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Schizophrenia

Disease Name : Schizophrenia, Symptoms : "behavioural disturbances : Extremely disorganized or abnormal motor behavior. This may show in a number of ways, from childlike silliness to unpredictable agitation. Behavior isnt focused on a goal, so its hard to do tasks. Behavior can include resistance to instructions, inappropriate or bizarre posture, a complete lack of response, or useless and excessive movement.", "delusion : These are false beliefs that are not based in reality. For example, you think that youre being harmed or harassed; certain gestures or comments are directed at you; you have exceptional ability or fame; another person is in love with you; or a major catastrophe is about to occur. Delusions occur in most people with schizophrenia.", "hallucinations : These usually involve seeing or hearing things that dont exist. Yet for the person with schizophrenia, they have the full force and impact of a normal experience. Hallucinations can be in any of the senses, but hearing voices is the most common hallucination.", "Speech disorders : Disorganized thinking is inferred from disorganized speech. Effective communication can be impaired, and answers to questions may be partially or completely unrelated. Rarely, speech may include putting together meaningless words that cant be understood, sometimes known as word salad.", "lack of interest in surroundings : This refers to reduced or lack of ability to function normally. For example, the person may neglect personal hygiene or appear to lack emotion (doesnt make eye contact, doesnt change facial expressions or speaks in a monotone). Also, the person may lose interest in everyday activities, socially withdraw or lack the ability to experience pleasure.", Signs : nan, Treatment : medication : Haloperidol , Risperidone/Respidon , Olanzapine , Educational programs for family members, significant others, and friends offer instruction about schizophrenia symptoms and treatments, and strategies for assisting the person with the illness. Increasing key supporters’ understanding of psychotic symptoms, treatment options, and the course of recovery can lessen their distress, bolster coping and empowerment, and strengthen their capacity to offer effective assistance. Family-based services may be provided on an individual basis or through multi-family workshops and support groups., Cognitive behavioral therapy, behavioral skills training, supported employment, and cognitive remediation interventions may help address the negative and cognitive symptoms of schizophrenia. ., Pathophysiology : Epidemiologic surveys identify several risk factors for schizophrenia, including genetic susceptibility, early developmental insults, winter birth, and increasing parental age. Genetic factors are involved in at least a subset of individuals who develop schizophrenia. Schizophrenia is observed in ~6.6% of all first-degree relatives of an affected proband. If both parents are affected, the risk for offspring is 40%. The concordance rate for monozygotic twins is 50%, compared to 10% for dizygotic twins. Schizophrenia-prone families are also at risk for other psychiatric disorders, including schizoaffective disorder and schizotypal and schizoid personality disorders, the latter terms designating individuals who show a lifetime pattern of social and interpersonal deficits characterized by an inability to form close interpersonal relationships, eccentric behavior, and mild perceptual distortions. Large scale genomewide association studies have identified >100 small effect risk loci and a few larger effect copy number variants, along with epigenetic effects. Pathways identified include ones involved in immunity, inflammation, and cell signaling., Epidemiology : 0.85% of individuals worldwide, Environmental factors that may be involved include living in poverty, stressful surroundings, and exposure to viruses or nutritional problems before birth, TREATABLE, Because experts still don’t know why schizophrenia happens, it’s impossible to prevent it or reduce your risk of it happening., Complications : delusion, hallucinations, social isolation, Diagnostics : Blood Glucose test, CSF EXAMINATION, EEG, Urinary Catecholamines, serum calcium Ca++, MRI, CT SCAN, THYROID PROFILE, Differential diagnosis : delusional thinking, Developmental defects, paranoid, personality disorder, Psychosis, disease description : Schizophrenia is a heterogeneous syndrome characterized by perturbations of language, perception, thinking, social activity, affect, and volition. There are no pathognomonic features. The syndrome commonly begins in late adolescence, has an insidious (and less commonly acute) onset, and, often, a poor outcome, progressing from social withdrawal and perceptual distortions to recurrent delusions and hallucinations. Patients may present with positive symptoms (such as conceptual disorganization, de

Schnyder Corneal Dystrophy

Disease Name : Schnyder Corneal Dystrophy, Symptoms : Corneal Sensations are decreased : Loss of corneal sensation may be more profound in advanced cases. Patients who are younger than 23 years demonstrate only a central corneal opacity , which may involve the entire stroma with or without central subepithelial cholesterol crystals., "Blurring of vision : Blurry vision thats worse in the morning and gets better later in the day.", "glare : Schnyders crystalline corneal dystrophy (SCCD) is a rare autossomal dominant condition characterized by abnormally increased deposition of cholesterol and phospholipids in the cornea leading to glare.", Signs : Corneal deposits : Corneal crystal : Bilateral cholesterol deposition in the anterior stroma. (Initial changes), corneal haziness and yellow infiltrates : Central corneal haze : Increased prevalence with age. (>40 years), Treatment : No treatment is available to stop progression. Phototherapeutic keratectomy can remove subepithelial crystals if they are affecting visual acuity. Penetrating keratoplasty can be performed in eyes with advance disease but the disease can recur in the graft., Pathophysiology : Schnyder corneal dystrophy (SCD) is also known as hereditary crystalline stromal dystrophy of Schnyder. Affected patients and non-affected members of the pedigrees may have hyperlipoproteinemia. Genetic locus is 1 p36 and the gene involved is UbiA prenyltransferase domain containing 1—UBIAD1. Inheritance is autosomal dominant. The dystrophy appears in early infancy or at birth or sometimes in the first decade of life. It is slowly progressive and usually asymptomatic. Signs include : • Round ring-shaped central corneal stromal opacities due to deposition of fine needle-like cholesterol crystals, which may be white to yellow or polychromatic in colour are characteristic lesions. • Corneal sensations decrease with age. • Visual acuity progressively decreases with age. Although scotopic vision may be remarkably good, photopic vision may be disproportionately decreased. • Glare which increase with age., Epidemiology : approximately 0.09% of the population., good, Complications : Atherosclerosis, Diagnostics : ophthalmoscopy, Differential diagnosis : cystinosis, hyperuricemia, multiple myeloma, Tyrosinemia, disease description : Schnyder corneal dystrophy (SCD)Schnyder corneal dystrophy (SCD) is also known as hereditary crystalline stromal dystrophy of Schnyder. Affected patients and non-affected members of the pedigrees may have hyperlipoproteinemia. Genetic locus is 1 p36 and the gene involved is UbiA prenyltransferase domain containing 1—UBIAD1. Inheritance is autosomal dominant.

Schwannoma (who Grade 1)

Disease Name : Schwannoma (who Grade 1), Symptoms : muscle weakness : Muscle weakness occurs when the schwannomas form on the peripheral nerves., Numbness : Numbness is a sign of pinched peripheral nerve., paresthesia : A sensation of pins-and-needles., Pain : Pain that’s aching, burning or sharp., lump : A visible lump that may feel tender when you put pressure on it., Signs : nan, Treatment : Stereotactic radiosurgery becomes necessary if the growing tumor is near vital blood vessels or nerves. Hearing preservation and tumor control show excellent results with treatment. More than 75% of the patients retain serviceable hearing. The radiation dose to the central cochlea should be less than 4.2 Gy., Tumor biopsy should be a consideration after confirming a nerve tumor on relevant imaging tests or nerve biopsy in case of aggressive peripheral neuropathy mimicking large nerve tumors. Schwannomas respond positively to local resection., Pathophysiology : Pathogenesis includes-May occur spontaneouslyCan occur in familial tumor syndromes, such as neurofibromatosis type 2 (NF2), schwannomatosis or Carney complex Loss of function of the tumor suppressor gene merlin (schwannomin)Direct genetic change involving the NF2 gene on chromosome 22 or secondarily to merlin inactivationCan occur in NF2 and spontaneous schwannomasCan cause other neoplasms including meningioma, mesothelioma, glioma multiforme and carcinomas of breast, colon and rectum, kidney (clear cell type), liver, prostate and skin, Epidemiology : 6%, The incidence of vestibular schwannomas in the USA is 1.2 cases per 100, 000/year., excellent, schwannomas can’t be prevented. In most cases, they happen randomly for unknown reasons. About 10% of cases are linked to certain genetic conditions that make it more likely that you’ll develop certain types of tumors.,,If you have a biological relative who’s been diagnosed with neurofibromatosis 2 (NF2), Schwannomatosis or Carney complex, talk to your healthcare provider. They may recommend genetic counseling to see if you also have the genetic condition., Complications : Meningitis, headache, Vestibular disorders, Diagnostics : MRI Brain, MRI, CT SCAN, Differential diagnosis : Chondroblastoma, Chordoma, Giant cell tumour, Malignant melanoma, neurofibroma, disease description : Schwannomas (also known as neuromas, neurinomas "of Verocay" and neurilemmomas) are benign, well-encapsulated, slow-growing nerve sheath tumors composed exclusively of Schwann cells derived from the neural crest.  The tumor can originate from any myelinated central or peripheral nerve with Schwann cells. The World Health Organization classifies schwannoma as a grade I benign tumor. Schwannomas are solitary in 90% of the cases. Multiple tumors in the same patient should bring attention to syndromic associations (neurofibromatosis type 2, schwannomatosis, and Carney complex)

Scleredema

Disease Name : Scleredema, Symptoms : infection : Type one is the acute type of scleroedema, and typically starts with an infection, most often Streptococcus pyogenes, the cause of tonsillitis. It mainly affects middle aged women and children. Hardening of the skin of the face and neck quickly develops and spreads to the upper trunk and arms. It usually improves spontaneously over six months to two years., multiple myeloma : Type 2 scleroedema is not associated with infection. It starts more slowly and persists. Abnormal levels of an abnormal paraprotein (immunoglobulin) in the blood may occur, sometimes due to multiple myeloma., diabetes mellitus : Type 3, scleroedema adultorum of Buschke, also called scleroedema diabeticorum, occurs in diabetics, particularly adult men. It is very persistent. The skin of the neck and upper back slowly thickens over months or years., "plaques : The affected areas are firm and woody plaques, sometimes slightly red or brown and often with a ‘peau dorange’ (orange-skin) appearance.", Signs : induration : Scleredema is an idiopathic condition with specific clincopathological findings, including symmetrical and diffuse nonpitting induration of the upper body and thickened dermis due to deposition of acid mucopolysaccharides., edema : Scleredema, or scleredema adultorum of Buschke, is a condition that mimics scleroderma and is characterized by firm, nonpitting edema that typically begins on the neck and spreads to the face, scalp, shoulders, and trunk. The hands and feet are characteristically spared (“inverse” in comparison to systemic sclerosis)., Treatment : Second line ,• Electron-beam radiotherapy ,• Photopheresis,• Intravenous immunoglobulin, Third line ,• Immunosuppresive agents, First line ,• Treatment of primary disease,• Phototherapy with UVA1, PUVA or narrow-band UVB,• Physical therapy, Pathophysiology : Extracellular Matrix Changes : The primary underlying abnormality in scleredema is an accumulation of abnormal collagen in the skins extracellular matrix. Collagen is a protein that provides structural support and elasticity to the skin. In scleredema, there is an excessive deposition of collagen in the dermal layer of the skin, leading to thickening and hardening of the affected areas.Inflammation : Inflammatory processes are thought to play a role in the development of scleredema. The exact trigger for the inflammation is unclear, but it may be related to infections, metabolic disturbances, or immune dysregulation. The inflammatory response can contribute to the activation of fibroblasts, which are cells responsible for producing collagen and other components of the extracellular matrix.Insulin Resistance : In some cases, scleredema has been associated with insulin resistance and diabetes mellitus. The relationship between insulin resistance and scleredema is not fully understood, but it is believed that insulin resistance may contribute to the accumulation of collagen and inflammation in the skin., Epidemiology : 2.5 percent, 8 to 56 individuals per million each year, variable, Regular exercise will not only help improve your overall physical and spiritual well-being, but it will also help keep your joints flexible and improve circulation,,When your joints hurt, avoid lifting heavy objects or performing chores that may place a strain on them, thus risking further injury.,,During the colder months, be sure to dress appropriately. Keeping your body warm and protected from the cold weather with boots, a hat, gloves and a scarf will help keep the blood vessels in your extremities open and your circulation flowing., Complications : dysarthria, dysphagia, hepatosplenomegaly, myositis, Diagnostics : Blood Glucose test, GLYCOSYLATED HB % HBAIC, ANTISTREPTOLYSIN O (ASO) TITRE, THROAT SWAB CULTURE, X RAY, electrophoresis with immunofixation, Differential diagnosis : Scleroderma crisis, scleromyxedema, disease description : Scleredema is a rare condition characterized by a non-pitting induration of the upper part of the body, associated with diabetes or with a history of infection or blood dyscrasia Scleredema is a symmetrical diffuse progressive non-pitting swelling and induration of the upper part of the body caused by a thickened dermis and deposition of mucin.

Sclerema Neonatorum

Disease Name : Sclerema Neonatorum, Symptoms : induration : Woody induration of the skin starts on the buttocks, thighs or calves and extends rapidly and symmetrically to involve almost the whole surface, with the exception of the palms, soles and genitalia., cutaneous symptoms : Sclerema neonatorum is typically characterized by hardening of the skin and subcutaneous tissues that subsequently bind to the underlying muscle and bone, compromising respiration and feeding and leading to death., Signs : nan, Treatment : First line , Treatment of the underlying medical condition(s) in a neonatal ,unit is the key to survival. , Second line , Systemic corticosteroids are probably not effective but there is ,evidence that repeated exchange transfusions and intravenous immunoglobulin may be helpful in some cases, Pathophysiology :  It has been recorded as already present at birth in infants subjected to placental insufficiency . The disorder does not seem to occur in otherwise healthy infants, and most characteristically develops during the course of one of a wide variety of severe illnesses, particularly serious infections, congenital heart disease and other major developmental defects . A proportion of these infants have been hypothermic, and occasionally sclerema has been described as a complication of neonatal cold injury . Nevertheless, cold does not appear to be an important aetiological factor in the majority of cases. Lipolytic mechanisms are poorly developed in the newborn, particularly in those born preterm. The maturation of these enzyme systems might be further compromised by major infection or hypoxia. It has been suggested that sclerema might reflect defective lipolysis within adipose tissue, which would result in failure of fat mobilization, and an impaired capacity to maintain body temperature. It has been reported that the ratio of saturated to unsaturated fatty acids is relatively high in the adipose tissue of all neonates, and that this ratio was even higher in an infant with sclerema. This would lead to a raised melting point, and it is possible that the induration of subcutaneous fat, which is the major clinical feature of sclerema, might reflect its solidification due to a fall in the temperature of the adipose tissue during peripheral circulatory collapse. In most cases the subcutaneous fat layer appears to be thickened due to an increased size of the individual lipocytes and to an increased width of the intersecting bands of connective tissue, probably due to oedema . There is very little evidence of fat necrosis and, generally, only the slightest indication of inflammation. The most characteristic histological feature of sclerema neonatorum is the presence of radially arranged, needle-shaped clefts in adipocytes and, occasionally, in multinucleate giant cells, reflecting the presence of crystals prior to processing., Epidemiology : It is very rare and its prevalence is unknown., 19 per 1000 live births in 2016 to 2019, an 82.9% decrease (P < 0.0001), mean 4% decrease per year., variable, Complications : Respiratory insufficiency, Diagnostics : HISTOPATHLOGY, Skin Biopsy With Immunofluorescence, Differential diagnosis : Cold panniculitis, Restrictive dermopathy, stiff skin syndrome, subcutaneous fat necrosis, disease description : Sclerema neonatorum is classified as a neonatal pannicultis. It usually affects gravely ill, preterm neonates in the first week of life. It manifests as a hardening of skin and subcutaneous adipose tissue to such an extent that it hinders feeding and respiration, and usually culminates in death. Age Sclerema neonatorum almost always appears during the first week of life, although it has occasionally been recorded later in infants born preterm.

Scleritis

Disease Name : Scleritis, Symptoms : Diminution of vision : I can lead to vision loss due to progressive inflammation of the ocular tissues., eye pain : Severe eye pain that responds poorly to painkillers is the main symptom of scleritis., headache : Deep-seated headaches., Lacrimation : Abnormal secretion of tears., REDNESS OF EYE : Redness of the sclera., photophobia : Intense sensitivity to light., Signs : WIDESPREAD INFLAMMATION OF THE SCLERA : Scleritis is the inflammation in the episcleral and scleral tissues with injection in both superficial and deep episcleral vessels. It may involve the cornea, adjacent episclera and the uvea and thus can be vision-threatening., one or two hard, purplish elevated immovable scleral nodules, usually situated near the limbus, NODULES ON SCLERA : In nodular disease, a distinct nodule of scleral edema is present. The nodules may be single or multiple in appearance and are often tender to palpation., Treatment : medication : Indomethacin , Cyclophosphamide , Methotrexate, I. Non-necrotizing scleritis. It is treated by : ,• Topical steroid eyedrops,• Systemic indomethacin 75 mg twice a day until,inflammation resolves. II. Necrotizing scleritis. It is treated by : ,• Topical steroids,• Oral steroids on heavy doses, tapered slowly.,• Immunosuppressive agents like methotrexate,or cyclophosphamide may be required in nonresponsive,cases.,• Subconjunctival steroids are contraindicated,because they may lead to scleral thinning and,perforation. B. Infectious scleritis,• Most of the time diagnosis is delayed and patients,are put on topical and oral steroids which worsen,the infective scleritis.,• Antimicrobial therapy, both with topical and oral,agents is required in an aggressive manner., 1.Surgical treatment, in the form of scleral patch graft,may be required to preserve integrity of the globe,in extensive scleral melt and thinning. 2.Surgical debridement, Pathophysiology : The pathophysiology of scleritis involves an immune-mediated inflammatory response that affects the scleral tissue.Immune Response : Scleritis is believed to have an autoimmune basis, where the bodys immune system mistakenly identifies the scleral tissue as foreign or abnormal. The immune system then mounts an inflammatory response against the scleral tissue, leading to the characteristic symptoms and signs of scleritis.Inflammatory Mediators : In the early stages of scleritis, inflammatory cells, such as neutrophils and lymphocytes, infiltrate the scleral tissue. These immune cells release various pro-inflammatory mediators, including cytokines and chemokines, which promote inflammation and attract more immune cells to the site of injury.Blood Vessel Involvement : Scleritis often affects the blood vessels in the sclera. There are two main types of scleritis based on the depth of blood vessel involvement : a. Anterior Scleritis : In this type, the inflammation primarily affects the superficial blood vessels in the sclera. It can be further divided into diffuse, nodular, and necrotizing subtypes based on the severity and pattern of inflammation.b. Posterior Scleritis : In posterior scleritis, the inflammation involves the deeper blood vessels and the adjacent tissue layers, such as the choroid (a layer of the eye containing blood vessels). Posterior scleritis is typically more challenging to diagnose and can be associated with more severe symptoms and complications.Tissue Damage : The inflammatory response and immune cell infiltration can cause damage to the scleral tissue. This can lead to thinning of the sclera, weakening of the eyes structural integrity, and potential complications such as scleral perforation (a hole in the sclera). Scleral thinning and perforation can result in severe visual impairment and even loss of vision., Epidemiology : The prevalence of scleritis has been estimated at 8 cases in 100 000, The incidence rates for episcleritis and scleritis were 15.39 and 5.54 per 100, 000 per year, respectively., variable, In many cases, you can’t prevent scleritis. But you can take good care of your eyes.,,You can reduce your risk of damaging your eyes by wearing the required eye protection when you’re at work or participating in certain contact sports.,,You can reduce your risk of eye infections by always making sure your hands are clean if you have to touch your eyes. Also, make sure you clean your contact lenses if you wear them., Complications : cataract, Secondary glaucoma, sclerosing keratitis, keratolysis, Diagnostics : COMPLEMENT 3(C3) LEVEL, Complete Blood Count CBC, Montoux test, ANCA, biopsy, MRI, CT SCAN, USG, Differential diagnosis : EPISCLERITIS, disease description : Scleritis refers to a inflammation of the sclera proper. It is a comparatively serious disease which may cause visual impairment and even loss of the eye if treated inadequately. Fortunately, its incidence is much less than that of episcleritis. It usually occurs in elderly patients (40-70 years) involving females more than the males.

Scleroderma Crisis

Disease Name : Scleroderma Crisis, Symptoms : constipation : In scleroderma, there is a weakening of the gut muscles and impaired motility. This can lead to constipation., heartburn : Chronic coughing that us Scleroderma in the Esophagus causes GERD. GERD may cause a burning sensation (heartburn) in your chest, throat, or mouth as food and acid return into the esophagus.ually is dry. Worsening cough is often the first sign of ILD scleroderma. As the ILD worsens shortness of breath develops, first with moderate activity but as things progress this may occur even with your normal daily activities and can be associated with feeling very tired with less energy., swelling : Swelling or puffiness in your hands or feet, often occurring in the morning., TELANGIECTASIA : Telangiectasia that appear as dilated loops of capillaries with the avascular areas (areas lacking blood vessels) on the fingernail folds are highly characteristic of scleroderma in your hands or feet, often occurring in the morning., ulceration : Digital ulcers occur because of poor blood flow to the fingertips which is in turn related to the narrowing of blood vessels that is the hallmark of all forms of systemic scleroderma., chronic cough : Chronic coughing that usually is dry. Worsening cough is often the first sign of ILD scleroderma. As the ILD worsens shortness of breath develops, first with moderate activity but as things progress this may occur even with your normal daily activities and can be associated with feeling very tired with less energy., Facial abnormalities : Facial skin becomes thin and taut, which leads to a mask-like appearance., alopecia : Alopecia (hair loss) may occur with scleroderma, if it affects the scalp. It may also occur due to the side effects of some treatments for scleroderma symptoms, such as chemotherapy., contractures of tissue : Patients with scleroderma may develop a characteristic claw deformity involving fixed flexion contractures of the interphalangeal joints, compensatory extension and sometimes hyperextension contractures of the metacarpophalangeal (MCP) joints, and an adduction contracture of the thumb., calcinosis : Calcinosis (calcium deposition under the skin) is common in patients with scleroderma, especially in people with limited disease and with overlap syndrome. Calcinosis can cause hand disability but is rarely associated with contractures., Signs : sclerodactyly : A condition called sclerodactyly, which is the thickening or hardening of the skin of the fingers and toes, also can occur. This may develop after the initial swelling goes away and may be followed by the shrinking or atrophy of skin., Treatment : SYSTEMIC SLERODERMA -Treatment aims to relieve symptoms and to slow disease progression. No treatment can cure the disease. Therapeutic strategies should have their basis on a person’s symptoms and the need to prevent complications. The use of different immunosuppressive drugs remains disappointing. Immunosuppressive therapy is reserved for diffuse SSc of recent diagnosis (less than 3 to 5 years) and patients with progressive PID. Its basis is on induction with cyclophosphamide then a relay by mycophenolate mofetil.,,LOCAL SCLERODERMA- ,Topical corticosteroids are the main treatment for plaque morphea. Generalized morphea may be treated with combination therapy of systemic steroids and methotrexate or with phototherapy. Linear scleroderma of the face or limbs generally requires the combination of systemic corticosteroids and methotrexate to avoid functional and/or esthetic disabilities, Pathophysiology : Three primary mechanisms contribute to the development of the scleroderma : vascular anomalies, excess fibrosis, and autoimmune phenomenon.Abnormal interactions between endothelial cells, fibroblasts, and lymphocytes (B and T) lead to microcirculatory vascular involvement. The endothelial cells produce large amounts of endothelin 1, causing vasoconstriction and fibroblast activation. Also, fibroblasts and activated endothelial cells produce reactive oxygen species that speed up vascular remodeling, leading to the obliteration of small vessels. Activated fibroblasts differentiate easily into myofibroblasts, which have increased collagen synthesis ability., Epidemiology : 7.2-33.9 cases per 100, 000 individuals, , Approximately one in 10, 000 individuals is affected. It is more common in women and most often develops around age 30 to 50., variable, There is no cure for scleroderma. However, there are medications that can reduce symptoms and organ damage,Limited scleroderma is usually treated with topical (applied to the skin) treatments such as moisturizers or topical corticosteroid creams.,Antibiotics can prevent bacterial infection of damaged parts of the intestines., Complications : musculoskeletal disorders, Diagnostics : ANA, Erythrocyte Sedimentation Rate (ESR), HISTOPATHLOGY, ECG, HRCT Thorax, kidney function test KFT, ENDOSCOPY, PULMONARY FUNCTION TEST(PFT), PHYSICAL EXAMINATION, Differential diagnosis : eosinophilic fasciitis, Fibrosis, Nephrogenic systemic fibrosis, disease description : Scleroderma is a chronic, autoimmune connective tissue disorder that is primarily characterized by thickening and hardening of the skin and other tissue. In localized scleroderma, the skin is the main organ system involved and muscles and bones may or may not be. In systemic scleroderma, internal organs such as the digestive tract, heart, lungs, and kidneys may be affected. The severity of this condition varies. This activity outlines the evaluation and management of scleroderma and highlights the role of the interprofessional team in managing patients with this condition.Life expectancy in patients with systemic sclerosis depends on the extent and severity of internal organ involvement.

Sclerosing Panniculitis

Disease Name : Sclerosing Panniculitis, Symptoms : induration : Sclerosing panniculitis is a chronic panniculitis characterized by skin induration and hyperpigmentation of one or both legs that often occurs in patients who have venous insufficiency., Pulmonary Embolism : Thrombosis caused by venous hypertension of the leg in sclerosing panniculitis causes pulmonary embolism, which leads to PH., plaques : The indurated plaques are often painful and the legs frequently have a characteristic “inverted wine bottle” appearance., Signs : nan, Treatment : nan, Pathophysiology : The pathophysiology of sclerosing panniculitis involves immune dysregulation and inflammation within the subcutaneous fat layer.Immune Dysregulation : The exact cause of sclerosing panniculitis is not fully understood, but it is believed to involve an abnormal immune response. In some cases, the immune system may mistakenly recognize the fat tissue as foreign or abnormal, leading to an immune attack against the adipocytes (fat cells) in the subcutaneous layer.Inflammatory Response : The immune attack triggers an inflammatory response within the subcutaneous fat tissue. Immune cells, such as lymphocytes and macrophages, infiltrate the affected area and release various pro-inflammatory cytokines and chemokines. These mediators promote inflammation and further recruit immune cells to the site of injury.Lipid Peroxidation : Inflammation in the adipose tissue can lead to the production of reactive oxygen species (ROS) and lipid peroxidation. Lipid peroxidation is the process of oxidative degradation of lipids, which can cause damage to cell membranes and cellular structures.Fibrosis and Scarring : The ongoing inflammation and lipid peroxidation can lead to fibrosis and scarring of the subcutaneous fat tissue. Fibrosis is the excessive deposition of connective tissue, mainly collagen, which replaces the normal fat cells. This fibrotic process results in hard, nodular, and tender subcutaneous masses, characteristic of sclerosing panniculitis.Triggers and Underlying Conditions : The exact triggers of sclerosing panniculitis remain unclear, but there is evidence to suggest that infections, medications, and autoimmune conditions may be associated with the development of the disease in some cases. Infections, especially viral infections like hepatitis, have been implicated as potential triggers. Certain medications, such as oral contraceptives, may also be associated with the development of sclerosing panniculitis in some individuals., Epidemiology : 0.6 to 2.5%, 3% and 1.5% in males and females, respectively, variable, Complications : CELLULITIS, Erysipelas, Diagnostics : HISTOPATHLOGY, skin lesion biopsy, Differential diagnosis : CARCINOID TUMORS, lymphoma, disease description : Sclerosing panniculitis is a relatively common form of long-term chronic panniculitis associated with chronic venous insufficiency and typically affecting the lower extremities of middle- aged or elderly women. This is manifested as a diffuse sclerosis and pigmentation of the skin and subcutaneous tissue (lipodermatosclerosis).

Sclerosing Stromal Tumour

Disease Name : Sclerosing Stromal Tumour, Symptoms : menstrual irregularities : Women suffers from menstrual irregularities in sclerosing stromal tumour., pelvic pain : Pelvic pain occurs mostly in the lower abdomen area. The pain might be steady, or it might come and go. It can be a sharp and stabbing pain in a specific spot, or a dull pain that is spread out. If the pain is severe, it might get in the way of your daily activities., ABDOMINAL MASS : An abdominal mass can be palpated., Signs : nan, Treatment : Complete surgical excision (oophorectomy)., Pathophysiology : FHL2-GLI2 fusions activate the Sonic hedgehog (SHH) pathway ., Epidemiology : Most common in the first 3 decades, 1.5% to 6% of ovarian stromal tumors, variable, Complications : nan, Diagnostics : CA 125, Frozen Section, Cytogenetics, MRI, CT SCAN, Immunostaining, Differential diagnosis : Fibroma, malignant epithelial ovarian tumours, METASTASES AT DIFFERENT SITES, disease description : Sclerosing stromal tumor is a benign stromal tumor that has a pseudolobular appearance resulting from alternating cellular and hypocellular areas.Sclerosing stromal tumor (SST) is an extremely rare benign ovarian neoplasm. It is a subtype of ovarian stromal neoplasm of sex chord-stromal origin that has distinctive clinical and pathological features, which differ from those of other stromal tumors (1). SST accounts for 2% to 6% of ovarian stromal tumors. These tumors occur predominantly in the second and third decade of life(2). Patients usually present with menstrual irregularities, pelvic pain, and an abdominal mass. SSTs are mostly hormonally inactive. If hormonally active, they are usually androgenic and occur most frequently during pregnancy

Scoliosis

Disease Name : Scoliosis, Symptoms : leg pain : In more severe cases, scoliosis can impact your sciatic nerve and cause pain to radiate down your leg., rib cage rigidity : With most scoliosis cases, the spine will rotate or twist in addition to curving side to side. This causes the ribs or muscles on one side of the body to stick out farther than those on the other side., Signs : One hip appears higher than the other : This occurs because as a scoliotic spine bends and twists, it pulls on the ribs and pelvis, distorting their position, and this can cause one hip to sit higher than the other and/or cause one hip to appear more rounded, while the other takes on a flatter appearance., TOP OF SHOULDERS ARE UNEVEN : The upper location of the scoliosis can result in one shoulder being pitched higher, with the other shoulder being forced downward, by the curve. The most common type of scoliosis is a right thoracic scoliosis, which can frequently lead to the right shoulder being higher than the left, Treatment : "NON SURGICAL METHODS- Milwaukee brace, Boston brace, Reissers turn-buckle cast, Localiser cast", Operative methods comprise,of fusion of the spine. In congenital scoliosis, ,simple fusion is sufficient. In idiopathic scoliosis, ,the spine is fused after achieving some correction,by stretching the spine, Pathophysiology : It is of two types : non-structural (transient) and structural (permanent).In structural scoliosis, the vertebrae, in addition to sideways tilt, are rotated along their long axis; in non-structural scoliosis they are not. Non-structural scoliosis : This is a mobile or transient scoliosis. It has three subtypes, as discussed below : • Postural scoliosis : It is the commonest overall type, often seen in adolescent girls. The curve is mild and convex, usually to the left. The main diagnostic feature is that the curve straightens completely when the patient bends forwards. • Compensatory scoliosis : In this type, the scoliosis is a compensatory phenomenon, occurring in order to compensate for the tilt of the pelvis (e.g., in a hip disease or for a short leg). The scoliosis disappears when the patient is examined in a sitting position (in case the leg is short) or when the causative factor is removed. • Sciatic scoliosis : This is as a result of unilateral painful spasm of the paraspinal muscles, as may occur in a case of prolapsed intervertebral disc. Structural scoliosis : It is a scoliosis with a component of permanent deformity. The following are the different subtypes : • Idiopathic : It is the commonest type of structural scoliosis. It may begin during infancy, childhood or adolescence. Infantile scoliosis begins in the first year of life, and is different from the other in that, it can be a resolving or progressive type. Scoliosis beginning later in life progresses at a variable rate, and leads to an ugly deformity. The deformity is most obvious in thoracic scoliosis because of the formation of a rib hump. In the lumbar region, even a moderate curve goes unnoticed because it gets masked by the compensatory curvature of the adjacent part of the spine. Idiopathic curves progress until the cessation of skeletal growth. • Congenital scoliosis : This type is always associated with some form of radiologically demonstrable anomaly of the vertebral bodies. These are : (i) hemivertebrae (only one-half of the vertebra grows); (ii) block vertebrae (two vertebral bodies fused); or (iii) an unsegmented bar (a bar of bone joining two adjacent vertebrae on one side, thereby preventing growth on that side). These curves grow, often at a very fast rate. Sometimes, there are associated anomalies in the growth of the neural structures, leading to a neurological deficit in the lower limbs. • Paralytic scoliosis : An unbalanced paralysis of the trunk muscles results in paralytic scoliosis of the spine. Poliomyelitis is the commonest cause in developing countries. Other common causes are cerebral palsy and muscular dystrophies. • Other pathologies : There are other causes of structural scoliosis such as neurofibromatosis which produces a sharp kyphoscoliosis. The main pathology is lateral curvature of a part of the spine. This is called the primary curve. The spine above or below the primary curve undergoes compensatory curvature in the opposite direction. These are called the compensatory or secondary curves . The lateral curvature is associated with rotation of the vertebrae. In curves of the thoracic spine, rotation of the vertebrae leads to prominence of the rib cage on the convex side, giving rise to a rib hump . Any part of the thoraco-lumbar spine may be affected. The pattern of the curve and its natural evolution are fairly constant for each site. The following types are recognised : (i) dorsal scoliosis; (ii) dorso-lumbar scoliosis; and (iii) lumbar scoliosis., Epidemiology : Prevalence of adult lumbar scoliosis has been reported to show a wide variability, ranging from 7.5% to 13.3%, 2-3 percent of the population, GOOD, Adult scoliosis cannot be prevented. In patients with idiopathic scoliosis, the cause of the condition is unknown. Degenerative scoliosis happens over time as the body ages. It is important to keep up with a regular low impact aerobic and core strengthening exercise program., Complications : back pain, nerve disorder, Diagnostics : MRI, X RAY, PHYSICAL EXAMINATION, Differential diagnosis : NEUROMUSCULAR DISORDER, spina bifida, Syringomyelia, disease description : Scoliosis is a sideways curvature of the spine that most often is diagnosed in adolescents. While scoliosis can occur in people with conditions such as cerebral palsy and muscular dystrophy, the cause of most childhood scoliosis is unknown.Most cases of scoliosis are mild, but some curves worsen as children grow.

