NEET-PG 2012 - Pharmacology Practice Questions

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: Which of the following is a centrally acting antihypertensive drug?

Methyldopa. ***Methyldopa*** - **Methyldopa** is a **prodrug** that is converted to **alpha-methylnorepinephrine** in the brain, which then stimulates **alpha-2 adrenergic receptors** in the brainstem. - This stimulation reduces **sympathetic outflow** from the central nervous system, leading to decreased heart rate, stroke volume, and peripheral vascular resistance, thus lowering blood pressure. *Phenoxybenzamine* - **Phenoxybenzamine** is an **alpha-1 and alpha-2 adrenergic receptor antagonist** (non-selective alpha blocker) that primarily acts peripherally. - It causes **vasodilation** by blocking alpha-1 receptors on smooth muscle, which reduces peripheral vascular resistance. *Propranolol* - **Propranolol** is a **non-selective beta-blocker** that primarily acts on peripheral beta-adrenergic receptors. - It reduces heart rate and cardiac output by blocking **beta-1 receptors** in the heart and can also affect beta-2 receptors in the lungs and vasculature. *Prazosin* - **Prazosin** is a **selective alpha-1 adrenergic receptor antagonist** that acts primarily on peripheral blood vessels. - It causes **vasodilation** in both arteries and veins by blocking alpha-1 receptors, which reduces both preload and afterload, lowering blood pressure.

Q: All are true regarding Sunitinib except which of the following?

It is excreted primarily in urine. ***It is excreted primarily in urine*** - **Sunitinib** is predominantly metabolized in the **liver** by CYP3A4 and primarily excreted in the **feces**, not urine. - Its major active metabolite, N-desethyl sunitinib, is also primarily eliminated via the fecal route. *It inhibits tyrosine kinase receptors* - **Sunitinib** is a **multitargeted receptor tyrosine kinase (RTK) inhibitor**. - It blocks several RTKs involved in tumor growth, angiogenesis, and metastatic progression, such as **VEGFR, PDGFR, KIT, and FLT3**. *It is used for the treatment of GIST* - **Sunitinib** is approved for the treatment of **imatinib-refractory** or **imatinib-intolerant gastrointestinal stromal tumors (GIST)**. - Its mechanism in GIST involves inhibiting KIT and PDGFR, which are often mutated and constitutively active in this cancer. *It is used for renal cell carcinoma* - **Sunitinib** is a standard first-line treatment for **advanced renal cell carcinoma (RCC)**. - Its efficacy in RCC is primarily due to its inhibition of VEGFR, which targets the high vascularity characteristic of kidney tumors.

Q: What is the primary cardiotoxic effect of bupivacaine?

Depressed pacemaker activity. ***Depressed pacemaker activity*** - **Bupivacaine** is a potent **local anesthetic** that blocks voltage-gated **sodium channels** in myocardial cells with **high affinity** and **slow dissociation kinetics**. - This prolonged channel blockade leads to decreased cardiac excitability and **depressed automaticity** of pacemaker cells, particularly affecting the **SA node** and **His-Purkinje system**. - Results in slowing of the **heart rate**, **bradyarrhythmias**, **conduction blocks**, and potentially **ventricular arrhythmias** or **asystole**. - Bupivacaine is **more cardiotoxic** than other local anesthetics due to its **lipophilicity** and prolonged binding to cardiac sodium channels. *Toxic compound damaging myocardial cells* - While **bupivacaine** is cardiotoxic, its primary mechanism is not direct **cellular damage** through cytotoxic effects, oxidative stress, or cell membrane lysis. - The toxicity is predominantly due to **electrophysiological effects** on ion channels, interfering with normal cardiac conduction and contractility. *Depressed neural control on heart* - **Bupivacaine's** cardiotoxicity primarily affects the **myocardium directly** through sodium channel blockade, rather than indirectly through the **autonomic nervous system**. - Although high systemic concentrations can affect the **central nervous system** (causing seizures and CNS depression), the direct cardiac effects occur independently of neural influence. *Vascular thrombosis and Myocardial ischemia* - **Bupivacaine** cardiotoxicity does not typically involve formation of **thrombi** or mechanisms leading to **myocardial ischemia** through coronary artery occlusion. - Its effects are predominantly on the **electrical conduction system**, **myocardial contractility**, and **cardiac ion channels**, not the vascular supply to the heart.

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 is not an alpha-blocker?

Atenolol. ***Atenolol*** - Atenolol is a **selective beta-1 adrenergic receptor blocker**, primarily used to treat hypertension, angina, and certain arrhythmias. - Its mechanism of action involves **blocking the effects of adrenaline** on the heart, leading to decreased heart rate and blood pressure, rather than affecting alpha receptors. *Indoramine* - Indoramine is an **alpha-1 adrenergic receptor blocker** used historically for hypertension. - It specifically **antagonizes alpha-1 receptors** in vascular smooth muscle, causing vasodilation. *Idazoxan* - Idazoxan is an **alpha-2 adrenergic receptor antagonist**, primarily used in research contexts. - It **blocks presynaptic alpha-2 receptors**, which can lead to an increase in norepinephrine release. *Prazosin* - Prazosin is a well-known **alpha-1 adrenergic receptor blocker** used to treat hypertension and benign prostatic hyperplasia (BPH). - It causes **vasodilation** by relaxing vascular smooth muscle, thus lowering blood pressure.

