Free practice final
Pharmacology practice final (free, with answers)
An intro pharmacology final usually covers pharmacokinetics (how the body absorbs, distributes, and eliminates a drug), pharmacodynamics (how a drug acts on its target), autonomic drugs, and the mechanisms and key adverse effects of the major drug classes. These 15 questions include the half-life and therapeutic index calculations that often appear. Try each question yourself before opening the answer, then use the explanation to link the drug's mechanism to its effects.
For exam practice only, not clinical advice. Drug and treatment decisions belong to licensed clinicians and current references.
Topics
- Pharmacokinetics
- Pharmacodynamics
- Autonomic Drugs
- Cardiovascular Drugs
- Anticoagulants
- Opioids and NSAIDs
- Antibiotics
15 questions
Try each one before you open its answer.
1. Nitroglycerin for acute angina is given as a sublingual tablet or spray rather than as a tablet to swallow. What is the main pharmacokinetic reason?
- A A swallowed dose would be absorbed into the portal circulation and largely inactivated by the liver before reaching the systemic circulation
- B The sublingual route gives a longer duration of action than a swallowed tablet
- C Nitroglycerin is too water-soluble to be absorbed from the intestine
- D Stomach acid converts nitroglycerin into a toxic metabolite
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Answer: A. A swallowed dose would be absorbed into the portal circulation and largely inactivated by the liver before reaching the systemic circulation
Drug absorbed from the intestine travels in the portal vein to the liver before reaching the rest of the body, and nitroglycerin is metabolized there so extensively that little of a swallowed dose would survive (a large first-pass effect). Veins under the tongue drain directly into the systemic circulation, bypassing the liver and giving a rapid onset.
2. Drug A and Drug B are agonists at the same receptor. Drug A can produce a maximal response of 100%, and 10 mg produces half of that maximum. Drug B can produce a maximal response of only 60%, and 1 mg produces half of its maximum. Which statement is correct?
- A Drug A is both more potent and more efficacious
- B Drug A is more potent, but Drug B is more efficacious
- C Drug B is both more potent and more efficacious
- D Drug B is more potent, but Drug A is more efficacious
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Answer: D. Drug B is more potent, but Drug A is more efficacious
Potency is about how much drug is needed for an effect, so Drug B, which needs a smaller dose for a half-maximal response, is more potent. Efficacy is the maximal effect a drug can produce, so Drug A is more efficacious, and Drug B is acting as a partial agonist. Clinically, greater efficacy usually matters more than greater potency.
3. Immediately after an IV bolus, the plasma concentration of a drug is 64 mcg/mL. The drug follows first-order elimination with a half-life of 4 hours. What will the plasma concentration be 12 hours later?
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Answer: 8 mcg/mL
12 hours is 3 half-lives, and each half-life halves the concentration: 64 → 32 → 16 → 8 mcg/mL. In first-order elimination, a constant fraction of the drug, not a constant amount, is removed per unit time.
4. Atropine blocks muscarinic acetylcholine receptors. Which effect would you expect in a patient given atropine?
- A Constricted pupils
- B Increased gastrointestinal motility
- C Urinary retention
- D Increased salivation
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Answer: C. Urinary retention
Blocking muscarinic receptors removes parasympathetic tone, so the bladder's detrusor muscle contracts less and urine is retained; dry mouth, dilated pupils, a faster heart rate, and slower gut motility follow for the same reason. Constricted pupils, more salivation, and faster gut motility are effects of muscarinic stimulation, the opposite of what atropine does.
5. A patient started on lisinopril, an ACE inhibitor, develops a persistent dry cough. What is the usual mechanism?
- A Angiotensin II accumulates and constricts the airways
- B ACE normally breaks down bradykinin, so bradykinin accumulates when ACE is inhibited
- C The drug blocks β2 receptors in bronchial smooth muscle
- D The drug causes fluid overload that leads to pulmonary edema
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Answer: B. ACE normally breaks down bradykinin, so bradykinin accumulates when ACE is inhibited
ACE converts angiotensin I to angiotensin II and also inactivates bradykinin, so inhibiting it lets bradykinin and related mediators build up in the airways and provoke cough. Angiotensin II receptor blockers (ARBs) do not interfere with bradykinin breakdown, so they cause this cough much less often. Bradykinin buildup is also linked to angioedema, a rare but serious effect of ACE inhibitors.
6. Drug X has an ED50 of 5 mg/kg and a TD50 of 50 mg/kg. Drug Y has an ED50 of 5 mg/kg and a TD50 of 15 mg/kg. Using therapeutic index = TD50 ÷ ED50, which drug has the narrower therapeutic index, and what is its value?
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Answer: Drug Y, with a therapeutic index of 3
Drug X's index is 50 ÷ 5 = 10, while Drug Y's is 15 ÷ 5 = 3. A smaller index means the toxic dose is closer to the effective dose, so a narrow-index drug leaves less margin for error and needs closer monitoring.
7. How does warfarin produce its anticoagulant effect?
- A It binds and directly inhibits thrombin
- B It enhances antithrombin, which then inactivates thrombin and factor Xa
- C It irreversibly inhibits cyclooxygenase in platelets
- D It blocks vitamin K recycling, so the liver makes fewer functional factors II, VII, IX, and X
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Answer: D. It blocks vitamin K recycling, so the liver makes fewer functional factors II, VII, IX, and X
Warfarin inhibits vitamin K epoxide reductase, and without reduced vitamin K the liver cannot finish activating (γ-carboxylating) factors II, VII, IX, and X. Because clotting factors already in the blood must be cleared first, its full effect takes several days, and it is monitored with the PT/INR. Dabigatran inhibits thrombin directly, heparin works through antithrombin, and aspirin inhibits platelet cyclooxygenase.
