Prokinetic Agents — MCQs
Which of the following is a guanylate cyclase agonist used in irritable bowel syndrome?
Which of the following antipsychotics is a partial D2 agonist?
Which of the following is not considered a prokinetic agent?
An 86-year-old lady presented with severe constipation. She was a known hypertensive on medications for 10 years. In clinic, her BP was 157/98 mm Hg with a heart rate of 58/min. On taking her BP in the supine position, it was found to be 90/60 mm Hg. She had a recent history of depression. She is taking atenolol, thiazide, imipramine, haloperidol, and docusate. What is the next best step in the management?
What is the mechanism of action of Tegaserod?
Which of the following is not a recognized use of alpha-2-agonists?
Prucalopride is a
What is the treatment for extrapyramidal side effects induced by Haloperidol?
Which of the following is not a prokinetic?
What is the drug that can be used for rheumatic fever prophylaxis in a patient with a history of allergy to Penicillin?
Prokinetic Agents Indian Medical PG Practice Questions and MCQs
Question 1: Which of the following is a guanylate cyclase agonist used in irritable bowel syndrome?
- A. Linaclotide (Correct Answer)
- B. Tegaserod
- C. Methyl naltrexone
- D. Lubiprostone
Explanation: ***Linaclotide*** - **Linaclotide** is an oral guanylate cyclase-C agonist approved for treating **constipation-predominant irritable bowel syndrome (IBS-C)** and **chronic idiopathic constipation (CIC)** [1]. - It works by increasing intracellular and extracellular **cyclic guanosine monophosphate (cGMP)**, leading to increased fluid secretion into the intestinal lumen and accelerated transit [1]. *Lubiprostone* - **Lubiprostone** is a **chloride channel activator**, specifically type 2 chloride channels, which enhances intestinal fluid secretion [1]. - It is used for **IBS-C** and **CIC**, but its mechanism of action is distinct from guanylate cyclase agonism [1]. *Tegaserod* - **Tegaserod** is a **5-HT4 receptor partial agonist** that was previously used for IBS-C in women [2], [3]. - Its prokinetic effects are mediated through serotonin receptors, not guanylate cyclase pathways [2]. *Methyl naltrexone* - **Methyl naltrexone** is a **peripherally acting mu-opioid receptor antagonist** used to treat **opioid-induced constipation** in advanced illness [1]. - It specifically blocks the constipating effects of opioids without crossing the blood-brain barrier, thus avoiding reversal of central opioid analgesia.
Question 2: Which of the following antipsychotics is a partial D2 agonist?
- A. Clozapine
- B. Quetiapine
- C. Ziprasidone
- D. Aripiprazole (Correct Answer)
Explanation: Aripiprazole - Aripiprazole is a D2 partial agonist [1][3], meaning it acts as an agonist in areas with low dopamine and an antagonist in areas with high dopamine [3]. - This unique mechanism helps to stabilize dopamine activity, leading to fewer extrapyramidal symptoms and hyperprolactinemia compared to typical antipsychotics. Clozapine - Clozapine is a D2 antagonist with a high affinity for D4 receptors and potent antagonism of 5-HT2A receptors; it is known for its efficacy in treatment-resistant schizophrenia [2]. - It carries a risk of severe side effects such as agranulocytosis [2] and myocarditis, requiring regular blood monitoring. Quetiapine - Quetiapine is primarily a D2 antagonist with significant antagonism at histamine H1 and alpha-1 adrenergic receptors, contributing to its sedative and orthostatic hypotensive effects. - It is known for its relatively low risk of extrapyramidal symptoms due to its rapid dissociation from D2 receptors. Ziprasidone - Ziprasidone is a D2 antagonist and a serotonin 5-HT1A agonist and 5-HT2C antagonist, contributing to its antidepressant and anti-anxiety effects. - It is associated with a risk of QTc prolongation, which necessitates cardiac monitoring in susceptible patients.
Question 3: Which of the following is not considered a prokinetic agent?
