Which local anesthetic is known for its vasoconstrictive properties?
Which of the following is the prototypical sympathomimetic agent with both alpha and beta-adrenergic activity?
What is the effect of adding epinephrine to lignocaine (a local anesthetic)?
Which amino acid-derived neurotransmitter is primarily targeted in the pharmacological treatment of depression?
Midazolam does not cause which of the following?
Drug of choice for Pneumocystis jirovecii in pregnancy?
What is the correct sequence of medication administration for pre-operative prophylaxis in pheochromocytoma?
What is the drug of choice for listeria meningitis?
What is the initial drug of choice for a suspected case of acute adrenal insufficiency?
Which drug is used as a treatment for sickle cell anemia by promoting fetal hemoglobin production?
NEET-PG 2012 - Pharmacology NEET-PG Practice Questions and MCQs
Question 81: Which local anesthetic is known for its vasoconstrictive properties?
- A. Lidocaine
- B. Chlorprocaine
- C. Procaine
- D. Cocaine (Correct Answer)
Explanation: ***Cocaine*** - Cocaine is unique among local anesthetics for its inherent **sympathomimetic** properties, leading to **vasoconstriction**. - This vasoconstriction is due to its ability to block the reuptake of **norepinephrine** and other catecholamines at adrenergic nerve terminals. *Procaine* - Procaine is an **ester-type** local anesthetic that typically causes **vasodilation**, which can lead to rapid systemic absorption and a shorter duration of action. - It does not possess any inherent vasoconstrictive properties. *Lidocaine* - Lidocaine, an **amide-type** local anesthetic, generally causes **vasodilation** at clinical concentrations. - Due to this vasodilatory effect, **epinephrine** is often added to lidocaine preparations to prolong its action and reduce systemic absorption. *Chlorprocaine* - Chlorprocaine is another **ester-type** local anesthetic known for its rapid onset and short duration of action. - It primarily causes **vasodilation**, similar to procaine, and has no intrinsic vasoconstrictive effects.
Question 82: Which of the following is the prototypical sympathomimetic agent with both alpha and beta-adrenergic activity?
- A. Epinephrine (Correct Answer)
- B. Isoproterenol
- C. Norepinephrine
- D. Dopamine
Explanation: ***Epinephrine*** - Epinephrine (adrenaline) is a potent direct-acting **sympathomimetic** that stimulates both **alpha and beta-adrenergic receptors**. - Its diverse effects on the cardiovascular, respiratory, and other systems make it the prototypical agent for demonstrating both receptor activities. *Norepinephrine* - While norepinephrine (noradrenaline) also acts on **alpha and beta-1 receptors**, its affinity for **beta-2 receptors** is significantly lower than epinephrine. - This results in a predominant effect on **vasoconstriction** and cardiac contractility rather than bronchodilation or peripheral vasodilation. *Isoproterenol* - Isoproterenol is a **non-selective beta-adrenergic agonist**, meaning it primarily stimulates **beta-1 and beta-2 receptors**. - It has minimal or no activity at **alpha-adrenergic receptors**, differentiating it from epinephrine's mixed activity. *Dopamine* - Dopamine's effects are **dose-dependent**; at low doses, it primarily stimulates **dopamine receptors** and at moderate doses, it activates **beta-1 receptors**. - At high doses, it can stimulate **alpha-adrenergic receptors**, but its primary and distinguishing characteristic is its agonism at **dopamine receptors**, which epinephrine does not share.
Question 83: What is the effect of adding epinephrine to lignocaine (a local anesthetic)?
- A. Increases distribution of local anesthetic
- B. Decreases absorption of local anesthetic (Correct Answer)
- C. Decreases duration of local anesthetic
- D. Increases metabolism of local anesthetic
Explanation: ***Decreases absorption of local anesthetic*** - Epinephrine causes **vasoconstriction** at the site of injection, which reduces the rate at which the local anesthetic is absorbed into the systemic circulation. - This slower absorption leads to a **higher concentration of the anesthetic** at the nerve fibers, prolonging its effect and reducing systemic toxicity. - This is the primary mechanism by which epinephrine enhances local anesthetic efficacy. *Increases distribution of local anesthetic* - The primary effect of epinephrine is to **localize the anesthetic** by reducing its systemic distribution. - This localization is achieved through **vasoconstriction**, which keeps the drug at the desired site rather than allowing it to distribute widely. *Decreases duration of local anesthetic* - By slowing absorption, epinephrine effectively **increases the duration of action** of the local anesthetic. - The anesthetic remains at the site of action for a longer period, providing **extended pain relief**. *Increases metabolism of local anesthetic* - Epinephrine does not directly affect the **metabolic rate** of local anesthetics. - The primary mechanism of metabolism for amides like lignocaine is in the **liver** by cytochrome P450 enzymes.
