FMGE 2019 — Pharmacology
27 Previous Year Questions with Answers & Explanations
Allopurinol inhibits which enzyme?
All of the following can result in gynecomastia except:
Mechanism of action of atropine in treatment of organophosphate poisoning is?
Which of the following is the shortest-acting corticosteroid?
Which of the following is a monoclonal antibody used in cancer treatment?
Hydrochlorothiazide works by inhibiting
Which of the following is an oral direct thrombin inhibitor?
What is the dose of mifepristone in emergency contraception?
Which of the following is the chemoprophylaxis of choice in a person who is on a journey to endemic malarial region?
Therapeutic drug monitoring is done for:
FMGE 2019 - Pharmacology FMGE Practice Questions and MCQs
Question 1: Allopurinol inhibits which enzyme?
- A. Lysyl oxidase
- B. Xanthine oxidase (Correct Answer)
- C. Cyclooxygenase
- D. Kinase
Explanation: ***Xanthine oxidase*** - Allopurinol is a **purine analog** that acts as a **competitive inhibitor** of the enzyme **xanthine oxidase**. - By inhibiting xanthine oxidase, allopurinol prevents the conversion of **hypoxanthine to xanthine** and subsequently to **uric acid**, thereby lowering serum uric acid levels. *Lysyl oxidase* - **Lysyl oxidase** is an enzyme involved in the **cross-linking of collagen and elastin**, crucial for the stability of connective tissues. - Its inhibition would not directly affect **uric acid metabolism** or be a mechanism of allopurinol's action. *Cyclooxygenase* - **Cyclooxygenase (COX)** is a key enzyme in the synthesis of **prostaglandins and thromboxanes** from arachidonic acid, mediating inflammation and pain. - **NSAIDs** are inhibitors of cyclooxygenase, not allopurinol. *Kinase* - **Kinases** are a broad class of enzymes that **catalyze the transfer of phosphate groups** from high-energy molecules (like ATP) to specific substrates. - While essential for many cellular processes, kinases are not the specific target of **allopurinol** in uric acid reduction.
Question 2: All of the following can result in gynecomastia except:
- A. Spironolactone
- B. Digoxin
- C. Aromatase inhibitors (Correct Answer)
- D. Sulphonamides
Explanation: ***Aromatase inhibitors*** - **Aromatase inhibitors** block the conversion of androgens to estrogens, thereby **decreasing estrogen levels** which would prevent rather than cause gynecomastia. - They are used in estrogen-sensitive breast cancers to reduce estrogen-dependent growth. *Spironolactone* - **Spironolactone** is an aldosterone antagonist that also possesses anti-androgenic effects and can inhibit androgen synthesis, leading to an **increased estrogen-to-androgen ratio** and gynecomastia. - It can also directly stimulate the estrogen receptor in male breast tissue. *Sulphonamides* - Certain **sulphonamides**, particularly sulfasalazine, have been associated with gynecomastia, possibly due to direct toxic effects on testicular function leading to a **relative increase in estrogen activity**. - While less common than with some other drugs, it can alter the estrogen-androgen balance. *Digoxin* - **Digoxin** can cause gynecomastia by mimicking estrogen physiologically or by inhibiting androgen production, leading to an **alteration in the estrogen-to-androgen ratio**. - The risk of gynecomastia is especially noted with prolonged use and higher doses of digoxin.
Question 3: Mechanism of action of atropine in treatment of organophosphate poisoning is?
- A. It inhibits secretion of acetylcholine
- B. It has antimuscarinic activity (Correct Answer)
- C. It is reactivator of acetylcholine esterase enzyme
- D. It is agonist of acetylcholine receptors
Explanation: ***It has antimuscarinic activity*** - **Organophosphate poisoning** leads to **excessive acetylcholine** at muscarinic receptors, causing symptoms like miosis, bradycardia, and increased secretions. - **Atropine** is a **competitive antagonist** at these muscarinic receptors, thereby blocking the effects of excess acetylcholine. *It inhibits secretion of acetylcholine* - Atropine does not directly inhibit the secretion of **acetylcholine** from nerve terminals. - Its action is postsynaptic, specifically at the **receptor level**. *It is reactivator of acetylcholine esterase enzyme* - **Pralidoxime (2-PAM)** and other **oximes** are the drugs that reactivate **acetylcholinesterase**. - Atropine does not reactivate the enzyme; it only blocks the effects of acetylcholine. *It is agonist of acetylcholine receptors* - An **agonist** would mimic the effects of acetylcholine, which would worsen the symptoms of organophosphate poisoning. - Atropine is an **antagonist**, meaning it blocks the receptors.
Question 4: Which of the following is the shortest-acting corticosteroid?
