Analgesics and Anti-inflammatory Drugs Practice Questions

Q: Monoamine oxidase inhibitors (MAOIs) should not be used concurrently with which of the following analgesics?

Pethidine. **Explanation:** The concurrent use of **Pethidine (Meperidine)** and **Monoamine Oxidase Inhibitors (MAOIs)** is strictly contraindicated due to the risk of a life-threatening drug interaction known as **Serotonin Syndrome** (or hyperpyretic coma). **Why Pethidine is the correct answer:** Pethidine acts as a weak serotonin reuptake inhibitor. MAOIs prevent the breakdown of serotonin. When combined, they cause a massive accumulation of serotonin in the synaptic cleft, leading to two distinct types of reactions: 1. **Excitatory Reaction:** Characterized by hyperpyrexia (high fever), agitation, muscle rigidity, convulsions, and cardiovascular instability. 2. **Depressive Reaction:** Characterized by respiratory depression, hypotension, and coma. **Why other options are incorrect:** * **Morphine:** It is primarily a pure mu-opioid agonist and does not significantly affect serotonin reuptake. It is generally considered safe to use with MAOIs, though caution is advised regarding potential potentiation of sedative effects. * **Pentazocine & Buprenorphine:** These are mixed agonist-antagonists. While they have complex receptor profiles, they do not possess the potent serotonergic activity required to trigger the classic MAOI interaction seen with Pethidine. **High-Yield Clinical Pearls for NEET-PG:** * **The "P" Rule:** Remember **P**ethidine + **P**henelzine (MAOI) = **P**yrexia. * **Metabolite Fact:** Pethidine is metabolized to **Norpethidine**, which is neurotoxic and can cause seizures (especially in renal failure). * **Other Serotonergic Opioids:** Besides Pethidine, **Tramadol**, **Tapentadol**, and **Dextromethorphan** should also be avoided with MAOIs to prevent Serotonin Syndrome. * **Clinical Presentation:** Look for the triad of cognitive changes (confusion), autonomic hyperactivity (tachycardia, diaphoresis), and neuromuscular abnormalities (clonus, tremors).

Q: Which of the following is a feature of a nonselective COX inhibitor but not of a selective COX-2 inhibitor?

Antiplatelet aggregatory effect. The correct answer is **B. Antiplatelet aggregatory effect**. ### **Explanation of the Correct Answer** The fundamental difference between nonselective NSAIDs and selective COX-2 inhibitors lies in their effect on **Thromboxane A2 (TXA2)**. * **Nonselective COX inhibitors** (e.g., Aspirin, Ibuprofen) inhibit **COX-1** in platelets. Since platelets lack a nucleus, they cannot synthesize new enzymes; thus, TXA2 production is inhibited for the life of the platelet (7–10 days). This leads to a potent antiplatelet effect. * **Selective COX-2 inhibitors** (e.g., Celecoxib, Etoricoxib) do not inhibit COX-1. Therefore, they do not affect platelet aggregation. In fact, by inhibiting PGI2 (prostacyclin) in the vascular endothelium without affecting TXA2, they may shift the balance toward a **pro-thrombotic state**, increasing cardiovascular risk. ### **Why Other Options are Incorrect** * **A. Analgesic effect:** Both classes are effective analgesics. Pain and inflammation are primarily mediated by COX-2 at the site of injury. * **C. Renal salt and water retention:** Both COX-1 and COX-2 are constitutively expressed in the kidneys. Inhibiting either can lead to decreased renal blood flow, sodium retention, and edema. * **D. Prolongation of labor:** Prostaglandins (PGE2 and PGF2α) are essential for uterine contractions. Both nonselective and selective inhibitors can delay the onset of labor. ### **High-Yield NEET-PG Pearls** * **Aspirin** is the only NSAID that binds **irreversibly** to the COX enzyme. * **Selective COX-2 inhibitors** are preferred in patients with a high risk of GI ulcers (as they spare the protective COX-1 in the gastric mucosa) but are **contraindicated** in patients with ischemic heart disease. * **Paracetamol (Acetaminophen)** is a poor anti-inflammatory because it is inactivated by peroxides at the site of inflammation.

Q: Tolerance develops to all of the following effects of opioids except?

