Pharmacology Examination MCQs – 51 MCQs | Kenya MBChB

51 Year 3: Basic Pharmacology II exam questions on Pharmacology Examination MCQs for medical students. Includes MCQs, answers, explanations and written question

This MCQ set contains 51 questions on Pharmacology Examination MCQs in the Year 3: Basic Pharmacology II unit. Each question includes the correct answer and a detailed explanation for active recall and exam preparation.

Q1: Question 1: A patient receives a drug dose of 500 mg daily. To express this dose normalized to body weight for a 70 kg patient, what unit would be most appropriate?

  1. A. mg/day
  2. B. mg/kg/day
  3. C. g/kg
  4. D. mg/L
  5. E. mg/kg/day

Correct answer: B – mg/kg/day

The dosage unit mg/kg/day includes both the dose per unit body weight and exposure duration, making it the standard unit in toxicology and pharmacology for comparing doses across individuals of different weights. For this patient, it would be approximately 7.14 mg/kg/day.

Q2: Question 2: The LD50 of a new compound is determined to be 200 mg/kg, while its ED50 is 20 mg/kg. What is the Therapeutic Index (TI) of this drug?

  1. A. 0.1
  2. B. 10C) 180
  3. C. 220
  4. D. 10

Correct answer: B – 10C) 180

The Therapeutic Index is calculated as LD50/ED50. In this case: 200/20 = 10. A TI of 10 indicates the drug has a reasonable margin of safety, as the lethal dose is 10 times higher than the effective dose. Drugs with higher TI values are generally considered safer.

Q3: Question 3: Which of the following best describes the "threshold dose" in a dose-response relationship?

  1. A. The dose at which 50% of the population shows a response
  2. B. The maximum dose that can be administered safely
  3. C. The dose below which no toxic response occurs or can be measured
  4. D. The dose that produces the maximum therapeutic effect
  5. E. The dose below which no toxic response occurs or can be measured

Correct answer: C – The dose below which no toxic response occurs or can be measured

The threshold dose represents the point where the body's ability to detoxify or repair effects is not yet exceeded. Below this dose, no observable adverse effects occur. This is a fundamental assumption in dose-response relationships for non-carcinogenic substances.

Q4: Question 4: A drug has an LD01 of 100 mg/kg and an ED99 of 80 mg/kg. What is the Margin of Safety (MOS)?

  1. A. 0.8
  2. B. 1.25
  3. C. 20
  4. D. 180
  5. E. 1.25

Correct answer: B – 1.25

The Margin of Safety is calculated as LD01/ED99 = 100/80 = 1.25. A MOS less than 1 would indicate that the dose causing lethality in 1% of the population overlaps with the dose needed for 99% effectiveness, which is dangerous. This drug has a narrow margin of safety.

Q5: Question 5: According to toxicity scales, a substance with an LD50 of 400 mg/kg would be classified as:

  1. A. Extremely toxic
  2. B. Moderately toxic
  3. C. Slightly toxic
  4. D. Relatively harmless
  5. E. Moderately toxic

Correct answer: B – Moderately toxic

The standard toxicity scale classifies substances with LD50 values between 50-500 mg/kg as moderately toxic. Extremely toxic substances have LD50 ≤ 50 mg/kg, slightly toxic 0.5-5 g/kg, and relatively harmless 5 g/kg.

Q6: : In dose-response curves, "potency" refers to:

  1. A. The maximum response a drug can produce
  2. B. The range of doses over which a drug produces increasing responses
  3. C. The plateau of the dose-response curve
  4. D. The duration of drug action
  5. E. The range of doses over which a drug produces increasing responses

Correct answer: B – The range of doses over which a drug produces increasing responses

Potency relates to the dose required to achieve a given response - more potent drugs require lower doses. It is reflected in the position of the dose-response curve along the dose axis. Efficacy (option C) refers to the maximum response, which is different from potency.

Q7: Question 7: NOAEL stands for:

  1. A. Normal Observed Adverse Effect Level
  2. B. No Observed Adverse Effect Level
  3. C. Nominal Observed Adverse Effect Limit
  4. D. Non-Observable Adverse Effect Level
  5. E. No Observed Adverse Effect Level

Correct answer: B – No Observed Adverse Effect Level

NOAEL is the highest dose point at which no adverse or toxic effects are observed in experimental studies. It is used along with LOAEL (Lowest Observed Adverse Effect Level) to establish safe exposure limits for chemicals and drugs.

