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Comprehensive Board Review Published by Foundatons of Medical Educaton, Inc Atlanta, GA, USA First Editon, 2021 Founda(ons of Emergency Medicine Kristen Grabow Moore COPYRIGHT Founda'ons Comprehensive Board Review Published by Founda8ons of Medical Educa8on, Inc Atlanta, GA, USA First Edi8on, 2021 Available for use under the Crea8ve Commons AHribu8on: NonCommercial-NoDeriva8ves 4.0 Interna8onal ISBN # 978-1-7365274-0-5 Founda8ons of Medical Educa8on, Inc. (FoME) publishes informa8on believed to be in agreement with the accepted standards of prac8ce at the date of publica8on. Due to the con8nual state of change in diagnos8c procedures, treatment, and drug therapy, FoME and the writer and editors are not responsible for any errors or omissions. In the prac8ce of Front Matter ii FOUNDATIONS Comprehensive Board Review First Edi8on, 2021 Author: Kristen Grabow Moore, MD, MEd Editors: Andrew KeHerer, MD, MA (2017) Adam Evans, MD (2018) Isabel Malone, MD (2019) Anwar Osborne, MD (2020) Front Matter iii Front Matter iv DEDICATION To the free open access medical educa8on (FOAMed) pioneers. You know who you are. Front Matter v ABOUT THIS BOOK The Founda8ons Comprehensive Board Review resource is intended to provide a high-yield, systems-based approach to studying for the Emergency Medicine In-Training Exam (ITE) and American Board of Emergency Medicine WriHen Board Exam. The first version, created in 2016, was developed as a comprehensive reservoir of test relevant informa8on based on a mul8tude of board review references. Each year, content has been edited by a recent emergency medicine resident while they study for the wriHen board exam. This review is divided by system with the highest yield (highest % on the test) first and the lower yield content topics towards the end. This is meant to be a free, open access resource that learners of emergency medicine can use for independent study. For a more interac8ve approach, consider following instruc8ons for flashcard review noted below. COPYRIGHT Available for use under the Crea8ve Commons AHribu8on: NonCommercial-NoDeriva8ves 4.0 Interna8onal LEARNING OPTIONS For instruc8ons on how to access Founda8ons Comprehensive Board Review using an interac8ve flashcard op8on, visit the Founda8ons of Emergency Medicine website. Learner Resources -> In-Training Exam Review www.founda8onsem.com Front Matter vi Contributors About the Author Kristen Grabow Moore, MD, MEd is an Assistant Professor for the Department of Emergency Medicine at Emory University. She is the Creator, Chief Execu8ve Officer and Editor-in-Chief of Founda8ons of Emergency Medicine (FoEM). Further informa8on about FoEM can be found at Andrew KeKerer, MD, MA Medical Educa8on Fellow Clinical Instructor Sec8on of Emergency Medicine Department of Emergency Medicine University of Chicago Beth Israel Deaconess Medical Center Harvard Medical School Anwar Osborne, MD, MPM Adam Evans, MD Associate Professor Staff Physician Department of Emergency Medicine Department of Emergency Medicine Department of Internal Medicine Montclair Hospital Medical Center Emory University Isabel Malone, MD about the illustrator Dr. Rahel Gizaw is a PGY-2 in the Emory School of Medicine Emergency Medicine Program. She has been providing scholarly illustrations for the department and shares many illustrations on her instagram page, @physiciandoodles. for inquiries: [email protected] Front Matter vii Table of Contents Cardiology 1 Trauma 13 Gastrointestinal 19 Pediatrics 27 Respiratory 36 HEENT 44 Neurology 50 Infectious Disease 56 Immunology 67 Toxicology 70 Environmental 83 OB/Gyn 91 Renal 100 Psychiatry 105 Musculoskeletal 111 Dermatology 119 Endocrine 124 Hematology & Oncology 131 Procedures 138 Grab Bag 145 References 150 Front Matter viii Front Matter ix Cardiology Cardiology Bizz Buzz What underlying pathologic Atherosclerotic plaque rupture → exposed endothelium → clot attaches process distinguishes → reduced blood flow; if cell death occurs (usually due to complete myocardial infarction from vascular obstruction) then positive trop and MI; if no cell death angina/unstable angina? occurs then negative trop and angina/unstable angina What is the difference Transmural: usually STEMI, large vessel affected, benefit from between transmural and non- thrombolytics/PCI; Non-Transmural: usually NSTEMI, smaller transmural infarction? subendocardial artery, may benefit from PCI but no thrombolytics What defines Unstable Angina? Stable Angina + pain at rest, new pain, increasing pain severity, hemodynamic changes with pain Acute chest pain at night, EKG Prinzmental's Angina (coronary spasm, most do not have CAD; treat with STEMI, all symptoms and with CCBs) EKG changes resolve with nitro? What are early to late EKG Hyperacute T's and Giant R (very early and transient), STE, STD changes with ACS? (ischemia or reciprocal), Q waves (1 square wide, 1/3 height QRS), TWI Biphasic T-wave in V2/V3 Wellen's Syndrome: biphasic (type A) or deeply inverted, symmetric (type B) TW in septal leads = early signal of proximal LAD lesion Chest Pain with STE V1-V4 with Anterior MI 2/2 LAD occlusion, may affect large territory of