Top 10 Drug interactions in long tern care facilities

Summarized by: Dr.S.Gunasakaran,MBBS,MD

Warfarin — NSAIDs*
Potential for serious gastrointestinal bleeding.
NSAIDs increase gastric irritation and erosion of the protective lining of the stomach, assisting in the formation of a GI bleed. Additionally, NSAIDs decrease the cohesive properties of platelets necessary in clot formation.

Warfarin — Sulfa drugs
Increased effects of warfarin, with potential for bleeding.
Currently, the mechanism for interaction with sulfa drugs is unknown; however, clinicians hypothesize that warfarin’s activity is prolonged due to a decreased production of vitamin K by intestinal flora affected by systemic antibiotic administration.

Warfarin — Macrolides
Increased effects of warfarin, with potential for bleeding.
Erythromycin inhibits the metabolism and subsequent clearance of warfarin from the body. The activity of warfarin may also be prolonged due to alterations in the intestinal flora and its production of vitamin K for clotting factor production.

Warfarin — Quinolones**
Increased effects of warfarin, with potential for bleeding.
The exact mechanism for the warfarin-quinolone drug interaction is unknown. Reduction of intestinal flora responsible for vitamin K production by antibiotics is probable as well as decreased metabolism and clearance of warfarin.

Warfarin — Phenytoin
Increased effects of warfarin and/or phenytoin.
Currently unknown, but one theory suggests a genetic basis involving liver metabolism of warfarin and phenytoin.

ACE inhibitors — Potassium supplements
Elevated serum potassium (hyperkalemia.
Inhibition of ACE results in decreased aldosterone production and potentially decreased potassium excretion.

ACE inhibitors — Spironolactone
Elevated serum potassium levels.
Unknown, possibly an additive effect. (Spironolactone being a potassium sparing diuretic, hence additive effect)

Digoxin — Amiodarone
Digoxin toxicity.
Multiple theories exist, but actual mechanism is unknown. Amiodarone may decrease the clearance of digoxin, resulting in prolonged digoxin activity. There may also be an additive effect on the sinus node of the heart.

Digoxin — Verapamil
Digoxin toxicity.
Synergistic effect of slowing impulse conduction and muscle contractility, leading to bradycardia and possible heart block.

Theophylline — Quinolones**
Theophylline toxicity.
Inhibition of hepatic metabolism of theophylline by the quinolones.

* NSAID class does not include COX-2 inhibitors
** Quinolones that interact include: ciprofloxacin, enoxacin, norfloxacin, and ofloxacin


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