on T phenomenon, this can result in Torsades de Pointes. Both congenital and drug-induced QT prolongation affect the cellular membrane in similar fashions by blocking the potassium channel. Torsades de Pointes is slightly different from ventricular fibrillation in that it can spontaneously resolve. However, Torsades de Pointes can ultimately progress into venticular fibrillation if left untreated., Epidemiology : Anywhere from one in 2, 000 people to one in 20, 000 people may have been born with a genetic problem that can lead to Torsades de Pointes., variable, You can reduce your risk of Torsades de Pointes in these ways : ,,Stop taking medicines that can cause Long QT syndrome. (Your provider can find an alternative.),Increase your levels of calcium, magnesium and potassium if your provider recommends it., Complications : sudden cardiac death, syncope, ventricular fibrillation, Diagnostics : ECG, ECG, Electrocardiography (EKG), Differential diagnosis : syncope, ventricular tachycardia, disease description : Torsades de pointes is a type of very fast heart rhythm (tachycardia) that starts in your heart’s lower chambers (ventricles). Unlike a normal pulse rate of 60 to 100 beats a minute, a fast heartbeat in your ventricles (ventricular tachycardia) is more than 100 beats a minute.

Torsion Of The Gall Bladder

Disease Name : Torsion Of The Gall Bladder, Symptoms : nausea, vomiting, fever, Signs : abdominal distension, ABDOMINAL MASS, Treatment : Early diagnostic imaging investigations and prompt cholecystectomy is the aim in order to achieve best patient outcome. Treatment consists of cholecystectomy with prior detorsion to avoid injury to the common duct, Pathophysiology : Shows a  floating gallbladder, with a long cystic duct, and a floating kidney, with cholelithiasis and perforation of the gall-bladder . Etiologically, two types of gallbladder have a tendency to undergo volvulus - those with a wide mesentery and those in which the mesentery covers only the cystic duct and artery. Both of these conditions allow the gallbladder to float and result in volvulus. Loss of fat and the liver atrophy that may occur with advancing age can cause an acquired gallbladder mesentery , Epidemiology : 65-75 year old group, and a 3 : 1 female predominance, GOOD, Complications : VOLVULUS, Diagnostics : MRI Abdomen, ultrasound, CT SCAN, Differential diagnosis : CHOLECYSTOSES, CHOLEDOCHAL CYST, CHOLELITHIASIS, disease description : Gallbladder torsion is defined as the rotation of the gallbladder on its mesentery along the axis of the cystic duct and cystic artery . It is an uncommon clinical entity and a difficult condition to diagnose preoperatively. Since its first description in 1898 by Wendell, there have been over 500 documented cases in the literature

Torsion Or Rupture Of Ovarian Cyst

Disease Name : Torsion Or Rupture Of Ovarian Cyst, Symptoms : Dizziness : Some women with an ovarian cyst feel lightheaded and dizzy. This usually occurs when the cyst has ruptured or become twisted, and your body reacts to the pain., nausea, vomiting, Frequent micturition : If the cysts press on the bladder, patients experience urinary frequency., Abdominal Pain : Ruptured ovarian cysts usually cause lower abdominal pain in one side, a known symptom of appendicitis., sever bleeding : A cyst that bursts open (ruptures) can cause severe pain and bleeding inside the pelvis., Signs : abdominal lump : Emergency surgery is needed when a cyst has burst and bled into the abdomen or there is ovarian torsion., Treatment : The gold standard to treat ovary torsion is surgery, and this is also the only way to confirm the torsion. There are two surgical methods, laparoscopy and laparotomy. A laparoscopic approach has become a popular procedure. However, if cancer of the ovary or fallopian tube is suspected, a laparotomy should be done . While performing the surgery, it is necessary to assess ovarian viability and preserve its function. The only way to determine the viability of a torsed ovary during surgery is by gross visual inspection. In the conventional view of point, dark and enlarged ovaries may have vascular and lymphatic congestion, and may seem nonviable. However, multiple studies have suggested that even those black or blue-like ovaries may retain ovarian function following detorsion. Postoperative follow-up with ultrasound showed over 80% of patients had normal follicular development after detorsion . Animal study showed that there may not be total occlusion of the artery in ovarian torsion even with venous and lymphatic congestion . In recent years, the mainstay of the treatment for ovarian torsion has been surgical evaluation and preserving ovarian function., Pathophysiology : Ovarian torsion occurs when an ovarian cyst or mass presents and rotates both the infundibulopelvic ligament and the UO ligament. The cyst or mass is usually a benign lesion over 5 cm in diameter. Torsion can also occur in normal ovaries, however, particularly in premenarchal girls who have elongated infundibulopelvic ligament. However, the occurrence of ovarian torsion may decrease thereafter because the ligament shortens when premenarchal girls mature to puberty., Epidemiology : 2%–15% of patients who had surgical treatment of adnexal masses had ovarian torsion., variable, Taking medications that contain hormones (such as birth control pills) will stop ovulation. Some studies suggest that the pill reduces the recurrence of certain cysts.,,Usually, ovarian cysts are harmless enough that prevention shouldn’t be a concern. Instead, take note of any symptoms that may indicate a cyst and tell your provider about them. Schedule regular pelvic exams so that your provider can find any cysts that require treatment., Complications : bleeding, anemia, septicemia, Diagnostics : Complete Blood Count CBC, Color Doppler, ultrasound, USG Pelvis, MRI PELVIS, Differential diagnosis : ABDOMINAL TRAUMA, abscess, appendicitis, DIVERTICULITIS, Ectopic pregnency, PID, Pyelonephritis, disease description : Ovarian torsion. Cysts that become large can cause the ovary to move. This increases the chance of painful twisting of the ovary (ovarian torsion). If this happens, you might have sudden, severe pelvic pain and nausea and vomiting. Ovarian torsion can also reduce or stop blood flow to the ovary.Cyst rupture. A cyst that bursts open (ruptures) can cause severe pain and bleeding inside the pelvis. The larger the cyst, the greater the risk of rupture. Vigorous activity that affects the pelvis, such as vaginal sex, also increases the risk of rupture.

Total Anomalous Pulmonary Venous Connection

Disease Name : Total Anomalous Pulmonary Venous Connection, Symptoms : Breathing difficulty : A baby with TAPVR may have breathing difficulty., Signs : "cyanosis : The babys skin may look gray or blue due to low oxygen levels.", Treatment : medication : Digoxin , Babies with TAPVR will need surgery to repair the defect. The age at which the surgery is done depends on how sick the child is and the specific structure of the abnormal connections between the pulmonary veins and the right atrium. The goal of the surgical repair of TAPVR is to restore normal blood flow through the heart. To repair this defect, doctors usually connect the pulmonary veins to the left atrium, close off any abnormal connections between blood vessels, and close the atrial septal defect., Surgery is done right away for newborns with obstructed total anomalous pulmonary venous return. Some of these children will need extracorporeal life support (ECMO) prior to surgery because of their blood flow instability., Pathophysiology : Supracardiac– In supracardiac TAPVR, the pulmonary veins come together and form an abnormal connection above the heart to the superior vena cava, which is a main blood vessel that brings oxygen-poor blood from the upper part of the body to the heart. In this type of TAPVR, a mixture of oxygen-poor and oxygen-rich blood returns to the right atrium through the superior vena cava.Cardiac – In cardiac TAPVR, the pulmonary veins meet behind the heart and connect to the right atrium. The coronary sinus, which is a vein that helps bring oxygen-poor blood from the heart muscle back to the heart, helps connect the pulmonary veins to the right atrium in this type of TAPVR.Infracardiac – In infracardiac TAPVR, the pulmonary veins come together and form abnormal connections below the heart. A mixture of oxygen-poor blood and oxygen-rich blood returns to the right atrium from the veins of the liver and the inferior vena cava, which is the main blood vessel that brings oxygen-poor blood from the lower part of the body to the heart., Epidemiology : The incidence of TAPVC ranges from 0.6 to 1.2 per 10, 000 live births . Among newborns with congenital heart disease, the incidence of TAPVC ranges between 0.7 and 1.5 percent, variable, NA, Complications : atrial septal defect, cyanosis, respiratory distress, Fetal death, Diagnostics : 2-D Echo, X RAY CHEST, CARDIAC CATHETERIZATION, Differential diagnosis : ATRIAL SEPTAL DEFECTS, mitral stenosis, mitral stenosis, VENTRICULAR SEPTAL DEFECTS, disease description : Total anomalous pulmonary venous return (TAPVR) is a rare congenital (present at birth) defect. With TAPVR, all four pulmonary veins do not connect normally to the left atrium. Instead, the four pulmonary veins drain abnormally to the right atrium (right upper chamber) through an abnormal (anomalous) connection.

Total Anomalous Pulmonary Venous Drainage

Disease Name : Total Anomalous Pulmonary Venous Drainage, Symptoms : failure to thrive, infections, Feeding Difficulty, Signs : heart murmur, Tachycardia, cyanosis, pulmonary edema, Treatment : The surgical principle is to re-establish the pulmonary ,venous drainage into the left atrium. The exact operative ,technique depends on the anatomy and type of TAPVD., Pathophysiology : the entire oxygenated blood from the lungs returns to the right atrium. Therefore, communication between the left and right atrium is crucial for survival in TAPVC. Mixing of the oxygenated and deoxygenated blood occurs in the right atrium, which is then shunted right to the left at the level of atria. Therefore, the left atrium and aorta get mixed blood,  which leads to cyanosis in patients with TAPVC., Epidemiology : (TAPVD) ,accounts for only l–2% of congenital heart disease., Complications : heart failure, hypertension, Diagnostics : ECG, doppler echocardiography, CARDIAC ANGIOGRAPHY, Differential diagnosis : acrocyanosis, mitral stenosis, disease description : the pulmonary venous drainage has become disconnected from the left atrium and drains into the systemic venous circulation at some other point (inferior vena cava, superior vena cava, coronary sinus or right atrium). Typically, TAPVD presents after the first week of life with cyanosis that is mild to moderate depending on pulmonary flow

Tourettes Syndrome

Disease Name : Tourettes Syndrome, Symptoms : involuntary movements : examples of motor tics include arm jerking, bending at the waist, eye blinking, twisting, jaw movements., tics : Tics — sudden, brief, intermittent movements or sounds — are the hallmark sign of Tourette syndrome. They can range from mild to severe. Severe symptoms might significantly interfere with communication, daily functioning and quality of life. Tics are classified as : Simple tics. These sudden, brief and repetitive tics involve a limited number of muscle groups. Complex tics. These distinct, coordinated patterns of movements involve several muscle groups., Signs : nan, Treatment : medication : Clonidine , Haloperidol , Risperidone/Respidon , Olanzapine , Guanfacine, Habit-reversal training (HRT), usually as the main component of comprehensive behavioral intervention for tics (CBIT) is the recommended treatment of choice in the United States practice parameter., Haloperidol and pimozide are the first-generation antipsychotics with the most data showing efficacy in reducing tic severity. However, their use is limited by potentially, Pathophysiology : TS is thought to be a genetic disorder, but no specific monogenic cause has yet been identified. Current evidence supports a complex inheritance pattern with an important contribution of de-novo, likely gene-disrupting variants. Four likely risk genes with multiple de novo damaging variants in unrelated probands include WWC1, CELSR3, NIPBL, and FN1. The risk of a family with one affected child having a second is about 25%. The pathophysiology of TS is not known, but alterations in dopamine neurotransmission, opioids, and second-messenger systems have been proposed. Some cases of TS may be the consequence of an autoimmune response to ß-hemolytic streptococcal infection (pediatric autoimmune neuropsychiatric disorder associated with streptococcal infection PANDAS); however, this entity remains controversial., Epidemiology : It predominantly affects males, 2 and 15 years (mean 7 years)., GOOD, Tourette syndrome isn’t preventable. But, early detection and treatment may prevent TS from worsening or lasting into adulthood., Complications : Sleep disturbances, Attention Deficit-hyperactivity disorder (ADHD), Obsessive-compulsive disorder (OCD), Autism spectrum disorder, Learning difficulty, Pain related to tics, especially headaches., Diagnostics : EEG, MRI Brain, PHYSICAL EXAMINATION, Differential diagnosis : akathisia, Chorea, "Huntingtons disease", Obsessive-compulsive disorder (OCD), stereotypies, disease description : Tourette Syndrome (TS) is a condition of the nervous system. TS causes people to have “tics”. Tics are sudden twitches, movements, or sounds that people do repeatedly. People who have tics cannot stop their body from doing these things. For example, a person might keep blinking over and over. 

Toxic Epidermal Necrolysis

Disease Name : Toxic Epidermal Necrolysis, Symptoms : blisters : TEN with spots is defined as widespread, irregularly shaped erythematous or purpuric macules with blistering that occurs on all or part of the macule. Blisters become more confluent and result in detachment of the epidermis and erosions on greater than 30% of the body surface area., erosions : It causes painful, blistering, peeling skin on at least 30% of the body, leading to open erosions. Open erosions may lead to dangerous complications such as sepsis, organ failure, infections or death., skin crusting : Sores, swelling and crusting on the mucous membranes, including the mouth, eyes and vagina, Signs : nan, Treatment : Treatment of TEN also might include one or a combination of medications that affect the whole body (systemic drugs), such as cyclosporine (Neoral, Sandimmune), etanercept (Enbrel) and intravenous immunoglobulin (IVIG). ,Fluid replacement and nutrition.,Wound care.,Breathing help.,Pain control.,Eye care., Pathophysiology : The most common cause of TEN is an abnormal reaction to medication. It’s also known as a dangerous type of drug rash, and is responsible for up to 95 percent of TEN cases.Often, the condition forms within the first 8 weeks of taking the drug., Epidemiology : incidence of 0.4 to 1.9 per million people annually worldwide., variable, You may be able to prevent TEN by seeking immediate medical care at the first signs of Stevens-Johnson syndrome., Complications : sepsis, Visual impairment, Lung infection, Diagnostics : HISTOLOGIC EXAMINATION, PHYSICAL EXAMINATION, Differential diagnosis : erythroderma., Staphylococcal scalded skin syndrome, toxic shock syndrome, disease description : Toxic epidermal necrolysis (TEN) is a rare, life-threatening skin reaction, usually caused by a medication. Its a severe form of Stevens-Johnson syndrome (SJS). In people with SJS, TEN is diagnosed when more than 30% of the skin surface is affected and the moist linings of the body (mucous membranes) have extensive damage.TEN is a life-threatening condition that affects people of all ages. TEN is usually treated in a hospital. While the skin heals, supportive care includes controlling pain, caring for wounds and making sure youre getting enough fluids. Recovery can take weeks to months.

Toxic Erythema Of Chemotherapy

Disease Name : Toxic Erythema Of Chemotherapy, Symptoms : pruritus of the skin, itching, Signs : paraesthesia, pruritic skin rash, Patients present with erythematous patches or oedematous plaques, typically distrib\x02uted on the acral skin and at the major fl exures (axillae, groins and inframammary folds)., plaques, patches, Treatment : There is no standardzsed treatment regimen for TEC. The treatment is symptomatic as the reaction usually spontaneously ,resolves with intense desquamation . Discontinuing treatment is needed if the skin reaction is severe., Pathophysiology : It has been proposed that TEC is caused by direct toxicity of a chemotherapeutic agent after it is excreted through the straight portion of the eccrine duct, the acrosyringium and the epidermis . The high density of eccrine glands in the palms and soles may explain, in part, the predilection of TEC to these sites. Other factors, including temperature gradient, friction, trauma and vascularity, may play a role in the distribution of skin signs in TEC 1 , 2 . TEC reactions are dose dependent. Pathology The histopathology of TEC will depend on the timing of the skin biopsy. Early histological features (within the fi rst 24 h of the eruption) include hyperplastic eccrine ducts with mitotic fi gures and multiple necrotic duct cells without associated keratinization. Late histological features (within 72–96 h of the eruption) include syringosquamous metaplasia, in which there is non-infl ammatory metaplastic transformation of the eccrine cuboidal epithelium into two or more layers of squamous cells with intraductal keratinization. Epidermal dysmaturation (loss of polarity of keratinocytes, multiple mitoses in the basal and suprabasal layers) may be observed in the epidermis after any cytoreductive therapy, and can occur in the absence of a rash., Epidemiology : There are no reliable data for the incidence or pr, Toxic erythema of chemotherapy can recur if the pa, Complications : loss of sensation on skin, Peripheral neuropathy, Diagnostics : BIOPSY FROM SKIN LESION, Differential diagnosis : Hypersensitivity-type reactions, toxic epidermal necrolysis, disease description : Toxic erythema of chemotherapy is the term used to describe a variety of overlapping cutaneous reactions to chemotherapy agents.Cutaneous toxicity can occur following treatment with many chemotherapeutic agents. Although a number of distinct dermatoses are described it has been suggested that the term ‘toxic erythema of chemotherapy’ (TEC) should be used to encompass the spectrum of eruptions triggered by anticancer drugs . As well as simplifying terminology, this designation embraces the overlapping clinical and histopathological features that occur in the chemotherapy-induced erythemas. TEC includes entities such as palmoplantar erythrodysaethesia, intertriginous eruption associated with chemotherapy and neutrophilic eccrine hidradenitis. Age and sex Toxic erythema of chemotherapy affects both sexes equally, and all ages.

Toxic Erythema Of The Newborn

Disease Name : Toxic Erythema Of The Newborn, Symptoms : erythema, Signs : Rashes, rashes on face, They are most profuse on the trunk, particularly the anterior trunk, but also commonly appear on the face and proximal parts of the limbs, especially the thighs., blotchy, macular erythema, pustules, Treatment : No treatment is needed., Pathophysiology : The cause is unknown. There is frequently an associated blood eosinophilia. This probably does not refl ect an allergic response as tissue eosinophilia is a non-specifi c feature of infl ammatory responses in neonates . The intrafollicular location of mature pustules has led to the suggestion that the infl ammatory response is elicited by some component of sebum . Scanning electron microscopy of neonatal skin shows that colonization of hair follicle epithelium by staphylococci is common in early life. Furthermore, accumulation of tryptase-expressing mast cells around the hair follicles in lesional skin has been recently demonstrated but its relation to the staphylococci and its signifi cance in toxic erythema remains unclear. Predisposing factors No predisposing factors are known. Pathology Histologically, the macular erythema shows oedema in the upper dermis, associated with a sparse and largely perivascular infl ammatory infi ltrate comprising principally of eosinophils. Papular lesions are characterized, in addition, by eosinophil infi ltration of the outer root sheath of one or more hair follicles, above the point of entry of the sebaceous duct. Pustular lesions show intrafollicular accumulation of eosinophils immediately below the stratum corneum. Smears of the pustule contents demonstrate infl ammatory cells, more than 90% of which are eosinophils 2 , 5 , 6–8 . There is an associated blood eosinophilia of up to 20% of the white cell count in around half the cases, and this is generally more marked when there is a prominent pustular element to the eruption. Causative organisms No pathogenic bacteria have been isolated from pustules. Environmental factors No environmental factors have been demonstrated. Clinical variants In more severe cases, urticarial papules arise within the erythematous areas or, occasionally, independently of them (particularly on the back and buttocks). These papules are, in about 10% of cases, Epidemiology : Thirty to 50% of children develop a degree of toxi, Spontaneous recovery occurs rapidly, usually withi, Complications : Acne, Diagnostics : Bacterial Culture& Sensitivity Routine Aerobic, Examination under Microscope, Viral cultures, Differential diagnosis : Herpes simplex, Miliaria, Varicella, disease description : Toxic erythema of the newborn is a common, transient, blotchy, red macular rash (sometimes with small pustules) seen in the fi rst few days of life. The most widely used term for this condition is inappropriate in view of the complete absence of any evidence of a toxic cause. Age It appears in the fi rst few days of life. Sex There is equal prevalence in most studies. Ethnicity It occurs in all racial groups. Associated diseases Blood eosinophilia is associated.

