WBR0938: Difference between revisions
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{{WBRQuestion | {{WBRQuestion | ||
|QuestionAuthor=William J Gibson (Reviewed by Serge Korjian) | |QuestionAuthor=William J Gibson (Reviewed by Serge Korjian) | ||
|ExamType=USMLE Step 1 | |ExamType=USMLE Step 1 |
Latest revision as of 02:07, 28 October 2020
Author | PageAuthor::William J Gibson (Reviewed by Serge Korjian) |
---|---|
Exam Type | ExamType::USMLE Step 1 |
Main Category | MainCategory::Pharmacology |
Sub Category | SubCategory::Cardiology |
Prompt | Prompt::A 60-year-old man attempts suicide by consuming his entire bottle of propranolol pills. He suffers extreme cardiovascular collapse and tonic-clonic seizures. Which of the following may serve as an antidote to his overdose? |
Answer A | AnswerA::Glucagon |
Answer A Explanation | AnswerAExp::Glucagon counteracts beta-blocker toxicity by increasing intracellular cAMP. |
Answer B | AnswerB::Epinephrine |
Answer B Explanation | AnswerBExp::Epinephrine can be administered in the case of anaphylaxis. |
Answer C | AnswerC::Digoxin |
Answer C Explanation | AnswerCExp::While digoxin has an inotropic effect, it is not appropriate for counteracting beta-blocker overdose. |
Answer D | AnswerD::Verapamil |
Answer D Explanation | AnswerDExp::Verapamil is a calcium channel blocker that can be used to treat cardiac arrhythmias. It is not an effective antidote for beta-blocker overdose. |
Answer E | AnswerE::Sotalol |
Answer E Explanation | AnswerEExp::Sotalol is both a non-selective beta-blocker and potassium channel blocker (Class III antiarrhythmic). It is not an effective antidote for beta-blocker overdose. |
Right Answer | RightAnswer::A |
Explanation | [[Explanation::Non-selective beta-blockers such as propranolol interfere with the binding of catecholamine stress hormones such as epinephrine to beta-adrenergic receptors at most sites (β1-adrenergic receptors are located mainly in the heart and in the kidneys; β2-adrenergic receptors are located mainly in the lungs, gastrointestinal tract, liver, uterus, vascular smooth muscle, and skeletal muscle; β3-adrenergic receptors are located in fat cells). Because beta blockers decrease activity in the SA-node, they can lead to bradycardia and first degree heart block. In addition to arrhythmias, beta-blocker overdose may cause CNS depression and seizures. At the molecular level, beta-blockade causes a decrease in intracellular levels of cAMP. Glucagon binds to its G protein-coupled receptor, which then activates adenylate cyclase to increase intracellular levels of cAMP. This cascade counteracts the effects of beta-blocker overdose. Educational Objective: Glucagon counteracts beta-blocker toxicity by increasing intracellular cAMP. |
Approved | Approved::Yes |
Keyword | WBRKeyword::Beta blocker, WBRKeyword::Beta-blocker, WBRKeyword::Overdose, WBRKeyword::Toxicity, WBRKeyword::Antidote, WBRKeyword::Glucagon, WBRKeyword::Heart block |
Linked Question | Linked:: |
Order in Linked Questions | LinkedOrder:: |