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WBR0000 + ( '''Educational Objective:''' '''References:''')
WBR0000000 + ( '''Educational Objective:''' '''References:''')
WBR1008 + ( '''Educational Objective:''' '''References:''')
WBR1151 + ( '''Educational Objective:''' '''References:''')
WBR1506 + ( '''Educational Objective:''' '''References:''')
WBR9876 + ( '''Educational Objective:''' '''References:''')

WBR0773 + (<img src="http://static.wikidoc.org/7/7 … <img src="http://static.wikidoc.org/7/73/Wjg_cachexia_illustration_12_30_14a.svg" width="700">This patient presents displays signs and symptoms consistent with cachexia, a syndrome that is characterized by the presence of anorexia, fat loss, skeletal muscle wasting, severe asthenia, and fatigue. An unintentional loss of greater than 10% loss of body weight over a 12 month period that is associated with an underlying disease constitutes the technical definition of cachexia. Affected patients have dyspnea and severe weakness on minimal exertion or even at rest. Cachexia typically arises in the setting of cancer and other chronic inflammatory conditions such as AIDs, tuberculosis and COPD. The weight loss in cachectic patients is caused by both a decrease in appetite and a hypermetabolic state caused by higher resting energy expenditure. The precise reasons that cancers evolve to consistently induce cachexia are unknown. One hypothesis is that cancers induce cachexia to generate more bioavailable nutrients (glucose and amino acids) to sustain rapid tumor growth. Another hypothesis is that cancers maintain a complex relationship with stromal and immune cells in which inflammatory cytokines play an essential role. In this model, a systemic side-effect of high levels of these cytokines in the bloodstream is cachexia.There is no scientific consensus on the specific cytokines responsible for inducing cachexia, but one of the prevailing candidates is TNF-alpha. TNF-alpha is sufficient to inhibit myocyte differentiation and induce myocyte atrophy in-vitro. Other mediators such as IL-6 and IFN-gamma may collaborate with TNF-alpha to promote cachexia. The only anti-cachexia drugs to date that have demonstrated benefit in phase III clinical trials are ghrelin analogues.Note: While TNF-alpha is firmly entrenched in the USMLE canon as the mediator of cachexia, evidence in favor of TNF-alpha has weakened over time. There is no strong evidence that levels of TNF-alpha are increased in the circulation of cancer patients with weight loss. Trials of anti-TNF-alpha antibodies (infliximab) in cancer patients have also failed to show any clinical benefit. On the other hand, evidence in favor of IL-6 as a cachexia mediator is mounting. Circulating levels of IL-6 correlate with weight loss and reduced survival in cancer patients. Still, for the purposes of USMLE Step 1, remember that cachexia is caused by TNF-alpha. '''Educational Objective:''' TNF-alpha (cachectin) is the main mediator of cachexia. '''References:''' Gordon JN, Green SR, Goggin PM. Cancer cachexia. Q J Med. 2005; 98:779-788. Fearon, Kenneth CH, David J. Glass, and Denis C. Guttridge. Cancer cachexia: mediators, signaling, and metabolic pathways. Cell metabolism 16.2 (2012): 153-166. Oliff, Allen, et al. Tumors secreting human TNF/cachectin induce cachexia in mice. Cell 50.4 (1987): 555-563. First Aid 2014 page 231xia in mice. Cell 50.4 (1987): 555-563. First Aid 2014 page 231)
WBR0835 + (A 38-year-old female with a facial rash, j … A 38-year-old female with a facial rash, joint pain and chest pain that changes with position suggests connective tissue disease induced pericarditis. The most common connective tissue disease causing pericarditis is Systemic lupus erythematosus (SLE). Electrocardiogram findings of diffuse ST segment elevation also points towards pericarditis. The most specific test to diagnose Systemic lupus erythematosus is Anti ds-DNA antibodies. '''Educational Objective:''' Anti ds-DNA is the most specific test for Systemic lupus erythematosus. Systemic lupus erythematosus is the most common connective tissue disease cause of Pericarditis.'''References:''' Page 183 Master the boards Step 2 CK second edition '''Educational Objective:''' '''References:'''ducational Objective:''' '''References:''')
