Desmopressin is preferred over vasopressin because it:
Which of the following has the least glucocorticoid activity?
Which of the following is the MOST CRITICAL indication for Acyclovir use during pregnancy?
What is the mode of action of azathioprine?
Resistance to Methotrexate develops due to?
What is a key difference between fosphenytoin and phenytoin?
Which of the following is NOT a mechanism of action of theophylline in bronchial asthma?
Omalizumab is primarily used in the treatment of which condition?
Which of the following is a selective serotonin and norepinephrine reuptake inhibitor?
What is the drug of choice for listeria meningitis?
NEET-PG 2012 - Pharmacology NEET-PG Practice Questions and MCQs
Question 61: Desmopressin is preferred over vasopressin because it:
- A. Is more potent and has little vasoconstrictor activity (Correct Answer)
- B. Is more potent than vasopressin
- C. Has little vasoconstrictor activity
- D. Is more selective for V2 receptors than vasopressin
Explanation: **Is more potent and has little vasoconstrictor activity** - **Desmopressin** is a synthetic analog of **vasopressin** (ADH) that is modified to have much higher selectivity for **V2 receptors** in the renal collecting ducts, leading to potent **antidiuretic effects** [1], [3]. - This selective action results in significantly **reduced vasoconstrictor activity** (mediated by V1 receptors) compared to natural vasopressin, making it safer for clinical use to manage water balance without significant cardiovascular side effects [1], [3]. *Is more potent than vasopressin* - While desmopressin is indeed more potent in its **antidiuretic effect** due to increased affinity for **V2 receptors**, this option alone doesn't specify the critical advantage of *reduced vasoconstrictor activity* [3]. - Its superior potency alone doesn't fully explain its preference over vasopressin, as the **side-effect profile** is a major consideration. *Has little vasoconstrictor activity* - This statement is true and highlights a key advantage of desmopressin, but it omits the fact that **desmopressin is also more potent** in its desired antidiuretic effect compared to natural vasopressin [1]. - Both the **potency** and **reduced vasoconstrictor activity** contribute to its superior clinical profile [3]. *Is more selective for V2 receptors than vasopressin* - **Desmopressin's increased selectivity** for **V2 receptors** is the mechanistic basis for its preferred properties, leading to both greater antidiuretic potency and reduced vasoconstriction [1], [4]. - However, the option "Is more potent and has little vasoconstrictor activity" describes the *clinical consequences* of this selectivity, which are the direct reasons for its preferred use [2].
Question 62: Which of the following has the least glucocorticoid activity?
- A. Fludrocortisone
- B. Cortisone (Correct Answer)
- C. Dexamethasone
- D. Betamethasone
Explanation: ***Cortisone*** - **Cortisone has the LEAST glucocorticoid activity** among the options listed. - It is a **prodrug** that must be converted to **hydrocortisone (cortisol)** by 11β-hydroxysteroid dehydrogenase in the liver to become active. - Its glucocorticoid potency is approximately **0.8** relative to hydrocortisone (when hydrocortisone = 1). - Due to variable hepatic conversion, it has **lower and less predictable glucocorticoid effects** compared to other agents. *Fludrocortisone* - Primarily used for its **potent mineralocorticoid activity** (125× that of hydrocortisone). - However, it retains **significant glucocorticoid activity** approximately **10-15 times** that of hydrocortisone. - Despite being marketed as a mineralocorticoid, its glucocorticoid potency is **considerably higher than cortisone**. *Dexamethasone* - **Highly potent synthetic glucocorticoid** with negligible mineralocorticoid activity. - Glucocorticoid potency is approximately **25-30 times** that of hydrocortisone. - Long duration of action (36-72 hours) and excellent CNS penetration. *Betamethasone* - **Highly potent synthetic glucocorticoid**, structurally similar to dexamethasone (differs only in stereochemistry at C-16). - Glucocorticoid potency is approximately **25-30 times** that of hydrocortisone. - Minimal mineralocorticoid activity, with similar clinical applications to dexamethasone.
Question 63: Which of the following is the MOST CRITICAL indication for Acyclovir use during pregnancy?