- A. Dopamine antagonist
- B. 5HT4 agonist
- C. Macrolides
- D. Diphenylmethane (Correct Answer)
Explanation: Diphenylmethane derivatives (e.g., bisacodyl, sodium picosulfate) are stimulant laxatives, not prokinetic agents. While they do increase colonic motility, they work by direct stimulation of the colonic mucosa and myenteric plexus, causing increased water secretion and peristalsis [3]. Prokinetic agents specifically enhance coordinated gastrointestinal motility through modulation of neurotransmitters (acetylcholine, dopamine, serotonin, motilin), whereas laxatives work through different mechanisms (osmotic effects, stimulation, bulk formation). Therefore, diphenylmethane derivatives are classified as laxatives, not prokinetics. Dopamine antagonist - Dopamine antagonists like metoclopramide and domperidone block D2 receptors in the chemoreceptor trigger zone and GI tract, enhancing acetylcholine release and promoting gastric emptying [2]. - They are commonly used as prokinetic agents and antiemetics [2]. 5HT4 agonist - 5HT4 agonists (e.g., cisapride, prucalopride) stimulate serotonin receptors in the enteric nervous system, increasing acetylcholine release and enhancing colonic motility [1]. - They are effective prokinetic agents for conditions like chronic constipation and gastroparesis [1]. Macrolides - Certain macrolide antibiotics, such as erythromycin, act as motilin receptor agonists at sub-antibiotic doses. - By mimicking motilin, they stimulate gastric and intestinal contractions (phase III of migrating motor complex), functioning as prokinetic agents.
Question 4: An 86-year-old lady presented with severe constipation. She was a known hypertensive on medications for 10 years. In clinic, her BP was 157/98 mm Hg with a heart rate of 58/min. On taking her BP in the supine position, it was found to be 90/60 mm Hg. She had a recent history of depression. She is taking atenolol, thiazide, imipramine, haloperidol, and docusate. What is the next best step in the management?
- A. Change atenolol and thiazide to calcium channel blocker and ACE inhibitor and add bisacodyl for constipation
- B. Change imipramine and haloperidol to fluoxetine and risperidone and add bisacodyl for constipation (Correct Answer)
- C. Only add bisacodyl for constipation and continue rest of the medications
- D. Discontinue all her medications and start her on steroids
Explanation: ***Change imipramine and haloperidol to fluoxetine and risperidone and add bisacodyl for constipation*** - The patient's presentation with **severe constipation** and **orthostatic hypotension** (supine BP 90/60 mmHg from 157/98 mmHg) strongly suggests drug-induced side effects. Older people are especially sensitive to drugs that can cause postural hypotension, and for any presenting problem in old age, the possibility that medication is a contributory factor should be considered [1]. Both **imipramine** (a tricyclic antidepressant) and **haloperidol** (an antipsychotic) have significant **anticholinergic effects**, which can cause severe constipation and worsen orthostatic hypotension. - Switching to **fluoxetine** (an SSRI with fewer anticholinergic effects) and **risperidone** (an atypical antipsychotic with less anticholinergic burden than haloperidol) would mitigate these side effects. Postural hypotension in older adults is defined as a drop in blood pressure of >20 mmHg systolic or >10 mmHg diastolic upon standing [2]. Adding **bisacodyl**, a stimulant laxative, directly addresses her severe constipation. *Change atenolol and thiazide to calcium channel blocker and ACE inhibitor and add bisacodyl for constipation* - While atenolol and thiazide can contribute to orthostatic hypotension, the primary drivers of her severe constipation and marked anticholinergic side effects are likely **imipramine** and **haloperidol**. - Changing the antihypertensive medications alone would not adequately address the severe constipation or the underlying pharmacological cause of her symptoms. *Only add bisacodyl for constipation and continue rest of the medications* - Simply adding a **laxative** without addressing the underlying drug-induced issues would not resolve the root cause of her severe constipation and orthostatic hypotension. Failure to recognise ADRs may lead to the use of further drugs to treat the problem, making matters worse [1]. - Continuing **imipramine** and **haloperidol** would perpetuate the significant anticholinergic side effects, leading to ongoing symptoms and potential complications. *Discontinue all her medications and start her on steroids* - **Discontinuing all medications** without a clear rationale is generally unsafe, especially in an elderly patient with multiple comorbidities like hypertension and depression. - **Steroids** are not indicated for constipation or orthostatic hypotension in this context and could introduce a new set of serious side effects.
Question 5: What is the mechanism of action of Tegaserod?
