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Sparganosis

Disease Name : Sparganosis, Symptoms : ocular changes : Ocular sparganosis depends on the exact location of spargana within the eye. It may present as eyelid redness, swelling, intraorbital mass, excessive lacrimation, itch or pain., Neurological symptoms : Larvae in the cerebral hemisphere can cause seizure, fatigue, limb weakness, confusion, headache, memory loss & cerebral haemorrhage., cutaneous symptoms : Cutaneous sparganosis occurs when sparganum larvae invade subcutaneous connective tissue and superficial muscles. Patients present with slowly growing, rubbery, subcutaneous nodules or tumours (0.5–5 cm). These are usually painless. Common sites are chest wall, lower extremities, cheek or scrotum., Signs : nan, Treatment : medication : Praziquantel , Praziquantel has ,limited success in the treatment of the disease, Treatment is by surgical removal and drainage, Pathophysiology : Adult Spirometra parasitize the gut of canines and felines. Eggs passed into water develop into procercoid larvae in copepod hosts of the genera Diaptomus and Cyclops. These are eaten by frogs, lizards, snakes, birds and some mammals, including mice and monkeys, in which the plerocercoid larvae develop, in muscle sheaths. Humans are infected either by the application of raw flesh to the skin or eye, usually as a medicinal poultice, or through eating uncooked flesh or drinking water containing infected copepods. Ingestion sparganosis occurs a variable amount of time after eating infected flesh, or drinking infected copepods. The larvae penetrate the intestine and develop into spargana, particularly in the subcutaneous tissues and muscle. The invaded areas become oedematous and form painful lumps, in the centres of which the white ribbon-like spargana move. Their death results in very intense inflammation with destruction of tissue and massive eosinophilia. Clinical variants : Application sparganosis. The spargana migrate into the inflamed part causing an immediate severe local pruritus. Subsequently, signs of sparganosis may be very hard to differentiate from those of the primary inflammation for which the flesh poultice was applied. Redness, pain and swelling increase in severity over a few days or very few weeks, and the worms become localized in small nodules surrounded by pus. Ocular sparganosis frequently results in panophthalmitis and loss of the globe. Sparganum proliferum. This is a rare form in which the sparganum branches and divides, producing thousands of mainly subcutaneous spargana, which form subcutaneous nodules and itchy papules. There may be a severe systemic illness with fever and eosinophilia., Epidemiology : The prevalence in frogs was on average 22.29%, ranging from 3.20% to 90.90%, poor, Spargana mainly infect through the mouth and wounds, so it is of great significance to publicize the prevention and treatment of sparganum., Complications : headache, seizures, hemiplegia, Diagnostics : MRI, Differential diagnosis : Brain tumors, Cysticercosis, orbital cellulitis, Tuberculoma, disease description : Sparganosis is a tissue infection with plerocercoid larvae or spargana of a number of species of pseudophyllidean tapeworms of the genus Spirometra. Patrick Manson described the first case, in Amoy, China in 1882. The Greek word sparganon means swaddling clothes, and describes the slender ribbon-like character of the larval worm. Once a human becomes infected, the larvae migrate into the subcutaneous tissue and develop into painful nodules.

Spectacle-frame Acanthoma

Disease Name : Spectacle-frame Acanthoma, Symptoms : "papules : Acanthoma fissuratum presents as a firm flesh-coloured papule that has a central furrow dividing the lesion in half (a coffee bean appearance). It is often painful, particularly if ulcerated.", LESIONS : The lesions are located where the glasses rest on the individual’s skin, most commonly, the lateral bridge of the nose or the retroauricular or superior auricular sulcus (behind the ear)., Signs : nan, Treatment : First line,Spectacle-frame acanthoma usually resolves after a few weeks or ,months if the patient discontinues wearing spectacles or changes ,are made to obviate the mechanical trauma. For example, a thin ,hydrocolloid or silicone dressing may be applied to the overlying ,skin as a cushion.,,Second line,Corticosteroids may be injected intralesionally.,,Third line,If necessary, the condition can be treated by surgical excision, electrosurgery and curettage., Pathophysiology : Friction between the skin and spectacles frame at the postauricular fold, or the lateral nose, can lead to localized epidermal hyperplasia. Histology shows acanthosis and hyperkeratosis of the epidermis, with a central depression and occasionally ulceration. In the dermis, there is often hyalinization of the collagen and a mild, mixed inflammatory infiltrate . Granulomatous change is not usually present.Upregulation of KGF (Keratinocyte Growth Factor) may cause the cell proliferationDefect in phosphorylase enzyme leads to intracellular glycogen accumulation, Epidemiology : canthomas occur equally in both sexes. Most cases occur in middle-aged persons, with a peak incidence between 50 and 60 years of age, variable, Avoid going outside from 10 a.m. to 4 p.m., when the sun is strongest.,Use a broad-spectrum sunscreen with SPF of 15 or higher.,Wear sun-protective clothing and hats when you’re outside.,Don’t use tanning beds., Complications : hypopigmentation, infection, Scarring, Diagnostics : biopsy, Differential diagnosis : Basal cell carcinoma, disease description : Spectacle-frame acanthoma is characterized by localized skin thickening in response to low-grade, chronic pressure from spectacle frames . It is often unilateral and occurs in the postauricular groove, or on the bridge of the nose, and is commonly mistaken for a basal cell carcinoma. Sex In a review of 27 published cases, males predominated 2. Predisposing factors Factors that contribute to the pathogenesis include the weight of the spectacles, minor derangement in local anatomy and maceration.

Spermatocytic Seminoma - Spermatocytic Seminoma Wi

Disease Name : Spermatocytic Seminoma - Spermatocytic Seminoma Wi, Symptoms : NODULES : In gross appearance spermatocytic seminomas consist of light greyish soft tissue, usually easily separable from the normal testis parenchyma but some tumours seem composed of smaller nodules., PAINLESS MASS : Spermatocytic seminoma is more frequently bilateral than seminoma and may be multifocal. The tumor involves only the testes and is not found in other locations where GCTs may occur in the male, or in the ovary in a female. The tumor usually manifests as a painless mass., Signs : nan, Treatment : Bleomycin, etoposide and cisplatin (BEP) chemotherapy has little effect on metastatic ST without sarcomatous differentiation, Orchiectomy, Pathophysiology : Testicular seminoma originates in the germinal epithelium of the seminiferous tubules. The disease is thought to result from the proliferation of immature spermatogonia. Arrested gonocyte maturation with the persistence of embryonic features and correspondingly increased genomic instability is the most probable model for the pathogenesis of CIS. The transition from the precursor lesion to invasive cancer is associated with a gain of the short arm of chromosome 12, Isochromosome i(12p), likely involving KRAS2 and possibly NANOG (pseudogenes). The exact mechanism is unknown. However, there is also an increased frequency of isozymes of 7, 15, 19, and X in seminoma., Epidemiology : 30% of patients are 30 - 39 years; 35% are 40 - 59 years; 35% are = 60 years, ~1% of germ cell tumors, Excellent, Complications : hair loss, anemia, Diagnostics : ELECTRON MICROSCOPY, Immunostaining, Differential diagnosis : classic seminoma, malignant lymphoma, solid embryonal carcinoma, disease description : Testicular cancers are classified based on their cell of origin : seminomatous, non-seminomatous, Leydig, Sertoli, choriocarcinoma, embryonal, teratoma, and yolk-sac derivatives. Seminoma and non-seminomatous lesions are frequently grouped as germ cell tumors and are notable for their responsiveness to chemotherapy compared to the other types. Seminoma accounts for about a third of all testicular germ cell malignancies and is one of the most treatable cancers, with a survival rate of 98% to 99% in early-stage disease

Spheroid Degeneration

Disease Name : Spheroid Degeneration, Symptoms : Reduced visual acuity : The majority of patients are asymptomatic. When lesions involve the central cornea, patients may experience reduced visual acuity., Signs : amber-coloured spheroidal granules (small droplets) accumulate at the level of Bowman’s membrane and anterior stroma in the interpalpebral zone : The clinical appearance is characterized by the presence of yellow or golden spherules or “droplets” at or beneath the corneal or conjunctival epithelium. The lesions are located in the superficial corneal stroma, Bowman’s membrane, subepithelium, and rarely in the epithelium in the advanced stage of the disease., Treatment : Only severe cases affecting vision need to be treated. In patients with central corneal involvement and reduced visual acuity, different treatments can be considered depending on the depth and density of the deposits. Treatments may include superficial keratectomy, phototherapeutic keratectomy, lamellar keratoplasty, or penetrating keratoplasty in the most severe cases., Pathophysiology : Cellular Injury and Degeneration : Spheroid degeneration is often observed in tissues that have undergone some form of injury or stress. This can include mechanical trauma, ischemia (reduced blood supply), hypoxia (oxygen deprivation), or toxic insults. The affected cells may undergo degenerative changes, leading to the formation of the characteristic eosinophilic spheroid structures.Disruption of Cellular Homeostasis : Underlying conditions that disrupt cellular homeostasis, such as infections, inflammation, or metabolic disturbances, can contribute to spheroid degeneration. These conditions can lead to cell dysfunction, altered cellular architecture, and the accumulation of cellular debris.Impaired Protein Handling and Clearance : Conditions that affect protein handling and clearance mechanisms within cells can lead to the accumulation of misfolded proteins or protein aggregates. This can result in cellular stress and damage, contributing to the formation of spheroid bodies.Microglial Activation in the CNS : In the central nervous system (CNS), spheroid degeneration is often associated with microglial activation. Microglia are immune cells in the CNS that respond to injury or disease. Activated microglia can phagocytose (engulf and remove) cellular debris, which may contribute to the formation of spheroid structures., Epidemiology : The prevalence of SDC was 10.7%, good, To Do : Although no known preventative measure was proven to reduce the occurrence, limiting sun exposure may reduce disease development and progression., Complications : KERATITIS, corneal erosions, Epithelial Basement Membrane Dystrophy of Cornea, Diagnostics : PHYSICAL EXAMINATION, ophthalmoscopy, Differential diagnosis : band keratopathy, Gelatinous Drop-Like Corneal Dystrophy (GDLD), Salzmann’s Nodular Degeneration, disease description : It typically occurs in men who work outdoors, especially in hostile climates. Its occurrence has been related to exposure to ultraviolet rays and/ or ageing and/or corneal disease. Spheroidal degeneration is a slowly progressive corneal and conjunctival disorder that occurs mostly in the interpalpebral region with homogenous, band-shaped, translucent, yellow-golden globular deposits

Spider Telangiectases

Disease Name : Spider Telangiectases, Symptoms : LESIONS : The lesions may briefly bleed on trauma but otherwise do not cause any symptoms or complications., Telangiectases – multiple, at characteristic sites (lips, oral cavity, fingers, nose) : Spider telangiectases are often located on the face, neck, and upper chest (this has been postulated to relate to the distribution of a large vein draining the heart, the superior vena cava). Spider telangiectases may also occur on the hands, arms, or other sites. Spider telangiectases vary in size and number, tending to be larger and more numerous in people with severe liver disease when other cutaneous signs of liver disease may be present such as palmar erythema, leukonychia, and jaundice. A central dilated arteriole may be present without radial capillaries, and the capillaries may vary in diameter, length, and number. They can also be star-shaped., Signs : nan, Treatment : First line Conservative approach (especially in children and pregnant ,patients),Many lesions resolve spontaneously,Identify and treat underlying disease,Cosmetic camouflag, Second line Electrodessication (small risk of a depressed scar if overtreated and ,may recur if undertreated),Laser : 585-nm pulsed dye laser produces a high rate of initial,clearance but may recur and require a second treatment. ,Laser is non-scarring but produces purpura,KTP 532-nm laser is also highly effective with no post-treatment ,purpura, Pathophysiology : The main vessel of the spider telangiectasis is an arteriole. The blood flows from this to the periphery, and then passes into a capillary network . The pressure in spider telangiectases rises to 40 mmHg. The lesions consist of a central, ascending, spiral, thick-walled arteriole which ends in a thin-walled ampulla just beneath the epidermis. From the ampulla, thin-walled branching channels radiate peripherally in the papillary dermis. Glomus cells have been described in the wall of the central arteriole. Therefore these lesions actually resemble microarteriovenous malformations. The high oestrogen states that predispose to the lesions (pregnancy and liver disease) are thought to induce vasodilatation of the central arteriole., Epidemiology : The condition has a higher prevalence in areas with extreme temperatures, low humidity, high wind, and presence of sand., variable, Protect your skin from the sun by applying sunscreen, and wearing sunglasses and a hat.,Use mild cleansers on your skin (such as those without dyes or fragrances).,Minimize your exposure to extreme hot or cold temperatures.,Avoid using topical steroids., Complications : THROMBOPHLEBITIS, Skin ulcers, Diagnostics : Thyroid Stimulating Hormone TSH, LIVER FUNCTION TEST LFT, HISTORY TAKING, skin lesion biopsy, Differential diagnosis : Acneiform eruptions, Basal cell carcinoma, Fabry Disease, insect bites, Scleroderma crisis, disease description : Spider veins are a colloquialism for telangiectasias and are the result of damaged small superficial blood vessels in the skin. They appear as thin purple, red, or blue lines and are most often found on the legs but may also occur elsewhere, particularly the face. Telangiectasias are also known as thread veins, venus flares, sunburst veins, stellate veins, and hyphen webs

Spina Bifida ( Neural Tube Defect )

Disease Name : Spina Bifida ( Neural Tube Defect ), Symptoms : weakness : Most children with spina bifida have some degree of weakness or paralysis in their lower limbs., Intellectual disability : Spina bifida might cause physical and intellectual disabilities that range from mild to severe. The severity depends on : The size and location of the opening in the spine. Whether part of the spinal cord and nerves are affected., Bone disorders : Orthopaedic malformations such as club feet or problems of the knees or hips., "cystic swelling in back : Spina bifida cystica is a more severe form of spina bifida that causes a visible cyst (fluid-filled sac) on the lower part of your babys back. This cyst is a symptom of spina bifida meningocele and myelomeningocele.", Signs : bowel/bladder dysfunction : Children born with Spina Bifida are almost always found to have a neurogenic bladder. This is because the nerves in the spinal cord that control the bladder did not form properly. This means that the bladder will have trouble storing urine in the bladder, emptying the bladder, or both., back pain : The type of back pain that those with spina bifida myelomeningocele feel is often described as extreme pain., Hydrocephalus : Hydrocephalus occurs due to a defect at the base of the brain, known as the "Arnold Chiari (Chiari 2) malformation." This is where parts of the brain push into the top part of the spinal canal., Treatment : People affected by spina bifida get around in different ways. These include walking without any aids or assistance; walking with braces, crutches or walkers; and using wheelchairs.,,People with spina bifida higher on the spine (near the head) might have paralyzed legs and use wheelchairs. Those with spina bifida lower on the spine (near the hips) might have more use of their legs and use crutches, braces, or walkers, or they might be able to walk without these devices.,Regular physical activity is important for all people, but especially for those with conditions that affect movement, such as spina bifida. CDC recommends 60 minutes of physical activity a day. There are many ways for people with spina bifida to be active, Sometimes when a baby has open spina bifida, or myelomeningocele doctors will perform surgery to close the spine before the baby is born, Pathophysiology : The three most common types of spina bifida are : Myelomeningocele-When people talk about spina bifida, most often they are referring to myelomeningocele. Myelomeningocele is the most serious type of spina bifida. With this condition, a sac of fluid comes through an opening in the baby’s back. Part of the spinal cord and nerves are in this sac and are damaged. This type of spina bifida causes moderate to severe disabilities, such as problems affecting how the person goes to the bathroom, loss of feeling in the person’s legs or feet, and not being able to move the legs. Meningocele-Another type of spina bifida is meningocele. With meningocele a sac of fluid comes through an opening in the baby’s back. But, the spinal cord is not in this sac. There is usually little or no nerve damage. This type of spina bifida can cause minor disabilities. Spina Bifida Occulta-Spina bifida occulta is the mildest type of spina bifida. It is sometimes called “hidden” spina bifida. With it, there is a small gap in the spine, but no opening or sac on the back. The spinal cord and the nerves usually are normal. Many times, spina bifida occulta is not discovered until late childhood or adulthood. This type of spina bifida usually does not cause any disabilities. Changes in dozens of genes in individuals with spina bifida and in those of their mothers may influence the risk of developing this type of neural tube defect. The best-studied of these genes is MTHFR, which provides instructions for making a protein that is involved in processing the vitamin folate (also called vitamin B9). A shortage (deficiency) of this vitamin is an established risk factor for neural tube defects like spina bifida. Changes in other genes related to folate processing and genes involved in the development of the neural tube have also been studied as potential risk factors for spina bifida. However, none of these genes appears to play a major role in causing the condition., Epidemiology : For unknown reasons, the prevalence of spina bifida varies among different geographic regions and ethnic groups. In the United States, this condition occurs more frequently in Hispanics and non-Hispanic whites than in African Americans., Spina bifida is one of the most common types of neural tube defect, affecting an estimated 1 in 2, 500 newborns worldwide, variable, Even though there is no known cause, experts believe spina bifida can be avoided with some simple measures to follow : ,1. Folic acid, a water-soluble B vitamin often found in leafy green vegetables, plays an important role in the prevention of spina bifida. During childbearing years, women should take a vitamin with 400 mcg (0.4 mg) folic acid every day. ,2. Tell your healthcare provider if you are taking any prescription and over-the-counter drugs, herbal and dietary supplements and vitamins.,3. Treat any fevers immediately with store brand acetaminophen or its brand name Tylenol®.,4. Avoid using hot tubs or saunas that overheat your body.,5. If you have diabetes or obesity, be sure to do your best to manage these conditions while you’re pregnant., Complications : Learning difficulty, Diagnostics : ALFA FETO PROTEIN AFP, ultrasound, CT SCAN, Triple marker test, Differential diagnosis : Chiari type 1 malformation, cord compression, disease description : Spina bifida is a condition that affects the spine and is usually apparent at birth. It is a type of neural tube defect (NTD). Spina bifida can happen anywhere along the spine if the neural tube does not close all the way. When the neural tube doesn’t close all the way, the backbone that protects the spinal cord doesn’t form and close as it should. This often results in damage to the spinal cord and nerves. Spina bifida might cause physical and intellectual disabilities that range from mild to severe. The severity depends on : The size and location of the opening in the spine. Whether part of the spinal cord and nerves are affected.

Spina Bifida

Disease Name : Spina Bifida, Symptoms : seizures, Pain, Signs : seizures, spasticity, Treatment : TREATMENT OF BASIC DEFECT, orthopaedic treatment to prevent and correct the,deformities, TT FOR INCONTINENCE., JOINT STABILISATIONS, MUSCLE POWER STRENGHTNENING, SUPPORT FOR WALKING, Pathophysiology : The defect varies in severity from a mere failure of fusion of the spinous processes, to a bony defect with a major aberration in the development of the neural elements. Accordingly, there are two main types of spina bifida : (i) spina bifida occulta; and (ii) spina bifida aperta. Spina bifida occulta : This is the mildest and the commonest. In this, the failure of the vertebral arches to fuse results in bifid spinous processes of vertebrae. The following are some of the important features : • Commonest site : This is common in the lumbosacral spine; S1 being the commonest site. • Externally, the skin may be normal or there may be tell tale signs in the form of a dimple in the skin, a lipomatous mass, a dermal sinus or a tuft of hair. Neurological impairment is not related to the severity of the bone defect. The commonest manifestation of neurological involvement is a muscle imbalance in the lower limbs with selective muscle wasting. This leads to foot deformities because of muscle imbalance; common ones being equinovarus or cavus. The cause of neural impairment may be : (i) tethering of the cord to the undersurface of the skin by a fibrous membrane (membrana reuniens); (ii) tethering of the cord to the filum terminale; (iii) bifid cord, transfixed with an antero-posterior bone bar (diastematomyelia); or (iv) defective neural development (myelodysplasia)., Epidemiology : 1 in 2, 500 newborns worldwide., GOOD, Folic acid, taken in supplement form starting at least one month before conception and continuing through the first trimester of pregnancy, greatly reduces the risk of spina bifida and other neural tube defects., Complications : Confusion, Hydrocephalus, scoliosis, Abnormal growth of nerve fibers, Diagnostics : CSF EXAMINATION, MRI, CT, X RAY, USG, Serum alpha-fetoprotein, Differential diagnosis : cord compression, Tethered Cord, disease description : Spina bifida is a birth defect that occurs when the spine and spinal cord dont form properly. Its a type of neural tube defect. The neural tube is the structure in a developing embryo that eventually becomes the babys brain, spinal cord and the tissues that enclose them .the neural tube forms early in pregnancy and it closes by the 28th day after conception. In babies with spina bifida, a portion of the neural tube doesnt close or develop properly, causing problems in the spinal cord and in the bones of the spine.

Spinal Injury

Disease Name : Spinal Injury, Symptoms : paraplegia : This paralysis affects all or part of the trunk, legs and pelvic organs., respiratory symptoms : Difficulty breathing, coughing or clearing secretions from your lungs., Sexual dysfunction : Changes in sexual function, sexual sensitivity and fertility., temperature instability : Loss of or altered sensation, including the ability to feel heat, cold and touch., Pain : Pain or an intense stinging sensation caused by damage to the nerve fibers in your spinal cord., quadriplagia : This means that your arms, hands, trunk, legs and pelvic organs are all affected by your spinal cord injury., Signs : nan, Treatment : Phase I Emergency care at the scene of accident,or in emergency department.,Phase II Definitive care in emergency department, ,or in the ward.,Phase III Rehabilitation, Harrington instrumentation – bilateral,• Luque instrumentation,• Hartshill rectangle fixation,• Pedicle screw fixation,• Moss Miami system, Pathophysiology : Spinal cord injuries are most often due to either direct trauma to the spinal cord or from compression due to fractured vertebrae or masses such as epidural hematomas or abscesses. Less commonly, the spinal cord may become injured due to compromise of blood flow, inflammatory processes, metabolic derangements, or exposure to toxins.Primary Injury  SCI results from initial insult such as mechanical forces to it, which is known as the primary injury. The most common mechanism of primary injury is a direct impact, and persistent compression typically occurs by bony fragments through fracture-dislocation injuries.Secondary InjurySecondary injury is a series of biological phenomena that begins within minutes and continue to self-immolation for weeks or months following the initial primary injury.  The acute phase of secondary injury begins after SCI and involves vascular damage, ionic imbalances, free-radical formation, the initial inflammatory response, and neurotransmitter accumulation (excitotoxicity).Immune Response Spinal Cord InjuryNeuroinflammation can be either beneficial or detrimental following SCI, providing time-point and the state of immune cells. The first three days following SCI, inflammatory events involve recruiting blood-born neutrophils resident microglia and astrocytes to the injury site., Epidemiology : The worldwide annual incidence of spinal cord injury is reported to be around 15 to 40 cases per million. The majority of these cases are young men and have SCI secondary to trauma. Approximately 55% of acute SCIs occur in the cervical region. Cervical spine SCI has a worse prognosis compared to SCI of other spinal levels, which is reflected in the decreased prevalence of cervical SCI in epidemiologic data, POOR, Because spinal cord injuries are often due to unpredictable events, the best you can do is reduce your risk. Some risk-reducing measures include : ,,always wearing a seatbelt while in a car,wearing proper protective gear while playing sports,never diving into water unless you’ve examined it first to make sure it’s deep enough and free of rocks, Complications : Cardiovascular Disease, respiratory problems, shock, sweating, temperature instability, musculoskeletal disorders, Diagnostics : ABG, X-Ray Spine, MRI, CT SCAN, Differential diagnosis : botulism, Hypoglycemia, Multiple Sclerosis, MYASTHENIA GRAVIS, tick paralysis, Transverse Myelitis, disease description : Spinal cord injury (SCI) is a serious medical condition, which often results in severe morbidity and permanent disability. It occurs when the axons of nerves running through the spinal cord are disrupted, leading to loss of motor and sensory function below the level of injury. Injury is usually the result of major trauma, and primary injury is often irreversible. These injuries are particularly costly and disabling as they disproportionately affect patients under 30-years-old, lead to significant functional impairment for the remainder of the individual’s life, and put the individual at risk for numerous complications leading to increased morbidity and mortality

Spinal Muscular Atrophies

Disease Name : Spinal Muscular Atrophies, Symptoms : Infants lie flaccid with little movement, unable to overcome gravity, and lack head control, respiratory distress : Between 6 weeks and 6 months of age, affected infants typically experience sudden onset of shortness of breath with progressive respiratory distress., Feeding Difficulty : Problems sucking and swallowing for people with SMA are usually caused by muscle weakness in the throat and mouth., severe hypotonia : They have extremely weak muscle tone at birth., symmetric generalized muscle weakness : Patients with all forms of SMA have diffuse symmetric proximal muscle weakness that is greater in the lower than upper limbs, and absent or markedly decreased deep tendon reflexes., Signs : Absence of deep tendon reflexes : Patients with all forms of SMA have absent or markedly decreased deep tendon reflexes., hypotonia, tongue fasciculations : Quivering of the tongue, a condition called tongue fasciculation, also may occur., bell-shaped chest : In SMA type I the pulmonary ribcage moves inward during inspiration rather than outward while the abdomen expands. This can lead to atelectasis of the upper lobes of the lungs and to underdevelopment of the upper chest wall, resulting in bell-shaped chest., frog-leg posture : Newborns with severe SMA type I will be born with tight joints and their legs may be fixed in a “frog” position., Treatment : Orally administered small molecules (RG7916 and LMI070) are also able to,promote exon 7 inclusion and are currently under investigation.,Another therapeutic approach is gene therapy (AVXS-101), to replace SMN1,and thus increase the production of the full-length SMN protein. Adenoassociated,viral vector (AAV-9) is able to transport a functional copy of SMN1,crossing the blood–brain barrier. An interim analysis of a phase I clinical trial of,intravenously administered AVXS-101 in SMA type I patients revealed a safety,profile and efficacy with achievement of motor milestones.,In terms of neuroprotective strategies, phase 2 studies with oral olesoxime,(TRO19622) in the SMA type II or nonambulant type III patient population,showed stabilization or improvement compared with placebo. Although the,primary endpoint was not met, olesoxime was safe and might be used in,combination with other drugs targeting other mechanisms of the disease. The,role of exercise as a neuroprotective measure is also under investigation. Current,clinical trials also include fast skeletal troponin activator (CK2127107), ,pyridostigmine, and 4-aminopyridine to enhance nerve or muscle function., Pathophysiology : The precise role SMN protein plays in neuronal function and development is not fully understood, and its subsequent absence causing such devastating deficits has so far eluded precise pathophysiological descriptions. SMN protein is found in all eukaryotic cells and has shown to play a crucial role in all cells with regards to homeostatic cellular pathways .Several hypotheses surrounding SMN protein and its role in SMA exist, two main hypotheses relate to SMN protein’s role in 1) The neuronal cytoplasm and 2) the neuronal nucleus. SMN protein in the cytoplasm has demonstrated a vital role in mRNA transport through axons, actin dynamics, and vesicle release in the synapse. In the nucleus, SMN protein forms small nuclear RNA’s (snRNA) and therefore plays a key role in the formation of the spliceosome, which removes introns in pre- mRNA into functional mRNA. This explanation hypothesizes the damage motor neurons specifically to either neuronal sensitivity to spliceosome malfunction directly or indirectly through incorrectly spliced mRNA creating dysfunctional proteins key to neuronal function,  Recent developments in the understanding of SMN protein regarding its ubiquitous presence and multiple functions in all eukaryotic cells have led to conclusions that SMA is not purely a motor neuron disorder with congenital heart disorder associations and sensory nerve pathology noted in type 1 SMA patients., Epidemiology : incidence of SMA is estimated to be 1 in 6, 000-10, , variable, SMA is an inherited disease. If you or your partner carries the mutated gene that causes SMA, a genetic counselor can explain the chances of your child having SMA or being a carrier.,,You may be able to take steps before pregnancy to lower the risk of passing on SMA. A process called preimplantation genetic diagnosis (PGD) identifies embryos that don’t have the mutated gene. Your doctor implants healthy embryos during in vitro fertilization (IVF). PGD ensures your child will have two healthy SMN1 genes and not get SMA., Complications : respiratory distress, Developmental delay in gross motor milestones, Diagnostics : CK (Creatine Kinase) test, HISTOPATHLOGY, Muscle Biopsy, EMG/NCS, GENETIC TESTING, CHEST X RAY, PLASMA CREATINE KINASE, Electrocardiography (EKG), Differential diagnosis : botulism, Duchenne muscular dystrophy, Guillain-Barre Syndrome, POMPE DISEASE, disease description : Spinal muscular atrophy is a genetic disorder characterized by weakness and wasting (atrophy) in muscles used for movement (skeletal muscles). It is caused by a loss of specialized nerve cells, called motor neurons that control muscle movement .The weakness tends to be more severe in the muscles that are close to the center of the body (proximal) compared to muscles away from the bodys center (distal). The muscle weakness usually worsens with age. There are many types of spinal muscular atrophy that are caused by changes in the same genes.

Spinal Stenosis

Disease Name : Spinal Stenosis, Symptoms : neck discomfort : Spinal stenosis in the neck can cause numbness, tingling or weakness in a hand, leg, foot or arm, problems with walking and balance, neck pain & problems with the bowel or bladder., lower back pain : Spinal stenosis in the lower back can cause pain or cramping in one or both legs. This happens when you stand for a long time or when you walk. Symptoms get better when you bend forward or sit. Some people also have back pain., Signs : nan, Treatment : "Nonsteroidal anti-inflammatory drugs (NSAIDs). If common pain relievers dont provide enough relief, prescription NSAIDs might be helpful.,Antidepressants. Nightly doses of tricyclic antidepressants, such as amitriptyline, can help ease chronic pain.,Anti-seizure drugs. Some anti-seizure drugs, such as gabapentin (Neurontin, Gralise), are used to reduce pain caused by damaged nerves.,Opioids. Medications such as oxycodone (Oxycontin, Roxicodone, others) and hydrocodone (Hysingla ER) can be habit-forming.", The condition may be treated successfully by surgical decompression alone with preservation of the ,facet joints., Pathophysiology : Spinal stenosis is a disease process that results from the narrowing of the vertebral spinal canal and the lateral recesses. This often leads to the compression of the structures located within the spinal canal, including the spinal cord, nearby nerve tissue, and cerebrospinal fluid. There are multiple factors that can lead to the narrowing. This includes bulging or protrusion of the intervertebral disc, herniation of the nucleus pulposus posteriorly, epidural fat deposition, hypertrophy of posterior longitudinal ligament, or the ligamentum flavum, and hypertrophy of the facet joints. Spinal cord injury can result in cord lead major complications such as myelopathic syndrome or cauda equina syndrome., Epidemiology : 1 per 1000 persons older than 65 years and about 5 of every 1000 persons older than 50 years, variable, As most causes of spinal stenosis are normal age-related “wear and tear” conditions, you can’t totally prevent spinal stenosis. But you can take certain steps to keep your spine healthy. They may help lower your risk or slow the progression of spinal stenosis. These steps include : ,,Eating healthy foods. Be sure you’re getting enough calcium in your diet to keep your bones strong.,Maintaining a weight that’s healthy for you.,Avoiding smoking or quitting smoking. Smoking damages your arteries, which can contribute to back pain and make it difficult for any injuries to heal.,Practicing good posture.,Exercising regularly. Keeping your muscles strong, especially your back and core muscles, helps to keep your spine healthy., Complications : Pain, nerve compression, Diagnostics : MRI, X RAY, CT SCAN, PHYSICAL EXAMINATION, Differential diagnosis : fracture, LUMBAR SPONDYLOSIS, Rheumatoid arthritis, SPONDYLOLISTHESIS, disease description : Spinal stenosis may be defined as any type of narrowing of the spinal canal, nerve root canal or intervertebral foramen. The resultant nerve root compression leads to nerve root ischaemia, presenting with back, buttock or leg pain provoked by exercise.

Spindle Cell/pleomorphic Lipoma

Disease Name : Spindle Cell/pleomorphic Lipoma, Symptoms : mobile swelling, Signs : nan, Treatment : Conservative surgical excision only, Pathophysiology : Pathology involves-Characterized by partial or whole chromosome 13 or 16 deletions.Breakpoints cluster around 13q14 where the RB1 gene resides.Part of the so called 13q / RB1 family of tumors, which includes myofibroblastoma and cellular angiofibroma., Epidemiology : Very rare in patients < 20 years,< 10% of cases occur in women, Uncommon compared with conventional lipoma (ratio = 1 : 60), variable, Lipomas (and many of the conditions that cause lipomas) are inherited. Since they’re passed down through families, it isn’t possible to prevent them. You can lower your risk of developing Madelung’s disease (a condition that causes lipomas to grow) by limiting the amount of alcohol you drink., Complications : ulceration, Embolism leading to acute ischaemia, Diagnostics : HISTOPATHLOGY, MRI, ELECTRON MICROSCOPY, Immunostaining, Differential diagnosis : Atypical lipomatous tumour/ Well differentiated li, Cellular angiofibroma, dermatofibrosarcoma protuberans, Myxoid liposarcoma, neurofibroma, Pleomorphic liposarcoma, schwannoma (who grade 1), Solitary fibrous tumour, disease description : Spindle cell lipoma and pleomorphic lipoma are benign adipocytic tumors, currently regarded as morphologic variants of a single neoplasmCompose approximately 1.5% of all lipomatous tumors First described in 1975 by Enzinger and Harvey

Spiny Keratoderma

Disease Name : Spiny Keratoderma, Symptoms : papules : Fine 1–2 mm papules that project from the palmoplantar surface are described as filiform, spiked, prickly, minute digitate or music box-like spines., Signs : nan, Treatment : Mechanical debridement, e.g. dermabrasion, may be more effective than topical keratolytics., Etretinate or actitretin have a temporary effect. Topical 5-fluorouracil ointment has been ,tried with differing results., Pathophysiology : The exact pathophysiology of spiny keratoderma may vary depending on the specific genetic mutation involved. However, many palmoplantar keratodermas, including spiny keratoderma, are thought to be caused by mutations in genes that are important for the normal functioning of the skin, specifically in regulating the balance between cell proliferation, differentiation, and cell death., Epidemiology : prevalence rate of 0.3-0.55%, variable, Complications : Juxta-articular myxoma, Diagnostics : HISTOPATHLOGY, PHYSICAL EXAMINATION, Differential diagnosis : Pitted keratolysis, porokeratosis, disease description : Spiny keratoderma (SK) is a rare condition of unknown aetiology and exists as a hereditary/benign or idiopathic form. Importantly, aquired digitate keratoses 4 need to be excluded. Brown described the first case as ‘punctuate keratotic projections’ (‘punctate keratoderma’), and since then the disease has been described under a variety of terms, of which ‘porokeratosis’ is a misleading misnomer.

