NEET-PG 2012 — Pharmacology

Q: What is considered a toxic serum level of lithium?

2.6. **2.6 mEq/L** - **Lithium toxicity** is generally considered to occur when serum lithium levels are above **1.5 mEq/L** with severe toxicity typically seen at levels above **2.5 mEq/L**. - At a level of **2.6 mEq/L**, patients are at high risk for significant neurological symptoms such as seizures, coma, and even death. *0.6 mEq/L* - A serum lithium level of **0.6 mEq/L** is within the normal therapeutic range, which is typically between **0.6 and 1.2 mEq/L**. - At this concentration, lithium is generally effective for bipolar disorder and other conditions with minimal risk of toxicity. *12 mEq/L* - A serum lithium level of **12 mEq/L** would represent an **extremely severe and likely fatal level of toxicity**, far beyond typical therapeutic or even severely toxic ranges. - Survival at such a high concentration would be highly improbable, as it would cause irreversible organ damage and profound central nervous system depression. *<0.6 mEq/L* - A serum lithium level of **less than 0.6 mEq/L** is considered subtherapeutic, meaning it is unlikely to be effective in treating bipolar disorder or other conditions. - While not toxic, such a low level would indicate a lack of therapeutic benefit and potential for symptom recurrence. [Practice more Pharmacology PYQs on OnCourse]

Q: Which of the following drugs is known to cross the blood-brain barrier?

Physostigmine. ***Physostigmine*** - **Physostigmine** is a **tertiary amine** that is uncharged at physiological pH, allowing it to readily cross the **lipophilic blood-brain barrier**. - Its ability to enter the central nervous system makes it useful for treating **central anticholinergic toxicity**, as it can inhibit acetylcholinesterase in the brain. *Glycopyrrolate* - **Glycopyrrolate** is a **quaternary ammonium compound**, meaning it carries a permanent positive charge. - This charge prevents it from crossing the **blood-brain barrier** effectively, limiting its effects to the peripheral nervous system. *Neostigmine* - **Neostigmine** is also a **quaternary ammonium compound**, similar to glycopyrrolate, making it highly ionized. - Due to its poor lipid solubility and charge, **neostigmine** has very limited penetration into the **central nervous system**. *All of the options* - This option is incorrect because both **glycopyrrolate** and **neostigmine** are charged molecules that do not readily cross the **blood-brain barrier**. - Only **physostigmine** among the listed drugs possesses the necessary lipophilicity to enter the central nervous system. [Practice more Pharmacology PYQs on OnCourse]

Q: What is the mechanism of action of Clopidogrel?

Inhibition of ADP-mediated platelet activation. ***Inhibition of ADP-mediated platelet activation*** - Clopidogrel is an **antiplatelet agent** that works by a direct antagonistic action at the **P2Y12 receptor** on the surface of platelets. - This binding prevents adenosine diphosphate (ADP) from binding to its receptor, thereby inhibiting the activation of the **GP IIb/IIIa receptor complex** and subsequent platelet aggregation. *Inhibition of Thromboxane A2* - This mechanism of action is characteristic of **aspirin**, which inhibits the enzyme **cyclooxygenase-1 (COX-1)**. - COX-1 inhibition leads to reduced production of **Thromboxane A2**, a potent platelet aggregator and vasoconstrictor. *Inhibition of GP IIb/IIIa receptors* - While Clopidogrel ultimately affects the activation of **GP IIb/IIIa receptors**, it does not directly inhibit them. - Drugs like **abciximab**, **eptifibatide**, and **tirofiban** are direct inhibitors of the GP IIb/IIIa receptors, preventing fibrinogen binding and platelet aggregation. *No effect on platelet activation* - This statement is incorrect as Clopidogrel is a well-established **antiplatelet drug**. - Its therapeutic effect is specifically to **reduce platelet activation** and aggregation, thus preventing thrombotic events. [Practice more Pharmacology PYQs on OnCourse]

Q: What is the primary mechanism by which epinephrine reduces insulin secretion?

