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Statins are the important medication in Myocardial Ischemia. Statins decrease the mortality risk in post-MI patients unlike other lipid lowering medication. They act by inhibiting HMG- Co A reductase and increasing Low density lipoprotein uptake. Side effects of statins are myositis, and elevation of liver enzymes. Statin induced hepatotoxicity can be a dangerous side effect of these drugs. Therefore, it is important to regularly monitor the liver enzymes aspartate transaminase, and alanine transaminase. While myositis is a very common complication of statin therapy, doses can be adjusted to a patient’s symptomatic tolerance without needing to monitor myoglobin or creatinine phopsphokinase levels.
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In patients on statins liver enzymes Aspartate and Alanine transaminases should be monitored regularly as statins cause elevation in the levels. Though statins also cause myositis,regular monitoring of Creatinine Phosphokinase of urine myoglobin is not indicated
'''References:''' Page 60 Master the boards Step 2 CK second edition<br/>
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Aspirin is the best initial therapy in all cases of myocardial infarction unless the patient has contraindications. Aspirin inhibits platelet aggregation and thus prevents occlusive thrombus formation in blood vessels.Aspirin is associated with a significant mortality benefit and is the most appropriate next step in this patient
'''Educational Objective:''' Aspirin inhibits platelet aggregation and thus further clot formation in coronary vessels.It offers a significant mortality benefit in both ST segment elevation myocardial infarction and unstable angina.It should be the first drug to be given to all patients with myocardial infarction.
'''References:''' Page 64, 68 Master the boards Step 2 CK second edition<br/>
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Electrocardiogram demonstrates an up to date image of the heart electrical activity. . Cardiac enzymes Troponin, Myoglobin and CK-MB start to rise after infarction of cardiac muscle with various kinetics.The first cardiac injury marker to rise is myoglobin at 1-4 hours and reaches baseline in 1-2 days. CK MB rises at 4-6 hours and becomes normal in 1-2 days. Finally,Troponin starts to rise at 4-6 hours and remains elevated for 10-14 days. Therefore, to diagnose a reinfarction, perform an electrocardiogram and measure CK-MB as the raised levels from previous infarction become normal on the second day.
'''Educational Objective:'''CK-MB returns to normal levels 2 days after infarction. Therefore, its is a useful diagnostic criterion for a second MI outside of a 2 day window. Electrocardiogram will help to confirm the diagnosis by showing new changes, particularly in the ST segments .
'''References:''' 66 Master the boards Step 2 Ck second edition<br/>
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Aspirin is always the best Initial therapy for myocardial Infarction unless the patient has contraindications, such as aspirin allergy. This patient has an aspirin allergy, as evidenced by anaphylaxis upon exposure previously. Antiplatelet therapy is still necessary, and the best choice for this patient is Clopidogrel . Clopidogrel blocks platelet aggregation by irreversibly inhibiting the ADP receptor on platelets.
'''Educational Objective:''' Clopidogrel is the next best alternative for the initial management of myocardial Infarction when the patient has contraindications for the use of Aspirin, such as allergy and anaphylaxis.
'''References:''' Page 64, 68 Master the boards step 2 CK second edition<br/>
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Management of myocardial infarction depends on the time between the onset of symptoms and arrival in the ER. Typical “door to needle time” (for thrombolysis) is said to be 30 minutes but the mortality benefit extends until 12 hours after the onset of pain. Thombolysis is considered the best option only when angioplasty is not feasible. Otherwise angioplasty is the best treatment and typical door to balloon time is less than 90 minutes. In this case, the onset of pain was 30 minutes ago and time of travel to the medical center with a catheterization lab is 30 minutes, so the patient could undergo catheterization with less than a 90 minute door to balloon time. Thus, the best choice here is to transfer the patient immediately to the nearest medical center
'''Educational Objective:''' Door to needle time for thrombolysis ought to be under 30 minutes but its mortality benefit extends until 12 hours after pain onset. Door to balloon time for angioplasty should be less than 90 minutes. The decision of whether to perform thrombolysis or angioplasty depends on whether or not a sufficiently low door to balloon time can be achieved.
