Property:Explanation
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Pacinian corpuscles are encapsulated specialized cells located beneath the dermis that respond to the sensation of vibration. Each corpuscle has an onion-shaped appearance with concentric layers that contain fluids. In the center of its concentricity, the corpuscle contains one primary afferent terminal fiber. The fluid inside the concentric layers is displaced upon the application of force on the Pacinian corpuscle and migrates towards the axonal terminal in the center. The Pacinian corpuscle is characterized by rapid adaptation, and despite sustained force, the axonal terminal only receives a transient force.<br/>
'''Educational Objective:''' Pacinian corpuscles are located in the dermal layer of the skin and are responsible for relaying the sensation of vibration from the skin.<br/>
'''References:''' Purves D, Augustine GJ, Fitzpatrick D, et al. Mechanoreceptors specialized to receive tactile information. in Neuroscience. 2nd ed. Sunderland (MA): Sinauer Associates; 2001. +
The experiment conducted by the lab technician assesses both precision and accuracy of his novel technique. Precision is defined as the consistency of a test; it measures its reproducibility and its reliability. It is optimally assessed when sample results from the same test are compared against each others (not against a reference standard). Lack of precision is a result of random error during experimentation. In contrast, accuracy measures the trueness or the validity of a test. It is optimally assessed by comparing sample results to a reference standard, not to other sample results of the same machine. Lack of accuracy is a result of systematic error during experimentation. As a result, all sample data will skew in a similar fashion from the true value due to the presence of an error that affects all the samples equally. In this vignette, the technician's novel method is accurate due to lack of systematic error but not precise due to the presence of a random error. As such, it is valid/true but not reproducible/reliable.<br/>
'''Educational Objective:''' Accuracy is measured by comparison of sample results to a reference standard. It assesses the trueness or validity of a technique or method and may be reduced by a systematic error. In contrast, precision is measured by comparison of sample results to other samples that have been similarly tested. It assesses the reproducibility or reliability of a technique or method and may be reduced by a random error.<br/>
'''References:''' First Aid 2014 page 54 +
Insulin is an anabolic hormone produced in the beta cells of the pancreas. It is involved in numerous processes in the body, such as fatty acid synthesis, protein synthesis, and glucose metabolism. In glucose metabolism, insulin is needed for the transport of glucose into cells in skeletal muscles and adipose tissue. Some organs (brain, RBCs, intestine, cornea, kidney, liver, and beta islet cells of the pancreas) do not require insulin for glucose uptake.
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Glucose transporters are required for uptake of glucose into many organs. There are several subtypes of glucose transporters:<br>
*GLUT-1: RBCs, brain cells, cornea<br>
*GLUT-2 - Has bidirectional activity: Renal tubular cells, small intestinal epithelial cells, liver cells, and pancreatic beta cells<br>
*GLUT-3: Neurons, placenta<br>
*GLUT-4 – Insulin-responsive transport: Skeletal muscle, adipose tissue
*GLUT-5: Intestinal epithelium<br/>
'''Educational Objective:''' In glucose metabolism, insulin is needed for the transport of glucose into cells in skeletal muscles and adipose tissue. Some organs (brain, RBCs, intestine, cornea, kidney, liver, and beta islet cells of the pancreas) do not require insulin for glucose uptake.<br/>
'''References:''' First Aid 2015 page 314 +
Behçet's disease a.k.a. Behçet's syndrome is a chronic multi-systemic vasculitis characterized by mucocutaneous, articular, neurological, gastrointestinal and ocular lesions. It involves a triad of symptoms that include recurring mouth ulcers (aphthous ulcers, canker sores), genital ulcers, and uveitis. Other ocular manifestations include iridocyclitis, retinal and choroidal vasculitis, optic neuritis and retinal vascular occlusion. It is common among Turkey, Asia and Middle-east population, and usually affects people in the 2nd and third decade of life.
