Biochemistry
2 questionsProlyl hydroxylase requires which cofactor?
GlcNAc-P-P-oligosaccharide is -
NEET-PG 2015 - Biochemistry NEET-PG Practice Questions and MCQs
Question 481: Prolyl hydroxylase requires which cofactor?
- A. Vitamin C (Correct Answer)
- B. Iron (Fe²⁺)
- C. Molybdenum
- D. Vitamin K1
Explanation: ***Vitamin C*** - **Prolyl hydroxylase** is an enzyme critical for the hydroxylation of proline residues during **collagen synthesis**. - **Vitamin C** (ascorbic acid) acts as an essential **cofactor**, reducing the ferric iron of the enzyme back to its ferrous state after each catalytic cycle, enabling continued activity. - The enzyme requires both **iron (Fe²⁺)** as a metal cofactor and **vitamin C** to maintain the iron in its reduced state. *Iron (Fe²⁺)* - While **iron** is indeed required by prolyl hydroxylase as a **metal cofactor**, the question asks for the cofactor, which specifically refers to **vitamin C**. - Iron functions as part of the enzyme's active site, but vitamin C is the reducing agent that keeps iron functional. - Vitamin C deficiency (scurvy) leads to defective collagen synthesis despite adequate iron. *Molybdenum* - **Molybdenum** is a cofactor for several human enzymes, including **xanthine oxidase** and **sulfite oxidase**. - However, it plays no direct role in the activity of prolyl hydroxylase. *Vitamin K1* - **Vitamin K1** is a crucial cofactor for **gamma-glutamyl carboxylase**, an enzyme involved in the carboxylation of glutamic acid residues in clotting factors. - It is not involved in the hydroxylation of proline by prolyl hydroxylase.
Question 482: GlcNAc-P-P-oligosaccharide is -
- A. Proteoglycan
- B. Glycoprotein (Correct Answer)
- C. Collagen
- D. Phospholipid
Explanation: ***Glycoprotein*** - **GlcNAc-P-P-oligosaccharide** refers to the **N-linked oligosaccharide precursor** that is synthesized on a **dolichol pyrophosphate** carrier (`-P-P`). This complex is characteristic of the initial stages of **N-linked glycosylation**, a process that forms glycoproteins. - **N-acetylglucosamine (GlcNAc)** is a crucial sugar residue found at the reducing end of this precursor, linking it to the dolichol carrier. *Proteoglycan* - Proteoglycans consist of a **core protein** covalently attached to long, unbranched **glycosaminoglycan (GAG)** chains, such as chondroitin sulfate or heparin. - While they contain sugar units, their structure and synthesis pathway are distinct from the GlcNAc-P-P-oligosaccharide described, which is specific to N-linked glycoprotein synthesis. *Collagen* - **Collagen** is a fibrous protein, primarily composed of a triple helix of polypeptide chains rich in **glycine, proline, and hydroxyproline**. - Although collagen undergoes some post-translational modifications like **glycosylation**, it does not involve the GlcNAc-P-P-oligosaccharide precursor in its typical synthesis. *Phospholipid* - **Phospholipids** are a major component of cell membranes, composed of a **hydrophilic head** (containing a phosphate group) and two **hydrophobic fatty acid tails**. - They are lipids and do not contain carbohydrate structures like GlcNAc-P-P-oligosaccharide.
Pharmacology
7 questionsPropranolol is most commonly prescribed as first-line therapy for which condition?
Which diuretic is known to cause the maximum potassium loss?
Hyoscine is an antagonist at which cholinergic receptor?
Which of the following is not a known side effect of amiodarone?
Which class of antihypertensive drugs is known to cause erectile dysfunction?
How do thiazides cause hypercalcemia?
Which diuretic is most likely to cause hyponatremia by impairing free water excretion?
NEET-PG 2015 - Pharmacology NEET-PG Practice Questions and MCQs
Question 481: Propranolol is most commonly prescribed as first-line therapy for which condition?