Scorpion Sting

Disease Name : Scorpion Sting, Symptoms : profuse sweating, vomiting, pulmonary edema, blurred or unstable vision, hypersalivation : Scorpion stings can result in excess cholinergic activity with symptoms of SALIVATION., Localised burning sensation : Most scorpion stings produce some local tissue reaction that is characterized by mild to moderate burning pain., paresthesia : Paresthesia refers to a burning or prickling sensation that is usually felt in the hands, arms, legs, or feet, but can also occur in other parts of the body., Pain, Signs : eyes are rolled, Tachycardia : Most scorpion stings are benign and patients present with tachycardia., shock : Reactions to these subsequent stings are sometimes severe enough to cause a life-threatening condition called anaphylaxis., Treatment : medication : Fentanyl, Midazolam, Prazosin , "The management of scorpion stings involves relief of,pain (paracetamol or ibuprofen), wound cleaning and,tetanus prophylaxis. These patients may be discharged,after observation for 4 hr to ensure lack of symptom,progression. Midazolam infusion helps provide sedation and relief,from muscle spasticity. Intravenous fentanyl is preferred,to morphine of pain relief, since it does not cause histamine,release. Prazosin is useful in the management of,vasoconstriction and hypertension associated with areceptor,stimulation, since it reduces preload without,causing tachycardia and increase in myocardial oxygen,demand. Patients with left ventricular dysfunction due to,hypertension may benefit from sodium nitroprusside,infusion or use of an angiotensin converting enzyme,inhibitor. Scorpion antivenom reverses the excitatory effects of,the venom and neutralizes circulating unbound venom,to minimize parasympathetic stimulation. Its use reduces,the duration of symptoms and the need for benzodiazepines.,Scorpion-specific F(ab) equine antivenom,should be administered as early as possible to patients,with Grade III or IV neurotoxicity.", Pathophysiology : Grade 1 involves local pain and paresthesias at the sting site. The puncture wound may not be noticeable in this grade. The "tap test" may confirm a providers suspicion of a sting by exilicauda by distracting the patient and tapping on the area of the sting, causing increased pain. This reaction does not occur with other species. Care is limited to analgesia. Historical and epidemiologic clues may also help in confirming a scorpion sting.Grade 2 involves local pain and paresthesias existing at the sting site as well as proximal to the sting site. Recommended care includes analgesia with optional anxiolytics if needed. More distant symptoms can radiate up to the same extremity or even to the contralateral limbs.Grade 3 includes grade 2 classification factors with added cranial nerve (increased oral secretions, blurry vision, rapid tongue movement, nystagmus), or skeletal neuromuscular dysfunction (flailing of the extremities and tetanus-like arching of the back) and can also be accompanied by autonomic dysfunction. Grade 3 envenomations can sometimes affect airways. Patients with Grade 3 stings require analgesia and anxiolytics as well as antivenom. Centruroides do sometimes produce autonomic dysfunction, and most commonly, symptoms include salivation, vomiting, bronchoconstriction, diaphoresis, and tachycardia. Parabuthus stings can also produce autonomic dysfunction, but uniquely, it can lead to urinary retention., Epidemiology : he estimated annual number of scorpion stings is 1.2 million leading to 3250 deaths, DEPENDS ON SEVERITY OF SYMPTOMS, Scorpions are more active at night, but people can get stung at any time. You can lessen your risk by wearing long sleeves, pants and gloves when you’re outside in areas where scorpions live. In these areas, it’s also a good idea to shake out your shoes and clothing before putting them on. In addition : ,,Wear protective footwear when you’re in an area where scorpions live.,Use caution when moving logs, lifting rocks or collecting firewood.,Don’t handle scorpions with your bare hands.,While camping, avoid sleeping directly on the ground.,Carry an epinephrine auto-injector (EpiPen®) if you know you have an allergy., Complications : death, respiratory distress, shock, MULTIORGAN FAILURE, Diagnostics : ABG, Complete Blood Count CBC, ECG, HISTORY TAKING, Differential diagnosis : botulism, diphtheria, insect bites, Toxicity, disease description : Scorpions are a common arthropod on every continent except Antarctica. If threatened, a scorpion may use its long, flexible tail to sting a potential predator. Frequently, people unknowingly come into contact with these species and experience the painful sensation of envenomation. While the vast majority of scorpion stings do not result in life-threatening situations, scorpion stings can produce life-threatening situations. When a victim of a scorpion sting presents to the emergency department, there are a few things to keep in mind to guide care for the patient safely

Scrofuloderma

Disease Name : Scrofuloderma, Symptoms : ulceration : Scrofuloderma usually presents as an undermined ulcer or discharging sinus, with surrounding induration and dusky red discoloration., NODULES : The clinical picture is characterized by the presence of subcutaneous, painless, slowly growing nodules that evolve to ulcers and fistulous tracts with drainage of serous, purulent, or caseous content., Signs : Initially bluish red, subcutaneous swellings that persist for several months and overlie an infected gland or joint. : A bluish-red nodule develops over the affected bone, joint or lymph node and multiple fistulae develop., Treatment : medication : Rifampicin/Rifampin, Isoniazid , Pyrazinamide , Antituberculous therapy should be commenced promptly., Pathophysiology :  The pathophysiology of scrofuloderma involves the following key processes : Tuberculous Infection : Scrofuloderma originates from an underlying tuberculous focus, such as a tuberculous lymph node or bone. Tuberculosis is caused by the bacterium Mycobacterium tuberculosis, which is an acid-fast bacillus that primarily infects the lungs (pulmonary tuberculosis). In some cases, the bacteria can spread to other parts of the body, leading to extrapulmonary tuberculosis, including cutaneous tuberculosis.Sinus Formation : As the tuberculous infection progresses in the lymph nodes or bones, caseous (cheesy) necrosis may develop. This necrotic material can erode and form sinus tracts or fistulae that connect the tuberculous focus to the skin surface. These sinus tracts provide a route for the tuberculous bacteria to spread to the skin, leading to scrofuloderma.Cutaneous Involvement : Once the bacteria reach the skin through the sinus tracts, they induce an immune response in the skin tissue. The bodys immune system attempts to contain and eliminate the bacteria, leading to the characteristic clinical features of scrofuloderma., Epidemiology : 1% to 1.5% of extrapulmonary tuberculosis, , variable, Prevention of cutaneous tuberculosis involves BCG vaccination; identification, separation, and treatment of the person who is a source of infection; and use of sterilized instruments, along with other steps. As immunodeficiency is the biggest cause of skin tuberculosis, one should try to avoid it by controlling diabetes and other diseases. In cases where drug therapy is the cause of immunodeficiency, pretesting and treating latent tuberculosis with antibiotics are indicated., Complications : Squamous carcinoma in situ, lymphedema, contractures of tissue, Diagnostics : FNAC, skin biopsy with immunohistochemistry, Mantoux test, Differential diagnosis : Actinomycosis, hidradenitis suppurativa, sporotrichosis, disease description : Scrofuloderma results from the direct invasion of the tubercle bacillus into the skin from an underlying contiguous tuberculous focus. Worldwide, it is the commonest form of cutaneous tuberculosis. It is most common in children and within the first three decades of life. Males were affected 1.5 times more than females in a recent series from India. Systemic tuberculosis and Sweet disease can coexist

Scrotal Calcinosis

Disease Name : Scrotal Calcinosis, Symptoms : itching : The nodules may sometimes be associated with itching., DISCHARGE : The nodule may break down to discharge chalky material., NODULES : The disease presents as slow-growing yellowish nodules in the scrotum, single to multiple in numbers, with varying sizes., Signs : nan, Treatment : The only treatment recommended for SC is surgery, which cures the aesthetic disorder and enables the confirmation of the diagnosis of SC on histologic examination. Surgical excision must be limited to the scrotal skin because the calcified nodules are localized in the dermis., Pathophysiology : Their origin has been debated : they have been said to arise from epidermoid cysts, , eccrine duct milia, eccrine epithelial cysts, dystrophy, of the dartos muscle, trauma and the presence of foreign bodies . Scrotal calcinosis may occur after meconium peritonitis, with leakage of meconium through the processus vaginalis, and in testicular tumours such as teratomas, gonadoblastomas and Leydig cell tumours . In endemic areas of onchocerciasis, calcified scrotal cysts may be caused by the living or dead nematodes, and patients have evidence of the disease elsewhere. Onchocercal nodules are more common., Epidemiology : 30% of adult dermatomyositis (DM) cases and in up to 20% to 40% of juvenile DM (JDM) case, variable, avoiding trauma, smoking cessation, decrease stress and exposure to the cold., Complications : Molluscum Contagiosum, Genital warts, milia, Diagnostics : HISTOPATHLOGY, USG, Differential diagnosis : angiokeratomas, Dermatomyositis, lipoma, neurofibroma, Raynaud phenomenon, disease description : Scrotal calcinosis is a relatively common, benign, idiopathic disorder presenting as solitary or multiple, hard, smooth, white papules or nodules on the scrotum, rarely the penis. Interestingly, these lesions are much rarer on the vulva. Occasionally, they may become secondarily inflamed or infected following trauma. Scrotal calcinosis may occur after meconium peritonitis, with leakage of meconium through the processus vaginalis, and in testicular tumours such as teratomas, gonadoblastomas and Leydig cell tumour. Other associations are trauma, self-injection with papaverine, Peyronie disease and cytotoxic chemotherapy . Metastatic calcinosis is due to renal failure and secondary hyperparathyroidism

Scurvy

Disease Name : Scurvy, Symptoms : bleeding : Bleeding under your skin (skin hemorrhages). You may develop a “scurvy rash” that shows up as red or blue spots on your skin., hair dryness : Dry, brittle hair that coils like a corkscrew., teeth problem : Loosened teeth that may fall out., gum pain : Swollen, bleeding gums that may become purple and spongy., Bruising easily : Easily bruised skin., Signs : anemia, Treatment : medication : Vitamin C/Ascorbic Acid, Vitamin C supplements of 100-200 mg/day orally or parenterally ensure rapid,and complete cure. The clinical improvement is seen within 1 week in most,cases, but the treatment should be continued for up to 3 mo for complete,recovery., Pathophysiology : A deficiency of vitamin C results in the clinical presentation of scurvy . Children fed predominantly heat-treated (ultrahigh-temperature or pasteurized) milk or unfortified formulas and not receiving fruits and fruit juices are at significant risk for symptomatic disease. Infants and children on highly restrictive diets, devoid of most fruits and vegetables, are at risk of acquiring severe vitamin C deficiency. Such diets are occasionally promoted with unsubstantiated claims of benefit in autism and other developmental disorders, In scurvy, there is defective formation of connective tissues and collagen in skin, cartilage, dentine, bone, and blood vessels, leading to their fragility. In the long bones, osteoid is not deposited by osteoblasts, cortex is thin, and the trabeculae become brittle and fracture easily. The early manifestations of vitamin C deficiency are irritability, loss of appetite, low-grade fever, musculoskeletal pain, and tenderness in the legs. These signs and symptoms are followed by leg swelling—most marked at the knees and the ankles—and pseudoparalysis . The infant might lie with the hips and knees semiflexed and the feet rotated outward. Subperiosteal hemorrhages in the lower-limb bones sometimes acutely increase the swelling and pain, and the condition might mimic acute osteomyelitis or arthritis. A “rosary” at the costochondral junctions and depression of the sternum are other typical features. The angulation of scorbutic beads is usually sharper than that of a rachitic rosary. Gum changes are seen in older children after teeth have erupted, manifested as bluish purple, spongy swellings of the mucous membrane, especially over the upper incisors. Anemia, a common finding in infants and young children with scurvy, is related to impaired iron absorption and coexistent hematopoietic nutrient deficiencies, including iron, vitamin B12 , and folate. Hemorrhagic manifestations of scurvy include petechiae, purpura, and ecchymoses at pressure points; epistaxis; gum bleeding; and the characteristic perifollicular hemorrhages. Other manifestations are poor wound and fracture healing, hyperkeratosis of hair follicles, arthralgia, and muscle weakness., Epidemiology : 5 to 45 percent, 3.9% in 2668 people in North India and 45.7% in 2970 from South India. 3 Only 10.8% in the North and 25.9% in the South meet the criteria. Vitamin C deficiency varies based on season and occurs more in men with, GOOD, You can prevent scurvy by getting the recommended daily allowance of vitamin C in your diet. The best sources of the nutrient are fresh fruits and vegetables. Good sources of vitamin C include : ,,Citrus fruits.,Tomatoes.,Potatoes.,Broccoli.,Strawberries.,Sweet peppers.,Speak to your healthcare provider before taking a vitamin C dietary supplement., Complications : nan, Diagnostics : Total Leucocyte Count (TLC), White Blood Cell count WBC, X RAY, PHYSICAL EXAMINATION, Differential diagnosis : Arthritis, MALIGNANCY, meningococcemia, osteomyelitis, poliomyelitis, rheumatic fever, Septic arthritis, Syphilis, disease description : Vitamin C is important for synthesis of collagen at the level of hydroxylation of lysine and proline in precollagen.Vitamin C functions to maintain the iron and copper atoms, cofactors of the metalloenzymes, in a reduced (active) state. Vitamin C is an important antioxidant (electron donor) in the aqueous milieu of the body. Vitamin C enhances nonheme iron absorption, the transfer of iron from transferrin to ferritin, and the formation of tetrahydrofolic acid and thus can affect the cellular and immunologic functions of the hematopoietic system. Humans depend on dietary sources for vitamin C. An adequate intake is 40 mg for ages 0-6 mo and 50 mg for 6-12 mo. For older children the recommended dietary allowance is 15 mg for ages 1-3 yr, 25 mg for 4-8 yr, 45 mg for 9-13 yr, and 65-75 mg for 14-18 yr. The recommended dietary allowances during pregnancy and lactation are 85 mg/day and 120 mg/day, respectively. The best food sources of vitamin C are citrus fruits and fruit juices, peppers, berries, melons, guava, kiwifruit, tomatoes, cauliflower, and green leafy vegetables. Vitamin C is easily destroyed by prolonged storage, overcooking, and processing of foods. Absorption of vitamin C occurs in the upper small intestine by an active process or by simple diffusion when large amounts are ingested. Vitamin C is not stored in the body but is taken up by all tissues; the highest levels are found in the pituitary and adrenal glands. The brain ascorbate content in the fetus and neonate is markedly higher than the content in the adult brain, a finding probably related to its function in neurotransmitter synthesis. When a mothers intake of vitamin C during pregnancy and lactation is adequate, the newborn will have adequate tissue levels of vitamin C related to active placental transfer, subsequently maintained by the vitamin C in breast milk or commercial infant formulas. Breast milk contains sufficient vitamin C to prevent deficiency throughout infancy. Neonates whose feeding has been delayed because of a clinical condition can also have ascorbic acid deficiency.

Sebaceoma

Disease Name : Sebaceoma, Symptoms : papules : Clinically sebaceomas are typically solitary, yellow-orange papules or nodules that range in size from 6 mm up to 3 cm in diameter., Signs : nan, Treatment : Once the diagnosis is established, no further treatment is needed,However, complete excision should be considered if the tumor is only partially biopsied or there is concern for basal cell carcinoma with sebaceous differentiation or sebaceous carcinoma., Pathophysiology : Sebaceous Glands : Sebaceous glands are specialized skin appendages responsible for producing sebum, an oily substance that lubricates the skin and hair. They are most commonly found in areas with a high density of hair follicles, such as the face, scalp, chest, and back.Abnormal Cell Proliferation : In sebaceoma, there is uncontrolled proliferation of sebaceous gland cells. The exact cause of this abnormal growth is not fully understood, but genetic mutations or alterations in cellular signaling pathways are believed to play a role.Formation of Tumor : As the sebaceous gland cells continue to grow and divide uncontrollably, they form a mass or tumor within the skin. The tumor consists of proliferating sebaceous gland cells and may be well-circumscribed.Benign Nature : Sebaceomas are typically considered benign tumors, meaning that they do not spread to other parts of the body (metastasize). However, they can be locally invasive and extend into nearby tissues. In some cases, sebaceomas may resemble other types of skin tumors or cancers, making accurate diagnosis and differentiation crucial., Epidemiology : Female to male ratio is 4 : 1,Wide age range but the majority of patients are in the sixth to ninth decades, variable, Complications : MALIGNANCY, Diagnostics : HISTOPATHLOGY, Immunostaining, Differential diagnosis : Basal cell carcinoma, Sebaceous adenoma, Sebaceous carcinoma, Trichoblastoma, disease description : Sebaceoma is a distinctive benign neoplasm of the adnexal epithelium with differentiation toward sebaceous structures; it presents as a circumscribed nodular lesion that is rarely diagnosed before a histological examination . Sebaceous carcinoma arising from sebaceoma is an extremely rare condition

Sebaceous Adenoma

Disease Name : Sebaceous Adenoma, Symptoms : papules : Patients with sebaceous adenomas typically experience a gradual onset of small, usually less than 0.5 cm in diameter (2-4 mm), smooth, yellow, sometimes speckled papules that may feature crusting or central umbilication. Typically, they grow on the skin of the face or scalp over the course of a few months and are asymptomatic., Signs : nan, Treatment : Because sebaceous adenomas are benign, treatment for most individuals is conservative management, although bothersome lesions can be removed for patient comfort.,Consider complete excision also if the lesion is partially biopsied or of clinical concern for carcinoma with sebaceous differentiation., Pathophysiology : Sebaceous Glands : Sebaceous glands are specialized skin appendages responsible for producing sebum, an oily substance that helps lubricate the skin and hair. These glands are most commonly found in areas with a high density of hair follicles, such as the face, scalp, chest, and back.Abnormal Cell Growth : In sebaceous adenoma, there is uncontrolled and localized growth of sebaceous gland cells. The exact cause of this abnormal growth is not fully understood, but genetic mutations or alterations in cellular signaling pathways are believed to play a role.Formation of Adenoma : As the sebaceous gland cells continue to proliferate, they form a well-circumscribed mass or adenoma within the skin. The tumor consists of proliferating sebaceous gland cells and may have varying appearances under the microscope.Benign Nature : Sebaceous adenomas are typically considered benign tumors, meaning that they do not spread to other parts of the body (metastasize). They are slow-growing and non-invasive, but they can be locally expansive and may extend into nearby tissues., Epidemiology : 0.1% of all salivary gland neoplasms and slightly less than 0.5% of all salivary adenomas, variable, You can’t prevent these bumps from forming, but certain skincare products may help reduce the chances of developing sebaceous hyperplasia : ,,Niacinamide : This form of vitamin B3 may help control the production of sebum and repair your skin’s protective barrier. It usually comes in serums you rub onto your skin or tablets that you swallow.,Retinol : This form of vitamin A is available by prescription and over the counter. It can help prevent clogging in your sebaceous glands. It’s usually in the form of a cream or serum that you put on your skin.,Salicylic acid : This product helps get rid of dead cells from the top layer of your skin. It also reduces swelling and redness. Salicylic acid typically comes in a lotion that you put on your skin., Complications : nan, Diagnostics : HISTOPATHLOGY, biopsy, HISTOLOGIC EXAMINATION, Immunostaining, Differential diagnosis : Basal cell carcinoma, Sebaceous hyperplasia, disease description : A sebaceous adenoma is a small, benign bump on a gland in your skin. Multiple sebaceous adenomas are called sebaceous hyperplasia. They often appear on your face or trunk.? A sebaceous adenoma is a small bump on a gland in your skin (sebaceous gland). It’s a harmless, benign tumor in a hair follicle .If you have several sebaceous adenomas, it’s called sebaceous hyperplasia.

Sebaceous Carcinoma

Disease Name : Sebaceous Carcinoma, Symptoms : crusting of the skin : Thickened, yellow or red crusty skin near your eyelashes., soreness : A sore that bleeds, doesn’t heal, or heals and then comes back., lump : Firm, round, yellow painless lump that resembles a pimple., TUMOURS : Sebaceous carcinoma tumors tend to affect your upper eyelids, which have many sebaceous glands. Tumors can also affect your lower eyelids., Signs : nan, Treatment : Wide local excision or Mohs micrographic surgery are the best initial treatment options,Sentinel lymph node biopsy for periorbital sebaceous carcinoma > 10 mm in diameter,Radiation therapy and systemic chemotherapy are only used for patients who are poor surgical candidates or those with recurrent or metastatic disease,Immunohistochemistry to evaluate for microsatellite instability (MSH2, MSH6, MLH1, PMS2) should be offered on sebaceous carcinoma specimens, especially extraocular ones, to screen for Muir-Torre syndrome,Evidence of orbital invasion on imaging necessitates exenteration., Complete surgical excision is required. Reports of excellent ,results with Mohs surgery suggest that this may be the treatment ,of choice, Pathophysiology :  The proportion of cells showing fat globules and the degree of cytoplasmic vacuolation are variable. The undifferentiated cells are of moderate size, with round centrally placed nuclei and rather basophilic cytoplasm, and they tend to group themselves in masses of a multilobular configuration. The differentiating cells tend to be more central. There are, in addition, cytological features of malignancy and evidence of an infiltrative growth pattern. Mitotic figures including atypical forms are frequent. Pagetoid infiltration of the epidermis is frequent, particularly in tumours arising around the eye. Demonstration of sebaceous differentiation by histochemistry is possible by the use of oil red O but it requires frozen sections and these are usually not available. By immunohistochemistry, sebaceous differentiation can be demonstrated by epithelial membrane antigen (EMA) but only in cells with good differentiation. Adipophilin and peripilin are more recently added immuno histochemical stains useful in demonstrating sebaceous differentiation. Peripilin seems to be more specific than adipophilin except in cases of carcinoma in situ with clear-cell change in which tumour cells are often positive for the former marker. Sebaceous carcinoma may rarely be associated with the Muir– Torre syndrome. The latter association is mainly seen with extraocular carcinomas and those tumours occurring outside the head and neck area., Epidemiology : Sebaceous carcinoma is a rare tumor, only 7 cases reported in literature., 5 year relative survival rate : 92.7%, 1. There should also be consideration of more frequent exams for transplant recipients with multiple risk factors for sebaceous carcinoma.,,2. Screening should also be considered for non-white patients, who may not be routinely surveilled for skin cancer, if they have multiple risk factors for sebaceous carcinoma.,,3. In addition, patients should be educated on the clinical appearance of sebaceous neoplasms (yellow/orange/red raised lesions, may ulcerate or bleed, often located on the face) in order to perform self-skin exams at home. ,,4. Further, to reduce risk for sebaceous carcinoma along with other skin cancer types, these high-risk populations (HIV positive, Muir-Torre syndrome, solid organ transplant recipients) should be advised about the importance of sun protection. ,,5. HIV testing should also be considered for patients with newly diagnosed sebaceous carcinoma, particularly when diagnoses occur before age 50 and when there are other risk factors for HIV infection such as intravenous drug use.,,6. If a virus is implicated in sebaceous carcinoma tumor development, then it may be possible to develop a vaccine to prevent infection and reduce cancer risk., Complications : Metastasis, Diagnostics : Frozen Section, HISTOPATHLOGY, biopsy, MRI, PHYSICAL EXAMINATION, Immunostaining, Differential diagnosis : Basal cell carcinoma, CHALAZION, dermoid cyst, inclusion cyst, keratoacanthoma, Papilloma, squamous cell carcinoma., disease description : Sebaceous carcinoma (SC) is a rare and aggressive malignancy that develops from the sebaceous glands. Sebaceous carcinoma is most common in the periocular area, head, and neck, but can occur anywhere in the body where sebaceous glands are present

Sebaceous Gland Hyperplasia, Adenoma And Carcinoma

Disease Name : Sebaceous Gland Hyperplasia, Adenoma And Carcinoma, Symptoms : LESIONS : Lesions are usually described as asymptomatic, soft, discrete, and yellow, with a surface that ranges from smooth to slightly verrucous. Patients may report one or multiple lesions at various locations on the face. Lesions may become red and irritated and bleed after scratching, shaving, or other trauma., Signs : nan, Treatment : First line,Cosmetic camouflage may be used.,Second line,If requested and appropriate, some physical treatments such as ,gentle cautery, cryotherapy or trichloroacetic acid can be used. ,Pulsed dye and 1450 nm diode lasers have also been advocated .,Third line,Oral isotretinoin has been reported to be of considerable benefit ,in extensive sebaceous gland hyperplasia . A therapeutic trial ,of oral isotretinoin may help to differentiate between sebaceous ,hyperplasia and multiple early basal cell carcinomas in transplant ,recipients, and may avoid multiple biopsies if there are many ,lesions.,Cyproterone actetate in combination with a combined oral contraceptive preparation has also been used with benefit to induce ,regression of sebaceous hyperplasia in females 8.,Photodynamic therapy using aminolaevulinic acid has also ,been shown to be useful for shrinking lesions of sebaceous hyperplasia., Pathophysiology : Pathophysiology- The whole pilosebaceous unit is enlarged compared with normal adjacent skin but otherwise appears normal. Familial cases presenting at a young age suggest the possibility of a genetic component., Epidemiology : Unknown but not uncommon., Unknown but not uncommon., good, Complications : nan, Diagnostics : HISTOPATHLOGY, biopsy, Differential diagnosis : Cowden syndrome, Sebaceous carcinoma, disease description : Sebaceous gland hyperplasia presents as scattered clinically obvious flesh-coloured to yellowish papules resulting from hypertrophy of sebaceous glands.

Seborrhoeic Dermatitis

Disease Name : Seborrhoeic Dermatitis, Symptoms : blepharitis : Blepharitis is inflammation of the eyelids. Blepharitis usually affects both eyes along the edges of the eyelids. Blepharitis commonly occurs when tiny oil glands near the base of the eyelashes become clogged, causing irritation and redness., flaking : Itchy white flakes of skin on your scalp (dandruff). When scratched, the flakes come loose, mix in with your hair, or fall onto your neck and shoulders., Redness : Redness in the folds and creases of your genitals, armpits and beneath your breasts., Skin rashes : Ring-shaped (annular) rash, for a type called petaloid seborrheic dermatitis. Rash that may look darker or lighter in people with brown or Black skin and redder in those with white skin., skin patches : Patches of greasy skin covered with flaky white or yellow scales or crust on the scalp, face, sides of the nose, eyebrows, ears, eyelids, chest, armpits, groin area or under the breasts, Signs : nan, Treatment : medication : Selenium sulfide, Terbinafine , Sertaconazole nitrate , Ketoconazole , Pimecrolimus, Keratolytic,agents such as urea, propylene glycol and lactic acid.Topical antifungals are the mainstay of therapy due to their safety in all ages.In addition to all azoles, newer azoles such as sertaconazole have been reported to be effective in treating SD. New formulations may also improve patient choice, such as a 2% ,ketoconazole foam.Topical use of the allylamines terbinafine and naftitine has been reported to be effective in SD, broad spectrum antifungal agent ciclopirox olamine is also effective topically in treating SD of the scalp and face. Selenium sulphide has been used to treat SD, Topical lithium gluconate has anti-inflammatory effects in SD, Topical corticosteroids may be used in combination with,antifungals for their additional anti-infl ammatory effect. Other active agents present in antidandruff shampoos include the antifungal agents zinc pyrithione and coal tar.antimicrobial peptides may provide another treatment option for SD, Pathophysiology : The pathophysiology includes-Disruption of the skin’s microbiotaAn impaired immune reaction to Malassezia spp. associated with a diminished T-cell response and activation of complement The increased presence of unsaturated fatty acids on the skin surfaceDisruption of cutaneous neurotransmittersAbnormal shedding of keratinocytesEpidermal barrier disturbances associated with genetic factors, Epidemiology : approximately 3 percent, variable, There’s little that can be done to prevent seborrheic dermatitis. Cradle cap is a natural, harmless condition. It can be simply treated at home. If you are a teenager or an adult with seborrheic dermatitis, you might be more prone if you have higher than normal levels of androgens, a higher level of lipids in your skin or have an overgrowth of the yeast that is always present on your skin’s surface.,,Some simple healthy things you can do to reduce your risk include getting plenty of rest, controlling your emotional stress and getting a daily small doses (minutes) of sunshine (UV light). Stay away from the midday sun.,,Always follow your healthcare provider’s instructions for using medicated shampoos and skin products. Under treatment or inappropriate treatment can result in flare-ups of your condition and return visits to your healthcare provider., Complications : erythroderma., Diagnostics : HIV, biopsy, TISSUE HISTOLOGY, Dermoscopy, Differential diagnosis : actinic keratosis, Melanoma, disease description : Seborrheic dermatitis (SD) is a common inflammatory skin disease presenting with a papulosquamous morphology in areas rich in sebaceous glands, particularly the scalp, face, and body folds. The infantile (ISD) and adult (ASD) variants reflect the condition’s bimodal occurrence.Infants are not usually troubled by seborrheic dermatitis, but it may cause significant parental anxiety, often appearing as firm, greasy scales on the crown and frontal regions of the scalp. It occurs in the first three months of life and is mild, self-limiting, and resolving spontaneously in most cases by the first year of life.ASD, on the other hand, is characterized by a relapsing and remitting pattern of disease and is ranked third behind atopic and contact dermatitis for its potential to impair the quality of life

Seborrhoeic Otitis Externa

Disease Name : Seborrhoeic Otitis Externa, Symptoms : scaling of skin : The seborrheic form is characterized by a lack of cerumen and by dry, scaly, red, or shiny skin in the ear canal, the eczematous form by moist, erythematous skin., Signs : nan, Treatment : medication : Salicylic acid , ear toilet, application of a cream containing ,salicylic acid and sulfur, Pathophysiology : The external auditory canal is covered by hair follicles and cerumen-producing glands. Cerumen provides a protective barrier and an acidic environment that inhibits bacterial and fungal growth .The inflammatory response in otitis externa is believed to be caused by a disruption of the normal pH and protective factors within the auditory canal. This includes a sequential process of damage to the epithelium, loss of protective wax, and accumulation of moisture that leads to a higher pH and bacterial growth., Epidemiology : Approximately 10% of people will develop otitis externa during their lifetime, and the majority of cases (95%) are acute, Otitis externa is a common condition and can occur in all age groups. It is uncommon in patients younger than 2 years old.it peaks around the age of 7-14., variable, "To help reduce your chances of developing otitis externa, you should avoid inserting cotton wool buds and other things into your ears (including your fingers), as this can damage the sensitive skin in your ear canal.,,If youre a regular swimmer, consider using ear plugs when swimming or wearing a swimming cap to cover your ears and protect them from water.,,You should also try to avoid getting water, soap or shampoo into your ears when you have a shower or bath.", Complications : PERICHONDRITIS, Myringitis Bullosa, Facial cellulitis and acute ethmoiditis, Diagnostics : Otoscopy, CT SCAN, Differential diagnosis : Acne vulgaris, candidiasis, ECZEMA, Impetigo, lupus erythematosus, psoriasis, tinea corporis, disease description : It is associated with seborrhoeic dermatitis of the scalp. Itching is the main complaint. Greasy yellow scales are seen in the external canal, over the lobule and postauricular sulcus. Treatment consists of ear toilet, application of a cream containing salicylic acid and sulfur, and attention to the scalp for seborrhoea.

Seborrhoeic

Disease Name : Seborrhoeic, Symptoms : They can occur on any body site but most frequently on the face and upper trunk. The fi rst evidence is slight hyperpigmentation, SKs can be pedunculated or acanthotic, smooth surfaced, domed and heavily pigmented. The surface of these SKs has numerous plugged follicular orifi ces, giving an almost cerebriform appearance, The superfi cial verrucous plaques vary from dirty yellow to black in colour and may have a typical ‘stuck-on’ appearance with a loosely adherent greasy keratin on the surface, SKs are commonly round or oval and their size varies from 1 mm to several centimetres. On the eyelids and major fl exures, SKs may be pedunculated and less keratotic., Signs : nan, Treatment : Pure trichloracetic acid application may also be helpful., First line,• Curettage, cryotherapy,Second line,• Ablative or non-ablative lasers,Third line,• Medium depth chemical peels, Pathophysiology :  Sunlight has been implicated in the causation of SKs. There is an accumulation of normal but immature keratinocytes between the basal layer and the keratinizing surface of the epidermis. Melanocyte proliferation may be present. Horn cysts are produced by immature keratinocytes. Coalescing horn cysts can be carried to the surface by the tide of epidermal cells. The surface may be verrucous and dermal papillae may be elongated. Marked papillomatosis will also cause an irregular ‘church steeple’ outer border which retains keratin. Conversely, the surface can be smooth and rounded, and the melanocyte population and degree of pigmentation might vary, so that the lesions may be deeply pigmented. The parenchymal cells are rather small and polygonal, possessing tonofibrils and intercellular bridges, and they are arranged in an orderly fashion. The three pathological variants are the solid, hyperkeratotic and reticular variants. The solid SK is the most common and displays a mass of immature keratinocytes seen mainly above the level of the surrounding epidermis. Occasional cystic areas containing fragments of stratum corneum are seen at these sites. The hyperkeratotic variety is rare and may be clinically mistaken for an actinic keratosis. The reticular form is a third variant, composed of strands of keratinocytes; this type is frequently seen as a fl at lesion on the face. The most important differential diagnosis for an irritated SK is an early invasive squamous cell carcinoma (SCC). Despite the presence of focal areas of whorls of keratinocytes in squamous eddies, mitotic figures are rare, and the base of the lesion shows a clear separation from dermal tissue, with no single-cell invasion Causative organisms The role of human papillomavirus in the causation of non-genital SK has been suggested but not established. FGFR3 mutations have been identified in 39–85% of human SK. It has been demonstrated that FGFR3 mutations are present in flat SKs which indicates that the mutations may be early genetic events in the pathogenesis of at least a subset of SK. Additionally, age has been identified as a major risk factor for the occurrence of somatic FGFR3 mutations in the skin, in line with the appearance of SK in mid to old age. Germline FGFR3 mutations detected in human skin tumours are associated with thanatophoric dysplasia, severe achondroplasia with developmental delay and acanthosis nigricans (SADDAN) syndrome and Crouzon syndrome. Benign epidermal naevi are histologically very similar to SK and show FGFR3 and PIK3CA oncogenic mutations as an underlying genetic basis. Activating FGFR3 mutations in human skin may provide proliferative signals for the keratinocytes in SK. Additionally, increased Ki-67 and antiapoptotic bcl-2 expression has been noted in SK. More recently, expression of DNp63a, the most abundantly expressed p63 isoform, has been found to be significantly increased in SK compared with normal skin, as have identifi - cation of activating PIK3CA mutations in 16% of SKs examined., Epidemiology : In studies from Australia, these lesions were iden, fair, Complications : nan, Diagnostics : Dermoscopy, Differential diagnosis : Acute Otitis Media, Carcinoma of the ear canal, foreign body, Furunculosis of meatus, psoriasis, disease description : A benign tumour composed of epidermal keratinocytes, displaying varying morphological features, frequently pigmented and more common in the elderly. Seborrhoeic keratoses (SK) are usually asymptomatic and can have pleomorphic features varying from pale superfi cial patches to darkly pigmented verrucous plaques.Age Seborrhoeic keratoses usually appear in the fi fth decade of life in patients living in temperate climates but the age of onset may be earlier in those residing in tropical regions. There is little tendency to spontaneous disappearance and new lesions may continue to appear for many years. Sex Males and females are equally affected.

Second Degree Cervical Descent With Cystocele2+ And Rectocele 3+

Disease Name : Second Degree Cervical Descent With Cystocele2+ And Rectocele 3+, Symptoms : sensation of heaviness : A sensation of pressure or fullness in your rectum or vagina., DYSPAREUNIA : Experiencing discomfort during intercourse., "bowel dysfunction : Feeling that your rectum hasnt completely emptied after pooping.", Signs : nan, Treatment : medication : Acridine Derivatives/Acriflavine, Pathophysiology : Second-Degree Cervical Descent : This refers to the descent of the cervix (the lower part of the uterus) into the vaginal canal. In a second-degree descent, the cervix is approximately halfway down the vaginal canal, but it does not protrude outside the vaginal opening.Pathophysiology : The pelvic floor muscles and ligaments that support the uterus may weaken over time due to factors such as aging, multiple childbirths, hormonal changes, obesity, chronic coughing, or chronic straining during bowel movements. Weakened support allows the uterus to descend into the vaginal canal, leading to second-degree cervical descent.Cystocele 2+ : A cystocele, also known as a bladder prolapse, occurs when the supportive tissues between the bladder and vaginal wall weaken, causing the bladder to bulge into the anterior vaginal wall.Pathophysiology : The weakening of the connective tissues and pelvic floor muscles supporting the bladder can be caused by factors similar to those mentioned above. As the supporting structures weaken, the bladder can descend into the vaginal canal, leading to a cystocele.Rectocele 3+ : A rectocele occurs when the supportive tissues between the rectum and vaginal wall weaken, causing the rectum to bulge into the posterior vaginal wall.Pathophysiology : Similar to cystocele, rectocele is caused by weakened pelvic floor muscles and connective tissues. As these structures weaken, the rectum can herniate into the posterior vaginal wall, leading to a rectocele., Epidemiology : 23%, variable, Complications : nan, Diagnostics : CYTOLOGY, URODYNAMIC TESTING, PHYSICAL EXAMINATION, Differential diagnosis : nan, disease description : The organs in our body are usually held firmly in place by connective tissue and muscles. For various reasons, though, the connective tissue in women’s pelvic floor may become weaker. As a result, one or more of the pelvic organs – including the womb (uterus), bladder and the last part of the bowel (rectum) – may slip down. This is called pelvic organ prolapse (also known as vaginal prolapse or genital prolapse). If the womb slips down, it is called uterine prolapse. Sometimes these organs slip down so far that the vagina or womb bulges out of the vaginal opening.The most common type of pelvic organ prolapse is bladder prolapse (also called cystocele) : Here, the bladder pushes down and against the wall of the vagina. But because the organs are connected to each other, they often drop down together. The treatment options for prolapses include pelvic floor exercises, vaginal pessaries and surgery.

Secondary Adrenal Insufficiancy

Disease Name : Secondary Adrenal Insufficiancy, Symptoms : anorexia, Malaise, decreased appetite, muscle weakness, vomiting, weight loss, Signs : abnormal facies, nystagmus, Orthostatic hypotension : A gradual decrease of cortisol levels often goes unnoticed which includes low blood pressure when standing or getting up., Hypotension, Treatment : medication : Hydrocortisone , Glucocorticoid replacement (one of the given regimens) : ,,Hydrocortisone 15 to 25 mg orally in two or three divided doses (the largest dose is taken early in the morning; typically 10 mg upon awakening in the morning, 5 mg early afternoon, 2.5 mg late afternoon), or,Prednisone 5 mg (2.5 to 7.5 mg) orally at bedtime, Pathophysiology : Hypothalamic Dysfunction : The process starts in the hypothalamus, a region of the brain that plays a crucial role in regulating hormone secretion. In secondary adrenal insufficiency, dysfunction in the hypothalamus can lead to a reduced secretion of corticotropin-releasing hormone (CRH), which is responsible for stimulating the release of adrenocorticotropic hormone (ACTH).Pituitary Dysfunction : With decreased CRH stimulation from the hypothalamus, the pituitary gland fails to secrete adequate levels of ACTH. ACTH is the hormone responsible for signaling the adrenal glands to produce cortisol.Adrenal Gland Response : In response to the reduced ACTH stimulation, the adrenal glands do not receive the appropriate signal to produce cortisol. Consequently, cortisol production is insufficient.Cortisol Deficiency : As a result of the reduced cortisol production, the body experiences a deficiency of this critical hormone. Cortisol plays a vital role in various physiological processes, including regulating metabolism, immune response, blood pressure, and stress response., Epidemiology : The prevalence of secondary adrenal deficiency is estimated to be between 150-280/million., variable, Prevention is centred around patient education. All patients should be educated on stress dosing and parenteral glucocorticoid administration. They should carry a steroid dependency alert card and wear a medical alert bracelet or similar identification., Complications : addisonian crisis, death, Hypoglycaemia, ABDOMEN PAIN, Diagnostics : ACTH, SERUM CORTISOL LEVEL, PLASMA ACTH LEVEL, CT SCAN, Differential diagnosis : Adrenal crisis, Congenital adrenal hyperplasia (CAH), eosinophilia, Histoplasmosis, hyperkalemia, Sarcoidosis, TUBERCULOSIS, disease description : Secondary adrenal insufficiency results from a decreased level of adrenocorticotrophin hormone (ACTH) released from the pituitary gland .The adrenal gland is made up of two parts, the cortex and the medulla. The adrenal cortex produces hormones necessary for normal body functioning; deficiency of these hormones results in adrenal insufficiency. The cortex is responsible for producing glucocorticoids, mineralocorticoids, and androgens. Destruction or dysfunction of the adrenal cortex mainly causes glucocorticoid and mineralocorticoid deficiency. Primary adrenal insufficiency is also known as autoimmune adrenalitis or Addison disease. Adrenal insufficiency ranges from mild nonspecific symptoms to life-threatening shock conditions. 

Secondary Amenorrhoea

Disease Name : Secondary Amenorrhoea, Symptoms : nipple discharge : Nipples may discharge in secondary amenorrhea., menstrual disturbances : The primary symptom of secondary amenorrhea is missing several menstrual periods in a row., vaginal dryness : secondary amenorrhoea causes vaginal dryness further leading to itching & irritation., Acne : It can present with mild acne., Hirsutism : Affected individuals experience excess hair growth across the body., Signs : nan, Treatment : medication : Oestradiol/Oestrogen, Medroxy Progesterone Acetate , Progesterone , Is the patient pregnant?, Is her serum prolactin level elevated? , Is there clinical evidence of oestrogen deficiency?, Does she have a positive response to the progesterone,challenge test?, Is it premature menopause?, What are the levels of her serum FSH and LH?, Pathophysiology : Hormonal Imbalances : Hormonal imbalances are a common cause of secondary amenorrhea. Disruptions in the delicate interplay between various hormones involved in the menstrual cycle can lead to anovulation (lack of ovulation) and subsequent absence of menstrual periods.a. Hypothalamic-Pituitary Dysfunction : Dysfunction in the hypothalamus or pituitary gland can lead to reduced secretion of gonadotropin-releasing hormone (GnRH) and gonadotropins (follicle-stimulating hormone, FSH, and luteinizing hormone, LH). The decrease in these hormones can result in inadequate stimulation of the ovaries, leading to anovulation and secondary amenorrhea. Causes of hypothalamic-pituitary dysfunction may include stress, excessive exercise, low body weight (e.g., in eating disorders), or tumors affecting these brain structures.b. Ovarian Dysfunction : The ovaries may not produce sufficient amounts of estrogen and progesterone due to ovarian failure or dysfunction. This can occur as a result of premature ovarian insufficiency (POI), polycystic ovary syndrome (PCOS), or ovarian surgery, among other causes.Structural Abnormalities : Anatomic abnormalities in the reproductive tract can also lead to secondary amenorrhea.a. Uterine Abnormalities : Conditions like Ashermans syndrome (intrauterine adhesions) or congenital malformations of the uterus can interfere with the normal menstrual flow and cause amenorrhea.b. Cervical Stenosis : Narrowing of the cervical canal can obstruct the passage of menstrual blood, leading to secondary amenorrhea.Systemic Conditions : Certain systemic disorders and chronic illnesses can disrupt the hormonal balance and lead to secondary amenorrhea.a. Thyroid Dysfunction : Thyroid disorders, such as hypothyroidism or hyperthyroidism, can affect the menstrual cycle through alterations in hormone levels.b. Pituitary or Hypothalamic Tumors : Tumors in the pituitary gland or hypothalamus can disrupt the normal production and secretion of hormones, including GnRH and gonadotropins, leading to amenorrhea.c. Chronic Illnesses : Chronic diseases like diabetes, inflammatory conditions, and autoimmune disorders can impact the hormonal regulation of the menstrual cycle., Epidemiology : 1.5–3% of the female population during reproductive years., 2-3% OF WOMEN, GOOD, Maintaining good overall health can help prevent some causes of secondary amenorrhea. Try to : ,,Follow a diet and exercise plan that’s healthy for you.,Be aware of your menstrual cycle (so you’ll know if you miss a period).,Get regular gynecological appointments, including having a pelvic exam and Pap test.,Get regular and adequate sleep., Complications : Cardiovascular Disease, Increased risk of fracture, Osteoporosis, pelvic pain, Diagnostics : PROLACTIN, GONADOTROPIN LEVEL, MRI, Serum LH Level Test, Serum FSH Level Test, USG, THYROID PROFILE, URINE PREGNANCY TEST, Differential diagnosis : anorexia, anxiety disorders, DEPRESSION, Prolactinoma, disease description : Secondary amenorrhoea is defined as amenorrhoea of 6 months or more in a woman with previous normal menstrual patterns in the absence of pregnancy and lactation (2–3% women).The most important cause of secondary amenorrhea is pregnancy, so it should be ruled out first. They should then ask about previous surgeries for Asherman syndrome.History of night sweats, sleep disturbance, and hot flushes for premature ovarian failure, history of chemotherapy, and radiation therapy for neoplasm should be obtained because these can also cause ovarian failure in young females. Polycystic ovary syndrome (PCOS) should be ruled out in accordance with the Rotterdam criteria.Vision test and sense of smell should be performed for pituitary adenoma and Kallman syndrome. A history of medication is very important because antipsychotics are one of the most common causes of high prolactin levels, which lead to amenorrhea. The use of contraception, cocaine,  opioids, antiepileptics can cause the failure of menstruation to occur, dieting,  strenuous exercise, history of weight loss, and anorexia nervosa can be determined by proper history taking to ascertain the cause of amenorrhea.