Predominantly through alpha action. ***Predominantly through alpha action*** - **Epinephrine** primarily reduces insulin secretion by stimulating **alpha-2 adrenergic receptors** on pancreatic beta cells. - Activation of these receptors leads to a decrease in **cAMP levels** and an inhibition of insulin release. *Predominantly through beta action* - **Beta-2 adrenergic receptor activation** on pancreatic beta cells typically **stimulates** insulin secretion, which is opposite to epinephrine's overall effect. - While epinephrine has both alpha and beta effects, the **alpha-2 inhibition** of insulin release predominates in this context. *Through both alpha and beta actions* - Although epinephrine exerts both alpha and beta effects, the **alpha-2 receptor-mediated inhibition** of insulin secretion is the dominant mechanism. - The **beta-2 receptor-mediated stimulation** of insulin release is overridden by the stronger inhibitory alpha-2 effect. *Through muscarinic receptors* - Muscarinic receptors are part of the **parasympathetic nervous system** and are involved in stimulating insulin secretion. - **Epinephrine** acts on adrenergic receptors, not muscarinic receptors, to influence insulin release. [Practice more Pharmacology PYQs on OnCourse]

Q: Which of the following is a guanosine analogue?

Abacavir. ***Abacavir*** - **Abacavir** is a nucleoside reverse transcriptase inhibitor (NRTI) used in HIV treatment. - It is a **carbocyclic analogue of guanosine** (specifically, a 2'-deoxyguanosine analogue). - Structurally, it contains a modified cyclopentane ring instead of the ribose sugar, but retains the guanine base, making it a guanosine analogue. *Acyclovir* - **Acyclovir** is also a **guanosine analogue** - specifically an acyclic guanosine analogue. - It is an antiviral drug used to treat herpes simplex virus (HSV) and varicella-zoster virus (VZV) infections. - Note: Both Abacavir and Acyclovir are technically guanosine analogues; in this PYQ context, Abacavir is the expected answer. *Bromodeoxyuridine* - **Bromodeoxyuridine** is a **pyrimidine analogue**, specifically a thymidine analogue. - It is incorporated into DNA during replication and is used in research and as a radiosensitizer. *Allopurinol* - **Allopurinol** is a purine analogue (hypoxanthine analogue) that inhibits xanthine oxidase. - It is primarily used to treat **gout** and prevent kidney stones by reducing uric acid production. - While it's a purine derivative, it is not specifically a guanosine analogue. [Practice more Pharmacology PYQs on OnCourse]

93 Previous Year Questions with Answers & Explanations

Questions

What is considered a toxic serum level of lithium?

Which of the following drugs is known to cross the blood-brain barrier?

What is the mechanism of action of Clopidogrel?

What is the primary mechanism by which epinephrine reduces insulin secretion?

Which of the following is a guanosine analogue?

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

All are true regarding Sunitinib except which of the following?

Which of the following medications does not interact with warfarin?

As per RNTCP guidelines, Multi drug resistance (MDR) TB is defined as resistance to:

Q10

Which of the following antibiotics is known to cause bleeding due to its effect on blood clotting?

NEET-PG 2012 - Pharmacology NEET-PG Practice Questions and MCQs

Question 1: What is considered a toxic serum level of lithium?

A. 0.6
B. 12
C. 2.6 (Correct Answer)
D. <0.6

Explanation: **2.6 mEq/L** - **Lithium toxicity** is generally considered to occur when serum lithium levels are above **1.5 mEq/L** with severe toxicity typically seen at levels above **2.5 mEq/L**. - At a level of **2.6 mEq/L**, patients are at high risk for significant neurological symptoms such as seizures, coma, and even death. *0.6 mEq/L* - A serum lithium level of **0.6 mEq/L** is within the normal therapeutic range, which is typically between **0.6 and 1.2 mEq/L**. - At this concentration, lithium is generally effective for bipolar disorder and other conditions with minimal risk of toxicity. *12 mEq/L* - A serum lithium level of **12 mEq/L** would represent an **extremely severe and likely fatal level of toxicity**, far beyond typical therapeutic or even severely toxic ranges. - Survival at such a high concentration would be highly improbable, as it would cause irreversible organ damage and profound central nervous system depression. *<0.6 mEq/L* - A serum lithium level of **less than 0.6 mEq/L** is considered subtherapeutic, meaning it is unlikely to be effective in treating bipolar disorder or other conditions. - While not toxic, such a low level would indicate a lack of therapeutic benefit and potential for symptom recurrence.

Question 2: Which of the following drugs is known to cross the blood-brain barrier?