Spiradenocarcinoma

Disease Name : Spiradenocarcinoma, Symptoms : NODULES : Spiradenomas are usually flesh-colored, gray, pink, purple, red, or blue nodules about 1 cm in diameter., LESIONS : The lesions tend to occur on the scalp, neck, and upper part of the torso., Tenderness : Spiradenomas tend to be soft and are sometimes tender to palpation., Signs : nan, Treatment : Excision and follow-up are required. Adjuvant chemoradiotherapy does not seem to alter the survivor rate., Pathophysiology : Genetics TP53 mutations have been described. These lesions usually show evidence of origin from a pre- existing benign spiradenoma. Necrosis, a high mitotic count, loss of the dual cell population, loss of infiltrating T lymphocytes and an infiltrative growth pattern are features that usually indicate malignant transformation., Epidemiology : 0.07 cases per million person-years, It is very rare.The incidence is extremely rare with total of 50 reported cases till date in literature and only 8 cases are associated with malignant transformation, poor, Complications : nan, Diagnostics : HISTOPATHLOGY, full thickness skin biopsy, Fine-needle aspiration biopsy, Differential diagnosis : Basal cell carcinoma, dermatofibroma, Epidermal Inclusion Cyst, leiomyoma, Poroma, disease description : Spiradenocarcinoma is a rare skin adnexal neoplasm with potential for aggressive behavior, classified histologically into low- and high-grade tumors. Morphologically, low-grade tumors are thought to behave more favorably. Limited information is available, however, with only 18 published cases. To study their clinical behavior, histological features, and the diagnostic value of immunohistochemistry, 19 morphologically low-grade spiradenocarcinomas were retrieved and compared with 21 spiradenomas and cylindromas. H&E-stained sections were reviewed, follow-up was obtained, and immunohistochemistry for Ki-67, p53 and, MYB was performed. The tumors were solitary, measuring 0.8–7?cm (median : 2.7?cm), with a predilection for the head and neck of elderly patients (median age : 72 years; range 53–92) without gender bias.

Spiradenoma

Disease Name : Spiradenoma, Symptoms : LESIONS : Lesion is usually solitary and painful and consists of a fi rm rounded bluish dermal nodule 3–50 mm in diameter. The usual site is on the front of the trunk and proximal limbs. Rare sites include the vulva, breast and external ear., Signs : nan, Treatment : Surgical excision should be complete, as there may be recurrence., Pathophysiology : The pathogenesis of the formation of spiradenomas is not completely understood. A defect in the tumor suppressor gene, CYLD,  is thought to contribute to their development in Brooke-Spiegler syndrome, which also features multiple cylindromas .A transition between cylindromas and spiradenomas has been shown to occur in patients with CYLD gene mutations. Derangements in intercellular bridge proteins that maintain epithelial organization, including claudin-4, cadherin, and beta-catenin,  have also been suggested as contributing to neoplasm formation.Two studies found intense nuclear immunoreactivity for beta-catenin in spiradenomas, supporting a role of alterations in the beta-catenin pathway in their development. Professionals postulate that an abnormal clone arising during embryogenesis produces multiple abnormal cells that result in presentations involving multiple nevoid, blaschkoid, or linear spiradenomas., Epidemiology : The incidence is extremely rare with total of 50 reported cases till date in literature and only 8 cases are associated with malignant transformation, The lesion is benign but may rarely recur locally, diagnosed in an asymptomatic woman on the basis of breast cancer prevention programme. Because of its rare incidence and lack of imaging workups, there are only two previous reports of malignant breast spiradenoma, Complications : nan, Diagnostics : HISTOPATHLOGY, MRI, PHYSICAL EXAMINATION, full thickness skin biopsy, Differential diagnosis : dermatofibroma, leiomyoma, Poroma, schwannoma, Spiradenoma, disease description : Spiradenomas are well-differentiated, benign, dermal neoplasms originating from the sweat glands. Most spiradenomas occur between the ages of 15 to 35 years. Typically, they present as small solitary nodules that can grow to several centimeters, often with a blue, gray, or purple hue.They are strikingly painful. Spiradenomas usually arise on the head, neck, and trunk; however, cases in other areas such as the breast have occurred. Spiradenomas with varying morphology like multiple linear, zosteriform, blaschkoid, and nevoid spiradenomas have also been reported. Spiradenomas can occur concomitantly with cylindromas, trichoepitheliomas,  and/or trichoblastomas. In patients with Brooke-Spiegler, multiple spiradenomas, cylindromas, and trichoepitheliomas can be seen.

Spirillum Minor Rat-bite Fever Or Sodoku

Disease Name : Spirillum Minor Rat-bite Fever Or Sodoku, Symptoms : Malaise, fever, Signs : maculopapular rash, regional lymphadenopathy, Treatment : medication : Amoxicillin and Clavulanic acid , Benzylpenicillin/ penicillin-G, Ceftriaxone , Avoid rodents, wash hands and face after contact and any scratches should be cleaned, and antiseptics applied. The effect of prophylactic chemoprophylaxis following rodent bites or scratches is unknown. Animal handlers, laboratory workers, sanitation, and sewer workers must take precautions against exposure. Wild rodents, dead or alive, should not be touched.,,Typically Intravenous Penicillin G at a dose of 200, 000 units every 4 hours or Ceftriaxone 1 gram intravenously daily should be administered. Once the patient improves clinically, the Intravenous medications can be transitioned to either Penicillin V 500 Mg four times a day or Ampicillin 500 mg four times a day or Amoxicillin 500 mg three times a day. The total duration of antibiotics is 2 weeks. In Penicillin allergic patients, Doxycycline 100 mg twice a day either intravenously or orally can be substituted., Pathophysiology : Because of the relatively low incidence and low mortality rate, little information describing the pathogenesis of S. moniliformis exists. The organism is capable of producing morphological findings not associated with bacterial infections. An autopsy of rat bite fever victims demonstrates erythrophagocytosis, hepatosplenomegaly, interstitial pneumonia, lymph node sinus hyperplasia, endocarditis, and myocarditis along with degenerative changes in the kidneys and liver. Radiological data suggest that rat-bite fever might cause damage to physes and acrophyses of bones, similar to frostbite induced damage. Biopsy of skin lesions in rat bite fever has demonstrated leukocytoclastic vasculitis., Epidemiology : rats are responsible for approximately 1%. The typical victim of rat bite fever is a child younger than five years old living in poverty. Pet store workers and laboratory technicians working with rats are also at risk. The risk of infection after a rat bite is about 10%, good, Complications : Adrenal Insufficiency, Meningitis, Endocarditis, LIVER ABSCESS, pneumonitis, Diagnostics : PHYSICAL EXAMINATION, Differential diagnosis : Brucellosis, Ehrlichiosis, "lymes disease", meningococcemia, Rickettsial Infection, disease description : Rat-bite fever, also known as streptobacillosis, spirillary fever,  bogger, and epidemic arthritic erythema, is a zoonotic illness, which is manifested by acute relapsing fever with migratory polyarthralgia. It is transmitted from rodents to humans either by rodent urine or from mucosal secretions. It is a rare disease and can be caused by two kinds of bacteria namely  Spirillum minus and Streptobacillus moniliformis. Both organisms are found as normal oral flora in rodents.

Spirochaetal Uveitis

Disease Name : Spirochaetal Uveitis, Symptoms : ocular defects : Due to the varying degrees of presentation patients may complain of blurry vision, floaters, light sensitivity, double vision, eye pain, and foreign body sensation., Signs : nan, Treatment : medication : Benzylpenicillin/ penicillin-G, Ceftriaxone , Azithromycin , the mainstay of treatment is systemic antibiotics, topically administered drugs are useful in alleviating acute ocular symptoms. Topical steroids, NSAIDs, mydriatics like atropine and lubricating agents are all helpful and can be used as indicated by the ophthalmologist.,,Systemic therapy is administered according to the stage of the disease. Patients with ocular syphilis are treated as neurosyphilis.,,The following are treatment protocols recommended by the center for disease control and prevention (CDC) : ,,Primary and secondary syphilis is treated with a single dose of intramuscular (IM) penicillin G benzathine 2.4 million units, or procaine penicillin, 2.4 million units IM daily, and probenecid, 1 g orally 4 times a day for 14 days. In patients who are allergic to penicillin, doxycycline 100 mg orally twice daily for 14 days or ceftriaxone 1 to 2 gm IM or intravenously (IV) daily for 10 to 14 days or tetracycline 100 mg orally 4 times daily for 14 days, can be used. Azithromycin has also been used.,Latent and tertiary syphilis, including neurosyphilis, is treated with aqueous crystalline penicillin G, 3 to 4 million units IV every 4 hourly for 10 to 14 days, or benzathine penicillin G, 2.4 million units IM weekly for 3 weeks. Ceftriaxone and azithromycin also have been used in patients allergic to penicillin.,Penicillin is the only antibiotic with documented efficacy for treating syphilis in pregnant patients. Pregnant females with syphilis who report penicillin allergy should be desensitized first and then treated with penicillin G., Pathophysiology : Syphilitic iritis manifests itself in two forms. A non-specific iritis or iridocyclitis, which can be granulomatous or non-granulomatous, occurs typically in the secondary stage of the disease, soon after the skin eruptions, usually within the first year after infection, but not before the third month. In light-coloured irides, prominently dilated iris vessels termed roseola, possibly due to treponemal emboli causing local vascular obstruction, dilatation and tortuosity have been noted to be a distinctive feature. Posterior synechiae form between the iris and the lens. The iritis lasts for 2–8 weeks and does not usually recur. In the absence of early antisyphilitic treatment it is seen in at least 3–4% of syphilitics, usually males, and is generally unilateral, but the fellow eye may become affected later. Treponema pallidum has been found in the aqueous. A ‘plastic’ iritis also occurs in congenital syphilis, usually as an accompaniment of interstitial keratitis. It also occurs in very young babies with congenital syphilis without any corneal complication, but usually with large nodules or gummata on the iris. Finally, an acute ‘plastic’ iritis may occur as a Jarisch– Herxheimer reaction 24–48 hours after the first therapeutic dose of penicillin, probably due to the flooding of the system with treponemal toxins. Finally, an acute ‘plastic’ iritis may occur as a Jarisch– Herxheimer reaction 24–48 hours after the first therapeutic dose of penicillin, probably due to the flooding of the system with treponemal toxins. Gummatous Iritis It occurs late in the secondary or rarely during the tertiary stage, and is characterized by the formation of yellowishred, heavily vascularized nodules near the pupillary and ciliary borders of the iris, but not in the intermediate region; they are usually multiple, vary in size from that of a pinhead upwards and are generally associated with much exudation and broad synechiae. Syphilitic Choroiditis and Chorioretinitis This may occur as disseminated choroiditis, peripheral choroiditis, diffuse chorioretinitis, pseudoretinitis pigmentosa, neuroretinitis, big blind spot syndrome, exudative maculopathy, uveal effusion, vasculitis, central retinal vein occlusion, retinal necrosis and, in HIV-infected individuals, lesions resembling placoid pigment epitheliopathy and atypical serpiginous choroidopathy. Vitritis is common and severe., Epidemiology : 24.9 cases per 100 000 person-years, good, Seeking proper treatment for an autoimmune disease or infection can help to prevent uveitis, Complications : cataract, CORNEAL OPACITIES, epiretinal membrane, Glaucoma, Macular edema, Optic Atrophy, Diagnostics : CSF EXAMINATION, rapid plasma reagin (RPR) tests, fluorescent treponemal antibody absorption (FTA-ABS) tests, treponemal haemagglutination (THA) tests, Differential diagnosis : Acute Retinal Necrosis, CHORIORETINITIS, retinitis, vasculitis, disease description :  The disease is most commonly transmitted sexually, and its clinical course is divided into primary, secondary, latent, and tertiary syphilis. Transplacental spread leads to congenital syphilis. Ocular manifestations can occur at any stage of the disease with varied clinical presentations because of which the disease is also known as the great imitator, as it can mimic a number of ocular diseases.

Spitz Naevus

Disease Name : Spitz Naevus, Symptoms : naevus : Their size ranges from a few millimetres to up to one or two centimetres in diameter. They usually appear on the face or limbs. Usually, a Spitz naevus is solitary, but sometimes they erupt as multiple lesions. A Spitz naevus grows rapidly for a few months. After the initial growth period, if untreated, it may remain static for years. A Spitz naevus may disappear spontaneously after some time. The atypical Spitz naevus or spitzoid naevus is so called because its features differ from those seen in the majority of Spitz naevi., papules : The classic Spitz naevus is typically a dome-shaped red, reddish-brown papule. A pigmented Spitz naevus is a tan or brown papule or nodule. A pigmented spindle cell tumour of Reed is a bluish or black papule., Signs : nan, Treatment : . Exceptions ,include large (>1 cm), nodular, ulcerated or rapidly growing ,lesions. The histological diagnosis of an atypical Spitz ,tumour should be approached more aggressively and treated ,with a wide margin resection following the guidelines of melanoma resection. Patients can be reassured that the lesion may in ,fact be benign, Pathophysiology : Most lesions are acquired, but up to 7% of Spitz naevi can occur congenitally. The ‘classic’ Spitz naevus typically is a symmetrical and well- defined compound naevus. Intraepidermal and intradermal forms have been also reported. There is a degree of epidermal hyperplasia overlying the naevus, without evidence of malignant intraepidermal pagetoid spreading of naevic cells. , Epidemiology : Approximately 50% of lesions occur in patients under the age of 14 ,years, 25% between the ages of 15 and 30, and 25% over the age ,of 30, Spitz naevi account for 1% of excised naevi in children, varible, Apply a broad-spectrum sunscreen with a sun protection factor (SPF) of at least 30 every day even when indoors,Don’t use tanning beds or sunlamps.,Try to do outdoor activities before 10 a.m. or after 4 p.m. when the sun’s rays are less strong. Seek shade if you must be outside during those hours.,Wear sun-protective clothes, including a wide-brimmed hat and large sunglasses when outdoors., Complications : nan, Diagnostics : HISTOPATHLOGY, full thickness skin biopsy, Dermoscopy, Differential diagnosis : dermatofibroma, HEMANGIOMA, KELOID., Melanoma, disease description : A Spitz nevus is a type of noncancerous (benign) mole that typically appears during childhood. It usually looks like a round pink bump. They can sometimes look flat or rough, or have a different color like blue, black or brown. A healthcare provider may also refer to a Spitz nevus as an epithelioid or spindle-cell nevus.It can be alarming to find a Spitz nevus on your child. They can look like melanoma, a life-threatening skin cancer. Fortunately, Spitz nevi (the plural form of nevus) aren’t skin cancer.

Spleen Infarction

Disease Name : Spleen Infarction, Symptoms : respiratory symptoms : Includes fever with chills & pleuritic chest pain., "shoulder pain : After the moment of rupture, pain from your ruptured spleen may seem to move to the left side of your chest or your left shoulder. This is called Kehrs sign.", Abdominal Pain : The most common presenting symptom is left-upper-quadrant abdominal pain (up to 70%)., abscesses : Septic thromboemboli may result in splenic abscesses, which present with sepsis and left upper abdominal pain., Signs : splenomegaly : Diseases which cause splenomegaly may place patients at risk for splenic infarction., Treatment : Treatment of splenic infarct is based primarily on the underlying causative disease state. Splenic infarct in the non-infectious setting may be treated with analgesics, hydration, anti-emetics and other means of supportive care. Hospital admission may be required to provide supportive treatment, monitoring, and further diagnostic testing if the underlying cause is not established. In patients with sickle cell hemoglobinopathies, treatment to correct hypoxia and acidosis may be required. In the case of septic emboli, patients may require intravenous antibiotics and further cardiac evaluation. In patients with the underlying hematologic disease or autoimmune disease, consultation with hematology, oncology or rheumatology may be indicated. Abdominal pain due to uncomplicated cases of splenic infarction resolve without intervention in 7-14 days., In the case of traumatic splenic injury, abnormal vasculature or hemodynamic instability, the surgical evaluation may be required. Dangerous complications of splenic infarct include pseudocyst formation, abscess, hemorrhage, splenic rupture, and aneurysm. In some instances, the infarcted splenic tissue may become infected and lead to abscess formation. Infarcted tissue may also undergo a hemorrhagic transformation. These complications warrant emergent surgical consultation., Pathophysiology : The splenic artery (branching off the celiac artery) supplies blood flow to the spleen in combination with the short gastric arteries (branches off of the left gastroepiploic artery).One of the most common causes of splenic infarction sickle hemoglobinopathies. In patients with sickle cell disease, episodes of hypoxia or acidosis cause red blood cells to transform into an abnormal shape leading to crystallization and occlusion of the vasculature. This process can lead to multiple infarctions beginning in childhood. Over time, multiple infarctions cause scarring and contraction of the spleen. This may ultimately result in complete splenic autoinfection by the time of adulthood.Diseases which cause splenomegaly may place patients at risk for splenic infarction. These diseases include chronic myelogenous leukemia, myelofibrosis, Gaucher disease, Malarial splenomegaly syndrome, AIDS with mycobacterium avium complex, Lymphoma.Rarely, abnormal splenic vascular anatomy may cause infarction., Epidemiology : 10 to 20% of splenic infarctions in patients, It accounts for 0.016% of admissions to an academic general hospital ., good, In patients undergoing surgery, it is important to ensure that the patient does get vaccinated against encapsulated organisms. For traumatic cases, the outlook is excellent but in patients with sickle cell disease or a chronic hematolgocial disorder, repeated episodes may occur., Complications : abscess, ANEURYSM, SPLENIC RUPTURE, hemorrhage, Diagnostics : LDH, LIVER FUNCTION TEST LFT, MRI, CT, Differential diagnosis : Cytomegalovirus (CMV), infectious mononucleosis, Infective endocarditis, leukemia, myelofibrosis, disease description : Splenic infarction may be the result of arterial or venous occlusion. Occlusion is usually caused by bland or septic emboli as well as venous congestion by abnormal cells. Infarction may involve a small segmental area of the spleen or may be global depending on which vessel is occluded. This occurrence is caused by a wide variety of underlying disease states with prognosis dependent on the causative illness.

Spleen Rupture

Disease Name : Spleen Rupture, Symptoms : Hypotension : Symptoms related to rapid drop in blood pressure includes lightheadedness, disorientation, blurred vision, paleness and faintness, anxiety & nausea., Signs : nan, Treatment : medication : Iron , Open surgical approach : Open surgical intervention is considered the gold standard approach for SAA repair. Techniques involving resection of an aneurysm with interposition bypass are ideal for aneurysms located in the proximal to the mid-splenic artery. Resection of an aneurysm can be combined with splenectomy in cases of a hostile abdomen or distal aneurysms located near the splenic hilum. Patients with ruptured splenic aneurysms should undergo urgent laparotomy and control of hemorrhage with ligation of an aneurysm. Preservation of the spleen is encouraged when possible, but splenectomy should be performed if adequate hemostasis is impossible to achieve otherwise.,,Endovascular approach : Endovascular intervention has gained a lot of popularity recently in managing aneurysms. Techniques vary according to the type of an aneurysm, location, whether preserving the splenic artery will be preserved, and the condition of collaterals. Fusiform true aneurysms are better treated with a stent graft (covered stent), while tortuous, saccular aneurysms are treated with aneurysmal coiling techniques. Pseudoaneurysms can be treated with embolization using liquid embolic agents to thrombose the inflow and outflow arteries or filling the sac itself. Distal splenic embolization should be avoided.,,Minimally invasive laparoscopic approach : The laparoscopic approach is a safe therapeutic alternative for cases of elective splenic aneurysm repair. Different techniques have been employed including ligation of the mid-splenic artery via stapling or clipping to splenectomy alone for distal SAAs near the hilum. Splenectomy with distal pancreatectomy may be necessary when the aneurysmal wall is severely inflamed and adherent to the tail of the pancreas. The laparoscopic approach carries the advantage of the rapid recovery, shorter hospital stay, and less postoperative pain compared with the open approach. The laparoscopic approach is also suitable and safe in pregnant SAA patients. Compared with the open approach, laparoscopic splenic aneurysm repair has a lower risk of preterm labor in these patients due to minimal manipulation of intra-abdominal contents., Pathophysiology : The exact etiology of slenic artery aneurysms is not established. Recent literature has suggested that true aneurysms develop secondary to arterial wall weakness due to several causes. These include atherosclerosis (32%), medial degeneration or dysplasia (24%), abdominal trauma (10%), hypertension, connective tissue diseases, and necrotizing vasculitis such as polyarteritis nodosa or Wegner granulomatosis. Pseudoaneurysms are periarterial hematomas that develop as a consequence of iatrogenic trauma or inflammatory processes such as chronic pancreatitis. Pseudoaneurysms lack a true wall hence they are more prone to rupture., Epidemiology : The prevalence of SAA in general population is reportedto be less than 1%, as most of the SAAs remain asymptomatic and therefore go undetected. A recent retrospective study found that 78% of SAAs occur in women. Mortality because of splenic aneurysm rupture in non-pregnant patients ranges from 25% to 40%. However, maternal mortality due to SAA rupture increases up to 75%, and fetal mortality increases as high as 95%, variable, "If youve been diagnosed with an enlarged spleen, ask your health care provider whether you need to avoid activities for several weeks that could cause it to rupture. These might include contact sports, heavy lifting and other activities that increase the risk of stomach trauma.", Complications : death, SPLENIC RUPTURE, Diagnostics : HISTOPATHLOGY, CT, USG, FOCUSED ASSESSMENT SONOGRAPHY IN TRAUMA(FAST), ANGIOGRAPHY, PHYSICAL EXAMINATION, Differential diagnosis : fracture, hemorrhage, LIVER TRAUMA, disease description : Splenic artery aneurysm is defined as a condition where there is a focal dilation in the diameter of the splenic artery that is 50% greater than the normal vessel diameter. This is the most common visceral artery aneurysm reported making up about 60% to 70% of patients diagnosed with visceral artery aneurysms.

Splenic Artery Aneurysm

Disease Name : Splenic Artery Aneurysm, Symptoms : Pain : Pain in the upper left part of your belly. This pain may radiate (spread) toward your left shoulder., pulsatile abdominal mass : Pulsating in your upper left belly., Ruptured spleen : If the aneurysm ruptures, symptoms include nausea and vomiting, pain in your upper belly, just below your ribs, pain in your left shoulder & symptoms of hypovolemic shock., Signs : nan, Treatment : medication : Iron , Endovascular intervention has gained a lot of popularity recently in managing aneurysms. Techniques vary according to the type of an aneurysm, location, whether preserving the splenic artery will be preserved, and the condition of collaterals. Fusiform true aneurysms are better treated with a stent graft (covered stent), while tortuous, saccular aneurysms are treated with aneurysmal coiling techniques. Pseudoaneurysms can be treated with embolization using liquid embolic agents to thrombose the inflow and outflow arteries or filling the sac itself. Distal splenic embolization should be avoided., Open surgical intervention is considered the gold standard approach for SAA repair. Techniques involving resection of an aneurysm with interposition bypass are ideal for aneurysms located in the proximal to the mid-splenic artery. Resection of an aneurysm can be combined with splenectomy in cases of a hostile abdomen or distal aneurysms located near the splenic hilum. Patients with ruptured splenic aneurysms should undergo urgent laparotomy and control of hemorrhage with ligation of an aneurysm. Preservation of the spleen is encouraged when possible, but splenectomy should be performed if adequate hemostasis is impossible to achieve otherwise., Pathophysiology : The exact etiology of slenic artery aneurysms is not established. Recent literature has suggested that true aneurysms develop secondary to arterial wall weakness due to several causes. These include atherosclerosis (32%), medial degeneration or dysplasia (24%), abdominal trauma (10%), hypertension, connective tissue diseases, and necrotizing vasculitis such as polyarteritis nodosa or Wegner granulomatosis. Pseudoaneurysms are periarterial hematomas that develop as a consequence of iatrogenic trauma or inflammatory processes such as chronic pancreatitis. Pseudoaneurysms lack a true wall hence they are more prone to rupture., Epidemiology : The prevalence of SAA in general population is reportedto be less than 1%, as most of the SAAs remain asymptomatic and therefore go undetected. A recent retrospective study found that 78% of SAAs occur in women. Mortality because of splenic aneurysm rupture in non-pregnant patients ranges from 25% to 40%. However, maternal mortality due to SAA rupture increases up to 75%, and fetal mortality increases as high as 95%, variable, It’s important to manage your medical conditions, including those that raise your risk for a splenic artery aneurysm. Talk with your provider about specific strategies based on the conditions you have. Some general tips include : ,,Take all your medications as prescribed.,Tell your provider any time you have new or changing symptoms.,Visit your provider for yearly checkups, and keep all your follow-ups.,,Also, lifestyle changes can help improve the health of all your blood vessels, including your splenic artery. Tips include : ,,Avoid smoking and tobacco use.,Eat a heart-healthy diet.,Exercise regularly, as recommended by your provider.,Limit alcohol consumption., Complications : death, SPLENIC RUPTURE, Diagnostics : MRI, CT, USG, Differential diagnosis : Marfan syndrome, Neurofibromatosis, Polyarteritis Nodosa, systemic lupus erythematosus (SLE), Takayasu Arteritis, disease description : Aneurysms involving the splenic artery are estimated to be identified at 0.04–1% of postmortem examinations. They are twice as common in women and are usually situated in the main arterial trunk. Although these are generally single, more than one aneurysm is found in one-quarter of cases. These may be a consequence of intra-abdominal sepsis and pancreatic necrosis, in particular.

Splenic Infarction

Disease Name : Splenic Infarction, Symptoms : Asymptomatic, left upper quadrant and left shoulder tip pain, Signs : nan, Treatment : Treatment ,is conservative, and splenectomy should be considered only ,when a septic infarct causes an abscess., Pathophysiology : nan, Epidemiology : nan, Complications : nan, Diagnostics : CECT, Differential diagnosis : CHEST TRAUMA, LIVER TRAUMA, TRAUMA TO THE GALL BLADDER AND EXTRAHEPATIC BILIAR, TRAUMATIC FAT NECROSIS, disease description : This condition commonly occurs in patients with a massively enlarged spleen from myeloproliferative syndrome, portal hypertension or vascular occlusion produced by previous surgical intervention (such as spleen-preserving distal pancreatectomy), pancreatic disease, splenic vein thrombosis or sickle cell disease.

Splenic Rupture

Disease Name : Splenic Rupture, Symptoms : Abdominal pain, tenderness, hypotension., Signs : Tachycardia, cold clammy skin, Hypotension, Treatment : nan, Pathophysiology : nan, Epidemiology : nan, Complications : nan, Diagnostics : nan, Differential diagnosis : CHEST TRAUMA, LIVER TRAUMA, TRAUMA TO THE GALL BLADDER AND EXTRAHEPATIC BILIAR, TRAUMATIC FAT NECROSIS, disease description : nan

Spondyloarthritides

Disease Name : Spondyloarthritides, Symptoms : back pain : Longstanding low back pain., back stiffness : Back pain and stiffness are typically worse at night and improve with exercise, finger deformity : Sausage-like appearance of fingers or toes., nail changes : Psoriasiform nail changes include changes of the nail matrix, such as pitting, nail plate crumbling, leukonychia and red spots in the lunula., uveitis : Uveitis is the most frequent extra-articular manifestation of axial spondyloarthritis (SpA), occurring in up to one-third of the patients. In the majority of patients, uveitis is acute, anterior and unilateral and presents with photosensitivity, sudden onset of pain and blurred vision., Joint swelling : Painful swelling of joints., cutaneous symptoms : Patients typically present with characteristic erythematous plaques with a coarse overlying scale on specific sites such as elbows, knees, scalp, umbilicus, rima ani and palms., Signs : nan, Treatment : medication : Indomethacin , Cortisone , The main pharmacologic therapy is a NSAID, usually in maximal doses (except in IBD associated arthritis), and at least two NSAIDs must be tried before advancing to the next class of pharmacologic agents, Pathophysiology : Enthesitis, or inflammation of the sites where the tendons or ligaments insert into the bone, is a key pathological finding in SpA .This finding differentiates it from rheumatoid arthritis and other inflammatory polyarthritides. As mentioned above, the major gene involved in several key pathogenic steps is HLA-B27. Several non-HLA genes have also been identified in disease pathogenesis. Environmental exposure of the immune system to microorganisms is also important. Several cytokines have been shown to participate in the inflammatory process. One of these cytokines is tumor necrosis factor (TNF) which is a target for a class of drugs used to treat the SpA. It is thought that microtrauma from stress also triggers inflammation at the enthesis,  These inflammatory processes lead to change in bone and pathologic new bone formation, which is seen in AS but not in rheumatoid arthritis., Epidemiology : 0.9 to 1.4%, , POOR, There’s no cure for spondyloarthritis, ,physical therapy,low-impact exercise,Smoking is a known cause of inflammation in the body. If you smoke, it’s important to consider quitting. Your doctor can help you find a smoking cessation program and other supportive resources that are right for you., Complications : Osteoporosis, uveitis, SPINAL INJURY, Diagnostics : CRP, MRI, Differential diagnosis : bone metastasis, Primary bone tumours, Spinal stenosis, disease description :  spondyloarthropathies (SpA) are a family of rheumatologic disorders that classically include1 : Ankylosing spondylitis (AS)Psoriatic arthritis (PsA)Inflammatory bowel disease (IBD) associated arthritisReactive arthritis (formerly Reiter syndrome; ReA)Undifferentiated SpA. Recently, these disorders have been differentiated further into three additional categories including non-radiographic axial SpA (nr-axSpA), peripheral SpA, and lastly, juvenile-onset SpA. This family of disorders shares several clinical features and has common genetic associations.Go to :

Spondyloepiphyseal Dysplasia

Disease Name : Spondyloepiphyseal Dysplasia, Symptoms : Arthritis : Arthritis and decreased joint mobility often develop early in life., Hearing loss : About one quarter of people with this condition have hearing loss., difficulty in breathing : Abnormal development of the chest can cause problems with breathing., vision abnormalities : Severe nearsightedness (high myopia) is common, as are other eye problems that can impair vision., KYPHOSCOLIOSIS : Abnormal curvature of the spine becomes more severe during childhood., Facial abnormalities : People with spondyloepiphyseal dysplasia congenita have mild changes in their facial features. The cheekbones close to the nose may appear flattened., cleft palate : Some infants are born with an opening in the roof of the mouth., spinal cord injury : Instability of the spinal bones (vertebrae) in the neck may increase the risk of spinal cord damage., short stature : People with spondyloepiphyseal dysplasia congenita have short stature from birth, with a very short trunk and neck and shortened limbs. Their hands and feet, however, are usually average-sized. Adult height ranges from 3 feet to just over 4 feet., Signs : nan, Treatment : Treatment is directed toward the specific symptoms that are apparent in each individual. Treatment may require the coordinated efforts of a team of specialists. Pediatricians, specialists in diagnosing and treating musculoskeletal disorders (orthopedic surgeons), specialists in diagnosing and treating eye disorders (ophthalmologists), rheumatologists, physical therapists and other healthcare professionals may need to systematically and comprehensively plan an affect child’s treatment. Genetic counseling may be of benefit for affected individuals and their families. Psychosocial support for the entire family is essential as well.,,Specific therapies are symptomatic and supportive. Physicians may carefully monitor affected infants to ensure prompt detection and appropriate prevention or corrective treatment of breathing (respiratory) difficulties. Regular eye (ophthalmologic) exams are required to detect and assess nearsightedness and to prevent retinal detachment. Retinal detachment can be repaired surgically. Standard physical therapy, which can improve joint motion and avoid muscle degeneration (atrophy), can be beneficial., Joint deformities,may require corrective osteotomies, and arthritis,of the hips or knees is managed with total joint,arthroplasty., Pathophysiology : The condition presents with two distinct phenotypes, due to a mutation in COL2A1 leading to impaired synthesis of type II collagen. SED congenita is the more severe form, characterized by an autosomal dominant inheritance pattern and average adult height of 90–165 cm. SED tarda is characterized by an X-linked recessive inheritance pattern and is associated with milder phenotypic changes. Since the onset of high definition antenatal ultrasonography, patients with SED congenita are often diagnosed in the perinatal period due to the degree of spinal and limb involvement. Maxillary flattening, facial abnormalities and cleft palate are common associations diagnosed in the postnatal period. Severe myopia, vitreous abnormalities and retinal detachment cause visual impairment, and hearing loss becomes obvious in early childhood. Atlantoaxial instability is a very significant association in patients with a diagnosis or suspected diagnosis of SED congenita. Patients should undergo radiological screening of the cervical spine and may require cervico-occipital fusion in the presence of significant instability to prevent cervical myelopathy. Thoracolumbar kyphoscoliosis, chest wall abnormalities with respiratory insufficiency and lumbar lordosis are commonly seen., Epidemiology : approximate incidence of 1 : 100 000., POOR, There’s no way to prevent SEDC. Some families who know they carry the COL2A1 mutation may choose not to have children., Complications : hip deformity, ocular defects, scoliosis, KYPHOSIS, Diagnostics : HISTOPATHLOGY, MRI, X RAY, CT SCAN, Differential diagnosis : Achondroplasia, DIASTROPHIC DYSPLASIA, disease description : ???Spondyloepiphyseal dysplasia is a form of skeletal dysplasia (osteochondrodysplasia), a broad term for a group of disorders characterized by abnormal growth or development of cartilage or bone. SEDC is characterized by distinctive skeletal malformations affecting the long bones of the arms and legs as well as the bones of the spine (vertebrae). Characteristic involvement includes underdevelopment and fragmentation of the bone and cartilage of the epiphyses, which are the rounded ends or “heads” of the long bones, and underdevelopment or malformation of the vertebrae. There are two main forms of spondyloepiphyseal dysplasia, SEDC and spondyloepiphyseal dysplasia tarda (SEDT).