Secondary Hyperparathyroidism

Disease Name : Secondary Hyperparathyroidism, Symptoms : loss of appetite : Some patients experience nausea, vomiting, and constipation, which may all cause a decreased appetite., Osteoporosis : If the parathyroid glands are producing too much parathyroid hormone then calcium will be released from bone stores. This has been shown to increase the risk of osteoporosis and broken bones by increasing the rate of bone turnover (the cycle of breakdown and renewal of bone)., polyuria : Hyperparathyroidism and polyuria can cause fatigue, excessive thirst, muscle weakness, belly pain, difficulty concentrating, and constipation., "kidney stone : Blood levels of calcium become too high, which leads to complications, including the kidney stones youve been having. Calcium kidney stones are the most likely to form.", joint pain : If the parathyroid This process is known as “bone turnover.” If you have secondary hyperparathyroidism, bone turnover is high. This means that the cells that remove bone are working more quickly than the cells that build new bone, causing your bones to become weak and brittle.are producing too much parathyroid hormone then calcium will be released from bone stores. This has been shown to increase the risk of osteoporosis and broken bones by increasing the rate of bone turnover (the cycle of breakdown and renewal of bone)., Abdominal Pain : SHPT causes abdominal pain., Signs : nan, Treatment : Standard management includes replacement of calcium and vitamin D and the reduction of phosphate levels by the use of phosphate binders. Treatment of this disease changed radically with the introduction,of calcimimetic drugs, such as cinacalcet. Calcimimetics,alter the set point of the CaR, thereby reducing the,constant stimulation of the parathyroid glands and lowering the PTH level, 1-subtotal parathyroidectomy, a total parathyroidectomy with autograft or a total parathyroidectomy without autograft.,2- Renal transplantation remains the only definite treatment for secondary hyperparathyroidism-, Pathophysiology : Hypocalcemia is the most important stimulus for increased secretion of PTH from parathyroid glands in SHPT. The increased stimulation also results in parathyroid hyperplasia. Increased PTH level results in increased calcium and phosphate absorption from the gut. PTH acts as a stimulus for increased osteoclast activity, which results in calcium and phosphorus resorption from the bone. PTH activates vitamin D in the kidneys to its active form. Vitamin D increases calcium and phosphorus absorption from the gut and calcium and phosphorus reabsorption in renal tubules,  vitamin D suppresses PTH secretion from parathyroid glands and regulates the calcium and phosphorus levels  .Fibroblast growth factor 23 (FGF-23) is secreted by osteocytes and plays an important role in phosphorus homeostasis by increasing phosphorus clearance in the renal tubules., Epidemiology : between 20% and 80%, about 100, 000 people in the United States develop primary hyperparathyroidism each yea, poor, prevention is therefore important and can be achieved initially by a combination of diet and calcium-containing phosphate binders, with later addition of calcitriol or alfacalcidol if parathyroid hormone control cannot be achieved or sustained., Complications : sepsis, Calciphylaxis, Diagnostics : Parathyroid Hormone (PTH), serum calcium Ca++, CT SCAN, USG, serum phosphate, Casanova test, vitamin d, Differential diagnosis : Hypoparathyroidism, PARATHYROID CARCINOMA, PERSISTENT HYPERPARATHYROIDISM, PRIMARY HYPERPARATHYROIDISM, RECURRENT HYPOPARATHYROIDISM, SECONDARY HYPERPARATHYROIDISM, disease description : Parathyroid hormone (PTH) is secreted by parathyroid glands and plays a role in calcium and skeletal metabolism. Important triggers for PTH secretion are hypocalcemia and hyperphosphatemia,  Secondary hyperparathyroidism (SHPT) is an increased secretion of PTH due to parathyroid hyperplasia caused by triggers such as hypocalcemia, hyperphosphatemia, or decreased active vitamin D. The increased PTH secretion, in turn, causes increased calcium in the blood by acting on bones, intestines, and kidneys.

Secondary Infertility

Disease Name : Secondary Infertility, Symptoms : unable to concieve : The main sign of secondary infertility is being unable to get pregnant after having one or more biological children., Signs : nan, Treatment : medication : Clomiphene citrate , Pathophysiology : Age-related Decline in Fertility : As a woman gets older, her fertility naturally declines due to a decrease in the number and quality of her eggs. This decline in fertility becomes more significant after the age of 35. While a couple may have successfully conceived in the past, advancing maternal age can lead to decreased ovarian reserve and reduced chances of conceiving again.Hormonal Imbalances : Hormonal imbalances in either the male or female partner can affect the ovulation process, sperm production, or the environment in the uterus. Conditions such as polycystic ovary syndrome (PCOS), thyroid disorders, or disorders of the hypothalamic-pituitary-gonadal axis can disrupt hormonal regulation and lead to fertility issues.Structural Abnormalities : Anatomic abnormalities in the reproductive tract of either partner can impede natural conception. For instance, in women, conditions such as uterine fibroids, endometrial polyps, or blocked fallopian tubes can hinder the transport of eggs or sperm. In men, structural issues with the testes or the vas deferens can affect sperm production or delivery.Ovulation Disorders : Women may experience irregular or absent ovulation, leading to infrequent or absent menstrual cycles. Conditions like PCOS, hypothalamic dysfunction, or premature ovarian insufficiency (POI) can result in ovulatory issues and contribute to infertility.Sperm Quality and Quantity : Male factors play a significant role in fertility. Problems with sperm count, motility, or morphology can reduce the likelihood of successful fertilization.Unidentified or Recurrent Infections : Infections in the reproductive tract can impair fertility. Untreated sexually transmitted infections (STIs) or chronic infections can lead to inflammation and damage to the reproductive organs, affecting conception.Lifestyle and Environmental Factors : Lifestyle choices such as smoking, excessive alcohol consumption, drug use, stress, and exposure to environmental toxins can impact fertility in both men and women., Epidemiology : (5.8%), about 12% of women trying for another child have trouble conceiving., variable, Complications : nan, Diagnostics : HISTORY TAKING, Differential diagnosis : nan, disease description : Secondary infertility is when you’re unable to get pregnant or carry a pregnancy to term after previously giving birth. To classify as secondary infertility, the previous birth must have occurred without help from fertility medications or treatments, like in vitro fertilization (IVF)Secondary infertility is just as common as primary infertility. It affects about 11% of couples in the United States.

Secondary Osteomyelitis

Disease Name : Secondary Osteomyelitis, Symptoms : fever, localized pain, localized swelling, LOCALIZED TENDERNESS, Signs : nan, Treatment : adequate initial treatment of,open fractures, and adherence to sterile operating,conditions for routine orthopaedic operations., Pathophysiology : Bone can get infected via the hematogenous route of infection through bacteremic seeding of bone from a distant source of infection, contiguous spread from surrounding tissue and joints, or direct inoculation of bone from trauma or surgery. Hematogenous osteomyelitis occurs more frequently in children compared to adults, and long bones are usually affected,  In adults, hematogenous osteomyelitis affects the vertebrae most commonly. Contiguous osteomyelitis in young adults usually occurs in the setting of trauma and related surgery, while in older adults, infection is typically related to decubitus ulcers and infected joint arthroplasties . Osteomyelitis associated with vascular insufficiency frequently occurs in the presence of underlying diabetes mellitus., Epidemiology : he incidence was higher in men for unknown reasons but increases with age, mainly due to an increase in the prevalence of comorbid factors such as diabetes mellitus and peripheral vascular disease, studies show an overall incidence of osteomyelitis of 21.8 cases per 100, 000 person-years, not specific, Reducing your risk of infection will also help your risk of developing osteomyelitis.,,In general, take precautions to avoid cuts, scrapes and animal scratches or bites, which give germs easy access to your body. If you or your child has a minor injury, clean the area immediately and apply a clean bandage., Complications : abscess, squamous cell carcinoma in situ, amyloidosis, Septic arthritis, Diagnostics : Erythrocyte Sedimentation Rate (ESR), HISTOPATHLOGY, PUS CULTURE, Total Leucocyte Count (TLC), biopsy, MRI, CT SCAN, USG, Differential diagnosis : BURSITIS, Gout, sickle cell anemia, disease description : Bone infection is called osteomyelitis. It is an acute or chronic inflammatory process involving the bone and its structures secondary to infection with pyogenic organisms, including bacteria, fungi, and mycobacteria. Interestingly, archeological finds showed animal fossils with evidence of bone infection, making this a relatively old disease. Osteomyelitis is a serious infection of the bone that can be either acute or chronic. It is an inflammatory process involving the bone and its structures caused by pyogenic organisms that spread through the bloodstream, fractures, or surgery

Seizure Disorders

Disease Name : Seizure Disorders, Symptoms : Confusion : Complex focal seizures can make a person with epilepsy confused or dazed. The person will be unable to respond to questions or direction for up to a few minutes. Secondary generalized seizures begin in one part of the brain, but then spread to both sides of the brain., seizures : Focal seizures affect a smaller area of your brain and stay in one hemisphere. These are also known as partial seizures, and auras — when they happen — come before these. Symptoms such as uncontrolled muscle movements may spread to different places on one side of your body, such as from one side of your face to the hand or foot on the same side. Focal seizures include the following subtypes : Simple focal seizures. Sometimes known as simple partial seizures, you’re aware of these when they happen. With this kind of seizure, the aura is the seizure itself and not just a warning sign. Complex focal seizures. These are sometimes known as complex partial seizures. These disrupt your awareness of what’s happening to or around you., jerking movements of the arms and legs : Myoclonic seizures usually appear as sudden brief jerks or twitches of the arms and legs. There is often no loss of consciousness., Signs : brisk tendon jerks : In a patient with spasticity, brisk tendon jerks sometimes accompanied by clonus and velocity dependent muscle hypertonia to stretch preferentially affecting certain muscle groups, are the effects of a combination of hyperexcitability of an afferent pathway to motor neurons and disturbed processing of other peripheral afferent pathways at the spinal cord level., Dystonia : Paroxysmal dystonia s a type of fluctuating dystonia characterized by repetitive and patterned twisting movements and abnormal postures lasting seconds to hours., extensor plantar response : Extensor plantar response occurs (Babinski sign) bilaterally, usually in the 5min subsequent to the seizure. The presence of urinary incontinence is frequent in GCTCS. Occasionally, there is a tongue injury, more often than not in the lateral regions., Treatment : medication : Oxcarbazepine , Phenobarbital/Phenobarbitone, Phenytoin , Valproic acid(sodium valproate)/ Divalproex Sodium, Ethosuximide , Lamotrigine , Carbamazepine, Diazepam , Clobazam, anti - epileptic medications, resective surgery- temporal lobectomy, cortical excision, hemispherectomy, corpus callosotomy, multiple subpial transection, vagus nerve stimulation, Pathophysiology : Everyone has some propensity to have seizures. The concept of a seizure threshold means that each individual exists on a seizure susceptibility continuum with many factors influencing that susceptibility. Medications, genetic factors, electrolyte abnormalities, sleep state, infections, brain inflammation, or injury from many causes may lead to an individual crossing that threshold with a resulting seizure. On a cellular level, seizures start with the excitation of susceptible cerebral neurons, which leads to synchronous discharges of progressively larger groups of connected neurons. Neurotransmitters are undoubtedly involved. Glutamate is the most common excitatory neurotransmitter, and gamma-aminobutyric acid (GABA) is an important inhibitory neurotransmitter. An imbalance of excess excitation and decreased inhibition initiates the abnormal electrical activity, , Epidemiology : between 4 and 10 per 1000 people., 5.59-10 per 1000., good if treated as required, Use safety belts, child passenger seats, airbags, bicycle helmets, and motorcycle helmets to reduce motor vehicle and traffic injuries.,,Step carefully. Falls are the leading cause of brain injury. Older adults and children have an increased chance of brain injuries from falls., Complications : cerebral palsy, death, mood disorders, Diagnostics : random blood sugar RBS, EEG, PET SCAN, lumbar puncture, MRI, NEUROLOGICAL EXAMINATION, Differential diagnosis : Convulsive concussion, convulsive syncope, movement disorders, disease description : A seizure is a sudden, uncontrolled electrical disturbance in the brain. It can cause changes in your behavior, movements or feelings, and in levels of consciousness. Having two or more seizures at least 24 hours apart that arent brought on by an identifiable cause is generally considered to be epilepsy.

Seizures In Newborn

Disease Name : Seizures In Newborn, Symptoms : seizures : Clonic seizures, which are rhythmic jerking movements that may involve the muscles of the face, tongue, arms, legs, or other regions. Tonic seizures, which are stiffening or tightening or muscle groups; the head or eyes may turn to one side, or the baby may bend or stretch one or more arms or legs. Myoclonic seizures, which are quick, single jerks involving one arm or leg or the whole body., ABNORMAL BODY MOVEMENTS : Myoclonic seizures are rapid, single or arrhythmic repetitive jerks. They may affect a finger, a limb or the whole body. They may mimic the Moro reflex and startling responses. They are more frequent in pre-term than full-term infants indicating, if massive, major brain injury and poor prognosis., Facial abnormalities : Repetitive facial movements, including sucking, chewing, or eye movements., poor feeding : The inability to take full oral feeds upon hospital discharge is an objective clinical sign that can identify infants with acute symptomatic neonatal seizures who are at high risk for impaired development at 24 months., Apnea : As a manifestation of a seizure, apnea is rare and most often is associated with other signs (change in heart rate, blood pressure, pupillary dilatation) that raise clinical suspicion., Signs : nan, Treatment : medication : Magnesium/Magnesium Sulphate, Phenobarbital/Phenobarbitone, Mannitol , Glucose/Dextrose, ntravenous administration of phenobarbitone 20 mg/kg body weight slowly over a ,period of 20 minutes is effective. A maintenance dose of 3–4 mg/kg body weight per day administered orally or IV ,for at least a period of 2 weeks or even longer. In resistant cases IV phenytoin (Dilantin), 15–20 mg/kg at the rate of ,1 mg/kg/min is administered. Maintenance dose of 3–4 mg/kg/day is divided 12 hourly. Fosphenytoin is preferred., Pathophysiology : The basic mechanism is excessive depolarization (excitation) of neurons within the CNS. Three possible reasons for excessive depolarization are proposed : (A) Failure of sodium-potassium pump operation; (B) Relative excess of excitatory neurotransmitter compared to the inhibitory ones. (C) Relative deficiency of inhibitory neurotransmitters. The neurons within the CNS undergo depolarization due to inward migration of sodium and repolarization due to efflux of potassium., Epidemiology : 2 in 1, 000 to 14 in 1, 000 live births., GOOD, To Do : ANTENATAL ASSESSMENT, Complications : nan, Diagnostics : ABG, Complete Blood Count CBC, URINE CULTURE, EEG, serum igG igM, TORCH Screening, kidney function test KFT, CSF CULTURE, BLOOD CULTURE, MRI, CT SCAN, USG, Differential diagnosis : benign neonatal sleep myoclonus, hyperekplexia, disease description : A seizure is a paroxysmal manifestation of neurological dysfunction (i.e. behaviors, motor or autonomic function). Overall incidence ranges from 2 in 1, 000 to 14 in 1, 000 live births. Pathophysiology : The basic mechanism is excessive depolarization (excitation) of neurons within the CNS. Three possible reasons for excessive depolarization are proposed : (A) Failure of sodium-potassium pump operation; (B) Relative excess of excitatory neurotransmitter compared to the inhibitory ones. (C) Relative deficiency of inhibitory neurotransmitters. The neurons within the CNS undergo depolarization due to inward migration of sodium and repolarization due to efflux of potassium.

Selective Iga Deficiency

Disease Name : Selective Iga Deficiency, Symptoms : GI disturbances : Various GI tract infections with viruses, bacteria, and G lamblia parasites manifest as chronic diarrhea with or without malabsorption. Biopsy specimens may show nodular lymphoid hyperplasia with flattened villi., Infections occur predominantly in the respiratory : Recurrent sinopulmonary infection is the most common illness associated with IgAD. Most upper and lower respiratory tract infections are caused by bacterial or viral pathogens characteristic of community-acquired pneumonia. Patients with concomitant IgG type 2 subclass deficiency may have a higher risk for recurrent infections from S pneumoniae, H influenzae, M catarrhalis, or Staphylococcus aureus., allergies : Food allergy and other atopic disorders, such as allergic conjunctivitis, rhinitis, urticaria, atopic dermatitis, and asthma, are common in patients with IgAD., Signs : nan, Treatment : medication : Human normal immunoglobulin , In IgA deficiency, the mainstay of treatment is the treatment of associated diseases. If the patient experiences recurrent infections, daily prophylactic antibiotics on a continuous or seasonal intermittent basis may be beneficial. In case of associated IgG subclass deficiency and/or specific antibody deficiency, immunoglobulin treatment via venous or subcutaneous route with a product that contains minimal IgA may be given. Standard treatment approach is entertained in case of an associated allergic disorder or autoimmune condition, Pathophysiology : In IgA deficiency, a maturation defect in B cells to produce IgA is commonly observed. Alterations in transmembrane activator and calcium modulator and cyclophilin ligand interactor gene appear to act as disease-modifying mutations in both IgA deficiency and common variable immunodeficiency, two diseases which probably lie in the same spectrum. Certain major histocompatibility complex haplotypes have been associated with susceptibility to IgA deficiency., Epidemiology : 1 : 2, 600 to 1 : 5, 300 in China, variable, IgA deficiency is a problem that may be passed down through your family, so you can’t do anything to prevent it. But you can limit the spread of germs and sickness by washing your hands often and staying away from large crowds. This is especially true during cold and flu season, Complications : BRONCHIECTASIS, PNEUMONIA, Diagnostics : PULMONARY FUNCTION TEST(PFT), SERUM IMMUNOGLOBULINS, Differential diagnosis : CHRONIC LYMPHOID LEUKEMIA (CLL), Common variable immunodeficiency disease (CVID), MYELOMA, disease description : Immunoglobulin A (IgA) deficiency is the most common primary immunodeficiency defined as decreased serum level of IgA in the presence of normal levels of other immunoglobulin isotypes. Most individuals with IgA deficiency are asymptomatic and identified coincidentally. However, some patients may present with recurrent infections of the respiratory and gastrointestinal tracts, allergic disorders, and autoimmune manifestations.

Selenium Deficiency

Disease Name : Selenium Deficiency, Symptoms : muscle pain, weakness, Signs : Arrhythmias, cardiomegaly, hypopigmentation of the hair and skin, Terry nails-like white nail beds, Treatment : For children less than 3 years of age, the recommended daily intake of selenium is 15–20 µg/day. Children 3–13 years of age require 20–40 µg/day. The recommended intake for adolescents and adults is 55 µg/day, but women who are pregnant or breastfeeding should increase to 60 and 70 µg/day, respectively. Parenteral selenium supplementation of 5–7 µg/kg/day can be used ,for acute correction of selenium deficiency., Pathophysiology : Keshan disease is congestive cardiomyopathy associated with heart failure, cardiac enlargement, electrocardiogram (ECG) abnormalities, gallop rhythm, and even cardiogenic shock. This is seen typically in children and women of child-bearing age.Of the 35 selenoproteins that have been identified so far, 3 of them are called Iodothyronine deiodinases, and they play a role in thyroid hormone metabolism. The thyroid contains the maximum concentration of selenium of all the organs in our bodiesGlutathione peroxidase (G-Px) is a selenium-dependent enzyme that protects cell membranes and lipid-containing organelles from peroxidative damage by inhibition and destruction. It acts in combination with vitamin E to maintain the integrity of the cell membranes, participating in redox reactions with hydrogen peroxide-producing glutathione., Epidemiology : GOOD, 1)consuming a lot of selenium-rich foods,2)testing the soil in food growing and harvesting sites to determine the concentration of selenium,3) eating a well-balanced diet and, if necessary, working with a doctor or dietitian to create a custom diet., Complications : cardiac dysfunction, Cardiomyopathy, Diagnostics : CT SCAN, SELENIUM, glutathione peroxidase activity, Differential diagnosis : Hepatic cirrhosis, KWASHIORKER, disease description : Selenium deficiency, also known as Keshan disease, is caused by inadequate intake, defective absorption or increased losses. In particular, glutathione peroxidase (G-Px), a selenoprotein, performs antioxidant activities that protect against reactive oxygen and nitrogen species. Iodothyronine deiodinases that convert inactive thyroxine (T4) to active thyroid hormone, triiodothyronine (T3), are selenium-dependen t.Selenium plays a role in the immune system functioning and the progression of HIV to AIDS.

Semicircular Lipoatrophy

Disease Name : Semicircular Lipoatrophy, Symptoms : Burning sensation of the skin, heavy legs, cramps or pain after exercising, Signs : band-like depressions, usually on the anterolateral thigh or thighs, Treatment : When a cause is identified and remedial action taken, spontaneous ,resolution generally occurs , in most cases after 9 months to 4 ,years, Pathophysiology : Presence of SL to impaired circulation in the upper leg as a consequence of a congenital abnormality in the lateral femoral circumflex artery. However, patients with arteritis or those whose quadriceps artery has been ligated do not develop SL., Epidemiology : 10-40%, excellent, Avoid wearing tight clothes when sitting for long periods of time.,Avoid wearing synthetic clothes.,In the case of upper limbs avoid compressive underwear or tucking up skirts.,Avoid wearing rubber soles on shoes and avoid shuffling., Complications : Polycystic Ovarian Syndrome, splenomegaly hepatomegaly, Diagnostics : MRI, Differential diagnosis : Acromegaly, Cushings syndrome, Panniculitis, disease description : Semicircular lipoatrophy is caused by mechanical injury to the subcutaneous fat inducing band-like depressions in the skin. It should be noted that mechanical injury to the subcutaneous fat, especially on the lower legs, can be a primary cause of fat injury . It is often followed by atrophic changes. Since the initial report , relatively few cases of semicircular lipoatrophy have been reported, but it is asymptomatic so may be underreported; several authors have commented that it may well not be rare It mainly occurs in women, aged between 20 and 40 years.

Seminoma

Disease Name : Seminoma, Symptoms : back pain : Lower back pain occurs if the tumor has spread to nearby lymph nodes., breast tenderness : It is due to the secretion of the hormone estrogen by the tumor., Testicular pain : Testicular pain, possibly with an acute onset, especially when an associated hydrocele prevents adequate physical examination., testicular tumor : A testis tumor may become metastatic and may manifest as large retroperitoneal and/or chest lesions, while the primary tumor is nonpalpable. Scrotal ultrasonography may locate the primary tumor., Signs : nan, Treatment : medication : Cisplatin , Etoposide, Bleomycin , Scrotal exploration and orchidectomy for,suspected testicular tumour., Pathophysiology : Testicular seminoma is a germ cell neoplasm originating from the seminiferous tubules, due to malignant transformation of primordial germ cells. The exact molecular derangements underlying this transformation are not clearly understood, but the most common genetic finding is the gain of genetic material from chromosome 12p. Some of the mutations noticed in germ cell tumors include BRAF, KIT, KRAS, NRAS, and TP53, although single-gene mutations are relatively uncommon,  Seminomas can be subdivided into one of three categories based on histology : classic, anaplastic, and spermatocytic. In testicular seminoma, alpha-fetoprotein (AFP) is in the normal range. If AFP is elevated and the presence of no seminomatous elements in histopathological specimens makes the diagnosis of non seminotaous germ cell tumor., Epidemiology : it accounts for less than 1% of all male tumors., The incidence of testicular tumors is rising from the past 20 years., POOR, Do the exam after a warm shower or bath. The warmth relaxes the skin of the scrotum, making it easier to feel for anything unusual.,Use both hands to examine each testicle. Place your index and middle fingers underneath the testicle and your thumbs on top. Roll the testicle between your thumbs and fingers, Complications : METASTASES AT DIFFERENT SITES, Diagnostics : HISTOPATHLOGY, HCG, PET SCAN, ultrasound, CT SCAN, Differential diagnosis : Epidermoid cyst, epididymitis, HYDROCELE, lymphoma, metastatic carcinoma, disease description : ?Testicular neoplasm is one of the most common causes of testicular mass. It occurs in approximately 5 per 100, 000 men, mainly in the age group of 15-34 years. Seminoma is a malignant germ cell tumor that involves most commonly the testicle or less frequently the mediastinum, the retroperitoneum, or other extra-gonadal sites. It is one of the treatable and curable cancers, with a survival rate of over 95% if discovered in early stages

Sengers Syndrome

Disease Name : Sengers Syndrome, Symptoms : cataract : Cataracts often develop shortly after birth or at the time of birth. It may be necessary to have early surgery if they are dense enough to impair vision., HYPERTROPHIC CARDIOMYOPATHY : A thickened heart muscle impairs its pumping ability., "Lactic acidosis : It is often seen following exercise that you develop lactic acidosis. Lactic acidosis is a buildup of lactic acid in your bloodstream. It happens when your body produces too much lactic acid and/or cant metabolize enough of the lactic acid it produces. Your liver and kidneys normally clear excess lactic acid from your body.", muscle weakness : The generalized muscle weakness can cause motor development to be delayed, despite normal intelligence., hypotonia : Hypotonia is the medical term for low muscle tone that doctors usually diagnose in infants. People sometimes call it floppy muscle syndrome. Usually, even when muscles relax, they have some contraction that provides some resistance to passive movement., Signs : nan, Treatment : Antenatal diagnosis : ,Prenatal genetic testing may be possible for families with affected children., Genetic counseling : nan,The reported mutations are transmitted in an autosomal recessive manner., Prenatal genetic testing may be possible for families with affected childr, Patients may require palliative care and a wheelchair for locomotion, medical management of cardiomyopathy with standard therapy., cataract surgery during infancy, Pathophysiology : This disease is caused by mutations in AGK or SLC25A4 genes. The AGK gene encodes the mitochondrial acylglycerol kinase which plays a role in the assembly of adenine nucleotide translocator. The SLC25A4 gene encodes the heart and muscle-specific isoform 1 of the mitochondrial adenine nucleotide translocator.In the majority of CCM patients mutations (nonsense, frame-shift, start codon or splice site) in the AGK gene have been identified. The AGK gene encodes the mitochondrial acylglycerol kinase which plays a role in the assembly of adenine nucleotide translocator (ANT), an essential component of the oxidative phosphorylation in mitochondria. Two patients with distinct autosomal recessive SLC25A4 mutations have been reported (one of whom had cardiomyopathy but not cataract). The SLC25A4 gene encodes the heart and muscle specific isoform 1 of the mitochondrial ANT. The etiology remains genetically unsolved in the rest of cases of CCM. The milder affected individuals carried either splice site or start codon mutations., Epidemiology : Prevalence : <1 / 1 000 000, variable, "Sengers syndrome is an autosomal recessive mitochondrial disorder and therefore cant be prevented.", Complications : cardiac failure, Physical disability, Diagnostics : Muscle Biopsy, PLATELET COUNT, 2-D Echo, TONOMETRY TEST, biopsy, doppler echocardiography, GENETIC TESTING, GENETIC TESTING, SERUM LACTATE, Urine analysis, ophthalmoscopy, Differential diagnosis : Barth syndrome, mitochondrial encephalo-cardio-myopathy, disease description : Sengers syndrome is an autosomal recessive mitochondrial disorder characterized by congenital cataracts, hypertrophic cardiomyopathy, skeletal myopathy, exercise intolerance, and lactic acidosis. Mental development is normal, but affected individuals may die early from cardiomyopathy. Skeletal muscle biopsies of 2 affected individuals showed severe mtDNA depletion. Most common age of presentation is birth to 2 years.

Senile Vaginitis

Disease Name : Senile Vaginitis, Symptoms : urine leakage, Urinary Tract Infection, vaginal dryness, Vaginal irritation, Vaginal Discharge, DYSPAREUNIA, Signs : nan, Treatment : systemic estrogen therapy ,may be considered if there is no contraindication. This ,improves the vaginal epithelium, raises glycogen content, ,and lowers vaginal pH.,Intravaginal application of estrogen cream by an ,applicator is also effective. About one-third of the vaginal ,estrogen is systemically absorbed., Pathophysiology : Vaginal atrophy occurs in conditions causing a diminished estrogen state. Estrogen typically stimulates exfoliation of vaginal epithelial cells, causing increased levels of glycogen in which vaginal flora lactobacilli convert into lactic acid. This process allows for the replacement of older vaginal epithelium, keeping the typical acidic pH of the vaginal canal. As estrogen levels decrease, this process is hindered, and the vaginal epithelium becomes atrophic with diminished secretions and a less acidic environment (pH >5) This, in turn, increases the risk of vaginal and urinary tract infections., Epidemiology : The worldwide prevalence of trichomoniasis is 174 million;, 10 to 40 percent of postmenopausal women, fair, Regular sexual activity help prevent genitourinary syndrome of menopause. Sexual activity increases blood flow to your vagina, which helps keep vaginal tissues healthy., Complications : endometrial changes, DYSPAREUNIA, Diagnostics : Gram Staining, White Blood Cell count WBC, Bacteria CELL CULTURE, HISTORY TAKING, PHYSICAL EXAMINATION, Differential diagnosis : vaginal atrophy, vulvovaginal atrophy, vulvovaginal candidiasis, disease description : Vaginitis in postmenopausal women is called atrophic vaginitis. The term is preferable to senile vaginitis. There is atrophy of the vulvovaginal structures due to estrogen deficiency. The vaginal defence is lost. Vaginal mucosa is thin and is more susceptible to infection and trauma. There may be desquamation of the vaginal epithelium which may lead to formation of adhesions and bands between the walls.A hypoestrogenic state may be part of natural physiological menopause or induced (secondary to surgical, radiation, or chemotherapy treatments). Premenopausal women may develop a temporary hypoestrogenic state while lactating. Other conditions, such as exposure to medications, radiation therapy, chemotherapy, or hypothalamic dysfunction, may also result in a hypoestrogenic state. Medications that may induce a hypoestrogenic state include Selective estrogen receptor modulators, Selective estrogen receptor degrader, and antigonadotropins.

Sensorineural Hearing Loss

Disease Name : Sensorineural Hearing Loss, Symptoms : impaired hearing : People with mild, moderate, or severe sensorineural hearing loss can still hear, but they may have trouble understanding sounds or need them to be louder in order to hear well. Those with profound hearing loss may not be able to hear any sounds except those that are very loud., tinnitus : Sensorineural tinnitus is defined as hearing a sound that has no physical correlate; hence the sound of tinnitus is often described as being a phantom (ghost) sound. Severe sensorineural tinnitus is a phantom sensation of sound that is often accompanied by an effect that is best described as suffering., Signs : nan, Treatment : Noise induced hearing loss can be prevented from further deteriora\x02tion if the person is removed from the noisy surroundings, Syphilis of the inner ear is treatable with high doses of ,penicillin and steroids with improvement in hearing. Hear\x02ing loss of hypothyroidism can be reversed with replacement ,therapy. Serous labyrinthitis can be reversed by attention to ,middle ear infection. Early management of Ménière’s disease,can prevent further episodes of vertigo and hearing loss. ,SNHL due to perilymph fistula can be corrected surgically by ,sealing the fistula in the oval or round window with fat.,Ototoxic drugs should be used with care and discontinued if ,causing hearing loss. In many such cases, it may be possible to ,regain hearing, total or partial, if the drug is stopped., Pathophysiology : Congenital It is present at birth and is the result of anomalies of the inner ear or damage to the hearing apparatus by prenatal or perinatal factors. Acquired It appears later in life. The cause may be genetic or nongenetic. The genetic hearing loss may manifest late (delayed onset) and may affect only the hearing, or be a part of a larger syndrome affecting other systems of the body as well (syndromal). Common causes of acquired SNHL include : 1. Infections of labyrinth—viral, bacterial or spirochaetal 2. Trauma to labyrinth or VIIIth nerve, e.g. fractures of temporal bone or concussion of the labyrinth or the ear surgery 3. Noise-induced hearing loss 4. Ototoxic drugs 5. Presbycusis 6. Ménière’s disease 7. Acoustic neuroma 8. Sudden hearing loss 9. Familial progressive SNHL 10. Systemic disorders, e.g. diabetes, hypothyroidism, kidney disease, autoimmune disorders, multiple sclerosis, blood dyscrasias., Epidemiology : 27 per 100, 000 in the United States and 2.4 per 100 000 in western China, ..., between 5-27 per 100, 000 people each year, with approximately 66, 000 new annual cases., GOOD, Avoid or limit exposure to excessively loud sounds,Turn down the volume of music systems,Move away from the source of loud sounds when possible,Use hearing protection devices when it is not feasible to avoid exposure to loud sounds or reduce them to a safe level, Complications : Tinnitus reduced hearing, Diagnostics : Complete Blood Count CBC, Rinne test, CT HEAD, Audiogram, BLOOD GLUCOSE, PHYSICAL EXAMINATION, Tympanometry, WEBER TEST, Schwabach test, Differential diagnosis : Alport Syndrome, Cytomegalovirus (CMV) infection, Hypoxia, "menieres disease", neonatal jaundice, disease description : Sensorineural hearing loss (SNHL) results from lesions of the cochlea, VIIIth nerve or central auditory pathways. It may be present at birth (congenital) or start later in life (acquired).Sensorineural hearing loss results from damage to the hair cells within the inner ear, the vestibulocochlear nerve, or the brains central processing centers. This differs from a conductive hearing loss, which results from the inability of sound waves to reach the inner ear

Sepsis

Disease Name : Sepsis, Symptoms : Severe infections, abdominal distension : The abdomen is often distended, with hypoactive-to-absent bowel sounds. This finding reflects a generalized ileus and may not be present if the infection is well localized., bleeding : If someone with ACS gets sepsis, they have a higher risk of having a GI bleed., Confusion : Sepsis-associated encephalopathy (SAE) describes acute cognitive dysfunction secondary to systemic or peripheral infection occurring outside of the central nervous system (CNS). Symptoms can range from mild confusion to coma and may precede the clinical signs of sepsis., "diarrhea : The bacteria cause inflammation of the gut or colon – colitis. This can lead to moderate-to-severe diarrhea, and sometimes sepsis, which can develop as the body tries to fight the infection. Sepsis, which was often called blood poisoning, is the bodys life-threatening response to infection.", lethargy : Some people with sepsis will experience long-term physical and psychological problems. This is known as post-sepsis syndrome. Symptoms of post-sepsis syndrome include : feeling lethargic or excessively tired., seizures : Patients with sepsis-associated encephalopathy (SAE) can develop convulsive or nonconvulsive seizures. The cytokine storm and the overwhelming systemic inflammation trigger the electric circuits that promote seizures., skin rash : Some patients who have sepsis develop a rash on their skin. The rash may be a reddish discoloration or small dark red dots seen throughout the body. Those with sepsis may also develop pain in the joints of the wrists, elbows, back, hips, knees, and ankles., vomiting, fever : Fever of 38 C / 100.4 F or more. Hypothermia of 36 C / 96.8 F or less., Oliguria : The reduction in glomerular filtration rate secondary to hypotension related to hypovolemia and decreased cardiac output are the mechanisms considered to be responsible for oliguria., Signs : apnoea : Disruption of normal circadian rhythm at the molecular level affects the severity of inflammation in sepsis, contributing to inflammatory response and affecting the duration of obstructive sleep apnoeas and an increase in mortality from sepsis., Slow pulse : Tachycardia is common in septic shock, but many patients with septic shock are relatively bradycardic., hypotonia : Hypotonia in sepsis or due to other illnesses like CHF also improves once the disease is treated., Acute Renal Failure : The inflammatory response during sepsis causes an adaptive response of the tubular epithelial cells. These alterations induce a downregulation of the cell function in order to minimize energy demand and to ensure cell survival. The result is reduced kidney function., cyanosis : Blueish discoloration of the lips and/or digits., hypothermia : Hypothermia is associated with higher mortality and an increased risk of persistent lymphopenia in septic patients, and it may be an early clinical predictor of sepsis-induced immunosuppression., Hypotension : Sepsis-induced hypotension is defined as mean arterial blood pressure <65mmHg, whereas septic shock was defined as maintained sepsis-induced hypotension despite adequate fluid resuscitation, which needs inotropic or vasopressor agents to restore perfusion abnormalities., Treatment : medication : Ampicillin , Cloxacillin Sodium , Cefotaxime , Ciprofloxacin , Amikacin , proper antibiotic coverage, Pathophysiology : Sepsis progressing to septic shock and multi-organ failure results from a worsening circulatory insufficiency characterized by hypovolemia, myocardial depression, increased metabolic demands, and vasoregulatory perfusion abnormalities. Classically, septic shock and inflammatory shock have been described as primarily systemic vasodilatation of both arteries and veins. This dilation reduces ventricular preload as well as afterload, by decreasing systemic vascular resistance. The typical hemodynamic pattern in septic shock consists of low cardiac filling pressures, or low central venous pressures (CVP), and low systemic vascular resistance (SVR). With low preload and afterload, cardiac output (CO) must increase to compensate, typically with increased heart rate (CO = Stroke Volume x Heart Rate).  This is also why sepsis is thought of as a distributive shock and is also known as hyper-dynamic or warm shock., Epidemiology : more than half of the patients in intensive care units in India suffer from sepsis, at least 1.7 million adults in the U.S. develop sepsis, and nearly 270, 000 die as a result, GOOD, Prevent infections that can lead to sepsis by : Cleaning scrapes and wounds and practicing good hygiene by washing hands and bathing regularly.,Get vaccinated against flu, pneumonia, and any other potential infections, Complications : sepsis, Diagnostics : BLOOD CULTURE test, ABG, Complete Blood Count CBC, CRP, Erythrocyte Sedimentation Rate (ESR), Gram Staining, X RAY CHEST, CT SCAN, PLATELETCRIT(PCT), Differential diagnosis : Adrenal Insufficiency, BURNS, cardiogenic shock, Pancreatitis, THYROTOXICOSIS, disease description : Bacterial sepsis is a life-threatening condition that arises when the body’s response to an infection injures its tissues and organs. Sepsis has recently been re-defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. This disease entity has had many iterations since that time, with the foundations for the modern understanding of sepsis coming about through breakthroughs in the late 19 century.  The development of antiseptic measures, the germ theory of disease, and bacteriology lead to the widely held belief that sepsis was a systemic infection resulting from a pathogenic organism invading the host that spreads via the bloodstream (i.e., septicemia). It was not until the further widespread use of antibiotics and the discovery of endotoxin that suggested the pathophysiology of sepsis was far more complex.

Septal Abscess

Disease Name : Septal Abscess, Symptoms : Common Cold : Symptoms include fever, general malaise, headache, difficulty breathing., nasal obstruction : A bilateral persistent nasal obstruction may also be present., nasal pain : Nasal septal abscess causes nasal pain & discomfort., Signs : nan, Treatment : augmentation rhinoplasty 2–3 months later., ANTIBIOTIC COVER, INCISION & DRAINAGE, Pus and necrosed pieces ,of cartilage are removed by suction., Pathophysiology : Mostly, it results from secondary infection of septal haematoma. Occasionally, it follows furuncle of the nose or upper lip. It may also follow acute infection such as typhoid or measles. There is severe bilateral nasal obstruction with pain and tenderness over the bridge of nose. Patient may also complain of fever with chills and frontal headache. Skin over the nose may be red and swollen. Internal examination of nose reveals smooth bilateral swelling of the nasal septum. Fluctuation can be elicited in this swelling. Septal mucosa is often congested. Submandibular lymph nodes may also be enlarged and tender., Epidemiology : between 0.8 and 1.6%, good, do not dig the nose, Complications : CAVERNOUS SINUS THROMBOSIS, perforation, BACTERIAL MENINGITIS, Diagnostics : PUS CULTURE, CT SCAN, rhinoscopy, Differential diagnosis : lymphoma, PNEUMONIA, TUBERCULOSIS, Wegener granulomatosis, disease description : Mostly, it results from secondary infection of septal haematoma. Occasionally, it follows furuncle of the nose or upper lip. It may also follow acute infection such as typhoid or measles.Nasal septal abscess is defined as a collection of purulent material between the cartilaginous or bony septum and the mucoperichondrium or mucoperiosteum.1 Nasal septal abscesses occur more commonly after minor nasal trauma1 but may also result from iatrogenic causes and sinonasal or dental infection. After minor nasal trauma, a hematoma may form secondary to the rupture of small blood vessels in the nasal septum. The hematoma separates the mucoperichondrium from the septal cartilage and forms an ideal medium for the colonization and growth of bacteria, leading to the formation of an abscess.

