Mechanism of action of allopurinol is
Which of the following drug causes postural hypotension commonly?
Which of the following is a carbonic anhydrase inhibitor?
Which of the following anti-epileptic drugs has the highest teratogenic potential?
Insulin of choice for the treatment of diabetic ketoacidosis is:
Praziquantel is used for the treatment of
A lady has taken medication for amoebiasis infection. She drank alcohol on the same day. She has nausea, vomiting, and dizziness. Which anti-amoebic drug could have led to interaction with alcohol to produce these symptoms?
Which drug is used as a spermicidal cream in contraceptives?
Which is the most cardiotoxic anti-cancer drug among the following?
Mechanism of action of exenatide in diabetes mellitus is
FMGE 2019 - Pharmacology FMGE Practice Questions and MCQs
Question 11: Mechanism of action of allopurinol is
- A. Recombinant uricase
- B. Decrease chemotaxis
- C. Increase uric acid excretion
- D. Xanthine oxidase inhibition (Correct Answer)
Explanation: ***Xanthine oxidase inhibition*** - **Allopurinol** acts as a **structural analog of hypoxanthine** and competitively inhibits the enzyme **xanthine oxidase**. - By inhibiting **xanthine oxidase**, allopurinol prevents the conversion of hypoxanthine to xanthine and then to uric acid, thereby **decreasing uric acid production**. *Recombinant uricase* - **Recombinant uricase** (e.g., rasburicase, pegloticase) is an enzyme that catalyzes the breakdown of existing uric acid into allantoin, a more soluble compound. - This mechanism is distinct from allopurinol, which **prevents uric acid formation**. *Decrease chemotaxis* - Medications that **decrease chemotaxis**, such as **colchicine**, work by interfering with the migration of neutrophils to sites of inflammation, which is useful in acute gout flares. - This is an **anti-inflammatory mechanism**, not related to uric acid synthesis or excretion. *Increase uric acid excretion* - Drugs that **increase uric acid excretion** are known as **uricosurics** (e.g., probenecid, lesinurad). - These agents act on the renal tubules to **inhibit uric acid reabsorption**, thus promoting its elimination from the body.
Question 12: Which of the following drug causes postural hypotension commonly?
- A. Alpha blocker (Correct Answer)
- B. Angiotensin receptor blockers
- C. Beta blocker
- D. ACE inhibitor
Explanation: ***Alpha blocker*** - **Alpha-1 adrenergic blockers** cause common postural hypotension by blocking **alpha-1 receptors** on vascular smooth muscle, leading to vasodilation and reduced peripheral vascular resistance. - This vasodilation, especially in the upright position, can cause blood to pool in the lower extremities, decreasing venous return to the heart and thus lowering blood pressure. *Angiotensin receptor blockers* - These drugs block the effects of **angiotensin II**, leading to vasodilation and decreased aldosterone secretion, typically causing a more gradual and less pronounced drop in blood pressure. - While they can cause hypotension, **postural hypotension** is less common and usually less severe compared to alpha blockers due to their different mechanism of action and less abrupt vasodilation. *Beta blocker* - **Beta-blockers** primarily reduce heart rate and myocardial contractility, thereby decreasing cardiac output, which can contribute to generalized hypotension. - They do not directly cause significant **vasodilation** in the same manner as alpha-blockers, making postural hypotension less common unless there are other contributing factors. *ACE inhibitor* - **ACE inhibitors** prevent the conversion of angiotensin I to **angiotensin II**, leading to vasodilation and reduced aldosterone. - They can cause hypotension, especially with the first dose or in volume-depleted patients, but **postural hypotension** is typically less frequent and severe than with alpha-blockers.
Question 13: Which of the following is a carbonic anhydrase inhibitor?
- A. Hydrochlorothiazide
- B. Mannitol
- C. Furosemide
- D. Acetazolamide (Correct Answer)
Explanation: ***Acetazolamide*** - Acetazolamide is a classic example of a **carbonic anhydrase inhibitor**, primarily used as a diuretic and for managing **glaucoma** and **altitude sickness**. - It works by inhibiting the enzyme **carbonic anhydrase** in the **proximal renal tubule**, reducing bicarbonate reabsorption and thus promoting diuresis. *Hydrochlorothiazide* - Hydrochlorothiazide is a **thiazide diuretic** that acts on the **distal convoluted tubule** to inhibit the reabsorption of sodium and chloride. - It is not a carbonic anhydrase inhibitor. *Mannitol* - Mannitol is an **osmotic diuretic** that works in the **proximal tubule** and **descending limb of Henle's loop** by creating an osmotic gradient. - It is not a carbonic anhydrase inhibitor and functions by drawing water into the renal tubule, leading to increased urine output. *Furosemide* - Furosemide is a **loop diuretic** that acts on the **thick ascending limb of the loop of Henle** by inhibiting the Na+-K+-2Cl- cotransporter. - It is one of the most potent diuretics but does not inhibit carbonic anhydrase.