Q8: Question 8: Allergic reactions differ from typical toxic responses because:

  1. A. They follow standard dose-response assumptions
  2. B. They result from the chemical directly acting on cells
  3. C. They result from immune system stimulation releasing natural chemicals
  4. D. They only occur at high doses
  5. E. They result from immune system stimulation releasing natural chemicals

Correct answer: C – They result from immune system stimulation releasing natural chemicals

Allergic reactions are immune-mediated responses where the chemical stimulates the body to release natural mediators (histamine, leukotrienes, etc.) that cause the observed effects. Unlike toxic responses, allergic reactions don't always comply with dose-response assumptions and can occur at very low doses in sensitized individuals.

Q9: Question 9: A drug with TD50 of 150 mg and ED50 of 50 mg would have what relationship?

  1. A. TD50/ED50 = 3, indicating a relatively safe therapeutic window
  2. B. TD50/ED50 = 0.33, indicating danger
  3. C. The drug cannot be used clinically
  4. D. The therapeutic index is 200
  5. E. TD50/ED50 = 3, indicating a relatively safe therapeutic window

Correct answer: A – TD50/ED50 = 3, indicating a relatively safe therapeutic window

The ratio of toxic dose to effective dose (150/50 = 3) represents the therapeutic index. A TI of 3 means the toxic dose is three times the effective dose. While not as safe as drugs with TI of 10 or higher, it still provides some margin for clinical use with careful monitoring.

Q10: Question 10: When comparing two drugs on a dose-response curve, if Drug A's curve is shifted to the left of Drug B's curve, this indicates:

  1. A. Drug A is more efficacious than Drug B
  2. B. Drug A is more potent than Drug B
  3. C. Drug A is safer than Drug B
  4. D. Drug A has a longer duration of action
  5. E. Drug A is more potent than Drug B

Correct answer: B – Drug A is more potent than Drug B

A leftward shift means Drug A produces the same effect at a lower dose than Drug B, indicating greater potency. Efficacy is determined by the height (maximum) of the curve, not its position along the x-axis.

Q11: Question 11: Tyramine produces its sympathomimetic effects primarily by which mechanism?

  1. A. Direct stimulation of alpha-1 receptors
  2. B. Inhibition of monoamine oxidase
  3. C. Causing release of norepinephrine via NET reversal
  4. D. Blocking acetylcholinesterase
  5. E. Causing release of norepinephrine via NET reversal

Correct answer: C – Causing release of norepinephrine via NET reversal

Tyramine is taken up into nerve terminals by NET (norepinephrine transporter) and causes catecholamine release through reverse transport. This indirect mechanism distinguishes it from direct-acting sympathomimetics that bind directly to adrenergic receptors.

Q12: Question 12: Why is tyramine normally inactive when consumed orally in food?

  1. A. It is not absorbed from the GI tract
  2. B. It undergoes extensive first-pass metabolism by MAO
  3. C. It is rapidly excreted by the kidneys unchanged
  4. D. It binds irreversibly to plasma proteins
  5. E. It undergoes extensive first-pass metabolism by MAO

Correct answer: B – It undergoes extensive first-pass metabolism by MAO

Tyramine has very low bioavailability because it is readily metabolized by monoamine oxidase (MAO) present in the gastrointestinal endothelium and liver. This explains why it only produces significant effects when MAO is inhibited or when administered parenterally.

Q13: Question 13: A patient taking a nonselective MAO inhibitor consumes aged cheese containing high tyramine levels. What is the most likely consequence?

  1. A. Severe hypotension and bradycardia
  2. B. Hypertensive crisis and tachycardia
  3. C. Respiratory depression
  4. D. No significant effect
  5. E. Hypertensive crisis and tachycardia

Correct answer: B – Hypertensive crisis and tachycardia

When MAO is inhibited, dietary tyramine is not metabolized and reaches the systemic circulation. This leads to massive norepinephrine release from nerve terminals, causing dangerous elevations in blood pressure and heart rate, known as the "tyramine reaction" or "cheese effect."

