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Tropical Ulcer

Disease Name : Tropical Ulcer, Symptoms : Burning pain, Malaise, fever, Pain, freezing, Signs : Ulcers with a slightly indurated edge that may be undermined, floor of the ulcer is covered by a foul-smelling greyish purulent slough., Treatment : Antibiotics such as tetracycline and metronidazole are used. Surgical debridement (removal of dead tissue) and skin grafts may have a role., Pathophysiology : nan, Epidemiology : nan, Complications : Squamous carcinoma in situ, TETANUS, osteomyelitis, Diagnostics : nan, Differential diagnosis : bacterial infection (sepsis), osteomyelitis, Trauma, disease description : Tropical ulcer is also called tropical phagedaenic (phagedenic) ulcer. This is a painful, rapidly enlarging sore, usually found on the lower limb of an individual living in a hot, humid tropical region.

Trypansomiasis

Disease Name : Trypansomiasis, Symptoms : behavioural disturbances : Behavioral changes, mood swings, and, in some patients, depression., Sleep disorders : Daytime somnolence followed by nighttime insomnia., fever : Intermittent fevers lasting one day to one week. The intervals between fevers can last days or months., Body Ache : General malaise, myalgia, arthralgias, and headache; usually 3 weeks after the bite., Neurological symptoms : Includes persistent headaches, seizures in children., chancre : In stage 1, painful skin chancre appears about 5-15 days after the bite, resolving spontaneously after several weeks., cutaneous symptoms : Transient urticarial, erythematous, or macular rashes 6-8 weeks after onset. Trypanids (ill-defined, centrally pale, evanescent, annular, or blotchy edematous erythematous macules on the trunk)., Signs : lymphadenopathy : Generalized or regional lymphadenopathy - Posterior cervical lymphadenopathy (Winterbottom sign) is characteristic of T brucei gambiense African trypanosomiasis., Treatment : medication : Pentamidine , Suramin sodium , Nifurtimox , Benznidazole , Pentamidine, the recommended drug for first stage T. b. gambiense infection, is available in the United States. The other drugs (suramin, melarsoprol, eflornithine, and nifurtimox when used in combination with eflornithine) used to treat African trypanosomiasis are not commercially available in the United States but can be obtained from CDC., Pathophysiology : A person will get East or West African trypanosomiasis if he or she is bitten by a tsetse fly infected with the Trypanosoma brucei rhodesiense or Trypanosoma brucei gambiense parasite respectively. The proportion of tsetse flies that are infected with these parasites is low. The tsetse fly is found only in rural Africa. Occasionally an infected pregnant woman may pass T. brucei gambiense infection to her baby. Other routes of transmission are possible though rare and poorly documented (sexual, blood transfusion and organ transplantation)., Epidemiology : 0.3%, incidence of gambiense HAT is less than 20, 000 cases., , variable, Currently there are few medically related prevention options for African trypanosomiasis (i.e. no vaccine exists for immunity). Although the risk of infection from a tsetse fly bite is minor (estimated at less than 0.1%), the use of insect repellants, wearing long-sleeved clothing, avoiding tsetse-dense areas, implementing bush clearance methods and wild game culling are the best options to avoid infection available for local residents of affected areas.,,Regular active surveillance, involving detection and prompt treatment of new infections, and tsetse fly control is the backbone of the strategy used to control sleeping sickness. Systematic screening of at-risk communities is the best approach, because case-by-case screening is not practical in endemic regions., Complications : fatigue, anemia, wasting, Diagnostics : CSF EXAMINATION, LYMPH NODE BIOPSY, IgM ELISA, PCR, Giemsa-stained blood films, Differential diagnosis : Ehrlichiosis, Malaria, TYPHOID FEVER, viral hepatitis, yellow fever, disease description : ?Trypanosomiasis is generally used to refer to African human trypanosomiasis, also known as African sleeping sickness. African sleeping sickness is an infectious disease caused by the parasite Trypanosoma brucei gambiense or Trypanosoma brucei rhodesiense and transmitted by the tsetse fly. This disease is distinct from Chagas disease, which is also known as American trypanosomiasis and is caused by Trypanosoma cruzi and transmitted by the Reduuvid insect vector. This activity reviews the evaluation and management of both African and American trypanosomiasis and highlights the role of interprofessional team members in collaborating to provide well-coordinated care and enhance outcomes for affected patients.

Tubal Blockage

Disease Name : Tubal Blockage, Symptoms : hearing disturbances, Hearing loss, tinnitus, vertigo, pain in ear, popping sensation, disturbances of equilibrium, Signs : perforation, Retracted Tympanic Membrane, congestion along the handle of malleus and the pars tensa, transudate behind the tympanic membrane, fluid level with conductive hearing loss, haemorrhages in subepithelial layer, haemotympanum, Treatment : symptomatic treatment and treatment of specific cause, Pathophysiology : Acute Acute tubal blockage Absorption of ME gases Negative pressure in ME Retraction of TM Transudate in ME/haemorrhage (acute OME) Prolonged Prolonged tubal blockage/dysfunction OME (thin watery or mucoid discharge) Atelectatic ear/perforation Retraction pocket/cholesteatoma Erosion of incudostapedial joint Eustachian tube obstruction can be mechanical, functional or both. Mechanical obstruction can result from (i) intrinsic causes such as inflammation or allergy or (ii) extrinsic causes such as tumour in the nasopharynx or adenoids. Functional obstruction is caused by collapse of the tube due to increased cartilage compliance, which resists opening of the tube or failure of active tubal-opening mechanism due to poor function of tensor veli palatini., Epidemiology : GOOD, Complications : hearing disturbances, fullness in ear, Diagnostics : Otoscopy, HSG TEST, Differential diagnosis : CHOLESTEATOMA, CHRONIC OTITIS MEDIA, CHRONIC SUPPURATIVE OTITIS MEDIA(ATTICO ANTRAL), disease description : Normally, eustachian tube is closed. It opens intermittently during swallowing, yawning and sneezing through the active contraction of tensor veli palatini muscle. Air, composed of oxygen, carbon dioxide, nitrogen and water vapour, normally fills the middle ear and mastoid. When tube is blocked, first oxygen is absorbed, but later other gases, CO2 and nitrogen also diffuse out into the blood. This results in negative pressure in the middle ear and retraction of tympanic membrane. If negative pressure is still further increased, it causes “locking” of the tube with collection of transudate and later exudate and even haemorrhagE

Tubercular Meningitis

Disease Name : Tubercular Meningitis, Symptoms : hemiparesis : TBM can lead to paralysis of one side of the body., Neurological symptoms : Headaches and behavioral changes may be noticed initially. Untreated, this disorder can lead to seizures, mental retardation., Stiff neck : Stiff neck is commonly seen in affected people., photophobia : TBM causes intense sensitivity to light., fever with chills : TBM causes fever with chills., Signs : "kernig sign positive : A positive test is the elicitation of pain or resistance with passive extension of the patients knees past 135 degrees in the setting of meningeal irritation.", pupillary dilation : Pupillary involvement may be due to the nerve involvement or due to pressure on the brain stem by dilation of third ventricle., Treatment : medication : Dexamethasone , Rifampicin/Rifampin, Ethambutol , Isoniazid , Pyrazinamide , The treatment of TB meningitis is isoniazid, rifampicin, pyrazinamide and ethambutol for two months, followed by isoniazid and rifampicin alone for a further ten months. Steroids help reduce the risk of death in those without HIV. Steroids can be used in the first six weeks of treatment, , Pathophysiology : The pathophysiology of tuberculous meningitis involves bacterial invasion of the brain parenchyma meninges or cortex, causing the formation of small subpial foci. These foci, termed Rich foci, are necrotic and expand as the colonies within them multiply. Tubercle (focal) rupture in the subarachnoid space causes meningitis., Epidemiology : "Approximately one-third of the worlds population is presumed to be infected with MTB.", 1%–5% of the approximately 10 million cases of TB worldwide., VARIABLE, Treating people who have signs of a non-active (dormant) TB infection can prevent its spread. A PPD test and other TB tests can be done to tell if you have this type of infection.,,Some countries with a high incidence of TB give people a vaccine called BCG to prevent TB. But, the effectiveness of this vaccine is limited, and it is not usually used in the United States. The BCG vaccine may help prevent severe forms of TB, such as meningitis, in very young children who live in areas where the disease is common., Complications : seizures, Stroke, hemiplegia, Diagnostics : CSF EXAMINATION, Erythrocyte Sedimentation Rate (ESR), HISTOPATHLOGY, Total Leucocyte Count (TLC), lumbar puncture, TUBERCULIN SKIN TEST, PCR, CHEST X RAY, NAAT TEST, ANGIOGRAPHY, Differential diagnosis : BACTERIAL MENINGITIS, Meningitis, sepsis, disease description : Tuberculous meningitis (TBM) manifests extrapulmonary tuberculosis caused by the seeding of the meninges with the bacilli of Mycobacterium tuberculosis (MTB). MTB is first introduced into the host by droplet inhalation infecting the alveolar macrophage. The primary infection localizes in the lung with dissemination to the lymph nodes. At this point in the infectious process, a high degree of bacteremia can seed the entire body. In tuberculous meningitis, the meninges are seeded by MTB and form sub-ependymal collections called Rich foci. These foci can rupture into the subarachnoid space and cause an intense inflammatory response that causes meningitis symptoms. The exudates caused by this response can encase cranial nerves and cause nerve palsies. They can entrap blood vessels causing vasculitis, and block cerebral spinal fluid (CSF) flow leading to hydrocephalus. These immune responses can lead to complications associated with tuberculous meningitis and chronic sequela in patients who recover from TBM. 

Tuberculoma

Disease Name : Tuberculoma, Symptoms : blindness, seizures, visual changes, Signs : raised intracranial pressure, Treatment : Antituberculous therapy is recommended for 1 yr ,(2 HRZE + 10 HR) as for tubercular meningitis along with ,corticosteroids for initial 6-8 weeks., Pathophysiology : nan, Epidemiology : fair, Complications : nan, Diagnostics : TUBERCULIN SKIN TEST, MRI, CT SCAN, Differential diagnosis : nan, disease description : Inflammatory granulomas are an important cause of raised intracranial pressure and partial seizures in childhood. These may be tubercular, parasitic, fungal or bacterial in origin. Neurocysticercosis and tuberculomas are the commonest granulomas.

Tuberculosis Of Small Intestine

Disease Name : Tuberculosis Of Small Intestine, Symptoms : Malaise, chronic cough, weight loss, constipation, diarrhea, profuse sweating, Signs : some patients may present with fistula-in-ano, Treatment : medication : Vitamin B6/Metadoxine/Pyridoxine, ANTI TUBERCULAR DRUGS, Symptomatic strictures are treated by the appropriate resection, ,e.g. local ileocolic resection or strictureplasty as an elective,procedure once the disease, Pathophysiology : There are two types : ulcerative and hyperplastic. In both types, there may be marked mesenteric lymphadenopathy. ?? Ulcerative type : When a patient with pulmonary tuberculosis swallows infected sputum, the organism colonises the lymphatics of the terminal ileum, causing transverse ulcers with typical undermined edges. The serosa is usually studded with tubercles. Histology shows caseating granuloma with giant cells This pathological entity, referred to as the ulcerative type, denotes a severe form of the disease in which the virulence of the organism overwhelms host resistance. ?? Hyperplastic type : This occurs when host resistance has the upper hand over the virulence of the organism. It is caused by drinking infected unpasteurised milk. There is a marked inflammatory reaction causing hyperplasia and thickening of the terminal ileum because of its abundance of lymphoid follicles, thus resulting in narrowing of the lumen and obstruction. Macroscopically, this type may be confused with Crohn’s disease. The small intestine shows areas of stricture and fibrosis, most pronounced at the terminal ileum ). As a result, there is shortening of the bowel with the caecum being pulled up into a subhepatic position, Epidemiology : GOOD, Complications : abdomen infection, Diagnostics : CRP, Erythrocyte Sedimentation Rate (ESR), SPUTUM CULTURE, Barium Imaging, USG ABDOMEN(W/A), X RAY CHEST, Interferon-Gamma Release Assays, Differential diagnosis : nan, disease description : Infection by Mycobacterium tuberculosis is common in the tropics. In these days of international travel and increased migration, tuberculosis in general and intestinal tuberculosis in particular are no longer clinical curiosities in non-endemic countries. Any patient, particularly one who has recently arrived from an endemic area and who has features of generalised ill health and altered bowel habit, should arouse suspicion for intestinal tuberculosis. The increased prevalence of human immunodeficiency virus (HIV) infection worldwide has also made tuberculosis more common.

Tuberculosis Of The Breast

Disease Name : Tuberculosis Of The Breast, Symptoms : Redness, DISCHARGE, Signs : abscess, swelling, sinuses, "Lump-irregular ill-defined; Peaud orange", a typical bluish appearance of surrounding skin w(th matted lymph nodes in the ipsilateral axilla, Treatment : medication : Alprostadil , Antituberculous drugs-I NH, rifampicin, ethambutol, pyrazinamide, Drainage of cold abscess., Pathophysiology : Usually associated with active pulmonary tuberculosis. Infection reaches through blood or retrograde lymphatic spread from lymph nodes of axilla. Common in lactation. Nipple and areola are not commonly involved. Lump-irregular ill-defined; Peaud orange; discharge, sinus, matted axillary nodes often with sinus are the features. Presents as a swelling in the breast with cold abscess, sinuses and a typical bluish appearance of surrounding skin w(th matted lymph nodes in the ipsilateral axilla., Epidemiology : It is relatively rare., Complications : nan, Diagnostics : AFB CULTURE, FNAC, Frozen Section, HISTOPATHLOGY, EXCISIONAL BIOPSY, Differential diagnosis : nan, disease description : It may be due to high resistance offered by mammary gland tissue to the survival and multiplication of the tubercle bacillus, a resistance similar to that offered by spleen and skeletal muscle

Tuberculosis Of The Hip

Disease Name : Tuberculosis Of The Hip, Symptoms : hip pain, hip stiffness, hip swelling, fever, weight loss, Signs : hip deformity, Treatment : medication : Methenamine , Rifampicin/Rifampin, Ethambutol , Isoniazid , Pyrazinamide , Streptomycin , Cycloserine , Conservative treatment : It consists of antitubercular,chemotherapy (page 184) and care of,the hip.,• Care of the hip : The affected hip is put to rest by,immobilisation using below-knee skin traction.,In addition to providing pain relief, this also,corrects any deformity by counteracting the,muscle spasm.,• General care, Operative treatment : The following operative,procedures may be indicated in TB of the hip-,• Joint debridement ,• Girdlestone arthroplasty ,• Arthrodesis ,• Corrective osteotomy ,• Total hip replacement, Pathophysiology : Osteoarticular TB is secondary to primary pathology in lungs, lymph nodes or any of the viscera. Through the hematogenous route, the bacteria reach either to synovium or bone. When it lodges first in synovium, the synovial membrane becomes swollen and congested. The granulation tissue from the synovium extends over the bone resulting in necrosis of sub chondral bone, sequetra and may be kissing lesion on either side of joint. The bacteria may also lodge first in the epiphyseal or metaphyseal region of the adjoining bones like head or neck of femur, greater trochanter or acetabulum to start the destructive process. It may start as extra articular or juxta articular lesion. When the disease starts as intraarticular, it progresses fast to involve the whole joint. An extra articular lesion can also progress further to involve the joint. Cold abscess that usually forms within the joint may perforate the capsule to present around the hip joint in the femoral triangle, medial, lateral or posterior aspects of thigh, ischio rectal fossa., Epidemiology : 15% of all cases of osteoarticular TB and is the most frequent site of bone involvement after the spine., not specific, Thorough debridement of infected tissues and postoperative antituberculous chemotherapy are the keys to lowering the potential risk of reactivation of TB., Complications : MUSCLE WASTING, Shortening of the leg, DEFORMITY, Diagnostics : Erythrocyte Sedimentation Rate (ESR), Total Leucocyte Count (TLC), X RAY, MRI PELVIS, Absolute Lymphocyte count, Mantoux test, Differential diagnosis : Coxa vara, Osteoarthritis, pseudogout, PSORIATIC ARTHRITIS, disease description : The TB of hip is still a common condition in developing countries. Early presentations are pain around hip and limp. Later the patient presents with deformities, shortening of limb and restriction of movements. The constitutional symptoms may or may not be present in all the cases.Tuberculosis (TB) of the musculoskeletal system, though accounts for only 1-3% of total TB cases, 1 however, as one fourth of all TB cases are in India, 2 the absolute number of cases with musculoskeletal TB become large. TB of hip constitutes 15-20% of the musculoskeletal system.1 The majority of cases of hip TB are presenting as painful, restricted movements of the hip and there comes, the dilemma of accurate diagnosis as several pathologies may mimic this presentation. For example in children, Perthes disease, juvenile rheumatoid arthritis, transient synovitis, bleeding disorders, pyogenic arthritis etc., has to be differentiated.

Tuberculosis Of The Knee

Disease Name : Tuberculosis Of The Knee, Symptoms : knee pain, knee stiffness, knee swelling, weight loss, Signs : fever, limping, Treatment : medication : Rifampicin/Rifampin, Ethambutol , Isoniazid , Pyrazinamide , Streptomycin , Cycloserine , Ethionamide , Conservative treatment : This consists of,antitubercular chemotherapy, general care and,local care of the part affected. It is started an all,cases and decision for surgery taken if indicated, ,as discussed later.,• Care of the knee : The knee is rested by applying,below-knee skin traction or an above-knee PoP,slab. This helps in the healing process, and also,takes care of the associated muscle spasm which,keeps the knee in a deformed position., Operative treatment : Following operative,procedures may be required in suitable cases : nan,• Synovectomy ,• Joint debridement ,• Arthrodesis, Pathophysiology : The disease may begin in the bone (osseous tuberculosis), usually in the femoral or tibial condyles, or more rarely in the patella. More commonly, the disease begins in the synovial membrane (synovial tuberculosis), leading to hypertrophy of the synovium. In early stages, the disease may be confined to the synovium without significant damage to the joint. Natural history : In later stages, the articular cartilage and bone are destroyed irrespective of the site of origin. In all types, there occurs synovial hypertrophy, synovial effusion and pus formation in the joint. The hypertrophied synovium spreads under and over the cartilage and destroys it. The cartilage may become detached, leaving the bone exposed. Long standing distension of the joint and destruction of the ligaments produces subluxation of the tibia. The tibia flexes, slips backwards and rotates externally on the femoral condyles (triple subluxation). Pus may burst out of the capsule to present as a cold abscess, and subsequently a sinus. Healing : If untreated, natures attempt at healing may result in fibrosis, and thereby stiffness of the joint in a deformed position. Healing is by fibrosis (fibrous ankylosis)., Epidemiology : (8%)., VARIABLE, Early diagnosis,Adequate treatment,reduces chances of dissemination, Complications : erosions, synovitis, Diagnostics : Erythrocyte Sedimentation Rate (ESR), Total Leucocyte Count (TLC), X RAY, CT SCAN, Mantoux test, Differential diagnosis : MALIGNANCY, Septic arthritis, disease description : Diagnosis of tubercular infection of bone and joints depends largely on suspicion of the diagnosis, and in an age where prevalence of the disease is rising, all clinicians should be aware of the potential of the infection. Joint TB may be suspected in a chronic case of joint pain, usually monoarticular. Although pulmonary TB may be absent, patients may demonstrate systemic symptoms of fatigue, lethargy, and weight loss. Pyrexia of unknown origin also may be a presenting feature.

Tuberculosis Of The Spine (potts Disease)

Disease Name : Tuberculosis Of The Spine (potts Disease), Symptoms : back pain : Back pain is the earliest and most common symptom of Pott disease, with patients usually experiencing this problem for weeks before seeking treatment. The pain caused by Pott disease can be spinal or radicular., fever : Potential constitutional symptoms of Pott disease include fever., Neurological symptoms : Neurologic abnormalities occur in 50% of cases and can include spinal cord compression with paraplegia, paresis, impaired sensation, nerve root pain, and/or cauda equina syndrome., "weight loss : Potts disease causes drastic weight loss.", Signs : "paraplegia : Potts disease causes inability to voluntarily move the lower parts of the body.", scoliosis : Scoliosis due to spinal tuberculosis is usually associated with cumulative sagittal and coronal plane imbalance., KYPHOSIS : Spinal tuberculosis is the most common cause of severe kyphosis., Treatment : medication : Rifampicin/Rifampin, Ethambutol , Isoniazid , Pyrazinamide , Streptomycin , Cycloserine , Ethionamide , Care of the affected part : This consists of protection,of the affected part from further damage, correction,of any deformities and prevention of joint,contractures. Once the disease is brought under,control, exercises to regain functions of the joint are,carried out. Care consists of the following : , a) Proper positioning of the joint,b) joint mobilisation,c) muscle strength building exercises, Operative intervention may be required in some cases. Following are some procedures commonly used : 1- biopsy 2- A bigger cold abscess may need aspiration or evacuation 3- Curettage of the lesion 4- Joint debridement 5- Synovectomy 6- Salvage operations 7- Decompression, Pathophysiology : Like tuberculosis of the bones and joints elsewhere in the body, TB of the spine is always secondary. The bacteria reach the spine via the haematogenous route, from the lungs or lymph nodes. It spreads via the para-vertebral plexus of veins i.e., Batsons plexus, which has free communication with the visceral plexus of the abdomen, a common site of tuberculosis. Types of vertebral tuberculosis : Lesions in the vertebrae may be of the following types : a) Paradiscal : This is the commonest type. In this, the contiguous areas of two adjacent vertebrae along with the intervening disc are affected. b) Central : In this type, the body of a single vertebra is affected. This leads to early collapse of the weakened vertebra. The nearby disc may be normal. The collapse may be a ‘wedging’ or ‘concertina’ collapse; wedging being commoner. c) Anterior : In this type, infection is localised to the anterior part of the vertebral body. The infection spreads up and down under the anterior longitudinal ligament. d) Posterior : In this type, the posterior complex of the vertebra i.e., the pedicle, lamina, spinous process and transverse process are affected., Epidemiology : "Potts spine accounts for 2% of all cases of TB, 15% of extrapulmonary, and 50% of skeletal TB.", not specific, "Potts disease can be prevented by controlling the spread of tuberculosis infection. Prevention of pulmonary tuberculosis is essential for the prevention of spinal tuberculosis.,,- BCG vaccination is recommended to all infants living in endemic areas of TB or having a high risk of exposure to TB.,- Travelers should avoid close contact or prolonged time with known TB patients in crowded, enclosed environments.", Complications : abscess, paraplegia, neurological problem, Diagnostics : Erythrocyte Sedimentation Rate (ESR), Antibody Serology Tests, biopsy, ELISA FOR ANTIBODY TITRE, MRI, CT SCAN, Mantoux test, molecular testing, Differential diagnosis : Aspergillosis, Cryptococcus neoformans, TREPONEMA PALLIDUM, disease description : Spinal tuberculosis (TB) or Potts spine is the commonest extrapulmonary manifestation of TB. It spreads through hematogenous route. Clinically, it presents with constitutional symptoms, back pain, tenderness, paraplegia or paraparesis, and kyphotic or scoliotic deformities. 

Tuberculosis Of Urinary Tract

Disease Name : Tuberculosis Of Urinary Tract, Symptoms : flank pain, dysuria, increased frequency of urination, Signs : nan, Treatment : medication : Rifampicin/Rifampin, Ethambutol , Isoniazid , Pyrazinamide , ANTI TUBERCULAR DRUGS, excision of dead tissue, e.g. partial nephrectomy,or nephrectomy, and reconstructive surgery, e.g. for,ureteric strictures, mainly distal ureteric, and surgery to the,bladder such as augmentation cystoplasty., Pathophysiology : Blood-borne organisms are deposited close to the glomeruli causing an inflammatory reaction. Macrophages react and granulomas are formed. If bacterial multiplication is checked, fibrous tissue is formed but if it is unchecked, tubercles result with later caseous necrosis. The healing process produces fibrous tissue and then calcium deposition follows. The lesions will eventually slough causing tuberculous bacilluria. The disease spreads through the collecting system and once a calyx is stenosed it is rare for the communication to be restored. Hypertension is rarely seen except when there is extensive renal destruction. Involvement of the ureter is an extension of renal TB commonly seen at the vesico-ureteric junction. Involvement of the bladder is again secondary to renal disease. It is seen around the ureteric orifice as inflammation, then bullous granulations and later as ulcers. It then progresses to the muscle which is replaced by fibrous tissue. Tubercles are infrequent. Involvement of the testis is usually secondary to epididymitis. Spread to the epididymis is usually blood-borne. The diagnosis is confirmed on a tuberculin test, or at least 3 consecutive early-morning specimens of urine are examined for acid-fast bacilli with a Ziehl–Neelsen stain and subsequently cultured. CT is the most sensitive modality for visualising renal calcifications and CT urography is more sensitive at identifying all manifestations of renal tuberculosis : ?? Early : ?? papillary necrosis (single or multiple) resulting in uneven caliectasis. ?? Progressive : ?? multifocal strictures can affect any part of the collecting system;, Epidemiology : GOOD, Complications : HYDRONEPHROSIS, hypertension, tissue calcification, Diagnostics : CT SCAN, CYSTOURETHROSCOPY, CT Urography, HYSTEROSALPINGOGRAPHY, Differential diagnosis : Acute prostatitis, epididymitis, MALIGNANCY, Urethritis, Urinary Tract Infection, disease description : Genitourinary tuberculosis (GUTB) accounts for 14% of non-pulmonary cases of TB. It is caused by dissemination of the organism through the bloodstream and is thus always secondary TB. There is either reinfection or reactivation of old TB...

Tuberous Sclerosis

Disease Name : Tuberous Sclerosis, Symptoms : behavioural disturbances : Common behavior problems may include hyperactivity, self-injury or aggression, or issues with social and emotional adjustment., "ocular changes : Growths can appear as white patches on the light-sensitive tissue at the back of the eye called the retina. These growths usually dont interfere with vision.", respiratory difficulties : Growths that develop in the lungs may cause coughing or trouble breathing, especially with physical activity or exercise. These lung tumors occur more often in females than in males., seizures : Growths in the brain may be linked with seizures. A seizure is often the first symptom of tuberous sclerosis. In small children, a common type of seizure called infantile spasm involves stiffening of the arms and legs and arching the back and head., dental problem : Teeth may have pits in the surface. Small growths may appear on the gums, inside of the cheeks and on the tongue., Learning difficulty : Tuberous sclerosis can result in developmental delays. Sometimes it limits the ability to think, reason and learn. Mental health conditions, such as autism spectrum disorder or attention-deficit/hyperactivity disorder (ADHD), also can occur., cutaneous symptoms : Skin changes are most common. These include patches of lighter skin and small areas of thickened, smooth or bumpy skin. On the forehead, skin can have raised, discolored areas. Small soft bumps under or around the nails may occur. Growths on the face that start in childhood and look like acne are common., Signs : nan, Treatment : medication : Prednisolone, Early intervention and special needs services can help children with developmental delays and behavior issues adapt to the classroom. This can help them meet their full potential. When needed, social, vocational and rehabilitation services may continue throughout life.,Mental health and behavior issues. Talking with a mental health provider may help people accept and adjust to living with tuberous sclerosis. A mental health provider also can help with behavior, social or emotional issues and suggest resources., "Anti-seizure medicines may be prescribed to control seizures. Other medicines may help manage heart rhythm problems, behavior problems or other symptoms. A medicine called everolimus (Afinitor, Zortress) may be used to treat certain types of brain and kidney growths that cant be removed with surgery. Using these medicines early in care may help reduce the risk of seizures. The topical ointment form of a medicine called sirolimus (Hyftor) may help treat acnelike skin growths.", "If a growth affects the function of a specific organ — such as the kidney, brain or heart — the growth may be removed with surgery. Sometimes surgery helps control seizures caused by brain growths that dont respond to medicine. Surgical procedures such as dermabrasion or laser treatment may improve the appearance of skin growths.", Pathophysiology : Tuberous sclerosis is a genetic disease that may affect almost every organ system. It involves mutations in genes (TSC1 and TSC2) that are responsible for the production of proteins that regulate cell division and growth in the body. When this balance is disrupted by the gene mutations, hamartomas may grow in the brain, skin, heart, kidney, liver, and lungs, affecting the function of these organs.TSC1 and TSC2 Gene MutationsThere are two specific gene mutations : TSC1 mutation occurs on chromosome 9 and is related to hamartin protein production.TSC2 is on chromosome 16 and affects tuberin protein production.It is these genes that are thought to cause the characteristic tumors of the condition. The gene mutation may be inherited or may occur spontaneously. Most cases present sporadically, with no known family history but approximately 1 in 3 patients inherit a defected TSC1 or TSC2 gene. If a parent has tuberous sclerosis, their children will carry a 50% risk of inheriting the disease. It follows an autosomal dominant inheritance pattern, and males and females are equally affected.Hamartin and Tuberin ProteinHamartin and tuberin play a role in a complex that controls cell growth and division in the body. The exact mechanism of pathology that leads to unregulated cell growth and the appearance of tumors is not clear, but it is thought to be due to changes in the signaling of mTOR. The proteins hamartin and tuberin are thought to modulate gene transcription and suppress tumor growth.Affected Areas and OrgansTuberous sclerosis causes tumors to grow in multiple locations. This results in a variation of the severity of the condition between individuals.Skin or nail lesions do not usually cause serious problems but can result in aesthetic effects.Tumors of the brain often cause seizures or developmental delays.Angiomyolipoma and cysts in the kidneys may affect renal function and renal failure may result. Some patients have symptoms similar to polycystic kidney disease, which has similar genetic characteristics.Cardiac rhabdomyomas that present in adults are not usually large enough to cause significant damage but they can be fatal in newborn infants.Pulmonary cysts and lymphangioleiomyomatosis can affect the lungs and are the most common cause of fatality, Epidemiology : approximately 1 in 6000 to 1 in 10, 000 live births, VARIABLE, There is no way to prevent or avoid tuberous sclerosis. If you have a family history of the disease and you want to have children, talk to your doctor. They may refer you to a genetic counselor or medical geneticist., Complications : Epilepsy, Polycystic kidney disease, Renal cell carcinoma, Diagnostics : ECG, EEG, ultrasound, GENETIC TESTING, MRI, CT SCAN, Fluorescence with Wood’s light, Differential diagnosis : Atonic Seizures, Autism spectrum disorder, Rhabdomyoma, seizures, disease description : Tuberous sclerosis (TOO-bur-us skluh-ROH-sis), also called tuberous sclerosis complex (TSC), is an uncommon genetic disorder that causes tumors to develop in many parts of the body. These tumors are not cancer. Noncancerous tumors, also called benign tumors, are overgrowths of cells and tissue that are not expected. Symptoms vary widely, depending on where the growths develop and how big they get.

Tubotympanic Type Of Csom

Disease Name : Tubotympanic Type Of Csom, Symptoms : Hearing loss : Hearing loss in CSOM can result from perforation of the tympanic membrane, disruption of ossicular chain (conductive hearing loss), outer hair cell damage caused by the diffusion of bacterial toxins into the inner ear (sensorineural hearing loss), or both (mixed hearing loss), mucopurulent ear discharge : Chronic otitis media Tubo-tympanic disease is characterized by intermittent episodes of profuse muco-purulent otorrhea. The discharge varies from fetid, purulent, and cheese-like to clear and serous., Signs : nan, Treatment : medication : Neomycin , Gentamicin , Polymyxin B, chloromycetin, Patients are instructed to keep water ,out of the ear during bathing, swimming and hair wash. ,Rubber inserts can be used. Hard nose blowing can also ,push the infection from nasopharynx to middle ear and ,should be avoided, 1. Aural toilet. Remove all discharge and debris from the ,ear. It can be done by dry mopping with absorbent cotton ,buds, suction clearance under microscope or irrigation (not forceful syringing) with sterile normal saline. Ear must be ,dried after irrigation., 1.Ear drops. Antibiotic ear drops containing neomycin, polymyxin, chloromycetin or gentamicin are used. ,They are combined with steroids which have local antiinflammatory effect. To use ear drops, patient lies down ,with the diseased ear up, antibiotic drops are instilled and ,then intermittent pressure applied on the tragus for antibiotic solution to reach the middle ear. This should be ,done three or four times a day.,2.Systemic antibiotics. They are useful in acute exacerbation of chronically infected ear, otherwise role of systemic ,antibiotics in the treatment of CSOM is limited., Surgical treatment. Aural polyp or granulations, if present, should be removed before local treatment with antibiotics. It will facilitate ear toilet and permit ear drops to be used ,effectively. An aural polyp should never be avulsed as it may be ,arising from the stapes, facial nerve or horizontal canal and ,thus lead to facial paralysis or labyrinthitis., Reconstructive surgery. Once ear is dry, myringoplasty ,with or without ossicular reconstruction can be done to ,restore hearing. Closure of perforation will also check ,repeated infection from the external canal., Pathophysiology : The tubotympanic disease remains localized to the mucosa and, that too, mostly to anteroinferior part of the middle ear cleft. Like any other chronic infection, the processes of healing and destruction go hand in hand. The pathological changes seen in this type of CSOM are : 1. Perforation of pars tensa. It is a central perforation and its size and position varies. 2. Middle ear mucosa. It may be normal when disease is quiescent or inactive. It is oedematous and velvety when disease is active. 3. Polyp. A polyp is a smooth mass of oedematous and inflamed mucosa which has protruded through a perforation and presents in the external canal. It is usually pale in contrast to pink, fleshy polyp seen in atticoantral disease. 4. Ossicular chain. It is usually intact and mobile but may show some degree of necrosis, particularly of the long process of incus. 5. Tympanosclerosis. It is hyalinization and subsequent calcification of subepithelial connective tissue. It is seen in remnants of tympanic membrane or under the mucosa of middle ear. It is seen as white chalky deposit on the promontory, ossicles, joints, tendons and oval and round windows. Tympanosclerotic masses may interfere with the mobility of these structures and cause conductive deafness. 6. Fibrosis and adhesions. They are the result of healing process and may further impair mobility of ossicular chain or block the eustachian tube. 1. Ear discharge. It is nonoffensive, mucoid or mucopurulent, constant or intermittent. The discharge appears mostly at time of upper respiratory tract infection or on accidental entry of water into the ear. 2. Hearing loss. It is conductive type; severity varies but rarely exceeds 50 dB.  In long standing cases, cochlea may suffer damage due to absorption of toxins from the oval and round windows and hearing loss becomes mixed type. 3. Perforation. Always central, it may lie anterior, posterior or inferior to the handle of malleus. It may be small, medium or large or extending up to the annulus, i.e. subtotal. 4. Middle ear mucosa. It is seen when the perforation is large. Normally, it is pale pink and moist; when inflamed it looks red, oedematous and swollen. Occasionally, a polyp may be seen., Epidemiology : 39 cases per 100, 000 persons in children and adolescents aged 15 years and younger, VARIABLE, Among the measures needed to prevent CSOM and its complications is a four step initiative known as HEAR—Hygiene of the ear, Early management of AOM, Antibiotics, and Raising awareness, Complications : Brain Abscess, petrositis, THROMBOPHLEBITIS, acute mastoiditis, FACIAL PARALYSIS, SUBDURAL ABSCESS, Diagnostics : Otoscopy, CT SCAN, Audiogram, Audiogram, Differential diagnosis : Acute Otitis Media, CHOLESTEATOMA, foreign body, Herpes Zoster, Langerhans cell histiocytosis (LCH), OTITIS EXTERNA, otitis media with effusiion, petrositis, Wegener granulomatosis, disease description : Chronic suppurative otitis media (CSOM) is a long-standing infection of a part or whole of the middle ear cleft characterized by ear discharge and a permanent perforation.  Tubotympanic. Also called the safe or benign type; it involves anteroinferior part of middle ear cleft, i.e. eustachian tube and mesotympanum and is associated with a central perforation. There is no risk of serious complications. 

