NEET-PG 2012 - Pharmacology Practice Questions

Q: What is the antidote for Ethylene Glycol?

Fomepizole. ***Fomepizole*** - **Fomepizole** is the primary and preferred antidote for ethylene glycol poisoning, as it competitively inhibits **alcohol dehydrogenase**, the enzyme responsible for metabolizing ethylene glycol into its toxic metabolites. - By blocking this enzyme, fomepizole prevents the formation of harmful compounds like **glycolic acid** and **oxalic acid**, which cause metabolic acidosis and kidney damage. - **Ethanol** is an alternative antidote that works by the same mechanism (competitive inhibition of alcohol dehydrogenase) and can be used when fomepizole is unavailable, though fomepizole is preferred due to better safety profile and easier dosing. *Barbiturate* - **Barbiturates** are a class of psychoactive drugs that act as central nervous system depressants, primarily used for sedation, anesthesia, and seizure control. - They have no role in neutralizing or metabolizing ethylene glycol or its toxic byproducts. *Acetylcysteine* - Acetylcysteine is an antidote primarily used for **acetaminophen (paracetamol) overdose**, where it replenishes glutathione stores and detoxifies its toxic metabolite, **NAPQI**. - It does not have any direct antidotal effect against ethylene glycol or its metabolites. *Ferric chloride* - **Ferric chloride** is a chemical compound used in various industrial processes, water treatment, and as a laboratory reagent. - It is highly corrosive and toxic if ingested, but it is not used as an antidote for any type of poisoning, including ethylene glycol.

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: 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 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: 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: Omalizumab is primarily used in the treatment of which condition?

Asthma. ***Asthma*** - **Omalizumab** is a **monoclonal antibody** that targets and binds to **immunoglobulin E (IgE)**, preventing it from binding to mast cells and basophils. - By reducing free IgE, omalizumab helps to prevent the release of inflammatory mediators, thereby **reducing allergic reactions and asthma symptoms**, particularly in patients with severe persistent allergic asthma. *Breast carcinoma* - **Omalizumab** is not indicated for the treatment of **breast carcinoma**; treatments for breast cancer typically involve chemotherapy, radiation, surgery, and targeted therapies specific to cancer cells. - Targeted therapies for breast cancer often focus on hormone receptors (e.g., **estrogen receptor**) or growth factor receptors (e.g., **HER2**), not IgE. *Rheumatoid arthritis* - **Omalizumab** is not used for **rheumatoid arthritis (RA)**; RA is an autoimmune disease primarily involving **T-cells and cytokines** like **TNF-alpha** and **IL-6**. - Treatment for RA typically includes **DMARDs** (disease-modifying antirheumatic drugs) and **biological agents** that target specific inflammatory pathways (e.g., **adalimumab**, **etanercept**). *Chronic obstructive pulmonary disease (COPD)* - **Omalizumab** is not indicated for **COPD**, which is primarily characterized by chronic inflammation of the airways and **emphysema**, largely caused by smoking. - COPD management focuses on bronchodilators, corticosteroids, and oxygen therapy, with no role for IgE-targeting therapy.

Q: Resistance to Methotrexate develops due to?

Increased production of dihydrofolate reductase (DHFR). ***Increased production of dihydrofolate reductase (DHFR)*** - Methotrexate acts by inhibiting **dihydrofolate reductase (DHFR)**, an enzyme essential for **folate metabolism** and DNA synthesis. - An **increased production of DHFR** (through gene amplification or overexpression) by cancer cells allows them to bypass the drug's inhibitory effects, leading to resistance. - This is the **most common mechanism** of methotrexate resistance. *Rapid proliferation of cancer cells* - While **rapid cell proliferation** is a characteristic of cancer, it doesn't directly explain resistance to methotrexate. - Methotrexate targets fast-dividing cells (S-phase specific), so rapid proliferation often makes them **more susceptible**, not resistant, as long as the drug's mechanism is effective. *Thymidylate kinase deficiency* - **Thymidylate kinase** is involved in the phosphorylation of **thymidine** to produce **dTMP** (deoxythymidine monophosphate). - A deficiency in this enzyme would likely hinder DNA synthesis, potentially increasing sensitivity to DNA-targeting agents, rather than causing resistance to methotrexate. *Thymidylate synthetase deficiency* - **Thymidylate synthetase** converts dUMP to dTMP using **5,10-methylene-THF** as a cofactor. - Methotrexate **indirectly inhibits** thymidylate synthetase by depleting tetrahydrofolate cofactor pools through DHFR inhibition. - A **deficiency** of this enzyme would not cause resistance; rather, **increased thymidylate synthetase** expression can be an alternative resistance mechanism, though less common than DHFR overexpression.

Q: Which steroid has the maximum mineralocorticoid activity?

Fludrocortisone. ***Fludrocortisone*** - **Fludrocortisone** is a synthetic corticosteroid specifically designed to have potent **mineralocorticoid activity**, with significant sodium-retaining properties. - Its high affinity for **mineralocorticoid receptors** distinguishes it from other steroids and makes it effective in treating conditions like **Addison's disease** and **postural orthostatic tachycardia syndrome (POTS)** due to its ability to retain sodium and water. *DOCA (Deoxycorticosterone acetate)* - While **DOCA** does possess significant **mineralocorticoid activity** and was historically used for this purpose, **fludrocortisone** is generally considered to have a stronger and more sustained effect in clinical practice. - **DOCA's** mineralocorticoid potency is substantial but slightly less than that of **fludrocortisone** when compared on a weight basis for equivalent sodium retention. *Prednisolone* - **Prednisolone** is primarily a **glucocorticoid** with potent anti-inflammatory and immunosuppressive effects. - It has minimal to negligible **mineralocorticoid activity** and is not used for salt retention purposes. *Triamcinolone* - **Triamcinolone** is a potent **glucocorticoid** with a long duration of action and is known for its strong anti-inflammatory properties. - It has virtually no **mineralocorticoid activity**, making it unsuitable for conditions requiring sodium retention.

Question 1

What is the antidote for Ethylene Glycol?

Accepted Answer

Fomepizole

Answer

Barbiturate

Answer

Acetylcysteine

Answer

Ferric chloride

Question 2

Which of the following medications does not interact with warfarin?

Accepted Answer

Benzodiazepines

Answer

Barbiturate

Answer

Oral contraceptive

Answer

Cephalosporins

Question 3

Which of the following has the least glucocorticoid activity?

Accepted Answer

Cortisone

Answer

Fludrocortisone

Answer

Dexamethasone

Answer

Betamethasone

Question 4

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

Accepted Answer

Venlafaxine

Answer

Fluoxetine

Answer

Sertraline

Answer

Aripiprazole

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

Omalizumab is primarily used in the treatment of which condition?

Accepted Answer

Asthma

Answer

Breast carcinoma

Answer

Rheumatoid arthritis

Answer

Chronic obstructive pulmonary disease (COPD)

Question 9

Resistance to Methotrexate develops due to?

Accepted Answer

Increased production of dihydrofolate reductase (DHFR)

Answer

Rapid proliferation of cancer cells

Answer

Thymidylate kinase deficiency

Answer

Thymidylate synthetase deficiency

Question 10

Which steroid has the maximum mineralocorticoid activity?

Accepted Answer

Fludrocortisone

Answer

DOCA

Answer

Prednisolone

Answer

Triamcinolone

NEET-PG 2012 — Pharmacology