Pharmacology Flashcards

A patient in the ICU is receiving vancomycin infusion and suddenly develops diffuse erythema, flushing, and hypotension without urticaria or bronchospasm. Which mechanism best explains this reaction, and what is the correct initial nursing action per SCFHS medication safety guidelines?

Answer: Red Man Syndrome (complement-independent mast cell degranulation) — slow the infusion rate and administer IV diphenhydramine

Red Man Syndrome is a rate-dependent, non-immune-mediated reaction caused by direct mast cell degranulation from rapid vancomycin infusion. It presents with flushing, erythema, and hypotension — but notably WITHOUT urticaria or bronchospasm (distinguishing it from true anaphylaxis). The correct intervention is to slow the infusion rate (minimum 60 minutes for 1g, ideally 90 minutes) and administer an antihistamine. Pre-medication with diphenhydramine before subsequent doses is recommended by Saudi MOH pharmacy protocols.

A 68-year-old Saudi male with chronic kidney disease (CrCl 22 mL/min) is prescribed metformin 1000 mg twice daily by a new resident for Type 2 diabetes. As the primary nurse, your priority concern regarding this prescription is:

Answer: Lactic acidosis risk, because metformin accumulates in renal impairment and inhibits hepatic lactate clearance

Metformin is contraindicated when CrCl < 30 mL/min (Saudi MOH and SFDA guidelines align with international standards). In renal impairment, metformin accumulates because it is renally cleared. This leads to mitochondrial inhibition of Complex I, reducing hepatic gluconeogenesis from lactate and causing life-threatening lactic acidosis. Metformin does not stimulate insulin secretion (it's not a secretagogue), does not cause hyperkalemia, and has no QT effect. The nurse must flag this as a critical prescribing error and withhold the dose pending physician review.

A patient is receiving heparin infusion for DVT treatment. The aPTT result comes back at 210 seconds (therapeutic range 60–100 seconds). The patient has no active bleeding. According to standard weight-based heparin nomogram protocols used in Saudi hospitals, the nurse should:

Answer: Stop the infusion for 1 hour, then reduce the rate by 3 units/kg/hour and recheck aPTT in 6 hours

When aPTT exceeds 2× the upper therapeutic limit (>200 seconds per most protocols) without bleeding, the standard weight-based heparin nomogram directs nurses to hold the infusion for 1 hour, reduce the rate by 3 units/kg/hour, and recheck aPTT in 6 hours. Protamine sulfate is reserved for active, life-threatening bleeding — not supratherapeutic values alone. Continuing unchanged is unsafe. A 50% rate reduction without holding may be used for lesser aPTT elevations but is not the protocol for values >200 seconds.

A nurse is preparing to administer digoxin 0.125 mg IV to a patient with atrial fibrillation and heart failure. Pre-administration assessment reveals: HR 58 bpm, serum potassium 3.1 mEq/L, serum digoxin level 1.8 ng/mL (therapeutic range 0.5–2.0 ng/mL). What is the most critical action before giving the dose?

Answer: Withhold digoxin and notify the physician — hypokalemia potentiates digoxin toxicity even within the therapeutic serum range

This is a high-stakes pharmacology concept: hypokalemia dramatically increases myocardial sensitivity to digoxin by competing at the Na⁺/K⁺-ATPase pump. A serum digoxin level of 1.8 ng/mL is 'therapeutic' in normokalemia, but becomes effectively toxic when K⁺ is 3.1 mEq/L. Saudi critical care and cardiac nursing protocols require that both hypokalemia (K⁺ < 3.5 mEq/L) and hypomagnesemia be corrected before administering digoxin. A bradycardic HR of 58 alone might warrant holding, but the electrolyte imbalance is the priority concern that must be escalated — the serum level alone does NOT confirm safety.

A patient receiving gentamicin (aminoglycoside) therapy develops tinnitus and a sensation of fullness in the ears on day 6 of treatment. Current trough level is 1.8 mcg/mL (acceptable: <2 mcg/mL) and renal function is normal. The most appropriate nursing response is:

Answer: Report findings immediately and advocate for audiometric evaluation — ototoxicity may precede measurable serum-level changes

Aminoglycoside-induced ototoxicity is insidious and can occur BEFORE trough levels become supratherapeutic. Gentamicin concentrates in the endolymph of the cochlea and vestibule, where it persists far longer than in plasma. Tinnitus and aural fullness are early cochleotoxicity warning signs. SCFHS pharmacology standards and Saudi MOH aminoglycoside stewardship protocols require immediate reporting and formal audiometric assessment. Continuing treatment despite these symptoms risks irreversible sensorineural hearing loss. Fluid intake and N-acetylcysteine do not address cochlear toxicity.

A 54-year-old female is prescribed warfarin for mechanical heart valve anticoagulation (target INR 2.5–3.5). She reports she has been regularly consuming large amounts of waraq al-khadra (dark leafy greens including spinach and parsley) as part of a Ramadan diet. Her INR today is 1.6. The pharmacokinetic explanation for this finding, and the most appropriate intervention, is:

Answer: Dietary vitamin K1 in leafy greens competes with warfarin at VKORC1, increasing clotting factor synthesis — adjust warfarin dose upward and counsel on consistent dietary intake

Warfarin acts by inhibiting Vitamin K epoxide reductase complex 1 (VKORC1), blocking recycling of vitamin K and thereby reducing synthesis of clotting factors II, VII, IX, and X. High dietary vitamin K1 (phylloquinone) intake from leafy greens directly counteracts this mechanism by saturating VKORC1 and increasing active vitamin K availability. The INR of 1.6 is below target for a mechanical valve (high thrombosis risk). The correct action is upward warfarin dose adjustment AND consistent dietary counseling — the patient should maintain consistent (not eliminate) leafy green intake, as fluctuation causes INR instability. CYP2C9 induction and GI binding are incorrect mechanisms.