- A. Dexamethasone
- B. Hydrocortisone (Correct Answer)
- C. Triamcinolone
- D. Deflazacort
Explanation: ***Hydrocortisone***- **Hydrocortisone** is considered a **short-acting corticosteroid** with a biological half-life of 8-12 hours [1].- It is a naturally occurring glucocorticoid, acting as a direct replacement for cortisol.- Among the given options, it has the shortest duration of action.*Dexamethasone*- **Dexamethasone** is a **long-acting corticosteroid** with a biological half-life of 36-72 hours.- Its potent and prolonged action makes it suitable for conditions requiring sustained anti-inflammatory or immunosuppressive effects.*Triamcinolone*- **Triamcinolone** is an **intermediate-acting corticosteroid** with a biological half-life typically ranging from 18-36 hours.- It is commonly used for its anti-inflammatory effects in conditions like allergies, asthma, and skin disorders.*Deflazacort*- **Deflazacort** is an **intermediate-acting corticosteroid** with a duration of action of approximately 12-18 hours.- It is a prodrug that is metabolized to 21-desacetyl deflazacort, the active form, often used in conditions like Duchenne muscular dystrophy and inflammatory disorders.
Question 5: Which of the following is a monoclonal antibody used in cancer treatment?
- A. Cisplatin
- B. Rituximab (Correct Answer)
- C. 5-fluorouracil
- D. Methotrexate
Explanation: ***Rituximab*** - **Rituximab** is a **chimeric monoclonal antibody** that targets the **CD20 protein** found on the surface of normal and malignant **B lymphocytes**. - It is widely used in the treatment of various **lymphomas** and **leukemias**, as well as autoimmune diseases, by inducing the death of CD20-positive B cells. *Cisplatin* - **Cisplatin** is a **platinum-based chemotherapy drug** that works by forming **DNA adducts**, leading to DNA damage and apoptosis of cancer cells. - It is used in various solid tumors but is not a monoclonal antibody; it's a **cytotoxic agent**. *5-fluorouracil* - **5-fluorouracil (5-FU)** is an **antimetabolite chemotherapy drug** that interferes with DNA and RNA synthesis, thereby inhibiting cell division. - It is a **pyrimidine analog** and not a monoclonal antibody. *Methotrexate* - **Methotrexate** is a **folate analog antimetabolite** that inhibits **dihydrofolate reductase**, interfering with DNA synthesis and cell proliferation. - It's a conventional chemotherapy agent and immunosuppressant, not a monoclonal antibody.
Question 6: Hydrochlorothiazide works by inhibiting
- A. Na+ Cl pump in late DCT
- B. Na+ K+ 2Cl pump in descending limb of loop of Henle
- C. Na+ K+ 2Cl pump in ascending limb of loop of Henle
- D. Na+ Cl pump in early DCT (Correct Answer)
Explanation: ***Na+ Cl pump in early DCT*** - **Hydrochlorothiazide** is a **thiazide diuretic** that acts primarily on the **early distal convoluted tubule (DCT)**. - It inhibits the **sodium-chloride cotransporter (NCC)**, leading to increased excretion of sodium, chloride, and water. *Na+ Cl pump in late DCT* - The **late DCT** and collecting duct are primarily involved in fine-tuning sodium reabsorption, influenced by **aldosterone**, not the primary site of action for thiazides. - The **epithelial sodium channel (ENaC)** and Na+/K+-ATPase are more prominent here. *Na+ K+ 2Cl pump in descending limb of loop of Henle* - The **descending limb of the loop of Henle** is primarily permeable to water, with no active ion pumps like **Na+ K+ 2Cl pump**. - Its main function is to concentrate the urine by allowing water to move out. *Na+ K+ 2Cl pump in ascending limb of loop of Henle* - **Furosemide** and other **loop diuretics** act on the **Na+ K+ 2Cl cotransporter (NKCC2)** in the **thick ascending limb of the loop of Henle**, not hydrochlorothiazide. - Inhibition here prevents significant reabsorption of sodium, potassium, and chloride, leading to potent diuresis.
Question 7: Which of the following is an oral direct thrombin inhibitor?
- A. Dabigatran (Correct Answer)
- B. Lepirudin
- C. Rivaroxaban
- D. Warfarin
Explanation: ***Dabigatran*** - **Dabigatran** is the correct answer because it is an **oral direct thrombin inhibitor (DTI)**, meaning it directly inhibits thrombin (factor IIa) to prevent clot formation. - It is one of the **novel oral anticoagulants (NOACs)**, used for conditions like atrial fibrillation and venous thromboembolism. *Lepirudin* - **Lepirudin** is a **direct thrombin inhibitor**, but it is administered **intravenously**, not orally. - It is typically used for **heparin-induced thrombocytopenia (HIT)** when heparin is contraindicated. *Rivaroxaban* - **Rivaroxaban** is an **oral anticoagulant**, but it is a **direct factor Xa inhibitor**, not a direct thrombin inhibitor. - This drug prevents the conversion of prothrombin to thrombin by inhibiting factor Xa. *Warfarin* - **Warfarin** is an **oral anticoagulant**, but it acts as a **vitamin K antagonist (VKA)**, inhibiting the synthesis of coagulation factors II, VII, IX, and X. - It does not directly inhibit thrombin, but rather reduces the production of thrombin precursors.