The underlying pathology is caused by an overactive immune system without an apparent infection. It is diagnosed according to the International Study Group diagnostic guidelines:
The presence of oral (aphthous) ulcers (any shape, size or number at least 3 times in any 12 months) plus 2 out of the next 4 "hallmark" symptoms:
- Genital ulcers (including anal ulcers and spots in the genital region and swollen testicles or epididymitis in men),
- Skin lesions (papulo-pustules, folliculitis, erythema nodosum, acne in post-adolescents not on corticosteroids),
- Eye inflammation (iritis, uveitis, retinal vasculitis, cells in the vitreous),
- Pathergy reaction (papule >2 mm dia. 24-48 hrs or more after needle-prick)
The current treatment is aimed at reducing the symptoms. Anti-inflammatory agents such as infliximab, etanercept which are anti-TNF agents and other drugs like interferon alfa-2a, azathioprine, colchicine, thalidomide, dapsone and rebamipide are useful alternatives.
Educational Objective: A history of recurrent mouth ulcers (aphthous ulcers, canker sores), genital ulcers, and uveitis is highly suggestive of Behçet's disease which is common among the Turkish, Asian, and middle-east population. It is a multi-systemic inflammatory disorder, and treated with anti-inflammatory agents and immunosuppressants.<br/>
'''Educational Objective:''' <br/>
'''References:''' +
The girl in this vignette has a condition known as Osteogenesis Imperfecta (OI). Osteogenesis imperfect (also known as brittle bone disease or "Lobstein syndrome") is an autosomal dominant bone disorder characterized by bones that are prone to fracture. People with OI are born with defective connective tissue, or without the ability to make it, usually because of a mutation in the genes coding for type-I pro-collagen i.e. COL1A1 and COL1A2. There are seven subtypes varying in severity, age of presentation, and clinical features. Classic signs and symptoms include: fractures after minor trauma, blue tint of the white part of the eye and deafness.
Type I collagen is found in bone, skin (dermis), tendon, dentin, fascia, cornea, late wound repair/mature scar, fibrous cartilage
Type II – Hyaline and elastic cartilage, vitreous body, nucleus pulposus
Type III – Skin, blood vessels, uterus, smooth muscle, liver, kidney, lung, spleen, fetal tissue, granulation tissue/early wound repair
Type IV – Basement membrane<br/>
'''Educational Objective:''' Defective type I collagen found in Osteogenesis Imperfecta is responsible for the brittle bones, lax ligaments and tendons. The characteristic blue-gray sclera is pathognomonic.<br/>
'''References:''' Forlino, Antonella, et al. "New perspectives on osteogenesis imperfecta." Nature Reviews Endocrinology 7.9 (2011): 540-557.<br>
First Aid 2015 page 76 +
Anorexia nervosa is a psychiatric eating disorder characterized by abnormal eating behavior, severe self-induced weight loss, and psychiatric co-morbidities.
Criteria for diagnosis include:
* Refusal to maintain body weight at or above a minimally normal weight for age and height: Weight loss leading to maintenance of body weight <85% of that expected or failure to make expected weight gain during period of growth, leading to body weight less than 85% of that expected
* Intense fear of gaining weight or becoming fat, even though under weight
* Disturbance in the way one's body weight or shape are experienced, undue influence of body weight or shape on self evaluation, or denial of the seriousness of the current low body weight
* Amenorrhea (at least three consecutive cycles) in post-menarchal girls and women. Amenorrhea is defined as periods occurring only following hormone (e.g., estrogen) administration.
People with anorexia have an intense preoccupation with thoughts of being fat, extreme fear of gaining weight, which causes them to try to maintain a very low weight. They will do almost anything to avoid gaining weight, including starving themselves or exercising too much. People with anorexia also have a distorted body image – they think they are fat when they are indeed extremely thin.
There are two types of anorexia nervosa:
* Restricting type: No binge-eating or purging behavior (self-induced vomiting or misuse of laxatives, diuretics, or enemas).
