MIDTERM REVIEW 2026/2027 | Latest Chamberlain College
Guide | Pass Guaranteed - A+ Graded
Part 1: Pharmacokinetics, Pharmacodynamics & Prescribing Principles
(Questions 1-18)
Q1: A 68-year-old patient with chronic kidney disease (eGFR 35 mL/min) is prescribed
metformin 1000mg twice daily for newly diagnosed type 2 diabetes. What is the primary
pharmacokinetic concern with this prescribing decision?
A. Metformin is primarily hepatically metabolized and will accumulate in liver disease
B. Metformin is renally excreted unchanged and requires dose reduction in CKD stage
3b
C. Metformin has a narrow therapeutic index and needs therapeutic drug monitoring
D. Metformin undergoes extensive first-pass metabolism and bioavailability increases in
CKD
Correct Answer: B [CORRECT]
Rationale: Metformin is eliminated renally without metabolism; in CKD stage 3b (eGFR
30-44), the FDA recommends avoiding starting metformin or using reduced doses with
caution due to accumulation risk and lactic acidosis. Option A is wrong because
metformin undergoes minimal hepatic metabolism. Option C is incorrect as metformin
has a wide therapeutic index. Option D is wrong because metformin has minimal
first-pass metabolism.
,Q2: Which cytochrome P450 enzyme is responsible for metabolizing approximately 50%
of all clinically used drugs and is the site of many significant drug-drug interactions?
A. CYP2C19
B. CYP2D6
C. CYP3A4
D. CYP1A2
Correct Answer: C [CORRECT]
Rationale: CYP3A4 is the most abundant hepatic CYP enzyme and metabolizes about
50% of marketed drugs. Strong inhibitors (ketoconazole, clarithromycin) and inducers
(rifampin, carbamazepine) of CYP3A4 cause many clinically significant interactions.
While CYP2C19, CYP2D6, and CYP1A2 are important, none match CYP3A4's metabolic
breadth.
Q3: A patient on warfarin (INR stable at 2.5) is started on TMP-SMX for a UTI. Five days
later, INR is 4.8. What is the mechanism behind this interaction?
A. TMP-SMX inhibits CYP2C9, reducing warfarin metabolism
B. TMP-SMX induces CYP1A2, increasing warfarin clearance
C. TMP-SMX displaces warfarin from albumin binding sites
D. TMP-SMX inhibits vitamin K absorption from the gut
Correct Answer: A [CORRECT]
,Rationale: TMP-SMX is a potent inhibitor of CYP2C9, the primary enzyme metabolizing
S-warfarin (the more potent isomer). This inhibition reduces warfarin clearance,
increasing INR. Option C describes a minor acute effect; albumin displacement is
transient. Option B is wrong (induction would lower INR). Option D is incorrect as
TMP-SMX doesn't affect vitamin K absorption.
Q4: When prescribing for a 78-year-old patient with multiple comorbidities, which
pharmacokinetic change of aging most consistently requires dose reduction across
drug classes?
A. Increased gastric pH affecting drug absorption
B. Decreased hepatic blood flow and phase I metabolism
C. Increased body fat percentage altering distribution
D. Decreased glomerular filtration rate
Correct Answer: D [CORRECT]
Rationale: Renal function declines approximately 1% per year after age 40; by age 80,
average GFR is 60-70 mL/min even with normal serum creatinine. This affects
elimination of many drugs (metformin, gabapentin, digoxin, low molecular weight
heparins) and consistently requires dose adjustment. While B and C occur, renal
impairment is most predictable and clinically significant.
Q5: A patient asks why they must take levothyroxine on an empty stomach, 30-60
minutes before breakfast. What is the primary pharmacokinetic rationale?
A. Food increases gastric acid destruction of the hormone
, B. Food decreases absorption by 40-50% through binding and delayed gastric emptying
C. Food induces CYP3A4 metabolism of levothyroxine in the gut wall
D. Food increases first-pass hepatic extraction of the drug
Correct Answer: B [CORRECT]
Rationale: Food, especially fiber, soy, and coffee, significantly reduces levothyroxine
bioavailability (by 40-50%) through physical binding and delayed gastric emptying.
Consistent administration timing ensures stable TSH levels. Options A, C, and D
describe mechanisms not relevant to levothyroxine pharmacokinetics.
Q6: Which pharmacodynamic concept explains why a patient on chronic beta-blocker
therapy for hypertension must taper the dose rather than stop abruptly?
A. Receptor upregulation and supersensitivity following chronic antagonism
B. Enzyme induction increasing drug metabolism over time
C. Accumulation of active metabolites with prolonged use
D. Development of IgE-mediated hypersensitivity with chronic exposure
Correct Answer: A [CORRECT]
Rationale: Chronic beta-blockade causes upregulation (increased density) of
beta-adrenergic receptors. Abrupt discontinuation leaves these supersensitive receptors
exposed to endogenous catecholamines, causing rebound hypertension, tachycardia,
and angina. This is a pharmacodynamic rebound phenomenon, not pharmacokinetic
tolerance or allergy.