Tubular Papillary Adenoma

Disease Name : Tubular Papillary Adenoma, Symptoms : Solitary nodule, Well circumscribed mass, Signs : nan, Treatment : Simple surgical excision., Pathophysiology : Studies hypothesize that the origin is renal tubular progenitor / stem cells.Renal tubular progenitor / stem cells increase upon renal injury or damage.Progenitor cells give rise to papillary adenoma, which in turn could be precursors to papillary RCC., Epidemiology : 40% in patients older than 70 years of age, 10% to 40%, excellent, NA, Complications : post-surgical complications, Diagnostics : ELECTRON MICROSCOPY, Incisional biopsy, Immunostaining, Differential diagnosis : Collecting duct carcinoma, Hidradenoma papilliferum, Metanephric adenoma, Microcystic adnexal carcinoma, Nipple adenoma, Papillary renal cell carcinoma, Syringocystadenoma papilliferum, disease description : Villous/tubulovillous adenomas are benign epithelial tumors usually detected in the colon. They often present by polyps elevated form the mucosa. These, mostly sporadic detected lesions can sometimes be a component of diseases such as familial adenomatous polyposis, Gardner’s syndrome and Peutz-Jegherz syndrome (1, 2). Villous/tubulovillous adenomas are rare in the common bile duct, and similar lesions of this localization are called papillary/tubulopapillary adenoma. General symptoms are bile duct obstruction and jaundice. They may be confused with common bile duct stones and malignant tumors during pre-operative evaluation 

Tubulointerstitial Nephritis

Disease Name : Tubulointerstitial Nephritis, Symptoms : Rashes : If the cause is an allergic reaction, symptoms may include a rash., weight gain : Weight gain occurs due to retaining fluid in different parts of the body leading to edema., fever : Tubulointerstitial Nephritis causes fever., flank pain : If the cause is pyelonephritis, symptoms may include pain in the lower back or side., cognitive impairment : People with severe kidney disease can develop cognitive symptoms like confusion or problems concentrating. These cognitive changes can develop for different reasons, such as damage to the small blood vessels in your brain or due to the buildup of waste products in your blood., Urine output Normal to decreased : When tubulointerstitial nephritis develops suddenly, the amount of urine produced may be normal or less than normal. Sometimes the amount of urine produced is excessive and people urinate more frequently and waken during the night to urinate (nocturia)., Signs : eosinophilia : The presence of eosinophilia (35% of patients) is considered as an another expression of this allergic-type reaction. Eosinophilia is significantly less common in NSAIDs-related AIN than in other types of drug-induced AIN., edema : Acute tubulointerstitial nephritis (ATIN) involves an inflammatory infiltrate and edema affecting the renal interstitium that often develops over days to months., hematuria : Urinalysis may show microscopic hematuria and/or sterile pyuria (with or without eosinophils)., Treatment : medication : Furosemide , Aside from steroid therapy, mycophenolate mofetil has been proposed as a possible treatment option in TIN., Current recommendations favor the use of oral prednisone in children,whose kidney function fails to improve after stopping the suspected agent.,Intravenous methylprednisolone is used in severe cases. Mycophenolate mofetil,has been found to be beneficial in steroid-unresponsive cases, Pathophysiology : Acute interstitial inflammatory reactions are associated with damage to the tubulointerstitium, leading to AKI associated with TIN. The high metabolic demand of the tubulointerstitium makes it particularly susceptible to injury because the inflammation and associated edema compromise renal blood flow, causing a decrease in glomerular filtration rate (GFR). In some situations, damage may lead to fibrosis., Epidemiology : TIN accounts for 2 % of native renal biopsies and up to 27 % of cases of unexplained kidney disease in adult patients, VARIABLE, "Often, the disorder cant be prevented. Avoiding or reducing your use of medicines that can cause this condition can help reduce your risk. If needed, your provider will tell you which medicines to stop or reduce.", Complications : Renal failure, Renal tubular acidosis, Diagnostics : Complete Blood Count CBC, Renal Biopsy, SERUM Creatinine, CT Abdomen, kidney function test KFT, Urine analysis, Urine analysis, Renal ultrasonography, Differential diagnosis : acute tubular necrosis(Kidney), Glomerulonephritis, URINARY TRACT OBSTRUCTION, disease description : Tubulointerstitial nephritis (TIN) is a group of immune-mediated inflammatory diseases that involves the interstitium and tubules. Inflammation of the kidney consists of the collection of inflammatory cells, fluid, and extracellular matrix surrounding the interstitium, along with the infiltration of tubular cells by inflammatory cells that define both tubules and interstitium pathology. It is one of the most important and major causes of acute kidney injury that subsequently leads to renal failure.

Tubulovillous Adenoma

Disease Name : Tubulovillous Adenoma, Symptoms : diarrhea : A large surface area of the villous adenomas further causes increased fluid secretion, which exceeds the reabsorption ability of the remaining normal rectal mucosa, resulting in chronic watery diarrhea., weight loss : Unintentional weight loss., Abdominal Pain : Polyps that are greater than 1 cm are more likely to cause symptoms like abdominal cramps., Signs : nan, Treatment : Endoscopic resection.,When possible, en bloc resection should be the goal for the management., Pathophysiology : Conventional adenoma carcinoma sequence with oncogene (KRAS) activation and tumor suppressor (APC,  SMAD4 and TP53) inactivation.Associated with chromosomal unstable colorectal cancer., Epidemiology : incidence of less than 1% of all duodenal tumors., VARIABLE, NA, Complications : rectal bleeding, Diagnostics : colonoscopy, Cytogenetics, Immunostaining, Differential diagnosis : Adenomas : Tubular adenoma, Lactating adenoma, Apoc, Cowden disease, inflammatory polyps, disease description :  Tubulovillous adenomas have between 25 and 75% villous features. Less than 25% villous features indicate a tubular adenoma. Adenomas are usually asymptomatic and found on routine colorectal cancer screening. Adenomas with villous features may be associated with a slight increase in the development of more advanced neoplasia or dysplasia compared to other types of adenomas

Tularemia

Disease Name : Tularemia, Symptoms : flu-like symptoms : Most cases of tularemia begin with rapid onset of nonspecific, flu-like symptoms including fever, chills, headaches, muscle pain (myalgia), joint pain (arthralgia), loss of appetite, and a general feeling of ill health (malaise)., organ damage : Tularemia has the potential to affect various organ systems of the body including the central nervous system, heart, and liver resulting in inflammation of the membranes surrounding the brain and spinal cord (meningitis), inflammation of the lining of the heart (endocarditis), and inflammation of the liver (hepatitis)., Oropharyngeal disorder : Infection through breathing in (inhalation) the bacterium may result in infection of the lungs (pneumonia), a collection of fluid around the lungs (pleural effusion), and lung abscesses. These cases are referred to as pneumonic tularemia. Eating undercooked, infected animal meat or drinking contaminated water may result in sore throat, nausea, vomiting, diarrhea, and abdominal pain. These cases are referred to as oropharyngeal tularemia. In rare cases, gastrointestinal bleeding may occur., cutaneous symptoms : . Infection through skin (e.g., tick bite or handling of infectious matter) may result in an ulcer or rash on the skin at the point of infection and swollen, painful lymph nodes (lymphadenopathy). These cases may be referred to as ulceroglandular tularemia. In some cases, individuals will have lymphadenopathy without any skin symptoms., Ocular symptoms : Tularemia can also affect the eyes resulting in inflammation of the delicate membrane that lines the eyes (conjunctiva), a condition called conjunctivitis. Conjunctivitis can cause pain, redness, and itching of the eyes. Nearby lymph nodes may be swollen and painful. These cases are referred to oculoglandular tularemia., Signs : nan, Treatment : medication : Doxycycline , Gentamicin , Streptomycin , Tetracycline , Gentamicin\t5 mg/kg IM or IV daily (with desired peak serum levels of at least 5 mcg/mL),,Ciprofloxacin\t400 mg IV or 500 mg PO twice daily,,Doxycycline\t100 mg IV or PO twice daily, Pathophysiology : F. tularensis is an obligate intracellular pathogen that enters and replicates within the cytoplasm of various host cells, including (but not limited to) macrophages, dendritic cells, and polymorphonuclear neutrophils. Upon entry into the human body, the organism multiplies locally, producing a skin ulcer after skin entry or destruction of bronchial tissues after inhalation and then spreading to local lymph nodes. Systemic spread can follow, with infected cells disseminating throughout the host to the liver, spleen, and lungs. Uncontrolled replication of F. tularensis leads to cell death, substantial tissue damage, and impairment of vital organs. The ability of F. tularensis to survive and replicate within host cells is essential for the development of tularemia. The bacterium does not produce toxins. By evading recognition by the innate immune system, F. tularensis can enter and proliferate within host cells. The atypical lipopolysaccharide of F. tularensis plays a key role in this process, exhibiting reduced endotoxicity and therefore failing to stimulate the host’s innate immunity. Rapid bacterial growth within host cells, followed by cell death, triggers a systemic inflammatory reaction that overwhelms the host defense system, culminating in extensive tissue injury. Inflammatory cell infiltration and various degrees of necrosis are histopathologic hallmarks of lymph node involvement. In the early stages of disease, infected lymph nodes may be characterized by follicular hyperplasia and inflammatory cell infiltration, whereas granulomatous lesions with areas of focal caseous necrosis, which may resemble tuberculous nodes (granulomatous form), are detected later in disease., Epidemiology : was highest in Wyoming (35.8 cases per 1 million population), far higher than the national average of 1 case per 1 million population in 2015, tenfold higher among some Native American populations, presumably because of higher rates of exposure., good, You can protect yourself by : ,,Not using bare hands to skin or dress wild animals,Avoiding sick or dead animals,Wearing clothing that covers exposed skin (tight at the wrists and ankles),Using insect repellents,Removing ticks promptly,Drinking clean water,Fully cooking wild meats, Complications : Meningitis, pericarditis, PNEUMONIA, osteomyelitis, Diagnostics : LYMPH NODE BIOPSY, BLOOD CULTURE, SEROLOGIC TEST, MICROSCOPIC AGGLUTINATION TEST, HISTORY TAKING, Differential diagnosis : Chlamydial Infections, diphtheria, "lymes disease", Malaria, Psittacosis, disease description : Tularemia, also known as rabbit fever, is an infectious disease caused by the bacterium Francisella tularensis.Symptoms may include fever, skin ulcers, and enlarged lymph nodes. Occasionally, a form that results in pneumonia or a throat infection may occur.The bacterium is typically spread by ticks, deer flies, or contact with infected animals. It may also be spread by drinking contaminated water or breathing in contaminated dust. It does not spread directly between people.Diagnosis is by blood tests or cultures of the infected site.Prevention is by using insect repellent, wearing long pants, rapidly removing ticks, and not disturbing dead animals.Treatment is typically with the antibiotic streptomycin. Gentamicin, doxycycline, or ciprofloxacin may also be used.

Tumor Lysis Syndrome

Disease Name : Tumor Lysis Syndrome, Symptoms : fatigue, hallucinations, loss of appetite, muscle cramps, muscle spasm, nausea, Numbness, palpitations, seizures, vomiting, flank pain, DARK URINE, Urine output-DECREASED, Signs : Hypocalcemia, Renal failure, Tetany, acidosis, hyperkalemia, Hyperphosphataemia, hyperuricemia, Ventricular arrhythmia, Treatment : medication : Allopurinol , Febuxostat, Urate Oxidase/Rasburicase/Pegloticase, HEMODIALYSIS, The standard preventive,approach consists of allopurinol and aggressive hydration. Intravenous allopurinol may be given in patients who cannot tolerate,oral therapy. Febuxostat, a potent nonpurine selective xanthine,oxidase inhibitor, is indicated for treatment of hyperuricemia. Rasburicase acts rapidly, decreasing uric acid levels within hours;,however, it may cause hypersensitivity reactions such as bronchospasm, ,hypoxemia, and hypotension. Rasburicase should also be,administered to high-risk patients for TLS prophylaxis., Pathophysiology : TLS is most often associated with the treatment of Burkitt’s lymphoma, acute lymphoblastic leukemia, and other rapidly proliferating lymphomas, but it also may be seen with chronic leukemias and, rarely, with solid tumors. This syndrome has been seen in patients with chronic lymphocytic leukemia after treatment with nucleosides like fludarabine and is increased in frequency in lymphoid neoplasms treated with venetoclax, a bcl-2 antagonist. TLS has been observed with administration of glucocorticoids, hormonal agents such as letrozole and tamoxifen, and monoclonal antibodies such as rituximab and gemtuzumab. TLS usually occurs during or shortly (1–5 days) after chemotherapy. Rarely, spontaneous necrosis of malignancies causes TLS. Hyperuricemia may be present at the time of chemotherapy. Effective treatment kills malignant cells and leads to increased serum uric acid levels from the turnover of nucleic acids. Owing to the acidic local environment, uric acid can precipitate in the tubules, medulla, and collecting ducts of the kidney, leading to renal failure. Lactic acidosis and dehydration may contribute to the precipitation of uric acid in the renal tubules. The finding of uric acid crystals in the urine is strong evidence for uric acid nephropathy. The ratio of urinary uric acid to urinary creatinine is >1 in patients with acute hyperuricemic nephropathy and <1 in patients with renal failure due to other causes. Hyperphosphatemia, which can be caused by the release of intracellular phosphate pools by tumor lysis, produces a reciprocal depression in serum calcium, which causes severe neuromuscular irritability and tetany. Deposition of calcium phosphate in the kidney and hyperphosphatemia may cause renal failure. Potassium is the principal intracellular cation, and massive destruction of malignant cells may lead to hyperkalemia., Epidemiology : 4.8%, Its incidence in patients with HMs varies from 30% to 69% depending on the relative proportions of patients with leukemia, lymphoma, and MM, VARIABLE, Hydration, electrolyte abnormalities, and renal replacement therapy,In patients with intermediate and high risk for TLS, vigorous hydration and assessment of fluid balance to keep urinary output >100 mL/h 24 hours before starting chemotherapy and through the duration of treatment are the key to management., Complications : cardiac arrhythmia, seizures, Uremia, oliguria in acute or chronic renal failure, Diagnostics : BLOOD UREA NITROGEN ( BUN ), Complete Blood Count CBC, LDH, Total Leucocyte Count (TLC), SERUM URIC ACID, ECG, serum potassium K+, serum calcium Ca++, CT SCAN, serum phosphate, URINE ANALYSIS (Volume), PHYSICAL EXAMINATION, Differential diagnosis : Gout, hypertension, insulin Resistance, Obesity, renal insufficiency, disease description : Tularemia, also known as rabbit fever, is an infectious disease caused by the bacterium Francisella tularensis.Symptoms may include fever, skin ulcers, and enlarged lymph nodes.Occasionally, a form that results in pneumonia or a throat infection may occur.The bacterium is typically spread by ticks, deer flies, or contact with infected animals. It may also be spread by drinking contaminated water or breathing in contaminated dust.  It does not spread directly between people.8 Diagnosis is by blood tests or cultures of the infected site.Prevention is by using insect repellent, wearing long pants, rapidly removing ticks, and not disturbing dead animals.Treatment is typically with the antibiotic streptomycin.Gentamicin, doxycycline, or ciprofloxacin may also be used.

Turners Syndrome

Disease Name : Turners Syndrome, Symptoms : chest deformity : A broad chest with widely spaced nipples may occur, which is sometimes referred to as “shield chest.”, "scoliosis : Turners Syndrome is a common congenital disorder caused by a missing X chromosome that presents with scoliosis.", Cubitus valgus deformity : Cubitus valgus (increased carrying angle) in a patient with Turner syndrome. The carrying angle of the elbow averages about 12 degrees in the general female population, and can be 20 to 30 degrees or more in patients with Turner syndrome., web neck : Obvious physical stigmata such as neck webbing affect only approximately 20% of girls with Turner syndrome (TS). The presence of neck webbing and shield crest are indicative of fetal lymphedema and highly correlated with congenital cardiovascular defects., short stature : The main symptom of Turner syndrome is short stature. Almost all females with TS grow more slowly than their peers during childhood and adolescence. Have delayed puberty and lack of growth spurts, resulting in an average adult height of 4 feet, 8 inches., Ocular symptoms : The most common impairments include refractive errors, strabismus, and amblyopia, Signs : nan, Treatment : medication : Oestradiol/Oestrogen, Somatropin , Pathophysiology : Approximately one-half of women with TS have a 45, X karyotype, about 20% have 45, X/46, XX mosaicism, and the remainder have structural abnormalities of the X chromosome such as X fragments, isochromosomes, or rings. The clinical features of TS result from haploinsufficiency of multiple X chromosomal genes (e.g., short stature homeobox, SHOX). However, imprinted genes also may be affected when the inherited X has different parental origins., Epidemiology : Turner syndrome is seen in about 1 in 2000 to 1 in 2500 live female births., fair, You can’t prevent Turner syndrome. It’s a congenital problem. It happens when a random error results in a missing or incomplete X chromosome. Parents can’t do anything to stop this error from happening., Complications : Aortic Dissection, Hearing loss, Hypothyroidism, neurocognitive disorders, diabetes mellitus, Diagnostics : Thyroid Stimulating Hormone TSH, Karyotype, GONADOTROPIN LEVEL, Differential diagnosis : Noonan syndrome, disease description : Turner syndrome, a condition that affects only females, results when one of the X chromosomes (sex chromosomes) is missing or partially missing. Turner syndrome can cause a variety of medical and developmental problems, including short height, failure of the ovaries to develop and heart defects.Turner syndrome may be diagnosed before birth (prenatally), during infancy or in early childhood. Occasionally, in females with mild signs and symptoms of Turner syndrome, the diagnosis is delayed until the teen or young adult years.Girls and women with Turner syndrome need ongoing medical care from a variety of specialists. Regular checkups and appropriate care can help most girls and women lead healthy, independent lives.

Typhoid Fever

Disease Name : Typhoid Fever, Symptoms : chills : "chills" in the context of typhoid fever, they\re likely referring to one of the common symptoms of the disease. Typhoid fever is caused by the bacterium Salmonella enterica serotype, diarrhea : In the context of typhoid fever, diarrhea can be severe and persistent, sometimes becoming bloody. This diarrhea is a result of the infection affecting the intestines, leading to inflammation and disruption of normal bowel function., headache : The headache in typhoid fever is often described as a generalized, persistent headache that can be quite severe., Abdominal Pain, anorexia : In the context of typhoid fever, anorexia can be a significant feature. Typhoid fever is caused by the bacterium Salmonella enterica serotype Typhi. It primarily spreads through contaminated food and water and is common in areas with poor sanitation., "vomiting : Vomiting can occur in the context of typhoid fever, although its not as common as some other symptoms like high fever, abdominal pain, and diarrhea. Typhoid fever is caused by the bacterium Salmonella Typhi, which primarily spreads through contaminated food and water.", fever, loose motion : Typhoid fever is caused by the bacterium Salmonella typhi, primarily spread through contaminated food and water., loss of appetite, nausea, Signs : Bradycardia : Bradycardia in the context of typhoid fever is generally a sign of a more severe infection or complications, especially if accompanied by other symptoms such as chest pain, dizziness, or fainting., epistaxis : Epistaxis, or nosebleeds, can occur in the context of typhoid fever, although it\s not a common symptom of the disease. Typhoid fever is primarily characterized by high fever, abdominal pain, headache, and a rash known as "rose spots." It\s caused by the bacterium Salmonella typhi, usually transmitted through contaminated food or water., Rashes : Rashes in the context of typhoid fever are not a typical symptom. Typhoid fever is primarily characterized by symptoms such as high fever, headache, stomach pain, weakness, and loss of appetite. Rashes are more commonly associated with other conditions like viral infections, allergic reactions, or certain bacterial infections like scarlet fever or meningitis., rose spots : In the context of typhoid fever, rose spots typically develop around the second week of illness. They are a characteristic sign that helps healthcare providers diagnose the disease. However, not all individuals with typhoid fever will develop rose spots, so other symptoms such as high fever, headache, weakness, abdominal pain, , splenomegaly : . In the context of typhoid fever, splenomegaly is a common finding. The spleen plays a crucial role in the immune response, particularly in filtering blood and removing old or damaged red blood cells., HEPATOMEGALY : in the context of typhoid fever. Typhoid fever is caused by the bacterium Salmonella enterica serotype Typhi, which primarily affects the gastrointestinal system but can also involve other organs, including the liver., Treatment : medication : Sulfamethoxazole and Trimethoprim (Co-trimoxazole), Amoxicillin and Clavulanic acid , Ceftriaxone , Azithromycin , "Fluoroquinolones. These antibiotics, including ciprofloxacin (Cipro), may be a first choice. They stop bacteria from copying themselves. But some strains of bacteria can live through treatment. These bacteria are called antibiotic resistant.,Cephalosporins. This group of antibiotics keeps bacteria from building cell walls. One kind, ceftriaxone, is used if there is antibiotic resistance.,Macrolides. This group of antibiotics keeps bacteria from making proteins. One kind called azithromycin (Zithromax) can be used if there is antibiotic resistance.,Carbapenems. These antibiotics also prevent bacteria from building cell walls. But they focus on a different stage of that process than the cephalosporins. Antibiotics in this category may be used with severe disease that doesnt respond to other antibiotics.", exteriorisation, closure of the perforation,and side-to-side ileotransverse anastomosis, ileostomy,or colostomy where the perforated bowel is exteriorised after refashioning the edges, Pathophysiology : Enteric fever is a misnomer, in that the hallmark features of this disease—fever and abdominal pain—are variable.  S. Paratyphi A is thought to cause milder disease than S. Typhi, with predominantly gastrointestinal symptoms. Early physical findings of enteric fever include rash (“rose spots”; 30%), hepatosplenomegaly (3–6%), epistaxis, and relative bradycardia at the peak of high fever (<50%). Rose spots make up a faint, salmon-colored, blanching, maculopapular rash located primarily on the trunk and chest. The rash is evident in ~30% of patients at the end of the first week and resolves without a trace after 2–5 days. Patients can have two or three crops of lesions, and Salmonella can be cultured from punch biopsies of these lesions. The faintness of the rash makes it difficult to detect in highly pigmented patients. The development of severe disease (which occurs in ~10–15% of patients) depends on host factors (host genetics, immunosuppression, acid suppression therapy, previous exposure, and vaccination), strain virulence and inoculum, and choice of antibiotic therapy. Gastrointestinal bleeding (10–20%) and intestinal perforation (1–3%) most commonly occur in the third and fourth weeks of illness and result from hyperplasia, ulceration, and necrosis of the ileocecal Peyer’s patches at the initial site of Salmonella infiltration . , Epidemiology : 21–27 million cases, EXCELLENT, The best way to reduce your risk of typhoid fever is to get vaccinated if you live in or are traveling to an area where it’s common. Hand washing and safe food handling are also important for limiting the spread of typhoid., Complications : internal bleeding, shock, Perforation of bowel, Diagnostics : BONE MARROW ASPIRATION, STOOL CULTURE, Total Leucocyte Count (TLC), TYPHIDOT IgG, WIDAL TEST, BLOOD CULTURE, HISTORY TAKING, Differential diagnosis : Amebiasis, Dengue, giardiasis, Leptospirosis, Malaria, disease description : Typhoid fever, also known as typhoid, is a disease caused by Salmonella serotype Typhi bacteria. Symptoms vary from mild to severe, and usually begin six to 30 days after exposure. Often there is a gradual onset of a high fever over several days.This is commonly accompanied by weakness, abdominal pain, constipation, headaches, and mild vomiting. Some people develop a skin rash with rose colored spots. In severe cases, people may experience confusion. Without treatment, symptoms may last weeks or months.Diarrhea may be severe, but is uncommon.Other people may carry it without being affected, but are still contagious. Typhoid fever is a type of enteric fever, along with paratyphoid fever. S. enterica Typhi is believed to infect and replicate only within humans.

Typical Abscence Seizures

Disease Name : Typical Abscence Seizures, Symptoms : LOSS OF CONSIOUSNESS : Absence seizures involve brief, sudden lapses of consciousness., blank stare : An absence seizure causes you to blank out or stare into space for a few seconds., Signs : rapid blinking of the eyelids : Rapid bilateral eye blinking (RBEB) is commonly seen during generalized absence seizures., Treatment : medication : Valproic acid(sodium valproate)/ Divalproex Sodium, The first line of treatment is with valproic acid or lamotrigine. Though ethosuximide may be helpful for absence seizures, it is not effective for generalized tonic-clonic seizures and, therefore, not the first line of treatment for a patient with both absence seizures and generalized tonic-clonic seizures.,,In view of the side-effects of valproic acid, such as teratogenicity and weight gain, it has to be used with caution in young female patients. Therefore lamotrigine may be the preferred agent in this group of patients. ,,Juvenile absence epilepsy is typically a pharmaco-responsive epilepsy syndrome but some medications may exacerbate seizures such as phenytoin, carbamazepine, oxcarbazepine, gabapentin, pregabalin, and vigabatrin, Pathophysiology : The relationship between genetic variation in the T-type calcium channel gene CACNA1H and childhood absence epilepsy is well established. Novel variants in the CACNA1H alter channel properties contributing to an individuals susceptibility to juvenile absence epilepsy but not sufficient to cause epilepsy on their own., Epidemiology : absence epilepsy prevalence was estimated to be 0.1 per 1000 persons by one study, VARIABLE, Unfortunately, there isn’t a way to prevent absence seizures, since genetics are thought to play a role in their cause., Complications : drowning, Learning difficulty, cognitive impairment, Diagnostics : EEG, MRI Brain, Differential diagnosis : Benign childhood epilepsy with centrotemporal spik, Childhood absence epilepsy, Juvenile Myoclonic Epilepsy, disease description : Typical absence seizures are characterized by sudden, brief lapses of consciousness without loss of postural control. The seizure usually lasts for only seconds, consciousness returns as suddenly as it was lost, and there is no postictal confusion. Although the brief loss of consciousness may be clinically inapparent or the sole manifestation of the seizure discharge, absence seizures are usually accompanied by subtle, bilateral motor signs such as rapid blinking of the eyelids, chewing movements, or small-amplitude, clonic movements of the hand

Ulcerative Colitis

Disease Name : Ulcerative Colitis, Symptoms : nausea, diarrhea : During an IBD flare, the lining of the intestine becomes inflamed and cannot absorb all fluid. This results in stools being loose and watery, or even entirely liquid. The looser stool can also move more rapidly through the colon, causing more frequent bowel movements., vomiting : People are more likely to experience nausea and vomiting if they have severe ulcerative colitis or if the condition involves more of the large intestine., fever : Fever is present in 40% of patients at the time of presentation., blood in stool : Rectal bleeding is a common symptom of UC. The condition causes small ulcerations in the lining of the large intestine, which then leads to blood appearing in the stools. Ulcers in the lining of the rectum and large intestine can also cause bloody stools., "weight loss : UC can affect a persons ability to digest food properly and absorb nutrients from it. Due to this, it can lead to serious vitamin deficiencies and malnutrition. Both of these effects can cause a person with UC to lose weight.", Abdominal Pain : The colon develops ulcers (open sores) that produce blood, pus, and mucus. The small intestine is rarely affected. The combination of inflammation and ulcers often causes abdominal discomfort, frequent bowel movements, and bloody stools., "Malaise : Fatigue is caused by the bodys response to inflammation in the colon.", Signs : Tenderness in lower abdomen, tenesmus : Up to 30% of people with ulcerative colitisexperience some tenesmus. In these cases, rectal tenesmus is a side effect of chronic inflammation in the lower bowel., "SACROILITIS : You may be more likely to have sacroiliitis if ulcerative colitis affects a large part of your colon or youve lived with IBD for many years.", anorexia, PRIMARY SCLEROSING CHOLANGITIS : A majority of people with primary sclerosing cholangitis also have inflammatory bowel disease, such as ulcerative colitis., Treatment : medication : Mercaptopurine, Infliximab, Sulfasalazine, Azathioprine , Mesalazine, Probiotics/Lactic-acid producing organisms, Rehydration,Supplementation of nutritional deficiencies (e.g., iron),Supplementation of nutrition : severe cases may warrant consideration of a feeding tube or parenteral nutrition, Colectomy is curative in patients with ulcerative colitis since the disease is restricted to the colon. Indications for surgery are a failure of medical therapy, intractable fulminant colitis, toxic megacolon, perforation, uncontrollable bleeding, intolerable side effects of medications, strictures, unresectable high-grade or multifocal dysplasia, cancer, or growth retardation in children. The procedure of choice is proctocolectomy with ileal pouch-anal anastomosis (IPAA); however, in patients who are ineligible for IPAA proctocolectomy with ileostomy is a viable alternative., Pathophysiology : UC is a mucosal disease that usually involves the rectum and extends proximally to involve all or part of the colon. About 40–50% of patients have disease limited to the rectum and rectosigmoid, 30–40% have disease extending beyond the sigmoid but not involving the whole colon, and 20% have a total colitis. Proximal spread occurs in continuity without areas of uninvolved mucosa. When the whole colon is involved, the inflammation extends 2–3 cm into the terminal ileum in 10–20% of patients. The endoscopic changes of backwash ileitis are superficial and mild and are of little clinical significance. Although variations in macroscopic activity may suggest skip areas, biopsies from normalappearing mucosa are usually abnormal. Thus, it is important to obtain multiple biopsies from apparently uninvolved mucosa, whether proximal or distal, during endoscopy. One caveat is that effective medical therapy can change the appearance of the mucosa such that either skip areas or the entire colon can be microscopically normal. With mild inflammation, the mucosa is erythematous and has a fine granular surface that resembles sandpaper. In more severe disease, the mucosa is hemorrhagic, edematous, and ulcerated long-standing disease, inflammatory polyps (pseudopolyps) may be present as a result of epithelial regeneration. The mucosa may appear normal in remission, but in patients with many years of disease it appears atrophic and featureless, and the entire colon becomes narrowed and shortened. Patients with fulminant disease can develop a toxic colitis or megacolon where the bowel wall thins and the mucosa is severely ulcerated; this may lead to perforation. Histologic findings correlate well with the endoscopic appearance and clinical course of UC. , Epidemiology : Worldwide, the highest incidence and prevalence of inflammatory bowel diseases are seen in Northern Europe and North America, Ulcerative colitis has a bimodal pattern of incidence. The main onset peaks between the age of 15 and 30 years. A second, and the smaller peak of incidence occurs between the age of 50 and 70 years., GOOD, When you’re in remission from ulcerative colitis, you’ll want to do everything you can to prevent a flare-up. Things that may cause a flare-up include : ,,Emotional stress : Get at least seven hours of sleep a night, exercise regularly and find healthy ways to relieve stress, such as meditation.,NSAID use : For pain relief or a fever, use acetaminophen (Tylenol®) instead of NSAIDs like Motrin® and Advil®.,Antibiotics : Let your healthcare provider know if antibiotics trigger your symptoms.,,Keep a careful eye on your child’s diet and nutrition. Their appetite may decrease during a flare-up and they might not eat enough to stay healthy and grow., Complications : Colorectal cancer, peritonitis, Toxic megacolon, Diagnostics : CRP, Erythrocyte Sedimentation Rate (ESR), Hb, HISTOPATHLOGY, colonoscopy, biopsy, X RAY, CT SCAN, flexible sigmoidoscopy, BACTERIOLOGY, Differential diagnosis : colon cancer, Crohn disease, Toxic megacolon, TUBERCULOSIS, viral gastroenteritis, disease description : Ulcerative colitis (UC) is an inflammatory bowel disease (IBD) characterized by chronic mucosal inflammation of the colon and cecum. Common symptoms include bloody diarrhea, abdominal pain, and fever. Laboratory findings typically show elevated inflammatory markers and the presence of autoantibodies (pANCA)

Undescended Testis

Disease Name : Undescended Testis, Symptoms : Absence of testis in the scrotum, asymptomatic initially., Signs : Non palpable testis, infertility, decreased scrotal folds/rugae, Treatment : orchidopexy,Surgery is recommended for congenital undescended testes between the ages of 6 and 18 months (AUA Guidelines)., Pathophysiology : One contributing mechanism for the reduced function of cryptorchid testes is temperature. It is also likely that transient hormone deficiencies may lead to a lack of testicular descent and impair the development of spermatogenic tissue., Epidemiology : 4 % BOYS, GOOD, There is no known way to prevent this condition., Complications : SEMINOMA, infertility, increased risk of infection or malignancy, Diagnostics : MRI, CT SCAN, USG, Laproscopy, Differential diagnosis : Ectopic testis, Retractile testes, vanishing testis, disease description : Undescended testicles (also known as cryptorchidism) is a condition in which one or both of a baby boys testicles (testes) have not moved down into their proper place in the scrotum.Undescended testicles move down on their own in about half of these babies by the time theyre 6 months old. If they dont, its important to get treatment. The testicles make and store sperm, and if they dont descend they could become damaged. This could affect fertility later in life or lead to other medical problems.

Undifferentiated Carcinoma With Osteoclast-like Gi

Disease Name : Undifferentiated Carcinoma With Osteoclast-like Gi, Symptoms : back pain, fatigue, nausea, weight loss, Abdominal Pain, Signs : anorexia, jaundice, Treatment : UC-OGC has a propensity to invade adjacent structures, although, complete resection of the tumor can prove curative when the tumor is limited to the pancreas., Pathophysiology : There is much debate in the literature as to the origin of the tumor, with many authors favoring mesenchymal origin, and others favoring epithelial origin. Consensus appears to be leaning toward an epithelial origin with some authors purporting that components of vimentin-positive carcinoma are mesenchymal transition from ductal cells. In reported cases, cytokeratin-positive ductal structures have been reported to comprise < 5% to 80% of the tumor. In a study by Luchini et al.,  it was purported that UC-OGC’s are variants of pancreatic ductal carcinoma (PDC) due to the presence of shared mutations in KRAS and other critical tumor suppressor genes commonly associated with PDC (TP53, CDKN2A and SMAD4)., Epidemiology : twice as likely to occur in females as in males, It constitutes less than 1% of pancreatic non-endocrine neoplasia, VARIABLE, Complications : nan, Diagnostics : CA 19.9, Endoscopic USG, Immunostaining, Differential diagnosis : Melanoma, Paraduodenal (groove) pancreatitis, disease description : Undifferentiated carcinoma of the pancreas with osteoclast-like giant cells (UC-OGC) is a rare and poorly described pancreatic malignancy. It is comprised of mononuclear, pleomorphic, and undifferentiated cells as well as osteoclast-like giant cells (OGC’s). This tumor can have a variable mix of anaplastic, sarcomatoid, and giant cell components. Undifferentiated carcinoma with osteoclast-like giant cells contains 2 cell populations : Large atypical multinucleated or mononuclear malignant cells and benign osteoclast-like giant cells .

