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Questions and Answers
What is the most widely prescribed digitalis glycoside in the U.S.?
What is the most widely prescribed digitalis glycoside in the U.S.?
What is the potentially fatal concentration of digoxin in the blood?
What is the potentially fatal concentration of digoxin in the blood?
In which part of the body does absorption of digitalis glycosides occur?
In which part of the body does absorption of digitalis glycosides occur?
What is the usual therapeutic range of digoxin in plasma concentration?
What is the usual therapeutic range of digoxin in plasma concentration?
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Which cardiovascular drug has played a prominent role in the therapy of congestive heart failure and supraventricular rhythm disturbances?
Which cardiovascular drug has played a prominent role in the therapy of congestive heart failure and supraventricular rhythm disturbances?
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What percentage of patients taking a digitalis preparation will experience toxicity?
What percentage of patients taking a digitalis preparation will experience toxicity?
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Which digitalis glycoside has less rapid and less complete absorption in the gastrointestinal tract?
Which digitalis glycoside has less rapid and less complete absorption in the gastrointestinal tract?
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(True/False): DGs bind to plasma proteins.
(True/False): DGs bind to plasma proteins.
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Which of the following is the most common manifestation in patients with ACE inhibitor overdoses?
Which of the following is the most common manifestation in patients with ACE inhibitor overdoses?
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What is the specific enzyme inhibited by ACE inhibitors?
What is the specific enzyme inhibited by ACE inhibitors?
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What is the primary cause of both ACE inhibitor-induced angioedema and cough?
What is the primary cause of both ACE inhibitor-induced angioedema and cough?
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What is the treatment for ACE inhibitor-induced angioedema involving the tongue, face, and oropharynx?
What is the treatment for ACE inhibitor-induced angioedema involving the tongue, face, and oropharynx?
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Which of the following is a predictable toxic effect of acute overdose with beta blockers?
Which of the following is a predictable toxic effect of acute overdose with beta blockers?
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What is suggested to be the mechanism underlying beta blocker-induced CNS toxicity?
What is suggested to be the mechanism underlying beta blocker-induced CNS toxicity?
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Which type of beta blockers are capable of producing serious toxicity?
Which type of beta blockers are capable of producing serious toxicity?
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What is a common manifestation of beta blocker poisoning in patients with significant cardiovascular toxicity?
What is a common manifestation of beta blocker poisoning in patients with significant cardiovascular toxicity?
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What is more common in children who have been poisoned by beta blockers?
What is more common in children who have been poisoned by beta blockers?
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What is the suggested treatment for patients with mild or quickly resolving beta blocker-induced angioedema?
What is the suggested treatment for patients with mild or quickly resolving beta blocker-induced angioedema?
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What is the most likely outcome of abrupt stoppage of beta blockers after chronic use?
What is the most likely outcome of abrupt stoppage of beta blockers after chronic use?
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What is the first-line therapy for β-blocker intoxication?
What is the first-line therapy for β-blocker intoxication?
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What is the mechanism of action of glucagon in β-blocker intoxication?
What is the mechanism of action of glucagon in β-blocker intoxication?
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How does atropine help in the management of β-blocker intoxication?
How does atropine help in the management of β-blocker intoxication?
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What is the most common toxic effect caused by calcium channel antagonists, particularly the dihydropyridines?
What is the most common toxic effect caused by calcium channel antagonists, particularly the dihydropyridines?
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How do dihydropyridines produce reflex increases in heart rate at therapeutic or moderate toxic doses?
How do dihydropyridines produce reflex increases in heart rate at therapeutic or moderate toxic doses?
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What is the effect of severe overdoses of calcium channel antagonists?
What is the effect of severe overdoses of calcium channel antagonists?
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What is a beneficial treatment for hypotension secondary to reduced systemic resistance and lowered cardiac output in calcium channel blocker overdose?
What is a beneficial treatment for hypotension secondary to reduced systemic resistance and lowered cardiac output in calcium channel blocker overdose?
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Which agent is beneficial in correcting hypotension secondary to reduced systemic resistance in calcium channel blocker overdose?
Which agent is beneficial in correcting hypotension secondary to reduced systemic resistance in calcium channel blocker overdose?
