Guanethidine is used in the treatment of which of the following conditions?
What is the primary therapeutic use of 5-HT1B/1D agonists?
Which enzyme is irreversibly inhibited by aspirin?
Side effects of thiazide diuretics include all of the following except?
Which of the following is an intermediate-acting insulin?
Long-term steroid ingestion leads to all of the following except:
Which antilipidemic drug reduces cholesterol levels by inhibiting cholesterol absorption?
Which sulphonamide has the longest acting duration?
All are true about ciprofloxacin except?
Which medication increases the efficacy of salmeterol when used together?
NEET-PG 2012 - Pharmacology NEET-PG Practice Questions and MCQs
Question 51: Guanethidine is used in the treatment of which of the following conditions?
- A. Ptosis
- B. Bell's palsy
- C. Thyrotoxic ophthalmopathy (Correct Answer)
- D. Horner's syndrome
Explanation: ***Thyrotoxic ophthalmopathy*** - Guanethidine is an **adrenergic neuron blocker** that can be used topically to reduce the sympathetic overactivity in the eye associated with thyrotoxicosis. - It helps alleviate symptoms like **retraction of the eyelids** and proptosis by blocking norepinephrine release from sympathetic nerve endings. *Ptosis* - **Ptosis** is primarily caused by weakness of the levator palpebrae superioris muscle or oculomotor nerve dysfunction, not sympathetic overactivity. - Guanethidine would not address the underlying muscular or neurologic deficit causing ptosis. *Bell's palsy* - **Bell's palsy** involves sudden, temporary weakness or paralysis of the muscles on one side of the face due to a dysfunction of the facial nerve. - Treatment typically involves corticosteroids and antivirals; guanethidine has no role in its management. *Horner's syndrome* - **Horner's syndrome** is characterized by miosis, ptosis, and anhidrosis, resulting from damage to the sympathetic nerve supply to the eye and face. - Guanethidine's mechanism of action would exacerbate, rather than treat, the existing sympathetic deficit in Horner's syndrome.
Question 52: What is the primary therapeutic use of 5-HT1B/1D agonists?
- A. Anti-anxiety medications
- B. Acute migraine treatment (Correct Answer)
- C. Anti-nausea medications for chemotherapy
- D. Drugs for gastroesophageal reflux disease (GERD)
Explanation: ***Acute migraine treatment*** - 5-HT1B/1D agonists, such as **triptans**, primarily work by causing **vasoconstriction of intracranial blood vessels** and inhibiting the release of pro-inflammatory neuropeptides. - This action directly alleviates the pain and associated symptoms of **acute migraine attacks**. *Anti-anxiety medications* - Anti-anxiety medications typically target neurotransmitter systems like **GABA** (e.g., benzodiazepines) or **serotonin reuptake** (e.g., SSRIs), not the 5-HT1B/1D receptors in this context. - While serotonin plays a role in anxiety, specific 5-HT1B/1D agonism does not lead to anxiolytic effects. *Anti-nausea medications for chemotherapy* - Anti-nausea medications used for chemotherapy-induced nausea and vomiting often target **5-HT3 receptors** (e.g., ondansetron) to block their pro-emetic effects. - 5-HT1B/1D agonists do not have primary anti-emetic properties useful in this setting. *Drugs for gastroesophageal reflux disease (GERD)* - GERD medications primarily focus on reducing stomach acid production (e.g., **proton pump inhibitors**, H2 blockers) or neutralizing it (antacids). - 5-HT1B/1D agonists do not directly influence gastric acid secretion or esophageal motility in a way beneficial for GERD.
Question 53: Which enzyme is irreversibly inhibited by aspirin?
- A. Lipooxygenase
- B. Cyclooxygenase (Correct Answer)
- C. Thromboxane synthase
- D. Phospholipase
Explanation: ***Cyclooxygenase*** - **Aspirin** irreversibly inhibits **cyclooxygenase (COX-1 and COX-2)** by acetylating a serine residue in the enzyme's active site. - This irreversible inhibition prevents the production of **prostaglandins, thromboxane**, and **prostacyclin**, thereby reducing inflammation, pain, fever, and platelet aggregation. *Lipooxygenase* - **Lipooxygenase** is involved in the synthesis of **leukotrienes**, which are mediators of inflammation and allergic responses. - Aspirin does not directly inhibit lipooxygenase; rather, it primarily targets the COX pathway. *Thromboxane synthase* - **Thromboxane synthase** is an enzyme downstream of COX, responsible for converting prostaglandin H2 into **thromboxane A2**. - While aspirin's effect on platelet aggregation is due to reduced thromboxane A2 synthesis via COX inhibition, it does not directly inhibit thromboxane synthase itself. *Phospholipase* - **Phospholipase A2** is responsible for releasing **arachidonic acid** from cell membrane phospholipids, which is the initial step in both the cyclooxygenase and lipooxygenase pathways. - Aspirin does not directly inhibit phospholipase A2; its action occurs later in the cascade.