'''References:''' Page 67, 68, 69 Master the boards step 2 CK second edition<br/>
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Management of myocardial infarction depends on the time between the onset of symptoms and arrival in the ER. Typical “door to needle time” (for thrombolysis) is said to be 30 minutes but the mortality benefit extends until 12 hours after the onset of pain. Thombolysis is considered the best option only when angioplasty is not feasible. Otherwise angioplasty is the best treatment and typical door to balloon time is less than 90 minutes. In this case, the onset of pain was 45 minutes ago and time of travel to the medical center with a catheterization lab is 60 minutes, so the patient could not undergo catheterization with less than a 90 minute door to balloon time. Thus, the best choice here is to initiate tPA therapy.
'''Educational Objective:''' Door to needle time for thrombolysis ought to be under 30 minutes but its mortality benefit extends until 12 hours after the onset of pain. Door to balloon time for angioplasty should be less than 90 minutes. The decision of whether to perform thrombolysis or angioplasty depends on whether or not a sufficiently low door to balloon time can be achieved.
'''References:''' Page 68, 69 Master the boards Step 2 CK second edition<br/>
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In this case, the anticipated door to balloon time is greater than 90 minutes which typically favors thrombolytic therapy. However, transfer to the medical center for angioplasty is correct in this case because thrombolysis is contraindicated. Contraindications for thrombolysis include major bleeding ( melena, brain hemorrhage), major surgery within last 2 weeks , and blood pressure over 180/110 .In these situations, angioplasty is the best choice even if door to balloon times exceed 90 minutes.
'''Educational Objective:''' Contraindications for thrombolysis include major bleeding (melena, brain hemorrhage), major surgery within last 2 weeks, and blood pressure over 180/110 , In these situations, angioplasty is the best choice even if door to balloon times exceed 90 minutes.
'''References:''' Page 67, 68,69 Master the boards step 2 CK second edition<br/>
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Complications of myocardial infarction is a high-yield topic for USMLE exams. Sinus bradycardia, heart block, ventricular tachycardia, ventricular fibrillation, valvular or septal rupture and pericarditis are complications of myocardial infarction.Dizziness,dyspnea and an electrocardiogram showing uncoordinated P and QRS suggest third degree heart block.
'''Educational Objective:''' Uncoordinated firing of the atria and ventricles accompanied by dizziness, and dyspnea strongly suggest third degree heart block .
'''References:'''Page 71, 551, 552, 553, 558 Master the boards Step 2 Ck second edition, Page 73 Master the boards Step 3 2009 edition.<br/>
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If a patient develops ventricular tachycardia or experiences continued chest pain following proper medical treatment for ST depression MI, percutanteous coronary angioplasty is the best option.
'''Educational Objective:''' If a patient develops ventricular tachycardia or experiences continued chest pain following proper medical treatment for ST depression MI, percutanteous coronary angioplasty is the best option.
'''References:''' Page 70,71 ,560 Master the boards Step 2 Ck second edition, Page 74 Master the boards Step 3 2009 edition<br/>
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Heparin, Glycoprotein IIb, IIIa inhibitors like Abciximab, tirofiban , Epifibatide and Angioplasty offer a significant mortality benefit in this patient.
'''Educational Objective:''' Heparin, Glycoprotein IIb, IIIa inhibitors like Abciximab, tirofiban , Epifibatide and Angioplasty offer great mortality benefits in ST depression or Non ST elevation myocardial infarction.
'''References:''' page 49 Master the boards Step 3 2009 edition, Page 69 Master the boards Step 2 CK second edition<br/>
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Patient can participate in sexual activity immediately post myocardial infarction if he is totally symptom free. Sildenafil and nitrates should never be combined as the risk of hypotension is greater because both are vasodilators.