Undifferentiated Endometrial Sarcoma

Disease Name : Undifferentiated Endometrial Sarcoma, Symptoms : vaginal bleeding : Abnormal vaginal bleeding between menstrual periods., Vaginal Discharge : Vaginal discharge that doesn’t improve with medication., Abdominal Pain : Patients typically present with abdominal pain., abdominal fullness : A feeling of abdominal fullness is typical in undifferentiated endometrial sarcoma., pelvic mass : Uterine cancer begins when healthy cells in the uterus change and grow out of control, forming a mass called a tumor., Signs : nan, Treatment : Adjuvant chemotherapy (gemcitabine / docetaxel or doxorubicin based regimens) is standard,Additional chemotherapy regimens may be used for recurrent / progressive disease,Response to chemotherapy is generally short lived, Complete surgical excision is first line treatment, if possible, Pathophysiology : The common acute lymphoblastic leukemia antigen (CALLA or CD10), a 90 to 110-kDa membrane-bound endopeptidase, is expressed on the cell surface of most cases of acute lymphoblastic leukemia, other types of leukemia, as well as lymphomas and nonhematopoietic neoplasms. This cell surface enzyme reduces cellular response to peptide hormones by regulating local peptide concentration. Thus, many hormone-sensitive and peptide-sensitive cells as well as their corresponding neoplasms express CD10 antigen, including normal endometrial stroma and ESS.Although CD10 has been considered a marker for ESS, some studies have shown that many other uterine neoplasms like uterine smooth muscle tumors, adenosarcomas, malignant Müllerian mixed tumors, rhabdomyosarcomas, endometrial carcinomas, endocervical adenocarcinomas, uterine tumors resembling ovarian sex cord tumors, perivascular round cell tumors, mesonephritic carcinomas, and gestational trophoblastic disease may express CD10., Epidemiology : Predominantly affects postmenopausal women, Annual incidence of ESS is 1-2 per million women., VARIABLE, Complications : death, Diagnostics : Immunostaining, Differential diagnosis : carcinosarcoma (malignant mullerian mixed tumour), Epithelioid leiomyosarcoma, Melanoma, Pleomorphic rhabdomyosarcoma, disease description : Undifferentiated uterine sarcoma is a diagnosis of exclusion applied to malignant mesenchymal tumors of the uterus with no lineage specific morphologic or immunohistochemical features and no entity defining molecular alterations.

Undifferentiated Ovarian Sarcoma

Disease Name : Undifferentiated Ovarian Sarcoma, Symptoms : constipation, Abdominal Pain, Signs : nan, Treatment : Surgical resection is the only curative treatment in early-stage ovarian undifferentiated carcinomas that has a favorable prognosis., Pathophysiology : Undifferentiated carcinomas of the ovary not exhibit characteristics that allow classified into any of the types of carcinoma of ovarian surface epithelium. Pure cases are rare and up to 80% of tumors classified as undifferentiated carcinomas may contain small foci of a recognizable subtype of carcinoma, usually serous or endometrioid adenocarcinoma. When strict pathological criteria are used, this diagnosis is very rare, comprising <1% of ovarian carcinomas. This neoplasm is so little differentiated that immunohistochemical reactions are negative for almost any marker and only focally positive for epithelial markers as in this case are found in a very small proportion.10 The clinical presentation is similar to that of other carcinomas and in 15% of cases are bilateral., Epidemiology : They account for ~ 4% of ovarian cancer, <0.6/100, 000, poor, NA, Complications : post-surgical complications, Diagnostics : CT SCAN, ELECTRON MICROSCOPY, Immunostaining, Differential diagnosis : Adult granulosa cell tumour, lymphomas, mesenteric tumors, small cell carcinoma, disease description : An aggressive high grade sarcoma that arises from the ovary. It is characterized by the presence of marked pleomorphism and nucleaThe WHO classification describes endometrial undifferentiated carcinomas (UCs) as malignant poorly differentiated endometrial carcinomas lacking any evidence of differentiation without any further characterization.r atypia in the neoplastic mesenchymal cells.

Unilateral Naevoid Telangiectasia

Disease Name : Unilateral Naevoid Telangiectasia, Symptoms : TELANGIECTASES : Clinically, UNT is characterized by multiple, unilateral, linearly arranged, blanching telangiectases in a dermatomal (most frequently involving the third and fourth cervical dermatomes) or Blaschkoid pattern., Signs : nan, Treatment : Cosmetic camouflage can be ,helpful, Pulsed dye laser can be effective but some authors have ,reported recurrence, Pathophysiology : Vascular malformations may result from a somatic mutation during embryologic development giving rise to distinct cell populations in a single individual. Paradominant inheritance, in which an autosomal mutation results in loss of heterozygosity and gives rise to a mosaic patch or twin spots, may explain the rare occurrence of telangiectatic nevi in several family members.  Whether these alterations include different concentrations of receptors for vasoactive substances or hormones remains to be determined. Telangiectasias are almost always limited to the skin, and associated gastric telangiectasias reported in one case may have been due to the underlying hepatic dysfunction., Epidemiology : more common in males than in females., VARIABLE, Complications : liver disease, high oestrogen state, Diagnostics : LIVER FUNCTION TEST LFT, biopsy, Differential diagnosis : angioma serpiginosum, Benign essential telangiectasia, erythema, disease description : A condition of telangiectasiae occurring in a Blaschkoid distribution on the skin. This condition was first described by Blaschko in 1899. It may be congenital or acquired aUnilateral nevoid telangiectasia (UNT) is a cutaneous condition consisting of congenital or acquired patches of superficial telangiectasias in a unilateral linear distribution.nd runs a benign course.

Unsafe Ear (atticoantral)

Disease Name : Unsafe Ear (atticoantral), Symptoms : Deafness : Atticoantral disease causes varying degrees of hearing loss., ear discharge : Clinically the patient usually presents with foul smelling continuous scanty otorrhea with occasional blood stained discharge., Signs : CHOLESTEATOMA : A cholesteatoma is a noncancerous skin growth in the middle section of your ear, behind the eardrum., Treatment : medication : Ciprofloxacin , in cases of annular osteitis due to chronic otitis media, regular aural toilet may be sufficient to prevent progression of this condition,however, the condition should be monitored assiduously,cholesteatomas may be fatal and should be treated aggressively, often requiring a mastoid exploration, Pathophysiology : The pathophysiology of CSOM is complex and multifactorial. Current theories suggest that CSOM is initiated by an episode of acute infection. The pathophysiology of CSOM begins with irritation and subsequent inflammation of the middle ear mucosa. The inflammatory response creates mucosal edema. Ongoing inflammation eventually leads to mucosal ulceration and consequent breakdown of the epithelial lining. The hosts attempt at resolving the infection or inflammatory insult manifests as granulation tissue, which can develop into polyps within the middle ear space. (A study by Wang et al suggested that in CSOM, T-cell–mediated cellular immunity plays a role in the formation of granulation tissue., Epidemiology : 5.2%, GOOD, Prevent common colds and other illnesses. Teach your children to wash their hands frequently and thoroughly and to not share eating and drinking utensils. Teach your children to cough or sneeze into their elbow. If possible, limit the time your child spends in group child care. A child care setting with fewer children may help. Try to keep your child home from child care or school when ill., Complications : Meningitis, facial nerve palsy, Diagnostics : HISTOPATHLOGY, MRI, CT SCAN, culture & sensitivity for ear discharge, Audiometry, Differential diagnosis : CHOLESTEATOMA, foreign body in ear, Langerhans-cell histiocytosis, Otitic hydrocephalus, petrositis, Wegener granulomatosis, disease description : In attico-antral chronic suppurative otitis media, there is a tympanic membrane perforation in the pars flaccida, involving the bony annulus. Bones affected in this condition are the tympanic ring, the ossicles, the mastoid air cells, the bony walls of the attic, aditus and antrum.

Unstable Angina

Disease Name : Unstable Angina, Symptoms : chest pain : Chest pain that feels crushing, pressure-like, squeezing, or sharp., fatigue : Affected individuals suffer from unexplained fatigue., sweating : Unstable angina causes excessive sweating., Pain : Pain that radiates to your upper extremities (usually on the left side) or back., "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 : hypertension : Prolonged hypertension promotes left ventricular hypertrophy which will eventually lead to heart failure (both systolic and diastolic). Eccentric hypertrophy leads to increased oxygen demand by the myocardium which can result in angina or ischemic symptoms., S3 and S4 gallop : It occurs as the atria push blood into a stiff ventricle. Therefore, this sound indicates that there may be an issue with the left ventricle, as it is inflexible., sinus tachycardia : These patients represent a unique subgroup of unstable angina, in which the mechanism responsible for ischemia is excessive increase in heart rate., Treatment : medication : Diltiazem , Verapamil, Glyceryl trinitrate (nitroglycerin) , Atorvastatin , Metoprolol , Enoxaparin sodium , Ramipril , Cardiac angiography is indicated in unstable angina if the patient has : ,,Cardiogenic shock, ,Depressed ejection fraction, ,Angina refractory to pharmacological therapy, ,New MITRAL REGURGITATION, ,Unstable arrhythmias., Pathophysiology : Unstable angina deals with blood flow obstacles causing a lack of perfusion to the myocardium. Initial perfusion starts directly from the heart into the aorta and subsequently into the coronary arteries which supply their respective portions of the heart. The left coronary artery will divide into the circumflex and the left anterior descending artery.  Subsequently, this will divide into much smaller branches. The right coronary will divide into smaller branches as well. Unstable angina results when the blood flow is impeded to the myocardium. Most commonly, this block can be from intraluminal plaque formation, intraluminal thrombosis, vasospasm, and elevated blood pressure.  Often a combination of these is the provoking factor.Factors that increase myocardial oxygen demand : ArrhythmiasFeverHypertensionCocaine useAortic stenosisAV shuntsAnemiaThyrotoxicosisPheochromocytomaCHF, Epidemiology : about six out of 10, 000 persons in the general population, fair, Some studies have shown that making a few lifestyle changes can prevent blockages from getting worse and may actually improve them. Lifestyle changes can also help prevent some angina attacks. Your provider may tell you to : ,,Lose weight if you are overweight,Stop smoking,Exercise regularly,Drink alcohol in moderation only,Eat a healthy diet that is high in vegetables, fruits, whole grains, fish, and lean meats. ,,Your provider will also recommend that you keep other health conditions such as high blood pressure, diabetes, and high cholesterol levels under control., Complications : Arrhythmias, cardiogenic shock, death, heart failure, Diagnostics : Complete Blood Count CBC, CPK, SERUM TROPONIN T(TROP T), SERUM TROPONIN- I(TROP I), ECG, MRI, Differential diagnosis : Aortic Dissection, PEPTIC ULCER DISEASE, pericarditis, PNEUMOTHORAX, Pulmonary Embolism, disease description : Unstable angina is chest discomfort or pain caused by an insufficient flow of blood and oxygen to the heart. It is part of the acute coronary syndromes and may lead up to a heart attack. Unstable angina with non-STEMI is a spectrum of disease that involves an imbalance of supply and demand of oxygen available to the myocardium

Urea Cycle Defects

Disease Name : Urea Cycle Defects, Symptoms : lethargy : Neonates with absent urea cycle enzyme activity typically present after the first 24 hours of life with lethargy which is caused by the rapid accumulation of ammonia and subsequent development of cytotoxic edema and seizure., Hyperammonemia : Symptoms of urea cycle disorder are the result of having too much ammonia in your blood Symptoms range from mild to severe and could include problems with cognitive development and intellectual challenges, behavioral changes, developmental delays, the buildup of fluid around your brain, spasticity, seizures& coma., Signs : nan, Treatment : medication : Lactulose , Neomycin , For neonates with hyperammonemia, the immediate treatment goal is a rapid lowering of ammonia and reducing dietary protein intake. Hemodialysis is very effective at reducing plasma ammonia and should immediately be initiated if elevated hyperammonemia is observed. Ammonia scavenger medications such as Ammonul IV are also useful. Ammonul IV acts by removing glycine and glutamate from plasma thereby their reducing contribution to ammonia formation., Pathophysiology : There has been considerable progress in understanding the pathophysiology of UCDs which may ultimately promote better medical interventions. Hyperammonemia is a key etiological factor in UCDs and plays a key role in CNS toxicity. Although complex, some important concepts are emerging.  The toxic effects of ammonia on the CNS are more severe in the developing brain than in the adult brain.  Whether the toxic effects of hyperammonemia are reversible or not depends upon the exposure time, the dose of hyperammonemia and the stage of neurological development. In the neonatal brain, hyperammonemia results in edema caused by swelling of astrocytes. The subsequent frequency and degree of swelling are key factors in determining the severity of CNS neurological disorders such as seizures, coma, and cognitive/motor deficits., Epidemiology : 1 in 35, 000 births, VARIABLE, You can’t prevent urea cycle disorder since it’s a genetic condition. If you plan on becoming pregnant and want to understand the risks of having a child with a genetic condition, talk to your provider about genetic testing., Complications : coma, brain damage, Diagnostics : biopsy, GENETIC TESTING, HISTORY TAKING, plasma ammonia, Amino acid level in blood, Differential diagnosis : anorexia, coma, hypothermia, lethargy, seizures, disease description : Urea cycle disorders are inborn errors of metabolism resulting from defects in one of the enzymes or transporter molecules involved in the hepatic removal of ammonia from the bloodstream. Removal of ammonia from the bloodstream normally occurs via its conversion to urea, which is then excreted by the kidneys. Consequently, urea cycle disorders lead to an accumulation of ammonia.

Ureaplasma Urealyticum Infection

Disease Name : Ureaplasma Urealyticum Infection, Symptoms : urethral irritation : Ureaplasma usually shows no symptoms in the early stages. However, when they occur, symptoms include inflammation of the urethra in both men and women., Genital infections : Urethritis can lead to pain during urination, a burning sensation and unusual discharge, plus redness and inflammation around the site of infection., Signs : nan, Treatment : Doxycycline is the drug of choice, but azithromycin is also used as a five-day course rather than a single dose that would be used to treat Chlamydia infection; streptomycin is an alternative, but is less popular because it must be injected. Penicillins are ineffective U. urealyticum does not have a cell wall, which is the drugs main target, Pathophysiology : Colonization and Adherence : Ureaplasma urealyticum has the ability to adhere to the mucosal surfaces of the urogenital tract, including the urethra, cervix, and reproductive organs. It does so by using adhesins, which are surface molecules that allow the bacteria to attach to host cells.Urease Enzyme Production : Ureaplasma urealyticum possesses an enzyme called urease, which hydrolyzes urea to produce ammonia and carbon dioxide. This process raises the pH of the local environment, making it less acidic. The increased pH can have various effects, including disrupting the balance of the normal vaginal or urethral flora and potentially promoting the growth of other microorganisms.Immune Response : Ureaplasma urealyticum infection can trigger an immune response from the hosts immune system. This immune response involves the activation of immune cells and the release of inflammatory mediators such as cytokines and chemokines. The immune response can contribute to the local inflammation and tissue damage associated with the infection.Inflammatory Effects : The presence of Ureaplasma urealyticum and the resulting immune response can lead to inflammation of the urogenital tissues. This inflammation can cause symptoms such as burning during urination, increased urinary frequency, genital discomfort, and, in some cases, pelvic inflammatory disease (PID) in women.Sexual Transmission : Ureaplasma urealyticum is considered a sexually transmitted bacterium, and sexual contact is a common mode of transmission. It can be passed between sexual partners, leading to infections in both males and females., Epidemiology : Only abstaining from sexual contact can prevent Ureaplasma transmission. But, some people may have Ureaplasma colonization without having sex.,,Ureaplasma is considered an opportunistic bacteria. Opportunistic bacteria may be able to make someone sick when an illness, stress, or other opportunity weakens the immune system and allows it to multiply and further invade the body.,,Getting treatment for medical conditions and having regular checkups with a doctor may help prevent these opportunities from occurring., Complications : nan, Diagnostics : PCR, CERVICAL SWAB CULTURE, Differential diagnosis : Chlamydial Infections, gonorrhea infection, disease description : Ureaplasma urealyticum is a type of bacteria that can cause infection of the urinary tract and vagina. It can be passed from mother to infant during birth, or be sexually transmitted. Ureaplasma urealyticum can be found in a majority of sexually active people, most of whom are asymptomatic

Uremia

Disease Name : Uremia, Symptoms : nan, Signs : nan, Treatment : Dialysis is indicated in a patient with symptomatic uremia (e.g., nausea, vomiting, hyperkalemia, metabolic acidosis) that is not treatable my medical means, and should be initiated as soon as possible, regardless of the patient’s GFR., Iron replacement should be initiated in patients with anemia of chronic kidney disease and underlying iron deficiency (as long as serum ferritin is greater than 100 mcg/mL). This can be done with dialysis treatments, or as oral therapy, if dialysis has not yet been initiated. Erythropoietic stimulating agents, such as erythropoietin or darbepoetin, may additionally be used in low doses (due to the increased risk of cardiovascular mortality) once hemoglobin levels reach below 10 g/dL., Pathophysiology : When the kidneys are not functioning properly, dysfunction can occur in acid-base homeostasis, fluid and electrolyte regulation, hormone production and secretion, and waste elimination. Altogether, these abnormalities can result in metabolic disturbances and ultimately conditions such as anemia, hypothyroidism, hypertension, acidemia, hyperkalemia, and malnutrition.Anemia associated with kidney disease is typically normocytic, normochromic, and hyperproliferative. It occurs as a result of decreased erythropoietin production by the failing kidneys. This is associated with a glomerular filtration rate (GFR) of less than 50 mL/min (unless the patient has diabetes, then they may have anemia at GFR less than 60mL/min) or when serum creatinine is greater than 2 mg/mL., Epidemiology : POOR, Complications : nan, Diagnostics : UREA CREATININE, USG KUB, SERUM ELECTROLYTE, ESTIMATED GLOMERULAR FILTRATION RATE (eGFR), Differential diagnosis : nan, disease description : Uremia is a clinical condition associated with worsening renal function. It is characterized by fluid, electrolyte, hormonal, and metabolic abnormalities. Uremia most commonly occurs in the setting of chronic and end-stage renal disease, but may also occur as a result of acute kidney injury.The literal meaning of uremia is “urine in the blood, ” and the condition develops most commonly in the setting of chronic and end-stage renal disease (ESRD), but may also occur as a result of acute kidney injury.Men are 1.2 times more likely than women to develop ESRD, though women are 1.7 times more likely to delay initiation of dialysis. Women are also more prone to the development of uremic symptoms at lower creatinine levels, due to the decreased amount of muscle mass and baseline serum creatinine levels that they have.

Ureteric Calculi

Disease Name : Ureteric Calculi, Symptoms : urinary disorders : Ureteral stones causes pink, red or brown urine, cloudy or foul-smelling urine, apersistent need to urinate, urinating more often than usual or urinating in small amounts., flank pain : Severe intermittent pain in your upper flank., Pain : Pain that spreads (radiates) to your lower abdomen., burning sensation : Burning sensation while urinating., fever with chills : A high temperature (fever) of 38C (100.4F) or over., Signs : nan, Treatment : medication : Diclofenac , Plenty of water orally. ,Diuretic-oral frusemide to flush the stone. ,Suitable antibiotics to control sepsis; antispasmodics to ,relieve pain. ,IV fluids-fast infusion of about 1.5 to 2 litres and injection ,frusemide 60 to 80 mg. Usually given for 3 to 5 days., 1.Upper third stone : nan,ESWL for stone in upper third ureter.,2.URS-Ureterorenoscopic stone removal : nan,3.Stone in middle third ureter. ,URS. ,Open ureterolithotomy. ,4.Stone in lower third ureter. ,URS. ,Dormia basketing : nan, Pathophysiology : The mechanism of stone formation include nucleation of stone constituent crystals, their growth or aggregation to a size that can interact with some intrarenal structure, their retention within the kidney or renal collecting system and further aggregation and/or secondary nucleation to form the clinical stone. The crystals form either in renal tubular fluid or in the renal interstitial fluid that is supersaturated with respect to these constituents, which in turn may be a consequence of increased excretion of stone constituent molecules, reduced urine volume, an alteration in urine pH, or a combination of these factors. The urine and, presumably, the tubular fluid of stone formers is often more highly supersaturated than that of normal healthy adults, which favors nucleation and growth of crystals., Epidemiology : prevalence of urolithiasis is 5%–19.1% i, 12% of men and 7% of women, VARIABLE, There are many ways to prevent ureteral stones : ,1. Drink more fluids.,2. Limit the amount of animal protein in your diet.,3. Limit the amount of sodium (salt) in your diet. ,4. Limit the amount of oxalate in your diet., Complications : HYDRONEPHROSIS, Urinary Tract Infection, Diagnostics : Complete Blood Count CBC, SERUM PHOSPHATE TEST, X RAY, CT SCAN, IVU, USG, PHYSICAL EXAMINATION, Differential diagnosis : ANEURYSM, cholecystitis, CHOLELITHIASIS, Nephrolithiasis, PID, Pyelonephritis, Renal cell carcinoma, small bowel obstruction, disease description : Ureterolithiasis, also known as ureteric calculi, is the presence or formation of stones within the ureters, which are the tubes responsible for the passage of urine from the kidneys to the bladder.

Ureterocele

Disease Name : Ureterocele, Symptoms : polyuria : Ureterocele makes the person urinate frequently., urinary disorders : Ureterocele leads to bad-smelling urine, blood in the urine., dysuria : Ureterocele causes pain during urination., fever with chills : Fever occurs when the patient develops UTI., Signs : nan, Treatment : medication : Moxifloxacin , Cystoscopic ureteric meatotomy with the removal of ,cyst wall. , In addition to that co-existing complications should be ,treated. , Often ureteric reimplantation is needed., Pathophysiology : Ureteral Valve Dysfunction : Ureterocele can arise due to a malfunctioning valve-like mechanism at the junction where the ureter enters the bladder. Normally, there is a one-way valve action that prevents urine from flowing back into the ureter from the bladder (vesicoureteral reflux). In some cases, this valve doesnt function properly, leading to urine retention and dilation of the ureter.Obstruction of Urine Flow : The ureterocele can act as a mechanical obstruction to the flow of urine from the ureter into the bladder. This obstruction can cause urine to accumulate within the ureter and the renal pelvis (the collecting area of the kidney), leading to dilation and potentially compromising kidney function.Hydroureter and Hydronephrosis : As urine accumulates behind the obstruction, the affected ureter and kidney become dilated. This condition is called hydroureter (dilation of the ureter) and hydronephrosis (dilation of the renal pelvis and calyces). If left untreated, severe hydronephrosis can lead to kidney damage and impairment of renal function.Urinary Stasis and Infection Risk : The stagnant urine behind the ureterocele can become a breeding ground for bacteria, increasing the risk of urinary tract infections (UTIs). Recurrent UTIs can further contribute to kidney damage and inflammation., Epidemiology : Ureteroceles occur in about 1 in 500 people., variable, Complications : kidney damage, kidney stone, Diagnostics : Complete Blood Count CBC, MRI, CT SCAN, INTRAVENOUS UROGRAM, CYSTOSCOPY, IVU, MICTURITION CYSTOURETHROGRAPHY, IV PYELOGRAM, contrast voiding cystourethrogram (VCUG), Differential diagnosis : BLADDER DIVERTICULA, disease description :  It is a cystic enlargement of the intramural portion of ureter due to congenital atresia of the ureteric orifice. Its wall contains mucous membrane only. It is common in females, often bilateral (10%).

Ureteropelvic Junction Obstruction

Disease Name : Ureteropelvic Junction Obstruction, Symptoms : nan, Signs : nan, Treatment : The anomaly is corrected by performing a pyeloplasty, in which the,stenotic segment is excised, and the normal ureter and renal pelvis are,reattached. Success rates are 91–98%. Pyeloplasty can be performed using,laparoscopic techniques, often robotic-assisted using the da Vinci robot, Pathophysiology : UPJ obstruction is the most common obstructive lesion in childhood and usually is caused by intrinsic stenosis. An accessory artery to the lower pole of the kidney also can cause extrinsic obstruction. The typical appearance on US is grade 3 or 4 hydronephrosis without a dilated ureter. UPJ obstruction most commonly manifests on antenatal sonography revealing fetal hydronephrosis; as a palpable renal mass in a newborn or infant; as abdominal, flank, or back pain; as a febrile UTI; or as hematuria after minimal trauma. Approximately 60% of cases occur on the left side; the male : female ratio is 2 : 1. UPJ obstruction is bilateral in only 10% of cases . In kidneys with UPJ obstruction, renal function may be significantly impaired from pressure atrophy, but approximately half of affected kidneys have relatively normal glomerular function. The anomaly is corrected by performing a pyeloplasty, in which the stenotic segment is excised, and the normal ureter and renal pelvis are reattached. Success rates are 91–98%. Pyeloplasty can be performed using laparoscopic techniques, often robotic-assisted using the da Vinci robot. Lesser degrees of UPJ narrowing might cause mild hydronephrosis, which usually is nonobstructive, and typically these kidneys function normally. The spectrum of UPJ abnormalities has been referred to as anomalous UPJ . Another cause of mild hydronephrosis is fetal folds of the upper ureter, which also are nonobstructive. The diagnosis can be difficult to establish in an asymptomatic infant in whom dilation of the renal pelvis is found incidentally in a prenatal US. After birth, the sonographic study is repeated to confirm the prenatal finding. A VCUG is necessary because 10–15% of patients have ipsilateral vesicoureteral reflux. Because neonatal oliguria can cause temporary decompression of a dilated renal pelvis, it is ideal to perform the first postnatal US after the 3rd day of life. Delaying the US may be impractical. If no dilation is found on the initial US, a repeat study should be performed at 1 mo of age. If the kidney shows grade 1 or 2 hydronephrosis and the renal parenchyma appears normal, a period of observation usually is appropriate, with sequential renal US studies to monitor the severity of hydronephrosis, and the hydronephrosis usually disappears. Antibiotic prophylaxis is not indicated for children with mild hydronephrosis. If the hydronephrosis is grade 3 or 4, spontaneous resolution is less likely, and obstruction is more likely to be present, particularly if the renal pelvic diameter is 3 cm. A diuretic renogram with MAG-3 is performed at 4-6 wk of age. If there is poor upper tract drainage or the differential renal function is poor, pyeloplasty is recommended. After pyeloplasty the differential renal function often improves, and improved drainage with furosemide stimulation is expected. If the differential function on renography is normal and drainage is satisfactory, the infant can be followed with serial US studies, even with grade 4 hydronephrosis. If the hydronephrosis remains severe with no improvement, a repeat diuretic renogram after 6-12 mo can help in the decision between continued observation and surgical repair. Prompt surgical repair is indicated in infants with an abdominal mass, bilateral severe hydronephrosis, a solitary kidney, or diminished function in the involved kidney. In unusual cases in which the differential renal function is < 10% but the kidney has some function, insertion of a percutaneous nephrostomy tube allows drainage of the hydronephrotic kidney for a few weeks to allow reassessment of renal function. In older children who present with symptoms, the diagnosis of UPJ obstruction usually is established by US and diuretic renography. The following entities should be considered in the differential diagnosis : megacalycosis, a congenital nonobstructive dilation of the calyces without pelvic or ureteric dilation; vesicoureteral reflux with marked dilation and kinking of the ureter; midureteral or distal ureteral obstruction when the ureter is not well visualized on the urogram; and retrocaval ureter., Epidemiology : nan, Complications : Pyelonephritis, Urinary Tract Infection, Diagnostics : CT Abdomen, X RAY, Renal ultrasonography, contrast voiding cystourethrogram (VCUG), Renal scintigraphy, Magnetic Resonance Urography, antegrade pyelogram, Differential diagnosis : POSTERIOR URETHRAL VALVES, disease description : UPJ obstruction is the most common obstructive lesion in childhood and usually is caused by intrinsic stenosis. An accessory artery to the lower pole of the kidney also can cause extrinsic obstruction. The typical appearance on US is grade 3 or 4 hydronephrosis without a dilated ureter. UPJ obstruction most commonly manifests on antenatal sonography revealing fetal hydronephrosis; as a palpable renal mass in a newborn or infant; as abdominal, flank, or back pain; as a febrile UTI; or as hematuria after minimal trauma.

Uretheral Caruncle

Disease Name : Uretheral Caruncle, Symptoms : Pain : Urethral caruncles causes pain, burning & bleeding., Carbuncle : Urethral caruncles are usually pink or red. If a blood clot has formed, they may turn purple or black. These growths are usually small, growing up to 1 centimeter (cm) in diameter. However, cases have been reported where they’ve have grown at least 2 cm in diameter. They typically sit on one side of the urethra (the posterior edge), and don’t go around the whole circle of the opening., Signs : nan, Treatment : medication : Oestradiol/Oestrogen, Local oestrogen cream may be preferred to oral ,hormone, The most common urethral caruncle treatments include : ,,Topical estrogen cream. Applying this cream helps restore your estrogen levels.,Anti-inflammatory medication. Your healthcare provider may also recommend a topical anti-inflammatory cream, such as a corticosteroid, to ease swelling and irritation., DIATHERMY EXCISION, Pathophysiology : Low estrogen is the only known risk factor for urethral caruncles. People with low estrogen have a higher chance of developing the condition.Estrogen keeps the skin in your genital area soft and flexible. When estrogen levels drop, you’re more prone to dry, thin skin that tears easily. Experts think this is why urethral caruncles are most common in people who’ve already gone through menopause., Epidemiology : 32%, . Of 14 cases of urethral caruncle in the paediatric age group described in the English literature, GOOD, Because urethral caruncles are associated with low levels of estrogen, hormone therapy could play a role in reducing your risk. Ask your healthcare provider about treatment options., Complications : dysuria, DYSPAREUNIA, Diagnostics : biopsy, CYSTOSCOPY, CYTOLOGY, USG, UROFLOWMETRY, HISTOLOGIC EXAMINATION, Differential diagnosis : cancer, urethral diverticula, disease description : A urethral caruncle is a benign fleshy outgrowth of the posterior urethral meatus. It is the most common lesion of the female urethra and occurs primarily in postmenopausal women. The lesion is typically asymptomatic, although some women present with vaginal bleeding.

Uretheritis

Disease Name : Uretheritis, Symptoms : itching : Itchiness at the tip of the urethra., dysuria : Intense pain during urination., DISCHARGE : Penile discharge, including pus and/or blood., Abdominal Pain : Urethritis causes pelvic pain., Signs : nan, Treatment : medication : Oestradiol/Oestrogen, Ampicillin , Tetracycline , diathermy excision, antibiotics such as ampicillin, tetracycline or ,cephalosporins may be used as indicated by culture., Pathophysiology : The lower urethra is usually affected, as vulvovaginitis is a common accompaniment. Vigorous and frequent sexual intercourse often aggravates the problem. Honeymoon cystitis is a distinct clinical entity following coital injury to the urethra and the bladder base. Menopausal women suffer from thinning of the vaginal epithelium and urethral lining due to oestrogen deficiency; these women are susceptible to trauma and infection which may lead to urethritis. Use of chemicals, deodorants, douches, vaginal contraceptives and tampons may lead to allergic or chemical reactions causing vulvovaginitis and urethritis., Epidemiology : Urethritis has an incidence of affecting 4 million Americans each year., GOOD, You can reduce your risk of developing urethritis by : ,,Doing things to avoid getting STIs, such as practicing safe sex and limiting the number of your sexual partners.,Getting regular tests for STIs if you’re sexually active.,Avoiding chemicals that may irritate your urethra.,Avoiding actions that may irritate your urethra., Complications : abscess, lymphangitis, vulvovaginitis, strictures, Diagnostics : PCR, NAAT TEST, culture of uretheral discharge, Differential diagnosis : Acute prostatitis, Cervicitis, Cystitis, epididymitis, PROCTITIS, Prostatic enlargement, vaginitis, disease description : Urethritis is inflammation of the urethra and is a lower urinary tract infection. The urethra is a fibromuscular tube through which urine exits the body in both males and females, and semen in males. Urethritis has a strong association with sexually transmitted infections (STIs).

Urethral Injury

Disease Name : Urethral Injury, Symptoms : bleeding : Physical examination may reveal blood at the meatus., Trauma : Trauma to the urethra can allow urine to leak into the tissues around it. This can cause swelling, inflammation, infection & pain in the belly Other signs of urethral trauma are : Not being able to pass urine Urine building up in the bladder Blood in the urine ("hematuria") For males, the most common sign of a problem is blood – even a drop – at the tip of the penis. Swelling and bruising of the penis, scrotum, and perineum may also occur, along with pain in that area., Signs : perineal bruising and haematoma : Blunt injuries to the anterior urethra, often the result of a “straddle injury” to the bulbar urethra, result in significant contusion to the spongiosus with possible significant hematoma of the perineum. For these reasons, immediate repair is contraindicated., Treatment : medication : Moxifloxacin , "When lower bougie is pulled out per ,urethrally, catheter tied to it will pass through urethra ,from above, to which Foleys catheter is tied and pulled ,up, so as to keep it in position. ,, Bladder is closed with a SPC using Malecots catheter Railroad technique", Pathophysiology : Injuries may affect either the anterior or posterior part of the urethra. In most cases, anterior urethral trauma is characterized as a blunt injury to the perineum — the area between the genitals and anus — since the urethra is located near the skin in this area. This type of trauma is often the result of straddle-like injuries, such as when a child forcefully straddles a bicycle or fence. Penetrating injuries to the anterior urethra, such as those from a gunshot wound, also may cause strictures or obstructions., Epidemiology : 20 pelvic fractures per 100, 000 population, these injuries are not uncommon., variable, Improper urethral catheter insertion is a source of preventable injury in male patients. ,,Iatrogenic urethral injuries are a substantial source of preventable morbidity in hospitalized male patients. Implementation of a nursing education program may significantly decrease the incidence of iatrogenic urethral injury and, thereby, improve patient safety.,,Avoiding injury to the pelvic area of the body, it may be possible to prevent some forms of urethral injury. ,,Taking care to avoid infection may also help prevent this condition., Complications : impotence, incontinence, strictures, Diagnostics : retrograde urethrogram (RUG), USG ABDOMEN(W/A), X RAY PELVIS, X RAY, CT SCAN, Differential diagnosis : Contusion, External genital injury, fracture, injury, Renal injury, disease description : Urethral injury is a relatively rare medical condition accounting for less than 1% of all emergency department visits in the United States. Injury patterns vary and encompass urethral crush, bruising, laceration, and transection. Urethral injuries are never life-threatening, but if left untreated can cause significant morbidity. 

Urethral Stricture

Disease Name : Urethral Stricture, Symptoms : RETENTION OF URINE : Some patients with severe urethral strictures are completely unable to urinate. This is referred to as urinary retention, and is a medical emergency., straining to void and a poor urinary stream : Many men with a stricture will have increasing discomfort with urinating and a slowing of the urinary stream. This can develop gradually and lead to pushing or straining to get urine out., burning micturation : Urethral stricture, or scarring, narrows the urethra and may cause inflammation or infection that causes a burning sensation at the tip., dysuria, hematuria : Patients who have urethral stricture most often present with obstructive voiding symptoms such as terminal hematuria., Suprapubic pain : Pain in the lower abdomen is often experienced by the patients., Prostatic enlargement : A urethral stricture can also cause inflammation of the prostate., Signs : Urinary Tract Infection : Over time, a urethral stricture can cause recurrent urinary tract infections (UTIs)., HESITANCY : It may feel like you have to urinate again right after a trip to the bathroom, or a frequent or urgent need to urinate., dribbling of urine : A hesitating start when urinating, a need to strain, a weak and trickling stream of urine, and dribbling at the end of urination are common symptoms of a partially obstructed urethra., Treatment : medication : Levofloxacin , "1. Intermittent dilatation : nan,Dilators used : nan,a. Listers dilator has got olive tip (blister). ,b. Gluttons dilator. ,c. Filiform bougies. ,2. Visual internal cystoscopic urethrotomy or stricturotomy.,3.External urethrotomy.,4.Urethroplasty", Pathophysiology : The pathophysiology is an injury to the urethral epithelium attributed to any of the specific etiologies causing a leak of urine to the corpus spongiosum or by direct trauma to the corpus spongiosum. Either of which initiates inflammation and fibrous changes of the corpus spongiosum. This form of fibrous tissue causes contraction compressing the urethral lumen. These also cause metaplasia of the urethral epithelium to stratified squamous epithelium, which is more affected by pressure changes and stretch causing tears in the mucosa, leading to a further leak of urine into the outer corpus spongiosum,  which causes fibrous changes and stricture. This process causes a vicious cycle of strictures and urethral injuries leading to further narrowing of the urethra, and so on., Epidemiology : Urethral stricture is much more common in males than in females., the incidence is estimated to be 229-627 per 100, 000 males, variable, By avoiding injury to the pelvic area of the body, it may be possible to prevent some forms of urethral stricture. Taking care to avoid infection may also help prevent this condition., Complications : BLADDER DIVERTICULA, urinary retention, recurrent UTIs, Diagnostics : URINE CULTURE, CYSTOURETHROGRAPHY, USG, USG, URETHROSCOPY, UROFLOWMETRY, MRI PELVIS, Differential diagnosis : Acute prostatitis, BLADDER STONE, recurrent UTIs, disease description : A urethral stricture involves scarring that narrows the tube that carries urine out of your body (urethra). A stricture restricts the flow of urine from the bladder and can cause a variety of medical problems in the urinary tract, including inflammation or infection.

