Analgesics and Anti-inflammatory Drugs Practice Questions

Q: Basiliximab acts by antagonism against which receptor?

CD 25. **Explanation:** **Basiliximab** is a chimeric monoclonal antibody used primarily as an induction agent in organ transplantation to prevent acute rejection. 1. **Why CD 25 is correct:** Basiliximab acts as a competitive antagonist to the **CD 25** receptor. CD 25 is the **alpha subunit of the Interleukin-2 (IL-2) receptor**, which is specifically expressed on the surface of activated T-lymphocytes. By binding to CD 25, Basiliximab prevents IL-2 from binding to its receptor, thereby inhibiting T-cell proliferation and activation—the key drivers of graft rejection. 2. **Why other options are incorrect:** * **CD 11a:** This is a component of LFA-1 (Lymphocyte Function-associated Antigen-1). **Efalizumab** (now withdrawn) was the monoclonal antibody targeting CD 11a. * **TNF (Tumor Necrosis Factor):** Drugs targeting TNF-alpha include **Infliximab, Adalimumab, and Etanercept**. These are used in autoimmune conditions like Rheumatoid Arthritis and Crohn’s disease, not as primary induction agents in transplant surgery. **High-Yield Clinical Pearls for NEET-PG:** * **Daclizumab** is another monoclonal antibody that targets CD 25 (though it was primarily used for Multiple Sclerosis before being withdrawn). * **Selectivity:** Unlike older immunosuppressants (like Cyclosporine), Basiliximab is highly selective because CD 25 is only expressed on *activated* T-cells, not resting ones. * **Adverse Effects:** It is generally well-tolerated; however, clinicians must monitor for hypersensitivity reactions and increased risk of opportunistic infections. * **Mnemonic:** "Basi-**LI**-ximab" targets the **I**nter-**L**eukin (IL-2) receptor.

Q: In which of the following conditions can a high dose of morphine be used without significant danger?

Myocardial infarction. **Explanation:** **Correct Option: C (Myocardial Infarction)** Morphine is the drug of choice for pain management in ST-elevation myocardial infarction (STEMI). At high doses, it provides profound analgesia and reduces anxiety (anxiolysis), which decreases sympathetic overactivity. Crucially, morphine acts as a **venodilator**, reducing preload and myocardial oxygen demand. In the controlled environment of a Cardiac Care Unit (CCU) with hemodynamic monitoring and ventilatory support available, high doses can be administered safely to manage cardiogenic pulmonary edema and severe ischemic pain. **Why other options are incorrect:** * **A. Gall bladder surgery:** Morphine causes contraction of the **Sphincter of Oddi**, increasing intrabiliary pressure. This can worsen biliary colic or complicate post-operative recovery in biliary surgeries. * **B. Labour:** Morphine readily crosses the placental barrier. High doses during labor can cause **neonatal respiratory depression** and may also prolong labor by decreasing uterine contractions. * **C. Head injury:** Morphine is strictly contraindicated in head injuries for two reasons: 1) It causes respiratory depression, leading to CO2 retention and subsequent cerebral vasodilation, which **increases intracranial pressure (ICP)**. 2) It causes miosis and sedation, which masks pupillary signs and neurological monitoring essential for assessing the patient's status. **High-Yield Clinical Pearls for NEET-PG:** * **Specific Antagonist:** Naloxone is the drug of choice for morphine overdose. * **Triad of Morphine Poisoning:** Coma, Pin-point pupil (miosis), and Depressed respiration. * **Tolerance:** Develops to most effects except **miosis** and **constipation**. * **Alternative in Biliary Colic:** Pethidine (Meperidine) is preferred as it has less effect on the Sphincter of Oddi and possesses atropine-like antispasmodic properties.

Q: Which route is not typically used by addicts for morphine administration?