WBR0836 + (A 50–year-old male with a history of diabe … A 50–year-old male with a history of diabetes, hypertension and smoking who suffers from leg pain on walking (Claudication) suggests peripheral arterial disease (PAD).Peripheral arterial disease occurs due to blockage of blood supply to any peripheral body parts but mostly involves lower limbs. Smoking is one of the major risk factors for peripheral arterial disease. Physical examination of the involved limb may show loss of hair, loss of sweat. The best initial test for diagnosing peripheral arterial disease is ankle brachial index, the ratio of blood pressure measured in the ankles and brachial arteries. Ankle brachial index value <0.9 indicates peripheral arterial disease. Treatment of PAD should include aspirin, cilostazol and smoking cessation.'''Educational Objective:''' Ankle brachial index is the best initial test in diagnosing peripheral arterial disease '''References:''' Page 102 Master the boards Step 2 CK 2nd edition, Page 71 Master the boards step 3, 2009 edition. '''Educational Objective:''' '''References:'''''Educational Objective:''' '''References:''')
WBR1095 + (A history of fever and seizures in a 11 mo … A history of fever and seizures in a 11 month old child is highly suggestive of an infection . Since the patient is from Haiti where malaria and other parasitic infection are endemic an empirical therapy of anti malarial should be started right away . Since the thick and thin smears are negative malaria is ruled out and other infectons should be thought about. The next step in the management is do a lumbar puncture and rule out other infection like meningitis from encephalitis.'''Educational objective''':Rule out encephalitis and meningitis before starting empirical therapy in a case of unknown sezirues with fever. Lumbar puncture is always the next best step in the management. '''Educational Objective:''' '''References:'''ducational Objective:''' '''References:''')
WBR0760 + (A minor is any individual of less than 18 … A minor is any individual of less than 18 years of age. Generally, a minor's parents have the right to refuse medical care for their child. But in the case of an emergency involving a minor, patient care must not be compromised despite family refusal. In emergency life-or-death situations, the physician must perform whatever it takes to save the minor's life regardless of the parent's decisions. The physician must not waste time calling for help or inquiring about legal issues in such emergency situations. On the contrary, physicians are protected by law to provide urgent care for minors. '''Educational Objective:''' In life-or-death situations, a minor's emergency care must not be withheld under any circumstance. '''References:'''d under any circumstance. '''References:''')
WBR0411 + (A minor is any individual under the age of … A minor is any individual under the age of 18 years. Generally, parental consent is required to treat minors. Parents may refuse the treatment of their minor children only when their refusal does not result in serious threat to the patient. If withholding treatment is dangerous to the patient and may result in adverse safety outcomes (e.g. life-threatening disease), the physician may initiate therapy on the basis of legal precedent. The physician may also treat minors without parental consent in the following cases: *Life-threatening conditions and parents cannot be contacted: Consent for treatment is implied*Emancipated minors (marriage or army)*Any of the following diagnoses: pregnancy, sexually transmitted infections, drugs abuse, or alcohol abuse '''Educational Objective:''' A minor is any individual under the age of 18 years. Although parental consent is generally required to treat minors, minors presenting with STI and who do not wish to inform their parents may be treated without parental consent. '''References:''' First Aid 2014 page 59ental consent. '''References:''' First Aid 2014 page 59)
