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{{WBRQuestion
{{WBRQuestion
|QuestionAuthor=William J Gibson
|QuestionAuthor=William J Gibson (Reviewed by Serge Korjian)
|ExamType=USMLE Step 1
|ExamType=USMLE Step 1
|MainCategory=Pharmacology
|MainCategory=Pharmacology
Line 8: Line 8:
|MainCategory=Pharmacology
|MainCategory=Pharmacology
|SubCategory=Cardiology
|SubCategory=Cardiology
|MainCategory=Pharmacology
|MainCategory=Pharmacology
|MainCategory=Pharmacology
|MainCategory=Pharmacology
|MainCategory=Pharmacology
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|SubCategory=Cardiology
|SubCategory=Cardiology
|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?
|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?
|Explanation=Beta-blockers such as propranolol interfere with the binding of catecholamine stress hormones such as epinephrine to beta-adrenergic receptors*.   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.
|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.
 
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.
 
*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.


Educational Objective: Glucagon counteracts beta-blocker toxicity by increasing intracellular cAMP.


References:
First Aid 2013 page 239 ; First Aid 2012 page 270


Weinstein RS, Cole S, Knaster HB, Dahlbert T (February 1985). "Beta blocker overdose with propranolol and with atenolol". Ann Emerg Med14 (2): 161–163


|AnswerA=Glucagon
|AnswerA=Glucagon
|AnswerAExp=Correct: Glucagon counteracts beta-blocker toxicity by increasing intracellular cAMP.
|AnswerAExp=Glucagon counteracts beta-blocker toxicity by increasing intracellular cAMP.
|AnswerB=Epinephrine
|AnswerB=Epinephrine
|AnswerBExp=Incorrect: Epinephrine can be administered in the case of anaphylaxis.
|AnswerBExp=Epinephrine can be administered in the case of anaphylaxis.
|AnswerC=Digoxin
|AnswerC=Digoxin
|AnswerCExp=Incorrect:  While digoxin has an inotropic effect, it is not appropriate for counteracting beta-blocker overdose.
|AnswerCExp=While digoxin has an inotropic effect, it is not appropriate for counteracting beta-blocker overdose.
|AnswerD=Verapamil
|AnswerD=Verapamil
|AnswerDExp=Incorrect: Verapamil is a calcium channel blocker that can be used to treat cardiac arrhythmias.  It is not an effective antidote for beta-blocker overdose.
|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.
|AnswerE=Sotalol
|AnswerE=Sotalol
|AnswerEExp=Incorrect: 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.
|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.
|EducationalObjectives=Glucagon counteracts beta-blocker toxicity by increasing intracellular cAMP.
|References=Weinstein RS, Cole S, Knaster HB, Dahlbert T (February 1985). "Beta blocker overdose with propranolol and with atenolol". Ann Emerg Med14 (2): 161–163
|RightAnswer=A
|RightAnswer=A
|WBRKeyword=Beta blocker, Beta-blocker, Overdose, Toxicity, Antidote, Glucagon, Heart block
|WBRKeyword=Beta blocker, Beta-blocker, Overdose, Toxicity, Antidote, Glucagon, Heart block
|Approved=Yes
|Approved=Yes
}}
}}

Revision as of 15:12, 11 March 2015

 
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.
References: Weinstein RS, Cole S, Knaster HB, Dahlbert T (February 1985). "Beta blocker overdose with propranolol and with atenolol". Ann Emerg Med14 (2): 161–163]]

Approved Approved::Yes
Keyword WBRKeyword::Beta blocker, WBRKeyword::Beta-blocker, WBRKeyword::Overdose, WBRKeyword::Toxicity, WBRKeyword::Antidote, WBRKeyword::Glucagon, WBRKeyword::Heart block
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