NEET-PG 2018 — Pharmacology

Q: What is the physiological dose of hydrocortisone (mg/m2/day)?

10-12 mg/m²/day. ***10-12 mg/m²/day*** - This range represents the typical **physiological replacement dose** of hydrocortisone, mimicking the body's natural cortisol production. - This dose is used for patients with **adrenal insufficiency** to maintain normal metabolic functions without causing significant side effects. *8-10 mg/m²/day* - This dose is slightly on the lower side of the accepted physiological range and might not be sufficient for complete replacement in all individuals. - While close, it is not the most commonly cited optimal physiological dose for hydrocortisone replacement. *15-18 mg/m²/day* - This dose is typically considered above the physiological replacement level and may begin to cause **mild corticosteroid side effects** with prolonged use. - It might be used for short periods or in specific conditions, but not as a standard physiological replacement. *20-25 mg/m²/day* - This dose is well above the physiological range and would be considered a **pharmacological dose** often used for its anti-inflammatory or immunosuppressive effects. - Prolonged use at this dose would likely lead to significant **corticosteroid side effects** such as Cushingoid features, osteoporosis, and hyperglycemia. [Practice more Pharmacology PYQs on OnCourse]

Q: Which drug requires continuous monitoring of prothrombin time?

Coumadin. ***Coumadin*** - **Coumadin (warfarin)** is an oral anticoagulant that inhibits vitamin K epoxide reductase, thereby reducing the synthesis of **vitamin K-dependent clotting factors** (II, VII, IX, X). - Its narrow therapeutic index and significant variability in dosage requirements necessitate continuous monitoring of the **prothrombin time (PT)**, reported as the **International Normalized Ratio (INR)**, to ensure efficacy and prevent bleeding complications. *Aspirin* - **Aspirin** is an antiplatelet agent that irreversibly inhibits cyclooxygenase-1 (COX-1), preventing the synthesis of thromboxane A2, which is crucial for platelet aggregation. - It does not directly affect the coagulation cascade or prothrombin time; its antiplatelet effects are typically monitored by patient response and bleeding time, though routine monitoring is not usually required for standard antiplatelet therapy. *Digoxin* - **Digoxin** is a cardiac glycoside used to treat heart failure and atrial fibrillation by increasing myocardial contractility and slowing AV nodal conduction. - Its therapeutic effects and potential toxicity are monitored through serum digoxin levels, electrolyte balance (especially potassium), and electrocardiograms for signs of dysrhythmias, not by prothrombin time. *Lepirudin* - **Lepirudin** is a direct thrombin inhibitor (DTI) used in patients with heparin-induced thrombocytopenia (HIT). - Its anticoagulant effect is typically monitored using the **activated partial thromboplastin time (aPTT)**, not prothrombin time. [Practice more Pharmacology PYQs on OnCourse]

Q: Mycoplasma is inherently resistant to which of the following antibiotic classes due to its lack of a peptidoglycan cell wall?

Ceftriaxone (a cephalosporin). ***Ceftriaxone (a cephalosporin)*** - Cephalosporins are **beta-lactam antibiotics** that inhibit **peptidoglycan cell wall synthesis** by binding to penicillin-binding proteins (PBPs) - *Mycoplasma* species **completely lack a peptidoglycan cell wall**, which is the primary target of all beta-lactam antibiotics - Therefore, cephalosporins (and all beta-lactams) are **inherently ineffective** against *Mycoplasma* infections - This is a classic example of **intrinsic resistance** due to absence of the drug target *Penicillins (e.g., Amoxicillin)* - While penicillins are also beta-lactam antibiotics that target cell wall synthesis, the question specifically asks about ceftriaxone - Penicillins are similarly ineffective against *Mycoplasma* for the same reason (lack of cell wall) - However, when given a specific drug example (ceftriaxone), it is the most precise answer *Aminoglycosides (e.g., Gentamicin)* - Aminoglycosides target the **30S ribosomal subunit** to inhibit **protein synthesis** - While they have **poor penetration** into *Mycoplasma* cells and limited clinical efficacy, the resistance is not due to lack of cell wall - The mechanism of reduced susceptibility is different from the intrinsic resistance seen with beta-lactams *Fluoroquinolones (e.g., Ciprofloxacin)* - Fluoroquinolones inhibit **DNA gyrase** and **topoisomerase IV**, enzymes essential for DNA replication - These antibiotics are **effective** against *Mycoplasma* species and are commonly used to treat *Mycoplasma* infections - They represent appropriate treatment options along with macrolides and tetracyclines [Practice more Pharmacology PYQs on OnCourse]

Q: At pKa = pH, what is the relationship between the ionic and non-ionic forms of a drug?

