FMGE 2025 - Pharmacology Practice Questions

Q: A patient came to the hospital with muscle weakness, diarrhea, and bradycardia. He was diagnosed with organophosphate poisoning for which atropine was administered. After atropine administration, which of the following changes are not seen?

Muscle weakness. ***Muscle weakness*** - Muscle weakness in organophosphate poisoning is a **nicotinic effect** caused by excessive acetylcholine at the **neuromuscular junction (NMJ)** - This leads to initial fasciculations followed by depolarization blockade and paralysis - **Atropine is a muscarinic antagonist** and has **no effect on nicotinic receptors** - Therefore, atropine does **not reverse muscle weakness** - this requires **pralidoxime** (2-PAM) to reactivate acetylcholinesterase - Muscle weakness is the change that is **NOT SEEN** after atropine administration *Bradycardia* - Bradycardia is a **muscarinic effect** on the heart (M2 receptors on SA node) - Atropine effectively blocks cardiac muscarinic receptors, leading to **increased heart rate** - This change (reversal of bradycardia) **IS SEEN** with atropine administration *Diaphoresis* - Excessive sweating is mediated by **muscarinic receptors** on eccrine sweat glands - Atropine blocks these receptors, causing **dry skin** (anticholinergic effect) - This change (cessation of sweating) **IS SEEN** with atropine *Nasal discharge* - Rhinorrhea (nasal secretions) is a **muscarinic effect** - part of SLUDGE syndrome - Atropine blocks glandular muscarinic receptors, causing **drying of secretions** - This change (reduction in nasal discharge) **IS SEEN** with atropine **Key Concept**: Atropine reverses only **muscarinic** effects (SLUDGE, bradycardia, bronchospasm) but NOT **nicotinic** effects (muscle weakness, fasciculations). Pralidoxime is needed for nicotinic symptoms.

Q: Mechanism of action of botulinum toxin is:

Inhibits the release of acetylcholine. ***Inhibits the release of Acetylcholine***- Botulinum toxin (BoNT) is a **zinc metalloprotease** that cleaves **SNARE proteins** (e.g., SNAP-25) essential for vesicular fusion and neurotransmitter release.- By preventing the exocytosis of **acetylcholine (ACh)** vesicles at the **neuromuscular junction**, BoNT causes irreversible chemical denervation and resulting **flaccid paralysis**.*Inhibits Elongation factor 2*- Inhibition of **Elongation factor 2 (EF-2)** targets the host cell's **protein synthesis** machinery, leading to cell death.- This mechanism is characteristic of toxins like **Diphtheria toxin** and *Pseudomonas aeruginosa* **Exotoxin A**, not botulinum toxin.*Inhibits the release of GABA*- While BoNT can inhibit the release of various neurotransmitters, its defining clinical effect of **flaccid paralysis** is primarily due to inhibition of **acetylcholine** at the peripheral neuromuscular junction.- Inhibition of **GABA** (an inhibitory neurotransmitter) in the CNS would typically lead to increased CNS excitability or spasms, which is contrary to the effects of botulism.*Increases cAMP*- Increasing intracellular **cAMP** levels, usually via activation of **adenylate cyclase**, is the mechanism used by toxins such as **cholera toxin** and **pertussis toxin**.- This mechanism primarily causes large fluid shifts (diarrhea) or cellular dysfunction (like impaired phagocytosis) and is unrelated to botulinum toxin's paralytic action.

Q: A 35-year-old male presents to the emergency department with complaints of blurred vision, dizziness, and severe headache after ingesting an unknown quantity of homemade alcohol earlier in the day. On examination, he is disoriented. Laboratory tests reveal severe metabolic acidosis with a high anion gap. Which metabolite is primarily responsible for the toxicity in this case?