* Binge-eating–purging type: The person regularly engages in binge-eating or purging behavior (self-induced vomiting or the misuse of laxatives, diuretics, or enemas).
Individuals with anorexia nervosa and bulimia nervosa share many similar features. In fact, the binge-eating-purging type of anorexia may be difficult to distinguish from bulimia nervosa. Some patients constantly cycle back and forth between the two disorders. In both disorders, individuals have an obsession with weight loss, an intense fear of weight gain, and over-concern with body weight and image. Both disorders can have self-imposed caloric restriction, food binging and purging. Anorexic individuals restrict their food intake far more than bulimic individuals do; thus anorexics are pathologically thin, whereas many bulimics have a normal weight. Bulimic individuals binge more than anorexic individuals.
Educational Objective: Anorexia nervosa is a psychiatric condition characterized by abnormal eating behavior, conscious restriction of food due to distorted body image of being fat. It it’s different from bulimia by the food restriction and distorted body image. Bulimic patients have uncontrolled eating habits which drives them into purging thereafter. The most common cause of death in anorexia nervosa is ventricular arrhythmias.<br/>
'''Educational Objective:''' <br/>
'''References:'''
Tourette's syndrome is a neuropsychiatric disorder characterized by multiple mannerisms known as tics. A tic is an unusual involuntary movement or sound that tends to be repetitive. Tics can start at any age, but are more common between the ages of 6 and 18 years. These tics characteristically wax and wane, but can worsen as the patient ages. Tics are typically worsened by anxiety, fatigue, excitement, and head injury.
''There are two main types of tics:''
#Motor tics – e.g. blinking, eye-rolling, grinding of teeth, head jerking, neck twisting.
#Vocal tics – Grunts, squeaks, coughing, barking, hiccuping, words or phrases.
The main etiology of tourette's syndrome is unknown but observational data suggest a dysfunction at the level of the basal ganglia. Tourette's syndrome patients are at higher risk of developing other psychiatric disorders including attention deficit hyperactive disorder (ADHD), learning difficulties, obsessive-compulsive disorder (OCD), depression, anxiety disorders, and sleep disorders. Despite this added risk, the majority of patients with Tourette syndrome have normal intelligence and no intellectual disability.<br/>
'''Educational Objective:''' Tourette's syndrome is a neuropsychiatric disorder characterized by tics (motor or vocal) and is associated with an increased risk of with ADHD, OCD, autistic spectrum disorders, and sleep disorders. Although patients have learning difficulties, majority of them have normal intelligence and no intellectual disability.<br/>
'''References:''' Kurlan R. Clinical practice. Tourette's Syndrome. N Engl J Med. 2010;363(24):2332-8. +
The use of creatinine clearance for the estimation of the glomerular filtration rate (eGFR) generally overestimates the true GFR due to the combined filtration and secretion of creatinine along the renal tubules. As such, inulin remains the gold standard for the estimation of the GFR because it is only filtered and not secreted. Cimetidine, an H2 receptor blocker, blocks tubular creatinine secretion. Because cimetidine blocks the tubular secretion of creatinine, the creatinine clearance is decreased. The use of cimetidine allows only the filtration of creatinine to occur by preventing its secretion. Thus, the estimation of GFR based on creatinine clearance is expected to become more accurate with the use of cimetidine and approximate inulin clearance or the true GFR. Inulin clearance is not affected by cimetidine.<br/>
'''Educational Objective:''' Cimetidine blocks the tubular secretion of creatinine, thus decreasing creatinine clearance. As such, creatinine will only be filtered and approximation of eGFR based on creatinine values becomes more accurate and closer to the true GFR.<br/>
'''References:''' Van Acker BA, Koomen GC, Koopman MG, et al. Creatinine clearance during cimetidine administration for measurement of glomerular filtration rate. Lancet. 1992;340(8831):1326-9. +
White coat hypertension is defined as high blood pressure in the clinic only, while being normal in the out-clinic setting. It is generally considered a benign condition. Nonetheless, accurate diagnosis of white coat hypertension is necessary before reassuring the patient. In this example, the patient reassures the physician that his blood pressure is measured using a calibrated sphygmomanometer by a nurse practitioner. As such, systemic errors due to inaccurate readings at home and the error in measurement technique can both be ruled out. 24-hour monitoring of the patient's blood pressure using a Holter monitor may be appropriate to rule out true hypertension before the diagnosis of white coat hypertension is made.
