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Purchase here: “The Complete EM Board Prep!”

📘 **”The Complete EM Board Prep” – Your Path to Excellence in Emergency Medicine** Welcome to the pinnacle of emergency medicine preparation! “The Complete EM Board Prep,” a meticulously designed, 1192-page masterpiece by Dr. Dwight Collman, MD, is your guide to prepare for board certification in emergency medicine. 🌟 **A Journey of Expertise** This resourceContinue reading “Purchase here: “The Complete EM Board Prep!””

Residents-In-Training Purchase Here: “The Complete EM Board Prep!”

Hey everyone! I just completed writing and illustrating my next text to prepare you for board certification and recertification. This is an 1192 page comprehensive approach to the qualifying, oral, and concert examinations. Remember, ABEM recertification is now every five years. I included thousands of questions with answers including new updated questions for each examinationContinue reading “Residents-In-Training Purchase Here: “The Complete EM Board Prep!””

ConCertTM Examination Prep by D Collman MD

Test Item 2/multiole questions:  What is the diagnosis?  Describe all of the findings.  Is this a pathognomonic study?  What is all the indicated management?  CT findings:  Bilateral frontal old SDHs seen as loss of bifrontal cortical gray matter with bifrontal hygromas; acute Rt frontal SDH [white crescent on right], brain laceration on right deep withinContinue reading “ConCertTM Examination Prep by D Collman MD”

Pathophysiology of Salicylate Toxicity: there are 9 potential end organs [systems] potentially affected: Disturbance of (1) hepatic function as well as direct hepatic injury (salicylate-induced hepatitis—an uncommon sequela), (2) acid-base mechanisms (uncoupling of oxidative phosphorylation with degradation or decay of ATP levels and induction of both lactic acidosis and ketoacidosis—the latter via accelerated lipolysis, i.e., a state of catabolism), (3) electrolyte imbalance (especially sodium and potassium homeostasis with hypokalemia promoting salicylate toxicity through continued renal tubular reabsorption of unionized salicylate), (4) pulmonary dysfunction including pulmonary edema (induced by several potential mechanisms—e.g., aspiration pneumonitis vs. leaky pulmonary-alveolar capillary syndrome [non-cardiogenic pulmonary edema]), (5) ototoxicity which may result from both vasoconstriction of tiny vessels perfusing the inner ear) in addition to biochemical alterations which affect auditory nerve transmission (the earliest, but nonspecific complaint indicative of toxicity is tinnitus), (6) disturbance of glucose homeostasis (including both hypoglycemia and possibly even more importantly, hypoglycorrachia, i.e., low CSF glucose concentration—hyperglycemia is also possible early in the course of acute salicylism), (7) myotoxicity from excessive heat and an inability to dispose of heat; this induces rhabdomyolysis, (8) hematologic manifestations including decreased platelet adhesion for primary hemostasis and hypoprothrobinogenemia, and (9) gastrointestinal toxicity including mucosal ulceration, (even frank ulceration or perforation) and bleeding.