Q: Which of the following is not a selective serotonin reuptake inhibitor?

Buspirone. ***Buspirone*** - **Buspirone** is an anxiolytic that primarily acts as a **serotonin 5-HT1A receptor partial agonist**, not an SSRI. - It does not significantly affect the reuptake of serotonin, distinguishing it from SSRIs. *Fluoxetine* - **Fluoxetine** is a well-known and widely used **SSRI**. - It works by selectively inhibiting the reuptake of serotonin, thereby increasing its concentration in the synaptic cleft. *Fluvoxamine* - **Fluvoxamine** is another antidepressant classified as an **SSRI**. - It is often used for the treatment of **obsessive-compulsive disorder (OCD)** due to its strong serotonin reuptake inhibition. *Citalopram* - **Citalopram** is an **SSRI** frequently prescribed for depression and anxiety disorders. - Its mechanism involves potent and selective inhibition of **serotonin reuptake**.

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: What is the best drug for open-angle glaucoma?

Latanoprost. Latanoprost - Latanoprost is a prostaglandin analog and is often considered a first-line treatment for open-angle glaucoma due to its efficacy in reducing intraocular pressure (IOP) and its once-daily dosing. - It works by increasing the outflow of aqueous humor through the uveoscleral pathway, thereby lowering IOP. Pilocarpine - Pilocarpine is a cholinergic agonist that causes miosis and ciliary muscle contraction [3], increasing the outflow of aqueous humor through the trabecular meshwork [4]. - While effective, its side effects (e.g., accommodative spasm, miosis) [1] and more frequent dosing make it generally a second-line or third-line agent for long-term management compared to prostaglandins. Physostigmine - Physostigmine is an acetylcholinesterase inhibitor that indirectly increases acetylcholine, mimicking cholinergic stimulation. - Although it can lower IOP, it is generally not used for open-angle glaucoma due to significant side effects and the availability of safer, more effective alternatives [1]. Apraclonidine - Apraclonidine is an alpha-2 adrenergic agonist [2] used primarily for short-term control of IOP, especially before or after ocular surgery, or as an adjunct therapy. - Its efficacy as a long-term monotherapy for open-angle glaucoma is limited by tachyphylaxis and potential for significant systemic side effects with chronic use.

Q: Which of the following best describes a Type B adverse drug reaction?

Unpredictable bizarre reaction. ***Unpredictable bizarre reaction*** - Type B reactions are **unpredictable**, **bizarre**, and not directly related to the drug's known pharmacological actions. - They often involve **immunological reactions** or genetic predispositions, such as allergies or idiosyncratic responses. *Augmented effect of drug* - This describes a **Type A** adverse drug reaction, which is predictable and results from an **exaggerated pharmacological effect** of the drug. - It is typically dose-dependent and can be managed by adjusting the dosage. *Effect seen on chronic use of drug* - This description can apply to several types of adverse reactions, but it commonly relates to **Type C (chronic) reactions**, where effects occur only after prolonged exposure. - These reactions might be due to **cumulative toxicity** or adaptive changes in the body. *Delayed effect of drug* - This aligns with **Type D (delayed) adverse drug reactions**, which manifest long after the drug exposure has ended or after a period of latency. - Examples include **carcinogenesis** or teratogenesis, occurring months or years later.

Question 1

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 2

Which of the following is a centrally acting antihypertensive drug?

Accepted Answer

Methyldopa

Answer

Phenoxybenzamine

Answer

Propranolol

Answer

Prazosin

Question 3

All are true regarding Sunitinib except which of the following?

Accepted Answer

It is excreted primarily in urine

Answer

It inhibits tyrosine kinase receptors

Answer

It is used for the treatment of GIST

Answer

It is used for renal cell carcinoma

Question 4

What is the primary cardiotoxic effect of bupivacaine?

Accepted Answer

Depressed pacemaker activity

Answer

Toxic compound damaging myocardial cells

Answer

Depressed neural control on heart

Answer

Vascular thrombosis and Myocardial ischemia

Question 5

Which of the following medications does not interact with warfarin?

Accepted Answer

Benzodiazepines

Answer

Barbiturate

Answer

Oral contraceptive

Answer

Cephalosporins

Question 6

Which of the following is not an alpha-blocker?

Accepted Answer

Atenolol

Answer

Indoramine

Answer

Idazoxan

Answer

Prazosin

Question 7

Which of the following is not a selective serotonin reuptake inhibitor?

Accepted Answer

Buspirone

Answer

Citalopram

Answer

Fluoxetine

Answer

Fluvoxamine

Question 8

Which enzyme is irreversibly inhibited by aspirin?

Accepted Answer

Cyclooxygenase

Answer

Lipooxygenase

Answer

Thromboxane synthase

Answer

Phospholipase

Question 9

What is the best drug for open-angle glaucoma?

Accepted Answer

Latanoprost

Answer

Pilocarpine

Answer

Physostigmine

Answer

Apraclonidine

Question 10

Which of the following best describes a Type B adverse drug reaction?

Accepted Answer

Unpredictable bizarre reaction

Answer

Augmented effect of drug

Answer

Effect seen on chronic use of drug

Answer

Delayed effect of drug

NEET-PG 2012 — Pharmacology