General Pharmacology Practice Questions

Q: Basiliximab is?

Anti CD25 monoclonal antibody. **Explanation:** **Basiliximab** is a chimeric monoclonal antibody that acts as a potent immunosuppressant. Its mechanism of action involves binding specifically to the **alpha subunit (CD25)** of the **Interleukin-2 (IL-2) receptor** expressed on the surface of activated T-lymphocytes. By competitively inhibiting the binding of IL-2 to its receptor, Basiliximab prevents T-cell proliferation and activation, which are critical steps in the cellular immune response against transplanted organs. **Analysis of Options:** * **Option A (Anti-CD3):** This refers to **Muromonab-CD3 (OKT3)**. It targets the CD3 complex on all T-cells, causing profound depletion. It is rarely used now due to "cytokine release syndrome." * **Option B (Correct):** Basiliximab (and Daclizumab) are specific **IL-2 receptor antagonists (Anti-CD25)**. * **Option C (IL-1 Receptor Antagonist):** This describes **Anakinra**, primarily used in the treatment of Rheumatoid Arthritis and Cryopyrin-associated periodic syndromes (CAPS). * **Option D (TNF-alpha Inhibitor):** This group includes drugs like **Infliximab, Adalimumab, and Etanercept**, used for autoimmune conditions like Crohn’s disease and Rheumatoid Arthritis. **High-Yield Clinical Pearls for NEET-PG:** * **Primary Indication:** Prophylaxis of **acute organ rejection** in renal transplantation (induction therapy). * **Key Advantage:** Unlike Muromonab-CD3, Basiliximab does not cause significant cytokine release syndrome because it only targets *activated* T-cells. * **Mnemonic:** "Basiliximab and Daclizumab are **25** letters combined" (to remember **CD25**). * **Chimeric vs. Humanized:** Basiliximab is **chimeric** (contains "-xi-"), whereas Daclizumab is **humanized** (contains "-zu-").

Q: Which of the following drugs is associated with tachyphylaxis?

Ephedrine. **Explanation:** **Tachyphylaxis** is a pharmacological phenomenon characterized by a rapid decrease in response to a drug after repeated administration over a short period. It is a form of "acute tolerance" that cannot be overcome by increasing the dose. **Why Ephedrine is the Correct Answer:** Ephedrine is a classic example of a drug that exhibits tachyphylaxis. It acts via a **mixed mechanism**: it directly stimulates adrenergic receptors and, more importantly, **indirectly** causes the release of stored norepinephrine (NE) from sympathetic nerve terminals. With repeated, frequent dosing, the readily releasable pools of NE become depleted. Once these stores are exhausted, subsequent doses of ephedrine produce a progressively diminishing effect, as there is no neurotransmitter left to release. **Analysis of Incorrect Options:** * **Dopamine:** While it is a catecholamine, it is primarily metabolized by MAO and COMT and does not typically demonstrate the rapid depletion-related tachyphylaxis seen with ephedrine. * **Haloperidol:** This is an antipsychotic (D2 blocker). Chronic use leads to **supersensitivity** or up-regulation of receptors (leading to tardive dyskinesia), rather than rapid tachyphylaxis. * **Propranolol:** As a beta-blocker, long-term use leads to **up-regulation** of receptors. Abrupt withdrawal can cause rebound hypertension or tachycardia, which is the opposite of tachyphylaxis. **High-Yield Clinical Pearls for NEET-PG:** * **Common drugs showing tachyphylaxis:** Ephedrine, Tyramine, Amphetamine, Nitroglycerin, Nicotine, and Nasal decongestants (e.g., Oxymetazoline). * **Mechanism:** For indirect sympathomimetics (Ephedrine/Amphetamine), the mechanism is **depletion of neurotransmitter stores**. For Nitrates, it involves the depletion of free sulfhydryl (-SH) groups. * **Distinction:** Unlike "Tolerance," which develops slowly (days/weeks), Tachyphylaxis develops **rapidly** (minutes/hours).

Q: Which of the following 5-HT receptors is not a G-protein coupled receptor?

