Practice 56 MCQs on Basic Pharmacology - Study Guide with OmpathStudy. Built for Kenyan medical and health students to revise key concepts and prepare for ex...
Q1. Pharmacodynamics includes the study of
Answer: Mechanisms of drug action
Explanation: Pharmacodynamics specifically studies the mechanisms of drug action and the biochemical and physiological effects of drugs on the body. Options B, C, and D describe pharmacokinetic processes (what the body does to the drug), while pharmacodynamics describes what the drug does to the body. ---
Q2. Which of the following physiological changes in the elderly may lead to the need to reduce the dose of a prescribed medication?
Answer: Decreased efficiency in drug biotransformation
Explanation: Elderly patients experience decreased hepatic enzyme activity and reduced liver blood flow, leading to decreased drug biotransformation. This results in prolonged drug half-life and increased drug accumulation, necessitating dose reduction to prevent toxicity. ---
Q3. What does the term "affinity" mean?
Answer: A measure of how tightly a drug binds to a receptor
Explanation: Affinity refers to the strength of the interaction between a drug and its receptor. High affinity means the drug binds strongly to the receptor, requiring lower concentrations to achieve binding. This is distinct from efficacy, which describes the ability to produce an effect once bound. ---
Q4. A pharmacological antagonist is a drug that
Answer: Binds to the receptors without directly altering their function
Explanation: An antagonist binds to a receptor but does not activate it. Instead, it blocks the receptor site, preventing endogenous ligands or agonists from binding and producing their effects. Antagonists have affinity but no intrinsic activity (efficacy). ---
Q5. Irreversible inhibition is due to
Answer: Covalent bond
Explanation: Irreversible inhibition occurs through covalent bond formation between the drug and its target. Covalent bonds are very strong and permanent, making the inhibition essentially irreversible. The effect only diminishes when new enzymes or receptors are synthesized. ---
Q6. Which of the following parameters is used to indicate the ability of a drug to produce the desired effect?
Answer: Efficacy
Explanation: Efficacy refers to the maximum response a drug can produce, regardless of dose. It indicates the drug's ability to produce the desired therapeutic effect. Potency refers to the dose required to produce a given effect, while efficacy describes the magnitude of that effect. ---
Q7. Drug receptors are found on
Answer: Plasma membranes and intracellular structures
Explanation: Drug receptors are located on plasma membranes (G-protein coupled receptors, ion channels, enzyme-linked receptors) and intracellularly (nuclear receptors for steroid hormones, thyroid hormones). This allows drugs to interact with various cellular components to produce therapeutic effects. --- ### AUTONOMIC NERVOUS SYSTEM
Q8. Nicotinic receptor sites do not include which of the following?
Answer: Bronchial smooth muscle
Explanation: Bronchial smooth muscle contains muscarinic receptors (M3), not nicotinic receptors. Nicotinic receptors are found at neuromuscular junctions (skeletal muscle), autonomic ganglia (both sympathetic and parasympathetic), and adrenal medulla. ---
Q9. Which of the following is the neurotransmitter agent normally released in the sinoatrial node (SAN) of the heart in response to an increase in blood pressure?
Answer: Acetylcholine
Explanation: When blood pressure increases, baroreceptors activate parasympathetic (vagal) output to the heart. The vagus nerve releases acetylcholine at the SA node, which binds to M2 muscarinic receptors, causing bradycardia and reduced cardiac output to lower blood pressure. ---
Q10. Which of the following drugs facilitates catecholamine transmitter release from adrenergic nerve endings?
Answer: Amphetamine
Explanation: Amphetamine is an indirect sympathomimetic that enters adrenergic nerve terminals and displaces stored norepinephrine, causing its release into the synaptic cleft. This mechanism is responsible for amphetamine's stimulant effects. Reserpine, in contrast, depletes catecholamine stores. ---
Q11. Full activation of the sympathetic nervous system, as in the fight-or-flight reaction, may occur during maximal exercise. Which of the following effects is most likely to occur?