- A. Treatment of disseminated herpes (Correct Answer)
- B. Treatment of chickenpox in the first trimester
- C. Prophylaxis for recurrent herpes during pregnancy
- D. Prevention of cytomegalovirus infection in pregnancy
Explanation: ***Treatment of disseminated herpes*** - **Disseminated herpes** in pregnancy is a severe, life-threatening condition for both the mother and the fetus, making acyclovir use critically indicated. - This systemic infection can lead to **visceral organ involvement**, **encephalitis**, and significantly increased maternal and fetal morbidity and mortality. - Immediate treatment with intravenous acyclovir is essential to prevent **multi-organ failure** and death. *Treatment of chickenpox in the first trimester* - While chickenpox in the first trimester can be serious, leading to **congenital varicella syndrome**, acyclovir's role here is primarily to mitigate maternal illness, not as critical as disseminated herpes. - The risk of congenital varicella syndrome for the fetus is relatively low (around 0.4%) after maternal infection in the first trimester. *Prophylaxis for recurrent herpes during pregnancy* - **Prophylactic acyclovir** in the third trimester is commonly used to prevent recurrent genital herpes and reduce the risk of **neonatal herpes**, but it is not as acutely critical as treating disseminated disease. - This intervention aims to prevent transmission during delivery rather than managing an immediate, life-threatening maternal or fetal condition. *Prevention of cytomegalovirus infection in pregnancy* - Acyclovir has **minimal activity against CMV** and is not indicated for CMV prevention or treatment. - **Ganciclovir** or **valganciclovir** are the antivirals used for CMV, not acyclovir.
Question 64: What is the mode of action of azathioprine?
- A. ↑ IL-2
- B. Decreased lymphophagocytic activity
- C. Wide-spread antitumor activity
- D. T-cell blockade (Correct Answer)
Explanation: ***T-cell blockade*** - Azathioprine is a **prodrug** that is metabolized into **6-mercaptopurine (6-MP)**, which then interferes with **purine synthesis** [1, 2]. - This interference inhibits the proliferation of **lymphocytes**, particularly **T-cells**, thereby blocking their immune response. *↑ IL-2* - An increase in **IL-2 (interleukin-2)** production would lead to enhanced T-cell proliferation and activity, which is the opposite effect of azathioprine. - **IL-2** is crucial for T-cell growth, differentiation, and survival, so drugs that increase it would boost, not suppress, the immune system. *Decreased lymphophagocytic activity* - This statement is not the primary mode of action of azathioprine. The drug's main effect is on the **synthesis of DNA and RNA** in rapidly dividing cells, including lymphocytes. - While immune suppression can indirectly affect various immune cell functions, the direct mechanism is not primarily a decrease in phagocytosis by lymphocytes. *Wide-spread antitumor activity* - Although 6-mercaptopurine, the active metabolite of azathioprine, is used in combination chemotherapy for some **hematological malignancies**, azathioprine itself is primarily known as an **immunosuppressant** in conditions like **autoimmune diseases** and **transplant rejection**. - Its antitumor activity is not typically described as "wide-spread," and its predominant use in pharmacology is for immune modulation.
Question 65: Resistance to Methotrexate develops due to?
- A. Rapid proliferation of cancer cells
- B. Thymidylate kinase deficiency
- C. Thymidylate synthetase deficiency
- D. Increased production of dihydrofolate reductase (DHFR) (Correct Answer)
Explanation: ***Increased production of dihydrofolate reductase (DHFR)*** - Methotrexate acts by inhibiting **dihydrofolate reductase (DHFR)**, an enzyme essential for **folate metabolism** and DNA synthesis. - An **increased production of DHFR** (through gene amplification or overexpression) by cancer cells allows them to bypass the drug's inhibitory effects, leading to resistance. - This is the **most common mechanism** of methotrexate resistance. *Rapid proliferation of cancer cells* - While **rapid cell proliferation** is a characteristic of cancer, it doesn't directly explain resistance to methotrexate. - Methotrexate targets fast-dividing cells (S-phase specific), so rapid proliferation often makes them **more susceptible**, not resistant, as long as the drug's mechanism is effective. *Thymidylate kinase deficiency* - **Thymidylate kinase** is involved in the phosphorylation of **thymidine** to produce **dTMP** (deoxythymidine monophosphate). - A deficiency in this enzyme would likely hinder DNA synthesis, potentially increasing sensitivity to DNA-targeting agents, rather than causing resistance to methotrexate. *Thymidylate synthetase deficiency* - **Thymidylate synthetase** converts dUMP to dTMP using **5,10-methylene-THF** as a cofactor. - Methotrexate **indirectly inhibits** thymidylate synthetase by depleting tetrahydrofolate cofactor pools through DHFR inhibition. - A **deficiency** of this enzyme would not cause resistance; rather, **increased thymidylate synthetase** expression can be an alternative resistance mechanism, though less common than DHFR overexpression.