'''Educational Objective:''' Patients post myocardial infarction can resume sexual activity immediately if they are symptom free. Sildenafil and Nitrates should not be combined as the risk of hypotension is increased with the combination
'''References:''' Page 74 Master the boards Step 2 CK Second edition<br/>
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The student's t-test is used to evaluate a significant difference between 2 means of continuous variables. In this study, the researchers are looking to compare the mean Δbody-weight between the 2 groups making the t-test the most appropriate choice. The t-test operates under the assumption that the population has a normal distribution. The t-test can be either independent (unpaired), used when two independent sets of similarly distributed samples one from each of the two groups being compared, or paired used in cases where the study population consists of matched pairs.<br/>
'''Educational Objective:''' The t-test is used to detect a statistically significant difference between the means of 2 groups.<br/>
'''References:''' Gerstman BB. Basic Biostatistics, Statistics for Public Health Practice/ Formula and Tables. Jones & Bartlett Learning; 2007. +
The classical treatment for patients with performance anxiety is a non-selective beta-blocker, most commonly propranolol. A key consideration in this question, other than the consistent clinical presentation, is the possibility of self-medication with a higher dose of propranolol given an upcoming stressful event. Beta-blocker toxicity manifests as bradycardia, hypotension, atrioventricular block, arrhythmias, and seizures. Given the non-selective nature of propranolol, bronchospasm is also a possible complication particularly in patients with pre-existing bronchospastic pulmonary disease. The ECG tracing may vary, showing anything from simple sinus bradycardia to third degree block (seen in this patient's tracing). The initial management for patients with propranolol toxicity includes activated charcoal; however, given the altered mental status of the patient, charcoal should be withheld. Along with initial fluid administration, glucagon is the treatment of choice for patients with beta-blocker toxicity. Glucagon increases heart rate and myocardial contractility, and improves atrioventricular conduction. These properties are unaffected by the presence of beta-blockers suggesting that glucagon's mechanism of action may bypass the beta-adrenergic receptor site. This may also explain why atropine and isoproterenol are not very effective in reversing the bradycardia and hypotension of beta-blocker overdose.<br/>
'''Educational Objective:''' Glucagon is the treatment of choice for patients with suspected or confirmed beta-blocker toxicity.<br/>
'''References:''' Peterson CD, Leeder JS, Sterner S. Glucagon therapy for beta-blocker overdose. Drug Intell Clin Pharm. 1984;18(5):394-8.<br>
Kerr GW, Mcguffie AC, Wilkie S. Tricyclic antidepressant overdose: a review. Emerg Med J. 2001;18(4):236-41. +
The mouse model presented is an experimental approach for the investigation of Huntington's disease. The disorder has an autosomal dominant inheritance with the HD gene (huntingtin protein) on chromosome 4p harboring an expansion of the CAG repeats. While healthy individuals may have up to 35 repeats, patients with Huntington's disease have 36 or more repeats. Patients initially present with personality alterations, mood disorders (commonly depression), and aggressiveness. This is later followed by dystonic posturing and rigidity, choreiform movements, and dementia.