Answer: Decreased renal blood flow
Explanation: During sympathetic activation, blood is redirected from non-essential organs (including kidneys and GI tract) to skeletal muscles, heart, and brain. This causes decreased renal blood flow. Other sympathetic effects include bronchodilation, decreased GI motility, mydriasis (pupil dilation), and tachycardia. ---
Q12. Mr. Otieno has been diagnosed with myasthenia gravis. You are considering treatment with pyridostigmine and neostigmine. Which adverse effect is associated with these two drugs?
Answer: Diarrhea
Explanation: Pyridostigmine and neostigmine are acetylcholinesterase inhibitors that increase acetylcholine levels at all cholinergic sites, including the GI tract. This leads to increased GI motility and secretions, causing diarrhea. Other cholinergic effects include bronchoconstriction, increased secretions, and bradycardia. ---
Q13. Probable signs of atropine overdose in toddlers include which one of the following?
Answer: Tachycardia
Explanation: Atropine is an antimuscarinic that blocks parasympathetic effects. Overdose presents with "hot as a hare, blind as a bat, dry as a bone, red as a beet, mad as a hatter." Tachycardia results from blockade of vagal (M2) receptors in the heart. Other signs include mydriasis, decreased secretions, and hyperthermia. ---
Q14. Which of the following is the most dangerous effect of belladonna alkaloids in infants and toddlers?
Answer: Hyperthermia
Explanation: Hyperthermia is the most life-threatening effect in children because belladonna alkaloids (atropine) block sweat glands, preventing heat dissipation. Children have less efficient thermoregulation and higher metabolic rates, making them particularly vulnerable to dangerous temperature elevations. ---
Q15. Which is the treatment of choice in a child with signs of anaphylaxis after being stung by three bees?
Answer: Epinephrine
Explanation: Epinephrine is the first-line treatment for anaphylaxis. It acts on α1 receptors (vasoconstriction to reverse hypotension), β1 receptors (increased cardiac output), and β2 receptors (bronchodilation). It also stabilizes mast cells, preventing further mediator release. Route: IM into anterolateral thigh. ---
Q16. Epinephrine causes a decrease in
Answer: Triglycerides in fat cells
Explanation: Epinephrine stimulates β3 receptors in adipose tissue, activating hormone-sensitive lipase, which breaks down triglycerides into free fatty acids and glycerol. This lipolysis provides energy substrates during the fight-or-flight response. Epinephrine increases cAMP, glucose, lactate, and free fatty acids. ---
Q17. Mr. Kamau, 54, had a cardiac transplant 6 months ago. His current blood pressure is 120/70 mmHg and heart rate is 100 bpm. Which of the following drugs would have the least effect on Mr. Kamau's heart rate?
Answer: Phenylephrine
Explanation: A transplanted heart is denervated (no sympathetic or parasympathetic innervation). It responds only to circulating catecholamines via direct receptor stimulation. Phenylephrine is a selective α1 agonist with no direct cardiac effects. Any heart rate changes would be indirect (reflex bradycardia from vasoconstriction), but reflexes are absent in denervated hearts. --- ### AUTACOIDS
Q18. In the synthesis of histamine, conversion of histidine to histamine is catalyzed by
Answer: L-histidine decarboxylase
Explanation: L-histidine decarboxylase is the enzyme responsible for converting L-histidine to histamine by removing the carboxyl group. This occurs primarily in mast cells, basophils, and gastric enterochromaffin-like cells. Histamine is then stored in granules until released by various stimuli. ---
Q19. Which receptor type is associated with first-generation H₁ receptor antagonists mediating urinary retention?
Answer: Cholinergic
Explanation: First-generation antihistamines have anticholinergic (antimuscarinic) properties in addition to H₁ blockade. Blockade of muscarinic receptors in the bladder detrusor muscle and internal sphincter leads to urinary retention. Other anticholinergic effects include dry mouth, constipation, and blurred vision. ---
Q20. Which of the following enzymes catalyzes the synthesis of acetylcholine?
