Ethanol alters the metabolism of warfarin. Two types of ethanol abuse are chronic ethanol abuse and binge ethanol drinking. How do these types of ethanol use alter warfarin metabolism? Chronic ethanol use _____ and binge ethanol drinking _____.
c. Increases warfarin metabolism, decreases warfarin metabolism. Chronic ethanol consumption can lead to increased hepatic metabolism of many medications that are cleared through the liver. Increased hepatic metabolism is related to enhanced enzyme function. Therefore, chronic ethanol users typically need higher-than-usual doses of warfarin to achieve therapeutic INRs. Acute ingestion of large amounts of ethanol at a time may inhibit warfarin metabolism. This may lead to elevated INRs and increase the risk of hemorrhagic complications. Moderate ingestion of ethanol does not seem to affect the metabolism of warfarin.
Which of the following drugs can significantly increase digoxin concentrations?
a. Amiodarone. Amiodarone significantly increases the levels of digoxin. Amiodarone decreases the clearance of digoxin and inhibits p-glycoprotein. Amiodarone can increase digoxin levels by 50% to 70%. This interaction can occur in the first days of therapy and a 50% dosage reduction is required immediately. Metoprolol does not increase the levels of digoxin; however, it can have synergistic effects on lowering heart rate and should be monitored closely. Simvastatin and fenofibrate do not alter the levels of digoxin.
Which of the following statements is true with regard to ACE inhibitors?
c. Sodium depletion is an important factor in the development of renal insufficiency associated with ACE inhibitors. Patients with hyponatremia, dehydration, and severe HF are most dependent on the maintenance of renal perfusion by angiotensin II–mediated vasoconstriction of the efferent arteriole. Prevention of hyponatremia by decreasing diuretics can reduce such risk. Numerous studies, including the Studies of Left Ventricular Dysfunction (SOLVD) treatment trial, Veterans’ Administration Heart Failure Trial (V-HeFT) II, and Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS), have shown ACE inhibitors to reduce mortality in patients with ischemic and nonischemic cardiomyopathy and mild-to-moderate HF. ACE inhibitors are considered to be associated with a class benefit; however, not all ACE inhibitors carry the FDA indication for HF. The ACE inhibitors that are approved for the treatment of HF include captopril, enalapril, lisinopril, quinapril, fosinopril, and ramipril. In 1998, the Assessment of Treatment with Lisinopril and Survival (ATLAS) trial showed that high doses of lisinopril were superior to low doses in decreasing risk of death or hospitalization. Therefore, an effort to use target doses used in clinical trials is important (e.g., captopril 50 mg thrice daily, enalapril 10 mg twice daily, and lisinopril 20 mg daily). Potassium retention of ACE inhibitors is caused by a reduction in the feedback of angiotensin II to stimulate aldosterone release. Caution is necessary when initiating a potassium supplement in a patient on ACE inhibitor therapy.
Match the properties with the associated β-blocking agents.
c. (1) ii; (2) iii; (3) i; (4) iv. Agents exhibiting α-blockade include labetalol and carvedilol. Agents with ISA are pindolol, penbutolol, carteolol, and acebutolol. Agents with membrane-stabilizing activity are propranolol, labetalol, and acebutolol. β1 -Selective agents include bisoprolol, betaxolol, atenolol, acebutolol, and metoprolol.
By which of the following mechanisms do diltiazem and verapamil slow ventricular rate in patients with AFib?
a. Diltiazem and verapamil decrease conduction velocity within the AV node and increase refractory period of nodal tissue. This then causes slowing of ventricular rate.
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