Conc. of drug is 50% ionic and 50% non-ionic. ***Conc. of drug is 50% ionic and 50% non-ionic*** - At **pKa = pH**, the concentrations of the **ionized** and **unionized** forms of a drug are equal as per the **Henderson-Hasselbalch equation**. - This means that exactly **half** of the drug molecules are in their charged (ionic) state, and the other half are in their uncharged (non-ionic) state. *Absorption of drug is 50% ionic and 50% non-ionic* - The amount of drug that is absorbed is dependent on the **non-ionic concentration** available at the absorption site, but this option incorrectly states that the *absorption itself* is 50% ionic. - Absorption primarily occurs for the **non-ionic, lipophilic form** as it can more readily cross cell membranes. *Conc. of drug is 75% ionic and 25% non-ionic* - This ratio would occur when the **pH** is either 0.5 units above the pKa for a weak acid or 0.5 units below the pKa for a weak base. - For example, if **pH = pKa + 0.5** (for a weak acid), approximately 75% would be ionic. *Conc. of drug is 25% ionic and 75% non-ionic* - This ratio would occur when the **pH** is either 0.5 units below the pKa for a weak acid or 0.5 units above the pKa for a weak base. - For example, if **pH = pKa - 0.5** (for a weak acid), approximately 25% would be ionic. [Practice more Pharmacology PYQs on OnCourse]

27 Previous Year Questions with Answers & Explanations

Questions

What is the mechanism of action of Curare drugs as muscle relaxants?

What is the physiological dose of hydrocortisone (mg/m2/day)?

Which drug requires continuous monitoring of prothrombin time?

Mycoplasma is inherently resistant to which of the following antibiotic classes due to its lack of a peptidoglycan cell wall?

At pKa = pH, what is the relationship between the ionic and non-ionic forms of a drug?

Endothelin primarily acts through which type of receptors?

Which drug is primarily used to promote fetal lung maturity?

Which drug decreases the bone resorption in osteoporosis?

What is mechanism of action of colchicine in acute gout?

Q10

Burkholderia cepacia is resistant to which of the following antibiotics?

NEET-PG 2018 - Pharmacology NEET-PG Practice Questions and MCQs

Question 1: What is the mechanism of action of Curare drugs as muscle relaxants?

A. Persistently depolarizing at Neuromuscular junction
B. Act competitively on Ach receptors blocking post-synaptically (Correct Answer)
C. Repetitive stimulation of Ach receptors on muscle end plate
D. Inhibiting the calcium channel on presynaptic membrane

Explanation: ***Act competitively on Ach receptors blocking post-synaptically*** - Curare-like drugs are **non-depolarizing neuromuscular blockers** that exhibit their effects by **competitively binding** to **nicotinic acetylcholine receptors** on the **postsynaptic membrane** of the neuromuscular junction. - This competitive binding prevents acetylcholine (ACh) from binding to its receptors, thereby inhibiting the generation of an **end-plate potential** and subsequent **muscle contraction**. *Persistently depolarizing at Neuromuscular junction* - This mechanism is characteristic of **depolarizing neuromuscular blockers** like **succinylcholine**, which first cause muscle fasciculations followed by paralysis due to persistent receptor activation and inactivation of voltage-gated sodium channels. - Curare-like drugs do not cause persistent depolarization; instead, they prevent depolarization by blocking ACh access to receptors. *Repetitive stimulation of Ach receptors on muscle end plate* - **Repetitive stimulation** of acetylcholine (ACh) receptors by ACh itself leads to muscle contraction, not relaxation. - Curare-like drugs *block* the ability of ACh to stimulate these receptors, thus preventing contraction. *Inhibiting the calcium channel on presynaptic membrane* - Inhibiting presynaptic calcium channels would reduce the **release of acetylcholine** from the presynaptic terminal. - While this would lead to muscle relaxation, it is not the primary mechanism of action for **curare-like drugs**, which act directly on the postsynaptic receptors.

Question 2: What is the physiological dose of hydrocortisone (mg/m2/day)?