Answer: Choline acetyltransferase
Explanation: Choline acetyltransferase (ChAT) catalyzes the synthesis of acetylcholine from acetyl-CoA and choline in the presynaptic nerve terminal. The reaction occurs in the cytoplasm, and acetylcholine is then transported into synaptic vesicles by vesicular acetylcholine transporter (VAChT). ---
Q21. Which of the following drugs inhibits the transport of choline into the nerve terminal?
Answer: Hemicholinium
Explanation: Hemicholinium blocks the sodium-dependent high-affinity choline transporter at the presynaptic membrane, preventing choline uptake. This depletes the substrate needed for acetylcholine synthesis, ultimately leading to neuromuscular blockade. It's used experimentally but not clinically. ---
Q22. Over-secretion of serotonin in carcinoid tumors results in
Answer: Diarrhoea
Explanation: Carcinoid syndrome, caused by serotonin-secreting tumors, produces excessive 5-HT₃ and 5-HT₄ receptor stimulation in the GI tract. This increases intestinal secretions and motility, leading to chronic diarrhea. Other symptoms include flushing, bronchoconstriction, and right-sided valvular heart disease. ---
Q23. An example of a widely distributed indole-ethylamine derived from tryptophan
Answer: Serotonin
Explanation: Serotonin (5-hydroxytryptamine, 5-HT) is synthesized from the amino acid tryptophan through hydroxylation and decarboxylation. It's an indole-ethylamine found in enterochromaffin cells (90%), platelets, and CNS neurons. It regulates mood, sleep, appetite, and GI motility. ---
Q24. What are the effects of serotonin on the cardiovascular system?
Answer: All of the above
Explanation: Serotonin has complex cardiovascular effects: (1) Vasodilation in skeletal muscle via 5-HT₇ receptors and NO release; (2) Reflex bradycardia from baroreceptor activation (Bezold-Jarisch reflex); (3) Vasoconstriction in splanchnic, renal, and pulmonary circulation via 5-HT₂ receptors. ---
Q25. Bradykinin causes
Answer: None of the above
Explanation: Bradykinin causes relaxation (not contraction) of vascular smooth muscle, leading to vasodilation and increased vascular permeability. It stimulates endothelial cells to release nitric oxide (NO) and prostacyclin (PGI₂), producing vasodilation. It also causes pain and is involved in inflammatory responses. --- ### ANTIMICROBIAL AGENTS
Q26. What is the mechanism of action of β-lactam antibiotics?
Answer: Inhibition of transpeptidase enzymes involved in peptidoglycan synthesis
Explanation: β-lactam antibiotics (penicillins, cephalosporins, carbapenems) bind to penicillin-binding proteins (PBPs), which are transpeptidase enzymes. This inhibits the cross-linking step in peptidoglycan synthesis, weakening the bacterial cell wall and causing cell lysis, particularly in actively dividing bacteria. ---
Q27. Which of the following β-lactam antibiotics is active against Pseudomonas aeruginosa?
Answer: Piperacillin
Explanation: Piperacillin is an extended-spectrum penicillin with anti-pseudomonal activity. It's often combined with tazobactam (a β-lactamase inhibitor) for broader coverage. Pseudomonas requires specific β-lactams with structural features allowing penetration through its outer membrane porins. ---
Q28. What is the primary mechanism of resistance to β-lactam antibiotics?
Answer: Enzymatic degradation by β-lactamases
Explanation: β-lactamases are enzymes that hydrolyze the β-lactam ring, rendering the antibiotic inactive. This is the most common resistance mechanism. Examples include penicillinases, extended-spectrum β-lactamases (ESBLs), and carbapenemases. β-lactamase inhibitors (clavulanic acid, tazobactam) can overcome this resistance. ---
Q29. Which antibiotic inhibits bacterial DNA synthesis by targeting DNA gyrase?