Toxic Multinodular Goiter

Disease Name : Toxic Multinodular Goiter, Symptoms : Nervousness, palpitations, tremor, weight loss, Signs : Tachycardia, Treatment : Radioiodine is generally the treatment of ,choice, Pathophysiology : nan, Epidemiology : nan, Complications : nan, Diagnostics : Thyroxine (T4) Test, Thyroid Stimulating Hormone TSH, USG Thyroid, THYROID SCAN, USG, Differential diagnosis : nan, disease description : nan

Toxic Shock Syndrome

Disease Name : Toxic Shock Syndrome, Symptoms : Gastrointestinal symptoms : Includes vomiting, watery diarrhea & nausea., Peeling of skin : Peeling of the skin on the soles of your feet or palms of your hands., Skin rashes : A sunburn-like rash is a characteristic sign of TSS. The rash develops within a few hours of TSS symptoms first appearing. Large portions of the skin may start peeling or flaking., fever with chills : Fever higher than 102°F (38.9°C)., Signs : Orthostatic hypotension : The first sign of this life-threatening condition can be dizziness when rising from a sitting or lying position ( orthostatic hypotension )., "strawberry tongue : Toxic shock syndrome (TSS) : Its rare, but this can sometimes cause strawberry tongue.", Treatment : medication : Benzylpenicillin/ penicillin-G, Clindamycin , Vancomycin , First line,•\tHaemodynamic resuscitation,•\tIV clindamycin +/– benzylpenicillin sodium (penicillin ,G) or vanocmycin,Second line,•\tFor severe cases, consider additional intravenous ,immunoglobulin (initial dose 2 g/kg, then 4 days of ,0.4 g/kg), "If you develop toxic shock syndrome, youll likely be hospitalized. In the hospital, youll : ,,Be treated with antibiotics while doctors seek the infection source,Receive medication to stabilize your blood pressure if its low and fluids to treat dehydration,Receive supportive care to treat other signs and symptoms", Surgery may be necessary to remove nonliving tissue from the site of infection or to drain the infection., Pathophysiology : Toxic shock syndrome can affect anyone. About half the cases of toxic shock syndrome associated with staphylococci bacteria occur in women of menstruating age; the rest occur in older women, men and children. Streptococcal toxic shock syndrome occurs in people of all ages.Toxic shock syndrome has been associated with : Having cuts or burns on your skinHaving had recent surgeryUsing contraceptive sponges, diaphragms, superabsorbent tampons or menstrual cupsHaving a viral infection, such as the flu or chickenpox, Epidemiology : incidence was 1.4/100K in 13–24 year-aged young women., variable, "You can take steps to lower your risk for toxic shock syndrome. Some of these include : ,,Use sanitary pads instead of tampons during menstrual periods or use pads at night. Switching from tampons to pads every other day or when the menstrual flow is heaviest may also help reduce your risk.,Change tampons every four to eight hours. If the flow is heavy, tampons may have to be changed more frequently.,Use a tampon with the lowest absorbency required for your flow.,Don’t use tampons when you aren’t menstruating.,Keep surgical incisions clean to avoid infection. See your healthcare provider if you notice unusual swelling, redness or heat near the wound.,Follow directions when using vaginal contraceptives such as sponges, caps or diaphragms.,Toxic shock syndrome is more likely to recur in people whove already had it. You should avoid using tampons during your period if youve recovered from a case of TSS.", Complications : Chronic renal failure, death, Respiratory Distress Syndrome, MULTIORGAN FAILURE, Disseminated lntravascular Coagulopathy, Diagnostics : Complete Blood Count CBC, URINE CULTURE, lumbar puncture, fluid microbiological culture, serum calcium Ca++, BLOOD CULTURE, plasma creatinine, Differential diagnosis : erythema multiforme, Kawasaki Disease, meningococcemia, scarlet fever, toxic epidermal necrolysis, disease description : Toxic shock syndrome is a rare, life-threatening complication of certain types of bacterial infections. Often toxic shock syndrome results from toxins produced by Staphylococcus aureus (staph) bacteria, but the condition may also be caused by toxins produced by group A streptococcus (strep) bacteria.

Toxic/nutritional Optic Neuropathy

Disease Name : Toxic/nutritional Optic Neuropathy, Symptoms : Loss of vision : Toxic and nutritional optic neuropathy both present with symmetric and progressive bilateral vision loss., photophobia : Intense sensitivity to light., loss of colour vision : General loss of color perception, particularly red., visual acuity : Loss of central or paracentral visual acuity., Signs : Central scotoma : Affected patients presents with central or cecocentral scotomas., Treatment : medication : Sodium bicarbonate , TREATMENT OF Tobacco amblyopia : ,• Complete cessation of tobacco and alcohol,consumption,• Hydroxocobalamin 1000 mg intramuscular,injections weekly for 10 weeks,• Care of general health and nutrition,• Vasodilators have also been tried,,TREATMENT OF Methyl alcohol amblyopia : 1. Gastric lavage to wash away the methyl alcohol,should be carried out immediately and at intervals,during the first few days, as the alcohol in the,system is continuously returned to stomach.,2. Administration of alkali to overcome acidosis,should be done in early stages. Soda bicarb may be,given orally or intravenously (500 ml of 5% solution).,3. Ethyl alcohol. It should also be given in early,stages. It competes with the methyl alcohol for the,enzyme alcohol dehydrogenase, thus preventing,the oxidation of methanol to formaldehyde. It,should be given in small frequent doses, 90 cc,every 3 hours for 3 days.,4. Eliminative treatment by diaphoresis in the form,of peritoneal dialysis is also helpful by washing,the alcohol and formaldehyde from the system.,5. Prognosis is usually poor; death may occur due to,acute poisoning. Blindness often occurs in those,who survive., Pathophysiology : Alcohols (commercial alcohol, methanol, and ethylene glycol) : Chronic alcoholism leads to vitamin B12 or folate deficiency. Over time, these deficiencies can cause accumulations of formic acid, which inhibits the electron transport chain and mitochondrial function. As a result, ATP production decreases and impairs the ATP-dependent axonal transport system. In methanol specifically, the drug can cause focal retrolaminar optic nerve delamination.Linezolid : Prolonged linezolid usage can interfere with mammalian ribosomes and lead to the disruption of mitochondrial oxidative phosphorylation and protein synthesis.Ethambutol : The chelating property of ethambutol has adverse effects on human cells. The exact mechanism is unknown, but it has been hypothesized that the induced optic neuropathy may possibly be due to a disruption of oxidative phosphorylation secondary to decreased free copper in the mitochondria or the inhibition of lysosomal activation due to the chelation of zinc. This damage is irreversible.Amiodarone : Amiodarone can interact with polar lipids and accumulate as inclusion bodies in the optic nerve, leading to optic disc swelling and induced optic neuropathy. Histological evaluation may reveal inclusion elements distributed in a lamellar fashion in the large axons of the optic nerve. In contrast, toxicity of amiodarone in peripheral nerves has been shown to induce loss of axons and demyelination. Sildenafil : Sildenafil acts as an inhibitor of phosphodiesterase and when used at high therapeutic doses, it can influence individual steps of the phototransduction process. It has been shown to increase the risk for NAION more than a direct toxicity to the optic nerve.Lead : Lead can bind to specific target proteins, which results in a change in protein structure and function. It can also bind to melanin in the retinal pigment epithelium, choroid, iris, and ciliary body with high affinity and disrupt cellular biochemistry. Recent evidence also indicates that it can induce oxidative stress that result in lipid peroxidation, DNA damage, and depletion of cell antioxidant defense systems. These events make the optic nerve susceptible to optic neuropathy. In addition, low-level lead exposure produces scotopic vision deterioration and rod and bipolar apoptopic cell death., Epidemiology : relatively uncommon and is primarily associated with specific medications, occupational exposures, or tobacco and alcohol use disorder., variable, Patients in whom ethambutol or isoniazid is indicated for tuberculosis need to have a baseline ophthalmologic examination before treatment is instituted and should be monitored by their ophthalmologist periodically as long as they are on the drug to detect any optic nerve toxicity as soon as possible. ,,Any patient for whom amiodarone is being considered for treatment requires a baseline ophthalmic examination before the drug is initiated. ,,Patients should seek assistance from their primary physician on methods to stop or reduce their smoking and/or alcohol intake., Complications : complete blindness, Diagnostics : FUNDOSCOPY, Optical coherence tomography (OCT), MRI, MRI, PHYSICAL EXAMINATION, Perimetry, Differential diagnosis : Acute Idiopathic Maculopathy, optic neuropathy, disease description : Toxic optic neuropathy (TON) refers to visual impairment due to optic nerve damage caused by a toxin. Toxic optic neuropathy is characterized by bilateral, usually symmetric vision loss, papillomacular bundle damage, central or cecocentral scotoma, and reduced color vision. 

Toxocara Endophthamitis

Disease Name : Toxocara Endophthamitis, Symptoms : pain in eyes, REDNESS OF EYE, photophobia, WATERING EYE, Signs : anterior uveitis and vitritis, Treatment : Topical cycloplegic mydriatic prevents posterior synechia formation and seclusio pupillae. Increased intraocular pressure can be controlled with topical antiglaucoma medications. The role of systemic anthelmintic drugs such as albendazole and thiabendazole is unclear. It is not proven to kill intraocular Toxocara. favorable results are seen in combination with oral corticosteroids., sometimes, the larva is seen migrating in the subretinal space. It can then be destroyed with laser photocoagulation over and around it. The laser can be done with a neodymium-doped yttrium aluminum garnet (Nd : YAG) frequency-doubled 532 nm green laser. The laser power can be in the range of 250 to 300 mW and 100 to 150 ms duration. The reaction should produce a white burn over the retina., Pathophysiology : Humans get infected after ingestion of eggs or larvae through contaminated vegetables or uncooked meat. Close contact with puppies or soil infested with embryonated eggs can lead to accidental ingestion of eggs. The perianal region of dogs is a reservoir of embryonated eggs. The dogs also harbor the eggs in their fur. According to a study, puppies harbor many eggs on their hair at densities higher than in the soil. Thus direct contact with puppies can lead to infection of T. canis.Sometimes people get infected after consumption of uncooked contaminated raw meat of chicken and cows. After ingestion, the eggs reach the small intestine. There they turn into larva. The larva penetrates the intestinal wall and enters the systemic circulation. The body tries to contain the infection by inciting an eosinophilic granuloma around the parasite.It tries to contain the Toxocara parasite within the granuloma. Toxocariasis can manifest in the form of visceral larva migrans and ocular toxocariasis. The clinical manifestation depends upon host immunity, the severity of inflammatory response, the quantity of larva ingested, and organ localization. Eosinophilia is often present in Toxocara infection. The greater the degree of exposure greater is the eosinophil count, Epidemiology : the antibody titer against Toxocara was found to be positive in 2.4% to 76.6% of individuals, Complications : angle closure glaucoma, cystoid macular edema, SYNECHIAE, Diagnostics : Complete Blood Count CBC, serum IgE level, Slit lamp examination, ultrasound, ELISA, Differential diagnosis : bilateral granulomatous panuveitis, ENDOPHTHALMITIS, retinoblastoma, Retinopathy of Prematurity, Toxoplasmosis, disease description : Ocular toxocariasis is a childhood disorder resulting from the ingestion of Toxocara ova. The patient may present with peripheral granuloma, posterior granuloma, or endophthalmitis. It is a serious ocular condition causing permanent vision loss, and it is an important differential diagnosis of retinoblastoma. It must be promptly diagnosed and treated after excluding other differential diagnoses to avoid the high morbidity associated with ocular toxocariasis. This activity reviews the evaluation and treatment of ocular toxocariasis and highlights the role of the interprofessional team in evaluating and treating patients with this condition.

Toxocariasis

Disease Name : Toxocariasis, Symptoms : systemic symptoms : Visceral larva migrans is caused by the migration of larvae through the internal organs of humans and the resulting inflammatory reaction. A constellation of symptoms develops, including fatigue, anorexia, weight loss, pneumonia, fever, cough, bronchospasm, abdominal pain, headaches, rashes, and, occasionally, seizures. Examination may reveal hepatomegaly, lymphadenitis, and/or wheezing. Occasionally, pleural effusions develop. Chronic urticaria has been described. Severe cases can lead to myocarditis or respiratory failure., Children : In children, covert toxocariasis is a mild, subclinical, febrile illness. Symptoms can include cough, difficulty sleeping, abdominal pain, headaches, and behavioral problems. Examination may reveal hepatomegaly, lymphadenitis, and/or wheezing., Ocular symptoms : Ocular larva migrans, which is caused by migration of larva into the posterior segment of the eye, tends to occur in older children and young adults. Patients may present with decreased vision, red eye, or leukokoria (white appearance of the pupil). Granulomas and chorioretinitis can be observed in the retina, especially at the macula. Unilateral visual loss, retinal fibrosis, retinoblastoma, and retinal detachment occur. Serum antibodies to Toxocara often are absent or present in low titers., Signs : nan, Treatment : It consists of periocular (posterior,sub-Tenon) injection of steroid and systemic,steroids., The standard treatment for toxocariasis is a five-day course of albendazole. This is sometimes supplemented with corticosteroids to suppress the allergic reaction to the roundworms., For OLM, surgery, steroids, and anthelminthic (anti-parasitic) chemotherapy are the preferred methods of treatment., Pars plana vitrectomy may be required in,unresponsive patients with endophthalmitis and in,patients with vitreous band formation., Pathophysiology : Ocular toxocariasis. It is ocular infestation by these larva and is almost always unilateral. Clinically, it can present as follows : ¦¦Toxocara chronic endophthalmitis. It usually presents with leucocoria due to marked vitreous clouding. The condition is seen in children between the age of 2–10 years and mimics retinoblastoma. ¦¦Posterior pole granuloma. It presents as a yellowwhite, round, solitary, raised nodule, about 1–2 disc diameter in size, located either at the macula or in the centrocaecal area. The condition is usually seen in children between 5 and 15 years of age, presenting with unilateral loss of vision. ¦¦Peripheral granuloma. It is situated anterior to the equator and may be associated with vitreous band formation. It may present from 6 to 40 years of age. Diagnosis is made on the basis of clinical feature and ELISA blood test., Epidemiology : Globally, the disease is more common in developing countries, with seroprevalence reported above 80% in children in parts of Nigeria., variable, You can prevent toxocariasis by taking some simple precautions. The most important thing you can do is practice good hand hygiene. Wash your hands with soap and water frequently, especially after touching animals and before eating.,,Other steps you can take to prevent the condition include : ,1. Pets - Make sure you dog or cat sees their veterinarian for checkups regularly. Keep your pet’s living area clean. Either bury your furry friend’s poop or bag it and throw it in the garbage. Make sure to wash your hands after picking up your pet’s poop.,,2. Children -Teach your children why it’s important to wash their hands. This is especially important after touching pets and playing outside., Complications : blindness, meningoencephalitis, unilateral loss of vision, Diagnostics : Complete Blood Count CBC, ELISA, direct microscopy, Differential diagnosis : Ascariasis, Onchocerciasis, schistosomiasis, Trichinosis, disease description : It is an infestation caused by an intestinal roundworm of dogs (Toxocara canis) and cats (Toxocara catis). The young children who play with dogs and cats or eat dirt are infested by ova of these worms. These ova develop into larva in the human gut, and then produce the condition visceral larva migrans (VLM).