Septal Hematoma

Disease Name : Septal Hematoma, Symptoms : nasal congestion : An untreated septal hematoma may lead to a hole in the area separating the nostrils, called a septal perforation. This can cause nasal congestion., dyspnea : Trouble breathing through your nose., Signs : nan, Treatment : medication : Ampicillin , Cloxacillin Sodium , Cefotaxime , Ciprofloxacin , Amikacin , proper antibiotic coverage, Pathophysiology : Sepsis progressing to septic shock and multi-organ failure results from a worsening circulatory insufficiency characterized by hypovolemia, myocardial depression, increased metabolic demands, and vasoregulatory perfusion abnormalities. Classically, septic shock and inflammatory shock have been described as primarily systemic vasodilatation of both arteries and veins. This dilation reduces ventricular preload as well as afterload, by decreasing systemic vascular resistance. The typical hemodynamic pattern in septic shock consists of low cardiac filling pressures, or low central venous pressures (CVP), and low systemic vascular resistance (SVR). With low preload and afterload, cardiac output (CO) must increase to compensate, typically with increased heart rate (CO = Stroke Volume x Heart Rate).  This is also why sepsis is thought of as a distributive shock and is also known as hyper-dynamic or warm shock., Epidemiology : 0.8% to 1.6%, GOOD, Prevent infections that can lead to sepsis by : Cleaning scrapes and wounds and practicing good hygiene by washing hands and bathing regularly.,Get vaccinated against flu, pneumonia, and any other potential infections, Complications : sepsis, Diagnostics : CT SCAN, Differential diagnosis : nasal polyps, Papilloma, Pyogenic granulomas, rhinitis, disease description : Bacterial sepsis is a life-threatening condition that arises when the body’s response to an infection injures its tissues and organs. Sepsis has recently been re-defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. This disease entity has had many iterations since that time, with the foundations for the modern understanding of sepsis coming about through breakthroughs in the late 19 century.  The development of antiseptic measures, the germ theory of disease, and bacteriology lead to the widely held belief that sepsis was a systemic infection resulting from a pathogenic organism invading the host that spreads via the bloodstream (i.e., septicemia). It was not until the further widespread use of antibiotics and the discovery of endotoxin that suggested the pathophysiology of sepsis was far more complex.

Septic Abortion

Disease Name : Septic Abortion, Symptoms : vaginal bleeding : Prolonged or heavy vaginal bleeding., Severe abdominal pain : Perforation of the uterus during the abortion typically causes severe abdominal pain., Vaginal Discharge : Foul or purulent cervical discharge., fever with chills : High fever, usually above 101 °F / 38 °C., Signs : hypothermia : Septic Abortion causes the body temperature to dip drastically., respiratory distress : The severe inflammatory responses induced by sepsis also increase vascular permeability, leading to acute pulmonary edema and resulting in acute respiratory distress syndrome (ARDS)., Oliguria : While systemic vasodilation in sepsis is predominant, macro- and microcirculatory alterations may diminish blood flow to certain regions of the kidney. This leads to the phenomenon, that despite an increase in renal blood flow (RBF), oliguria followed by AKI may rapidly develop., Hypotension : In women who have a septic abortion, blood pressure may become dangerously low, resulting in septic shock., Treatment : medication : Sulfamethoxazole and Trimethoprim (Co-trimoxazole), Piperacillin and tazobactum , Ampicillin , Gentamicin , Clindamycin , Metronidazole , GENERAL MANAGEMENT : ,Hospitalization is essential for all cases of septic abortion. The patient is kept in isolation., To take high vaginal or cervical swab for culture, drug sensitivity test and Gram stain.,? Vaginal examination is done to note the state of the abortion process and extension of the,infection.,? Overall assessment of the case and the patient is leveled in accordance with the clinical grading.,Investigation protocols, Pathophysiology : The microorganisms involved in the sepsis are usually those normally present in the vagina (endogenous). The microorganisms are : (a) Anaerobic—Bacteroides group (fragilis), anaerobic Streptococci, Clostridium welchii and tetanus bacillus. (b) Aerobic—Escherichia coli (E. coli), Klebsiella, Staphylococcus, Pseudomonas and group A beta-hemolytic Streptococcus (usually exogenous), methicillin-resistant Staphylococcus aureus (MRSA). Mixed infection is more common. The increased association of sepsis in unsafe induced abortion is due to the fact that : (1) proper antiseptic and asepsis are not taken, (2) incomplete evacuation and (3) inadvertent injury to the genital organs and adjacent structures, particularly the bowels. In the majority (80%), the organisms are of endogenous origin and the infection is localized to the conceptus without any myometrial involvement. In about 15%, the infection either produces localized endomyometritis surrounded by a protective leukocytic barrier, or spreads to the parametrium, tubes, ovaries or pelvic peritoneum. In about 5%, there is generalized peritonitis and/or endotoxic shock., Epidemiology : 10% of abortions, POOR, Primary prevention of septic abortion includes access to effective and acceptable contraception; access to safe, legal abortion in case of contraceptive failure; and appropriate medical management of abortion.,,,Avoiding unintended pregnancy,,Pregnancy places women at risk for illness and death., Complications : hyperbilirubinemia, Thrombocytopenia, Oliguria, MULTIORGAN FAILURE, Diagnostics : ultrasound, BLOOD CULTURE, CT SCAN, Electrocardiography (EKG), Differential diagnosis : appendicitis, ENDOMETRITIS, Incomplete Abortion, Influenza, Pyelonephritis, disease description : Any abortion associated with clinical evidences of infection of the uterus and its contents is called septic abortion. Although clinical criteria vary, abortion is usually considered septic when there are : (1) rise of temperature of at least 100.4°F (38°C) for 24 hours or more, (2) offensive or purulent vaginal discharge and (3) other evidences of pelvic infection such as lower abdominal pain and tenderness.

Septic Shock

Disease Name : Septic Shock, Symptoms : lethargy, altered sensorium : Sepsis-associated delirium (SAD) is a cerebral manifestation commonly occurring in patients with sepsis and is thought to occur due to a combination of neuroinflammation and disturbances in cerebral perfusion, the blood brain barrier (BBB) and neurotransmission., fever : Fever of 38 C / 100.4 F or more., Oliguria : Inflammation and sepsis is another important mechanism for oliguria as demonstrated by the fact, that sepsis is often accompanied by oliguria., Signs : crackles, Acute Renal Failure : Sepsis-associated acute kidney injury (S-AKI) is a common complication in hospitalized and critically ill patients, which increases the risk of developing chronic comorbidities and is associated with extremely high mortality., bounding pulses : A bounding pulse is a strong throbbing felt over one of the arteries in the body. It is due to a forceful heartbeat., coma : Impaired consciousness in the form of excessive somnolence, stupor, or coma is more often seen in the presence of multiorgan dysfunction and refractory septic shock. Patients with SAE have a level of consciousness that is out of proportion to any sedative treatment they might be receiving., hepatitis : Hypoxic hepatitis (HH) may be the cause of fulminant hepatitis. In septic shock, an increase in blood flow and cardiac output is not enough to compensate increased hepatic oxygen demand. 34 Decreased hepatic blood flow in shock does not always cause HH; it may occur in patients with normal blood pressure., hypothermia : Hypothermia is associated with higher mortality and an increased risk of persistent lymphopenia in septic patients, and it may be an early clinical predictor of sepsis-induced immunosuppression., poor peripheral pulses : With the progression of septic shock into the uncompensated stage, hypotension ensues, and patients may present with cool extremities, delayed capillary refill (more than three seconds), and thready pulses, also known as cold shock., Tachycardia, tachypnoea : Tachypnea is a common and often underappreciated feature of sepsis. It is an indicator of pulmonary dysfunction and is commonly found in pneumonia and acute respiratory distress syndrome (ARDS), both of which are associated with increased mortality in sepsis., wide pulse pressure : A hyperdynamic circulation during sepsis, anaphylaxis or liver failure, when there are severe vasodilation and increased cardiac output, can also lead to a widened pulse pressure., Treatment : medication : Dopamine , Dobutamine , Noradrenaline/Norepinephrine, guidelines are derived from the Surviving Sepsis Campaign Guidelines ,,Source Control,,Broad-spectrum antibiotics within one hour of diagnosis for all patients. Initial empiric anti-infective therapy should have activity against all likely pathogens and adequate penetration of source tissue. ,Removal of infected/necrotic tissue, if it is the source of septic shock, i.e. patients with cellulitis, abscess, infected devices, purulent wounds.,Management of Shock 19,,Measures most effective if achieved within the first six hours of diagnosis,Restore central venous pressure (CVP) to 8 mmHg to 12 mmHg,Restore mean arterial pressure (MAP) greater than 65 mmHg,Restore superior vena cava saturation to 70% or mixed venous saturation to 65%,Fluid resuscitation with crystalloid (NS or albumin) and colloid (blood products) up to 80 ml/kg,Mechanical ventilation to reduce metabolic demand,First-line vasoactive agents (epinephrine in cold shock versus norepinephrine in warm shock) when fluid-refractoryNote : dopamine as a first-line agent has fallen out of favor given its inhibitory effect on the HPA axis, namely prolactin and growth hormone, which can confer immunologic dysfunction ,Enhancing Host Response,,Corticosteroids indicated in vasoactive-refractory shock and or in patients with low (unstimulated) basal cortisol levels less than 150 ug/L) ,Addition of vasopressin indicated in vasoactive-refractory shock, Pathophysiology : The pathophysiology of septic shock involves a complex interplay of immune, inflammatory, and coagulation responses. Heres an overview of the key processes involved : Infection and Immune Response : The process begins with an infection, typically caused by bacteria, but it can also be triggered by fungi, viruses, or other pathogens.Immune cells, such as macrophages and neutrophils, recognize the invading pathogens and release pro-inflammatory cytokines (e.g., interleukin-1, interleukin-6, and tumor necrosis factor-alpha) to signal the immune system.Systemic Inflammation : The release of pro-inflammatory cytokines leads to a systemic inflammatory response, also known as a cytokine storm.Blood vessels become leaky, causing fluid and immune cells to enter surrounding tissues. This can lead to edema and hypotension.Vasodilation and Hypotension : In response to the cytokine storm, blood vessels dilate and become permeable, leading to decreased vascular resistance and increased capillary leak.Vasodilation contributes to a decrease in blood pressure (hypotension), which reduces blood flow to vital organs.Endothelial Dysfunction : The inner lining of blood vessels, called the endothelium, becomes damaged due to the inflammatory response.Dysfunction of the endothelium can lead to impaired regulation of blood flow, increased clotting, and compromised barrier function., Epidemiology : The incidence of sepsis and severe sepsis have risen over the past decade from approximately 600, 000 to over 1, 000, 000 hospitalizations per year from 2000 through 2008, poor, Get regular vaccinations against viral infections that may cause sepsis.,Practice good hygiene.,Care for and clean any open or gaping wounds.,Follow medical advice on managing bacterial infections.,Treat fungal and parasitic infections as soon as symptoms appear.,Control diabetes, if relevant.,Avoid smoking., Complications : acute liver failure, acute respiratory distress syndrome, Mesentric Ischemia, myocardial damage, Diagnostics : Complete Blood Count CBC, PLATELET COUNT, Serum Bilirubin (Total ), PT/INR, CT SCAN, SERUM LACTIC ACID LEVEL, HIGH SENSITIVITY C-REACTIVE PROTEIN (HS-CRP), Differential diagnosis : acute respiratory distress syndrome, cardiogenic shock, DIC, DISTRIBUTIVE SHOCK, shock, disease description :  Septic shock, the most severe complication of sepsis, carries high mortality. In response to an inciting agent, pro-inflammatory and anti-inflammatory arms of the immune system are activated in concert with the activation of monocytes, macrophages, and neutrophils that interact with the endothelium through pathogen recognition receptors to elaborate cytokines, proteases, kinins, reactive oxygen species, and nitric oxide.

Serotonin Deficiency

Disease Name : Serotonin Deficiency, Symptoms : behavioural disturbances : Includes obsessive-compulsive disorder (OCD), panic disorder, suicidal behavior, post-traumatic stress disorder (PTSD), social anxiety disorder., Neurological symptoms : Includes anxiety, depressed mood, aggression, impulsive behavior, insomnia, dementia and cognitive decline., Signs : nan, Treatment : SSRIs, such as escitalopram (Cipralex) and fluoxetine (Prozac),selective norepinephrine reuptake inhibitors (SNRIs), such as duloxetine (Cymbalta) and venlafaxine (Effexor XR),monoamine oxidase inhibitors (MAOIs), such as isocarboxazid (Marplan) and phenelzine (Nardil), Pathophysiology : The pathophysiology of serotonin deficiency involves complex interactions between genetics, neurobiology, and environmental factors. Heres an overview of the key aspects : Genetics : Genetic factors can influence the production, release, reuptake, and receptor sensitivity of serotonin.Polymorphisms in genes that encode for enzymes involved in serotonin synthesis and metabolism (such as tryptophan hydroxylase and monoamine oxidase) can impact serotonin levels.Neurotransmitter Synthesis and Release : Serotonin is derived from the amino acid tryptophan, which is obtained from the diet.Tryptophan is converted into serotonin through a series of enzymatic reactions, and any disruption in these pathways can lead to reduced serotonin levels.Serotonin is released from neurons into synapses to transmit signals between nerve cells. Reduced release of serotonin can lead to decreased signaling in serotonin pathways.Reuptake and Transport : After being released into the synapse, serotonin is typically taken back up into the presynaptic neuron through a process called reuptake.Dysregulation of serotonin reuptake, which is a key mechanism of action for selective serotonin reuptake inhibitors (SSRIs), can result in lower serotonin availability in the synapse.Receptor Sensitivity and Signaling : Serotonin exerts its effects by binding to specific receptors on target neurons.Reduced sensitivity of serotonin receptors or changes in receptor distribution can result in altered neurotransmission and contribute to symptoms of serotonin deficiency., Epidemiology : nan, Complications : nan, Diagnostics : plasma serotonin level, Differential diagnosis : nan, disease description : nan

Serous Adenocarcinoma

Disease Name : Serous Adenocarcinoma, Symptoms : bloating : Persistently feeling bloated and full is one of the most common early signs of serous adenocarcinoma., bladder dysfunction : It is possible for patients with serous adenocarcinoma to present with issues that mimic bladder problems. These problems include urinary retention and/or distention., Abdominal Pain : Serous adenocarcinoma causes intense pelvic pain., abdominal fullness : Difficulty eating or feeling full quickly., POSTMENOPAUSAL BLEEDING : As with other forms of endometrial cancer, postmenopausal bleeding is the most common presenting symptom for uterine serous carcinoma. Because many women with uterine serous carcinoma have extrauterine disease at diagnosis, presenting symptoms may also include abdominal pain or bloating as in ovarian serous carcinomas., Signs : nan, Treatment : Surgery is the first treatment for almost all women with endometrial cancer. The operation includes removing the uterus, fallopian tubes, and ovaries. (This is called a total hysterectomy bilateral salpingo-oophorectomy or TH/BSO). Lymph nodes from the pelvis and around the aorta may also be removed (a pelvic and para-aortic lymph node dissection LND or sampling) and tested for cancer spread. Pelvic washings may be done, too., Pathophysiology : Pathophysiology involves-Hereditary predisposition in 15 - 20% of cases involving BRCA genes : BRCA1 germline mutations cause 50% lifetime risk of ovarian cancer at average age of ~50 yearsBRCA2 germline mutations causes lower lifetime risk (10 - 35%) at a later age (average ~55 years)Associated with homologous recombination defectsHereditary predisposition in 6% of women with Fanconi anemiaA significant proportion arise in the fallopian tube and spread to the ovaries and peritoneum, Epidemiology : represents less than 10% of all endometrial cancers., variable, Consider taking birth control pills. Taking birth control pills reduces the risk of ovarian cancer., Complications : hysterectomy, Diagnostics : CT SCAN, USG, Immunostaining, Differential diagnosis : clear cell adenocarcinoma, Endometrial cancer, disease description : Uterine serous adenocarcinoma (USC) is rare and invasive cancer. This cancer is more often reported in the ovary, the fallopian tube, and the endometrium than uterine cervix. No matter where the tumor is located, the tumor exhibits similar histological characteristics.

Serous Cystadenocarcinoma

Disease Name : Serous Cystadenocarcinoma, Symptoms : abdominal discomfort, Abdominal Pain, ABDOMINAL MASS, Signs : nan, Treatment : medication : Gemcitabine hydrochloride, Capecitabine, Erlotinib, Surgery (cystectomy or oophorectomy), Pathophysiology : Initiation and Genetic Mutations : The exact cause of serous cystadenocarcinoma is not fully understood, but genetic mutations are thought to play a significant role.Mutations in tumor suppressor genes (such as TP53) and oncogenes (such as KRAS) can accumulate in ovarian epithelial cells, disrupting normal cellular processes and promoting uncontrolled cell growth.Cellular Transformation and Dysplasia : Accumulation of genetic mutations can lead to cellular transformation, where normal ovarian epithelial cells acquire characteristics of cancer cells.Dysplastic changes can occur, including alterations in cell shape, size, and nuclear features.Cell Proliferation and Tumor Formation : Dysregulated signaling pathways, such as the PI3K/AKT pathway, can promote cell proliferation and survival, contributing to the formation of tumors.These tumors can initially appear as cystic growths on the surface of the ovaries or within ovarian cysts.Invasion and Metastasis : Cancer cells can invade surrounding tissues and structures, including the pelvic cavity and nearby organs.Cancer cells can also shed into the abdominal cavity, leading to the potential for distant metastasis to organs such as the liver, lungs, and lymph nodes.Angiogenesis : Tumors require a blood supply to sustain their growth. Cancer cells can stimulate the formation of new blood vessels (angiogenesis) to ensure a nutrient and oxygen supply to the growing tumor.Immune Evasion and Tumor Microenvironment : Cancer cells can manipulate the immune system to avoid detection and destruction by immune cells.The tumor microenvironment, which includes immune cells, fibroblasts, and extracellular matrix components, plays a crucial role in tumor growth, invasion, and metastasis., Epidemiology : Serous ovarian cystadenocarcinomas account for ~25% of serous tumors., Account for the largest proportion of malignant ovarian tumors, representing over 50-80% of all malignant epithelial ovarian tumors, variable, Surgical risk reduction, particularly RRSO, plays an important role in the prevention of ovarian carcinoma in high-risk women., Complications : Ovarian Cyst, CYST RUPTURE, Diagnostics : CA 125, CT SCAN, USG, Differential diagnosis : HYDROSALPINX, Mesonephric cyst, Polycystic Ovarian Syndrome, disease description : Epithelial neoplasms of the ovary account for 60% of all ovarian tumors and 40% of benign tumors .They classify as benign, borderline, or malignant tumors. Ovarian cystadenomas are common benign epithelial neoplasms which carry an excellent prognosis. The two most frequent types of cystadenomas are serous and mucinous cystadenomas whereas endometrioid and clear cell cystadenomas are rare. Despite advances in imaging studies, the establishment of a definitive diagnosis of cystadenomas is primarily by histopathological examination of the surgical specimen. This review will focus on ovarian cystadenomas and their histopathological features.

Serous Cystadenoma

Disease Name : Serous Cystadenoma, Symptoms : bloating, discomfort, pelvic pain, Signs : nan, Treatment : nan, Pathophysiology : Heres an overview of the pathophysiology of serous cystadenomas : Origins and Cellular Changes : Serous cystadenomas are believed to arise from the exocrine portion of the pancreatic tissue. The exact cause of their formation is not fully understood, but its thought to involve genetic mutations or alterations in specific signaling pathways.Fluid Accumulation : The hallmark of serous cystadenomas is the formation of cystic structures filled with a watery, serous fluid. This fluid accumulation occurs due to increased secretion of fluid by the lining epithelial cells of the cysts and/or impaired drainage of this fluid, leading to cyst expansion.Cellular Proliferation : The lining epithelial cells of the cysts undergo proliferation, contributing to the enlargement of the cysts. The exact mechanisms triggering this proliferation are still being investigated., Epidemiology : Benign serous tumors of the ovary represent 16% of all ovarian epithelial neoplasms, variable, Complications : CYST RUPTURE, PSEUDOMYXOMA PERITONEII, Diagnostics : CA 125, MRI, CT SCAN, CT SCAN, USG, Immunostaining, Differential diagnosis : HYDROSALPINX, mucinous cystadenoma, Polycystic Ovarian Syndrome, disease description : Ovarian cystadenomas are common benign epithelial neoplasms which carry an excellent prognosis. The two most frequent types of cystadenomas are serous and mucinous cystadenomas.Epithelial neoplasms of the ovary account for 60% of all ovarian tumors and 40% of benign tumors.1 They classify as benign, borderline, or malignant tumors. Ovarian cystadenomas are common benign epithelial neoplasms which carry an excellent prognosis. The two most frequent types of cystadenomas are serous and mucinous cystadenomas whereas endometrioid and clear cell cystadenomas are rare. Despite advances in imaging studies, the establishment of a definitive diagnosis of cystadenomas is primarily by histopathological examination of the surgical specimen. This review will focus on ovarian cystadenomas and their histopathological features.

Serous Otitis Media

Disease Name : Serous Otitis Media, Symptoms : Hearing loss : Serous otitis media (SOM) is a common inflammatory process of the middle ear, frequent in early childhood. It is commonly accompanied by mild to moderate hearing loss (HL)., "DELAYED SPEECH : If there are delays in your childs speech or language development because of fluid, these delays usually disappear once the ear fluid goes away on its own or ear tubes are inserted. If a delay persists, your child should be referred to a speech-language pathologist for evaluation and treatment, as necessary.", BALANCE PROBLEM : Fluid in the middle ear can cause imbalance and spinning vertigo., Signs : nan, Treatment : 1-Decongestants,2-Antihistaminic and steroids,3-Antibiotics,4-Middle Ear Aeration, 1-Myringotomy and Aspiration of Fluid,2- Grommet Insertion-If myringotomy and aspiration ,combined with medical measures have not helped and ,fluid recurs,3-Tympanotomy or Cortical Mastoidectomy,4-Surgical Treatment of Causative Factor, Pathophysiology :  Heres an overview of the pathophysiological processes involved : Eustachian Tube Dysfunction : The Eustachian tube is a small tube that connects the middle ear to the back of the throat. Its primary function is to regulate pressure and ventilate the middle ear, allowing for equalization of air pressure on both sides of the eardrum. In serous otitis media, dysfunction of the Eustachian tube can occur, leading to inadequate ventilation and impaired drainage of fluid from the middle ear.Fluid Accumulation : When the Eustachian tube is not functioning properly, it can lead to a negative pressure within the middle ear. This negative pressure can cause fluid (serous fluid, mucus, or other secretions) to accumulate in the middle ear space. The fluid buildup can affect the mobility of the eardrum and the tiny bones (ossicles) within the middle ear.Inflammation and Mucosal Changes : Eustachian tube dysfunction and fluid accumulation can trigger an inflammatory response in the middle ear. The mucosal lining of the middle ear becomes swollen and may produce excessive mucus. This inflammatory process further impairs the normal functioning of the Eustachian tube., Epidemiology : OME is more prevalent during the winter months, corresponding to higher patient rates of upper respiratory infections., The disease commonly affects children between the ages of 1 and 6. There is a higher prevalence at the age of 2, which drops after the age of 5., variable, Helping your child reduce the risk of ear infections can help prevent OME., Complications : Hearing loss, Diagnostics : Otoscopy, X Ray skull, CT SCAN, Mastoid X-Ray, Impedance Audiometry, Tuning Fork Tests, Differential diagnosis : CHRONIC OTITIS MEDIA, Herpes Zoster, OTITIS EXTERNA, OTITIS MEDIA WITH EFFUSION, disease description : Otitis media with effusion (OME) is a condition in which there is fluid in the middle ear, but no signs of acute infection. As fluid builds up in the middle ear and Eustachian tube, it places pressure on the tympanic membrane. The pressure prevents the tympanic membrane from vibrating properly, decreases sound conduction, and therefore results in a decrease in patient hearing. Chronic OME is defined as OME that persists for 3 or more months on examination or tympanometry, although some clinicians recommend reserving the term, ‘chronic otitis media’ for patients in which the tympanic membrane has perforated.

Serrated Adenoma

Disease Name : Serrated Adenoma, Symptoms : bleeding, pain in abdomen radiating to back, Diarrhea or constipation, Signs : nan, Treatment : Polypectomy or endoscopic mucosal resection,Recommendations are to completely remove all serrated lesions proximal to the sigmoid colon and all serrated lesions > 5 mm in the rectosigmoid colon.,Lesions > 1 cm in size or with high grade dysplasia should be managed clinically like a high risk adenoma., Pathophysiology : Origins and Molecular Changes : Serrated adenomas are thought to arise from the crypts (small glands) that line the colon and rectum. The development of serrated adenomas is associated with specific genetic and epigenetic changes in the cells lining the crypts. These changes can lead to alterations in cell growth, differentiation, and signaling pathways.Serrated Pathway : Serrated adenomas are often considered to be part of a distinct pathway in colorectal carcinogenesis known as the "serrated pathway." This pathway is thought to contribute to a subset of colorectal cancers that have unique molecular and clinical features. The serrated pathway is characterized by abnormalities in DNA methylation, which can lead to the silencing of tumor suppressor genes and activation of oncogenes.BRAF Mutation : A significant proportion of serrated adenomas harbor mutations in the BRAF gene, specifically the V600E mutation. This mutation is associated with the activation of signaling pathways that promote cell proliferation and survival. BRAF mutations are more commonly found in serrated lesions compared to other types of colorectal polyps.Microsatellite Instability : Some serrated adenomas may exhibit microsatellite instability (MSI), which is a condition characterized by errors in DNA replication. MSI can result in the accumulation of mutations in genes involved in DNA repair, cell cycle control, and apoptosis, further contributing to the development of cancer.Wnt Signaling : Similar to other types of colorectal polyps, the Wnt signaling pathway plays a role in the pathogenesis of serrated adenomas. Aberrant activation of the Wnt pathway can lead to the overgrowth of cells and the formation of polyps., Epidemiology : Prevalence of sessile serrated adenoma increases slightly with age, Account for approximately 3 - 9% of all colorectal polyps and 10 - 25% of all serrated polyps, variable, Some risk factors for adenomas are not controllable. However, you can improve your chances of staying healthy by getting regular health screenings. If you have a higher risk of developing an adenoma, ask your healthcare provider how often you should receive screenings.,,You can also improve your health by : ,,Avoiding smoking.,Eating plenty of fruits, vegetables and whole grains.,Exercising regularly.,Limiting alcohol consumption., Complications : bleeding, Diagnostics : Cytogenetics, CT SCAN, CT SCAN, Immunostaining, Immunostaining, Differential diagnosis : Adenomas : Tubular adenoma, Lactating adenoma, Apoc, tubulovillous adenoma, disease description : It is characterized by epithelial dysplasia with serration of the crypt luminal surface and prominent infolding of the epithelium. Other cytological features include central, elongated nuclei, mild pseudostratification, and eosinophilic cytoplasm.

Sertoli Cell Tumour, Stromal-leydig Cell Tumour

Disease Name : Sertoli Cell Tumour, Stromal-leydig Cell Tumour, Symptoms : amenorrhoea, ascites, Irregular menstruation, pelvic pain, Hirsutism, Clitoromegaly, Signs : nan, Treatment : Platinum based adjuvant chemotherapy has also been reported in patients with moderately and poorly differentiated tumors, heterologous mesenchymal elements, advanced stage or rupture., Genetic counseling and germline DICER1 mutation testing is recommended., Conservative fertility sparing surgery (unilateral salpingo-oophorectomy) and staging procedure (with or without lymphadenectomy) is usually performed in young patients with stage I tumors.,Older patients who do not wish to preserve fertility typically undergo bilateral salpingo-oophorectomy, total hysterectomy and complete surgical staging., Pathophysiology : Pathophysiology-May occur sporadically or in patients with DICER1 syndromeRare tumor predisposition syndrome caused by germline mutations in DICER1, a gene encoding the RNase III enzyme in the microRNA maturation pathway.Other tumors and disorders associated with DICER1 syndrome include pleuropulmonary blastoma, cystic nephroma, multinodular goiter and botryoid embryonal rhabdomyosarcoma, among others.Germline mutation is generally a truncating mutation; may occur anywhere in the gene.Second hit somatic mutation is a focused hotspot missense mutation affecting the RNase IIIb domain of DICER1.Sporadic Sertoli-Leydig cell tumors (moderately and poorly differentiated) harbor somatic mutations at the same hotspot of DICER1 gene.Somatic hotspot DICER1 mutations are present in approximately half of all cases (range : 15 - 97%), 61 - 69% of which also have germline DICER1 mutations., Epidemiology : accounting for < 0.5% of all ovarian neoplasms and 1 - 2% of pediatric ovarian cancers, variable, Complications : erectile dysfunction, Gynecomastia, hypogonadism, infertility, Diagnostics : SERUM TESTOSTERONE LEVEL, Cytogenetics, Cytogenetics, Cytogenetics, ultrasound, CT SCAN, Immunostaining, Immunostaining, Differential diagnosis : Endometrioid carcinoma, tubular Krukenberg tumor, disease description : Sertoli–Leydig cell tumors (SLCTs) are rare tumors, accounting for less than 0.5% of all ovarian cancers . The varying histopathology and differentiation of this tumor present difficulties with proper diagnosis and development of optimal treatment regimens. The prevalence of Sertoli–Leydig tumors with hepatoid differentiation is exceedingly uncommon with few published case reports, resulting in an additional diagnostic dilemma. We report the case of a Sertoli–Leydig cell tumor found in a 40 years old female with intermediate differentiation and heterologous elements including endometrioid and hepatoid differentiation with alpha-fetoprotein expression.

Severe Acute Malnutrition

Disease Name : Severe Acute Malnutrition, Symptoms : Cardiac Disease : Palpitations, light headedness, dizziness, and chest pain can be indications that serious cardiac complications have developed. Some of these include myocardial atrophy, mitral valve prolapse, pericardial effusion, sinus bradycardia, orthostatic hypotension, and even sudden cardiac death., CNS disturbances : Cognitive deficits as a result of generalized brain atrophy. Numbness and tingling can also occur., Gastrointestinal symptoms : Constipation, diarrhea, fullness, and abdominal pain are all indicators of potential gastrointestinal complications from such diagnosis as gastroparesis, superior mesenteric artery (SMA) syndrome, liver disease, and functional bowel disorders., Bone disorders : Usually painless, sarcopenia and bone loss (osteopenia and osteoporosis) are complications from severe malnutrition. However, osteoporosis may be irreversible with significant malnutrition, and severe fractures can occur with low bone density., Endocrine disturbances : Symptoms from endocrine complications are often vague but can reflect low leptin levels, growth hormone resistance, elevated serum cortisol levels, euthyroid sick syndrome, hypoglycemia, and resultant amenorrhea., Pulmonary disorders : The development of shortness of breath and fevers can be revealing of a spontaneous pneumothorax and pneumomediastinum, aspiration pneumonia, in concert with abnormal pulmonary function tests., cutaneous symptoms : Manifestations include xerosis, acrocyanosis, lanugo hair growth, brittle hair and nails and unexplained hypercarotenemia., Signs : BAGGY PANT APPEARANCE : There might be folds of skin on the buttocks and thighs that make it look as if the child is wearing “baggy pants Children with severe acute under nutrition has very low weight for their height and severe muscle wasting and they may also have nutritional edema–characterized by swollen feet, face and limbs., edema : Low protein levels in the blood caused by malnutrition, kidney and liver disease can cause edema. The proteins help to hold salt and water inside the blood vessels so fluid does not leak out into the tissues., angular stomatitis : Angular stomatitis (AS) has classically been linked with deficiencies of riboflavin, other B group vitamins and iron. Potential functional consequences of riboflavin deficiency in humans include decreases in motor skills and attention span, and reduced absorption or utilisation of iron., anemia : Anemia is associated with micronutrient deficiencies such as vitamin B-12 and B-9, as well as different infectious diseases that primarily attack the red blood cells. Likewise, iron deficiency shares 50% of all causes of anemia, and it is basically linked with poor dietary intake., visible severe wasting : Severe acute malnutrition is defined in these guidelines as the presence of oedema of both feet or severe wasting (weight-for-height/length <-3SD or mid-upper arm circumference < 115 mm)., mid upper arm circumference below 11.5cm : MUAC less than 110mm (11.0cm), RED COLOUR, indicates Severe Acute Malnutrition (SAM)., hair discoloration : Hair becomes thin and fragile with bands of loss of pigmentation., pigmentation on skin : They occur in patchy distribution with flaking of the skin often described as “flaky paint dermatosis.”, Treatment : medication : Magnesium/Magnesium Sulphate, Folic acid / Vitamin B9, Potassium/Potassium Salts, Ampicillin , Ceftriaxone , Amikacin , Vitamin A (Retinol), Iron , Zinc/Zinc Sulphate, Glucose/Dextrose, Asymptomatic hypoglycemia,Give 50 ml of 10% glucose or sucrose solution orally or by nasogastric tube followed by first feed,Feed with starter F-75 every 2 hourly day and night,Symptomatic hypoglycemia,Give 10% dextrose IV 5 ml/kg,Follow with 50 ml of 10% dextrose or sucrose solution by nasogastric tube. Severe dehydration with shock is treated with intravenous,fluids. Ideally, Ringer lactate with 5% dextrose should be,used as rehydrating fluid. If not available, half normal,saline (N /2) with 5% dextrose or Ringer lactate alone can,be used,Feed with starter F-75 every 2 hourly day and night,Start appropriate antibiotics. Use reduced osmolarity ORS with potassium supplements for rehydration and maintenance. Give supplemental potassium at 3-4 mEq/kg/ day for at least 2 weeks,On day l, give 50% magnesium sulphate (equivalent to 4 mEq/ml) IM once (0.3 ml/kg; maximum of 2,ml). Treat with parenteral ampicillin 50 mg/kg/ dose 6 hourly for at least 2 days followed by oral,amoxicillin 15 mg/kg 8 hourly for 5 days and gentamicin 7.5 mg/kg or arnikacin 15-20 mg/kg,IM or IV once daily for 7 days,If no improvement occurs within 48 hr, change to IV cefotaxime (100-150 mg/kg/day 6-8 hourly) or,ceftriaxone (50-75 mg/kg/day 12 hourly),If other specific infections are identified, give appropriate antibiotics., Pathophysiology : Severe acute malnutrition is defined as severe wasting and/or bilateral edema. Severe wasting is extreme thinness diagnosed by a weight-for-length (or height) < -3 SD of the WHO Child Growth Standards. In children ages 6-59 mo, a mid-upper arm circumference <115 mm also denotes extreme thinness : a colorbanded tape is a convenient way of screening children in need of treatment. Children with severe acute malnutrition have had a diet insufficient in energy and nutrients relative to their needs. The magnitude of the deficits will differ depending on the duration of inadequacy, quantity and diversity of food consumed, presence of antinutrients (e.g., phytate), individual variation in requirements, and number and severity of coexisting infections and their duration. Infections can lead to profound nutrient deficits and imbalances : For example, amino acids are diverted to form acute-phase proteins, and potassium, magnesium, vitamin A, and zinc are lost through diarrhea, and losses of glycine and taurine are linked to small bowel bacterial overgrowth. Ingested microbes can cause villous atrophy and loss of nutrients from maldigestion and malabsorption, as well as disruption of gut barrier function leading to microbial translocation, chronic immune activation, and altered gut microbiome (environmental enteric dysfunction). Deficits can also arise from increased nutrient utilization in response to noxae (e.g., cysteine and methionine to detoxify dietary cyanogens). Pathophysiology When a childs intake is insufficient to meet daily needs, physiologic and metabolic changes take place in an orderly progression to conserve energy and prolong life. This process is called reductive adaptation . Fat stores are mobilized to provide energy. Later, protein in muscle, skin, and the gastrointestinal tract is mobilized. Energy is conserved by reducing physical activity and growth, reducing basal metabolism and the functional reserve of organs, and reducing inflammatory and immune responses. These changes have important consequences : ? The liver makes glucose less readily, making the child more prone to hypoglycemia. It produces less albumin, transferrin, and other transport proteins. It is less able to cope with excess dietary protein and to excrete toxins. Heat production is less, making the child more vulnerable to hypothermia. The kidneys are less able to excrete excess fluid and sodium, and fluid easily accumulates in the circulation, increasing the risk of fluid overload. The heart is smaller and weaker and has a reduced output, and fluid overload readily leads to death from cardiac failure. Sodium builds up inside cells due to leaky cell membranes and reduced activity of the sodiumpotassium pump, leading to excess body sodium, fluid retention, and edema.  Potassium leaks out of cells and is excreted in urine, contributing to electrolyte imbalance, fluid retention, edema, and anorexia. Loss of muscle protein is accompanied by loss of potassium, magnesium, zinc, and copper. The gut produces less gastric acid and enzymes. Motility is reduced, and bacteria may colonize the stomach and small intestine, damaging the mucosa and deconjugating bile salts. Digestion and absorption are impaired. Cell replication and repair are reduced, increasing the risk of bacterial translocation through the gut mucosa. ? Immune function is impaired, especially cellmediated immunity. The usual responses to infection may be absent, even in severe illness, increasing the risk of undiagnosed infection. Red blood cell mass is reduced, releasing iron, which requires glucose and amino acids to be converted to ferritin, increasing the risk of hypoglycemia and amino acid imbalances. If conversion to ferritin is incomplete, unbound iron promotes pathogen growth and formation of free radicals. Micronutrient deficiencies limit the bodys ability to deactivate free radicals, which cause cell damage. Edema and hair/skin changes are outward signs of cell damage. Pathological changes in malnutrition in various organ systems Upper gastrointestinal tract- Mucosa shiny and atrophic, papillae of tongue flattened Small and large intestine-Mucosa and villi atrophic; brush border enzymes reduced; hypotonic, rectal prolapse Liver- Fatty liver, deposition of triglycerides Pancreas-Exocrine secretion depressed; endocrine function less severely affected; glucagon production reduced; insulin levels low; atrophy and degranulation or hypertrophy of islets seen Endocrine system-Elevated growth hormone; thyroid involution and fibrosis; adrenal glands atrophic and cortex thinned; increased cortisol; catecholamine activity unaltered Lymphoreticular system- Thymus involuted; loss of distinction between cortex and medulla; depletion of lymphocytes; paracortical areas of lymph nodes depleted of lymphocytes; germinal centers smaller and fewer Central nervous system-Head circumference and brain growth retarded; changes seen in the dendritic arborization and morphology of dendritic spines; cerebral atrophy on CT /MRI; abnormalities in auditory brainstem potentials and visual evoked potentials Cardiovascular system-Changes in cardiac volume, muscle mass and electrical properties of the myocardium; systolic function affected more than diastolic function Marasmus It results from rapid deterioration in nutritional status. Acute starvation or acute illness over a borderline nutritional status could precipitate this form of undernutrition. It is characterized by marked wasting of fat and muscle as these tissues are consumed to make energy. i. The main sign is severe wasting. The child appears very thin (skin and bones) and has no fat. There is severe wasting of the shoulders, arms, buttocks and thighs ii. The loss of buccal pad of fat creates the aged or wrinkled appearance that has been referred to as monkey facies. Baggy pants appearance refers to loose skin of the buttocks hanging down. Axillary pad of fat may also be diminished iii. Affected children may appear to be alert in spite of their condition iv. There is no edema Kwashiorkor It usually affects children aged 1--4 yr. The main sign is pitting edema, usually starting in the legs and feet and spreading, in more advanced cases, to the hands and face. Because of edema, children with kwashiorkor may look healthy so that their parents view them as well fed. i. General appearance. Child may have a fat sugar baby appearance. ii. Edema. It ranges from mild to gross and may represent up to 5-20% of the body weight. iii. Muscle wasting. It is always present. The child is often weak, hypotonic and unable to stand or walk. iv. Skin changes. The skin lesions consist of increased pigmentation, desquamation and dyspigmentation. Pigmentation may be confluent resemblingflaky paint or in individual enamel spots. The distribution is typically on buttocks, perineum and upper thigh. Petechiae may be seen over abdomen. Outer layers of skin may peel off and ulceration may occur. The lesions may sometimes resemble burns. v. Mucous membrane lesions. Smooth tongue, cheilosis and angular stomatitis are common. Herpes simplex stomatitis may also be seen. vi. Hair. Changes include dyspigmentation, loss of characteristic curls and sparseness over temple and occipital regions. Hairs also lose their lustre and are easily pluckable. A flag sign which is the alternate bands of hypopigmented and normally pigmented hair pattern is seen when the growth of child occurs in spurts. vii. Mental changes. Includes unhappiness, apathy or irritability with sad, intermittent cry. They show no signs of hunger and it is difficult to feed them. viii. Neurological changes. These are seen during recovery. ix. Gastrointestinal system. Anorexia, sometimes with vomiting, is the rule. Abdominal distension is characteristic. Stools may be watery or semisolid, bulky with a low pH and may contain unabsorbed sugars. x. Anemia. It may also be seen, as in mild PEM, but with greater severity. xi. Cardiovascular system. The findings include cold, pale extremities due to circulatory insufficiency and are associated with prolonged circulation time, bradycardia, diminished cardiac output and hypotension. xii. Renal Junction. Glomerular filtration and renal plasma flow are diminished. There is aminoaciduria and inefficient excretion of acid load. Marasmic Kwashiorkor It is a mixed form of PEM and manifests as edema occurring in children who may or may not have other signs of kwashiorkor and have varied manifestations of marasmus., Epidemiology : 1-3% of adult testicular neoplasms and 3% of testicular tumors in infants and children., <0.5% of all primary ovarian neoplasms, variable, Special nutritious foods directly meet the increased nutrient requirements of children at risk for wasting; assistance to vulnerable households, in the form of cash or food, enables households to better meet the food, health, and other needs of household members and may increase resilience; water, sanitation, and hygiene (WASH) and health interventions help prevent and address illness and hence reduce wasting risk. ,Programs should address the most important causes in given contexts, be feasible to implement at scale, and assess implementation, coverage, and outcomes., Complications : No dehydration, Hypoglycaemia, hypothermia, infections, Diagnostics : Complete Blood Count CBC, CSF EXAMINATION, Peripheral Blood Smear, ECG, Montoux test, X RAY CHEST, serum potassium K+, PLASMA D DIMER ELISA, SERUM MAGEISIUM, BLOOD CULTURE, CHEST X RAY, CT SCAN, SERUM SODIUM LEVEL, BLOOD GLUCOSE, PCR tests, Differential diagnosis : Chronic Pancreatitis, Kwashiorkor, MARASMUS, nephrotic syndrome, No dehydration, disease description : Severe acute malnutrition (SAM) among children 6-59 months of age is defined by World Health Organization (WHO) and UNICEF as any of the following : (i) weightfor- height below -3 standard deviation (SD or Z scores) of the median WHO growth reference; (ii) visible severe wasting; (iii) presence of bipedal edema; or (iv) mid upper arm circumference below 11.5 cm. This classification is used to identify children at high-risk of death. Children having SAM require urgent attention and management in the hospital. In a child below 6 months of age, the MUAC cannot be used, and SAM should be diagnosed in the presence of (i), (ii) or (iii).