WBR1128 + (A physician is bound ethically and legally … A physician is bound ethically and legally to maintain patient information confidentiality. He is not supposed to discuss this information with anyone, unless specifically requested by the patient. General principles for exceptions to Confidentiality are: * Potential physical harm to others is serious and imminent * Likelihood of harm to self is great * No alternative means exists to warn or to protect those at risk * Physicians can take steps to prevent harm In the scenarios mentioned above, the patient diagnosed with HIV needs to inform his girlfriend about his condition. If not it is physicians duty to inform her to prevent harm. '''Educational Objective:''' A physician is bound ethically and legally to maintain patient information confidentiality. There are a few important cases in which the physician may share patient information. '''References:''' First Aid 2014 Page 59,60ay share patient information. '''References:''' First Aid 2014 Page 59,60)
WBR259 + (A spinal epidural abscess threatens the sp … A spinal epidural abscess threatens the spinal cord or cauda equina by compression and also by vascular compromise (see images below). If untreated, an expanding suppurative infection in the spinal epidural space impinges on the spinal cord, producing sensory symptoms and signs, motor dysfunction, and, ultimately, paralysis and death. This patient is having cauda equina signs and immediate surgical consultation and operative decompression is the first step in management. All other answers are appropriate in the meantime, but after steps towards surgical release are taken. '''Educational Objective:''' '''References:'''ducational Objective:''' '''References:''')
WBR0540 + (A subdural hematoma is characterized by th … A subdural hematoma is characterized by the rupture of a bridging vein. Because the venous pressure system is a low-presure system as compared to the arterial system, the build-up of blood following subdural hematoma is slow and gradual increase in hematoma size develops over a prolonged period of time. On CT scan, subdural hematoma appears as a crescent-shaped hemorrhage that does not cross the falx cerebra but may cross the suture lines. '''Educational Objective:''' Upon CT scan, subdural hematoma, resulting from a rupture of bridging veins, appears as a crescent-shaped hemorrhage that crosses the suture lines but is unable to cross the falx cerebri. '''References:''' First Aid 2014 page 462. '''References:''' First Aid 2014 page 462)
WBR0706 + (According to the current CDC recommendatio … According to the current CDC recommendation, CSF should be examined before the start of treatment in case of patients diagnosed with syphilis of unknown duration, or late latent syphilis. Patients with CD4 < 350 mm3, and RPR titer greater than 1:32 considered high risk patients for neurosyphilis. Neurosyphilis can present early with CSF changes without neurological manifestations. '''Educational Objective:''' '''References:'''''Educational Objective:''' '''References:''')
WBR0323 + (Acetylation of core histones, such as H2A, … Acetylation of core histones, such as H2A, H2B, H3, and H4, plays a major role in the regulation of transcription in eukaryotic cells. The acetylation of lysine residues at the tails of histones neutralizes its positively charge and decreases its affinity for DNA. Consequently, the alteration of nucleosomal conformation facilitates the transcription at the level of chromatin templates. '''Educational Objective:''' Histone acetylation is crucial in the regulation of eukaryotic transcriptional activity. '''References:''' Struhl K. Histone acetylation and transcriptional regulatory mechanisms. Genes Dev. 1998;12:599-606.nal regulatory mechanisms. Genes Dev. 1998;12:599-606.)