Toxoplasmosis

Disease Name : Toxoplasmosis, Symptoms : flu-like symptoms : Includes fever, sore throat, muscle aches, headaches., respiratory symptoms : Includes breathing problems, fever & cough., Skin rashes : Lesions may be telangiectatic macules, papules, or vesicles., Neurological symptoms : Includes confusion, poor coordination, seizures & changes in alertness., Congenital disorders : Congenital toxoplasmosis is passed from a pregnant person to the fetus. Some babies won’t have any symptoms at birth, but are at high risk for developing them later on. These symptoms may include jaundice, rash, hepatosplenomegaly, retinochoroiditis, calcium deposits in their brain, hydrocephalus, microcephaly, seizures, delays in motor skill development, learning delays or differences & ocular toxoplasmosis., Ocular symptoms : The toxoplasma parasites may infect tissues of the inner eye. Symptoms may include eye pain, p Symptoms may include & floaters., Signs : lymphadenopathy : Lymphadenitis is the most common clinical form of toxoplasmosis., Treatment : medication : Folinic acid (Leucovorin calcium), Pyrimethamine , Sulfadiazine , Azithromycin , Clindamycin , In addition to the regular drug treatment, eye disease also may be treated with anti-inflammatory steroids called glucocorticosteroids., "Pyrimethamine (Daraprim). This fights infections caused by microscopic organisms. It can block the bodys use of folic acid. Other possible side effects with long-term use include bone marrow suppression and liver toxicity.,Leucovorin calcium helps correct the effects of pyrimethamine on folic acid activity.,Sulfadiazine is an antibiotic often prescribed with pyrimethamine. Other medication includes clindamycin (Cleocin), azithromycin (Zithromax) and others.", Treatment for infants,Drug treatment for infants may last 1 to 2 years. Regular and frequent follow-up appointments are needed to watch for side effects, vision problems, and physical, intellectual and overall development., Pathophysiology : Upon the host’s ingestion of either tissue cysts containing bradyzoites or oocysts containing sporozoites, the parasites are released from the cysts by the digestive process. Bradyzoites are resistant to the effect of pepsin and invade the host’s gastrointestinal tract. Within enterocytes (or other gut-associated cells), the parasites undergo morphologic transformation, giving rise to invasive tachyzoites. From the gastrointestinal tract, parasites disseminate to a variety of organs, particularly lymphatic tissue, skeletal muscle, myocardium, retina, placenta, and the CNS. At these sites, the parasite infects host cells, replicates, and invades the adjoining cells. In this fashion, the hallmarks of the infection develop : cell death and focal necrosis surrounded by an acute inflammatory response. In the immunocompetent host, both the humoral and the cellular immune responses control infection; parasite virulence and tissue tropism may be strain specific. Tachyzoites are sequestered by a variety of immune mechanisms, including induction of parasiticidal antibody, activation of macrophages with radical intermediates, production of interferon  (IFN), and stimulation of CD8+ cytotoxic T lymphocytes. These antigen-specific lymphocytes are capable of killing both extracellular parasites and target cells infected with parasites., Epidemiology : United States, 13.2% of individuals >6 years old, not specific, Safe food preparation and hand washing are the most important things you can do to help prevent toxoplasmosis.,,Follow safe freezing and cooking practices before eating meat.,Peel fruits and vegetables or wash thoroughly before eating.,Wash cutting boards, counters, utensils and dishes with soapy water after use.,Don’t drink unpasteurized milk.,Don’t eat raw or undercooked clams, oysters or mussels.,Don’t drink untreated water.,Wear gloves when gardening and while working with soil or sand. Wash hands with soap and water afterward.,Cover outdoor sandboxes.,Don’t feed cats raw or undercooked meats.,Change cat litter daily. Wear gloves and wash your hands with soap and water afterward.,Keep cats indoors.,If you’re pregnant or have a compromised immune system : ,,Avoid changing cat litter yourself if possible.,If you must change cat litter, wear disposable gloves and wash your hands thoroughly afterward.,Don’t adopt a new cat or take in a stray cat, Complications : ENCEPHALITIS, Pancreatitis, Lung infection, Diagnostics : biopsy, BLOOD CULTURE, PCR, ELISA, CT SCAN, IgG ANTIBODY AND IgM ANTIBODY, IgA ANTIBODY, molecular testing, Differential diagnosis : Cytomegalovirus (CMV), encephalopathy, Herpes simplex encephalitis, lymphoma, disease description : Toxoplasmosis is an infection with a parasite called Toxoplasma gondii. People often get the infection from eating undercooked meat. You can also get it from contact with cat feces. The parasite can pass to a baby during pregnancy.

Tracheitis

Disease Name : Tracheitis, Symptoms : myalgia, sore throat, post nasal drip, Rhinorrhoea, fever, dyspnea, Signs : respiratory distress, Tachycardia, stridor, Treatment : Treatment of bacterial tracheitis includes a prompt assessment for airway compromise first. The need for intubation is common with reported rates ranging from 38% to 100% of patients in various studies, Antibacterial management should be prompt and include broad-spectrum coverage, including MRSA. Gram stain results, if obtained, can focus on antibiotic selection, but broad coverage should be initially chosen until culture results are obtained. Current guidelines recommend a 10-day to 14-day antibiotic course, although no formal studies have investigated the recommended time length of antimicrobial treatment. The first-line treatments suggested include amoxicillin-clavulanic acid, ceftriaxone plus nafcillin or vancomycin, clindamycin plus a third-generation cephalosporin, or ampicillin-sulbactam., Pathophysiology : In bacterial tracheitis, opportunistic bacteria invade damaged tracheal mucosa, made of pseudostratified columnar epithelium, and stimulate local and systemic inflammatory responses. In otherwise healthy patients, this is presumed to be precipitated by a viral upper respiratory infection, while in patients with an indwelling tracheostomy tube, it can also be due to seeding from a colonized tracheostomy appliance.Local responses in the tracheal mucosa cause edema, thick mucopurulent secretions, ulceration, and mucosal sloughing, which can predispose the patient to subglottic narrowing, tracheal narrowing, and/or airway obstruction.Systemic inflammation leading to sepsis is rare but can occur in immunocompromised patients. Staphylococcus aureus has been the most commonly implicated pathogen, although reports suggest M. catarrhalis is becoming more common, especially in younger children, Epidemiology : The annual incidence of bacterial tracheitis varies between countries, with an estimated incidence of 0.1 to 1 case(s) per 100, 000 children., Complications : acute respiratory distress syndrome, aspiration pneumonia, encephalopathy, Hypoxia, cardiopulmonary arrest, airway obstruction, Diagnostics : ECG, Laryngoscopy, USG ABDOMEN(W/A), X RAY CHEST, X RAY CHEST, BRONCHOSCOPY, Differential diagnosis : Acute Epiglottits, amyloidosis, angioedema, diphtheria, foreign body, oropharyngeal candidiasis, disease description : Bacterial tracheitis (BT), also known as bacterial croup or laryngotracheobronchitis, was first described in medical literature in the 1920s, despite the name not being coined until the 1970s.Bacterial tracheitis is a potentially lethal infection of the subglottic trachea. It is often a secondary bacterial infection preceded by a viral infection affecting children, most commonly under age six It can also be rarely seen spontaneously in the adult population, and tracheostomy-dependent patients of any age. Concern for airway protection is the mainstay of treatment as thick, mucopurulent secretions can cause airway narrowing and obstruction.On presentation, this must be distinguished from other causes of airway obstruction to allow for more expedited treatment. Treatment is aimed at the protection of the airway, assessing the need for diagnostic and/or therapeutic endoscopy, and antimicrobial therapy.

Tracheoesophageal Fistula (tef)

Disease Name : Tracheoesophageal Fistula (tef), Symptoms : choking, polyhydramnios, VENTRICULAR SEPTAL DEFECTS, Congenital heart disease, Signs : cyanosis, respiratory distress, Feeding Difficulty, DROOLING OF SALIVA, excessive drooling with froathing, Treatment : The baby should be nursed supine or in an upright,position and esophageal pouch should be gently sucked every five minutes, or continuously using a slow suction,device. Intravenous fluids should be administered and,infection, if any should be treated., Surgical repair should,be undertaken as early as possible, Pathophysiology : Upper part of esophagus is developed from retropharyngeal segment and the lower part from pregastric segment of the first part of the primitive gut. At four weeks of gestation, the laryngotracheal groove is formed. Later, two longitudinal furrows develop to separate the respiratory primordium from the esophagus. Deviation or altered cellular growth in this septum results in formation of tracheoesophageal fistulae. Incidence is 1 in 4000 live births. In the most common variety (over 80% of cases), the upper part of the esophagus ends blindly and the lower part is connected to the trachea by a fistula., Epidemiology : Incidence is 1 in 4000 live births, variable, Because people are born with congenital TEF, there’s no way to prevent it from happening. And since most cases of acquired TEF are caused by cancer and infections, there’s no known way to reduce your risk for the condition., Complications : aspiration pneumonia, respiratory distress, Diagnostics : Karyotype, ultrasound, BARIUM ESOPHAGOGRAM, X RAY ABDOMEN, Oral cavity examination, Differential diagnosis : esophageal stricture, GASTRO OESOPHAGEAL REFLUX DISEASE, PERFORATION OF OESOPHAGUS, disease description : A tracheoesophageal fistula (TEF) is an abnormal connection between your esophagus and trachea. The condition is often congenital, which means it happened during fetal development. TEF may also be acquired in adulthood due to cancer, infection or trauma. Treatment involves surgery to close the fistula.

Trachoma

Disease Name : Trachoma, Symptoms : blepharitis : Trachoma causes eyelids to become swollen., "discharge from eyes : Theres watery discharge from the eyes.", eye pain : Trachoma causes intense eye pain., Lacrimation : Patients experience teary eyes in trachoma., red eyes : Red and irritated eyes is experienced by the affected individuals., visual disturbances : Trachoma is the most common infectious cause of blindness worldwide., photophobia : Sensitivity to light is prevalent in trachoma., Signs : Conjunctival scarring : Conjunctival scarring with ensuing trichiasis and entropion result in corneal scarring and eventual blindness., Herbert follicles : Trachoma infection causes follicular conjunctivitis, sometimes involving the cornea and limbus. When infectious follicles heal, they are replaced by rounded, depressed, or flat scars (ie, Herbert pits) as seen in this patient., Progressive pannus : A pannus is young vascularized connective tissue (granulation tissue) growing into the cornea beyond the gray zone with its normal limbal arcade. There is also an aberrant lash in the upper lid that is part of the trachoma afflicting this eye., Conjunctival Concretions : A conjunctival concretion is a benign entity characterized by single or multiple discrete yellowish-white deposits of varying size. They may be idiopathic and are generally a finding in elderly individuals or secondary to chronic conjunctival inflammation like in trachoma., Treatment : medication : Azithromycin , Doxycycline , Erythromycin , Tetracycline , Sulfacetamide, A. Treatment of active trachoma,Antibiotics for treatment of active trachoma may be,given locally or systemically, but topical treatment is,preferred because : ,• It is cheaper, ,• There is no risk of systemic side-effects, and,• Local antibiotics are also effective against bacterial,conjunctivitis which may be associated with,trachoma., B. Treatment of trachoma sequelae,1. Concretions should be removed with a hypodermic,needle.,2. Trichiasis may be treated by epilation, electrolysis,or cryolysis.,3. Cicatricial entropion should be corrected,surgically.,4. Conjunctival xerosis should be treated by artificial,tears., Pathophysiology : The World Health Organization (WHO) has identified five stages in the development of trachoma : Inflammation — follicular. The early infection has five or more follicles — small bumps that contain lymphocytes, a type of white blood cell — visible with magnification on the inner surface of your upper eyelid (conjunctiva).Inflammation — intense. In this stage, your eye is now highly infectious and becomes irritated, with a thickening or swelling of the upper eyelid.Eyelid scarring. Repeated infections lead to scarring of the inner eyelid. The scars often appear as white lines when examined with magnification. Your eyelid may become distorted and may turn in (entropion).In-turned eyelashes (trichiasis). The scarred inner lining of your eyelid continues to deform, causing your lashes to turn in so that they rub on and scratch the transparent outer surface of your eye (cornea).Corneal clouding (opacity). The cornea becomes affected by an inflammation that is most commonly seen under your upper lid. Continuous inflammation compounded by scratching from the in-turned lashes leads to clouding of the cornea., Epidemiology : GOOD, Improving access to water supplies and sanitation services is key to stopping trachoma. Other strategies include improving crowded housing and getting rid of fly populations. Authorities throughout the world are making efforts to putting these actions into place to try to eliminate trachoma and trachoma blindness everywhere. The primary prevention strategy has an acronym — SAFE : ,,Surgery to repair advanced disease.,Antibiotics for infections.,Facial cleansing to stop the spread.,Environmental changes like improved access to clean water and sanitation services.,,On a personal level, you can do some things to protect yourself if you live in an area where trachoma exists, or if you visit an area with trachoma. These include : ,,Pay attention to your hygiene. Make sure you clean your face well, removing any trace of discharge from your eyes and nose.,Wash your hands well. Do this especially if you’re around children.,Don’t share towels or bedding.,If possible, avoid areas where there are flies., Complications : chronic dacryocystitis, CORNEAL ULCER, ENTROPION, trichiasis, Scarring, Diagnostics : ANTIGEN DETECTION ELISA, PCR, GIEMSA STAINED CONJUNCTIVAL SMEAR, MICROIMMUNOFLUORESCENCE, Differential diagnosis : conjunctivitis, follicular conjunctivitis, disease description : Trachoma is a bacterial infection that affects your eyes. Its caused by the bacterium Chlamydia trachomatis. Trachoma is contagious, spreading through contact with the eyes, eyelids, and nose or throat secretions of infected people. It can also be passed on by handling infected items, such as handkerchiefs.

Tractional Retinal Detachment

Disease Name : Tractional Retinal Detachment, Symptoms : Vision loss, floaters, flashes of light., Signs : Presence of vitreoretinal bands, Retinal breaks are usually absent and configuration of the detached area is concave., Highest elevation of the retina occurs at sites of vitreoretinal traction., Retinal mobility is severely reduced and shifting fluid is absent., Treatment : • Surgery is difficult and requires pars plana,vitrectomy to cut the vitreoretinal tractional bands,and internal tamponade with either a long-acting,gas or silicon oil, Pathophysiology : Clinical features Photopsia and floaters are not complained. Tractional retinal detachment is characterised by : • Presence of vitreoretinal bands with lesions of the causative disease. • Retinal breaks are usually absent and configuration of the detached area is concave. • Highest elevation of the retina occurs at sites of vitreoretinal traction. • Retinal mobility is severely reduced and shifting fluid is absent., Epidemiology : NOT SO GOOD, Complications : nan, Diagnostics : ophthalmoscopy, Fundus fluorescein angiography (FFA), Differential diagnosis : nan, disease description : Tractional retinal detachment (TRD) occurs due to retina being mechanically pulled away from its bed by the contraction of fibrous tissue in the vitreous (vitreoretinal tractional bands). Etiology TRD is associated with the following conditions : • Post-traumatic retraction of scar tissue especially following penetrating injury, • Proliferative diabetic retinopathy, • Post-haemorrhagic retinitis proliferans, • Retinopathy of prematurity, • Plastic cyclitis, • Sickle cell retinopathy, • Proliferative retinopathy in Eales’ disease, • Vitreomacular traction syndrome, • Incontinentia pigmenti, • Retinal dysplasia, and • Toxocariasis.

Transaldolase Deficiency

Disease Name : Transaldolase Deficiency, Symptoms : antimongoloid palpebral fissures : The antimongoloid slant of the palpebral fissures and the rudimentary, inferiorly placed lateral canthal ligaments are almost uniform., CIRRHOSIS : Liver cirrhosis is associated with increased apoptosis of hepatocytes and transaldolase is a regulator in apoptosis signaling processing – therefore transaldolase deficiency can result in liver cirrhosis.8, hepatosplenomegaly : Hepatosplenomegaly is the simultaneous enlargement of both the liver (hepatomegaly) and the spleen (splenomegaly)., Thrombocytopenia : Thrombocytopenia is a condition characterized by abnormally low levels of platelets, also known as thrombocytes, in the blood. Low levels of platelets in turn may lead to prolonged or excessive bleeding., "Coagulopathy : Coagulopathy is a condition in which the bloods ability to coagulate (form clots) is impaired.", Cutis laxa : Cutis laxa is a group of rare connective tissue disorders in which the skin becomes inelastic and hangs loosely in folds., Signs : nan, Treatment : There is no established treatment for transaldolase deficiency in humans. Recent work in a knockout mouse model of transaldolase deficiency has demonstrated a benefit to supplementation with the glutathione precursor N-acetylcysteine (NAC) (Hanczko et al. 2009), Pathophysiology : Less than ten cases have been reported in the literature so far, all involving children born to consanguineous parents of Turkish and Arabic origin. The deletion of Ser171 leads to inactivation and proteasome-mediated degradation of TALDO1. The deletion of Ser171 leads to inactivation and proteasome-mediated degradation of TALDO1. D-glyceraldehyde 3-phosphate + D-sedoheptulose 7-phosphate <=> D-fructose 6-phosphate + D-erythrose 4-phosphate, Epidemiology : Prevalence : <1 / 1 000 000, Less than ten cases have been reported in the literature so far, all involving children born to consanguineous parents of Turkish and Arabic origin., Poor, "Inheritance : Autosomal recessive and therefore cant be prevented.", Complications : hepatosplenomegaly, Liver dysfunction, Thrombocytopenia, anemia, Diagnostics : Complete Blood Count CBC, DNA analysis for mutation, ELISA, Differential diagnosis : enzyme deficiency, disease description : Transaldolase deficiency is an inborn error of the pentose phosphate pathway that presents in the neonatal or antenatal period with hydrops fetalis, hepatosplenomegaly, hepatic dysfunction, thrombocytopenia, anemia, and renal and cardiac abnormalities.

Transient Abnormalities In Liver Function

Disease Name : Transient Abnormalities In Liver Function, Symptoms : bleeding : Frequent nosebleeds and bleeding gums. Easy bruising and difficulty in stopping small bleeds., Gastrointestinal symptoms : Includes nausea, vomiting, loss of appetite., hematemesis : Presence of blood in vomitus., jaundice : Symptoms include dark urine, pale-coloured stools or very dark/black tarry stools, yellowing of the whites of the eyes and the skin., Malaise : Generally feeling unwell and tired all the time., PALMAR ERYTHEMA : Blotchy red palms., Sleep disturbances : Disturbed sleep patterns., Pain : Pain in the liver area., Neurological symptoms : Includes forgetfulness, memory loss, confusion and drowsiness, subtle change in personality, trembling hands, writing becomes difficult, spidery and small staggering gait when walking; tendency to fall., spider angiomas : Spider-like small blood capillaries on the skin above waist level., fever with chills : Fevers with high temperature and shivers., Signs : ascites : Ascites is a condition in which fluid collects in spaces within your abdomen., clubbing : Ends of fingers become wider/thicker., Treatment : Lifestyle changes : You can use your diet to help manage certain types of liver disease. If you have fatty liver disease, avoiding alcohol, limiting fat and calories and increasing fiber intake can help. Alcohol-related liver disease can improve with abstinence from alcohol., Medications : Healthcare providers treat some types of liver disease with medication. You may take medicine for viral infections like hepatitis or inherited conditions like Wilson disease., Liver transplant : When liver disease progresses to liver failure, a liver transplant may be the best treatment option. A transplant replaces your liver with a healthy liver., Pathophysiology : liver disease represents a continuous and progressive process of hepatic fibrosis, liver tissue architectural distortion, and regeneration nodule formation. While fibrosis is usually irreversible, but it can be reversible in the initial stage of development. The transition time point of reversible fibrosis to irreversible fibrosis is still not completely understood. In chronic liver disease, if not treated, the endpoint is usually irreversible fibrosis, regeneration nodule formation, and development of cirrhosis liver. The common pathway is initiated by hepatic stellate cells (HSC), which usually are vitamin A storing dormant cells found in space between sinusoids and hepatocytes. In response to chronic liver injury, HSC gets activated into proliferative fibrogenic myofibroblast and upregulates the expression of inflammatory receptors such as chemokine receptors, ICAM-1, and other inflammatory mediators by releasing chemokines and other leukocyte chemoattractants. This pro-inflammatory phase or initiation phase also changes gene and phenotypic expression of the liver cells, making them more responsive to these inflammatory cytokines, and perpetuation of activated HSC cells results in the accumulation of ECM and progressive fibrosis., Epidemiology : About 5.5 million people in the U.S. have chronic liver disease or cirrhosis., About 1 in 10 Americans (30 million in total) have some type of liver disease., Variable, You can take steps to prevent some types of liver disease — especially those affected by your diet and lifestyle. If you are at risk for liver disease, your provider may recommend lifestyle changes including : ,,1. Avoiding or limiting alcohol.,2. Avoiding foods and drinks that contain trans fats or high-fructose corn syrup.,3. Carefully managing your intake of prescription and over-the-counter medications to avoid liver damage, as medications like acetaminophen (Tylenol®) are a common cause of liver injury.,4. Getting regular exercise.,5. Limiting consumption of red meat.,You can minimize the likelihood of contracting viral hepatitis by practicing safe sex and not sharing needles., Complications : ascites, HEPATIC ENCEPHALOPATHY, hepatorenal syndrome, Diagnostics : GENRAL BLOOD PICTURE, LIVER FUNCTION TEST LFT, biopsy, Differential diagnosis : Cardiomyopathy, COR PULMONALE, Hyperplasia, pericarditis, Sarcoidosis, schistosomiasis, Thrombosis, disease description : There are many types of liver disease, which can be caused by infections, inherited conditions, obesity and misuse of alcohol. Over time, liver disease may lead to scarring and more serious complications. Early treatment can help heal the damage and prevent liver failure.Your liver is your body’s second-largest organ (after the skin). It sits just under your ribcage on the right side and is about the size of a football. The liver separates nutrients and waste as they move through your digestive system. It also produces bile, a substance that carries toxins out of your body and aids in digestion.The term “liver disease” refers to any of several conditions that can affect and damage your liver. Over time, liver disease can cause cirrhosis (scarring). As more scar tissue replaces healthy liver tissue, the liver can no longer function properly. Left untreated, liver disease can lead to liver failure and liver cancer.