Urinary Fistula

Disease Name : Urinary Fistula, Symptoms : urinary incontinence : Vesicovaginal fistula (VVF) is an abnormal opening between the bladder and the vagina that results in continuous and unremitting urinary incontinence., FOUL SMELLING DISCHARGE : If you have a vaginal fistula that opens to your rectum or colon, you most likely have foul-smelling discharge or gas coming from your vagina., Abdominal Pain : A colovesical fistula is an open connection between the colon and bladder. A thick wall of tissue normally separates the two. Fecal matter from the colon can enter the bladder through this colovesical fistula, causing painful infections and other complications., dribbling of urine : Fistulas can cause severe urinary incontinence because the urine can bypass the urethra and the sphincter, which normally regulate the flow of urine. They can lead to constant, or almost constant, urine leakage., leaking from vagina : Urine and other fluid leaking from the vagina., Signs : nan, Treatment : Treatment is difficult. Surgical exploration-transvaginal repair in ,low fistula. Suprapubic repair if fistula is high. Often urinary ,diversion is needed., Some simple fistulas may be able to heal on their own. This might be possible when the fistula is small and the tissue around the fistula is healthy. For instance, where tissue has not been damaged by radiation therapy or cancer., URETERIC REIMPLANTATION, Pathophysiology : Damage to the tissues of the urinary tract, pelvic region or vagina can create the conditions for a fistula. Urinary fistulas can develop from an injury or accident, a surgery, radiation treatment or (less often) by an infection. The fistula may open after tissue breaks down over time, from days to years., Epidemiology : 50, 000 to 100, 000 women develop fistula annually, GOOD, Obstetric fistula is preventable; it can largely be avoided by : ,delaying the age of first pregnancy;,the cessation of harmful traditional practices; and.,timely access to obstetric care., Complications : URETHRAL STRICTURE, Diagnostics : SERUM Creatinine, USG Pelvis, CYSTOURETHROGRAPHY, CYSTOSCOPY, Differential diagnosis : hematuria, pelvic abscess, urethral diverticula, Urinary incontinence, disease description : A urinary fistula can be an abnormal opening between urinary tract organs that process urine and carry it out of the body (kidneys, ureter tubes, bladder, urethra). Urinary fistulas can also form an abnormal connection between a urinary tract organ and another nearby organ such as the vagina or colon. Vagina/urinary organ connections are often called vaginal fistulas.

Urinary Tract Infection

Disease Name : Urinary Tract Infection, Symptoms : "behavioural disturbances : Behavior changes and causes that seem to affect ones personality may include sleeping issues, anxiety, depression, confusion, aggression, delusions, hallucinations and paranoia.", nocturia : Even without increased nighttime urine production, reduced bladder capacity and increased urinary frequency can give rise to nocturia. Urinary tract infections (UTIs) can cause a person to feel that they need to urinate frequently., urinary urgency : Urinary urgency can sometimes indicate a urinary tract infection., fever : A high temperature (fever) of 38ºC (100.4ºF) or above., dysuria : It causes a burning sensation, pain and/or discomfort., hematuria : This condition happens when the kidneys or other parts of the urinary tract let blood cells leak into urine., increased frequency of urination : Urinary tract infections (UTIs) can cause a person to feel that they need to urinate frequently., Signs : nan, Treatment : medication : Amoxicillin and Clavulanic acid , Ceftriaxone , Cefotaxime , Nitrofurantoin , Sulfamethoxazole + Trimethoprim Co-trimoxazole , PERCUTANEOUS DRAINAGE IN COMPLICATED UTI, "DIFFERS IN DIFFERENT TYPES OF UTIS", Pathophysiology : Infection of the bladder. usually caused by Escherichia coli (E. coli). E. coli is a type of bacteria commonly found in the gastrointestinal (GI) tract. But sometimes other bacteria are the cause.Having sex also may lead to a bladder infection, but you dont have to be sexually active to develop one. All women are at risk of bladder infections because of their anatomy. In women, the urethra is close to the anus. And the urethral opening is close to the bladder. This makes it easier for bacteria around the anus to enter the urethra and to travel to the bladder.Infection of the urethra. GI bacteria spread from the anus to the urethra. An infection of the urethra can also be caused by sexually transmitted infections. They include herpes, gonorrhea, chlamydia and mycoplasma. This can happen because womens urethras are close to the vagina., Epidemiology : 150 million persons per year, GOOD, The following lifestyle changes can help prevent urinary tract infections : nan, Complications : kidney damage, sepsis, Recurrent infection, strictures, Diagnostics : Complete Blood Count CBC, Erythrocyte Sedimentation Rate (ESR), URINE CULTURE, CT Abdomen, USG KUB, BLOOD CULTURE, URINE MICROSCOPY, URINARY RBC, IVU, URINARY FLOW RATE, POST VOIDAL RESIDUAL URINE, Differential diagnosis : HERPES SIMPLEX, PID, Pyelonephritis, Renal Stone, vaginitis, disease description : A urinary tract infection (UTI) is an infection in any part of the urinary system. The urinary system includes the kidneys, ureters, bladder and urethra. Most infections involve the lower urinary tract — the bladder and the urethra.

Urocanase Deficiency

Disease Name : Urocanase Deficiency, Symptoms : hematuria : A tremor present when the limbs are active, either when outstretched in a certain position or throughout a voluntary movement., hematuria : A type of ataxia characterized by the impairment of the ability to coordinate the movements required for normal walking. Gait ataxia is characteirzed by a wide-based staggering gait with a tendency to fall., hematuria : An abnormal gait pattern in which persons stand and walk with their feet spaced widely apart. This is often a component of cerebellar ataxia., hematuria : Cerebellar ataxia refers to ataxia due to dysfunction of the cerebellum. This causes a variety of elementary neurological deficits including asynergy (lack of coordination between muscles, limbs and joints), dysmetria (lack of ability to judge distances that can lead to under- or overshoot in grasping movements), and dysdiadochokinesia (inability to perform rapid movements requiring antagonizing muscle groups to be switched on and off repeatedly)., hematuria : Dysarthric speech is a general description referring to a neurological speech disorder characterized by poor articulation., hematuria : Horizontal nystagmus made apparent by looking to the right or to the left., hematuria : Increased susceptibility to infections., Signs : nan, Treatment : There is no cure for Urocanase Deficiency Disorder, since it is a genetic condition. Treatment is usually given to manage the signs and symptoms and any complication that develops., Pathophysiology : Enzyme Deficiency : Urocanase deficiency is caused by a genetic mutation that affects the urocanase enzyme. Urocanase is responsible for converting urocanic acid, an intermediate product in the breakdown of histidine, into another compound called imidazolone propionic acid. Mutations in the urocanase gene lead to reduced or absent activity of the enzyme, preventing the normal conversion of urocanic acid.Histidine Metabolism Disruption : Histidine is an essential amino acid obtained from the diet and plays a role in protein synthesis and various biochemical pathways. In individuals with urocanase deficiency, the breakdown of histidine is impaired, leading to the accumulation of urocanic acid in the body.Accumulation of Urocanic Acid : Urocanic acid, which is normally rapidly converted by urocanase, starts to accumulate in the body due to the enzyme deficiency. Elevated levels of urocanic acid can be detected in urine and, to a lesser extent, in blood and other body fluids., Epidemiology : In the US, there are less than 1, 000 with this disease., variable, there are no known prevention methods, Complications : encephalopathy, Diagnostics : urine organic acids, Differential diagnosis : nan, disease description : Encephalopathy due to urocanase deficiency is an extremely rare histidine metabolism disorder characterized by urocanic aciduria and other variable manifestations including intellectual deficit and intermittent ataxia in the 4 cases reported to date.

Urothelial Carcinoma In Situ - Non-invasive Papill

Disease Name : Urothelial Carcinoma In Situ - Non-invasive Papill, Symptoms : loss of appetite : leading to weight loss, fever, hematuria : Papillary urothelial carcinoma begins by affecting the urothelial cells within the bladder or the lower parts of the kidneys, where urine pools before moving on to the bladder through the ureters., Signs : nan, Treatment : Adjuvant : usually not indicated for low grade,Mitomycin C, Surgical : transurethral resection, Pathophysiology : Normal urothelium, through loss of chromosome 9, becomes hyperplasiaFollowed by further genetic alterations, such as mutations in FGFR3, which activates mitogen activated protein (MAP) kinase pathway, leading to development of low grade noninvasive papillary urothelial carcinomaOther genetic alterations :  PIK3CA, loss of 11p or CCND1, Epidemiology : M : F = 3 : 1, Incidence : 5 per 100, 000 people per year, variable, Don’t smoke,Workers in industries that use certain organic chemicals have a higher risk of bladder cancer. Workplaces where these chemicals are commonly used include the rubber, leather, printing materials, textiles, and paint industries.,Drink plenty of liquids,Eat lots of fruits and vegetables, Complications : fatigue, Urinary Tract Infection, weight loss, Metastasis, Diagnostics : PET SCAN, biopsy, CT SCAN, CYSTOSCOPY, USG, Differential diagnosis : Carcinoma in situ, INVERTED PAPILLOMA, Urothelial dysplasia, Urothelial papilloma, disease description : Neoplastic proliferation of the urothelium in a papillary configuration, with no invasion through the basement membrane.It involves low grade architectural and cytologic abnormality, absence of high grade features, such as irregular nuclei with frequent, prominent nucleoli and mitoses, pleomorphism.

Urothelial Papilloma

Disease Name : Urothelial Papilloma, Symptoms : BLADDER OUTLET OBSTRUCTION : Bladder outlet obstruction (BOO) is a blockage at the base of the bladder. It reduces or stops the flow of urine into the urethra., dysuria : Urothelial papilloma causes painful urination., painless heamaturia : One of the cardinal symptoms of urothelial papilloma is presence of blood in urine., Signs : nan, Treatment : Inverted urothelial papillomas of the upper urinary tracts are even less common than bladder lesions. However, when the upper urinary tracts are involved, the lesions tend to be sizeable. Treatment of smaller upper tract inverted urothelial papillomas can be with ureteroscopy, but larger lesions may require percutaneous access for direct resection, partial ureterectomy, or even nephrectomy., Resection : transurethral resection of bladder tumor (TURBT), Pathophysiology : Targeted next generation sequencing (NGS) and whole exome sequencing (WES) showed Activating mutations involving the MAPK / ERK pathway, in particular KRAS and HRAS genes, are common alterationsKRAS mutations more frequent than HRASMutations in chromatin modifiers (often associated with urothelial carcinoma) are rareLow tumor mutational burdenNo APOBEC (apolipoprotein B mRNA editing catalytic polypeptide-like) mutational signature (identified in about 70% of muscle invasive urothelial carcinomas)Other earlier studies have shownFGFR3 mutations in 75%TERT promoter mutation in 46% (12/26)However, these findings have not been replicated in the newer study using NGS and WES, Epidemiology : M : F - 1.9 : 1, Rare urothelial neoplasm, comprises ~1% of all papillary bladder neoplasm, variable, Complications : obstruction, dysuria, hematuria, Diagnostics : CT SCAN, USG, Immunostaining, Differential diagnosis : adenomas, CARCINOID TUMORS, Cystitis, Cystitis, Papilloma, Urothelial carcinoma, disease description :  Urothelial papilloma is an uncommon benign exophytic neoplasm composed of a delicate fibrovascular core covered by normal-appearing urothelium. 1, 2 The posterior or lateral walls close to the ureteric orifices and the urethra are the most common locations

Urticaria Pigmentosa

Disease Name : Urticaria Pigmentosa, Symptoms : blisters : In young children, it is common for the mastocytosis patches to blister when rubbed. If many patches are rubbed or activate spontaneously at the same time, the infant may become irritable, but is uncommon for severe symptoms to arise. Over time, the mastocytosis becomes less itchy and eventually the patches fade away. By the teenage years, most patches will have gone., skin patches : Maculopapular cutaneous mastocytosis most often affects infants, with the first patches appearing at a few months of age. They patches are often confused with moles or with insect bites at first, but the lesions persist and gradually increase in number for several months or years. They can appear on any part of the body including the scalp, face, trunk and limbs., systemic symptoms : Sometimes patients can have systemic symptoms (such as flushing, itching, low blood pressure, anaphylactic shock, diarrhoea and bleeding from the gastrointestinal tract), which suggest the presence of systemic mastocytosis., LESIONS : Maculopapular cutaneous mastocytosis can sometimes develop for the first time in an adult. Just a few lesions may appear, or many. The lesions can be unsightly and itchy. Unfortunately, in adults, urticaria pigmentosa tends to persist long-term., Signs : nan, Treatment : nan, Pathophysiology : Mast Cell Proliferation : In urticaria pigmentosa, there is an excessive proliferation of mast cells within the skin. These mast cells are derived from bone marrow precursors and migrate to the skin where they accumulate. The exact cause of this abnormal proliferation is not fully understood but is believed to involve genetic factors.Mast Cell Activation : Mast cells are immune cells that play a crucial role in allergic and inflammatory responses. In urticaria pigmentosa, these mast cells are hyperactive and prone to activation. Various triggers, such as physical friction, temperature changes, certain medications, and emotional stress, can lead to mast cell degranulation.Histamine Release : When mast cells are activated, they release numerous inflammatory mediators, with histamine being one of the most prominent. Histamine causes blood vessels to dilate, leading to increased blood flow and leakage of fluid into the surrounding tissues. This results in the characteristic skin lesions seen in urticaria pigmentosa, often referred to as "urticaria" or hives.Skin Lesions : Urticaria pigmentosa is characterized by small reddish-brown or yellowish-brown lesions on the skin, which can appear anywhere on the body. These lesions can be raised, itchy, and can take on a hive-like appearance. Scratching or rubbing the lesions, even mildly, can trigger mast cell degranulation and worsen the symptoms., Epidemiology : 45% to 75%, , variable, There is no sure way to prevent UP. The inherited form is very rare, and even when the child has the abnormal gene, they may not ever develop UP.,,However, you can prevent the disorder from getting worse. Try the following methods : ,,Help your child from scratching or rubbing their irritated skin to prevent the lesions from spreading.,Avoid hot baths to keep from drying out their skin and making the itching worse. Bathing in lukewarm (or cool) Aveeno oil baths have been shown to control itching.,Avoid itchy, irritating clothing. Try cotton or other light fabrics instead.,Keep fingernails short.,Have them wear light cotton gloves to bed to prevent scratching., Complications : nan, Diagnostics : BONE DENSITY, full thickness skin biopsy, Differential diagnosis : Atopic dermatitis, Urticarial vasculitis, disease description : Urticaria pigmentosa is a skin disease that produces patches of darker skin and very bad itching. Hives can develop when these skin areas are rubbed.Urticaria pigmentosa is most common in children. It can also occur in adultsMastocytosis is a disorder characterized by mast cell accumulation, commonly in the skin, bone marrow, gastrointestinal (GI) tract, liver, spleen, and lymphatic tissues. The World Health Organization (WHO) divides cutaneous mastocytosis into three main presentations. The first has solitary or few (less than or equal to 3) lesions called “mastocytomas.” The second involves multiple lesions ranging from less than 10 to greater than 100 which is referred to as “urticaria pigmentosa” (UP). The last presentation involves diffuse cutaneous involvement.

Urticaria

Disease Name : Urticaria, Symptoms : angioedema : Painful swelling around the eyes, cheeks or lips., Urticarial rashes : Urticaria appears as raised, well-circumscribed areas of erythema (redness) and edema (swelling) involving the dermis and epidermis that are very pruritic (itchy)., wheal and flare effects : Batches of welts (wheals) that can arise anywhere on the body. Welts that might be red, purple or skin-colored, depending on your skin color. Welts that vary in size, change shape, and appear and fade repeatedly., Signs : nan, Treatment : medication : Prednisolone, First line therapies (antihistamines),Second line therapies-Oral corticosteroids are effective in severe urticaria at high doses, ,e.g. prednisolone 0.5 mg/kg/day and may be used as rescue treatment over 1–3 days.,Third line therapies (immunomodulatory),Fourth line treatment-omalizumab (anti-IgE) have shown very good results in H1 antihistamine unresponsive chronic spontaneous urticaria, Pathophysiology : Weals are due to release of chemical mediators from tissue mast cells and circulating basophils. These chemical mediators include histamine, platelet-activating factor and cytokines. The mediators activate sensory nerves and cause dilation of blood vessels and leakage of fluid into surrounding tissues. Bradykinin release causes angioedema.Several hypotheses have been proposed to explain urticaria. The immune, arachidonic acid and coagulation systems are involved, and genetic mutations are under investigation.Chronic spontaneous urticaria is mainly idiopathic (cause unknown). An autoimmune cause is likely. About half of investigated patients carry functional IgG autoantibodies to immunoglobulin IgE or high-affinity receptor FceRIa., Epidemiology : Chronic spontaneous urticaria affects 0.5–2% of the population; in some series, two-thirds are women., variable, Your healthcare provider can use the results of allergy tests to help you figure out which substances bring on acute hives. Once you know your triggers, you can avoid them. You may want to : ,,Cut certain food products out of your diet.,Reduce exposure to airborne allergens.,Switch to detergents and soaps without scents or dyes.,Avoid extreme changes in temperature.,Relax and take a break when you’re stressed or overworked.,Wear loose-fitting, lightweight clothing., Complications : Anaphylaxis, Diagnostics : CRP, Radioallergosorbent test (RAST), Skin Prick test, Differential diagnosis : Bullous impetigo, Juvenile xanthogranuloma, Urticaria, disease description : The term ‘urticaria’ is being used increasingly to describe a disease that may present with short-lived itchy weals, angio-oedema or both.It may be spontaneous or inducible. There may be overlap between patterns of urticaria.Urticaria appears as raised, well-circumscribed areas of erythema (redness) and edema (swelling) involving the dermis and epidermis that are very pruritic (itchy), as shown in the image below. Acute urticaria can be caused by allergic reactions to foods, drugs, cosmetics, or soaps; infections; insect bites, stings, or exposure; environmental factors; latex; undue skin pressure, cold, or heat; emotional stress; and exercise, among other factors. It may be acute (< 6 wk) or chronic (>6 wk). Urticaria may be confused with a variety of other dermatologic diseases that are similar in appearance and are also pruritic; usually, however, it can be distinguished from these diseases by an experienced clinician. Urticaria is not contagious, unless the swollen hives themselves contain a pathogen.

Urticarial Vasculitis

Disease Name : Urticarial Vasculitis, Symptoms : Urticarial vasculitis : Patients most often present with classical indurated wheals that can be difficult to distinguish clinically from chronic idiopathic urticaria . However, unlike the latter, which is characterized by lesions that generally resolve within 2 to 8 hours and by definition within 24 hours, lesions of urticarial vasculitis last >24?h, often persisting for several days, and may leave behind a residual ecchymotic hyperpigmentation that is not seen in chronic idiopathic urticaria., Signs : nan, Treatment : First line treatments Second line treatments Third line treatments,Non-sedating H1,antihistamines,Non-steroidal anti-,inflammatory drugs,Dapsone,Colchicine,Hydroxychloroquine,Short trials of,corticosteroids,Azathioprine,Ciclosporin,Mycophenolate mofetil,Methotrexate,Intravenous immunoglobulins,Cyclophosphamide,?Interleukin Agonists,??Omalizumab, Pathophysiology : nan, Epidemiology : nan, Complications : nan, Diagnostics : Anti HBe Antibody ELISA, ANTI NUCLEAR ANTI BODY(ANA), COMPLEMENT 3(C3) LEVEL, Complete Blood Count CBC, Erythrocyte Sedimentation Rate (ESR), BIOPSY FROM SKIN LESION, URINE ANALYSIS (Volume), Differential diagnosis : Urticaria, disease description : Urticarial vasculitis is a rare disease characterized by continued wealing associated with histopathological evidence of leucocytoclastic vasculitis. If associated with systemic involvement, urticarial vasculitis can lead to substantial morbidity

Uterine Cancer

Disease Name : Uterine Cancer, Symptoms : Vaginal Discharge : Vaginal discharge that is watery, pink, or white instead of red., POSTMENOPAUSAL BLEEDING : Bleeding after menopause is a sign of uterine cancer., intermenstrual bleeding : Approximately 90% of people with uterine cancer experience abnormal vaginal bleeding. This symptom occurs in people with uterine cancer experiencing premenopause, perimenopause, and postmenopause and is considered the most common symptom., Signs : nan, Treatment : Surgery is usually the primary treatment for endometrial cancer. You’ll most likely have a hysterectomy, with the surgeon removing your uterus and cervix. There are three types of hysterectomy procedures : ,,Total abdominal hysterectomy : The surgeon makes an incision (cut) in your abdomen to access and remove your uterus.,Vaginal hysterectomy : The surgeon removes your uterus through your vagina.,Radical hysterectomy : If cancer has spread to your cervix, you may need a radical hysterectomy. The surgeon removes your uterus and the tissues next to your uterus. The surgeon also removes the top part of your vagina, next to your cervix.,Minimally invasive hysterectomy : The surgeon makes multiple small incisions (cuts) to remove your uterus. This may be done robotically., Pathophysiology : Researchers aren’t sure of the exact cause of uterine cancer. Something happens to create changes in cells in your uterus. The mutated cells grow and multiply out of control, which can form a mass called a tumor., Epidemiology : Endometrial cancer is a type of cancer that begins as a growth of cells in the uterus. The uterus is the hollow, pear-shaped pelvic organ where fetal development happens.,,Endometrial cancer begins in the layer of cells that form the lining of the uterus, called the endometrium. Endometrial cancer is sometimes called uterine cancer. Other types of cancer can form in the uterus, including uterine sarcoma, but they are much less common than endometrial cancer.,,Endometrial cancer is often found at an early stage because it causes symptoms. Often the first symptom is irregular vaginal bleeding. If endometrial cancer is found early, surgically removing the uterus often cures it., variable, Most of the time, you can’t prevent uterine cancer. But you can take steps to reduce your risk by : ,,Managing diabetes.,Maintaining a weight that’s healthy for you.,Talking to your provider about using progesterone-based or combined estrogen and progesterone hormonal contraceptives. These medications can offer some protection against uterine cancer., Complications : bleeding, infertility, Diagnostics : CA 125, TVS (Transvaginal ultrasound), MRI, CT SCAN, CT SCAN, HYSTEROSCOPY, ENDOMETRIAL BIOPSY, Differential diagnosis : adenomyosis, endometrial hyperplasia., Endometrial polyp, FIBROID UTERUS, ovulatory dysfunction, disease description : ?Uterine cancer is a general term that describes cancers of your uterus. Uterine cancer can refer to either endometrial cancer, uterine sarcoEndometrial cancer is a type of cancer that begins as a growth of cells in the uterus. The uterus is the hollow, pear-shaped pelvic organ where fetal development happens.Endometrial cancer begins in the layer of cells that form the lining of the uterus, called the endometrium. Endometrial cancer is sometimes called uterine cancer. Other types of cancer can form in the uterus, including uterine sarcoma, but they are much less common than endometrial cancer.Endometrial cancer is often found at an early stage because it causes symptoms. Often the first symptom is irregular vaginal bleeding. If endometrial cancer is found early, surgically removing the uterus often cures it.ma or other rare forms of cancer that can arise in your uterus.

Uterine Fibroids

Disease Name : Uterine Fibroids, Symptoms : "bloating : The exact cause of bloating with uterine fibroids isnt fully understood, but it likely relates to the fibroids putting pressure on nearby organs, such as the bladder or intestines.", constipation : Constipation can sometimes occur in the context of uterine fibroids due to their size and location. Large fibroids can press against the rectum, leading to difficulty in passing stools. Additionally, hormonal changes associated with fibroids can contribute to bowel irregularities, i, pelvic pain : Pelvic pain in the context of uterine fibroids is a common concern for many women. Fibroids are non-cancerous growths that can develop in the uterus and vary in size. When they grow large or press against other organs, they can cause discomfort or pain., "heavy menstrual bleeding : heavy menstrual bleeding in the context of uterine fibroids, its essential to consult with your healthcare provider. They can evaluate your symptoms, conduct tests if necessary, and discuss treatment options.", Signs : spotting : Spotting in the context of uterine fibroids can occur due to various reasons. Uterine fibroids are non-cancerous growths in the uterus that can cause symptoms like heavy menstrual bleeding, pelvic pain, and pressure on the bladder or rectum., pain during sex : Experiencing pain during sex in the context of uterine fibroids is a common concern for many individuals. Uterine fibroids are noncancerous growths in the uterus that can vary in size and location. When fibroids are located near the surface of the uterus or close to the cervix, they can sometimes cause discomfort or pain during sexual intercourse., Treatment : medication : Leuprolide/Leuprorelin, Tranexamic acid , Ibuprofen , <p><span style="color : rgb(13, 13, 13); font-family : Söhne, ui-sans-serif, system-ui, -apple-system, &quot;Segoe UI&quot;, Roboto, Ubuntu, Cantarell, &quot;Noto Sans&quot;, sans-serif, &quot;Helvetica Neue&quot;, Arial, &quot;Apple Color Emoji&quot;, &quot;Segoe UI Emoji&quot;, &quot;Segoe UI Symbol&quot;, &quot;Noto Color Emoji&quot;; font-size : 16px; white-space-collapse : preserve;">Surgical removal of fibroids while preserving the uterus, often recommended for women who want to maintain fertility.</span><br></p>, Pathophysiology : Fibroids are a result of the inappropriate growth of uterine smooth muscle tissue or myometrium. Their growth is dependent on estrogen and progesterone levels. The underlying pathophysiology is uncertain., Epidemiology : 20–30% of females, most often in women aged 30–50, the estimated incidence of fibroids in women by age 50 was 70% for white women and reached over 80% black women, prognosis of uterine fibroids varies extensively f, It might not be possible to prevent uterine fibroids. But only a small percentage of these tumors need treatment.,,You might be able to lower your fibroid risk with healthy lifestyle changes. Try to stay at a healthy weight. Get regular exercise. And eat a balanced diet with plenty of fruits and vegetables., Complications : Urinary Tract Infection, infertility, pelvic pain, heavy menstrual bleeding, miscarriages, Diagnostics : ultrasound, MRI, CT SCAN, HYSTEROSALPINGOGRAPHY, HYSTEROSCOPY, Differential diagnosis : adenomyosis, Endometrial polyps, Endometriosis, Ovarian Cyst, Pelvic Inflamatory Disease, disease description : Uterine fibroids or leiomyomata are the most common benign tumor affecting women. Fibroids originate from uterine smooth muscle cells (myometrium) whose growth is primarily dependent on the levels of circulating estrogen. Further information regarding the pathogenesis of fibroids is poorly understood. Fibroids can either present as an asymptomatic incidental finding on imaging, or symptomatically. Common symptoms include abnormal uterine bleeding, pelvic pain, disruption of surrounding pelvic structures(bowel and bladder), and back pain. Uterine fibroids typically are seen in three significant locations : subserosal (outside the uterus), intramural (inside the myometrium), and submucosal (Inside the uterine cavity).

Uterine Prolapse

Disease Name : Uterine Prolapse, Symptoms : hematuria : The most common complaint of female patients with uterine prolapse is the visualization or sensation of a bulge in the vaginal area, associated with vaginal pressure., hematuria : the sensation of incomplete bladder emptying, and dyspareunia., Signs : nan, Treatment : medication : Acridine Derivatives/Acriflavine, Early pregnancy — the pessary should be placed inside ,up to 18 weeks when the uterus becomes sufficiently ,enlarged to sit on the brim of the pelvis.,\x02 Puerperium — to facilitate involution.,\x02 Patients absolutely unfit for surgery specially with short ,life expectancy.,\x02 Patient’s unwillingness for operation.,\x02 While waiting for operation.,\x02 Additional benefits : Improvement of urinary symptoms ,(voiding problems, urgency)., Anterior colporrhaphy., Paravaginal defect repair,Vaginal repair of enterocele with PFR, McCall culdoplasty , Moskowitz procedure, Pathophysiology : Normal : External os lies at the level of ischeal spines. No prolapse  First degree : The uterus descends down from its normal anatomical position but the external os still remains above the introitus Second degree : The external os protrudes outside the vaginal introitus but the uterine body still remains inside the vagina. Third degree : (Syn : Procidentia, Complete prolapse) : The uterine cervix and body and the fundus descends to lie outside the introitus.  Procidentia involves prolapse of the uterus with eversion of the entire vagina., Epidemiology : "To reduce the risk of uterine prolapse, try to : ,,Prevent constipation. Drink plenty of fluids and eat high-fiber foods, such as fruits, vegetables, beans and whole-grains.,Avoid heavy lifting. If you have to lift something heavy, do it correctly. Correct lifting uses the legs instead of the waist or back.,Control coughing. Get treatment for a chronic cough or bronchitis. Dont smoke.,Avoid weight gain. Talk with your doctor about your ideal weight and get advice on how to lose weight, if you need to.", Complications : Anterior prolapse, Posterior vaginal prolapse, Diagnostics : USG Pelvis, CT PELVIS, MRI PELVIS, Differential diagnosis : abscess, cystocele, enterocele, rectocele, disease description : Uterine prolapse occurs when pelvic floor muscles and ligaments stretch and weaken until they no longer provide enough support for the uterus. As a result, the uterus slips down into or protrudes out of the vagina.

Uterine Rupture

Disease Name : Uterine Rupture, Symptoms : hematuria : begins with a “ripping” sensation. Subsequent contracts are often quite painful., hematuria : Pink, red, or brown urine can imply the presence of red blood cells, Signs : nan, Treatment : RESUSCITATION & LAPROTOMY, Pathophysiology : SPONTANEOUS During pregnancy : It is indeed rare for an apparently uninjured uterus to give way during pregnancy. The causes are : (1) Previous damage to the uterine walls following dilatation and curettage operation or manual removal of placenta. (2) Rarely in grand multiparae due to thin uterine walls. (3) Congenital malformation of the uterus (bicornuate variety) is a rare possibility. (4) In Couvelaire uterus. Spontaneous rupture during pregnancy is usually complete, involves the upper segment and usually occurs in later months of pregnancy. On rare occasion, spontaneous rupture may occur even in early months. During labor : Spontaneous rupture which occurs predominantly in an otherwise intact uterus during labor is due to : Obstructive rupture—This is the end result of an obstructed labor. The mechanism of rupture has already been described in. The rupture involves the lower segment and usually extends through one lateral side of the uterus to the upper segment.Nonobstructive rupture—Grand multiparae are usually aff ected and rupture usually occurs in early labor. Weakening of the walls due to repeated previous births as mentioned earlier may be the responsible factor. Th e rupture usually involves the fundal area and is complete. SCAR RUPTURE : With the liberal use of primary cesarean section, scar rupture constitutes significantly to the overall incidence of uterine rupture. The incidence of lower segment scar rupture is about 1–2%, while that following classical one is 5–10 times higher. Uterine scar, following operation on the nonpregnant uterus such as myomectomy or metroplasty hardly rupture as the wound heals well because the uterus remains quiescent following operation. Uterine scar following hysterotomy behaves like that of a classical scar and is of growing concern. During pregnancy : Classical cesarean or hysterotomy scar is likely to give way during later months of pregnancy. The weakening of such scar is due to implantation of the placenta over the scar and consequent increased vascularity. Right angle stretching effect by the increased transverse diameter of the enlarging uterus puts an additional effect in disruption of the upper segment scar. Lower segment scar rarely ruptures during pregnancy During pregnancy : Classical cesarean or hysterotomy scar is likely to give way during later months of pregnancy. The weakening of such scar is due to implantation of the placenta over the scar and consequent increased vascularity. Right angle stretching effect by the increased transverse diameter of the enlarging uterus puts an additional effect in disruption of the upper segment scar. Lower segment scar rarely ruptures during pregnancy. During labor : The classical or hysterotomy scar or cornual resection for ectopic pregnancy is more vulnerable to rupture during labor. Although rare, lower segment scar predominantly ruptures during labor. IATROGENIC OR TRAUMATIC During pregnancy : (1) Injudicious administration of oxytocin. (2) Use of prostaglandins for induction of abortion or labor. (3) Forcible external version especially under general anesthesia. (4) Fall or blow on the abdomen. During labor : (1) Internal podalic version—especially following obstructed labor. (2) Destructive operation. (3) Manual removal of placenta. (4) Application of forceps or breech extraction through incompletely dilated cervix. (5) Injudicious administration of oxytocin for augmentation of labor.. Pathologically, it is customary to distinguish between complete and incomplete rupture depending on whether the peritoneal coat is involved or not. So far from the treatment point of view, it matters little. In incomplete rupture, the peritoneum remains intact. Incomplete rupture usually results from rupture of the lower segment scar or extension of a cervical tear into the lower segment with formation of a broad ligament hematoma. Complete rupture usually occurs following disruption of the scar in upper segment. It may also be due to spontaneous rupture of both obstructive and nonobstructive type. SITES : Spontaneous nonobstructive rupture usually involves the upper segment and often involves the fundus. Whereas, in obstructive type, the rupture involves the anterior lower segment transversely and often extends upward along the lateral uterine wall. The margins are ragged and necrosed. On occasion, the posterior wall may be involved due to friction with the sacral promontory. Not infrequently, the tear extends downward to involve the cervix and the vaginal wall (colporrhexis). The bladder may be involved, at times. Rupture over the previous scar is almost always located at the site of the scar. The margins of the ruptured cesarean scar are usually clean and look fibrosed. The rent over the lower segment scar may extend to one or both the sides to involve the major branches of uterine vessels. The morbid pathology of traumatic rupture following destructive operation or internal version is almost similar to that met in spontaneous obstructive variety. This may at times be indistinguishable., Epidemiology : 1 in 2, 000 to 1 in 200 deliveries1 in 2, 000 to 1 i, POOR, Complications : Haemorrhage, signs of shock, Diagnostics : Complete Blood Count CBC, TVS (Transvaginal ultrasound), USG ABDOMEN(W/A), Differential diagnosis : nan, disease description : Disruption in the continuity of the all uterine layers (endometrium, myometrium and serosa) any time beyond 28 weeks of pregnancy is called rupture of the uterus. Small rupture to the wall of the uterus in early months is called perforation either instrumental or perforating hydatidiform mole. Rupture of a rudimentary pregnant horn has got a special clinical entity and is grouped in ectopic pregnancy.

