Pharmacology Examination MCQs | MCQ Quiz | OmpathStudy Kenya

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?

Accepted Answer

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.

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?

Accepted Answer

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.

Question 3

Which of the following best describes the "threshold dose" in a dose-response relationship?

Accepted Answer

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.

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)?

Accepted Answer

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.

Question 5

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

Accepted Answer

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.

Question 6

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

Accepted Answer

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.

Question 7

NOAEL stands for:

Accepted Answer

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.

Question 8

Allergic reactions differ from typical toxic responses because:

Accepted Answer

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.

Question 9

A drug with TD50 of 150 mg and ED50 of 50 mg would have what relationship?

Accepted Answer

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.

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:

Accepted Answer

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.

Question 11

Tyramine produces its sympathomimetic effects primarily by which mechanism?

Accepted Answer

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.

Question 12

Why is tyramine normally inactive when consumed orally in food?

Accepted Answer

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.

Question 13

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

Accepted Answer

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."

Question 14

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

Accepted Answer

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.

Question 15

Cocaine blocks the reuptake of neurotransmitters by inhibiting which transporters?

Accepted Answer

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.

Question 16

Tricyclic antidepressants like imipramine would be expected to:

Accepted Answer

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.

Question 17

Which statement about cocaine's cardiovascular toxicity is correct?

Accepted Answer

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.

Question 18

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

Accepted Answer

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.

Question 19

Why does tyramine NOT produce psychoactive effects when administered systemically?

Accepted Answer

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.

Question 20

Lisdexamfetamine (Vyvanse®) is considered a prodrug because:

Accepted Answer

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.

Question 21

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

Accepted Answer

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.

Question 22

The combination of cocaine and ethanol in the body produces:

Accepted Answer

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.

Question 23

Which enzyme catalyzes the conversion of L-histidine to histamine?

Accepted Answer

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.

Question 24

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

Accepted Answer

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.

Question 25

H2 receptor antagonists like ranitidine reduce gastric acid secretion by:

Accepted Answer

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).

Question 26

First-generation H1 antihistamines like diphenhydramine cause sedation because they:

Accepted Answer

Cross the blood-brain barrier and block central H1 receptors — First-generation antihistamines are lipophilic and readily cross the blood-brain barrier, blocking H1 receptors in the CNS that mediate wakefulness and alertness. Second-generation antihistamines (like cetirizine, loratadine) are more polar and penetrate the brain poorly, causing minimal sedation.

Question 27

A unique side effect of cimetidine (but not other H2 blockers) in males is:

Accepted Answer

Gynecomastia and decreased libido — Cimetidine has anti-androgenic effects and increases prolactin secretion, which can lead to gynecomastia (breast enlargement), decreased libido, and impotence in males. This is specific to cimetidine and does not occur with other H2 blockers like ranitidine or famotidine.

Question 28

Which H1 antihistamine also has significant 5-HT (serotonin) antagonist properties?

Accepted Answer

Cyproheptadine — Cyproheptadine is unique among H1 antihistamines in having potent 5-HT antagonist activity, particularly at 5-HT2 receptors. This dual action makes it useful for conditions beyond typical allergies, such as migraine prophylaxis and treatment of serotonin syndrome.

Question 29

Which G-protein type is coupled to H1 receptors?

Accepted Answer

Gq (phospholipase C activation) — H1 receptors couple to Gq proteins, which activate phospholipase C (PLC). This produces IP3 and DAG as second messengers. IP3 increases intracellular Ca2+, leading to smooth muscle contraction, while DAG activates protein kinase C.

Question 30

The "flare" component of histamine's triple response is mediated by:

Accepted Answer

Axon reflex causing arteriolar dilation — The flare is a bright red area extending irregularly beyond the initial flush, caused by arteriolar dilation via axon reflex. This is a neurogenic response where sensory nerve stimulation causes reflex vasodilation in surrounding vessels.