Answer: Ciprofloxacin
Explanation: Ciprofloxacin is a fluoroquinolone that inhibits bacterial DNA gyrase (topoisomerase II) and topoisomerase IV. These enzymes are essential for DNA replication, transcription, and repair. Inhibition leads to DNA strand breaks and bacterial cell death. Fluoroquinolones are bactericidal. ---
Q30. Which aminoglycoside has the least resistance due to enzymatic modification?
Answer: Amikacin
Explanation: Amikacin is semi-synthetic and structurally modified to resist most aminoglycoside-modifying enzymes (phosphotransferases, acetyltransferases, adenylyltransferases). This makes it effective against aminoglycoside-resistant organisms. It's often reserved for serious infections when other aminoglycosides fail. ---
Q31. What is the mechanism of action of vancomycin?
Answer: Binds to D-Ala-D-Ala termini, preventing peptidoglycan cross-linking
Explanation: Vancomycin is a glycopeptide that binds to the D-alanyl-D-alanine terminus of peptidoglycan precursors in the bacterial cell wall. This prevents transpeptidase from accessing its substrate, blocking peptidoglycan synthesis and cross-linking. It's bactericidal against Gram-positive bacteria, especially MRSA. ---
Q32. What is the primary mechanism of action of azole antifungals?
Answer: Disruption of ergosterol synthesis by inhibiting lanosterol 14α-demethylase
Explanation: Azole antifungals (fluconazole, itraconazole, voriconazole) inhibit the fungal cytochrome P450 enzyme lanosterol 14α-demethylase, blocking ergosterol synthesis. Ergosterol is essential for fungal cell membrane integrity. Its depletion and accumulation of toxic sterol precursors disrupt membrane function. ---
Q33. What is the primary target of neuraminidase inhibitors like oseltamivir?
Answer: Neuraminidase enzyme on influenza virus
Explanation: Oseltamivir (Tamiflu) inhibits viral neuraminidase, an enzyme that cleaves sialic acid residues, allowing newly formed virions to bud from infected cells. Inhibition prevents viral release and spread to adjacent cells, limiting infection progression. Effective against both influenza A and B if started within 48 hours. ---
Q34. Acyclovir selectively inhibits viral replication by
Answer: Incorporating into viral DNA and causing chain termination
Explanation: Acyclovir is a guanosine analog phosphorylated by viral thymidine kinase to its active triphosphate form. It's incorporated into viral DNA by viral DNA polymerase, causing chain termination. Selectivity comes from preferential phosphorylation by viral (not cellular) thymidine kinase. ---
Q35. Which class of antiretrovirals prevents HIV integration into the host genome?
Answer: Integrase strand transfer inhibitors (INSTIs)
Explanation: INSTIs (dolutegravir, raltegravir, bictegravir) block HIV integrase, the enzyme responsible for inserting viral DNA into the host chromosome. This prevents viral replication and establishment of latent infection. INSTIs are highly effective, well-tolerated, and form the backbone of modern ART regimens. ---
Q36. What is the most common adverse effect of zidovudine?
Answer: Myelosuppression
Explanation: Zidovudine (AZT) commonly causes bone marrow suppression, leading to anemia and neutropenia, especially with prolonged use or high doses. This occurs because it affects rapidly dividing bone marrow cells. Regular monitoring of complete blood counts is essential during treatment. ---
Q37. Which antibiotic is known for causing "Red Man Syndrome" when infused too quickly?
Answer: Vancomycin
Explanation: Red Man Syndrome is a histamine-mediated reaction causing flushing, pruritus, and erythema of the face, neck, and upper torso. It results from rapid vancomycin infusion causing mast cell degranulation. Prevention involves slow infusion (over 60 minutes) and premedication with antihistamines if necessary. ---
Q38. Which of the following antibiotics targets the bacterial 50S ribosomal subunit?