WBR0265 + (Acute exposures to sound pressure levels a … Acute exposures to sound pressure levels above 180 dB result in traumatic rupture of the tympanic membrane and conductive hearing loss. The rupture should repair spontaneously unless infection occurs. If the loss persists for more than 3 months, surgical repair is possible.'''Educational Objective:'''Acute exposures to sound pressure levels above 180 dB result in traumatic rupture of the tympanic membrane and a temporary conductive hearing loss, which reverses either spontaneously or by surgical repair. '''Educational Objective:''' '''References:'''ducational Objective:''' '''References:''')
WBR0185 + (Acute lymphoblastic leukemia (ALL) is the … Acute lymphoblastic leukemia (ALL) is the most common childhood malignancy, accounting for approximately 30% of all cancers in patients younger than 14 years of age. It is a clonal lymphoid stem cell disease. The classical presentation of patients with ALL includes fatigue, recurrent infections, bony pain, weight loss, easy bruisability, petechiae, dyspnea on exertion, and hepatosplenomegaly. t(12;21) translocation is the most common chromosomal anomaly in childhood leukemias and is exclusively found in patients with Pre-B-ALL (approximately 25% of these patients). The translocation generates TEL-AML1 (ETV6-RUNX1) fusion gene, which is associated with a more favorable prognosis as evidenced by a significantly lower relapse rate. Evaluation of this and other prognostic markers helps in selecting low toxicity versus high toxicity therapies. '''Educational Objective:''' The t(12;21) translocation is a good prognostic marker in cases of acute lymphoblastic leukemia. '''References:''' Romana SP, Mauchauffé M, Le coniat M, et al. The t(12;21) of acute lymphoblastic leukemia results in a tel-AML1 gene fusion. Blood. 1995;85(12):3662-70. Borkhardt A, Cazzaniga G, Viehmann S, et al. Incidence and clinical relevance of TEL/AML1 fusion genes in children with acute lymphoblastic leukemia enrolled in the German and Italian multicenter therapy trials. Associazione Italiana Ematologia Oncologia Pediatrica and the Berlin-Frankfurt-Münster Study Group. Blood. 1997;90(2):571-7.rlin-Frankfurt-Münster Study Group. Blood. 1997;90(2):571-7.)
WBR0930 + (Acute promyelocytic leukemia (APML) is a r … Acute promyelocytic leukemia (APML) is a rare subset of acute myeloid leukemia (AML). APML is characterized by a chromosomal translocation involving the retinoic acid receptor-alpha gene on chromosome 17 (RARA). APML cells undergo a differentiation arrest, which can be reversed with all-trans retinoic acid. Arsenic is thought to act by inhibiting the enzyme thioredoxin reductase, an enzyme that is essential for cell growth and survival and that is upregulated in APML cells. Histologically, APML is notable for leukemic cells containing rod-like cytoplasmic inclusions called “Auer rods”. Treatment of APML can precipitate release of these inclusions causing disseminated intravascular coagulopathy (DIC). Prolonged therapy with arsenic trioxide, a known carcinogenic agent, increases the risk of certain cancer particularly squamous cell carcinoma of the skin as well as angiosarcoma of the liver. '''Educational Objective:''' Angiosarcoma is a potential late complication of exposure to arsenic. '''References:''' Watts JM, Tallman MS. Acute promyelocytic leukemia: what is the new standard of care?. Blood Rev. 2014;28(5):205-12. Pershagen G. The carcinogenicity of arsenic. Environ Health Perspect. 1981;40:93-100.enicity of arsenic. Environ Health Perspect. 1981;40:93-100.)
WBR0380 + (Acute tubulointerstitial nephritis (ATIN) … Acute tubulointerstitial nephritis (ATIN) is a common cause of acute kidney injury. The most common etiologies of ATIN include drugs such as antimicrobials, NSAIDs, and analgesics, immunologic diseases, and infections. Clinical presentation of ATIN is very variable ranging from asymptomatic renal functional decline to a syndrome that includes rash, fever, and livido reticularis. Work-up often reveals pyuria and eosinophiluria with eosinophil casts. However, non-invasive techniques have clear limitations in the diagnosis of ATIN and renal biopsy is often essential. The hallmark of ATIN on biopsy is the presence of inflammatory