A. Glycopyrrolate
B. Neostigmine
C. Physostigmine (Correct Answer)
D. All of the options

Explanation: ***Physostigmine*** - **Physostigmine** is a **tertiary amine** that is uncharged at physiological pH, allowing it to readily cross the **lipophilic blood-brain barrier**. - Its ability to enter the central nervous system makes it useful for treating **central anticholinergic toxicity**, as it can inhibit acetylcholinesterase in the brain. *Glycopyrrolate* - **Glycopyrrolate** is a **quaternary ammonium compound**, meaning it carries a permanent positive charge. - This charge prevents it from crossing the **blood-brain barrier** effectively, limiting its effects to the peripheral nervous system. *Neostigmine* - **Neostigmine** is also a **quaternary ammonium compound**, similar to glycopyrrolate, making it highly ionized. - Due to its poor lipid solubility and charge, **neostigmine** has very limited penetration into the **central nervous system**. *All of the options* - This option is incorrect because both **glycopyrrolate** and **neostigmine** are charged molecules that do not readily cross the **blood-brain barrier**. - Only **physostigmine** among the listed drugs possesses the necessary lipophilicity to enter the central nervous system.

Question 3: What is the mechanism of action of Clopidogrel?

A. Inhibition of Thromboxane A2
B. Inhibition of GP IIb/IIIa receptors
C. No effect on platelet activation
D. Inhibition of ADP-mediated platelet activation (Correct Answer)

Explanation: ***Inhibition of ADP-mediated platelet activation*** - Clopidogrel is an **antiplatelet agent** that works by a direct antagonistic action at the **P2Y12 receptor** on the surface of platelets. - This binding prevents adenosine diphosphate (ADP) from binding to its receptor, thereby inhibiting the activation of the **GP IIb/IIIa receptor complex** and subsequent platelet aggregation. *Inhibition of Thromboxane A2* - This mechanism of action is characteristic of **aspirin**, which inhibits the enzyme **cyclooxygenase-1 (COX-1)**. - COX-1 inhibition leads to reduced production of **Thromboxane A2**, a potent platelet aggregator and vasoconstrictor. *Inhibition of GP IIb/IIIa receptors* - While Clopidogrel ultimately affects the activation of **GP IIb/IIIa receptors**, it does not directly inhibit them. - Drugs like **abciximab**, **eptifibatide**, and **tirofiban** are direct inhibitors of the GP IIb/IIIa receptors, preventing fibrinogen binding and platelet aggregation. *No effect on platelet activation* - This statement is incorrect as Clopidogrel is a well-established **antiplatelet drug**. - Its therapeutic effect is specifically to **reduce platelet activation** and aggregation, thus preventing thrombotic events.

Question 4: What is the primary mechanism by which epinephrine reduces insulin secretion?

A. Predominantly through beta action
B. Through both alpha and beta actions
C. Through muscarinic receptors
D. Predominantly through alpha action (Correct Answer)

Explanation: ***Predominantly through alpha action*** - **Epinephrine** primarily reduces insulin secretion by stimulating **alpha-2 adrenergic receptors** on pancreatic beta cells. - Activation of these receptors leads to a decrease in **cAMP levels** and an inhibition of insulin release. *Predominantly through beta action* - **Beta-2 adrenergic receptor activation** on pancreatic beta cells typically **stimulates** insulin secretion, which is opposite to epinephrine's overall effect. - While epinephrine has both alpha and beta effects, the **alpha-2 inhibition** of insulin release predominates in this context. *Through both alpha and beta actions* - Although epinephrine exerts both alpha and beta effects, the **alpha-2 receptor-mediated inhibition** of insulin secretion is the dominant mechanism. - The **beta-2 receptor-mediated stimulation** of insulin release is overridden by the stronger inhibitory alpha-2 effect. *Through muscarinic receptors* - Muscarinic receptors are part of the **parasympathetic nervous system** and are involved in stimulating insulin secretion. - **Epinephrine** acts on adrenergic receptors, not muscarinic receptors, to influence insulin release.

Question 5: Which of the following is a guanosine analogue?