Spondylolisthesis

Disease Name : Spondylolisthesis, Symptoms : back pain : Persistent lower back pain., muscle spasm : Muscle spasms in the hamstring., muscle spasm : Spondylolisthesis causes back stiffness., Numbness : Spondylolisthesis can also cause numbness in the foot and weakness in the muscles supplied by the affected nerve., difficulty in walking : Difficulty walking or standing for long periods., Signs : nan, Treatment : VWhen,symptoms are mild, they are adequately relieved,by conservative methods, such as a brace and spinal,exercises. When symptoms are moderately severe,or more, especially if these hamper the activity of,the patient, an operation may be required., decompression,of the compressed nerves if any, followed by,fusion of the affected segments of the spine, Pathophysiology : Any process that can weaken the supports keeping vertebral bodies aligned can allow spondylolisthesis to occur. As one vertebra moves relative to the adjacent vertebrae, local pain can occur from mechanical motion or radicular or myelopathic pain can occur due to compression of the exiting nerve roots or spinal cord, respectively. Pediatric patients are more likely to increase spondylolisthesis grade when going through puberty. Older patients with lower grades I or II spondylolistheses are less likely to progress to higher grades over time., Epidemiology : Current estimates for prevalence are 6 to 7% for isthmic spondylolisthesis by the age of 18 years, and up to 18% of adult patients undergoing MRI of the lumbar spine. Grade I spondylolisthesis accounts for 75% of all cases. Spondylolisthesis most commonly occurs at the L5-S1 level with an anterior translation of the L5 vertebral body on the S1 vertebral body. The L4-5 level is the second most common location for spondylolisthesis., GOOD, You can take steps to reduce your risk of spondylolisthesis : ,,- Do regular exercises for strong back and abdominal muscles.,- Maintain a healthy weight. Excess weight puts added stress on your lower back.,- Eat a well-balanced diet to keep your bones well-nourished and strong., Complications : KYPHOSIS, Diagnostics : MRI, CT SCAN, plain radiograph, PHYSICAL EXAMINATION, Differential diagnosis : Radiculopathy, disease description : Spondylolisthesis is the slippage of one vertebral body with respect to the adjacent vertebral body causing mechanical or radicular symptoms or pain. It can be due to congenital, acquired, or idiopathic causes. Spondylolisthesis is graded based on the degree of slippage of one vertebral body on the adjacent vertebral body. Spondylolisthesis is a condition that occurs when one vertebral body slips with respect to the adjacent vertebral body causing radicular or mechanical symptoms or pain

Spontaneous Bacterial Peritonitis

Disease Name : Spontaneous Bacterial Peritonitis, Symptoms : abdominal discomfort, fever, ALTERED MENTAL STATUS, Abdominal Pain, Signs : ascites : Patients who develop SBP typically have large ascitic fluid volume., Treatment : medication : Meropenem , Ceftriaxone , Ciprofloxacin , Metronidazole , Empiric antibiotic therapy, such as intravenous third-generation cephalosporin, should be started in all patients with suspected SBP and a PMN count of greater than 250 cells/microliter on ascitic fluid analysis. Exceptions to this rule include patients with recent beta-lactam antibiotic exposure or diagnosis of SBP in a nosocomial setting. Antibiotics should be chosen based on the results of susceptibility testing in these cases., Pathophysiology : The majority of the isolated organisms in SBP (90%) are gram-negative enteric organisms (e.g.,  Escherichia coli or Klebsiella pneumoniae), which suggests that the primary source of contamination is the gastrointestinal (GI) tract. Enterotoxin is also frequently isolated from ascitic fluid, further supporting the theory that bacteria involved in SBP migrate transmurally from the intestinal lumen (i.e., bacterial translocation).An alternatively proposed mechanism of contamination involves hematogenous spread, from a distant source, such as a urinary tract infection, in individuals predisposed to the disease by a weakened immune system (i.e., immunocompromised).  Patients with cirrhosis typically have an elevated level of bacterial overgrowth in the GI tract, mainly due to a prolonged intestinal transit time. This, coupled with reduced protein production by a cirrhotic liver (e.g., low complement levels in both the serum and ascites) and poor phagocytic and reticuloendothelial system function, results in a decreased ability to clear microorganisms from the system, thereby further contributing to bacterial overgrowth, migration, and expansion within the ascites fluid., Epidemiology : Approximately 10 to 25% of patients with ascites will develop SBP, and the condition is associated with a 20% in-hospital rate of mortality., variable, It is important to prevent spontaneous bacterial peritonitis in people at high risk of developing it, because it is associated with a significant risk of death. Antibiotics are often used in people with advanced liver disease and ascites as a means to help prevent spontaneous bacterial peritonitis, but it is unclear whether they are effective and if effective, which antibiotic is the most effective., Complications : liver failure, Renal failure, sepsis, Diagnostics : BLOOD CULTURE test, Differential Leucocyte Count DLC, Total Leucocyte Count (TLC), URINE CULTURE, ASCITIC FLUID TAP, PHYSICAL EXAMINATION, Differential diagnosis : appendicitis, DIVERTICULITIS, Mesenteric ischemia, perforation, PERINEPHRIC ABSCESS, Pyelonephritis, disease description : Spontaneous bacterial peritonitis (SBP) is a term used to describe acute infection of ascites, an abnormal accumulation of fluid in the abdomen without a distinct or identifiable source of infection .SBP virtually always occurs in patients with cirrhosis and ascites and is suspected when the patients present with abdominal pain, fever, or altered mental status. There are not accepted diagnostic criteria for SBP, and a minority of patients also presents without apparent abdominal pain.

Sporotrichosis

Disease Name : Sporotrichosis, Symptoms : cutaneous symptoms : The first symptom of cutaneous (skin) sporotrichosis is usually a small, painless bump that can develop any time from 1 to 12 weeks after exposure to the fungus. The bump can be red, pink, or purple, and usually appears on the finger, hand, or arm where the fungus has entered through a break in the skin. The bump will eventually grow larger and may look like an open sore or ulcer that is very slow to heal. Additional bumps or sores may appear later near the original one., respiratory symptoms : Pulmonary (lung) sporotrichosis is rare. Symptoms include cough, shortness of breath, chest pain, and fever., Signs : nan, Treatment : medication : Terbinafine , Itraconazole , First line ,• Itraconazole 100–200 mg/day until clinical recovery (at ,least 3 months) , Or ,• Terbinafi ne 250 mg/day until clinical recovery (at least ,3 months) , Second line ,• Potassium iodide at an initial dose of 5 drops daily of satu\x02rated solution increasing slowly to 4–6 mL daily, Pathophysiology : S. schenckii is a dimorphic fungus existing in hyphal form at temperatures less than 37 degrees and as a yeast at temperatures greater 37 degrees. S. schenckii is found on soil, marine animals, moss, wood, and decaying vegetation. A virulence factor is a feature of the organism that enhances microbial growth. Some virulence factors of S. schenckii include thermotolerance, ergosterol peroxide, and melanin. The ergosterol peroxide found in the fungus is formed to evade reactive oxygen species during phagocytosis., Epidemiology : In the highlands of Peru, the incidence of sporotrichosis is approximately 1 case per 1000 people, Sporotrichosis can affect anyone regardless of age or gender as it depends on occupational exposure., not life threatening, You can lower the chance of getting sporotrichosis by wearing protective clothing such as gloves and long sleeves when touching plant matter that can cause minor cuts or scrapes.people have gotten sporotrichosis from contact with cats. This form of sporotrichosis (Sporothrix brasiliensis) has not been found in the United States.,,Be careful with unfamiliar animals, particularly cats. Cat bites and scratches can spread the fungus that causes sporotrichosis, and other diseases. This fungus is most often spread by stray cats and pet cats that are allowed outdoors., Complications : Arthritis, infections, Bone infection, Breathing difficulty, Diagnostics : Complete Blood Count CBC, FUNGAL CULTURE, PCR, MRI, ELISA, Examination under Microscope, Differential diagnosis : Blastomycosis dermatology, Chromoblastomycosis, Cutaneous Leishmaniasis, Mycobacterial infection, psoriasis, pyoderma gangrenosum, disease description : Sporothrix schenckii, S. schenckii, is a dimorphic fungus that can cause Sporotrichosis. S. schenckii exists in either a hyphal form at temperatures less than 37 degrees Celsius or as a budding yeast at 37 degrees Celsius or greater. This characteristic morphology is important in identifying the conversion from mold to yeast. There are different strains of S. schenckii, with S. schenckii complex being most commonly found in America, Asia, and Africa. S. brasilienis has been found in Brazil and is known to be transmitted from infected cats. S. Mexicana and S. globose have also been identified throughout the world.

Sprain

Disease Name : Sprain, Symptoms : swelling : The sprained part has intense swelling & tenderness., Pain : The sprained ankle causes intense pain., restricted joint movement : Limited ability to move the affected joint., Signs : nan, Treatment : All sprains are treated initially with rest, ,ice therapy, compression bandage, elevation (RICE)., Suitable analgesics and anti-inflammatory medication, Pathophysiology : The ankle joint is composed of the articulation of the tibia, fibula, and talus , The joint is stabilized by three ligamentous systems : the lateral ligament complex, the medial deltoid ligament, and the syndesmotic ligaments. The most common ankle injury occurs with inversion of the ankle which stresses the lateral ligament complex. The three ligaments that compose the lateral complex are the anterior talofibular (ATFL), the calcaneofibular (CFL), and posterior talofibular (PTFL) and they tend to be injured in this order with the anterior talofibular ligament being injured most commonly. The ATFL is the weakest ligament of the lateral ligament complex, and approximately 70% of lateral ankle sprains involve only this ligament and a mechanicsm of plantar flexion and inversion.  The CFL is injuries more commonly in dorsiflexion and inversion mechanisms. The posterior talofibular ligament is the least commonly injured of the lateral ligament complex. The medial deltoid ligament is the strongest of the ankle ligaments and tends to be injured with eversion injuries.  Isolated deltoid ligament injuries are extremely rare.  The superficial deltoid complex limits talar abduction moments, while the deep deltoid complex limits external rotation of the talus on the distal tibia., Epidemiology : up to 40% of patients sustaining a lateral ankle sprain note persistent symptoms, recurrent sprains, and chronic lateral ankle instability, good, Though sprains can happen to anyone, there are a few ways you can reduce the risk of a sprain. These tips include : ,,Avoid exercising or playing sports when tired or in pain.,Maintain a healthy weight and well-balanced diet to keep muscles strong.,Wear shoes that fit properly and be sure any sports equipment is also fitting well.,Practice safety measures to prevent falls.,Do stretching exercises daily or prior physical therapy exercises to maintain strength and balance.,Warm up and stretch before doing any physical activity., Complications : CHRONIC PAIN, Diagnostics : MRI, X RAY, X RAY, Differential diagnosis : Ankle sprain, fracture, injury, disease description : Acute ankle sprains are commonly seen in both primary care and sports medicine practices as well as emergency departments and can result in significant short-term morbidity, recurrent injuries, and functional instability. Although nonoperative treatment is often successful in achieving satisfactory outcomes, correct diagnosis and treatment is important at the time of initial evaluation to mitigate the risks of recurrent instability.  Appropriate treatment can limit the impact of long-term detrimental effect such as chronic recurrent ankle instability, arthritic progression, and long-term disability

Squamous Cell Carcinoma (epithelioma)

Disease Name : Squamous Cell Carcinoma (epithelioma), Symptoms : nasal obstruction, infiltrating nodule or an ulcer with rolled out edges affecting side of nose or columella, Signs : nan, Treatment : Early lesions respond to radiotherapy, more advanced ,lesions or those with exposure of bone or cartilage require ,wide surgical excision and plastic repair of the defect. Enlarged regional lymph nodes will require block dissection, Pathophysiology : It occurs as an infiltrating nodule or an ulcer with rolled out edges affecting side of nose or columella. Nodal metastases are seen in 20% of cases. Early lesions respond to radiotherapy; more advanced lesions or those with exposure of bone or cartilage require wide surgical excision and plastic repair of the defect. Enlarged regional lymph nodes will require block dissection.., Epidemiology : POOR, Complications : nan, Diagnostics : nan, Differential diagnosis : Actinic keratoses, Basal cell carcinoma, Blastomycosis dermatology, Bowen disease, keratoacanthoma, Melanoma, Warts, disease description : This is the second most common malignant tumour (11%), equally affecting both sexes in 40–60 age group.

Squamous Cell Carcinoma Of Conjunctiva

Disease Name : Squamous Cell Carcinoma Of Conjunctiva, Symptoms : Red eye, growth on the eye, vision changes., Signs : focal thickening of the epithelium with overlying hyperkeratotic plaque, , Papillomatous form appears as well-defined soft vascularised mass, Gelatinous form appears as an ill-defined translucent thickening, Treatment : Topical chemotherapy with mitomycin, Cryotherapy to surrounding tissue., excision with surrounding 2-4,mm of normal tissue is the treatment of choice., Radical excision including enucleation and even,exentration may be needed along with postoperative,radiotherapy in advanced cases of SCC., Pathophysiology : Ocular Surface Squamous Neoplasia Ocular surface squamous neoplasia (OSSN) is the term coined to denote the wide spectrum of dysplastic changes involving epithelium of conjunctiva, cornea and limbus. It includes squamous dysplasia, carcinomain- situ i.e. corneal and conjunctival intraepithelial neoplasia (CIN) and squamous cell carcinoma(SCC). CIN is characterised by partial to full thickness intraepithelial neoplasia with an intact basement membrane without involvement of the underlying substantia propria. While, SCC occurs when neoplastic cells penetrate the basement membrane and invade the underlying stroma. Very few CIN progress to SCC. Since OSSN usually arise at the limbus, so it has been postulated that various predisposing factors probably act on the stem cells causing their abnormal maturation and proliferation resulting in OSSN (Stem cell theory), Epidemiology : nan, Complications : nan, Diagnostics : MRI, Differential diagnosis : nan, disease description : Squamous cell carcinoma (epithelioma). It usually occurs at the transitional zones, i.e., at limbus and the lid margin. The tumour invades the stroma deeply and may be fixed to underlying tissues. Histologically, it is similar to squamous cell carcinomas occurring elsewhere. Now it is also included in ocular surface squamous neoplasia (OSSN).

Squamous Cell Carcinoma Of Eyelid

Disease Name : Squamous Cell Carcinoma Of Eyelid, Symptoms : Lump on the eyelid, ulceration, bleeding., Signs : Ulcerated, scaly, erythematous plaque like growth with elevated and indurated margins of eyelid, Fungating or polypoid verrucous lesion in eyelid, Treatment : Radiotherapy and cryotherapy should be given,only in inoperable cases for palliation., Local surgical excision of the tumour,along with a 3 mm surrounding area of normal,skin with primary repair is the treatment of choice.,Mohs’ microsurgical technique or frozen section,biopsy should be adopted for complete removal., Pathophysiology : It commonly arises from the lid margin (mucocutaneous junction) in elderly patients de novo or from pre-existing lesion such as actinic keratosis, Bowen’s disease and radiation dermatosis. It affects lower lids more frequently. Risk factors include sun exposure, radiation, fair skin, injury or other irritative insults. There is a male predilection. It is metastasized in preauricular and submandibular lymph nodes. It is characterised by an irregular downward proliferation of epidermal cells into the dermis. In well-differentiated form, the malignant cells have a whorled arrangement forming epithelial pearls which may contain laminated keratin material in the centre., Epidemiology : nan, Complications : METASTASES AT DIFFERENT SITES, Diagnostics : MRI, Differential diagnosis : nan, disease description : It forms the second commonest malignant tumour of the lid. Its incidence (5%) is much less than the basal cell carcinoma.

Squamous Cell Carcinoma Of Lung

Disease Name : Squamous Cell Carcinoma Of Lung, Symptoms : Hoarseness : Chest pain is most likely to develop during the later stages of lung cancer. It occurs especially when taking a deep breath or coughing., Hoarseness : If a tumor grows into the nerve supplying the vocal cords, you might develop a hoarse voice., chronic cough : Tumors can irritate your airways and trigger your cough reflex & cause persistent cough., hemoptysis : Coughing up blood from your respiratory tract is a common symptom of lung cancer., hemoptysis : Coughing up blood from your respiratory tract is a common symptom of lung cancer. 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., weight loss : unexplained weight loss, shortness of breath : Shortness of breath if the tumor obstructs the major airways or causes fluid to accumulate around the lungs., Signs : nan, Treatment : For 1B, surgical resection with adjuvant chemotherapy is considered in some cases if the tumor size is greater than 4 cm. Stage II is treated by surgery followed by chemotherapy; usually, lobectomy is preferred, but in poor surgical candidates, sub-lobar resection can be considered. In stages I and II, radiation therapy is considered if there are positive margins post-surgically and also in poor surgical candidates.,,Most stage III tumors are unresectable. Stage IIIA, which is definitely staged during resection surgery, can be considered followed by adjuvant chemotherapy but chemotherapy with radiation is the usual choice. For stage IIIB, combined chemotherapy and radiation are used., Pathophysiology : Genetic Mutations : SCC of the lung is often associated with specific genetic mutations, many of which are caused by exposure to tobacco smoke. Mutations in genes such as TP53, EGFR, and KRAS are common in SCC and can disrupt normal cellular pathways involved in growth regulation, DNA repair, and cell death.Cellular Proliferation and Tumor Growth : Genetic mutations lead to uncontrolled cell proliferation and division. These cancer cells form a tumor mass within the lung tissue. As the tumor grows, it can obstruct airways and impair lung function.Invasion and Metastasis : Cancer cells from the primary tumor can invade surrounding lung tissue and structures, such as blood vessels and lymph nodes. The tumor can also spread to distant sites in the body, such as other organs (metastasis), through the bloodstream or lymphatic system.Angiogenesis : To sustain their growth, cancer cells promote the growth of new blood vessels (angiogenesis) into the tumor mass. This ensures a supply of oxygen and nutrients, supporting further tumor growth and metastasis.Tumor Microenvironment : The tumor microenvironment includes various cell types, immune cells, and signaling molecules that interact with cancer cells. In SCC of the lung, the tumor microenvironment can contribute to tumor progression by promoting inflammation, suppressing the immune response, and providing signals that support cancer cell survival and invasion., Epidemiology : 14.4 per 100, 000 individuals, variable, "Theres no sure way to prevent lung cancer, but you can reduce your risk if you : nan,1. Dont smoke - Talk to your children about not smoking so that they can understand how to avoid this major risk factor for lung cancer. Begin conversations about the dangers of smoking with your children early so that they know how to react to peer pressure.,,2. Stop smoking - Stop smoking now. Quitting reduces your risk of lung cancer, even if youve smoked for years. Talk to your doctor about strategies and stop-smoking aids that can help you quit. Options include nicotine replacement products, medications and support groups.,,3. Avoid secondhand smoke - If you live or work with a smoker, urge him or her to quit. At the very least, ask him or her to smoke outside. Avoid areas where people smoke, such as bars and restaurants, and seek out smoke-free options.,,4. Test your home for radon - Have the radon levels in your home checked, especially if you live in an area where radon is known to be a problem. High radon levels can be remedied to make your home safer. For information on radon testing, contact your local department of public health or a local chapter of the American Lung Association.,,5. Avoid carcinogens at work. Take precautions to protect yourself from exposure to toxic chemicals at work. ,,6. Eat a diet full of fruits and vegetables. Choose a healthy diet with a variety of fruits and vegetables. Food sources of vitamins and nutrients are best. ,,7. Exercise most days of the week. If you dont exercise regularly, start out slowly. Try to exercise most days of the week.", Complications : nan, Diagnostics : HISTOPATHLOGY, Differential diagnosis : nan, disease description : Squamous cell carcinoma (SCC) of the lung, also known as epidermoid carcinoma, is a form of lung cancer. There are two types of lung cancer : small lung cell cancer (SCLC) and non-small cell lung cancer (NSCLC). Squamous cell carcinoma is a type of non-small cell carcinoma. It’s the most common form of lung cancer in men, and it’s more common in men than in women. It’s usually caused by smoking tobacco. Squamous cell carcinoma is named after squamous cells, which are types of cells that are flat and thin and look like fish scales. They’re found in many different parts of your body. A squamous cell carcinoma can happen anywhere you have squamous cells.

Squamous Cell Carcinoma

Disease Name : Squamous Cell Carcinoma, Symptoms : skin patches : An area of skin that’s flat, scaly and red that’s larger, about 1 inch (2.5 centimeters)., Wound : A wound or sore that won’t heal, or a sore that heals and then comes back., NODULES : A firm bump on the skin, called a nodule. The nodule might be the same color as the skin, or it might look different. It can look pink, red, black or brown, depending on skin color., Signs : leukoplakia : White or pale spots in your mouth, on your tongue, gums or cheeks., LESIONS : A lesion on your lower lip where the tissue becomes pale, dry and cracked, Treatment : Topical chemotherapy with mitomycin, Cryotherapy to surrounding tissue., excision with surrounding 2-4,mm of normal tissue is the treatment of choice., Radical excision including enucleation and even,exentration may be needed along with postoperative,radiotherapy in advanced cases of SCC., Pathophysiology : Genetic Mutations : The development of SCC is often associated with genetic mutations, primarily caused by exposure to ultraviolet (UV) radiation from the sun or other sources. These mutations can affect the DNA of squamous cells, disrupting the normal regulation of cell growth and division.Dysregulated Cell Proliferation : The genetic mutations can lead to the loss of control over cell proliferation. Normal cells have mechanisms that regulate their growth, preventing them from dividing uncontrollably. In SCC, mutated cells can bypass these regulatory mechanisms, leading to uncontrolled cell division and the formation of a tumor.Invasion and Metastasis : As the tumor grows, cancer cells can invade nearby tissues and structures. SCC cells may produce enzymes that break down the surrounding tissue barriers, allowing them to penetrate into deeper layers of the skin or even into blood vessels and lymphatic vessels. This enables the cancer cells to spread to distant parts of the body, a process known as metastasis.Angiogenesis : To sustain their rapid growth, cancer cells need a blood supply. They can stimulate the growth of new blood vessels through a process called angiogenesis. This ensures a steady supply of nutrients and oxygen to the growing tumor., Epidemiology : An estimated 1.8 million cases of SCC are diagnosed in the U.S. each year, variable, While you can’t prevent all types of squamous cell carcinoma, you can take steps to reduce your risk by : ,,Avoiding excessive sun exposure.,Avoid using tanning beds.,Using sunscreen when you’re outdoors.,Wearing protective clothing and accessories from the sun, including sunglasses, hats and clothing with UPF protection.,Stopping smoking.,Avoid exposing yourself to chemicals without wearing personal protective equipment.,If you notice changes to your skin, contact your healthcare provider or visit a dermatologist for a professional skin exam., Complications : death, Diagnostics : HISTOPATHLOGY, CT/MRI, Differential diagnosis : Adenocarcinoma of lung, large cell carcinoma, Small cell lung cancer, disease description : Squamous cell carcinoma (epithelioma). It usually occurs at the transitional zones, i.e., at limbus and the lid margin. The tumour invades the stroma deeply and may be fixed to underlying tissues. Histologically, it is similar to squamous cell carcinomas occurring elsewhere. Now it is also included in ocular surface squamous neoplasia (OSSN).

Squamous Cell Carcinomal

Disease Name : Squamous Cell Carcinomal : Acantholytic, Spindle-ce, Symptoms : TUMOURS : The tumor is mostly composed of large keratinocytes with abundant pale eosinophilic (glassy) cytoplasm., Signs : nan, Treatment : medication : Topotecan , Doxorubicin (Liposomal), Immunotherapy if inoperable, Mohs, surgical excision with adequate margins, especially for high risk squamous cell carcinoma,Also curettage, electrodessication, cryotherapy, radiation therapy., Pathophysiology : Cutaneous squamous cell carcinoma appears to develop through a multistep process UV radiation, mutations involving genes (such as TP53, CDKN2A, NOTCH1 and NOTCH2, EGFR and TERT) and molecular pathways (RAS / RAF / MEK / ERK and PI3K / AKT / mTOR) have been shown to play an important role in the pathogenesis., Epidemiology : 2-4% of SCC which affects mainly the sun-exposed areas of the skin, M > F,Incidence : 5 - 499 per 1, 000 individuals depending on the latitude, variable, Complications : nan, Diagnostics : Immunostaining, Differential diagnosis : squamous papilloma, verruca vulgaris, verrucous hyperplasia, disease description : Spindle cell squamous cell carcinoma (SpSCC), also known as sarcomatoid squamous cell carcinoma (SCC), is a biphasic variant of SCC consisted of a mesenchymal component of sarcomatoid spindle cell proliferation and an epithelial component of SCC 1. Cutaneous SpSCC is very rare and only 11 cases have been reported in Korea 2-4. It can cause diagnostic and therapeutic problems particularly when the SCC component is minimal or absent because of ulceration or necrosis.In-transit metastasis and satellite lesion (satellitosis) mean intralymphatic or, less frequently, angiotrophic tumor spread; these terms differ only in the distance of spread. When a regional metastasis is within 2 cm (an arbitrary cutoff) from the tumor, it is defined as satellitosis, whereas a regional metastasis beyond 2 cm is defined as in-transit metastasis 5-7. The concept and clinical significance of in-transit metastasis and satellitosis have been established for melanoma, but they are very rare in other skin malignancies; overall only 59 in-transit metastases from SCCs have been reported Here the author reports an exceptionally aggressive cutaneous case of SpSCC, in which the patient showed a satellite lesion and recurrent in-transit metastases.

Squamous Cell Carcinoma

Disease Name : Squamous Cell Carcinoma : Verrucous Carcinoma, Basa, Symptoms : lymphadenopathy : Painful nonmalignant lymphadenopathy can be seen with concurrent infection or inflammation. Tumors most often grow around the lymph nodes rather than metastasizing to them. If metastases do occur, they usually remain limited to the regional lymph nodes, cutaneous lesions : Lesions are usually slow growing, exophytic, and locally invasive. Lesions may exhibit hyperkeratosis, ulceration, and sinuses that may drain foul-smelling discharge and cause pain, bleeding, and difficulty walking. Lesions can often be misdiagnosed for plantar warts that grow slowly into a large exophytic mass., Genital lesions : The Buschke-Löwenstein tumor usually manifests as an exophytic tumor of the genital or perianal area, with ulceration and sometimes fistulae and sinuses. They typically manifest as large, exophytic, nonhealing, cauliflowerlike lesions with a verrucous or ulcerated surface. The Buschke-Löwenstein tumor usually can only be differentiated from ordinary condylomata based on histologic findings. These tumors tend to infiltrate deeply, and recurrence is common. The Buschke-Löwenstein tumor is preferentially seen in men and immunocompromised patients. It commonly occurs on the glans penis, mainly in uncircumcised men. In females, this tumor is most often found on the vulva., Oral squamous cell carcinoma : The oral cavity is the most common site of occurrence of verrucous carcinoma and represents 2-12% of all oral carcinomas. Early lesions appear as white, translucent patches on an erythematous base. They may develop in previous areas of leukoplakia, lichen planus, chronic lupus erythematosus, cheilitis, candidiasis, or submucous fibrosis. The more fully developed lesions are white, soft, cauliflowerlike papillomas with a pebbly surface that may extend and coalesce over large areas of the oral mucosa. Ulceration, fistulation, and local invasion into soft tissues and bone (eg, mandible) may occur. Oroaerodigestive verrucous carcinoma most commonly occurs on the buccal mucosa., Signs : nan, Treatment : medication : Cisplatin , Carboplatin, Methotrexate, Paclitaxel, Docetaxel, Cetuximab, Surgical excision, radiation therapy if poor surgical candidate (although 30% of radiated tumors become poorly differentiated and aggressive), Pathophysiology : Verrucous Carcinoma : Verrucous carcinoma is a rare subtype of squamous cell carcinoma (SCC) that typically develops on the oral mucosa, genitalia, or plantar surfaces of the feet. It is characterized by a warty, exophytic growth pattern and tends to be less aggressive and less likely to metastasize compared to conventional SCC. The exact pathophysiology of verrucous carcinoma is not fully understood, but it is thought to involve a combination of genetic mutations and interactions with the local microenvironment.Pathophysiological factors include : HPV Infection : Verrucous carcinoma of the genitalia is often associated with human papillomavirus (HPV) infection. Certain HPV strains, particularly types 6 and 11, are implicated in the development of these lesions.Chronic Irritation : In some cases, chronic irritation or inflammation of the affected tissue may contribute to the development of verrucous carcinoma. This is particularly evident in verrucous carcinoma of the oral cavity, where factors such as tobacco use, poor oral hygiene, and denture-related trauma may play a role.Genetic Mutations : Like other types of SCC, verrucous carcinoma may involve genetic mutations that lead to uncontrolled cell proliferation and impaired regulation of apoptosis (cell death).Local Immune Response : The immune response within the tumor microenvironment can influence the growth and behavior of verrucous carcinoma. The immune systems interactions with the tumor cells and surrounding tissues may impact the progression of the disease.Basal Cell Carcinoma (BCC) : Basal cell carcinoma is the most common type of skin cancer, originating from the basal cells in the outermost layer of the epidermis. It is often associated with chronic sun exposure and is characterized by slow growth and a low potential for metastasis. The pathophysiology of BCC involves multiple genetic and molecular abnormalities.Pathophysiological factors include : Sonic Hedgehog (SHH) Pathway Activation : The majority of BCC cases are associated with mutations in the Sonic Hedgehog (SHH) signaling pathway. This pathway plays a critical role in embryonic development and tissue repair, but its dysregulation in adults can lead to uncontrolled cell proliferation and tumor formation.Loss of Tumor Suppressor Genes : Mutations in tumor suppressor genes, such as PTCH1 and TP53, are frequently found in BCC. These mutations disrupt the normal regulation of cell growth and division.Ultraviolet (UV) Radiation Exposure : Chronic exposure to UV radiation from sunlight is a major risk factor for BCC. UV radiation damages DNA and increases the likelihood of genetic mutations that contribute to cancer development.Immunosuppression : Weakened immune surveillance, such as in individuals with suppressed immune systems (e.g., organ transplant recipients), can increase the risk of BCC development., Epidemiology : 5% of intraoral carcinomas, 11.0 per 100, 000 men and women per year, Complications : nan, Diagnostics : HISTOPATHLOGY, Immunostaining, Differential diagnosis : ANGIOSARCOMA, kaposi sarcoma, Leiomyosarcoma, Malignant melanoma, Sebaceous carcinoma, disease description : Also called Ackerman tumorLocally invasive, may recur (as nonverrucal types) but nonmetastasizing.5% of intraoral carcinomas.Men, ages 60+ years; associated with chewing tobacco, snuff dipping or heavy smoking.Not associated with alcohol abuse; HPV found in 28% but unclear if relevant.20% coexist with typical squamous cell carcinoma - these cases have risk of metastasis.Enlarged lymph nodes are reactive, due to trauma or infection.

Squamous Intraepithelial Neoplasia

Disease Name : Squamous Intraepithelial Neoplasia, Symptoms : Redness, vaginal bleeding, itching, Burning, Vaginal Discharge, Abdominal Pain, Signs : nan, Treatment : Avoid genital contact with another person whenever possible.,Stick to the screening guidelines that are right for your age and risk level.,Use condoms and dental dams., Topical treatments : You may apply some medicine directly to your skin. The creams or ointments may contain chemotherapy, hormones or substances to stimulate your immune system., Cryotherapy : Extreme cold, achieved with liquid nitrogen, can treat some lesions, such as anal or genital warts. Cryotherapy freezes away abnormal tissue.,Laser treatment : A powerful laser uses light to burn away abnormal tissue.,Excisional surgery : Your healthcare provider may recommend cutting the abnormal tissue out of your body. For cervical dysplasia, you may need a loop electrosurgical excision procedure (LEEP) or a cold knife cone (CKC) excision., Pathophysiology : The pathophysiology of squamous intraepithelial neoplasia involves a series of cellular changes driven by persistent infection with high-risk human papillomavirus (HPV) types and other genetic and environmental factors. Heres an overview of the pathophysiological processes involved : HPV Infection : Persistent infection with high-risk HPV, particularly types 16 and 18, is the primary risk factor for the development of squamous intraepithelial neoplasia. HPV is a sexually transmitted virus that infects the epithelial cells of the cervix. The virus can integrate its DNA into the host cells genome, leading to alterations in cellular function and proliferation.Disruption of Normal Cell Cycle Regulation : High-risk HPV infection interferes with the normal regulation of the cell cycle in cervical epithelial cells. The viral oncoproteins E6 and E7 play a key role in this process. E6 targets the tumor suppressor protein p53 for degradation, while E7 binds to and inactivates the retinoblastoma (Rb) protein. These actions disrupt the cell cycle control and apoptosis (programmed cell death) mechanisms, leading to uncontrolled cell proliferation.Progression to Dysplasia : Over time, the persistent infection and genetic alterations caused by high-risk HPV lead to the formation of abnormal cells in the cervical epithelium. These cells are characterized by their altered appearance, disorganized growth, and loss of normal tissue architecture. The progression from normal cervical tissue to squamous intraepithelial neoplasia is categorized into different grades (CIN 1, CIN 2, and CIN 3), representing increasing degrees of severity.Potential for Invasion : If left untreated, high-grade squamous intraepithelial neoplasia (CIN 2 and CIN 3) may progress to invasive squamous cell carcinoma. The accumulation of additional genetic mutations and changes in cellular behavior can lead to the infiltration of cancer cells into deeper layers of the cervical tissue and potentially metastasis to other parts of the body., Epidemiology : 138 out of 1, 800 cases (7.7 %)., variable, The best way to prevent squamous intraepithelial lesions is by getting the HPV vaccine. Girls and boys ages 9 to 14 can get the HPV vaccine series, which is two or three shots spaced two to 12 months apart. If you get the vaccine when you’re older, between ages 15 and 45, you’ll need three doses. If you’re older than 46, talk to your healthcare provider before getting the HPV vaccine.,,Other ways to reduce your risk of HPV include : ,,Avoid genital contact with another person whenever possible.,Stick to the screening guidelines that are right for your age and risk level.,Use condoms and dental dams., Complications : nan, Diagnostics : PAP SMEAR, Colposcopy, biopsy, Differential diagnosis : atrophy, squamous metaplasia, transitional metaplasia, disease description : A squamous intraepithelial lesion (SIL) is an area of abnormal tissue on the skin inside of your body. It can affect the cervix, vagina, vulva, anus, penis or back of the throat. These lesions are precancers, which means they’re not cancer but have the potential to become cancer and spread to other tissues.

Squamous Papilloma

Disease Name : Squamous Papilloma, Symptoms : LESIONS : A single lesion is most common and appears as a soft, pedunculated mass (supported on a stem or stalk) with numerous finger-like projections. The projections may be long and pointy or short and rounded if keratin (skin-forming protein) has built-up around the lesion. Less keratinised lesions are pink or red in colour and resemble a raspberry, whilst heavily keratinised lesions are white and look like the head of a cauliflower., Signs : nan, Treatment : The treatment of choice is complete surgical excision including the base of the lesion and a small marginal area to prevent recurrence. The use of laser treatments has also been proposed to eliminate oral squamous cell papilloma, rather than the surgical scalpel., Pathophysiology : Papillomas arise from the skin or some mucosal surfaces depending on the different types of Human Papillomavirus involved and their affinity to different sites. For example, conjunctival papilloma is caused by HPV infection type 6, 11, 16, 33, and 45, which is somewhat dissimilar to genital warts caused by types 2, 3, 6, 11, 16, 18, and 30-32 and cutaneous papillomas (types 1-4 and 26-29).Infection is established in the basal cell layers of the epithelium, but this involves the expression of a limited part of the viral genome. Its not until the basal cells develop and move externally through the different layers of the skin of the stratum spinosum and granulosum, that the virus begins to replicate itself, and the lesion becomes infectious.Normally papillomavirus infects the epidermis in sites near the site of entry, but self inoculation often occurs, and the virus can infect farther sites. This phenomenon is known as the Koebner phenomenon. It has been observed that the immune system has an important role in controlling the spread of the virus, as, despite the virus infecting the intraepidermal cells that are considered "hard-to-reach" by the immune system, it was found that papillomas tend to reactivate and are more extensive in immunocompromised individuals., Epidemiology : 0.01 to 0.45 %, The incidence was 0.13% in 2000 and increased to 0.57% in 2013 (P < 0.0001), variable, preventive measures need to be exercised by explaining to patients about the 9-valent HPV vaccine to treat or limit the spread of laryngeal papilloma., Complications : Hydrocephalus, Recurrent infection, Diagnostics : Biopsy Large, SPECULUM EXAMINATION, Differential diagnosis : inflammatory polyps, squamous cell carcinoma., disease description : Squamous papilloma is an exophytic overgrowth and projection of the soft tissue associated with human papillomavirus (HPV), with the function of the surrounding structures spared. It is usually benign and asymptomatic, appears as pedunculated, sessile or verrucous, and usually depends on its location. Squamous papillomas are traditionally divided into two types : Isolated-solitary and multiple-recurring. The former is usually found in an adults oral cavity, while the latter is mostly found in a childs laryngo tracheobronchial complex.