Severe Acute Respiratory Syndrome (sars)

Disease Name : Severe Acute Respiratory Syndrome (sars), Symptoms : dry cough : SARS causes dry cough., flu-like symptoms : SARS usually begins with flu-like signs and symptoms — fever, chills, muscle aches, headache and occasionally diarrhea., dyspnea : It occurs when tiny, elastic air sacs (alveoli) in your lungs experience fluid buildup, leading to shortness of breath, rapid breathing, and gasping for air., fever with chills : Fever of 100.4°F (38.0°C) or higher., Signs : nan, Treatment : in mild cases-quarantine of suspected contacts for 10 days;, Personal preventive measures to prevent spread of the virus include frequent hand washing using soap or alcohol-based disinfectants. For those with a high risk of contracting the disease, such as health care workers, use of personal protective equipment, including a mask, goggles and an apron is mandatory. Whenever possible, household contacts should also wear a mask., symptomatic management, immuneboosters-vit c, vit b12, vit d3, calcium,severe cases may require intubation and ICU care,,Antibiotics to treat bacteria that cause pneumonia (until bacterial pneumonia is ruled out or if there is bacterial pneumonia in addition to SARS) and to treat bacterial infections that could occur in addition to SARS, Pathophysiology : The SARS coronavirus (SARS-CoV) uses the angiotensin-converting enzyme 2 (ACE2) receptor for entry into its host,  SARS-CoV recognizes the host ACE2 receptor through the viruss receptor-binding domain. Mutation in this domain may allow this and other coronaviruses to cause new and increased cross-species infections , he virus concentrates in the lungs and small bowel, which are areas with a high density of its receptors,  Specifically, the alveolar epithelium shows the highest focus of infection. The infection leads to serous pleural effusions, pulmonary edema, and consolidations with relative sparing of the upper respiratory tract , he lung injury is thought to be due to an out-of-control immune response by the host leading to excess quantities of pro-inflammatory cytokines., Epidemiology : China had the majority of cases (83%), while in the United States, there were only 27 probable cases identified and no noted deaths or secondary cases. The outbreak in total led to 8096 cases, with 774 deaths attributed, variable, washing hands frequently or cleaning with an alcohol-based detergent,avoiding touching the eyes, mouth, and nose with unclean hands,covering the mouth and nose with a tissue when coughing or sneezing,avoiding sharing food, drinks, and utensils,staying at least 3 feet away from other people,regularly cleaning surfaces with disinfectant, Complications : leukopenia, pulmonary hypertension, Rhabdomyolysis, Thrombocytopenia, Diagnostics : Arterial Blood Gas Analysis(ABG), PLATELET COUNT, X RAY CHEST, SERUM ANTIBODY/TOXIN, White Blood Cell count WBC, X RAY, Differential diagnosis : Haemophilus influenzae, Hantavirus pulmonary syndrome, Influenza, Respiratory syncytial virus, Varicella, disease description : A new and rapidly progressive respiratory syndrome termed severe acute respiratory syndrome (SARS) was identified by the World Health Organization (WHO) , Severe acute respiratory syndrome (SARS) is a contagious and sometimes fatal respiratory illness. SARS first appeared in China in November 2002. Within a few months,  SARS spread worldwide, carried by unsuspecting travelers.SARS showed how quickly infection can spread in a highly mobile and interconnected world. On the other hand, a collaborative international effort allowed health experts to quickly contain the spread of the disease. There has been no known transmission of SARS anywhere in the world since 2004.

Severe Acute Respiratory Syndrome

Disease Name : Severe Acute Respiratory Syndrome, Symptoms : sore throat, fever, dyspnea, lethargy, myalgia, Signs : crackles, INCREASE HEART RATE, Treatment : medication : Paracetamol/Acetaminophen, Noscapine , Fexofenadine , Budesonide , Levosulpiride/Sulpiride, Low-dose corticosteroids, like prednisolone at 0.5–1.0 mg/kg/day, are usually used in infections and ARDS. On the other hand, pulse doses of methylprednisolone at 0.5–1.0 g/day have been widely used in SARS, especially when patients deteriorated clinically in the second week., Pathophysiology : nan, Epidemiology : 18.4%, The attack rate for SARS-CoV ranges from 10.3% to 60% or 2.4 to 31.3 cases/1000 exposure-hours, variable, "Researchers are working on several types of vaccines for SARS, but none has been tested in humans. If SARS infections reappear, follow these safety guidelines if youre caring for someone who may have a SARS infection : ,,1. Wash your hands.,2.Wear disposable gloves. ,3. Wear a surgical mask. ,4. Wash personal items. ,5. Disinfect surfaces.", Complications : nan, Diagnostics : Complete Blood Count CBC, X RAY CHEST, ABG PO2, ABG PCO2, BODY FLUID CULTURE, RT PCR AMPLIFICATION, DIRECT IMMUNOFLORESCENCE ASSAY, INDIRECT IMMUNOFLORESCENCE ASSAY, Differential diagnosis : Hantaviral Disease, Influenza, Perinatal varicella, Respiratory syncytial virus, disease description : ARS is an airborne virus and can spread through small droplets of saliva in a similar way to the cold and influenza. It was the first severe and readily transmissible new disease to emerge in the 21st century and showed a clear capacity to spread along the routes of international air travel.SARS can also be spread indirectly via surfaces that have been touched by someone who is infected with the virus. Most patients identified with SARS were previously healthy adults aged 25–70 years. A few suspected cases of SARS have been reported among children under 15 years. The case fatality among persons with illness meeting the current WHO case definition for probable and suspected cases of SARS is around 3%. 

Severe Combined Immunodeficiency (scid)

Disease Name : Severe Combined Immunodeficiency (scid), Symptoms : CHRONIC DIARRHEA : Persistent diarrhea resulting in failure to thrive is a common problem in children with SCID., failure to thrive : Due to recurrent infections, children with SCID do not grow and gain weight as expected (failure to thrive). SCID may be caused by genetic changes in any of several genes and can be inherited in an X-linked recessive (most commonly) or autosomal recessive manner., infections : Other bacterial, viral, or fungal infections that can be serious and hard to treat, such as ear infections (acute otitis media), sinus infections (sinusitis), skin rashes, meningitis, pneumonia., Pulmonary disorders : Frequent and often very severe respiratory infections such as pneumonia commonly occurs in affected children., cutaneous symptoms : The skin may be involved in children with SCID. The skin may become chronically infected with the same fungus (candida) that infects the mouth and causes thrush., Signs : MUCOCUTANEOUS CANDIDIDASIS : Chronic mucocutaneous candidiasis (CMC) is characterized by recurrent or persistent infections affecting the nails, skin and oral and genital mucosae caused by Candida spp., mainly Candida albicans. CMC is an infectious phenotype in patients with inherited or acquired T-cell deficiency., Treatment : The most common treatment for SCID is an allogeneic bone marrow transplant, which will introduce normal infection-fighting cells into your child’s body, Pathophysiology : The best-known form of autosomal recessive SCID is caused by adenosine deaminase (ADA) deficiency,   in which infants lack the ADA enzyme necessary for T-cell survival. X-linked SCID, which is caused by mutations in a gene on the X chromosome, primarily affects male infants. Boys with this type of SCID have white blood cells that grow and develop abnormally. As a consequence, they have low numbers of T Cell and natural killer cell and their B cell do not function., Epidemiology : nearly 30% of all cases, 1 in 60, 000 newborns and it is estimated that one-quarter to one-third of these cases are X-linked SCID, variable, Restricted contact with other people to prevent exposure to new infections, Complications : septic shock, Bleeding disorders, MULTIORGAN FAILURE, Diagnostics : X RAY CHEST, Differential diagnosis : HIV, WISKOTT-ALDRICH SYNDROME, disease description : Severe combined immunodeficiency (SCID) is a group of rare disorders caused by mutations in different genes involved in the development and function of infection-fighting immune cells. Infants with SCID appear healthy at birth but are highly susceptible to severe infections. The condition is fatal, usually within the first year or two of life, unless infants receive immune-restoring treatments, such as transplants of blood-forming stem cells, gene therapy, or enzyme therapy. More than 80 percent of SCID infants do not have a family history of the condition. However, development of a newborn screening test has made it possible to detect SCID before symptoms appear, helping ensure that affected infants receive life-saving treatments.

Severe Dehydration

Disease Name : Severe Dehydration, Symptoms : CNS disturbances : Includes headache, delirium and confusion., constipation : Dehydration is a common cause of constipation. When a person becomes dehydrated, their intestines cannot add enough water to stools. Dehydration results in hard, dry, lumpy stools that are difficult to pass. Drinking plenty of water can help to ease or resolve the symptoms and avoid a person getting constipated., Dizziness : One of the potential symptoms of dehydration is dizziness. You may feel lightheaded or woozy. In some cases, you may also feel as if you or your surroundings are spinning or tilting. This is known as vertigo., fatigue : As dehydration sets in, your blood pressure drops, leading to poor circulation and reduced blood flow to your brain. This causes feelings of sleepiness., loss of appetite : Loss of appetite but maybe craving sugar., DARK URINE : Dark urine is most commonly due to dehydration., "Hypotension : When the body doesnt have enough water, the amount of blood in the body (blood volume) decreases. This can cause blood pressure to drop.", flushed face : Dehydration can often cause redness in the face, due to your body beginning to overheat., Signs : Heart rate-Tachycardia, with bradycardia in most severe cases : Dehydration is known to decrease orthostatic tolerance and cause tachycardia., Breathing-deep : Not taking in enough fluids can impact your ability to breathe deeply and cause significant respiratory distress if you are severely dehydrated., eyes-Deeply sunken : Lack of proper hydration can lead to sunken eyes, especially in children., Quality of pulses-Weak, thready, or impalpable : Patients who are severely dehydrated can present with weak thread pulses, and delayed capillary refill., tear-absent : Inability to produce tearscan be a sign of not having enough fluid in the body., "Mouth and tongue-Parched : When youre not hydrating properly, your body starts to conserve the fluid it has. Thats why one of the first signs of dehydration shows up in the mouth as decreased saliva production. This is why your tongue might feel dry and even swollen.", skinfold-Recoil in >2 sec : A decrease in skin turgor is a late sign of dehydration., Treatment : REHYDRATION THERAPY-Malnourished infants may benefit from smaller-volume, frequent boluses of 10 mL/kg body weight due to reduced capacity to increase cardiac output with larger volume resuscitation. Infants (<12 months) and children (12 mo to 5 yr) without malnutrition : Give 20-30 mL/kg boluses of intravenous isotonic crystalloid solution (e.g., normal saline solution) over 30-60 min. Repeat boluses as necessary to restore adequate perfusion. Then give 70 mL/kg over 2.5-5 hr. (Note the slower infusion times are for infants.) Reassess the infant or child frequently and adjust infusion rate if needed. Switch to ORS, breast milk, and feed as described for some dehydration, when the child can drink, perfusion is adequate, and mental status is normal. Adjust electrolytes and administer dextrose based on chemistry values,REPLACEMENT,OF LOSSES,DURING,MAINTENANCE-Infants and,children : ,<10 kg body,weight : 50-,100 mL ORS,for each,diarrheal stool,or vomiting,episode, up to,~500 mL/day,>10 kg body,weight : 100-,200 mL ORS,for each,diarrheal stool,or vomiting,episode; up to,~1 L/day,Adolescents,and adults : ,Ad libitum, up,to ~2 L/day,Replace losses,as above as,long as, Pathophysiology : Fluid Loss : Dehydration can result from various factors, such as inadequate fluid intake, excessive fluid loss (through sweating, vomiting, diarrhea, or excessive urination), or a combination of both. The body relies on a balance of fluids to function properly, and when this balance is disrupted, dehydration can occur.Disruption of Electrolyte Balance : Fluid loss leads to an imbalance in electrolytes, which are minerals in the body that carry an electrical charge and play a crucial role in various physiological processes. Sodium, potassium, chloride, and bicarbonate are important electrolytes. Electrolytes are essential for maintaining proper fluid balance, nerve function, muscle contraction, and other vital functions.Effects on Blood Volume and Pressure : As fluid is lost from the body, blood volume decreases. This reduction in blood volume can lead to decreased blood pressure, which can have various systemic effects. Reduced blood flow to vital organs can impair their function and lead to symptoms such as dizziness, lightheadedness, and rapid heart rate.Impact on Kidney Function : Dehydration can affect kidney function. The kidneys play a crucial role in maintaining fluid and electrolyte balance by filtering waste products and excess substances from the blood and excreting them as urine. In response to dehydration, the kidneys conserve water by reducing urine output. This can lead to concentrated urine and potentially contribute to the formation of kidney stones., Epidemiology : Yes, you can prevent dehydration by keeping track of how much fluid you drink. Drink water throughout the day, including at meals. Avoid soda, alcohol and caffeinated drinks. One way to make sure you’re properly hydrated is to check your pee. If it’s clear, pale or straw-colored, it’s OK. If it’s darker than that, keep drinking.,,To avoid dehydration, active people — people playing a sport or exercising — should drink at least 16 to 20 ounces (oz.) of fluids one to two hours before an outdoor activity. After that, you should consume six to 12 ounces of fluid every 10 to 15 minutes when you’re outside. When you’re finished with the activity, you should drink more. To replace what you’ve lost, drink at least another 16 to 24 ounces., Complications : seizures, Urinary disturbances, kidney dysfunction, HYPOVOLEMIA, Diagnostics : ultrasound, BUN / SR.CREATININE RATIO, Urine analysis, Differential diagnosis : Chronic hyponatremia, Diabetic Ketoacidosis, shock, disease description :  Dehydration results when water losses from the body exceed water replacement. It may be caused by failure to replace obligate water losses.Severe hydration is a medical emergency. It’s important to know how to recognize this advanced state of dehydration and know what to do.

Severe Dengue

Disease Name : Severe Dengue, Symptoms : headache : The dengue head- ache has some features in common with migraine, because it is most commonly throbbing and is usually associated with nausea, photophobia and phonophobia, loss of appetite : Appetite loss may be a symptom of dengue., respiratory symptoms : Respiratory symptoms, such as cough, sore throat, and rhinorrhea, can occur., skin rash : A flat, red rash may appear over most of the body 2 to 5 days after the fever starts. A second rash, which looks like the measles, appears later in the disease. Rash in dengue fever is a maculopapular or macular confluent rash over the face, thorax, and flexor surfaces, with islands of skin sparing. The rash typically begins on Day 3 and persists 2-3 days., weakness : Acute neuromuscular weakness may occur due to dengue infection. rash may appear over most of the body 2 to 5 days after the fever starts. A second rash, which looks like the measles, appears later in the disease., fever : Dengue fever begins with a sudden high fever, often as high as 105°F (40.5°C), 4 to 7 days after the infection., Bleeding disorders : Mild hemorrhagic manifestations (eg, petechiae, bleeding gums, epistaxis, menorrhagia, hematuria)., Body Ache : Severe dengue causes arthralgias, myalgias., retro-orbital pain : Pain behind the eyes., Signs : collapse : Circulatory collapse and multiorgan failure, called dengue shock syndrome, may develop rapidly 2 to 6 days after onset., flushed face : A sensitive and specific indicator of dengue fever., Treatment : immediate evaluation of vital signs and degrees of hemoconcentration, ,dehydration, and electrolyte imbalance. Close monitoring is essential for at least,48 hr because shock may occur or recur precipitously, usually several days after,the onset of fever, Patients who are cyanotic or have labored breathing should be,given oxygen.. Rapid intravenous replacement of fluids and electrolytes can,frequently sustain patients until spontaneous recovery occurs. Normal saline is,more effective than the more expensive Ringer lactated saline in treating shock.,When the pulse pressure is =10 mm Hg or when elevation of the hematocrit,persists after the replacement of fluids, plasma or colloid preparations are,indicated. Oral rehydration of children who are being monitored is useful.,Prophylactic platelet transfusions have not been shown to reduce the risk of,hemorrhaging or improve low platelet counts and may be associated with,adverse effects., Pathophysiology : Dengue Virus Infection : Dengue is caused by the dengue virus, which is transmitted to humans through the bite of infected Aedes mosquitoes, primarily Aedes aegypti. The virus enters the bloodstream and targets various cells, including immune cells and endothelial cells lining blood vessels.Immune Response and Cytokine Storm : The immune system responds to the dengue virus by releasing various signaling molecules called cytokines. In severe dengue, an excessive and uncontrolled immune response, often referred to as a "cytokine storm, " can occur. This immune response can lead to increased vascular permeability, leakage of fluid from blood vessels, and tissue damage.Vascular Leakage : One of the hallmarks of severe dengue is increased vascular permeability, which can result from the effects of cytokines on endothelial cells. As blood vessels become more permeable, plasma leaks into the surrounding tissues, leading to a decrease in circulating blood volume and potentially causing hypovolemic shock.Hemorrhage and Coagulopathy : Severe dengue can lead to abnormalities in blood clotting and coagulation. The virus and the immune response can affect platelet function, impair the clotting cascade, and lead to a tendency for bleeding. This can result in manifestations such as petechiae (small red or purple spots on the skin), ecchymosis (bruising), and internal bleeding.Organ Dysfunction : The immune response and vascular changes associated with severe dengue can impact the function of various organs, including the liver, heart, lungs, and kidneys. Liver involvement can lead to increased levels of liver enzymes and impaired blood clotting factors. Cardiovascular and pulmonary manifestations can contribute to shock and respiratory distress., Epidemiology : "About half of the worlds population is now at risk of dengue with an estimated 100–400 million infections occurring each year", variable, The two main ways to protect yourself from dengue are through avoiding mosquito bites and vaccination.,,1. Mosquito protection.,2. Dengue vaccine., Complications : Convulsions, prolonged asthenia, mental depression, ventricular extrasystoles, Diagnostics : PLATELET COUNT, alanine transaminase (ALT), ultrasound, CHEST X RAY, CT SCAN, HEMATOCRIT(PCV), AST (SGOT), tourniquet test, Differential diagnosis : Chikungunya, Influenza, Malaria, MEASLES, yellow fever, Zika Virus Disease, disease description : Dengue hemorrhagic fever and dengue shock syndrome comes under severe dengue.Dengue hemorrhagic fever occurs where multiple types of dengue virus are simultaneously or sequentially transmitted. It is endemic in tropical America, Asia, the Pacific Islands, and parts of Africa, where warm temperatures and the practices of water storage in homes plus outdoor breeding sites result in large, permanent populations of A. aegypti

Severe Digoxin Or Digitoxin Intoxication

Disease Name : Severe Digoxin Or Digitoxin Intoxication, Symptoms : Confusion : Digitoxin intoxication can lead to confusion., Gastrointestinal symptoms : Includes anorexia, nausea, vomiting, diarrhoea and abdominal pain., lethargy : Digitoxin intoxication causes a person to feel extremely lethargic., Signs : nan, Treatment : nan, Pathophysiology : Mechanism of Action : Both digoxin and digitoxin are cardiac glycosides, which means they have a direct effect on the hearts electrical and mechanical activity. They inhibit the sodium-potassium pump (Na+/K+ ATPase) in cardiac cells, leading to an increase in intracellular sodium levels. This sodium accumulation indirectly affects calcium levels within the cells, leading to increased intracellular calcium concentrations. This alteration in calcium dynamics enhances myocardial contractility and slows down electrical conduction in the heart.Toxic Effects on Heart Function : Arrhythmias : One of the most concerning effects of severe intoxication is the development of arrhythmias, such as ventricular tachycardia, ventricular fibrillation, and heart block. These arrhythmias can be life-threatening and contribute to hemodynamic instability.Bradycardia : While cardiac glycosides can enhance contractility, they can also slow down the heart rate, leading to bradycardia (slow heart rate). In severe intoxication, this bradycardia can be pronounced and contribute to inadequate cardiac output.Altered Conduction : Conduction abnormalities can occur due to the effects of cardiac glycosides on the electrical system of the heart. This can result in prolonged PR intervals and other electrocardiographic changes.Electrolyte Imbalance : Severe intoxication can lead to electrolyte imbalances, particularly low levels of potassium (hypokalemia), which can increase the risk of digoxin toxicity. Hypokalemia enhances the binding of digoxin to its target site on the sodium-potassium pump, increasing its toxic effects.Gastrointestinal Effects : Toxic levels of digoxin and digitoxin can affect the gastrointestinal system, leading to symptoms such as nausea, vomiting, and abdominal pain. Gastrointestinal disturbances can contribute to fluid and electrolyte imbalances., Epidemiology : 4.1%, Approximately 1% of patients with heart failure treated with digoxin develop toxicity. Additionally, 1% of adverse drug effects in patients greater than age 40 are due to digoxin toxicity; the incidence rises to greater than 3% in patients over age 85, variable, Complications : nan, Diagnostics : nan, Differential diagnosis : Bidirectional ventricular tachycardia, disease description : digoxin is a cardiac glycoside that historically was used for "dropsy" (edema) and is currently used as an inotrope to improve systolic dysfunction in patients with congestive heart failure (CHF) and as an atrioventricular nodal blocking agent for managing atrial tachydysrhythmias. Digoxin may improve the quality of life in CHF patients, but it does not confer a mortality benefit, and its narrow therapeutic index limits its utility. Digoxin toxicity can present acutely, by an intentional or accidental overdose (i.e., therapeutic misadventure), or chronically, such as when patients on digoxin develop an acute kidney injury. Similar toxicity can occur after exposure to cardioactive steroids in plants such as oleander, red squill, or dogbane or from animals such as Bufo toads

Severe Eosinophilic Asthma

Disease Name : Severe Eosinophilic Asthma, Symptoms : "chest tightness : The immune system can cause the airways to become inflamed and swollen when theyre around certain irritants. This can lead to chest tightness, pressure, or pain.", eosinophilia : People with eosinophilic asthma will have a high eosinophil count (at least 150 cells/ul but generally over 300 cells/ul). High eosinophils with asthma does not always mean that a person has eosinophilic asthma., Sinusitis : Chronic symptoms of sinus infections, such as stuffy nose, nasal drainage, and a reduced sense of smell., wheezing : Wheezing may result from localized or diffuse airway narrowing or obstruction from the level of the larynx to the small bronchi. The airway narrowing may be caused by bronchoconstriction, mucosal edema, external compression, or partial obstruction by a tumor, foreign body, or tenacious secretions., shortness of breath : Increased mucus in the airways can cause spasms of the bronchial tubes, making it difficult to breathe., cough : Most people with asthma have a dry cough, one that does not produce mucous. This happens when the airways constrict in response to an irritant and is a feature of asthma., Signs : nan, Treatment : nan, Pathophysiology : Eosinophilic Inflammation : In eosinophilic asthma, there is an excessive and chronic inflammatory response in the airways, driven by the presence of eosinophils. Eosinophils release inflammatory mediators, such as cytokines and leukotrienes, that contribute to airway inflammation and hyperresponsiveness.Allergic and Non-Allergic Triggers : Eosinophilic asthma can be triggered by both allergic and non-allergic factors. Allergic triggers, such as pollen, dust mites, and animal dander, can lead to an immune response involving eosinophils. Non-allergic triggers, such as viral infections and environmental pollutants, can also contribute to eosinophilic inflammation.Th2-Mediated Immune Response : Eosinophilic asthma is often associated with a Th2-mediated immune response. This type of immune response involves the production of specific cytokines, such as interleukin-4 (IL-4), interleukin-5 (IL-5), and interleukin-13 (IL-13), which promote eosinophil recruitment and activation.Airway Remodeling : Chronic inflammation in eosinophilic asthma can lead to structural changes in the airways, a process known as airway remodeling. This can involve thickening of the airway walls, increased mucus production, and changes in the smooth muscle surrounding the airways. Airway remodeling contributes to airflow limitation and increased susceptibility to asthma symptoms., Epidemiology : It is estimated that approximately 10% of all asthma is categorized as severe and that approximately 50% of all asthma is eosinophilic, approximately 10% of all asthma is categorized as severe, variable, Complications : nan, Diagnostics : ABG, Complete Blood Count CBC, ECG, X RAY CHEST, TRANSCUTANEOUS OXIMETRY, spirometry, Differential diagnosis : nan, disease description : Eosinophilic asthma is like other forms of asthma in that people with the condition suffer from inflamed airways, blocked by fluid and mucus and experience spasms that make it difficult to breathe.Unlike other kinds of asthma, however, eosinophilic asthma involves abnormally high levels of a particular type of white blood cell called eosinophils.Eosinophils are part of the immune system and help the body fight off infection. However, high levels of eosinophils can cause inflammation in the airways, affecting the sinuses and nasal passages as well as the lower airways.In general, as the level of eosinophils increases, inflammation and other symptoms of asthma become more severe.This form of asthma most often develops in people between the ages of 25 and 35. People with eosinophilic asthma usually do not suffer from allergies. This condition can be difficult to treat and may have a detrimental effect on an individual’s quality of life.

Severe Hyperuricaemia

Disease Name : Severe Hyperuricaemia, Symptoms : Gout : Gout, sometimes called gouty arthritis, occurs in about 20 percent of people with hyperuricemia. A rapid drop in uric acid levels can also trigger gout. Gout can appear as isolated attacks, or flares. Symptoms of gout may include severe pain in your joints, joint stiffness, difficulty moving affected joints, redness and swelling & misshapen joints., kidney stone : Uric acid crystals can cause a buildup of stones in your kidneys. Often, the stones are small and are passed in your urine. Sometimes, they can become too large to pass and block parts of your urinary tract. Symptoms of kidney stones include pain in abdomen, nausea, increased urge to urinate, pain when urinating, difficulty urinating, hematuria & foul-smelling urine., Signs : nan, Treatment : The initial goal in acute gouty arthritis is to provide symptomatic relief from pain. Indomethacin and other nonsteroidal anti-inflammatory drugs (NSAIDs) are the drugs of choice. NSAIDs are prescribed for approximately a 7- to 10-day course or until 3-4 days after all signs of inflammation have resolved. ,Probenecid, which is a uricosuric drug, inhibits the tubular reabsorption of filtered and secreted urate, thereby increasing urate excretion. The ideal candidates for probenecid therapy are those with a 24-hour urine uric acid excretion of less than 800 mg, no history of nephrolithiasis, and good kidney function (creatinine clearance >80 mL/min). The starting dose for probenecid is 250 mg twice a day, which can be increased gradually to a maximum daily dose of 3 g/d., Pathophysiology : Heres an overview of the pathophysiological factors contributing to severe hyperuricemia : Overproduction of Uric Acid : Genetic Factors : Genetic variations can lead to overproduction of uric acid due to alterations in enzymes involved in its synthesis. Mutations in the PRPS1, HPRT1, and G6PD genes, for example, can lead to excessive production of uric acid.Dietary Factors : Consumption of purine-rich foods, such as organ meats, seafood, and certain types of alcohol (especially beer), can contribute to increased uric acid production.Impaired Renal Excretion : Genetic Factors : Genetic mutations affecting renal transporters involved in uric acid excretion, such as URAT1 and ABCG2, can lead to reduced elimination of uric acid by the kidneys.Insulin Resistance : Conditions like obesity and insulin resistance have been associated with impaired renal excretion of uric acid. Insulin resistance can disrupt the normal function of renal transporters, leading to elevated uric acid levels.Purine Metabolism and Uric Acid Formation : Purine Breakdown : Uric acid is a byproduct of the breakdown of purines, which are nitrogen-containing compounds found in certain foods and in the bodys cells. Excessive purine breakdown, whether due to increased intake or increased cell turnover, can contribute to hyperuricemia.Alcohol Consumption : Alcohol, especially beer and spirits, can increase uric acid production and decrease its excretion by the kidneys, leading to hyperuricemia., Epidemiology : It is estimated as much as 21% of the general population and 25% of hospitalized patients have asymptomatic hyperuricemia, variable, The best way to prevent hyperuricemia is by following a diet and exercise plan that’s healthy for you. Limiting how often you eat or drink foods and beverages high in purines will help you keep your uric acid levels low. It will also help you maintain good overall health.,,Talk to your provider about which kinds of foods or drinks you should avoid, and how often it’s OK to have certain high-purine foods or drinks., Complications : nan, Diagnostics : URINE 24 Hour VOLUME, Renal ultrasonography, Joint aspiration, Differential diagnosis : Diabetic Ketoacidosis, Hemolytic anemia, Hodgkin lymphoma, Hyperparathyroidism, Hypothyroidism, Nephrolithiasis, disease description : Hyperuricemia is an elevated uric acid level in the blood. The normal upper limit is 6.8mg/dL, and anything over 7 mg/dL is considered saturated, and symptoms can occur.This elevated level is the result of increased production, decreased excretion of uric acid, or a combination of both processes.  Elevated uric acid can also be seen in accelerated purine degradation in high cell turnover states (hemolysis, rhabdomyolysis, and tumor lysis) and decreased excretion (renal insufficiency and metabolic acidosis). Hyperuricemia can lead to gout and nephrolithiasis. It has also been implicated as an indicator for diseases like metabolic syndrome, diabetes mellitus, cardiovascular disease, and chronic renal disease.

Severe Initial Genital Herpes

Disease Name : Severe Initial Genital Herpes, Symptoms : flu-like symptoms : During the first outbreak (called primary herpes), you may experience flu-like symptoms. These include body aches, fever, and headache., sore mouth : Cold sores around their lips, mouth or tongue. They may look crusty or like fluid-filled blisters., soreness : Sores on the genitals or around the anus., ulcer : Painful ulcers that form when blisters rupture and ooze or bleed., DISCHARGE : Discharge from the urethra & vagina., scabs : Scabs that form as the ulcers heal., Signs : nan, Treatment : nan, Pathophysiology : nan, Epidemiology : Nationwide, 11.9 % of persons aged 14 to 49 years have HSV-2 infection, 572, 000 new genital herpes infections in the United States in a single year, variable, "Prevention of genital herpes is the same as preventing other sexually transmitted infections.,,Have one long-term sexual partner who has been tested for STIs and isnt infected.,Use a condom or dental dam during sexual activity. These reduce the risk of disease, but they dont prevent all skin-to-skin contact during sex.,Dont have sex when a partner with genital herpes has symptoms.", Complications : nan, Diagnostics : nan, Differential diagnosis : candidiasis, Chancroid, Granuloma Inguinale, Herpes Zoster, Syphilis, disease description : Genital herpes is a common sexually transmitted infection (STI). The herpes simplex virus (HSV) causes genital herpes. Genital herpes can often be spread by skin-to-skin contact during sexual activity.Some people infected with the virus may have very mild symptoms or no symptoms. They can still able to spread the virus. Other people have pain, itching and sores around the genitals, anus or mouth.There is no cure for genital herpes. Symptoms often show up again after the first outbreak. Medicine can ease symptoms. It also lowers the risk of infecting others. Condoms can help prevent the spread of a genital herpes infection.

Severe Pneumonia/very Severe Pneumonia

Disease Name : Severe Pneumonia/very Severe Pneumonia, Symptoms : chest indrawing : Chest indrawing occurs because of the contraction of the thoracic accessory muscles(6). Any condition that causes either reduced lung compliance, like pneumonia causes chest indrawing., chest pain : Sharp or stabbing chest pain that gets worse when you breathe deeply or cough., Gastrointestinal symptoms : Includes nausea, vomiting or diarrhea., fever : Fever may rise as high as a dangerous 105 degrees F, with profuse sweating and rapidly increased breathing and pulse rate., cough with sputum : A classic sign of bacterial pneumonia is a cough that produces thick, blood-tinged or yellowish-greenish sputum with pus., mental changes : Pneumonia can also cause confusion, forgetfulness, or a sudden change in mental ability in adults over 65., Signs : convulsion : Pneumonia is considered to be a common complication of generalized tonic–clonic seizures (GTCS) and is caused by the aspiration of secretions as airway protective reflexes are inhibited by the seizure., stridor : Stridor is a noisy or high-pitched sound with breathing. It is a sign that the upper airway is partially blocked. It may involve the nose, mouth, sinuses, voice box (larynx), or windpipe (trachea)., Treatment : medication : Meropenem , Piperacillin and tazobactum , Amoxicillin and Clavulanic acid , Chloramphenicol , VAP and HaP is in accordance with the ATS/IDSA guidelines. It is much more prolonged, complicated, and involves the use of broad-spectrum antibiotics as compared to the management of CAP, Pathophysiology : Pathologically, lobar pneumonia is the acute exudative inflammation of a lung lobe. It has the following four advanced stages if left untreated;Congestion :  In this stage, pulmonary parenchyma is not fully consolidated, and microscopically, the alveoli have serous exudates, pathogens, few neutrophils, and macrophages.Red hepatization :  In this stage,  the lobe becomes consolidated, firm, and liver-like. Microscopically, there is fibrin and serous exudate, pathogens, neutrophils, and macrophages. The capillaries are congested, and the alveolar walls are thickened.Gray hepatization :  The lobe is still liver-like in consistency but gray in color due to suppurative and exudate-filled alveoli.Resolution :  After a week, it starts resolving as lymphatic drainage or a productive cough clears the exudate., Epidemiology : Pneumonia accounts for 14% of all deaths of children under 5 years old, killing 740 180 children in 2019, average, The best way to prevent pneumonia is to get vaccinated against bacteria and viruses that commonly cause it. There are also everyday precautions you can take to help reduce your risk of pneumonia.,,Vaccines for pneumonia - There are two types of vaccines (shots) that prevent pneumonia caused by pneumococcal bacteria. ,1. Pneumococcal vaccines. ,2. Vaccinations against viruses : As certain viruses can lead to pneumonia, getting vaccinated against COVID-19 and the flu can help reduce your risk of getting pneumonia.,3. Childhood vaccinations : If you have children, ask their healthcare provider about other vaccines they should get., Complications : Meningitis, respiratory failure, sepsis, metastatic disease, empyema, Lung Fibrosis, Diagnostics : BLOOD CULTURE test, ABG, C- REACTIVE PROTEIN TEST, Complete Blood Count CBC, Erythrocyte Sedimentation Rate (ESR), X RAY CHEST, CULTURE OF BAL(BRONCHOALVEOLAR LAVAGE) FLUID, CHEST X RAY, CT SCAN, CT PULMONARY ANGIOGRAM, Differential diagnosis : Asthma, Atelectasis, BRONCHIECTASIS, BRONCHIOLITIS, Epiglottitis, disease description : Pneumonia has been defined as an infection of the lung parenchyma. Rather than looking at it as a single disease, health care professionals must remember that pneumonia is an umbrella term for a group of syndromes caused by a variety of organisms resulting in varied manifestations and sequelaeAny pneumonia acquired outside of a hospital in a community setting. Any pneumonia acquired 48 hours after being admitted in an inpatient setting such as a hospital and not incubating at the time of admission is considered as HAP. This classification helps clear the confusion surrounding the terms healthcare-associated and hospital-acquired pneumonia.