Uveitis With Ankylosing Spondylitis

Disease Name : Uveitis With Ankylosing Spondylitis, Symptoms : acute, recurrent, non-granulomatous type of iridocyclitis, Signs : nan, Treatment : medication : Naproxen , Phenylbutazone, Long-term aspirin or,indomethacin may decrease the recurrences., Pathophysiology : Uveitis associated with ankylosing spondylitis is characteristically an acute, recurrent, non-granulomatous type of iridocyclitis. The disease usually affects one eye at a time., Epidemiology : nan, Complications : nan, Diagnostics : nan, Differential diagnosis : acute angle-closure glaucoma, conjunctivitis, CORNEAL ULCER, SCLERITIS, disease description : Ankylosing spondylitis is an idiopathic chronic inflammatory arthritis, usually involving the sacroiliac and posterior inter-vertebral joints. The disease affects young males (20–40 years) who are positive for HLA-B27. About 30 to 35% patients with ankylosing spondylitis develop uveitis.

Uveitis

Disease Name : Uveitis, Symptoms : eye pain : Uveitis is inflammation of the middle layer of the eye, called the uvea or uveal tract. It can cause eye pain., floaters in eyes : Affected individuals experience floaters., photophobia : Light sensitivity is intense in uveitis., blurred vision : The blurring of vision in uveitis lasts up to 8 weeks., Signs : nan, Treatment : "Eyedrops are usually not enough to treat inflammation beyond the front of the eye, so a corticosteroid injection in or around the eye or corticosteroid tablets (taken by mouth) may be necessary.,Drugs that control spasms,antibiotics, antiviral medications or other medicines, with or without corticosteroids, to bring the infection under control.,immunosuppressive drugs if your uveitis affects both eyes, doesnt respond well to corticosteroids or becomes severe enough to threaten your vision.", "Vitrectomy. Surgery to remove some of the vitreous in your eye is rarely used to diagnose or manage the condition.,A medication-releasing implant. For people with difficult-to-treat posterior uveitis, a device thats implanted in the eye may be an option. This device slowly releases corticosteroid into the eye for two to three years.", Pathophysiology : Inflammation of the uvea fundamentally has the same characteristics as any other tissue of the body, i.e., a vascular and a cellular response. However, due to extreme vascularity and looseness of the uveal tissue, the inflammatory responses are exaggerated and thus produces special results. Pathologically, inflammations of the uveal tract may be divided into suppurative (purulent) and non-suppurative (non-purulent) varieties. Wood has further classified non-suppurative uveitis into nongranulomatous and granulomatous types. Although morphologic description is still of some value, the rigid division of uveitis by Wood into these two categories has been questioned on both clinical and pathological grounds. Certain transitional forms of uveitis have also been recognised. Some of these (e.g., phacoanaphylactic endophthalmitis and sympathetic ophthalmia) showing pathological features of granulomatous uveitis are caused by hypersensitivity reactions. While uveitis due to tissue invasion by leptospirae presents with manifestation of nongranulomatous uveitis. Nonetheless, the classification is often useful in getting oriented towards the subject of uveitis, its workup and therapy. , Epidemiology : The prevalence of uveitis ranged from 152 per 100, 000 persons in China, to 173 per 100, 000 persons in South Korea (14), to 194 per 100, 000 persons in Taiwan (15). The prevalence from studies in India ranged from 317 per 100, 000 (16) to 730 per 100, 000 (17)., variable, Healthcare providers usually don’t know what causes most cases of uveitis. There isn’t much you can do to prevent the disease.,,Doing what you can to maintain good eye health is always wise. Getting care for diseases, infections or other health conditions linked to uveitis can help protect your vision. You can also lower your risk by quitting smoking., Complications : Glaucoma, Macular edema, Retinal damage, permanent vision loss, cataracts, Diagnostics : FUNDOSCOPY, Optical coherence tomography (OCT), Slit lamp examination, TONOMETRY TEST, Fluorescein angiography, Differential diagnosis : nan, disease description : Uveitis is inflammation inside your eye. Inflammation usually happens when your immune system is fighting an infection. Sometimes uveitis means your immune system is fighting an eye infection — but it can also happen when your immune system attacks healthy tissue in your eyes. Uveitis can cause problems like pain, redness, and vision loss.Uveitis damages the part of the eye called the uvea — but it often affects other parts of the eye, too. Sometimes uveitis goes away quickly, but it can come back. And sometimes it’s a chronic (long-term) condition. It can affect 1 eye or both eyes.

Vaccinia

Disease Name : Vaccinia, Symptoms : redness on skin : The initial clinical signs of the infection are focal red skin areas., Common Cold : General symptoms similar to those of a cold such as sneezing, stuffy nose, runny nose, sore throat, coughing, post-nasal drip, watery eyes & rarely fever., Signs : nan, Treatment : Care after vaccination should include adequate coverage of the ,vaccination site and avoidance of close contact with individuals ,who are immunosuppressed or atopic., Supportive treatment such as pain relief,• Vaccinia immune globulin intravenous (VIGIV)* can be given and most effective when administered,early in the course of illness.,• When VIGIV is inadequate or not readily available, Tecovirimat*, Cidofovir*, and Brincidofovir may,be considered as secondary or alternative treatment, though none of these are currently FDA,approved. Clinicians can also consider antiviral treatment in consultation with their LHJ, WA DOH,CD Epi and CDC., Pathophysiology : Poxviruses are unique among DNA viruses because they replicate only in the cytoplasm of the host cell, outside of the nucleus. Therefore, the large genome is required for encoding various enzymes and proteins involved in viral DNA replication and gene transcription. During its replication cycle, VV produces four infectious forms which differ in their outer membranes : intracellular mature virion (IMV), the intracellular enveloped virion (IEV), the cell-associated enveloped virion (CEV) and the extracellular enveloped virion (EEV). Although the issue remains contentious, the prevailing view is that the IMV consists of a single lipoprotein membrane, while the CEV and EEV are both surrounded by two membrane layers and the IEV has three envelopes. The IMV is the most abundant infectious form and is thought to be responsible for spread between hosts. On the other hand, the CEV is believed to play a role in cell-to-cell spread and the EEV is thought to be important for long range dissemination within the host organism., Epidemiology : Approximately 15%--25% of affected vaccinees with this complication die, and 25% have permanent neurological sequelae, variable, Vaccination with vaccinia virus has been directly responsible for the successful eradication of smallpox (variola)., Complications : ENCEPHALITIS, Diagnostics : PCR, full thickness skin biopsy, Differential diagnosis : erythema multiforme, Impetigo, disease description : Vaccinia virus (VACV or VV) is a large, complex,  enveloped virus belonging to the poxvirus family. It has a linear, double-stranded DNA genome approximately 190 kbp in length, which encodes approximately 250 genes. The dimensions of the virion are roughly 360 × 270 × 250 nm, with a mass of approximately 5–10 fg. The vaccinia virus is the source of the modern smallpox vaccine, which the World Health Organisation used to eradicate smallpox in a global vaccination campaign in 1958–1977. Although smallpox no longer exists in the wild,  vaccinia virus is still studied widely by scientists as a tool for gene therapy and genetic engineering.

Vaginal Cancer

Disease Name : Vaginal Cancer, Symptoms : Vaginal Discharge : Vaginal discharge that’s watery, bloody or foul-smelling., dysuria : Vaginal cancer causes painful urination., pelvic pain : Along with dysuria, patientes experience intense pelvic pain., DYSPAREUNIA : It is defined as persistent or recurrent genital pain that occurs just before, during or after sex., POSTCOITAL BLEEDING : Postcoital bleeding can be one of the first indications of vaginal cancer., post menopausal bleed : Vaginal bleeding after menopause., Signs : nan, Treatment : medication : Dactinomycin (Actinomycin D), Ifosfamide /Isophosphamide, Cisplatin , Cyclophosphamide , Vincristine, Immunotherapy is a treatment that uses the patient’s immune system to fight cancer. Substances made by the body or made in a laboratory are used to boost, direct, or restore the body’s natural defenses against cancer. This cancer treatment is a type of biologic therapy., local excision biopsy, CO2 laser and local application of,5-fluorouracil cream, Radiation therapy is a cancer treatment that uses high-energy x-rays or other types of radiation to kill cancer cells or keep them from growing. There are two types of radiation therapy : ,,External radiation therapy uses a machine outside the body to send radiation toward the area of the body with cancer.,Internal radiation therapy uses a radioactive substance sealed in needles, seeds, wires, or catheters that are placed directly into or near the cancer., Wertheim hysterectomy with total colpectomy, , Pathophysiology : Vaginal cancer is not common. There are two main types of vaginal cancer : Squamous cell carcinoma : Cancer that forms in the thin, flat cells lining the inside of the vagina. Squamous cell vaginal cancer spreads slowly and usually stays near the vagina, but may spread to the lungs, liver, or bone. This is the most common type of vaginal cancer.Adenocarcinoma : Cancer that begins in glandular cells. Glandular cells in the lining of the vagina make and release fluids such as mucus. Adenocarcinoma is more likely than squamous cell cancer to spread to the lungs and lymph nodes. A rare type of adenocarcinoma (clear cell adenocarcinoma) is linked to being exposed to diethylstilbestrol (DES) before birth. Adenocarcinomas that are not linked with being exposed to DES are most common in women after menopause., Epidemiology : less than 0.2% of all cancers in women, DEPENDS ON THE STAGE OF CANCER, You can’t prevent vaginal cancer, but you can reduce your risk.,,Get regular pelvic exams and Pap tests. Talk with your provider about how regularly you should be receiving routine checks from your gynecologist.,Get the HPV vaccine. Talk to your provider about getting vaccinated against HPV. Currently, there are three FDA-approved vaccines available, Gardasil, Gardasil 9 and Cervarix.,Don’t smoke. Smoking increases your risk of all cancers, including vaginal cancer., Complications : Haemorrhage, METASTASES AT DIFFERENT SITES, Diagnostics : PET SCAN, MRI, CT SCAN, CYSTOSCOPY, Differential diagnosis : Basal cell carcinoma, CANCER CERVIX, candidiasis, CARCINOMA RECTUM, cutaneous melanoma, Mycosis fungoides, squamous cell carcinoma., disease description : Vaginal cancer is a disease in which malignant (cancer) cells form in the vagina.Older age and having an HPV infection are risk factors for vaginal cancer.Signs and symptoms of vaginal cancer include pain or abnormal vaginal bleeding.Tests that examine the vagina and other organs in the pelvis are used to diagnose vaginal cancer.Certain factors affect prognosis (chance of recovery) and treatment options.

Vaginismus

Disease Name : Vaginismus, Symptoms : hyperaesthesia, pelvic pain, DYSPAREUNIA, HYMEN LACERATIONS, VAGINAL SORENESS, Signs : painful intercourse, anxiety disorders, Treatment : BOTH THE PARTNERS ARE COUNSELLED PROPERLY, Botulinum neurotoxin type A injection into levator ani,muscle 4 weekly improves vaginismus., If a rigid hymen appreciated as a sickle-like band resistant to,stretching is encountered under anaesthesia, the operation of,perineotomy (or Fenton’s operation) should be performed, Pathophysiology : In primary vaginismus there is no organic lesion present, whereas in secondary vaginismus some obvious painful lesion in the region of the genital tract can be found on examination. In primary vaginismus, when the patient is being examined and an attempt is made to inspect the vulva by separating the labia, a muscle spasm is induced whereby the thighs are drawn together, the levator muscles become tonically contracted and the patient cries out and endeavours to push the medical attendant away from her. In secondary vaginismus, a minor degree of spasm is induced by painful local lesions such as small infected lacerations of the hymen, urethral caruncle, vulvitis, or a sequela of vaginal operations for the repair of prolapse when, as a result of the operation, the calibre of the introitus and the vagina is narrowed. The operation scar is naturally sensitive for some weeks after the repair, and premature attempts at coitus are painful. It is thus easy for organic dyspareunia to lead to a protective spasm in order to avoid the pain of coitus. The spasm is not unlike that seen in primary vaginismus, although it is never of the same degree. Removal of the cause will cure this condition, whereas true vaginismus requires prolonged therapy and the results are not always satisfactory., Epidemiology : GOOD, To Do : PROPER COUNSELLING OF BOTH THE PARTNERS ,Coitus should not be attempted until the perineotomy wound has healed soundly, usually in 3 or 4 weeks., Complications : nan, Diagnostics : BIMANUAL EXAMINATION, Differential diagnosis : nan, disease description : Vaginismus is regarded as hyperaesthesia which leads to spasm of the sphincter vagina and the levator ani muscles during attempted coitus or when an attempt is made to examine the patient vaginally.

Vaginitis

Disease Name : Vaginitis, Symptoms : vaginal bleeding : Bleeding related to vaginitis is usually light., itching : The infection causes extreme vaginal itching., Vaginal Discharge : A heavy vaginal discharge that may be yellow-gray or green in color., dysuria : Painful urination is commonly experienced by the patients., DYSPAREUNIA : It is a persistent or recurrent genital pain that occurs just before, during or after sex., Signs : nan, Treatment : medication : Doxycycline , Fluconazole , Metronidazole , Vulvar hygiene : Proper wiping (front to back) will ,reduce rectal flora to invade the vulvovaginal area. Sitz baths are very helpful in relieving symptoms ,(baking soda in water).,Avoiding chemical irritants—soaps, shampoos, etc., To keep the local area dry., To wear cotton undergarments., To reduce the overgrowth of pathogenic bacteria, ,Amoxicillin 20–40 mg/kg/day in 3 divided doses is ,effective., In refractory cases, estrogen locally as cream twice ,daily for 3 weeks is effective to improve the vaginal ,defense and to promote healing, Pathophysiology : Changing any element of the vaginal ecology can alter the population characteristics of the vaginal bacteria. Changes in hormonal status, as previously mentioned with estrogen, can greatly shift the makeup of the flora. Menses can act as a nutrient base for some bacterial species leading to their overgrowth, but there is no clear evidence that this is associated with pathogens or infection. Broad-spectrum antibiotic use can lead to alteration of the vaginal bacterial flora leading to Candida species overgrowth. Douching and unprotected vaginal intercourse can increase pH as well., Epidemiology : Vaginitis is common in adult women and uncommon in prepubertal girls. Bacterial vaginosis accounts for 40-50% of vaginitis cases;, good, There are certain things that you can do to decrease your chance of getting vaginitis.,,1. Avoid wearing clothes that hold in heat and moisture.,2. Avoid staying in a wet bathing suit or sweaty workout clothes for too long.,3. Try yogurt and probiotics containing lactobacillus.,4. Avoid cleaning your vagina with heavily perfumed soaps or sprays. ,5. Don’t douche.,6. Use condoms and dental dams. ,7. Ask your healthcare provider about the benefits of taking hormones.,8. Get regular screenings., Complications : SEXUALLY TRANSMITTED DISEASE, Diagnostics : Gram Staining, X RAY PELVIS, X RAY PELVIS, BACTERIOLOGY, Differential diagnosis : Cervicitis, HERPES SIMPLEX, Pinworm infestation, urinary tract infections, disease description : Vaginitis is an inflammation of the vagina that can result in discharge, itching and pain. The cause is usually a change in the balance of vaginal bacteria or an infection. Reduced estrogen levels after menopause and some skin disorders also can cause vaginitis.

Valley Fever

Disease Name : Valley Fever, Symptoms : flu-like symptoms : Includes fever, cough, body ache. fatigue. muscle pain, headache., Gastrointestinal symptoms : Includes loss of appetite, nausea & vomiting., jaundice : Hemorrhagic fever, which occurs in less than 1% of all RVF patients. Symptoms of hemorrhaging may begin with jaundice and other signs of liver impairment, followed by vomiting blood, bloody stool, or bleeding from gums, skin, nose, and injection sites., organ damage : It can spread to your skin, bones, joints, liver, pancreas, kidneys and brain., brain problem : When coccidioidomycosis spreads to your brain, you can develop coccidioidal meningitis, a life-threatening condition., Signs : nan, Treatment : Fluconazole.,Itraconazole.,Amphotericin B (AmB)., Pathophysiology : Anyone who breathes in the fungus can get infected, but Valley fever is most common in adults over age 60.Certain people are also at higher risk : People with weakened immune systems, which can be caused by certain medications or diseases like HIV/AIDS.Pregnant people in their third trimester.People living with diabetes.Blacks and Filipinos.People who have jobs that expose them to soil dust.Anyone who’s recently traveled or moved to an area where the fungus lives.About 20, 000 people are diagnosed with Valley fever each year. It’s most common in California and Arizona.The Coccidioides fungus breaks apart into microscopic reproductive parts (spores) that travel through the air you breathe. They settle into the airways in your lungs where they grow into larger clusters of more spores (spherules).The spherules can break apart and send more spores out into other parts of your lungs and sometimes other parts of your body. Those spores can grow into spherules of more spores and keep spreading the fungus in your body., Epidemiology : 161.1 per 100, 000 population in 2020 and stayed relatively even at 159.8 per 100, 000 population in 2021, while incidence in California dipped to 16.9 per 100, 000 in 2020 before rising to 20.7 per 100, 000 in 2021, variable, - It’s very difficult to avoid breathing in the fungus Coccidioides in areas where it’s common in the environment. ,,- People who live in these areas can try to avoid spending time in dusty places as much as possible. People who are at risk for severe Valley fever (such as people who have weakened immune systems, pregnant women, people who have diabetes, or people who are Black or Filipino) may be able to lower their chances of developing the infection by trying to avoid breathing in the fungal spores.,,- Avoid activities that involve close contact to dirt or dust, including yard work, gardening, and digging.,,- Use air filtration measures indoors.,,- Clean skin injuries well with soap and water to reduce the chances of developing a skin infection, especially if the wound was exposed to dirt or dust.,,- Take preventive antifungal medication if your healthcare provider says you need it., Complications : severe pneumonia\\/very severe pneumonia, Diagnostics : Skin test, PCR, X RAY, Differential diagnosis : anemia, Blastomycosis dermatology, granuloma, Histoplasmosis, LUNG ABSCESS, lymphoma, disease description : An infection with the fungus coccidioides.The coccidioides fungus is found in soil and causes infection when inhaled. People with suppressed immune systems are particularly at risk.The initial form is often mild, with few symptoms. When symptoms do occur, they may resemble those of the flu, including fever, cough, chills and chest pain.Mild cases clear up on their own. If symptoms dont improve, antifungal medication may be necessary

Valvular Heart Disease

Disease Name : Valvular Heart Disease, Symptoms : fatigue : Fatigue in such patients is intense., "palpitations : Palpitations (irregular or rapid heartbeats caused by problems with the hearts electrical system) can sometimes be a symptom of valvular heart disease.", chest discomfort : Chest discomfort, especially when you exert yourself., edema : Swelling of the ankles, feet or abdomen., heart murmurs : In adults, worrisome heart murmurs are usually due to heart valve problems that develop later in life. A murmur is caused by turbulent or abnormal blood flow across your heart valves. If blood is flowing more rapidly than normal, it can cause an innocent heart murmur., shortness of breath : Increasing shortness of breath, especially with physical activity or lying down., Signs : nan, Treatment : In many patients, this compensatory mechanism cannot be maintained indefinitely, and systolic function begins to decline as a result of the pressure overload. If LV systolic dysfunction is present, it often improves after aortic valve replacement (AVR). ,Percutaneous balloon valvotomy of the aortic valve may be a reasonable option for the treatment of adolescents and young adults with noncalcified aortic valves., Pathophysiology : Valve conditions may be congenital, arise from inflammation, or occur due to complications from infections. Mild or moderate disease is usually asymptomatic at first, but due to the progressive and degenerative nature of the disease, may eventually become severe and lead to heart failure and death if left untreated. In general, VHD is related to aging. Prevalence is increasing as the U.S. population ages and lives longer. Aortic stenosis is the most common valve disease in the United States, followed by mitral regurgitation, aortic regurgitation, and mitral stenosis., Epidemiology : About 2.5% of the U.S. population has valvular heart disease, variable, Although you can’t change some risk factors, like growing older, there are things you can do that may reduce your risk of heart valve disease. These include : ,,Getting treatment quickly for infections.,Being physically active.,Eating healthy foods.,Staying at a healthy weight.,Continuing to take medicine for high blood pressure and/or high cholesterol if you have those conditions.,Not using tobacco products.,Not using recreational drugs, especially IV drugs which increase your risk for heart valve infection., Complications : cardiac failure, Stroke, Diagnostics : 2-D Echo, X RAY CHEST, cardiac HR MRI, CARDIAC MRI, Differential diagnosis : aortic stenosis, coronary artery disease, restrictive cardiomyopathy, RHEUMATIC HEART DISEASE, disease description : Valvular heart disease (VHD) is characterized by damage to or a congenital defect in one or more heart valves : mitral, aortic, tricuspid, and pulmonary. Heart valves have a single function : to permit unobstructed forward blood flow through the heart. Damaged or defective valves can cause two types of problems : either they fail to open properly (a condition called stenosis) impeding blood flow, or they leak (a condition called regurgitation) permitting back flow. Regurgitation occurs because a valve does not close tightly, which allows blood to flow back into the previous chamber from where it came. Mitral regurgitation is most often due to prolapse, a condition in which the valve leaflets bulge into the left atrium during a heartbeat. Stenosis occurs when the heart valve cannot fully open because the valve flaps, or ring, have become thick, stiff, or fused together, preventing sufficient supply of blood to flow through the valve.

Varicella Zoster

Disease Name : Varicella Zoster, Symptoms : flu-like symptoms : Includes fever, body ache, tiredness, headache, loss of appetite., Rashes : Raised bumps called papules, which break out over a few days. Small fluid-filled blisters called vesicles, which form in about one day and then break and leak. Crusts and scabs, which cover the broken blisters and take a few more days to heal., Signs : nan, Treatment : medication : Valaciclovir , Famciclovir , Aciclovir , Acyclovir (800 mg by mouth five times daily), valacyclovir,(1 g three times daily), or famciclovir (250 mg three times daily) for,5–7 days is recommended for adolescents and adults with chickenpox of =24 h duration. (Valacyclovir is licensed for use in children,and adolescents. Famciclovir is recommended but not licensed for,varicella.) Likewise, acyclovir therapy may be of benefit to children,<12 years of age if initiated early in the disease (<24 h) at a dose of,20 mg/kg every 6 h., Pathophysiology : Transmission occurs readily by the respiratory route; the subsequent localized replication of the virus at an undefined site (presumably the nasopharynx) leads to seeding of the lymphatic/reticuloendothelial system and ultimately to the development of viremia. Viremia in patients with chickenpox is reflected in the diffuse and scattered nature of the skin lesions and can be confirmed in selected cases by the recovery of VZV from the blood or routinely by the detection of viral DNA in either blood or lesions by polymerase chain reaction (PCR). Vesicles involve the corium and dermis, with degenerative changes characterized by ballooning, the presence of multinucleated giant cells, and eosinophilic intranuclear inclusions. Infection may involve localized blood vessels of the skin, resulting in necrosis and epidermal hemorrhage. With the evolution of disease, the vesicular fluid becomes cloudy because of the recruitment of polymorphonuclear leukocytes and the presence of degenerated cells and fibrin. Ultimately, the vesicles either rupture and release their fluid (which includes infectious virus) or are gradually reabsorbed. Recurrent Infection The mechanism of reactivation of VZV that results in herpes zoster is unknown. The virus infects dorsal root ganglia during chickenpox, where it remains latent until reactivated. Histopathologic examination of representative dorsal root ganglia during active herpes zoster demonstrates hemorrhage, edema, and lymphocytic infiltration. Latent virus been detected in sensory (dorsal, cranial, and enteric) ganglia. Active replication of VZV in other organs, such as the lung or the brain, can occur during either chickenpox or herpes zoster but is uncommon in the immunocompetent host. Pulmonary involvement is characterized by interstitial pneumonitis, multinucleated giant cell formation, intranuclear inclusions, and pulmonary hemorrhage. , Epidemiology : excellent, The best way to prevent chickenpox is to get the chickenpox vaccine. Everyone—including children, adolescents, and adults—should get two doses of chickenpox vaccine if they have never had chickenpox or were never vaccinated., Complications : PNEUMONIA, secondary infection, Diagnostics : PCR, MRI, DIRECT FLORESCENT ANTIBODY TESTING, Viral cultures, Differential diagnosis : Dermatitis herpetiformis, Impetigo, insect bites, Small pox, disease description : Varicella-zoster virus (VZV) causes two distinct clinical syndromes : varicella (chickenpox) and herpes zoster (shingles). Chickenpox, a ubiquitous and extremely contagious infection, is usually a benign illness of childhood characterized by an exanthematous vesicular rash. With reactivation of latent VZV (which is most common after the sixth decade of life), herpes zoster presents as a dermatomal vesicular rash and is usually associated with severe pain.

Varicocele

Disease Name : Varicocele, Symptoms : testicular atrophy : Testicular atrophy refers to a condition wherein the testicles gradually shrink in size., Pain : A dull, aching pain or discomfort is more likely when standing or late in the day. Lying down often relieves pain., infertility : A varicocele may lead to difficulty fathering a child, but not all varicoceles cause infertility., scrotal swelling : If a varicocele is large enough, a mass like a "bag of worms" may be visible above the testicle. A smaller varicocele may be too small to see but noticeable by touch., Signs : nan, Treatment : percutaneous embolisation,of the gonadal veins is the usual first-line intervention., Microscopic varicocelectomy. The surgeon makes a tiny incision low in the groin. Using a powerful microscope, the surgeon identifies and ligates several small veins. The procedure usually lasts 2 to 3 hours.,Laparoscopic varicocelectomy. The surgeon performs the procedure using a video camera and surgical tools attached to tubes that pass through a few very small incisions in the lower abdomen. Because the network of veins are less complex above the groin, there are fewer veins to ligate. The procedure usually last 30 to 40 minutes., Pathophysiology : The veins draining the testis and the epididymis form the pampiniform plexus. The veins gradually join each other as they traverse the inguinal canal and at, or near, the inguinal ring, there are only one or two testicular veins, which pass upwards within the retroperitoneum. The left testicular vein empties into the left renal vein while the right empties into the inferior vena cava below the right renal vein. The testicular veins usually have valves near their terminations, but these are sometimes absent. There is an alternative (collateral) venous return from the testes through the cremasteric veins, which drain mainly into the inferior epigastric veins., Epidemiology : 15–20% of adult, Approximately 15-20% of the healthy fertile male population is estimated to have varicoceles, GOOD, Medical experts aren’t sure what causes varicoceles to develop. As a result, they’re not sure how you can prevent them., Complications : infertility, Diagnostics : ultrasound, Differential diagnosis : epididymitis, HYDROCELE, Inguinal Hernias, Spermatocele, TORSION OF TESTIS, Trauma, disease description : A varicocele is an abnormal dilatation and tortuosity of the veins of the spermatic cord. Although varicoceles are common in the general population and are frequently found on routine physical examinations, they represent the most common correctable cause of male factor infertility. Varicoceles are also often incidental findings on imaging studies, particularly scrotal ultrasound.

Varicose Veins

Disease Name : Varicose Veins, Symptoms : swelling : Your legs, ankles and feet can swell and throb., Pain : Legs may be painful, achy or sore, especially behind your knees. You might have muscle cramps., itching : The area around varicose veins may itch., Veins become tortuous and engorged : Twisted, swollen, rope-like veins are often blue or purple. They appear just below the surface of the skin on your legs, ankles and feet. They can develop in clusters. Tiny red or blue lines (spider veins) may appear nearby., heaviness in legs : Muscles in your legs may feel tired, heavy or sluggish, especially after physical activity., Signs : "ECZEMA : Varicose eczema, also known as venous, gravitational or stasis eczema, is a long-term skin condition that affects the lower legs. Its common in people with varicose veins. Varicose eczema tends to be a long-term problem. However, treatments are available to help keep it under control.", EXERCISE INTOLERANCE : High-impact exercises like jogging and jumping can increase blood pressure in the legs, which can feel uncomfortable., pigmentation on skin : Varicose veins, skin discoloration occurs during the more advanced stages of venous reflux. The initial redness is from inflammation. As blood continues to pool under the skin, the breakdown of red blood cells causes the skin damage to advance and take on a tan or reddish-brown appearance., ulceration : Venous ulcers typically occur because of damage to the valves inside the leg veins., edema : Poor circulation brought on by varicose veins may lead to edema., TORTOUS VEINS : Varicose veins are tortuous, widened veins in the subcutaneous tissues of the legs and are often easily visible. Their valves are usually incompetent so that reflux of blood occurs, and the resulting venous hypertension can cause symptoms., Visible palpable dilated and tortuous veins in the subcutis : Varicose veins are tortuous, widened veins in the subcutaneous tissues of the legs and are often easily visible. Their valves are usually incompetent so that reflux of blood occurs, and the resulting venous hypertension can cause symptoms., Telangiectases (spider veins : Spider veins, also known as telangiectasias or thread veins, are prominent clusters of damaged small blood vessels in the skin. They can appear as red, blue, or purple tortious lines bulging and branching out from a central locus resulting in a spider-like appearance., lipodermatosclerosis : Lipodermatosclerosis is a consequence of localized chronic inflammation and fibrosis of the skin and subcutaneous tissue of the lower part of the leg. The skin changes will often occur at the “gaiter area” above the medial malleolus., Treatment : Self-care — such as exercise, raising the legs when sitting or lying down, or wearing compression stockings — can help ease the pain of varicose veins and might prevent them from getting worse.,Wearing compression stockings all day is often the first approach to try. The stockings squeeze the legs, helping veins and leg muscles move blood more efficiently. The amount of compression varies by type and brand.,,Compression stockings are available at most pharmacies and medical supply stores. Prescription-strength stockings also are available and may be covered by insurance if varicose veins are causing symptoms., Offer endothermal ablation and endovenous laser treatment of ,the long saphenous vein,If endothermal ablation is unsuitable, offer ultrasound-guided,foam sclerotherapy,If ultrasound-guided foam sclerotherapy is unsuitable, offer ,surgery. If incompetent varicose tributaries are to be treated, ,consider treating them at the same time, "Sclerotherapy. A health care provider injects the varicose veins with a solution or foam that scars and closes those veins. In a few weeks, treated varicose veins should fade.,,The same vein might need to be injected more than once. Sclerotherapy doesnt require anesthesia and can be done in a health care providers office.,,Laser treatment. Laser treatment sends strong bursts of light onto the vein, which makes the vein slowly fade and disappear. No cuts or needles are used.,Catheter-based procedures using radiofrequency or laser energy. This procedure is the preferred treatment for larger varicose veins. A health care provider inserts a thin tube (catheter) into an enlarged vein and heats the tip of the catheter using either radiofrequency or laser energy. As the catheter is removed, the heat destroys the vein by causing it to collapse and seal shut.,High ligation and vein stripping. This procedure involves tying off a vein before it joins a deep vein and removing the vein through small cuts. This is an outpatient procedure for most people. Removing the vein wont keep blood from flowing in the leg because veins deeper in the leg take care of the larger volumes of blood.,Ambulatory phlebectomy (fluh-BEK-tuh-me). A health care provider removes smaller varicose veins through a series of tiny skin punctures. Only the parts of the leg that are being pricked are numbed in this outpatient procedure. Scarring is generally minimal.", Pathophysiology : A myriad of intrinsic and extrinsic factors contribute to the formation of varicose veins, including age, gender, pregnancy, obesity, height, race, diet, occupation, history of deep vein thrombosis (DVT), and genetics. The primary pathologies related to varicose veins are; 1) elevated venous pressure in the extremities and 2) defective or incompetent valves resulting in reflux and, thus, elevated venous pressure in the extremity. Whether venous hypertension and valvular incompetence occur before the irreversible alterations of venous wall development or the reverse is still inconclusive. Several pathophysiological mechanisms, including hypoxia, cellular hyperplasia, and dysregulated apoptosis, might affect and change the combination of the extracellular matrix in the involved vein at the cellular level.   Incompetent venous valves result in the backward transmission of the pressure gradient. The pressure gradient would be transmitted from the deep to the superficial venous system via the saphenofemoral junction (SFJ) and perforator veins. The most common site for the incompetent venous valve is the below-knee great saphenous vein. Moreover, venous hypertension has been correlated with the severity of the disease. Any conditions with increased intraabdominal pressure, including pregnancy and obesity in individuals with incompetent lower leg valves, might impose a higher risk for varicose veins. A limited number of genetic disorders have been correlated with varicose veins disease. Accordingly, the correlation between Klippel-Trenaunay syndrome and varicose vein disease has been well established. Moreover, mutations in FOXC2, thrombomodulin (THBD), and desmuslin (SYNM) may alter vein function and impose the risk of varicose vein development., Epidemiology : between 10-30% of the population., The incidence of varicose veins is unknown, variable, You may not be able to prevent varicose veins. You can reduce your chances of developing them by living an active, healthy lifestyle. Healthcare providers recommend many of the same measures to prevent and treat varicose veins : ,,1. Avoid long periods of standing.,2. Elevate your legs. ,3. Maintain a healthy weight.,4. Quit tobacco use.,5. Stay active.,6. Try compression stockings.,8. Wear clothes that fit properly., Complications : deep vein thrombosis, Pulmonary Embolism, THROMBOPHLEBITIS, Thrombosis, Pain, venous ulceration, Diagnostics : VENOUS COLOUR DOPPLER, X RAY, Differential diagnosis : CELLULITIS, deep vein thrombosis, lymphedema, stasis dermatitis, disease description : Varicose veins are a common condition caused by weak or damaged vein walls and valves. Veins have one-way valves inside them that open and close to keep blood flowing toward the heart. Weak or damaged valves or walls in the veins can cause blood to pool and even flow backwards. This is called reflux. Varicose vein entity includes a vast majority of clinical and pathological manifestations, from limited leg discomfort to swelling and non-healing ulcers.