- A. Atrioventricular (AV) block
- B. Hypertension (high blood pressure)
- C. Cardiac arrest
- D. Thyrotoxicosis (excessive thyroid hormones) (Correct Answer)
Explanation: ***Thyrotoxicosis (excessive thyroid hormones)*** - **Propranolol** is commonly prescribed as **first-line symptomatic therapy** for **thyrotoxicosis** to manage symptoms such as **tachycardia, tremors, palpitations, and anxiety**. - It works by **blocking peripheral conversion of T4 to T3** and providing rapid **symptomatic relief** through beta-blockade. - While it does not treat the underlying thyroid disorder, it is the **immediate first-line agent** for symptom control while definitive treatment (antithyroid drugs, radioiodine, or surgery) is being arranged. - **Clinical pearl:** Propranolol is preferred over selective beta-blockers due to its additional effect on T4 to T3 conversion. *Hypertension (high blood pressure)* - **Propranolol** is **NOT a first-line agent** for hypertension in current guidelines (JNC 8, ESC/ESH). - First-line agents include **ACE inhibitors, ARBs, thiazide diuretics, and calcium channel blockers**. - Non-selective beta-blockers like propranolol are typically **third-line or later** due to unfavorable metabolic effects and side effect profile. - Selective beta-blockers (atenolol, metoprolol) may be used in specific hypertension scenarios, but propranolol is rarely first-line. *Atrioventricular (AV) block* - **Propranolol** is **absolutely contraindicated** in **AV block** as it further slows conduction through the AV node. - Beta-blockers can precipitate **complete heart block** in patients with pre-existing conduction abnormalities. *Cardiac arrest* - **Propranolol** is **contraindicated** in acute management of **cardiac arrest** as it reduces cardiac contractility and can worsen outcomes. - Cardiac arrest management involves **CPR, defibrillation, epinephrine, and amiodarone**.
Question 482: Which diuretic is known to cause the maximum potassium loss?
- A. Spironolactone
- B. Furosemide (Correct Answer)
- C. Thiazide diuretics
- D. Acetazolamide
Explanation: ***Furosemide*** - Furosemide is a **loop diuretic** that inhibits the Na-K-2Cl cotransporter in the **thick ascending limb of the loop of Henle**, leading to significant excretion of sodium, chloride, potassium, and water. - Its potent diuresis and impact on potassium reabsorption result in a **high risk of hypokalemia**. *Thiazide* - Thiazide diuretics inhibit the **Na-Cl cotransporter** in the **distal convoluted tubule**, causing moderate sodium and water excretion, and some potassium loss. - While they can cause hypokalemia, their effect on potassium excretion is generally **less pronounced than loop diuretics**. *Acetazolamide* - Acetazolamide is a **carbonic anhydrase inhibitor** that acts primarily in the **proximal tubule**, inhibiting bicarbonate reabsorption and leading to increased excretion of bicarbonate, sodium, potassium, and water. - The potassium loss is due to increased delivery of sodium to the collecting duct, leading to enhanced potassium secretion, but it is typically **less severe than with loop diuretics**. *Spironolactone* - Spironolactone is a **potassium-sparing diuretic** that acts as an **aldosterone antagonist** in the collecting duct, inhibiting sodium reabsorption and potassium secretion. - Instead of causing potassium loss, spironolactone actually **conserves potassium** and can lead to hyperkalemia.
Question 483: Hyoscine is an antagonist at which cholinergic receptor?
- A. Muscarinic (Correct Answer)
- B. Nicotinic
- C. Both
- D. None of the above
Explanation: ***Muscarinic*** - **Hyoscine** (scopolamine) is a well-known **antagonist** at **muscarinic cholinergic receptors**. - It blocks the action of **acetylcholine** at these receptors, leading to its anticholinergic effects like treating motion sickness and reducing secretions. *Nicotinic* - **Hyoscine** does not primarily act on **nicotinic cholinergic receptors**. - Drugs acting on nicotinic receptors include **neuromuscular blockers** (e.g., succinylcholine, rocuronium) and **ganglionic blockers**, which have different clinical applications. *Both* - While some drugs may have activity at both receptor types, **hyoscine's primary and clinically significant antagonism is at muscarinic receptors**. - Its therapeutic effects are attributed almost exclusively to its **muscarinic blockade**. *None of the above* - This option is incorrect because **hyoscine is a clear antagonist at muscarinic cholinergic receptors**. - Its widespread use in medicine is based on this specific pharmacological action.
