ATI RN
Chapter 11 principles of pharmacology Questions
Question 1 of 5
You receive a call from a frantic mother whose 3-year-old son ate a handful of her amitriptyline (a weak acid). You instruct the mother to take her son to the emergency department where he is given bicarbonate (in addition to other measures). What is the most likely explanation for bicarbonate administration in this case?
Correct Answer: C
Rationale: Bicarbonate hastens amitriptyline elimination via ion trapping in urine (C). As a weak base (pKa ~9.4), amitriptyline is protonated (ionized) in alkaline urine (pH >8), reducing tubular reabsorption, speeding excretion in overdose. Option A is incorrect; acidification (ammonium chloride) suits bases, not acids here. Option B is false; trapping occurs in urine, not blood. Option D is wrong; no chemical inactivation occurs. This pH-dependent strategy, critical in TCA overdose, leverages Henderson-Hasselbalch to mitigate CNS/cardiac toxicity, a key toxicologic intervention.
Question 2 of 5
A 54-year-old man hurt his lower back while lifting his garage door a month ago. His pain has been somewhat lessened by taking naproxen almost daily for 3 weeks. He began to have epigastric pain with meals 3 days ago. Taking an extra dose of naproxen does not alleviate his epigastric pain. This unfortunate side effect is caused by naproxen inhibiting which enzyme?
Correct Answer: A
Rationale: Naproxen's epigastric pain results from COX-1 inhibition (A), reducing protective gastric prostaglandins, leading to mucosal damage (e.g., gastritis). COX-2 (B) targets inflammation, less GI impact. Lipoxygenase (C) and phospholipase Aâ‚‚ (D) aren't NSAID targets. Thromboxane synthase (original E) is downstream. COX-1's constitutive role, critical in GI protection, explains naproxen's common side effect, necessitating antacids or PPIs, a key consideration in chronic NSAID use.
Question 3 of 5
The following drugs are partial agonists:
Correct Answer: D
Rationale: Buprenorphine (D) is a partial agonist at μ-opioid receptors, producing submaximal analgesia with a ceiling effect, useful in addiction treatment. Isoprenaline (A) is a full $\beta$-agonist. Morphine (B) is a full opioid agonist. Flumazenil (C) is a benzodiazepine antagonist. Oxprenolol (original E) is a partial $\beta$-agonist, also correct but D is chosen. Partial agonists like buprenorphine balance efficacy and safety, limiting maximal response despite receptor occupancy, a key feature in opioid pharmacodynamics, contrasting full agonists in potency and overdose risk.
Question 4 of 5
In repeated (chronic or multiple) dosing:
Correct Answer: A
Rationale: If the dosing interval exceeds the half-life (A), minimal accumulation occurs (e.g., penicillin G, tâ‚/â‚‚ ~30 min, dosed q6h), as drug clears before the next dose. Option B is false; 50\% is ~1 half-life, 97\% is ~5. Option C is true (peak = 2 × trough at tâ‚/â‚‚ dosing). Option D is correct (loading speeds steady state). Option E (original) about gentamicin is true but specific. This principle, critical in chronic therapy, prevents toxicity, guiding interval selection.
Question 5 of 5
The following drugs are absorbed predominantly through active transport systems:
Correct Answer: C
Rationale: Levodopa (C) is absorbed via active transport (L-amino acid transporter) in the small intestine, critical for Parkinson's delivery. Paracetamol (A) and phenytoin (B) use passive diffusion. Methyldopa (D) also uses active transport, correct but C is chosen. Lithium (original E) is passive. Active transport, saturable and energy-dependent, enhances levodopa's uptake, a key pharmacokinetic feature, overcoming passive limitations.