Educational Objective:
White coat hypertension is defined as high blood pressure in the clinic only, whereas it normalizes in the out-clinic setting.<br/>
'''Educational Objective:''' <br/>
'''References:''' +
Carcinoid tumors are neuroendocrine serotonin-secreting tumors arising from the Kulchitsky cells in the crypts of Liberkuhn. They are commonly present in the GI tract and grow as nodules in the submucosa, especially in the appendix, ileum, and rectum. Patients typically have high levels of urinary 5-hydroxyindoleacetic acid (5-HIAA), a by-product of serotonin. Carcinoid tumors may present at virtually any age; the median age of diagnosis is in the range of 55-65 years of age.
Carcinoid tumors may remain asymptomatic in the majority of cases. Symptoms usually arise in the case of metastasis beyond the GI tract, when the liver is unable to metabolize the secreted serotonin. Excess serotonin is responsible for the non-specific symptoms that often occur late in the disease, including diarrhea in more than 80% of the cases. Other common symptoms are cutaneous flushing, erythema, cyanosis, dyspnea due to bronchospasm, abdominal pain, and right-sided cardiac valvulopathy and heart failure. When symptoms become present, carcinoid tumors are then called "carcinoid syndrome".
Diagnosis is often difficult, since the tumor may not be easily visualized on routine imaging techniques, which are best at identifying metastasized tumors. Small bowel series may be helpful in diagnosing early carcinoid tumors. Pathological findings, including electron microscopy, are needed to visualize characteristic findings of carcinoid tumors, which are cells that contain secretory granules containing serotonin. Treatment is generally by resection of tumor and pharmacologic therapy, including somatostatin. Prognosis depends on the location, pathological findings of the tumor, and metastasis. Small localized tumors have excellent prognosis with 90% 5-year survival rate. Diagnosis and treatment must take into consideration the probability of metastasis.<br/>
'''Educational Objective:''' Carcinoid syndrome is characterized by diarrhea, cutaneous flushing, right-sided cardiac valvulopathy, and pulmonary wheezing. Patients have elevated levels of urinary 5-HIAA. On electron microscopy, carcnoid tumors have cells that contain membrane-bound granules that secrete serotonin.<br/>
'''References:''' Ha J, Tan WA. Gastrointestinal carcinoid tumors: a review. J Gastroint Dig Syst. 2012; 2(2):107-14<br>
Kulke MH, Mayer RJ. Carcinoid tumors. N Engl J Med. 1999; 340(11):858-68
The patient is diagnosed with Reye's syndrome, a form of acute hepatic encephelopathy in children characterized by altered mental status associated with hyperammonenia, hypoglycemia, and lactic acidemia. Diffuse edema on neurological imaging is also characteristic of Reye's syndrome. In children, Reye's syndrome is associated with administration of aspirin for viral infections (e.g. VZV). Reye's syndrome is thought to be caused by the presence of non-uniform loss of enzymatic activity in the mitochondria within cells in the liver and the brain, such as the loss of activity of pyruvate carboxylase. Exposure to chemical products that alter the intra-mitochondrial matrix, as well as low ATP:ADP ratio, leads to the inhibition of the proper protein synthesis required by the mitochondria and development of Reye's syndrome.<br/>
'''Educational Objective:''' Reye's syndrome is an acute hepatic encephalopathy typically seen in children following ingestion of aspirin. It is characterized by altered level of consciousness and altered metabolic blood panel. Reye's syndrome is due to a mitochondrial dysfunction with characteristic pleomorphic mitochondria in the liver and the brain that have reduced enzymatic activity.<br/>