Stable Angina Pectoris

Disease Name : Stable Angina Pectoris, Symptoms : chest pain, Dizziness, sweating, chest heaviness, chest discomfort, CHEST PAIN ON EXERTION, Signs : bilateral chest fine crepitation, S3 S4 heart sound, Treatment : medication : Diltiazem , Glyceryl trinitrate (nitroglycerin) , Isosorbide dinitrate , Isosorbide Mononitrate , Amlodipine , Metoprolol , Aspirin/Acetylsalicylic acid, angioplasty, stunting and bypass surgery, First-line Treatment Includes Lifestyle Modifications-,Tobacco cessation will result in the biggest risk reduction, Cholesterol reduction, Blood pressure control, Diabetes mellitus management, Weight loss, Aerobic exercise.,Pharmacologic- Aspirin : Determine the risk of coronary heart disease in each patient. In low-risk individuals, the use of aspirin for primary prevention decreases the risk of nonfatal MI without benefit in all-cause mortality and nonfatal stroke, HMG-CoA reductase inhibitor : Statin therapy in high, moderate, and low-risk primary prevention subjects, ACE-inhibitor/angiotensin receptor blocker (ARB) : May be used in primary prevention to assist in blood pressure control and recommended in the setting of high-risk individuals or known cardiovascular disease for cardioprotective efforts., Pathophysiology : Endothelial cells line the coronary arteries; these cells are responsible for regulating vascular tone and preventing intravascular thrombosis. Any disruption in these two functions can lead to coronary heart disease. Multiple mechanisms can result in injury or impairment of the endothelial lining. These mechanisms include, but are not limited to, stress, hypertension, hypercholesterolemia, viruses, bacteria, and immune complexes. Endothelial injury triggers an immune response, which ultimately leads to fibrous tissue formation. Smooth muscle remodeling/fibrous caps can lead to coronary artery stenosis or even acute coronary syndrome. Coronary artery stenosis is the most common cause of myocardial ischemia. During times of increased myocardial oxygen demand, the stenosis prevents adequate myocardial oxygen supply. Four main factors contribute to oxygen demand : heart rate, systolic blood pressure, myocardial wall tension, and myocardial contractility. In states of increased demand such as illness, stress, and exercise – we rely on the body’s ability to up-regulate myocardial oxygen supply appropriately. , Epidemiology : dipends on stage and treatment, Complications : death, Myocardial infarction, unstable angina, Diagnostics : HDL - Cholesterol, LDL - Cholesterol, SERUM TROPONIN T(TROP T), SERUM TROPONIN- I(TROP I), 2-D Echo, Coronary Angiography, ECG, CT, Differential diagnosis : acute myocardial infarction, Acute Pericarditis, PNEUMONIA, Pulmonary Embolism, unstable angina, disease description : Stable angina, also is known as typical angina or angina pectoris, is a symptom of myocardial ischemia. Stable angina is characterized by chest discomfort or anginal equivalent that is provoked with exertion and alleviated at rest or with nitroglycerin. This is often one of the first manifestations or warning signs of underlying coronary disease. This episodic clinical syndrome is due to transient myocardial ischemia.Various diseases that cause myocardial ischemia and the numerous forms of discomfort. Males constitute ~70% of all patients with angina pectoris and an even greater proportion of those aged <50 years. It is, however, important to note that angina pectoris in women is often atypical in presentation

Staphylococcal Infections

Disease Name : Staphylococcal Infections, Symptoms : Sinusitis, abscess, otitis media, PNEUMONIA, skin infection, Signs : LUNG ABSCESS, CELLULITIS, FURUNCLE, Impetigo, NECROTISING FASCIITIS, Treatment : The drug of choice for treating MSSA infections is cloxa\x02cillin. Other alternatives are first generation cephalo\x02sporins (cephalexin, cefadroxil or cefazolin), second ,generation cephalosporins (cefuroxime) and coamoxiclav, ,clindamycin. If MRSA infections are proven or suspected, ,drugs like vancomycin, linezolid and teicoplanin are ,required., surgical ,drainage and antibiotics., Pathophysiology : Etlopathogenesls Staphylococci are functionally classified on basis of production of an enzyme and virulence factor coagulase. Coagulase positive staphylococcus is termed as S. aureus while S. saprophyticus and S. epidermidis are important coagulase negative staphylococci (CONS). CONS usually colonize the skin of all people and S. aureus the nares, axilla and perineum of around 20-25% of the population. Staphylococcal infection is acquired usually by direct contact with an infected patient or carrier and sometimes contaminated objects. Airborne spread is less common. Predisposing factors for staphylococcal infections include breach in the mucocutaneous barrier, previous viral infections such as measles, depressed immunity and prosthetic material such as shunts, central venous catheters and prosthetic joints., Epidemiology : nan, Complications : nan, Diagnostics : Blood Culture Aerobic, Differential diagnosis : nan, disease description : Staphylococcus a gram-positive coccus is a very common cause of both community acquired and nosocornial disease in children.

Staphylococcal Scalded Skin Syndrome

Disease Name : Staphylococcal Scalded Skin Syndrome, Symptoms : blisters : Following the rash, the formation of large fluid-filled blisters occur in areas of friction (such as axillae, groin, and buttocks), the centre of the face and body orifices (such as the nose and ears). Fluid contents range from a sterile cloudy fluid to frank yellow pus. Blisters easily rupture leading to the top layer of the skin (epidermis) peeling off easily, often in large sheets. Exposure of the underlying, moist, reddish tissue leaves the skin with a burned-like appearance., Skin rashes : Within 24–48 hours, a painful widespread red rash develops on the face and flexural regions (groin, axillae, and neck), then spreads rapidly to other parts of the body including the arms, legs, and trunk. In newborns, lesions can be found around the umbilical cord., systemic symptoms : SSSS tends to start with nonspecific symptoms in children; this may include irritability, lethargy, and fever., Signs : Nikolsky sign : Gentle rubbing of the skin causes exfoliation., Treatment : medication : Clindamycin , Vancomycin , Tobramycin sulfate , First line,•\tFlucoxacillin,•\tClindamycin,•\tTemocillin,•\tTigecycline,•\tDaptomycin,First line treatments if MRSA is suspected,•\tVancomycin,•\tTobramycin, Pathophysiology : Staphylococcal Scalded Skin Syndrome is caused by toxin-producing strains of Staphylococcus bacteria. These toxins target the desmoglein 1 complex in the zona granulosa of the epidermis, resulting in skin exfoliation. It can range from a mild localized form to exfoliation of the entire body. Those with previous antibodies are more likely to have the localized form. The resultant skin loss predisposes patients to hypothermia and a large volume fluid loss, as well as, the potential for additional or worsening infections.The exfoliative toxins target desmoglein, which is an important keratinocyte that plays a critical role in cell to cell adhesion. This protein is only found in the superficial epidermis. The relative concentration of desmoglein varies in the skin. It is believed that in patients with renal failure the exotoxins are not excreted and thus contribute to disease. Adults rarely develop the syndrome because of antibodies to the exotoxin. Staphylococcal scalded skin syndrome can be mistaken for bullous impetigo. Both cause blistering skin lesions caused by the staphylococcus exotoxin, but in the latter, the exotoxins remain localized to the site of infection. In staphylococcal scalded skin syndrome, the exotoxins are spread via the systemic circulation to distant sites. Further staphylococcal scalded skin syndrome can be differentiated from toxic epidermal necrolysis by the fact the former is intraepidermal, whereas in TENS there is necrosis of the entire epidermal layer., Epidemiology : 45·1 cases per million U.S. infants age < 2 years and 20·9 cases per million U.S. infants who were 1 year old., GOOD, "Staph bacteria is very hardy and can survive extreme temperatures, dryness, and even stomach acid. Scalded skin syndrome can be prevented by preventing the spread of the bacteria. Taking the following precautions can help : nan,,Frequently wash your hands. ,Bathe or shower daily.,Keep wounds, cuts, and rashes clean and covered.,Dont share towels, sheets, or personal items if someone in your family has a staph infection.", Complications : Renal failure, sepsis, Dehydration, Diagnostics : BLOOD CULTURE test, Erythrocyte Sedimentation Rate (ESR) test, HISTOPATHLOGY, PUS CULTURE, X RAY CHEST, SERUM ELECTROLYTE, Microbiological skin swabs, Differential diagnosis : Bullous impetigo, CELLULITIS, Kawasaki Disease, scarlet fever, toxic shock syndrome, disease description : Staphylococcal Scalded Skin Syndrome, also known as Ritter disease is a disease characterized by denudation of the skin caused by exotoxin producing strains of the Staphylococcus species, typically from a distant site. It usually presents 48 hours after birth and is rare in children older than six years. It may also present in immunocompromised adults or those with severe renal disease The disorder is characterized by significant exfoliation of skin following cellulitis. The severity may vary from a few blisters to system exfoliation leading to marked hypothermia and hemodynamic instability.

Staphylomas

Disease Name : Staphylomas, Symptoms : Defective vision, visual disturbances, Signs : anterior surface of the eye protrudes outward, Eyeball is slightly proptosed, Treatment : Inflammatory diseases which affect the outer coats of the,eye such as scleritis, corneal ulcer and keratomalacia from,vitamin A deficiency or rheumatoid arthritis with prevention,of secondary glaucoma should be promptly treated to,prevent the formation of staphylomas., Local excision and,repair with a corneal and scleral patch graft can be performed.,Large, unsightly blind eyes can be treated with,staphylectomy and keratoplasty, or enucleated and replaced,with an implant, depending on the extent of involvement,and degree of cosmetic disfigurement., Pathophysiology : 1. Anterior Staphyloma This can be partial or total, depending on whether part or whole of the cornea is affected. The most common cause is a sloughing corneal ulcer which perforates and heals with the formation of a pseudocornea by the organization of exudates and laying down of fibrous tissue. It is lined internally by the iris and externally by newly formed epithelium. The anterior chamber is flat and later secondary glaucoma may supervene. Gradually the weak anterior surface of the eye protrudes outward leading to an anterior staphyloma. 2. Intercalary Staphyloma This is located at the limbus and is lined by the root of the iris and the anteriormost part of the ciliary body. It is seen externally from the limbus to up to 2 mm behind the limbus. The usual causes are lesions that produce weakening of the globe in this region such as perforating injuries of the peripheral cornea, marginal corneal ulcer, anterior scleritis, scleromalacia perforans, complicated cataract surgery with poor wound apposition and secondary glaucoma. 3. Ciliary Staphyloma This affects the ciliary zone that includes the region up to 8 mm behind the limbus. Here the ciliary body is incarcerated in the region of scleral ectasia and has a bluish colour with a lobulated surface. Developmental glaucoma, endstage primary or secondary glaucoma, scleritis and trauma to the ciliary region of the eye are some of the conditions that lead to a ciliary staphyloma. 4. Equatorial Staphyloma This occurs at the equatorial region of the eye with incarceration of the choroid. The equatorial region is approximately 14 mm behind the limbus and is inherently relatively weak owing to the passage of the venae vorticosae. Scleritis, degenerative myopia and chronic uncontrolled glaucoma are conditions that may lead to equatorial staphyloma. 5. Posterior Staphyloma This affects the posterior pole of the eye and is lined by the choroid. Degenerative high axial myopia is the most common cause. The ectatic portion is not visible externally but can be detected by fundoscopy and B-scan ultrasonography. Indirect ophthalmoscopy shows a posterior outward curvature of the globe detected as a crescentic shadow in the macular region. The retinal vessels are seen to change direction, dipping down into the region. The staphylomatous region may appear pale due to degenerative changes in the retina, retinal pigment epithelium and sometimes choroid., Epidemiology : nan, Complications : nan, Diagnostics : FUNDOSCOPY, ophthalmoscopy, Differential diagnosis : nan, disease description : A staphyloma is a clinical condition characterized by an ectasia of the outer coats (cornea, or sclera or both) of the eye with an incarceration of the uveal tissue. The basic underlying pathology is a weakening of the eye wall, which can be caused by many inflammatory or degenerative diseases involving these structures. Most commonly the diseases causing a weakening of the globe are accompanied by a raised intraocular pressure and both contribute to the development of the staphyloma. Depending on the site affected, staphyloma can be classified as (i) anterior, (ii) intercalary, (iii) ciliary, (iv) equatorial and (v) posterior.

Stargardt Disease

Disease Name : Stargardt Disease, Symptoms : VISION DEFICITS : Vision deterioration is rapidly progressive; its age of onset highly variable, but it most often occurs between childhood and adolescence or early adulthood., vision abnormalities : Color vision in Stargardt patients is typically compromised. Using Hardy-Rand-Rittler or Ishihara color plates it is possible to detect a mild red-green dyschromatopsia in patients with Stargardt disease. Moreover, when these patients are submitted to a Farnsworth-Munsell Hue Test, a tritan axis (or short wavelength) deviation may be noted., Signs : nan, Treatment : nan, Pathophysiology : Genetic Mutations : Stargardt disease is primarily caused by mutations in the ABCA4 gene (ATP-binding cassette subfamily A member 4), also known as the ABCR gene. This gene provides instructions for producing a protein that plays a crucial role in the transport of vitamin A derivatives (retinoids) within the photoreceptor cells of the retina. Mutations in the ABCA4 gene lead to dysfunctional or absent ABCA4 protein, disrupting the normal processing of retinoids.Accumulation of Lipofuscin : In healthy retinal cells, the ABCA4 protein helps remove toxic waste products, including a substance called lipofuscin, which is a mixture of lipids and proteins. Lipofuscin accumulates within the retinal pigment epithelium (RPE) cells of individuals with Stargardt disease due to the impaired function of the ABCA4 protein. The accumulation of lipofuscin is particularly prominent in the macula, which is crucial for high-acuity vision.Oxidative Stress and Photoreceptor Degeneration : The accumulated lipofuscin is photosensitive and can undergo photooxidation upon exposure to light. This process generates reactive oxygen species and other damaging byproducts, leading to oxidative stress and cellular damage within the RPE cells and photoreceptor cells. Over time, this oxidative stress contributes to the degeneration of these cells, ultimately leading to the loss of central vision.Secondary Inflammation and Immune Response : The accumulation of lipofuscin and retinal degeneration trigger an inflammatory response in the retina. Immune cells are recruited to the site of damage, which can further contribute to tissue damage and photoreceptor cell death., Epidemiology : The prevalence is estimated at 1/8, 000 - 1/10, 000. Both sexes are equally affected., variable, You can’t prevent Stargardt disease. It’s an inherited condition., Complications : nan, Diagnostics : nan, Differential diagnosis : Age-related macular degeneration, Autosomal Dominant Stargardt-like Macular Dystrophies, Pattern Dystrophy, disease description : Stargardt disease is an eye disease that causes vision loss in children and young adults. It is an inherited disease, meaning it is passed on to children from their parents.Stargardt disease is often called juvenile macular dystrophy. In people with Stargardt disease, special light-sensing cells in the macula, called photoreceptors, die off. Central, or detailed, vision becomes blurry or has dark areas. It may also be difficult to see colors well.

Status Asthmaticus

Disease Name : Status Asthmaticus, Symptoms : dry 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., speech disturbances : An inability to speak more than one or two words at a time may also be observed in the later stages of an acute asthma episode., dyspnea : Patients with status asthmaticus have severe dyspnea that has developed over hours to days., wheezing : Patients are usually tachypneic upon examination and, in the early stages of status asthmaticus, may have significant wheezing. Initially, wheezing is heard only during expiration, but wheezing later occurs during expiration and inspiration., Confusion : Decreased level of alertness, such as severe drowsiness or confusion, during an asthma attack., Abdominal Pain : This may be due to the dysfunction of the smooth muscle in the gastrointestinal and respiratory systems occurring at the same time., Signs : nan, Treatment : nitial treatment consists of 2.5 mg of albuterol (0.5 mL of a 0.5% solution in 2.5 mL normal saline) by nebulization every 20 minutes for 60 minutes (three doses) followed by treatments hourly during the first several hours of therapy. Interestingly, Idris and colleagues demonstrated that even in patients with severe disease, 4 puffs of albuterol (0.36 mg) delivered with a metered-dose inhaler (MDI) and spacer were as effective as a 2.5-mg dose by nebulization. , ipratropium bromide with 5 mg of albuterol by nebulizer resulted in greater improvement in FEV1 than albuterol alone.,Magnesium inhibits calcium-mediated smooth muscle constriction, decreases acetylcholine release in the neuromuscular junction, and affects respiratory muscle force generation.,A true shunt in acute asthma averages only 1.5% of pulmonary blood flow. Therefore, oxygen supplementation need in status asthmaticus is an infrequent and low dose. Refractory hypoxemia in status asthmaticus should trigger a search for complications like pneumonia, atelectasis, or barotrauma. Heliox is a mixture of 70 : 30 or 60 : 40 helium : oxygen decreases airway resistance and turbulence and reduces work of breathing and inspiratory muscle fatigue., Pathophysiology : Airway Inflammation : Asthma is characterized by chronic airway inflammation, involving various immune cells, such as eosinophils, mast cells, and T lymphocytes. In status asthmaticus, this inflammation becomes intensified and sustained. Inflammatory mediators, such as histamines, leukotrienes, and cytokines, are released, leading to increased vascular permeability, airway edema, and mucus production.Bronchoconstriction : The inflammation and activation of immune cells in the airways cause the smooth muscle surrounding the bronchioles to contract excessively (bronchoconstriction). This leads to a narrowing of the airway lumen and reduced airflow. Bronchoconstriction is a central factor contributing to the characteristic wheezing, shortness of breath, and difficulty exhaling seen in asthma.Mucus Hypersecretion : Inflammation triggers an overproduction of mucus in the airways. The excessive mucus, combined with the narrowed airways, can obstruct airflow further, making it difficult for air to pass in and out of the lungs.Airway Remodeling : Over time, chronic inflammation and repeated bronchoconstriction can lead to structural changes in the airways, a process known as airway remodeling. This involves thickening of the airway walls, increased deposition of extracellular matrix proteins, and hypertrophy (enlargement) of airway smooth muscle. Airway remodeling contributes to the persistence of airflow obstruction, even during periods of exacerbation.Impaired Gas Exchange : As the airflow obstruction worsens, ventilation-perfusion mismatch occurs, leading to impaired gas exchange in the lungs. Oxygen delivery to the bloodstream is compromised, and carbon dioxide elimination is impaired. This can result in hypoxemia (low blood oxygen levels) and hypercapnia (elevated blood carbon dioxide levels), which can have systemic effects on various organs.Respiratory Muscle Fatigue : The increased effort required to breathe against the obstructed airways can lead to fatigue of the respiratory muscles, including the diaphragm and intercostal muscles. This fatigue further contributes to inadequate ventilation and worsening respiratory distress., Epidemiology : This equals about 1 in 13 people. Nearly 21 million U.S. adults ages 18 and older have asthma., variable, There’s no way to completely prevent severe asthma attacks if you have asthma. However, there are several things you can do to greatly reduce your risk of having one.,,The most important step is sticking with the treatment plan recommended by your doctor. Even if your symptoms seem to be improving and you aren’t having any attacks, don’t stop any treatments until your doctor tells you to do so.,,Other preventive measures you can take include : ,1. Using a peak flow monitor.,2. Monitoring your triggers.,3.Carrying an extra inhaler.,4. Talking to friends and family., Complications : nan, Diagnostics : ABG, ECG, PULMONARY FUNCTION TEST(PFT), Differential diagnosis : Chronic Obstructive Pulmonary Disease, heart failure, disease description : Status asthmaticus is a medical emergency, an extreme form of asthma exacerbation characterized by hypoxemia, hypercarbia, and secondary respiratory failure. All patients with bronchial asthma are at risk of developing an acute episode with a progressive severity that is poorly responsive to standard therapeutic measures, regardless of disease severity or phenotypic variant. This is also known as status asthmaticus.If not recognized and managed appropriately, asthmatics portends the risk of acute ventilatory failure and even death.Despite advances in pharmacotherapy and access to early diagnosis and treatment of asthma itself, it remains one of the most common causes of emergency department visits. No single clinical or diagnostic index has been known to predict clinical outcomes in status asthmaticus. Hence, a multi-pronged and time-sensitive approach combining symptoms and signs, assessing airflow and blood gas, and a rapid escalation of treatment based on initial treatment response is favored to diagnose and manage the condition.

Status Epilepticus

Disease Name : Status Epilepticus, Symptoms : seizures : This form involves seizure activity without convulsions or uncontrolled shaking and muscle movements throughout your body. Some minor muscle movements may still happen, but they’re usually small twitches or slow, repetitive motions with a hand or part of your face. Absence seizures and other kinds of focal seizures — which affect only a limited part of the brain — can cause nonconvulsive SE., frothing from mouth : During a convulsion, one can not swallow one own saliva due to impaired consciousness. Also, there is heavy breathing, which leads to the formation of froth (bubbles of saliva) at the mouth. Foaming or frothing at the mouth occurs when excess saliva pools in the mouth or lungs and is mixed with air, creating foam., convulsive disorders : Convulsive SE : This form involves uncontrolled shaking or convulsing on both sides of your body. Generalized tonic-clonic seizures are a key type of seizure that can turn into SE., Signs : nan, Treatment : medication : Phenytoin , Levetiracetam , Pentobarbitone/Pentobarbital , Midazolam, Diazepam , There are four goals of therapy : (i) ensure adequate vitals, ,systemic and cerebral oxygenation, (ii) terminate seizure,activity, (iii) prevent seizure recurrence, and (iv) establish,the diagnosis and treat the underlying disorder.,Secure the airway, maintain oxygenation, ensure perfusion, ,obtain intravenous access and protect the patient,from hypoglycemia, hyperthermia and injury. Head and neck should be positioned to keep the airway open. If,necessary, airway should be suctioned. Oxygen by nasal,cannula or mask, if needed, is administered, endotracheal,intubation may be required. Two IV access should be,established. Blood samples should be sent for laboratory,studies, and 10-25% dextrose (2 ml/kg) should be given,empirically. Systolic BP should be maintained at normal,levels. Hyperthermia occurs frequently in SE; temperature,should be recorded and treated promptly., Pathophysiology : Excitatory-Inhibitory Imbalance : Normally, the brain maintains a delicate balance between excitatory and inhibitory neurotransmitters, such as glutamate (excitatory) and gamma-aminobutyric acid (GABA, inhibitory). During a seizure, there is an excessive release of excitatory neurotransmitters and a decreased inhibitory activity, leading to a hyperexcitable state of neurons.Sustained Neuronal Hyperactivity : In status epilepticus, seizures continue without interruption, resulting in sustained neuronal hyperactivity. The repetitive firing of neurons can lead to a cycle of self-sustaining seizures, as each seizure episode can lower the seizure threshold and make subsequent seizures more likely.Energy Depletion : The intense and prolonged neuronal firing in status epilepticus increases the demand for energy in the brain. This demand can outstrip the brains ability to supply energy in the form of glucose and oxygen. The resulting energy depletion can impair cellular function and lead to an imbalance in ion concentrations (e.g., sodium, potassium) across cell membranes.Neuronal Injury and Excitotoxicity : Prolonged seizures can lead to neuronal injury and excitotoxicity. Excitotoxicity occurs when excessive glutamate release overactivates glutamate receptors, leading to calcium influx and triggering a cascade of events that damage neurons, including the activation of enzymes that break down cellular components.Blood-Brain Barrier Disruption : The prolonged seizure activity and neuronal injury can disrupt the blood-brain barrier, which normally separates the brain from circulating blood and helps maintain a stable brain environment. The breach of the blood-brain barrier can lead to increased permeability and allow harmful substances to enter the brain.Systemic Effects : Status epilepticus can have systemic effects on the body, including cardiovascular changes such as hypertension and tachycardia. Additionally, metabolic imbalances can occur, including lactic acidosis and electrolyte disturbances.Neuroinflammation : Prolonged seizures can trigger an inflammatory response in the brain, involving the release of inflammatory molecules and the activation of immune cells. Neuroinflammation can contribute to further neuronal damage and exacerbate the pathophysiological processes.Timely intervention is crucial in status epilepticus to halt the ongoing seizure activity and prevent potential long-term damage. Treatment typically involves the administration of antiseizure medications, such as benzodiazepines, followed by other antiepileptic drugs and supportive measures. In some cases, intravenous anesthetics or other interventions may be necessary to achieve seizure control. If you suspect someone is experiencing status epilepticus, seek immediate medical assistance., Epidemiology : The overall incidence of SE is 9.9 to 41 per 100, 000/year, GOOD, Seizures can happen for many reasons, many of which happen unpredictably. Because of this, there’s no way to prevent seizures and SE completely. But there are ways to reduce your risk of having a seizure. Doing so makes it less likely that you’ll have a seizure that can turn into SE. Ways you can reduce your chances of having a seizure include : ,,1. Having rescue medications available.,2. Eating a balanced diet and maintaining a weight that’s healthy for you. ,3. Treating infections.,4.Wearing safety equipment.,5. Avoiding alcohol, prescription and recreational drug misuse.,6. Managing your health conditions., Complications : developmental neurological abnormality, Stroke, Subarachnoid Hemorrhage, recent head trauma, Diagnostics : Arterial Blood Gas Analysis(ABG), Blood Urea, EEG, MRI Brain, lumbar puncture, SERUM ELECTROLYTE, serum calcium Ca++, CT HEAD, URINE TOXIN SCREEN, CT, plasma creatinine, BLOOD GLUCOSE, Differential diagnosis : Ischemic Stroke, Trauma, disease description : Status epilepticus is a neurological emergency requiring immediate evaluation and management to prevent significant morbidity or mortality. Previously, status epilepticus was defined as a seizure with a duration equal to or greater than 30 minutes or a series of seizures in which the patient does not regain normal mental status between seizures. The Neurocritical Care Society guidelines from 2012 revised the definition to a seizure with 5 minutes or more of continuous clinical and/or electrographic seizure activity or recurrent seizure activity without recovery between seizures

Stemi

Disease Name : Stemi, Symptoms : chest pain : ST-elevation myocardial infarction (STEMI) presents with central chest pain that is classically heavy in nature, like a sensation of pressure or squeezing., Gastrointestinal symptoms : ST-elevation myocardial infarction(STEMI) can present with gastrointestinal symptoms such as abdominal pain, nausea & vomiting., palpitations : The presence of Q waves may indicate a prior myocardial infarction as the etiology of the palpitations, "shortness of breath : If your heart isnt pumping enough oxygen-containing blood around the body, your body responds by breathing faster to try to get more oxygen into your body, making you feel short of breath.", Signs : diaphoresis : A probable explanation of profuse sweating in STEMI is stimulation of the sympathetic nervous system as a protective phenomenon in response to pain., systolic flow murmer : This murmur may be due to the rupture of a papillary muscle, the rupture of the interventricular septum, papillary muscle dysfunction, or acute left ventricular dilatation., Treatment : medication : Glyceryl trinitrate (nitroglycerin) , Metoprolol , Morphine, Aspirin/Acetylsalicylic acid, angiography , angioplasty, stunting , ballooning, bypass, Pathophysiology : For an acute thrombotic coronary event to cause ST-segment elevation on a surface ECG, there needs to be a complete and persistent occlusion of blood flow. Coronary athersclerosis and presence of high risk thin cap fibroatheroma (TCFA) can result in sudden onset plaque rupture. This results in changes in vascular endothelium resulting in cascade of platelet adhesion , activation and aggregartion resulting in thrombosis formation. Coronary artery occlusion in animal models shows a "wave-front" of myocardial injury that spreads from the sub-endocardial myocardium to the sub-epicardial myocardium resulting in a transmural infarction that appears as an ST elevation on surface ECG .Myocardial damage occurs as soon as the blood flow is interrupted which makes timely management a necessity. Sudden onset acute ischmemia can result in severe microvascualr dysfunction., Epidemiology : 64.37/1000 people in men aged 29-69 years, not specific, "There are several things you can do that will help prevent a heart attack. Perhaps the most important of them is to get a yearly physical. This annual visit with your primary care provider (sometimes called a checkup or wellness visit) is one of the most important ways to catch problems early. Conditions like high blood pressure or diabetes may not cause symptoms until theyre advanced, but a healthcare provider can easily catch them during an annual checkup.,,There are several other steps — many of which your primary care provider can offer guidance and resources about — that you can take : ,,Maintain a healthy weight.,Eat a balanced diet.,Get at least 150 minutes per week of moderate-intensity exercise (or higher).,If you use tobacco products, quit as soon as possible.,Manage your health, especially conditions like high cholesterol, high blood pressure and diabetes (this includes taking your medication regularly, not just when you remember).,However, because of the factors that you can’t change — especially your age and family history — preventing a heart attack isn’t always possible. Even so, it may be possible to delay when a heart attack happens. Recovering from a heart attack — or virtually any illness, for that matter — is also easier when you’re healthy.", Complications : mitral regurgitation, VENTRICULAR SEPTAL DEFECTS, Diagnostics : CPK MB, SERUM TROPONIN T(TROP T), SERUM TROPONIN- I(TROP I), ECG, trans thoracic 2D ECHO, CT ANGIOGRAPHY, CT SCAN, CARDIAC MRI, CARDIAC ANGIOGRAPHY, Differential diagnosis : anginal pain, myocarditis, non-ST-segment elevation myocardial infarction (NSTEMI), pericarditis, disease description : An acute ST-elevation myocardial infarction (STEMI) is an event in which transmural myocardial ischemia results in myocardial injury or necrosis. The current 2018 clinical definition of myocardial infarction (MI) requires the confirmation of the myocardial ischemic injury with abnormal cardiac biomarkers. It is a clinical syndrome involving myocardial ischemia, EKG changes and chest pain.

Stenosis & Atresia Of Nares

Disease Name : Stenosis & Atresia Of Nares, Symptoms : choking, difficulty in breathing, Feeding Difficulty, mouth breathing, Signs : nan, Treatment : reconstructive,plastic procedures, Pathophysiology : Accidental or surgical trauma to the nasal tip or vestibule can lead to web formation and stenosis of anterior nares. In Young’s operation, vestibular skin flaps are raised to create deliberate closure of nares in the treatment of atrophic rhinitis. Destructive inflammatory lesions of nose also cause stenosis. Earlier, several cases of vestibular stenosis resulted from smallpox. Congenital atresia of anterior nares due to noncanalization of epithelial plug is a rare condition. Stenosis of nares can be corrected by reconstructive plastic procedures., Epidemiology : GOOD, Complications : difficulty in breathing, Diagnostics : CT SCAN, DIRECT ENDOSCOPIC INSPECTION, Flexible Nasopharyngoscopy, Differential diagnosis : nan, disease description : Accidental or surgical trauma to the nasal tip or vestibule can lead to web formation and stenosis of anterior nares. In Young’s operation, vestibular skin flaps are raised to create deliberate closure of nares in the treatment of atrophic rhinitis. Destructive inflammatory lesions of nose also cause stenosis. Earlier, several cases of vestibular stenosis resulted from smallpox

Steroid-induced Glaucoma

Disease Name : Steroid-induced Glaucoma, Symptoms : eye pain : Steroid-induced glaucoma causes intense eye pain., headache : Increase in the IOP causes headaches., visual defects : Blurred vision may be due to corneal edema or steroid-induced posterior subcapsular cataract., Signs : Splinter haemorrhages present on or near the optic disc margin : Disc hemorrhages have been observed more frequently in early compared with advanced glaucoma and in patients with normal-tension rather than high-pressure glaucoma., Atrophy of retinal nerve fibre layer : Retinal nerve fiber layer atrophy is associated with visual field loss over time in glaucoma suspect and glaucomatous eyes., Thinning of neuroretinal rim : Neuroretinal rim thinning (NRR) is a characteristic glaucomatous optic disc change., increased intraocular pressure : Intraocular pressure (IOP) increase usually occurs 3 to 6 weeks following topical steroid use., Scotoma (defect in the visual field) : Glaucomatous visual field defects are basically comprised of four major patterns : an isolated scotoma, an arcuate scotoma, a nasal step, and generalized depression., Marked cupping of optic disc : Patients are suspicious for glaucoma based on optic nerve findings, such as large cups or asymmetric cupping –difference in cup size between the right and left eye. The optic nerve cup at left is larger than the optic nerve cup at right., Nasal shifting of retinal vessels : It is possible that the shift in retinal vessels seen in glaucoma is a result of the loss of retinal nerve fibers and thinning of the prelaminar tissue. This reduction in tissue could cause the vessels to be located more nasally and have a nasal orientation in relation to the nerve., Lamellar dot sign the pores in the lamina cribrosa : The laminar dot sign is one classical optic nerve head sign of glaucoma in inspections of the lamina cribrosa area. It is the visible grey pores or fenestrae that develop by the loss of neural tissue and deep optic disc cupping, exposing the underlying lamina cribrosa tissue., Treatment : medication : Timolol , • Discontinuation of steroids. IOP may normalise,within 10 days to 4 weeks in 98% of cases.,• Medical therapy with 0.5% timolol maleate is,effective during the normalisation period., • Filtration surgery is required occasionally in,intractable cases., Pathophysiology : Steroid-induced glaucoma is considered to be a type of secondary open-angle glaucoma, caused by increased resistance to the outflow of aqueous at the level of the trabecular meshwork. In this condition, there is increased production and decreased destruction of the extracellular matrix of the trabecular meshwork. There is increased deposition of glycosaminoglycans, fibronectin, elastin, and Type IV collagen and reduced activity of matrix metalloproteinases. Trabecular meshwork cells have glucocorticoid receptors, and steroids may act on them to alter cell migration and phagocytosis. This reaction causes decreased cellularity of the trabecular meshwork and increased extracellular matrix deposition, thus increasing aqueous outflow resistance and a rise in IOP. Glaucoma may develop if the IOP elevation is of sufficient magnitude and duration, thus leading to progressive damage to the optic nerve and visual field., Epidemiology : more than 30% of individuals show a moderate rise of IOP (6 to 15 mmHg) after topical cortisone use, variable, Listed below are some ways by which you can prevent steroid-Induced glaucoma : ,,1.Regular dilated eye exam : ,Regular eye exams are always suggested. It helps in detecting glaucoma in its early stages, much before any significant damage occurs. Patients with glaucoma have to attend frequent screenings.,,2.Check your family history : ,Since you’re at an increased rate of developing glaucoma if you have a family history of it, it is advised that you should take all necessary precautions to avoid it in the best possible way.,,3.Take prescribed eye drops : ,Eye Drops meant for treating glaucoma result in reducing the high eye pressure. Hence, after doctor’s consultation, eye drops should be taken.,,4.Exercise safely : ,Moderate and regular exercise may help in reducing eye pressure. You can have a talk with your doctor about an appropriate exercise program.,,5.Eye protection : ,Wear eye protection if you are playing high-speed games or using power tools.,,6.Necessary information sharing : ,While testing, the doctor might ask specific questions like if you experience eye redness, headache, multi-colored halos, etc. They can also enquire about previous surgeries or illnesses. It is better to inform the doctor so that your further medication goes in the right direction.,,Time plays a crucial role while dealing with steroid-Induced glaucoma as any delay can lead to severe consequences. Hence, immediate measures should be taken to deal with this eye disorder., Complications : blindness, Diagnostics : GONIOSCOPY, Slit lamp examination, TONOMETRY TEST, Perimetry, Differential diagnosis : angle closure glaucoma, Glaucoma, Glaucoma, Glaucoma, Glaucoma, Glaucoma, disease description : Steroids are one of the most commonly prescribed drugs, used mainly in the treatment of various autoimmune and inflammatory conditions. Although it has numerous benefits, steroid usage can cause many adverse effects on the eye, the most important being steroid-induced glaucoma and cataract. Steroid-induced iatrogenic glaucoma was described for the first time in the 1950s with the observation of glaucoma following the use of systemic adrenocorticotropic hormones and topical or systemic steroids. 