LV, septum STD II, III, aVL and conduction sysytem (high grade blocks, wide complex bradycardias), commonly have shock, possible ruptures Chest Pain with STE I, aVL, V5, Lateral MI 2/2 LAD vs LCx occlusion, may affect LV V6 with STD V1 Chest Pain with STE II, III, aVF Inferior MI 2/2 occlusion of PDA (RCA > LCx), may affect AV node with STD V1-V4 (usually transient narrow complex bradycardias), may cause papillary muscle rupture Chest Pain with STE III > II and Right Ventricular MI, should get R-sided leads (STE in V4R, V5R), 2/2 V1 > V2 proximal RCA lesion, associated with Inferior MI Chest Pain with STD V1-3 Posterior MI, get posterior leads to dx (req only 0.5 mm elevation for STEMI dx), 2/2 occlusion of Posterior Descending (RCA > L circ) What meets STEMI criteria for V2-V3: ≥2mm in MEN ≥ 40yrs, ≥2.5mm in MEN < 40yrs, or ≥ 1.5mm in leads V2-V3 versus all other WOMEN; All other leads: STE at the J-point of ≥ 1mm in two contiguous leads? lead What distinguishes Type I- Type I: MI caused by acute atherothrombotic CAD, usually due to Type V MI? plaque rupture or erosion; Type II: MI 2/2 mismatch of oxygen supply and demand; Type III: typical MI presentation but death before biomarkers obtained; Type IV: MI 2/2 PCI; Type V: MI 2/2 CABG Cardiology 2 How can you detect MI in Sgarbossa Criteria: STE >1mm with concordant (same direction) QRS, patients with paced rhythm or concordant STD >1mm V1-V3, STE >5mm with discordant (opposite old LBBB direction) QRS (modified Sgarbossa changes this last rule to discordant STE >25% preceding S wave) What is unique about the With Inferior MI, always consider RV involvement and get right-sided management of Inferior MIs? EKG leads What is unique about the They are preload dependent and will become very hypotensive with management MI with right- nitroglycerin - avoid this, give IVF for hypotension ventricular involvement? What are potential early arrhythmia, shock 2/2 pump failure or valve dysfunction complications (<24hr) of MI? What are potential late Thromboembolism, myocardial rupture, valve rupture, CHF, pericarditis complications (>24hr) of MI? Pleuritic chest pain 4wks after Dressler's syndrome: autoimmune pericarditis, typically 2-6wks s/p MI. Tx MI? it with NSAIDs like any other pericarditis What artery typically supplies the SA- RCA 60%, LCx 40%; AV- RCA 90%, LCx 10%; concern for SA node and AV node? bradycardias if Inferior MI Cardiac Tamponade after MI Myocardial wall rupture, give IVF and dispo to OR What EKG finding is classic in Electrical Alternans Cardiac Tamponade? Shock + new murmur after Papillary muscle rupture, Rx- reduce afterload and dispo to OR; same recent treatment if septal wall rupture MI What is unique about the With Inferior MI, always consider RV involvement and get right-sided management of Inferior MIs? EKG leads What potential treatments for Defibrillation for VF/VT (30% mortality reduction), Aspirin (25% mortality AMI have been shown to reduction) reduce mortality? What is the only True aspirin allergy (anaphylaxis) contraindication to aspirin in ACS? What is better for treatment of PCI is better. Thrombolytics should only be considered if PCI is not STEMI, thrombolytics or PCI? available at center within 90min or after transfer within 120min What EKG changes are STEMI (STE >2mm for men, >1.5mm for women in V2-3, STE >1mm included under indications for in 2+ other leads), STD V1-3 (posterior MI), old LBBB + Sgarbossa thrombolysis? What are absolute Any previous brain bleed or known mass, ischemic stroke or closed contraindications for head injury within 3mo, known bleeding disorder, current active thrombolysis? bleeding, major surgery in the last 2 months, BP > 180/110 *after treatment, suspected aortic dissection Cardiology 3 What are concerning Intracranial hemorrhage (1/70 to 1/100, >50% mortality), major bleeding complications of thrombolysis (e.g. GI bleed) in 5% and how often do they occur? What potential treatments for Defibrillation for VF/VT (30% mortality reduction), Aspirin (25% mortality AMI have been shown to reduction) reduce mortality? What EKG changes may occur Accelerated idioventricular rhythm, NSVT, PVCs; these should be with reperfusion? transient, are overall benign and do not require additional treatment What is the appropriate First treat with benzos, aspirin, nitrates, calcium channel blockers or treatment of ST elevation after alpha blockers (e.g. phentolamine) for HTN, thrombolysis only if ST cocaine use? does not return to baseline after these treatments What is the appropropriate Benzos, CCBs or phentolamine; NO Beta Blockers (may theoretically treatment for HTN after cocaine lead to unopposed alpha stimulation and worsened HTN) use? What are key risk factors for Diseased valves, artificial valves, IV drug use, dental extractions Infective Endocarditis? What EKG changes may occur Accelerated idioventricular rhythm, NSVT, PVCs; these should be with reperfusion? transient, are overall benign and do not require additional treatment What is the appropriate First treat with benzos, aspirin, nitrates, calcium channel blockers or treatment of ST elevation after alpha blockers (e.g.
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