NEET-PG 2012 - Pharmacology Practice Questions

Q: Which of the following is a selective serotonin and norepinephrine reuptake inhibitor?

Venlafaxine. ***Venlafaxine*** - **Venlafaxine** is a commonly used antidepressant that inhibits the reuptake of both **serotonin** and **norepinephrine**, making it an SNRI. - Its dual mechanism of action can be effective for a broad range of depressive and anxiety disorders. *Fluoxetine* - **Fluoxetine** is a **selective serotonin reuptake inhibitor (SSRI)**, primarily affecting serotonin levels in the brain. - It does not significantly inhibit norepinephrine reuptake and, thus, is not classified as an SNRI. *Sertraline* - **Sertraline** is another widely prescribed antidepressant that is also a **selective serotonin reuptake inhibitor (SSRI)**. - It works mainly by increasing serotonin availability in the synaptic cleft. *Aripiprazole* - **Aripiprazole** is an **atypical antipsychotic** medication, often used as an adjunct therapy for depression, but its primary mechanism is partial agonism at dopamine D2 and serotonin 5-HT1A receptors, and antagonism at serotonin 5-HT2A receptors. - It is not classified as a selective serotonin and norepinephrine reuptake inhibitor.

Q: Which of the following has the least glucocorticoid activity?

Cortisone. ***Cortisone*** - **Cortisone has the LEAST glucocorticoid activity** among the options listed. - It is a **prodrug** that must be converted to **hydrocortisone (cortisol)** by 11β-hydroxysteroid dehydrogenase in the liver to become active. - Its glucocorticoid potency is approximately **0.8** relative to hydrocortisone (when hydrocortisone = 1). - Due to variable hepatic conversion, it has **lower and less predictable glucocorticoid effects** compared to other agents. *Fludrocortisone* - Primarily used for its **potent mineralocorticoid activity** (125× that of hydrocortisone). - However, it retains **significant glucocorticoid activity** approximately **10-15 times** that of hydrocortisone. - Despite being marketed as a mineralocorticoid, its glucocorticoid potency is **considerably higher than cortisone**. *Dexamethasone* - **Highly potent synthetic glucocorticoid** with negligible mineralocorticoid activity. - Glucocorticoid potency is approximately **25-30 times** that of hydrocortisone. - Long duration of action (36-72 hours) and excellent CNS penetration. *Betamethasone* - **Highly potent synthetic glucocorticoid**, structurally similar to dexamethasone (differs only in stereochemistry at C-16). - Glucocorticoid potency is approximately **25-30 times** that of hydrocortisone. - Minimal mineralocorticoid activity, with similar clinical applications to dexamethasone.

Q: Which of the following drugs acts directly to induce an erection without the need for sexual stimulation?

Alprostadil. ***Alprostadil***- **Alprostadil** is a **prostaglandin E1** analog that can directly induce vasodilation in the penile arteries, leading to an erection without sexual stimulation [1].- It is typically administered via **intracavernosal injection** or as a **urethral suppository**.*Sildenafil*- **Sildenafil** is a **PDE5 inhibitor** that works by enhancing the effects of **nitric oxide**, which is released in response to sexual stimulation [2, 3].- It requires **sexual arousal** to be effective, as it doesn't directly initiate the erectile process [2, 3].*Tadalafil*- Similar to sildenafil, **tadalafil** is also a **PDE5 inhibitor** that works by increasing cGMP levels and promoting smooth muscle relaxation [2, 3].- Its action is dependent on the release of **nitric oxide** triggered by sexual stimulation [2, 3].*Testosterone*- **Testosterone** is a hormone involved in sex drive and overall erectile function over time, but it does not directly or acutely induce an erection.- Its primary role in erectile dysfunction is in cases of **hypogonadism**, and it requires sexual stimulation for its effects on erection.

Q: Which of the following medications does not interact with warfarin?

Benzodiazepines. ***Benzodiazepines*** - **Benzodiazepines** are generally considered safe to use with warfarin as they are extensively metabolized in the liver, but they do not typically alter the **cytochrome P450 enzymes** responsible for warfarin metabolism. - They also do not interfere with **vitamin K recycling** or **platelet function**, which are key mechanisms through which other drugs interact with warfarin. *Barbiturate* - **Barbiturates** are **potent inducers of hepatic enzymes**, particularly CYP2C9, which is responsible for metabolizing warfarin. - This enzyme induction leads to **increased warfarin metabolism**, reducing its anticoagulant effect and necessitating higher warfarin doses. *Oral contraceptive* - **Oral contraceptives** can **reduce the anticoagulant effect of warfarin** by inducing clotting factors or inhibiting warfarin metabolism. - This interaction can increase the risk of **thromboembolic events** in patients on warfarin. *Cephalosporins* - Certain **cephalosporins**, especially those with a **methylthiotetrazole (MTT) side chain** (e.g., Cefamandole, Cefoperazone, Moxalactam), can **inhibit vitamin K epoxide reductase**. - This inhibition leads to a **decrease in vitamin K-dependent clotting factors**, thus potentiating the anticoagulant effect of warfarin and increasing bleeding risk.