Question 8: What is the dose of mifepristone in emergency contraception?
- A. 25 mg
- B. 200 mcg
- C. 200 mg
- D. 10 mg (Correct Answer)
Explanation: ***10 mg*** - **10 mg is the WHO-recommended dose** of mifepristone for emergency contraception. - This single dose is **equally effective** as higher doses (25-50 mg) and works primarily by **delaying or inhibiting ovulation**. - It has been validated through **multiple international clinical trials** and is the standard regimen used globally. - When taken within **72-120 hours** of unprotected intercourse, it significantly reduces pregnancy risk. *25 mg* - While 25 mg of mifepristone has been studied for emergency contraception and shows efficacy, it is **not the standard recommended dose**. - The **10 mg dose is preferred** as it achieves similar efficacy with potentially fewer side effects and lower cost. - Some countries may use 25 mg, but **WHO guidelines recommend 10 mg** as the optimal dose. *200 mg* - A 200 mg dose of mifepristone is typically utilized for **medical abortion regimens**, often in combination with a prostaglandin analog (misoprostol). - This dosage achieves a different pharmacological effect, leading to **detachment of the embryo** and uterine contractions. - This is **far higher than needed** for emergency contraception purposes. *200 mcg* - **Mifepristone is not dosed in micrograms** (mcg) for emergency contraception or medical abortion; it is measured in milligrams (mg). - This unit and dosage are more commonly associated with other medications, such as **misoprostol** when used for obstetric indications. - 200 mcg would be 0.2 mg, which is **subtherapeutic** for any mifepristone indication.
Question 9: Which of the following is the chemoprophylaxis of choice in a person who is on a journey to endemic malarial region?
- A. Doxycycline
- B. Mefloquine
- C. Chloroquine
- D. Atovaquone-proguanil (Correct Answer)
Explanation: ***Atovaquone-proguanil*** - **First-line choice** for malaria chemoprophylaxis in travelers to endemic regions according to WHO and CDC guidelines - Highly effective against **drug-resistant *P. falciparum***, including chloroquine and mefloquine-resistant strains - **Excellent tolerability** with minimal side effects compared to other antimalarials - **Convenient dosing schedule**: started 1-2 days before travel and continued for only **7 days after** leaving the endemic area (shorter post-travel duration than alternatives) - Well-tolerated with few contraindications, making it suitable for most travelers *Doxycycline* - Effective alternative for malaria prophylaxis as a **tetracycline antibiotic** - Provides additional protection against **leptospirosis** and traveler's diarrhea - However, associated with **photosensitivity reactions** (sunburn risk), **GI upset**, and **esophageal irritation** - Contraindicated in **pregnancy** and **children <8 years** due to effects on teeth and bone - Requires daily dosing starting 1-2 days before until **4 weeks after travel** (longer duration) *Mefloquine* - Once-weekly dosing offers convenience for long-term travelers - Effective against most *P. falciparum* strains - Major limitation: significant **neuropsychiatric side effects** including anxiety, depression, dizziness, and rarely psychosis - Contraindicated in those with **psychiatric history**, seizure disorders, or cardiac conduction abnormalities - Must be started **2-3 weeks before travel** to assess tolerance *Chloroquine* - Historically the first-line agent but now limited by widespread **chloroquine resistance** - Only effective in few remaining areas with **chloroquine-sensitive *P. vivax*** or *P. falciparum* (parts of Central America, Middle East) - Well-tolerated with once-weekly dosing - Not appropriate for most endemic malarial regions in Africa, Southeast Asia, or South America
Question 10: Therapeutic drug monitoring is done for:
- A. Aspirin
- B. Heparin
- C. Phenytoin (Correct Answer)
- D. Metformin
Explanation: ***Phenytoin*** - **Phenytoin** has a **narrow therapeutic window**, meaning the difference between an effective and a toxic dose is small, necessitating close monitoring. - Its **variable absorption** and **nonlinear pharmacokinetics** (saturable metabolism) make individual dosing adjustments critical to maintain therapeutic levels and avoid toxicity. *Aspirin* - **Aspirin** is generally not monitored via plasma levels for its analgesic or antiplatelet effects, as its therapeutic effects are often observed at doses where plasma monitoring is not practical or necessary. - Its primary therapeutic use as an **antiplatelet agent** is evaluated by clinical outcomes rather than drug concentration. *Heparin* - **Heparin** is monitored using coagulation tests like **aPTT (activated partial thromboplastin time)** or anti-Xa levels to assess its anticoagulant effect, not direct drug concentration. - Therapeutic drug monitoring for heparin focuses on its **pharmacodynamic effects** on the clotting cascade rather than its absolute plasma concentration. *Metformin* - **Metformin** has a relatively **wide therapeutic index** and its efficacy is primarily measured by reductions in blood glucose and HbA1c, not by plasma drug concentrations. - It is excreted largely unchanged by the kidneys, and dose adjustments are typically made based on **renal function** and glycemic control.