A. 20-25 mg/m²/day
B. 15-18 mg/m²/day
C. 10-12 mg/m²/day (Correct Answer)
D. 8-10 mg/m²/day

Explanation: ***10-12 mg/m²/day*** - This range represents the typical **physiological replacement dose** of hydrocortisone, mimicking the body's natural cortisol production. - This dose is used for patients with **adrenal insufficiency** to maintain normal metabolic functions without causing significant side effects. *8-10 mg/m²/day* - This dose is slightly on the lower side of the accepted physiological range and might not be sufficient for complete replacement in all individuals. - While close, it is not the most commonly cited optimal physiological dose for hydrocortisone replacement. *15-18 mg/m²/day* - This dose is typically considered above the physiological replacement level and may begin to cause **mild corticosteroid side effects** with prolonged use. - It might be used for short periods or in specific conditions, but not as a standard physiological replacement. *20-25 mg/m²/day* - This dose is well above the physiological range and would be considered a **pharmacological dose** often used for its anti-inflammatory or immunosuppressive effects. - Prolonged use at this dose would likely lead to significant **corticosteroid side effects** such as Cushingoid features, osteoporosis, and hyperglycemia.

Question 3: Which drug requires continuous monitoring of prothrombin time?

A. Coumadin (Correct Answer)
B. Digoxin
C. Aspirin
D. Lepirudin

Explanation: ***Coumadin*** - **Coumadin (warfarin)** is an oral anticoagulant that inhibits vitamin K epoxide reductase, thereby reducing the synthesis of **vitamin K-dependent clotting factors** (II, VII, IX, X). - Its narrow therapeutic index and significant variability in dosage requirements necessitate continuous monitoring of the **prothrombin time (PT)**, reported as the **International Normalized Ratio (INR)**, to ensure efficacy and prevent bleeding complications. *Aspirin* - **Aspirin** is an antiplatelet agent that irreversibly inhibits cyclooxygenase-1 (COX-1), preventing the synthesis of thromboxane A2, which is crucial for platelet aggregation. - It does not directly affect the coagulation cascade or prothrombin time; its antiplatelet effects are typically monitored by patient response and bleeding time, though routine monitoring is not usually required for standard antiplatelet therapy. *Digoxin* - **Digoxin** is a cardiac glycoside used to treat heart failure and atrial fibrillation by increasing myocardial contractility and slowing AV nodal conduction. - Its therapeutic effects and potential toxicity are monitored through serum digoxin levels, electrolyte balance (especially potassium), and electrocardiograms for signs of dysrhythmias, not by prothrombin time. *Lepirudin* - **Lepirudin** is a direct thrombin inhibitor (DTI) used in patients with heparin-induced thrombocytopenia (HIT). - Its anticoagulant effect is typically monitored using the **activated partial thromboplastin time (aPTT)**, not prothrombin time.

Question 4: Mycoplasma is inherently resistant to which of the following antibiotic classes due to its lack of a peptidoglycan cell wall?

A. Penicillins (e.g., Amoxicillin)
B. Ceftriaxone (a cephalosporin) (Correct Answer)
C. Aminoglycosides (e.g., Gentamicin)
D. Fluoroquinolones (e.g., Ciprofloxacin)

Explanation: ***Ceftriaxone (a cephalosporin)*** - Cephalosporins are **beta-lactam antibiotics** that inhibit **peptidoglycan cell wall synthesis** by binding to penicillin-binding proteins (PBPs) - *Mycoplasma* species **completely lack a peptidoglycan cell wall**, which is the primary target of all beta-lactam antibiotics - Therefore, cephalosporins (and all beta-lactams) are **inherently ineffective** against *Mycoplasma* infections - This is a classic example of **intrinsic resistance** due to absence of the drug target *Penicillins (e.g., Amoxicillin)* - While penicillins are also beta-lactam antibiotics that target cell wall synthesis, the question specifically asks about ceftriaxone - Penicillins are similarly ineffective against *Mycoplasma* for the same reason (lack of cell wall) - However, when given a specific drug example (ceftriaxone), it is the most precise answer *Aminoglycosides (e.g., Gentamicin)* - Aminoglycosides target the **30S ribosomal subunit** to inhibit **protein synthesis** - While they have **poor penetration** into *Mycoplasma* cells and limited clinical efficacy, the resistance is not due to lack of cell wall - The mechanism of reduced susceptibility is different from the intrinsic resistance seen with beta-lactams *Fluoroquinolones (e.g., Ciprofloxacin)* - Fluoroquinolones inhibit **DNA gyrase** and **topoisomerase IV**, enzymes essential for DNA replication - These antibiotics are **effective** against *Mycoplasma* species and are commonly used to treat *Mycoplasma* infections - They represent appropriate treatment options along with macrolides and tetracyclines

Question 5: At pKa = pH, what is the relationship between the ionic and non-ionic forms of a drug?