Sexual Problem

Disease Name : Sexual Problem, Symptoms : libido : Lack of interest in or desire for sex., Sexual dysfunction : In females, the symptoms are inability to achieve orgasm, inadequate vaginal lubrication before and during intercourse & inability to relax the vaginal muscles enough to allow intercourse., Sexual dysfunction : In males, the symptoms are erectile dysfunction, absent or delayed ejaculation despite enough sexual stimulation & inability to control the timing of ejaculation., DYSPAREUNIA : Pain with intercourse., Signs : nan, Treatment : nan, Pathophysiology : Erectile Dysfunction (ED) : Physiological Factors : ED can result from impaired blood flow to the penis, often due to conditions such as atherosclerosis (narrowing of blood vessels), hypertension, diabetes, and hormonal imbalances.Neurological Factors : Conditions affecting the nerves that control penile erection, such as multiple sclerosis or spinal cord injuries, can contribute to ED.Psychological Factors : Anxiety, stress, depression, and performance anxiety can interfere with the neural signals and hormonal pathways necessary for achieving and maintaining an erection.Premature Ejaculation (PE) : Neurobiological Factors : Altered serotonin levels in the brains neural circuits that control ejaculation can lead to PE. Serotonin plays a role in delaying ejaculation, and low levels can contribute to rapid ejaculation.Psychological Factors : Anxiety, stress, and relationship issues can lead to heightened arousal and decreased control over ejaculation.Female Sexual Dysfunction (FSD) : Physiological Factors : FSD can result from hormonal imbalances (e.g., menopause), gynecological conditions, and chronic illnesses affecting sexual function.Psychological Factors : Emotional factors like stress, depression, anxiety, and body image concerns can negatively impact sexual desire and arousal.Hypoactive Sexual Desire Disorder (HSDD) : Hormonal Factors : HSDD may be related to hormonal imbalances, such as low levels of testosterone, estrogen, or other hormones involved in sexual desire.Neurological Factors : Brain neurotransmitters and pathways related to sexual desire, such as dopamine and norepinephrine, can play a role in HSDD.Psychological Factors : Psychological and emotional factors, including stress, depression, and interpersonal conflicts, can contribute to reduced sexual desire.Orgasmic Disorders : Physiological Factors : Conditions affecting the nerves, blood flow, or pelvic muscles necessary for orgasm can lead to orgasmic disorders.Psychological Factors : Stress, anxiety, past traumas, and relationship issues can interfere with the ability to achieve orgasm.Vaginismus and Dyspareunia : Vaginismus involves involuntary muscle contractions in the vaginal wall, making penetration painful or impossible.Dyspareunia refers to painful intercourse.Both conditions can be influenced by psychological factors, past traumatic experiences, and physical factors such as infections, hormonal imbalances, or anatomical abnormalities.Interplay of Factors : Many sexual problems have complex interactions between physiological, psychological, and interpersonal factors. For example, psychological stress can lead to hormonal changes that affect sexual function, while physical conditions can trigger psychological distress.Its important to note that sexual problems can have a significant impact on ones quality of life and overall well-being. Treatment often involves a multidisciplinary approach, including medical interventions (such as medications, hormone therapy, or surgery), psychotherapy, and addressing underlying psychological or relational issues. Open communication with healthcare professionals and, if applicable, with a partner, can be key to understanding and addressing the pathophysiology of sexual problems., Epidemiology : 15.77%, Sexual dysfunctions are highly prevalent, affecting about 43% of women and 31% of men., variable, "Some types of sexual dysfunction cannot be prevented. However, you may be able to reduce your risk of certain types of dysfunction by working to prevent diseases that can lead to dysfunction. Adopting certain healthy habits may reduce your risk. For example : ,,Stop smoking or dont start,Get regular exercise, including aerobic exercise,Maintain a healthy weight,Eat a well-balanced diet,Limit alcohol intake to a maximum of two drinks per day,Dont use illegal drugs,If you have chronic diseases, like heart disease or diabetes, take steps to control your condition and improve your overall health,If you are taking medications that can cause sexual dysfunction , ask your doctor whether you can switch to another drug that doesnt have a side effect of sexual dysfunction. (Dont ever stop taking prescribed medication without your doctors approval.)", Complications : nan, Diagnostics : nan, Differential diagnosis : DEPRESSION, hypogonadism, loss of Libido, disease description : Sexual dysfunction is a problem that can happen during any phase of the sexual response cycle. It prevents you from experiencing satisfaction from sexual activity.The sexual response cycle traditionally includes excitement, plateau, orgasm and resolution. Desire and arousal are both part of the excitement phase of the sexual response. It’s important to know women don’t always go through these phases in order.

Shigellosis

Disease Name : Shigellosis, Symptoms : diarrhea : Diarrhea, which can be watery, bloody and/or contain mucus or pus., Abdominal Pain : Shigellosis causes a temperature over 102°F., Abdominal Pain : Shigellosis causes intense abdominal pain., vomiting : Vomiting can occur but is not common., Signs : nan, Treatment : medication : Azithromycin , Ciprofloxacin , Antimotility drugs such as loperamide, paregoric or diphenoxylate are not recommended for patients with Shigella infection as they may prolong the infection and increase the shedding of the organism, Pathophysiology : Once ingested,  Shigella enters the small intestine and multiplies then enters the large intestine. Shigella causes cell injury and resulting complications by direct invasion of colonic mucosa and production of enterotoxins. In the large intestine, it invades using transcytosis and transports through basolateral epithelium using M cells which are mainly responsible for immune activation of intestinal lymphoid tissue by antigen recognition .Following transcytosis, it induces macrophages and cellular apoptosis .This results in the release of inflammatory cytokines such as IL-1 and IL-18 which results in intestinal inflammation and subsequent activation of the innate immune system. Shigella is released from the macrophages after following apoptosis and inflammation. It continues to invade the adjacent epithelium and the immune system by using the intercellular actin polymerization process .Another mechanism for cell injury by Shigella is through the production of enterotoxin 1 and 2 which plays a part in impaired fluid and nutrient absorption causing Shigella-associated diarrhea., Epidemiology : 99% of cases occurring in the developing world and the highest prevalences in the most impoverished areas, where personal and general hygiene is below standard, good, You can lessen your risk of getting or spreading shigellosis in the following ways : ,,Wash your hands with soap and water thoroughly and often, especially before and after eating, after using the bathroom and changing diapers, before preparing food, and after coming into contact with an infected person.,Wash foods well and cook them well.,Avoid swallowing water in pools, lakes or ponds.,Throw away soiled diapers in a lined garbage can with a lid.,Follow safe food and water instructions when traveling in other countries.,Wait for a week after your partner has recovered from diarrhea before engaging in sexual activities.,Researchers are working on vaccines against Shigella bacteria but haven’t developed one yet., Complications : rectal bleeding, seizures, sepsis, severe diarrhoea, Diagnostics : BLOOD CULTURE test, Complete Blood Count CBC, STOOL CULTURE, LIVER FUNCTION TEST LFT, kidney function test KFT, MICROSCOPIC AGGLUTINATION TEST, PCR, ELISA, STOOL EXAMINATION, Differential diagnosis : aeromonas infection, Clostridium difficile infection, infection, infection, TYPHOID FEVER, disease description : Shigella is a non-spore-forming, gram-negative bacterium that, unlike E. coli, is nonmotile and does not produce gas from sugars, decarboxylate lysine, or hydrolyze arginine. Some serovars produce indole, and occasional strains utilize sodium acetate. Shigella dysenteriae, Shigella flexneri, Shigella boydii, and Shigella sonnei (serogroups A, B, C, and D, respectively) can be differentiated on the basis of biochemical and serologic characteristics. The human intestinal tract represents the major reservoir of Shigella, which is also found (albeit rarely) in the higher primates. Because excretion of shigellae is greatest in the acute phase of disease, the bacteria are transmitted most efficiently by the fecal–oral route via hand carriage; however, some outbreaks reflect foodborne or waterborne transmission. In impoverished areas, Shigella can be transmitted by flies. Shigellosis can also be transmitted sexually.

Shock

Disease Name : Shock, Symptoms : altered sensorium : Altered mental status is a common clinical sign of systemic hypoperfusion in cardiogenic shock and is associated with poor outcome. It is also associated with several biochemical findings that reflect inadequate tissue perfusion, of which low arterial pH is independently associated with altered mental status., chest pain : Because cardiogenic shock usually results from a severe heart attack, people may also experience heart attack symptoms. These include : Pressure, fullness or a squeezing pain in the center of your chest that lasts for more than a few minutes., "Hypoglycaemia : Hypoglycemic shock, occurs when a persons blood sugar drops extremely low.", polydipsia : Shock makes a person feel extremely thirsty., septic shock : Septic shock is a life-threatening condition that happens when your blood pressure drops to a dangerously low level after an infection., Oliguria : Oliguria is a frequent manifestation of shock. The decreased urine output is not simply due to hypoperfusion and dysfunction, but also a renal compensatory response to decreased blood flow, Neurological symptoms : You may also experience some neurological symptoms like confusion, agitation, or lethargy (drowsiness), which occur due to decreased blood flow to the brain., Signs : delayed capillary refilling time : CRT may or may not be prolonged in patients with class II shock but will undoubtedly be prolonged in both class III and IV shock., Tachycardia : Tachycardia is typically the first abnormal vital sign of hemorrhagic shock. As the body attempts to preserve oxygen delivery to the brain and heart, blood is shunted away from extremities and nonvital organs. This causes cold and modeled extremities with delayed capillary refill., poor peripheral pulses : Patients with decompensated shock have feeble or absent peripheral pulse., tachypnea (rapid breathing) : There will be tachypnea, but in hypovolemic shock the effort of breathing is only mildly increased., comatose patients, Hypotension : In the later stages of shock due to progressive volume depletion, cardiac output also decreases and manifest as hypotension., Treatment : medication : Dobutamine , Noradrenaline/Norepinephrine, Phenylephrine , FLUID & PROPER HYDRATION, Administration of inotropic or chronotropic,agents, Pathophysiology : Hypoxia at the cellular level causes a series of physiologic and biochemical changes, resulting in acidosis and a decrease in regional blood flow, which further worsens the tissue hypoxia. In hypovolemic, obstructive, and cardiogenic shock, there is a decrease in cardiac output and decreased oxygen transport. In distributive shock, there is decreased peripheral vascular resistance and abnormal oxygen extraction. Excitement is a spectrum of physiologic changes, ranging from early stages, which are reversible to the final stages, which are irreversible with multiorgan failure and death. Generally, shock has the following three stages : Pre-shock or compensated shock - As the name suggests, this stage is characterized by compensatory mechanisms to counter the decrease in tissue perfusion, including tachycardia, peripheral vasoconstriction, and changes in systemic blood pressure Shock - During this stage, most of the classic signs and symptoms of shock appear due to early organ dysfunction, resulting from the progression of the pre-shock stage as the compensatory mechanisms become insufficient. End-organ dysfunction - This is the final stage, leading to irreversible organ dysfunction, multiorgan failure, and death In hypovolemic, obstructive, and cardiogenic shock, there is a decrease in cardiac output and decreased oxygen transport. In distributive shock, there is decreased peripheral vascular resistance and abnormal oxygen extraction. Excitement is a spectrum of physiologic changes, ranging from early stages, which are reversible to the final stages, which are irreversible with multiorgan failure and death. Generally,  shock has the following three stages : Pre-shock or compensated shock - As the name suggests, this stage is characterized by compensatory mechanisms to counter the decrease in tissue perfusion, including tachycardia, peripheral vasoconstriction, and changes in systemic blood pressureShock - During this stage, most of the classic signs and symptoms of shock appear due to early organ dysfunction, resulting from the progression of the pre-shock stage as the compensatory mechanisms become insufficient.End-organ dysfunction - This is the final stage, leading to irreversible organ dysfunction, multiorgan failure,  and death, Epidemiology : 76 per 100 000 person-years, POOR, "Dont smoke, and avoid secondhand smoke. If you smoke, the best way to reduce your heart attack risk is to quit.,Maintain a healthy weight,Eat less cholesterol and saturated fat.,Use less salt,Cut back on sugar.,Limit alcohol,Exercise regularly. Exercise can lower your blood pressure and improve the overall health of your blood vessels and heart. Get at least 150 minutes of moderate aerobic activity or 75 minutes of vigorous aerobic activity a week", Complications : Acute Renal Failure, cardiovascular collapse, Severe Acute Respiratory Syndrome (SARS), Coagulopathy, MULTIORGAN FAILURE, Diagnostics : Arterial Blood Gas Analysis(ABG), Complete Blood Count CBC, ECG, X RAY CHEST, CT SCAN, Differential diagnosis : Acute Pancreatitis, Adrenal crisis, Anaphylaxis, Arrhythmias, heart failure, Hemolytic Uremic Syndrome, Myocardial infarction, Poisoning, disease description : Shock is a life-threatening manifestation of circulatory failure.  Circulatory shock leads to cellular and tissue hypoxia resulting in cellular death and dysfunction of vital organs. Effects of shock are reversible in the early stages, and a delay in diagnosis and/or timely initiation of treatment can lead to irreversible changes, including multiorgan failure (MOF) and death.

Short Chain 3-hydroxyacyl-coa Dehydrogenase Deficiency

Disease Name : Short Chain 3-hydroxyacyl-coa Dehydrogenase Deficiency, Symptoms : Gastrointestinal symptoms : Initial signs and symptoms of this disorder typically occur during infancy or early childhood and can include poor appetite, vomiting, diarrhea., Hypoglycaemia : Short chain 3-Hydroxyacyl-CoA dehydrogenase deficiency cause low blood glucose., seizures : Individuals with 3-hydroxyacyl-CoA dehydrogenase deficiency are also at risk for complications such as seizures., hypotonia : Affected individuals have muscle weakness., Signs : nan, Treatment : medication : L-Carnitine , Your baby’s primary doctor may work with a metabolic doctor to care for your child. Your doctor may also suggest that you meet with a dietician familiar with M/SCHADD.,,Certain treatments may be advised for some children but not others. When necessary, treatment is usually needed throughout life. The following are treatments that may be recommended for some children with SCHADD.,1- Avoid going a long time without food.,2-Sometimes a low fat, high carbohydrate food plan is recommended.,3- L-carnitine supplementaion, Pathophysiology : Mutations in the HADH gene lead to inadequate levels of an enzyme called 3-hydroxyacyl-coenzyme A dehydrogenase. Medium-chain and short-chain fatty acids cannot be metabolized and processed properly without sufficient levels of this enzyme. As a result, these fatty acids are not converted to energy, which can lead to characteristic features of this disorder, such as lethargy and hypoglycemia. Medium-chain and short-chain fatty acids or partially metabolized fatty acids may build up in tissues and damage the liver, heart, and muscles, causing more serious complications.This condition is inherited in an autosomal recessive pattern, which means two copies of the gene in each cell are altered. Most often, the parents of an individual with an autosomal recessive disorder each carry one copy of the altered gene but do not show signs and symptoms of the disorder., Epidemiology : less than ten cases described worldwide., Treatment may improve the long-term prognosis., "Cant be prevented since it is is an inherited condition.", Complications : seizures, Diagnostics : Protein, Differential diagnosis : Cardiomyopathy, Hypoglycemia, metabolic acidosis, Primary Carnitine Deficiency, Systemic Primary Carnitine Deficiency, disease description : 3-hydroxyacyl-CoA dehydrogenase deficiency is an inherited condition that prevents the body from converting certain fats to energy, particularly during prolonged periods without food (fasting). Short-chain 3-hydroxyacyl-CoA dehydrogenase (HADH, SCHAD) deficiency (OMIM #231530) represents a recently described disorder of mitochondrial fatty acid beta-oxidation, with less than ten cases described worldwide. 

Short Qt Syndrome

Disease Name : Short Qt Syndrome, Symptoms : palpitations : Heart palpitations occurs in almost 1 in 3 people., sudden cardiac death : For some people (around 2 in 5), the first sign of SQTS unfortunately is cardiac arrest or sudden cardiac death, an unexpected stoppage of heart function due to ventricular fibrillation or ventricular tachycardia, both dangerous arrhythmias of the bottom chambers (ventricles) of the heart., Signs : atrial fibrillation : About 4 in 5 people with SQTS have atrial fibrillation (AFib). Atrial fibrillation is an irregular heart rhythm where the electrical signals in your heart’s top chambers (atria) don’t fire properly., syncope : Syncope occurs in about 1 in 4 people., Treatment : medication : Amiodarone , Quinidine , Propranolol , The treatment for short QT syndrome is aimed at preventing abnormal heart rhythms and reducing the risk of sudden cardiac death. It has been difficult to experimentally test potential treatments as the condition is very rare, so the evidence for treatment effectiveness comes largely from consensus opinion. In addition to treating the person identified as having the condition, screening of family members may be recommended., Pathophysiology : Mutations in the KCNH2, KCNJ2, and KCNQ1 genes can cause short QT syndrome. These genes provide instructions for making channels that transport positively charged atoms (ions) of potassium out of cells. In cardiac muscle, these ion channels play critical roles in maintaining the hearts normal rhythm. Mutations in the KCNH2, KCNJ2, or KCNQ1 gene increase the activity of the channels, which enhances the flow of potassium ions across the membrane of cardiac muscle cells. This change in ion transport alters the electrical activity of the heart and can lead to the abnormal heart rhythms characteristic of short QT syndrome. Some affected individuals do not have an identified mutation in the KCNH2, KCNJ2, or KCNQ1 gene. Changes in other genes that have not been identified may cause the disorder in these cases., Epidemiology : At least 70 cases have been identified worldwide since the condition was discovered in 2000., The incidence of SQTS in the general population remains unclear., Variable, There’s no way to prevent SQTS. Because it’s genetic, you can’t control whether you get it.,,If you have SQTS, it’s important to see a cardiologist (heart doctor) regularly. A cardiologist monitors your heart health. They can help you reduce your risk of severe SQTS complications, such as sudden cardiac death., Complications : Arrhythmias, Cardiac arrest, syncope, Diagnostics : Coronary Angiography, ECG, GENETIC TESTING, Differential diagnosis : sudden death, disease description : Short QT syndrome (SQTS) is an extremely rare genetic disorder that causes an irregular heart rhythm. In SQTS, your heart muscle doesn’t take as long as usual to recover between beats. The part of your heartbeat called the QT interval is irregularly short.SQTS can cause arrhythmias in which you may feel dizziness, fainting or heart palpitations. They may even cause cardiac arrest (your heart stops) and sudden cardiac death, in severe cases. If you have signs of SQTS, it’s essential to see a healthcare provider for treatment.

Sialadenitis

Disease Name : Sialadenitis, Symptoms : Salivation : Decreased saliva (a symptom of both acute and chronic sialadenitis)., fever : The gland may sometimes become infected, leading to fever., Salivary gland enlargement : Enlargement, tenderness and discoloration of one or more salivary glands., Signs : nan, Treatment : Acute sialadenitis : Most cases receive treatment with conservative medical management; this includes hydration, warm compresses, and massage, pain relief with analgesics (e.g., NSAIDs), sialogogues. Empiric antibiotic therapy starts with amoxicillin/clavulanate or clindamycin., Chronic sialadenitis : Medical management is with hydration, oral hygiene, pain relief, sialogogues. In cases of infection, broad-spectrum antibiotics are added. In the case of sialolithiasis, salivary gland stone removal should take place, using interventional sialendoscopy or direct surgical removal., Pathophysiology : Major risk factors for sialadenitis include reduced salivary secretion and duct obstruction. Hyposecretion of saliva can occur in dehydrated people, postoperative patients, immunocompromised, and undernourished. Medications that decrease salivary flow like antihistaminics, diuretics, beta-blockers can predispose to sialadenitis. Decreased salivary production can occur in patients with a history of radiation to the head and neck region, long-standing xerostomia (e.g., Sjogren syndrome), and those with chronic illness. Salivary duct obstruction is usually due to sialolithiasis, ductal stricture, ductal foreign body, and external compression of the duct .Other risk factors include old age, poor oral hygiene, postoperative state, intubation, use of anticholinergic agents, Stasis of salivary flow through the ducts and parenchyma promotes acute suppurative infection. Retrograde contamination of salivary ducts and parenchymal tissues by bacteria inhabiting the oral cavity is common. Usually, submandibular sialadenitis is polymicrobial. Staphylococcus aureus is the most frequently isolated organism. Other bacterias include Streptococcus viridans,  Haemophilus influenza,  Enterobacteriaceae spp, and anaerobes like Prevotella,  Fusobacterium spp,  Peptostreptococcus. Viral sialadenitis can result from mumps, parainfluenza, Epstein-Barr virus, HIV., Epidemiology : exact prevalence of submandibular sialadenitis is not clear. Submandibular gland sialadenitis accounts for about 10% of all cases of sialadenitis, variable, You may not be able to prevent sialadenitis completely. But there are a few things you can do to reduce your risk : ,,Drink plenty of water.,Practice good oral hygiene.,Eat a diet that’s healthy for you.,Avoid smoking and using other tobacco products., Complications : abscess, recurrence, Diagnostics : Cranial Ultrasonography, MRI, CT SCAN, CT SCAN, Differential diagnosis : Cat scratch disease, CIRRHOSIS, Mumps, Sarcoidosis, Sjogren’s Syndrome, TUBERCULOSIS, disease description : Submandibular glands are major paired salivary glands. It is located in the submandibular triangle covered by the investing layer of deep cervical fascia. Mylohyoid muscle separates the superficial and deep lobe of the glands. Submandibular glands drain into the mouth via Wharton’s duct, which courses between the sublingual gland and hyoglossus muscle; it opens through a small opening lateral to the frenulum on the floor of the mouth. Submandibular glands are major paired salivary glands. It is located in the submandibular triangle covered by the investing layer of deep cervical fascia. Mylohyoid muscle separates the superficial and deep lobe of the glands. Submandibular glands drain into the mouth via Wharton’s duct, which courses between the sublingual gland and hyoglossus muscle; it opens through a small opening lateral to the frenulum on the floor of the mouth.

Sialidosis

Disease Name : Sialidosis, Symptoms : CNS disturbances : Individuals with sialidosis type I also experience muscle twitches (myoclonus), difficulty coordinating movements (ataxia), leg tremors, and seizures. The myoclonus worsens over time, causing difficulty sitting, standing, or walking., coarse facial features : Distinctive “coarse” facial features associated with sialidosis type II may include a high forehead, flattened bridge of the nose, a long groove on the upper lip (long philtrum), upturned nostrils (anteverted nares), and puffy eyelids. Some affected children may have overgrowth of the gums (gingival hypertrophy) and an abnormally large tongue (macroglossia)., gait disturbances : Initially, affected individuals experience problems walking., eye problem : Affected individuals may experience loss of clarity of vision (visual acuity) and may develop impaired color vision and night blindness. Rapid, involuntary eye movements (nystagmus) and clouding (opacity) of the cornea may also occur., BONE DEFORMITY : Sialidosis causes dysostosis multiplex which is a rare disease of congenital origin characterized by chondrodystrophic skeletal changes and deposition of a lipid-like substance in many of the body tissues. Bone deformities associated with dysostosis multiplex include premature closure (fusion) of the fibrous joints (sutures) between certain bones of the skull, a thickened skullcap (calvaria), an enlarged skull, widely spaced teeth, thickened collarbones (clavicles), and abnormalities of the ribs, pelvic bones, certain long bones and other bones of the body., Signs : cherry red spot : Signs of sialidosis type I include the development of distinct red spots in the eyes known as cherry-red macules. Cherry red macules are spots that form on the retina, the thin membrane that lines the back of the eyes. The retinas sense light and convert it to nerve signals, which are then relayed to the brain through the optic nerve., hepatosplenomegaly : Children with sialidosis type II may develop an abnormally enlarged liver or splen., Treatment : There is no specific therapy for sialidosis. Treatment is directed toward the specific symptoms that are apparent in each individual. Anti-seizure medications (anti-convulsants) may be used to treat myoclonic seizures, but are not always effective.,,Genetic counseling may be of benefit for affected individuals and their families. Other treatment is symptomatic and supportive., Pathophysiology : The NEU1 gene contains instructions for creating (encoding) an enzyme known as neuraminidase (alpha-neuraminidase) which is necessary for the proper breakdown (metabolism) of certain glycoproteins, substances that play various vital roles in the body. Glycoproteins are proteins that contain oligosaccharides, which are long sugar chains. Without proper levels of functional neuraminidase, oligosaccharides abnormally accumulate in and damage various tissues and organs of the body. Mutations of the NEU1 gene result in the lack of production of the neuraminidase enzyme or the production of a defective, inactive form of the enzyme., Epidemiology : The prevalence of sialidosis (types 1 and 2 combined) has been estimated at approximately 1/5, 000, 000-1/1, 500, 000 live births., rare, variable, This condition is inherited in an autosomal recessive pattern. It occurs because of a genetic mutation in the NEU1 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 : Life threatening infections, Diagnostics : MRI, Urine analysis, full thickness skin biopsy, Differential diagnosis : Galactosialidosis, disease description : Sialidosis is a severe inherited disorder that affects many organs and tissues, including the nervous system. This disorder is divided into two types, which are distinguished by the age at which symptoms appear and the severity of features.Sialidosis type I, also referred to as cherry-red spot myoclonus syndrome, is the less severe form of this condition. Sialidosis type II, the more severe type of the disorder, is further divided into congenital, infantile, and juvenile forms

Sialolethiases

Disease Name : Sialolethiases, Symptoms : dysphagia : Dysphagia is presented in extended lesions., facial pain : Facial pain or swelling, usually under your jaw or around your ear., trismus : Trismus refers to muscle spasms in your temporomandibular joint., Xerostomia : Sialolithiasis causes dry mouth., lump : A painful lump under your tongue., Signs : intermittent swelling of the involved gland : Most patients present with pain, swelling, and tenderness of the involved salivary gland., Treatment : Management of sialolithiasis should begin with conservative measures, including massaging the salivary gland, nonsteroidal anti-inflammatory drugs (NSAIDs), and sialogogues. Signs of infection, including cervical adenopathy, purulent discharge from the salivary ducts, or erythema surrounding the salivary ducts, indicate the need for antibiotic therapy, Stones in peripheral part of submandibular or parotid ,ducts can be removed intraorally, while those at the hilum or in the parenchyma require excision of the gland., Pathophysiology : Calculi may form in the ducts of submandibular or parotid glands. They are formed by the deposition of calcium phosphate on the organic matrix of mucin or cellular debris. About 90% of the stones are seen in the submandibular but only 10% in the parotid. Stones may form in the duct or parenchyma of the gland. The presenting feature is intermittent swelling of the involved gland, and pain due to obstruction to outflow of saliva. Sometimes, a stone is visible at the duct opening or can be palpated intraorally. About 80% of the stones are radio-opaque and can be seen on appropriate X-rays Sialography may be required for radiolucent stones. Stones in peripheral part of submandibular or parotid ducts can be removed intraorally, while those at the hilum or in the parenchyma require excision of the gland. Diagnosis of radiolucent stones is a challenge. If palpation does not reveal a stone, contrast sialography, ultrasound, magnetic resonance sialography or digital subtraction sialography can be attempted. Recently sialoendoscopy has been used both to diagnose and treat such stones., Epidemiology : The incidence of sialolithiasis is estimated at 1 in 10000 to 1 in 30000 individuals., GOOD, Complications : atrophy, Bacterial infection, Fibrosis, Diagnostics : X Ray skull, MRI, CT SCAN, SIALOGRAPHY, Differential diagnosis : CELLULITIS, Herpes Zoster, neoplasms, disease description : Calculi may form in the ducts of submandibular or parotid glands. They are formed by the deposition of calcium phosphate on the organic matrix of mucin or cellular debris. About 90% of the stones are seen in the submandibular but only 10% in the parotid. Stones may form in the duct or parenchyma of the gland..

Sickle Cell Anemia

Disease Name : Sickle Cell Anemia, Symptoms : delayed growth and sexual development : Red blood cells provide the body with the oxygen and nutrients needed for growth. A shortage of healthy red blood cells can slow growth in infants and children and delay puberty in teenagers., infections : Sickle cells can damage the spleen, increasing vulnerability to infections. Infants and children with sickle cell anemia commonly receive vaccinations and antibiotics to prevent potentially life-threatening infections, such as pneumonia., swelling : The swelling is caused by sickle-shaped red blood cells blocking blood circulation in the hands and feet., Pain : Periodic episodes of extreme pain, called pain crises, are a major symptom of sickle cell anemia. Pain develops when sickle-shaped red blood cells block blood flow through tiny blood vessels to your chest, abdomen and joints., vision abnormalities : Tiny blood vessels that supply the eyes can become plugged with sickle cells. This can damage the retina — the portion of the eye that processes visual images — and lead to vision problems., Signs : "anemia : Sickle cells break apart easily and die. Red blood cells usually live for about 120 days before they need to be replaced. But sickle cells typically die in 10 to 20 days, leaving a shortage of red blood cells (anemia). Without enough red blood cells, the body cant get enough oxygen and this causes fatigue.", Treatment : medication : Hydroxycarbamide (Hydroxyurea), Intubation and mechanical ventilation may be required in whom cerebrovascular accidents have occurred, or with acute chest syndrome. Exchange blood transfusions are indicated in cases of cerebrovascular accidents and acute chest syndrome., Hydration and analgesia are the mainstays of treatment in a pain crisis. Narcotic analgesia is most frequently used. Hydration is corrected orally if the patient is not vomiting and can tolerate oral fluids. In severe dehydration, intravenous fluids are required. Care is taken not to overload the patient and accurate intake-output monitoring should be ensured. Blood transfusion is useful in patients in aplastic crisis and acute sequestration crisis. Oxygen supplementation is of benefit if the patient has hypoxia., Pathophysiology : Sickle cell anemia is characterized by two major components : Hemolysis and vaso-occlusive crises (VOC). The defect in the beta-globin gene makes the sickle hemoglobin (HbS) molecule susceptible to converting into rigid, elongated polymers in a deoxygenated state. The sickling process is cyclical initially, where sickle erythrocytes oscillate between the normal biconcave shape and the abnormal crescent shape (acquired under low oxygen pressure). However, there comes a time when the change becomes irreversible, and the sickle erythrocytes develop a permanent sickle shape increasing the risk for hemolysis and VOC. All variants of SCD share the same pathophysiology leading to polymerization of the HbS component., Epidemiology : 1-40 per cent., 1 to 40 per cent^10, DEPENDS ON SEVERITY OF SYMPTOMS, If you carry the sickle cell trait, seeing a genetic counselor before trying to conceive can help you understand your risk of having a child with sickle cell anemia. A genetic counselor can also explain possible treatments, preventive measures and reproductive options., Complications : Cerebrovascular accident, congestive heart failure (CHF), splenomegaly, Stroke, osteomyelitis, Diagnostics : Hb, Peripheral Blood Smear, PLATELET COUNT, Serum Bilirubin (Total ), SICKLE CELL TEST, ECG, X RAY CHEST, White Blood Cell count WBC, X RAY, Differential diagnosis : Acute leukemia, Polycythemia vera, Septic arthritis, systemic lupus erythematosus (SLE), Thalassemia, disease description : Sickle cell anemia is an autosomal recessive disease that results from the substitution of valine for glutamic acid at position 6 of the beta-globin gene. Patients who are homozygous for the HbS gene have sickle cell disease. Patients who are heterozygous for the HbS gene have sickle trait. The gene frequency for sickle cell anemia in India is 4.3%. Deoxygenation of the heme moiety of sickle hemoglobin leads to hydrophobic interactions between adjacent sickle hemoglobin (HbS) molecules that aggregate into larger polymers. Sickle red blood cells are less deformable and obstruct the microcirculation, resulting in tissue hypoxia, which further promotes sickling. These red blood cells are rapidly hemolyzed and have a life span of only 10-20 days.

Sickle-cell Retinopathy

Disease Name : Sickle-cell Retinopathy, Symptoms : peripheral arteriolar occlusion and ischaemia. : The retinal changes in NPSR occur secondary to vaso-occlusion and local ischemia. Occlusion of retinal vasculature first appears in the peripheral retina as “salmon patches”, which represent retinal hemorrhage from superficial blood vessels., Signs : VITREOUS HAEMORRHAGE : Patients with sickle cell disease generally maintain good vision until they progress to Goldberg Stage IV disease, when vitreous hemorrhage occurs due to vitreous contraction on sea-fan neovascular complexes. The avascular peripheral retina in SCD is thin and therefore prone to retinal breaks., Neovascularization : The fundus of a patient with sickle cell retinopathy can have characteristic non-neovascular and/or neovascular signs. Non-neovascular signs include hemorrhage in one or more layers of the retina., peripheral arteriovenous anastomoses : The peripheral retina may show retinal vascular loops, pigmentary changes, retinal vascular anastomoses, retinal vascular occlusions, and retinal whitening. Retinal vascular anastomoses are dilated capillary connections between the arterioles and venules and represent stage II of proliferative sickle cell retinopathy., tractional retinal detachment : Retinal traction detachment is an ocular complication of many systemic disorders, including DM, HTN, sickle cell disease, and premature birth., Treatment : • Panretinal photocoagulation (PRP) is effective in,regressing the neovascularization., Pars plana vitrectomy is required for vitreoretinal,tractional bands., Pathophysiology : In sickle cell disease, polymerization of HbS occurs under conditions of hypoxia, leading to aggregation of the stiff HbS molecules, damaging the RBC cell membrane and cytoskeleton, and producing the characteristic sickle-shaped red blood cells. These sickle-shaped red blood cells are rigid and less deformable. They have a longer transit time across the capillaries of the retina and choroid and increased endothelial adhesion, causing damage to the blood vessels. The endothelium is thought to produce adhesion molecules, and there is also the release of inflammatory mediators, all of which produce vascular occlusion. Repeated vaso-occlusive episodes presumably lead to the production of angiogenic factors such as vascular endothelial growth factor and fibroblast growth factor, which subsequently give rise to proliferative retinopathy.Thalassemia is characterized by the absent or reduced production of hemoglobin chains, leading to inefficient erythropoiesis, which itself can cause ocular damage. However, iron overload due to repeated transfusions and iron chelators can also add on to the ocular damage., Epidemiology : sickle cell disease and is reportedly seen in 0.5% of patients with HbSS disease and about 2.5% of patients with HbSC disease., variable, Drugs that prevent new blood vessel formation can be injected into the eye in select patients.,Laser treatment of large areas of ischemia (blood vessel blockage) can prevent the release of factors that promote abnormal blood vessels., Complications : macular hole, RETINAL DETACHMENT, VITREOUS HAEMORRHAGE, Diagnostics : RETINOSCOPY, Slit lamp examination, Fluorescein angiography, Differential diagnosis : BRANCH RETINAL VEIN OCCLUSION , chronic kidney disease, Eales’ disease, hypertension, disease description : Hemoglobinopathy refers to genetic disorders which are characterized by the inheritance of either an abnormal hemoglobin as in sickle cell disease or an insufficient production of hemoglobin chains as in thalassemia. A Detroit physician who was studying Italian children with severe anemia, poor growth, and early death first discovered thalassemia in 1925. Ocular involvement in beta thalassemia can occur because of the disease itself, because of the iron overload as a result of blood transfusions, or because of desferrioxamine used to treat the iron overload.

Signet-ring Stromal Tumour

Disease Name : Signet-ring Stromal Tumour, Symptoms : abnormal uterine bleeding, pelvic pain, Abdominal Pain, Signs : nan, Treatment : Surgical excision (oophorectomy), Pathophysiology : Pathophysiology is unknown. Hypothesized to arise from ovarian stromal cells or multifocal conversion of a fibroma., Epidemiology : < 20 cases reported to date, Rare.Account for ~1% of all ovarian tumours, variable, Complications : nan, Diagnostics : Cytogenetics, CT SCAN, Immunostaining, Immunostaining, Differential diagnosis : BRENNER TUMOR, Fibroma, Krukenberg tumor, disease description : Signet-ring stromal tumor (SRST) of the ovary is an extremely rare neoplasm , Signet-ring stromal tumor (SRST) of the ovary , The Ovarian SRSTs are currently classified as sex cord stromal ovarian tumors within the spectrum of thecoma-fibromas, and are non-functioning distinctive stromal tumors characterized by the proliferation of stroma and signet-ring cell appearance due to the cytoplasmic vacuoles

Silent Thyroiditis

Disease Name : Silent Thyroiditis, Symptoms : diarrhea, fatigue, heat intolerance, hyperactivity, Increased appetite, Malaise, weakness, weight loss, Signs : Tachycardia, tremor, gynaecomastia, Treatment : medication : Propranolol , Levothyroxine/Tetra idothyronine, Treatment is based on symptoms. Medicines called beta-blockers may be used to relieve rapid heart rate and excessive sweating and thyroxin for hhypothyroidism., Pathophysiology : In most types of thyroiditis, there are three phases, including : 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 : It occurs in about 5 to 10% of postpartum women., good, 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 : thyroiditis, Thyroid storm, Myxedema, Diagnostics : Erythrocyte Sedimentation Rate (ESR), TPOAb (Thyroid peroxidase antibodies), ultrasound, THYROID SCAN, THYROID PROFILE, Differential diagnosis : "De Quervains thyroiditis", "Hashimotos thyroiditis", "Riedels thyroiditis", disease description : Thyroiditis is inflammation of your thyroid gland. Your thyroid is a small, butterfly-shaped gland located at the front of your neck under your skin. It’s a part of your endocrine system and controls many of your body’s important functions by producing and releasing certain hormones.