Question 66: What is a key difference between fosphenytoin and phenytoin?
- A. Can be used in absence seizures
- B. Can be mixed with saline (Correct Answer)
- C. Can be given orally
- D. It is the drug of choice for myoclonic seizures
Explanation: **Can be mixed with saline** - **Fosphenytoin** is a water-soluble prodrug that is converted to phenytoin in the body; its solubility allows it to be **mixed with saline** solutions for intravenous administration, minimizing the risk of precipitation. - Unlike phenytoin, fosphenytoin's formulation avoids the need for propylene glycol, which is associated with adverse cardiovascular effects and makes phenytoin incompatible with saline. *Can be used in absence seizures* - Neither **fosphenytoin nor phenytoin** is effective for treating **absence seizures**, and they can sometimes worsen them. - **Ethosuximide** or **valproic acid** are the drugs of choice for absence seizures. *Can be given orally* - While **phenytoin** is commonly available in oral forms (capsules, chewable tablets, suspension), **fosphenytoin** is primarily designed for **parenteral administration** (intravenous or intramuscular). - Fosphenytoin is a prodrug that is rapidly converted to phenytoin *in vivo*, but it is not typically available or indicated for direct oral administration. *It is the drug of choice for myoclonic seizures* - Neither **fosphenytoin nor phenytoin** is the drug of choice for **myoclonic seizures**; they can exacerbate this type of seizure. - **Valproic acid** and **levetiracetam** are preferred treatments for myoclonic seizures due to their broader spectrum of activity.
Question 67: Which of the following is NOT a mechanism of action of theophylline in bronchial asthma?
- A. Adenosine receptor antagonism
- B. Increased histone deacetylation
- C. Phosphodiesterase inhibition
- D. Beta-2 receptor stimulation (Correct Answer)
Explanation: ***Beta-2 receptor stimulation*** - Theophylline is a **non-selective phosphodiesterase inhibitor** and an **adenosine receptor antagonist**, but it does not directly stimulate beta-2 receptors. - **Beta-2 receptor agonists** like salbutamol or formoterol are the medications that work by stimulating these receptors to cause bronchodilation. *Phosphodiesterase inhibition* - Theophylline inhibits **phosphodiesterase enzymes**, leading to an increase in intracellular **cAMP** levels. - This increase in **cAMP** promotes bronchodilation by relaxing airway smooth muscle. *Adenosine receptor antagonism* - Theophylline acts as an antagonist at **adenosine receptors**, particularly A1 and A2B. - Antagonism of adenosine receptors can reduce bronchoconstriction and inflammatory mediator release, contributing to its anti-asthmatic effects. *Increased histone deacetylation* - Theophylline, particularly at lower concentrations, increases the activity of **histone deacetylase (HDAC)**. - This action helps to **repress inflammatory gene expression**, which is a unique anti-inflammatory mechanism separate from its bronchodilatory effects.
Question 68: Omalizumab is primarily used in the treatment of which condition?