- A. 5HT3 receptor antagonist
- B. Dopamine D2 receptor antagonist
- C. 5HT4 receptor agonist (Correct Answer)
- D. NK1 receptor antagonist
Explanation: ***5HT4 receptor agonist*** - Tegaserod is a **selective serotonin 5-HT4 receptor partial agonist** that facilitates the release of neurotransmitters. - This action **stimulates the peristaltic reflex** and intestinal secretion, thereby accelerating intestinal transit and alleviating symptoms of **irritable bowel syndrome with constipation (IBS-C)**. *5HT3 receptor antagonist* - **5-HT3 receptor antagonists** (e.g., ondansetron) are primarily used as **antiemetics** to prevent nausea and vomiting. - They work by blocking serotonin's action at 5-HT3 receptors in the gastrointestinal tract and the **chemoreceptor trigger zone** in the brain. *Dopamine D2 receptor antagonist* - **Dopamine D2 receptor antagonists** (e.g., metoclopramide) are used as **prokinetics** and antiemetics due to their ability to block dopamine's inhibitory effect on gastrointestinal motility. - They increase **gastric emptying** and intestinal transit, but this is not the primary mechanism of tegaserod. *NK1 receptor antagonist* - **Neurokinin-1 (NK1) receptor antagonists** (e.g., aprepitant) are primarily used for their **antiemetic properties**, particularly in chemotherapy-induced nausea and vomiting. - They block the action of **substance P** at the NK1 receptor, which is involved in the emetic reflex.
Question 6: Which of the following is not a recognized use of alpha-2-agonists?
- A. Glaucoma
- B. Hypertension
- C. Sedation
- D. Benign Hyperplasia of prostate (Correct Answer)
Explanation: ***Correct Answer: Benign Hyperplasia of prostate*** - Alpha-2-agonists are **NOT** used to treat **benign prostatic hyperplasia (BPH)**; this condition is typically managed with **alpha-1-blockers** (e.g., tamsulosin, alfuzosin) or 5-alpha-reductase inhibitors. - Alpha-1-blockers relax the smooth muscle in the prostate and bladder neck, improving urine flow, which involves a different receptor mechanism than alpha-2-agonists. - Alpha-2-agonists would not provide therapeutic benefit for BPH. *Incorrect: Glaucoma* - Alpha-2-agonists (e.g., **brimonidine**, **apraclonidine**) **are** used to treat **glaucoma** by reducing aqueous humor production and increasing uveoscleral outflow. - This action helps to **lower intraocular pressure**, a primary goal in glaucoma management. *Incorrect: Hypertension* - Central-acting alpha-2-agonists (e.g., **clonidine**, **methyldopa**) **are** used as **antihypertensive agents**. - They reduce sympathetic outflow from the central nervous system, leading to decreased heart rate, vasodilation, and consequently, **lower blood pressure**. *Incorrect: Sedation* - Alpha-2-agonists like **dexmedetomidine** and **clonidine** **are** commonly used for **sedation** in critically ill patients, especially in intensive care units. - They produce sedation, analgesia, and anxiolysis without causing significant respiratory depression, making them valuable in certain clinical settings.
Question 7: Prucalopride is a
- A. 5HT4 agonist (Correct Answer)
- B. 5HT2b agonist
- C. 5HT2b antagonist
- D. 5HT1a partial agonist
Explanation: ***5HT4 agonist*** - **Prucalopride** is a highly selective, high-affinity **5HT4 receptor agonist** used to treat chronic idiopathic constipation. - Its activation of **5HT4 receptors** in the enteric nervous system stimulates gut motility and promotes colonic transit. *5HT2b agonist* - Agonism of **5HT2b receptors** is not the primary mechanism of action for prucalopride. - While 5HT2b receptors are present in the GI tract, their activation is not the therapeutic target for constipation relief with prucalopride. *5HT2b antagonist* - Prucalopride's therapeutic effect is due to agonism, not antagonism, of serotonin receptors. - Antagonism of **5HT2b receptors** would likely have different or even opposing effects on gut motility compared to prucalopride. *5HT1a partial agonist* - **5HT1a partial agonism** is characteristic of some anxiolytics and antidepressants, but not prucalopride. - This receptor subtype is primarily involved in central nervous system functions, not the direct regulation of gastrointestinal motility targeted by prucalopride.
Question 8: What is the treatment for extrapyramidal side effects induced by Haloperidol?