Q14: Question 14: Amphetamine's mechanism of action differs from tyramine in that amphetamine:

  1. A. Only releases dopamine, not norepinephrine
  2. B. Acts as a direct agonist at adrenergic receptors
  3. C. Crosses the blood-brain barrier to produce CNS effects
  4. D. Is metabolized by MAO in the gut
  5. E. Crosses the blood-brain barrier to produce CNS effects

Correct answer: C – Crosses the blood-brain barrier to produce CNS effects

Unlike tyramine, amphetamine can cross the blood-brain barrier and produce central nervous system stimulation. Both are indirectly acting sympathomimetics that cause catecholamine release, but amphetamine's CNS penetration is responsible for its stimulant and abuse potential.

Q15: Question 15: Cocaine blocks the reuptake of neurotransmitters by inhibiting which transporters?

  1. A. Only NET (norepinephrine transporter)
  2. B. Only DAT (dopamine transporter)
  3. C. NET, DAT, and SERT (all three monoamine transporters)
  4. D. Only voltage-gated sodium channels
  5. E. NET, DAT, and SERT (all three monoamine transporters)

Correct answer: C – NET, DAT, and SERT (all three monoamine transporters)

Cocaine is a non-selective inhibitor that blocks all three monoamine reuptake transporters: NET (norepinephrine), DAT (dopamine), and SERT (serotonin). This results in increased synaptic concentrations of all three neurotransmitters, contributing to its stimulant and addictive properties.

Q16: Question 16: Tricyclic antidepressants like imipramine would be expected to:

  1. A. Enhance the effects of tyramine
  2. B. Antagonize the effects of indirectly acting sympathomimetics
  3. C. Increase MAO activity
  4. D. Have no effect on sympathomimetic drugs
  5. E. Antagonize the effects of indirectly acting sympathomimetics

Correct answer: B – Antagonize the effects of indirectly acting sympathomimetics

Imipramine blocks NET, preventing the uptake of indirectly acting sympathomimetics like tyramine into nerve terminals. Since these drugs must enter the nerve terminal to cause catecholamine release, blocking NET antagonizes their effects. This is an important drug interaction.

Q17: Question 17: Which statement about cocaine's cardiovascular toxicity is correct?

  1. A. It only causes hypotension
  2. B. It produces bradycardia through vagal stimulation
  3. C. It can cause both tachycardia and hypertension due to increased sympathetic outflow
  4. D. Cardiovascular effects only occur with chronic use
  5. E. It can cause both tachycardia and hypertension due to increased sympathetic outflow

Correct answer: C – It can cause both tachycardia and hypertension due to increased sympathetic outflow

Cocaine blocks monoamine reuptake, leading to increased norepinephrine at sympathetic nerve terminals. This causes simultaneous tachycardia and hypertension. Additionally, at higher doses, cocaine's sodium channel blocking effects can contribute to arrhythmias and cardiac toxicity.

Q18: Question 18: Repeated administration of tyramine leads to rapidly developing tolerance (tachyphylaxis) because:

  1. A. MAO activity increases
  2. B. NET transporters are downregulated
  3. C. The readily releasable pool of catecholamines becomes depleted
  4. D. Adrenergic receptors become desensitized
  5. E. The readily releasable pool of catecholamines becomes depleted

Correct answer: C – The readily releasable pool of catecholamines becomes depleted

Tyramine releases catecholamines from a small cytoplasmic "readily releasable" pool. With repeated exposure, this pool becomes depleted faster than it can be replenished, resulting in tachyphylaxis. This is characteristic of indirectly acting sympathomimetics.

Q19: Question 19: Why does tyramine NOT produce psychoactive effects when administered systemically?

  1. A. It is too rapidly metabolized
  2. B. It does not cross the blood-brain barrier
  3. C. It has no affinity for CNS receptors
  4. D. It is actively pumped out of the brain
  5. E. It does not cross the blood-brain barrier

Correct answer: B – It does not cross the blood-brain barrier

Tyramine and other monoamines cannot cross the blood-brain barrier due to tight junctions in cerebral capillaries and high concentrations of MAO and dopa decarboxylase in the capillary endothelium. This results in only peripheral sympathomimetic effects.