All of the above. **Explanation:** The development of tolerance is a hallmark of chronic opioid use, but it does not occur uniformly across all physiological systems. Tolerance refers to the need for increasing doses to achieve the same pharmacological effect. **Why "All of the above" is correct:** In pharmacology, opioids follow a specific pattern regarding tolerance. While tolerance develops rapidly to effects like euphoria, sedation, and respiratory depression, there are certain effects to which the body **never** (or very minimally) develops tolerance. These are often referred to as the "Exceptions to Opioid Tolerance." 1. **Constipation (Option A):** Opioids act on $\mu$-receptors in the myenteric plexus, decreasing GI motility. This effect persists indefinitely regardless of the dose or duration of use. 2. **Miosis (Option B):** Pinpoint pupils (due to stimulation of the Edinger-Westphal nucleus) remain a consistent sign of opioid use/overdose because tolerance does not develop to the miotic effect. 3. **Convulsions (Option C):** At high doses (especially with Pethidine due to its metabolite norpethidine), opioids can induce seizures. Tolerance does not develop to this excitatory effect. **Clinical Pearls & High-Yield Facts for NEET-PG:** * **Mnemonic for No Tolerance:** "**M-C-C**" (**M**iosis, **C**onstipation, **C**onvulsions). * **Highest Tolerance:** Develops to Euphoria, Analgesia, Sedation, and Respiratory depression. * **Clinical Significance:** Because tolerance does *not* develop to constipation, patients on long-term opioids (e.g., palliative care) must be started on a prophylactic stimulant laxative. * **Diagnostic Sign:** Miosis is a diagnostic "tell" in the ER for opioid overdose, as it persists even in chronic addicts.

Q: Which of the following is a common side effect of colchicine?

Diarrhea. **Explanation:** **Colchicine** is a unique anti-inflammatory agent primarily used for the management of acute gouty arthritis and prophylaxis. Its mechanism of action involves binding to tubulin, which inhibits microtubule polymerization [1]. This disrupts leukocyte migration, chemotaxis, and phagocytosis. **Why Diarrhea is the Correct Answer:** The most common and dose-limiting side effect of colchicine is **gastrointestinal distress**, specifically **diarrhea**, nausea, and vomiting [2]. This occurs because colchicine inhibits the rapid turnover of intestinal mucosal cells (which are highly dependent on microtubule-mediated mitosis). Diarrhea often serves as a clinical "stop signal," indicating that the maximum tolerated dose has been reached [2]. **Analysis of Incorrect Options:** * **A. Neutropenia:** While chronic high-dose colchicine can cause bone marrow suppression (leading to agranulocytosis or aplastic anemia), it is a rare, toxic effect rather than a "common" side effect. * **B. Asthma:** Colchicine does not cause bronchospasm or asthma. In fact, drugs like NSAIDs (via leukotriene shunting) are more commonly associated with drug-induced asthma. * **C. Fever:** Fever is not a side effect of colchicine; rather, colchicine is sometimes used to treat Familial Mediterranean Fever (FMF) [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Binds to tubulin $\rightarrow$ inhibits microtubule assembly $\rightarrow$ arrests mitosis in metaphase [1]. * **Drug of Choice:** Colchicine is the drug of choice for **prophylaxis** of gout and for **Familial Mediterranean Fever** [1]. * **Toxicity:** Acute overdose can lead to multi-organ failure. Chronic use may cause **myopathy** and **neuropathy**, especially when combined with statins. * **Contraindication:** It should be avoided in patients with severe renal or hepatic impairment [2].

Q: Methotrexate is used in all the following conditions except?