Huntington's disease is often used as a classical example of anticipation i.e. earlier manifestation of the disease due to further expansion of the CAG repeats in subsequent affected generations. A classical finding in these patients is atrophy of the caudate nucleus which is often evident on brain imaging. Atrophy of the caudate leads to decreased GABA and acetylcholine, with increased dopamine due to disrupted dopaminergic regulation in the basal ganglia. The disordered neurotransmitter balance is responsible for the characteristic symptoms of chorea and mood changes.<br/>
'''Educational Objective:''' Huntington's disease is an autosomal dominant disorder caused by a CAG trinucleotide expansion in the HD gene on chromosome 4p. It is characterized by caudate atrophy leading to a decrease in GABA and acetylcholine, and an increase in dopamine.<br/>
'''References:''' First Aid 2013 page 461<br>
Menalled LB, Sison JD, Dragatsis I, Zeitlin S, Chesselet MF. Time course of early motor and neuropathological anomalies in a knock-in mouse model of Huntington's disease with 140 CAG repeats. J Comp Neurol. 2003;465(1):11-26.<br>
Crow TJ, Baker HF, Cross AJ, et al. Monoamine mechanisms in chronic schizophrenia: post-mortem neurochemical findings. Br J Psychiatry. 1979;134:249-56. +
This patient is likely having a non-STEMI given the presentation and EKG changes. He would benefit from the medical therapy mentioned and also from anticoagulation. Therefore, a dose of SC low molecular weight heparin would be the most important next step in management. Cardiac markers should be obtained, if they are positive, then a definite diagnosis of MI will be made and consultation with a cardiologist is warranted for further intervention.<br/>
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Potter’s Syndrome is a triad of clubbed feet, pulmonary hypoplasia, and cranial anomalies. Oligohydramnios, commonly associated with bilateral renal agenesis, can give rise to Potter’s syndrome. Other causes of oligohydramnios include ureteral or urethral atresia, polycystic kidney disease, renal hypoplasia, and uteroplacental insufficiency. The incidence of Potter’s syndrome is related to the degree of oligohydramnios and to the gestational age at which rupture takes place. Approximately 50% of infants with rupture at 19 weeks’ gestation or earlier are affected with Potter’s syndrome.<br/>
'''Educational Objective:''' Oligohydramnios, commonly caused by bilateral renal agenesis, can give rise to Potter’s syndrome. The latter is characterized by the triad of: Clubbed feet, pulmonary hypoplasia, and facial anomalies.<br/>
'''References:''' Medina TM, Hill DA. Preterm premature rupture of membranes: Diagnosis and management. Am Fam Phys. 2006; 73(4):659-664. +
Bilateral renal cortical necrosis is a rare phenomenon caused by significantly diminished renal arterial perfusion secondary to vascular injury, spasm, or coagulopathy. Sepsis, disseminated intravascular coagulation (DIC), and pregnancy-related complications are typical inciting events for renal cortical necrosis. Other causes include drugs and blunt trauma. Contrast-enhanced computed tomography (CT) is the imaging of choice to diagnose renal cortical necrosis. CT scan reveals acutely hypo-dense areas in the renal cortex bilaterally with enhancement of subcapsular and juxtamedullary areas. Care should be taken with these patients as further injury from contrast media administration is possible. Chronic kidney disease develops up to 50% of patients requiring long term dialysis and transplantation. Partial recovery of renal function is a possibility in certain patients. The mortality rate from renal cortical necrosis exceeds 50% in untreated patients.<br/>
'''Educational Objective:''' Bilateral renal cortical necrosis is a rare complication of pregnancy-related medical conditions and sepsis. Contrast-enhanced CT scan is the imaging reveals bilateral renal infarcts that confirms the diagnosis.<br/>
'''References:''' Chervu I, Koss M, Campese VM. Bilateral renal cortical necrosis in two patients with Neisseria meningitidis sepsis. Am J Nephrol. 1991;11(5):411-5 +
Seborrheic keratosis resembles flattened or raised warts, but have no viral origins and may exhibit a variety of colors, from pink or yellow through brown and black. Because only the top layers of the epidermis are involved, seborrheic keratoses are often described as having a "stuck-on" appearance. Darkly pigmented lesions can be hard to distinguish from nodular melanomas. If in doubt, a skin biopsy should be performed.<br/>
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This patient is in severe respiratory distress with evidence of hypoxemia despite high flow oxygen, cyanosis and altered mentation. She most likely developed ACEI induced angioedema. The most important next step in management is intubation to save her life. You can then proceed with IV steroids and antihistamines. It’s also reasonable to call her primary care physician as soon as possible to confirm the diagnosis. IV normal saline will be of little use in treating this condition unless she develops hypotension.<br/>
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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.<br/>
'''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.<br/>
'''References:''' Rossert J. Drug-induced acute interstitial nephritis. Kidney Int. 2001;60(2):804-17.<br>
Praga M, Gonzalez E. Acute Interstitial Nephritis. Kidney International. 2010; 77:956-961