'''References:''' Van Coster RN, De Vivo DC, Blake D, et al. Adult Reye's syndrome: a review with new evidence for a generalized defect in intramitochondrial enzyme processing. Neurology. 1991; 41(11):1815-21.<br>
Davies NW, Sharief MK, Howard RS. Infection-associated encephalopathies - their investigation, diagnosis, and treatment. J Neurol. 2006; 253:833-45.<br>
Glasgow JF. Reye's syndrome: the case for a causal link with aspirin. Drug Saf. 2006; 29(12):1111-21. +
The mechanism of action of nystatin closely resembles that of amphotericin B. It binds to ergosterol molecules, which are major components of the fungal cell membrane. This leads to pore formation in the cell membrane causing potassium leakage and eventual fungal cell death. In the curve depicting the growth of strain B of Candida tropicalis, the continued growth despite the addition of Nystatin can be explained by a structural mutation in the ergosterol molecule leading to resistance to the effects of Nystatin. The curve of strain A shows a decrease in growth compatible with sensitivity to Nystatin.<br/>
'''Educational Objective:''' Nystatin shares the same mechanism of action of amphotericin B. It binds to ergosterol molecules in the fungal cell membrane leading to pore formation and cell death.<br/>
'''References:''' Borgers M. Mechanism of Action of Antifungal Drugs, with Special Reference to the Imidazole Derivatives. Clinical Infectious Diseases. 1980;2(4):520-534. +
In this vignette, the patient is put on Amikacin, an aminoglycoside antibiotic. A reported class effect of cephalosporins is the synergistic effect on nephrotoxicity when combined with aminoglycosides. Initially, the strongest evidence came from the combination of cephalothin and gentamicin or tobramycin. The increased risk of renal dysfunction with this combination is seen mostly in critically ill patients and those with pre-existing renal disease. Large doses of cephalosporins have also been associated with increased risk for nephrotoxicity.
Despite initial reports of aminoglycoside toxicity being potentiated by cephalosporins, animal studies have shown the opposite. The exact mechanism of synergistic kidney toxicity is not known. Still, it is best to avoid using this combination of antibiotics unless clinically indicted with no other alternatives.<br/>
'''Educational Objective:''' The combination of cephalosporins and aminoglycosides should be avoided due to the synergistic effect on nephrotoxicity.<br/>
'''References:''' Rankin GO, Sutherland CH. Nephrotoxicity of aminoglycosides and cephalosporins in combination. Adverse Drug React Acute Poisoning Rev. 1989;8(2):73-88.<br>
First Aid 2015 page 182 (Cephalosporins) <br>
First Aid 2015 page 184 (Aminoglycosides) +
The retinoblastoma ''RB'' gene product, Rb, is a protein responsible in part for maintaining cells in G1 and inhibiting G1-to-S progression. For the retinoblastoma protein to be active, however, it needs to be in the hypophosphorylated form. Hyperphosphorylation of the retinoblastoma protein by cyclin-dependent kinases (CDKs) renders it inactive, favoring to G1-to-S progression. An inactive Rb protein can also lead to the development of uncontrolled cellular proliferation. Many factors can result in retinoblastoma hyperphosphorylation, the most common of which is UV radiation. This is in part the mechanism for squamous cell carcinoma, which is characterized by marked atypia at all levels of the epidermis with formation of keratin pearls, and prominent intercellular bridges.<br/>
'''Educational Objective:''' The Rb protein is a modulator of the cell cycle required to inhibit G1-to-S progression. Hyperphosphorylation of the Rb protein renders it inactive.<br/>
'''References:''' Buchkovich K, Duffy LA, Harlow E. The retinoblastoma protein is phosphorylated during specific phases of the cell cycle. Cell. 1989;58(6):1097-105. +