A. Absorption of drug is 50% ionic and 50% non-ionic
B. Conc. of drug is 25% ionic and 75% non-ionic
C. Conc. of drug is 75% ionic and 25% non-ionic
D. Conc. of drug is 50% ionic and 50% non-ionic (Correct Answer)

Explanation: ***Conc. of drug is 50% ionic and 50% non-ionic*** - At **pKa = pH**, the concentrations of the **ionized** and **unionized** forms of a drug are equal as per the **Henderson-Hasselbalch equation**. - This means that exactly **half** of the drug molecules are in their charged (ionic) state, and the other half are in their uncharged (non-ionic) state. *Absorption of drug is 50% ionic and 50% non-ionic* - The amount of drug that is absorbed is dependent on the **non-ionic concentration** available at the absorption site, but this option incorrectly states that the *absorption itself* is 50% ionic. - Absorption primarily occurs for the **non-ionic, lipophilic form** as it can more readily cross cell membranes. *Conc. of drug is 75% ionic and 25% non-ionic* - This ratio would occur when the **pH** is either 0.5 units above the pKa for a weak acid or 0.5 units below the pKa for a weak base. - For example, if **pH = pKa + 0.5** (for a weak acid), approximately 75% would be ionic. *Conc. of drug is 25% ionic and 75% non-ionic* - This ratio would occur when the **pH** is either 0.5 units below the pKa for a weak acid or 0.5 units above the pKa for a weak base. - For example, if **pH = pKa - 0.5** (for a weak acid), approximately 25% would be ionic.

Question 6: Endothelin primarily acts through which type of receptors?

A. Calcium receptors
B. General receptor type (GPCRs)
C. Endothelin receptor type B (ETB)
D. Endothelin receptor type A (ETA) (Correct Answer)

Explanation: ***Endothelin receptor type A (ETA)*** - **ETA receptors** are primarily responsible for the **vasoconstrictive effects** of endothelin-1 in various tissues, leading to increased vascular tone and blood pressure. - Activation of **ETA receptors** on vascular smooth muscle cells mediates signaling pathways that result in **smooth muscle contraction**. *Endothelin receptor type B (ETB)* - **ETB receptors** have dual roles, mediating both **vasoconstriction** (via smooth muscle ETB) and **vasodilation** (via endothelial ETB, stimulating nitric oxide and prostacyclin release). - They also play a significant role in **clearance of endothelin-1** from circulation. *General receptor type (GPCRs)* - While **endothelin receptors (ETA and ETB)** are indeed **G protein-coupled receptors (GPCRs)**, "General receptor type (GPCRs)" is too broad and not the most specific answer for how endothelin *primarily acts*. - Endothelin's specific effects are mediated through its dedicated subtypes of GPCRs, not the general class. *Calcium receptors* - **Calcium receptors** (e.g., calcium-sensing receptors) are involved in sensing extracellular calcium levels and regulating calcium homeostasis. - Endothelin's mechanism involves **intracellular calcium mobilization** *after* receptor activation, but it does not act *through* calcium receptors.

Question 7: Which drug is primarily used to promote fetal lung maturity?

A. Folic acid
B. Dexamethasone (Correct Answer)
C. Beclomethasone

Explanation: ***Dexamethasone*** - **Dexamethasone** is a synthetic glucocorticoid that rapidly crosses the placenta and stimulates the maturation of fetal lung surfactant production. - It significantly reduces the incidence and severity of **respiratory distress syndrome (RDS)** in preterm infants when administered to the mother. - **Antenatal corticosteroids** (dexamethasone or betamethasone) are given to mothers at risk of preterm delivery between 24-34 weeks of gestation. *Folic acid* - **Folic acid** is a B vitamin crucial for cell growth and DNA synthesis, primarily used to prevent **neural tube defects** in developing fetuses. - It does not have a direct role in promoting fetal lung maturity or surfactant production. *Beclomethasone* - **Beclomethasone** is an inhaled corticosteroid primarily used for the long-term management of **asthma** in children and adults. - While it is a corticosteroid, it is not typically used for systemic administration to the mother to promote fetal lung maturity due to its primary delivery method (inhalation) and limited systemic bioavailability compared to dexamethasone or betamethasone.

