FPGEE Exam Flashcards
7 cards from real FPGEE practice questions. Tap to flip, then mark Knew It or Still Learning — missed cards come back until you master them.
Read the first 7 FPGEE Exam flashcards as text
A patient develops signs of serotonin syndrome after being prescribed linezolid while already on sertraline. Which symptom BEST distinguishes serotonin syndrome from neuroleptic malignant syndrome?
Answer: Hyperreflexia and clonus
Hyperreflexia and clonus are hallmark features of serotonin syndrome and are generally absent in neuroleptic malignant syndrome, which features lead-pipe rigidity instead.
Which class of antihypertensives is CONTRAINDICATED in bilateral renal artery stenosis?
Answer: ACE inhibitors
ACE inhibitors (and ARBs) block angiotensin II-mediated efferent arteriolar constriction, which is the compensatory mechanism maintaining GFR in bilateral renal artery stenosis, leading to acute kidney injury.
A drug has a half-life of 8 hours. How long will it take to reach approximately 94% of steady-state concentration with regular dosing?
Answer: 32 hours
It takes approximately 4 half-lives to reach ~94% of steady state; 4 × 8 hours = 32 hours.
Which antiepileptic drug works primarily by blocking voltage-gated sodium channels and is first-line for focal seizures?
Answer: Carbamazepine
Carbamazepine blocks voltage-gated sodium channels, stabilizing neuronal membranes, and is a first-line agent for focal (partial) seizures.
A compounding pharmacist needs to prepare an isotonic solution. What is the approximate freezing point depression of normal saline (0.9% NaCl)?
Answer: -0.52°C
Normal saline (0.9% NaCl) has a freezing point depression of -0.52°C, which equals the freezing point depression of blood, making it isotonic.
Which metabolic pathway is PRIMARILY responsible for phase II conjugation of acetaminophen under normal dosing conditions?
Answer: Glucuronidation and sulfation
Under therapeutic doses, acetaminophen is primarily metabolized by glucuronidation (~55%) and sulfation (~30%); CYP2E1-mediated oxidation to NAPQI becomes significant only in overdose when conjugation pathways are saturated.
What is the primary mechanism by which aminoglycosides cause nephrotoxicity?
Answer: Accumulation in proximal tubular cells causing cellular damage
Aminoglycosides accumulate in proximal tubular epithelial cells through endocytosis, causing mitochondrial dysfunction, oxidative stress, and tubular necrosis.