Sickle cell anemia. ### Explanation **1. Why Sickle Cell Anemia is the Correct Answer:** Methotrexate (MTX) is a folate antagonist that inhibits **dihydrofolate reductase (DHFR)**, leading to a decrease in DNA synthesis. It is primarily used as a Disease-Modifying Anti-Rheumatic Drug (DMARD) and a chemotherapeutic agent. It has **no role** in the management of Sickle Cell Anemia. The drug of choice for reducing the frequency of vaso-occlusive crises in Sickle Cell Anemia is **Hydroxyurea**, which works by increasing the levels of Fetal Hemoglobin (HbF). **2. Why the other options are incorrect:** * **Psoriasis:** MTX is a standard systemic treatment for severe, recalcitrant psoriasis. It works by inhibiting the rapid proliferation of epidermal cells (keratinocytes) and providing systemic anti-inflammatory effects. * **Rheumatoid Arthritis (RA):** MTX is the **"Anchor Drug"** and the first-line DMARD for RA. It reduces joint destruction and slows disease progression by inhibiting cytokine production and increasing extracellular adenosine. * **Ankylosing Spondylitis:** While TNF-inhibitors are preferred for axial disease, MTX is frequently used as a DMARD to manage peripheral joint involvement in patients with Ankylosing Spondylitis. **3. High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Action:** Competitive inhibition of DHFR; at low doses (for RA), it also increases **Adenosine**, which acts as a potent anti-inflammatory mediator. * **Toxicity:** The most common side effect is mucosal ulceration (stomatitis). The most serious are **hepatotoxicity** (cirrhosis) and **pulmonary fibrosis**. * **Rescue Therapy:** **Leucovorin (Folinic acid)** is used to "rescue" normal cells from MTX toxicity by bypassing the inhibited DHFR enzyme. * **Contraindication:** It is highly **teratogenic** (causes neural tube defects) and must be stopped at least 3 months before conception in both men and women.

Q: Which of the following drugs causes the least sedation?

Loratadine. **Explanation:** The question tests the classification of antihistamines based on their ability to cross the blood-brain barrier (BBB) and their sedative potential. **1. Why Loratadine is the correct answer:** Loratadine is a **Second-generation H1-antihistamine**. These drugs are characterized by high molecular weight and low lipid solubility, which prevents them from crossing the BBB effectively. Furthermore, they are substrates for the P-glycoprotein efflux pump, which actively removes them from the CNS. Consequently, they lack central sedative effects and are often referred to as "non-sedating antihistamines." **2. Why the other options are incorrect:** * **Hydroxyzine, Promethazine, and Chlorpheniramine** are all **First-generation H1-antihistamines**. * These agents are highly lipid-soluble and easily cross the BBB. * Once in the CNS, they block H1 receptors in the tuberomammillary nucleus (the arousal center), leading to significant sedation. * **Promethazine** and **Hydroxyzine** are particularly potent sedatives, often used clinically for their hypnotic or anti-anxiety properties. **3. High-Yield Clinical Pearls for NEET-PG:** * **Second-generation H1 blockers:** Loratadine, Cetirizine, Fexofenadine, Desloratadine. * **Fexofenadine** is considered the "least sedating" of all, as it has virtually zero CNS penetration. * **Cetirizine** is a second-generation drug but is unique because it can cause mild sedation in a small percentage of patients (it is the most sedating of the non-sedating group). * **First-generation drugs** also possess significant **anti-cholinergic** side effects (dry mouth, urinary retention, blurred vision), which are largely absent in second-generation agents.

Q: All are effects of morphine EXCEPT:

Hyperalgesia. **Explanation:** Morphine is the prototype opioid agonist acting primarily on **$\mu$-opioid receptors**. The correct answer is **Hyperalgesia** because morphine is an **analgesic** (relieves pain); it does not typically cause increased sensitivity to pain (hyperalgesia) as a primary pharmacological effect. While "Opioid-Induced Hyperalgesia" (OIH) can occur with chronic high-dose use or rapid titration, it is considered a paradoxical side effect rather than a standard physiological effect of the drug. **Analysis of Options:** * **Miosis (A):** Morphine stimulates the **Edinger-Westphal nucleus** of the 3rd cranial nerve, leading to "pin-point pupils." This is a diagnostic sign of opioid overdose as tolerance does not develop to this effect. * **Delayed gastric emptying (B):** Opioids increase smooth muscle tone but decrease propulsive rhythmic contractions in the GI tract. This leads to delayed gastric emptying and constipation (via $\mu$-receptors in the myenteric plexus). * **Respiratory depression (C):** This is the most dangerous side effect. Morphine reduces the sensitivity of the brainstem respiratory centers to carbon dioxide ($CO_2$). **High-Yield Clinical Pearls for NEET-PG:** 1. **Mnemonic for Morphine Effects:** **"MORPHINE"** – **M**iosis, **O**ut of it (sedation), **R**espiratory depression, **P**neumonia (aspiration), **H**ypotension, **I**nfrequent stools (constipation), **N**ausea, **E**mesis. 2. **Tolerance:** Tolerance develops to most effects **EXCEPT** Miosis and Constipation. 3. **Contraindication:** Morphine is contraindicated in **Head Injury** because it causes $CO_2$ retention, leading to cerebral vasodilation and increased intracranial pressure. 4. **Biliary Colic:** Morphine can aggravate biliary colic by causing spasm of the **Sphincter of Oddi**.