Question 84: Which amino acid-derived neurotransmitter is primarily targeted in the pharmacological treatment of depression?
- A. Histamine
- B. None of the options
- C. Serotonin (Correct Answer)
- D. Acetylcholine
Explanation: ***Serotonin*** - **Serotonin** is an amino acid-derived neurotransmitter (from **tryptophan**) known to play a crucial role in mood regulation, sleep, appetite, and other functions, making it a primary target for **antidepressant medications**. - Medications like **Selective Serotonin Reuptake Inhibitors (SSRIs)** increase serotonin levels in the brain to alleviate symptoms of depression. *Histamine* - **Histamine** is an amino acid-derived neurotransmitter (from **histidine**) primarily involved in allergic reactions, inflammation, and regulating wakefulness. - While it has some central nervous system effects, its primary role is not directly in the treatment of **depression**. *Acetylcholine* - **Acetylcholine** is a neurotransmitter involved in muscle contraction, learning, memory, and attention, and is not derived from amino acids; it is synthesized from **choline** and acetyl-CoA. - It is not directly used for treating **depression**, although imbalances can play a role in cognitive aspects of some psychiatric disorders. *None of the options* - This option is incorrect because **Serotonin** is indeed an amino acid-derived neurotransmitter (from tryptophan) targeted for treating **depression**. - Many antidepressant drugs work by modulating **serotonergic pathways**.
Question 85: Midazolam does not cause which of the following?
- A. Anterograde amnesia
- B. Decreased cardiovascular effects as compared to propofol
- C. Causes tachyphylaxis during high dose infusions
- D. Retrograde amnesia (Correct Answer)
Explanation: ***Retrograde amnesia*** - Midazolam, a benzodiazepine, primarily causes **anterograde amnesia** [2], meaning patients have difficulty forming new memories after drug administration. - It does not significantly affect memories formed **before drug administration** (retrograde amnesia). *Anterograde amnesia* - Midazolam is well-known for its ability to induce **anterograde amnesia**, which is often a desirable effect in procedural sedation [2]. - This effect helps patients forget unpleasant or painful procedures performed while under its influence. *Causes tachyphylaxis during high dose infusions* - Prolonged or high-dose infusions of midazolam can lead to **tachyphylaxis**, requiring increased doses to achieve the same effect [1]. - This phenomenon is due to the **down-regulation or desensitization of GABA-A receptors** with continuous stimulation. *Decreased cardiovascular effects as compared to propofol* - Midazolam generally causes **less pronounced cardiovascular depression** (e.g., hypotension) compared to propofol, especially in standard sedative doses [1]. - This makes midazolam a safer option for sedation in some patients with **fragile cardiovascular statuses**.
Question 86: Drug of choice for Pneumocystis jirovecii in pregnancy?
- A. Primaquine
- B. Dapsone
- C. Pentamidine
- D. Trimethoprim-sulfamethoxazole (SMZ/TMP) (Correct Answer)
Explanation: ***Trimethoprim-sulfamethoxazole (SMZ/TMP)*** - Despite being a **folate antagonist**, SMZ/TMP is considered safe and the **drug of choice** for treating **Pneumocystis jirovecii pneumonia (PJP)** in pregnant women, particularly as the benefits outweigh the risks. - It is recommended to supplement with **folic acid** during treatment to mitigate potential teratogenic risks, although these risks are generally low. *Primaquine* - **Primaquine** is primarily used for the treatment of **Plasmodium vivax** and **Plasmodium ovale malaria**, specifically targeting hypnozoites in the liver. - It is contraindicated in pregnancy due to the risk of **hemolytic anemia** in the fetus, especially if the fetus has **glucose-6-phosphate dehydrogenase (G6PD) deficiency**. *Dapsone* - **Dapsone** is used in the treatment of **leprosy**, **dermatitis herpetiformis**, and as an alternative for **PJP prophylaxis** in HIV-positive patients. - While it can be used for PJP prophylaxis, its efficacy for **active PJP treatment** is lower than SMZ/TMP, and it carries risks of **hemolytic anemia** and **methemoglobinemia**, particularly in pregnancy. *Pentamidine* - **Pentamidine** is an alternative treatment for **PJP**, especially in patients who cannot tolerate SMZ/TMP. - It is typically reserved for **severe cases** or as a second-line agent due to its potential for **significant toxicity**, including hypotension, nephrotoxicity, and hypoglycemia, which can be particularly concerning in pregnancy.
