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Increase in glyburide dose as amitriptyline is hepatically cleared
11%
3/28
Recent NSAID use as amitriptyline is renally cleared
4%
1/28
Increase in glyburide dose as digoxin is hepatically cleared
7%
2/28
Increase in glyburide dose as digoxin is renally cleared
21%
6/28
Recent NSAID use as digoxin is renally cleared
57%
16/28
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This patient presents with blurry vision, diarrhea, and premature ventricular complexes (PVCs) on EKG, which are classic findings for chronic digoxin toxicity. The patient's recent NSAID use likely caused a fall in renal clearance and a buildup of digoxin. In addition to blurry vision (including changes in color vision) and gastrointestinal distress, digoxin toxicity can cause many cardiac arrhythmias ranging from premature ventricular contractions to bradycardia, atrial tachyarrhythmias with AV block, and ventricular arrhythmias. Other EKG changes include increased PR intervals, decreased QT intervals, ST segment scooping, and T wave inversions. Heart failure patients are at additional risk for digoxin toxicity because furosemide can cause a slight hypokalemia (which this patient has) that makes patients more susceptible to digoxin toxicity. Because digoxin is predominantly excreted by the kidneys, acute kidney injury or chronic renal failure may also lead to chronic digoxin toxicity in these patients. Figure A demonstrates premature ventricular complexes, the most common EKG abnormality seen in digoxin toxicity. Incorrect Answers: Answers 1-2: The toxidrome of an anticholinergic medications such as amitriptyline would present as constipation rather than diarrhea. Other common features of TCA overdose include tachycardia, hyperthermia, sedation or confusion, dilated pupils, dry mouth, nausea and vomiting, and urinary retention. Classic findings on electrocardiogram include prolongation of the QRS, abnormal morphology of the QRS, R' wave in AVR, and AV block or bundle branch blocks. Treatment is sodium bicarbonate. Answer 3: Digoxin is predominantly excreted by the kidneys. In addition, glyburide is a sulfonylurea and a CYP450 inducer. Increasing the dose of a CYP450 inducer would lead to sub-therapeutic levels of drugs metabolized by the CYP450 system rather than supra-therapeutic. Answer 4: Digoxin is not primarily metabolized through the CYP450 system. In addition, because glyburide is a CYP450 inducer, increasing the dose of glyburide would lead to a sub-therapeutic level of digoxin rather than supra-therapeutic. Bullet Summary: Chronic digoxin toxicity is characterized by blurry vision, gastrointestinal symptoms, and life-threatening cardiac arrhythmias. Because digoxin is primarily excreted by the kidneys, digoxin toxicity may be precipitated by acute kidney injury or renal failure. Patients with heart failure, particularly those on loop diuretics like furosemide, are at particular risk because the hypokalemia caused by the furosemide predisposes to digoxin toxicity.
4.7
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