Question 484: Which of the following is not a known side effect of amiodarone?
- A. Peripheral neuropathy
- B. Hyperthyroidism
- C. Hyperglycemia (Correct Answer)
- D. Skin discoloration
Explanation: ***Hyperglycemia*** - **Hyperglycemia** is generally **not recognized** as a direct or common side effect of amiodarone. - Amiodarone's primary action is on cardiac ion channels, and its metabolic effects typically involve thyroid function, not glucose regulation. *Hyperthyroidism* - Amiodarone contains **iodine**, which can induce **thyroid dysfunction**, including both hypo- and hyperthyroidism. - **Amiodarone-induced hyperthyroidism (AIH)** can occur due to increased thyroid hormone synthesis or destructive thyroiditis. *Peripheral neuropathy* - **Neurological side effects**, including **peripheral neuropathy**, are known to occur with chronic amiodarone use. - Symptoms often include **paresthesias**, weakness, and sensory loss in the extremities. *Skin discoloration* - Prolonged use of amiodarone can lead to **bluish-gray skin discoloration**, particularly in sun-exposed areas. - This is due to the **accumulation of amiodarone** and its metabolites in the skin.
Question 485: Which class of antihypertensive drugs is known to cause erectile dysfunction?
- A. Calcium channel blocker
- B. ACE inhibitors
- C. AT1 receptor antagonists
- D. Beta-blockers (Correct Answer)
Explanation: ***Beta-blockers*** - **Beta-blockers** are the antihypertensive class most commonly associated with **erectile dysfunction** - Mechanism: Reduced cardiac output, decreased peripheral blood flow, central nervous system effects reducing libido, and blockade of β2-mediated vasodilation - **Non-selective beta-blockers** (propranolol, nadolol) have higher incidence of ED compared to selective β1-blockers (metoprolol, atenolol) - Newer vasodilating beta-blockers (nebivolol, carvedilol) have lower risk of sexual dysfunction *Calcium channel blockers* - Generally have **neutral or minimal effect** on erectile function - May even improve ED in some patients due to **vasodilatory properties** - Side effects include peripheral edema and headache, but not sexual dysfunction *ACE inhibitors* - Associated with **lower risk of erectile dysfunction** compared to other antihypertensives - May have neutral or even protective effects on sexual function - Preferred choice for hypertensive patients with existing sexual dysfunction concerns - Common side effects: dry cough and angioedema (not related to sexual function) *AT1 receptor antagonists* - **ARBs have neutral to potentially beneficial effects** on sexual function - Considered an excellent alternative for patients experiencing sexual side effects with other antihypertensive medications - Some studies suggest they may improve erectile function in hypertensive patients
Question 486: How do thiazides cause hypercalcemia?
- A. Decreased calcium excretion (Correct Answer)
- B. Increased parathyroid hormone secretion
- C. Decreased calcitonin secretion
- D. Increased calcium absorption
Explanation: ***Decreased calcium excretion*** - Thiazides inhibit the **Na-Cl co-transporter** in the **distal convoluted tubule**, leading to increased reabsorption of calcium [1], [2]. - This increased reabsorption of calcium is mediated by a low intracellular sodium concentration, which enhances the activity of the **Na+/Ca2+ exchanger** on the basolateral membrane [1]. *Increased parathyroid hormone secretion* - Thiazides **do not directly stimulate** parathyroid hormone (PTH) secretion; instead, they *decrease* calcium excretion, which would typically *lower* PTH levels through negative feedback. - Elevated PTH would lead to increased bone resorption and kidney calcium reabsorption, but this is not the **primary mechanism** for thiazide-induced hypercalcemia [2]. *Decreased calcitonin secretion* - **Calcitonin** is a hormone that *lowers* blood calcium levels, and its decrease would theoretically contribute to hypercalcemia. - However, thiazides have **no direct effect** on calcitonin secretion, making this an unlikely primary mechanism. *Increased calcium absorption* - While increased calcium absorption from the gut can contribute to hypercalcemia, thiazides do **not directly increase intestinal calcium absorption**. - Their primary action for influencing calcium levels is within the **kidney**, specifically on reabsorption, not absorption from the GI tract [1], [2].