5-HT3. ### Explanation The correct answer is **5-HT3**. **1. Why 5-HT3 is the correct answer:** Serotonin (5-HT) receptors are categorized into seven families (5-HT1 to 5-HT7). Among these, the **5-HT3 receptor** is the only exception that is a **ligand-gated ion channel** (ionotropic receptor) [2]. It is a pentameric selective cation channel that, when activated, leads to the rapid depolarization of neurons via the influx of Na⁺ and K⁺ ions [1]. It is primarily located in the Area Postrema (Chemoreceptor Trigger Zone - CTZ) and the gastrointestinal tract [3]. **2. Why the other options are incorrect:** * **5-HT1:** These are G-protein coupled receptors (GPCRs) linked to **Gi/o** proteins, which inhibit adenylyl cyclase and decrease cAMP levels [1], [2]. * **5-HT2:** These are GPCRs linked to **Gq/11** proteins, which activate the phospholipase C (PLC) pathway, leading to increased IP3 and DAG [1]. * **5-HT4:** These are GPCRs linked to **Gs** proteins, which stimulate adenylyl cyclase and increase cAMP levels [1]. (Note: 5-HT5, 5-HT6, and 5-HT7 are also GPCRs). **3. High-Yield Clinical Pearls for NEET-PG:** * **Antiemetics:** 5-HT3 antagonists (e.g., **Ondansetron**, Granisetron) are the drugs of choice for chemotherapy-induced nausea and vomiting (CINV) [3]. * **Prokinetics:** 5-HT4 agonists (e.g., **Prucalopride**, Tegaserod) are used to treat chronic constipation as they stimulate the peristaltic reflex [3]. * **Migraine:** 5-HT1B/1D agonists (**Triptans**) are used for acute migraine attacks by causing cranial vasoconstriction. * **Mnemonic:** Remember "**3 is Free**" (as in free-flowing ions) or "**3 is the odd one out**" to recall that 5-HT3 is the only ionotropic serotonin receptor.

Q: Which microsomal enzyme is involved in the metabolism of omeprazole?

CYP 2C19. **Explanation:** **Omeprazole**, a Proton Pump Inhibitor (PPI), is primarily metabolized in the liver by the cytochrome P450 system. The major enzyme responsible for its metabolism is **CYP2C19**, which converts omeprazole to 5-hydroxyomeprazole. A smaller portion is metabolized by CYP3A4 to omeprazole sulfone. **Analysis of Options:** * **CYP2C19 (Correct):** This is the principal enzyme for omeprazole metabolism. Genetic polymorphism of CYP2C19 is clinically significant; "poor metabolizers" (common in Asian populations) exhibit higher plasma concentrations and better therapeutic responses to PPIs compared to "rapid metabolizers." * **CYP2A:** This subfamily (specifically CYP2A6) is primarily involved in the metabolism of nicotine and coumarin, not PPIs. * **CYP2C8:** This enzyme is involved in the metabolism of drugs like paclitaxel, amodiaquine, and pioglitazone. * **CYP2B:** Specifically CYP2B6, this enzyme is responsible for metabolizing drugs such as bupropion and efavirenz. **High-Yield Clinical Pearls for NEET-PG:** 1. **Drug Interaction:** Omeprazole is a known **inhibitor of CYP2C19**. It can decrease the activation of **Clopidogrel** (a prodrug that requires CYP2C19 for conversion to its active form), potentially increasing the risk of cardiovascular events. 2. **Stereoisomerism:** **Esomeprazole** (the S-isomer of omeprazole) is less dependent on CYP2C19, leading to more predictable bioavailability and fewer drug interactions. 3. **Other CYP2C19 Substrates:** Phenytoin, Voriconazole, and Warfarin (minor).

Q: Which of the following is NOT a prodrug?

Lisinopril. **Explanation:** A **prodrug** is a pharmacologically inactive compound that must undergo metabolic conversion (usually in the liver) to become an active metabolite. **Why Lisinopril is the correct answer:** Most ACE inhibitors are prodrugs (e.g., Enalapril converts to Enalaprilat) to improve oral bioavailability. However, **Lisinopril** and **Captopril** are the two major exceptions; they are active drugs themselves and do not require hepatic activation. This makes them preferred in patients with liver dysfunction. **Analysis of Incorrect Options:** * **Levodopa:** It is the metabolic precursor of **Dopamine**. Since dopamine cannot cross the blood-brain barrier, Levodopa is administered and then converted to active dopamine in the CNS by the enzyme DOPA decarboxylase. * **Carbimazole:** This antithyroid drug is a prodrug that is rapidly converted to its active form, **Methimazole**, which inhibits the synthesis of thyroid hormones. * **Prednisolone:** While **Prednisone** is a prodrug (converted to Prednisolone in the liver), **Prednisolone** itself is the active metabolite. *Note: In some contexts, Prednisolone is considered active, but it can further convert to other metabolites; however, compared to the other options, it is frequently tested as the active form vs. Prednisone.* **High-Yield Clinical Pearls for NEET-PG:** * **ACE Inhibitor Mnemonic:** All ACE inhibitors are prodrugs **EXCEPT** Captopril and Lisinopril. * **Common Prodrugs to Remember:** Enalapril, Ramipril, Valacyclovir (to Acyclovir), Clopidogrel, Cyclophosphamide, and Sulfasalazine. * **Advantage of Prodrugs:** They often have better absorption, reduced side effects at the site of administration, or a longer duration of action.