Question 8: Which drug decreases the bone resorption in osteoporosis?

A. Teriparatide
B. Risedronate (Correct Answer)
C. Cortisone
D. Cimetidine

Explanation: ***Risedronate*** - **Risedronate** is a **bisphosphonate**, a class of drugs that inhibits osteoclast activity, thereby decreasing **bone resorption**. - By reducing the rate at which bone is broken down, it helps to preserve **bone mineral density** in patients with osteoporosis. *Teriparatide* - **Teriparatide** is a **parathyroid hormone analog** that primarily works by stimulating **osteoblast activity** to promote new bone formation. - While it treats osteoporosis, its primary mechanism is **anabolic** (bone building), not directly decreasing bone resorption as its main effect. *Cortisone* - **Cortisone** is a **glucocorticoid** that can actually *worsen* osteoporosis by increasing **bone resorption** and decreasing **bone formation** with long-term use. - It is used to treat inflammatory conditions, not to decrease bone resorption for osteoporosis. *Cimetidine* - **Cimetidine** is an **H2-receptor antagonist** used to reduce stomach acid production, commonly for conditions like GERD or ulcers. - It has no known effect on **bone metabolism** or **osteoporosis**.

Question 9: What is mechanism of action of colchicine in acute gout?

A. Inhibition of purine metabolism
B. Inhibition of uric acid conversion
C. Migration of leukocytes
D. Inhibition of leukocyte migration and microtubule function (Correct Answer)

Explanation: ***Inhibition of leukocyte migration and microtubule function*** - Colchicine works by disrupting **microtubule polymerization**, which interferes with the **motility and activity of neutrophils and other inflammatory cells** [1]. - Its anti-inflammatory effect in acute gout is primarily due to the inhibition of **leukocyte migration and phagocytosis of urate crystals**, thereby reducing the inflammatory response [1]. - The mechanism involves binding to **tubulin**, preventing microtubule assembly, which affects multiple cellular processes including chemotaxis and cell division [1]. *Inhibition of purine metabolism* - This mechanism is associated with drugs like **allopurinol**, which inhibit **xanthine oxidase** to reduce uric acid production [2]. - Colchicine does not directly inhibit **purine metabolism** or uric acid synthesis; its effect is on the inflammatory response, not uric acid formation [1]. *Inhibition of uric acid conversion* - This mechanism refers to **uricosuric agents** like probenecid that increase renal excretion of uric acid. - Colchicine's action is primarily anti-inflammatory, not related to uric acid metabolism or excretion [1]. *Migration of leukocytes* - While this is partially correct, as colchicine does inhibit **leukocyte migration**, this option is incomplete. - The complete mechanism must include its action as a **microtubule inhibitor**, which is the underlying basis for all its cellular effects including inhibition of migration, phagocytosis, and inflammatory mediator release [1].

Question 10: Burkholderia cepacia is resistant to which of the following antibiotics?

A. Trimethoprim-sulfamethoxazole
B. Cefotetan (Correct Answer)
C. Ceftazidime
D. Temocillin

Explanation: ***Cefotetan*** - *Burkholderia cepacia* shows **consistent resistance** to second-generation cephalosporins and cephamycins like **cefotetan**. - This organism is intrinsically resistant to **aminoglycosides** (gentamicin, tobramycin) and **polymyxins** (colistin), and shows variable resistance to many beta-lactams. - Among the options provided, cefotetan represents the most consistently ineffective agent. *Ceftazidime* - **Ceftazidime** (third-generation cephalosporin) shows **variable susceptibility** with *B. cepacia*. - While resistance is common, it is **not uniform**, and ceftazidime is sometimes used in **combination therapy** for B. cepacia infections. - Not considered a classic example of intrinsic resistance. *Trimethoprim-sulfamethoxazole* - **TMP-SMX** is the **first-line treatment** for *Burkholderia cepacia* infections. - It demonstrates good activity and is the preferred antimicrobial agent for this organism. - Resistance can develop but is not intrinsic. *Temocillin* - **Temocillin** (carboxypenicillin) has demonstrated activity against *B. cepacia*. - Used particularly in Europe for treating infections caused by this organism. - Not an antibiotic to which *B. cepacia* shows consistent resistance.