Q: What is the primary reason for using a combination of four drugs in Anti-Koch's Treatment (AKT) for tuberculosis?

To decrease the risk of resistance due to mutation.. ***To decrease the risk of resistance due to mutation*** - **Tuberculosis bacteria** can spontaneously develop resistance to a single drug through **random genetic mutations**. - Using multiple drugs simultaneously significantly reduces the probability that a bacterium will spontaneously develop resistance to **all drugs** in the regimen. - This is the **primary rationale** for multi-drug therapy in TB, as emphasized by WHO guidelines. *To decrease the risk of resistance due to conjugation* - **Conjugation** is a mechanism of horizontal gene transfer in bacteria, primarily involving the transfer of plasmids. - While important for antibiotic resistance in some bacteria, it is **not the primary mechanism** of resistance development in *Mycobacterium tuberculosis*. - TB resistance develops mainly through **chromosomal mutations**, not plasmid transfer. *To enhance overall treatment efficacy* - While multi-drug regimens do enhance treatment efficacy by targeting different bacterial populations (actively dividing, slow-growing, dormant), this is a **consequence** of the multi-drug approach. - The **primary reason** for using four drugs specifically is to prevent the emergence of **drug-resistant mutants**. - Enhanced efficacy is achieved *because* resistance is prevented, making this a secondary benefit. *To simplify treatment* - A four-drug regimen actually makes treatment more **complex** due to multiple pills, potential drug interactions, and increased side effects. - The complexity is a necessary trade-off for **resistance prevention** and treatment success.

Q: What is the mechanism of action of quinolones?

Inhibit DNA gyrase. ***Inhibit DNA gyrase*** - Quinolones, particularly **fluoroquinolones**, exert their bactericidal effect by targeting **bacterial DNA gyrase (topoisomerase II)** and **topoisomerase IV**. - This inhibition prevents the uncoiling and replication of bacterial DNA, leading to cell death. *Bind to 30S ribosomal subunit* - This mechanism is characteristic of **aminoglycosides** and **tetracyclines**, which disrupt bacterial protein synthesis. - Quinolones do not interfere with ribosomal function but rather with **DNA replication**. *Bind to bacterial cell membrane* - This is the mechanism of action for **polymyxins** and **daptomycin**, which disrupt the integrity of the bacterial cell membrane. - Quinolones specifically target **intracellular enzymes** involved in DNA handling. *Inhibit tetrahydrofolate reductase* - This enzyme name in the option is technically imprecise; **trimethoprim** actually inhibits **dihydrofolate reductase**, which is part of the **sulfonamide-trimethoprim (Bactrim)** combination. - This pathway is involved in **folic acid synthesis**, crucial for bacterial DNA and RNA production, a mechanism distinct from quinolones.

Q: Which enzyme is irreversibly inhibited by aspirin?

Cyclooxygenase. ***Cyclooxygenase*** - **Aspirin** irreversibly inhibits **cyclooxygenase (COX-1 and COX-2)** by acetylating a serine residue in the enzyme's active site. - This irreversible inhibition prevents the production of **prostaglandins, thromboxane**, and **prostacyclin**, thereby reducing inflammation, pain, fever, and platelet aggregation. *Lipooxygenase* - **Lipooxygenase** is involved in the synthesis of **leukotrienes**, which are mediators of inflammation and allergic responses. - Aspirin does not directly inhibit lipooxygenase; rather, it primarily targets the COX pathway. *Thromboxane synthase* - **Thromboxane synthase** is an enzyme downstream of COX, responsible for converting prostaglandin H2 into **thromboxane A2**. - While aspirin's effect on platelet aggregation is due to reduced thromboxane A2 synthesis via COX inhibition, it does not directly inhibit thromboxane synthase itself. *Phospholipase* - **Phospholipase A2** is responsible for releasing **arachidonic acid** from cell membrane phospholipids, which is the initial step in both the cyclooxygenase and lipooxygenase pathways. - Aspirin does not directly inhibit phospholipase A2; its action occurs later in the cascade.

Q: Which of the following antiepileptic drugs is most classically associated with causing hirsutism?

Phenytoin. ***Phenytoin*** - **Phenytoin** is the **most classically associated** antiepileptic drug with **hirsutism**, which is abnormal/excessive growth of hair [1]. - The mechanism involves changes in **androgen metabolism** and stimulation of hair follicle growth. - Other cosmetic side effects include **gingival hyperplasia** and **coarsening of facial features** [1].*Valproate* - Valproate can paradoxically cause both **hair loss (alopecia)** and **hirsutism**, particularly in women and children. - However, phenytoin has a **stronger and more classical association** with hirsutism. - Valproate is also known for **weight gain**, **hepatotoxicity**, **pancreatitis**, and **teratogenicity**.*Carbamazepine* - Carbamazepine's common side effects include **drowsiness**, **dizziness**, **diplopia**, and **hyponatremia**. - It is not classically linked to **hirsutism** as a prominent adverse effect. - Can cause **agranulocytosis** and **Stevens-Johnson syndrome** in rare cases.*Phenobarbitone* - Phenobarbitone is an older antiepileptic drug associated with **sedation**, **cognitive impairment**, and **dependence**. - It does not commonly cause **hirsutism**. - Also causes **enzyme induction** leading to multiple drug interactions.

