NEET-PG 2015 - Pharmacology Practice Questions

Q: Acetaminophen [Paracetamol] induced liver toxicity is due to which metabolite?

NAPQI. ***NAPQI*** - **N-acetyl-p-benzoquinone imine (NAPQI)** is a highly reactive and toxic metabolite produced during acetaminophen metabolism, especially in overdose situations [1, 3]. - When glutathione stores are depleted due to excessive NAPQI formation, this metabolite covalently binds to hepatic macromolecules, causing **hepatocellular damage and necrosis** [1, 3].*N-acetylcysteine* - **N-acetylcysteine (NAC)** is the antidote for acetaminophen overdose, not the toxic metabolite itself [2, 3]. - NAC works by replenishing hepatic **glutathione stores**, which helps detoxify NAPQI and prevent liver injury [2, 3].*Co-Q* - **Coenzyme Q10 (CoQ10)** is an endogenous antioxidant and electron carrier in the mitochondrial respiratory chain. - It is not a metabolite of acetaminophen and plays no direct role in acetaminophen-induced liver toxicity.*Cytochrome 'C'* - **Cytochrome c** is a protein involved in the electron transport chain in mitochondria and plays a critical role in apoptosis. - While cellular damage from NAPQI can eventually lead to cytochrome c release and apoptosis, cytochrome c itself is not a metabolite of acetaminophen or the direct cause of toxicity.

Q: Which of the following is the most characteristic sexual side effect of SSRIs?

Delayed ejaculation. ***Delayed ejaculation*** - **Delayed ejaculation** is a common and characteristic sexual side effect of SSRIs due to their impact on serotonin pathways involved in sexual response. - This effect can lead to significant distress and non-adherence to treatment, and often requires dose adjustment or switching to an alternative antidepressant. *Erectile dysfunction* - While **erectile dysfunction** can occur with SSRIs, it is a less specific and less consistently reported sexual side effect compared to ejaculatory dysfunction. - Many factors, including underlying mood disorder and comorbidities, can contribute to erectile dysfunction, making it less characteristic of SSRI use alone. *Retrograde ejaculation* - **Retrograde ejaculation** is a condition where semen enters the bladder during orgasm, and while it can be a side effect of some medications (e.g., alpha-blockers), it is not a hallmark sexual side effect of SSRIs. - SSRIs primarily affect the process of emission and expulsion, leading more commonly to delayed or absent ejaculation rather than retrograde flow. *Anxiety* - **Anxiety** is generally a *primary symptom* of the conditions SSRIs are prescribed to treat, such as depression or anxiety disorders, not a sexual side effect of the medication itself. - Although SSRIs can initially cause or worsen anxiety in some patients before therapeutic effects are seen, this is a systemic side effect, not a sexual one.

Q: What is the mechanism of action of ticagrelor?

Reversible inhibition of ADP action. ***Reversible inhibition of ADP action*** - **Ticagrelor** is a **P2Y12 receptor antagonist** that works by preventing ADP from binding to its receptor on platelets [2]. - This binding is **reversible**, meaning ticagrelor can dissociate from the receptor, allowing for some recovery of platelet function over time [2]. *Irreversible inhibition of ADP action* - **Clopidogrel** and **prasugrel** are examples of **irreversible P2Y12 inhibitors**, forming a permanent bond with the receptor [2]. - Irreversible inhibition leads to a longer duration of platelet inhibition, as new platelets must be generated for function to return [2]. *Reversible inhibition of GPIIb/IIIa* - **GPIIb/IIIa inhibitors** like **eptifibatide** and **tirofiban** block the final common pathway of platelet aggregation by preventing fibrinogen binding [1]. - While their action is reversible, they target a *different* mechanism than ticagrelor. *Irreversible inhibition of GPIIb/IIIa* - **Abciximab** is a GPIIb/IIIa inhibitor that binds **irreversibly** (or with very slow dissociation) to the receptor [1]. - Unlike reversible GPIIb/IIIa inhibitors, abciximab is a monoclonal antibody with a prolonged antiplatelet effect [1]. - This is still an incorrect answer as ticagrelor targets the P2Y12 receptor, not GPIIb/IIIa.