Transient Aquagenic Keratoderma

Disease Name : Transient Aquagenic Keratoderma, Symptoms : pruritus, itching, Signs : papules, typically show a subtle keratoderma appearing after a few minutes of immersion of their hands in water or after sweating, plaques, Treatment : Treatment with 20% aluminium chloride hexahydrate followed by ,urea cream , or botulinum toxin may lead to significant ,improvement., Pathophysiology : Most cases of transient aquagenic keratoderma (TAK) appear to be acquired, but autosomal recessive or dominant cases have been described. The disease may be associated with the use of cyclo-oxygenase 2 inhibitors. The relationship with other diseases such as asthma is unknown. It may be differentiated from hereditary papulotranslucent acrokeratoderma (MIM 101840), in which lesions are persistent once they appeared. Affected individuals aged 6–45 years, more often women, typically show a subtle keratoderma appearing after a few minutes of immersion of their hands in water or after sweating. Only in some patients are the soles affected. One characteristic sign might be that patients bring with them a vessel to immerse their hands in water (‘hands in the bucket’ sign). The painful, burning or itching, whitish papular lesions are associated with dilated acrosyringeal ostia, which can be seen by dermoscopy. Lesions subside shortly after drying the hands, leaving minimal hyperkeratosis in the centre of the palms. Differential diagnosis : Transient aquagenic keratoderma should be differentiated from other keratodermas that are sensitive to exposure to water, e.g. Bothnia type NEPPK. Importantly, aquagenic wrinkling of the palms is associated with cystic fibrosis (in about 50% of affected patients) and can be observed in up to 10% of heterozygous CFTR gene mutation carriers, , Epidemiology : nan, Complications : Hyperhidrosis, pruritus, Diagnostics : HISTOLOGIC EXAMINATION, Differential diagnosis : Non-epidermolytic palmoplantar keratoderma, disease description : Aquagenic keratoderma (AK) is a rare acquired condition consisting in recurrent and transient white papules and plaques associated with a burning sensation, pain, pruritus and/or hyperhidrosis on the palms and more rarely, soles triggered by sweat or contact with water.

Transient Erythroblastopenia Of Childhood

Disease Name : Transient Erythroblastopenia Of Childhood, Symptoms : CONGENITAL MALFORMATION, failure to thrive, lethargy, PALENESS OF BODY, breathlessness, Dizziness, pallor, Signs : anemia, Treatment : nan, Pathophysiology : nan, Epidemiology : nan, Complications : nan, Diagnostics : Reticulocyte Count, hemoglobin HB, THROMBOCYTE COUNT, Differential diagnosis : nan, disease description : Transient erythroblastopenia of childhood (TEC ) is the most common acquired red cell aplasia occurring in children. It is more prevalent than congenital hypoplastic anemia (Diamond-Blackfan anemia, DBA). This syndrome of severe, transient hypoplastic anemia occurs mainly in previously healthy children between 6 mo and 3 yr of age.

Transient Ischaemic Attacks

Disease Name : Transient Ischaemic Attacks, Symptoms : aphasia : Difficulty with or loss of speaking ability., diplopia : Diplopia refers to seeing two images and is due either to ocular misalignment, in which case it disappears when either eye is occluded or to an optical problem, in which case it is termed monocular diplopia and does not disappear with monocular viewing., dysarthria : Slurred or garbled speaking., headache : Headaches are usually sudden & severe., neurological disturbances : Includes confusion, amnesia, coma., vertigo : Affected individuals suffer from dizziness., vertigo : Affected individuals suffer from dizziness.s., MOOD CHANGES : Emotional instability and personality changes., hemiplegia : One-sided weakness or paralysis., Signs : nan, Treatment : In selected cases, a procedure called carotid angioplasty, or stenting, is an option. This procedure involves using a balloon-like device to open a clogged artery and placing a small wire tube (stent) into the artery to keep it open., Anti-platelet drugs.,Anticoagulants. These drugs include heparin and warfarin (Jantoven). They affect clotting-system proteins instead of platelet function. Heparin is used for a short time and is rarely used in the management of TIAs., If you have a moderately or severely narrowed neck (carotid) artery, your provider may suggest carotid endarterectomy (end-ahr-tur-EK-tuh-me). This preventive surgery clears carotid arteries of fatty deposits (atherosclerotic plaques) before another TIA or stroke can occur. An incision is made to open the artery, the plaques are removed and the artery is closed., Pathophysiology : A TIA has the same origins as that of an ischemic stroke, the most common type of stroke. In an ischemic stroke, a clot blocks the blood supply to part of the brain. In a TIA, unlike a stroke, the blockage is brief, and there is no permanent damage.The underlying cause of a TIA often is a buildup of cholesterol-containing fatty deposits called plaques (atherosclerosis) in an artery or one of its branches that supplies oxygen and nutrients to the brain.Plaques can decrease the blood flow through an artery or lead to the development of a clot. A blood clot moving to an artery that supplies the brain from another part of the body, most commonly from the heart, also may cause a TIA., Epidemiology : 1-3 cases per 100, 000 in those younger than 35 years to as many as 1500 cases per 100, 000 in those older than 85 years, variable, Sometimes, but not always. Many TIAs happen for preventable reasons. But a TIA can also happen for unpredictable or unexpected reasons.,,You can do many things to reduce your risk of having an ischemic stroke. While this doesn’t mean you can prevent a stroke, it can lower your risk. Actions you can take include : ,,See a primary care provider yearly for a checkup (this can detect symptomless concerns like high blood pressure and Type 2 diabetes sooner).,Reach and maintain a weight that’s healthy for you.,Manage what you eat (your primary care provider can guide you on this).,Stop using tobacco products (or don’t start using them in the first place).,Use alcohol only in moderation and avoid nonmedical drug use.,Take prescription medications exactly as instructed.,Manage any chronic conditions you have (such as high blood pressure, Type 2 diabetes and high cholesterol)., Complications : blindness, Speech Difficulties, Diagnostics : 2-D Echo, MRI, CT SCAN, Carotid Angiography, PHYSICAL EXAMINATION, Doppler ultrasound, Differential diagnosis : Haemorrhage, Meningitis, Meningococcal Meningitis, Multiple Sclerosis, syncope, disease description : A transient ischemic attack (TIA) is a stroke that lasts only a few minutes. It occurs when the blood supply to part of the brain is briefly interrupted.TIA symptoms, which usually occur suddenly, are similar to those of stroke but do not last as long. Most symptoms of a TIA disappear within an hour, although they may persist for up to 24 hours. Symptoms can include : Numbness or weakness in the face, arm, or leg, especially on one side of the bodyTrouble seeing in one or both eyesDifficulty with walking, dizzinessConfusion or difficulty in talking or understanding speechLoss of balance and coordination

Transposition Of The Great Vessels

Disease Name : Transposition Of The Great Vessels, Symptoms : pulse deficit : The pulse is weak in affected infants., Tachycardia : Infants presents with rapid heart rate., poor feeding : Infants struggle to feed further leading to weight loss & failure to thrive., Breathing difficulty : Infants often experience laboured breathing., Signs : cardiomegaly : Cardiomegaly with increased pulmonary vascular markings may be found if a ventricular septal defect is present., cyanosis : Bluish skin, lips and nails from not getting enough oxygen-rich blood., systolic murmur : A single second heart sound (S2) and a systolic ejection murmur may be present., Treatment : Prostagladin El can help reduce cyanosis in selected cases,by keeping the PDA open., 1.Balloon atrial septostomy,,2. Septostomy,,3. Arterial switch operation, Pathophysiology : In patients with TGA the oxygenated pulmonary venous blood recirculates in the lungs whereas the systemic venous blood recirculates in the systemic circulation. The pulmonary artery saturation is thus always higher than the aortic saturation. Survival depends on the mixing available between the two circulations. In patients with intact ventricular septum, the mixing site is the atrial communication. Generally, the atrial communication is the patent foramen ovale and this being small, the mixing is very poor . The neonates become symptomatic due to severe hypoxemia and systemic acidosis soon after birth. Presence of a VSD of adequate size results in good mixing. As the fetal pulmonary vasculature regresses, the pulmonary blood flow increases and results in congestive failure around 4-10 weeks of age. The failing left ventricle as well as the large pulmonary blood flow increase the left atrial pressure. The patients, therefore, have pulmonary venous hypertension as well. The mixing with a large VSD can be so good that at times cyanosis can be missed. The presence of a large VSD equalizes pressures in the two ventricles as well as the great arteries. The pulmonary artery also carries a large flow. Patients with TGA and a large VSD develop pulmonary vascular obstructive disease (Eisenmenger physiology) early in life., Epidemiology : 20-30 per 100, 000 live births, variable, If you have a family history of congenital heart defects or if you already have a child with one, consider talking with a genetic counselor and a cardiologist experienced in congenital heart defects before getting pregnant., Complications : heart failure, Hypoxia, PULMONARY ARTERIAL HYPERTENSION, Diagnostics : CARDIAC CATHETERIZATION, X RAY, CHEST RADIOGRAPH, Electrocardiography (EKG), Differential diagnosis : tetralogy of fallot, total anomalous pulmonary venous connection, tricuspid atresia, Truncus Arteriosus, disease description : Transposition of the great arteries (TGA) is a serious, rare heart problem in which the two main arteries leaving the heart are reversed. The condition is present at birth, which means its a congenital heart defect?.Symptoms of transposition of the great arteries after birth include : Blue or gray skin. Depending on the babys skin color, these color changes may be harder or easier to see.Weak pulse.Lack of appetite.Poor weight gain.

Transverse Myelitis

Disease Name : Transverse Myelitis, Symptoms : "leg weakness : Some people notice heaviness in the legs, or that theyre stumbling or dragging one foot. Others may develop severe weakness or even total paralysis.", Numbness : Some people with transverse myelitis report sensations of numbness, tingling, coldness or burning. Some are especially sensitive to the light touch of clothing or to extreme heat or cold. You may feel as if something is tightly wrapping the skin of your chest, abdomen or legs., "Pain : Transverse myelitis pain may begin suddenly in your lower back. Sharp pain may shoot down your legs or arms or around your chest or abdomen. Pain symptoms vary based on the part of your spinal cord thats affected.", bladder dysfunction : This may include needing to urinate more frequently, urinary incontinence, difficulty urinating., Signs : Areflexia, priapism : A sudden loss of sympathetic tone to the pelvic vasculature following SCI causes an increase in the parasympathetic tone and uncontrolled arterial blood flow into the penile sinusoidal spaces. Lesions and injuries of the cervical spinal cord are most frequently associated with priapism., spasticity : Patients with transverse myelitis are at risk of developing spasticity., "flaccid paralysis : Acute flaccid myelitis (AFM) is a rare neurological condition that causes your muscles and reflexes to become weak. It often affects your upper limbs and can affect the muscles you need to breathe as well. Because of this, its important to seek medical care as soon as possible if you or your child develop symptoms.", allodynia : Most people with transverse myelitis report heightened sensitivity to heat, cold, or touch; for some a light touch with a finger may cause significant pain., Treatment : medication : Cyclophosphamide , Rituximab, Methyl prednisolone , A psychotherapist can use talk therapy to treat anxiety, depression, sexual dysfunction, and other emotional or behavioral issues from coping with transverse myelitis., plasma exchange, There are no standards for the treatment of TM. Available evidence suggests that,modulation of the immune response may be effective in decreasing the severity,and duration of the condition. The use of high-dose steroids, particularly,methylprednisolone, is the initial approach to treatment of the childhood forms,of TM. If there is a poor response to high-dose steroids, other therapeutic,approaches for acute intervention include intravenous immunoglobulin and,plasma exchange. If the TM is secondary to an underlying antibody-driven,disorder, treatments such as rituximab or cyclophosphamide can be considered.,Long-term prophylactic therapy is recommended for children with recurrent,forms of the disease., Pathophysiology : They often have a history of an infectious disease, possibly of viral or mycoplasmal origin, or of an immunization within the few weeks preceding the development of their neurologic difficulties. The clinical loss of function is often severe and may seem complete. Although a slow recovery (weeks to months) is common in these cases, it is likely to be incomplete. The likelihood of independent ambulation in young children is approximately 40%. The pathologic findings of perivascular infiltration with mononuclear cells imply an infectious or inflammatory basis. Overt necrosis of the spinal cord may be seen and may be tied to specific etiologies, including infectious etiologies such as enterovirus infection. In older children, the syndrome may be different, and outcomes may vary by etiology. Although the onset is also rapid, with a nadir in neurologic function occurring between 2 days and 2 wk, recovery is more rapid and more likely to be complete. In a small but important number of cases, necrosis and irreversible injury may occur. The condition can be associated with underlying etiologies, including systemic vasculitic entities (e.g., SLE), antibody-mediated CNS disorders (e.g., AQP4-Ab or MOG-Ab-associated NMOSD), infectious etiologies (e.g., mycoplasma, enterovirus), or idiopathic disease. Pathologic or imaging examinations show acute inflammation with demyelination in some cases. There is no sex or familial predisposition in those with idiopathic TM. , Epidemiology : A bimodal age distribution is observed in those younger than 5 yr and older than 10 yr., estimated to affect around 2 per million children , GOOD, Unfortunately, transverse myelitis can’t be prevented., Complications : sensory disturbances, bladder dysfunction, Diagnostics : CSF EXAMINATION, MRI Brain, MRI Spine, lumbar puncture, MRI, Differential diagnosis : abscesses, neoplasms, spondylitis, disease description : Transverse myelitis is an inflammation of part of the spinal cord. The exact cause is often not known, but it sometimes happens after infections or in people with autoimmune diseases.Common symptoms are back or neck pain, weakness or sensation changes in the arms or legs, or loss of bladder or bowel control.Treatment with steroids or other drugs doesnt cure transverse myelitis, but it might relieve symptoms. Some people recover fully, while others might have minor or more serious long-term problems.

Traumatic Brain Injury

Disease Name : Traumatic Brain Injury, Symptoms : bleeding : Traumatic Subarachnoid Hemorrhage (tSAH) is bleeding into the space that surrounds the brain. This space is normally filled with cerebrospinal fluid (CSF), which acts as a floating cushion to protect the brain. Traumatic SAH occurs when small arteries tear during the initial injury., unconsciousness : Concussion or mTBI is defined as a loss of consciousness of less than 30 minutes or amnesia lasting less than 24 hours, or any period of altered mental status at the time of injury., vomiting : Vomiting is one of many effects that may occur after traumatic brain injury. Like all secondary effects, vomiting can range from mild, isolated episodes, to severe, persistent nausea and vomiting., cognitive impairment : Includes profound confusion, agitation, slurred speech & coma., Signs : convulsion : A seizure that occurs within 1 week of a TBI is called an early posttraumatic seizure. About 25% of people who have an early posttraumatic seizure will have another seizure months or years later. This is called epilepsy. A seizure that occurs more than 1 week after a TBI is called a late posttraumatic seizure., dilated pupils : Pupil dilation is thought to be the result of uncal herniation causing mechanical compression of the IIIrd cranial nerve and subsequent brain stem compromise., CSF RHINORRHOEA : Cerebrospinal fluid (CSF) rhinorrhea is a condition where the fluid that surrounds the brain leaks into the nose and sinuses. Head trauma can make a hole in the membranes that hold this fluid., anemia : Severe anemia is common after acute moderate to severe TBI, developing during the first 48 h after the trauma., Treatment : Counseling for emotional support. Many individuals experience stress and worries about their recovery. They may find that it is more difficult to get back to their work and hobbies than anticipated. Therefore, counseling is often very helpful in conjunction with other medical treatments., Rehabilitation, including physical, occupational and speech therapy., Rest. Talk to your doctor about how long to rest after a TBI. Depending on the type of TBI, some may need to rest for 1 to 2 days before going back to their typical activities. More severe head injuries may require longer periods of rest., Return to typical activities. For milder head injuries, sometimes if people rest for too long after their head injury, they may have more difficulty returning to work, school, and other activities like socializing and hobbies. For more severe injuries, returning to activities too soon can make symptoms worse. Talk to your doctor for specific recommendations., People with mild to moderate TBIs may only need minimal treatment. Your care may involve a short period of rest from sports, school or work. Symptoms should improve within a few weeks., Surgery to treat bleeding in the brain (intracranial hemorrhage) or reduce pressure from brain swelling., Pathophysiology : ConcussionThis is usually a mild TBI without any gross structural damage and occurs secondary to a nonpenetrating TBI. It usually results from acceleration/deceleration forces occurring secondary to a direct blow to the head. It causes a transient altered mental status, which can range from confusion to loss of consciousness. This cannot be diagnosed with a routine computed tomogram (CT) scan or magnetic resonance imaging (MRI) scan. Special sequence MRI like diffusion tensor imaging and functional MRI may result in earlier diagnosis of concussion.Extra-axial HematomaExtra-axial hematomas include both epidural hematomas (EDH) and subdural hematomas (SDH). EDH usually results from bleeding from the middle meningeal artery and its branches or a fracture and is usually acute.SDH can result from the bleeding of a bridging vein and can be acute or chronic.ContusionContusions (bruising of the brain) can be a coup or contrecoup type. Coup contusions occur at the site of impact, whereas contrecoup injuries typically take place on the contralateral side of impact, usually the basi-frontal lobe and anterior temporal lobe.Traumatic Subarachnoid Hemorrhage (SAH)Subarachnoid hemorrhage is most commonly caused by trauma and results from the tearing of small capillaries with blood subsequently entering into the subarachnoid space. It commonly occurs over the convexity, whereas SAH secondary to aneurysmal rupture occurs in the basal cisterns.Diffuse Axonal Injury (DAI)This can underlie mild to moderate TBI and potentially results from any shearing, stretching, or twisting injuries to the neuronal axons. This phenomenon is mainly seen at the junction of the gray and white matter where neuronal axons are entering a more dense, fatty (myelinated), and less fluid-filled white matter. Such shearing forces cause the neuronal axon to be stretched, and the subsequent damage to the cytoskeleton may lead to axonal swelling, increased permeability, calcium influx, detachment, and axonal death. Diffuse laminar necrosis is typically seen on autopsy., Epidemiology : 1.5 to 2 million persons are injured and 1 million succumb to death every year in India., Variable, Many TBIs aren’t preventable. They happen without warning due to an accident or fall. But you can take these steps to avoid some incidents that commonly cause TBIs : ,,Monitor medicines : Ask your doctor or pharmacist to review your prescription and over-the-counter medications, including supplements. Be sure you know which ones might make you dizzy, sleepy and more prone to falls. You may be able to change medications.,Have clear vision : Get regular eye exams so you can see well enough to prevent falls and injuries. Arrange good lighting at home to light the way.,Fall-proof your home : Remove rugs that are tripping hazards. Install stair handrails and bathtub grab bars. And if you have young children, install window guards on high windows and safety gates on stairs. Be aware of toys and pets underfoot.,Be smart behind the wheel : Buckle everyone up with seat belts, and use car seats or booster seats for children. Don’t drive if you’re drowsy or under the influence.,Put on a helmet : Protect your head when you play sports like hockey or football or when you bike, skate, ski or snowboard. And wear a helmet when you ride a motorcycle, scooter, ATV or horse.,Stay active : Activities like yoga, tai chi and strength training build muscle and improve balance.,Use a walking assist device : Walkers and canes can help you be steadier on your feet., Complications : deep vein thrombosis, Hydrocephalus, infection, insomnia, spasticity, Stroke, Vessel injury, Diagnostics : Complete Blood Count CBC, MRI Head, SINGLE-PHOTON EMISSION COMPUTED TOMOGRAPHY (SPECT), CT HEAD, CT SCAN, Differential diagnosis : Alzheimers Disease, aneurysms, hematomas, Hydrocephalus, Stroke, disease description : Traumatic Brain Injury (TBI) may result from anywhere between a simple blow to the head to a penetrating injury to the brain. In the United States, around 1.7 million people suffer TBI with older adolescents (ages 15 to 19 years) and older adults (ages 65 years and older) among the most likely to sustain a TBI. The frontal and temporal areas of the brain are the main areas involved. Mild TBI (mTBI), also known as brain concussion, initially considered as a benign event, has galvanized tremendous attention for some of its adverse neuropsychological outcomes in civilians (e.g., athletes who play contact sports) as well as military personnel. Moderate to severe TBI is a primary cause of injury-induced death and disability. In the United States, It has an annual incidence of approximately 500 in 100, 000. However, around 80% of all TBI cases are categorized as mild head injuries.