Steroid-modified Tinea

Disease Name : Steroid-modified Tinea, Symptoms : Red, scaly rash, often in skin folds., Signs : bruise-like brownish discoloration, concentric rings of erythema, Steroid-modified eyelid infection may closely resemble a sty, rashes on skin, Eczematous skin lesions, Scaling, Treatment : medication : Terbinafine , Itraconazole , Whatever site is affected, it is often best to treat steroid-modified ,ringworm with oral therapy, allowing a few applications of topical ,steroid to continue until the terbinafine or itraconazole has begun ,to take effect. It is wise to use 1% hydrocortisone cream or at least ,a weaker steroid than that originally prescribed, and also to warn ,the patient about a possible rebound in spite of these measures. ,Follow-up to ensure steroid cream has been stopped and cure ,obtained is mandatory., Pathophysiology : Normally, the clinical diagnosis of tinea depends heavily on the inflammatory changes involved. This inflammatory response may be almost totally suppressed by corticosteroids, systemic or topical. At the same time, it is probable that the resistance to infection mediated by the immune response, especially the cell- mediated response, is diminished by corticosteroids. In this situation, the patient suffers doubly : the infection is less likely to be diagnosed, and the patient has been rendered more susceptible to that infection. With patients on systemic steroids (perhaps treated with additional immunosuppressive agents or irradiation), the degree of modification is often minor, but even in these cases it may be sufficient to mislead, especially on the face. With topical steroids, the degree of modification can be profound. The usual sites where this problem occurs are the groins, lower legs, face and hands, but tinea circinata elsewhere may be steroid treated. The history is characteristic. The patient is often satisfied initially with the treatment. Itching is controlled and the inflammatory signs settle. But there is a relapse on stopping treatment, with varying rapidity. Further applications bring renewed relief and the cycles are repeated. In the groins, the patient may develop few persistent nodules, which become unsuppressible by the steroid preparation., Epidemiology : RELAPSING, Complications : Majocchi granuloma, Diagnostics : nan, Differential diagnosis : Candidosis, disease description : These are ringworm infections modified by corticosteroids (systemic or topical) prescribed for some pre-existing pathology or given mistakenly for the treatment of misdiagnosed tinea. With patients on systemic steroids (perhaps treated with additional immunosuppressive agents or irradiation), the degree of modifi cation is often minor, but even in these cases it may be suffi - cient to mislead, especially on the face. With topical steroids, the degree of modification can be profound. The usual sites where this problem occurs are the groins, lower legs, face and hands, but tinea circinata elsewhere may be steroid treated.In India, a dermatophyte species often identified as Trichophyton mentagrophytes has been reported as the cause of these breakthrough infections.13 Genetic sequencing of Trichophyton isolates causing multidrug-restraint tinea in North India suggests that they are highly related and belong to a unique clade indistinguishable from T. mentagrophytes/T. interdigitale

Stevens-johnson Syndrome And Toxic Epidermal Necro

Disease Name : Stevens-johnson Syndrome And Toxic Epidermal Necro, Symptoms : blisters : Within a few days, the skin begins to blister and peel, forming very painful raw areas called erosions that resemble a severe hot-water burn. The skin erosions usually start on the face and chest before spreading to other parts of the body., dysphagia : This condition also damages the mucous membranes, including the lining of the mouthwhich can cause trouble with swallowing., flu-like symptoms : Includes fever, sore throat, mouth, headache., eye problem : SJS/TEN often affects the eyes as well, causing irritation and redness of the conjunctiva., Signs : nan, Treatment : Systemic treatment in acute phase includes : ,Removal (e.g., causative drugs) or treatment (e.g., of,causative infection) of the inciting factor : ,• Intravenous immunoglobulin, ,• Role of systemic steroids is controversial, ,• Maintenance of hydration, and,• Debridement and replacement of sloughing skin.,Ocular treatment during acute phase includes : ,• Topical tear drops and prevention of exposure, ,• Topical antibiotics and steroid eyedrops, and,• Pseudomembrane peel and symblepharon lysis,with glass rod or moistened cotton swab should,be done daily., Pathophysiology : The initial step for Stevens-Johnson syndrome/toxic epidermal necrolysis may be interaction/binding of a drug-associated antigen or metabolite with the major histocompatibility complex (MHC) type 1 or cellular peptide to form an immunogenic compound. The exact mechanism is speculative.Stevens-Johnson syndrome/toxic epidermal necrolysis is T–cell-mediated.CD8+ cells are present in blister fluid and may induce keratinocyte apoptosis.Other cells of the innate immune system play a role.CD40 ligand cells are also present and may induce the release of TNF–alpha, nitrous oxide, interleukin 8 (IL-8), and cell adhesion antibodies. TNF–alpha also induces apoptosis.Both Th1 and Th2 cytokines are present.Other cells implicated in Stevens-Johnson syndrome/toxic epidermal necrolysis include macrophages, neutrophils, and natural killer (NK) cells.The pharmacologic interaction of drugs with the immune system could result in binding of the responsible drug to MHC-1 and the T cell receptor. An alternative theory is a pro-hapten concept, in which drug metabolites become immunogenic and stimulate the immune system., Epidemiology : SJS/TEN is a rare disease, affecting 1 to 2 per million people each year. Stevens-Johnson syndrome (the less severe form of the condition) is more common than toxic epidermal necrolysis., variable, Special attention should be given to the prevention of ocular complications. Early referral to an ophthalmologist is mandatory for assessment of the extent of eye involvement and prompt treatment with topical steroids., Complications : Corneal perforation, trichiasis, corneal ulceration, formation of symblepharon, Corneal neovascularization, Diagnostics : Complete Blood Count CBC, LIVER FUNCTION TEST LFT, kidney function test KFT, BIOPSY FROM SKIN LESION, Differential diagnosis : acute graft versus host disease, erythema multiforme, Pemphigus Vulgaris, Staphylococcal scalded skin syndrome, toxic shock syndrome, disease description : ?Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN) is a severe skin reaction most often triggered by particular medications. Although Stevens-Johnson syndrome and toxic epidermal necrolysis were once thought to be separate conditions, they are now considered part of a continuum .SJS/TEN often begins with a fever and flu-like symptoms. Within a few days, the skin begins to blister and peel, forming very painful raw areas called erosions that resemble a severe hot-water burn. 

Strain

Disease Name : Strain, Symptoms : swelling, Pain, Tenderness, muscle spasm, Redness, PAIN ON WALKING, Signs : nan, Treatment : At first, treatment of both sprains and strains usually involves resting the injured area, icing it, wearing a bandage or device that compresses the area, and medicines. Later treatment might include exercise and physical therapy.,\tNSAID AND ANTI INFLAMMETORY DRUG REST, ICE PACKING, COMPRESSION BAND, ELEVATION (RICE), Pathophysiology : nan, Epidemiology : good, Complications : nan, Diagnostics : X RAY AP VIEWS, Differential diagnosis : nan, disease description : Strain is a physical effect of stress, in this case tensile stress associated with some stretching of the ligaments; in colloquial usage, ‘strained ligament’ is often meant to denote an injury somewhat more severe than a ‘sprain’, which possibly involves tearing of some fibres.A strain is a stretched or torn muscle or tendon. Tendons are tissues that connect muscle to bone. Twisting or pulling these tissues can cause a strain. Strains can happen suddenly or develop over time. Back and hamstring muscle strains are common. Many people get strains playing sports. Symptoms include pain, muscle spasms, swelling, and trouble moving the muscle.

Streptocerciasis/mansonellosis

Disease Name : Streptocerciasis/mansonellosis, Symptoms : papules, fatigue, headache, respiratory difficulties, Skin rashes, visual disturbances, fever, Abdominal Pain, Signs : lymphadenopathy, hypopigmented macules, arthralgia, dermatitis, pruritus, edema, corneal lesions, Treatment : medication : Ivermectin , Diethylcarbamazine , First line,•\tDiethylcarbamazine 6 mg/kg/day for 12 days,Second line,•\tIvermectin (150 µg/kg single dose), Pathophysiology : Streptocerciasis causes a subcutaneous filariasis in humans. The disease is transmitted by biting midges (Culicoides). Adult worms reside in the dermis of the upper trunk and shoulder region and the microfilariae are found in the skin. Most individuals with M. streptocera are asymptomatic. The most common complaint is pruritus. The skin rash is rather similar to that seen with onchocerciasis, with acute or lichenified itching papules. More widespread lichenification may also occur, and hypopigmented macules are common. Secondary enlargement of the local lymph nodes is seen in many patients., Epidemiology : ~40%, variable, There have been no studies of chemoprophylaxis for prevention of streptocerciasis. Although specific control programs have not been attempted, mass drug administration campaigns for W. bancrofti and O. volvulus control in Africa may help to dampen transmission of M. streptocerca., Complications : nan, Diagnostics : Microscopy For Microfilaria, RT PCR, EOSINOPHILS, Differential diagnosis : Granuloma multiforme, LEPROSY, Onchocerciasis, disease description : Streptocerciasis is an infection caused by the filarial nematode, Mansonella streptocerca. The disease is seen mainly in parts of west and central Africa in rainforest areas, where it may be found in the majority of the population. Chimpanzees in the endemic area may also be infected. There remains much unknown about M. streptocerca, including its prevalence in endemic areas. The disease, however, is known to be a common parasite with cutaneous manifestations. The disease causes a subcutaneous filariasis, with Loa loa and Onchocerca volvulus being the other two causes in humans.

Stress Disorder

Disease Name : Stress Disorder, Symptoms : mood disturbances, Feelings of anxiety, Sleep disturbances, Irritability, Night terrors, flashback, Signs : amnesia, Treatment : medication : Topiramate , Hydrocortisone , Sertraline, Venlafaxine , paroxetine, BENZODIAZEPINE, COUNSELLING & EXPRESSIVE PSYCHOPTHERAPY, Pathophysiology : It is hypothesized that in PTSD there is excessive release of norepinephrine from the locus coeruleus in response to stress and increased noradrenergic activity at projection sites in the hippocampus and amygdala. These changes theoretically facilitate the encoding of fear-based memories. Greater sympathetic responses to cues associated with the traumatic event occur in PTSD, although pituitary adrenal responses are blunted. In addition to fear learning, changes in threat detection (insula overactivity), executive function, emotional regulation and contextual learning have been documented., Epidemiology : GOOD, To Do : Risk factors for the development of PTSD include a past psychiatric history and personality characteristics of high neuroticism and,extroversion., Complications : nan, Diagnostics : nan, Differential diagnosis : Mental disturbances including depression, disease description : Psychiatric disorders are common in medical practice and may present either as a primary disorder or as a comorbid condition. The prevalence of mental or substance use disorders in the United States is ~30%, but only one-third of affected individuals are currently receiving treatment. Global burden of disease statistics indicates that 4 of the 10 most important causes of morbidity and attendant health care costs worldwide are psychiatric in origin. Changes in health care delivery underscore the need for primary care physicians to assume responsibility for the initial diagnosis and treatment of the most common mental disorders. Prompt diagnosis is essential to ensure that patients have access to appropriate medical services and to maximize the clinical outcome. Validated patient-based questionnaires have been developed that systematically probe for signs and symptoms associated with the most prevalent psychiatric diagnoses and guide the clinician into targeted assessment. The Primary Care Evaluation of Mental Disorders (PRIME-MD; and a self-report form, the Patient Health Questionnaire) and the Symptom-Driven Diagnostic System for Primary Care (SDDS-PC) are inventories that require only 10 min to complete and link patient responses to the formal diagnostic criteria of anxiety, mood, somatoform, and eating disorders and to alcohol abuse or dependence.

Striate (and Focal) Palmoplantar Keratoderma(15959

Disease Name : Striate (and Focal) Palmoplantar Keratoderma(15959, Symptoms : knee pain, Cardiac Disease, Signs : Hyperhidrosis, hyperkeratosis, woolly hair, linear pattern of skin thickening on the palms and flexor aspects of the fingers, Treatment : medication : Acitretin, Several reports point to good response to systemic acitretin treatment and/or application of high percentage urea creams., Pathophysiology : Initially, autosomal dominant striate keratoderma was mapped to the desmosomal cadherin cluster on 18q12.1. SPPK has been shown to result from haploinsufficiency for desmoglein 1 due to heterozygous mutations in DSG1. Heterozygous mutations in DSG1 are not exclusively associated with a striate pattern of hyperkeratosis as they have also been found to cause focal and diffuse PPK. Moreover, since carriers of heterozygous mutations in DSG1 display PPK only while the offsprings of two such heterozygous carriers can be affected by a life-threatening condition known as SAM syndrome (see earlier), DSG1 mutations are actually inherited in a semidominant fashion. The second SPPK locus on 6p21 is linked to dominant nonsense mutations in the desmoplakin gene (DSP) also leading to haploinsufficiency. The majority of genetic reports on isolated striate keratoderma show dominant DSG1 mutations, whereas there are several reports on striate or focal keratoderma with cardiac involvement due to recessive (or dominant) DSP mutations (see Carjaval syndrome later). Finally, there is one report on a frameshift mutation in the V2 tail domain of keratin 1. The mutation is similar to those being reported for ICM., Epidemiology : 1.17 cases per 100, 000 population., variable, Complications : nan, Diagnostics : ELECTRON MICROSCOPY, HISTOLOGIC EXAMINATION, Differential diagnosis : nan, disease description : Isolated SPPK is usually transmitted as an autosomal dominant trait and is caused by defects in at least three different genes. It is associated with a spectrum of Mendelian diseases of the desmosomes. Most important, keratoderma with cardiomyopathy should be excluded.

Stricture Of The Bile Duct

Disease Name : Stricture Of The Bile Duct, Symptoms : Malaise, nausea, vomiting, weight loss, Obstructive jaundice, Signs : nan, Treatment : Medical management of biliary strictures is largely restricted to addressing complications from biliary obstructions and sometimes treatment of the causative agent. Therefore, analgesics, empiric antibiotics, plus hemodynamic support with intravenous fluids with or without vasopressors and inotropes are often instituted where applicable.24 Also common are therapies aimed at reducing the effects of increasing bilirubinemia. These efforts are often supportive and in preparation for definitive therapy.Other forms of medical treatment could be aimed at the prevention of further complications like excessive bleeding due to a coagulopathy as well as deep vein thrombosis and sepsis in the early postoperative period., There are varying options for operative or interventional management. These options can be accomplished via endoscopy, open surgery, or percutaneously., Pathophysiology : Biliary strictures are characterized by narrowing of a segment of the bile duct associated with proximal ductal dilatation. Obstruction of bile flow leads to elevation of serum bilirubin levels with clinical and laboratory features of obstructive jaundice. Stasis of bile is a major risk factor for ascending cholangitis.As observed from magnetic resonance cholangiopancreatography (MRCP) or endoscopic retrograde cholangiopancreatography (ERCP), benign strictures have tapered margins with smooth and symmetric borders. On the other hand, malignant strictures have shouldering of the margins with irregular and asymmetric borders. Malignant strictures involve a long segment as opposed to benign, which involves shorter segments. Malignant strictures appear to enhance on contrast-enhanced cross-sectional imaging.The strictures can be classified according to the Strasberg-Bismuth classification. Classification helps in guiding management.Type E injuries lead to strictures of the hepatic ducts, which are further defined by the proximal extent.E1 : Common hepatic duct division greater than 2 cm from the bifurcation.E2 : Common hepatic duct division less than 2 cm from the bifurcation.E3 : Common bile duct division at the bifurcation.E4 : Hilar stricture involves confluence and loss of communication between the right and left hepatic duct.E5 : Involves aberrant right hepatic duct with concomitant stricture of the common hepatic duct, Epidemiology : good, Complications : CHOLANGIOCARCINOMA, cholangitis, CIRRHOSIS, LIVER ABSCESS, septicemia, Diagnostics : ERCP, MRCP, CT SCAN, CT SCAN, USG, CHOLANGIOGRAPHY, PERCUTANEOUS TRANSHEPATIC CHOLANGIOGRAPHY, Differential diagnosis : ACALCULOUS CHOLECYSTITIS, CHOLECYSTOSES, CHOLEDOCHAL CYST, CHOLELITHIASIS, PRIMARY SCLEROSING CHOLANGITIS, disease description : Biliary strictures or bile duct strictures refer to segments of narrowing of the intrahepatic or extrahepatic biliary ductal system. When narrowed, they impede the normal antegrade flow of bile, causing proximal dilatation resulting in clinical and pathological sequelae of biliary obstruction. Patients with chronic biliary strictures present a unique challenge when malignancy is suspected.

Stridor

Disease Name : Stridor, Symptoms : respiratory difficulties, respiratory distress, hoarseness of voice, stridor, wheezing, SNORING, fever, Signs : nan, Treatment : TREATMENT OF THE CAUSE, Pathophysiology : Stridor may arise from lesions of nose, tongue, mandible, pharynx, larynx or trachea and bronchi. Common causes of stridor in infants and children are given below : 1. Nose. Choanal atresia in newborn. 2. Tongue. Macroglossia due to cretinism, haemangioma or lymphangioma, dermoid at base of tongue, lingual thyroid. 3. Mandible. Micrognathia, Pierre-Robin syndrome. In these cases, stridor is due to falling back of tongue. 4. Pharynx. Congenital dermoid, adenotonsillar hypertrophy, retropharyngeal abscess, tumours. 5. Larynx. (a) Congenital. Laryngeal web, laryngomalacia, cysts, vocal cord paralysis, subglottic stenosis. (b) Inflammatory. Epiglottitis, laryngotracheitis, diphtheria, tuberculosis. (c) Neoplastic. Haemangioma and juvenile multiple papillomas, carcinoma in adults. (d) Traumatic. Injuries of larynx, foreign bodies, oedema following endoscopy, or prolonged intubation. (e) Neurogenic. Laryngeal paralysis due to acquired lesions. (f) Miscellaneous. Tetanus, tetany, laryngismus stridulus. 6. Trachea and bronchi (a) Congenital. Atresia, stenosis, tracheomalacia. (b) Inflammatory. Tracheobronchitis. (c) Neoplastic. Tumours of trachea. (d) Traumatic. Foreign body, stenosis trachea (e.g. following prolonged intubation or tracheostomy). 7. Lesions outside respiratory tract (a) Congenital. Vascular rings (cause stridor and dysphagia), oesophageal atresia, tracheo-oesophageal fistula, congenital goitre, cystic hygroma. (b) Inflammatory. Retropharyngeal and retro-oesophageal abscess. (c) Traumatic. FB oesophagus (secondary tracheal compression). (d) Tumours. Masses in neck., Epidemiology : GOOD, Complications : nan, Diagnostics : CT SCAN, Direct Laryngoscopy, Flexible Fiberoptic Laryngoscopy, Soft Tissue Lateral View Neck Radiographs, ANGIOGRAPHY, PHYSICAL EXAMINATION, Differential diagnosis : ACUTE LARYNGITIS, diphtheria, Epiglottitis, Peritonsillar abscess, retropharyngeal abscess, disease description : Stridor is noisy respiration produced by turbulent airflow through the narrowed air passages. It may be heard during inspiration, expiration or both.. Inspiratory stridor is often produced in obstructive lesions of supraglottis or pharynx, e.g. laryngomalacia or retropharyngeal abscess. • Expiratory stridor is produced in lesions of thoracic trachea, primary and secondary bronchi, e.g. bronchial foreign body, and tracheal stenosis. • Biphasic stridor is seen in lesions of glottis, subglottis and cervical trachea, e.g. laryngeal papillomas, vocal cord paralysis and subglottis stenosis. 1. Time of onset. To find whether cause is congenital or acquired. 2. Mode of onset. Sudden onset (foreign body, oedema), gradual and progressive (laryngomalacia, subglottic haemangioma, juvenile papillomas). 3. Duration. Short (foreign body, oedema, infections), long (laryngomalacia, laryngeal stenosis, subglottic haemangioma, anomalies of tongue and jaw). 4. Relation to feeding. Aspiration in laryngeal paralysis, oesophageal atresia, laryngeal cleft, vascular ring, foreign body oesophagus..5. Cyanotic spells. Indicate need for airway maintenance. 6. Aspiration or ingestion of a foreign body. 7. Laryngeal trauma. Blunt injuries to larynx, intubation, endoscopy..

Stroke

Disease Name : Stroke, Symptoms : diplopia : Diplopia, or double vision, can occur as a result of a stroke. When certain parts of the brain that control eye movements are affected by a stroke, it can lead to problems with coordinating the movement of the eyes, resulting in seeing double images, headache : A sudden, severe headache, which may be accompanied by vomiting, dizziness or altered consciousness., Signs : "aphasia : Aphasia is a communication disorder that can occur after a stroke, usually due to damage to the language centers of the brain, typically in the left hemisphere. It can affect a persons ability to speak, understand speech, read, write, or use numbers.", slurred speech : In the context of a stroke, slurred speech typically occurs when the part of the brain responsible for controlling speech and language is affected by the stroke. This can happen due to a blockage (ischemic stroke) or bleeding (hemorrhagic stroke) in the blood vessels supplying the brain., paralysis : Patients may develop sudden numbness, weakness or paralysis in the face, arm or leg. This often affects just one side of the body., Treatment : medication : Heparin , Mannitol , Aspirin/Acetylsalicylic acid, Pathophysiology : The pathophysiology of stroke is complex and involves numerous processes, including : energy failure, loss of cell ion homeostasis, acidosis, increased intracellular calcium levels, excitotoxicity, free radical-mediated toxicity, generation of arachidonic acid products, cytokine-mediated cytotoxicity, complement activation, disruption of the blood-brain barrier (BBB), activation of glial cells, and infiltration of leukocytes .These are interrelated and co-ordinated events, which can lead to ischemic necrosis, which occurs in the severely affected ischemic-core regions. Within a few minutes of a cerebral ischemia, the core of brain tissue exposed to the most dramatic blood flow reduction, is mortally injured, and subsequently undergoes necrotic cell death. This necrotic core is surrounded by a zone of less severely affected tissue which is rendered functionally silent by reduced blood flow but remains metabolically active .  Necrosis is morphologically characterized by initial cellular and organelle swelling, subsequent disruption of nuclear, organelle, and plasma membranes, disintegration of nuclear structure and cytoplasmic organelles with extrusion of cell contents into the extracellular space . , Epidemiology : prevalence of stroke escalates with age. The lifetime risk of all types of stroke is higher in women; however, this is attributed to longer life expectancy., 105 to 152/100, 000 persons per year, variable, "Many stroke prevention strategies are the same as strategies to prevent heart disease. In general, healthy lifestyle recommendations include : nan, , Controlling high blood pressure (hypertension). This is one of the most important things you can do to reduce your stroke risk. If youve had a stroke, lowering your blood pressure can help prevent a subsequent TIA or stroke. Healthy lifestyle changes and medications are often used to treat high blood pressure.,Lowering the amount of cholesterol and saturated fat in your diet. Eating less cholesterol and fat, especially saturated fat and trans fats, may reduce buildup in the arteries. If you cant control your cholesterol through dietary changes alone, your doctor may prescribe a cholesterol-lowering medication.,Quitting tobacco use. Smoking raises the risk of stroke for smokers and nonsmokers exposed to secondhand smoke. Quitting tobacco use reduces the risk of stroke.,Managing diabetes. Diet, exercise and losing weight can help you keep your blood sugar in a healthy range. If lifestyle factors dont seem to be enough to control your diabetes, your doctor may prescribe diabetes medication.,Maintaining a healthy weight. Being overweight contributes to other stroke risk factors, such as high blood pressure, cardiovascular disease and diabetes.,Eating a diet rich in fruits and vegetables. A diet containing five or more daily servings of fruits or vegetables may reduce the risk of stroke. The Mediterranean diet, which emphasizes olive oil, fruit, nuts, vegetables and whole grains, may be helpful.,Exercising regularly. Aerobic exercise reduces the risk of stroke in many ways. Exercise can lower blood pressure, increase the levels of good cholesterol, and improve the overall health of the blood vessels and heart. It also helps you lose weight, control diabetes and reduce stress. Gradually work up to at least 30 minutes of moderate physical activity — such as walking, jogging, swimming or bicycling — on most, if not all, days of the week.,Drinking alcohol in moderation, if at all. Heavy alcohol consumption increases the risk of high blood pressure, ischemic strokes and hemorrhagic strokes. Alcohol may also interact with other drugs youre taking. However, drinking small to moderate amounts of alcohol, such as one drink a day, may help prevent ischemic stroke and decrease the bloods clotting tendency. Talk to your doctor about whats appropriate for you.,Treating obstructive sleep apnea (OSA). Your doctor may recommend a sleep study if you have symptoms of OSA — a sleep disorder that causes you to stop breathing for short periods repeatedly during sleep. Treatment for OSA includes a device that delivers positive airway pressure through a mask to keep the airway open while you sleep.,Avoiding illegal drugs. Certain street drugs, such as cocaine and methamphetamine, are established risk factors for a TIA or a stroke.", Complications : Pulmonary Embolism, DVT, Diagnostics : Complete Blood Count CBC, Erythrocyte Sedimentation Rate (ESR), PLATELET COUNT, RBC Count, Total Leucocyte Count (TLC), CHEST X RAY, Differential diagnosis : Hypoglycemia, intracranial hemorrhage, Intracranial tumour haemorrhage, migraine, Multiple Sclerosis, syncope, disease description : Stroke is a life-threatening condition that happens when part of your brain doesn’t have enough blood flow. This most commonly happens because of a blocked artery or bleeding in your brain. Without a steady supply of blood, the brain cells in that area start to die from a lack of oxygen.

Stromal Tumour With Minor Sex Cord Elements

Disease Name : Stromal Tumour With Minor Sex Cord Elements, Symptoms : bleeding pv, Abdominal Pain, Signs : ABDOMINAL MASS, Treatment : nan, Pathophysiology : Genetic Mutations : Like many types of tumors, genetic mutations play a role in the pathophysiology of stromal tumors with minor sex cord elements. Specific genetic alterations in the affected cells can disrupt normal cellular functions, including growth regulation and differentiation.Hormonal Influences : Sex cord-stromal tumors, including those with minor sex cord elements, are often hormone-producing tumors. They may produce hormones such as estrogen, progesterone, and androgens. These hormones can contribute to the growth and development of the tumor and its associated features.Cellular Differentiation : The presence of both stromal and sex cord elements suggests a disruption in the normal differentiation pathways of ovarian cells. Abnormal signaling pathways and interactions between different cell types can lead to the mixed histological appearance of these tumors.Tumor Microenvironment : The tumor microenvironment, including the presence of various immune cells, blood vessels, and signaling molecules, can influence tumor growth and behavior. Interactions between the stromal and sex cord elements within the tumor microenvironment may contribute to tumor progression.Molecular Pathways : Research into the molecular pathways involved in ovarian sex cord-stromal tumors is ongoing. Alterations in certain signaling pathways, such as the Wnt/ß-catenin pathway, have been implicated in the pathogenesis of these tumors., Epidemiology : The yearly adjusted incidence rate is 3.7/1000 000, variable, Complications : nan, Diagnostics : Examination under Microscope, Differential diagnosis : Brenner tumour, Prostate cancer, disease description : Ovarian stromal tumor with minor sex cord elements is a rare tumor. It is composed of predominantly Sex cord-stromal tumors are groups of tumors composed of granulosa cells, theca cells,  Sertoli cells, Leydig cells, and fibroblasts of stromal origin, singly or in various combinations. These tumors have variable clinicopathologic fetaures and biologic behavior, which may pose a diagnostic challenge. tumor with scattered minor sex cord elements in less than 10% of the tumor area. 

Strongyloidiasis

Disease Name : Strongyloidiasis, Symptoms : Gastrointestinal symptoms : Gastrointestinal symptoms are vague, including epigastric abdominal cramping, indigestion, anorexia, weight loss, nausea, vomiting, chronic diarrhea, constipation, pruritus ani, bloating and, rarely, small bowel obstruction. In classic cases, diarrhea is profuse, watery, and mucoid. Periods of alternation between diarrhea and constipation may occur. Malabsorption of fat and vitamin B-12 has been reported in chronic infections and has been successfully treated by deworming. Prolonged malabsorption of both fat and protein can lead to a celiac-like syndrome, characterized by steatorrhea, hypoalbuminemia, and peripheral edema., respiratory symptoms : Migration of the larvae through the lungs produces a pneumonitis that resembles Loeffler syndrome. Symptoms include a productive cough, at times with blood-streaked sputum, dyspnea, and fever. Strongyloidiasis can also produce a clinical syndrome that mimics either asthma or pneumonia. In severe (disseminated) disease, pneumonitis may cause hemoptysis and difficulty in breathing. In addition, cough, hemoptysis, dyspnea, wheezing, pleuric pain, tachypnea can occur, and acute respiratory distress syndrome (ARDS) may require mechanical ventilation., Neurological symptoms : An altered mental status, focal seizures, meningitis, brain abscess or nuchal rigidity may indicate central nervous (CNS) involvement. Symptoms of meningitis may include headache, nausea, vomiting, and, in extreme cases, coma. Granulomatous hepatitis and parasitic invasion of the heart, kidney, peritoneum, lymph nodes, pancreas, prostate, ovaries, thyroid, or parathyroid may be present in disseminated disease., cutaneous symptoms : Skin penetration by infective larvae can elicit ground itch, a cutaneous eruption of pruritic papulovesicular lesions. Typically, skin penetration is on the feet but may be at any site that contacted infected soil (eg, around the anus within 12 cm or anywhere on the trunk and thighs). Larva currens (racing larvae), the pathognomonic rash of Strongyloides infection, is an intensely pruritic linear or serpiginous urticarial rash that may consist of one or more such bands and creeps 5 cm/h to 15 cm/h up the body. The rash, likely an allergic response to the migrating filariform larvae, often manifests as a pruritic wheal or linear urticaria. This dermatologic manifestation may last hours to days but in autoinfection cycles can recur over weeks, months, and years. In an individual who has already been sensitized, a second, creeping, urticarial rash may appear, which is caused by an allergic reaction to the larvae penetrating the skin. Excoriation and impetigo are common., Signs : nan, Treatment : medication : Albendazole , Ivermectin , Ivermectin does not kill the Strongyloides larvae, but only the adult worms. As a result, repeat dosing is necessary., Pathophysiology : The life cycle of S. stercoralis has three components : direct, indirect, and autoinfection. In the direct cycle,  the rhabditiform larva from stool matures into filariform larvae in the soil and penetrates the skin to travel to the lungs and eventually the gastrointestinal system. The indirect cycle follows, where eggs are excreted and returned to the soil to live as free-living adults or develop into filariform larvae or reinvade the host through the perianal skin. This reinvasion characterizes the autoinfection cycle, where the infective filariform larva completes its formation in the host’s intestines.Direct contact of intact skin with contaminated soil results in inoculation of the larva which then migrates through lymphatics and venules to reach pulmonary circulation and then alveoli. Larvae are then coughed up proximally into the trachea and then swallowed from the upper respiratory tract into the gastrointestinal tract. Within the intestine, they mature and eggs are produced by females.Eggs may pass intact through stoolEggs may hatch in the intestine and pass in stool as rhabditiform larvaOr produce infective filariform larva prematurely,   which then reinvades the host either via intestinal wall or perianal skin to create a perpetual cycle of infection known as autoinfection., Epidemiology : 8.1%, variable, Some ways you can reduce your risk for strongyloidiasis include : ,,Wear protective clothing when you’re around soil in areas where Strongyloides lives. This includes shoes and gloves.,Be especially cautious in areas with inadequate sanitation. This increases the risk of Strongyloides contaminating the soil.,If you’re going to have a procedure or start medication that will weaken your immune system, ask your provider about testing for infections. If they diagnose you with strongyloidiasis, you can treat it while you still have a strong immune system. This can prevent hyperinfection., Complications : Neurological symptoms, Diagnostics : serum IgE level, ELISA FOR ANTIBODY TITRE, STOOL EXAMINATION, DUODENAL MUCOSAL BIOPSY, Differential diagnosis : Asthma, CHOLERA, Chronic Obstructive Pulmonary Disease, DIVERTICULITIS, Ileus, INFLAMMATORY BOWEL DISEASES, Loeffler syndrome, peritonitis, disease description : Strongyloidiasis is a disease caused by the intestinal nematodes Strongyloides stercoralis or Strongyloides fuelleborni. The more common agent,  Stercoralis stercoralis, is a helminth transmitted by soil and can cause severe disease in immunocompromised individuals.

