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Chapter 11 principles of pharmacology Questions
Question 1 of 5
A researcher is studying the bioavailability of commonly used antimuscarinics to treat irritable bowel syndrome. Medication A is administered in a $100 \mathrm{mg}$ daily dose orally and $60 \mathrm{mg}$ of the drug is absorbed from the gastrointestinal tract unchanged. Thus, the bioavailability of Medication A is
Correct Answer: B
Rationale: The bioavailability of Medication A is $60\%$ (B). Bioavailability (F) = (Amount absorbed unchanged / Dose) × 100 = (60 mg / 100 mg) × 100 = $60\%$. Options A (50\%), C (70\%), D (80\%), and E (90\%, original) miscalculate. This reflects the fraction reaching systemic circulation intact (e.g., avoiding first-pass metabolism), typical for antimuscarinics (e.g., hyoscyamine), guiding dosing for IBS, where GI absorption and hepatic metabolism determine efficacy, a key pharmacokinetic metric.
Question 2 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 3 of 5
A 24-year-old primigravid female's water breaks at 39 weeks gestation. Twenty-four hours later, she is having regular contractions 3 min apart. Her labor lasts $8 \mathrm{~h}$. At the hospital, she gives birth to a baby boy, who initially appeared healthy. Within the next $12 \mathrm{~h}$, the baby boy begins to have temperature fluctuations, difficulty breathing, and reduced movements. You suspect neonatal sepsis, so IV gentamicin plus ampicillin is started. Gentamicin and ampicillin are commonly used together because the combined effect is greater than the additive effects of both alone. This increased effectiveness is an example of what principle?
Correct Answer: D
Rationale: Synergy (D) describes gentamicin and ampicillin's combined effect exceeding their additive sum in neonatal sepsis. Gentamicin (aminoglycoside) disrupts protein synthesis, enhancing ampicillin's (beta-lactam) cell wall inhibition, improving bactericidal action against pathogens (e.g., E. coli). Agonism (A) is receptor activation. Anergy (B) is immune unresponsiveness. Symbiosis (C) is ecological. Synergy, critical in infections, leverages complementary mechanisms, reducing resistance and improving outcomes, a key antibiotic strategy.
Question 4 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 5 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.