Anatomy
1 questionsSertoli cells are derived from -
NEET-PG 2015 - Anatomy NEET-PG Practice Questions and MCQs
Question 491: Sertoli cells are derived from -
- A. Genital swelling
- B. Coelomic epithelium (Correct Answer)
- C. Primordial germ cells
- D. Germinal epithelium
Explanation: Sertoli cells are derived from the **coelomic epithelium** (surface epithelium) of the urogenital ridge during gonadal development. - The coelomic epithelium proliferates to form the **primitive sex cords** (medullary cords in males), and cells within these cords differentiate into Sertoli cells. - These cells are essential for **spermatogenesis**, providing structural support and nutrition to developing germ cells, and producing **anti-Müllerian hormone (AMH)** which causes regression of Müllerian ducts in male development [1]. *Germinal epithelium* - This is an **outdated term** previously used for the surface epithelium of the gonad, based on the misconception that it gave rise to germ cells. - Modern embryology uses the term **coelomic epithelium** or surface epithelium instead. - While historically used, this terminology is no longer preferred in current medical literature. *Genital swelling* - **Genital swellings** (labioscrotal swellings) are external mesodermal structures that develop into the **scrotum** in males or **labia majora** in females. - These are external genitalia components and are not the source of internal testicular cells like Sertoli cells. *Primordial germ cells* - **Primordial germ cells (PGCs)** originate from the epiblast, migrate via the hindgut to the developing gonads, and differentiate into **spermatogonia** (males) or **oogonia** (females) [1]. - They form the **germ cell lineage** (gametes), not somatic support cells like Sertoli cells, which are of coelomic epithelial origin.
Biochemistry
4 questionsWhich of the following statements about the enzymes involved in the conversion of glucose to glucose-6-phosphate in glycolysis is true?
Enzyme deficient in Hers disease -
Fumarate is formed from which amino acid?
Citrate synthase is inhibited by -
NEET-PG 2015 - Biochemistry NEET-PG Practice Questions and MCQs
Question 491: Which of the following statements about the enzymes involved in the conversion of glucose to glucose-6-phosphate in glycolysis is true?
- A. Glucokinase is induced by insulin. (Correct Answer)
- B. Hexokinase is specific for glucose.
- C. Glucokinase is inhibited by glucose-6-phosphate.
- D. Hexokinase has a high Km for glucose.
Explanation: ***Glucokinase is induced by insulin.*** - **Insulin** promotes glucose uptake and utilization in the liver and pancreatic beta cells, where glucokinase is primarily expressed. - Induction of **glucokinase** by insulin ensures that glucose is efficiently phosphorylated and trapped within hepatocytes when blood glucose levels are high. - This is a key mechanism for postprandial glucose homeostasis. *Incorrect: Hexokinase is specific for glucose.* - **Hexokinase** is NOT specific for glucose; it can phosphorylate various hexoses including **fructose**, **mannose**, and **galactose**. - Its broad substrate specificity distinguishes it from glucokinase, which has greater specificity for glucose. *Incorrect: Glucokinase is inhibited by glucose-6-phosphate.* - Unlike **hexokinase**, which is subject to product inhibition by glucose-6-phosphate, **glucokinase is NOT inhibited** by its product. - This lack of feedback inhibition allows glucokinase to continue phosphorylating glucose even when glucose-6-phosphate levels are elevated, which is appropriate for its role as a glucose sensor in liver and pancreatic beta cells. *Incorrect: Hexokinase has a high Km for glucose.* - **Hexokinase** has a **low Km** (~0.1 mM) for glucose, meaning it has high affinity and is saturated at normal blood glucose levels. - In contrast, **glucokinase** has a high Km (~10 mM), allowing it to respond proportionally to changes in blood glucose concentration.