Question 14: Which of the following anti-epileptic drugs has the highest teratogenic potential?
- A. Carbamazepine
- B. Phenytoin
- C. Valproate (Correct Answer)
- D. Lamotrigine
Explanation: ***Correct: Valproate*** - **Valproate has the highest teratogenic potential** among all anti-epileptic drugs, with a **10-20% risk of major congenital malformations** - **Neural tube defects** (spina bifida) occur in **1-2% of exposed pregnancies**, which is 10-20 times higher than the general population - Other significant risks include **cardiac malformations, craniofacial abnormalities**, and **neurodevelopmental disorders** (autism spectrum disorder, reduced IQ) - **Fetal valproate syndrome** is a recognized clinical entity - Current guidelines strongly recommend **avoiding valproate in women of childbearing potential** unless no alternatives exist *Incorrect: Carbamazepine* - Has teratogenic risks but significantly **lower than valproate** (2-5% risk of major malformations) - Associated with **neural tube defects** (0.5-1% risk, lower than valproate) - Considered a safer alternative when valproate must be avoided *Incorrect: Phenytoin* - Causes **fetal hydantoin syndrome** with characteristic features: craniofacial anomalies, nail/digital hypoplasia, growth restriction, and developmental delay - Teratogenic risk is **moderate** (approximately 5-10% risk of major malformations) - Risk is significant but **lower than valproate** *Incorrect: Lamotrigine* - Considered **one of the safest anti-epileptic drugs** during pregnancy - Low teratogenic risk with **major malformation rate of 2-3%** (close to baseline population risk) - Slight increased risk of **oral clefts** at higher doses - **Preferred choice** for women of childbearing potential requiring anti-epileptic therapy
Question 15: Insulin of choice for the treatment of diabetic ketoacidosis is:
- A. Insulin lispro
- B. Insulin glargine
- C. NPH insulin
- D. Regular Insulin (Correct Answer)
Explanation: ***Regular Insulin*** - **Regular insulin** is the insulin of choice for treating **diabetic ketoacidosis (DKA)** because it can be administered intravenously. - Its **short onset of action** and predictable duration allow for rapid and precise titration in a critical care setting. *Insulin lispro* - **Insulin lispro** is a **rapid-acting insulin analog** typically used for mealtime coverage, which has a very quick onset and short duration. - While it acts quickly, its primary use is not for the continuous intravenous infusion required in DKA management. *Insulin glargine* - **Insulin glargine** is a **long-acting insulin analog** designed to provide basal insulin replacement. - It has a prolonged duration of action and a slow, sustained release profile, making it unsuitable for the rapid correction needed in DKA. *NPH insulin* - **NPH insulin** is an **intermediate-acting insulin** that has a delayed onset and peak effect. - Its insoluble nature and variable absorption make it inappropriate for the acute, immediate intravenous insulin therapy required in DKA.
Question 16: Praziquantel is used for the treatment of
- A. Schistosomiasis (Correct Answer)
- B. Rhinosporidiosis
- C. Strongyloidiasis
- D. Trichomoniasis
Explanation: ***Schistosomiasis*** - **Praziquantel** is the primary drug for treating all species of **schistosomiasis**, effectively killing adult worms [1], [2]. - It works by increasing the **calcium permeability** of the worm's cells, leading to muscle contraction and paralysis [2]. *Rhinosporidiosis* - **Rhinosporidiosis** is a fungal infection, and its treatment typically involves **surgical excision** of the lesions. - Antifungal agents like **dapsone** may be used as an adjuvant therapy, but praziquantel is not indicated. *Strongyloidiasis* - **Strongyloidiasis** is caused by the nematode *Strongyloides stercoralis*, and the preferred treatment is **ivermectin** [3]. - **Albendazole** is an alternative treatment option, but praziquantel is ineffective against this parasite [2], [3]. *Trichomoniasis* - **Trichomoniasis** is a sexually transmitted infection caused by the protozoan *Trichomonas vaginalis*. - It is effectively treated with **metronidazole** or **tinidazole**, while praziquantel has no activity against this protozoan.
Question 17: A lady has taken medication for amoebiasis infection. She drank alcohol on the same day. She has nausea, vomiting, and dizziness. Which anti-amoebic drug could have led to interaction with alcohol to produce these symptoms?