Q: Which of the following antibiotics is known to cause bleeding due to its effect on blood clotting?

Moxalactam. Moxalactam - Moxalactam is a **third-generation cephalosporin** known to cause **hypoprothrombinemia** and platelet dysfunction, leading to an increased risk of bleeding. - This effect is due to its **N-methylthiotetrazole (NMTT) side chain**, which inhibits vitamin K-dependent clotting factor synthesis. Cefaloridine - This is a **first-generation cephalosporin** that does not have the NMTT side chain and is not commonly associated with significant bleeding risks. - Its primary adverse effect of concern is **nephrotoxicity** at high doses, rather than coagulopathy. Ceftazidime - Ceftazidime is a **third-generation cephalosporin** primarily used for *Pseudomonas aeruginosa* infections but does **not contain the NMTT side chain** responsible for bleeding complications. - While broad-spectrum, it generally has a favorable safety profile concerning coagulation. *Cefazolin* - Cefazolin is a **first-generation cephalosporin** [1] widely used for surgical prophylaxis and skin infections [1], and it does **not interfere with coagulation** pathways. - Its main side effects are typical for penicillin-related antibiotics, such as hypersensitivity reactions [1],[2].

Q: Which of the following medications is known to cause increased renin levels with prolonged use?

Enalapril. ***Enalapril*** - **Enalapril** is an **ACE inhibitor** which blocks the conversion of angiotensin I to angiotensin II, leading to decreased levels of angiotensin II [1]. - Reduced angiotensin II levels remove the **negative feedback** on renin release from the juxtaglomerular cells, thus increasing renin secretion [1], [2]. *Clonidine* - Clonidine is a **central alpha-2 adrenergic agonist** that reduces sympathetic outflow from the central nervous system. - This reduction in sympathetic activity leads to a **decrease in renin release**, as sympathetic stimulation normally promotes renin secretion [3]. *Methyldopa* - Methyldopa is a **central alpha-2 adrenergic agonist** that works similarly to clonidine by reducing sympathetic tone. - It consequently causes a **decrease in plasma renin activity** due to reduced sympathetic stimulation of the juxtaglomerular apparatus [3]. *Propranolol* - Propranolol is a **non-selective beta-blocker** that blocks beta-1 receptors in the juxtaglomerular cells of the kidney. - This blockade **inhibits the release of renin** stimulated by sympathetic activity, leading to reduced renin levels [3].

Question 1

Which of the following is a selective serotonin and norepinephrine reuptake inhibitor?

Accepted Answer

Venlafaxine

Answer

Fluoxetine

Answer

Sertraline

Answer

Aripiprazole

Question 2

Which of the following has the least glucocorticoid activity?

Accepted Answer

Cortisone

Answer

Fludrocortisone

Answer

Dexamethasone

Answer

Betamethasone

Question 3

Which of the following drugs acts directly to induce an erection without the need for sexual stimulation?

Accepted Answer

Alprostadil

Answer

Sildenafil

Answer

Tadalafil

Answer

Testosterone

Question 4

Which of the following medications does not interact with warfarin?

Accepted Answer

Benzodiazepines

Answer

Barbiturate

Answer

Oral contraceptive

Answer

Cephalosporins

Question 5

What is the primary reason for using a combination of four drugs in Anti-Koch's Treatment (AKT) for tuberculosis?

Accepted Answer

To decrease the risk of resistance due to mutation.

Answer

To decrease the risk of resistance due to conjugation.

Answer

To enhance overall treatment efficacy.

Answer

To simplify treatment.

Question 6

What is the mechanism of action of quinolones?

Accepted Answer

Inhibit DNA gyrase

Answer

Inhibit tetrahydrofolate reductase

Answer

Bind to 30S ribosomal subunit

Answer

Bind to bacterial cell membrane

Question 7

Which enzyme is irreversibly inhibited by aspirin?

Accepted Answer

Cyclooxygenase

Answer

Lipooxygenase

Answer

Thromboxane synthase

Answer

Phospholipase

Question 8

Which of the following antiepileptic drugs is most classically associated with causing hirsutism?

Accepted Answer

Phenytoin

Answer

Valproate

Answer

Carbamazepine

Answer

Phenobarbitone

Question 9

Which of the following antibiotics is known to cause bleeding due to its effect on blood clotting?

Accepted Answer

Moxalactam

Answer

Cefaloridine

Answer

Cefazolin

Answer

Ceftazidime

Question 10

Which of the following medications is known to cause increased renin levels with prolonged use?

Accepted Answer

Enalapril

Answer

Clonidine

Answer

Methyldopa

Answer

Propranolol

NEET-PG 2012 — Pharmacology