Q: Tacrolimus acts by inhibiting which of the following?

T–Cell proliferation. **Explanation:** **Tacrolimus** is a potent immunosuppressant belonging to the class of **calcineurin inhibitors**. **Mechanism of Action (Why C is correct):** Tacrolimus binds to an intracellular protein called **FK-binding protein (FKBP-12)**. This complex inhibits **calcineurin**, a phosphatase enzyme required for the dephosphorylation of the **Nuclear Factor of Activated T-cells (NFAT)**. Without dephosphorylation, NFAT cannot enter the nucleus to promote the transcription of **Interleukin-2 (IL-2)**. Since IL-2 is the primary cytokine responsible for the growth and differentiation of T-lymphocytes, its suppression directly leads to the inhibition of **T-cell proliferation**. **Analysis of Incorrect Options:** * **Option A:** Drugs like Azathioprine and Mycophenolate Mofetil (antimetabolites) inhibit DNA/RNA synthesis, not Tacrolimus. * **Option B:** Tacrolimus inhibits cytokine production (cell-mediated immunity) rather than directly blocking the formation of anti-lymphocyte antibodies. * **Option D:** Since A and B are incorrect, this option is invalid. **High-Yield Clinical Pearls for NEET-PG:** * **Potency:** Tacrolimus is roughly 100 times more potent than Cyclosporine. * **Side Effects:** While similar to Cyclosporine, Tacrolimus has a **higher incidence of Nephrotoxicity and Neurotoxicity** (tremors, seizures) and is more likely to cause **Post-transplant Diabetes Mellitus (PTDM)**. * **Cosmetic Advantage:** Unlike Cyclosporine, Tacrolimus **does not** cause hirsutism or gum hyperplasia. * **Drug of Choice:** It is the preferred agent for preventing rejection in liver and kidney transplants.

Q: Which of the following drugs is implicated in causing urinary retention?

Meperidine. **Explanation:** **Correct Option: B. Meperidine** Meperidine (Pethidine) is a synthetic opioid analgesic. While most opioids can cause urinary retention by increasing the tone of the bladder sphincter and decreasing the detrusor muscle's excitability, Meperidine has a distinct pharmacological profile. It possesses significant **anticholinergic (atropine-like) properties**. Anticholinergic drugs inhibit the parasympathetic nervous system, leading to relaxation of the detrusor muscle and contraction of the internal urethral sphincter, which directly results in acute urinary retention. **Incorrect Options:** * **A & D (Lisinopril & Losartan):** Lisinopril (an ACE inhibitor) and Losartan (an ARB) primarily affect the Renin-Angiotensin-Aldosterone System (RAAS). Their main side effects include hyperkalemia and renal impairment, but they do not typically cause urinary retention. * **C (Terazosin):** This is an **alpha-1 blocker**. It is actually used to *treat* urinary retention associated with Benign Prostatic Hyperplasia (BPH) by relaxing the smooth muscles of the bladder neck and prostate. **High-Yield NEET-PG Pearls:** * **Meperidine Metabolism:** It is metabolized to **normeperidine**, which is neurotoxic and can cause tremors, myoclonus, and **seizures** (especially in renal failure). * **Mydriasis:** Unlike most opioids that cause miosis (pinpoint pupils), Meperidine can cause mydriasis due to its anticholinergic effect. * **Drug Interaction:** Meperidine is contraindicated with **MAO inhibitors** as it can precipitate a life-threatening **Serotonin Syndrome**. * **Other drugs causing retention:** Tricyclic antidepressants (TCAs), first-generation antihistamines, and antiparkinsonian drugs (due to anticholinergic effects).