- A. Breast carcinoma
- B. Asthma (Correct Answer)
- C. Rheumatoid arthritis
- D. Chronic obstructive pulmonary disease (COPD)
Explanation: ***Asthma*** - **Omalizumab** is a **monoclonal antibody** that targets and binds to **immunoglobulin E (IgE)**, preventing it from binding to mast cells and basophils. - By reducing free IgE, omalizumab helps to prevent the release of inflammatory mediators, thereby **reducing allergic reactions and asthma symptoms**, particularly in patients with severe persistent allergic asthma. *Breast carcinoma* - **Omalizumab** is not indicated for the treatment of **breast carcinoma**; treatments for breast cancer typically involve chemotherapy, radiation, surgery, and targeted therapies specific to cancer cells. - Targeted therapies for breast cancer often focus on hormone receptors (e.g., **estrogen receptor**) or growth factor receptors (e.g., **HER2**), not IgE. *Rheumatoid arthritis* - **Omalizumab** is not used for **rheumatoid arthritis (RA)**; RA is an autoimmune disease primarily involving **T-cells and cytokines** like **TNF-alpha** and **IL-6**. - Treatment for RA typically includes **DMARDs** (disease-modifying antirheumatic drugs) and **biological agents** that target specific inflammatory pathways (e.g., **adalimumab**, **etanercept**). *Chronic obstructive pulmonary disease (COPD)* - **Omalizumab** is not indicated for **COPD**, which is primarily characterized by chronic inflammation of the airways and **emphysema**, largely caused by smoking. - COPD management focuses on bronchodilators, corticosteroids, and oxygen therapy, with no role for IgE-targeting therapy.
Question 69: Which of the following is a selective serotonin and norepinephrine reuptake inhibitor?
- A. Fluoxetine
- B. Venlafaxine (Correct Answer)
- C. Sertraline
- D. Aripiprazole
Explanation: ***Venlafaxine*** - **Venlafaxine** is a commonly used antidepressant that inhibits the reuptake of both **serotonin** and **norepinephrine**, making it an SNRI. - Its dual mechanism of action can be effective for a broad range of depressive and anxiety disorders. *Fluoxetine* - **Fluoxetine** is a **selective serotonin reuptake inhibitor (SSRI)**, primarily affecting serotonin levels in the brain. - It does not significantly inhibit norepinephrine reuptake and, thus, is not classified as an SNRI. *Sertraline* - **Sertraline** is another widely prescribed antidepressant that is also a **selective serotonin reuptake inhibitor (SSRI)**. - It works mainly by increasing serotonin availability in the synaptic cleft. *Aripiprazole* - **Aripiprazole** is an **atypical antipsychotic** medication, often used as an adjunct therapy for depression, but its primary mechanism is partial agonism at dopamine D2 and serotonin 5-HT1A receptors, and antagonism at serotonin 5-HT2A receptors. - It is not classified as a selective serotonin and norepinephrine reuptake inhibitor.
Question 70: What is the drug of choice for listeria meningitis?
- A. Ampicillin (Correct Answer)
- B. Cefotaxime
- C. Ciprofloxacin
- D. Ceftriaxone
Explanation: ***Ampicillin*** - **Ampicillin** is the **drug of choice** for *Listeria monocytogenes* meningitis due to its excellent in vitro activity and good central nervous system penetration. - It is often used in combination with an **aminoglycoside** (e.g., gentamicin) for synergistic bactericidal activity, especially in severe cases, though gentamicin does not penetrate the CSF well. *Cefotaxime* - **Third-generation cephalosporins** like cefotaxime have poor activity against *Listeria monocytogenes* due to the organism's intrinsic resistance to these agents. - While effective against many other bacterial causes of meningitis (e.g., *S. pneumoniae*, *N. meningitidis*), it is not appropriate for *Listeria*. *Ceftriaxone* - Similar to cefotaxime, **ceftriaxone** is a third-generation cephalosporin and is **ineffective** against *Listeria monocytogenes* due to the lack of penicillin-binding protein (PBP) affinity. - Its use for *Listeria* meningitis would lead to treatment failure. *Ciprofloxacin* - **Ciprofloxacin**, a fluoroquinolone, is generally **not recommended** as a first-line treatment for *Listeria* meningitis, despite some in vitro activity. - Its use is typically reserved for patients with severe allergies to penicillins, and even then, **trimethoprim-sulfamethoxazole** is usually preferred as an alternative to ampicillin.