Question 54: Side effects of thiazide diuretics include all of the following except?
- A. Hypokalemia
- B. Erectile dysfunction
- C. Hyponatremia
- D. Hypocalcemia (Correct Answer)
Explanation: ***Hypocalcemia*** - Thiazide diuretics are known to cause **hypercalcemia** (increased calcium reabsorption), NOT hypocalcemia, due to their action on the distal convoluted tubule. - This property makes them useful in treating conditions like **idiopathic hypercalciuria** and **calcium-containing kidney stones**. - The mechanism involves enhanced passive calcium reabsorption in the proximal tubule and active reabsorption in the distal tubule. *Hyponatremia* - Thiazide diuretics impair the kidney's ability to dilute urine and reabsorb sodium in the distal tubule, leading to **increased sodium excretion** and potential hyponatremia. - This effect is more pronounced in **elderly patients** and those with increased free water intake. - Hyponatremia is one of the most common electrolyte disturbances with thiazides. *Hypokalemia* - Thiazides increase the delivery of sodium and water to the collecting duct, leading to increased activity of the **renin-angiotensin-aldosterone system** and enhanced potassium secretion. - This results in **potassium wasting** and hypokalemia, which may require potassium supplementation or combination with potassium-sparing diuretics. *Erectile dysfunction* - Thiazide diuretics can cause **erectile dysfunction** through mechanisms including effects on vascular smooth muscle, reduced blood flow, and possible hormonal effects. - This is a common side effect reported in male patients using these medications for hypertension and may affect compliance.
Question 55: Which of the following is an intermediate-acting insulin?
- A. Insulin lispro
- B. NPH insulin (Correct Answer)
- C. Insulin glargine
- D. Regular insulin
Explanation: ***NPH insulin*** - **NPH (Neutral Protamine Hagedorn) insulin** is characterized by its intermediate duration of action, typically peaking in 4-12 hours and lasting up to 24 hours [1]. - This intermediate profile is achieved by combining insulin with **protamine**, which slows its absorption from the subcutaneous injection site [1]. *Insulin lispro* - **Insulin lispro** is a **rapid-acting insulin** analog, designed to act very quickly after injection, typically within 15-30 minutes [1, 2]. - Its quick onset and short duration make it suitable for dosing **immediately before meals** to control post-prandial glucose levels [1]. *Regular insulin* - **Regular insulin** is a **short-acting insulin**, with an onset of action around 30-60 minutes and a peak effect typically within 2-4 hours. - It is often administered **30 minutes before meals** and can also be used intravenously in acute situations like diabetic ketoacidosis. *Insulin glargine* - **Insulin glargine** is a **long-acting insulin** analog, providing a prolonged and relatively peakless effect over 24 hours [1, 2]. - Its primary role is to provide **basal insulin coverage**, mimicking the body's continuous background insulin production [1, 2].
Question 56: Long-term steroid ingestion leads to all of the following except:
- A. Avascular necrosis of head of femur
- B. Growth retardation
- C. Hypoglycemia (Correct Answer)
- D. Cataract
Explanation: ***Hypoglycemia*** - Chronic steroid use primarily leads to **hyperglycemia** due to increased **gluconeogenesis** and **insulin resistance**, not hypoglycemia. - Steroids raise blood glucose levels, potentially inducing or worsening **diabetes mellitus**. *Avascular necrosis of head of femur* - Long-term steroid use is a well-established risk factor for **avascular necrosis**, particularly affecting the **femoral head**. - This occurs due to impaired blood supply to the bone, leading to its death. *Cataract* - **Posterior subcapsular cataracts** are a known ocular complication of prolonged systemic corticosteroid therapy. - The mechanism involves direct effects of steroids on lens metabolism and protein aggregation. *Growth retardation* - In children, chronic corticosteroid therapy can suppress growth, leading to **growth retardation**. - This is due to interference with **growth hormone secretion** and direct effects on bone formation.
Question 57: Which antilipidemic drug reduces cholesterol levels by inhibiting cholesterol absorption?