Q: Which of the following is an example of topical administration producing only local effects (not systemic)?

Topical corticosteroid cream. ***Topical corticosteroid cream*** - When applied to the skin for conditions like dermatitis, topical corticosteroids primarily exert their effects at the site of application, reducing **local inflammation** and itching. - While systemic absorption can occur with potent steroids over large areas, typical use aims for **localized action** without significant systemic effects. *Sublingual nitroglycerin* - This route is designed for **rapid systemic absorption** through the oral mucosa, bypassing first-pass metabolism to quickly treat angina. - The goal is a **widespread vasodilatory effect** throughout the body, not a local one within the mouth. *Transdermal patch* - Transdermal patches, such as those for nicotine or fentanyl, are specifically designed to deliver medication **systemically** through the skin into the bloodstream over a prolonged period. - They provide a **sustained release** and systemic therapeutic effect throughout the body. *Rectal diazepam* - Administered rectally, diazepam is absorbed into the systemic circulation to produce **CNS effects** such as sedation, anxiolysis, or anticonvulsant activity. - Although the administration is local, the intended clinical effect is **systemic** and widespread throughout the body.

Q: How do thiazides cause hypercalcemia?

Decreased calcium excretion. ***Decreased calcium excretion*** - Thiazides inhibit the **Na-Cl co-transporter** in the **distal convoluted tubule**, leading to increased reabsorption of calcium [1], [2]. - This increased reabsorption of calcium is mediated by a low intracellular sodium concentration, which enhances the activity of the **Na+/Ca2+ exchanger** on the basolateral membrane [1]. *Increased parathyroid hormone secretion* - Thiazides **do not directly stimulate** parathyroid hormone (PTH) secretion; instead, they *decrease* calcium excretion, which would typically *lower* PTH levels through negative feedback. - Elevated PTH would lead to increased bone resorption and kidney calcium reabsorption, but this is not the **primary mechanism** for thiazide-induced hypercalcemia [2]. *Decreased calcitonin secretion* - **Calcitonin** is a hormone that *lowers* blood calcium levels, and its decrease would theoretically contribute to hypercalcemia. - However, thiazides have **no direct effect** on calcitonin secretion, making this an unlikely primary mechanism. *Increased calcium absorption* - While increased calcium absorption from the gut can contribute to hypercalcemia, thiazides do **not directly increase intestinal calcium absorption**. - Their primary action for influencing calcium levels is within the **kidney**, specifically on reabsorption, not absorption from the GI tract [1], [2].

Q: What effect does morphine have on muscle tone?

Increased muscle tone. ***Increased muscle tone*** - Morphine **increases skeletal muscle tone** and can cause muscle rigidity, particularly with rapid IV administration (truncal rigidity). - It significantly increases **smooth muscle tone** in various organs including the sphincter of Oddi (causing biliary colic), bladder sphincter (causing urinary retention), and GI tract (causing constipation). - This increased tone in sphincters and smooth muscle is a well-documented effect mediated through **opioid receptor activation**. *Bradycardia (not increased heart rate)* - Morphine typically causes **bradycardia** (decreased heart rate) due to vagal stimulation and central effects, not tachycardia. - Increased heart rate would be atypical and not a primary pharmacological effect of morphine. *Miosis (not mydriasis)* - Morphine characteristically causes **miosis** (pinpoint pupils) due to stimulation of the Edinger-Westphal nucleus of the oculomotor nerve. - Mydriasis (dilated pupils) is seen with anticholinergics or sympathomimetics, not opioids. *Respiratory depression (not stimulation)* - Morphine causes **respiratory depression**, not stimulation, by reducing the responsiveness of brainstem respiratory centers to CO2. - This is one of the most dangerous adverse effects and the primary cause of death in opioid overdose.