Answer: Azithromycin
Explanation: Azithromycin is a macrolide antibiotic that binds to the 23S rRNA of the bacterial 50S ribosomal subunit, inhibiting protein synthesis by blocking translocation. Other 50S inhibitors include chloramphenicol, clindamycin, and linezolid. This prevents bacterial growth (bacteriostatic effect). ---
Q39. Which antibiotic is associated with gray baby syndrome when used in neonates?
Answer: Chloramphenicol
Explanation: Gray baby syndrome occurs in neonates due to immature hepatic glucuronyl transferase, leading to chloramphenicol accumulation. Features include abdominal distension, vomiting, cyanosis, cardiovascular collapse, and gray skin discoloration. It can be fatal. Chloramphenicol is contraindicated in neonates. ---
Q40. Which drug is used as prophylaxis for influenza A and B?
Answer: Oseltamivir
Explanation: Oseltamivir can be used for post-exposure prophylaxis and seasonal prophylaxis against both influenza A and B. Amantadine only covers influenza A and has significant resistance. Acyclovir and ganciclovir target herpesviruses, not influenza. ---
Q41. Which antibiotic is associated with gray baby syndrome when used in neonates?
Answer: Chloramphenicol
Explanation: Gray baby syndrome occurs in neonates due to immature hepatic glucuronyl transferase, leading to chloramphenicol accumulation. Features include abdominal distension, vomiting, cyanosis, cardiovascular collapse, and gray skin discoloration. It can be fatal. Chloramphenicol is contraindicated in neonates. ---
Q42. What is the first-line treatment regimen for drug-sensitive tuberculosis?
Answer: Isoniazid + Rifampin + Pyrazinamide + Ethambutol
Explanation: The standard first-line regimen (RIPE therapy) consists of Rifampin, Isoniazid, Pyrazinamide, and Ethambutol for 2 months (intensive phase), followed by Rifampin and Isoniazid for 4 months (continuation phase). This combination prevents resistance and ensures cure. ---
Q43. What is the primary adverse effect of isoniazid?
Answer: Hepatotoxicity
Explanation: Isoniazid can cause hepatotoxicity, ranging from asymptomatic transaminase elevation to acute liver failure. Risk factors include age 35, alcohol use, and concurrent hepatotoxic drugs. Monitoring liver function tests is essential. Pyridoxine (vitamin B6) is co-administered to prevent peripheral neuropathy. ---
Q44. Which of the following drugs is used in the new injectable-free regimen for drug-resistant TB?
Answer: Bedaquiline
Explanation: Bedaquiline is an oral ATP synthase inhibitor used in MDR-TB and XDR-TB regimens, replacing injectable aminoglycosides. WHO now recommends all-oral regimens containing bedaquiline, linezolid, fluoroquinolones, and other agents to improve tolerability and adherence while maintaining efficacy. ---
Q45. What is the major adverse effect of ethambutol?
Answer: Optic neuritis
Explanation: Ethambutol can cause dose-dependent optic neuritis, presenting with decreased visual acuity, red-green color blindness, and central scotomas. It's usually reversible if detected early and the drug is discontinued. Baseline and monthly visual acuity and color vision testing are recommended. ---
Q46. Which of the following antibiotics inhibits bacterial folic acid synthesis?
Answer: Trimethoprim
Explanation: Trimethoprim inhibits bacterial dihydrofolate reductase, blocking tetrahydrofolate synthesis, which is essential for purine and DNA synthesis. Combined with sulfamethoxazole (which inhibits dihydropteroate synthase), it provides sequential blockade of the folic acid pathway, producing synergistic bactericidal activity. ---
Q47. Which cephalosporin has the best CNS penetration and is used for bacterial meningitis?
Answer: Ceftriaxone
Explanation: Ceftriaxone is a third-generation cephalosporin with excellent CSF penetration, especially in inflamed meninges. It's effective against common meningitis pathogens (S. pneumoniae, N. meningitidis, H. influenzae) and has a long half-life allowing once or twice-daily dosing. ---
Q48. Which of the following is a concentration-dependent antibiotic?
