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Quizzes > Health & Medicine > Diseases & Conditions

Test Your Knowledge: Digoxin Therapy & Digitalis Toxicity Quiz

Think you know digoxin toxicity treatment? Dive in and master digitalis toxicity symptoms now!

Difficulty: Moderate
2-5mins
Learning OutcomesCheat Sheet
Paper art illustration of heart, digoxin tablets and antidote quiz text on coral background

This digoxin quiz helps you confirm which medication reverses digitalis toxicity and recognize key symptoms and treatment steps. Quick questions cover dosing, interactions, and when to reach for the antidote. Use it to check gaps before an exam or shift, then review our cardiac meds guide or try another pharmacology quiz .

Which agent is the first-line antidote for severe digoxin toxicity?
Digoxin-specific antibody fragments (Digoxin Immune Fab)
Atropine
Calcium gluconate
Magnesium sulfate
Digoxin-specific antibody fragments (Digoxin Immune Fab) bind circulating digoxin, neutralizing its effects and allowing renal excretion. They are the treatment of choice for life-threatening toxicity such as severe arrhythmias or hyperkalemia.
What electrolyte disturbance commonly exacerbates digoxin toxicity?
Hypernatremia
Hypermagnesemia
Hyperkalemia
Hypocalcemia
Hyperkalemia often occurs in acute digoxin toxicity because digoxin inhibits the Na+/K+-ATPase pump, leading to extracellular potassium accumulation. High serum potassium also worsens toxicity and is an indication for antibody therapy.
Which of the following is NOT a typical sign of chronic digoxin toxicity?
Nausea and vomiting
Bradycardia
Hyperreflexia
Yellow-green vision changes
Chronic digoxin toxicity often presents with gastrointestinal symptoms, visual disturbances (xanthopsia), and bradyarrhythmias, but not hyperreflexia. Neuromuscular irritability is not characteristic of digoxin excess.
What is the mechanism of action of digoxin in the heart?
Blockade of L-type calcium channels
Inhibition of phosphodiesterase
Inhibition of Na+/K+-ATPase pump
Beta-1 adrenergic receptor blockade
Digoxin inhibits the Na+/K+-ATPase pump in cardiac myocytes, increasing intracellular sodium which indirectly increases calcium via the sodium-calcium exchanger, enhancing contractility.
Which organ plays the primary role in the elimination of digoxin?
Lungs
Kidney
Liver
Intestine
Digoxin is primarily excreted unchanged by the kidneys. Renal impairment thus increases digoxin half-life and risk of toxicity.
At what serum potassium level is digoxin toxicity most dangerous?
6.5 mEq/L
5.5 mEq/L
3.0 mEq/L
4.0 mEq/L
Serum potassium above 5.0 mEq/L in the setting of acute digoxin toxicity indicates severe poisoning and is an indication for digoxin-specific antibody therapy. Hyperkalemia reflects pump blockade and cellular potassium leakage.
Which ECG finding is most characteristic of digoxin effect (not toxicity)?
Scooped ST segments
Flattened T waves
Delta waves
Prolonged QT interval
A 'scooped' or 'hockey stick' ST depression is a classic sign of digoxin effect at therapeutic levels, not necessarily toxicity. It reflects altered repolarization currents.
Which of the following medications can increase digoxin levels by reducing its renal clearance?
Amiodarone
Rifampin
Spironolactone
Phenytoin
Amiodarone reduces digoxin clearance and displaces it from tissues, raising serum levels and risk of toxicity. Dosing adjustments of digoxin are recommended when starting amiodarone.
Which clinical scenario most strongly indicates the need for digoxin immune Fab?
Mild nausea and anorexia
Dry mouth and thirst
Chronic fatigue and blurred vision
Acute ventricular tachycardia with hyperkalemia
Life-threatening arrhythmias (e.g., VT) combined with hyperkalemia are clear indications for digoxin immune Fab to neutralize toxin rapidly. Less severe symptoms are managed supportively.
True or False: Activated charcoal is useful in acute digoxin overdose if given within 1 hour.
True
False
Activated charcoal can bind digoxin in the GI tract if administered early (within ~1 hour), reducing absorption. However, its utility is limited after that window.
Which symptom is more typical of acute rather than chronic toxicity?
Chronic GI upset
Visual halos
Gradual weight loss
Sudden-onset bradyarrhythmias
Acute digoxin toxicity often manifests with abrupt severe bradyarrhythmias and hyperkalemia, whereas chronic toxicity shows milder GI and visual symptoms.
What effect does hypomagnesemia have on digoxin toxicity risk?
No effect
Increases risk
Decreases risk
Only affects efficacy, not toxicity
Low magnesium levels sensitize the heart to digoxin, increasing the risk of arrhythmias. Hypomagnesemia should be corrected in toxicity management.
Which of the following is a contraindication to digoxin immune Fab therapy?
Cardiac arrest
Known hypersensitivity to ovine proteins
Hyperkalemia
Life-threatening arrhythmia
Digoxin immune Fab is derived from sheep (ovine). A known allergy to sheep proteins is a contraindication due to risk of anaphylaxis. Severe toxicity otherwise warrants its use.
Which drug interaction can decrease digoxin toxicity risk by increasing gut motility?
Clarithromycin