Traumatic Fat Necrosis

Disease Name : Traumatic Fat Necrosis, Symptoms : skin retraction : Fat necrosis of the breast most commonly presents as a mass. The mass is often firm and there may be skin retraction, thickening or tethering., lump : It may feel like a fatty lump or like a hard nodule. A lump occurs in the first stage of fat necrosis. As fat cells die, they release their oily contents, which collect into a pocket called an oil cyst. Over time, the walls of the cyst can calcify, causing them to harden. When cysts begin to break down, they may flatten., Tenderness : It usually doesn’t, but occasionally, the area may feel a little tender. Subcutaneous fat necrosis associated with panniculitis is more often painful because this type involves chronic inflammation., bumps under the skin : You may see a lump or bump under your skin. If much of the fat under your skin has died, it might appear dimpled or to sag. In your breast, fat necrosis might cause your nipple to sink in. When dying fat cells release inflammatory compounds, they can cause your skin to appear red or bruised, or to thicken., Signs : nan, Treatment : Healthcare providers use many of the same methods to remove fat necrosis as they would use to take a biopsy. In some cases, a biopsy taken for diagnostic purposes may also serve to remove your fat necrosis. Methods include : ,,Fine needle aspiration. This method uses a long, thin needle and syringe to extract cells, tissue and fluids without cutting your skin. The needle can be used to drain an oil cyst, which causes the lump to deflate.,Vacuum-assisted core needle biopsy. This method uses a wider, hollow needle to extract pieces of tissue through a small incision. Using ultrasound or X-ray imaging to guide the needle, healthcare providers attach a vacuum device to suction tissue through the chamber, similar to liposuction. This method can be done under local anesthesia.,Excision biopsy. A surgical cut to remove the tissue is a last resort, as surgery can cause further fat necrosis. However, some cases may require excision — for example, if the lump is too big to suck through a needle or if there’s a high suspicion of cancer. This operation may be done under local or general anesthesia. It leaves a small scar., If the fat necrosis contains oily fluid, it may need to be aspirated using a needle to relieve any patient discomfort. In the case of a solid mass and/or breast distortion, treatment options depend on the size of the anticipated defect after excision. A small defect may be addressed with either excision alone or excision with fat grafting and/or local tissue rearrangement. For a large defect such as those due to partial flap loss after reconstruction, a more significant tissue debridement and reconstruction may be necessary., Pathophysiology : Fat necrosis can also occur in other fatty areas such as your abdomen, buttocks and thighs as a result of medical or cosmetic procedures. For example, a tummy tuck may injure your abdominal fat tissue. Fat transfer procedures, such as the Brazilian butt lift (BBL), which take fat from one area and move it to another area, may injure the grafted fat along the way, causing necrosis and failure of the grafted tissue.A severe case of acute pancreatitis can sometimes cause fat necrosis in the fatty tissue surrounding your pancreas. When corrosive pancreatic enzymes leak into your body, they can inflame and irritate the surrounding tissues. Pancreatic fat necrosis usually affects your abdominal region, but occasionally, it can infiltrate the subcutaneous fat layer under your skin and spread throughout your body (panniculitis)., Epidemiology : (21 to 70%), The incidence of fat necrosis of the breast is estimated to be 0.6%, representing 2.75% of all breast lesions., variable, Avoid trauma, Complications : infection, Cosmetic disfigurement, Diagnostics : FNAC, mammography, biopsy, MRI, X RAY, EXCISIONAL BIOPSY, CT SCAN, USG, Differential diagnosis : Breast carcinoma, BREAST CYSTS , Fibroadenoma, phyllodes tumor, disease description : Fat necrosis is a form of necrosis that is caused by the action of lipases on adipocytes.In fat necrosis, the enzyme lipase releases fatty acids from triglycerides. The fatty acids then complex with calcium to form soaps. These soaps appear as white chalky deposits.It is usually associated with trauma of the pancreas or acute pancreatitis. It can also occur in the breast, 5 the salivary glands and neonates after a traumatic delivery

Traumatic Paraplegia

Disease Name : Traumatic Paraplegia, Symptoms : Numbness : Decreased sensation in the arms and or legs., respiratory symptoms : Respiratory impairment following spinal cord injury (SCI) is more severe in high cervical injuries, and is characterised by low lung volumes and a weak cough secondary to respiratory muscle weakness., weakness : Weakness in the arms and or legs., CHRONIC PAIN : Severe pain or pressure in the neck or back., Signs : bladder dysfunction : Although bladder and bowel sphincter tone may allow the paralyzed individual to maintain continence of urine and feces, the cord injury prevents the individual from contracting the bladder and relaxing the sphincters to facilitate elimination. Retained urine or feces is the most common cause of autonomic dysreflexia., Treatment : Phase I Emergency care at the scene of accident,and in the emergency department,Phase II Definitive care on in-patient basis,Phase III Rehabilitation, Surgery to treat swelling, remove lesions, or remove embedded objects.,Spinal cord alignment surgery.,Secondary surgeries to treat muscle injuries.,Medications to reduce your risk of infection and blood clots.,Physical therapy to help you regain as much function as possible., Pathophysiology : The displaced vertebra may either damage the cord (very unlikely), the cord along with the nerve roots lying by its side or the roots alone. Pathologically, damage to neural structures may be a cord concussion, cord transection or root transection . Cord concussion : In this type, the disturbance is one of functional loss without a demonstrable anatomical lesion. Motor paralysis (flaccid), sensory loss and visceral paralysis occur below the level of the affected cord segment. Recovery begins within 8 hours, and eventually the patient recovers fully. Cord transection : In this type, the cord and its surrounding tissues are transected. The injury is anatomical and irreparable. Initially, the motor paralysis is flaccid because the cord below the level of injury is in a state of ‘spinal shock’. After some time, however, the cord recovers from shock and acts as an independent structure, without any control from the higher centres. In this state, though the cord manifests reflex activity at spinal level, there is no voluntary control over body parts below the level of injury. There is total loss of sensation and autonomic functions below the level of injury. The appearance of signs suggestive of reflex cord activity i.e., bulbo-cavernosus reflex, anal reflex and plantar reflex, without recovery of motor power or sensations is an indicator of cord transection. These reflexes usually appear within 24 hours of the injury. In a few days or weeks, the flaccid paralysis (due to spinal shock) becomes spastic, with exaggerated tendon reflexes and clonus. Involuntary flexor spasms at different joints and spasticity leads to contractures. Sensation and autonomic functions never return. Root transection : Spinal nerve roots may be damaged alone in injuries of the lumbar spine, or in addition to cord injury, in injuries of the dorso-lumbar spine. Neurological damage in nerve root injury is similar to that in cord transection except that in the former residual motor paralysis remains permanently flaccid and regeneration is theoretically* possible. A discrepancy between the neurological and skeletal levels may occur in spinal injuries below D10 level because the roots descending from the segments higher than the affected cord level may also be transected, thereby producing a higher neurological level than expected. Incomplete lesions : Occasionally, the neurological lesion may be incomplete i.e., affecting only a portion of the cord. In these cases, there is evidence of neurological sparing distal to the injury (perianal sensation sparing is common). Such sparing is an indication of a favourable prognosis. Incomplete lesions may be of the following types. a) Central cord lesion : This is the commonest incomplete lesion. There is initial flaccid weakness followed by a lower motor neurone type of paralysis of the upper limbs and upper motor neurone (spastic) paralysis of the lower limbs, with preservation of bladder control and perianal sensations (sacral sparing). b) Anterior cord lesion : There is complete paralysis and anaesthesia but deep pressure and position sense are retained in the lower limbs (dorsal column sparing). c) Posterior cord lesion : It is a very rare lesion. Only deep pressure and proprioception are lost. d) Cord hemi-section (Brown-Sequard syndrome) : There is ipsilateral paralysis and contralateral loss of pain sensation.Cervical spine : In these injuries, the segmental level of the cord transection nearly always corresponds to the level of bony damage. A high cervical cord transection (above C5) is fatal because all the respiratory muscles (thoracic and diaphragmatic) are paralysed. Transection at the C5 segment results in paralysis of the muscles of the upper limbs, thorax, trunk, and lower limbs, with loss of sensation and visceral functions. With transection at level below the C5 segment, some muscles of the upper limbs are spared, resulting in characteristic deformities, depending upon the level. Thoracic lesion (between T1 and T10) : In cord transection from T1 to T10, trunk and lower limb muscles are paralysed. At the tenth thoracic vertebra, the corresponding cord segment is L1, so in injuries at this level, only the lower limbs are affected. Dorso-lumbar lesions (between D11 and L1) : Between 11th dorsal and 1st lumbar vertebrae lie all the lumbar and sacral segments along with their nerve roots. Hence, injuries at this level cause cord transection with or without involvement of nerve roots. This is the cause of difference in neurological deficit in fractures and fracture-dislocations with apparently similar X-ray appearances. In injuries of the cord with nerve root transection, paralysis in the lower limbs is mixed (UMN+LMN type). It is important to differentiate it from a lesion of cord transection with root escape, as the latter has a better prognosis. Lesions below L1 : This area of the canal has only bunch of nerve roots, which subsequently emerge at successive levels of the lumbo-sacral spine. Thus, injury in this area results in root damage, resulting in flaccid paralysis, sensory loss and autonomic disturbances in the distribution of the affected roots., Epidemiology : 50 per 100 000 population, 40 to 80 cases per million population, POOR, Avoid injuries, Complications : deep vein thrombosis, MUSCLE ATROPHY, spasticity, bladder dysfunction, bowel dysfunction, Diagnostics : CT/MRI, MRI, CT SCAN, Differential diagnosis : Spinal Neoplasia, thoracolumbar spine trauma, disease description : Traumatic paraplegia is caused by a lesion of the spinal cord which occurs after a trauma, e.g. vertebral fracture causing a puncture to the spinal cord. The most common causes of SCI in the world are traffic accidents, gunshot injuries, knife injuries, falls and sports injuries. 

Traumatic Rupture

Disease Name : Traumatic Rupture, Symptoms : tinnitus, pain in ear, DISCHARGE, nystagmus, vertigo, Epiphora, Signs : OTALGIA, Treatment : when edges of perforation ,get inverted towards the middle ear-edges of perforation repositioned and splinted, Pathophysiology : Tympanic membrane may be ruptured by : (a) Trauma due to a hair pin, matchstick or unskilled attempts to remove a foreign body. (b) Sudden change in air pressure, e.g. a slap or a kiss on the ear or a sudden blast. Forceful Valsalva may rupture a thin atrophic membrane. (c) Pressure by a fluid column, e.g. diving, water sports or forceful syringing. (d) Fracture of temporal bone., Epidemiology : GOOD, Complications : vertigo, FACIAL PARALYSIS, SENSORINEURAL HEARING LOSS, Diagnostics : Examination under Microscope, Differential diagnosis : Acute Otitis Media, CHOLESTEATOMA, OTITIS EXTERNA, disease description : Tympanic membrane may be ruptured by : (a) Trauma due to a hair pin, matchstick or unskilled attempts to remove a foreign body. (b) Sudden change in air pressure, e.g. a slap or a kiss on the ear or a sudden blast. Forceful Valsalva may rupture a thin atrophic membrane. (c) Pressure by a fluid column, e.g. diving, water sports or forceful syringing. (d) Fracture of temporal bone.

Tremor

Disease Name : Tremor, Symptoms : tremor, Signs : nan, Treatment : medication : Primidone , Propranolol , Pathophysiology : Tremor consists of alternating contractions of agonist and antagonist muscles in an oscillating, rhythmic manner. It can be most prominent at rest (rest tremor), on assuming a posture (postural tremor), on actively reaching for a target (kinetic tremor), or on carrying out a movement (action tremor). Tremor may also be characterized based on distribution, frequency, amplitude, and related neurologic dysfunction., Epidemiology : depends on cause of tremor, Complications : nan, Diagnostics : EEG, Differential diagnosis : ANXIETY, panic attacks, Parkinson’s Disease, disease description : Hyperkinetic movement disorders are characterized by involuntary movements unaccompanied by weakness. This term is somewhat arbitrary and potentially misleading as hypokinetic disorders such as Parkinson’s disease (PD) are often accompanied by tremor which is a hyperkinetic feature, and hyperkinetic disorders such as dystonia may manifest slow movements because of the severe muscle contractions. Nonetheless, the terms continue to be used because of convention. The major hyperkinetic movement disorders and the diseases with which they are associated are considered in this section.

Trench Fever

Disease Name : Trench Fever, Symptoms : headache : Affected individuals suffer from severe headaches., soreness : Trench fever causes soreness of the muscles of the legs and back., fever : The disease is classically a five-day fever of the relapsing type, rarely exhibiting a continuous course. The incubation period is relatively long, at about two weeks. The initial fever is usually followed in a few days by a single, short rise but there may be many relapses between periods without fever., hyperesthesia : Hyperesthesia of the shin. Hyperesthesia is a neurological condition that causes a person extreme sensitivity to touch, pain, pressure, and thermal sensations., Signs : splenomegaly : Trench fever episodes may involve spleen enlargement., Treatment : "Optimal management for trench fever is uncertain due to limited published data. The recommended treatment depends on the patients presentation. For acute or chronic infection, doxycycline 200mg for four weeks daily in combination with gentamicin 3 mg/kg intravenously once daily for the first 14 days. If gentamicin is not an option due to availability, allergies, or other contraindications, rifampin 300 mg twice a day for the first 14 days is recommended.", Pathophysiology : Bartonella quintana is carried predominately by a vector body louse as it reproduces in the intestinal lumen. The infected louse transmits the disease via inoculation of contaminated feces into exposed skin or conjunctivae. The Medical Research Committee, set up by the American Red Cross, documented this transmission route in 1918. Hence, expedited transmission can be detected in crowded living conditions and poor hygiene, such as homelessness and its associated alcohol abuse., Epidemiology : more than 1 million soldiers during World War I and is often linked to those suffering from homelessness and/or poor hygiene, spontaneous recovery, Trench fever can present as non-specific symptoms but should be considered in patients known to live in clustered areas with inadequate hygiene. It is essential to find all Bartonella species, including B. quintana, in blood culture-negative endocarditis to avoid further treatment delay. Consider utilizing polymerase chain reaction in addition to blood culture for diagnosis. Consider adding an aminoglycoside, especially in severely ill patients with endocarditis who are at risk for Bartonella quintana infection., Complications : Angiomatosis, chest pain, Endocarditis, shortness of breath, Diagnostics : Bacteria Culture Test, ELISA, RT PCR, PCR tests, Differential diagnosis : Leptospirosis, Malaria, Rocky Mountain spotted fever, typhus, disease description : Trench fever is an infection caused by Bartonella quintana, which is an aerobic gram-negative rod bacteria. It can vary in presentation, from non-specific symptoms such as fever, rash, malaise, and lumbago to bacteremia, endocarditis, and bacillary angiomatosis.

