NEET-PG 2015

1414 Questions — Page 49 of 142

Biochemistry

5 questions

Q481

Transport of lipids from the intestine to other tissues is by -

Q482

Which method is used to separate a mixture of lipids?

Q483

Bile acids are synthesized from ?

Q484

Most abundant source of fuel in starvation -

Q485

Most important carbohydrate store for maintaining blood glucose homeostasis -

NEET-PG 2015 - Biochemistry NEET-PG Practice Questions and MCQs

Question 481: Transport of lipids from the intestine to other tissues is by -

A. Chylomicrons (Correct Answer)
B. LDL
C. HDL
D. VLDL

Explanation: ***Chylomicrons*** - **Chylomicrons** are the **largest lipoprotein particles** that transport **dietary (exogenous) lipids** from the **intestine** to peripheral tissues - They are synthesized in **intestinal enterocytes** after fat absorption and enter the bloodstream via the **lymphatic system (thoracic duct)** - They carry **triglycerides (85-95%), cholesterol, phospholipids, and fat-soluble vitamins** (A, D, E, K) - **Apolipoprotein B-48** is the characteristic structural protein of chylomicrons - After delivering triglycerides to tissues (via lipoprotein lipase), chylomicron remnants are taken up by the **liver** *LDL (Low-Density Lipoprotein)* - LDL transports **cholesterol from the liver to peripheral tissues** (not from intestine) - It carries **endogenous cholesterol**, not dietary lipids from the intestine - Often called "**bad cholesterol**" due to its role in atherosclerosis - Contains **Apolipoprotein B-100** *HDL (High-Density Lipoprotein)* - HDL performs **reverse cholesterol transport** - moving excess cholesterol from peripheral tissues **back to the liver** - It does **not transport lipids from the intestine** to tissues - Called "**good cholesterol**" for its protective cardiovascular role - Contains **Apolipoprotein A-I and A-II** *VLDL (Very-Low-Density Lipoprotein)* - VLDL is synthesized in the **liver** (not intestine) and transports **endogenous triglycerides** to peripheral tissues - It carries lipids **from the liver**, not from the intestine - VLDL is converted to IDL and then LDL after losing triglycerides - Contains **Apolipoprotein B-100**

Question 482: Which method is used to separate a mixture of lipids?

A. Electrophoresis
B. Chromatography (Correct Answer)
C. Isoelectric focusing
D. PAGE

Explanation: ***Chromatography*** - **Chromatography** (e.g., thin-layer chromatography, gas chromatography, high-performance liquid chromatography) is widely used to separate lipids based on differences in their **polarity**, **molecular weight**, or **solubility** in various solvents. - This method allows for the isolation and identification of different lipid classes and individual lipid species from a complex mixture. *Electrophoresis* - **Electrophoresis** separates molecules based on their **charge** and **size** in an electric field, making it more commonly used for proteins and nucleic acids. - Lipids are generally **uncharged** or have very low charge, which makes them poorly suited for separation by standard electrophoretic methods without modification. *Isoelectric focusing* - **Isoelectric focusing** is a type of electrophoresis that separates molecules based on their **isoelectric point (pI)**, which is the pH at which a molecule has no net charge. - This technique is primarily used for **proteins** and **peptides**, as lipids typically lack ionizable groups necessary for establishing a distinct pI. *PAGE* - **PAGE** (Polyacrylamide Gel Electrophoresis) is a common method used to separate **proteins** and **nucleic acids** based on their size and charge. - Lipids are **hydrophobic** and do not readily migrate through an aqueous polyacrylamide gel matrix, making PAGE unsuitable for their direct separation.

Question 483: Bile acids are synthesized from ?

A. Heme
B. Ribulose
C. Arachidonic acid
D. Cholesterol (Correct Answer)

Explanation: ***Cholesterol*** - **Bile acids** are derivatives of **cholesterol**, synthesized in the liver through a multi-step enzymatic pathway. - The conversion of cholesterol to bile acids is a primary mechanism for the excretion and transport of cholesterol from the body. *Heme* - **Heme** is a component of hemoglobin and myoglobin, primarily involved in oxygen transport and storage. - Its degradation product is **bilirubin**, which forms part of bile but is distinct from bile acids. *Ribulose* - **Ribulose** is a 5-carbon sugar, playing a key role in the **pentose phosphate pathway** and the **Calvin cycle** in photosynthesis. - It is not a precursor for bile acid synthesis. *Arachidonic acid* - **Arachidonic acid** is a polyunsaturated fatty acid that serves as a precursor for **eicosanoids** (prostaglandins, thromboxanes, and leukotrienes). - These molecules are involved in inflammation and immune responses but are unrelated to bile acid synthesis.

Question 484: Most abundant source of fuel in starvation -

A. Liver glycogen
B. Muscle glycogen
C. Adipose tissue (Correct Answer)
D. Blood glucose

Explanation: ***Adipose tissue*** - **Adipose tissue** stores **triglycerides**, which are hydrolyzed into fatty acids and glycerol to serve as the body's primary energy source during prolonged starvation. - The energy reserve in adipose tissue is significantly larger than glycogen stores, providing **sustained fuel** for days or weeks. *Liver glycogen* - **Liver glycogen** is a readily available source of glucose but is rapidly depleted within **12-24 hours** during starvation. - Its primary role is to maintain **blood glucose levels** for glucose-dependent tissues like the brain. *Muscle glycogen* - **Muscle glycogen** is used primarily for **muscle contraction** and cannot be directly released into the bloodstream to maintain blood glucose levels. - While it's a significant energy reserve for working muscles, it does not contribute to systemic fuel needs during starvation. *Blood glucose* - **Blood glucose** is the immediate circulating fuel, but it is tightly regulated and its levels decrease during starvation as glycogen stores are depleted. - It is not an abundant stored source of fuel but rather a transport form of energy.

Question 485: Most important carbohydrate store for maintaining blood glucose homeostasis -

A. Blood glucose
B. Glycogen in adipose tissue
C. Hepatic glycogen (Correct Answer)
D. None of the options

Explanation: ***Hepatic glycogen*** - The liver contains **100-120g of glycogen**, which is the most crucial carbohydrate store for **maintaining blood glucose homeostasis**. - **Hepatic glycogen** can be mobilized and released as glucose into the bloodstream to supply all body tissues, especially during fasting. - Although muscle glycogen is quantitatively larger (~400-500g), it cannot contribute to blood glucose as muscle lacks glucose-6-phosphatase. - The liver's unique ability to release free glucose makes hepatic glycogen the **most metabolically important** carbohydrate store. *Blood glucose* - **Blood glucose** (~5g total in circulation) represents carbohydrates available for immediate energy, not a storage form. - This is far too small to be considered a major carbohydrate reserve. *Glycogen in adipose tissue* - **Adipose tissue** primarily stores **fat (triglycerides)**, with negligible glycogen content. - Adipose tissue plays virtually no role in carbohydrate storage. *None of the options* - This is incorrect because **hepatic glycogen** is indeed the most important carbohydrate store for glucose homeostasis.

Obstetrics and Gynecology

1 questions

Q481

Which drug is contraindicated before delivery of the baby (during first and second stages of labor)?

Pharmacology

4 questions

Q481

Which class of antihypertensive drugs is known to cause erectile dysfunction?

Q482

Which diuretic is most likely to cause hyponatremia by impairing free water excretion?

Q483

Which ACE inhibitor is safe in renal failure?

Q484

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 481: 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 482: 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 483: 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 484: 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.