Amiodarone
Metoclopramide
Verapamil
Metoclopramide enhances gastrointestinal motility, reducing digoxin absorption and potentially lowering toxicity risk. Other listed drugs increase levels.
Which of these is NOT a known mechanism by which digoxin immune Fab reverses toxicity?
Binding free digoxin in plasma
Increasing hepatic metabolism of digoxin
Reducing tissue binding of digoxin
Forming Fab-digoxin complexes eliminated by kidneys
Digoxin immune Fab works by binding digoxin in the circulation, forming complexes excreted renally and decreasing tissue-receptor interaction. It does not increase hepatic metabolism.
In an elderly patient with renal impairment, which change to digoxin half-life is expected?
No change
Becomes less than 12 hours
Shortened from 36 to 24 hours
Extended from 36 to 48 - 72 hours
Renal impairment prolongs digoxin elimination, extending its half-life from ~36 hours to up to 48 - 72 hours, increasing toxicity risk. Dose adjustments and monitoring are essential.
Which laboratory finding distinguishes acute from chronic digoxin toxicity?
Serum digoxin level >2.0 ng/mL
Elevated bilirubin
Elevated BUN
Serum potassium >5.0 mEq/L
Hyperkalemia (>5.0 mEq/L) is more characteristic of acute digoxin overdose due to Na+/K+ pump blockade. Chronic toxicity usually shows normal or low potassium.
Which rhythm disturbance is an indication for urgent digoxin immune Fab despite normal potassium?
Sinus bradycardia
Mobitz I second-degree AV block
Atrial fibrillation with rapid ventricular response
Ventricular tachycardia
Ventricular tachycardia in digoxin toxicity is life-threatening and requires prompt Fab therapy, even if serum potassium is not elevated. Lower-degree blocks and AFib are managed supportively first.
After administration of digoxin immune Fab, which change is expected in serum total digoxin levels?
Become undetectable
Increase due to complexed digoxin
Remain unchanged
Decrease immediately
Total serum digoxin appears to rise post-Fab because assays detect both free and bound drug. Clinical improvement, not levels, guides further therapy.
Which condition may reduce the effectiveness of digoxin immune Fab therapy?
High digoxin volume of distribution
Metabolic alkalosis
Concurrent administration of activated charcoal
Hypokalemia
A large digoxin volume of distribution means more drug is tissue-bound, so Fab may not immediately neutralize all toxin, delaying effect. Plasma-bound digoxin is more readily neutralized.
Which of these is a documented adverse effect of digoxin immune Fab?
Pulmonary fibrosis
Severe hypotension
Rebound hyperkalemia
Hypokalemia
Digoxin Fab can precipitate hypokalemia and hypomagnesemia as digoxin is displaced intracellularly. Electrolytes must be monitored after infusion.
Which dosing metric best predicts the required dose of digoxin immune Fab?
Height of patient
Baseline serum creatinine
Patient weight alone
Total ingested dose of digoxin
Dose of Fab is calculated based on the estimated total body load of digoxin ingested or the serum digoxin concentration × volume of distribution. Weight alone is insufficient.
Which of these pharmacokinetic properties of digoxin contributes to risk of chronic toxicity?
High hepatic clearance
Low bioavailability
Rapid distribution half-life
Narrow therapeutic index
Digoxin's narrow therapeutic index means small changes in dose or clearance can lead to toxicity. Other properties are less contributory.
Which drug class is most likely to interact with digoxin by reducing its renal clearance?
Loop diuretics
Beta-agonists
ACE inhibitors
Statins
ACE inhibitors can decrease renal perfusion and GFR, reducing digoxin clearance and raising levels. Monitoring is warranted.
Which physiological state increases digoxin binding to Na+/K+-ATPase, heightening toxicity?
Hypoglycemia
Hypernatremia
Alkalemia
Acidemia
Acidic pH increases digoxin affinity for Na+/K+-ATPase, potentiating its effects and risk of toxicity. Correcting acidemia can mitigate this.
True or False: Fab fragments may cause rebound toxicity days after administration.
False
True
Rebound toxicity can occur as Fab-digoxin complexes dissociate or if tissue stores release digoxin. Patients require monitoring for up to a week.
Which marker best correlates with severity of acute digoxin poisoning?
Amount ingested
Baseline echocardiogram
Serum digoxin level alone
Time since last dose
Amount ingested is more predictive of acute toxicity severity than serum level measured soon after ingestion. Early levels may lag behind tissue distribution.
Which pharmacodynamic change occurs in chronic digoxin users that may delay recognition of toxicity?
Downregulation of beta-receptors
Increased P-glycoprotein activity
Upregulation of Na+/K+-ATPase
Enhanced hepatic metabolism
Chronic digoxin exposure can upregulate Na+/K+-ATPase receptors, requiring more drug for effect and masking early toxicity until doses accumulate.
Which genetic polymorphism may alter digoxin pharmacokinetics and affect toxicity risk?
CYP3A4*1B
CYP2D6 poor metabolizer
SLCO1B1 variants
ABCB1 (MDR1) variants
Polymorphisms in ABCB1, encoding P-glycoprotein, affect digoxin transport and clearance, altering serum levels and toxicity risk.