infiltrates within the interstitium. The mainstay of treatment of drug-induced ATIN is discontinuation of the offending medication and administration of a short course of corticosteroids in order to limit the progression to ESRD in some patients. Recovery ranges widely. Approximately 50% of patients fail to fully recover normal renal function. Several prognostic factors have been studied to determine the eventual outcome of renal function in patients with ATIN. Histologic findings such as diffuse interstitial infiltration and extensive interstitial fibrosis have been linked to poorer renal outcomes. The most important prognostic factors are the duration of acute renal failure and renal function 2-3 weeks after the diagnosis. The severity of renal failure at diagnosis is of no prognostic significance. '''Educational Objective:''' Drug-induced acute tubulointerstitial nephritis is the most common cause of acute tubulointerstitial nephritis. Antimicrobials and NSAIDs are commonly attributed to drug-induced AIN. Transformation of interstitial cellular infiltrates into fibrosis is the most important prognostic factor in determining the outcome of AIN. '''References:''' Rossert J. Drug-induced acute interstitial nephritis. Kidney Int. 2001;60(2):804-17. Praga M, Gonzalez E. Acute Interstitial Nephritis. Kidney International. 2010; 77:956-961rstitial Nephritis. Kidney International. 2010; 77:956-961)
WBR0321 + (Adenosine deaminase deficiency, the likely … Adenosine deaminase deficiency, the likely culprit in this patient, is an important cause of severe combined immunodeficiency (SCID). SCID is a syndrome encompassing a group of rare congenital disorders characterized by B cell and T cell deficiency. All forms of SCID are inherited, most common of which is X-linked. X-linked SCID is caused by a deficiency of IL-2 receptor gamma leading to a failure in the development and differentiation of T and B cells. Adenosine deaminase deficiency is the second most common cause of SCID. Adenosine deaminase is coded for by a gene on chromosome 20 and is essential for the breakdown of purines. Loss of this enzyme leads to the accumulation of dATP causing feedback inhibit the activity of ribonucleotide reductase. As ribonucleotide reductase is essential for dNTP synthesis, DNA replication would cease and lymphocyte proliferation is subsequently inhibited. Accordingly, patients with SCID present early in childhood with failure to thrive and recurrent infections by viruses, bacteria and fungi. Work-up may reveal thymic aplasia and loss of germinal centers on lymph node biopsy. Currently, the only curative treatment for SCID is bone marrow transplantation despite several controversial attempts at introducing gene therapy as an alternative (mainly due to the high incidence of leukemias). '''Educational Objective:''' Adenosine deaminase deficiency is a common cause of severe combined immunodeficiency (SCID). '''References:''' Weinberg K, Parkman R. Severe combined immunodeficiency due to a specific defect in the production of interleukin-2. N Engl J Med. 1990;322(24):1718-23. Parkman R, Gelfand EW, Rosen FS, Sanderson A, Hirschhorn R. Severe combined immunodeficiency and adenosine deaminase deficiency. N Engl J Med. 1975;292(14):714-9. First Aid 2014 page 68. Engl J Med. 1975;292(14):714-9. First Aid 2014 page 68.)
WBR1010 + (Amiodarone augment the anticoagulant effec … Amiodarone augment the anticoagulant effect caused by warfarin, and results in an increase in international normalized ratio (INR) and increased risk of bleeding. The enhanced anticoagulant effect that happens when amiodarone and warfarin are prescribed is due to amiodarone induced cytochrome P450 inhibition.Coagulopathy might manifest as epistaxis, gingival bleeding, hematemesis, hematuria, hematochezia, menometrorrhagia, ecchymosis, petechial hemorrhages, intracranial hemorrhages, or bleeding that is disproportionate to the level of the injuryThe effects of interaction with amiodarone do not peak until seven weeks after the initiation of concomitant therapy. A mean reduction of 35% in the dose of warfarin, and frequent follow up of INR and prothrombin time is needed when amiodarone used with warfarin.'''Reference''': "The incidence, magnitude, and time course of the amiodarone-warfarin interaction.",journal = Arch Intern Med, volume = 148, issue = 8, month = Aug, year = 1988, PMID = 3401099. '''Educational Objective:''' '''References:'''ducational Objective:''' '''References:''')