Question 31

Betahistine, a histamine analog, is used clinically to treat:

Accepted Answer

Vertigo in Meniere's disease — Betahistine is a histamine H1 receptor agonist and H3 receptor antagonist used to reduce vertigo attacks in Meniere's disease. It is thought to work by improving microcirculation in the inner ear, though its exact mechanism remains unclear.

Question 32

Promethazine differs from other H1 antihistamines by also possessing:

Accepted Answer

Alpha-adrenergic blocking and local anesthetic properties — Promethazine is a phenothiazine derivative with multiple actions: H1 antagonism, alpha-adrenergic blockade, local anesthetic effects, and antimuscarinic activity. This explains its use in motion sickness, as an antiemetic, and its stronger sedative properties.

Question 33

Second-generation antihistamines like cetirizine and loratadine cause less sedation because they:

Accepted Answer

Are more polar and penetrate the brain poorly — Second-generation antihistamines are more polar (less lipophilic) than first-generation drugs, resulting in minimal blood-brain barrier penetration and reduced CNS effects. They maintain peripheral H1 blocking activity while causing minimal sedation.

Question 34

Cimetidine can increase plasma levels of other drugs because it:

Accepted Answer

Inhibits cytochrome P450 enzymes (particularly 2D6) — Cimetidine inhibits several cytochrome P450 enzymes, reducing the metabolism of many drugs (warfarin, phenytoin, theophylline, etc.) and potentially increasing their plasma levels and toxicity. This is unique to cimetidine among H2 blockers and represents a significant drug interaction concern.

Question 35

What percentage of the body's serotonin is stored in enterochromaffin cells of the GI tract?

Accepted Answer

90% — Approximately 90% of the body's serotonin is synthesized and stored in enterochromaffin cells of the gastrointestinal tract. Only about 10% is found in platelets and the CNS. Despite this distribution, GI serotonin does not cross the blood-brain barrier.

Question 36

Which enzyme catalyzes the rate-limiting step in serotonin synthesis?

Accepted Answer

Tryptophan hydroxylase — Tryptophan hydroxylase converts dietary tryptophan to 5-hydroxytryptophan in the rate-limiting step of serotonin synthesis. This is then converted to serotonin (5-HT) by amino acid decarboxylase.

Question 37

The 5-HT3 receptor differs from other serotonin receptors in that it is a:

Accepted Answer

Ligand-gated ion channel — 5-HT3 is the only serotonin receptor that is a ligand-gated ion channel (specifically for Na+ and K+). All other 5-HT receptors (5-HT1, 5-HT2, 5-HT4, 5-HT5, 5-HT6, 5-HT7) are G-protein coupled receptors.

Question 38

Ondansetron is used as an antiemetic primarily because it:

Accepted Answer

Blocks 5-HT3 receptors in the chemoreceptor trigger zone — Ondansetron is a selective 5-HT3 receptor antagonist. Blocking 5-HT3 receptors in the chemoreceptor trigger zone and vagal afferents effectively prevents nausea and vomiting, particularly from chemotherapy and post-operative settings.

Question 39

Sumatriptan is effective in treating acute migraine attacks because it:

Accepted Answer

Acts as a 5-HT1D agonist decreasing serotonin release — Sumatriptan is a selective 5-HT1D receptor agonist. Activation of presynaptic 5-HT1D receptors inhibits serotonin release and causes vasoconstriction of cranial vessels, both contributing to relief of acute migraine symptoms.

Question 40

Which metabolite of serotonin is measured in urine to assess serotonin metabolism?

Accepted Answer

5-Hydroxyindoleacetic acid (5-HIAA) — Serotonin is metabolized by monoamine oxidase (MAO) to 5-HIAA, which is excreted in urine. Elevated urinary 5-HIAA is a diagnostic marker for carcinoid tumors, which secrete excessive amounts of serotonin.

Question 41

Which 5-HT receptor subtype functions as an autoreceptor regulating serotonin release?