Sturge-weber Syndrome

Disease Name : Sturge-weber Syndrome, Symptoms : Hypothyroidism : Patients with Sturge-Weber syndrome carry the additional risk of developing hypothalamic-pituitary dysfunction, secondary to their central nervous system dysfunction., migraine : Sturge-Weber syndrome is known to be associated with migraine attacks and prolong aura even without cerebral infarction., seizures : At least three-quarters of children with Sturge-Weber syndrome will have seizures. These are caused by the growth of blood vessels on the surface of the brain. Seizures usually start before your baby is 1., Intellectual disability : Some individuals have learning disabilities with problems focusing similar to attention-deficit/hyperactivity disorder (ADHD)., Signs : HEMANGIOMA : Sturge-Weber syndrome (SWS) is a neurocutaneous syndrome, characterized by the association of facial port-wine hemangiomas in the trigeminal nerve distribution area, with vascular malformation(s) of the brain (leptomeningeal angioma) with or without glaucoma., port-wine birthmark involving the forehead and upper eyelid : In people with Sturge-Weber syndrome, the port-wine birthmark is most often on the face, typically on the forehead, temple, or eyelid. The port-wine birthmark is usually only on one side of the face but can be on both sides. Over time, the skin within the port-wine birthmark can darken and thicken., Buphthalmos : In individuals with Sturge-Weber syndrome, glaucoma typically develops either in infancy or early adulthood and can cause vision impairment. In some affected infants, the pressure can become so great that the eyeballs appear enlarged and bulging., Treatment : Topical medication is considered first for late-onset glaucoma. The surgery is considered for patients with early-onset glaucoma and associated angle abnormalities and includes goniotomy or trabeculotomy, Pulsed-dye laser therapy often provides excellent clearing,of the PWB, particularly if it is located on the forehead., The surgical procedures for Sturge-Weber syndrome include hemispherectomy or focal resection of the seizure focus. Patients with bilateral involvement are typically not good candidates for surgery., Pathophysiology : Somatic Mutation : The exact cause of Sturge-Weber Syndrome is not fully understood, but it is believed to result from a somatic mutation that occurs sporadically during early embryonic development. This mutation affects the GNAQ gene, which plays a role in regulating cell signaling pathways.Vascular Abnormalities : Sturge-Weber Syndrome is characterized by the presence of vascular malformations, particularly in the brain and skin. The most common vascular abnormality is a capillary-venous malformation, also known as a port-wine stain. These malformations are caused by abnormal blood vessel development and can lead to issues with blood flow and drainage.Leptomeningeal Angiomatosis : One of the hallmarks of Sturge-Weber Syndrome is leptomeningeal angiomatosis, which involves the presence of abnormal blood vessels (angiomas) within the leptomeninges, the membranes covering the brain and spinal cord. These angiomas can disrupt the normal flow of cerebrospinal fluid and lead to increased intracranial pressure.Seizures and Neurological Symptoms : The leptomeningeal angiomatosis in the brain can cause a variety of neurological symptoms, including seizures, developmental delays, cognitive impairment, and neurological deficits. Seizures are a common and often early symptom of Sturge-Weber Syndrome, typically presenting in infancy.Ocular Involvement : Sturge-Weber Syndrome can also affect the eyes, leading to glaucoma, a condition characterized by increased pressure within the eye. Glaucoma can result from abnormal blood vessel development in the eye and can contribute to vision impairment or blindness.Hemiatrophy : Another characteristic feature of Sturge-Weber Syndrome is hemiatrophy, which involves the progressive shrinking and loss of brain tissue on one side of the brain. Hemiatrophy can lead to motor deficits, weakness, and other neurological problems.Potential Secondary Complications : The chronic vascular abnormalities in Sturge-Weber Syndrome can lead to secondary complications such as stroke, intellectual disabilities, and neurologic deterioration over time.Treatment for Sturge-Weber Syndrome is typically aimed at managing symptoms and preventing complications. This may involve anticonvulsant medications to control seizures, glaucoma management, rehabilitation therapies, and other supportive measures. Early intervention and a multidisciplinary approach involving neurologists, ophthalmologists, and other specialists are important for optimizing outcomes for individuals with Sturge-Weber Syndrome.Its important to note that Sturge-Weber Syndrome varies widely in its presentation and severity among individuals. If you suspect that you or someone you know may have Sturge-Weber Syndrome, its crucial to seek evaluation and guidance from a medical professional., Epidemiology : Approximately 1 in 20, 000 to 50, 000 live births ar, variable, SWS gene mutations occur sporadically (for no clear reason). There is no proven way to prevent Sturge-Weber syndrome., Complications : Glaucoma, Buphthalmos, Diagnostics : MRI Brain, PET SCAN, CT HEAD, CT SCAN, ophthalmoscopy, Differential diagnosis : arterial damage, HEMANGIOMA, Weber syndrome, disease description : Sturge-Weber syndrome (SWS) is a segmental vascular neurocutaneous disorder with a constellation of symptoms and signs characterized by capillary malformation in the face (port-wine birthmark) and brain (leptomeninges), as well as abnormal blood vessels of the eye leading to glaucoma. Patients present with seizures, hemiparesis, stroke-like episodes, headaches, and developmental delay. Approximately 1 in 20, 000 to 50, 000 live births are affected with SWS.

Styalgia

Disease Name : Styalgia, Symptoms : pain on swallowing, throat pain, Signs : dysphagia, PAINFUL JAW MOVEMENT, Treatment : Symptomatic styloid process can be excised by,transoral or cervical approach., Pathophysiology : It is due to elongated styloid process or calcification of stylohyoid ligament. A normal styloid process is 25 mm; if greater than 30 mm, it is considered to be elongated. Patient complains of pain in tonsillar fossa and upper neck which radiates to the ipsilateral ear. It gets aggravated on swallowing. Diagnosis can be made by transoral palpation of the styloid process in the tonsillar fossa, by a radiograph (such as anteroposterior view with open mouth or lateral view of skull) or by a CT scan with 3D reconstruction. Many persons may have elongated styloid process but remain asymptomatic and do not need treatment. Symptomatic styloid process can be excised by transoral or cervical approach., Epidemiology : GOOD, Complications : nan, Diagnostics : X Ray skull, X RAY, CT SCAN, PALPATION, Differential diagnosis : nan, disease description : It is due to elongated styloid process or calcification of stylohyoid ligament. A normal styloid process is 25 mm; if greater than 30 mm, it is considered to be elongated. Patient complains of pain in tonsillar fossa and upper neck which radiates to the ipsilateral ear. It gets aggravated on swallowing. Diagnosis can be made by transoral palpation of the styloid process in the tonsillar fossa, by a radiograph (such as anteroposterior view with open mouth or lateral view of skull) or by a CT scan with 3D reconstruction. Many persons may have elongated styloid process but remain asymptomatic and do not need treatment. Symptomatic styloid process can be excised by transoral or cervical approach.

Stye

Disease Name : Stye, Symptoms : pain in eyes, photophobia, Signs : swelling of eyelid, firm, red, tender swelling at the lid margin associated with marked oedema, Treatment : • Antibiotic eye drops (3–4 times a day) and eye,ointment (at bed time) should be applied to control,the infection.,• Systemic anti-inflammatory and analgesics relieve,pain and reduce oedema.,• Systemic antibiotics should be used for early,control of infection., • Evacuation of the pus should be done by epilating,the involved cilia, when the pus point is formed.,• Surgical incision is required rarely for a large,abscess., Pathophysiology : 1. Predisposing factors are as below : • Age. It is more common in children and young adults (though no age is bar) and in patients with eye strain due to muscle imbalance or refractive errors. • Habitual rubbing of the eyes or fingering of the lids and nose, chronic blepharitis and diabetes mellitus are usually associated with recurrent styes. • Metabolic factors, chronic debility, excessive intake of carbohydrates and alcohol also act as predisposing factors. 2. Causative organism commonly involved is staphylococcus aureus. Symptoms include acute pain associated with swelling of lid, mild watering and photophobia. Signs are as follows : • Stage of cellulitis is characterised by localised, firm, red, tender swelling at the lid margin associated with marked oedema . Usually, there is one stye, but occasionally, these may be multiple. • Stage of abscess formation is characterised by a visible pus point on the lid margin in relation to the affected cilia., Epidemiology : GOOD, Complications : abscess, stye, Diagnostics : nan, Differential diagnosis : nan, disease description : A stye, also known as a hordeolum, is a common problem involving the eye seen in both primary and urgent care setting. It is a painful, acute infectious process of the upper or lower eyelid. Classically a hordeolum appears as a small pustule along the margin of the eyelid and can be differentiated from a chalazion which tends to involve less of an inflammatory response and follows a more chronic courseIt is an acute suppurative inflammation of lash follicle and its associated glands of Zeis or Moll.

Sub Conjunctival Haemorrhage

Disease Name : Sub Conjunctival Haemorrhage, Symptoms : Redness, headache, red eyes, vomiting, COUGHING, Signs : HAEMORRHAGE IN CONJUNCTIVA, Treatment : medication : Vitamin C/Ascorbic Acid, Dilute brimonidine and oxymetazoline have been indicated to improve patient comfort and decrease the incidence of SCH after intravitreal injections, Pathophysiology : Subconjunctival hemorrhage results from bleeding of the conjunctival or episcleral blood vessels and subsequently leaks into the subconjunctival space. Blood vessels can wear and tear over time. The elastic and connective tissues become fragile with age and underlying comorbidities which can result in the ease of spread of the hemorrhage in the elderly. Traumatic SCH is more localized to the site of impact compared to spontaneous. There is a predilection for SCH to develop on the temporal aspect of the eye since the bulbar conjunctiva of the temporal aspect is larger than the nasal aspect. Other reasons include increased incidence of conjunctivochalasis, protection of the nose on the nasal aspect, and more difficulty detecting projectiles on the temporal aspect. The inferior aspect was noted to have an increased incidence of SCH compared to superior likely to blood gravitating downwards after insult, Epidemiology : SCH offers a good visual prognosis after resolutio, Complications : conjunctivitis, EPISCLERITIS, Diagnostics : HISTOPATHLOGY, Slit lamp examination, VISUAL ACUITY TEST, COAGULATION PROFILE, Differential diagnosis : nan, disease description : Subconjunctival Hemorrhage (SCH) is a disorder that can occur for the most part from benign situations. However, there are certain times when subconjunctival hemorrhages can occur as a manifestation of a more dangerous underlying diagnosis, especially if persistent or recurrent.  Subconjunctival Hemorrhage is generally painless but can appear as diffusely hyperemic.

Subacute Primary Angle-closure

Disease Name : Subacute Primary Angle-closure, Symptoms : Coloured halos, browache and eyeache on the affected side, headache, ocular pain, visual disturbances, Signs : unilateral transient blurring of vision, Treatment : Patients assessed to be at risk of angle closure (AC) warrant prophylactic laser peripheral iridotomy. Prior to laser therapy, a parasympathomimetic like pilocarpine is helpful to induce pupil miosis and iris stromal thinning so that laser may be more easily performed. The a2-agonists like brimonidine work quickly to lower IOP and may be used prior to and/or after laser peripheral iridotomy to prevent an IOP spike. Topical steroids instilled four times daily for a week after laser are beneficial in reducing post-laser intraocular inflammation., Treatment of choice is Peripheral laser iridotomy., Pathophysiology : Anatomy of the Eye : In a healthy eye, there is a clear fluid called aqueous humor that circulates within the eye to provide nourishment and maintain intraocular pressure. The fluid is produced by the ciliary body and flows through the pupil into the anterior chamber of the eye.Drainage Angle and Trabecular Meshwork : The drainage angle of the eye refers to the area where the cornea (clear front surface of the eye) meets the iris (colored part of the eye). The trabecular meshwork, a delicate tissue located at this angle, is responsible for draining the aqueous humor out of the eye. This drainage process helps regulate intraocular pressure.Closure of the Drainage Angle : In subacute primary angle-closure glaucoma, the drainage angle becomes progressively narrow due to anatomical changes in the eye. This can happen because the iris is pushed forward, blocking the trabecular meshwork and obstructing the outflow of aqueous humor. As a result, fluid accumulates in the eye, leading to an increase in intraocular pressure.Intraocular Pressure (IOP) Increase : The accumulation of aqueous humor leads to an elevation in intraocular pressure. Increased IOP can compress the blood vessels that nourish the optic nerve and can potentially cause damage to the optic nerve fibers, leading to glaucomatous optic neuropathy., Epidemiology : 0.6%, variable, Laser iridotomy is also used to treat persons suspected of having primary angle closure in order to prevent the development of glaucoma, a condition in which the eye’s optic nerve is damaged, Complications : blindness, Visual field loss, Diagnostics : FUNDOSCOPY, GONIOSCOPY, TONOMETRY TEST, slit-lamp biomicroscopic examination, Gonioscopic examination, Fincham’s test, Differential diagnosis : central retinal vein occlusion, EPISCLERITIS, malignant glaucoma, disease description : Glaucoma is a progressive optic neuropathy associated with elevated intraocular pressures. Glaucoma results in visual field loss, and in its end-stage, may lead to complete blindness. Anatomically, glaucoma is classified into open-angle glaucoma and closed-angle glaucoma. A closed-angle is an anatomical configuration in which there is a mechanical blockage of the trabecular meshwork by the peripheral iris. Etiologically, it can be classified as primary or secondary angle closure. Primary angle-closure is not associated with any other ocular condition, while secondary angle closure is associated with one or more other ocular conditions.

Subacute Sclerosing Panencephalitis

Disease Name : Subacute Sclerosing Panencephalitis, Symptoms : CNS depression : Jerking movemenAreas of the brain that control breathing, heart rate, and blood pressure are damaged. This leads to coma and then death.ts are replaced by writhing (twisting) movements and rigidity. Death may occur from complications., uncontrollable movements : There may be uncontrolled movement problems including jerking and muscle spasms. Other symptoms that may occur in this stage are loss of vision, dementia, and seizures., cognitive impairment : There may be personality changes, mood swings, or depression. Fever and headache may also be present. This stage may last up to 6 months., jerking movements of the arms and legs : Jerking movements are replaced by writhing (twisting) movements and rigidity. Death may occur from complications., Signs : nan, Treatment : medication : Vitamin A (Retinol), 1) ANTIVIRAL DRUGS.\,\,2) Maintenance of hydration, \,oxygenation, and comfort are goals of therapy. Antipyretics for comfort and\,fever control are useful. For patients with respiratory tract involvement, airway\,humidification and supplemental oxygen may be of benefit. Oral rehydration is\,effective in most cases, but severe dehydration may require intravenous therapy., Pathophysiology : A person must be directly infected with the measles virus to cause subacute sclerosing panencephalitis. It has been found that wild strains causing the measles have a tri-residue motif, which infers an increased ability to spread, which is not present in lab-adapted strains used for vaccines. Thus, SSPE remains solely a complication of the wild type measles infection. The latency period varies from 7-10 years with shorter latency periods observed with children infected with the measles virus under the age of 2 or intrafamilial measles cases.The measles virus has a tropism for lymphocytes in the lower respiratory tract and epithelial cells in the upper respiratory tract.Measles virus initially infects immune cells within the respiratory tract, which carry the infection to local lymph nodes. From the lymphatic system, various organs and tissues are infected through cellular fusion, causing syncytium formation, also known as Warthin-Finkeldey cells. As epithelial cells are destroyed secondary to the infection, the cells slough off and are expelled via coughing and sneezing. This allows for the airborne transmission of the measles virus to another host., Epidemiology : SSPE is a rare disease and generally follows the prevalence of measles in a population., The incidence in the United States in 1960 was 0.61 cases per\,million persons younger than age 20 yr., FATAL, Immunization against measles is the only known prevention for SSPE. The measles vaccine has been highly effective in reducing the numbers of affected children.,,Measles immunization should be done according to the recommended American Academy of Pediatrics and Centers for Disease Control schedule., Complications : infection, Diagnostics : CSF EXAMINATION, MRI Head, EEG, biopsy, CT SCAN, Differential diagnosis : LEUKODYSTROPHY, neoplasms, VIRAL ENCEPHALITIS, disease description : Subacute Sclerosing Panencephalitis (SSPE) is a rare complication due to persistent measles infection. This neurological sequela typically presents in early adolescence and has a progressive course with a high mortality rate , Vaccination implementation has been effective in reducing the number of Measles cases, thereby reducing cases of SSPE. However, measles remains endemic in many countries with poor access to vaccinations. Also, there has been a re-emergence of measles in industrialized countries due to vaccination refusal.

Subacute Thyroiditis

Disease Name : Subacute Thyroiditis, Symptoms : arthralgia, diarrhea, fatigue, painful swelling, Restlessness, sore throat, throat pain, fever, Irritability, Malaise, Signs : enlarged and tender goitre, Treatment : medication : Prednisolone, Aspirin/Acetylsalicylic acid, In some patients, no treatment is required. For many, analgesic therapy for relief of pain can be achieved with non-steroidal anti-inflammatory agents. If this fails, prednisone administration should be employed with daily doses of 20-40 mg prednisone. After one to 2 weeks of this treatment, the osage is tapered over a period of 6 weeks. Most patients have no recrudescence of symptoms, but occasionally this does occur and the dose must be increased again. The recurrence rate of painful subacute thyroiditis after cessation of prednisolone therapy is about 20%. Beta blocking agents are usually administered for relief of thyrotoxic symptoms in the initial stage of SAT., Pathophysiology : The thyroid shows a characteristic patchy inflammatory infiltrate with disruption of the thyroid follicles and multinucleated giant cells within some follicles. The follicular changes progress to granulomas accompanied by fibrosis. Finally, the thyroid returns to normal, usually several months after onset. During the initial phase of follicular destruction, there is release of Tg and thyroid hormones, leading to increased circulating T4 and T3 and suppression of TSH. During this destructive phase, radioactive iodine uptake is low or undetectable. After several weeks, the thyroid is depleted of stored thyroid hormone and a phase of hypothyroidism typically occurs, with low unbound T4 (and sometimes T3 ) and moderately increased TSH levels. Radioactive iodine uptake returns to normal or is even increased as a result of the rise in TSH. Finally, thyroid hormone and TSH levels return to normal as the disease subsides., Epidemiology : nan, Complications : nan, Diagnostics : Erythrocyte Sedimentation Rate (ESR), Free T3, Free T4, Thyroid Stimulating Hormone TSH, Radionuclide Imaging technique, THYROID SCAN, Differential diagnosis : Pharyngitis, disease description : This is also termed de Quervain’s thyroiditis, granulomatous thyroiditis, or viral thyroiditis. The diagnosis of subacute thyroiditis is often overlooked because the symptoms can mimic pharyngitis. The peak incidence occurs at 30–50 years, and women are affected three times more frequently than men

Subarachnoid Hemorrhage

Disease Name : Subarachnoid Hemorrhage, Symptoms : fatigue : SAH can lead to physical difficulties, such as fatigue., neck pain : This is often accompanied by stiffness or tenderness in the neck., vertigo : Benign paroxysmal positional vertigo (BPPV) is the most prevalent form of peripheral vertigo and is common in posttraumatic patients., vomiting : This may be present in the early stages of the condition., Muscle ache : Subarachnoid Hemorrhage causes muscle aches, especially in your neck and shoulders., photophobia : Subarachnoid Hemorrhage causes patients to become sensitive to light., LOSS OF CONSIOUSNESS : Loss of consciousness has been shown to be present in around 40% of those with spontaneous SAH., VISION DEFICITS : Vision changes, including double vision, blind spots or temporary vision loss in one eye., MOOD CHANGES : Personality changes (PC) comprise a common and debilitating illness that accompanies many neurological disorders, including non-traumatic subarachnoid hemorrhage (SAH)., Signs : amnesia : One of the major neurologic functions that can be affected by a SAH is memory., Treatment : endovascular coiling or direct surgical clipping of the IA. Patients are typically treated with both medical and interventional options., Pathophysiology : Hemodynamic stress is the initiating factor for intracranial aneurysm (IA) formation. The observation best illustrates that IAs occur at arterial junctions, bifurcations, or abrupt vascular angles where excessive hemodynamic stresses are exerted on arterial walls. The typical locations include the bifurcation of the basilar artery at the junction of the ipsilateral posterior inferior cerebellar artery (PICA), vertebral artery, and the anterior communicating artery. Large unruptured aneurysms compress the adjacent cerebral tissue causing neurological signs. However, the rupture of these lesions creates a state of reduced blood flow and vasospasm leading to cerebral ischemia. The pathophysiological mechanisms by which these lesions are formed and eventually rupture are not fully understood. The hemodynamic stress to the vessel wall caused by increased blood pressure and other risk factors promotes the formation and rupture of IA., Epidemiology : 7.9 (95% CI, -9.0) per 100 000 person-years, 9 per 100 000 person-years., variable, The majority of subarachnoid hemorrhage cases are due to head trauma and/or a ruptured brain aneurysm. Because of this, the best way you can try to avoid experiencing SAH is to manage your risk factors for these two situations.,,To try to prevent head trauma, always wear a helmet when riding a bike or motorcycle or when playing high-risk sports. Always drive safely and follow traffic laws. If you’re prone to falls, work with a physical or occupational therapist to learn how to try to prevent them and make your home safer.,,To lower your risk of developing a brain aneurysm and/or to prevent an existing aneurysm from rupturing, talk to your healthcare provider about steps you can take to stay healthy. They’ll likely recommend the following : ,,Manage high blood pressure with medications and lifestyle changes.,Quit smoking.,Exercise regularly (and moderately) without excessive heavy lifting. (Heavy exertion or straining can cause an aneurysm to burst.),Eat a balanced diet.,Get help for alcohol or substance use disorders and don’t use cocaine or other stimulant drugs., Complications : Hydrocephalus, seizures, cerebral infraction, Diagnostics : lumbar puncture, CT ANGIOGRAPHY, CT SCAN, Differential diagnosis : hemorrhage, Meningitis, Meningitis, NEUROSARCOIDOSIS, disease description : Overall, about 20% of strokes are hemorrhagic, with SAH and Intracerebral hemorrhage (ICH) each accounting for 10% .Subarachnoid space is described as a space between the arachnoid membrane and the pia mater. It consists of the cerebrospinal fluid and the blood vessels that supply different areas of the brain. A subarachnoid hemorrhage (SAH) is defined as the accumulation of blood in the space between the arachnoid membrane and the pia mater around the brain referred to as the subarachnoid space.  The etiology of SAH can be either nontraumatic (about 85% are secondary to aneurysm rupture) or traumatic in nature. In this review, we shall discuss the various aspects of nontraumatic SAH. Most nontraumatic causes of SAH (~ 85%) are caused by the rupture of an intracranial aneurysm. The remaining 15-20% of patients presenting with SAH do not have a vascular lesion on the initial digital subtraction angiography.

Subcorneal Pustular Dermatosis

Disease Name : Subcorneal Pustular Dermatosis, Symptoms : Pustules, erythema, pruritus., Signs : PUSTULE, distribution is mainly in the flexures of the trunk and proximal limbs, including axillae, groins, submammary area, neck and inframammary and apron area, Lesions are oval, pea-sized flaccid pustules on a normal or erythematous base, Treatment : medication : Dapsone , Etanercept , Ketoconazole , Acitretin, First line : , Dapsone 50–150 mg daily is the treatment of choice leading to,either a partial or a complete response.,,Second line : , Some cases respond to potent topical or oral corticosteroids but,overall these are not particularly effective. Acitretin and tacalcitol have been used effectively.,,Third line : , Ketoconazole has been reported to be of benefit. There are,also reports of effective use of anti-TNF therapy alone or,in combination, including etanercept. Adalimumab was,combined with mycophenolate mofetil in a case of IgA pemphigus and response to infliximab was dramatic but short-lived,in one intractable case and highly effective in another two,reports, one associated with lupus where infliximab was combined with prednisolone and azathioprine and another ,where it was used in combination with acitretin and intermittent,systemic corticosteroids., Pathophysiology : The pathogenesis is obscure. The condition is characterized by subcorneal accumulation of neutrophils. It has also occurred at injection sites of GM-CSF in a patient with IgA myeloma. Excessive production of TNF-a has also been linked with the lesions as has neutrophil activation. Thus, subcorneal pustular dermatosis has much in common with other neutrophilic dermatoses. However, it has also been considered to overlap with pemphigus although in most cases immunofluorescence is negative. In a subgroup, IgA is deposited in the upper dermis and is directed against the extracellular domains of desmocollin 1. The relationship between intercellular IgA pemphigus and classical subcorneal pustular dermatosis is unclear. Pathology Biopsies from early lesions show a perivascular inflammatory infiltrate with occasional eosinophils. The pustules sit on the surface of the epidermis rather than within it, spongiosis and spongiotic pustules are absent and acantholysis is only seen in old lesions., Epidemiology : although serious associated disease may have a wor, Complications : nan, Diagnostics : Skin Biopsy With Immunofluorescence, Differential diagnosis : Dermatitis herpetiformis, Impetigo, Pustular psoriasis, disease description : Subcorneal pustular dermatosis is a rare neutrophilic dermatosis, with sterile subcorneal pustules typically affecting the flexural areas of the trunk and proximal extremities.

Subcutaneous Fat Necrosis Of The Newborn

Disease Name : Subcutaneous Fat Necrosis Of The Newborn, Symptoms : ulceration, DISCHARGE, painful lesions, Scarring, failure to thrive, seizures, Irritability, Signs : plaques, Nodular thickening of the subcutaneous tissues, nodules are present at buttocks, thighs, shoulders, back, cheeks and arms., subcutaneous nodules, poor feeding, Treatment : medication : Furosemide , Prednisolone, Risedronate/Risedronic Acid, No treatment is generally required as the condition spontaneously ,resolves over several weeks., dietary ,restriction of calcium and vitamin D, In resistant cases bisphosphonates can be ,used, Pathophysiology : The pathogenesis of subcutaneous fat necrosis of the newborn is not entirely known. The organization of neonatal fat with high saturated fatty acids and its higher melting point in comparison with adult fat leads to a tendency for solidification and crystallization. In regards to the extracutaneous abnormalities observed in SCFN, hypercalcemia is considered to be secondary to the granulomatous essence of SCFN, with increased macrophage activity, with subsequent expression of 1-alpha-hydroxylase, improving the intestinal absorption of calcium and its mobilization from bones after converting 25-hydroxyvitamin D3 to the active 1, 25-dihydroxyvitamin D3. Thrombocytopenia appears concurrently with the development of subcutaneous nodules. It is deemed to be caused by peripheral platelet sequestration, and dyslipidemias are caused by the mobilization of fatty acids from adipose tissue, Epidemiology : The majority of patients (90%) were born at more than 37 weeks gestational age, with an average birth weight of 3455 g, good, Subcutaneous fat necrosis of the newborn is , Complications : Transient thrombocytopenia, hypercalcaemia, Diagnostics : HISTOPATHLOGY, serum calcium Ca++, DOPPLER FLOW VELOCITY WAVEFORM ANALYSIS, skin lesion biopsy, Differential diagnosis : Sclerema neonatorum, disease description : Subcutaneous fat necrosis of the newborn is an uncommon and transient disorder of neonates in which focal areas of fat necrosis cause nodular skin lesions.

Subcutaneous Mycosis

Disease Name : Subcutaneous Mycosis, Symptoms : DISCHARGE, warty plaque, Signs : disc-shaped masses have a uniform hard consistency, overlying skin may be tense, oedematous, desquamating, hyperpigmented or normal, granulomas, ulceration, pustules, patches, Treatment : medication : Sulfamethoxazole and Trimethoprim (Co-trimoxazole), Itraconazole , Itraconazole is useful in this condition. Lesions also usually respond to oral treatment with potassium iodide given ,in similar doses to those used in sporotrichosis. There is ,some evidence that co-trimoxazole can be used in addition in ,conidiobolomycosis., Pathophysiology : In their natural environment, both causative fungi B. ranarum and C. coronatus are associated with decaying vegetation and the gastro-intestinal tracts of frogs., Epidemiology : nan, Complications : nan, Diagnostics : HISTOPATHLOGY, Differential diagnosis : nan, disease description : This is a localized, subcutaneous and predominantly tropical mycosis characterized by chronic, woody swelling of subcutaneous tissue.There are three general types of subcutaneous mycoses : chromoblastomycosis, mycetoma, and sporotrichosis. All appear to be caused by traumatic inoculation of the etiological fungi into the subcutaneous tissue. Chromoblastomycosis is a subcutaneous mycosis characterized by verrucoid lesions of the skin (usually of the lower extremities); histological examination reveals muriform cells (with perpendicular septations) or so-called “copper pennies” that are characteristic of this infection. Chromoblastomycosis is generally limited to the subcutaneous tissue with no involvement of bone, tendon, or muscle. 

Subdural Abscess

Disease Name : Subdural Abscess, Symptoms : "amblyopia : Amblyopia is a type of poor vision that usually happens in just 1 eye but less commonly in both eyes. It develops when theres a breakdown in how the brain and the eye work together, and the brain cant recognize the sight from 1 eye.", headache : Initially focal and later generalized is caused by subdural empyema., seizures : Subdural empyema causes seizures., fever : Temperature above 38°C (100.5°F) is experienced in this condition., mental changes : Includes confusion, drowsiness, stupor, or coma., mental changes : Subdural empyema causes hemiplegia which is paralysis of the muscles of the lower face, arm, and leg on one side of the body. In addition to motor problems other losses may occur eg. sensation, memory, cognition. The most common cause of hemiplegia is stroke, which damages the corticospinal tracts in one hemisphere of the brain., Signs : nan, Treatment : series of burr holes or a craniotomy is done to,drain subdural empyema, Intravenous antibiotics are administered,to control infection. Once infection is under,control, attention is paid to causative ear disease which,may require mastoidectomy., Pathophysiology : Subdural empyema most often occurs due to the direct extension of local infection. The infection can spread to the intracranial compartment due to the valveless diploic veins of Breschet. As a result, blood may flow in either direction, causing the spread of bacterial infection intracranially. They can also occur after cranial surgical procedures secondary to the inoculation of microorganisms into the subdural space, further developing into a subdural empyema., Epidemiology : Intracranial subdural empyema usually affects children and young adults. Males are more commonly affected, with a male to female ratio of 3 : 1,Intracranial subdural empyemas are much less common than brain abscesses., GOOD, Complications : CAVERNOUS SINUS THROMBOSIS, Cerebral oedema, Hydrocephalus, seizures, sepsis, Diagnostics : Complete Blood Count CBC, MRI Head, CT HEAD, MRI, ophthalmoscopy, Differential diagnosis : Brain Abscess, Brain tumors, Meningitis, disease description : Intracranial subdural empyema is a loculated collection of pus in the subdural space between the dura mater and the arachnoid. Due to the skull being a confined cavity, intracranial subdural empyema can lead to severe symptoms or even death by direct compression and injury of the brain. Prompt diagnosis and adequate treatment can, in most cases, prevent these types of complications resulting in better outcomes.Subdural empyema is usually a complication of purulent meningitis in infants, whereas, in older children, it is commonly secondary to direct extension from contiguous foci. The mechanism of the development in infants is through infection of sterile, reactive subdural effusions secondary to meningitis. In adults, subdural empyema secondary to bacterial meningitis is rare.

Subependymoma (who Grade 1)

Disease Name : Subependymoma (who Grade 1), Symptoms : seizures : Subependymoma (who grade 1) an lead to seizures., TUMOURS : Subependymomas are indolent, benign tumors of the central nervous system typically arising in the ventricular spaces. Subependymomas most often arise in the fourth and the lateral ventricles., FOCAL NEUROLOGICAL DEFICITS : A focal neurologic deficit is a problem with nerve, spinal cord, or brain function. It affects a specific location, such as the left side of the face, right arm, or even a small area such as the tongue. Speech, vision, and hearing problems are also considered focal neurological deficits., csf malformation : Patients with symptomatic masses have been reported to present with cerebrospinal fluid (CSF) obstruction., Signs : nan, Treatment : Excision is usually curative, occasionally radiation therapy., Pathophysiology : Ependymal Cell Abnormalities : Ependymal cells are specialized glial cells that line the ventricles of the brain and the central canal of the spinal cord. They play a role in producing cerebrospinal fluid (CSF) and maintaining the fluid balance within the central nervous system. Mutations or genetic alterations in ependymal cells may lead to abnormal cellular growth and division, contributing to the formation of a subependymoma.Cellular Proliferation : Subependymomas are characterized by slow cellular proliferation. Abnormal ependymal cells may undergo uncontrolled division and form a mass or tumor. However, unlike higher-grade tumors, subependymomas tend to have a lower rate of cell division and less aggressive growth.Cellular Differentiation : Subependymomas are thought to originate from differentiated ependymal cells that have undergone changes in their genetic or molecular makeup. These changes can lead to altered cellular behavior and the formation of a distinct tumor mass within the ventricles or central canal.Genetic Mutations : The specific genetic mutations or alterations that drive the development of subependymomas are not yet fully understood. Genetic studies are ongoing to identify potential molecular markers associated with these tumors., Epidemiology : 2%, variable, Complications : nan, Diagnostics : MRI Head, NEUROIMAGING, Immunostaining, Differential diagnosis : central neurocytoma (who grade 2), choroid plexus papilloma (who grade 1), ependymoma, Metastasis, subependymal giant cell astrocytoma (who grade 1), disease description : Subependymomas are benign slow-growing tumors of ependymal origin that account for less than 10% of ependymal neoplasms. Subependymomas most commonly occur in the fourth and fifth decades of life where they appear in the fourth and lateral ventricles. Because of their intimacy with the ventricular system, subependymomas cause ventricular obstruction, resulting in symptoms associated with increased intracranial pressure. On MRI studies, subependymomas are circumscribed, nodular nonenhancing mass lesions attached to the ventricular wall.

Subglottic Haemangioma

Disease Name : Subglottic Haemangioma, Symptoms : difficulty in breathing : Subglottic hemangiomas may form a large mass in the airway below the vocal cords, causing varying degrees of airway obstruction. They grow rapidly for at least 12 to 18 months followed by slow shrinking., chronic cough : Persistent cough that may sound like croup., stridor : Subglottic hemangiomas should be considered in any child with recurrent, persistent and/or progressive, inspiratory or biphasic stridor., Signs : nan, Treatment : medication : Dexamethasone , Prednisolone, Lasers and microdebridement of the subglottic hemangioma carries the risk of scarring which may lead to subglottic stenosis.,Steroids may improve symptoms but put the child at risk of many side effects. Steroid use is only advised for short periods of time., Tracheostomy and observation, as many haemangiomas involute spontaneously.CO2 laser excision, if lesion is small, Pathophysiology : Vascular Malformation : Subglottic hemangioma is considered a vascular malformation, specifically a type of infantile hemangioma. Infantile hemangiomas are the most common benign tumors of infancy and childhood. These tumors are characterized by an abnormal proliferation of blood vessels.Developmental Origins : The exact cause of subglottic hemangioma is not fully understood, but it is believed to arise during fetal development or shortly after birth. Genetic factors and disturbances in the normal processes of blood vessel development are thought to play a role in the formation of subglottic hemangioma.Proliferation of Blood Vessels : In subglottic hemangioma, there is an overgrowth of blood vessels within the subglottic region. The blood vessels can become enlarged and disorganized, leading to the formation of a mass or tumor.Clinical Presentation : Subglottic hemangioma often becomes symptomatic during the first few months of life. As the tumor grows, it can lead to narrowing of the airway, causing respiratory symptoms such as stridor (high-pitched breathing sound), hoarseness, coughing, and difficulty breathing. Severe cases of airway obstruction can lead to respiratory distress, especially during periods of increased activity or illness.Natural Course : Infantile hemangiomas, including subglottic hemangiomas, have a characteristic natural course of growth and regression. They typically undergo a period of rapid growth during the first several months of life, followed by a slower phase of regression. Many subglottic hemangiomas start to shrink and involute on their own as the child grows older, leading to a gradual improvement in symptoms., Epidemiology : approximately 10, 000 out of 100, 000 infants., 4% to 5% of the pediatric population, , variable, AVOID SMOKING, Complications : dysphagia, Diagnostics : biopsy, CT SCAN, USG, Direct Laryngoscopy, Differential diagnosis : laryngo-tracheo-bronchitis, subglottic stenosis, tracheal papillomatosis, disease description : Subglottic hemangioma is a rare condition that can be potentially life threatening because of airway obstruction. It is common for subglottic hemangioma to be misdiagnosed as croup initially.  Infants with a subglottic hemangioma and cutaneous facial hemangiomas in a "beard" distribution should be evaluated for PHACE syndrome. Endoscopic laser resection is effective for subglottic hemangioma but carries a chance of subglottic stenosis, up to 25% .  a benign tumor of infancy that can cause severe obstruction of the airway. Overall, infantile hemangiomas affect 4% to 5% of the pediatric population, making them the most common type of head and neck tumor in children

Subinvolution

Disease Name : Subinvolution, Symptoms : abdominal cramp : Subinvolution causes irregular cramps in the affected individuals., abdominal discharge : Abnormal lochial discharge is caused by subinvolution. Lochia is the vaginal discharge you have after giving birth. It contains a mix of blood, mucus and uterine tissue. It has a stale, musty odor like menstrual period discharge and can last several weeks., uterine bleeding : During the process of physiological subinvolution, bleeding from the uterus is regulated by several factors and mechanisms, for example, myometrial contraction and local decidual and systemic coagulation factors leading to the minimalization of blood loss after delivery., Signs : nan, Treatment : medication : Ampicillin , Methergine, 1) Antibiotics in endometritis, (2) Exploration of the uterus in retained products, ,(3) Pessary in prolapse or retroversion. Methergine, so often prescribed to enhance the involution process, ,is of little value in prophylaxis., Pathophysiology : The uterus is the most common organ affected in subinvolution. As it is the most accessible organ to be measured per abdomen, the uterine involution is considered clinically as an index to assess subinvolution., Epidemiology : 13.3% of 26.023 patients, GOOD, Complications : abdominal distension, Diagnostics : Complete Blood Count CBC, PT/PC/INR, USG ABDOMEN(W/A), MRI PELVIS, Differential diagnosis : ENDOMETRITIS, GESTATIONAL TROPHOBLASTIC DISEASES (GTD), disease description : Subinvolution of placental sites (SPSs) is a rare but severe cause of secondary postpartum haemorrhage (PPH). SPS is characterised by the abnormal persistence of large, dilated, superficially modified spiral arteries in the absence of retained products of conception.