WBR0501 + (Amiodarone is a class III antiarrhythmic d … Amiodarone is a class III antiarrhythmic drug that has effects of class Ia, II, III, and IV antiarrhythmics. Electrophysiological effects of amiodarone include prolongation of phase 3 of the action potential (repolarization) leading to an increase in AP duration, and increase of the refractory period causing a decrease in the heart rate. Amiodarone also increases the QT interval, however, it is not associated with an increase risk of torsade de pointes. Amiodarone has a chemical structure that closely resembles thyroxine, which replaces thyroxine at its receptor. The molecule also inhibits the action of type 1 5'-deiodinase that is responsible for the peripheral conversion of T4 to T3. Several other pathological effects on the thyroid gland and its hormones have been described including cytotoxic effects, and inhibition of feedback regulation. Clinically, these effects may manifest as either hypo- or hyperthyroidism, which is the main reason for the close follow-up of thyroid function among patients receiving amiodarone. Amiodarone also has several other side-effects including interstitial fibrosis, corneal deposits, peripheral neuropathy, and skin discoloration. The bluish skin discoloration (ceruloderma) associated with skin deposits of amiodarone is also known as "blue-man syndrome". It most commonly involves the face and is also associated with severe corneal deposits. It resolves within weeks to months of amiodarone discontinuation. '''Educational Objective:''' Amiodarone is a class III antiarrhythmic associated with hypo or hyperthyroidism and bluish-grey discoloration with prolonged use. '''References:''' Zimetbaum P. Amiodarone for atrial fibrillation. N Engl J Med. 2007;356(9):935-41. Enseleit F, Wyss CA, Duru F, Noll G, Ruschitzka F. Images in cardiovascular medicine. The blue man: amiodarone-induced skin discoloration. Circulation. 2006;113(5):e63. First Aid 2013 page 303n. Circulation. 2006;113(5):e63. First Aid 2013 page 303)
WBR1011 + (Amiodarone is the ant arrhythmic agent of … Amiodarone is the ant arrhythmic agent of choice that is used to treat ventricular arrhythmias and atrial fibrillation. Amiodarone augment the anticoagulant effect caused by warfarin, and results in an increase in international normalized ratio (INR) and increased risk of bleeding. The effects of interaction with amiodarone do not peak until seven weeks after the initiation of concomitant therapy. A mean reduction of 35% in the dose of warfarin, and frequent follow up of INR and prothrombin time is needed when amiodarone used with warfarin. '''Reference''':"The incidence, magnitude, and time course of the amiodarone-warfarin interaction.", journal = Arch Intern Med, volume = 148, issue = 8, month = Aug, year = 1988, PMID = 3401099. '''Educational Objective:''' '''References:'''ducational Objective:''' '''References:''')
WBR1026 + (Amiodarone-induced hypothyroidism (AIH) is … Amiodarone-induced hypothyroidism (AIH) is believed to result from the inability of the thyroid to escape from the Wolff-Chaikoff effect. Amiodarone is a benzofuranic-derivative iodine-rich drug, the large amount of iodide released during the metabolism of amiodarone leads to an adaptive blockage of further thyroidal iodide uptake and thyroid hormone biosynthesis, the so-called Wolff-Chaikoff effect.The reported incidence of AIH varies widely, ranging from 6% in countries with low iodine intake to 13% in countries with a high dietary iodine intake. The risk of developing hypothyroidism is independent of the daily or cumulative dose of amiodarone. However, the risk is greater in the elderly and in female patients, probably as a result of a higher prevalence of underlying thyroid abnormality. The relative risk of developing AIH was found to be 13-fold higher in female patients with positive thyroid microsomal or thyroglobulin antibodies, as compared with men without thyroid antibodies.'''Reference'''*"Effects of amiodarone on thyroid function.",journal = Ann Intern Med, volume = 126, issue = 1, month = Jan, year = 1997,PMID = 8992925.*"Amiodarone and the thyroid: a practical guide to the management of thyroid dysfunction induced by amiodarone therapy.", journal = Heart, volume = 79, issue = 2, month = Feb, year = 1998,PMID = 9538302.*"Incidence, predictability, and pathogenesis of amiodarone-induced thyrotoxicosis and hypothyroidism.",journal = Am J Med, volume = 91, issue = 5, month = Nov, year = 1991, PMID = 1951413. '''Educational Objective:''' '''References:'''ducational Objective:''' '''References:''')