Question 492: Enzyme deficient in Hers disease -
- A. Muscle phosphorylase
- B. Liver phosphorylase (Correct Answer)
- C. Acid maltase
- D. Debranching enzyme
Explanation: ***Liver phosphorylase*** - Hers disease, also known as Glycogen Storage Disease Type VI, is specifically caused by a deficiency of **liver phosphorylase**. - This enzyme is crucial for the breakdown of **glycogen in the liver**, leading to an inability to release glucose into the bloodstream during fasting. *Muscle phosphorylase* - Deficiency of **muscle phosphorylase** (myophosphorylase) causes **McArdle disease** (Glycogen Storage Disease Type V), which primarily affects muscle energy. - Patients typically present with exercise intolerance, muscle pain, and cramps, not the hepatic symptoms seen in Hers disease. *Acid maltase* - Deficiency of **acid maltase** (also known as alpha-glucosidase) is responsible for **Pompe disease** (Glycogen Storage Disease Type II), a lysosomal storage disorder. - This enzyme deficiency leads to glycogen accumulation in lysosomes in various tissues, including muscle, liver, and heart, causing muscle weakness and cardiomyopathy. *Debranching enzyme* - A deficiency in the **debranching enzyme** (amylo-1,6-glucosidase) causes **Cori disease** or **Forbes disease** (Glycogen Storage Disease Type III). - This results in the accumulation of abnormally structured glycogen with short outer branches in the liver, muscle, and heart.
Question 493: Fumarate is formed from which amino acid?
- A. Methionine
- B. Valine
- C. Histidine
- D. Tyrosine (Correct Answer)
Explanation: ***Tyrosine*** - **Tyrosine** is a **glucogenic and ketogenic amino acid** that is catabolized to acetoacetate and fumarate. - **Fumarate** then enters the **citric acid cycle (Krebs cycle)**, whereas acetoacetate is a ketone body. *Methionine* - **Methionine** is an **essential amino acid** and a precursor for **S-adenosylmethionine (SAM)**, a methyl donor in many reactions. - Its catabolism produces **succinyl CoA**, not fumarate, through a series of steps via propionyl CoA. *Valine* - **Valine** is a **branched-chain amino acid (BCAA)** that is exclusively **glucogenic**. - Its catabolism ultimately leads to the formation of **succinyl CoA**, which can enter the citric acid cycle. *Histidine* - **Histidine** is an **essential amino acid** that is catabolized to **formiminoglutamate (FIGLU)**. - FIGLU is then converted to **glutamate**, which can eventually be deaminated to α-ketoglutarate, a citric acid cycle intermediate, but not directly fumarate.
Question 494: Citrate synthase is inhibited by -
- A. Insulin
- B. Glucagon
- C. ADP
- D. ATP (Correct Answer)
Explanation: ***ATP*** - **Citrate synthase**, a key enzyme in the Krebs cycle, is inhibited by **high levels of ATP**, indicating a high energy state in the cell. - This allosteric inhibition helps regulate the metabolic flux through the cycle, slowing it down when energy is abundant. *ADP* - **ADP** typically signifies a low energy state and would generally act as an **activator** rather than an inhibitor for metabolic pathways that produce ATP. - In this context, ADP would promote the activity of enzymes involved in energy generation, including those in the Krebs cycle. *Insulin* - **Insulin** is a hormone that promotes fuel storage and utilization, generally **activating** metabolic pathways rather than directly inhibiting enzymes like citrate synthase. - Its primary role is to regulate blood glucose levels and promote glucose uptake and utilization. *Glucagon* - **Glucagon** is a hormone that mobilizes fuel from storage and is typically associated with **catabolic processes**, often increasing metabolic activity in response to low blood glucose. - It does not directly inhibit citrate synthase; its main actions are on glucoregulation.
Pharmacology
4 questionsWhich class of antihypertensive drugs is known to cause erectile dysfunction?
Which diuretic is most likely to cause hyponatremia by impairing free water excretion?
Which ACE inhibitor is safe in renal failure?
Which of the following agents requires the MOST caution when combined with spironolactone due to increased risk of hyperkalemia:
NEET-PG 2015 - Pharmacology NEET-PG Practice Questions and MCQs
Question 491: 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 492: 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
Question 493: Which ACE inhibitor is safe in renal failure?