Q: Which of the following statements about glucocorticoids is true?

Glucocorticoids downregulate MHC class II expression.. ***Glucocorticoids downregulate MHC class II expression.*** - Glucocorticoids exert **immunosuppressive effects** by reducing the expression of **MHC class II molecules** on antigen-presenting cells. - This downregulation impairs the ability of antigen-presenting cells to activate **CD4+ T-helper cells**, thereby suppressing adaptive immune responses. *Glucocorticoids directly activate T-helper cells.* - Glucocorticoids do not directly activate T-helper cells; rather, they have an **inhibitory effect** on T-cell function and proliferation. - They tend to promote **T-cell apoptosis** and reduce cytokine production, thus dampening T-helper cell responses. *Glucocorticoids have no effect on immune cells.* - This statement is incorrect as glucocorticoids have profound and widespread **immunosuppressive and anti-inflammatory effects** on various immune cells. - They influence the function, proliferation, and survival of **lymphocytes, macrophages, and granulocytes**. *Glucocorticoids enhance the activity of cytotoxic T cells.* - Glucocorticoids generally **suppress immune responses**, including the activity of **cytotoxic T cells (CTLs)**, rather than enhancing it. - They tend to inhibit the production of **interleukins** necessary for CTL activation and proliferation.

Q: Fastest receptor mediated action is through?

Intrinsic ion channels. ***Intrinsic ion channels*** - Receptors that are also **ion channels** (ligand-gated ion channels) allow direct and rapid ion flow across the membrane upon ligand binding, leading to immediate changes in membrane potential. - This direct mechanism bypasses complex intracellular signaling cascades, resulting in the **fastest cellular response** compared to other receptor types. *Cell surface receptors* - This is a broad category that includes **G protein-coupled receptors** and **receptor tyrosine kinases**, which typically involve more complex and slower signaling pathways. - While located on the cell surface, not all receptors in this category mediate action as quickly as intrinsic ion channels. *Receptor tyrosine kinases* - These receptors initiate signaling by **phosphorylating tyrosine residues** on target proteins, triggering a cascade of intracellular events that take time to manifest. - Their action involves **multiple phosphorylation steps** and protein interactions, making their response slower compared to direct ion channels. *Intracellular receptors* - These receptors, such as **steroid hormone receptors**, are located in the cytoplasm or nucleus and require their ligands to diffuse across the cell membrane. - The activated receptor then typically translocates to the nucleus to regulate gene transcription, a process that is much **slower** due to gene expression and protein synthesis.

Q: Thymidine is responsible for resistance to which antibiotic ?

Sulfonamide. ***Sulfonamide*** - **Thymidine** can contribute to **sulfonamide resistance** because sulfonamides interfere with **folate metabolism** and the subsequent synthesis of purines and pyrimidines, including thymidine. - An excess of thymidine can bypass the metabolic block caused by sulfonamides, allowing bacteria to continue DNA synthesis and grow. *Erythromycin* - **Erythromycin** resistance is primarily mediated by **methylation of ribosomal RNA**, which prevents the antibiotic from binding to the 50S ribosomal subunit. - It does not directly involve thymidine or the folate synthesis pathway. *Tetracycline* - Resistance to **tetracyclines** is commonly due to **efflux pumps** that actively pump the drug out of the bacterial cell or **ribosomal protection proteins** that prevent tetracycline binding. - Thymidine production or metabolism is not a mechanism of tetracycline resistance. *Nitrofurantoin* - **Nitrofurantoin** resistance typically involves **mutations** in bacterial enzymes (like **nitrofuran reductase**) that are responsible for activating the drug into its active form. - These mutations prevent the drug from becoming bactericidal, and thymidine does not play a role in this mechanism.

Q: Which of the following combinations does not show synergistic action?

