WBR0938
| 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:: |