Q: All of the following drugs can cross the placenta EXCEPT:

Heparin. **Explanation:** The transfer of drugs across the placenta is primarily governed by **Fick’s Law of Diffusion**. For a drug to cross the placental barrier, it typically needs to be lipid-soluble, non-ionized, and have a low molecular weight (usually <500–600 Daltons). **Why Heparin is the Correct Answer:** **Heparin** is a large, highly polar (negatively charged) polysaccharide molecule with a high molecular weight (approx. 15,000 Daltons). Due to its **large size and high ionization**, it cannot cross the placental barrier. Consequently, heparin (and its derivative, LMWH) is the anticoagulant of choice during pregnancy as it poses no teratogenic risk to the fetus. **Why the Other Options are Incorrect:** * **Phenytoin:** An antiepileptic that is lipid-soluble and easily crosses the placenta. It is associated with **Fetal Hydantoin Syndrome**. * **Diazepam:** A benzodiazepine that is highly lipid-soluble. It crosses the placenta rapidly and can lead to "Floppy Infant Syndrome" if given near term. * **Morphine:** An opioid analgesic that is relatively small and lipid-soluble. It crosses the placenta and can cause neonatal respiratory depression or withdrawal symptoms (NAS). **NEET-PG High-Yield Pearls:** * **Warfarin vs. Heparin:** Unlike Heparin, **Warfarin** has a low molecular weight and crosses the placenta, making it highly teratogenic (causing Fetal Warfarin Syndrome/Chondrodysplasia punctata). * **Rule of Thumb:** "Large, charged molecules stay put." Insulin and Heparin are classic examples of drugs that do **not** cross the placenta. * **Crucial Exception:** Most antibodies (IgG) are large but cross the placenta via active transport, not passive diffusion.

Q: Pseudocholinesterase acts on which of the following substances?

Mivacurium. **Explanation:** The question tests your knowledge of drug metabolism via specific esterases. **Mivacurium**, a short-acting non-depolarizing neuromuscular blocker, is primarily metabolized by **Pseudocholinesterase** (also known as Butyrylcholinesterase or Plasma Cholinesterase). This is clinically significant because patients with a genetic deficiency of this enzyme (atypical pseudocholinesterase) will experience prolonged muscle paralysis and apnea after receiving Mivacurium or Succinylcholine. **Analysis of Incorrect Options:** * **Esmolol:** This ultra-short-acting beta-blocker is metabolized by **Red Blood Cell (RBC) esterases**, not plasma pseudocholinesterase. * **Atracurium:** It undergoes degradation via **Hofmann elimination** (a spontaneous non-enzymatic chemical process dependent on pH and temperature) and, to a lesser extent, hydrolysis by non-specific esterases. * **Remifentanil:** This opioid is metabolized by **non-specific tissue and plasma esterases**, allowing for its rapid offset regardless of pseudocholinesterase levels. **High-Yield Clinical Pearls for NEET-PG:** * **Pseudocholinesterase substrates:** Succinylcholine, Mivacurium, Cocaine, and Procaine. * **RBC Esterase substrates:** Esmolol. * **Hofmann Elimination:** Characteristic of Atracurium and Cisatracurium; safe in renal and hepatic failure. * **Dibucaine Number:** Used to screen for pseudocholinesterase deficiency. A low number (<20) indicates an abnormal enzyme and high risk for prolonged apnea.

Question 1

Basiliximab is?

Accepted Answer

Anti CD25 monoclonal antibody

Answer

Anti CD3 monoclonal antibody

Answer

IL1 receptor antagonist

Answer

TNF alpha inhibitor

Question 2

Which of the following drugs is associated with tachyphylaxis?

Accepted Answer

Ephedrine

Answer

Dopamine

Answer

Haloperidol

Answer

Propranolol

Question 3

Which of the following 5-HT receptors is not a G-protein coupled receptor?

Accepted Answer

5-HT3

Answer

5-HT1

Answer

5-HT2

Answer

5-HT4

Question 4

Which microsomal enzyme is involved in the metabolism of omeprazole?

Accepted Answer

CYP 2C19

Answer

CYP 2A

Answer

CYP 2C8

Answer

CYP 2B

Question 5

Which of the following adverse effects can persist long after the offending drug has been withdrawn?

Accepted Answer

Tardive dyskinesia

Answer

Paradoxical tachycardia

Answer

Malignant hyperthermia

Answer

Gynaecomastia

Question 6

Which of the following is a common cause of electrolyte abnormalities?

Accepted Answer

Aluminum Hydroxide (Al(OH)3)

Answer

Potassium Chloride (KCl)

Answer

0.9% Sodium Chloride (NaCl)

Answer

Sodium Bicarbonate (NaHCO3)

Question 7

Which of the following is NOT a prodrug?

Accepted Answer

Lisinopril

Answer

Levodopa

Answer

Carbimazole

Answer

Prednisolone

Question 8

Allergic reactions depend on all except:

Accepted Answer

Dosage of the drug received

Answer

Previous exposure to the drug

Answer

Pharmacological action of the drug

Answer

Antigen-antibody reaction

Question 9

All of the following drugs can cross the placenta EXCEPT:

Accepted Answer

Heparin

Answer

Phenytoin

Answer

Diazepam

Answer

Morphine

Question 10

Pseudocholinesterase acts on which of the following substances?

Accepted Answer

Mivacurium

Answer

Esmolol

Answer

Atracurium

Answer

Remifentanil

General Pharmacology — MCQs

General Pharmacology — MCQs

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