Simple Allergic Conjunctivitis

Disease Name : Simple Allergic Conjunctivitis, Symptoms : photophobia : Some types of conjunctivitis can cause a condition called keratitis. Keratitis is where your cornea (the front of your eye) becomes swollen. This can be painful and make your eyes sensitive to light (photophobia)., burning sensation in eyes : People with all forms of allergic conjunctivitis develop intense itching and burning in both eyes., Watery mucus : Watery or white, stringy mucus discharge is produced in allergic conjunctivitis., Signs : conjunctival hyperaemia : Conjunctival hyperemia is caused by a pathological vasodilatory response of the microvasculature in response to inflammation due to a myriad of infectious and non-infectious etiologies., eyelid oedema : The conjunctiva becomes red and sometimes swells, giving the surface of the eyeball a puffy appearance. The eyelids may become intensely itchy. Rubbing and scratching leads to eyelid skin redness, swelling, and a crinkly appearance., conjunctival chemosis : Chemosis is swelling of the tissue that lines the eyelids and surface of the eye (conjunctiva). Chemosis is swelling of the eye surface membranes because of accumulation of fluid. This symptom is often related to an allergic response., Papillary reaction : Giant Papillary Conjunctivitis : Symptoms consistent with simple allergic conjunctivitis often give way to worsening itch and discharge that becomes thick mucus instead of clear and watery. Patients usually report worsening pain and blurry vision with the increased sense of foreign body (contact lenses, sutures)., Treatment : medication : Ketotifen Fumarate , Sodium Cromoglycate , Carboxymethyl cellulose , Naphazoline, 1. Elimination of allergens if possible.,2. Topical vasoconstrictors like naphazoline, ,antizoline and tetrahydrozoline provide immediate,decongestion.,3. Artificial tears like carboxymethyl cellulose,provide soothing effect.,4. Mast cell stabilizers such as sodium cromoglycate,and nedocromil sodium are very effective in,preventing recurrences in atopic cases.,5. Dual action antihistamines and mast cell stabilizers,such azilastine, olopatidine and ketotifen are very,effective for exacerabations.,6. Steroid eyedrops should be avoided. However, ,these may be prescribed for short duration in,severe and non-responsive patients.,7. Systemic antihistaminic drugs are useful in acute,cases with marked itching.,8. Desensitization has been tried without much,rewarding results. However, a trial may be given,in recurrent cases., Pathophysiology : Simple allergic conjunctivitis (acute, seasonal, and perennial) is an immunoglobulin E (IgE) mediated hypersensitivity reaction (type I) and resultant mast cell degranulation secondary to direct contact with an allergen to the ocular surface. As such, there is an immediate and delayed phase of the reaction mediated by different inflammatory modulators. The exact mechanism involved in vernal keratoconjunctivitis is not well understood. Still, there is likely an IgE mediated hypersensitivity and T cell involvement in the reaction. Atopic keratoconjunctivitis appears to be a combination of delayed-type (type IV) and immediate (type I) hypersensitivity to an ocular allergen exposure. Giant papillary conjunctivitis occurs secondary to direct mechanical irritation/injury and subsequent immune response (type I and type IV). The foreign object may become coated with different allergens or injury epithelial tissue and allow deeper exposure to allergens and provoke an immunological response., Epidemiology : 12.22%, between 10% to 30% of the general population., good, The best way to prevent allergic conjunctivitis is to avoid exposure to environmental triggers, but this can be hard to do.,,Depending on the trigger, it may help if you : ,,use only scent-free soaps and detergents,install an air purifier in your home,vacuum and dust regularly,limit the carpets, soft toys, curtains, and soft furnishings in your home, Complications : Chemosis of conjunctiva, Diagnostics : fluorescein staining, Differential diagnosis : ANGULAR BACTERIAL CONJUNCTIVITIS, bacterial conjunctivitis, VIRAL CONJUNCTIVITIS, disease description : Allergic conjunctivitis is a common, under-appreciated, and largely benign process. It is rarely vision-threatening but can significantly decrease the quality of life for patients. There are three subtypes of simple allergic conjunctivitis : acute, seasonal, and perennial. There is considerable overlap with atopic conjunctivitis (vernal and atopic keratoconjunctivitis) and giant papillary conjunctivitis in both treatment and certain aspects of pathophysiology. As such, these are all considered to be ocular allergies. Initial treatment strategies can be similar, although outcomes and rates of complications vary

Simple Bone Cyst

Disease Name : Simple Bone Cyst, Symptoms : swelling : Simple bone cyst causes swelling & tenderness at the affected site., Pain : Most children with unicameral bone cysts are asymptomatic or have mild symptoms close to where the cyst is located, such as slight pain., pathological fracture : These cysts are in contact with the growth plate. They can grow large enough to weaken bone and cause fracture., Signs : nan, Treatment : medication : Methyl prednisolone , Small asymptomatic lesions in upper extremities are usually followed up with serial plain radiographs. Larger lesions at risk for fracture, symptomatic lesions, and lower extremity lesions typically receive treatment with curettage or aspiration and injection (corticosteroids, bone marrow aspirates, bone matrix, and other materials). Pathological fractures in the upper extremity generally have conservative treatment. The priority of therapy is to treat the fracture first, typically by immobilization for 4 to 6 weeks. However, unstable fracture or fracture in weight-bearing areas like in the lower extremity, treatment involves both fracture fixation and treatment of the bone cyst, curettage and bone grafting, Pathophysiology : When in the active phase, the cysts tend to arise near the physis (growth plate) and maintain their growth potential; however, as the cysts become more latent, they begin to migrate away from the physis and can remain as a static bone defect or may gradually resolve over time., Epidemiology : The annual prevalence is 0.3 per 100.000 individuals, 0.15 cases per one million per year, GOOD, There is no way to prevent unicameral bone cysts because providers aren’t sure why they occur., Complications : Arthritis, pathological fracture, Diagnostics : X RAY, X RAY, Histopathological examination, Differential diagnosis : eosinophilic granulomatosis, Giant cell tumor of bone, malignant tumors, Osteoblastoma, disease description : Unicameral bone cysts (UBCs) or simple bone cyst are common benign tumor-like bone lesions. They are also known as simple or solitary bone cysts. Most benign bone tumors have a characteristic appearance on radiographs. Their appearance can aid in diagnosis and decrease unnecessary additional imaging or invasive diagnostic procedures. They are typically asymptomatic and found on imaging incidentally. However, when symptomatic, it is usually as a result of a pathologic fracture causing pain, swelling, or deformity.  Treatment is not required unless the bone cyst is large and leads to deformity or symptoms, or there is an impending fracture.

Simple Cystic Disease

Disease Name : Simple Cystic Disease, Symptoms : polyuria : Simple kidney cysts causes frequent urination., fever : When the cysts become affected infected, affected individuals experience fever., DARK URINE : Dark urine means the kidney cyst that has burst or become infected., Abdominal Pain : Simple liver cysts are fluid-filled cavities in the liver. Usually, they cause no signs or symptoms and need no treatment. However, they may become large enough to cause pain or discomfort in the upper right part of the abdomen., Signs : nan, Treatment : The majority of cysts do not need any intervention or follow-up. If a cyst becomes infected, antibiotics are necessary., If a cyst is so large that it is exerting mass effect or pressure on another organ, the two most common procedures for treating simple kidney cysts are (1) aspiration and sclerotherapy and (2) laparoscopic surgery to remove the cyst. Ethanol is most commonly used in sclerotherapy, Pathophysiology : The exact pathophysiology for renal cysts is unclear. Diverticula on the distal tubule of the nephron may be the starting point for cyst formation. The basal membrane involution with age, combined with a degree of urinary obstruction, may result in simple cyst formation., Epidemiology : 5% of the general population, good, "Simple kidney cysts cant be prevented. You can reduce your risk by drinking plenty of water and making sure you use less than 2, 300 mg of sodium a day (less than 1, 500 mg if you are older than 51, African-American, or have high blood pressure or long-term kidney disease).", Complications : infected cyst, Diagnostics : URINE MICROSCOPY, MRI, CT, CT SCAN, USG, Differential diagnosis : NEUROBLASTOMA, renal disease, disease description : A cyst is a closed pouch or sac filled with air or liquid. Kidneys are bean-shaped organs located in the lower back that help to control the amount of salt and water in the body. They also remove waste products by filtering the blood and making urine.Inside the kidneys are small working parts called nephrons. Each nephron is made up of a filter and a tube. As blood flows through the kidneys to be filtered, the nephrons remove extra water and waste products, which leave the body as urine.

Simple Hyperaemia Of Conjunctiva

Disease Name : Simple Hyperaemia Of Conjunctiva, Symptoms : eye pain : Simple hyperaemia of conjunctiva causes slight pain., GRITTINESS : Foreign body sensation is experienced by affected individuals., photophobia : Light sensitivity is experienced by the patients., Signs : nan, Treatment : medication : Adrenaline (Epinephrine), Naphazoline, • Removal of the cause of hyperaemia, e.g., in acute,transient hyperaemia the removal of irritants (e.g., ,misdirected cilia) gives prompt relief., Symptomatic relief may be achieved by use of,topical decongestants (e.g., 1 : 10000 adrenaline,drops) or naphazoline drops., Pathophysiology : It may be acute and transient, or recurrent and chronic. 1. Acute transient hyperaemia. It results due to temporary irritation caused by : i. Direct irritants such as a foreign body, misdirected cilia, concretions, dust, chemical fumes, smoke, stormy wind, bright light, extreme cold, extreme heat and simple rubbing of eyes with hands. ii. Reflex hyperaemia due to eye strain, from inflammations of nasal cavity, lacrimal passages and lids. iii. Hyperaemia associated with systemic febrile conditions. iv. Nonspecific inflammation of conjunctiva. 2. Recurrent or chronic hyperaemia. It is often noticed in chronic smokers, chronic alcoholics, people residing in dusty, ill ventilated rooms, workers exposed to prolonged heat, in patients sufffering from rosacea and insomnia or otherwise having less sleep., Epidemiology : 135 cases per 10, 000 population annually, GOOD, "Dont touch your eyes with your hands.,Wash your hands often.,Use a clean towel and washcloth daily.,Dont share towels or washcloths.,Change your pillowcases often.,Throw away your eye cosmetics, such as mascara.,Dont share eye cosmetics or personal eye care items.", Complications : Corneal perforation, Diagnostics : RAPID ANTIGEN DETECTION, Differential diagnosis : EPISCLERITIS, Glaucoma, KERATITIS, SCLERITIS, disease description : Conjunctival hyperemia is caused by a pathological vasodilatory response of the microvasculature in response to inflammation due to a myriad of infectious and non-infectious etiologies. It is one of the most common contributors in ocular complaints that prompts visits to medical centers.

Simple Renal Cyst

Disease Name : Simple Renal Cyst, Symptoms : abdominal discomfort, palpable mass, Signs : tender abdomen, Treatment : Health care professionals usually don’t treat simple kidney cysts that aren’t causing symptoms. However, you may be asked to have regular ultrasounds to watch your simple kidney cysts for signs of change or problems., "Kidney is exposed. The cyst is aspirated and a portion of ,the cyst wall is removed (Kirwin s operation) and cavity ,is filled with perinephric fat. ,- Occasionally if the cyst is in one of the poles, partial ,nephrectomy is done. ,, Laparoscopic approach.", Pathophysiology : The exact pathophysiology for renal cysts is unclear. Diverticula on the distal tubule of the nephron may be the starting point for cyst formation. The basal membrane involution with age, combined with a degree of urinary obstruction, may result in simple cyst formation., Epidemiology : Approximately 25% of people who are 40 years or older and approximately 50% of people 50 years and older have simple kidney cysts, variable, "Simple kidney cysts cant be prevented. You can reduce your risk by drinking plenty of water and making sure you use less than 2, 300 mg of sodium a day (less than 1, 500 mg if you are older than 51, African-American, or have high blood pressure or long-term kidney disease).", Complications : infection, Diagnostics : CT Abdomen, ultrasound, MRI, CT, IVU, Differential diagnosis : NEUROBLASTOMA, RECURRENT HYPOPARATHYROIDISM, RENAL CALCULI, RENAL CARBUNCLE, RENAL ECTOPIA, RENAL TUBERCULOSIS, SIMPLE RENAL CYST, Surgery, disease description : A simple kidney cyst is the most common type of renal cyst. It is a fluid-filled sac that originates from the surface of the kidney. One or more simple cysts may form within the same kidney. These cysts are usually asymptomatic and detected incidentally upon radiological exams of the abdomen ,  A simple kidney cyst is a pocket of fluid that originates from the surface of the kidney and is contained by a thin wall. One or more simple cysts may form within the kidneys. The simple cyst is the most common type of renal cyst.

Sindbis Virus Infection

Disease Name : Sindbis Virus Infection, Symptoms : flu-like symptoms : Includes fever (mild), malaise, fatigue & body pain., Skin rashes : The rash is initially widespread and maculopapular., joint pain : Chronic joint pain is common., Signs : nan, Treatment : There is no specific treatment for the virus infection but rest and ,pain control are advised., Pathophysiology : The disease occurs in places and at times of mosquito breeding. The features of the infection appear between 1 and 2 weeks after inoculation by mosquito bite. Non-specific features of malaise, mild fever, headache and musculoskeletal aches can be followed rapidly by a more definite peripheral arthritis and a widespread rash which is often itchy. The eruption consists of small papules and macules up to 1 cm in diameter, most abundant on the trunk, thighs and limbs. There is relative sparing of the hands, feet and face. The rash clears within a week. Arthralgia often lasts for several months and persists for over a year in half those affected., Epidemiology : The incidence and prevalence of SINV infection varies considerably between different parts of the country, being highest in eastern and central Finland., GOOD, Protection against mosquitos is the mainstay of prevention in Sindbis virus prevalent areas. There is no prophylaxis or vaccine to prevent the infection., Complications : arthralgia, Diagnostics : ELISA FOR ANTIBODY TITRE, RT PCR, Differential diagnosis : ASEPTIC MENINGITIS, disease description : The Sindbis virus can be regarded as the prototype togavirus causing a mosquito-borne viral fever. Sindbis virus infection can occur in any individual in contact with mosquitos. However, the incidence is higher in some parts of the world. In Sweden, the disease is more common in rural areas and in individuals with obesity, hypertension or with a history of cerebrovascular disease.Phylogenetic analysis indicates that there is one major genetic cluster of western SIN virus strains in Africa and another in Australia and Asia. There is evidence of some geographic mixing of western strains of SIN virus that suggest long-distance transport via migrating birds. There is no vaccine available. Since many of the mosquito vectors breed in extensive rice fields, large-scale control would be expensive

Sinus Tachycardia

Disease Name : Sinus Tachycardia, Symptoms : Feelings of anxiety, palpatation, Signs : nan, Treatment : medication : Diltiazem , Verapamil, Clonidine , Metoprolol , Propranolol , Nifedipine , Ivabradine, Catheter ablation of the sinus node has,been performed, Pathophysiology : Sinus p waves are characterized by a frontal plane axis directed inferiorly and leftward, with positive p waves in leads II, III, and aVF; a negative p wave in aVR; and an initially positive biphasic p wave in V1. Normal sinus rhythm has a range of rates between 60–100 beats/min. Sinus tachycardia (>100 beats/min) typically occurs in response to sympathetic stimulation and vagal withdrawal, whereby the rate of spontaneous depolarization of the sinus node increases and the focus of earliest activation within the node typically shifts more leftward and closer to the superior septal aspect of the crista terminalis, thus producing taller p waves in the inferior limb leads when compared to normal sinus rhythm. Sinus bradycardia is defined as rates less than 60 beats/min; however, bradycadia can be normal during sleep and in fit individuals., Epidemiology : not specified, Complications : nan, Diagnostics : ECG, trans thoracic 2D ECHO, Differential diagnosis : nan, disease description : there are two types of sinus tachycardia 1- physiologic sinus tachycardia 2- non physiologic sinus tachycardia 1- Physiologic Sinus Tachycardia The sinus node is comprised of a group of cells dispersed within the superior aspect of the thick ridge of muscle known as the crista terminalis where the posterior smooth atrial wall derived from the sinus venosus meets the trabeculated anterior portion of the right atrium (Fig. 242-1). Sinus p waves are characterized by a frontal plane axis directed inferiorly and leftward, with positive p waves in leads II, III, and aVF; a negative p wave in aVR; and an initially positive biphasic p wave in V1. Normal sinus rhythm has a range of rates between 60–100 beats/min. Sinus tachycardia (>100 beats/min) typically occurs in response to sympathetic stimulation and vagal withdrawal, whereby the rate of spontaneous depolarization of the sinus node increases and the focus of earliest activation within the node typically shifts more leftward and closer to the superior septal aspect of the crista terminalis, thus producing taller p waves in the inferior limb leads when compared to normal sinus rhythm. Sinus bradycardia is defined as rates less than 60 beats/min; however, bradycadia can be normal during sleep and in fit individuals. Sinus tachycardia is considered physiologic when it is an appropriate response to exercise, stress, or illness. Sinus tachycardia can be difficult to distinguish from focal atrial tachycardia (see below) that originates near the sinus node. A causative factor (such as exertion) and a gradual increase and decrease in rate favor sinus tachycardia, whereas abrupt onset and offset favor atrial tachycardia. The distinction can be difficult and occasionally requires extended ECG monitoring or even invasive electrophysiology study. Treatment for physiologic sinus tachycardia is aimed at the underlying condition, but frequently no therapy is necessary. 2- Nonphysiologic Sinus Tachycardia Inappropriate sinus tachycardia is an uncommon condition in which the sinus rate increases spontaneously at rest or out of proportion to physiologic stress or exertion and is within a spectrum of ill-defined conditions associated with autonomic dysregulation. Affected individuals are often women in the third or fourth decade of life. Fatigue, dizziness, and even syncope may accompany palpitations, which can be disabling. Additional symptoms of chest pain, headaches, and gastrointestinal upset are common. It must be distinguished from appropriate sinus tachycardia and from focal atrial tachycardia. The distinction between physiologic sinus tachycardia due to an anxiety disorder and inappropriate sinus tachycardia can be difficult. Therapy is often ineffective or poorly tolerated. Careful titration of beta blockers and/or calcium channel blockers may reduce symptoms. Clonidine and serotonin reuptake inhibitors have also been used. Ivabradine, a drug that blocks the If current that causes sinus node depolarization, is now approved in the United States for use in heart failure, but it has also been effective in the treatment of inappropriate sinus tachycardia. Catheter ablation of the sinus node has been performed, but long-term control of symptoms is usually poor, and it often leaves young individuals with a permanent pacemaker. Postural orthostatic tachycardia syndrome (POTS) is characterized by symptomatic sinus tachycardia that occurs with postural change from a supine position to standing. The sinus rate increases by 30 beats/ min or to >120 beats/min within 10 min of standing and in the absence of hypotension. Symptoms are often similar to those in patients with inappropriate sinus tachycardia. POTS is sometimes due to autonomic dysfunction following a viral illness and may resolve spontaneously over 3–12 months. Volume expansion with salt supplementation, oral fludrocortisone, compression stockings, and the a-agonist midodrine, often in combination, can be helpful. Exercise training has also been purported to improve symptoms.

Sitosterolaemia

Disease Name : Sitosterolaemia, Symptoms : Arthritis, Impaired growth, Premature onset of cardiovascular disease, Signs : anaemia, Thrombocytopenia, tendon xanthomas, Tuberous xanthomata, Treatment : medication : Ezetimibe , The first step in treatment is significant dietary modifications. This includes a major reduction in the intake of plant sterols and shellfish sterols. Common examples include vegetable oils, nuts, and avocados. Patients often experience a measurable reduction in serum sterol levels and cholesterol levels following the dietary intervention.,,Medications are generally required to fully control the chronic disease process of sitosterolemia. At a dosage of 10 mg per day, ezetimibe is approved by the United States Food and Drug Administration (FDA) for the treatment of sitosterolemia. It works directly by blocking plant sterol entry and consequently lowers serum plant sterol levels. Other medication options include bile-acid binding resins such as cholestyramine, surgical intervention with an ileal bypass was reserved for severe cases., Pathophysiology : This condition results from mutations in the genes ABCG5 or ABCG8 , which encode the proteins sterolin-1 and sterolin-2 in enterocytes and hepatocytes. Sterolin-1 and sterolin-2 act together to form a lipid transporter that is thought to facilitate immediate excretion of any plant sterols absorbed across the small intestinal brush border. Defective function thereby allows a much greater absorption of plant sterols into the body, principally ß-sitosterol but also sitostanol, campesterol and stigmasterol., Epidemiology : true prevalence remains unknown. Some estimates show the prevalence may be as high as 1 in 50, 000., variable, Complications : aortic stenosis, arthralgia, Arthritis, CIRRHOSIS, Hemolytic anemia, Myocardial infarction, splenomegaly, Thrombocytopenia, Atherosclerosis, Diagnostics : Complete Blood Count CBC, LIPID PROFILE, GENETIC TESTING, CT SCAN, serum plant sterol concentrations, Differential diagnosis : Cerebrotendinous Xanthomatosis, Familial Hypercholesterolemia, hypertriglyceridaemia, Tangier disease, disease description : Sitosterolemia is a rare lipid disorder that is characterized by the accumulation of plant sterols in the blood. It is autosomal recessive and often presents in early childhood. Clinically, it can be misdiagnosed as familial hypercholesterolemia, and overlap between the two disorders creates a diagnostic challenge for physicians. Those with sitosterolemia absorb significantly higher amounts of plant sterols and stanols than healthy patients. This can lead to hypercholesterolemia and subsequent premature atherosclerosis. Patients can develop severe coronary artery disease, myocardial infarction, and other complications quite early in life if this condition is left untreated

Sixth Nerve Palsy

Disease Name : Sixth Nerve Palsy, Symptoms : diplopia : Double vision or diplopia when looking side to side is the most common symptom of sixth nerve palsy. You may notice this vision impairment when both eyes are open or when you’re looking at something in the distance. Sometimes, double vision occurs when looking in the direction of the damaged eye. It’s also possible to have sixth nerve palsy without double vision., headache : Sixth nerve palsy cause headaches., Hearing loss : Depending on the other structures affected, you might have symptoms such as : Hearing loss., eye problem : Because each eye has its own lateral rectus muscle and sixth cranial nerve, sixth nerve palsy can affect one or both eyes. Your symptoms and the severity of the condition depend on whether both eyes are affected., Strabismus : Also called crossed eyes, poor eye alignment is when your eyes don’t look in the same direction at the same time., Signs : nan, Treatment : nan, Pathophysiology : Nerve Compression or Ischemia : Vascular Compression : Compression of the sixth cranial nerve along its course by adjacent blood vessels or structures can lead to nerve dysfunction. This compression can result from conditions such as aneurysms, tumors, or vascular malformations.Ischemia : Reduced blood flow (ischemia) to the sixth cranial nerve or the area of the brainstem responsible for controlling the nerves function can also lead to palsy. Ischemia can result from conditions like diabetes, hypertension, or vascular diseases.Inflammation and Autoimmune Disorders : Idiopathic Intracranial Hypertension (IIH) : Increased pressure within the skull can lead to damage or compression of cranial nerves, including the sixth nerve. IIH is often associated with obesity and may result in nerve dysfunction.Inflammatory Conditions : Inflammatory disorders like multiple sclerosis can affect the myelin sheath surrounding the nerve or the nerve itself, leading to palsy.Autoimmune Disorders : Autoimmune conditions that cause inflammation of blood vessels, such as vasculitis, can lead to nerve damage and palsy.Head Trauma : Direct Injury : Trauma to the head or the area around the eye can lead to damage of the sixth cranial nerve or its associated structures, resulting in palsy.Neurological Disorders : Increased Intracranial Pressure : Conditions that cause increased pressure within the skull, such as brain tumors or hydrocephalus, can lead to nerve dysfunction.Brainstem Lesions : Lesions or damage to the brainstem, where the sixth cranial nerve originates, can disrupt nerve signals and lead to palsy.Infection : Infections of the brainstem, such as brainstem encephalitis, or infections affecting the cranial nerves can lead to nerve dysfunction.Microvascular Ischemia : Diabetes : Microvascular complications of diabetes can lead to nerve damage, including the sixth cranial nerve.Hypertension : High blood pressure can affect the blood vessels supplying the nerve, leading to ischemia and dysfunction., Epidemiology : incidence to be 11.3/100 000, variable, This condition is inherited in an autosomal recessive pattern. It occurs because of a , genetic mutation in the ABCG5 or ABCG8 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 : nan, Diagnostics : nan, Differential diagnosis : ANEURYSM, diabetes mellitus, hypertension, MYASTHENIA GRAVIS, THYROID EYE DISEASE, disease description : Sixth nerve palsy occurs when the sixth cranial nerve is damaged or doesnt work right. Its also known as the abducens nerve. This condition causes problems with eye movement.The sixth cranial nerve sends signals to your lateral rectus muscle. This is a small muscle that attaches to the outer side of your eye. When this muscle contracts, your eye moves away from your nose. Each eye has its own lateral rectus muscle served by its own cranial nerve.The sixth nerve emerges from the lower part of your brain. It travels a long way before reaching the lateral rectus. Damage at any point along its path can cause the nerve to work poorly or not at all. Because the lateral rectus muscle can no longer contract properly, your eye turns inward toward your nose.Sometimes, sixth nerve palsy happens without any other symptoms. This is called isolated sixth nerve palsy. Other times, sixth nerve palsy may come with other symptoms. This is called nonisolated sixth nerve palsy.Sometimes, sixth nerve palsy is present from birth. It can also result from other problems that happen later on. In children, injury is a leading cause. In adults, stroke is one of the most common causes. It is relatively rare.

Sjogren’s Syndrome

Disease Name : Sjogren’s Syndrome, Symptoms : dry eyes, dry mouth, Signs : nan, Treatment : nan, Pathophysiology : Primary Sjogren’s syndrome consists of xerostomia and xerophthalmia and is due to involvement of salivary and lacrimal glands. Parotid is the most often involved gland. It has also been called as benign lymphoepithelial lesion of parotid or Mikulicz’s disease. Both sexes are equally involved. Secondary Sjogren’s syndrome consists of three major components : (i) keratoconjunctivitis sicca (due to involvement of lacrimal gland); (ii) xerostomia (due to involvement of salivary glands and minor mucous glands of the oral cavity); (iii) autoimmune connective tissue disorder, usually the rheumatoid arthritis, sometimes the systemic lupus erythematosus (SLE). In scleroderma or polymyositis, there is often a bilateral swelling of the salivary glands. Moreover, 90% of the cases occur in females. Sjogren’s syndrome histopathologically shows destruction of acini and lymphocytic infiltration and has therefore earned the name of lymphoepithelial lesion., Epidemiology : GOOD, Complications : nan, Diagnostics : Erythrocyte Sedimentation Rate (ESR), biopsy, MRI, Rheumatoid Factor Test, PHYSICAL EXAMINATION, SS-A antibody, SS-B antibody, Differential diagnosis : Dehydration, lymphoma, Mumps, Rheumatoid arthritis, rosacea, Sarcoidosis, Scleroderma crisis, disease description : Lymphoepithelial sialadenitis is an autoimmune disorder involving exocrine glands of the body. It may be primary or secondary.

Sjögren Syndrome

Disease Name : Sjögren Syndrome, Symptoms : "dry eyes : Your eyes might burn, itch or feel gritty — as if theres sand in them.", "Xerostomia : Your mouth might feel like its full of cotton, making it difficult to swallow or speak.", joint pain : Sjögren syndrome causes joint pain, swelling and stiffness., Salivary gland enlargement : Swollen salivary glands — particularly the set located behind your jaw and in front of your ears Skin rashes or dry skin., "cutaneous symptoms : People with Sjogrens may be more susceptible to a rash, especially after spending time in the sun. Skin problems that occur with the condition may present as : xerosis, or dry, rough skin. small “blood spots” or purpura on the lower legs due to vasculitis, or inflammation of the blood vessels.", respiratory symptoms : Includes chronic cough, wheezing, chest burning/ tightness, and shortness of breath, especially on exertion., "vaginal dryness : Even though vaginal dryness is a common occurrence during menopause, women with Sjögrens syndrome report this symptom 2-3 times more often than comparably aged women without Sjögrens syndrome. Vaginal atrophy develops during menopause as a consequence of a marked decline in serum levels of estrogen.", vision abnormalities : Dry eyes can lead to light sensitivity, blurred vision and corneal damage., Signs : nan, Treatment : medication : Prednisolone, Symptomatic treatment for the dryness of the eyes is best accomplished by lubricating agents, such as 0.5% methylcellulose eye drops ,instilled frequently. Artificial saliva can be prescribed, and steam ,inhalations or an air humidifier may help dryness of the respiratory,tract. Systemic ,corticosteroids are effective in reducing parotid swelling, but rarely ,increase parotid or lacrimal secretion. Chloroquine or hydroxychloroquine sulphate by mouth have been found useful by some authors but not by others. The annular ,erythema may be controlled by prednisolone 10–20 mg/day or by ,dapsone. There is no single therapy that helps hyperglobulinaemic ,purpura., Pathophysiology : The characteristic lesion of Sjogren syndrome is focal lymphocytic sialadenitis (FLS). FLS is a lesion of exocrine glands. Foci of lymphocyte-rich mononuclear cells infiltrate exocrine glandular tissue adjacent to blood vessels and excretory ducts. The foci are comprised predominantly of T lymphocytes. However, B lymphocytes, plasma cells, and other cell types are seen. With more severe disease the foci may become confluent. The infiltrating mononuclear cells, humoral factors such as antibodies and cytokines, or both are hypothesized to cause exocrine gland dysfunction resulting in diminished tear production by the lacrimal glands and diminished saliva production by salivary glands. Also, exocrine glands outside the head and neck may be involved resulting in skin, tracheobronchial and vaginal dryness as well as lung and kidney dysfunction. Rarely, malignant transformation of B lymphocytes can result in non-Hodgkin lymphoma. Immune complexes may deposit in skin, joints and other organs resulting in a systemic vasculitis., Epidemiology : prevalence of 3 in 100 to 1 in 1000, 1 has rarely been reported from India., 0.5% to 1.0% of the population., VARIABLE, Because no one knows exactly what causes Sjögren’s syndrome or other autoimmune diseases, there is no known way to prevent it., Complications : BRONCHIECTASIS, lymphoma, wheezing, Diagnostics : ANA, ANTI dsDNA TITRE, Schirmer-I test, Differential diagnosis : nan, disease description : Primary Sjogren syndrome is a systemic autoimmune disorder commonly presenting with dryness involving the eyes and mouth due to inflammation and resultant pathology of the lacrimal and salivary glands. Up to one-half of affected individuals also develop extra-glandular involvement in organs such as the joints, skin, lungs, gastrointestinal (GI) tract, nervous system, and kidneys. This condition is frequently associated with other autoimmune disorders including rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Sjogren syndrome is managed by replacing moisture at affected glandular sites and diminishing the autoimmune response locally as well as systemically.

Small Cell Carcinoma Of Lung

Disease Name : Small Cell Carcinoma Of Lung, Symptoms : chest pain : Chest pain that is often worse with deep breathing, coughing, or laughing., facial swelling : Facial swelling can sometimes be a complication of lung cancer. It can occur when tumors in the lungs obstruct the flow of blood in a blood vessel known as the superior vena cava., Hoarseness : Some people with lung cancer can develop a hoarse voice. It may be caused by the cancer pressing on a nerve in the chest called the laryngeal nerve. If this nerve is squashed, one of the vocal cords in your throat can become paralysed, leading to a hoarse voice., difficulty in breathing : This feeling of starving for oxygen is also known as “air hunger.” More than 50 percent of people with advanced stage cancer, and between 50 and 75 percent of people with lung cancer, experience dyspnea. It becomes more common in the final six weeks of life for people with advanced stage cancer., chronic cough : Chronic cough that doesn’t go away or worsens., hemoptysis : The source of hemoptysis is often from a bronchial arterial bleed within the tumor, less frequently from tumor erosion into the pulmonary artery (PA), and rarely from systemic arterial rupture., Signs : nan, Treatment : Novel agents for SCLC are currently under investigation and include immunotherapies and targeted therapies previously approved for NSCLC and other malignancies. Immunotherapies include immune checkpoint inhibitors Nivolumab (PD-1 inhibitor antibody), Pembrolizumab (anti-PD1 antibody), Ipilimumab (CTLA-4 inhibitor antibody). Targeted therapies in clinical trials include Rovalpituzumab tesirine (Delta-like protein three antibody-drug conjugate)., The remainder of limited stage patients is treated with concurrent chemotherapy and radiation. Cisplatin and etoposide is the current standard of care. The addition of radiation to chemotherapy significantly increases local control and overall survival. The early incorporation of RT with CT has been shown to further increase overall survival compared to late incorporation. Prophylactic cranial irradiation (PCI) is indicated for patients with a complete or partial response to therapy. PCI significantly increases overall survival and decreases the incidence of brain metastases., While the majority of patients present with locally advanced disease, a small minority may present with T1-2N0 disease. These patients may be candidates for lobectomy with mediastinal sampling or dissection. If surgery demonstrates mediastinal nodal involvement, adjuvant chemoradiation is indicated. If they are not surgical candidates, stereotactic ablative body therapy (SABR) may be employed. Adjuvant cisplatin-based systemic therapy typically follows both local approaches, The mainstay of therapy for patients with the extensive stage is systemic chemotherapy. Patients who have a complete or partial response to therapy can be evaluated for consolidative thoracic RT. This therapy has been associated with an increase in overall survival and is typically well tolerated. PCI is also indicated for ES and has been associated with an increase in survival with a decrease in brain metastases incidence. There is currently no role for the addition of consolidation radiation to limited volume metastatic sites., Pathophysiology : SCLC is divided into the 2 subtypes : oat cell carcinoma and combined-SCLC. Combined SCLC is defined as SCLC with non-small cell components such as squamous cell or adenocarcinoma.SCLC carcinogenesis can occur by various pathways that disrupt normal DNA repair mechanisms. Common mutations in SCLC include loss of RB1 tumor suppressor gene and TP53(17p13) mutations which decrease the pro-apoptotic activity of cancer cells. Almost all SCLC tumors have a deletion in a section of the short arm of chromosome 3p which contains the tumor suppressor gene FHIT. , Epidemiology : 9.8% WORLDWIDE, variable, Avoiding tobacco is the best way to prevent small cell lung cancer. Giving your lungs a chance to heal reduces your risk of developing small cell lung cancer. If you smoke tobacco and want to quit, ask a healthcare provider about smoking cessation treatment and programs., Complications : hypercalcemia, MYASTHENIA GRAVIS, Diagnostics : HISTOPATHLOGY, PET SCAN, biopsy, CT, BRONCHOSCOPY, SPUTUM CYTOLOGY, Differential diagnosis : CARCINOID TUMORS, granuloma, Hamartoma, Lung cancer, lymphoma, disease description : Lung cancer is the second most diagnosed cancer in the United States. It is the leading cause of cancer death in both men and women, accounting for approximately a quarter of all cancer deaths. Lung cancer is histologically divided into 2 main types : small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC).Lung cancer is the second most diagnosed cancer in the United States. It is the leading cause of cancer death in both men and women, accounting for approximately a quarter of all cancer deaths. Lung cancer is histologically divided into 2 main types : small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC). SCLC comprises about 15% of lung cancer while NSCLC comprises approximately 85%. Since the late 1980s, there has been a decline in the incidence of lung cancer coincident with a decline in smoking, the leading cause of lung cancer.

Small Cell Carcinoma

Disease Name : Small Cell Carcinoma : Combined Small Cell Carcinom, Symptoms : hemoptysis, dyspnoea, cough, Signs : nan, Treatment : SCLC is mostly treated by chemotherapeutics, which may be also important in C-SCLC. We retrospectively assessed the clinical characteristics of 7 C-SCLC cases after surgery in Zhejiang Cancer Hospital from 2007 to 2010. One patient received no chemotherapy, and showed reduced survival compared with other stage IIIA patients administered chemotherapeutics. This suggests that chemo therapy is significant for C-SCLC, and correlated with survival time., Surgical treatment may be applied in stage IA, IB, IIA, IIB, and IIIA NSCLC cases; among SCLC patients, only those classified as T1-2N0M0 are eligible for surgical treatment according to NCCN guidelines. Studies confirmed that use of surgery, and particularly lobectomy, yields optimal local control and results in a higher survival rate in patients with early stage SCLC., Pathophysiology : nan, Epidemiology : New cases IN U. S : 221, 200., The incidence of C-SCLC ranges from 5% to 28% in different studies, and is related to the type of specimens used., variable, Complications : nan, Diagnostics : LDH, X RAY, Differential diagnosis : CARCINOID TUMORS, inflammation, malignant lymphoma, Malignant melanoma, disease description : Combined small-cell lung carcinoma (C-SCLC) is defined by the World Health Organization (WHO) as small-cell carcinoma (SCLC) combined with additional components that consist of any of the histological types of non-small-cell lung carcinoma (NSCLC); usually adenocarcinoma (ADC), squamous-cell carcinoma (SCC), large-cell carcinoma (LCC), large-cell neuroendocrine carcinoma (LCNEC), or less commonly spindle-cell carcinoma or giant cell carcinoma.

Small Pox

Disease Name : Small Pox, Symptoms : flu-like symptoms : The symptoms of smallpox begin with a high fever, head and body aches, weakness., Rashes : Rash that starts in your mouth and spreads to your face, then to the rest of your body., pustules : A few days later, flat, red spots appear on the body. They may start in the mouth and on the tongue and then spread to the skin. The face, arms and legs are often affected first, followed by the torso, hands and feet. Within a day or two, many of the spots turn into small blisters filled with clear fluid. Later, the blisters fill with pus. These sores are called pustules. Scabs form 8 to 9 days later and eventually fall off, leaving deep, pitted scars., Abdominal Pain : Infected people may have severe abdominal pain., Signs : nan, Treatment : Vaccination has been successful in the eradication of smallpox globally., Pathophysiology : After viral entry through the oropharynx or nasopharynx, the virus migrates to regional lymph nodes where it begins replication.  An initial viremia occurs on day 3 to 4 after infection, and the virus further disseminates to the bone marrow, spleen, and additional lymph node chains.  A secondary viremia occurs between day 8 to 12 after infection and coincides with the onset of fever and clinical evidence of illness. At this stage, the virus becomes localized in the oropharyngeal mucosa and small blood vessels of the dermis, resulting in the onset of rash and clinical infectiousness., Epidemiology : Smallpox was fatal in up to 30% of cases, In 1980, the World Health Assembly declared smallpox eradicated (eliminated), and no cases of naturally occurring smallpox have happened since., VARIABLE, Smallpox can be prevented by smallpox vaccines, also called vaccinia virus vaccines. The vaccines are made from a virus called vaccinia, which is a poxvirus similar to smallpox, but less harmful., Complications : blindness, Diagnostics : ELISA FOR ANTIBODY TITRE, PCR, Differential diagnosis : chickenpox, Eczema herpeticum, MONKEYPOX, VACCINIA, disease description : Smallpox is the first human infectious disease to be successfully eradicated worldwide. It remains of clinical concern because of the potential for release and weaponization. Smallpox is a member of the viral family poxvirus, genus orthopoxvirus, and species variola virus. Smallpox is the first human infectious disease to be successfully eradicated worldwide, and the World Health Assembly certified its global eradication in 1980, It remains of clinical importance because of concerns about the potential for release and weaponization.Smallpox is the first human infectious disease to be successfully eradicated worldwide. It remains of clinical concern because of the potential for release and weaponization. Smallpox is a member of the viral family poxvirus, genus orthopoxvirus, and species variola virus. Smallpox is the first human infectious disease to be successfully eradicated worldwide, and the World Health Assembly certified its global eradication in 1980,  It remains of clinical importance because of concerns about the potential for release and weaponization. 

Smiths Fracture (reverse Of Colles Fracture)

Disease Name : Smiths Fracture (reverse Of Colles Fracture), Symptoms : "wrist deformity : Typically, individuals with a Smiths fracture may also present with swelling, pain, and decreased range of motion in the wrist.", wrist joint pain : Inability to move your wrist without pain., Signs : nan, Treatment : Careful decision-making is required to determine treatment via conservative closed reduction and casting vs. operative measures, which include percutaneous fixation, external fixation, or open reduction internal fixation (ORIF). To guide this, established criteria for acceptable alignment. Indications for operative management include,,Dorsal or volar comminution,Intra-articular involvement,Instability post-reduction,Surface angulation greater than 20 degrees,Articular surface step-off over 2 mm,Radial shortening greater than 5 mm, Pathophysiology : Mechanical Force and Trauma : Traumatic Impact : Smiths fracture typically occurs as a result of a fall onto an outstretched hand (FOOSH) or a direct impact to the back of the hand or wrist.Force Transmission : The force of impact is transmitted through the hand and wrist bones, causing stress and potential fractures.Deformation of the Radius Bone : Anterior Displacement : In a Smiths fracture, the distal end of the radius bone is pushed or displaced in an anterior direction, towards the palm of the hand.Volar Tilt : The fracture often results in volar (palmar) angulation of the distal fragment, leading to the characteristic "dinner fork" or "garden spade" deformity.Impact on Surrounding Structures : Soft Tissue Injury : The traumatic force can cause damage to surrounding soft tissues, including ligaments, tendons, and blood vessels.Ligament and Tendon Injuries : The forceful displacement of the bone may cause injury to the surrounding ligaments and tendons, potentially leading to instability and impaired wrist function., Epidemiology : "Compared to other types of wrist breaks, Smith fractures are rare. Theyre only around 5% of all broken wrists.", good, Breaking your wrist almost always happens accidentally. Because falls are by far the most common cause of wrist fractures, make sure your home and workspace are free from clutter that could trip you or others. Make sure the adults older than 50 in your life practice good fall prevention, too.,,Talk to your healthcare provider about osteoporosis and how you can prevent bone loss with the right diet, exercise routine and regular bone density screening, as well., Complications : Stiffness of joint, Malunion, Subluxation of joint, "Sudecks osteodystrophy", Rupture of the extensor pollicis longus tendon, Diagnostics : X RAY AP VIEWS, X RAY, PHYSICAL EXAMINATION, Differential diagnosis : "COLLES FRACTURE", fracture, GALEAZZI FRACTURE-DISLOCATION, disease description : A Smith fracture is an eponym for an extraarticular fracture of the distal radius featuring a volar displacement or angulation of the distal fragment. It is also known as a reverse Colles fracture since the more common Colles fracture features a dorsal displacement of the distal fracture fragment. The Smith fracture was named by Irish surgeon Robert William Smith in 1847.