Question 487: Which diuretic is most likely to cause hyponatremia by impairing free water excretion?
- A. Loop diuretics
- B. Acetazolamide
- C. Amiloride
- D. Thiazide diuretics (Correct Answer)
Explanation: ***Thiazide diuretics*** - **Thiazide diuretics** inhibit the **Na-Cl cotransporter in the distal convoluted tubule (DCT)**, impairing the kidney's ability to dilute urine and excrete free water - This impaired urinary dilution leads to **water retention relative to sodium**, resulting in **dilutional hyponatremia** - **Most common in elderly patients**, those on low-salt diets, or with pre-existing volume depletion - **Mechanism**: By blocking sodium reabsorption in the DCT (a key site for urinary dilution), thiazides prevent the generation of free water, leading to hyponatremia when water intake continues *Loop diuretics* - **Loop diuretics** inhibit the **Na-K-2Cl cotransporter in the thick ascending limb of Henle**, causing significant diuresis - They impair the medullary concentration gradient, **enhancing free water excretion** - **Less likely to cause hyponatremia** compared to thiazides because they promote rather than impair free water clearance - When hyponatremia occurs with loop diuretics, it's usually due to concurrent SIADH or excessive free water intake *Acetazolamide* - **Acetazolamide** is a **carbonic anhydrase inhibitor** acting primarily on the **proximal tubule** - Causes **bicarbonate and sodium excretion**, leading to mild diuresis - Main side effect is **metabolic acidosis** (type 2 RTA) - **Does not significantly impair free water excretion**, making hyponatremia uncommon *Amiloride* - **Amiloride** is a **potassium-sparing diuretic** that blocks **epithelial sodium channels (ENaC) in the collecting duct** - Weak diuretic effect, primarily used to prevent potassium loss - **Does not impair urinary dilution mechanisms**, so hyponatremia is rare - Main concern is **hyperkalemia**, especially with ACE inhibitors or in renal insufficiency
Physiology
1 questionsWhat is the PRIMARY mechanism by which the Na+-Ca2+ exchanger functions in cardiac muscle cells?
NEET-PG 2015 - Physiology NEET-PG Practice Questions and MCQs
Question 481: What is the PRIMARY mechanism by which the Na+-Ca2+ exchanger functions in cardiac muscle cells?
- A. Na+-Ca2+ exchanger requires ATP directly
- B. Na+-Ca2+ exchanger acts to remove Ca2+ from heart muscle cells (Correct Answer)
- C. The Na+-Ca2+ exchanger operates in reverse mode during normal cardiac contraction
- D. The Na+-Ca2+ exchanger primarily moves Ca2+ into cardiac muscle cells during systole
Explanation: ***Na+-Ca2+ exchanger acts to remove Ca2+ from heart muscle cells.*** - The primary function of the **Na+-Ca2+ exchanger (NCX)** in cardiac muscle is to **extrude calcium from the cell** into the extracellular space. - It uses the electrochemical gradient of **sodium (Na+)** which flows into the cell, to power the removal of **calcium (Ca2+)** from the cell, contributing to muscle relaxation during diastole. *The Na+-Ca2+ exchanger operates in reverse mode during normal cardiac contraction* - While it can theoretically operate in reverse, its **primary physiological role** during normal cardiac contraction is forward mode (Ca2+ extrusion). - Reverse mode operation (Ca2+ influx) is typically seen under specific conditions, such as **pathological states** or severely altered intracellular Na+ concentrations. *Na+-Ca2+ exchanger requires ATP directly* - The **Na+-Ca2+ exchanger** is a **secondary active transporter** and does not directly use ATP. - Its energy comes from the **electrochemical gradient of Na+**, which is maintained by the **Na+/K+-ATPase** (primary active transport, which *does* use ATP). *The Na+-Ca2+ exchanger primarily moves Ca2+ into cardiac muscle cells during systole.* - Moving **Ca2+ into the cell** during systole would primarily be the role of **L-type calcium channels** on the sarcolemma. - The NCX's main role is to **reduce intracellular Ca2+** after contraction, facilitating relaxation during diastole.