Variegate Porphyria

Disease Name : Variegate Porphyria, Symptoms : CNS disturbances : The central nervous system is often affected with insomnia, restlessness, agitation, confusion, hallucinations and convulsions. The level of sodium in the blood may decrease and cause convulsions., Gastrointestinal symptoms : Nausea, vomiting, constipation (occasionally diarrhea) and trouble urinating may also occur during acute attacks. These symptoms are due to effects on the nerves of the bowel and bladder., Hepatocellular carcinoma : Individuals with variegate porphyria are at an increased risk for developing a form of liver cancer known as hepatocellular carcinoma. There is also risk of developing chronic kidney disease., DARK URINE : The urine may be reddish due to increased porphyrins, and dark due to porphobilin, which is a brownish degradation product of PBG., Abdominal Pain : Symptoms during an attack may include intense abdominal discomfort or pain, which is usually constant, lasting hours to days, but may be cramping., paralysis : The level of sodium in the blood may decrease and cause convulsions. The peripheral nerves are affected, leading to severe pain in the extremities, back or chest and, especially with more prolonged attacks, paralysis of muscles. This may progress to involve all extremities and the muscles that control breathing., cutaneous symptoms : Chronic skin abnormalities result from photosensitivity, a condition in which the skin is abnormally sensitive to sunlight, causing blistering skin lesions. Symptoms include abnormally fragile skin, blisters (bullae), milia, which are tiny, white bumps or cysts, and excessive hair growth (hypertrichosis). Blisters are slow to heal and can scar leaving patches of skin that are abnormally dark (hyperpigmentation) or light (hypopigmentation). Skin symptoms may be less common in individuals who live in nontropical climates. Some individuals with variegate porphyria only develop skin abnormalities, others only develop neurological symptoms and some have both., Signs : nan, Treatment : The key to successful management of the skin disease is photoprotection with sun avoidance using clothes, hats and gloves. Opaque,sunscreens, containing pigmentary grade titanium dioxide or zinc,oxide sometimes with the addition of iron oxide, are protective ,against Soret wavelength light., ß-Carotene and canthaxanthin have,also been claimed to provide limited protection in some patients, , Liver transplantation has been successfully used to cure ,variegate porphyria., Pathophysiology : Variegate porphyria is caused by an autosomal dominant inherited deficiency of protoporphyrinogen oxidase. In addition to causing photosensitization, accumulated coproporphyrinogen and protoporphyrinogen also inhibit PBG deaminase, the probable mechanism for acute attacks in VP. It is perhaps unexpected that the accumulated copro- and protoporphyrin should cause PCT-like upper dermal blistering rather than EPP-like acute pain. This is likely to be because, although hydrophobic porphyrins predominate in the plasma, hydrophilic porphyrins, especially uroporphyrin, predominate in the skin. This local accumulation is thought to result from secondary local photo-inactivation of UROD in the skin by coproporphyrin. In addition, the protoporphyrin in VP is conjugated to a peptide which may reduce its phototoxicity., Epidemiology : prevalence is around 0.5–1/100 000, 1 in 100, 000 individuals in the general population in European populations, variable, Prevention of primary manifestations : Acute neurovisceral attacks are less likely to occur if exacerbating factors are corrected or avoided. Recurrent premenstrual acute attacks can be prevented with gonadotropin-releasing hormone analogs; weekly or biweekly hemin infusions to prevent frequent noncyclical attacks may be effective, but experience is lacking. Prevention of the skin manifestations requires protection from sunlight., Complications : Peripheral neuropathy, respiratory failure, areflexic quadriparesis, Diagnostics : MRI, STOOL EXAMINATION, Urine analysis, Differential diagnosis : porphyria, Pseudoporphyria, systemic lupus erythematosus (SLE), disease description : This is a rare inherited disease usually characterized by photo- induced skin fragility and blistering, which may cause acute attacks.Variegate porphyria (VP) is both a cutaneous porphyria (with chronic blistering skin lesions) and an acute porphyria (with severe episodic neurovisceral symptoms). The most common manifestation of VP is adult-onset cutaneous blistering lesions (subepidermal vesicles, bullae, and erosions that crust over and heal slowly) of sun-exposed skin, especially the hands and face. Other chronic skin findings include milia, scarring, thickening, and areas of decreased and increased skin pigmentation. Facial hyperpigmentation and hypertrichosis may occur. Cutaneous manifestations may improve in winter and be less prevalent in northern regions and in dark-skinned individuals. Acute neurovisceral symptoms can occur any time after puberty, but less often in the elderly

Vasculitis Syndrome

Disease Name : Vasculitis Syndrome, Symptoms : flu-like symptoms : Includes fever, body ache, headache, fatigue, coughing & trouble breathing., Gastrointestinal symptoms : If your stomach or intestines are affected, you may experience pain after eating. Ulcers and perforations are possible and may result in blood in the stool., numbness of the extremities : Some types of vasculitis can cause numbness or weakness in a hand or foot. The palms of the hands and soles of the feet might swell or harden., lung damage : You may develop shortness of breath or even cough up blood if vasculitis affects your lungs., ear problem : Dizziness, ringing in the ears and abrupt hearing loss may occur., cutaneous symptoms : Bleeding under the skin can show up as red spots. Vasculitis can also cause lumps or open sores on your skin., Ocular symptoms : Vasculitis can make your eyes look red and itch or burn. Giant cell arteritis can cause double vision and temporary or permanent blindness in one or both eyes., Signs : nan, Treatment : medication : Sulfamethoxazole and Trimethoprim (Co-trimoxazole), Cyclophosphamide , Rituximab, Methotrexate, Sometimes, vasculitis causes an aneurysm — a bulge or ballooning in the wall of a blood vessel. This bulge may need surgery to reduce the risk of it rupturing. Blocked arteries also may require surgical treatment to restore blood flow to the affected area., Pathophysiology : Generally, most of the vasculitic syndromes are assumed to be mediated at least in part by immunopathogenic mechanisms that occur in response to certain antigenic stimuli. However, evidence supporting this hypothesis is for the most part indirect and may reflect epiphenomena as opposed to true causality. Furthermore, it is unknown why some individuals might develop vasculitis in response to certain antigenic stimuli, whereas others do not. It is likely that a number of factors are involved in the ultimate expression of a vasculitic syndrome. These include the genetic predisposition, environmental exposures, and the regulatory mechanisms associated with immune response to certain antigens. Although immune complex formation, antineutrophil cytoplasmic antibodies (ANCAs), and pathogenic T lymphocyte responses have been among the prominent hypothesized mechanisms, it is likely that the pathogenesis of individual forms of vasculitis is complex and varied.  Cryoglobulinemic vasculitis is strongly associated with hepatitis C virus infection; hepatitis C virions and hepatitis C virus antigen-antibody complexes have been identified in the cryoprecipitates of these patients (see “Cryoglobulinemic Vasculitis”). The mechanisms of tissue damage in immune complex–mediated vasculitis resemble those described for serum sickness. In this model, antigen-antibody complexes are formed in antigen excess and are deposited in vessel walls whose permeability has been increased by vasoactive amines such as histamine, bradykinin, and leukotrienes released from platelets or from mast cells as a result of IgE-triggered mechanisms. The deposition of complexes results in activation of complement components, particularly C5a, which is strongly chemotactic for neutrophils. The terminology of cytoplasmic ANCA (cANCA) refers to the diffuse, granular cytoplasmic staining pattern observed by immunofluorescence microscopy when serum antibodies bind to indicator neutrophils. The terminology of perinuclear ANCA (pANCA) refers to the more localized perinuclear or nuclear staining pattern of the indicator neutrophils. The major target for pANCA is the enzyme myeloperoxidase; other targets that can produce a pANCA pattern of staining include elastase, cathepsin G, lactoferrin, lysozyme, and bactericidal/permeability-increasing protein. However, only antibodies to myeloperoxidase have been convincingly associated with vasculitis., Epidemiology : 10.3 per 100, 000, The annual incidence rate of IgA vasculitis is between 3.5 (in Japan) and 26.7 (in Scotland) per 100, 000 persons aged <15 years, GOOD, You can’t prevent vasculitis because experts don’t know what causes it. There’s no way to know if someone will develop it., Complications : infection, organ damage, Loss of vision, blood clot formation, aneurysms, Diagnostics : Complete Blood Count CBC, PET SCAN, ANCA, biopsy, MRI, CT SCAN, Fluorescein angiography, Differential diagnosis : gonococcal infection, Histoplasmosis, Infective endocarditis, disease description : Vasculitis involves inflammation of the blood vessels. The inflammation can cause the walls of the blood vessels to thicken, which reduces the width of the passageway through the vessel. If blood flow is restricted, it can result in organ and tissue damage.

Vasomotor Rhinitis

Disease Name : Vasomotor Rhinitis, Symptoms : nasal irritation : Vasomotor (nonallergic) rhinitis is inflammation of nasal tissues that results in sneezing, nasal congestion, runny nose or postnasal drip., anosmia : Diminished sense of smell., Signs : nan, Treatment : medication : Fluticasone , Beclometasone , Budesonide , Levocetirizine, Avoidance of physical factors which provoke symptoms, e.g. sudden change in temperature, humidity, ,blasts of air or dust, polyp, deviated nasal septum, should also be corrected.,2. Excessive rhinorrhoea, not corrected by medical therapy,and bothersome to the patient, can be relieved by,sectioning the parasympathetic secretomotor fibres to,nose (vidian neurectomy)., Pathophysiology : Nasal mucosa has rich blood supply. Its vasculature is similar to the erectile tissue in having venous sinusoids or “lakes” which are surrounded by fibres of smooth muscle which act as sphincters and control the filling or emptying of these sinusoids. Sympathetic stimulation causes vasoconstriction and shrinkage of mucosa, while parasympathetic stimulation causes vasodilation and engorgement. Overactivity of parasympathetic system also causes excessive secretion from the nasal glands. Autonomic nervous system is under the control of hypothalamus and therefore emotions play a great role in vasomotor rhinitis. Autonomic system is unstable in cases of vasomotor rhinitis. Nasal mucosa is also hyper-reactive and responds to several nonspecific stimuli, e.g. change in temperature, humidity, blasts of air, small amounts of dust or smoke., Epidemiology : worldwide prevalence approaching 320 million., GOOD, There’s no way to prevent vasomotor rhinitis. You can lower your risk by avoiding triggers known to cause rhinitis., Complications : nasal polyps, Sinusitis, HYPERTROPHIC RHINITIS, Diagnostics : CT SCAN, Nasal endoscopy, allergy skin test, Differential diagnosis : drug induced rhinitis, gustatory rhinitis, senile rhinitis, disease description : It is nonallergic rhinitis but clinically simulating nasal allergy with symptoms of nasal obstruction, rhinorrhoea and sneezing. One or the other of these symptoms may predominate. The condition usually persists throughout the year and all the tests of nasal allergy are negative..

Venezuelan Equine Encephalomyelitis Virus Disease

Disease Name : Venezuelan Equine Encephalomyelitis Virus Disease, Symptoms : headache : Severe headache with or without associated photophobia may also be reported., Neurological symptoms : Children are at particular risk to progress to clinical CNS involvement, especially encephalitis. Symptoms of CNS involvement include disorientation, somnolence, nuchal rigidity, convulsions, inappropriate antidiuretic hormone (ADH) secretion, paralysis, coma, and death., INFLUENZA LIKE ILLNESS : Venezuelan equine encephalitis virus infection manifests as influenzalike symptoms approximately 1-6 days after infection. Typical initial symptoms of infection include fatigue, weakness, malaise, fever, chills, myalgia, lumbosacral pain, nausea, vomiting, and prostration., Signs : nan, Treatment : Currently, no specific treatment exists for any of the encephalitic arboviruses, including Venezuelan equine encephalitis. Treatment is supportive or palliative. Most infections are self-limiting, though neurological sequelae may persist., Pathophysiology : Several species of mosquitos are capable of transmitting both the enzootic and epizootic strains of VEEV. Ochlerotatus taeniorhynchus appears to be the primary mosquito vector during epizootics, while Culex species transmit enzootic strains. Mosquitos feed on infected rodents or equines, infecting the mosquito midgut. Following initial infection, the virus matures and disseminates to secondary organs, including the salivary glands. Virus accumulates in the salivary glands, and blood-feeding releases virions through the mosquito salivary ducts into the new host. The virus then gains entry to a host cell and replicates in the cellular cytoplasm. Infected equines are viral amplification hosts for epizootic strains, while sylvatic rodents are the primary reservoir hosts for enzootic strains. Infected equines and humans develop high viremia loads that can, in turn, be a source of further mosquito infections. Infected horses shed the virus in body fluids, and humans can then become infected by direct contact or aerosolized fluids. , Epidemiology : VEE can occur in all age groups, and there is usually no sex bias during outbreaks.112 equine cases of EEE were reported from 16 States, variable, The diagnosis and treatment of Venezuelan equine encephalitis require a multidisciplinary approach. Healthcare providers in endemic areas must maintain a high degree of suspicion for the diagnosis. Patients will require supportive care for any degree of disease they develop, from mild illness to fulminant encephalitis. Following recovery, some patients will suffer from neurological sequelae and will require continued support from healthcare providers and the community., Complications : Confusion, seizures, Intellectual disability, Diagnostics : CSF EXAMINATION, lumbar puncture, ELISA, Differential diagnosis : BACTERIAL MENINGITIS, Chikungunya, eastern equine encephalitis, LYME BORRELIOSIS, Malaria, disease description : Venezuelan equine encephalitis virus is a mosquito-borne viral pathogen that causes Venezuelan equine encephalitis or encephalomyelitis (VEE). VEE can affect all equine species, such as horses, donkeys, and zebras. After infection, equines may suddenly die or show progressive central nervous system disorders. Humans also can contract this disease. Healthy adults who become infected by the virus may experience flu-like symptoms, such as high fevers and headaches. People with weakened immune systems and the young and the elderly can become severely ill or die from this disease.

Venous Leg Ulcers

Disease Name : Venous Leg Ulcers, Symptoms : leg cramps : The leg has a feeling of heaviness and cramping., pedal edema : Venous leg ulcers are often accompanied by swelling of your feet and ankles (oedema), which is caused by fluid., itching : venous leg ulcers causes intense itching., Skin color changes. : The area of the venous ulcer turns a dark red, purple, or brown, and there is hardened skin., Signs : dermatitis : Stasis dermatitis is a change in the skin that results from the pooling of blood in the veins of the lower leg. Ulcers are open sores that can result from untreated stasis dermatitis. This photograph shows a red to brownish discoloration just above the ankle, known as stasis dermatitis., ulceration : They usually develop on the inside of the leg, just above the ankle., VARICOSE VEINS : Varicose veins can increase the risk of developing venous ulcers., hyperpigmentation at site : It is thought that the pigmentation is mainly due to haemosiderin or melanin deposition., Treatment : Compression therapy, either using bandages or stockings, are the mainstay in the treatment of VLUs., synthetic dressings, Pathophysiology : Chronic venous insufficiency and VLU result from peripheral venous hypertension or chronic ambulatory venous hypertensionory venous hypertension. They exclusively occur in humans. Gravitation, upright walk and dysfunctional venous ejection during leg motion or dysfunctional venous drainage due to obstruction (e.g. chronic occlusion, obesity, pregnancy) are prerequisites to the development CVI and VLUs. All forms of neuromuscular diseases and/or ankle and knee joint dysfunction can induce CVI and VLUs.Obesity raises the intra-abdominal pressure, which impedes venous drainage. Pathology There is sclerosing panniculitis with non-specific skin ulceration.The epidermis is acanthotic, while the dermis is thickened and fibrotic. The subpapillary veins are elongated with wall thickening (pseudo-increased due to more cross-sections of tortuous vessels., Epidemiology : point prevalence of 0.1%., The lifetime incidence of leg ulcers is around 1%, variable, Preventive care can help you avoid a venous stasis ulcer. If you’ve had one in the past, these steps can lower the risk of ulcers recurring (returning) after treatment.,,Venous ulcer prevention includes : ,,Keeping up with treatments for chronic conditions like high blood pressure that affect vein health.,Maintaining a healthy weight.,Quitting smoking.,Taking blood thinners (anticoagulants), if prescribed, to avoid blood clots., Complications : sepsis, CHRONIC PAIN, impairment of quality of life, systemic infection, local wound infection, s, secondary squamous cell carcinoma, secondary lymphoedema (periulcer lymphoedema, Diagnostics : CT SCAN, DOPPLER USG, Differential diagnosis : Ulcers, Ulcers, Ulcers, vasculitis, disease description : Venous leg ulcers are chronic skin ulcers at the gaiter area that result from chronic peripheral venous hypertension. They Introduction, Venous leg ulcer, Mixed leg ulcer , Arterial leg ulcer Hypertensive ischaemic leg ulcer represent the most advanced grade of chronic venous insufficiency (CVI).

Venous Thromboembolism

Disease Name : Venous Thromboembolism, Symptoms : Arrhythmias : PE leads to rapid heart beats., chest pain : Chest pain or discomfort that worsens when you take a deep breath or when you cough., hemoptysis : Infarction of lung tissue with hemoptysis can occur in numerous diseases. Pulmonary emboli often present with hemoptysis as a result of ischemic pulmonary parenchymal necrosis., LOSS OF CONSIOUSNESS : Loss of consciousness may also be an atypical clinical manifestation of pulmonary embolism., blood clot formation : Symptoms include swelling, redness, warmth & pain., shortness of breath : Sudden shortness of breath is seen in patients of PPE., Signs : nan, Treatment : medication : Heparin , fondaparinux sodium/ Fondaparin sodium, Warfarin , Rivaroxaban, Dabigatran Etexilate, Low-molecular-weight Heparins, Inferior vena cava filter-,When anticoagulants cannot be used or don’t work well enough, a filter can be inserted inside the inferior vena cava (a large vein that brings blood back to the heart) to capture or trap an embolus (a clot that is moving through the vein) before it reaches the lungs.,,Thrombectomy/Embolectomy-,In rare cases, a surgical procedure to remove the clot may be necessary. Thrombectomy involves removal of the clot in a patient with DVT. Embolectomy involves removal of the blockage in the lungs caused by the clot in a patient with PE., Anticoagulants (commonly referred to as “blood thinners”) are the medications most commonly used to treat DVT or PE. Although called blood thinners, these medications do not actually thin the blood. They reduce the ability of the blood to clot, preventing the clot from becoming larger while the body slowly reabsorbs it, and reducing the risk of further clots developing., Pathophysiology : The three factors described by Virchow over a century ago are still relevant in the development of venous thrombosis. These are - contact of blood with an abnormal surface (e.g. endothelial damage); - abnormal flow (e.g. stasis); - abnormal blood (e.g. thrombophilia). There are many predisposing causes for VTE. The most important factor is a hospital admission for treatment of a medical or surgical condition. Injury, especially fractures of the lower limb and pelvis, pregnancy and the oral contraceptive pill are other well-recognised predisposing factors. Endothelial damage is now known to be critically important. The interaction of the endothelium with inflammatory cells, or previous deep vein damage, renders the endothelial surface hypercoagulable and less fibrinolytic. Stasis is a predisposing factor seen in many of the conditions, especially in the postoperative period, in patients with heart failure and in those with arterial ischaemia., Epidemiology : ~1–2 per 1, 000 person-years, 1 per 10, 000 persons per year in young adults (<25 years old) to 1 per 100 persons per year in the elderly (>75 years), POOR, Venous thromboembolism has many risk factors, and not all of them can be managed. But in general, movement is the easiest prevention. Since most DVTs occur in the legs, you can mitigate a lot of risk by keeping blood circulating in your legs. If you sit a lot for work or travel, make sure to get up and walk or exercise your leg muscles periodically to keep blood from pooling. If you’ve been sick or you’re recovering from surgery, getting up and moving as soon as you can will help reduce the risk of clots. Exercise will also help you keep stress levels down and maintain a healthy weight, which are other contributing factors., Complications : Pulmonary Embolism, Diagnostics : D-DIMER, pulmonary angiography, contrast venography, MRI, DUPLEX ULTRASONOGRAPHY, X RAY, Differential diagnosis : Arthritis, CELLULITIS, hematomas, lymphedema, Trauma, disease description : Venous thromboembolism (VTE), a term referring to blood clots in the veins, is an underdiagnosed and serious, yet preventable medical condition that can cause disability and death.A venous thromboembolism is a blood clot that blocks the flow of blood through your veins. A VTE can be stuck in the deep veins of the legs or arms (deep vein thrombosis) or travel through the veins to the lungs (pulmonary embolism). A VTE that blocks the lungs is life-threatening.

Ventilator-associated Pneumonia

Disease Name : Ventilator-associated Pneumonia, Symptoms : hypoxaemia : Decreasing amounts of oxygen in the blood., fever : Acute Respiratory Distress Syndrome (ARDS) is one of the major complications that can occur in patients receiving mechanical ventilation; such complications can lead to longer duration of mechanical ventilation., fever : Among mechanically ventilated patients, fever could have a detrimental effect on gas exchange, and increases in cardiac output and oxygen consumption driven by fever tend to worsen hypoxemia., DISCHARGE : Ventilator-associated pneumonia includes clinical signs of purulent tracheal discharge., Signs : nan, Treatment : medication : Piperacillin and tazobactum , Ceftazidime , Cefepime Hydrochloride , Levofloxacin , Pathophysiology : There are few mechanisms suggested for development of ventilator-associated pneumonia : (1) most commonly it is thought to be a progression from colonization of the upper airway, leading to tracheal colonization, then tracheitis, and finally pneumonia. This depends on the number, type, and virulence of the bacteria as well as natural host defenses such as mechanical factors and humoral and cellular immunity. Mechanical defenses, such as ciliary motion and mucus secretion, can be altered in an intubated patient. Artificial airway inhibits gag reflex and ciliary functions and provides a substrate for growth of biofilm which acts as a reservoir for pathogens. This biofilm can be dislodged and delivered to the lower respiratory tract through mechanical suctioning or high-pressure airflow, leading to pneumonia in a susceptible host. , Epidemiology : vary between 6 and 52 cases per 100 patients, POOR, 1. Minimize ventilator exposure.,2. Provide excellent oral hygiene care.,3. Coordinate care for subglottic suctioning. ,4. Maintain optimal positioning and encourage mobility.,5. Ensure adequate staffing., Complications : pulmonary haemorrhage, Diagnostics : BLOOD CULTURE test, CHEST X RAY, CT SCAN, Differential diagnosis : aspiration pneumonia, Bacterial pneumonia, heart failure, Pneumocystis jirovecii, PNEUMONIA, disease description : Ventilator-associated pneumonia is defined as pneumonia occurring more than 48 h after patients have been intubated and received mechanical ventilation. Diagnosing VAP requires a high clinical suspicion combined with bedside examination, radiographic examination, and microbiologic analysis of respiratory secretions.

Ventricular Fibrillation

Disease Name : Ventricular Fibrillation, Symptoms : chest pain : Chest pain occur within minutes to 1 hour before the collapse., Dizziness : A heart that beats too fast or too slow can cause dizziness., nausea : Patients may demonstrate signs of acute MI such as nausea., shortness of breath : V-fib causes acute shortness of breath., Signs : Tachycardia : A dangerous condition related to ventricular tachycardia is ventricular fibrillation (V-fib). In V-fib , the lower heart chambers contract in a very rapid and uncoordinated manner. This irregular rhythm happens most often in people with heart disease or a prior heart attack., Treatment : "Cardiopulmonary resuscitation (CPR). CPR mimics the pumping motion of the heart. It keeps blood flowing through the body. First call 911 or your local emergency number. Then start CPR by pushing hard and fast on the persons chest — about 100 to 120 compressions a minute. Let the chest rise completely between compressions. Continue CPR until an automated external defibrillator (AED) is available or emergency medical help arrives.", "Defibrillation. This treatment is also called cardioversion. An automated external defibrillator (AED) delivers shocks through the chest wall to the heart. It can help restore a regular heart rhythm. As soon as an AED is available, apply it and follow the prompts. If youre not trained to use an AED, a 911 operator or another emergency medical operator may be able to give you instructions. Public-use AEDs are programmed to recognize ventricular fibrillation and send a shock only when needed.", "Implantable cardioverter-defibrillator (ICD). An ICD is a battery-powered unit thats implanted under the skin near the collarbone — similar to a pacemaker. The ICD continuously monitors the heart rhythm. If the device detects an episode of ventricular fibrillation, it sends shocks to stop it and reset the hearts rhythm.,Cardiac ablation. This procedure uses heat or cold energy to create tiny scars in the heart to block the irregular heart signals that cause ventricular fibrillation. Its most often done using thin, flexible tubes called catheters inserted through the veins or arteries. It may also be done during heart surgery.,Coronary angioplasty and stent placement. If ventricular fibrillation is caused by a heart attack, this procedure may reduce the risk of future episodes of ventricular fibrillation.,,The health care provider inserts a long, thin tube (catheter) through an artery, usually in the groin, to a blocked artery in the heart. A balloon on the tip of the catheter briefly inflates to widen the artery. This restores blood flow to the heart. A metal mesh stent may be placed into the artery to help it stay open.,,Coronary bypass surgery. This open-heart surgery redirects blood around a section of a blocked or partially blocked artery in the heart. It may be done if ventricular fibrillation is caused by coronary artery disease. During bypass surgery, the surgeon takes a healthy blood vessel from the leg, arm or chest. Its connected below and above the blocked artery or arteries in the heart. This creates a new pathway for blood flow.", Pathophysiology : Disorganized Electrical Activity : VF begins when the hearts normal electrical conduction system becomes disrupted. This disruption can be caused by various factors, such as ischemia (inadequate blood supply), electrolyte imbalances, or structural abnormalities in the heart.Reentry Circuits : In many cases, VF is initiated by the formation of reentry circuits. These are abnormal electrical pathways within the heart that allow electrical impulses to circulate in a continuous loop. When these reentry circuits are present, the electrical signals can become chaotic and uncoordinated, leading to the disorganized electrical activity seen in VF.Cellular Dysfunction : VF is associated with dysfunction at the cellular level within the heart muscle (myocardium). During VF, individual cardiac muscle cells may fire rapidly and independently, causing a lack of coordinated contraction. This can be caused by alterations in the ion channels responsible for generating and propagating electrical signals within the heart cells.Wavefront Collision : In VF, multiple wavefronts of electrical activity collide and interact within the ventricles. These collisions can further disrupt the normal electrical conduction pattern of the heart and contribute to the chaotic nature of the arrhythmia.Loss of Synchronous Contraction : As VF progresses, the normal coordinated contraction of the ventricles is lost. Instead of the ventricles contracting in a synchronized manner to pump blood effectively, they quiver or fibrillate, leading to inadequate blood flow., Epidemiology : VF incidence was 2.0% in women (81/4091) and 2.7% in men (278/10315), generally occurring in ~10% of cases. The incidence of VF varies by setting and age., variable, Prevention focuses on diagnosing and treating the underlying medical conditions that cause V-fib. Certain medicines can be used to reduce the risk of recurrence.,,Implantable cardiac defibrillators are devices that are implanted within the body that can shock the heart back to normal rhythm within seconds if V-fib is present. Although this device does not necessarily prevent V-fib, it can rapidly and automatically diagnose and treat this potentially fatal heart rhythm.,,If you are at risk for V-fib, you should wear a medical ID and let friends and loved ones know what to do in an emergency., Complications : Embolic events, Diagnostics : 2-D Echo, ECG, X RAY CHEST, ANGIOGRAM, MRI, CT SCAN, Differential diagnosis : Pulseless electrical activity, Tachycardia, torsade de pointes, disease description : Ventricular fibrillation is a type of irregular heart rhythm (arrhythmia). During ventricular fibrillation, the lower heart chambers contract in a very rapid and uncoordinated manner.Ventricular fibrillation is a type of irregular heart rhythm (arrhythmia). During ventricular fibrillation, the lower heart chambers contract in a very rapid and uncoordinated manner. As a result, the heart doesnt pump blood to the rest of the body.Ventricular fibrillation is an emergency that requires immediate medical attention. Its the most frequent cause of sudden cardiac death.

Ventricular Septal Defects

Disease Name : Ventricular Septal Defects, Symptoms : sweating : The infants sweat intensely., exertional dyspnea : Shortness of breath, especially when exercising., Signs : failure to thrive : Some babies with a ventricular septal defect become tired while feeding and do not eat enough to gain weight. This leads to failure to thrive., PANSYSTOLIC MURMUR : The murmur of VSD is typically pan-systolic best heard in the left lower sternal border; it is harsh and loud in small defects but softer and less intense in large ones. Handgrips increase afterload, increasing the strength of the murmur., tachypneic : Moderately-sized defects can cause congestive heart failure, which is characterized by an abnormally rapid rate of breathing (tachypnea), wheezing, unusually fast heartbeat (tachycardia), enlarged liver (hepatomegaly), and/or failure to thrive., frequent chest infections : They can also be prone to respiratory infections., palpable thrill : A very small VSD can cause a palpable thrill (vibration on the chest), parasternal heave : Larger VSDs may cause a parasternal heave., Treatment : medication : Furosemide , Digoxin , Captopril , Percutaneous device VSD closure is reserved for those whose surgery is very risky due to severe PAH, multiple comorbidities, and those who had prior cardiothoracic surgery such as residual or recurrent VSD., Surgical repair reduces the risk for endocarditis, might improve PAH, and overall it increases survival. Without PAH, the operative mortality rate is approximately 1%. Complications include residual or recurrent VSD, valvular incompetence such as tricuspid regurgitation and aortic insufficiency, arrhythmias, LV dysfunction, and progression of PAH. The arrhythmias which accompany VSD repair include atrial fibrillation, complete heart block, and uncommonly, ventricular tachycardia. The main contraindication for surgical VSD closure is the presence of irreversible PAH; this is due to the high surgical perioperative mortality and pulmonary complications.,Angioplastic stenting, Pathophysiology : The interventricular septum is an asymmetric curved structure due to the pressure difference in ventricular chambers. It is composed of five parts : the membranous, muscular (frequently referred to as trabecular), infundibular, atrioventricular, and the inlet.Failure of development or fusion of one of the above components during morphogenesis of the embryonic heart results in a VSD in the corresponding component. Different anatomic locations and histologic variations of VSDs have led to several classifications and nomenclature systems. Complexities in describing VSDs and multiple synonyms have been improved after a new unified classification was established and categorized VSDs into four major groups : Type 1 : (infundibular, outlet),  Type 2 : (membranous),  Type 3 : (inlet or atrioventricular canal),  Type 4 : (muscular, trabecular).The main pathophysiologic mechanism of VSD is shunt creation between the right and left ventricles. The amount of blood shunted and the direction of the shunted blood determine the hemodynamic significance of the VSD. These factors are governed by the size, location of the VSD, and pulmonary vascular resistance., Epidemiology : Isolated VSD accounts for 37% of all congenital heart disease in children. The incidence of isolated VSD is about 0.3% of newborns. Because as many as 90% may eventually close spontaneously; the incidence is significantly lower in adults. VSDs have no gender predilection., variable, Because there aren’t any known causes for VSD, prevention isn’t usually possible. However, you can decrease the risk by avoiding alcohol use and certain anti-seizure medications during pregnancy., Complications : Eisenmenger Syndrome, Endocarditis, heart failure, Diagnostics : 2-D Echo, ECG, CARDIAC CATHETERIZATION, MRI, CHEST X RAY, CT SCAN, Differential diagnosis : atrial septal defect, disease description : VSD are the most common congenital anomaly recognized at birth, however, they account for only about 10% of CHD in the adult, due to the high rate of spontaneous closure of small VSDs during the early years of life. Large VSDs usually cause symptoms of heart failure and poor somatic growth, and are most often closed before adulthood.

Vernal Keratoconjunctivitis

Disease Name : Vernal Keratoconjunctivitis, Symptoms : Lacrimation : Excessive watering of eyes., "blepharospasm : Blepharospasm is blinking or other eyelid movements, like twitching, that you cant control.", grittiness in eyes : VKC leads to foreign body sensations in the eyes., mild photophobia : The eyes become sensitive to light., stringy (ropy) discharge : VKC causes ropy discharge., Signs : Subepithelial scarring, Punctate epithelial keratitis : They begin as punctate epithelial erosions which coalesce to form macroerosions which then develop into shield ulcers which can be self-limiting or develop further consequences such as bacterial keratitis. Plaques form when inflammatory debris accumulates at the base of a shield ulcer., Ulcerative vernal keratitis (shield ulceration) : Shield ulcers form when superficial punctate keratitis–associated VKC leads to a break in the corneal epithelium., Pseudogerontoxon : Pseudogerontoxon is a lesion that resembles a small segment of arcus senilis or gerontoxon and is seen in many individuals with limbal vernal or atopic keratoconjunctivitis., Vernal corneal plaques : Corneal plaque is a rare complication of vernal keratoconjunctivitis. These plaques usually do not resolve with standard conservative measures. Failure to epithelialize may be a result of the plaque material extending below the edges of adjacent epithelium., Treatment : medication : Sodium Cromoglycate , Tacrolimus , Azelastine , Betamethasone , Carboxymethyl cellulose/ CARBOXYMETHYLCELLULOSE SODIUM, Fluorometholone , Ketorolac trometamol, Acetylcysteine (N-acetylcysteine) , 1. Topical steroids. These are effective in all forms of,spring catarrh. However, their use should be minimised, ,as they frequently cause steroid induced glaucoma.,2. Mast cell stabilizers such as sodium cromoglycate,(2%) drops 5 times a day are quite effective in,controlling VKC, especially atopic cases. 3. Dual action antihistamines and mast cell stabilizers,such as azelastine, olopatidine and ketotifen are very,effective for control and prevention of exacerbations. 4. NSAIDs eye drops such as ketorolac and diclofenac,give added benefits. 5. Topical cyclosporine (0.5 to 1%), the immunemodulator, ,is indicated when steroids are ineffective, ,inadequate, or poorly tolerated, or when given as a,steroid-sparing agent in patients with severe disease.,6. Tacrolimus (0.03% ointment) is another immunemodulator, ,which can be useful in refractory cases. Systemic therapy,1. Oral antihistaminics may provide some relief from,itching in severe cases.,2. Oral steroids for a short duration have been,recommended for advanced, very severe, nonresponsive,cases., Severe shield ulcer resistant to medical therapy may,need surgical treatment in the form of debridement, ,superficial keratectomy, excimer laser therapeutic,keratectomy as well as amniotic membrane,transplantation to enhance re-epithelialization., Pathophysiology : Vernal keratoconjunctivitis (VKC) has long been considered an atopic disorder, mainly type-I IgEmediated hypersensitivity reaction to pollen allergens. However, now it is believed that pathogenesis of VKC is characterized by Th2 lymphocyte alteration and that the exaggerated IgE response to common allergens is a secondary event. Pathology- 1. Conjunctival epithelium undergoes hyperplasia and sends downward projections into the subepithelial tissue. 2. Adenoid layer shows marked cellular infiltration by eosinophils, plasma cells, lymphocytes and histiocytes. 3. Fibrous layer shows proliferation which later on undergoes hyaline changes. 4. Conjunctival vessels also show proliferation, increased permeability and vasodilation. All these pathological changes lead to formation of multiple papillae in the upper tarsal conjunctiva., Epidemiology : .2–10.6 cases per 10000 population, GOOD, Using air conditioning or moving to a cooler climate may help prevent the problem from getting worse in the future., Complications : Vernal keratopathy, Diagnostics : HISTOPATHLOGY, EOSINOPHILS, Differential diagnosis : allergic conjunctivitis, atopic keratoconjunctivitis, GIANT PAPILLARY CONJUNCTIVITIS, perennial allergic conjunctivitis, disease description : VKC is a recurrent, bilateral, interstitial, self-limiting, allergic inflammation of the conjunctiva having a periodic seasonal incidence.Vernal keratoconjunctivitis (VKC) is a seasonally recurring, bilateral, and severe form of allergic inflammation affecting the ocular surface. This relatively uncommon type of allergic eye disease can cause severe damage to the ocular surface, leading to corneal scarring and vision loss if not treated properly.