8. A patient with respiratory depression from a long-acting opioid wakes up and breathes normally after naloxone, but about an hour later becomes drowsy again with slow, shallow breathing. What is the most likely explanation?
- A Naloxone is a partial agonist that depresses breathing on its own
- B Naloxone wears off before the opioid does, so the opioid's effect returns
- C The patient has become tolerant to naloxone
- D Naloxone slows the liver's metabolism of the opioid
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Answer: B. Naloxone wears off before the opioid does, so the opioid's effect returns
Naloxone is a competitive antagonist that displaces opioids from μ receptors, but its effect is shorter-lived than that of many opioids, especially long-acting ones. As naloxone is cleared, opioid still in the body binds the receptors again and respiratory depression can return, which is why patients are observed after reversal.
9. Organophosphate insecticide poisoning causes heavy salivation, sweating, bronchial secretions, a slow heart rate, and pinpoint pupils. Which enzyme do organophosphates inhibit?
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Answer: Acetylcholinesterase
With acetylcholinesterase blocked, acetylcholine is not broken down and builds up at muscarinic and nicotinic synapses, overstimulating them. The muscarinic signs are the opposite of atropine's effects, which is why atropine is a classic antidote.
10. Why is a nonselective beta blocker such as propranolol generally avoided in patients with asthma?
- A It blocks β2 receptors in bronchial smooth muscle, which can cause bronchoconstriction
- B It stimulates α1 receptors in the airways, causing mucosal swelling
- C It blocks the breakdown of bradykinin in the lungs
- D It slows the heart so much that the lungs receive too little blood
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Answer: A. It blocks β2 receptors in bronchial smooth muscle, which can cause bronchoconstriction
Stimulation of β2 receptors relaxes bronchial smooth muscle, so blocking them can trigger bronchospasm in reactive airways. Cardioselective (β1-selective) blockers such as metoprolol carry less of this risk, although their selectivity decreases at higher doses. Blocking bradykinin breakdown is how ACE inhibitors cause cough.
11. A patient taking an ACE inhibitor and a diuretic has a serum potassium of 6.1 mEq/L (normal 3.5 to 5.0 mEq/L). Which diuretic is the most likely contributor?
- A Furosemide
- B Hydrochlorothiazide
- C Spironolactone
- D Acetazolamide
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Answer: C. Spironolactone
Spironolactone blocks aldosterone receptors in the collecting duct, so less Na⁺ is reabsorbed and less K⁺ is secreted into the urine; ACE inhibitors also lower aldosterone, adding to the effect. Loop diuretics, thiazides, and acetazolamide deliver more Na⁺ to the collecting duct, which increases K⁺ loss and tends to cause hypokalemia.
12. A patient receiving a continuous IV infusion of unfractionated heparin develops serious bleeding. Which agent specifically reverses heparin's anticoagulant effect?
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Answer: Protamine sulfate
Protamine is a strongly positively charged protein that binds the negatively charged heparin molecule and neutralizes it. Vitamin K reverses warfarin, not heparin, and heparin's effect is monitored with the aPTT.
13. A single dose of aspirin reduces platelet aggregation for several days, but the antiplatelet effect of ibuprofen wears off within about a day. What explains the difference?
- A Aspirin irreversibly acetylates COX-1, and platelets have no nucleus to make new enzyme
- B Aspirin selectively inhibits COX-2, the main COX enzyme in platelets
- C Aspirin is stored inside platelets and released slowly over several days
- D Aspirin blocks the platelet ADP receptor
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Answer: A. Aspirin irreversibly acetylates COX-1, and platelets have no nucleus to make new enzyme
Aspirin permanently acetylates COX-1, stopping that platelet from making thromboxane A₂ for the rest of its 7- to 10-day life span, so recovery depends on new platelets being made. Ibuprofen inhibits COX reversibly, so its effect ends as the drug is cleared. Blocking the ADP (P2Y12) receptor is how clopidogrel works.
14. A patient is receiving gentamicin, an aminoglycoside, for a serious Gram-negative infection. Which pair of adverse effects is most characteristic of this drug class?
- A Tendon rupture and QT prolongation
- B Tooth discoloration and photosensitivity
- C Nephrotoxicity and ototoxicity
- D Gray baby syndrome and bone marrow suppression
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Answer: C. Nephrotoxicity and ototoxicity
Aminoglycosides block bacterial protein synthesis at the 30S ribosomal subunit, but they also accumulate in renal tubule cells and the inner ear, damaging both. That is why kidney function, hearing and balance, and drug levels are monitored during therapy. The other pairs are classic for fluoroquinolones, tetracyclines, and chloramphenicol, in that order.
15. Statins such as atorvastatin lower LDL cholesterol by inhibiting which enzyme, the one that catalyzes the rate-limiting step of cholesterol synthesis?
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Answer: HMG-CoA reductase
With less cholesterol made in the liver, hepatocytes add more LDL receptors and pull more LDL out of the blood. The classic adverse effects are muscle pain or myopathy, rarely progressing to rhabdomyolysis, and elevated liver enzymes.