WBR1025 + (Amiodarone-induced hypothyroidism (AIH) is … Amiodarone-induced hypothyroidism (AIH) is believed to result from the inability of the thyroid to escape from the Wolff-Chaikoff effect. Amiodarone is a benzofuranic-derivative iodine-rich drug, the large amount of iodide released during the metabolism of amiodarone leads to an adaptive blockage of further thyroidal iodide uptake and thyroid hormone biosynthesis, the so-called Wolff-Chaikoff effect.The reported incidence of AIH varies widely, ranging from 6% in countries with low iodine intake to 13% in countries with a high dietary iodine intake.The risk of developing hypothyroidism is independent of the daily or cumulative dose of amiodarone. However, the risk is greater in the elderly and in female patients, probably as a result of a higher prevalence of underlying thyroid abnormality. The relative risk of developing AIH was found to be 13-fold higher in female patients with positive thyroid microsomal or thyroglobulin antibodies, as compared with men without thyroid antibodies. '''Reference''':*"Effects of amiodarone on thyroid function.", journal = Ann Intern Med, volume = 126, issue = 1, month = Jan, year = 1997, PMID = 8992925*"Amiodarone and the thyroid: a practical guide to the management of thyroid dysfunction induced by amiodarone therapy.", journal = Heart, volume = 79, issue = 2, month = Feb, year = 1998, PMID = 9538302 .*"Incidence, predictability, and pathogenesis of amiodarone-induced thyrotoxicosis and hypothyroidism.", journal, volume = 91, issue = 5, month = Nov, year = 1991, PMID = 1951413 '''Educational Objective:''' '''References:'''ducational Objective:''' '''References:''')
WBR0079 + (Amiodarone-induced hypothyroidism (AIH) is … Amiodarone-induced hypothyroidism (AIH) is believed to result from the inability of the thyroid to escape from the '''Wolff-Chaikoff''' effect. Amiodarone is a benzofuranic-derivative iodine-rich drug, the large amount of iodide released during the metabolism of amiodarone leads to an adaptive blockage of further thyroidal iodide uptake and thyroid hormone biosynthesis, the so-called '''Wolff-Chaikoff''' effect.The reported incidence of AIH varies widely, ranging from 6% in countries with low iodine intake to 13% in countries with a high dietary iodine intake.The risk of developing hypothyroidism is independent of the daily or cumulative dose of amiodarone. However, the risk is greater in the elderly and in female patients, probably as a result of a higher prevalence of underlying thyroid abnormality. The relative risk of developing AIH was found to be 13-fold higher in female patients with positive thyroid microsomal or thyroglobulin antibodies, as compared with men without thyroid antibodies.'''Reference''':*"Effects of amiodarone on thyroid function.", journal = Ann Intern Med, volume = 126, issue = 1, month = Jan, year = 1997, PMID = 8992925.*"Amiodarone and the thyroid: a practical guide to the management of thyroid dysfunction induced by amiodarone therapy.", journal = Heart, volume = 79, issue = 2, month = Feb, year = 1998, PMID = 9538302.*"Incidence, predictability, and pathogenesis of amiodarone-induced thyrotoxicosis and hypothyroidism." journal = Am J Med, volume = 91, issue = 5, month = Nov, year = 1991, PMID = 1951413. '''Educational Objective:''' '''References:'''ducational Objective:''' '''References:''')