Verrucous Carcinoma

Disease Name : Verrucous Carcinoma, Symptoms : Wart-like growths, often in genital areas., Signs : papillomatous lesion : Florid oral papillomatosis (FOP) is a rare disorder of the oral cavity and lips, characterised by the presence of multiple and multifocal papillomatous and verruciform growths that form confluent plaques and vegetation., Treatment : Treatment in the early stage of the disease is usually successful. ,Etretinate therapy (200 mg/day) or chemotherapy with bleomycin ,may reduce the lesion bulk . Treatment can also be with photodynamic therapy, laser, interferon a or imiquimod., The use of radiotherapy is ,controversial since in numerous reported cases this has produced ,an anaplastic squamous cell carcinoma., Surgical or laser excision is favoured, Pathophysiology : Florid oral papillomatosis Florid oral papillomatosis is a rare but well-defi ned clinical entity of unknown pathogenesis. Risk factors include possible association with HPV, tobacco, and chronic infl ammation or irritation. Florid oral papillomatosis is essentially a verrucous carcinoma, a clinicopathological variant of squamous cell carcinoma also known by a confusing array of names such as Ackerman tumour, Buschke–Loewenstein tumour, epithelioma cuniculatum, carcinoma cuniculatum and cutis papillomatosis carcinoides of Gottron., Epidemiology : about 2, 000 out of 100, 000 people in the U.S. had verrucous carcinoma in their oral cavity., variable, You can reduce your risk of developing verrucous carcinoma by avoiding tobacco products and drinking less alcohol. Try to quit smoking or vaping, too., Complications : Metastasis, Diagnostics : PAP SMEAR, biopsy, MRI, CT SCAN, Differential diagnosis : Hyperplasia, squamous cell carcinoma., squamous papilloma, disease description : Verrucous carcinoma (Ackerman tumour) is an uncommon warty white neoplasm that is rarely ulcerated, sometimes called carcinoma cuniculatum. It may develop from proliferative verrucous leukoplakia.Verrucous carcinoma is a low-grade variant of squamous cell carcinoma with specific morphologic, cytokinetic and clinical features. Despite low mitotic activity and slow growth, it can infiltrate adjacent tissues in advanced stages but does not metastasize. The most frequently affected site is the oral cavity

Verrucous Haemangioma

Disease Name : Verrucous Haemangioma, Symptoms : itching, LESIONS : lesions initially are non-keratotic, soft and bluish-red in colour., plaques : well-circumscribed linear vascular plaques and vary from a few centimetres to 25 cm in diameter, Signs : nan, Treatment : NdYAG laser for plaques and pulsed dye laser for,patches can help improve the appearance and relieve symptoms., Surgery is the treatment of choice, Pathophysiology : The pathogenesis is not understood. The lesions show overlying epidermal hyperkeratosis, papillomatosis and irregular acanthosis with underlying dilated capillary vascular channels in the dermis and also often in the subcutis. The vessels are organized in a diffuse or lobular pattern., Epidemiology : 2.6% of newborns younger than 2 weeks and in 10% of children younger than 1 year, variable, Currently there are no specific methods or techniques to prevent the formation of a Verrucous Hemangioma., Complications : infection, ulceration, Diagnostics : VENOUS MRI, MRI, full thickness skin biopsy, Differential diagnosis : angiokeratomas, kaposi sarcoma, disease description : This is a congenital vascular anomaly made up of a dermal and subcutaneous capillary vascular component with an overlying warty surface. There has been some debate as to whether it should be classified as a vascular neoplasm, though recent evidence supports the original view that it should be regarded as a vascular malformation

Vesicular Stomatitis Virus Infection

Disease Name : Vesicular Stomatitis Virus Infection, Symptoms : Mouth ulceration : If you look inside the mouth, you will see blanched and raised vesicles or blister-like lesions on the inner surfaces of the lips, gums, tongue, and/or dental pad. These blister-like lesions can also form on the lips, nostrils, coronary band, prepuce, vulva, and teats. The blisters will swell and break open, which causes mouth pain, discomfort, and reluctance to eat or drink., INFLUENZA LIKE ILLNESS : Includes headache, fever, myalgia, and weakness., weight loss : Blisters in the mouth restricts the patients from consuming food, hence leading to weight loss., Signs : nan, Treatment : There are no specific antiviral agents. Treatment consists of supportive care including the prevention or treatment of secondary infections. A mild antiseptic mouthwash may reduce the pain associated with oral lesions. Nutritional support is provided if eating is impaired., Pathophysiology : The infection can cause vesicles which are intraepithelial. Intranuclear inclusions are present in infected cells. The incubation period is 2 days after which there is fever with myalgia and malaise. This is occasionally followed by mild stomatitis with vesicles on the gums and buccal and pharyngeal mucosa, and lymphadenitis. Some patients develop vesicles of the fingers., Epidemiology : from 5% to more than 90%, Recovery is usually complete within a week, Outbreaks of vesicular stomatitis can be explosive, but effective methods of control are poorly defined, as the epidemiology of the infection is uncertain and frequently there is little response even in the face of epizootics. Avoidance of pastures known to be sites of transmission may help avoid infection. Because of the potential for arthropod-borne transmission, fly control is often advocated, and animal quarantine and movement restrictions are frequently imposed. In temperate zones, epizootics occur at such infrequent intervals that concern wanes during inter-epizootic periods. Both inactivated and live-attenuated virus vaccines have been developed, but are not used widely., Complications : ENCEPHALITIS, Diagnostics : SEROLOGIC TEST, molecular testing, Differential diagnosis : Foot and mouth disease, disease description : Vesicular stomatitis is an arbovirus which infects horses and cattle in the Americas, Asia and Africa. It is generally mild but can mimic foot and mouth disease. It is occasionally transmitted to humans by direct or indirect contact with infected animals.

Vestibular Neuronitis

Disease Name : Vestibular Neuronitis, Symptoms : nystagmus : It is a condition in which your eyes make rapid, repetitive, uncontrolled movements — such as up and down (vertical nystagmus), side to side (horizontal nystagmus) or in a circle (rotary nystagmus)., vertigo : Vestibular neuritis is an inner ear disorder that causes symptoms such as sudden, severe vertigo., vomiting : Persistent vertigo can lead to nausea & vomiting., BALANCE PROBLEM : This inflammatory disorder, probably caused by a virus, can affect the nerves in the balance portion of your inner ear. Symptoms are often severe and persistent, and include nausea and difficulty walking., Signs : Gait disturbance : Unilateral vestibular dysfunctions usually show postural sway and a tendency to fall toward the affected side during gait, which suggests a more lateral displacement of CoM toward the CoP of the affected side., Treatment : medication : Dimenhydrinate , Prochlorperazine , Promethazine , Atropine/ Atropine methonitrate, Diazepam , Intratympanic gentamicin therapy (chemical labyrinthectomy, Decompression of endolymphatic sac. (b) Endolymphatic shunt operation, Sacculotomy (Fick’s operation), Section of vestibular nerve, Ultrasonic destruction of vestibular labyrinth., Labyrinthectomy., ntermittent Low-Pressure Pulse Therapy Meniett Device Therapy, Pathophysiology : Vestibular neuritis is believed to be an inflammatory disorder selectively affecting the vestibular portion of the 8th cranial nerve. The cause is presumed to be of viral origin (e.g., the reactivation of latent HSV infection), but other causes of vascular etiology and immunologic in origin are proposals. Vestibular damage appears to have a predilection for the superior portion of the vestibular labyrinth (supplied by the superior division of the vestibular nerve) over the inferior aspect of the vestibular labyrinth (supplied by the inferior portion of the vestibular nerve). The underlying mechanism is unclear, but this phenomenon may be explainable by anatomical differences between the two vestibular divisions., Epidemiology : Usually about 10-15% of the ani- mals show clinical signs of the disease, self limiting(good), Because viruses cause vestibular neuritis, you can’t always prevent the condition. However, you can reduce your risk by making sure you’re up to date on all of your vaccines., Complications : Dizziness, nausea, vertigo, vomiting, BALANCE PROBLEM, Diagnostics : MRI, CT SCAN, PHYSICAL EXAMINATION, Differential diagnosis : benign paraoxysmal positional vertigo, "menieres disease", migraine, disease description : Vestibular neuritis, also known by the name vestibular neuronitis, is thought to be caused by inflammation of the vestibular portion of the eighth cranial nerve and classically presents with vertigo, nausea, and gait imbalance. It is believed to be associated with preceding or accompanying viral infection. It is considered a benign, self-limited condition that typically lasts several days, but can take weeks to months for all vestibular symptoms to completely resolve. Vestibular neuritis is a clinical diagnosisIt is characterized by severe vertigo of sudden onset with no cochlear symptoms. Attacks may last from a few days to 2 or 3 weeks. It is thought to occur due to a virus that attacks vestibular ganglion.

Vibrio Vulnificus Infections

Disease Name : Vibrio Vulnificus Infections, Symptoms : blisters : Fluid-filled blisters on your skin that are large, discolored or painful., diarrhea : Watery diarrhea, often accompanied by stomach cramping, nausea, vomiting, and fever, Flu-like illness : Includes fever with chills, headache, body ache., Hypotension : For bloodstream infection, vibrio vulnificus infections causes dangerously low blood pressure., wound infection : For wound infection, which may spread to the rest of the body : fever, redness, pain, swelling, warmth, discoloration, and discharge (leaking fluids)., cutaneous symptoms : Most patients infected with V vulnificus have bullous skin lesions, which are found on the trunk and the lower extremities. These hemorrhagic bullae can progress to necrotic ulcerations, which require surgical debridement. Edema can be present., Signs : nan, Treatment : medication : Ceftazidime , Ciprofloxacin , Tetracycline , The main treatment is large doses of ceftazidime, ciprofloxacin or ,tetracycline and surgical debridement where necessary. Treatment ,should be initiated as early as possible as there is a case fatality ,rate of 50%., surgical debridement where necessary, Pathophysiology : The morphology of Vibrionaceae contributes significantly to its virulence. Structurally V. vulnificus is a flagellated motile halophilic bacillus with a capsular polysaccharide (CPS), a lipopolysaccharide (LPS), and specific flagellin homologous proteins (FHPs).Capsular polysaccharides in the organism’s capsule resist host gastric acid attack, and further trigger the release of host cytokines, such as tumor necrosis factor (TNF) and interleukins-8 and interleukin-6. V. vulnificus infection blocks complement activation as well as inhibits opsonization, both necessary for bacterial eradication. Capsular polysaccharides are also are implicated in neutrophil and macrophage dysfunction. Surface pili facilitate the attachment to host cells. Flagellar elements (FHPs) are required for the development of Vibrio biofilm. Biofilm development is essential for V. vulnificus’s cytotoxicity as well as environmental survival. V. vulnificus lipopolysaccharides mediate septic shock through the release of cytokines and pyrogens., Epidemiology : Approximately 100 V vulnificus infections are reported each year in the US, The countries with the most documented cases of V. vulnificus are the United States, South Korea, Taiwan, Japan, and Mexico., FATAL, You can reduce your risk of Vibrio vulnificus infection by following safe food and wound care practices, including : ,,Don’t eat raw or undercooked shellfish, especially oysters.,Keep cooked and uncooked shellfish (and their juices) separate to avoid contamination.,Wash your hands after preparing or handling raw shellfish. Wearing gloves can provide an extra layer of protection.,Avoid contact with seawater and brackish water if you have a wound or break in your skin or have had a recent piercing, tattoo or surgery. If you can’t avoid contact, protect any wounds with waterproof covering.,Wash wounds thoroughly if they’ve been in contact with seawater or raw shellfish or its juices., Complications : septicaemia, Diagnostics : Gram Staining, PCR, HISTORY TAKING, Differential diagnosis : erythema multiforme, necrosis, pemphigoid gestations, Pemphigus Vulgaris, Steven-Johnson syndrome, disease description : Certain non-cholera vibrios have been found to cause severe cellulitis. Vibrio vulnificus is the best known of these organisms. It is found in warm seawater areas such as around the gulf of Mexico, South America, Asia and Australia and may invade via the gastrointestinal tract, for instance, after eating raw oysters, or contaminate superficial wounds.

Villoglandular Adenocarcinoma

Disease Name : Villoglandular Adenocarcinoma, Symptoms : Vaginal Discharge : Watery, bloody vaginal discharge that may be heavy and have a foul odor., DYSPAREUNIA : Patients complain of pain during/after sex., "post coital bleeding : Theres abnormal bleeding from the vagina.", Signs : nan, Treatment : The standard treatment for advanced adeno-squamous cervical cancer is chemo radiation., Treatment modalities range from cone biopsies to simple and radical hysterectomy with or without pelvic lymph node dissection and pre-postoperative radiation therapy, Pathophysiology : HPV is well recognized and its role in cervical carcinogenesis has been proven. To the best of our knowledge, only 3 studies have referred to the association between VGPA and HPV infection.  In one study, 3 patients presented with HPV infection, mainly type 16, and 2 of these presented with a mixed type. Considering these positive results in the present patients, and in accordance with previous studies, it is reasonable to support HPV infection, particularly high-risk types, in the molecular pathogenesis of this unusual cervical adenocarcinoma., Epidemiology : Villoglandular papillary adenocarcinoma (VGPA) is a rare but well-differentiated subtype of cervical adenocarcinoma, which accounts for 3.7–4.8% of cervical adenocarcinomas, good, Complications : recurrence, Diagnostics : TISSUE BIOPSY, CT SCAN, Differential diagnosis : cervical leiomyoma, CERVICAL POLYP, Endocervical adenocarcinoma, Vaginal cancer, disease description : Villoglandular papillary adenocarcinoma (VPA) is a very rare subtype of adenocarcinoma of the uterine cervix, but a well-recognized variant of cervical adenocarcinoma with a favorable prognosis and generally occurring in women of child-bearing age.Villoglandular papillary adenocarcinoma (VPA) is a very rare subtype of adenocarcinoma of the uterine cervix, but a well-recognized variant of cervical adenocarcinoma with a favorable prognosis and generally occurring in women of child-bearing age. Herein, we report a case of VPA diagnosed and managed successfully with conservative measure. This management is particularly desirable in young women to preserve reproductive capability.

Vincent Infection

Disease Name : Vincent Infection, Symptoms : Halitosis : Vincent disease causes extremely bad breath., mouth deformity : There’s a yellow-white or gray membrane or film on the skin between the teeth., gingival bleeding : It has a sudden onset with gingiva showing punched-out crater-like ulcerations, covered with a whitish pseudomembrane, surrounded by a demarcated zone of erythema., Signs : nan, Treatment : medication : Sodium bicarbonate , Erythromycin , Metronidazole , Penicillin, attention to dental hygiene, Pathophysiology : Impaired host immunologic response due to immunocompromised state or malnutritionDisruption of normal oral flora with predominance of invasive anaerobic bacteria (Treponema spp.,  Selenomonas spp.,  Fusobacterium spp., and Prevotella intermedia) (2)Loss of integrity and necrosis of the gingival mucosa and interdental papillaeIncreased bacterial attachment with active herpesvirus infection, Epidemiology : prevalence is <1%, GOOD, Good dental hygiene is the best way to prevent trench mouth. Ask your dentist how often you should floss and brush your teeth.,,Trench mouth is linked to general health habits like coping with stress, getting enough sleep, eating well and not smoking., Complications : Malaise, Dehydration, malodorous breath, Diagnostics : THROAT SWAB CULTURE, Blood smear, PHYSICAL EXAMINATION, Differential diagnosis : Desquamative gingivitis, gingivitis, gingivostomatitis, infectious mononucleosis, Pemphigus Vulgaris, disease description : This is trench mouth, a progressive painful infection with ulceration, swelling and sloughing off of dead tissue from the mouth and throat due to the spread of infection from the gums.Vincent gingivitis, also called Vincent infection, Vincent stomatitis, acute necrotizing ulcerative gingivitis, Vincent angina, or trench mouth, acute and painful infection of the tooth margins and gums that is caused by the symbiotic microorganisms Bacillus fusiformis and Borrelia vincentii. The chief symptoms are painful, swollen, bleeding gums; small, painful ulcers covering the gums and tooth margins; and characteristic fetid breath. The ulcers may spread to the throat and tonsils. Fever and malaise may also be present. Vincent gingivitis can occur after a prolonged failure to brush one’s teeth, though there are many other predisposing factors, such as vitamin deficiencies, emotional stress, and so on. The infection is readily treated by bed rest, the administration of penicillin or other antibiotics, and the use of antiseptic mouth rinses. Regular tooth brushing is the chief preventive measure.

Viral Encephalitis

Disease Name : Viral Encephalitis, Symptoms : Neurological symptoms : Includes behavior changes, confusion, difficulty speaking or moving, loss of consciousness, memory issues, seizures & photophobia., physical signs : Includes fever, headache, joint pain, muscle weakness & stiff neck., Signs : nan, Treatment : medication : Paracetamol/Acetaminophen, Ganciclovir , Foscarnet , Aciclovir , Antiviral medicines commonly used to treat encephalitis include : ,,Acyclovir (Zovirax).,Ganciclovir (Zirgan).,Foscarnet (Foscavir).,Intravenous or oral corticosteroids.,Intravenous immunoglobulin.,Plasma exchange., Pathophysiology : Viruses invade the host at a site outside the CNS and replicate. Most then reach the spinal cord and brain hematogenously. HSV, rabies, and herpes zoster virus are important exceptions to this. They travel to the CNS from nerve endings in a retrograde manner. Once in the brain, the virus and the host’s inflammatory response disrupt neural cell function. On gross examination, there us usually cerebral edema, vascular congestion, and hemorrhage. Infiltration with leukocytes or microglial cells is also a common feature. With EEE and JE, the extent of necrosis can be significant.Following arbovirus encephalitis, calcification often is seen, especially in children.Herpes simplex tends to produce focal necrotic lesions with obvious intranuclear inclusions., Epidemiology : In the United States, there are an estimated ~20, 000 cases of encephalitis ,per year, although the actual number of cases is likely to be significantly ,larger,The incidence of viral encephalitis is 3.5 to 7.5 per 100, 000 people, with the highest incidence in the young and elderly., variable, You can stay current with vaccines for diseases that cause encephalitis, such as the measles, mumps and rubella (MMR) injection., Complications : death, hypoxaemia, INTRACEREBRAL HEMORRHAGE, Hypotension, Diagnostics : HISTOPATHLOGY, BRAIN BIOPSY, ECG, lumbar puncture, CSF CULTURE, PCR, MRI, CT SCAN, PHYSICAL EXAMINATION, Differential diagnosis : Brain Abscess, ENCEPHALITIS, MALIGNANCY, metabolic encephalopathy, neurosyphilis, seizures, TUBERCULOSIS, disease description : Encephalitis is defined as an inflammation of the brain caused either by infection, usually with a virus, or from a primary autoimmune process.Infectious encephalitis can be viral, bacterial, fungal, protozoal, or helminthic in etiology. The etiology of many cases of encephalitis remains unknown despite extensive workup. Viruses are the most prevalent identified cause, accounting for about 70% of confirmed cases of encephalitis.

Viral Esophagitis

Disease Name : Viral Esophagitis, Symptoms : sore mouth : Viral esophagitis causes soreness in the mouth., Swallowing defect : Patients usually complain about odynophagia and/or dysphagia., heartburn : The most common type of esophagitis occurs when acids and digestive agents escape your stomach and reflux into your esophagus, irritating and eroding the mucous lining (mucosa). This may happen if you have frequent acid reflux or if you vomit frequently., retrosternal pain : Retrosternal chest pain refers to pain that occurs in the space behind the sternum., Signs : nan, Treatment : medication : Ganciclovir , Pantoprazole , Aciclovir , For HSV esophagitis, treatment is oral or intravenous acyclovir and Foscarnet for those who are non-responders. CMV esophagitis is treated with Gancyclovir or Valganciclovir. Treatment of complications like stenosis or stricture may require endoscopic dilation. Addition of topical anesthesia like topical lidocaine (e.g. GI cocktail) and opioids may help in ulcers related pain. NSAIDs must be avoided as it may exacerbate symptoms, Pathophysiology : Infectious esophagitis : Infection esophagitis can be caused by bacterial, fungal, parasitic and viral micro-organisms. Bacterial esophagitis is the least common of all. Candida albicans infection is the most common cause of infectious esophagitis. The first step in the pathophysiology involves colonization with mucosal adherence and proliferation. The second step involves impairing the host defense mechanisms. C. Albicans is a normal component of oral flora, but it can become a problem if their number increases (e.g., with the use of antibiotics) or if the patient is immunosuppressed (e.g., by therapy with corticosteroids). Herpes simplex virus (HSV) is the most common cause of viral esophagitis. It infects the squamous epithelium leading to vesicles and then ulcerations. Cytomegalovirus (CMV), Epstein-Barr (EBV) and varicella-zoster (VZV) are other viral causes of viral esophagitis., Epidemiology : For infectious esophagitis, the numbers are not very easy to define. One thing that is certain is that is way more prevalent in patients who are immunocompromised such as HIV-infected patients and patients with hematological malignancies., variable, If you have a weak immune system, try to avoid contact with people who have an infection with any of the organisms mentioned above., Complications : aspiration pneumonia, laryngitis, strictures, BARRETT ESOPHAGUS, PERFORATION OF ESOPHAGUS, Diagnostics : Complete Blood Count CBC, HISTOPATHLOGY, Upper GI Endoscopy, CT SCAN, Differential diagnosis : Acute coronary syndromes, angina pectoris, PEPTIC ULCER DISEASE, PEPTIC ULCER DISEASE, Pulmonary Embolism, disease description : Esophagitis refers to inflammation or injury to the esophageal mucosa. There are many causes of esophagitis and essentially the presentation is similar which include retrosternal chest, heartburn, dysphagia or odynophagiaMultiple etiologies for esophagitis have been identified such as reflux esophagitis, Medication (Pills) induced esophagitis, infectious , eosinophilic and radiation esophagitisInfection esophagitis can be caused by bacteria, viruses, fungal and parasitic microorganisms with the least common being bacteria and the most common being fungal.?

Viral Gastroenteritis

Disease Name : Viral Gastroenteritis, Symptoms : abdominal cramp : Viral gastroenteritis causes severe abdominal cramps., myalgia : Viral gastroenteritis causes occasional muscle aches., vomiting : Viral gastroenteritis affected patients experience nausea & vomiting., fever : Mild fever is common in viral gastroenteritis, but high fever (greater than 39 C) should trigger concern for causes that are not viral in origin., loose motion : Watery, usually non-bloody diarrhea — bloody diarrhea usually means severe infection., Signs : nan, Treatment : The disease is self-limited, and oral rehydration therapy is generally adequate. If severe dehydration develops, IV fluid therapy is indicated. No specific antiviral therapy is available., Pathophysiology : The exact sites and cellular receptors for attachment of viral particles have not been determined. Data suggest that carbohydrates that are similar to human histo-blood group antigens and are present on the gastroduodenal epithelium of individuals with the secretor phenotype may serve as ligands for the attachment of Norwalk virus. Additional studies must more fully elucidate norovirus–carbohydrate interactions, including potential strain-specific variations. After the infection of volunteers, reversible lesions are noted in the upper 1465 jejunum, with broadening and blunting of the villi, shortening of the microvilli, vacuolization of the lining epithelium, crypt hyperplasia, and infiltration of the lamina propria by polymorphonuclear neutrophils and lymphocytes. The lesions persist for at least 4 days after the resolution of symptoms and are associated with malabsorption of carbohydrates and fats and a decreased level of brush-border enzymes. Adenylate cyclase activity is not altered. No histopathologic changes are seen in the stomach or colon, but gastric motor function is delayed, and this alteration is believed to contribute to the nausea and vomiting that are typical of this illness., Epidemiology : 2% to 9%, 11.37 million episodes of acute gastroenteritis (AGE) in children < 5 years annually in India, , poor, You can reduce your risk of getting stomach flu or spreading it to others by practicing good hygiene.,This includes : ,,Handwashing. Good handwashing is the most important defense against stomach flu viruses since hand sanitizer isn’t always effective. It’s especially important after going to the bathroom or changing a diaper and before coming into contact with food.,Cleaning. Wash and disinfect any surfaces or materials that you or the infected person has touched. Use bleach and water (up to 25 tablespoons per gallon) to disinfect surfaces, especially in the bathroom. Use the high heat setting on your washing machine for bed linens and clothes.,Safe food handling. Food may be contaminated with stomach flu viruses, bacteria or other organisms. Safe food prep can help reduce this risk. People already infected with stomach flu should avoid handling food for others, if possible., Complications : shock, Dehydration, Diagnostics : STOOL CULTURE, BARIUM SWALLOW, PCR, ELISA, CT SCAN, ELECTRON MICROSCOPY, PHYSICAL EXAMINATION, enzyme immunoassays (EIAs), Differential diagnosis : Food poisoning, gastroenteritis, disease description : Viral gastroenteritis is an inflammation, swelling, and irritation of the inside lining of your gastrointestinal tract. A virus causes this illness. It can infect your stomach, small intestine, and large intestine.Viral gastroenteritis is very common. In most cases, it lasts only a few days and doesn’t require treatment. The biggest danger is dehydration from loss of fluid due to diarrhea and vomiting.

Virilisation

Disease Name : Virilisation, Symptoms : libido : Virilization causes abnormally high libido in women., deepening of the voice : Virilization causes deepening of the voice in women., menstrual irregularities : Menstrual irregularities is one of the earliest symptoms showing up., "Acne : Theres development of acne on chest, back, face, hairline, underarms, groin.", Male-pattern baldness : Virilization can cause women to develop masculine traits, such as male pattern baldness and excessive facial and body hair growth., Signs : nan, Treatment : nan, Pathophysiology : Hypersecretion of Androgens : One of the primary causes of virilization is the excessive production of androgens. This can occur in conditions such as : Polycystic Ovary Syndrome (PCOS) : PCOS is a common hormonal disorder in women where the ovaries produce higher levels of androgens than normal, leading to irregular menstrual cycles, ovarian cysts, and virilization symptoms.Adrenal Tumors : Tumors in the adrenal glands can lead to the overproduction of androgens, resulting in virilization.Congenital Adrenal Hyperplasia (CAH) : CAH is a group of genetic disorders that affect the adrenal glands ability to produce cortisol and aldosterone. In some cases, this can lead to excess androgen production and virilization.Exogenous Androgen Exposure : Virilization can also occur due to the introduction of external sources of androgens, such as anabolic steroids or androgen-containing medications. These substances can disrupt the hormonal balance and lead to the development of masculine traits.Hormonal Imbalances : Various hormonal imbalances can affect the androgen-to-estrogen ratio in the body, leading to virilization. For example : Ovarian Tumors : Certain ovarian tumors, known as androgen-secreting tumors, can produce excessive androgens and lead to virilization.Ovarian Hyperthecosis : This condition involves the presence of luteinized ovarian stromal cells that produce androgens in excess.Receptor Sensitivity and Resistance : Sometimes, the bodys tissues may exhibit increased sensitivity to androgens, even at normal or slightly elevated levels. Alternatively, there can be resistance to the effects of androgens. These abnormalities can lead to virilization despite relatively normal androgen levels., Epidemiology : incidence of 2 cases per one million persons per year, which are equally divided among adenomas and carcinomas., variable, Early prenatal treatment of the mother with dexamethasone can prevent virilization of female genitalia., Complications : nan, Diagnostics : nan, Differential diagnosis : Congenital adrenal hyperplasia (CAH), disease description : Virilization or masculinization is the biological development of adult male characteristics in young males or females. Most of the changes of virilization are produced by androgens.Virilization is most commonly used in three medical and biology of sex contexts : prenatal biological sexual differentiation, the postnatal changes of typical chromosomal male (46, XY) puberty, and excessive androgen effects in typical chromosomal females (46, XX). It is also the intended result of androgen replacement therapy in males with delayed puberty and low testosterone

Virilism

Disease Name : Virilism, Symptoms : libido : Virilization causes abnormally high libido in women., deepening of the voice : Virilization causes deepening of the voice in women., "Acne : Theres development of acne on chest, back, face, hairline, underarms, groin.", Male-pattern baldness : Virilization can cause women to develop masculine traits, such as male pattern baldness., menstrual irregularity : Menstrual irregularities is one of the earliest symptoms showing up., Signs : fusion of the labia majora : Labial fusion is when the small inner lips around the entrance to the vagina become sealed together., Hirsutism : Excessive hair growth is common in women suffering from virilism., "Hypertrophy of the clitoris : An enlarged clitoris describes a clitoris thats larger than it should be.", Treatment : medication : Oestradiol/Oestrogen, Cortisone , A regular maintenance dose of oestrogen is usually ,effective in restoring some of the secondary sex charac\x02teristics, e.g. breast development. Additional intermittent progesterone therapy prevents breast and uterine ,malignancy.,n The most effective treatment of facial hirsutism is ,shaving and cosmetics., "MCINDOES OPERATION", Pathophysiology : Adrenal hyperplasia is usually congenital; delayed virilizing adrenal hyperplasia is a variant of congenital adrenal hyperplasia. Both are caused by a defect in hydroxylation of cortisol precursors, most commonly 21-hydroxylase deficiency, or the much milder condition of 11beta-hydroxylase deficiency.; cortisol precursors accumulate and are shunted into the production of androgens. The defect is only partial in delayed virilizing adrenal hyperplasia, so clinical disease may not develop until adulthood., Epidemiology : prevalence of <1/1, 000, 000, GOOD, Since the 1980s, antenatal treatment with dexamethasone has been recommended in high-risk pregnancies to minimise the risk of virilising the female genitalia of affected fetuses. To be effective, this treatment requires implementation in early pregnancy, prior to the commencement of autonomous fetal adrenal androgen synthesis., Complications : Oily skin, Irregular menstruation, Acne, Diagnostics : SERUM TESTOSTERONE LEVEL, SERUM ESTROGEN LEVEL, USG, NEUTROPHILS, Differential diagnosis : androgen-secreting ovarian tumor, ovarian stromal thecomatosis, disease description : Virilization is a condition in which a female develops characteristics associated with male hormones (androgens), or when a newborn has characteristics of male hormone exposure at birth.?

Visceral Larva Migrans

Disease Name : Visceral Larva Migrans, Symptoms : FAILURE TO GAIN WEIGHT, lymphadenopathy : itching, lymphadenopathy : swollen lymph node, muscle pain, fever, dyspnea, Signs : eosinophilia : Visceral larva migrans is usually a relatively benign disease, characterized chiefly by sustained eosinophilia., HEPATOMEGALY : An enlarged liver is commonly seen in visceral larva migrans., Treatment : medication : Albendazole , Mebendazole , Diethylcarbamazine , First line,•\tAlbendazole 800 mg PO twice daily × 2 weeks,•\tWith prednisolone if clinically warranted,Second line,•\tMebendazole (not recommended in patients with ,ocular and neurological disease as it does not cross ,the blood–brain barrier) 200 mg PO twice daily × ,5 days,Third line,•\tDiethylcarbamazine 4 mg/kg/day × 21 days, Pathophysiology : Your body responds to a Toxocara infection by producing extra immune cells in your blood. An increase in blood flow and immune cells to the affected area causes inflammation. Which symptoms you experience depends on how much inflammation your immune system creates in response to a Toxocara infection.Toxocariasis is the medical term for a Toxocara infection. The main presentations of toxocariasis include : Visceral larva migrans : Affects internal organs, including your liver, lungs and heart.Ocular larva migrans : May cause inflammation in your eyes and can lead to vision loss.Neurotoxocariasis : Affects your brain and spinal cord. It can cause severe inflammation, seizures and an altered mental state (encephalopathy). This type of infection is rare., Epidemiology : High prevalences range of 55.8 and 82 % were observed in Miraj and Calcutta, respectively, variable, You can prevent visceral larva migrans with the following steps : ,,Don’t eat food grown in dirt that might be contaminated with dog or cat poop.,Keep an eye on your children when they’re playing outside. Don’t let them put dirt in their mouth.,Wash fruits and vegetables before you eat them.,Practice good hand washing techniques. Teach your children to wash their hands before they eat and after they play outside or touch pets.,Restrict your pets to designated areas to poop and properly dispose of their bagged poop or litter.,Take your pets to the vet regularly for parasite screenings and deworming., Complications : myocarditis, PNEUMONIA, pulmonary fibrosis, uveitis, Diagnostics : Complete Blood Count CBC, ELISA, CT SCAN, Differential diagnosis : Ascariasis, Asthma, Dracunculiasis, FILARIASIS, HYMENOLEPIASIS, Urticaria, Urticaria, disease description : Visceral larva migrans is usually a mild condition. It’s caused by a parasitic roundworm called Toxocara that lives in dogs and cats. It usually affects children who play in dirt contaminated with pet poop.Children younger than six are more commonly infected with Toxocara that cause visceral larva migrans.People who have cats and dogs are more likely to experience visceral larva migrans.If you live in a warm climate, you’ll have a higher risk of ingesting Toxocara because their eggs can survive longer in infected soil when it’s hot.

Visceral Spasm

Disease Name : Visceral Spasm, Symptoms : CNS disturbances : Strong emotional reactions are also common presenting signs and may include anxiety, anguish and a sense of impending doom., Malaise : Visceral pain should be suspected when vague midline sensations of malaise are reported by a patient., autonomic dysfunction : The pain is typically associated with involvement of the autonomic nervous system. Some of these symptoms include pallor, sweating, nausea, vomit, changes in vital signs including blood pressure, heart rate and/or temperature., visceral spasm : True visceral pain is characterized as a vague, diffuse, and poorly defined sensation., Signs : nan, Treatment : nan, Pathophysiology : nan, Epidemiology : 28% of cancer-related pain, variable, Complications : nan, Diagnostics : ENDOSCOPY, PHYSICAL EXAMINATION, Differential diagnosis : Myocardial ischemia, Urinary colic, disease description : Visceral pain is pain related to the internal organs that is perceived in the midline of the body.  Unlike somatic pain — pain that occurs in tissues such as the muscles, skin, or joints — visceral pain is often vague, happens every so often, and feels like a deep ache or pressure.?More than 20% of the worlds population suffer from visceral pain. 