Formic acid. ***Formic acid***- The severe clinical toxicity, including **high anion gap metabolic acidosis**, visual impairment (e.g., blurred vision, blindness), and central nervous system depression, is primarily due to the accumulation of **formic acid** (formate), which is the final toxic metabolite of methanol [1].**Formic acid** inhibits **cytochrome c oxidase** in the retina and brain, leading to cytotoxic hypoxia, specifically affecting the optic nerve and basal ganglia.*Methanol*- **Methanol** itself causes mild inebriation and CNS depression, but it is relatively non-toxic; the severe symptoms arise only after its metabolism begins [2].The signs and symptoms (blurred vision, severe acidosis) that lead to presentation typically occur after a latent period (12-24 hours) as the relatively slow conversion of methanol to **formate** occurs [2].*Formaldehyde*- **Formaldehyde** is the intermediate metabolite formed from methanol via **alcohol dehydrogenase (ADH)**; however, it is rapidly converted to formic acid by **aldehyde dehydrogenase (ALDH)** [1].Due to its rapid metabolism, **formaldehyde** does not accumulate significantly and is therefore not the major culprit responsible for the sustained **high anion gap acidosis** and end-organ damage seen clinically.*Acetic acid*- **Acetic acid** is the final, non-toxic metabolite of **ethanol** metabolism (ethanol -> acetaldehyde -> acetic acid).Ingestion of methanol does not result in the production of **acetic acid**, and this substance plays no role in the clinical picture of methanol poisoning.

Q: In paracetamol poisoning, N-acetylcysteine is administered as an antidote. How does it act to prevent toxicity?

Restores glutathione levels. ***Restores glutathione levels*** - NAC acts as a **precursor** to the synthesis of **glutathione (GSH)**, which is essential for detoxifying the toxic metabolite of paracetamol, **NAPQI**. - By restoring GSH levels, NAC allows **NAPQI** to be conjugated and safely excreted, preventing **hepatocellular necrosis**. *Inhibits the toxin* - NAC does not directly inhibit the formation or activity of the toxic metabolite **NAPQI**, but rather boosts the body's capacity to detoxify it. - The primary mechanism is replenishment of the depleted endogenous antioxidant and detoxifying agent, **glutathione**. *Removes the toxin* - NAC does not increase the clearance or physical removal of paracetamol or its metabolites from the system (unlike measures such as **gastric lavage** or hemodialysis). - Its role is conversion: it helps convert the highly reactive **NAPQI** metabolite into a benign, excretable compound directly within the liver. *Neutralizes liver enzymes* - NAC's mechanism is not focused on neutralizing liver enzymes, but on preventing **NAPQI** from causing **covalent binding** and damage to these enzymes and other cellular macromolecules. - Paracetamol toxicity leads to damage due to **oxidative injury** and depletion of defenses, not primarily due to unwanted enzyme neutralization.

Q: A patient with osteoarthritis, for the last 3 months, has been taking ibuprofen and has developed occult GI bleeding. Which is correct about the cause?

PGE-2 and prostacyclin production were reduced. ***PGE-2 and prostacyclin production were reduced***- NSAIDs like **ibuprofen** inhibit cyclooxygenase-1 (**COX-1**), which is responsible for synthesizing protective prostaglandins like **PGE2** and **prostacyclin (PGI2)** in the GI mucosa.- The loss of these protective factors impairs the mucosal barrier's ability to withstand acid, leading to ulceration, erosion, and subsequent **occult GI bleeding**. *Increased acid production*- NSAIDs primarily cause mucosal injury by reducing protective factors, not by significantly increasing **basal acid production**.- Although excess acid facilitates damage, the core mechanism of NSAID injury is the loss of **prostaglandin-mediated cytoprotection**. *PGE-1 and prostacyclin production were reduced*- While **prostacyclin (PGI2)** reduction is key, **PGE2** (not PGE1) is the major endogenous prostaglandin responsible for maintaining gastric mucosal integrity in humans.- Misrepresenting the primary protective prostaglandin (PGE2 vs PGE1) makes this option medically less precise than the former. *Mucosal injury due to inhibition of COX-2*- The severe gastrointestinal side effects, including bleeding and ulceration, are predominantly due to the inhibition of the constitutive **COX-1 isoenzyme**.- Selective **COX-2 inhibitors** (coxibs) were specifically designed to minimize GI toxicity by sparing the protective functions of COX-1.

Q: A patient with schizophrenia, developed muscular dystonia and was treated for it. The patient now presents with complaints of dry mouth, dizziness, and hypotension. What is the most likely drug causing these side effects?