Accepted Answer

5-HT1D — 5-HT1B and 5-HT1D receptors function as presynaptic autoreceptors. When activated, they inhibit further serotonin release via negative feedback. This is the mechanism by which sumatriptan works in migraine - it activates 5-HT1D autoreceptors to reduce excessive serotonin release.

Question 42

Metoclopramide acts as a prokinetic agent primarily through:

Accepted Answer

5-HT4 receptor agonism — Metoclopramide is a 5-HT4 receptor agonist that enhances GI motility by stimulating acetylcholine release in the enteric nervous system. It also has dopamine D2 antagonist and 5-HT3 antagonist properties, contributing to its antiemetic effects.

Question 43

The majority of serotonin's metabolism occurs through which pathway?

Accepted Answer

Oxidation by MAO to 5-HIAA — Most secreted serotonin is either taken back up into neurons or metabolized by monoamine oxidase (MAO) to 5-hydroxyindoleacetic acid (5-HIAA), which is then excreted in urine. Elevated urinary 5-HIAA indicates increased serotonin production, as seen in carcinoid syndrome.

Question 44

Which G-protein and second messenger system is activated by 5-HT2 receptors?

Accepted Answer

Gq → IP3 and DAG increase — 5-HT2 receptors (including 5-HT2A, 5-HT2B, 5-HT2C) couple to Gq proteins, activating phospholipase C to produce IP3 (releases Ca2+) and DAG (activates PK

Question 45

Buspirone's anxiolytic effects are mediated through:

Accepted Answer

Partial agonism at 5-HT1A receptors — Buspirone is a partial agonist at 5-HT1A receptors, which mediates its anxiolytic effects. Unlike benzodiazepines, it doesn't enhance GABA activity, has no sedative or muscle relaxant properties, and takes several weeks to produce therapeutic effects.

Question 46

Methysergide is used in migraine prophylaxis but can cause which serious adverse effect with long-term use?

Accepted Answer

Retroperitoneal and cardiac valve fibrosis — Methysergide, a non-selective 5-HT antagonist, can cause serious fibrotic complications including retroperitoneal fibrosis, pleuropulmonary fibrosis, and cardiac valve fibrosis with prolonged use. Due to this risk, it requires drug holidays and is now rarely used.

Question 47

Which enzyme releases arachidonic acid from cell membrane phospholipids, initiating eicosanoid synthesis?

Accepted Answer

Phospholipase A2 — Phospholipase A2 is the enzyme that cleaves arachidonic acid from membrane phospholipids. This is the first and crucial step in eicosanoid biosynthesis, occurring during inflammation, allergy, and cell injury. The released arachidonic acid is then metabolized by COX or lipoxygenase pathways.

Question 48

Thromboxane A2 (TXA2) produced by platelets primarily causes:

Accepted Answer

Vasoconstriction and promotion of platelet aggregation — TXA2 is synthesized by platelets via the cyclooxygenase pathway and is a potent vasoconstrictor and platelet aggregator. This is crucial for hemostasis. Aspirin's antiplatelet effect comes from irreversibly inhibiting COX in platelets, thereby preventing TXA2 synthesis.

Question 49

Leukotrienes LTC4, LTD4, and LTE4 are collectively known as cysteinyl leukotrienes because they:

Accepted Answer

Contain the amino acid cysteine in their structure — These leukotrienes are called cysteinyl leukotrienes due to the presence of the amino acid cysteine in their chemical structure. They are potent bronchoconstrictors and play a major role in asthma pathophysiology, which is why leukotriene receptor antagonists like montelukast are effective asthma treatments.

Question 50

Prostacyclin (PGI2) synthesized by vascular endothelium has effects that are opposite to TXA2, specifically:

Accepted Answer

It causes vasodilation and inhibits platelet aggregation — PGI2 and TXA2 have opposing actions, creating a balance in hemostasis. While TXA2 (from platelets) promotes vasoconstriction and aggregation, PGI2 (from endothelium) causes vasodilation and inhibits aggregation. This balance is important in maintaining vascular homeostasis.

Pharmacology Examination MCQs | MCQ Quiz | OmpathStudy Kenya

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