Wiskott-Aldrich Syndrome (WAS) is a rare X-linked disorder characterized by thrombocytopenia, recurrent infections, eczema, and increased risk of hematopoietic malignancies. WAS is a primary immunodeficiency syndrome with multiple affected cell lines including lymphocytes, neutrophils, and monocytes. The defect is due to a mutation in the WAS gene on the X chromosome and a defective WAS protein that combines with signaling molecules and alters the actin cytoskeleton. The WAS protein may act as support for signaling molecules in a complex cascade to regulate the cytoskeleton, or alternatively may depolymerize actin directly. Patients with WAS usually seek medical care for signs of thrombocytopenia including GI bleeding or unusual bruising. Eczema is usually an accompanying sign. Lab studies classically reveal decreased IgM levels and elevated IgE.<br/>
'''Educational Objective:''' Wiskott-Aldrich Syndrome (WAS) is characterized by thrombocytopenia, recurrent infections, and eczema due to a defect in the WAS gene an important player in the cascade that regulates the cytoskeleton.<br/>
'''References:''' Snapper SB, Rosen FS. The Wiskott-Aldrich syndrome protein (WASP): roles in signaling and cytoskeletal organization. Annu Rev Immunol. 1999;17:905-29. +
Scurvy is a relatively rare disease occuring in patients with severe vitamin C deficiency. As vitamin C is essential for the hydroxylation of proline and lysine residues during collagen synthesis, its deficiency leads signs of collagen abnormality. Patients initially complain of nonspecific malaise and fatigue that progresses to bony pain and dyspnea. Physical exam reveals multiple bruises compatible with a decrease in collagen synthesis in the skin. Other signs include swollen gums, poor wound healing, and anemia. Scurvy is usually seen only in patients with very poor nutrition since vitamin C is redundantly present in most diets. Patients at risk for scurvy include those who are elderly or alcoholic, those with chronic malnutrition, and men living alone, termed "widower scurvy". Treatment is usually restricted to vitamin C supplementation and supportive care.<br/>
'''Educational Objective:''' Vitamin C is important in the hydroxylation of proline and lysine residues during collagen synthesis. Vitamin C deficiency lead to scurvy characterized by ecchymoses, swollen gums, and poor wound healing.<br/>
'''References:''' Kumar V, Abbas AK, Fausto N, Aster JC. Environmental and nutritional diseases. In: Kumar V, Abbas AK, Fausto N, Aster JC, eds. Robbins and Cotran Pathologic Basis of Disease. 8th ed. Philadelphia, PA: Elsevier Saunders; 2009:chap 9. +
Ehlers-Danlos Syndrome is a rare, inherited disorder that is heterogeneous in presentation and pathologic mechanisms. Six subtypes of Ehlers-Danlos exist each having distinct mutations affecting collagen synthesis. The classical types of Ehlers-Danlos involve mostly collagen type 1 and collagen type 4. One of the most studied pathological mechanisms of Ehlers-Danlos is a mutation affecting lysyl-oxidase, an enzyme responsible for collagen crosslinking in the extracellular matrix. Ehlers-Danlos classically presents with skin hyperextensibility, cutaneous fragility, joint hypermobility, and vascular anomalies. Physical exam also showns poor wound healing with "fish mouth" re-opened scars, or classic "cigarette paper" like scars which are poorly healed thin and fragile skin. The most dangerous subtype involves type 4 collagen and leads to increased risk of visceral perforation and arterial rupture. Mutations often involve the COL-A genes.<br/>
'''Educational Objective:''' Ehlers-Danlos is a rare inherited disorder with certain forms characterized by defective corss-linking of collagen fibers.<br/>
'''References:''' Mao JR, Bristow J. The Ehlers-Danlos syndrome: on beyond collagens. J Clin Invest. 2001;107(9):1063-9.<br>
