ACTUAL EXAM WITH COMPLETE
QUESTIONS AND CORRECT DETAILED
ANSWERS (100% VERIFIED ANSWERS)
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Foundations of Prescribing & Pharmacokinetics/Pharmacodynamics (Questions 1-20)
1. Q: What are the four key components of the "Four P's" model for safe prescribing?
A: Patient, Preparation, Product, Prescription. It emphasizes a systematic approach to minimize
errors.
2. Q: A drug with a high hepatic extraction ratio will primarily be affected by changes in
what physiological parameter?
A: Hepatic blood flow. Drugs with high extraction are flow-dependent; reduced blood flow (e.g.,
heart failure) significantly decreases clearance.
3. Q: What does a narrow therapeutic index (NTI) signify, and name two classic NTI drugs.
A: It signifies a small difference between the effective dose and the toxic dose, requiring close
monitoring. Examples: Warfarin, Digoxin, Lithium, Phenytoin, Levothyroxine.
4. Q: Describe the primary clinical implication of a drug being a potent CYP3A4 inhibitor.
A: It can significantly increase the plasma levels of other drugs metabolized by the CYP3A4
pathway, leading to toxicity. Example: Ketoconazole inhibiting metabolism of simvastatin,
causing rhabdomyolysis risk.
5. Q: What is the "first-pass effect"?
A: The metabolism of an orally administered drug by the liver and intestinal wall before it
reaches systemic circulation, often reducing its bioavailability.
6. Q: How does protein binding affect drug dynamics?
A: Only the unbound (free) drug is pharmacologically active. Conditions like hypoalbuminemia
can increase free drug levels, raising the risk of toxicity even with normal total drug doses.
, 7. Q: What is the Beers Criteria?
A: A list of potentially inappropriate medications for older adults due to high risk of adverse
effects, drug-disease interactions, or limited efficacy in this population.
8. Q: Define "stepped care" in pharmacotherapy.
A: A treatment approach starting with safer, first-line agents and escalating to more potent or
risky drugs only if treatment goals are not met (e.g., hypertension: start with ACEi/ARB or
thiazide, then add CCB).
9. Q: What is the primary goal of Phase IV (Post-Marketing Surveillance) clinical trials?
A: To monitor a drug's long-term safety, efficacy, and rare adverse effects in a larger, more
diverse population under real-world conditions.
10. Q: A patient with renal impairment requires a dose adjustment for a drug that is
primarily renally excreted. What two pharmacokinetic parameters are most critical to
consider?
A: Creatinine Clearance (CrCl) and the drug's elimination half-life.
11. Q: What is the difference between a side effect and an adverse drug reaction (ADR)?
A: A side effect is a known, often predictable, and usually mild effect (e.g., dry mouth from
antihistamines). An ADR is any harmful, unintended reaction to a drug, which can be
unpredictable and severe.
12. Q: Explain the concept of "tolerance" as it relates to pharmacology.
A: A diminished response to a drug over time, requiring increased doses to achieve the same
effect (common with opioids, nitrates, benzodiazepines).
13. Q: What does "black box warning" (BBW) mean?
A: The strictest FDA-required warning on a drug's labeling, indicating a significant risk of serious
or life-threatening adverse effects.
14. Q: Why is creatinine clearance (CrCl) a better indicator of renal function for dosing
than serum creatinine alone?
A: CrCl accounts for age, weight, and gender, providing a more accurate estimate of glomerular
filtration rate (GFR), especially in elderly or malnourished patients.
15. Q: What is the role of P-glycoprotein (P-gp) in drug interactions?
A: P-gp is an efflux transporter that pumps drugs out of cells. Inhibitors (e.g., verapamil,
quinidine) can increase absorption and bioavailability of P-gp substrates (e.g., digoxin).
, 16. Q: Define "bioequivalence."
A: When a generic drug has the same rate and extent of absorption (bioavailability) as its brand-
name counterpart, allowing for therapeutic substitution.
17. Q: In pediatrics, why is drug dosing often based on body surface area (BSA)?
A: BSA correlates better with metabolic processes and organ size (like hepatic and renal
function) than weight or age alone, leading to more accurate dosing.