Trench Foot

Disease Name : Trench Foot, Symptoms : erythema : In the setting of cold exposure, vascular changes resulting in poor blood flow can result in the feet becoming erythematous or cyanotic., Numbness : The first symptoms of trench foot include tingling and itching which can progress to numbness. Your feet may feel prickly or heavy, like blocks of wood. Because of this, you may have difficulty walking. Your feet may be bright red. But they’ll soon turn pale, clammy and white as your blood vessels narrow., temperature instability : Your skin may become overly sensitive to changes in temperature and the lightest touch., Signs : nan, Treatment : Treatment for trench foot includes gentle rewarming of your foot. Rapid rewarming can cause severe pain and swelling. To get rid of trench foot, your healthcare provider will also clean your foot and keep it dry and warm. Additional treatment includes resting and elevating your foot above your heart. This can help prevent new wounds and blisters.,,Your healthcare provider may prescribe an antibiotic to prevent any infections. You may receive a tetanus booster shot. For pain, you can take nonsteroidal anti-inflammatory drugs (NSAIDs) or acetaminophen. But your healthcare provider may prescribe a medication called amitriptyline., Pathophysiology : The pathological changes are those of dependent oedema and lymphovenous stasis. Perivascular inflammation occurs and in severe cases arterial occlusion and ischaemic necrosis. There is damage to both myelinated and unmyelinated nerve fibres., Epidemiology : Official statistics put the casualty figure for the condition at around 75, 000 for the British and 2, 000 for the Americans., Changes may persist for months or years., Trench foot is very preventable. The following precautions may help prevent you from developing the condition : ,,Change out of wet socks and shoes/boots as soon as possible.,Let your feet air-dry and make sure your feet stay dry.,Keep your feet elevated when possible.,Change into a new pair of socks at least once a day.,Wear properly fitting boots or shoes., Complications : swelling, Sensory neuropathies, Diagnostics : X RAY, PHYSICAL EXAMINATION, Differential diagnosis : CELLULITIS, FROSTBITE, disease description : Trench foot is a condition you can develop if you stand in a cold, wet environment for an extended period of time. Symptoms of trench foot include numbness, pain, redness and swelling. Trench foot occurs when cold temperatures and moisture combine, causing restricted blood flow to your foot?. 

Trichiasis

Disease Name : Trichiasis, Symptoms : eyes irritation, Lacrimation, pain in eyes, photophobia, FOREIGN BODY SENSATION IN EYE, Signs : Conjunctival congestion, Misdirected cilia, Treatment : 1.Epilation, 2.Electrolysis, 3.Diathermy, 4.Cryoepilation, , When many cilia are misdirected,operative treatment similar to cicatricial entropion,should be employed., Pathophysiology : Any condition causing entropion will cause trichiasis, trachoma and spastic entropion being among the most common, while other causes are blepharitis, pemphigoid and scars resulting from injuries, chemical burns, operations, or destructive inflammations such as Stevens– Johnson syndrome and diphtheria. A few of the lashes may be affected or the condition may be due to entropion involving the whole margin of the lid. It may also be caused by congenital distichiasis. Symptoms. These include foreign body sensation and photophobia. Patient may feel troublesome irritation, pain and lacrimation. Signs. Examination reveals : • Misdirected cilia one or more touching the cornea. • Reflex blepharospasm and photophobia occur when cornea is abraded. • Conjunctiva may be congested. • Signs of causative disease viz. trachoma, blepharitis, etc. may be present., Epidemiology : GOOD, Complications : CORNEAL OPACITIES, corneal abrasions, corneal vascularisation, non-healing corneal ulcer, Diagnostics : VISUAL ACUITY TEST, ophthalmoscopy, Differential diagnosis : blepharitis, CHEMICAL INJURIES TO EYE, severe erythema multiforme, Trachoma, disease description : It refers to inward misdirection of cilia (which rub against the eyeball) with normal position of the lid margin. Pseudotrichiasis. The inward turning of lashes along with the lid margin (seen in entropion) is called pseudotrichiasis.

Trichilemmoma

Disease Name : Trichilemmoma, Symptoms : papules, Signs : a characteristic ‘cobblestone’ appearance of the oral epithelium, multiple skin tags, squamous papillomas and sclerotic fi bromas (storiform collagenomas), Treatment : surgical excision to carbon dioxide laser tissue ablation for multiple cases., Pathophysiology : Pathology These lesions are well-circumscribed lobular tumours extending down from the epidermis and often connected to a hair follicle. Tumour cells display prominent clear cytoplasm secondary to the deposition of glycogen. The presence of glycogen can be confi rmed with a positive periodic acid–Schiff (PAS) stain, which becomes negative after treatment with diastase. There is an irregular enclosing PAS-positive diastase-resistant membrane. In a number of cases, there is prominent hyperplasia of the surface epithelium, with hypergranulosis, clumping of keratohyalin granules and hyperkeratosis. This suggests induction of some lesions by HPV. A viral aetiology has been confi rmed by demonstration of HPV DNA by polymerase chain reaction in some but not in all cases of the tumour . Trichilemmomas are often found within a naevus sebaceous. A variant of trichilemmoma, described as desmoplastic trichilemmoma, is more rarely seen. The periphery of this lesion has histological features identical to those of ordinary trichilemmoma, but towards the centre there are strands of squamous cells embedded in a desmoplastic stroma. This stroma appears to contain type I collagen and tenascin but not laminin or type IV collagen. This results in an infi ltrative appearance that may be confused with a squamous cell carcinoma, particularly in small biopsy samples. Genetics Mutations of the PTEN tumour suppressor gene on chromosome 10q23 are found in Cowden syndrome. The number of mutations identifi ed is large and continues to increase . It seems that the benign lesions in Cowden syndrome occur without loss of the second PTEN allele while the malignant tumours require inactivation of both alleles and additional somatic mutations . Only rarely sporadic trichilemmomas show loss of PTEN, Epidemiology : The incidence of this condition is estimated to 1 , Solitary trichilemmoma is a relatively common lesi, The lesion although benign can recur if treated by, Complications : nan, Diagnostics : nan, Differential diagnosis : nan, disease description : This lesion is classically considered to be a proliferation of the external root sheath of the hair follicle. However, immunohistochemical studies with different molecular weight keratins normally expressed by different components of the hair follicle have not only confi rmed the latter but suggest that the lesion also displays infundibular keratinization. Age Lesions usually present in young and middle-aged adults. Sex The solitary variant shows no sex predilection but lesions in patients with Cowden syndrome show a slight female predominance

Trichinellosis

Disease Name : Trichinellosis, Symptoms : abdominal cramp : Abdominal discomfort and cramps may occur., Cardiac Disease : Cardiac system involvement occurs during the third week of infection. Death may result from congestive heart failure and/or arrhythmias., Flu-like illness : Includes fever, headaches, chills, muscle soreness., Gastrointestinal symptoms : The intestinal phase usually causes symptoms in the first week of illness. Diarrhea is the most common symptom. Constipation, anorexia, and diffuse weakness may occur. Occasionally, severe enteritis due to a massive inoculum of Trichinella species occurs. Symptoms typically last 2-7 days but may persist for weeks. With certain Trichinella species and in certain population groups and geographic regions, the disease may not progress beyond the intestinal stage. Nausea is reported in 15% of patients, vomiting in 3%, and diarrhea in 16%., respiratory difficulties : Patients present with dyspnea, a cough, and hoarseness., eye problem : Trichinellosis causes pain and swelling around the eyes., Neurological symptoms : Approximately 52% of patients present with headaches; other symptoms include deafness, ocular disturbances, weakness, and monoparesis., Signs : maculopapular rash : Maculopapular rash in cervical, scapular, and dorsal regions caused by Trichinella spp. infection., Treatment : medication : Noscapine , Albendazole , Mebendazole , Prednisolone, Acamprosate calcium, Pathophysiology : When a human or animal eats meat that contains infective Trichinella larvae, the acid in the stomach dissolves the hard covering of the cyst around the larvae and releases the worms. The worms pass into the small intestine and, in 1–2 days, become mature. After mating, adult females lay eggs. Eggs develop into immature worms, travel through the arteries, and are transported to muscles. Within the muscles, the worms curl into a ball and encyst (become enclosed in a capsule). The life cycle repeats when meat containing these encysted worms is consumed by another human or animal., Epidemiology : an estimated 10, 000 cases of trichinellosis occur every year, poor, You can’t tell if the meat you’re eating has worms just by looking at it. Parasites can only be seen with a microscope. However, there are several things you can do to reduce your risk of being infected with trichinosis. One basic thing is to always wash your hands with soap and water before and after you touch raw meat or any food.,,1. Cooking - Be sure you cook any meat you eat, especially pork and wild game, thoroughly. Use a food thermometer to cook it to recommended temperatures, after washing your thermometer with soap and water.,2. Freezing. ,3. Other processing - U.S. cases of trichinosis in previous years were caused by eating undercooked pork, but a successful education campaign reduced those numbers., Complications : ENCEPHALITIS, heart failure, myocarditis, pneumonitis, Diagnostics : Complete Blood Count CBC, CPK, EOSINOPHILS - ABSOLUTE COUNT, ECG, X RAY CHEST, biopsy, CT SCAN, serum creatine phosphokinase, Rbc antibody screen, Differential diagnosis : Dermatomyositis, gastroenteritis, periorbital cellulitis, POLYMYOSITIS, disease description : Trichinellosis, also called trichinosis, is caused by eating raw or undercooked meat of animals infected with the larvae of a species of worm called Trichinella. Infection occurs commonly in certain wild carnivorous (meat-eating) animals such as bear or cougar, or omnivorous (meat and plant-eating) animals such as domestic pigs or wild boar.

Trichinosis

Disease Name : Trichinosis, Symptoms : Malaise, muscle pain, sweating, vomiting, fever, Abdominal Pain, paralysis of the muscles of the tongue, jaw and respiration, Signs : conjunctivitis, maculopapular rash, periorbital swelling, splinter haemorrhages beneath the nails, Treatment : medication : Albendazole , Mebendazole , Management of the disease with systemic symptoms including central nervous system involvement, cardiac inflammation or pulmonary infiltration consists of combined use of ,a corticosteroid and an antiparasitic agent. Corticosteroids ,are life saving in suppressing allergic reaction at the height ,of larval spread. Mebendazole and albendazole reduce the ,severity of infection if given early enough in the acute disease, but albendazole is possibly more effective. However, once the parasites are encysted in muscle, antiparasitics ,are ineffective., Pathophysiology : Humans acquire the disease by eating raw or undercooked meat infected by Trichinella spiralis – such as bush pig in Africa, polar and black bear meat in Alaska and the Arctic. Entire polar expeditions have died of the infection after eating polar bear. Pathology Intestinal infection causes partial villous atrophy and mucosal and submucosal inflammation. The deposition of larvae in muscles is associated with oedema, loss of cross striations and basophilic degeneration. The coiled larvae are surrounded by an inflammatory infiltrate of lymphocytes and macrophages until they become encapsulated. Encysted larvae of Trichinella spiralis are ingested in meat, hatch in the duodenum, penetrate the submucosa and within 5 days have matured and mated and started producing 200– 2000 invasive larvae, which reach muscles where they become encysted and infective to a fresh host within 21 days. The adult worms live less than 2 months. Cysts may calcify, but the larvae remain viable for many years and can outlive their dead host by 10 days., Epidemiology : An estimated 10, 000 cases occur worldwide annually., variable, Complications : hair loss, hearing disturbances, heart failure, menstrual irregularities, still-birth, Diagnostics : Erythrocyte Sedimentation Rate (ESR), stool microscopy, ELISA, EOSINOPHILS, Differential diagnosis : Ascariasis, Gnathostomiasis, Hookworm Infestation, Lymphatic Filariasis, schistosomiasis, Strongyloidiasis, disease description : Trichinosis is an infection of the intestine and muscle, with Trichinella spiralis, a natural worldwide parasite of a wide range of carnivores. The human is normally an end host. A variety of allergic phenomena characterize human infection.

Trichoblastoma

Disease Name : Trichoblastoma, Symptoms : papules : It typically presents as a solitary mass of small skin-coloured to brown or blue-black papules or nodules, usually 1-2 cm in diameter. They most commonly occur on the face and scalp of adults around 40-50 years of age., LESIONS : Lesions are found within naevus sebaceous and trichoblastoma is regarded as the most common neoplasm occurring in this hamartoma., Signs : nan, Treatment : Complete excision is often desirable as exclusion of a basal cell ,carcinoma may be diffi cult in small biopsies., Trichoblastoma is a benign follicular tumour that requires no treatment. However, because of its association with basal cell carcinoma and the chance that it may transform into trichoblastic carcinoma, additional biopsy or complete surgical excision or Mohs micrographic surgery should be considered if there is uncertainty about the diagnosis.,,Occasionally true trichoblastomas may be excised for cosmetic reasons or if they occur in functionally sensitive areas. Treatment options include curettage and electrodesiccation or surgical excision., Pathophysiology : Nests of basophilic basaloid cells with a lobular architecture and prominent induction of stroma are seen in the dermis and/or subcutaneous tissue. Focal evidence of follicular differentiation is seen, but this usually consists of less mature structures than those seen in trichoepithelioma. Characteristically, condensation of cellular stroma is seen around aggregates of basaloid cells but true follicular papillae are not usually formed, as the stroma does not invaginate into the epithelial component. Mitotic fi gures vary and may be frequent. Usually, the tumour is not connected to the epidermis. According to the degree of follicular differentiation and the amount of stroma induced, lesions have been subclassifi ed into different categories, including trichogenic and trichoblastic fi bromas. However, all tumours in this category are best classifi ed as variants of trichoblastoma. Some tumours display sebaceous and even ductal (apocrine) differentiation confi rming the theory that they differentiate towards the folliculosebaceous and apocrine germ. , Epidemiology : Both sexes are affected eadults around 40-50 years of age..qually., Trichoblastoma and syringocystadenoma papilliferum were the most frequent benign tumors, occurring in 7.4% and 5.2% of cases, good, NA, Complications : post-surgical complications, Diagnostics : Immunostaining, Differential diagnosis : Basal cell carcinoma, disease description : Trichoblastoma is a rare, slow-growing, benign cutaneous tumor derived from follicular germinative cells 1-3. Headington first illustrated trichoblastoma in 1970 as a follicular differentiated neoplasm 4. In 1993, Ackerman et al. further described trichoblastoma to include all follicular germinative cell-derived benign cutaneous tumors 5, 6.The main differential diagnosis for trichoblastoma is basal cell carcinoma, since the two resemble one another both clinically and dermoscopically . Basal cell carcinoma, first described in 1827 by Jacob, is the most common malignancy worldwide, accounting for 75% of all cutaneous malignancies . Basal cell carcinoma is derived from basal cells of the epidermis, and rare subtypes such as infundibulocystic basal cell carcinoma originate from hair follicle-derived cells . While basal cell carcinoma rarely metastasizes, it is locally invasive. In contrast, trichoblastoma rarely undergoes a malignant transformation into trichoblastic carcinoma, which is a locally invasive and metastatic tumor

Trichodysplasia Spinulosa

Disease Name : Trichodysplasia Spinulosa, Symptoms : eruptions : Trichodysplasia spinulosa presents as an eruption of flesh coloured follicular papules each with a central keratin spine. These are usually located over the nose and forehead, but can more rarely affect other areas of the body including the ears and trunk., alopecia : Trichodysplasia spinulosa can result in hair loss (localised alopecia)., madarosis : This most commonly affects the eyebrows but can also affect eyelashes., Signs : nan, Treatment : medication : Valganciclovir , Cidofovir , Tazarotene, Epigallocatechin gallate, Antiviral treatment has been successful ,in some patients and one patient responded to surgery followed by topical tazarotene.,,,,First line,•\tReduction of immunosuppression : if feasible,•\tOral valganciclovir : successful response has been reported in ,four patients,•\tTopical cidofovir : four of five patients who were treated ,improved,Second line,•\tTopical tazarotene : one patient improved with topical tazarotene ,after skin lesions were shaved off under local anaesthesia 11,Third line,•\tOne patient treated with a topical compound of aciclovir, ,2-deoxy-d-glucose, and epigallocatechin (green tea extract) ,showed improvement., Topical cidofovir 3% has been recommended as a first-line treatment for trichodysplasia spinulosa based on a trend of treatment success in case reports. Topical cidofovir as a possible treatment is further supported by in vitro evidence that cidofovir inhibits human polyomavirus replication. Oral valganciclovir has also been effective in several cases and is more accessible than topical cidofovir but lacks the evidentiary support of in vitro or in vivo studies showing activity against human polyomavirus. Regarding reducing immunosuppressive therapy, the risk of sub-therapeutic dosing, transplant rejection, and progression or relapse of underlying disease often outweighs the benefit of reversing trichodysplasia spinulosa., Pathophysiology : Hypotheses about the potential pathophysiology of trichodysplasia spinulosa are as follows : symptomatic reactivation of latent TSPyV due to immunosuppression, repeat exposure to TSPyV while immunosuppressed, and fulminant primary infection with TSPyV while immunosuppressed., Epidemiology : Due to the rarity of this condition and the limited number of case reports, there is insufficient data to establish valid patterns of geographic distribution., variable, NA, Complications : FACIAL DYSMORPHISM, pruritus, Diagnostics : Immunofluorescence, Antibody Serology Tests, PCR, ELECTRON MICROSCOPY, Differential diagnosis : Lichen spinulosus, Trichostasis spinulosa, disease description : Trichodysplasia spinulosa is a rare dermatologic condition characterized by painless erythematous papules on the face with folliculocentric keratin spines. This condition is unique to patients with trichodysplasia spinulosa-associated polyomavirus (TSPyV) in the setting of immunosuppression. 

Tricholemmoma

Disease Name : Tricholemmoma, Symptoms : papules : Trichilemmoma typically presents as a solitary papule or mass of small skin-coloured papules that are 1-5 cm in diameter. These lesions slowly grow over time and tend to form small plaques that may resemble a wart/verruca or a cutaneous horn. They most commonly occur around the central part of the face, ears and neck, but also occur on the forearms and hands., solitary plaque : Solitary trichilemmomas are relatively common benign follicular tumours and occur in both male and females usually between 20-80 years of age. Desmoplastic trichilemmomas, a subtype of trichilemmoma, mainly occurs in white males around 50 years old. Lesions of this subtype are usually less than 1 cm in diameter and occur mainly on the face, neck and scalp, and sometimes on the chest and vulva., Signs : nan, Treatment : curettage and electrodesiccation,surgical excision,Mohs micrographic surgery .,carbon dioxide laser therapy, Topical 5-fluorouracil,Oral retinoids, Shave biopsy,Surgical excision, Pathophysiology : Derived from the outer root sheath of the hair follicle .Defects in the PTEN pathway have been associated with CS, Bannayan-Riley-Ruvalcaba syndrome, Proteus or Proteus-like syndrome, adult Lhermitte-Duelos disease, and autism-like disorders associated with macrocephaly. While the exact relationship between PTEN gene mutations and the development of trichilemmomas is unknown, defects in the PTEN pathway cause disordered cellular growth, which is likely involved in the pathogenesis of trichilemmomas., Epidemiology : Cowden syndrome is thought to affect 1/200, 000 to 1/250, 000 people. The penetrance of this autosomal dominant disorder is nearly complete, with almost 90% of patients affected with mucocutaneous lesions by age 20; however, the onset of skin signs can vary from 4 to 75 years., Their true incidence is hard to determine and is probably underestimated. Approximately 40 cases per 100, 000 c, variable, NA, Complications : post-surgical complications, Diagnostics : BIOPSY FROM SKIN LESION, Dermoscopy, Differential diagnosis : Basal cell carcinoma, Molluscum Contagiosum, Squamous cell carcinoma, disease description : Trichilemmoma, also called tricholemmoma is a benign tumour originating from the outer root sheath of the hair follicle. Diagnosis depends on careful histopathological examination of a skin biopsy.Trichilemmoma often occurs alongside other skin lesions such as trichoblastoma, sebaceous adenoma and sebaceous naevus. Occasionally trichilemmoma may appear as a new growth within a sebaceous naevus lesion.Multiple trichilemmoma on the face is often associated with Cowden disease, a rare inherited condition characterized by multiple types of skin tumours which can be found throughout different body systems. Although multiple trichilemmoma associated with Cowden disease is very rare, it is important to re-evaluate patients for this disease if a diagnosis of trichilemmoma is confirmed.