- A. Barbiturates
- B. SSRIs
- C. Benzodiazepines
- D. Anticholinergic drugs (Correct Answer)
Explanation: ***Anticholinergic drugs (effective treatment)*** - **Anticholinergic medications**, such as **benztropine** or **diphenhydramine**, are the primary treatment for **acute extrapyramidal symptoms (EPS)** like dystonia and parkinsonism induced by antipsychotics like haloperidol. - They work by **blocking muscarinic acetylcholine receptors**, helping to restore the balance between dopamine and acetylcholine in the basal ganglia. *Benzodiazepines (used for anxiety and muscle relaxation)* - While benzodiazepines can offer some relief for **akathisia** (a form of EPS characterized by restlessness) due to their sedative and muscle relaxant properties, they are **not the first-line treatment for other acute EPS** such as dystonia or parkinsonism. - They primarily enhance **GABAergic transmission** and are effective for anxiety and seizure control rather than direct antagonism of EPS mechanisms. *Barbiturates (used as sedative-hypnotic drugs)* - **Barbiturates** are strong central nervous system depressants used for sedation, anesthesia, and seizure control, but are **not indicated for the treatment of EPS**. - Their significant **sedative and addictive potential**, along with a narrow therapeutic index, makes them unsuitable for this purpose. *SSRIs (used for depression and anxiety)* - **SSRIs (Selective Serotonin Reuptake Inhibitors)** are antidepressants that work by increasing serotonin levels in the brain and are used to treat depression, anxiety, and obsessive-compulsive disorder. - They **do not have a direct role** in ameliorating dopamine-acetylcholine imbalance responsible for haloperidol-induced EPS.
Question 9: Which of the following is not a prokinetic?
- A. Macrolides
- B. D2 blocker
- C. 5HT4 agonist
- D. Loperamide derivative (Correct Answer)
Explanation: **Loperamide derivative** - **Loperamide** is an **opioid receptor agonist** that acts on the mu-opioid receptors in the gut, primarily to **decrease gastrointestinal motility** and treat diarrhea. - Its mechanism of action directly opposes that of prokinetic agents, which aim to increase GI motility. *Macrolides* - Certain macrolide antibiotics, particularly **erythromycin**, act as **motilin receptor agonists** at low doses. - This agonism leads to increased gastric motility and can be used as a prokinetic in conditions like gastroparesis. *D2 blocker* - **Dopamine D2 receptor antagonists** (e.g., **metoclopramide**, **domperidone**) block the inhibitory effect of dopamine on cholinergic smooth muscle. - This blockade enhances acetylcholine release, leading to increased gastrointestinal motility and prokinetic effects. *5HT4 agonist* - **Serotonin 5-HT4 receptor agonists** (e.g., **cisapride**, **prucalopride**) stimulate the release of acetylcholine and other excitatory neurotransmitters in the enteric nervous system. - This action promotes increased gastrointestinal motility, making them effective prokinetic agents.
Question 10: What is the drug that can be used for rheumatic fever prophylaxis in a patient with a history of allergy to Penicillin?
- A. Erythromycin (Correct Answer)
- B. Amoxicillin
- C. Streptomycin
- D. Sulfasalazine
Explanation: ***Erythromycin*** - **Erythromycin** is a macrolide antibiotic that is a suitable alternative for **rheumatic fever prophylaxis** in patients with a documented allergy to penicillin. - It effectively covers *Streptococcus pyogenes*, the causative agent of group A streptococcal (GAS) pharyngitis that precedes rheumatic fever. *Amoxicillin* - **Amoxicillin** is a penicillin-class antibiotic and would be contraindicated in a patient with a **penicillin allergy**, as it carries a high risk of cross-reactivity and allergic reaction. - Using amoxicillin in this scenario could lead to severe hypersensitivity reactions, compromising patient safety. *Streptomycin* - **Streptomycin** is an aminoglycoside antibiotic primarily used for infections like **tuberculosis** and severe bacterial endocarditis. - It is not indicated for the treatment of *Streptococcus pyogenes* infections or for **rheumatic fever prophylaxis**. *Sulfasalazine* - **Sulfasalazine** is an anti-inflammatory and immunomodulatory drug primarily used in the management of **inflammatory bowel disease** and **rheumatoid arthritis**. - It has no antimicrobial activity against *Streptococcus pyogenes* and is therefore not used for **rheumatic fever prophylaxis**.
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free