- A. Captopril
- B. Enalapril
- C. None of the options
- D. Benazepril (Correct Answer)
Explanation: ***Benazepril*** - Among the listed ACE inhibitors, benazepril has the **most favorable excretion profile** in renal failure with approximately **50% renal and 50% hepatic elimination** (dual excretion pathway). - This balanced elimination reduces the risk of drug accumulation compared to predominantly renally excreted ACE inhibitors. - While dose adjustment may still be needed in **severe renal impairment**, benazepril is considered the **safest option among those listed** for patients with renal dysfunction. - **Note:** Fosinopril (not listed here) has true 50/50 dual elimination and requires no dose adjustment in renal failure, making it the ideal choice in clinical practice. *Captopril* - This ACE inhibitor undergoes predominantly **renal excretion (95%)** as unchanged drug and metabolites. - Requires significant **dose reduction** in renal failure to prevent accumulation and adverse effects including **hyperkalemia** and **hypotension**. - Less safe than benazepril in renal impairment due to heavy dependence on renal elimination. *Enalapril* - Enalapril is a prodrug converted to **enalaprilat**, with approximately **90% renal excretion**. - Dose adjustment is mandatory based on **creatinine clearance** in patients with renal failure. - Higher risk of accumulation and toxicity compared to dual-elimination ACE inhibitors like benazepril.
Question 494: Which of the following agents requires the MOST caution when combined with spironolactone due to increased risk of hyperkalemia:
- A. ACE inhibitors (Correct Answer)
- B. Beta-blockers
- C. Amlodipine
- D. Chlorothiazide
Explanation: ***ACE inhibitors*** - Spironolactone is a **potassium-sparing diuretic** that increases potassium levels by blocking aldosterone's effects in the collecting duct [1]. - **ACE inhibitors** also decrease aldosterone production [2], leading to reduced potassium excretion and a significant risk of **severe hyperkalemia** when combined with spironolactone [1, 2].*Beta-blockers* - While beta-blockers can cause a slight increase in plasma potassium by inhibiting cellular potassium uptake, this effect is generally modest and does not pose a major hyperkalemia risk when co-administered with spironolactone. - Their primary interaction concerns blood pressure and heart rate, not direct potassium handling.*Amlodipine* - Amlodipine is a **calcium channel blocker** that primarily causes vasodilation and does not significantly alter potassium balance. - Therefore, it does not substantially increase the risk of hyperkalemia when used concurrently with spironolactone.*Chlorothiazide* - Chlorothiazide is a **thiazide diuretic** that promotes potassium excretion, leading to a risk of hypokalemia. - When combined with spironolactone, a potassium-sparing diuretic, these agents can **partially offset each other's effects** on potassium balance, potentially reducing the risk of hyperkalemia compared to ACE inhibitors.
Physiology
1 questionsThe major role of 2,3-bisphosphoglycerate in RBCs is -
NEET-PG 2015 - Physiology NEET-PG Practice Questions and MCQs
Question 491: The major role of 2,3-bisphosphoglycerate in RBCs is -
- A. Acid-base balance
- B. Reversal of glycolysis
- C. Release of oxygen (Correct Answer)
- D. Binding of oxygen
Explanation: ***Release of oxygen*** - **2,3-bisphosphoglycerate (2,3-BPG)** binds allosterically to **deoxyhemoglobin**, stabilizing its T (tense) state. - This binding reduces hemoglobin's affinity for oxygen, promoting the **release of oxygen** to tissues. *Acid-base balance* - While red blood cells play a role in **acid-base balance** through the bicarbonate buffer system, 2,3-BPG's primary role is not buffering. - The **chloride shift** and **carbonic anhydrase** are more directly involved in RBC acid-base regulation. *Reversal of glycolysis* - 2,3-BPG is an intermediate of the **Rapoport-Luebering shunt**, a side pathway of glycolysis. - It does not reverse glycolysis but rather is produced during glycolysis to serve a specific function in oxygen transport. *Binding of oxygen* - 2,3-BPG **decreases** hemoglobin's affinity for oxygen, thus promoting its *release* from hemoglobin, not its binding. - Oxygen binding to hemoglobin occurs primarily at the **heme iron** without 2,3-BPG.