Penicillin plus tetracycline. ***Penicillin plus tetracycline*** - This combination is generally **antagonistic** or **indifferent**, not synergistic. Penicillin is a cell wall synthesis inhibitor that works best on actively growing bacteria, while tetracycline is a bacteriostatic protein synthesis inhibitor that can reduce bacterial growth, thereby diminishing penicillin's effect. - The combination is usually avoided as the **bacteriostatic action of tetracycline** can counteract the **bactericidal action of penicillin**, leading to reduced efficacy, especially in infections requiring rapid bacterial clearance. *Penicillin plus sulfonamide* - This combination can show synergism in some contexts, particularly as sulfonamides inhibit **folate synthesis**, while penicillin inhibits **cell wall synthesis**. - While not a classic synergistic pair for all infections, their mechanisms of action are distinct, and they can sometimes be used together, although specific synergistic effects are more limited compared to other pairs. *Streptomycin plus penicillin* - This is a classic example of **synergistic action**, particularly in conditions like **enterococcal endocarditis**. - Penicillin damages the bacterial cell wall, allowing **streptomycin** (an aminoglycoside) to more easily penetrate the cell and act on ribosomal targets, leading to enhanced bactericidal effect. *Rifampicin plus dapsone* - This combination is a cornerstone of **multi-drug therapy for leprosy**, demonstrating clear synergy against *Mycobacterium leprae*. - **Rifampicin** inhibits bacterial RNA synthesis, and **dapsone** inhibits folate synthesis, attacking different essential bacterial pathways which, when combined, are more effective and reduce the development of resistance.

Question 1

Acetaminophen [Paracetamol] induced liver toxicity is due to which metabolite?

Accepted Answer

NAPQI

Answer

Co-Q

Answer

Cytochrome 'C'

Answer

N-acetylcysteine

Question 2

Which of the following is the most characteristic sexual side effect of SSRIs?

Accepted Answer

Delayed ejaculation

Answer

Retrograde ejaculation

Answer

Erectile dysfunction

Answer

Anxiety

Question 3

What is the mechanism of action of ticagrelor?

Accepted Answer

Reversible inhibition of ADP action

Answer

Irreversible inhibition of ADP action

Answer

Reversible inhibition of GPIIb/IIIa

Answer

Irreversible inhibition of GPIIb/IIIa

Question 4

Which of the following is an example of topical administration producing only local effects (not systemic)?

Accepted Answer

Topical corticosteroid cream

Answer

Sublingual nitroglycerin

Answer

Transdermal patch

Answer

Rectal diazepam

Question 5

How do thiazides cause hypercalcemia?

Accepted Answer

Decreased calcium excretion

Answer

Increased parathyroid hormone secretion

Answer

Decreased calcitonin secretion

Answer

Increased calcium absorption

Question 6

What effect does morphine have on muscle tone?

Accepted Answer

Increased muscle tone

Answer

Respiratory stimulation

Answer

Decreased muscle tone

Answer

Mydriasis

Question 7

Which of the following statements about glucocorticoids is true?

Accepted Answer

Glucocorticoids downregulate MHC class II expression.

Answer

Glucocorticoids directly activate T-helper cells.

Answer

Glucocorticoids have no effect on immune cells.

Answer

Glucocorticoids enhance the activity of cytotoxic T cells.

Question 8

Fastest receptor mediated action is through?

Accepted Answer

Intrinsic ion channels

Answer

Intracellular receptors

Answer

Cell surface receptors

Answer

Receptor tyrosine kinases

Question 9

Thymidine is responsible for resistance to which antibiotic ?

Accepted Answer

Sulfonamide

Answer

Erythromycin

Answer

Tetracycline

Answer

Nitrofurantoin

Question 10

Which of the following combinations does not show synergistic action?

Accepted Answer

Penicillin plus tetracycline

Answer

Streptomycin plus penicillin

Answer

Rifampicin plus dapsone

Answer

Penicillin plus sulfonamide

NEET-PG 2015 — Pharmacology