Q: Which of the following is NOT a contraindication in the therapy with opioids?

Use in severe constant pain. **Explanation:** **1. Why "Use in severe constant pain" is the correct answer:** Severe constant pain is the **primary clinical indication** for opioid therapy, not a contraindication. Opioids (like Morphine and Fentanyl) are the gold standard for managing moderate-to-severe acute pain (e.g., myocardial infarction, post-operative pain) and chronic cancer pain. They act on $\mu$-receptors in the CNS to raise the pain threshold and alter the emotional perception of pain. **2. Why the other options are Contraindications:** * **Head Injury:** Opioids cause respiratory depression, leading to CO₂ retention. CO₂ is a potent cerebral vasodilator which increases cerebral blood flow and **increases intracranial pressure (ICP)**. This can mask neurological signs (like pupillary changes) and worsen the clinical condition. * **Impaired Pulmonary Function:** Opioids decrease the sensitivity of the brainstem respiratory center to CO₂. In patients with COPD, asthma, or respiratory failure, this can precipitate fatal respiratory depression. * **Agonist with Mixed Agonist-Antagonist:** Administering a mixed agent (e.g., Pentazocine or Nalbuphine) to a patient already on a pure $\mu$-agonist (e.g., Morphine) can antagonize the analgesic effects and **precipitate withdrawal symptoms** in opioid-dependent individuals. **NEET-PG High-Yield Pearls:** * **Biliary Colic:** Opioids (except Pethidine) can cause contraction of the Sphincter of Oddi, potentially worsening biliary pain. * **Pin-point pupil (Miosis):** A classic sign of opioid overdose; it occurs due to stimulation of the Edinger-Westphal nucleus. * **Tolerance:** Develops to most effects except **miosis and constipation**. * **Antidote:** Naloxone is the drug of choice for acute opioid poisoning.

Question 1

Monoamine oxidase inhibitors (MAOIs) should not be used concurrently with which of the following analgesics?

Accepted Answer

Pethidine

Answer

Pentazocine

Answer

Buprenorphine

Answer

Morphine

Question 2

Which of the following is a feature of a nonselective COX inhibitor but not of a selective COX-2 inhibitor?

Accepted Answer

Antiplatelet aggregatory effect

Answer

Analgesic effect

Answer

Renal salt and water retention

Answer

Prolongation of labor

Question 3

Tolerance develops to all of the following effects of opioids except?

Accepted Answer

All of the above

Answer

Constipation

Answer

Miosis

Answer

Convulsions

Question 4

Which of the following is a common side effect of colchicine?

Accepted Answer

Diarrhea

Answer

Neutropenia

Answer

Asthma

Answer

Fever

Question 5

Methotrexate is used in all the following conditions except?

Accepted Answer

Sickle cell anemia

Answer

Psoriasis

Answer

Rheumatoid arthritis

Answer

Ankylosing spondylitis

Question 6

Which of the following drugs causes the least sedation?

Accepted Answer

Loratadine

Answer

Hydroxyzine

Answer

Promethazine

Answer

Chlorpheniramine

Question 7

All are effects of morphine EXCEPT:

Accepted Answer

Hyperalgesia

Answer

Miosis

Answer

Delayed gastric emptying

Answer

Respiratory depression

Question 8

Tacrolimus acts by inhibiting which of the following?

Accepted Answer

T–Cell proliferation

Answer

DNA and RNA synthesis

Answer

Anti–lymphocyte antibody formation

Answer

All of the above

Question 9

Which of the following drugs is implicated in causing urinary retention?

Accepted Answer

Meperidine

Answer

Lisinopril

Answer

Terazosin

Answer

Losartan

Question 10

Which of the following is NOT a contraindication in the therapy with opioids?

Accepted Answer

Use in severe constant pain

Answer

Use in a head injury patient

Answer

Use in impaired pulmonary function

Answer

Use of an agonist with a mixed agonist-antagonist

Analgesics and Anti-inflammatory Drugs — MCQs

Analgesics and Anti-inflammatory Drugs — MCQs

On this page

Practice by Chapter

Want unlimited practice?