Oral. **Explanation:** The primary goal of drug abuse is to achieve a rapid "rush" or intense euphoria. This is directly dependent on the **speed of onset** and the **peak plasma concentration** of the drug in the brain [1]. **Why Oral is the Correct Answer:** Morphine has a significant **first-pass metabolism** in the liver when taken orally. This results in low bioavailability (approximately 20-40%) and a slow, gradual increase in blood levels [2]. For an addict, the oral route fails to produce the immediate "high" or "kick" desired, making it the least preferred route for abuse. **Analysis of Incorrect Options:** * **Intravenous (IV):** This is the most common route for advanced addicts [1]. It provides 100% bioavailability and an almost instantaneous peak concentration in the brain, leading to an immediate, intense euphoria. * **Subcutaneous (SC):** Often referred to as **"skin popping,"** this route is frequently used by addicts when their veins become sclerosed or difficult to access due to repeated IV injections. * **Intramuscular (IM):** This route provides faster absorption than the oral route and avoids first-pass metabolism, making it a viable alternative for users when intravenous access is unavailable. **High-Yield Clinical Pearls for NEET-PG:** * **Skin Popping:** Look for multiple circular, atrophic scars on the extremities in a patient with a history of drug abuse; this is a classic sign of subcutaneous morphine/heroin injection [3]. * **Complications:** IV drug use is a major risk factor for **Infective Endocarditis** (commonly involving the Tricuspid valve) and blood-borne pathogens like **HIV and Hepatitis B/C**. * **Triad of Opioid Overdose:** Pinpoint pupils (miosis), respiratory depression, and altered mental status (coma) [3]. * **Antidote:** Naloxone (pure opioid antagonist) is the treatment of choice for acute toxicity [3].

Q: Rofecoxib was withdrawn due to which of the following reasons?

Ischemic heart disease. **Explanation:** **Rofecoxib**, a selective COX-2 inhibitor, was voluntarily withdrawn from the global market in 2004 following the **APPROVe trial**, which demonstrated a significantly increased risk of **Ischemic Heart Disease (IHD)** and myocardial infarction. **Why Option A is correct:** The underlying mechanism involves an imbalance between prostanoids. COX-2 is the primary enzyme responsible for producing **Prostacyclin (PGI2)** in the vascular endothelium, which is a potent vasodilator and inhibitor of platelet aggregation. Selective COX-2 inhibitors suppress PGI2 without affecting **Thromboxane A2 (TXA2)** (produced by COX-1 in platelets), which is a vasoconstrictor and pro-aggregatory agent. This shift toward a pro-thrombotic state leads to increased cardiovascular events like MI and stroke. **Why other options are incorrect:** * **B. Renal complications:** While COX-2 inhibitors can cause fluid retention and worsen hypertension (similar to non-selective NSAIDs), this was not the primary reason for withdrawal. * **C. Liver adenoma:** This is not a recognized side effect of Rofecoxib; hepatic toxicity is more commonly associated with drugs like high-dose Paracetamol or Nimesulide. * **D. Gastric ulcer:** Selective COX-2 inhibitors were actually developed to *reduce* the risk of gastric ulcers compared to traditional NSAIDs. **High-Yield NEET-PG Pearls:** * **VIGOR Trial:** First major study to highlight the GI benefits but also the CV risks of Rofecoxib. * **Valdecoxib** was also withdrawn for similar CV risks and serious skin reactions (Stevens-Johnson Syndrome). * **Celecoxib** remains on the market but carries a "black box warning" for cardiovascular and gastrointestinal risks. * **Contraindication:** Avoid selective COX-2 inhibitors in patients with established ischemic heart disease or stroke.

Q: Which uricosuric drug is not used in acute gout?