Vitamin B12 Deficiency

Disease Name : Vitamin B12 Deficiency, Symptoms : Ataxia : Ataxia, or impaired balance and coordination, is a neurological symptom that can be caused by B12 deficiency. As such, a person with B12 deficiency may have difficulty walking and balancing., Depressive symptoms : B12 deficiency is associated with a greater risk of developing depression. Having low levels of B12 can cause elevated levels of a sulfur-containing amino acid called homocysteine. In turn, this may contribute to the development of depression by increasing oxidative stress, DNA damage, and cell death in the body., erectile dysfunction : Men with B12 deficiency may experience erectile dysfunction as a result of increased levels of homocysteine in the body., fatigue : Low vit B12 makes one feel tired. As such, having inadequate B12 levels can decrease normal red blood cell production, which can impair oxygen delivery., Gastrointestinal symptoms : A B12 deficiency may also cause diarrhea, nausea, constipation, bloating, gas, and other gastrointestinal symptoms. These issues can affect both adults and children., headache : Headaches are among the most commonly reported symptoms related to B12 deficiency in both adults and kids., muscle weakness : B12 deficiency negatively impacts motor and sensory nerve function, which can cause muscle cramps and weakness., PALENESS OF BODY : Like the condition called iron deficiency anemia, anemia related to B12 deficiency may make your skin pale due to a lack of fully-matured, healthy red blood cells in the body. B12 deficiency can also cause a condition called jaundice, which makes your skin and the whites of your eyes take on a yellowish color due to high levels of bilirubin., mental changes : In addition to depressive symptoms, low or deficient B12 levels may lead to other mental conditions, including psychosis and mood disorders., vision abnormalities : B12 deficiency may cause vision disturbances, possibly due to damage to the optic nerve., paresthesia of hand & foot : Many adults and kids who have B12 deficiency report experiencing paresthesia, a burning or pins-and-needles sensation in certain areas of the body like the hands and feet. Unfortunately, this symptom of B12 deficiency overlaps with symptoms related to diabetic neuropathy — nerve damage caused by high blood sugar that can cause pain and numbness in the extremities. People with diabetes taking metformin are at a higher risk of developing B12 deficiency because this medication can reduce vitamin B12 absorption in the body., oral pain : In people with this deficiency, glossitis can appear alongside stomatitis, which is characterized by sores and inflammation in the mouth. Even though glossitis and stomatitis are common in people with B12 deficiency-related anemia, they can also occur without anemia and can be a sign of an early B12 deficiency., Signs : nan, Treatment : "If you have pernicious anemia or have trouble absorbing vitamin B12, youll need shots of this vitamin at first. You may need to keep getting these shots, take high doses of a supplement by mouth, or get it nasally after that.,,If you dont eat animal products, you have options. You can change your diet to include vitamin B12-fortified grains, a supplement or B12 injections, or a high-dose oral vitamin B12 if you are deficient.,,Older adults who have a vitamin B12 deficiency will likely have to take a daily B12 supplement or a multivitamin that contains B12.", Pathophysiology : With age, it can become harder to absorb this vitamin. It can also happen if you have had weight loss surgery or another operation that removed part of your stomach, or if you drink heavily.You may also be more likely to develop vitamin B12 deficiency if you have : Atrophic gastritis, in which your stomach lining has thinnedPernicious anemia, which makes it hard for your body to absorb vitamin B12Conditions that affect your small intestine, such as Crohns disease, celiac disease, bacterial growth, or a parasiteAlcohol misuse or heavy drinking can make it harder for your body to absorb nutrients or prevent you from eating enough calories. One sign that you lack enough B12 may be glossitis, or a swollen, inflamed tongue., Epidemiology : at least 47% i, Vitamin B12 deficiency in the US and the UK is estimated to occur in about 6 percent of those under the age of 60, and 20 percent of those over the age of 60., variable, Most people can prevent vitamin B12 deficiency by consuming foods and drinks that have vitamin B12.,,Options for consuming vitamin B12 include : ,1. Animal food products. ,2. Fortified foods.,3. Vitamin B12 dietary supplements.,,Other things you can do to help prevent vitamin B12 deficiency include : ,1. Avoid alcohol.,2. Do your best to manage your digestive disease., Complications : Memory loss, paraesthesia, Diagnostics : Complete Blood Count CBC, serum Vitamin B12 level, Schilling test, Differential diagnosis : FOLATE DEFICIENCY, Multiple Sclerosis, Myelopathy, Syphilis, Toxicity, disease description : Even though the vitamin is found in many foods, B12 insufficiency and deficiency are relatively common. This is often due to limited dietary intake, malabsorption, certain medical conditions, or the use of B12-depleting medicationsFor reference, B12 levels above 300 pg/mL are considered normal, levels of 200–300 pg/mL are considered borderline, and levels below 200 pg/mL are considered deficient

Vitamin B2 Deficiency

Disease Name : Vitamin B2 Deficiency, Symptoms : conjunctivitis : Vitamin B2, Riboflavin, is awarded special importance from the B vitamin family to eye health due to its role in helping the retina receive light. Deficiency of which leads to conjuctivitis., fatigue : Vitamin B12 deficiency can cause pronounced symptoms of exhaustion and fatigue, even in the low normal range., glossitis : The glossitis in vitamin B2 deficiency is described as magenta., DEPRESSION : It has been associated with psychological effects including depression., Ocular symptoms : It has also been associated with visual disturbances including night blindness, migraine headaches & photophobia., Signs : angular stomatitis : Angular stomatitis (AS) has classically been linked with deficiencies of riboflavin, other B group vitamins and iron., cheilitis : Research reveals 90 percent of angular cheilitis is caused due to poor diet. Vitamin deficiency is the most common cause of cheilitis. The absence of vitamin B2 in the body slows down the metabolism of fats, proteins, and carbohydrates and decreases energy production., dermatitis : It can affect the skin by causing skin crack, itching, and dermatitis around the mouth., Treatment : Riboflavin supplements come in 25 mg, 50 mg, and 100 mg tablets. According to the National Institutes of Health, the recommended daily nutrient intake of riboflavin is 1.3 mg for men, 1.1 mg for women, 1.3 mg for male adolescents (age 14 to 18), and 1.0 mg for female adolescents (age 14 to 18). Recommendations are that pregnant women take 1.4 mg, and breastfeeding women take 1.6 mg. For infants age of 0 to 6 months old is 0.3 mg, 7 to 12 months is 0.4 mg, 1 to 3 years old is 0.5 mg, 4 to 8 years old is 0.6 mg, and 9 to 13 years is 0.9 mg. It is important to take riboflavin supplements with meals because absorption levels increase with food. If oral supplementation is not possible, then injections are an option, Pathophysiology : Riboflavin deficiency may develop as a result of decreased dietary intake, malabsorption and phototherapy. Adolescents, the elderly, alcoholics and individuals with eating disorders are at risk for inadequate nutritional intake. Breastfed infants of riboflavin-deficient mothers, as well as infants weaned to non- milk products, are also at risk. Impaired absorption of riboflavin has been associated with bariatric surgery and the use of various medications, including chlorpromazine or other tricyclics. Borate can complex with riboflavin, increase urinary excretion of riboflavin and inhibit riboflavin-dependent enzymes. In the setting of protein–energy malnutrition, riboflavin deficiency may worsen due to increased renal loss. Finally, phototherapy for neonatal hyperbilirubinaemia causes photodecomposition of riboflavin., Epidemiology : Riboflavin deficiency is relatively uncommon in the developed world but in developing countries mild deficiency can be seen in up to 50% of the population., EXCELLENT, Supplements can be used to increase the amount of B2 consumed, however should be only on prescription., Complications : DEPRESSION, liver degeneration, Diagnostics : erythrocyte glutathione reductase, Differential diagnosis : anaemia, cataracts, Cleft Lip with Cleft Palale, fatigue, MALIGNANCY, migraine, Night blindness, disease description : Vitamin B2 (riboflavin) is a water-soluble B-complex vitamin. It is an essential co-factor for cellular oxidation-reduction reactions and vitamin B6 metabolism. Riboflavin exists as two biologically active forms – flavin mononucleotide (FMN) and flavin-adenine dinucleotide (FAD). These co-enzymes, along with a small percentage of free riboflavin, are found in milk, dairy products, meats, fatty fish, eggs, green leafy vegetables, whole grains and enriched breads. Dietary FMN and FAD are both hydrolysed to riboflavin, then actively absorbed in the proximal small intestine . A deficiency in riboflavin can lead to various cutaneous, mucosal and ocular manifestations, the so-called oculo-orogenital syndrome.

Vitamin B3 Deficiency

Disease Name : Vitamin B3 Deficiency, Symptoms : CHRONIC DIARRHEA : Chronic diarrhea, sometimes bloody., Gastrointestinal symptoms : Includes abdominal pain and indigestion, loss of appetite, nausea, vomiting., Rashes : Thick, scaly pigmented rash on skin exposed to sunlight., Neurological symptoms : Includes mood changes, depression, tremors or numbness and tingling in the hands and feet, delirium and dementia., Oral ulcers : Mouth sores and a red, swollen tongue., Signs : nan, Treatment : The recommended daily intake of niacin is 13–20 mg, depending ,on age and gender.,Treatment includes 500 mg/day of nicotinamide or nicotinic ,acid over several weeks. Nicotinamide is preferred because nicotinic acid can cause headaches and flushing. Neuropsychiatric ,symptoms improve within the first 24–48 h of treatment, while ,cutaneous disease may require weeks to remit., Pathophysiology : Decreased dietary intake, defective absorption of niacin or tryptophan, and impaired conversion of tryptophan to niacin predispose individuals to the development of niacin deficiency. Individuals with alcoholism, eating disorders, and presumed food allergies are at risk for inadequate intake. Malabsorption can occur in the setting of inflammatory bowel disease, gastroenterostomy, subtotal gastrectomy, jejunoileitis and gastric bypass surgery. Genetics : Hartnup disease is a rare autosomal recessive disorder characterized by a defective neutral amino acid transport system, resulting in malabsorption of tryptophan, thus giving rise to niacin deficiency. It is caused by mutations in the SLC6A19 gene, which encodes a neutral amino acid transporter expressed in the intestine and kidneys. Hartnup disease presents with cerebellar ataxia, psychiatric symptoms, aminoaciduria and pellagra., Epidemiology : Niacin deficiency was noted in almost one third of women and 6% of children in this country, can be fatal if not treated, The prevention of vitamin B3 deficiency can be achieved by consuming food items rich in vitamin B3 such as red meat, fish, fortified bread, cereals, poultry, peanuts, and enriched pasta., Complications : neurological problem, Diagnostics : VITAMIN B3/NICOTINIC ACID, Urine analysis, Differential diagnosis : Acute cutaneous lupus erythematosus, Crohn disease, Discoid lupus erythematosus, Porphyria Cutanea Tarda, Ulcerative Colitis, disease description : A severe niacin deficiency leads to pellagra, a condition that causes a dark, sometimes scaly rash to develop on skin areas exposed to sunlight; bright redness of the tongue; and constipation/diarrhea.

Vitamin B6 Deficiency

Disease Name : Vitamin B6 Deficiency, Symptoms : cheilosis : Cheilosis, which is characterized by sore, red and swollen lips with cracked mouth corners, can result from B6 deficiency. Cracked areas may bleed and become infected. In addition to being very painful, having cracked and sore lips can make activities like eating and talking difficult., fatigue : A vitamin B6 deficiency can leave you feeling unusually tired and sluggish. A big reason is vitamin B6’s role in helping make hemoglobin deficiency of which causes extreme fatigue.., glossitis : The glossy, smooth surface of the tongue is due to the loss of papillae. Those are the bumps on your tongue. Glossitis can cause problems chewing, swallowing and talking., Peripheral neuropathy : Deficiency of B6 can cause nerve damage called peripheral neuropathy. Symptoms may include burning, shooting and tingling pain in your arms, legs, hands and feet. Some describe it as a “pins and needles” feeling. The nerve damage may also result in clumsiness, balance problems and difficulty walking., seizures : Without enough B6, you don’t make adequate amounts of the calming neurotransmitter GABA, so your brain may become overstimulated. Seizures can cause symptoms such as muscle spasms, rolling eyes and jerky arms or legs. Sometimes people have rapid, uncontrollable shaking (convulsions) or lose consciousness., immune deficiency : Nutrient deficiencies, including B6, can disrupt the immune system. More specifically, a deficiency in B6 can result in the decreased production of antibodies needed to fight infections. A B6 deficiency may also reduce your body’s production of white blood cells, including T cells. These cells regulate immune function, helping it respond appropriately., Skin rashes : Vitamin B6 deficiency is one cause of a red, itchy rash called seborrheic dermatitis. The rash can appear on your scalp, face, neck and upper chest. It’s known for its oily, flaky appearance and may cause swelling or white patches., MOOD CHANGES : Shortfalls of B6 may affect your mood, sometimes contributing to depression, anxiety, irritability and increased feelings of pain. That’s because B6 is involved in the making of several neurotransmitters, such as serotonin and gamma-aminobutyric acid (GABA). Both serotonin and GABA help control anxiety, depression and feelings of pain., Signs : nan, Treatment : The recommended daily intake of vitamin B6 is 0.1–2 mg, depending on age and gender.,Treatment of vitamin B6 deficiency includes stopping any inciting medications and supplementation with pyridoxine 100 mg ,daily. Mucosal lesions resolve within days, while cutaneous and ,haematological manifestations improve over weeks and neurological sequelae over months., Pathophysiology : Factors contributing to vitamin B6 deficiency include decreased dietary intake, malabsorption and medications. Alcoholics are particularly prone to poor dietary intake. Individuals with Crohn disease and coeliac disease may suffer from malabsorption. Certain medications bind to vitamin B6 and act to increase its excretion or decrease its activity, including isoniazid, hydralazine, penicillamine and oral contraceptives. Vitamin B6 deficiency has also been reported in patients undergoing haemodialysis., Epidemiology : prevalence rates of 11-24%, GOOD, A varied, adequate diet will prevent vitamin B6 deficiency. Fish, organ meats, poultry, potatoes, grains, fortified cereals, soy products, legumes, and non-citrus fruits all are good sources of vitamin B6., Complications : seizures, Diagnostics : VITAMIN B6/P5P, HISTORY TAKING, PHYSICAL EXAMINATION, pyridoxal-5-phosphate, Differential diagnosis : anemia, beriberi, cheilosis, glossitis, porphyria, stomatitis, disease description : Vitamin B6 deficiency is associated with microcytic anemia, electroencephalographic abnormalities, dermatitis with cheilosis (scaling on the lips and cracks at the corners of the mouth) and glossitis (swollen tongue), depression and confusion, and weakened immune function 

Vitamin B9 Deficiency

Disease Name : Vitamin B9 Deficiency, Symptoms : Neurological symptoms : Includes memory loss, difficulty concentrating, confusion & problems with judgment., anemia : Symptoms includes paleness, dyspnea, irritability & dizziness., oral infection : Symptoms includes tender, red tongue, mouth ulcers, reduced sense of taste., Signs : nan, Treatment : Most adults need 400 micrograms (mcg) of folic acid each day. Your healthcare provider will let you know how much you should take.,,Your healthcare provider will also advise you to eat a healthy, balanced diet. A balanced diet includes fruits, vegetables and other foods that contain folate or are enriched with folic acid., Pathophysiology : One of the most common causes of folate deficiency is not eating a healthy, balanced diet. A healthy diet includes foods that naturally contain folate or are enriched with folic acid. Other causes of folate deficiency can include : Digestive system diseases : Your digestive system doesn’t absorb folic acid well if you have a disease such as Crohn’s disease or celiac disease.Excessive alcohol use : People who drink large amounts of alcohol sometimes substitute alcohol for food. As a result, they don’t get enough folate.Overcooking your fruits and vegetables : When you overcook, the heat can destroy the naturally occurring folate in your produce.Hemolytic anemia : A blood disorder that occurs when your red blood cells are destroyed and can’t be replaced fast enough.Certain medications : Some anti-seizure drugs and ulcerative colitis drugs interfere with the proper absorption of folate.Kidney dialysis : A treatment for people with kidney failure. , Epidemiology : 39.8% of all adolescent had folate deficiency, variable, The best way to prevent folate deficiency is to eat a healthy diet that includes foods that contain folate or folic acid. ,Folate can be found naturally in : ,,Peas, beans and legumes.,Citrus fruits.,Dark green leafy vegetables.,Liver.,Seafood.,Eggs and dairy.,Meat and poultry., Complications : Alzheimers Disease, Cardiovascular Disease, Dementia, infertility, anemia, DEPRESSION, Diagnostics : Complete Blood Count CBC, HISTORY TAKING, Differential diagnosis : ALCOHOLIC LIVER DISEASE, anemia, Hypothyroidism, disease description : A folate deficiency is rare because it is found in a wide range of foods. Folate is the natural form of vitamin B9, water-soluble and naturally found in many foods. It is also added to foods and sold as a supplement in the form of folic acid; this form is actually better absorbed than that from food sources—85% vs. 50%, respectively.

Vitamin D Deficiency

Disease Name : Vitamin D Deficiency, Symptoms : Hypoparathyroidism : Patients with prolonged and severe vitamin D deficiency can experience symptoms associated with secondary hyperparathyroidism, including bone pain, arthralgias, myalgias, fatigue, muscle twitching (fasciculations), and weakness, fracture : Fragility fractures may result from chronic vitamin D deficiency, leading to osteoporosis., Signs : nan, Treatment : Sun exposure and UV light therapy may be useful in correcting vitamin D deficiency., The recommended daily intake of vitamin D is 200–600 IU, ,depending on age. Most experts agree that individuals without ,adequate sun exposure require 800–1000 IU daily.,For patients older than 1 year of age, supplementation with ,50 000 IU of vitamin D2 weekly for 8 weeks is a cost effective method ,of correcting vitamin D deficiency. Alternatively, taking 1000 IU of ,vitamin D3 or 3000 IU of vitamin D2 daily may also be effective.,For patients under 1 year of age, 1000–5000 IU of vitamin D2 ,should be given daily until radiological abnormalities normalize. ,All breastfed infants should be supplemented with 400 IU of vitamin D daily as prophylaxis. d-a-tocopheryl polyethylene ,glycol-1000 succinate, a vitamin E compound, has been successfully used to treat hepatic rickets, Pathophysiology : Vitamin D deficiency is commonly caused by decreased vitamin D synthesis, malabsorption and poor dietary intake. Decreased endogenous vitamin D synthesis occurs in individuals with increased melanin pigment and/or decreased sun exposure. In some cultures, shielding of the skin with clothing is mandated, and therefore prevents adequate UV light exposure. The use of sunscreen can theoretically reduce vitamin D synthesis; however, studies have demonstrated that real-life application of sunscreens does not result in significant vitamin D deficiency. Fat malabsorption states, including coeliac disease, cystic fibrosis, pancreatic disease, biliary disease and gastric bypass surgery, may predispose individuals to vitamin D deficiency. Liver disease, renal disease and anticonvulsants can also interfere with vitamin D metabolism. Inadequate dietary intake of vitamin D is observed in exclusively breastfed infants, preterm infants (due to lower stores and higher demand) and the elderly or disabled. Genetics There are two inherited autosomal recessive forms of vitamin D-dependent rickets. Type I involves a defect in vitamin D 1a- hydroxylase of the kidneys, while type II is associated with defects in the vitamin D receptor, resulting in end-organ resistance to physiological amounts of 1, 25-hydroxyvitamin D., Epidemiology : 14-59%, variable, The best way to prevent vitamin D deficiency is to ensure you’re getting enough vitamin D in your diet and/or through sun exposure. But be careful about being in the sun for too long without sunscreen. Excessive sun exposure puts you at an increased risk for skin cancer., Complications : osteopenia, Osteoporosis, Diagnostics : Parathyroid Hormone (PTH), serum calcium Ca++, serum phosphate, VITAMIN D3, HISTORY TAKING, Differential diagnosis : CYSTIC FIBROSIS, Dietary supplement, liver disease, disease description : Vitamin D deficiency can lead to a loss of bone density, which can contribute to osteoporosis and fractures (broken bones).Severe vitamin D deficiency can also lead to other diseases. In children, it can cause rickets. Rickets is a rare disease that causes the bones to become soft and bend.

Vitamin D Dependent Rickets

Disease Name : Vitamin D Dependent Rickets, Symptoms : CNS disturbances : Irritability, tetany or seizures, and failure to thrive, are typical in the first few months of life., frontal bossing : Frontal bossing (develops in later stages) is an unusually prominent forehead. It is sometimes associated with a heavier than normal brow ridge., leg deformity : Long-bone deformities is commonly experienced by affected individuals., hypotonia : Weak muscle tone is the first sympon to show up., Signs : nan, Treatment : "Most cases of rickets can be treated with vitamin D and calcium supplements. Follow your childs doctors directions as to dosage. Too much vitamin D can be harmful.,,Your childs doctor will monitor your childs progress with X-rays and blood tests.,,If your child has a rare inherited disorder that causes low amounts of phosphorus, supplements and medication may be prescribed.,,For some cases of bowleg or spinal deformities, your doctor might suggest special bracing to position your childs body appropriately as the bones grow. More-severe skeletal deformities might require surgery.", Pathophysiology : The term “vitamin D dependent rickets” describes a group of genetic disorders that are characterized by early-onset rickets due to the inability to maintain adequate concentrations of active forms of vitamin D or a failure to respond fully to activated vitamin D. Although the term is now admittedly a pathophysiological misnomer, there remains clinical relevance for its continued use, as patients have a lifelong “dependency” on administration of specialized regimens of vitamin D replacement. , Epidemiology : 1 in 200, 000 children., variable, Rickets can easily be prevented by eating a diet that includes vitamin D and calcium, spending some time in sunlight, and if necessary, taking vitamin D supplements., Complications : seizures, Failure to grow, Bone deformities, Dental defects, Diagnostics : Parathyroid Hormone (PTH), serum calcium Ca++, CT SCAN, serum phosphate, Differential diagnosis : Achondroplasia, CELIAC DISEASE, fanconi syndrome, Hypoparathyroidism, injury, renal insufficiency, disease description : Vitamin D-dependent rickets is a disorder of bone development that leads to softening and weakening of the bones (rickets). There are several forms of the condition that are distinguished primarily by their genetic causes : type 1A (VDDR1A), type 1B (VDDR1B), and type 2A (VDDR2A).

Vitreous Haemorrhage

Disease Name : Vitreous Haemorrhage, Symptoms : floaters in eyes, sudden painless loss of vision, Signs : BOAT SHAPED HAEMORRHAGE WHICH IS RED IN COLOUR, VITREOUS HAEMORRHAGE, black shadows against the red glow in small haemorrhages, presence of blood in the vitreous cavity, reddish mass in the vitreous, Treatment : nan, Pathophysiology : nan, Epidemiology : nan, Complications : nan, Diagnostics : nan, Differential diagnosis : nan, disease description : nan

Vitreous Opa Cities

Disease Name : Vitreous Opa Cities, Symptoms : floaters in eyes, visual disturbances, Signs : leucocoria : Leucocoria, also known as white pupillary reflex, is a medical condition characterized by the abnormal appearance of a white reflection from the retina of the eye., Photopsia : Photopsia refers to the perception of flashes of light or visual disturbances in the absence of any external light source., Treatment : Persistent hyperplastic primary vitreous (PHPV) treatment : pars plana lensectomy and,excision of the membranes with anterior vitrectomy,provided the diagnosis is made early., Pathophysiology : The vitreous gel, which consists of collagen fibers, fills the vitreous chamber undergoing syneresis and contraction (shrinking) due to age and mechanical factors. Fibers are intertwined within the vitreous and are attached to the surface of the retina. Over time, the vitreous shrinks, and these fibers pull on the retinal surface. Often these fibers break and allow the vitreous to separate and continue shrinking. Eventually, the vitreous cannot fill the volume of the cavity it sits within. This leads to the separation of the vitreous from the retina, creating vitreous floating in its chamber. If this process happens gradually, the symptoms are typically mild and can go unnoticed. If the process of separation is violent, on an isolated portion of the retina, or there is the presence of abnormal adhesion between the vitreous and retina, the PVD can tear retinal vessels or the retina itself., Epidemiology : POOR, Complications : nan, Diagnostics : CT Orbit, Slit lamp examination, USG, Indirect ophthalmoscopic examination, Differential diagnosis : nan, disease description : Since vitreous is a transparent structure, any relatively nontransparent structure present in it will form an opacity and cause symptoms of floaters. Common conditions associated with vitreous opacities are described below. Muscae volitantes These are physiological opacities and represent the residues of primitive hyaloid vasculature. Patient perceives them as fine dots and filaments, which often drift in and out of the visual field, against a bright background (e.g., clear blue sky). Persistent hyperplastic primary vitreous (PHPV) It results from failure of the primary vitreous structure to regress combined with the hypoplasia of the posterior portion of vascular meshwork. Clinical features. PHPV may be anterior or posterior, most often elements of both are present. Common features are : ¦¦Leucocoria (whitish pupillary reflex) is the most common presenting feature of both anterior and posterior PHPV. ¦¦Microphthalmia is often associated with PHPV. ¦¦Tractional retinal detachment and retinal folds are features of posterior PHPV. ¦¦Associated anomalies include congenital cataract, shallow anterior chamber, angle closure glaucoma, long ciliary processes and recurrent intraocular haemorrhage. ¦¦PHPV is almost always unilateral. Bilateral cases are rare and may be associated with trisomy 13 (Patau syndrome), trisomy 22, Norries disease and Walkers Warburg syndrome. Inflammatory vitreous opacities These consist of exudates poured into the vitreous in patients with anterior uveitis (iridocyclitis), posterior uveitis (choroiditis), pars planitis, pan uveitis and endophthalmitis. Vitreous aggregates and condensation with liquefaction It is the commonest cause of vitreous opacities. Condensation of the collagen fibrillar network is a feature of the vitreous degeneration which may be senile, myopic, post-traumatic or post-inflammatory in origin. Amyloid degeneration It is a rare condition in which amorphous amyloid material is deposited in the vitreous as a part of the generalised amyloidosis. These vitreous opacities are linear with footplate attachments to the retina and the posterior lens surface. Asteroid hyalosis It is characterised by small, white rounded bodies suspended in the vitreous gel. These are formed due to accumulation of calcium-containing lipids. Asteroid hyalosis is a unilateral, asymptomatic condition usually seen in old patients with healthy vitreous. There is a genetic relationship between this condition, diabetes and hypercholesterolaemia. The genesis is unknown and there is no effective treatment. Synchysis scintillans (Cholestrolosis bulbi) In this condition, vitreous is laden with small white angular and crystalline bodies formed of cholesterol. It affects the damaged eyes which have suffered from trauma, vitreous haemorrhage or inflammatory disease in the past. In this condition vitreous is liquid and so, the crystals sink to the bottom, but are stirred up with every movement to settle down again with every pause. This phenomenon appears as a beautiful shower of golden rain on ophthalmoscopic examination. Since, the condition occurs in a damaged eye, it may occur at any age. The condition is generally symptomless, and untreatable. Red cell opacities These are caused by small vitreous haemorrhages or leftouts of the massive vitreous haemorrhage. Tumour cells opacities These may be seen as free floating opacities in some patients with retino-blastoma, and reticulum cell sarcoma and intraocular lymphomas.

Vocal Nodule

Disease Name : Vocal Nodule, Symptoms : vocal fatigue, hoarseness of voice : They make your voice hoarse and change the sound of your voice., voice change : It may sound raspy or breathy too., pain in the neck on prolonged phonation : General neck pain or a shooting pain that travels from ear to ear., cough : Frequent coughing, throat clearing or general fatigue., Signs : nan, Treatment : medication : Pantoprazole , vocal rest, proper use of voice, large nodules or,nodules of long standing in adults. They are excised with,precision under operating microscope either with cold instruments,or laser avoiding any trauma to the underlying,vocal ligament, Pathophysiology : They appear symmetrically on the free edge of vocal cord, at the junction of anterior one-third, with the posterior two-thirds, as this is the area of maximum vibration of the cord and thus subject to maximum trauma and. Their size varies from that of pin-head to half a pea. They are the result of vocal trauma when person speaks in unnatural low tones for prolonged periods or at high intensities. They mostly affect teachers, actors, vendors or pop singers. They are also seen in school going children who are too assertive and talkative. Pathologically, trauma to the vocal cord in the form of vocal abuse or misuse causes oedema and haemorrhage in the submucosal space. This undergoes hyalinization and fibrosis. The overlying epithelium also undergoes hyperplasia forming a nodule. In the early stages, the nodules appear soft, reddish and oedematous swellings but later they become greyish or white in colour. Patients with vocal nodules complain of hoarseness. Vocal fatigue and pain in the neck on prolonged phonation are other common symptoms., Epidemiology : 2.29% to 16.9%, good, To reduce your risk of developing a vocal cord lesion, you should avoid : ,,Singing or talking excessively if you have an upper respiratory infection.,Talking excessively or speaking loudly without adequately resting your voice.,Drinking alcohol excessively and consuming too much caffeine (which dry out your vocal cords).,Smoking or being in smoke-filled rooms.,,You can also put healthy habits into place to care for your vocal cords and reduce your risk of getting sick., Complications : Hoarseness, multiple tones, loss of voice, Diagnostics : HISTOPATHLOGY, Laryngoscopy, CT SCAN, Differential diagnosis : Epidermoid cyst, mucous retention cysts, Vocal cord cysts, Vocal fold papillomas, disease description : Vocal cord nodules (referred to as “vocal fold” nodules by physicians) are growths that form on the vocal cords. These bumps are benign (noncancerous) and are similar to calluses that can form on the hands.

Vocal Polyp

Disease Name : Vocal Polyp, Symptoms : vocal fatigue, hoarseness of voice, dyspnea, Signs : diplophonia (double voice) : simultaneous presence in the voice of two separate tones, heard as distinctly different in pitch., Treatment : surgical excision under operating,microscope followed by speech therapy, Pathophysiology : Both vocal cord nodules and polyps can be caused by different forms of trauma, including singing (particularly in professional singers), screaming, cheerleading, and excessive talking (such as that by a teacher, coach, salesperson or radio personality). Other causes include extra muscle tension when speaking, smoking, alcohol use, sinusitis, allergies, and rarely, hypothyroidism., Epidemiology : The prevalence of vocal nodules was 1.31%, (0.3–0.6%), GOOD, To Do : VOICE REST & REHABILITATION, Complications : Hoarseness, Scarring, Painful phonation\\/voice use, Diagnostics : HISTOPATHLOGY, Laryngoscopy, CT SCAN, Indirect Laryngoscopy, HISTORY TAKING, Differential diagnosis : Epidermoid cyst, intubation granuloma, mucous retention cyst, Vocal fold papillomas, disease description : Vocal cord lesions are benign (non-cancerous) growths that may include nodules, polyps and cysts. Vocal trauma or overuse is associated with these lesions.Vocal cord nodules, vocal cord cysts, and vocal cord polyps are noncancerous growths or bumps, like calluses on your vocal cords. They can cause your voice to sound raspy, breathy, or hoarse. Your voice may crack or cut in and out as the bumps prevent your vocal cords from vibrating normally.

Vogt-koyanagi-harada (vkh) Syndrome

Disease Name : Vogt-koyanagi-harada (vkh) Syndrome, Symptoms : eye pain : Very deep pain in the eyes is a characteristic of Vogt-Koyanagi-Harada (VKH) Syndrome., headache : Vogt-Koyanagi-Harada disease is initially characterized by headaches., uveitis : These symptoms are usually followed in a few weeks by eye inflammation (uveitis) and blurring of vision., vertigo : Persistent dizziness coupled with nausea is experienced by the patients., cutaneous symptoms : Skin changes may include the development of smooth, white patches in the skin caused by the loss of pigment-producing cells (vitiligo). These white patches are usually distributed over the head, eyelids and torso. The chronic stage can last for several months to several years., Ocular symptoms : The chronic stage follows in a few weeks. This stage is characterized by changes in the eyes and skin. The changes in the eyes may include loss of color in the layer of the eye filled with blood vessels that nourish the retina (choroid), as well as the development of small yellow nodules in parts of the retina., Signs : nan, Treatment : medication : Cyclosporine/Ciclosporine, Dexamethasone , Azithromycin , Cyclophosphamide , Azathioprine , Prednisolone, Betamethasone , Atropine/ Atropine methonitrate, Phenylbutazone, Standard treatment of Vogt-Koyanagi-Harada disease is the use of high-dose systemic steroid drugs initially and often followed by immunosuppressive therapy., Pathophysiology : As a response to an environmental factor, Th1 mediated inflammation develops against melanocytes. Tyrosinase peptide is a known target of T-cells, specifically in melanocytes expressing HLA DRB1-04*05. Comparing the tyrosinase peptide and a cytomegalovirus peptide has shown that homology exists between the two proteins. Other studies have shown EBV DNA by PCR in CSF of patients with VKH.This inflammatory cascade leads to the formation of non-necrotizing granulomas in affected organs. In the eye, these are seen as sub-retinal pigment epithelial (RPE) aggregates named Dalen-Fuchs nodules, which may also be seen in other granulomatous processes, especially sympathetic ophthalmia., Epidemiology : There are regional differences in the prevalence of VKH among patients presenting with uveitis – it is the most common cause of uveitis in India (prevalence 21.08%) and the second most common in Thailand., variable, VKH, when caught early, can be effectively managed and treated by the appropriate specialties as part of a care team that includes primary care physicians, emergency room physicians, and specialists in low vision, otorhinolaryngology, ophthalmology, and audiology., Complications : cataract, Glaucoma, Diagnostics : CSF EXAMINATION, HISTOPATHLOGY, MRI Brain, Optical coherence tomography (OCT), Slit lamp examination, Fluorescein angiography, ERG, Differential diagnosis : Alport Syndrome, Choroidal Melanoma, Infectious Posterior Uveitis, Sarcoidosis, Sympathetic Ophthalmia, systemic lupus erythematosus (SLE), disease description : It is an idiopathic multisystem disorder which includes cutaneous, neurological and ocular lesions. The disease is comparatively more common in Japanese Vogt-Koyanagi-Harada disease (VKH) is a central nervous system condition that specifically affects vision and hearing. Descriptions of this disease date back to the 12 century, but the disease is named after three 20 century physicians who described the collective manifestations of this disease. Alfred Vogt initially described bilateral iridocyclitis and eyebrow depigmentation in 1906, followed by Yoshizo Koyanagi’s 1926 description of bilateral serous detachments in association with cerebrospinal fluid (CSF) pleocytosis. Einosuke Harada identified the integumentary symptoms of the condition shortly thereafter. The disease presents with signs and symptoms of a loss of immune tolerance to melanocytes within the meninges, eyes, skin, hair, and earswho are usually positive for HLA-DR4 and DW15.

Vohwinkel Syndrome And Bart–pumphrey Syndrome

Disease Name : Vohwinkel Syndrome And Bart–pumphrey Syndrome, Symptoms : Hearing loss : The hearing loss associated with Bart-Pumphrey syndrome ranges from moderate to profound and is typically present from birth (congenital)., nail disorders : People with Bart-Pumphrey syndrome typically have a white discoloration of the nails (leukonychia); the nails may also be thick and crumbly., cutaneous symptoms : Affected individuals often have wart-like (verrucous) skin growths called knuckle pads on the knuckles of the fingers and toes. They may also have thickening of the skin on the palms of the hands and soles of the feet (palmoplantar keratoderma). The skin abnormalities generally become noticeable during childhood., Signs : nan, Treatment : Appropriate rehabilitation (hearing aids, speech therapy, language training, cochlear implantation, educational programmes) for the hearing loss are important to achieve auditory ,speech recognition effectively., Vohwinkel syndrome has been successfully treated by etretinate, acitretin and the cicatricial bands released surgically., Pathophysiology : Connexin 26 is expressed in the cochlea where it may permit the recycling of potassium to endolymph. In skin, the protein is found in palmoplantar epidermis and sweat glands, and is up-regulated in conditions such as psoriasis. Patients homozygous for mutations preventing any expression of connexin 26 have no discernible skin phenotype, indicating that dominant negative or gain-of-function effects may be involved in the pathogenesis of cutaneous manifestations of mutations in GJB2. There are various mechanisms which may underlie the phenotypic effects of connexin gene mutations : mutant proteins are sometimes unable to form functional gap junction channels; in other cases, aberrant trafficking of mutant proteins may prevent some of them reaching the cell surface membrane and lead to their accumulation in organelles triggering ER stress response; finally, mutant proteins may exert deleterious effects on other connexins’ function (e.g. c.del42E has been shown to exert a dominant negative effect on the wild-type connexin 43)., Epidemiology : Bart-Pumphrey syndrome is a rare disorder; its exact prevalence is unknown., variable, NA, Complications : hearing impairment, Diagnostics : GENETIC TESTING, HISTOLOGIC EXAMINATION, hearing tests, Differential diagnosis : knuckle pads, leukonychia, Olmsted syndrome, Papillon-Lefevre syndrome, Papillon-Lefevre syndrome, disease description : Bart-Pumphrey syndrome (BPS) is an autosomal dominant disorder characterized by sensorineural hearing loss, palmoplantar keratoderma, knuckle pads, and leukonychia, which show considerable phenotypic variability.

Volkmann’s Ischaemia

Disease Name : Volkmann’s Ischaemia, Symptoms : severe pain in the forearm, unable to move the fingers fully, Stretch pain : Pain occurs with passive stretching of the flexor, Swelling over the fingers, numbness over the fingers : there is a decreased sensation (paresthesia) and there is an observable motor deficit (paresis), tenderness over the fingers, PULSELESSNESS : It is possible that the pulsations can not be felt in the swollen arm, mainly in the distal part (pulselessness)., Signs : nan, Treatment : Volkmann’s ischaemia is an emergency,of the highest order. The following actions need to,be taken urgently in a suspected case : ,• Any external splints or bandages that might be,causing constriction are removed.,• The forearm is elevated and the child encouraged,to move fingers.,• If no improvement occurs within 2 hours, an,urgent decompression of the tight compartment,is necessary. This is done by a fasciotomy – an,operation where the deep fascia covering the,flexor muscles of the forearm is slit along its,entire length, Pathophysiology : Volkmann’s ischaemia is the result of diminished blood supply to the flexor muscles of the forearm. The muscles supplied by the anterior interosseous artery, a branch of brachial artery, are most susceptible to ischaemic damage because this artery is an end-artery*. Most commonly affected muscles are the flexor pollicis longus and medial half of flexor digitorum profundus. The muscle ischaemia leads to compartment syndrome, Epidemiology : poor, varies greatly from case to case, Complications : nan, Diagnostics : X RAY AP VIEWS, X RAY, x ray lateral view, Differential diagnosis : nan, disease description : This is an ischaemic injury to the muscles and nerves of the flexor compartment of the forearm. It is caused due to occlusion of the brachial artery by a supracondylar fracture.