- A. Nitazoxanide
- B. Paromomycin
- C. Metronidazole (Correct Answer)
- D. Diloxanide
Explanation: ***Metronidazole*** - **Metronidazole** is well-known for causing a **disulfiram-like reaction** when consumed with alcohol. - This reaction leads to a rapid accumulation of **acetaldehyde**, manifesting as nausea, vomiting, flushing, headache, and dizziness. *Nitazoxanide* - **Nitazoxanide** is an oral anti-infective agent used for protozoal infections, but it is **not associated with a disulfiram-like reaction** with alcohol. - Its mechanism of action involves interfering with the **pyridoxine ferredoxin oxidoreductase enzyme**, which is distinct from alcohol metabolism. *Paromomycin* - **Paromomycin** is an aminoglycoside antibiotic primarily used for luminal amoebiasis and is **poorly absorbed from the GI tract**. - It does **not typically interact with alcohol** or cause disulfiram-like reactions. *Diloxanide* - **Diloxanide furoate** is a luminal amoebicide primarily used for asymptomatic cyst passers. - It is **not known to cause a disulfiram-like reaction** or significant interactions with alcohol.
Question 18: Which drug is used as a spermicidal cream in contraceptives?
- A. Gossypol
- B. Clomiphene
- C. Nonoxynol-9 (Correct Answer)
- D. Centchroman
Explanation: **Nonoxynol-9** - **Nonoxynol-9** is a common **spermicide** used in many contraceptive products like creams, foams, and gels. - It works by damaging the **sperm cell membrane**, effectively immobilizing and killing sperm. *Gossypol* - **Gossypol** is a natural compound found in cotton plants that has been studied for its potential as a **male contraceptive**. - It works by inhibiting **spermatogenesis** but has not been approved for widespread use due to toxicity concerns like **hypokalemia**. *Clomiphene* - **Clomiphene** is a **selective estrogen receptor modulator (SERM)** used to induce ovulation in women who are infertile due to anovulation. - It stimulates the release of **gonadotropins** (FSH and LH) from the pituitary gland, leading to follicular development. *Centchroman* - **Centchroman** (also known as Ormeloxifene) is a **non-steroidal oral contraceptive** used in India. - It acts as a **selective estrogen receptor modulator** in the uterus, disrupting the implantation process.
Question 19: Which is the most cardiotoxic anti-cancer drug among the following?
- A. Cyclophosphamide
- B. Tamoxifen
- C. Imatinib
- D. Anthracyclines (Correct Answer)
Explanation: ***Anthracyclines*** - **Anthracyclines** (e.g., doxorubicin, daunorubicin) are notorious for causing **dose-dependent cardiotoxicity**, leading to **irreversible dilated cardiomyopathy** and **heart failure**. - Their cardiotoxic effect is primarily due to the generation of **reactive oxygen species** and interference with cardiac topoisomerase IIβ. *Cyclophosphamide* - Cyclophosphamide can cause cardiotoxicity, particularly at **high doses**, manifesting as **hemorrhagic myocardial necrosis** or **pericarditis**. - However, its cardiotoxicity is generally considered **less frequent and severe** than that of anthracyclines. *Tamoxifen* - Tamoxifen is primarily associated with an **increased risk of thromboembolic events** and **endometrial cancer**. - While some cardiac effects like **QT prolongation** can occur, it is not considered a primary cardiotoxic agent leading to cardiomyopathy. *Imatinib* - Imatinib, a **tyrosine kinase inhibitor**, has been linked to **cardiac dysfunction** including heart failure in some patients. - However, the incidence and severity of cardiotoxicity with imatinib are **lower** compared to anthracyclines, which are broadly cardiotoxic.
Question 20: Mechanism of action of exenatide in diabetes mellitus is
- A. It is DPP-4 inhibitor and results in decreased breakdown of GLP
- B. It is amylin analogue and decreases glucagon
- C. It is analogue of GLP released from gut and increases glucose dependent insulin secretion (Correct Answer)
- D. It inhibits SGLT-2 and causes glucosuria
Explanation: ***It is analogue of GLP released from gut and increase glucose dependant insulin secretion*** - **Exenatide** is a **glucagon-like peptide-1 (GLP-1) receptor agonist**, mimicking the action of naturally occurring GLP-1 [1]. - It stimulates **glucose-dependent insulin secretion**, suppresses glucagon release, slows gastric emptying, and promotes satiety, all contributing to improved glycemic control [2]. *It inhibits SGLT-2 and cause glucosuria* - This describes the mechanism of **sodium-glucose co-transporter 2 (SGLT-2) inhibitors**, such as empagliflozin or canagliflozin, which promote glucose excretion in urine. - **Exenatide** does not directly affect renal glucose reabsorption. *It is DPP-4 inhibitor and result in decreased breakdown of GLP* - This mechanism belongs to **dipeptidyl peptidase-4 (DPP-4) inhibitors** (e.g., sitagliptin, saxagliptin), which prevent the rapid degradation of endogenous GLP-1, thus prolonging its action [1]. - **Exenatide** directly activates GLP-1 receptors rather than modulating the enzyme that breaks down endogenous GLP-1 [1]. *It is amylin analogue and decrease glucagon* - This describes **pramlintide**, an amylin analogue used in diabetes management, which primarily suppresses postprandial glucagon secretion, slows gastric emptying, and promotes satiety. - While **exenatide** also decreases glucagon, its primary mechanism is via GLP-1 receptor agonism [2].