Sulfinpyrazone. **Explanation:** The management of gout is divided into two distinct phases: **Acute Gouty Arthritis** (treatment of inflammation) and **Chronic Gout** (lowering serum uric acid levels). **Why Sulfinpyrazone is the correct answer:** Sulfinpyrazone is a **uricosuric agent**. It works by inhibiting the reabsorption of uric acid in the proximal convoluted tubules of the kidney, thereby increasing uric acid excretion. Uricosuric drugs (and Xanthine Oxidase inhibitors like Allopurinol) should **never** be initiated during an acute attack. Rapid fluctuations in serum uric acid levels can cause the mobilization of urate crystals from tissue stores, which paradoxically worsens and prolongs the acute inflammatory episode. **Analysis of Incorrect Options:** * **A. NSAIDs:** These are the first-line treatment for acute gout. They act by inhibiting prostaglandin synthesis, thereby reducing pain and inflammation. (Note: Aspirin is avoided as it can interfere with uric acid excretion). * **B. Colchicine:** This is a classic drug for acute gout. It inhibits microtubule polymerization and leukocyte migration to the joint, effectively halting the inflammatory response. * **C. Corticosteroids:** These are used in acute gout when NSAIDs or Colchicine are contraindicated (e.g., in renal failure) or when the attack is polyarticular. They provide potent anti-inflammatory relief. **NEET-PG High-Yield Pearls:** * **The "Golden Rule":** Never start or stop urate-lowering therapy (ULT) during an acute attack. If a patient is already on ULT when an attack starts, continue it at the same dose. * **Probenecid:** Another uricosuric drug; like Sulfinpyrazone, it is contraindicated in patients with a history of renal stones (urolithiasis). * **Drug of Choice:** NSAIDs (specifically Indomethacin or Naproxen) are generally preferred over Colchicine due to the latter's narrow therapeutic index and GI side effects.

Q: Which of the following statements about cetirizine is false?

It has good central nervous system penetration.. **Explanation:** **1. Why Option C is the correct (False) statement:** Cetirizine is a **second-generation H1-antihistamine**. Unlike first-generation agents (e.g., diphenhydramine), second-generation drugs are characterized by their **high polar nature** and low lipid solubility. This prevents them from crossing the blood-brain barrier (BBB) effectively. Therefore, cetirizine has **poor central nervous system (CNS) penetration**, resulting in minimal sedation compared to older antihistamines [1, 2]. **2. Analysis of Incorrect Options:** * **Option A:** This is true. Cetirizine belongs to the second generation of H1 blockers, which are preferred for allergic rhinitis and urticaria due to their longer duration of action and lack of anticholinergic side effects. * **Option B:** This is true. Cetirizine is the active acid metabolite of **hydroxyzine** (a first-generation antihistamine) [1]. * **Option D:** This is true. Beyond blocking H1 receptors, cetirizine possesses additional anti-inflammatory properties, including the inhibition of mast cell degranulation and the release of histamine and other inflammatory mediators. **Clinical Pearls for NEET-PG:** * **Levocetirizine** is the R-enantiomer of cetirizine, offering higher potency and potentially fewer side effects. * While classified as "non-sedating," cetirizine is the **most sedative** among the second-generation agents (more so than fexofenadine or loratadine). * It is primarily excreted unchanged in the urine; hence, dose adjustment is required in **renal impairment**. * Unlike terfenadine or astemizole, cetirizine does **not** cause QTc prolongation or Torsades de Pointes.

Q: Which of the following drugs reduces the activity of phospholipase A2?

Prednisolone. **Explanation:** The correct answer is **Prednisolone**. **Mechanism of Action:** Prednisolone is a glucocorticoid. Corticosteroids exert their anti-inflammatory effects by inducing the synthesis of **Lipocortin-1 (Annexin A1)**. Lipocortin-1 directly inhibits the enzyme **Phospholipase A2 (PLA2)**. Since PLA2 is responsible for releasing arachidonic acid from membrane phospholipids, its inhibition prevents the formation of all downstream inflammatory mediators, including prostaglandins, thromboxanes, and leukotrienes. **Analysis of Incorrect Options:** * **A. Alprostadil:** This is a synthetic analogue of **Prostaglandin E1 (PGE1)**. It acts as a vasodilator and is used clinically to maintain the patency of the ductus arteriosus or to treat erectile dysfunction. It does not inhibit PLA2. * **B. Aspirin:** This is a Non-Steroidal Anti-Inflammatory Drug (NSAID) that acts further down the cascade. It **irreversibly inhibits Cyclooxygenase (COX-1 and COX-2)** enzymes, preventing the conversion of arachidonic acid into prostaglandins. * **C. Ibuprofen:** Like aspirin, this is an NSAID. It **reversibly inhibits COX-1 and COX-2**. It has no effect on Phospholipase A2. **NEET-PG High-Yield Pearls:** * **Corticosteroids** are the only class that inhibits both the COX and LOX pathways by acting at the level of PLA2. * **Zileuton** inhibits 5-Lipoxygenase (LOX), while **Montelukast/Zafirlukast** are leukotriene receptor antagonists. * **Aspirin** is unique among NSAIDs for its irreversible inhibition (via acetylation) of the COX enzyme, which is why its anti-platelet effect lasts for the life of the platelet (7–10 days).