Benzotropine. ***Benzotropine***- This drug is an **anticholinergic agent** administered specifically to treat **extrapyramidal symptoms (EPS)** like acute muscular dystonia caused by antipsychotics.- **Dry mouth** is a characteristic manifestation of its peripheral **anticholinergic side effects**, while **dizziness and hypotension** can occur due to central effects or potentiation of adrenergic blockade, particularly when co-administered with antipsychotics.*Risperidone*- Although Risperidone (an atypical antipsychotic) commonly causes EPS and strong **orthostatic hypotension** due to **alpha-1 adrenergic blockade** (dizziness/hypotension), it has moderate anticholinergic activity, making it less likely to be the sole cause of prominent dry mouth.- The patient's presentation suggests a new medication was introduced *after* the dystonia developed; Risperidone was likely the cause of the *initial* dystonia.*Haloperidol*- Haloperidol, a high-potency typical antipsychotic, is a common cause of **muscular dystonia** (EPS).- It has relatively **low anticholinergic activity** and is therefore an improbable cause of severe **dry mouth** compared to agents like Benzotropine.*Propranolol*- Propranolol is a **beta-blocker** typically used to treat antipsychotic-induced **akathisia** or tremor, not acute dystonia.- Its most prominent side effects are related to beta-blockade, such as **bradycardia** and fatigue; it is not routinely associated with significant **dry mouth**.

Q: A child accidentally took a bottle full of iron tablets. Which of the drugs is used as an antidote for iron poisoning?

Deferoxamine. ***Deferoxamine***- It is the standard **chelating agent** administered via intravenous or intramuscular routes for treating life-threatening acute **iron overdose** (toxicity) [1].- It binds strongly to free **ferric iron (Fe3+)** in the circulation, forming the non-toxic, water-soluble complex *ferrioxamine* which is then excreted in the urine [1].*Luspatercept*- This is an **erythroid maturation agent** used to treat **anemia** associated with *myelodysplastic syndromes* (MDS) and *beta-thalassemia*.- It functions by modulating the **TGF-β signaling pathway** to reduce ineffective erythropoiesis, not by direct heavy metal chelation.*Deferiprone*- This is an **oral iron chelator** primarily used for the management of **chronic iron overload**, often seen in patients receiving frequent blood transfusions (e.g., thalassemia).- While it removes iron, it is generally less effective and not the first-line choice for the management of acute life-threatening pediatric poisoning, where **intravenous Deferoxamine** is mandatory.*DMSA*- DMSA (Succimer) is a heavy metal chelating agent primarily indicated for poisoning by **lead**, **arsenic**, and **mercury**.- It is administered orally and is structurally distinct from iron chelators like deferoxamine, making it unsuitable for treating acute iron toxicity.

Q: A child is brought to the hospital with pinpoint pupils and difficulty breathing after playing at home. What is the most likely substance the child accidentally ingested?

Opioid. ***Opioid*** - Opioid toxicity classically causes the triad of **miosis (pinpoint pupils)**, **respiratory depression**, and **altered mental status**. - The difficulty breathing is a critical sign of opioid overdose due to reduced sensitivity of the brainstem's respiratory centers to **carbon dioxide**. - In a home setting, accidental ingestion of prescription opioid medications (morphine, codeine, oxycodone) is a common pediatric emergency. *Organophosphate* - While organophosphates cause **miosis** (pinpoint pupils) due to excessive parasympathetic stimulation, they typically cause a cholinergic crisis with copious secretions (salivation, lacrimation) and **bronchospasm** (wet lungs). - The clinical picture usually includes muscle weakness, fasciculations, and the pronounced **SLUDGE** syndrome (Salivation, Lacrimation, Urination, Defecation, GI distress, Emesis), which differentiates it from isolated respiratory depression and miosis. - More commonly associated with agricultural or pesticide exposure rather than typical home ingestion. *Atropine* - Atropine is an anticholinergic agent that causes the opposite effects, specifically **mydriasis (dilated pupils)**, dry skin, and tachycardia (anticholinergic toxidrome). - Patients present with flushed, dry skin, urinary retention, hyperthermia, and altered mental status ("hot as a hare, blind as a bat, dry as a bone, red as a beet, mad as a hatter"). - Would not cause pinpoint pupils or the respiratory depression seen in this case. *Benzodiazepine* - Benzodiazepines can cause **respiratory depression** and CNS depression, but they do not typically cause **miosis (pinpoint pupils)**. - Pupils are usually normal or slightly dilated with benzodiazepine overdose. - The absence of pinpoint pupils makes this diagnosis unlikely in this clinical presentation.

Q: A 12-year-old child presents with palpitations, tremors, dry mouth, heart rate 130 bpm, respiratory rate 34/min. Which of the following substances is most likely responsible?