- A. Ezetimibe (Correct Answer)
- B. Orlistat
- C. Cholestyramine
- D. Statins
Explanation: ***Ezetimibe*** - **Ezetimibe** selectively inhibits the **Niemann-Pick C1-Like 1 (NPC1L1) protein**, which is responsible for plant sterol and cholesterol absorption in the small intestine. - This action leads to a reduction in **LDL-C** levels by decreasing the amount of cholesterol available to the liver. *Orlistat* - **Orlistat** is a **lipase inhibitor** that prevents the absorption of dietary fats by inhibiting gastric and pancreatic lipases. - While it aids in weight loss and can indirectly improve lipid profiles, its primary mechanism is *not* direct inhibition of cholesterol absorption. *Cholestyramine* - **Cholestyramine** is a **bile acid sequestrant** that binds to bile acids in the intestine, preventing their reabsorption. - This increases the excretion of bile acids, prompting the liver to synthesize more bile acids from cholesterol, thereby lowering cholesterol levels, but it does *not* directly inhibit cholesterol absorption. *Statins* - **Statins** (HMG-CoA reductase inhibitors) are considered first-line agents for lowering cholesterol by inhibiting the **rate-limiting step in cholesterol synthesis** in the liver. - Their primary action is to reduce endogenous cholesterol production, not to block cholesterol absorption from the gut.
Question 58: Which sulphonamide has the longest acting duration?
- A. Sulfadiazine
- B. Sulphadoxine (Correct Answer)
- C. Sulfamethoxazole
- D. Sulfamethiazole
Explanation: ***Sulphadoxine*** - **Sulphadoxine** is known for its **exceptionally long elimination half-life**, which is due to its high plasma protein binding and slow renal excretion. - This property allows for **once-weekly dosing**, making it one of the longest-acting sulfonamides, often used in combinations for malaria prophylaxis or treatment. *Sulfadiazine* - **Sulfadiazine** has an intermediate half-life, typically requiring **multiple daily doses**. - It is commonly used for infections like **toxoplasmosis** and **nocardiosis**. *Sulfamethoxazole* - **Sulfamethoxazole** has an intermediate half-life, usually requiring **twice-daily administration**. - It is most famously co-formulated with **trimethoprim** (as co-trimoxazole) for a broad range of bacterial infections. *Sulfamethiazole* - **Sulfamethiazole** is a **short-acting sulfanilamide derivative** with a rapid elimination, meaning it would require frequent dosing. - It is not commonly used systemically due to its short duration of action.
Question 59: All are true about ciprofloxacin except?
- A. More active at acidic pH (Correct Answer)
- B. DNA gyrase inhibition
- C. Contraindicated in pregnancy
- D. Second generation fluoroquinolone
Explanation: ***More active at acidic pH*** - Fluoroquinolones, including ciprofloxacin, exhibit **reduced antibacterial activity in acidic environments**. Their efficacy is generally better at **neutral or alkaline pH**. - This is clinically relevant as fluoroquinolones may have **reduced effectiveness in acidic sites** like the stomach or acidic urine. - The optimal antibacterial activity occurs at physiological or slightly alkaline pH. *DNA gyrase inhibition* - Ciprofloxacin, like other fluoroquinolones, exerts its antibacterial effect by inhibiting **bacterial DNA gyrase (topoisomerase II)** and **topoisomerase IV**. - This inhibition prevents DNA replication and repair, leading to bacterial cell death. *Contraindicated in pregnancy* - Ciprofloxacin is generally **contraindicated in pregnancy** due to concerns about potential harm to the developing fetus, particularly effects on **cartilage development**. - However, it may be used in specific, life-threatening situations if the benefit outweighs the potential risk. *Second generation fluoroquinolone* - Ciprofloxacin is classified as a **second-generation fluoroquinolone**. - This class includes agents with improved activity against Gram-negative bacteria and some atypical organisms.
Question 60: Which medication increases the efficacy of salmeterol when used together?
- A. Corticosteroid (Correct Answer)
- B. Theophylline
- C. Ipratropium
- D. Sodium cromoglycate
Explanation: ***Corticosteroid*** - **Corticosteroids** act synergistically with **beta-2 agonists** like salmeterol by increasing the number and sensitivity of beta-2 receptors on bronchial smooth muscle cells. - They also reduce inflammation, which contributes to airway hyperresponsiveness, thereby improving the overall efficacy of bronchodilators. *Theophylline* - **Theophylline** is a methylxanthine that causes bronchodilation through inhibition of phosphodiesterase, but it is not directly synergistic with **salmeterol** in potentiating its primary action. - While both treat airway obstruction, their mechanisms are distinct, and theophylline has a narrow therapeutic index with significant side effects. *Ipratropium* - **Ipratropium** is an **anticholinergic bronchodilator** that blocks muscarinic receptors, leading to bronchodilation. - Its mechanism of action is different from that of **salmeterol (a beta-2 agonist)**, and while they can be used together for additive bronchodilation, ipratropium does not directly increase the efficacy of salmeterol itself. *Sodium cromoglycate* - **Sodium cromoglycate** is a **mast cell stabilizer** that prevents the release of inflammatory mediators, primarily used for asthma prophylaxis. - It does not have direct bronchodilatory effects and does not enhance the bronchodilatory action of **salmeterol**.