In renal failure, why might smaller, divided doses of Fab fragments be preferred?
To match slower renal elimination of complexes
To reduce immunogenicity
To avoid volume overload
To prevent rapid hypokalemia
In renal failure, Fab-digoxin complexes clear more slowly. Divided dosing prevents accumulation of immunocomplexes and associated adverse effects.
Which monitoring parameter requires adjustment after Fab administration?
Serum amylase
Serum digoxin assay for free drug
Liver function tests
Coagulation profile
Standard digoxin assays measure total drug (free + bound). Specialized assays or assays after Fab clearance are needed to measure free digoxin.
Which ion channel effect contributes to digoxin's arrhythmogenic potential?
Increased inward calcium current
Reduced sodium current
Enhanced funny current (If)
Enhanced transient outward K+ current
By increasing intracellular calcium, digoxin can trigger delayed afterdepolarizations and arrhythmias. This calcium overload is pro-arrhythmic.
Why is intravenous calcium administration controversial in digoxin toxicity with hyperkalemia?
May precipitate digoxin-induced arrhythmias
Leads to hypotension
Increases digoxin binding
Worsens hyperkalemia
Calcium can exacerbate digoxin-induced calcium overload and precipitate severe arrhythmias ('stone heart'). Current practice is cautious use only if life-threatening.
Which new investigational antidote is in development as an alternative to Fab fragments?
Synthetic ion exchanger resin
Monoclonal anti-digoxin antibody
Small-molecule Na+/K+-ATPase blocker
Recombinant P-glycoprotein enhancer
Monoclonal anti-digoxin antibodies are being studied to neutralize digoxin with potentially lower immunogenicity and more consistent supply than ovine Fab fragments.
Which clinical trial endpoint is most relevant when evaluating new digoxin antidotes?
Reduction in serum digoxin levels
Improvement in ejection fraction
Time to resolution of life-threatening arrhythmias
Decrease in hospitalization duration
The critical outcome in acute toxicity is resolution of life-threatening arrhythmias. While serum levels matter, clinical endpoints drive safety.
Which off-label use of digoxin immune Fab has been explored in severe poisoning by other cardiac glycosides?
Lily of the valley toxicity
Taxine alkaloid poisoning
Veratrum alkaloid poisoning
Aconite toxicity
Cases of severe toxicity from lily of the valley (contains digitalis-like compounds) have been treated successfully with digoxin Fab due to cross-reactivity.
True or False: Hemodialysis is effective for removing digoxin in severe toxicity.
True
False
Digoxin has a large volume of distribution and is highly tissue-bound, making hemodialysis ineffective for its removal. Fab fragments remain the treatment of choice.
Which electrolyte should be corrected first in severe digoxin toxicity?
Phosphate
Sodium
Magnesium
Calcium
Magnesium repletion helps stabilize cardiac membranes and suppress digoxin-induced arrhythmias. It should be corrected before or along with potassium.
Which advanced clearance technique has been trialed for digoxin removal when Fab is unavailable?
Lipid emulsion therapy
Continuous renal replacement therapy
High-flux hemofiltration
Hemoperfusion with activated charcoal
Intravenous lipid emulsion has been used anecdotally to 'trap' lipophilic drugs like digoxin and reduce free concentrations when Fab is unavailable. Evidence remains limited.
Which structural feature of digoxin allows it to be a substrate for P-glycoprotein?
Three sugar moieties
Ethylenic side chain
Unsaturated lactone ring
Steroid backbone
The trisaccharide sugar component of digoxin interacts with P-glycoprotein transporters, affecting absorption and excretion.
In a digoxin-poisoned patient with cardiogenic shock, which mechanical support might bridge until Fab effect?
Ventricular assist device
Impella device
ECMO
IABP (intra-aortic balloon pump)
IABP can improve coronary perfusion and reduce afterload in cardiogenic shock from digoxin toxicity, buying time for Fab to work. ECMO is less commonly used.
Which advanced imaging modality can help differentiate digoxin toxicity from myocardial ischemia?
Echocardiographic strain imaging
CT coronary angiography
Cardiac MRI with late gadolinium enhancement
Nuclear stress test
Cardiac MRI can demonstrate myocardial edema or fibrosis patterns distinct from ischemic injury. Digoxin toxicity may show diffuse changes rather than territorial infarction.
Which research direction holds promise for genetic prediction of digoxin response?
Serum proteomics
Whole-body metabolomics
MicroRNA profiling
Exosomal lipidomics
MicroRNA signatures may regulate P-glycoprotein expression and predict digoxin pharmacokinetics, offering personalized dosing and toxicity risk assessment.
True or False: Novel engineered sheep Fab with humanized Fc region reduces immunogenicity.
True
False
Humanized Fc regions on engineered Fab fragments decrease antibody formation and allergic reactions compared to purely ovine products. This is an area of active investigation.
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Study Outcomes