Q: Which of the following statements about baricitinib is FALSE?

Approved for use in moderate to severe Crohn's disease. **Explanation:** **Baricitinib** is a selective and reversible inhibitor of **Janus Kinase (JAK) 1 and 2**. It modulates the signaling pathway of various cytokines (like IL-6, IFN-γ) involved in inflammatory processes. **Why Option B is False (Correct Answer):** While several JAK inhibitors are used in Inflammatory Bowel Disease (IBD), Baricitinib is **not** currently approved for Crohn’s disease. **Upadacitinib** and **Tofacitinib** are the JAK inhibitors typically used in IBD (specifically Ulcerative Colitis). Baricitinib is primarily indicated for **Rheumatoid Arthritis (RA)**, **Alopecia Areata**, and severe **COVID-19**. **Analysis of Other Options:** * **Option A (True):** Baricitinib is an **oral** small-molecule drug, offering an advantage over injectable biological DMARDs. * **Option C (True):** JAK inhibitors are known to cause metabolic alterations, including **hyperlipidemia** (increased LDL, HDL, and triglycerides). Monitoring lipid profiles is mandatory during treatment. * **Option D (True):** Baricitinib is primarily excreted by the kidneys. Dose reduction is required if GFR is between 30-60 mL/min, and it is contraindicated if GFR <30 mL/min. It should also be used with caution in hepatic impairment. **High-Yield NEET-PG Pearls:** 1. **Mechanism:** JAK-STAT pathway inhibition. 2. **Black Box Warning:** Increased risk of serious infections (TB, fungal), malignancies, and **thromboembolism** (DVT/PE). 3. **Specific Indication:** It is the first FDA-approved systemic treatment for **Alopecia Areata**. 4. **Drug Interaction:** Its serum concentration increases when co-administered with **Probenecid** (due to inhibition of OAT3 transporter).

Q: Long term use of pethidine is avoided because a metabolite of pethidine is associated with which of the following?

Seizures. **Explanation:** Pethidine (Meperidine) is a synthetic opioid analgesic. Unlike most opioids, it is not recommended for long-term or chronic pain management due to its metabolic profile. **1. Why Seizures is the Correct Answer:** Pethidine is metabolized in the liver via N-demethylation to its active metabolite, **Norpethidine**. Norpethidine has a longer half-life (15–20 hours) than pethidine (3 hours) and possesses significant **CNS stimulant** properties. With repeated dosing or in patients with renal impairment, norpethidine accumulates, leading to CNS toxicity characterized by tremors, muscle twitches, hyperreflexia, and ultimately, **grand mal seizures**. **2. Analysis of Incorrect Options:** * **A. Constipation:** While pethidine causes less constipation than morphine (due to its mild anticholinergic activity), it is not the reason its *long-term* use is specifically contraindicated. * **B. Dependence:** All mu-opioid agonists carry a risk of dependence; however, this is a class effect and not specifically linked to a toxic metabolite. * **C. Respiratory depression:** This is a common acute side effect of all opioids. While norpethidine can contribute to toxicity, the specific limiting factor for long-term use is the excitatory neurotoxicity (seizures), not respiratory depression. **High-Yield Clinical Pearls for NEET-PG:** * **Anticholinergic effects:** Pethidine is the only opioid that causes **mydriasis** (due to its atropine-like structure) instead of the classic "pinpoint pupil" (miosis). * **Tachycardia:** Unlike other opioids that cause bradycardia, pethidine can cause tachycardia. * **Drug Interaction:** Pethidine is strictly contraindicated with **MAO inhibitors**, as it can precipitate a life-threatening **Serotonin Syndrome** (hyperpyrexia, coma, and convulsions). * **Renal Caution:** Always avoid pethidine in patients with renal failure due to rapid norpethidine accumulation.