Trichomoniasis

Disease Name : Trichomoniasis, Symptoms : Burning pain : Burning after ejaculation or painful urination., Irritation : Irritation or itching inside the penis., Redness : Genital redness, burning and itching., Vaginal Discharge : A large amount of a thin, often foul-smelling discharge from the vagina — which might be clear, white, gray, yellow or green., DISCHARGE : Froth-like discharge from your penis., DYSPAREUNIA : Pain or discomfort during intercourse., Signs : nan, Treatment : medication : Tinidazole , Ornidazole , Povidone iodine , Your health care provider may recommend one large dose (megadose) of either metronidazole (Flagyl), tinidazole (Tindamax) or secnidazole (Solosec). You only take these oral medications one time., Pathophysiology : There is no doubt that this infection is sexually transmissible but, in some instances, it can be acquired by inadequate hygiene or the use of an infected person’s towels, bath or clothes. Its ingress to the vagina is favoured by a low general resistance and when the pH is raised as during a menstrual period (pH 5–6). It is not uncommon during pregnancy and is often associated with gonococcal infection. The Trichomonas vaginalis is a protozoan, actively motile and slightly larger than a leucocyte and is anaerobic. Three types of trichomonas are known. Men may harbour Trichomonas vaginalis in the urethra and prostate. A trichomonad has four anterior flagella and one posterior flagella, and they move along the mucous membrane. The posterior flagella are responsible for motility., Epidemiology : s 16%, GOOD, If you’re sexually active, you can take these steps to protect yourself against getting or spreading trich and other STIs : ,,Use condoms.,Get tested routinely for trich and other STIs.,Get treated if you have trich or other STIs.,Tell your sexual partners if you have trich so they can get tested and treated.,Engage in a monogamous relationship with one sexual partner.,Limit your number of sexual partners., Complications : low birth weight, Premature rupture of membranes, preterm labour, Diagnostics : Peripheral Blood Smear, PCR, NAAT TEST, Examination under Microscope, Differential diagnosis : bacterial vaginosis, PID, vaginitis, disease description : Trichomoniasis is a common sexually transmitted infection caused by a parasite. In women, trichomoniasis can cause a foul-smelling vaginal discharge, genital itching and painful urination.Men who have trichomoniasis typically have no symptoms. Pregnant women who have trichomoniasis might be at higher risk of delivering their babies prematurely.Treatment for trichomoniasis is taking an antibiotic — either metronidazole (Flagyl), tinidazole (Tindamax) or secnidazole (Solosec). To prevent being infected again, all sexual partners should be treated at the same time. You can reduce your risk of infection by using condoms correctly every time you have sex

Trichomycosis Axillaris

Disease Name : Trichomycosis Axillaris, Symptoms : sweating : Trichomycosis axillaris causes sweaty, smelly armpits. Sweat is also discoloured yellow, red or black, and may stain clothing ., NODULES : Trichomycosis axillaris is a superficial bacterial infection of underarm hair. The disease is characterised by 1–2 mm yellow, red or black concretions encircling the hair shaft, which make the hair appear beaded or thicker. Yellow concretions are the most common, whilst red and black are found in tropical climates., hair loss : Hair loss is rare, and is due to bacteria invadind and destroying the hair shaft., Signs : nan, Treatment : In general therapy of trichomycosis, many authors consider that the most effective treatment consist in shaving of the affected area for a period of 2-3 weeks, but the use of a concomitant treatment, such as sulfur soaps, is also recommended. ,Topical treatments containing any of the following : 3% sulfur, 2% formalin, 1% mercury (II) chloride (or mercuric chloride) or 2% sodium hypochlorite, as well as topical antibiotics with fusidic acid, erythromycin and clindamycin, may also be used., The use of an effective antiperspirant such as aluminium chloride ,is a rapid means of therapy., Pathophysiology : Studies using transmission and scanning electron microscopy have shown that the concretions consist almost exclusively of tightly packed bacteria. They grow within and between the cuticular cells and may invade the cortex. Cultural studies have shown a variety of different biochemical types of aerobic corynebacteria to be involved and not the single species, C. tenuis, as was at one time believed. These biotypes probably reflect the range of resident coryneform types in the normal axilla. It has been shown that changes in the chemical environment of these organisms may induce pigment production, perhaps explaining the different colours of the nodules, which are not attributable to different bacterial strains., Epidemiology : incidence of the condition of 23%, after examining 100 consecutive patients in the United States., Chronic but fluctuates in severity, You should be able to stop your trichomycosis from coming back if you follow good hygiene and keep your underarms clean and dry. Use antiperspirant daily and after washing to reduce excess moisture and the collection of bacteria. Using antibacterial soap can also help to eliminate bacteria., Complications : secondary infection, Diagnostics : Potassium hydroxide (KOH) mount, Fluorescence with Wood’s light, direct microscopy, Differential diagnosis : Black piedra, PEDICULOSIS PUBIS, disease description : Trichomycosis is asymptomatic, superficial infection, which is generally caused by a coryneform-actinomycetes bacteria which, from the very first reports, has been called Corynebacterium tenuis. While on rare occasions the pubic, scrotal and intergluteal hairs may also be affected, this infection predominantly affects the hairs of the axilla, and thus the condition is referred to as “trichomycosis axillaris.”

Tricuspid Regurgitation

Disease Name : Tricuspid Regurgitation, Symptoms : Arrhythmias : Tricuspid regurgitation causes irregular heart rhythms., swelling : Swelling in the abdomen, legs or neck veins, shortness of breath : Shortness of breath with activity., Signs : ascites : Chronically, tricuspid regurgitation leads to RV volume overload, which results in right-sided congestive heart failure (CHF). This manifests as ascites., PANSYSTOLIC MURMUR : The pansystolic murmur associated with tricuspid regurgitation is high pitched and is loudest in the fourth intercostal space in the parasternal region. The murmur is usually augmented during inspiration and is reduced in intensity and duration in the standing position and during a Valsalva maneuver., strong pulsations in abdomen : An unusually strong pulse in your neck or near your liver., Treatment : Drugs to remove extra fluids from the body (diuretics),Drugs to control irregular heartbeats (anti-arrhythmics),Other drugs to treat or control heart failure, TR may resolve following mitral,valvotomy. In those patients undergoing surgery for the,MR, the tricuspid valve can be inspected and tricuspid,annuloplasty or repair performed if needed., Tricuspid valve repair.,Tricuspid valve replacement.,Catheter procedure., Pathophysiology : The tricuspid valve sits between the hearts two right chambers. The tricuspid valve consists of three thin flaps of tissue (called cusps, or leaflets). These valve flaps open to let blood flow from the upper right chamber (right atrium) to the lower right chamber (right ventricle). The valve flaps then close tightly to prevent the blood from moving backward.In tricuspid valve regurgitation, the tricuspid valve doesnt close tightly. As a result, blood leaks backward into the right atrium., Epidemiology : the prevalence of moderate and severe TR is estimated to be around 1, 600, 000, Tricuspid regurgitation (TR) occurs in 65–85% of the population, GOOD, It’s not always possible to prevent this condition, which has many possible causes. But you can take some steps to lower your risk.,,Many different forms of heart disease can cause tricuspid regurgitation. So, keeping your heart as healthy as possible can help lower your risk of heart diseases that lead to a leaky valve. Here are some tips.,,Follow a heart-healthy eating plan, like the Mediterranean Diet.,Build up to at least 150 minutes of moderate-intensity exercise per week.,Avoid all tobacco products.,Avoid or limit alcohol.,See a healthcare provider for a yearly check-up., Complications : atrial fibrillation, heart failure, Diagnostics : 2-D Echo, ECG, doppler echocardiography, CHEST X RAY, CT SCAN, Differential diagnosis : ascites, atrial fibrillation, cardiogenic shock, CIRRHOSIS, Dilated cardiomyopathy, Ebstein Anomaly, heart failure, Marfan syndrome, mitral regurgitation, disease description : Tricuspid valve regurgitation is a type of heart valve disease in which the valve between the two right heart chambers (right ventricle and right atrium) doesnt close properly. As a result, blood leaks backward into the upper right chamber (right atrium).

Tricuspid Stenosis

Disease Name : Tricuspid Stenosis, Symptoms : Arrhythmias : Tricuspid stenosis causes abnormal heart rhythms., fatigue : Fatigue, due to limited cardiac output, may be present., Gastrointestinal symptoms : Systemic venous congestion leads to abdominal discomfort and swelling., heart murmur : The murmur of tricuspid stenosis is mid-diastolic at the left lower sternal border., edema : Edema of the abdomen, legs, ankles or feet., dyspnea : Dyspnea may be present but is not severe unless concomitant mitral valve disease is present., Signs : nan, Treatment : Mechanical valves in the tricuspid position,are more prone to thromboembolic complications than in other positions.,Percutaneous tricuspid balloon valvotomy for isolated severe,TS without significant TR is very rarely performed., Patients with TS generally exhibit marked systemic venous congestion; salt restriction, bed rest, and diuretic therapy are required,during the preoperative period., Surgical relief of the TS should be carried out, preferably at the time of surgical mitral valvotomy or mitral valve replacement,(MVR) for mitral valve disease, in patients with moderate or severe TS who have mean diastolic pressure gradients exceeding ~4 mmHg and tricuspid orifice areas <1.5–2 cm2, TS is almost always accompanied by significant TR. Operative repair may permit substantial improvement of tricuspid valve function. If repair cannot be accomplished, the tricuspid valve may have to be replaced. Meta-analysis,has shown no difference in overall survival between mechanical and tissue valve replacement. Mechanical valves in the tricuspid position are more prone to thromboembolic complications than in other positions. Percutaneous tricuspid balloon valvotomy for isolated severe TS without significant TR is very rarely performed., Pathophysiology : A diastolic pressure gradient between the right atrium (RA) and right ventricle (RV) defines TS. It is augmented when the transvalvular blood flow increases during inspiration and declines during expiration. A mean diastolic pressure gradient of 4 mmHg is usually sufficient to elevate the mean RA pressure to levels that result in systemic venous congestion. Unless sodium intake has been restricted and diuretics administered, this venous congestion is associated with hepatomegaly, ascites, and edema, sometimes severe. In patients with sinus rhythm, the RA a wave may be extremely tall and may even approach the level of the RV systolic pressure. The y descent is prolonged. The cardiac output (CO) at rest is usually depressed, and it fails to rise during exercise. The low CO is responsible for the normal or only slightly elevated left atrial (LA), pulmonary artery (PA), and RV systolic pressures despite the presence of MS. Thus, the presence of TS can mask the hemodynamic and clinical features of any associated MS., Epidemiology : Tricuspid stenosis is rare, occurring in less than 1% of the population., GOOD, In many cases, you can’t prevent tricuspid valve disease. But if you have a condition that may cause it, seek treatment and follow your healthcare provider’s instructions., Complications : death, heart failure, Diagnostics : Complete Blood Count CBC, 2-D Echo, ECG, CHEST X RAY, CT SCAN, Differential diagnosis : aortic regurgitation, ATRIAL MYXOMA, constrictive pericarditis, mitral regurgitation, mitral stenosis, restrictive cardiomyopathy, tricuspid atresia, tricuspid regurgitation, disease description : Tricuspid stenosis (TS) is a very rare valvular abnormality occurring due to the narrowing of the tricuspid valve. It results in an elevated gradient between the right atrium and right ventricle, systemic congestion, and failure to augment right ventricle output. The isolated occurrence is rare, and tricuspid stenosis usually accompanies other valvular abnormalities. It most often co-exists with mitral valve pathology, especially in patients with rheumatic heart disease.

Trigeminal Neuralgia

Disease Name : Trigeminal Neuralgia, Symptoms : facial pain : Pain that occurs with facial spasms. Pain in areas supplied by the trigeminal nerve, including the cheek, jaw, teeth, gums, lips, or less often the eye and forehead. Pain affecting one side of the face at a time., severe pain : Episodes of severe, shooting or jabbing pain that may feel like an electric shock. Spontaneous attacks of pain or attacks triggered by things such as touching the face, chewing, speaking or brushing teeth. Attacks of pain lasting from a few seconds to several minutes. Pain in areas supplied by the trigeminal nerve, including the cheek, jaw, teeth, gums, lips, or less often the eye and forehead., Signs : nan, Treatment : "Anticonvulsants. Doctors usually prescribe carbamazepine (Tegretol, Carbatrol, others) for trigeminal neuralgia, and its been shown to be effective in treating the condition. Other anticonvulsant drugs that may be used to treat trigeminal neuralgia include oxcarbazepine (Trileptal, Oxtellar XR), lamotrigine (Lamictal), valproate and phenytoin (Dilantin, Phenytek, Cerebyx). Other drugs, including clonazepam (Klonopin), topiramate (Qsymia, Topamax, others), pregabalin (Lyrica) and gabapentin (Neurontin, Gralise, Horizant), also may be used.,Antispasmodic agents. Muscle-relaxing agents such as baclofen (Gablofen, Lioresal, Ozobax) may be used alone or in combination with carbamazepine. Side effects may include confusion, nausea and drowsiness.,Botox injections. Small studies have shown that onabotulinumtoxinA (Botox) injections may reduce pain from trigeminal neuralgia in people who are no longer helped by medications.", Microvascular decompression. ,Brain stereotactic radiosurgery (Gamma knife). In this procedure, a surgeon directs a focused dose of radiation to the root of your trigeminal nerve. This procedure uses radiation to damage the trigeminal nerve and reduce or eliminate pain. Relief occurs gradually and may take up to a month., Pathophysiology : In trigeminal neuralgia, also called tic douloureux, the trigeminal nerves function is disrupted. Usually, the problem is contact between a normal blood vessel — in this case, an artery or a vein — and the trigeminal nerve at the base of your brain. This contact puts pressure on the nerve and causes it to malfunction.While compression by a blood vessel is one of the more common causes of trigeminal neuralgia, there are many other potential causes as well. Some may be related to multiple sclerosis or a similar disorder that damages the myelin sheath protecting certain nerves. Trigeminal neuralgia can also be caused by a tumor compressing the trigeminal nerve.A variety of triggers may set off the pain of trigeminal neuralgia, including : ShavingTouching your faceEatingDrinkingBrushing your teethTalkingPutting on makeupBreeze lightly blowing over your faceSmilingWashing your face, Epidemiology : incidence was estimated to be 5.5 per 100, 000 person-years, variable, Unfortunately, trigeminal neuralgia isn’t preventable. But you can prevent painful episodes by avoiding certain activities that cause severe, intense pain. There’s also nothing to suggest that trigeminal neuralgia is brought on by stress., Complications : double vision in eyes, Jaw pain, Diagnostics : MRI, MRI, PHYSICAL EXAMINATION, NEUROLOGICAL EXAMINATION, Differential diagnosis : Dental pain, neuropathy, disease description : Trigeminal neuralgia (TN), also known as tic douloureux, is a type of chronic pain disorder that involves sudden, severe facial pain. It affects the trigeminal nerve, or fifth cranial nerve, which provides feeling and nerve signaling to many parts of the head and face. TN is a type of neuropathic pain, typically caused by a nerve injury or nerve lesion.

Trigger Finger And Thumb

Disease Name : Trigger Finger And Thumb, Symptoms : soreness : Soreness in your palm near the base of your fingers or thumb. This pain is usually worse when you’re gripping or grasping something., lump : Tender lump in the palm of your hand., popping sensation : A snapping or popping feeling when you move your fingers or thumb. It might feel like your affected digits are “catching” or getting stuck as they move., pain in finger : Pain and stiffness when flexing your fingers or thumb in toward your palm., Signs : nan, Treatment : medication : Hydrocortisone , Initial treatment for a trigger finger is usually nonsurgical.,,Rest. Resting your hand and avoiding activities that make it worse may help to resolve the problem.,,Splinting. Wearing a splint at night to keep the affected finger or thumb in a straight position while you sleep may be helpful.,,Exercises. Gentle stretching exercises can help decrease stiffness and improve range of motion in the involved digit.,,Medications. Over-the-counter medications, such as acetaminophen and nonsteroidal anti-inflammatory drugs (NSAIDs), can help relieve pain and inflammation.,,Steroid injections. Corticosteroid, or cortisone, is a powerful anti-inflammatory agent that can be injected into the tendon sheath at the base of the affected digit. In many cases, a steroid injection can resolve the condition., ULTRASONIC RADIATION (INITIAL STAGES), splitting of the tight tendon sheath may be,required., Surgical procedure. The surgical procedure for trigger finger is usually trigger finger release., Pathophysiology : Initially, the only symptom is pain at the base of the affected finger, especially on trying to passively extend the finger. As the sheath further thickens, the contained tendon gets swollen proximal to it.The swollen segment of the tendon does not enter the sheath when an attempt is made to straighten the finger from the flexed position. This is called ‘locking of finger’. This locking can be overcome either by a strong effort in which case the finger extends with a snap-like trigger of a pistol or by extending the finger passively with other hand., Epidemiology : prevalence is roughly 2 percent in the general population, , GOOD, The best way to prevent trigger finger is to avoid overusing your hands, fingers and thumbs. To prevent trigger finger : ,,Learn the proper posture or technique for sports or work activities.,Ease into new exercises or activities to avoid injury.,Take breaks if you’re doing a repetitive task that puts a lot of stress on your hands., Complications : stiffness, pain during movement, Diagnostics : ultrasound, X RAY, PHYSICAL EXAMINATION, Differential diagnosis : DEFORMITY, hypoplasia, disease description : Trigger finger makes a finger get stuck in a bent position. It may straighten suddenly with a snap. The fingers most often affected are the ring finger and the thumb, but the condition can affect any finger.Trigger finger happens when the tendon that controls that finger cant glide smoothly in the sheath that surrounds it. This may occur if part of the tendon sheath becomes swollen or if a small lump forms on the tendon.The condition is most common in women over the age of 50. You may be at higher risk of trigger finger if you have diabetes, low thyroid function or rheumatoid arthritis.