Answer: Aminoglycosides
Explanation: Aminoglycosides exhibit concentration-dependent killing—higher peak concentrations produce greater bactericidal activity and longer post-antibiotic effect. Dosing strategy aims for high peak levels (Cmax/MIC 8-10) while minimizing trough levels to reduce toxicity. Beta-lactams and vancomycin are time-dependent antibiotics. ---
Q49. Which antiviral drug is used as post-exposure prophylaxis for HIV?
Answer: Tenofovir + Emtricitabine + Dolutegravir
Explanation: Post-exposure prophylaxis (PEP) for HIV uses a three-drug regimen, typically tenofovir/emtricitabine (NRTIs) plus dolutegravir (INSTI). It must be initiated within 72 hours of exposure and continued for 28 days. This combination is highly effective at preventing HIV transmission. ---
Q50. Which tuberculosis drug requires co-administration with pyridoxine to prevent neuropathy?
Answer: Isoniazid
Explanation: Isoniazid interferes with pyridoxine (vitamin B6) metabolism by inhibiting pyridoxal phosphokinase. This can cause peripheral neuropathy, especially in high-risk patients (diabetics, alcoholics, malnourished, pregnant women). Pyridoxine 25-50 mg/day supplementation prevents this adverse effect. ---
Q51. Which of the following tuberculosis drugs has the highest risk of inducing hyperuricemia?
Answer: Pyrazinamide
Explanation: Pyrazinamide inhibits renal tubular secretion of uric acid, leading to hyperuricemia in most patients. This can precipitate acute gout in susceptible individuals. Other adverse effects include hepatotoxicity and arthralgias. Uric acid levels should be monitored during treatment. --- ### ANESTHETICS & ANALGESICS
Q52. Which of the following prostaglandins is primarily responsible for vasodilation?
Answer: PGE2
Explanation: PGE2 is a potent vasodilator that also increases vascular permeability, causes fever (acts on hypothalamus), and sensitizes nociceptors to pain. PGF2α causes vasoconstriction and bronchoconstriction. Thromboxane A2 causes vasoconstriction and platelet aggregation. ---
Q53. Which prostaglandin analog is used for gastric ulcer prevention in NSAID users?
Answer: Misoprostol
Explanation: Misoprostol is a synthetic PGE1 analog that protects gastric mucosa by increasing bicarbonate and mucus secretion, decreasing acid secretion, and maintaining mucosal blood flow. It prevents NSAID-induced ulcers but causes diarrhea and is contraindicated in pregnancy (abortifacient properties). ---
Q54. What is the mechanism of action of propofol?
Answer: GABA-A receptor agonist
Explanation: Propofol enhances GABA-A receptor activity, increasing chloride conductance and causing neuronal hyperpolarization. This produces rapid onset of anesthesia with smooth induction and quick recovery. Side effects include hypotension (vasodilation), respiratory depression, and pain on injection. ---
Q55. What is the mechanism of action of ketamine?
Answer: NMDA receptor antagonist
Explanation: Ketamine is a non-competitive NMDA (glutamate) receptor antagonist that produces "dissociative anesthesia"—patients appear awake but are unresponsive to pain. It maintains cardiovascular stability and respiratory drive, making it useful in hemodynamically unstable patients. Side effects include hallucinations and increased salivation. ---
Q56. Which intravenous anesthetic is preferred for patients at risk of hypotension?
Answer: Etomidate
Explanation: Etomidate has minimal cardiovascular effects and maintains hemodynamic stability, making it ideal for patients with cardiovascular compromise or hypovolemia. However, it can suppress adrenal steroid synthesis (inhibits 11β-hydroxylase) with prolonged use and causes myoclonus and pain on injection. --- --- ## SECTION B: SHORT ANSWER QUESTIONS