WBR1027 + (Amiodarone-induced thyrotoxicosis (AIT) oc … Amiodarone-induced thyrotoxicosis (AIT) occurs in 2–12% of patients on chronic amiodarone treatment. In patients with pre-existing thyroid abnormalities, thyrotoxicosis is believed to result from:*Type I AIT is believed to result from iodine-induced excessive thyroid hormone synthesis.*Type II AIT results from glandular damage with consequent release of preformed thyroid hormones into the circulation. It is usually self-limiting, which may be explained by the dose-dependent cytotoxic effect of amiodarone.'''Reference''':*"Effects of amiodarone on thyroid function.",journal = Ann Intern Med, volume = 126, issue = 1, month = Jan, year = 1997, PMID = 8992925.*"Amiodarone and the thyroid: a practical guide to the management of thyroid dysfunction induced by amiodarone therapy.", journal = Heart, volume = 79, issue = 2, month = Feb, year = 1998, PMID = 9538302. '''Educational Objective:''' '''References:'''ducational Objective:''' '''References:''')
WBR0680 + (Amoebic cysts in a patient with bloody dia … Amoebic cysts in a patient with bloody diarrhea and abdominal pain is diagnostic of amoebic dysentery. Amebic dysentery is most common among travelers to developing countries and may be confused with traveler's diarrhea (although it is usually more severe). Intestinal amoebiasis is a parasitic infection, and eosinophilia is one of the classical signs observed among infected patients. Eosinophils play a major role in controlling parasitic infections by producing major basic protein and peroxidase. Eosinophils are induced to grow and to differentiate by specific cytokines, namely interleukin (IL)-5. Other cytokines play different pro-inflammatory roles, such as IL-8 in neutrophil chemotaxis and IL-4 in differentiation into Th2 cells, whereas others have anti-inflammatory roles, such as IL-10 and TGF-beta that are secreted by Treg cells. '''Educational Objective:''' IL-5 is activated in parasitic infections to enhance growth and differentiation of eosinophils. '''References:''' Takatsu K, Nakajima H. IL-5 and eosinophilia. Curr Opin Immunol. 2008;20(3):288-94. First Aid 2015 page 207mmunol. 2008;20(3):288-94. First Aid 2015 page 207)
WBR0703 + (Ampicilline-associated maculopapular rash … Ampicilline-associated maculopapular rash in patients with infectious mononucleosis is a well know phenomenon. It is caused by the circulating IgG and IgM targeting penicillin derivatives causing this immune vasculitic rash '''Educational Objective:''' '''References:'''ducational Objective:''' '''References:''')
WBR0572 + (Amyotrophic lateral sclerosis (ALS or Lou … Amyotrophic lateral sclerosis (ALS or Lou Gehrig disease) is a progressive neurodegenerative disorder of the central and peripheral motor systems. The hallmark of ALS is the presence of signs and symptoms that suggest the simultaneous involvement of upper motor and lower motor neuron disease. Notably, ALS does not affect the sensory, cognitive, or oculomotor nervous systems. Manifestations of ALS vary, and symptoms may suggest prognosis and progression. Presentations may have a limb-onset, bulbar-onset, or less commonly pure upper/lower motor neuron involvement. Patients may develop of limb spasticity, weakness, fasciculations, wasting, and hyperreflexia. In addition, bulbar symptoms may include spastic dysarthria that causes distorted nasal speech, flaccid dysarthria, brisk gag/jaw jerks, or dysphagia. This patient has signs and symptoms consistent with ALS. Fasciculations and muscle atrophy are signs of lower motor neuron involvement, whereas rigidity, hyperreflexia marked by a positive Babinski test, and stuttered speech are signs of upper motor neuron involvement. Weakness in his extremities may be signs of either upper or lower motor neuron involvement. The cause of ALS is unknown, but some have speculated a role of superoxide dismutase 1 defects in the pathogenesis of the disease. The majority of patients with ALS die within 30 months of onset of symptoms, and less than 20% survive beyond 5 years. The management of ALS is very limited, riluzole has demonstrated modest improvement in survival among ALS patients. '''Educational Objective:''' ALS is a progressive neurodegenerative disorder characterized by involvement of upper and lower motor neuron systems. In the spinal cord, ALS is caused by lesions that typically involve the white and grey matters. '''References:''' Kiernan MC, Vucic S, Cheah BC, et al. Amyotrophic lateral sclerosis. Lancet. 2011;377:942-55. First Aid 2014 page 467. Lancet. 2011;377:942-55. First Aid 2014 page 467)

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