Trimethylaminuria

Disease Name : Trimethylaminuria, Symptoms : unpleasant odour, Signs : foul smelling skin, Halitosis, foul smell from mouth, fishy smell, fishy odour, Treatment : A diet low in carnitine and choline may help. Egg yolks, legumes, ,red meats, fish and beans should be avoided, Short courses of metronidazole or neomycin Charcoal and copper ,chlorophyllin, Pathophysiology : Affected individuals are unable to oxidize trimethylamine, which is produced by the intestinal bacterial degradation of choline and carnitine in food, to the odourless trimethylamine N-oxide. This can occur as a primary problem, as a result of a mutation in the flavin-containing mono-oxygenase3 (FMO3) gene. Secondary trimethylaminuria can occur when there is an increased burden of trimethylamine, and is seen when there is an increased production of it from its precursors by gut bacteria in conditions such as blind loop syndrome, uraemia and liver disease, Epidemiology : nan, Complications : stress disorder, Diagnostics : Urine analysis, Differential diagnosis : liver failure, olfactory disturbances, Uremia, disease description : This disorder results from excessive amounts of the offensively smelling tertiary amine trimethylamine appearing in eccrine and apocrine sweat, breath and urine, and imparting an unpleasant rotting fish smell to sufferers

Triosephosphate Isomerase Deficiency

Disease Name : Triosephosphate Isomerase Deficiency, Symptoms : Cardiomyopathy : Weakness of the heart can occur in triosephosphate isomerase deficiency., Dystonia : Dystonia is the name for a group of movement disorders that is generally characterized by involuntary muscle contractions that force the body into abnormal, sometimes painful, movements and positions (postures)., Hemolytic anemia : The disorder is characterized by hemolytic anemia. Hemolytic anemia occurs before birth (neonatally) in approximately half of the cases. Hemolytic anemia is a condition characterized by low levels of circulating red blood cells (erythrocytes) that occurs because red blood cells are prematurely destroyed and the bone marrow cannot compensate for the loss. Hemolytic anemia may cause fatigue, lightheadedness, yellowing of the skin and whites of the eyes (jaundice), pale skin color, and difficulty breathing., seizures : Affected individuals may also develop seizures., Neurological symptoms : Progressive neurological symptoms are seen in infants with TPI deficiency usually between 6 and 30 months of age. Such symptoms include diminished muscle tone (hypotonia), weakness, muscular wasting or degeneration (amyotrophy), lack of deep tendon reflexes, and involuntary muscle spasms (spasticity) that result in slow, stiff movements of the legs., Breathing difficulty : Breathing difficulties occur due to paralysis of the muscle that separates the stomach and the diaphragm., Signs : splenomegaly : TPI causes spleen enlargement., Treatment : Genetic counseling may be of benefit for affected people and their families, Specific therapies may include blood transfusions to treat hemolytic anemia during episodes of red blood cell destruction (hemolysis) and assisted ventilation to treat paralysis of the diaphragm., Other treatment is symptomatic and supportive, Pathophysiology : Mutations in the TPI1 gene cause triosephosphate isomerase deficiency. This gene provides instructions for making an enzyme called triosephosphate isomerase 1. This enzyme is involved in a critical energy-producing process known as glycolysis. During glycolysis, the simple sugar glucose is broken down to produce energy for cells. Death of red and white blood cells, nerve cells in the brain, and cardiac muscle cells leads to the signs and symptoms of triosephosphate isomerase deficiency., Epidemiology : approximately 40 cases have been reported in the scientific literature, Poor, "Triosephosphate isomerase deficiency is a rare autosomal recessive metabolic disorder and therefore cant be prevented.", Complications : Cardiomyopathy, respiratory failure, Respiratory infections, Diagnostics : RBC Count, Serum Bilirubin Indirect, GENETIC TESTING, HISTORY TAKING, Differential diagnosis : GB syndrome, Glucose phosphate isomerase (GPI) deficiency, disease description : Triosephosphate isomerase deficiency is a disorder characterized by a shortage of red blood cells (anemia), movement problems, increased susceptibility to infection, and muscle weakness that can affect breathing and heart function.

Triphalangeal Thumb

Disease Name : Triphalangeal Thumb, Symptoms : thumb deformity : The triphalangeal thumb has a different appearance than normal thumbs. The appearance can differ widely; the thumb can be a longer thumb or thumb strength can be diminished., clinodactyly : The thumb can be deviated in the radio-ulnar plane., polydactyly : There is often a combination with radial polydactyly., Signs : nan, Treatment : The aim of surgical treatment is to reconstruct or correct the anatomic anomalies to obtain greater function and a more acceptable appearance., Pathophysiology : Triphalangeal thumb is a rare congenital anomaly in which the thumb has three phalanges. Clinical presentation of triphalangeal thumb can vary considerably and can be present in both hands or unilateral. The thumb can be long with a finger-like appearance. The presence of clinodactyly depends on the shape of the extra phalanx varying from wedge-shaped to rectangular. Various joints, ligaments, muscles, and tendons can be hypoplastic or absent, with varying degrees of stiffness or instability., Epidemiology : 1 in 25, 000 live births., variable, NA, Complications : post-surgical complications, Diagnostics : X RAY, PHYSICAL EXAMINATION, Differential diagnosis : nan, disease description : A triphalangeal thumb is a thumb with three phalanges. The thumb often appears long and fingerlike, and can sometimes be in the same plane as the other fingers. Anatomically, the extra phalanx can have different shapes.Triphalangeal thumb is a rare congenital anomaly in which the thumb has three phalanges. Clinical presentation of triphalangeal thumb can vary considerably and can be present in both hands or unilateral. The thumb can be long with a ?nger-like appearance. The presence of clinodactyly depends on the shape of the extra phalanx varying from wedge-shaped to rectangular. Various joints, ligaments, muscles, and tendons of the ?rst ray can be hypoplastic or absent, with varying degrees of stiffness or instability

Trisomy 13/patau Syndrome

Disease Name : Trisomy 13/patau Syndrome, Symptoms : Cardiac Disease : About 80 percent of infants with Trisomy 13 Syndrome also have congenital heart defects, such as atrial or ventricular septal defects or patent ductus arteriosus (PDA). In infants with PDA, the channel that is present between the pulmonary artery and the aorta during fetal development fails to close after birth., Gastrointestinal symptoms : GI problems in children with trisomy 13 can include umbilical hernias and inguinal hernias. Omphaloceles, where part of the intestines are outside the body, occurs in some cases., seizures : Trisomy 13 affected individuals are susceptible to developing seizures., Microphthalmia : Individuals with trisomy 13 often have very small or poorly developed eyes., physical signs : Physical symptoms of trisomy 13 include Cleft lip or cleft palate, difficulty gaining weight, polydactyly, ears forming low on the head, growth abnormalities in the arms and legs, hypotonia, microcephaly, lower jaw & ery small, close together or underdeveloped eyes., Signs : nan, Treatment : Additional treatments may be performed including specialized dietary feeds, seizure prophylaxis, prophylactic antibiotics for urinary tract infections, and the use of hearing aids, At delivery, infants diagnosed with Patau syndrome may need post-delivery oxygenation and ventilation; this may require intubation or tracheostomy due to facial defects. Patients with cardiac defects may require cardiac surgery to repair common cardiac abnormalities. Other surgeries may be indicated for common defects including herniorrhaphy, cleft lip repair, feeding tube placement, or corrective orthopedic surgeries., Pathophysiology : An extra copy of chromosome 13 causes the defects in Patau syndrome. Advanced maternal age is a risk factor for this pathology because of the increased frequency of nondisjunction in meiosis. This extra copy of chromosome 13 disrupts normal embryonic development and leads to multiple defects.Most cases of trisomy 13 are not inherited and result from random events during the formation of eggs and sperm in healthy parents. An error in cell division called nondisjunction results in a reproductive cell with an abnormal number of chromosomes. For example, an egg or sperm cell may gain an extra copy of chromosome 13. If one of these atypical reproductive cells contributes to the genetic makeup of a child, the child will have an extra chromosome 13 in each cell of the body., Epidemiology : the chance of having a child with this condition increases as a woman gets older, Trisomy 13 occurs in about 1 in 16, 000 newborns., variable, NA, Complications : CONGENITAL MALFORMATION, death, Diagnostics : USG, PHYSICAL EXAMINATION, Differential diagnosis : Down syndrome, trisomy 18/edward syndrome, disease description : Trisomy 13, also called Patau syndrome, is a chromosomal condition associated with severe intellectual disability and physical abnormalities in many parts of the body. Individuals with trisomy 13 often have heart defects, brain or spinal cord abnormalities, very small or poorly developed eyes (microphthalmia)

Trisomy 18/edward Syndrome

Disease Name : Trisomy 18/edward Syndrome, Symptoms : "head deformity : Trisomy 18/Edwards syndrome causes abnormally shaped head.", mouth deformity : Infants have small mouth & jaw., hypotonia : The infants have decreased muscle tone., organ damage : Major internal organs functioning differently is commonly seen., "Club foot : Trisomy 18/Edwards syndrome causes clubfoot.", cognitive impairment : Issues with cognitive development (intellectual disabilities), which are typically severe., Signs : nan, Treatment : Support is available to you, your family and your child diagnosed with Edwards syndrome (trisomy 18), especially to help cope with the loss of your child or help you navigate your child’s complex diagnosis., Feeding management : Nasogastric tube feeding and gastrostomy feeding are considered to address the feeding issues. Gastroesophageal reflux can be initially managed with medical therapy and later with surgical options if refractory, Cardiac management : Diuretics, digoxin are used for heart failure. Palliative and corrective cardiac surgery are recommended for complex congenital heart defects.,Infections : Treat infections like respiratory infections, pneumonia, Urinary tract infection, and otitis media with the standard approach. ,Orthopedic management may be required, particularly for scoliosis due to the hemivertebra., Pathophysiology : The Edwards syndrome phenotype appears to be associated with three copies of two critical regions in the long arm of chromosome 18, 18q12.1 to 18q21.2, and 18q22.3 to 18qter. Severe mental retardation in Edwards syndrome may be associated with trisomy of 18q12.1 to 18q21.2. The trisomy of the short arm of chromosome 18 (18p) does not seem to cause any of the major features of Edwards syndrome., Epidemiology : The condition is more common during pregnancy (1 out of every 2, 500 pregnancies), but most (at least 95%) fetuses don’t survive full term due to complications from the diagnosis, so pregnancies can end in miscarriage or babies are stillborn., Edwards syndrome (trisomy 18) occurs in an estimated 1 out of every 5, 000 to 6, 000 live births., variable, Edwards syndrome (trisomy 18) is the result of a genetic mutation and there’s no way to prevent the condition. However, if you qualify for a combination of genetic testing and in vitro fertilization (preimplantation genetic testing), you can significantly reduce the chance of having a child with Edwards syndrome (trisomy 18). If you plan on becoming pregnant and want to understand your risk of having a child with a genetic condition, talk with your healthcare provider about genetic testing., Complications : Cardiorespiratory arrest, developmental delay, low birth weight, Thymic hypoplasia, WILMS TUMOR, Adrenal hypoplasia congenita, Hodgkin lymphoma, Diagnostics : Beta HCG, ultrasound, AMNIOTIC FLUID EXAMINATION, Serum alpha-fetoprotein, NEUROLOGICAL EXAMINATION, Differential diagnosis : CHARGE Syndrome, trisomy 13/patau syndrome, disease description : Edwards syndrome (trisomy 18) is a genetic condition that causes physical growth delays during fetal development. Life expectancy for children diagnosed with Edwards syndrome is short due to several life-threatening complications of the condition. Children who survive past their first year may face severe intellectual challenges.

Tropical Pulmonary Eosinophilia

Disease Name : Tropical Pulmonary Eosinophilia, Symptoms : fatigue : The cough is followed by extreme fatigue., fever : Tropical pulmonary eosinophilia causes low-grade fever., chronic cough : A persistent or recurrent cough that is aggravated at night., dyspnea : Affected individuals complain of difficulty in breathing., Signs : lymphadenopathy : Some people with this disease may also have enlarged lymph nodes in the neck, axillae or inguinal areas., Treatment : medication : Diethylcarbamazine , The confirmed case of tropical pulmonary eosinophilia is treated with diethylcarbamazine (DEC) for 21 days. DEC is active against both microfilariae and adults. Signs and symptoms respond dramatically with DEC, which is the characteristic of TPE., Pathophysiology : There are several theories postulated for the pathogenesis of TPE, but the exact mechanism is still unclear. Eosinophils play a central role in the pathogenesis of TPE. The microfilariae are periodically released from the lymphatic system, which gets trapped within the pulmonary microcirculation. This triggers an immune response by releasing eosinophils. Eosinophil degranulates releasing eosinophilic cationic protein (ECP), eosinophil-derived neurotoxin (EDN), major basic proteins (MBP), and eosinophil peroxidase (EPO), which helps in the clearance of microfilariae as well as causes lung damage. Compliment activation and opsonization by antifilarial antibodies also help in microfilariae clearance. It is postulated that MBP-2 is associated with airway hyperactivity and interleukin (IL)-4 induces while interferon (IFN)-gamma suppresses the airway hyperactivity induced by microfilariae. Microfilariae in pulmonary circulation also generate an overactive systemic and pulmonary TH2 response resulting in increased levels of IL-4, IL-5, filarial-specific IgG, IgM, IgE antibodies, and massive pulmonary eosinophilia., Epidemiology : prevalence both in immunocompromised and immunocom- petent individuals., less than 1% of individuals with filariasis will develop TPE., variable, The eradication of lymphatic filariasis can lower the incidence rate of tropical pulmonary eosinophilia. The WHO recommends an elimination strategy for lymphatic filariasis by interrupting the transmission cycle. This strategy includes the administration of ivermectin with DEC or albendazole annually to the people of endemic regions. Since adult worms remain viable for years, the drug should be given for 4 to 6 years. The mosquito control strategy is also used to eliminate the vector causing lymphatic filariasis., Complications : Pulmonary dysfunction, Diagnostics : Complete Blood Count CBC, EOSINOPHILS - ABSOLUTE COUNT, HISTOPATHLOGY, CT CHEST, CHEST X RAY, PULMONARY FUNCTION TEST(PFT), STOOL EXAMINATION, SERUM SPECIFIC IgE TESTING, HISTORY TAKING, PHYSICAL EXAMINATION, Differential diagnosis : allergic rhinitis, BRONCHIAL ASTHMA, Churg-Strauss Syndrome, disease description : Tropical pulmonary eosinophilia (TPE) is a hyperresponsive pulmonary syndrome in response to trapped microfilariae within the lung tissue characterized by nocturnal cough, dyspnea, and wheezing. Travel history to a lymphatic filariasis endemic region, peripheral eosinophilia >3, 000/mm3, and elevated serum IgE and antifilarial antibodies level is crucial for diagnosis. Treatment with diethylcarbamazine has an excellent response. Despite treatment, mild interstitial lung disease has been found to persist in some patients.

Tropical Sprue

Disease Name : Tropical Sprue, Symptoms : anorexia : People with this disorder may also experience a profound loss of appetite., diarrhea : The symptoms of Tropical Sprue may include diarrhea with stools that are abundant, pale and foul-smelling., mouth deformity : Inflammation of the mouth and tongue, a scaly appearance on the lips and at the angles of the mouth are commonly presented by affected people., sore tongue : Affected individuals presents a sore tongue., fever : Tropical spruce causes high fever., Night blindness : Vitamin A deficiency in patients of tropical sprue leads to night blindness., Depressive symptoms : Sometimes mental depression may occur., Signs : anemia : People with this disorder may develop anemia characterized by the presence of abnormally enlarged blood cells (megaloblastic) in the bone marrow., Treatment : medication : Sulfamethoxazole and Trimethoprim (Co-trimoxazole), Erythromycin , Pathophysiology : Because tropical sprue responds to antibiotics, the consensus is that it may be caused by one or more infectious agents. Nonetheless, the etiology and pathogenesis of tropical sprue are uncertain. First, its occurrence is not evenly distributed in all tropical areas; rather, it is found in specific locations, including southern India, the Philippines, and several Caribbean islands (e.g., Puerto Rico, Haiti), but is rarely observed in Africa, Jamaica, or Southeast Asia. Second, an occasional individual does not develop symptoms of tropical sprue until long after having left an endemic area. For this reason, celiac disease (often referred to as celiac sprue) was originally called nontropical sprue to distinguish it from tropical sprue. Third, multiple microorganisms have been identified in jejunal aspirates, with relatively little consistency among studies. Klebsiella pneumoniae, Enterobacter cloacae, and E. coli have been implicated in some studies of tropical sprue, while other studies have favored a role for a toxin produced by one or more of these bacteria. Fourth, the incidence of tropical sprue appears to have decreased substantially during the past two or three decades, perhaps in relation to improved sanitation in many tropical countries during this time. Some have speculated that the reduced occurrence is attributable to the wider use of antibiotics in acute diarrhea, especially in travelers to tropical areas from temperate countries. Fifth, the role of folic acid deficiency in the pathogenesis of tropical sprue requires clarification. Folic acid is absorbed exclusively in the duodenum and proximal jejunum, and most patients with tropical sprue have evidence of folate malabsorption and depletion. Although folate deficiency can cause changes in small-intestinal mucosa that are corrected by folate replacement, several earlier studies reporting that tropical sprue could be cured by folic acid did not provide an explanation for the “insult” that was initially responsible for folate malabsorption. The clinical pattern of tropical sprue varies in different areas of the world (e.g., India vs Puerto Rico). Not infrequently, individuals in southern India initially report the occurrence of acute enteritis before the development of steatorrhea and malabsorption. In contrast, in Puerto Rico, a more insidious onset of symptoms and a more dramatic response to antibiotics are seen than in some other locations. Tropical sprue in different areas of the world may not be the same disease, and similar clinical entities may have different etiologies., Epidemiology : This disease affects 5–10% of the population in some tropical areas., GOOD, There is no known prevention for tropical sprue other than avoiding tropical locations., Complications : growth retardation in children, VITAMIN DEFICIENCIES, MINERAL DEFICIENCIES, Diagnostics : Complete Blood Count CBC, Upper GI Endoscopy, STOOL FAT LEVEL, D-xylose test, Breath test, Differential diagnosis : capillariasis, cryptosporidiosis, giardiasis, Strongyloidiasis, disease description : Tropical sprue is a malabsorption syndrome characterized by chronic diarrhea, weight loss, and malabsorption of nutrients. It occurs in travelers to the tropical regions or the natives of the tropics. To avoid the complications and morbidity associated with this condition, it must be promptly diagnosed and treated.