Q20: Question 20: Lisdexamfetamine (Vyvanse®) is considered a prodrug because:

  1. A. It is already active when administered
  2. B. It must be hydrolyzed by red blood cells to release active dextroamphetamine
  3. C. It inhibits drug metabolism
  4. D. It prevents amphetamine synthesis
  5. E. It must be hydrolyzed by red blood cells to release active dextroamphetamine

Correct answer: B – It must be hydrolyzed by red blood cells to release active dextroamphetamine

Lisdexamfetamine is an inactive prodrug consisting of dextroamphetamine bound to L-lysine. After oral absorption (~96% bioavailability), it is hydrolyzed by red blood cells to release the active dextroamphetamine, providing more controlled and sustained stimulant effects.

Q21: Question 21: Reserpine would antagonize the effects of indirectly acting sympathomimetics like tyramine if given:

  1. A. Simultaneously
  2. B. Several hours to days before tyramine
  3. C. Immediately after tyramine
  4. D. Reserpine does not affect tyramine's actions
  5. E. Several hours to days before tyramine

Correct answer: B – Several hours to days before tyramine

Reserpine depletes catecholamines from nerve terminals by inhibiting VMAT (vesicular monoamine transporter). Since tyramine works by releasing stored catecholamines, it cannot work if the stores are depleted. However, depletion takes time to develop, so reserpine must be given well in advance.

Q22: Question 22: The combination of cocaine and ethanol in the body produces:

  1. A. Enhanced cocaine metabolism and shorter effects
  2. B. Cocaethylene, with longer half-life and similar toxicity
  3. C. Complete antagonism of cocaine's effects
  4. D. Immediate cardiovascular collapse
  5. E. Cocaethylene, with longer half-life and similar toxicity

Correct answer: B – Cocaethylene, with longer half-life and similar toxicity

When cocaine and ethanol are consumed together, they undergo transesterification in the liver to form cocaethylene, which has a half-life of 3-4 hours (longer than cocaine's ~50 min) and shares similar pharmacology. This prolongs the "high" and may increase cardiotoxicity.

Q23: Question 23: Which enzyme catalyzes the conversion of L-histidine to histamine?

  1. A. Monoamine oxidase
  2. B. Histidine decarboxylase
  3. C. Catechol-O-methyltransferase
  4. D. Tyrosine hydroxylase
  5. E. Histidine decarboxylase

Correct answer: B – Histidine decarboxylase

Histidine decarboxylase is the enzyme responsible for synthesizing histamine from the amino acid L-histidine. This occurs primarily in mast cells, basophils, and enterochromaffin cells in the stomach.

Q24: Question 24: The "triple response" following intradermal histamine injection consists of all of the following EXCEPT:

  1. A. Red spot (flush) at injection site
  2. B. Bright red flare extending beyond the flush
  3. C. Localized wheal formation
  4. D. Vasoconstriction of surrounding vessels
  5. E. Vasoconstriction of surrounding vessels

Correct answer: D – Vasoconstriction of surrounding vessels

The triple response includes: 1) flush (capillary/venule dilation), 2) flare (arteriolar dilation via axon reflex), and 3) wheal (increased capillary permeability causing edema). Vasoconstriction does not occur; all three components involve vasodilation and increased permeability.

Q25: Question 25: H2 receptor antagonists like ranitidine reduce gastric acid secretion by:

  1. A. Directly inhibiting the proton pump
  2. B. Blocking histamine stimulation of parietal cell H2 receptors
  3. C. Increasing prostaglandin synthesis in gastric mucosa
  4. D. Neutralizing already secreted acid
  5. E. Blocking histamine stimulation of parietal cell H2 receptors

Correct answer: B – Blocking histamine stimulation of parietal cell H2 receptors

H2 blockers competitively antagonize histamine at H2 receptors on gastric parietal cells, preventing the histamine-mediated activation of adenylyl cyclase and subsequent stimulation of the proton pump. They do not directly block the pump itself (that's the mechanism of PPIs like omeprazole).

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