Smith-lemli-opitz Syndrome

Disease Name : Smith-lemli-opitz Syndrome, Symptoms : cataract : Vision problems can occur, including cataracts., finger deformity : Most babies have differences in their fingers and/or toes. This includes fused toes (2-3 syndactyly) and extra fingers or toes (polydactyly)., Facial abnormalities : Individuals with SLOS have specific facial features. Their eyes may appear to be drooping (ptosis). There can also be a fold in the inner corner of the eye (epicanthal folds) and wrinkles on the eyelids. Children with SLOS can have a small nose and nostril differences (anteverted nares). Other common facial features include differences of the upper lip, a small jaw and large ears., "cleft palate : Microcephaly which is seen in patients affected by Smith-Lemli-Opitz syndrome is a birth defect where a babys head is smaller than expected when compared to babies of the same sex and age. Babies with microcephaly often have smaller brains that might not have developed properly.", "cleft palate : Smith-Lemli-Opitz syndrome causes cleft palate in infants. A cleft palate is an opening or split in the roof of the mouth that occurs when the tissue doesnt fuse together during development in the womb. A cleft palate often includes a split (cleft) in the upper lip (cleft lip) but can occur without affecting the lip.", Growth retardation : Infants with Smith-Lemli-Opitz syndrome tend to grow more slowly than other infants., Signs : Autism spectrum disorder : Many affected children have the characteristic features of autism, a developmental condition that affects communication and social interaction., Treatment : medication : Simvastatin , Early educational intervention is important for learning and developmental disabilities., Some children may require surgery to correct cleft palate, heart defects and genital anomalies., Pathophysiology : Smith-Lemli-Opitz syndrome is caused by mutations in the DHCR7 gene, which provides instructions for making an enzyme called 7-dehydrocholesterol reductase. This enzyme is responsible for the final step in the production of cholesterol. Cholesterol is a waxy, fat-like substance that is produced in the body and obtained from foods that come from animals (particularly egg yolks, meat, poultry, fish, and dairy products). Cholesterol is necessary for normal embryonic development and has important functions both before and after birth. It is a structural component of cell membranes and the protective substance covering nerve cells (myelin). Additionally, cholesterol plays a role in the production of certain hormones and digestive acids. Mutations in the DHCR7 gene reduce or eliminate the activity of 7-dehydrocholesterol reductase, preventing cells from producing enough cholesterol. A lack of this enzyme also allows toxic byproducts of cholesterol production to build up in the blood, nervous system, and other tissues. The combination of low cholesterol levels and an accumulation of other substances likely disrupts the growth and development of many body systems. It is not completely understood, however, how either abnormality leads to the specific features of Smith-Lemli-Opitz syndrome., Epidemiology : 1 in 20, 000-60, 000 births among Caucasians., variable, "This condition is inherited in an autosomal recessive pattern and therefore, cant be prevented.", Complications : Malformation, Diagnostics : HISTOPATHLOGY, ECG, GENETIC TESTING, TOTAL SERUM PROTEIN LEVEL, Differential diagnosis : cleft palate, desmosterolosis, Hypospadiasis, polydactyly, disease description : Smith–Lemli–Opitz syndrome is an inborn error of cholesterol synthesis. It is an autosomal recessive, multiple malformation syndrome caused by a mutation in the enzyme 7-Dehydrocholesterol reductase encoded by the DHCR7 gene. Smith-Lemli-Opitz syndrome is a developmental disorder that affects many parts of the body. This condition is characterized by distinctive facial features, small head size (microcephaly), intellectual disability or learning problems, and behavioral problems.

Smooth Muscle Tumour Of Uncertain Malignant Potent

Disease Name : Smooth Muscle Tumour Of Uncertain Malignant Potent, Symptoms : nan, Signs : nan, Treatment : myomectomy or hysterectomy, total hysterectomy as first approach or as complete surgical staging, Pathophysiology : Cellular Origin and Growth : Smooth Muscle Cells : STUMP tumors originate from abnormal growth or proliferation of smooth muscle cells. These cells are responsible for the involuntary contractions of various organs.Uncontrolled Proliferation : The exact trigger for the uncontrolled growth of smooth muscle cells in STUMP is not fully understood. Genetic mutations and alterations in signaling pathways that regulate cell growth and division may play a role., Epidemiology : Usually occurs in women of reproductive age or postmenopausal women, Rare., variable, Complications : nan, Diagnostics : MRI, USG, immunohistochemistry, Histopathological examination, Differential diagnosis : Genital leiomyoma, leiomyosarcoma, disease description : Smooth muscle tumors of uncertain malignant potential (STUMP) are mesenchymal uterine tumors lying between benign leiomyomas and leiomyosarcomas. The term “STUMP” contains a heterogeneous group of rare tumors. There is lack of clinicopathologic details and follow-up data of these neoplasm. STUMP cannot be classified as benign or malignant.

Snake Bite

Disease Name : Snake Bite, Symptoms : Redness : Redness, swelling and tissue damage, or complete destruction, in the area of the bite., respiratory symptoms : Respiratory paralysis and pulmonary edema can be due to either elapid or viper bites, whereas pulmonary complications of coagulopathy are exclusively reported with viper bites., weakness : Weakness in your muscles and numbness in the face or limbs., Pain : Sharp, throbbing, burning pain around the bite that you may not feel for a little while after the bite. You may also feel pain all the way up whichever limb was affected, such as in the groin for a bite on the leg or the armpit for a bite on the arm. But not everyone feels pain. For example, a bite from a coral snake can be almost painless at first, but still deadly., vision abnormalities : Neurotoxic pa- ralysis may also begin within the first hour of snake bites and is seen first as ptosis, then blurred vision and diplopia., kidney faliure : Pathogenesis of kidney injury due to snake envenomation includes ischaemia secondary to decreased kidney blood flow caused by systemic bleeding and vascular leakage, proteolytic degradation of the glomerular basement membrane by snake venom metalloproteinases (SVMPs), Signs : "bleeding : They can cause bleeding or interfere with the bloods ability to clot.", Hypotension : Snake venom PLA2s can lower blood pressure through the production of arachidonic acid, a precursor of cyclooxygenase metabolites (prostaglandins or prostacyclins)., Treatment : medication : Neostigmine , Atropine/ Atropine methonitrate, Edrophonium chloride, airway, breathing, and circulation, Fluid resuscitation with isotonic saline (20–40,mL/kg IV) should be initiated if there is any evidence of hemodynamic,instability, and a trial of 5% albumin (10–20 mL/kg IV) may,be undertaken if the response to saline infusion is inadequate. Vasopressors,(e.g., norepinephrine, dopamine) should be added only if,venom-induced shock persists after aggressive volume resuscitation,and antivenom administration., Pathophysiology : Snake venoms are highly variable and complex mixtures of enzymes, polypeptides, glycoproteins, and other constituents. Among the deleterious components are proteolytic enzymes that cause local tissue necrosis, affect the coagulation pathway at various steps, and impair organ function. Hemorrhagins cause vascular leakage, resulting in fluid shifts and spontaneous local and systemic bleeding. Hyaluronidases promote the spread of venom through connective tissue. Myocardial depressant factors reduce cardiac output, and bradykinins cause vasodilation and hypotension. Neurotoxins act at various sites of the neuromuscular junction to block transmission and cause muscle paralysis. Most snake venoms have multisystem effects on their victims. After a venomous snakebite, the time to symptom onset and clinical presentation can be quite variable and depends on the species involved, the anatomic location of the bite, and the amount of venom injected. Envenomations by most viperids and some elapids with necrotizing venoms cause progressive local pain, soft-tissue swelling, and ecchymosis. Hemorrhagic or serum-filled vesicles and bullae may develop at the bite site over a period of hours to days. In serious bites, tissue loss can be significant. Systemic findings are extremely variable and can include generalized fatigue, nausea, changes in taste, mouth numbness, tachycardia or bradycardia, hypotension, muscle fasciculations, pulmonary edema, renal dysfunction, and spontaneous hemorrhage from essentially any anatomic site. Envenomations by neurotoxic elapids, such as kraits (Bungarus species), many Australian elapids (e.g., death adders Acanthophis species and tiger snakes Notechis species), some cobras (Naja species), some viperids (e.g., the South American rattlesnake Crotalus durissus, and certain Indian Russell’s vipers Daboia russelii), cause neurologic dysfunction. Early findings may consist of nausea and vomiting, headache, paresthesias or numbness, and altered mental status. Victims may develop cranial nerve abnormalities (e.g., ptosis, difficulty swallowing), followed by peripheral motor weakness. Severe envenomation may result in muscle paralysis, including the muscles of respiration, and lead to death from respiratory failure and aspiration. Sea snake envenomation results in local pain (variable), generalized myalgias, trismus, rhabdomyolysis, and progressive flaccid paralysis; these manifestations can be delayed for several hours., Epidemiology : 421, 000–1, 841, 000 envenomations and 20, 000–94, 000 , 1.2 million and 5.5 million snakebites, TREATABLE, Most snakebites occur between April and October, when outdoor activities are popular. You can avoid snakebites by taking the following steps : ,,Avoid places where snakes may live. These places include tall grass or brush, rocky areas, fallen logs, bluffs, swamps, marshes, and deep holes in the ground.,,When moving through tall grass or weeds, poke at the ground in front of you with a long stick to scare away snakes.,,Watch where you step and where you sit when outdoors.,,Wear loose, long pants and high, thick leather or rubber boots.,,Shine a flashlight on your path when walking outside at night.,,Never handle a snake, even if you think it is dead. Recently killed snakes may still bite by reflex., Complications : Acute Renal Failure, death, gangrene, ischaemia, necrosis, respiratory failure, shock, Serum sickness, compartment syndrome, Coagulopathy, Diagnostics : ABG, ECG, CHEST X RAY, PHYSICAL EXAMINATION, Differential diagnosis : Anaphylaxis, deep venous thrombosis, septic shock, Serum sickness, wound infection, disease description : A snakebite is an injury caused by the bite of a snake, especially a venomous snake. A common sign of a bite from a venomous snake is the presence of two puncture wounds from the animals fangs. Sometimes venom injection from the bite may occur. This may result in redness, swelling, and severe pain at the area, which may take up to an hour to appear. Vomiting, blurred vision, tingling of the limbs, and sweating may result. Most bites are on the hands, arms, or legs. Fear following a bite is common with symptoms of a racing heart and feeling faint. The venom may cause bleeding, kidney failure, a severe allergic reaction, tissue death around the bite, or breathing problems. Bites may result in the loss of a limb or other chronic problems or even death.

Sneddon Syndrome

Disease Name : Sneddon Syndrome, Symptoms : headache, vertigo, Signs : hypertension, peripheral neuropathies, cutaneous livedo, Treatment : There is no specific treatment for Sneddon syndrome. Treatment is symptomatic and supportive, but there are no standardized treatment protocols or guidelines. Due to the rarity of the disease, there are no treatment trials that have been tested on a large group of patients. Various treatments have been reported in the medical literature as part of single case reports or small series of patients. Treatment trials would be very helpful to determine the long-term safety and effectiveness of specific medications and treatments for individuals with Sneddon syndrome.,,Anti-aggregants such as aspirin or direct oral anticoagulants (DOAC) or vitamin K-antagonsists such as warfarin may be given to thin the blood and to prevent the formation of blood clots. Some physicians recommend that individuals with Sneddon syndrome without antiphospholipid antibodies should be treated in a less aggressive manner through antiplatelet therapy with aspirin and patients with antiphospholipid antibodies should receive DOAC or warfarin with an international normalize ratio (INR) target of 2 to 3. But even with heart valve involvement, antiplatelet therapy was not inferior in comparison to anticoagulation. And always the risk of microbleeds and intracerebral hemorrhage must be taken into account.,,The use of anti-inflammatory or immunosuppressive therapies is discussed controversial, but may be considered in patients with biopsy or laboratory findings indicative of an inflammation. Always the association with an autoimmune disorder like lupus must be excluded., Pathophysiology : The exact pathophysiology of Sneddon syndrome remains incompletely understood, but there are several theories and mechanisms that have been proposed : Vascular Damage and Thrombosis : One of the central features of Sneddon syndrome is the involvement of small- to medium-sized blood vessels. It is thought that endothelial dysfunction (impairment of the inner lining of blood vessels) plays a key role. Endothelial damage can lead to inflammation and activation of platelets, which in turn contributes to the formation of blood clots within the affected vessels. These blood clots can obstruct blood flow, leading to tissue ischemia (lack of blood supply) and subsequent cerebrovascular events.Immune-Mediated Mechanisms : Autoimmune processes have been suggested as a potential contributor to Sneddon syndrome. Some individuals with the syndrome have been found to have antiphospholipid antibodies, which are associated with an increased risk of blood clot formation. These antibodies can target phospholipids, a component of cell membranes, leading to disruption of normal endothelial function and increased clotting tendencies.Genetic Factors : While there is currently limited understanding of the genetic basis of Sneddon syndrome, genetic predisposition may play a role in its development. Genetic factors could influence the susceptibility to endothelial damage, immune dysregulation, or other aspects of the pathophysiological processes involved.Inflammatory Processes : Chronic inflammation is believed to contribute to the pathophysiology of Sneddon syndrome. Inflammation can lead to endothelial dysfunction and create a pro-thrombotic (pro-clotting) environment within blood vessels. Additionally, inflammation can promote the recruitment of immune cells to affected areas, further contributing to vessel damage., Epidemiology : One estimate places the incidence at approximately one out of 250, 000 individuals in the general population., There’s no way to prevent Sneddon syndrome.,In many cases, Sneddon syndrome causes neurological changes like memory loss and difficulty speaking that progressively worsen. In some cases, people with Sneddon syndrome are diagnosed with early-onset dementia., Complications : hemiparesis, hypertension, visual defects, fits, later cognitive changes, Diagnostics : EEG, CT/MRI, MRI, ARTERIOGRAPHY, skin lesion biopsy, Differential diagnosis : cutaneous polyarteritis nodosa, Fabry Disease, lupus erythematosus, disease description : Sneddon syndrome (SS) is characterized by livedo racemosa, recurrent ischemic strokes, and often progressive vascular dementia. After exclusion of more common causes of stroke, livedo reticularis may be a clue to the aetiology of ischaemic stroke, leading to a diagnosis of Sneddon syndrome

Snoring

Disease Name : Snoring, Symptoms : Excessive daytime sleepiness, fatigue, headache, Irritability, SNORING, Signs : DEPRESSION, Treatment : Avoidance of alcohol, sedatives and hypnotics.,2. Reduction of weight.,3. Sleeping on the side rather than on the back, Performing uvulopalatoplasty (UPP) surgically with,cold knife or assisted with radiofrequency (RAUP) or,laser (LAUP)., Pathophysiology : Muscles of pharynx are relaxed during sleep and cause partial obstruction. Breathing against obstruction causes vibrations of soft palate, tonsillar pillars and base of tongue producing sound. Sound as loud as 90 dB has been recorded during snoring. Snoring may be primary, i.e. without association with obstructive sleep apnoea (OSA) or complicated, i.e. associated with OSA. Primary snoring is not associated with excessive daytime sleepiness and has apnoea–hypnoea index of less than five. Sites of snoring may be soft palate, tonsillar pillars or hypopharynx. It may vary from patient to patient and even in the same patient thus making surgical correction a difficult decision. Sometimes sites of snoring are multiple even in the same patient., Epidemiology : To Do : Avoidance of alcohol, sedatives and hypnotics.,Reduction of weight,Sleeping on the side rather than on the back, Complications : Cerebrovascular accident, hypertension, Myocardial infarction, DEPRESSION, sleepiness, Diagnostics : CT/MRI, X RAY, Differential diagnosis : Asthma, Chronic Obstructive Pulmonary Disease, DEPRESSION, Gastroesophageal reflux disease (GERD), Hypothyroidism, obstructive sleep apnea, disease description : Snoring is the hoarse or harsh sound that occurs when air flows past relaxed tissues in your throat, causing the tissues to vibrate as you breathe. Nearly everyone snores now and then, but for some people it can be a chronic problem. Sometimes it may also indicate a serious health condition. In addition, snoring can be a nuisance to your partner.

Snyder-robinson Syndrome

Disease Name : Snyder-robinson Syndrome, Symptoms : developmental delay : Males with Snyder-Robinson syndrome have delayed development., Osteoporosis : Osteoporosis develops which can result in numerous fractures without a causative event., hypotonia : Weakness or "floppiness" (hypotonia) typically becomes apparent in infancy, and the loss of muscle tissue continues with age., Speech Difficulties : Speech often develops late, and speech difficulties are common. Some affected individuals never develop any speech., Intellectual disability : The intellectual disability can range from mild to profound., KYPHOSCOLIOSIS : Most affected individuals also develop an abnormal side-to-side and back-to-front curvature of the spine., Facial abnormalities : Snyder-Robinson syndrome is associated with distinctive facial features, including a prominent lower lip; a high, narrow roof of the mouth or an opening in the roof of the mouth (a cleft palate); and differences in the size and shape of the right and left sides of the face (facial asymmetry)., Gait disturbance : People with this condition often have difficulty walking; most have an unsteady gait., Signs : nan, Treatment : medication : Calcium carbonate , There is no treatment which effectively treats Snyder-Robinson syndrome. Initially, as SRS results from a lack of spermine being produced by cells within the body, it was thought spermine supplementation might treat the disorder. However, this approach has proved to be unsuccessful. Thus, treatment is directed towards alleviating some of the symptoms of SRS. Speech, physical, occupational therapies have been helpful but results have varied, Treatment of seizures can be attempted with various drugs. However, success with any one drug has been variable and some seizures have been refractory to treatment., Pathophysiology : This gene provides instructions for making an enzyme called spermine synthase his enzyme is involved in the production of spermine, which is a type of small molecule called a polyamine. Polyamines have many critical functions within cells. Studies suggest that these molecules play roles in cell growth and division, the production of new proteins, the repair of damaged tissues, the function of molecules called ion channel, and the controlled self-destruction of cells (apoptosis)Polyamines appear to be necessary for normal development and function of the brain and other parts of the body. Mutations in the SMS gene greatly reduce or eliminate the activity of spermine synthase, which decreases the amount of spermine in cells. A shortage of this polyamine clearly impacts normal development, including the development of the brain, muscles, and bones, but it is unknown how it leads to the specific signs and symptoms of Snyder-Robinson syndrome., Epidemiology : Snyder-Robinson syndrome is a rare condition; its prevalence is unknown., About 10 affected families have been identified worldwide., variable, "Snyder-Robinson syndrome (SRS) is an X-linked intellectual disability syndrome. Therefore cant be prevented.", Complications : gait disturbances, Osteoporosis, Diagnostics : GENETIC TESTING, enzyme marker test, Differential diagnosis : cerebral palsy, Glycerol kinase deficiency, Prader-Willi syndrome, disease description : Snyder-Robinson syndrome is a condition characterized by intellectual disability, muscle and bone abnormalities, and other problems with development. It occurs exclusively in males. Males with Snyder-Robinson syndrome have delayed development and intellectual disability beginning in early childhood. The intellectual disability can range from mild to profound. Speech often develops late, and speech difficulties are common. Some affected individuals never develop any speech.

Soft Tissue Chondroma

Disease Name : Soft Tissue Chondroma, Symptoms : lump : Soft tissue chondromas most commonly develop during middle age. Although they rarely measure more than 3 cm in diameter, they are often noticeable, appearing as nodules or lumps in the small bones of the fingers, hands, toes, and feet. Most patients have a single tumor or mass that is not painful., Signs : nan, Treatment : Both periosteal chondromas and soft tissue chondromas are easily identified as distinct and separate masses and can be surgically removed., Pathophysiology : Metaplasia : One of the prevailing theories is that soft tissue chondromas develop through a process called metaplasia. Metaplasia involves the transformation of one type of mature cell into another type of cell that is not normally found in that tissue. In the case of soft tissue chondromas, it is thought that pluripotent mesenchymal stem cells or fibroblasts undergo metaplasia and differentiate into cartilage cells (chondrocytes) within the soft tissues.Trauma or Chronic Irritation : Some researchers suggest that soft tissue chondromas may arise in response to trauma or chronic irritation to a specific area of soft tissue. Repetitive microtrauma or chronic inflammation could lead to changes in the local cellular environment, promoting the transformation of local cells into chondrocytes.Genetic Factors : Genetic factors may also play a role in the development of soft tissue chondromas. Alterations or mutations in certain genes involved in cell growth, differentiation, and tissue development could contribute to the formation of these tumors.Dysregulation of Cartilage Formation : Abnormalities in the processes that regulate cartilage formation and growth could lead to the development of soft tissue chondromas. Dysregulation of signaling pathways involved in cartilage development, such as the hedgehog signaling pathway, could potentially contribute to tumor formation., Epidemiology : The prevalence of enchondromas is approximately 12, 000 - 24, 000 per 100, 000 individuals of benign bone tumors and 3000-10, 000 of all bone tumors., The incidence is only about 1.5% of all benign tumors, variable, Complications : nan, Diagnostics : GENETIC TESTING, MRI, X RAY, Differential diagnosis : BURSITIS, Giant cell tumour, disease description : Soft tissue chondromas are not connected to bone. They most often form on the tendons that attach muscles to bone or to the tendon sheaths that keep tendons in place next to bone. Soft tissue chondromas also sometimes grow out of the joint capsule, a dense, fibrous tissue that encloses a joint and provides stability.

Solar Retinopathy

Disease Name : Solar Retinopathy, Symptoms : eye pain : Pain in the eye., headache : Patients affected by solar retinopathy experiences episodes of intense headaches., visual changes : More serious symptoms of solar retinopathy include changes in vision, such as blurry vision., Loss of vision : Partial or total loss of vision in one or both eyes., photophobia : Sensitivity to light is complained by the patients., Signs : nan, Treatment : There is no effective treatment for photoretinitis, so,emphasis should be on prevention. Eclipse viewing,should be discouraged unless there is proper use,of protective eye wear filters (which absorb UV and,infrared wavelengths)., Pathophysiology : Solar radiations damage the retina through : ¦¦Photochemical effects produced by UV and visible blue light, and ¦¦Thermal effects may enhance the photochemical effects. The long visible wavelength and infrared rays from the sun are absorbed by the pigment epithelium producing a thermal effect. Therefore, severity of lesion varies directly with the degree of pigmentation of the fundus, duration of exposure and the climatic conditions during exposure. • Persistence of negative after-image of the sun, progressing later into a positive scotoma and metamorphopsia. • Decreased vision (6/12–6/60) (unilateral or bilateral) which develops within 1 to 4 hours after solar exposure, usually improves to 6/6–6/12 within six months. Initially, the fundus may appear normal. Shortly after exposure a small yellow spot with grey margin may be noted in the foveolar and parafoveolar region. The typical lesion, which appears later, consists of a central burnt-out hole in the pigment epithelium surrounded by aggregation of mottled pigment. Ophthalmoscopically, it appears as a bean- or kidney-shaped pigmented spot with yellowish white centre in the foveal region. In worst cases, typical macular hole may appear., Epidemiology : 0.01%, Solar retinopathy is caused by prolonged or high intensity ... Men have a slightly higher incidence of solar retinopathy than women., vaiable, The RANZCO advises that the only way to guarantee the prevention of solar retinopathy is to avoid exposure through direct sungazing of any kind.,,If people decide to use eclipse glasses, it is important to minimise the risks., Complications : scotoma, Loss of visual acuity, Diagnostics : Optical coherence tomography (OCT), PHYSICAL EXAMINATION, ophthalmoscopy, Differential diagnosis : Cystoid macular oedema, macular hole, disease description : Solar retinopathy also known as photoretinitis, or eclipse retinopathy, refers to retinal injury induced by direct or indirect sun viewing. Solar retinopathy is associated with religious sun gazing, solar eclipse observing, telescopic solar viewing, sun bathing and sun watching in psychiatric disorders.

Solar Urticaria

Disease Name : Solar Urticaria, Symptoms : allergic reaction : If the hives cover a lot of your skin, you may have other allergy symptoms, such as low blood pressure, headache, nausea, wheezing, difficulty breathing & fainting., "Mucosal damage : A stinging, itchy rash develops within minutes after a short period (less than 30 minutes) of sun exposure. The rash may look like weals and be red and swollen. Often the rash affects areas of exposed skin that are normally shielded from sunlight by clothing, e.g. back. The face and upper sides of the hands that are constantly exposed to the sun may be unaffected or only slightly affected. This may be put down to acclimatisation or hardening of these chronically exposed areas.", "itchy rashes : A stinging, itchy rash develops within minutes after a short period (less than 30 minutes) of sun exposure. The rash may look like weals and be red and swollen. Often the rash affects areas of exposed skin that are normally shielded from sunlight by clothing, e.g. back. The face and upper sides of the hands that are constantly exposed to the sun may be unaffected or only slightly affected. This may be put down to acclimatisation or hardening of these chronically exposed areas.", Signs : nan, Treatment : Antihistamines are most effective at reducing ,or abolishing weal and fl are, although not immediate or delayed ,erythema., Doxepin 27 , ketotifen, chromoglycate and montelukast may also ,be benefi cial in individual patients although, due to the rarity of ,the condition, these agents have not been thoroughly evaluated.,Ciclosporin, systemic glucocorticoids and other immunosuppressants ,may be effective in some patients and ineffective in others. For severely affected patients, particularly if the intradermal ,test is positive, plasmapheresis may be benefi cial, Pathophysiology : Solar urticaria pathophysiology is not entirely understood. It is an immediate hypersensitivity reaction, which might be IgE-mediated, occurring after exposure to the sun. The radiation may activate an endogenous substance called a chromophore, which could be present in the serum and/or the dermis, turning it into an immunologically active photo allergen. This later induces the degranulation of mast cells, resulting in lesions of urticaria. The intradermal positive reaction after injection of the patient’s irradiated serum is consistent with the hypothesis of a circulating chromophore.Certain radiation wavelengths (usually long ones) may inhibit the immunological reaction induced by other wavelengths (usually short ones). This is called the double spectrum of action.Occasionally, solar urticaria is triggered by an exogenous substance, such as some medications. Some examples include atorvastatin, chlorpromazine, tetracycline, or oral contraceptives., Epidemiology : only about 4% of patients with photosensitive disorders are reported, more than 650 cases have been described worldwide., variable, There are some things you can do to prevent or reduce your risk for solar urticaria.,,Limit your sun exposure, and especially stay out of the sun between 10 a.m. and 4 p.m. when the sun is strongest.,Talk with your doctor about phototherapy treatment which may help to desensitize you.,If your rash is related to a particular medication, ask your doctor if there is an alternative.,Wear closely woven clothes with maximum coverage, such as long sleeves, long pants, or long skirts.,Consider wearing sun protective clothing with a UPF protection factor greater than 40, which blocks UV better than sunscreens.,Wear a broad-spectrum sunscreen on any exposed skin, and reapply regularly.,Wear sunglasses and a hat with a broad brim when outdoors.,Use a sun umbrella., Complications : Urticaria, Diagnostics : HISTOPATHLOGY, Patch Test, full thickness skin biopsy, Differential diagnosis : dermatitis, lupus erythematosus, disease description : Solar urticaria is a chronic acquired photosensitivity disorder. It consists of recurrent episodes of urticaria rash developed on areas of the skin exposed to sunlight. Despite being usually a benign condition, it may be extremely disabling, thus limiting everyday activities and severely altering the quality of life of patient?s

Solid Pseudo Papillary Carcinoma

Disease Name : Solid Pseudo Papillary Carcinoma, Symptoms : jaundice : Jaundice is a condition produced when excess amounts of bilirubin circulating in the blood stream dissolve in the subcutaneous fat causing a yellowish appearance of the skin and the whites of the eyes., TUMOURS : Solid pseudopapillary tumors often manifest late, and the masses are large with mean size of 10 cm., ABDOMINAL MASS : A feeling of heaviness is felt in the lower abdomen., Signs : nan, Treatment : Surgical resection., Pathophysiology : Cellular Origin : SPC is believed to arise from pancreatic progenitor cells that have the potential to differentiate into various cell types within the pancreas. These cells might undergo genetic mutations or epigenetic changes that lead to the development of a solid pseudopapillary tumor.Genetic Alterations : Studies have identified certain genetic alterations in SPC, including mutations in the CTNNB1 gene (encoding ß-catenin) and inactivation of the APC gene. These mutations can lead to the dysregulation of the Wnt signaling pathway, which plays a role in cell proliferation and differentiation. Dysregulated Wnt signaling may contribute to the uncontrolled growth of tumor cells in SPC.Epithelial-Mesenchymal Transition (EMT) : EMT is a process through which epithelial cells acquire characteristics of mesenchymal cells, leading to increased migratory and invasive properties. Its been suggested that SPC may undergo EMT, contributing to its ability to infiltrate surrounding tissues and metastasize to distant organs.Hormonal Influences : Some studies have suggested a possible hormonal influence on the development of SPC, given its higher incidence in young women. Estrogen receptors have been found in SPC cells, and estrogen-related pathways might contribute to tumor growth., Epidemiology : The male to female ratio is 1 : 10, incidence of 0.13% to 2.7% of all pancreatic tumors., variable, Complications : pancreatic pseudocyst, Diagnostics : MRI, CT, Immunostaining, Differential diagnosis : acinar cell carcinoma, Pancreatic neuroendocrine tumors, pancreatoblastoma, disease description : Solid pseudopapillary tumors (SPTs) of the pancreas are rare neoplasms with low malignant potential. SPTs have been associated with several other names, including Frantz tumors, Hamoudi tumors, and papillary cystic neoplasm. SPTs are notable for their high prevalence among women, most commonly occurring in the third decade of life and earlier

Solid Pseudopapillary Neoplasm

Disease Name : Solid Pseudopapillary Neoplasm, Symptoms : TUMOURS : Solid pseudopapillary tumors often manifest late, and the masses are large with mean size of 10 cm., Signs : nan, Treatment : For the unresectable SPNs (too large or widespread metastasis), radio-therapy is suggested, as the tumours are radiosensitive, complete surgical resection, Pathophysiology : Cellular Origin : SPN is thought to arise from pluripotent progenitor cells in the pancreas that have the ability to differentiate into various cell types. These cells may undergo genetic mutations or epigenetic changes that drive the formation of SPN.Genetic Alterations : Studies have identified specific genetic mutations in SPN, including mutations in the CTNNB1 gene (ß-catenin gene) and inactivation of the APC (adenomatous polyposis coli) gene. The CTNNB1 gene is a key component of the Wnt signaling pathway, which regulates cell proliferation and differentiation. Mutations in this pathway can lead to uncontrolled cell growth and tumor formation. The activation of the Wnt/ß-catenin pathway is a hallmark of SPN and contributes to its unique histological features.Epithelial-Mesenchymal Transition (EMT) : SPN may undergo an epithelial-mesenchymal transition, a process in which epithelial cells acquire characteristics of mesenchymal cells. This transition can enhance the tumors ability to invade surrounding tissues and metastasize. EMT-related markers have been identified in SPN tissue samples, supporting the involvement of this process.Hormonal and Hormone Receptor Expression : Estrogen and progesterone receptors are often expressed in SPN cells, suggesting a potential hormonal influence on tumor development. The presence of hormone receptors may contribute to the higher incidence of SPN in young women and could play a role in tumor growth.Aberrant Differentiation and Cellular Architecture : SPN is characterized by a combination of solid and pseudopapillary architectural patterns. The solid areas consist of poorly differentiated cells with high mitotic activity, while the pseudopapillary areas have a more organized arrangement. The factors contributing to this unique differentiation pattern are still being studied., Epidemiology : Usually presents in the third to fourth decade of life, 0.9%-2.7% of all exocrine pancreatic neoplasms and 5% of cystic pancreatic neoplasms, poor, Complications : nan, Diagnostics : MRI, CT SCAN, immunohistochemistry, Histopathological examination, Differential diagnosis : acinar cell carcinoma, Pancreatic neuroendocrine tumors, pancreatoblastoma, disease description : Low malignant potential tumors with unclear cell of origin and pathogenesisMay be derived from pluripotent stem cells of the genital ridges that become attached to the pancreas during embryogenesis 

Solitary Fibrous Tumour And Haemangiopericytoma (

Disease Name : Solitary Fibrous Tumour And Haemangiopericytoma (, Symptoms : painless, slow-growing mass that is firm or hard., Signs : nan, Treatment : nan, Pathophysiology : Paracentric inversion involving chromosome 12q, resulting in NAB2-STAT6 gene fusion. NAB2-STAT6 fusions converts NAB2 from transcriptional repressor to activator Altered NAB2 function leads to constitutive (deregulated) expression of early growth response 1 (EGR1) target genes, including IGF2, FGFR1, Epidemiology : nan, Complications : nan, Diagnostics : MRI, CT SCAN, Differential diagnosis : nan, disease description : Fibroblastic tumor characterized by haphazardly arranged spindled to ovoid cells, prominent staghorn vasculature and NAB2-STAT6 gene rearrangement

Some Dehydration

Disease Name : Some Dehydration, Symptoms : fatigue, Restlessness, IRRITABLE, Thirsty; eager to drink, Eyes-Slightly sunken, Mouth and tongue-Dry, vomiting, loose motion, Signs : HEART RATE-Normal to increased, Quality of pulses-Normal to decreased, Breathing-Normal; fast, Tears-Decreased, Skinfold-Recoil in <2 sec, Capillary refill-PROLONGED, Extremities-COOL, Urine output-DECREASED, Treatment : medication : Oral Rehydration Salts , REHYDRATION THERAPY-Infants ‡ and children : ORS, 50-100 mL/kg over 3-4 hr. Continue,breast feeding. After 4 hr, give food every 3-4 hr for children who,normally receive solid foods.,REPLACEMENT,OF LOSSES,DURING,MAINTENANCE-Infants and,children : ,<10 kg body,weight : 50-,100 mL ORS,for each,diarrheal stool,or vomiting,episode, up to,~500 mL/day, Pathophysiology : Dehydration causes a decrease in total body water in both the intracellular and extracellular fluid volumes. Volume depletion closely correlates with the signs and symptoms of dehydration. The total body water (TBW) in humans is distributed in two major compartments. 2/3rd the of TBW is in the intracellular compartment and the other 1/3rd is distributed between interstitial space (75%) and plasma (25%). The total body water is higher in infants and children as compared to the adults. In infants, it is 70% of the total weight, whereas it is 65% and 60% respectively in children and adults. As indicated earlier dehydration is total water depletion with respect to the sodium and volume depletion is the decrease in the circulation volume. Volume depletion is seen in acute blood loss and burns, whereas distributive volume depletion is seen in sepsis and anaphylaxis. In much of the literature, the distinction between dehydration and volume depletion is a blur.Metabolic acidosis is seen in infants and children with dehydration, the pathophysiology of which is multifactorial.1. excess bicarbonate loss in the diarrhea stool or in the Urine is certain types of renal tubular acidosis2. Ketosis secondary to the glycogen depletion seen in starvation which sets in infants and children much earlier when compared to adults.3. Lactic acid production secondary to poor tissue perfusion4. Hydrogen ion retention by the kidney from decreased renal perfusion and decreased glomerular filtration rate.In children with pyloric stenosis have very unique electrolyte abnormalities from the excessive emesis of gastric contents. This is seen mostly in the older children. They loose chloride, sodium, potassium in addition to volume resulting in hypochloremic, hypokalemic metabolic alkalosis. Kidney excretes base in the form of Hco3 ion to maintain acid-base balance of loss of Hydrogen ion in the emesis in the form of hydrogen chloride. It is interesting to note that kidney also excretes hydrogen ion to save sodium and water, which could be the reason for aciduria., Epidemiology : good, Dehydration happens when your body loses or uses more fluids than it takes in. When it happens, your body isn’t able to do all the things it’s supposed to. It’s especially dangerous in older people and young children, ,,The best way to avoid dehydration is to drink plenty of fluids, especially if you’re in a hot climate or you’re playing or working in the sun. Be aware of how much fluid you’re losing through sweat and when you pee. Drink enough to keep up with what you’re getting rid of., Complications : death, Lactic acidosis, ALTERED MENTAL STATUS, Hypotension, kidney dysfunction, Diagnostics : ABG, Differential diagnosis : Acute Gastroenteritis, hypernatremia, hypokalemia, HYPOVOLEMIA, metabolic acidosis, pyloric stenosis, disease description : Dehydration occurs when you use or lose more fluid than you take in, and your body doesnt have enough water and other fluids to carry out its normal functions. If you dont replace lost fluids, you will get dehydrated.Anyone may become dehydrated, but the condition is especially dangerous for young children and older adults.The most common cause of dehydration in young children is severe diarrhea and vomiting. Older adults naturally have a lower volume of water in their bodies, and may have conditions or take medications that increase the risk of dehydration.

Sotos Syndrome

Disease Name : Sotos Syndrome, Symptoms : CNS disturbances : People with Sotos syndrome often have intellectual disability, and most also have neurodevelopmental disorders. Conditions that commonly occur in people with Sotos syndrome include autism spectrum disorder, attention-deficit/hyperactivity disorder (ADHD), phobias, obsessions and compulsions, tantrums, and impulsive behaviors., jaundice : Some infants with this disorder experience yellowing of the skin and whites of the eyes., hypotonia : Weak muscle tone (hypotonia) may delay other aspects of early development, particularly motor skills such as sitting and crawling., Speech Difficulties : Problems with speech and language are also common. Affected individuals often have a stutter, a monotone voice, and problems with sound production., Facial abnormalities : Characteristic facial features include a long, narrow face; a high forehead; flushed (reddened) cheeks; and a small, pointed chin. In addition, the outside corners of the eyes may point downward (down-slanting palpebral fissures). This facial appearance is most notable in early childhood., scoliosis : Symptoms of Sotos syndrome can include an abnormal side-to-side curvature of the spine., Signs : nan, Treatment : Treatment for Sotos syndrome varies based on the severity of the diagnosis and aims to alleviate symptoms of the condition. Treatment for Sotos syndrome includes : ,,Educational support (special education program).,Participating in therapy (behavioral, physical, speech).,Taking medications to manage symptoms (ADHD, anxiety).,Using hearing aids.,Wearing a back brace or undergoing surgery for scoliosis.,Wearing glasses.,Early intervention for developmental delays and other symptoms related to Sotos syndrome generally helps children reach their full potential., Pathophysiology : Sotos syndrome is the result of a genetic mutation — a change in a gene that makes it not work the way it should. About 95% of cases of Sotos syndrome occur due to a new genetic mutation in an egg or sperm cell. New genetic mutations happen randomly. While less likely to occur, children can inherit the condition if one parent carries the mutated gene and passes it to their child (autosomal dominant); if a parent has Sotos syndrome, any child born to them will have a 50% chance of inheriting it., Epidemiology : Sotos syndrome is a rare condition that affects an estimated 1 in every 14, 000 births. Often, Sotos syndrome shares the same symptoms as other conditions. For this reason, many cases go undiagnosed., poor, There is no way to prevent most cases of Sotos syndrome. It’s a rare condition caused by a genetic mutation that happens unexpectedly. If you have Sotos syndrome, or if you plan on becoming pregnant, talk with your healthcare provider about genetic testing to assess your risk of having a child with a genetic condition., Complications : Hearing loss, seizures, heart problem, vision abnormalities, scoliosis, kidney dysfunction, Diagnostics : GENETIC TESTING, MRI, PHYSICAL EXAMINATION, Differential diagnosis : Acromegaly, fragile x syndrome, HOMOCYSTINURIA, Marfan syndrome, Neurofibromatosis, disease description : Sotos syndrome is a disorder characterized by a distinctive facial appearance, overgrowth in childhood, and learning disabilities or delayed development of mental and movement abilities. Characteristic facial features include a long, narrow face; a high forehead; flushed (reddened) cheeks; and a small, pointed chin. People with Sotos syndrome often have intellectual disability, and most also have behavioral problems. Frequent behavioral issues include autism spectrum disorder, attention-deficit/hyperactivity disorder (ADHD), phobias, obsessions and compulsions, tantrums, and impulsive behaviors. Problems with speech and language are also common