TCA (tricyclic antidepressant). ***TCA (tricyclic antidepressant)***- The constellation of tachycardia (palpitations, HR 130 bpm), tremors, and dry mouth suggests a severe mixed toxidrome, highly characteristic of a TCA overdose.- TCAs exhibit potent **anticholinergic effects** (dry mouth, tachycardia) combined with severe **sodium channel blockade** (contributing to CNS symptoms like tremors and cardiovascular instability) resulting in this critical presentation [1].*Lithium*- Lithium toxicity primarily presents with progressive **neurological symptoms** like ataxia, coarse tremors, lethargy, and seizures.- While tremor is present, the severe **tachycardia** and pronounced **dry mouth** are not typical primary features of the lithium toxidrome.*Opioid*- Opioid toxicity is defined by the classic triad of **miosis** (pinpoint pupils), **respiratory depression** (bradypnea), and altered consciousness.- The patient is profoundly **tachycardic** (130 bpm) and **tachypneic** (34/min), which directly contradicts the expected findings of an opioid overdose.*Propranolol*- Propranolol is a **beta-blocker**, and its overdose typically causes **bradycardia**, hypotension, and potential non-cardiogenic pulmonary edema.- The patient's presentation of significant **tachycardia** (130 bpm) rules out poisoning by a beta-blocking agent.

Question 1

A patient came to the hospital with muscle weakness, diarrhea, and bradycardia. He was diagnosed with organophosphate poisoning for which atropine was administered. After atropine administration, which of the following changes are not seen?

Accepted Answer

Muscle weakness

Answer

Nasal discharge

Answer

Bradycardia

Answer

Diaphoresis

Question 2

What is the mechanism of action of botulinum toxin?

Accepted Answer

Inhibits acetylcholine release from the presynaptic terminal

Answer

Blocks the postsynaptic acetylcholine receptor

Answer

Inhibits acetylcholine reuptake

Answer

Inhibits acetylcholinesterase

Question 3

Mechanism of action of botulinum toxin is:

Accepted Answer

Inhibits the release of acetylcholine

Answer

Increases cAMP

Answer

Inhibits the release of GABA

Answer

Inhibits Elongation Factor 2

Question 4

A 35-year-old male presents to the emergency department with complaints of blurred vision, dizziness, and severe headache after ingesting an unknown quantity of homemade alcohol earlier in the day. On examination, he is disoriented. Laboratory tests reveal severe metabolic acidosis with a high anion gap. Which metabolite is primarily responsible for the toxicity in this case?

Accepted Answer

Formic acid

Answer

Formaldehyde

Answer

Acetic acid

Answer

Methanol

Question 5

In paracetamol poisoning, N-acetylcysteine is administered as an antidote. How does it act to prevent toxicity?

Accepted Answer

Restores glutathione levels

Answer

Removes the toxin

Answer

Neutralizes liver enzymes

Answer

Inhibits the toxin

Question 6

A patient with osteoarthritis, for the last 3 months, has been taking ibuprofen and has developed occult GI bleeding. Which is correct about the cause?

Accepted Answer

PGE-2 and prostacyclin production were reduced

Answer

PGE-1 and prostacyclin production were reduced

Answer

Increased acid production

Answer

Mucosal injury due to inhibition of COX-2

Question 7

A patient with schizophrenia, developed muscular dystonia and was treated for it. The patient now presents with complaints of dry mouth, dizziness, and hypotension. What is the most likely drug causing these side effects?

Accepted Answer

Benzotropine

Answer

Propranolol

Answer

Risperidone

Answer

Haloperidol

Question 8

A child accidentally took a bottle full of iron tablets. Which of the drugs is used as an antidote for iron poisoning?

Accepted Answer

Deferoxamine

Answer

DMSA

Answer

Deferiprone

Answer

Luspatercept

Question 9

A child is brought to the hospital with pinpoint pupils and difficulty breathing after playing at home. What is the most likely substance the child accidentally ingested?

Accepted Answer

Opioid

Answer

Benzodiazepine

Answer

Atropine

Answer

Organophosphate

Question 10

A 12-year-old child presents with palpitations, tremors, dry mouth, heart rate 130 bpm, respiratory rate 34/min. Which of the following substances is most likely responsible?

Accepted Answer

TCA (tricyclic antidepressant)

Answer

Opioid

Answer

Propranolol

Answer

Lithium

FMGE 2025 — Pharmacology