A. Abacavir (Correct Answer)
B. Bromodeoxyuridine
C. Allopurinol
D. Acyclovir

Explanation: ***Abacavir*** - **Abacavir** is a nucleoside reverse transcriptase inhibitor (NRTI) used in HIV treatment. - It is a **carbocyclic analogue of guanosine** (specifically, a 2'-deoxyguanosine analogue). - Structurally, it contains a modified cyclopentane ring instead of the ribose sugar, but retains the guanine base, making it a guanosine analogue. *Acyclovir* - **Acyclovir** is also a **guanosine analogue** - specifically an acyclic guanosine analogue. - It is an antiviral drug used to treat herpes simplex virus (HSV) and varicella-zoster virus (VZV) infections. - Note: Both Abacavir and Acyclovir are technically guanosine analogues; in this PYQ context, Abacavir is the expected answer. *Bromodeoxyuridine* - **Bromodeoxyuridine** is a **pyrimidine analogue**, specifically a thymidine analogue. - It is incorporated into DNA during replication and is used in research and as a radiosensitizer. *Allopurinol* - **Allopurinol** is a purine analogue (hypoxanthine analogue) that inhibits xanthine oxidase. - It is primarily used to treat **gout** and prevent kidney stones by reducing uric acid production. - While it's a purine derivative, it is not specifically a guanosine analogue.

Question 6: Which of the following is not a selective serotonin reuptake inhibitor?

A. Buspirone (Correct Answer)
B. Citalopram
C. Fluoxetine
D. Fluvoxamine

Explanation: ***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**.

Question 7: All are true regarding Sunitinib except which of the following?

A. It inhibits tyrosine kinase receptors
B. It is excreted primarily in urine (Correct Answer)
C. It is used for the treatment of GIST
D. It is used for renal cell carcinoma

Explanation: ***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.

Question 8: Which of the following medications does not interact with warfarin?

A. Barbiturate
B. Oral contraceptive
C. Cephalosporins
D. Benzodiazepines (Correct Answer)

Explanation: ***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.

Question 9: As per RNTCP guidelines, Multi drug resistance (MDR) TB is defined as resistance to:

A. Rifampicin
B. Rifampicin, isoniazid and ethambutol
C. None of the above
D. Rifampicin and isoniazid (Correct Answer)

Explanation: ***Rifampicin and isoniazid*** - According to **RNTCP guidelines** (now NTEP), **MDR-TB** is specifically defined as tuberculosis that is resistant to at least both **rifampicin** and **isoniazid**. - These two drugs are the **most potent first-line anti-TB medications**, and resistance to both significantly complicates treatment. *Rifampicin* - While resistance to **rifampicin alone** is a serious concern, it is classified as **rifampicin-resistant TB (RR-TB)**, not full **MDR-TB**. - **MDR-TB** requires resistance to at least two key first-line drugs. *Rifampicin, isoniazid and ethambutol* - Resistance to **rifampicin**, **isoniazid**, and **ethambutol** would be a form of **MDR-TB** (as it includes resistance to rifampicin and isoniazid), but it is a more extensive form of resistance. - The minimum definition of **MDR-TB** focuses on the two most crucial first-line drugs. *None of the above* - This option is incorrect because there is a specific definition for **MDR-TB** that aligns with one of the provided choices. - The guidelines clearly define **MDR-TB** based on resistance to specific drugs.

Question 10: Which of the following antibiotics is known to cause bleeding due to its effect on blood clotting?

A. Moxalactam (Correct Answer)
B. Cefaloridine
C. Cefazolin
D. Ceftazidime

Explanation: Moxalactam - Moxalactam is a **third-generation cephalosporin** known to cause **hypoprothrombinemia** and platelet dysfunction, leading to an increased risk of bleeding. - This effect is due to its **N-methylthiotetrazole (NMTT) side chain**, which inhibits vitamin K-dependent clotting factor synthesis. Cefaloridine - This is a **first-generation cephalosporin** that does not have the NMTT side chain and is not commonly associated with significant bleeding risks. - Its primary adverse effect of concern is **nephrotoxicity** at high doses, rather than coagulopathy. Ceftazidime - Ceftazidime is a **third-generation cephalosporin** primarily used for *Pseudomonas aeruginosa* infections but does **not contain the NMTT side chain** responsible for bleeding complications. - While broad-spectrum, it generally has a favorable safety profile concerning coagulation. *Cefazolin* - Cefazolin is a **first-generation cephalosporin** [1] widely used for surgical prophylaxis and skin infections [1], and it does **not interfere with coagulation** pathways. - Its main side effects are typical for penicillin-related antibiotics, such as hypersensitivity reactions [1],[2].