18. Q: What is a "prodrug"? Provide an example.
A: An inactive compound that must be metabolized in the body to become active. Example:
Codeine (prodrug) is metabolized to morphine (active drug) via CYP2D6.
19. Q: What does a low volume of distribution (Vd) indicate about a drug?
A: The drug is largely confined to the plasma and has poor tissue penetration (e.g., highly
protein-bound drugs like warfarin).
20. Q: What is the significance of a drug's half-life in determining dosing interval?
A: Dosing intervals are typically set at one half-life to maintain steady-state concentrations with
minimal fluctuation. For drugs with long half-lives (e.g., fluoxetine), once-daily or less frequent
dosing is possible.
Cardiovascular & Renal Pharmacology (Questions 21-35)
21. Q: What is the first-line drug class for uncomplicated hypertension in most patients,
according to JNC-8?
A: Thiazide diuretics, ACE inhibitors (ACEIs), Angiotensin II Receptor Blockers (ARBs), or Calcium
Channel Blockers (CCBs).
22. Q: Why must pregnancy be ruled out before starting a woman on an ACE inhibitor or
ARB?
A: These drugs are teratogenic (Pregnancy Category D) and can cause fetal injury, including skull
hypoplasia, renal failure, oligohydramnios, and death, especially in the 2nd and 3rd trimesters.
23. Q: What is the most critical monitoring parameter when initiating amiodarone?
A: Regular pulmonary function monitoring (e.g., chest X-ray, PFTs) and thyroid function tests due
to risks of pulmonary toxicity and thyroid dysfunction.
24. Q: A patient on metoprolol presents with dizziness and a heart rate of 48 bpm. What is
the immediate action?
, A: Withhold the next dose of metoprolol, assess blood pressure and symptoms, and evaluate for
other causes of bradycardia.
25. Q: What is the mechanism of action and primary use of spironolactone?
A: It is a potassium-sparing diuretic and aldosterone antagonist. Used for heart failure (reduces
mortality), hypertension, and conditions like ascites or hypokalemia.
26. Q: Why is a "statin" drug typically dosed at night?
A: Because the body synthesizes most cholesterol at night, and older statins (like simvastatin,
lovastatin) with short half-lives are more effective with evening dosing.
27. Q: What is the antidote for heparin overdose?
A: Protamine sulfate (1 mg neutralizes ~100 units of heparin).
28. Q: What is the antidote for warfarin overdose in a bleeding patient?
A: For acute reversal: Prothrombin Complex Concentrate (PCC) or Fresh Frozen Plasma (FFP) for
immediate effect, supplemented with Vitamin K for sustained reversal.
29. Q: What is the "6 P's" mnemonic for signs of statin-induced myopathy?
A: Pain, Power loss (weakness), Peripheral neuropathy, Paresthesias, Pee color change (dark
urine from myoglobinuria), Profile elevation (elevated CK).
30. Q: What electrolyte abnormality is a major concern with loop diuretics like
furosemide?
A: Hypokalemia. Also hypomagnesemia, hypocalcemia, and hypochloremic metabolic alkalosis.
31. Q: What is the key difference between "rhythm control" and "rate control" strategies
in atrial fibrillation?
A: Rhythm control aims to restore and maintain normal sinus rhythm (using antiarrhythmics like
amiodarone, flecainide). Rate control aims to simply control ventricular response rate (using
beta-blockers, non-DHP CCBs like diltiazem) without correcting the underlying rhythm.
32. Q: Why is clopidogrel sometimes ineffective (a phenomenon called "clopidogrel
resistance")?
A: Often due to genetic polymorphisms in the CYP2C19 enzyme required to activate the
prodrug. Poor metabolizers have reduced antiplatelet effect.
33. Q: Name the preferred beta-blocker for a patient with heart failure with reduced
ejection fraction (HFrEF).
A: Carvedilol, metoprolol succinate (Toprol-XL), or bisoprolol. These are proven to reduce
mortality in HFrEF.