Question 87: What is the correct sequence of medication administration for pre-operative prophylaxis in pheochromocytoma?
- A. Beta blockade followed by alpha blockade
- B. Simultaneous alpha and beta blockade
- C. Alpha blockade followed by beta blockade (Correct Answer)
- D. Alpha blockade only
Explanation: ***Alpha blockade followed by beta blockade*** - **Alpha blockade** should always be initiated first to control **hypertension** and prevent a **hypertensive crisis** during surgery. This is critical because pheochromocytoma causes excessive catecholamine release, leading to profound vasoconstriction. - **Beta blockade** is then added only after adequate alpha blockade has been achieved to control **tachycardia** and arrhythmias, preventing **unopposed alpha-adrenergic stimulation** which could paradoxically worsen hypertension. *Simultaneous alpha and beta blockade* - Administering both simultaneously is dangerous because **beta blockade** can mask the effects of inadequate alpha blockade. - This can lead to **unopposed alpha-adrenergic stimulation** after beta blockade, causing severe **vasoconstriction** and hypertensive crisis. *Beta blockade followed by alpha blockade* - Initiating with **beta blockade** without prior **alpha blockade** is absolutely contraindicated in pheochromocytoma. - This can lead to severe and potentially fatal **hypertension** due to **unopposed alpha-adrenergic stimulation** as beta blockade prevents vasodilation. *Alpha blockade only* - While essential for initial management, **alpha blockade alone** might not fully control all symptoms, especially **tachycardia** and **arrhythmias** caused by high circulating catecholamine levels. - Adding a **beta blocker** after achieving adequate alpha blockade helps in controlling these cardiac effects, optimizing patient preparation for surgery.
Question 88: 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.
Question 89: What is the initial drug of choice for a suspected case of acute adrenal insufficiency?
- A. Norepinephrine
- B. Hydrocortisone (Correct Answer)
- C. Dexamethasone
- D. Fludrocortisone
Explanation: ***Hydrocortisone*** - This is the initial drug of choice due to its **combined mineralocorticoid and glucocorticoid activity**, which effectively replaces the deficient hormones in acute adrenal insufficiency. - It also has a **rapid onset of action** crucial for stabilizing patients in an adrenal crisis. *Norepinephrine* - This is a **vasopressor** used to manage **severe hypotension or shock** by increasing peripheral vascular resistance. - While hypotension is a feature of adrenal insufficiency, norepinephrine does not address the underlying hormonal deficiency directly and is not the primary treatment. *Dexamethasone* - Dexamethasone is a **potent glucocorticoid** and can be used in adrenal insufficiency, but it lacks significant **mineralocorticoid activity**. - Its longer half-life might make it less ideal for immediate, titratable replacement compared to hydrocortisone in an acute setting. *Fludrocortisone* - Fludrocortisone is a **pure mineralocorticoid** primarily used for long-term replacement therapy to manage sodium and potassium balance in adrenal insufficiency. - It does not have sufficient glucocorticoid activity to address the immediate, life-threatening aspects of acute adrenal crisis.
Question 90: Which drug is used as a treatment for sickle cell anemia by promoting fetal hemoglobin production?
- A. Trypsin
- B. Hydroxyurea (Correct Answer)
- C. L-glutamine
- D. Glucose 6-phosphate dehydrogenase
Explanation: ***Hydroxyurea*** - **Hydroxyurea** is the primary drug used to treat sickle cell anemia by promoting **fetal hemoglobin (HbF)** production - It is a **ribonucleotide reductase inhibitor** that increases HbF levels, which reduces sickling of red blood cells - Clinical benefits include reduced frequency of **vaso-occlusive crises**, decreased need for transfusions, and improved survival - Mechanism: Increases **HbF** production, which dilutes the abnormal **HbS** and prevents polymerization *Trypsin* - **Trypsin** is a **proteolytic enzyme** involved in protein digestion in the gastrointestinal tract - It has no role in the treatment of **sickle cell anemia** or in promoting **fetal hemoglobin** production *L-glutamine* - **L-glutamine** is an **amino acid** (not a drug that promotes HbF) approved for sickle cell disease - Its mechanism involves reducing **oxidative stress** by increasing NAD+ levels and improving red blood cell energy metabolism - It reduces complications but does not primarily work by increasing **fetal hemoglobin** production *Glucose 6-phosphate dehydrogenase* - **G6PD** is an **enzyme** in the **pentose phosphate pathway**, not a therapeutic agent - **G6PD deficiency** causes hemolytic anemia but is unrelated to sickle cell disease treatment or fetal hemoglobin production