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Which of the following is NOT a clinical feature of digoxin intoxication?
Which of the following is NOT a clinical feature of digoxin intoxication?
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What is the major route of elimination for digoxin?
What is the major route of elimination for digoxin?
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Which microorganism in the colon may require larger doses of digitalis to achieve therapeutic serum concentrations?
Which microorganism in the colon may require larger doses of digitalis to achieve therapeutic serum concentrations?
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What is the mechanism through which digitalis glycosides produce a positive inotropic effect on the heart?
What is the mechanism through which digitalis glycosides produce a positive inotropic effect on the heart?
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Which drug reduces the elimination of cardiac glycosides or displaces digoxin from tissue-binding sites?
Which drug reduces the elimination of cardiac glycosides or displaces digoxin from tissue-binding sites?
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What is the antidote indicated for ingestion of greater than 10 mg digoxin by an adult?
What is the antidote indicated for ingestion of greater than 10 mg digoxin by an adult?
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What is the effect of gut flora metabolizing digoxin?
What is the effect of gut flora metabolizing digoxin?
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What is the half-life of digitoxin?
What is the half-life of digitoxin?
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What is the primary cause of accidental overdose in children?
What is the primary cause of accidental overdose in children?
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Study Notes
Digitalis Glycosides
- Digoxin is the most widely prescribed digitalis glycoside in the U.S.
- The potentially fatal concentration of digoxin in the blood is above 5 ng/mL.
- Absorption of digitalis glycosides occurs in the small intestine.
- The usual therapeutic range of digoxin in plasma concentration is 0.5-2 ng/mL.
- Digoxin has played a prominent role in the therapy of congestive heart failure and supraventricular rhythm disturbances.
- Around 20% of patients taking a digitalis preparation will experience toxicity.
Digitalis Glycoside Pharmacology
- Digitalis glycosides have less rapid and less complete absorption in the gastrointestinal tract, especially digitoxin.
- DGs bind to plasma proteins.
- The major route of elimination for digoxin is through the kidneys.
- The Eubacterium lentum microorganism in the colon may require larger doses of digitalis to achieve therapeutic serum concentrations.
Mechanism of Action
- Digitalis glycosides produce a positive inotropic effect on the heart by inhibiting the Na+/K+-ATPase pump.
- Quinidine reduces the elimination of cardiac glycosides or displaces digoxin from tissue-binding sites.
Toxicity and Treatment
- The antidote indicated for ingestion of greater than 10 mg digoxin by an adult is Digoxin Immune Fab (DIF).
- Gut flora metabolizing digoxin can reduce its efficacy.
- Accidental overdose in children is the primary cause of digitalis toxicity.
ACE Inhibitors
- ACE inhibitors inhibit the angiotensin-converting enzyme.
- The primary cause of both ACE inhibitor-induced angioedema and cough is bradykinin potentiation.
- Treatment for ACE inhibitor-induced angioedema involving the tongue, face, and oropharynx includes antihistamines and corticosteroids.
Beta Blockers
- The most common manifestation of beta blocker poisoning in patients with significant cardiovascular toxicity is bradycardia.
- In children who have been poisoned by beta blockers, hypoglycemia is more common.
- The suggested treatment for patients with mild or quickly resolving beta blocker-induced angioedema is antihistamines and corticosteroids.
- The first-line therapy for β-blocker intoxication is activated charcoal and atropine.
- Glucagon is used to treat β-blocker intoxication by increasing the force of contraction of the heart.
- Atropine helps in the management of β-blocker intoxication by counteracting the bradycardic effects.
Calcium Channel Antagonists
- The most common toxic effect caused by calcium channel antagonists, particularly the dihydropyridines, is hypotension.
- Dihydropyridines produce reflex increases in heart rate at therapeutic or moderate toxic doses.
- Severe overdoses of calcium channel antagonists can cause cardiac arrest.
- Calcium gluconate is a beneficial treatment for hypotension secondary to reduced systemic resistance and lowered cardiac output in calcium channel blocker overdose.
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Description
Test your knowledge of the treatment options for digitalis toxicity, including the administration of IV fluids, IV insulin, dextrose, sodium bicarbonate, oral ion-exchange resins, and specific treatments for digitalis-induced arrhythmias.