Subluxated Lens

Disease Name : Subluxated Lens, Symptoms : VISION DEFICITS, Asymptomatic, Signs : Iridodonesis i.e., tremulousness of iris can be demonstrated., Treatment : The practical options to manage subluxated lenses include (1) removal of the entire crystalline lens, including its capsule, and implantation of either an anterior chamber IOL or fixation of a posterior chamber IOL to the iris or the sclera using sutures or biologic glue and (2) preservation and suture fixation of the lens capsule to the scleral wall using a capsule-stabilizing device. There are two kinds of stabilizing devices : equator- and capsule-supporting devices., Pathophysiology : Blunt trauma can lead to either subluxation or dislocation of the crystalline lens. In lens subluxation, zonular filaments are broken, and the lens is no longer held securely in place but remains in the pupillary aperture. Lens dislocation occurs following complete disruption of the zonular filaments and displacement of the lens from the pupil. Trauma is the leading cause of lens dislocation., Epidemiology : nan, Complications : nan, Diagnostics : VISUAL ACUITY TEST, Differential diagnosis : HOMOCYSTINURIA, Marfan syndrome, disease description : Partial displacement of lens from its normal position.

Subluxation Or Dislocation Of The Acromioclavicula

Disease Name : Subluxation Or Dislocation Of The Acromioclavicula, Symptoms : Pain, Joint swelling, Signs : nan, Treatment : 1- Grades I&II injuries are treated by rest in a,triangular sling and analgesics.,2- Grade III - surgical,repair, Pathophysiology : There are two main mechanisms of acromioclavicular joint injury direct : direct blow or fall onto the shoulder with an adducted arm results in a superior force onto the acromion with clavicular movement restricted at the sternoclavicular joint results in the acromion pushed forcibly inferiorly and medially with respect to the clavicleindirect : can occur from a fall onto an outstretched hand or elbow resulting in the humerus being pushed into the acromion, which in turn results in lower-grade injuries typically involving the AC ligaments but sparing the coracoclavicular ligament, Epidemiology : GOOD, Complications : Osteoarthritis, Diagnostics : X RAY, X RAY, Differential diagnosis : DISLOCATION OF THE SHOULDER, shoulder pain, disease description : This is an uncommon injury, caused by a fall on the outer prominence of the shoulder.The injury may result in a partial or complete rupture of the acromio-clavicular or coracoclavicular ligaments. Acromio-clavicular joint injuries are divided into three grades depending upon their severity Grade I : Minimal strain to acromio-clavicular ligament and joint capsule Grade II : Rupture of acromio-clavicular ligament and joint capsule Grade III : Rupture of acromio-clavicular ligament, joint capsule and coraco-clavicular ligaments

Submandibular Gland Tumour

Disease Name : Submandibular Gland Tumour, Symptoms : Numbness : Weakness or numbness in your face, neck, jaw or mouth., trismus : Difficulty opening your mouth fully or moving your facial muscles., Pain : Persistent pain in your face, neck, jaw or mouth., difficulty in swallowing : Submandibular gland tumous causes dysphagia., lump : A lump or swelling on or near your jaw or in your neck or mouth., Signs : nan, Treatment : "Chemotherapy is a drug treatment that uses medications to kill cancer cells. Chemotherapy isnt currently used as a standard treatment for salivary gland cancer, but researchers are studying its use.", "If youre diagnosed with salivary gland cancer, your doctor may recommend radiation therapy. Radiation therapy uses high-powered energy beams, such as X-rays and protons, to kill cancer cells. During radiation therapy, you lie on a table while a machine moves around you, directing high-powered beams at specific points on your body.", "Removing a portion of the affected salivary gland, if your tumor is small.,Removing the entire salivary gland, if you have a larger tumor.,Removing lymph nodes in your neck. Your surgeon may recommend removing some lymph nodes from your neck if your salivary gland tumor is cancerous and theres a risk that the cancer has spread to the lymph nodes. ,Reconstructive surgery. After surgery to remove the tumor, your doctor may recommend reconstructive surgery to repair the area.", Pathophysiology : Mucoepidermoid carcinoma arises from the epithelium of the interlobular and intralobular salivary ducts. The most common genetic finding is the chromosomal translocation t(11;19)(q21 : p13), leading to the fusion of MECT1 and MAML2 genes, which is responsible for disrupting the NOTCH signaling pathway. This translocation is found in 50% to70% of patients with MEC and is more often seen in low-grade tumors associated with a better prognosis. Over 50% of Adenoid Cystic Carcinoma (AdCC) tumors contain the t(6;9)(q22-23;p23-24) translocation, which fuses the MYB protooncogene on chromosome 6q to the NFIB gene on chromosome 9p, resulting in an overexpression of MYB-NFIB fusion oncogene and worse prognosis., Epidemiology : Salivary gland malignancies make up 0.5 to 1.2% of all cancers and 5% of head and neck cancers, variable, Certain viral infections, such as Epstein-Barr virus (EBV), human immunodeficiency virus (HIV), and human papillomavirus (HPV), might be linked to an increased risk of salivary gland cancers. Avoiding exposure to these viruses might help lower your risk., Complications : facial nerve palsy, Diagnostics : PET SCAN, MRI, MRI, CT, TRUCUT BIOPSY, USG GUIDED FNAC, Differential diagnosis : BACTERIAL SIALADENITIS, NEOPLASMS, Sialadenitis, Soft tissue disorder, VASCULAR DISORDER, disease description : Salivary gland tumors are growths of abnormal cells (tumors) that begin in the salivary glands .Salivary gland tumors are a rare group of complex, heterogenous histologies that are located in the parotid gland, submandibular gland, sublingual gland, and minor salivary glands of the upper aerodigestive tract.

Submucous Fibrosis

Disease Name : Submucous Fibrosis, Symptoms : decrease mouth opening, INTOLERANCE TO SPICY FOOD, vesicle formation, soreness of mouth, Signs : erythema, trismus, Fibrosis, Scarring, superficial ulcers, Fibrotic bands, Treatment : medication : Dexamethasone , Avoid irritant factors, e.g. areca nuts, pan, tobacco, ,pungent foods, etc., PHYSIOTHERAPY & EXERCISES-Encourage jaw opening exercises, Treat existent anaemia or vitamin deficiencies, Simple release of fibrosis and skin grafting, Bilateral tongue flaps, Nasolabial flaps, Island palatal mucoperiosteal flap, Bilateral radial forearm free flap., Surgical excision and buccal fat pad graft.,7. Superficial temporal fascia flap and split-skin graft.,8. Coronoidectomy and temporal muscle myotomy., Pathophysiology : PATHOGENESIS Histopathology in early cases of OSF shows presence of polymorphonuclear leukocytes, eosinophils and a few lymphocytes while advanced cases show lymphocytes and plasma cells. Immunochemistry of inflammatory cells showed higher population of activated T-lymphocytes especially the T-helper/inducer lymphocytes but minor population of B-cells and macrophages. Later studies also showed significant increase in number of T-lymphocytes, macrophages and high CD4+ to CD8+ lymphocyte ratio in the subepithelial connective tissue suggesting that OSF is a cellular immune response. Small number of B-lymphocytes suggests minor role of humoral immunity in OSF. In advanced stages, there was severe fibrosis and loss of vascularity in the lamina propria and submucosa. The process may extend deeper into muscle layers also. Activated macrophages and T-lymphocytes produce fibrogenic cytokines which act on mesenchymal cells to produce fibrosis. Also certain cytokines liberated by T-lymphocytes upregulate synthesis of collagen but downregulate collagenase production further promoting fibrosis. It is thus believed that OSF is due to increased production of collagen and its decreased degradation in subepithelial layers of the oral mucosa. PATHOLOGY The basic change is fibroelastotic transformation of connective tissues in lamina propria associated with epithelial atrophy, sometimes preceded by vesicle formation. In later stages, when fibrosis is marked, there is progressive trismus and difficulty to protrude the tongue. Leukoplakia and squamous cell carcinoma may be associated with submucous fibrosis possibly because of common aetiological factors involved. It is a premalignant condition and malignant transformation has been seen in 3-7.6% of cases., Epidemiology : POOR, To Do : INCLUDE VIT C IN DIET,Avoid irritant factors, e.g. areca nuts, pan, tobacco, ,pungent foods, etc.,3. Treat existent anaemia or vitamin deficiencies.,4. Encourage jaw opening exercises. Not To Do : AVOID ARECA NUTS,TOBACCO CONSUMPTION, Complications : MALIGNANCY, Diagnostics : HISTOPATHLOGY, biopsy, USG, Immunochemistry test, Oral cavity examination, Differential diagnosis : leukoplakia, plummer vinson syndrome, Scleroderma crisis, submucous fibrosis, disease description : Oral submucous fibrosis (OSF) is a chronic insidious process characterized by juxtaepithelial deposition of fibrous tissue in the oral cavity and pharynx. The condition was first described in India by Joshi in 1953. The disease is widely seen in India, Pakistan, Taiwan, Sri Lanka, Nepal and Thailand due to habit of betel-nut chewing..

Subphrenic Abscess

Disease Name : Subphrenic Abscess, Symptoms : respiratory symptoms : Subphrenic abscess presents with cough, increased respiratory rate with shallow respiration, diminished or absent breath sounds, hiccups, dullness in percussion, tenderness over the 8th–11th ribs, fever, chills., shoulder pain : Shoulder pain is experienced by the affected individuals., dyspnea : Due to the presence fluid between the diaphragm, subphrenic abscess causes dyspnea., Abdominal Pain : Subphrenic abscess causes upper quadrant pain., Signs : Tenderness : Costal margin tenderness is seen in subphrenic abscess., Treatment : medication : Ceftriaxone , Fluconazole , Metronidazole , "Management of subphrenic abscess includes antibiotics, drainage of the abscess, and general care of the patient.,,Broad-spectrum parenteral antibiotics should be initiated empirically at the time of diagnosis, which should cover both aerobes and anaerobes. Later, the antibiotics can be modified as per culture and sensitivity. Early initiation of antibiotics improves outcomes. Combination therapy or a single broad-spectrum antibiotic can be initiated. Cephalosporins with metronidazole can be considered as the initial choice. In immunosuppressed patients, antifungals covering candida may be indicated. The antifungal of choice depends on the patients general condition. Azoles are preferred if the patient is stable and if cultures show sensitivity to azoles. In critically ill patients and non-albicans candida, echinocandins like anidulafungin are the drug of choice", Pathophysiology : The diaphragm, an intrathoracic organ, separates the thoracic and abdominal cavities and is covered by pleura and peritoneum, as it is both extrapleural and extraperitoneal. The subphrenic space is divided by the falciform ligament.The subphrenic space is divided into five regions : The intraperitoneal space above the liver, limited medially by the falciform ligament, is a common location for pyogenic and amebic abscess; appendicitis or pelvic infections can localize here, ascending through the paracolic gutter.The intraperitoneal space below the liver (Rutherford Morison’s kidney pouch) communicates with the right gutter and is home to infections from the stomach and duodenal perforations and empyema of the gallbladder.Above the liver, the intraperitoneal perisplenic space may become infected from stomach perforation, cancer, splenectomy, or colon resection.The lesser peritoneal sac behind the pancreas and the left kidney is limited below by the transverse colon. Infection in this area is usually caused by perforation on the posterior wall of the stomach.Above the liver space, the “bare area” is bounded above and behind by the diaphragm. It is affected by extraperitoneal infections like retrocecal or retroperitoneal appendicitis, kidney abscesses, or from the retroperitoneal portion of the duodenum., Epidemiology : The actual frequency of primary subphrenic abscess is not known and is thought to be very rare. It constituted 13% in one case series, good, CT guided drainage with interventional radiology is highly effective and can prevent the morbidity and mortality associated with surgical drainage., Complications : Pleurisy, PLEURAL EFFUSION, LUNG ABSCESS, Fistula, Diagnostics : ABG, Hb, CT Abdomen, USG ABDOMEN(W/A), CT SCAN, CT SCAN, Differential diagnosis : fever, Ileus, INFLAMMATORY BOWEL DISEASES, unexplained fever, disease description : Subphrenic abscesses represent infected collections bounded above by the diaphragm, and below by the transverse colon and mesocolon, and the omentum. They typically arise from abdominal surgery, trauma, or local inflammation in the space between the liver, intestines, and lungs, making drainage a challenge.

Sucla2-& Suclg1-related Mitochondrial Dna Depletion Syndrome (mds)

Disease Name : Sucla2-& Suclg1-related Mitochondrial Dna Depletion Syndrome (mds), Symptoms : Dystonia : Dystonia is a movement disorder that causes the muscles to contract involuntarily. This can cause repetitive or twisting movements. The condition can affect one part of your body (focal dystonia), two or more adjacent parts (segmental dystonia), or all parts of your body (general dystonia), MUSCLE ATROPHY : Muscular atrophy caused by SUCLA2-& SUCLG1-related Mitochondrial DNA depletion syndrome (MDS) is the decrease in size and wasting of muscle tissue. Muscles that lose their nerve supply can atrophy and simply waste away., psychomotor retardation : Psychomotor retardation involves a slowing down of thought and a reduction of physical movements in an individual. It can cause a visible slowing of physical and emotional reactions, including speech and affect., hypotonia : SUCLA2-& SUCLG1-related Mitochondrial DNA depletion syndrome (MDS) causes decreased muscle tone., Feeding Difficulty, SENSORINEURAL HEARING LOSS : Sensorineural hearing impairment is experienced by the affected individuals., Growth retardation : Postnatal growth restriction implies a growth arrest in a newborn who is no longer able to follow the previous intrauterine trend and it has been related to neurodevelopment impairment., Signs : nan, Treatment : There is no cure for Mitochondria Depletion Syndrome. Genetic testing is important to identify the specific cause of the syndrome. Clinical trials for MDS are becoming more frequent and may offer therapies targeting the specific genetic causes of the disorder, or be broader based therapies to increase mitochondrial content in cells., Other therapies that support mitochondrial enzyme deficiencies that arise in these conditions, such as mitochondrial supplement medications consisting of amino acids, antioxidants, and vitamins may help patients with metabolic disorders like MDS., In some cases of liver failure, liver transplant may be an option., Pathophysiology : MDS are due to defects in mtDNA maintenance caused by mutations in nuclear genes, which function in either maintaining the mitochondrial nucleotide pool (TK2,  DGUOK,  SUCLA2,  SUCLG1,  RRM2B, and TYMP) or by mutations in genes associated with mtDNA replication (POLG and C10orf2). The function of the MPV17 gene remains unclear. Unlike nuclear DNA, which replicates with each cell division, mtDNA replicates continuously and independently of cell division. dNTPs can be synthesized via either the de novo pathway, which is cell cycle-regulated, thereby operative only in S-phase cells or the salvage pathway in which dNTPs are produced by utilizing pre-existing deoxynucleosides to synthesize DNA precursors. As mtDNA synthesis is continuous throughout the cell cycle, the salvage pathway becomes essential for mtDNA maintenance. TK2,  DGUOK,  SUCLA2,  SUCLG1,  RRM2B, and TYMP encode proteins that maintain the mitochondrial dNTP pool mainly through salvage pathways; therefore, mutations in any of these genes result in depleting the mitochondria from DNA building blocks with subsequent mtDNA depletion.SUCLA2 and SUCLG1 encode subunits of succinyl CoA ligase (SUCL). SUCL is a mitochondrial tricarboxylic acid cycle enzyme that catalyzes the reversible conversion of succinyl-CoA and ADP or GDP to succinate and adenosine triphosphate or guanosine triphosphate. SUCL is composed of an alpha subunit, encoded by SUCLG1 and a beta subunit, encoded by either SUCLA2 or SUCLG2. The alpha subunit forms a heterodimer with either of its beta subunits, resulting in an ADP-forming SUCL and a GDP-forming SUCL, respectively. SUCL also forms a complex with the mitochondrial nucleoside diphosphate kinase, and the lack of this complex formation in SUCL deficiency has been suggested to disturb the kinase function, resulting in decreased mtDNA synthesis leading to mtDNA depletion. , Epidemiology : between 1 : 5, 000 and 1 : 10, 000 live births, Poor, "Are a genetically and clinically heterogeneous group of autosomal recessive disorders and therefore cant be prevented.", Complications : Epilepsy, liver failure, seizures, developmental regression, Diagnostics : biopsy, GENETIC TESTING, Differential diagnosis : Demyelinating form of charcot-marie-tooth disease, Epilepsy, Limb-Girdle Muscular Dystrophies, MYASTHENIA GRAVIS, Myotonic Muscular Dystrophy, renal tubulopathy, Sengers syndrome, disease description : Mitochondrial DNA (mtDNA) depletion syndromes (MDS) are a genetically and clinically heterogeneous group of autosomal recessive disorders that are characterized by a severe reduction in mtDNA content leading to impaired energy production in affected tissues and organs. In MDS, fewer functioning mitochondria produce less energy, limiting the ability of cells to work properly.

Sudden Cardiac Arrest

Disease Name : Sudden Cardiac Arrest, Symptoms : chest pain : Some people have chest pain during the initial seconds of sudden cardiac arrest. Pressure, fullness, burning or tightness in the chest. Crushing or searing pain that spreads to the back, neck, jaw, shoulders, and one or both arms. Pain that lasts more than a few minutes, gets worse with activity, goes away and comes back, or varies in intensity., palpitations : Cardiac arrest happens when your heart stops beating or beats so fast that it stops pumping blood., vomiting, loss of consciousness : Usually, the first sign of SCA is loss of consciousness (fainting). This happens when the heart stops beating., shortness of breath : Sudden cardiac arrest causes dyspnea., Signs : nan, Treatment : "SCA is an emergency. A person having SCA needs to be treated with a defibrillator right away. A defibrillator is a device sends an electric shock to the heart. The electric shock can restore a normal rhythm to a heart thats stopped beating. To work well, it needs to be done within minutes of the SCA", may have an angioplasty or coronary artery bypass surgery. These procedures help restore blood flow through narrowed or blocked coronary arteries.an implantable cardioverter defibrillator (ICD)., Pathophysiology : After a myocardial infarction, the risk of sudden cardiac death is highest during the first months due to fatal tachyarrhythmias, re-infarction, or myocardial rupture. Ventricular fibrillation (VF) and ventricular tachycardia (VT) were initially thought to be the most common causes of out-of-hospital cardiac arrest. More recent studies show pulseless, electrical activity (PEA) and asystole as more frequent. Approximately 50% of patients initially have asystole, and 19% to 23% have PEA as the first identifiable rhythm. Immediately following OHCA the blood flow to the brain slows to essentially zero and ultimately leading to death., Epidemiology : In elite athletes with an incidence of 1 : 8, 253 per year, variable, You can reduce your risk in many ways, such as : ,,Keeping your regular follow-up appointments with your healthcare provider.,Making healthy lifestyle changes such as losing weight and eating a low-fat diet.,Avoiding smoking and other tobacco products.,Taking medications your healthcare provider prescribes for high cholesterol or arrhythmia.,Getting an implantable cardioverter defibrillator (ICD) if your healthcare provider recommends it.,Having procedures or surgery your healthcare provider recommends, such as angioplasty or catheter ablation.,Taking genetic testing if recommended by your physician to look for potential causes of sudden cardiac death.,Teaching your family the importance of immediate care and learning CPR.,,High school and college athletes should have a heart screening every two years. This should include an evaluation of their personal and family history (updated annually) and a physical exam. Their sports physician may recommend additional testing such as an electrocardiogram if there are any concerning findings on an initial evaluation.,,If your healthcare provider suspects a heart problem, you should get a referral to a cardiologist., Complications : death, Diagnostics : ECG, CT SCAN, HISTORY TAKING, Differential diagnosis : angina pectoris, aortic stenosis, Atherosclerosis, Dilated cardiomyopathy, Ebstein Anomaly, Myocardial infarction, disease description : Sudden cardiac death (SCD) is death due to a cardiovascular cause that occurs within one hour of the onset of symptoms. A sudden cardiac arrest occurs when the heart stops beating or is not beating sufficiently to maintain perfusion and life. Emergency treatment for sudden cardiac arrest includes cardiopulmonary resuscitation (CPR) and shocks to the heart with a device called an automated external defibrillator (AED). Survival is possible with fast, appropriate medical care.Sudden cardiac arrest isnt the same as a heart attack. A heart attack happens when blood flow to a part of the heart is blocked. Sudden cardiac arrest is not due to a blockage. However, a heart attack can cause a change in the hearts electrical activity that leads to sudden cardiac arrest

Sudden Hearing Loss

Disease Name : Sudden Hearing Loss, Symptoms : Deafness, Signs : nan, Treatment : medication : Prednisolone, bed rest, HYPERBARIIC O2 THERAPY, Inhalation of carbogen (5% CO2 + 95% O2). It increases,cochlear blood flow and improves oxygenation., Pathophysiology : Most often the cause of sudden deafness remains obscure, in which case it is called the idiopathic variety. In such cases, three aetiological factors are considered—viral, vascular or the rupture of cochlear membranes. Spontaneous perilymph fistulae may form in the oval or round window. Other aetiological factors which cause sudden deafness and must be excluded are listed below. Remember the mnemonic “In The Very Ear Too No Major Pathology.” 1. Infections. Mumps, herpes zoster, meningitis, encephalitis, syphilis, otitis media. 2. Trauma. Head injury, ear operations, noise trauma, barotrauma, spontaneous rupture of cochlear membranes. 3. Vascular. Haemorrhage (leukaemia), embolism or thrombosis of labyrinthine or cochlear artery or their vasospasm. They may be associated with diabetes, hypertension, polycythaemia, macroglobinaemia or sickle cell trait. 4. Ear (otologic). Ménière’s disease, Cogan’s syndrome, large vestibular aqueduct. 5. Toxic. Ototoxic drugs, insecticides. 6. Neoplastic. Acoustic neuroma. Metastases in cerebellopontine angle, carcinomatous neuropathy. 7. Miscellaneous. Multiple sclerosis, hypothyroidism, sarcoidosis. 8. Psychogenic., Epidemiology : half the patients of idiopathic sensorineural hear, Complications : Deafness, Diagnostics : Erythrocyte Sedimentation Rate (ESR), Pure tone audiometry (PTA), Rinne test, LIPID PROFILE, CT Scan Temporal Bone, THYROID PROFILE, Differential diagnosis : acoustic neuroma, h/o Drug intake, Hypothyroidism, "menieres disease", Meningitis., Multiple Sclerosis, Mumps, otitis media, trauma, disease description : Sudden SNHL is defined as 30 dB or more of SNHL over at least three contiguous frequencies occurring within a period of 3 days or less. Mostly it is unilateral. It may be accompanied by tinnitus or temporary spell of vertigo.

Sulfite Oxidase Deficiency

Disease Name : Sulfite Oxidase Deficiency, Symptoms : seizures : Babies with classic ISOD have seizures that are difficult to treat., vision abnormalities : Affected individuals who survive past infancy usually develop displacement of the lenses of the eyes., Facial abnormalities : Abnormalities in facial features also become increasingly pronounced with lack of normal head growth. These facial differences include a relatively long and narrow face; deep-set, widely-spaced eyes; elongated openings of the eyes (palpebral fissures); puffy cheeks; a small nose; a large space between the nose and upper lip (a long philtrum); and thick lips. Babies with cla, quadriplagia : They have muscle stiffness that results in paralysis of the arms and legs., Microcephaly–capillary malformation syndrome : Because development of the brain is impaired, the head does not grow at the same rate as the body, so it appears that the head is getting smaller as the body grows (progressive microcephaly)., opisthotonus : Episodes of muscle spasms that cause backward arching of the spine is seen in the affected infants., Signs : nan, Treatment : Gastrostomy tube placement to manage difficulties with swallowing., No treatment exists for the underlying metabolic defect. Symptomatic treatment can include : antiepileptic drugs (AEDs) for seizures; medications to reduce spasticity; and early consideration of gastrostomy tube placement to manage difficulties with swallowing, assure adequate caloric intake, and reduce risk of aspiration. Other measures can include vigorous chest physiotherapy to prevent respiratory complications. Treatment of vomiting, gastroesophageal reflux, and aspiration pneumonia are per routine., Pathophysiology : ISOD is caused by mutations in the SUOX gene. This gene provides instructions for making an enzyme called sulfite oxidase, which helps break down protein building blocks (amino acids) that contain sulfur when they are no longer needed. Specifically, sulfite oxidase is involved in the final step of this process, in which sulfur-containing molecules called sulfites are converted to other molecules called sulfates by adding an oxygen atom (a process called oxidation). The SUOX gene mutations that cause ISOD impair the function of sulfite oxidase, preventing complete breakdown of sulfur-containing amino acids. As a result, sulfites and other compounds left over from the partial breakdown process abnormally accumulate in the body. Researchers suggest that the nervous system is especially sensitive to this abnormal accumulation, and excessive levels of sulfite compounds that are toxic to the brain are thought to result in the brain damage that occurs in ISOD. It is unclear why most affected individuals have the classic form of the condition while a smaller number develop the milder late-onset form. Classic ISOD is characterized in the first few hours to days of life by intractable seizures, feeding difficulties, and rapidly progressive encephalopathy manifest as abnormal tone (especially opisthotonus, spastic quadriplegia, and pyramidal signs) followed by progressive microcephaly and profound intellectual disability. Lens subluxation or dislocation, another characteristic finding, may be evident after the newborn period. Children usually die during the first few months of life. Late-onset ISOD manifests between ages six and 18 months and is characterized by ectopia lentis (variably present), developmental delay/regression, movement disorder characterized by dystonia and choreoathetosis, ataxia, and (rarely) acute hemiplegia due to metabolic stroke. The clinical course may be progressive or episodic. In the episodic form encephalopathy, dystonia, choreoathetosis, and/or ataxia are intermittent., Epidemiology : 50 affected individuals have been described in the medical literature., More than 356, 000 people have an out-of-hospital cardiac arrest in the United States every year, POOR, "This condition is inherited in an autosomal recessive pattern and therefore cant be prevented.", Complications : encephalopathy, paralysis, Diagnostics : MRI Brain, CT HEAD, MRI, Amino acid level in blood, Differential diagnosis : Glycine encephalopathy, molybdenum cofactor deficiency, Pyridoxine-dependent epilepsy, disease description : Isolated sulfite oxidase deficiency (ISOD) is a disorder of the nervous system, with a severe "classic" form that starts in the newborn period and a milder, late-onset form that begins later in infancy or early childhood.Sudden cardiac death (SCD) is death due to a cardiovascular cause that occurs within one hour of the onset of symptoms. A sudden cardiac arrest occurs when the heart stops beating or is not beating sufficiently to maintain perfusion and life. This activity examines the evaluation, diagnosis, and management of sudden cardiac death and the role of team-based interprofessional care for affected patients.

Superficial Fibromatoses (palmar / Plantar)

Disease Name : Superficial Fibromatoses (palmar / Plantar), Symptoms : Pain : The most common symptom of a plantar fibroma is pain on the bottom of your foot, usually in the arch., subcutaneous nodules : Plantar fibromatosis typically presents as small soft issue nodules on the sole of the foot, frequently multiple and bilateral., Signs : nan, Treatment : Palmar fibromatosis,Observation, excision or incision of contracture band,Often recurs,Surgical treatment is necessary if the contracture results in functional disability and the total flexion deformity is greater than 30°, Plantar fibromatosis,Conservative measures should be used prior to recommending surgery ,Observation, surgery if symptomatic, complete fasciectomy has fewer recurrences (0 - 50%) than local excision (57 - 100%) and wide excision (8 - 80%) ,Wide excision : 2 - 3 cm margin, Pathophysiology : Palmar fibromatosisProliferation of fibroblasts, their differentiation into myofibroblasts and the production of the extracellular matrixProposed roles of fibroblast growth factor (FGF), wingless / integrated (WNT) and transforming growth factor beta (TGF-ß) in disease progression Plantar fibromatosisProliferative phase : increased fibroblastic activity and cellular proliferationActive phase : nodule formation occursResidual phase : collagen deposition, scar formation and tissue contracture., Epidemiology : Palmar fibromatosis,Most common type of superficial fibromatosis (1 - 2% of population),Prevalence increases with age (~20% of population at age 65),M : F = 3 - 4 : 1,Plantar fibromatosis,Prevalence not currently understood M > F, variable, Complications : nan, Diagnostics : MRI, MRI, USG, USG, Differential diagnosis : Calcifying aponeurotic fibroma, Epithelioid sarcoma, kaposi sarcoma, Melanoma, Synovial sarcoma, disease description : Palmar fibromatosisBenign disordered nodular proliferative process of palmar aponeurosis, surrounding adipose and occasionally dermis, due to fibroblasts, myofibroblasts and fibrocytes with subsequent formation of nodulesPlantar fibromatosis.Benign disordered nodular proliferative process of plantar aponeurosis and surrounding adipose tissue due to fibroblasts, myofibroblasts and fibrocytes with subsequent formation of nodules.

Superficial Migratory Thrombophlebitis

Disease Name : Superficial Migratory Thrombophlebitis, Symptoms : Pain in extremities : In superficial thrombophlebitis, acute-onset pain and swelling usually occur over a previous varicose vein. At times, this pain and swelling, which is often associated with warm erythema, can appear even without an obvious underlying varicosity. Swelling and pain in an upper extremity are suggestive of thrombosis., Signs : erythema : Phlebitis is an inflammation of the vein, which may bring with it erythema., Treatment : medication : Enoxaparin sodium , Dalteparin, ANTICOAGULATION, Pathophysiology : Superficial thrombophlebitis starts with microscopic thrombosis. When there is venous turbulence or stasis, vessel wall injuries, abnormal coagulability, or vessel wall injuries, microthrombi could propagate and subsequently form macroscopic thrombi. Vascular endothelial injury reliably results in thrombus formation by triggering an inflammatory response that results in immediate platelet adhesion. Platelet aggregation is mediated by thrombin and thromboxane A2., Epidemiology : 0.3 to 0.6 per 1000 person-years in younger patients and 0.7 to 1.5 per 1000 person-years in older patients., variable, can prescribe medications like blood thinners, which can stop a clot from forming in the first place.,Tobacco use. Quit using tobacco (including vaping or smokeless tobacco products). If you don’t use tobacco, don’t start.,Stay hydrated. Drinking enough fluids can help lower your risk of developing thrombophlebitis., Complications : Pulmonary Embolism, DVT, Diagnostics : Complete Blood Count CBC, DUPLEX ULTRASONOGRAPHY, CECT CHEST, Differential diagnosis : CELLULITIS, erythema nodosum, lymphangitis, Nodular vasculitis, Polyarteritis Nodosa, disease description : Migratory thrombophlebitis or thrombophlebitis migrans is an inflammatory reaction of the vein accompanied by a thrombus. It is characterized by the involvement of one vein group first, then improving and followed by the involvement of other vein groups.Thrombophlebitis is an inflammatory reaction of the vein accompanied by a thrombus. Migratory thrombophlebitis or thrombophlebitis migrans is characterized by the involvement of one vein group first, then improving and followed by the involvement of other vein groups. Sometimes several veins in different locations can be involved simultaneously. Superficial and deep veins both may be affected.Idiopathic thrombophlebitis migrans occurs between the ages of 25 and 50 years; the average age is about 40. Men are affected three times more than that of women and occur in otherwise healthy adults.

Superficial Punctate Keratitis (spk)

Disease Name : Superficial Punctate Keratitis (spk), Symptoms : eye pain : Superficial punctate keratitis causes intense eye pain., Lacrimation : The eyes become extremely watery., Loss of vision : Superficial punctate keratitis causes the vision to decrease., photophobia : Superficial punctate keratitis makes the affected individuals sensitive to light., Signs : multiple, spotty lesions in the superficial layers of cornea : Superficial punctate keratitis is an eye disorder caused by death of small groups of cells on the surface of the cornea., Treatment : 1. Topical steroids have a marked suppressive effect.,2. Artificial tears have soothing effect.,3. Specific treatment of cause should be instituted whenever possible e.g., antiviral drugs in cases of,herpes simplex., Pathophysiology :  1. Viral infections are the chief cause. Of these more common are : herpes zoster, adenovirus infections, epidemic keratoconjunctivitis, pharyngoconjunctival fever and herpes simplex. 2. Chlamydial infections include trachoma and inclusion conjunctivitis. 3. Toxic lesions e.g., due to Staphylococcal toxin in association with blepharoconjunctivitis. 4. Trophic lesions e.g., exposure keratitis and neuroparalytic keratitis. 5. Allergic lesions e.g., vernal keratoconjunctivitis. 6. Irritative lesions e.g., effect of some drugs such as idoxuridine. 7. Disorders of skin and mucous membrane, such as acne rosacea and pemphigoid. 8. Dry eye syndrome, i.e., keratoconjunctivitis sicca. 9. Specific type of idiopathic SPK e.g., Thygeson’s superficial punctate keratitis and Theodore’s superior limbic keratoconjunctivitis. 10. Photo-ophthalmia. Morphological types 1. Punctate epithelial erosions (multiple superficial erosions). 2. Punctate epithelial keratitis. 3. Punctate subepithelial keratitis. 4. Punctate combined epithelial and subepithelial keratitis. 5. Filamentary keratitis. Superficial punctate keratitis may present as different morphological types as enumerated above. Punctate epithelial lesions usually stain with fluorescein, rose bengal and other vital dyes. The condition mostly presents with acute pain, photophobia and lacrimation; and is usually associated with conjunctivitis., Epidemiology : "Superficial punctate keratitis (SPK) is damage to the cells of the corneas ... in their 20s and 30s and has a higher incidence in females.", variable, "Choose daily wear contacts and take them out before going to sleep.,Wash, rinse and dry your hands thoroughly before handling your contacts.,Follow your eye care providers recommendations for taking care of your lenses.,Use only sterile products that are made specifically for contact lens care, and use lens care products made for the type of lenses you wear.,Replace your contact lenses as recommended.,Replace your contact lens case every 3 to 6 months.", Complications : blindness, Scarring, Diagnostics : Slit lamp examination, Rose Bengal staining, Differential diagnosis : Molluscum Contagiosum, Sjögren syndrome, VIRAL CONJUNCTIVITIS, disease description : Superficial punctate keratitis is characterised by occurrence of multiple, spotty lesions in the superficial layers of cornea. It may result from a number of conditions, identification of which (causative condition Superficial punctate keratitis is an eye disorder caused by death of small groups of cells on the surface of the cornea (the clear layer in front of the iris and pupil).) might not be possible most of the times.