  1. Identify the Antidote -

    Recognize digoxin immune Fab as the primary medication that reverses digitalis toxicity and understand its clinical application.

  2. Recognize Toxicity Symptoms -

    List the common digitalis toxicity symptoms, including gastrointestinal, cardiac, and neurological signs, to support timely diagnosis.

  3. Explain Mechanisms of Action -

    Describe how digoxin immune Fab binds free digoxin molecules and facilitates safe elimination to neutralize toxicity.

  4. Differentiate Treatment Strategies -

    Compare the role of specific antidote medication versus supportive measures in the comprehensive management of digitalis toxicity.

  5. Apply Clinical Reasoning -

    Use quiz scenarios to select appropriate interventions for digoxin toxicity and reinforce decision-making skills in digoxin therapy treatment.

  6. Reinforce Digoxin Safety -

    Recall best practices for monitoring serum levels and adjusting dosage to prevent digitalis toxicity and optimize patient outcomes.

Cheat Sheet

  1. Mechanism of Digitalis Toxicity -

    Digoxin inhibits the Na+/K+ ATPase pump in cardiac myocytes, increasing intracellular calcium and enhancing contractility, but excess levels lead to arrhythmias and digitalis toxicity symptoms like nausea and blurred vision. Use the mnemonic "D-I-G" for Digoxin: D for Digestion upset, I for Inverted vision, and G for GI disturbances. Grasping this mechanism forms the basis for all digoxin toxicity treatment strategies.

  2. Clinical Presentation and Lab Monitoring -

    Early signs of toxicity include bradycardia, heart blocks, hyperkalemia and yellow halos around lights; these digitalis toxicity symptoms can escalate rapidly. Monitor serum digoxin levels (therapeutic range: 0.5 - 2.0 ng/mL) and electrolytes frequently, with levels drawn 6 - 8 hours post-dose for best accuracy. University guidelines stress vigilant lab checks to guide digoxin therapy adjustments.

  3. Primary Antidote: Digoxin Immune Fab -

    Digoxin immune Fab (Digibind, DigiFab) is the medication that reverses digitalis toxicity and is the gold standard digitalis antidote medication; it binds free digoxin molecules into complexes excreted renally. Calculate required vials using the formula: (serum digoxin concentration [ng/mL] × patient weight [kg]) / 100. Immediate administration of this antidote is key in severe digoxin toxicity treatment.

  4. Supportive Measures and Electrolyte Correction -

    In tandem with digoxin immune Fab, correct hyperkalemia with insulin and dextrose or sodium bicarbonate, and treat hypomagnesemia with IV magnesium sulfate; avoid calcium chloride to prevent paradoxical cardiac toxicity. These steps are critical components of comprehensive digoxin toxicity treatment and can stabilize patients until the antidote takes effect. Familiarize yourself with advanced cardiac life support guidelines for best outcomes.

  5. Preventing Recurrence and Patient Education -

    Educate patients on factors increasing toxicity risk, such as renal impairment, drug interactions (e.g., verapamil, amiodarone), and fluctuating electrolytes; stress adherence to prescribed digoxin doses and regular lab monitoring. Use the mnemonic "KEEP SAFE" (Kidney function, Electrolytes, Evaluate interactions, Patient adherence) to reinforce key points. Effective education reduces readmissions and ensures safer digoxin therapy.

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