Q: Which of the following is NOT a first-line drug for treating neuropathic pain?

Opioids. **Explanation:** Neuropathic pain results from damage or dysfunction of the somatosensory nervous system [2]. Unlike nociceptive pain, it responds poorly to conventional analgesics like NSAIDs and is managed using drugs that modulate neurotransmission. **Why Opioids are the Correct Answer:** According to international guidelines (IASP/NeuPSIG), **Opioids** (e.g., Morphine, Oxycodone) are considered **second-line or third-line treatments**. While effective, they are not first-line due to significant risks of dependence, tolerance, opioid-induced hyperalgesia [3], and the potential for misuse. They are generally reserved for patients who fail to respond to first-line agents or for acute exacerbations of severe neuropathic pain. **Analysis of Incorrect Options (First-line Agents):** * **Gabapentin (and Pregabalin):** These are Calcium channel $\alpha_2\delta$ ligands. They reduce the release of excitatory neurotransmitters (Glutamate, Substance P) and are first-line for Post-herpetic neuralgia and Diabetic neuropathy [1]. * **Duloxetine (and Venlafaxine):** These are SNRIs (Serotonin-Norepinephrine Reuptake Inhibitors). They enhance the descending inhibitory pain pathways and are first-line, especially for painful diabetic neuropathy [1]. * **Lidocaine (Topical):** Topical 5% lidocaine patches are considered first-line for **localized** neuropathic pain, such as Post-herpetic neuralgia (PHN), due to their excellent safety profile and minimal systemic absorption. **NEET-PG High-Yield Pearls:** * **Tricyclic Antidepressants (TCAs):** Amitriptyline is also a first-line agent [2] but should be used cautiously in the elderly due to anticholinergic side effects. * **Trigeminal Neuralgia:** The drug of choice is **Carbamazepine** (not Gabapentin). * **Mechanism of Gabapentin:** It does *not* act on GABA receptors; it binds to the $\alpha_2\delta$ subunit of voltage-gated calcium channels.

Question 1

Basiliximab acts by antagonism against which receptor?

Accepted Answer

CD 25

Answer

CD 11a

Answer

TNF

Answer

All of the above

Question 2

In which of the following conditions can a high dose of morphine be used without significant danger?

Accepted Answer

Myocardial infarction

Answer

Gall bladder surgery

Answer

Labour

Answer

Head injury

Question 3

Which route is not typically used by addicts for morphine administration?

Accepted Answer

Oral

Answer

Intravenous

Answer

Intramuscular

Answer

Subcutaneous

Question 4

Rofecoxib was withdrawn due to which of the following reasons?

Accepted Answer

Ischemic heart disease

Answer

Renal complication

Answer

Liver adenoma

Answer

Gastric ulcer

Question 5

Which uricosuric drug is not used in acute gout?

Accepted Answer

Sulfinpyrazone

Answer

NSAIDs

Answer

Colchicine

Answer

Corticosteroids

Question 6

Which of the following statements about cetirizine is false?

Accepted Answer

It has good central nervous system penetration.

Answer

It is a second-generation antihistamine.

Answer

It is a metabolite of hydroxyzine.

Answer

It inhibits the release of histamine.

Question 7

Which of the following drugs reduces the activity of phospholipase A2?

Accepted Answer

Prednisolone

Answer

Alprostadil

Answer

Aspirin

Answer

Ibuprofen

Question 8

Which of the following statements about baricitinib is FALSE?

Accepted Answer

Approved for use in moderate to severe Crohn's disease

Answer

Oral JAK inhibitor

Answer

Increases triglycerides

Answer

Dose reduction is required in renal and hepatic impairment

Question 9

Long term use of pethidine is avoided because a metabolite of pethidine is associated with which of the following?

Accepted Answer

Seizures

Answer

Constipation

Answer

Dependence

Answer

Respiratory depression

Question 10

Which of the following is NOT a first-line drug for treating neuropathic pain?

Accepted Answer

Opioids

Answer

Lidocaine

Answer

Gabapentin

Answer

Duloxetine

Analgesics and Anti-inflammatory Drugs — MCQs

Analgesics and Anti-inflammatory Drugs — MCQs

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