Supracondylar Fracture Of The Humerus

Disease Name : Supracondylar Fracture Of The Humerus, Symptoms : elbow injury : The clinical presentation of a supracondylar humerus fracture (SCHF) is that of a painful swollen elbow that the patient is hesitant to move. The elbow may appear angulated and the upper extremity shortened., elbow pain : SCHF causes intense pain in the fractured elbow., Signs : nan, Treatment : Non-operative management involves immobilization in a collar and cuff or an above-elbow cast with the elbow in 80-90 degrees of flexion for three to four weeks., Surgical management is indicated for displaced Gartland II and Gartland III fractures. Urgent surgical management is indicated for patients with neurovascular compromise, compartment syndrome, and open fractures. For closed injuries, surgical management involves closed reduction and percutaneous pinning with K-wires. Open reduction may be required for failed closed reduction, irreducible fractures, and for vascular exploration. Orthopedic surgeons managing these intricate fracture patterns with potential concomitant neurovascular injuries should ensure that they can handle the associated injuries and have a vascular surgeon on hand for assistance during the surgery., Pathophysiology : The fracture line extends transversely through the distal metaphysis of humerus just above the condyles. Types : A supracondylar fracture may be of extension or flexion type, depending upon the displacement of the distal fragment The extension type is the commoner of the two. In this, the distal fragment is extended (tilted backwards) in relation to the proximal fragment. In the flexion type, the distal fragment is flexed (tilted forwards) in relation to the proximal fragment. Subsequent text is limited to the commoner, extension type of supracondylar fracture. Displacements : Commonly, a supracondylar fracture is displaced. The distal fragment may be displaced in the following directions : (i) posterior or backward shift; (ii) posterior or backward tilt; (iii) proximal shift; (iv) medial or lateral shift; (v) medial tilt; and (vi) internal rotation., Epidemiology : 177.3 per 100 000, good, In lateral external fixation of supracondylar humeral fractures, ,care should be taken to avoid iatrogenic radial nerve palsy , It is recommended to place the proximal Shanz pin under direct vision,with a drill sleeve, 2cm proximal to the fracture line to prevent,injury to the radial nerve which crosses the lateral supracondylar,ridge of the humerus at the diaphyseal-metaphyseal junction, Complications : Malunion, NERVE INJURY, Injury to the brachial artery, Diagnostics : X RAY, X RAY, Differential diagnosis : Distal humeral fractures, olecranon fractures, soft tissue injury, disease description : Supracondylar fractures of humerus are the most common type of elbow fractures in children accounting for up to 60% of elbow fractures. This activity reviews the mechanism of injury, classification, and management of these injuries in the pediatric population and highlights the role of the interprofessional team in evaluating and improving the care of patients with this condition.This is one of the most serious fractures in childhood as it is often associated with complications. MECHANISM The fracture is caused by a fall on an out-stretched hand. As the hand strikes the ground, the elbow is forced into hyperextension resulting in fracture of the humerus above the condyles.They most frequently occur in children aged 5 to 7 years. The median age is approximately six years. Boys are affected equally to girls. Extension-type fractures are much more common than flexion-type fractures.Flexion-type fractures are more prevalent in older children. These injuries often occur in the non-dominant upper extremity.

Supraventricular Tachycardia

Disease Name : Supraventricular Tachycardia, Symptoms : EXERCISE INTOLERANCE, sudden death, chest pain, Dizziness, palpitations, syncope, dyspnea, Signs : atrial fibrillation, atrial flutter, ventricular fibrillation, Treatment : medication : Diltiazem , Adenosine , Pathophysiology : nan, Epidemiology : nan, Complications : nan, Diagnostics : ECG, trans thoracic 2D ECHO, Differential diagnosis : nan, disease description : Supraventricular tachycardia (SVT) is a condition where your heart suddenly beats much faster than normal. Its not usually serious, but some people may need treatment

Sustained Ventricular Tachycardia

Disease Name : Sustained Ventricular Tachycardia, Symptoms : Palpitations, dizziness, syncope., Signs : Tachycardia, Treatment : medication : Amiodarone , Adenosine , 299). If hypotension, impaired consciousness, or pulmonary,edema are present, QRS synchronous electrical cardioversion,should be performed, Pathophysiology : nan, Epidemiology : NOT SPECIFIED, Complications : nan, Diagnostics : ECG, trans thoracic 2D ECHO, CARDIAC MRI, Differential diagnosis : supraventricular tachycardia, disease description : Sustained monomorphic ventricular tachycardia (VT) presents as a wide QRS tachycardia that has the same QRS configuration from beat to beat indicating an identical sequence of ventricular depolarization for each beat. VT originates from a stable focus or reentry circuit. In structural heart disease, the substrate is often an area of patchy replacement fibrosis due to infarction, inflammation or prior cardiac surgery that creates anatomical or functional reentry pathways. Less commonly, VT is related to reentry or automaticity in a diseased Purkinje system. Idiopathic VT occurs in the absence of structural heart disease and is due to a focal region of automaticity or reentry involving a portion of the Purkinje system.

Sweet Syndrome

Disease Name : Sweet Syndrome, Symptoms : arthralgia : Arthralgias and non-erosive inflammatory arthritis have been reported., myalgia : Sweet syndrome leads to muscle aches., fever : Fever is almost always present, especially in drug-induced Sweet syndrome., Oral lesions : Oral lesions are seen in affected individuals., non itchy erythematous plaques : Non-itchy, sometimes tender, erythematous plaques and papules most commonly distributed on the arms, upper body, head and neck., Ocular symptoms : The ocular manifestations of Sweet syndrome include periorbital and orbital inflammation, dacryoadenitis, conjunctivitis, episcleritis, scleritis, limbal nodules, peripheral ulcerative keratitis, iritis, glaucoma, and choroiditis., Signs : nan, Treatment : medication : Colchicine , Cyclosporine/Ciclosporine, Clofazimine , Dapsone , Iodine (Sodium iodide, potassium iodide) , First line ,• Systemic corticosteroids (0.5–1 mg/kg for 4–6 weeks),• Potent topical or intralesional corticosteroids may be tried ,for mild localized disease, Pathophysiology : The exact pathogenesis of Sweet syndrome is not known.Some genetic factors such as HLA-B54 in the Japanese population,  MEFV gene mutation in familial Mediterranean fever patients,  and chromosome 3q abnormalities have been observed in patients with Sweet syndrome .Theories regarding the pathogenesis of Sweet syndrome include hypersensitivity to eliciting bacterial, viral, or tumor antigen that may trigger neutrophil activation and infiltration leading to Sweet syndrome. Another theory suggests the role of cytokines and chemokines such as G-CSF, GM-CSF, IL-1, and interferon-gamma with a higher level of these cytokines reported in patients with Sweet syndrome. Studies for circulating immune complexes, complement activation, and tissue bound immunoglobulins have been negative and not shown to be pathognomic in Sweet syndrome., Epidemiology : To date, several hundred cases have been reported., The incidence of AML in patients with Sweet syndrome was 4%, variable, Because doctors don’t know what causes Sweet syndrome, it is not possible to prevent it., Complications : infection, Diagnostics : Complete Blood Count CBC, CRP, LIVER FUNCTION TEST LFT, THYROID PROFILE, full thickness skin biopsy, Differential diagnosis : allergic contact dermatitis, "Behcets syndrome/disease", CELLULITIS, erythema multiforme, erythema nodosum, HERPES SIMPLEX, Leukocytoclastic vasculitis, pyoderma gangrenosum, disease description : Sweet syndrome is an inflammatory dermatosis characterized by non-itchy, sometimes tender, erythematous plaques and papules most commonly distributed on the arms, upper body, head and neck. Sweet syndrome is the end point of unrestricted neutrophil production with consequent infiltration of the skin and in some cases other organs. A predisposition to this could be either acquired or genetic.Three main types of Sweet syndrome are now recognized as follows : • Classical. • Malignancy associated. • Drug induced.

Swine Flu

Disease Name : Swine Flu, Symptoms : GI disturbances : Some people with H1N1 flu virus have also reported vomiting and diarrhea., sore throat : A sore throat caused by swine flu is a lot more painful than having a regular sore throat., fever : A rising fever is also one of the popular symptoms that are associated with swine flu., Muscle ache : Swine flu causes intense body aches., cough : A person suffering from swine flu experiences symptoms of barking cough., Signs : INCREASE HEART RATE : Critically ill patients with H1N1 infection frequently exhibit right heart dilatation and failure., Treatment : medication : Ibuprofen , Paracetamol/Acetaminophen, Oseltamivir , Some of the same antiviral drugs that are used to treat seasonal flu also work against H1N1 Swine Flu. Oseltamivir (Tamiflu) and zanamivir (Relenza), Pathophysiology : H1N1 swine flu is an acute disease that infects the upper respiratory tract and can cause inflammation of the upper respiratory passages, trachea, and possibly the lower respiratory tract. The known incubation period for H1N1 swine flu ranges from 1 to 4 days, with the average around 2 days in most individuals, but some individuals, it may be as long as 7 days. The contagious period for adults starts about 1 day before symptoms develop and lasts around 5 to 7 days after the person develops symptoms. The contagious period may be longer in individuals with weakened immune systems and children .The acute symptoms of uncomplicated infections persist for three to seven days, and the disease is mostly self-limited in healthy individuals, but malaise and cough can persist for up to 2 weeks in some patients. Patients with more severe disease may require hospitalization, and this may increase the time of infection to around 9 to 10 days. The bodys immune reaction to the virus and the interferon response are the causes of the viral syndrome which includes high fever, coryza, and myalgia. Patients with chronic lung diseases, cardiac disease and who are currently pregnant are at higher risk of severe complications such as viral pneumonia, superimposed bacterial pneumonia, hemorrhagic bronchitis, and possibly death. These complications can potentially develop within 48 hours from the onset of symptoms. The replication of the virus occurs primarily in the upper and lower respiratory tract passages from the time of inoculation and peaks around 48 hours in most patients. The recommended time of isolation of the infected patient is around 5 days., Epidemiology : 700 million to 1.4 billion people—or 11 to 21 percent of the global population of 6.8 billion at the time., variable, "The best way to prevent swine flu (H1N1) is to get your annual flu vaccine. The flu vaccine has helped protect against swine flu since 2010.,,Other ways to prevent getting and spreading swine flu (H1N1) include : ,,Cover your nose and mouth with a tissue when you sneeze or cough.,If you don’t have a tissue, sneeze or cough into your elbow.,Wash your hands with soap and water.,Don’t touch your eyes, nose or mouth.,Avoid people who are sick.,Stay home if youre sick.,Don’t share personal items such as cups, straws and utensils.", Complications : Asthma, respiratory failure, Diagnostics : H1N1 DETECTION, Total Leucocyte Count (TLC), X RAY CHEST, RT PCR, Differential diagnosis : acute respiratory distress syndrome, ADENOVIRUS INFECTION, Cytomegalovirus (CMV), Dengue, infection, disease description : H1N1 Swine flu is a subtype of influenza A virus (a communicable viral disease), which causes upper, and potentially, lower respiratory tract infections in the host it infects, resulting in symptoms such as nasal secretions, chills, fever, decreased appetite, and possibly lower respiratory tract disease. H1N1 swine influenza is a common infection in pigs worldwide, and that is why it is also known as swine flu. H1N1 swine flu leads to respiratory disease that can potentially infect the respiratory tract of pigs. Sometimes, people who are closely associated with pigs or in the proximity of pigs have developed swine flu (zoonotic swine flu). Swine influenza viruses can potentially cause infections in humans if antigenic characteristics of the virus change through reassortment. When this happens, transmission from person-to-person is usually inefficient. Influenza A pandemics such as the ones in 1918 and 2009 can occur if the transmission from person-to-person becomes efficient.

Swyers Syndrome

Disease Name : Swyers Syndrome, Symptoms : amenorrhoea, delay in appearance of secondary sexual characters, Signs : nan, Treatment : medication : Oestradiol/Oestrogen, Progesterone , Cyclical oestrogen and ,progestogen can induce menstruation. Conception with in ,vitro fertilization (IVF) using donor eggs is a possibility, Pathophysiology : Undeveloped testes do not secrete testosterone and MIF resulting in the development of female genital organs and female phenotype. The woman presents with primary amenorrhoea, absence of secondary sex characters and female external genitalia. Cyclical oestrogen and progestogen can induce menstruation. Conception with in vitro fertilization (IVF) using donor eggs is a possibility. The gonads (testis) have 30% risk to undergo malignancy and should be removed., Epidemiology : 1 in 80, 000 births, variable, Additionally, preventive measures may also be taken in order to prevent the development of cancer. ,,Swyer syndrome is treated with hormonal replacement therapy, including the replacement of estrogen and progesterone, the two main hormones that are produced by the ovaries., Complications : Hearing loss, heart problem, vision abnormalities, Diagnostics : SERUM TESTOSTERONE, USG, Differential diagnosis : androgen insensitivity syndrome, Gonadal suppression, lipoid congenital adrenal hyperplasia, Turners syndrome, disease description : Swyer syndrome is a condition that affects sex development. Sex development usually follows a particular path based on an individuals chromosomes; however, in Swyer syndrome, sex development is not typical for the affected individuals chromosomal pattern. Chromosomes contain the genetic instructions for how the body develops and functions.

Sydenhams Chorea

Disease Name : Sydenhams Chorea, Symptoms : CNS disturbances : In addition to choreic movements, individuals with Sydenham chorea may develop muscle weakness, slurred speech (dysarthria), diminished muscle tone (hypotonia), tics, obsessions, compulsions, inattention, anxiety, labile mood, and decreased verbal output., movement disorders : The abnormal movements in Sydenham chorea range from subtle symptoms, affecting coordination and tasks such as writing, to severe symptoms, disrupting walking, talking, and performing basic tasks such as dressing, eating, or simply holding objects. Choreic movements may fluctuate through the day. In most cases, chorea disappears during sleep., Rheumatoid arthritis : Because Sydenham chorea is a complication of rheumatic fever, some individuals will have additional symptoms of joint arthritis or arthralgia., heart problem : Sydenham chorea causes inflammation of the heart valves causing permanent damage to the valves., Signs : Chorea : Sydenham chorea is a rare neurological disorder characterized by sudden onset chorea, usually in childhood. Chorea is defined as random-appearing, continuous (while awake), involuntary movements which can affect the entire body. This often includes the face and tongue., Treatment : medication : Valproic acid(sodium valproate)/ Divalproex Sodium, Carbamazepine, Prednisolone, Penicillin, The child should be protected from injury;,bedding should be well padded. These children may be,treated with chlorpromazine, haloperidol, sodium,valproate or carbamazepine. Drugs are maintained at,minimum doses required for symptom suppression. Antistreptococcal,prophylaxis with penicillin G should be,given to prevent recurrence of rheumatic activity., Pathophysiology : Most authorities believe SD to be an autoimmune disease that is triggered by a streptococci infection, subsequently resulting in a hypersensitivity humoral reaction to the infection and cross-reactivity streptococci antigens and human tissue antigens through antigen mimicry. The stimulated antibodies target the basal ganglia brain cells in the host and cause a diffuse inflammatory process in the corpus striatum, mainly the caudate nucleus. The symptoms of SD are caused by an imbalance between the dopaminergic system, intrastriatal cholinergic system, and the inhibitory gamma-aminobutyric acid (GABA) system., Epidemiology : 20–30% ..., SELF LIMITING, Timely strep throat and rheumatic fever treatment may lower the risk of this condition.,,If your child has had Sydenham chorea, being on antibiotics until adulthood can lower the risk of recurrent streptococcal infections, as well as the risk of heart disease. The long-term focus of treatment is to prevent permanent damage to heart valves due to heart disease., Complications : SYDENHAMS CHOREA, Diagnostics : ANTISTREPTOLYSIN O (ASO) TITRE, MRI Brain, PET SCAN, CT SCAN, Differential diagnosis : atrophy, hemorrhage, Huntington’s disease, "lymes disease", Surgery, disease description : Sydenham chorea (SD),   is a manifestation of rheumatic fever (RF), occurring in up to 40% of patients with RF. It is uncommon in the United States but occurs at a much higher frequency in developing countries. It is thought to be an autoimmune process that is the result of antigenic mimicry between central nervous system basal ganglia cells and Group A B-hemolytic Streptococci antigens. Anti-basal ganglia antibodies that result from the antigenic mimicry attack portions of the brain and are responsible for the pathological findings and symptoms. SD is much less common today than in the past, but when it does occur, the symptoms are less severe and the relapses are less frequent

Symblepharon

Disease Name : Symblepharon, Symptoms : diplopia, Lagophthalmos, Restricted Ocular movements, Signs : ENTROPION, Cosmetic disfigurement, squint, Treatment : Curative treatment consists of symblepharectomy.The raw area created may be covered by : ,• Mobilising the surrounding conjunctiva in mild,cases.,• Conjunctival or buccal mucosal graft is required,in severe cases.,• Amniotic membrane transplantation (AMT), also,gives good results., Pathophysiology : This is a condition where adhesion of the lid to the globe takes place. Any cause which produces raw surfaces on two opposed areas of the palpebral and bulbar conjunctiva will lead to adhesion if the areas are allowed to remain in contact during the process of healing, e.g. burns from heat or chemical injury, Stevens–Johnson syndrome, ulcers, diphtheria, operations, etc. Bands of fibrous tissue are thus formed, stretching between the lid and the globe, involving the cornea if this has also been injured. The bands may be narrow, but are more frequently broad, and may extend into the fornix so that the lid is completely adherent to the eyeball over a considerable area (symblepharon posterior). Bands limited to the anterior parts not involving the fornix are called symblepharon anterior. However, total symblepharon. in which the lids are completely adherent to the globe, is rare. Pronounced adhesions cause impairment of mobility of the eye resulting in diplopia. The adhesion may be so intimate that it is impossible to close the lids efficiently resulting in lagophthalmos with its baneful consequences. There is often extensive disfigurement., Epidemiology : GOOD, Complications : diplopia, corneal ulceration, CONJUNCTIVAL DISORDERS, Diagnostics : nan, Differential diagnosis : nan, disease description : This is a condition where adhesion of the lid to the globe takes place. Any cause which produces raw surfaces on two opposed areas of the palpebral and bulbar conjunctiva will lead to adhesion if the areas are allowed to remain in contact during the process of healing, e.g. burns from heat or chemical injury, Stevens–Johnson syndrome, ulcers, diphtheria, operations, etc.

Symmetrical Drug-related Intertriginous And Flexur

Disease Name : Symmetrical Drug-related Intertriginous And Flexur, Symptoms : papules, Signs : sharply demarcated erythema of the gluteal/perianal area and/or V-shaped erythema of the inguinal area;, vesicles, pustules, Treatment : Treatment is symptomatic. The offending drug should be withdrawn ,and avoided in the future. No active therapy is required although ,topical or systemic glucocorticoids may hasten recovery, Pathophysiology : Pathophysiology In SDRIFE, immunohistological findings on skin biopsies have shown an infiltration of CD4+ T cells in the dermis. The delayed latency and occasional positivity on patch testing to causative drugs support a type IV delayed hypersensitivity reaction. Systemic drugs induce SDRIFE without prior skin sensitization and without cross-reactivity to known contact allergens. The reason for the peculiar distribution of the reaction is unknown. Postulated explanations include a preferential trafficking of activated memory T cells to these sites as a form of recall phenomenon from previous physical/inflammatory insult. Although excretion of drugs or their metabolites in the site has been postulated, there is no syringotropic inflammation which argues against a central role for sweat glands in the pathogenesis . Pathology There is significant heterogeneity in SDRIFE . Features that have been described include : superficial perivascular lymphocytic infiltrate, which may also include neutrophils and eosinophils, spongiosis and vacuolar degeneration of the basal cells., Epidemiology : The reaction improves quickly on withdrawal of the, Complications : nan, Diagnostics : Skin Prick test, Patch Test, Differential diagnosis : Contact dermatitis, Hailey–Hailey disease, Tinea cruris, disease description : A benign and self-limiting drug eruption characterized by symmetrical involvement of the gluteal and intertriginous areas, occurring in the absence of systemic involvement.SDRIFE is a distinctive drug eruption characterized by symmetrical eruption of the gluteal region, thighs and other intertriginous areas such as the axillae, knees, elbows and neck. Previously, such cases were called drug-induced baboon syndrome – a form of systemic allergic contact dermatitis . The term SDRIFE was proposed in 2004 as a culturally more neutral term, and also to reflect a spectrum of involvement beyond the gluteal region. Reported in all ages. Male preponderance

Sympathetic Ophthalmitis

Disease Name : Sympathetic Ophthalmitis, Symptoms : Loss of vision : Typically, reduction of near vision is an early symptom. The onset can be insidious or acute., Ocular inflammatory condition : Patients typically present with non-specific symptoms of ocular inflammation, including blurred or decreased vision, pain, photophobia and conjunctival injection., Signs : nan, Treatment : medication : Atropine/ Atropine methonitrate, When there is hope of saving useful vision : Immediate expectant treatment with topical as well,as systemic steroids and antibiotics along with,topical atropine should be started.,Sympathetic ophthalmia (SO) is a bilateral granulomatous panuveitis following accidental or surgical trauma to 1 eye. Systemic corticosteroid therapy is first-line therapy, but immunosuppressive agents are commonly required for longer-term treatment., EXCISION OF EYE WHEN THERE IS NO CHANCE OF SAVING USEFUL VISION., Pathophysiology : Various theories have been put forward. Most accepted one is allergic theory, which postulates that the uveal pigment acts as an allergen and excites plastic uveitis in the sound eye. It is characteristic of granulomatous uveitis, i.e., there is : • Nodular aggregation of lymphocytes, plasma cells, epitheloid cells and giant cells scattered throughout the uveal tract. • Dalen-Fuchs’ nodules are formed due to proliferation of the pigment epithelium (of the iris, ciliary body and choroid) associated with invasion by the lymphocytes and epitheloid cells. • Sympathetic perivasculitis. Retina shows perivascular cellular infiltration. I. Exciting (injured) eye. It shows clinical features of persistent low grade plastic uveitis, which include ciliary congestion, lacrimation and tenderness. Keratic precipitates may be present at the back of cornea (dangerous sign). ll. Sympathizing (sound) eye. It is usually involved after 4–8 weeks of injury in the other eye. Earliest reported case is after 9 days of injury. Most of the cases occur within the first year. However, delayed and very late cases are also reported. Sympathetic ophthalmitis, almost always, manifests as acute plastic iridocyclitis. Rarely it may manifest as neuroretinitis or choroiditis., Epidemiology : the prevalence of sympathetic ophthalmia is widely cited to be 0.03 out of 100, 000 per year, 0.044% at minimum., VERY POOR, "There has been debate regarding the only known means of preventing sympathetic ophthalmia, i.e. removal of the injured eye shortly after the traumatizing event. The goal of enucleation or evisceration is to prevent exposure of uveal and retinal tissue to the immune system. Enucleation has historically been then treatment modality of choice out of concern that evisceration might leave behind residual uveal tissue. However, an evisceration is easier and quicker to perform, and arguably has better functional and cosmetic results. To support the argument that evisceration is a viable alternative are case series of positive outcomes. Also, the logical argument that since evisceration is a viable treatment option in non-trauma-causes, then the uveal tissue left behind on routine, non-trauma-related eviscerations likely isnt sufficient to promote a SO response; otherwise, one would expect higher rates of SO following all eviscerations. Finally, some authors argue against removing the eye because of the rarity of SO and the effective modern treatment options. Also, the exciting eye may also have useful vision after therapy. There is no known benefit to removing the exciting eye after the onset of sympathetic ophthalmia.", Complications : Keratic precipitates present at the back of cornea, ACUTE IRIDOCYCLITIS, Diagnostics : HISTOPATHLOGY, ophthalmoscopy, Fundus fluorescein angiography (FFA), Differential diagnosis : RETINAL DETACHMENT, Vogt-Koyanagi-Harada (VKH) Syndrome, disease description : Sympathetic ophthalmitis is a serious bilateral granulomatous panuveitis which follows a penetrating ocular trauma. The injured eye is called exciting eye and the fellow eye which also develops uveitis is called sympathizing eye. Very rarely, sympathetic ophthalmitis can also occur following an intraocular surgery. Incidence of sympathetic ophthalmitis has markedly decreased in the recent years due to meticulous repair of the injured eye utilizing microsurgical techniques and use of the potent steroids.

Symptomatic Intestinal Or Invasive Amoebiasis

Disease Name : Symptomatic Intestinal Or Invasive Amoebiasis, Symptoms : colitis : Amebic colitis is gradual in onset, with symptoms presenting over 1-2 weeks; this pattern distinguishes this condition from bacterial dysentery. Diarrhea is the most common symptom. Patients with amebic colitis typically present with cramping abdominal pain, watery or bloody diarrhea, and weight loss or anorexia. Rectal bleeding without diarrhea can occur, especially in children. Chronic amebic colitis is clinically similar to inflammatory bowel disease (IBD). Recurrent episodes of bloody diarrhea and vague abdominal discomfort develop in 90% of patients with chronic amebic colitis who have antibodies to E histolytica., Signs : nan, Treatment : nan, Pathophysiology : Transmission and Colonization : Amoebiasis is commonly transmitted through the ingestion of contaminated food or water containing the cyst form of the parasite. Once ingested, the cysts travel to the intestines, where they release the active trophozoite form of the parasite. Trophozoites colonize the large intestine (colon) and may initially exist as commensals without causing symptoms.Tissue Invasion and Pathogenicity : In some cases, trophozoites of E. histolytica can become pathogenic and invade the intestinal mucosa, leading to tissue damage. The trophozoites adhere to the intestinal lining and can produce proteolytic enzymes, such as cysteine proteinases, which allow them to penetrate the epithelial barrier and cause tissue destruction. This can result in the formation of flask-shaped ulcers in the colon, leading to symptoms such as diarrhea, abdominal pain, and bloody stools.Local and Systemic Inflammatory Response : The invasion of intestinal tissues triggers an immune response, involving the recruitment of immune cells like neutrophils and macrophages to the site of infection. This inflammatory response contributes to the symptoms and tissue damage associated with amoebiasis.Extraintestinal Spread (Invasive Amoebiasis) : In some cases, trophozoites can penetrate the intestinal wall and enter the bloodstream, leading to extraintestinal or invasive amoebiasis. They can disseminate to other organs, most commonly the liver, through the portal circulation. Liver abscesses can form as a result of the immune response and tissue destruction. Patients with invasive amoebiasis may experience fever, right upper quadrant abdominal pain, and other systemic symptoms., Epidemiology : 3-23% in asymptomatic population, 0.64-11% in symptomatic patients and 1-17.5% in HIV-infected patients., variable, Complications : nan, Diagnostics : STOOL CULTURE, colonoscopy, ELISA, PCR tests, Differential diagnosis : cholecystitis, DIVERTICULITIS, Hepatitis A, pericarditis, salmonellosis, disease description : Amebiasis or amoebic dysentery is a common parasitic enteral infection. It is caused by any of the amoebas of the Entamoeba group. Amoebiasis may present with no symptoms or mild to severe symptoms, including abdominal pain, diarrhea, or bloody diarrhea. Severe complications may include inflammation and perforation, resulting in peritonitis. People affected may develop anemia.If the parasite reaches the bloodstream, it can spread through the body and end up in the liver, causing amoebic liver abscesses. Liver abscesses can occur without previous diarrhea. Diagnosis is typically by stool examination using a microscope. An increased WBC count may be present. The most accurate test is specific antibodies in the blood.Prevention of amoebiasis is by improved sanitation. Two treatment options are possible, depending on the location. Amoebiasis in tissue is treated with metronidazole, tinidazole, nitazoxanide, dehydroemetine, or chloroquine. A luminal infection is treated with diloxanide furoate or iodoquinoline. Effective treatment may require a combination of medications. Infections without symptoms require treatment, but infected individuals can spread the parasite to others.

Syndrome Of Inappropriate Diuresis

Disease Name : Syndrome Of Inappropriate Diuresis, Symptoms : Confusion, headache, vomiting, anorexia, coma, nausea, Signs : nan, Treatment : medication : Fludrocortisone , Demeclocycline , Pathophysiology : nan, Epidemiology : nan, Complications : nan, Diagnostics : SERUM Sodium Na+, URINARY SODIUM Na+, Plasma Aldosterone, Differential diagnosis : nan, disease description : nan

Synovial Chondromatosis

Disease Name : Synovial Chondromatosis, Symptoms : joint pain, Joint swelling, Signs : nan, Treatment : Management of primary synovial chondromatosis is surgery. Current arthroscopic surgical techniques allow for arthroscopic surgical management, however, occasionally open procedures may be necessary. Removal of loose bodies with partial synovectomy of the involved joints results in decreased pain, improved mechanical function, and decreased swelling in most cases. Open procedures have similar results, but surgical morbidity is greater. Post-operative management includes a progressive range of motion and strengthening of peri-articular muscle groups, Pathophysiology : X-ray examination reveals irregularly shaped loose bodies within a synovial joint. This number varies anywhere from two or three loose bodies to several dozens. They present in varied sizes and several loose bodies may combine to form larger bodies. The number of intraarticular lesions is greater in the primary type than the secondary type. The gross and microscopic evaluation of the loose bodies reveals lobulated masses of hyaline cartilage surrounded by a layer of synovial tissue. The hyaline cartilage is hypercellular, and the cells are often atypical. These atypical changes are multinucleated cells, myxoid degeneration of matrix, crowding of cell nuclei, and large nuclei. In long-standing disease, the lobules can undergo peripheral ossification. High levels of bone morphogenic protein have been found in the loose cartilaginous bodies and synovial tissue. The loose bodies may create pathological mechanical wear on joint surfaces and result in various types of erosion of articular surfaces. The process is classified as a benign neoplastic rather than a metaplastic lesion., Epidemiology : The exact prevalence is unknown, but the disorder , It has incidence of 1 : 100, 000 and occurs de novo, Complications : nan, Diagnostics : MRI, X RAY, Differential diagnosis : nan, disease description : Synovial chondromatosis typically presents with large joint effusion(s), and joints may appear deformed due to swelling or synovial hypertrophy. Synovial chondromatosis can result in severe disability and dysfunction. However, most cases are benign and this condition rarely undergoes malignant transformation. The initial diagnosis of synovial chondromatosis is made through thorough history and physical examination and radiological evaluation of an affected joint. Involved joints are painful at rest and pain is worsened with motion. The range of motion is usually decreased, and x-ray evaluation reveals multiple loose radio-opaque chondroid bodies of varied sizes within the joint.

Synovial Sarcoma

Disease Name : Synovial Sarcoma, Symptoms : Pain : A sudden sharp pain in your hip, knee, ankle or shoulder., lump : A painless lump that appears on your hip, knee, ankle or shoulder., Signs : nan, Treatment : Chemotherapy may be used when synovial sarcoma cannot be completely removed by surgery or when it has spread., Surgery is the first choice of treatment for synovial sarcomas. When all of the tumor is removed and there is no sign of cancer anywhere else in the body, there is a better chance of survival. Success of the surgery depends on the size of the tumor and its location in the body., Pathophysiology : The word synovial is a misnomer in synovial sarcoma, as the development of the tumor is not limited to the synovium and can originate anywhere in the body. The pathognomonic translocation between chromosomes X and 18 leads to the expression of several SS18 : SSX fusion proteins described in this tumors pathogenesis. SS18 : SSX1 and SS18 : SSX2 (and rarely SS18 : SSX4) are the fusion proteins expressed in 95% of patients diagnosed with SS and are essential in establishing the diagnosis. The fusion proteins bind to the BAF complex (BRG1- or HBRM-associated factors), which displaces the tumor suppressor BAF47. The modified BAF complex leads to the activation of Sox2 (sex-determine region Y-box 2), which is necessary for the proliferation of synovial sarcoma., Epidemiology : Synovial sarcoma accounts for 5% to 10% of soft-tissue tumors., variable, Unfortunately, there aren’t ways to prevent synovial sarcoma. That’s because it’s likely caused by changes in your chromosomes, and that’s not something you can control.,,One thing you can control is being aware of changes in your body. A lump on your legs and arms that doesn’t go away or is painful might be something your healthcare provider should check. Finding synovial sarcoma early improves your chances of a full recovery., Complications : metastatic disease, Diagnostics : biopsy, MRI, X RAY, EXCISIONAL BIOPSY, CT SCAN, USG, Cardiac MRI with gadolinium contrast, Differential diagnosis : dermatofibrosarcoma protuberans, Epithelioid sarcoma, Ewing sarcoma, Fibrosarcoma, tumors, tumors, tumors, disease description : Synovial sarcoma (SS) is a mesenchymal tumor with partial epithelial differentiation. It is commonly seen in older children and younger adults. The presence of t(X;18)(p11.2;q11.2) is a pathognomonic feature of synovial sarcoma. Synovial sarcoma is the most well-established translocation-associated sarcoma, and several molecular techniques are used to determine this translocation. It is a very aggressive malignancy with a high potential for metastasis. Like other soft-tissue sarcomas (STS), surgical resection (to achieve microscopic negative margins) along with perioperative radiotherapy remains the cornerstone of treatment. The role of neoadjuvant or adjuvant chemotherapy remains controversial in adults but is utilized regularly in the pediatric population.

Syphilis Of The Joints

Disease Name : Syphilis Of The Joints, Symptoms : swelling, fever, joint pain, Signs : joint tenderness, Treatment : medication : Penicillin, rest and medical treatment, Pathophysiology : nan, Epidemiology : not specific, To Do : Control of venereal and nonvenereal treponematoses is based upon active surveillance and treatment of contacts. Penicillin treatment eradicates all stages, including congenital infection in pregnancy. Not To Do : Avoid close contact with the infected person, Complications : nan, Diagnostics : Complete Blood Count CBC, Erythrocyte Sedimentation Rate (ESR), PUS CULTURE, BLOOD CULTURE, X RAY, Differential diagnosis : candidiasis, Chancroid, condyloma acuminatum, Genital warts, Urethritis, disease description : The joint may be affected early or late in congenital syphilis. Early : During infancy, osteochondritis in the juxtaepiphyseal region results in breakdown of the bone and cartilage. Late : A manifestation of congenital syphilis, ‘Clutton’s joints’ is a painless synovitis occurring at puberty. It most commonly affects the knee and elbow, mostly bilaterally.ACQUIRED SYPHILIS The joints may be affected in the secondary and tertiary stages of acquired syphilis. In the secondary stage, transient polyarthritis and polyarthralgia involving the larger joints occur. In tertiary stage, gummatous arthritis occurs where the larger joints are most often involved. Neuropathic (Charcot’s) joint is an indirect consequence of syphilis.