Wenstrup RJ, Florer JB, Willing MC, et al. COL5A1 haploinsufficiency is a common molecular mechanism underlying the classical form of EDS. Am J Hum Genet. 2000;66(6):1766-76. +
Ehlers-Danlos Syndrome is a rare inherited disease that is heterogeneous in presentation and pathologic mechanisms. Six subtypes of Ehlers-Danlos exist with each having distinct mutations affecting collagen synthesis. One of the most studied pathological mechanisms of Ehlers-Danlos is a mutation affecting lysyl-oxidase, an enzyme responsible for collagen crosslinking in the extracellular matrix. Lysyl-oxidase requires copper as a cofactor to function effectively. Ehlers-Danlos classically presents with skin hyperextensibility, cutaneous fragility, joint hypermobility, and vascular anomalies.<br/>
'''Educational Objective:''' Ehlers-Danlos is a rare inherited disorder with certain forms characterized by defective corss-linking of collagen fibers due to abnormal lysyl-oxidase. Lysyl oxidase requires copper as a cofactor.<br/>
'''References:''' Wenstrup RJ, Florer JB, Willing MC, et al. COL5A1 haploinsufficiency is a common molecular mechanism underlying the classical form of EDS. Am J Hum Genet. 2000;66(6):1766-76.<br>
Mao JR, Bristow J. The Ehlers-Danlos syndrome: on beyond collagens. J Clin Invest. 2001;107(9):1063-9. +
The murmur described here is the classic murmur of mitral stenosis, a diastolic murmur after an opening snap. An immigrant patient with a fever treated with penicillin should raise suspicion for rheumatic fever. During pregnancy, plasma volume increases, thereby increasing blood flow through the narrowed mitral valve and causing pregnancy related cardiomyopathy. Other special features of mitral stenosis are due to pressure of enlarged left atrium on adjacent tracts. For example,dysphagia may occur due to pressure on esophagus, hoarseness of voice occurs due to pressure on recurrent laryngeal nerve and cough occurs due to pressure on the bronchus. Transthoracic echocardiogram is the best initial diagnostic test for all valvular diseases.Diuretics are the best initial therapy for mitral stenosis.
'''Educational Objective:''' An immigrant pregnant patient with a diastolic murmur after an opening snap is the classic presentation of mitral stenosis due to rheumatic fever
'''References:''' Page 29,30,86,87 Master the boards Step 2 CK second edition, Page 65,119 Master the boards step 3 2009 edition, http://www.wikidoc.org/index.php/Mitral_stenosis_history_and_symptoms C. Michael Gibson, M.S., M.D<br/>
'''Educational Objective:''' <br/>
'''References:''' +
An abnormal backward flow of blood through the mitral valve causes mitral regurgitation. Hypertension, myocardial infarction, papillary muscle rupture or any other condition leading to dilation of the heart causes mitral regurgitation. Mitral regurgitation is characterized by a pansystolic murmur at the cardiac apex that radiates to axilla and increases in intensity on leg raising, squatting and handgrip. Dyspnea on exertion is the most common presentation. Transthoracic echocardiogram is the best initial diagnostic test for all valvular diseases. Angiotensisn converting enzyme inhibitors, angiotenisn receptor blockers and nifedipine are the best initial therapy but surgery is indicated when ejection fraction drops below 60% and left ventricular end systolic diameter is more than 40mm.
'''Educational Objective''' In mitral regurgitation angiotensisn converting enzyme inhibitors, angiotenisn receptor blockers and nifedipine are the best initial therapy but surgery is indicated when ejection fraction drops below 60% and left ventricular end systolic diameter is more than 40mm.
'''References''' Page 65,66 Master the boards step 3 2009 edition, page 89,90 Master the boards step 2 CK second edition.<br/>
'''Educational Objective:''' <br/>
'''References:''' +