Vitamins and Coenzymes — MCQs

Vitamins and Coenzymes Indian Medical PG Practice Questions and MCQs

Question 731: All of the following are true about Vitamin K EXCEPT:

A. Requires bile salts for absorption
B. Synthesized in large amounts by the liver (Correct Answer)
C. Functions in carboxylation reactions
D. Essential for blood clotting

Explanation: ***Synthesized in large amounts by the liver*** - Vitamin K is primarily obtained from **dietary sources** and synthesized by **gut bacteria**, not in large amounts by the liver. - The liver is crucial for the **storage** and **utilization** of Vitamin K in synthesizing clotting factors, but not its primary production. *Requires bile salts for absorption* - Vitamin K is a **fat-soluble vitamin**, and like other fat-soluble vitamins (A, D, E), its absorption in the intestines requires the presence of **bile salts**. - Conditions that impair bile production or flow (e.g., biliary obstruction, cholestasis) can lead to **Vitamin K deficiency**. *Functions in carboxylation reactions* - Vitamin K acts as a **cofactor** for the enzyme **gamma-glutamyl carboxylase**, which catalyzes the carboxylation of glutamic acid residues. - This carboxylation is essential for activating a variety of **proteins**, including clotting factors. *Essential for blood clotting* - Vitamin K is critical for the synthesis of several **coagulation factors** in the liver, specifically factors **II (prothrombin), VII, IX, and X**. - It works by enabling the carboxylation of these factors, which allows them to bind calcium and participate in the **clotting cascade**.

Question 732: Which coenzyme is essential for pyruvate carboxylase activity?

A. Thiamine
B. NAD+
C. CoA
D. Biotin (Correct Answer)

Explanation: ***Biotin*** - **Biotin** (vitamin B7) is a crucial coenzyme for **carboxylase enzymes**, including **pyruvate carboxylase**. - It acts as a **CO2 carrier**, facilitating the carboxylation of pyruvate to **oxaloacetate** in gluconeogenesis. *Thiamine* - **Thiamine pyrophosphate** is a coenzyme for enzymes involved in **decarboxylation reactions**, such as pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase. - It is not directly involved in the carboxylation activity of pyruvate carboxylase. *NAD+* - **NAD+** (nicotinamide adenine dinucleotide) is a coenzyme primarily involved in **redox reactions** as an electron acceptor. - While important in many metabolic pathways, it does not function as a coenzyme for carboxylase activity. *CoA* - **Coenzyme A** is essential for carrying acyl groups, particularly in the formation of **acetyl-CoA** which enters the citric acid cycle. - Although acetyl-CoA is an allosteric activator of pyruvate carboxylase, CoA itself is not a coenzyme for its catalytic activity.

Question 733: Due to which of the following enzyme deficiency, vitamin C cannot be synthesised in humans?

A. L-Gulonolactone reductase
B. L-Glucuronic acid oxidase
C. L-Gulonic acid reductase
D. L-Gulonolactone oxidase (Correct Answer)

Explanation: ***L-Gulonolactone oxidase*** - This enzyme is **deficient in humans**, guinea pigs, and some primates, preventing the conversion of **L-gulono-γ-lactone to L-ascorbic acid (vitamin C)**, the final step in vitamin C synthesis. - The absence of functional L-gulonolactone oxidase (due to a mutation in the GULO gene) makes **ascorbic acid (vitamin C)** an essential dietary nutrient for humans. *L-Gulonolactone reductase* - This enzyme is not part of the vitamin C synthesis pathway and its deficiency is not the reason for the inability to synthesize vitamin C in humans. - Reductase enzymes typically add electrons/hydrogen, whereas the critical missing step requires an oxidase. *L-Glucuronic acid oxidase* - This enzyme is part of the **glucuronic acid pathway**, but its deficiency does not directly impair the synthesis of vitamin C. - The glucuronic acid pathway primarily detoxifies xenobiotics and endogenous compounds and contributes to **UDP-glucuronic acid** synthesis. *L-Gulonic acid reductase* - This enzyme catalyzes the conversion of **L-gulonate to L-gulonolactone**, a step *prior* to the one blocked in humans through the deficiency of L-gulonolactone oxidase. - While it is part of the overall pathway, its deficiency is not the ultimate reason humans cannot synthesize vitamin C; rather, it is the inability to convert L-gulono-γ-lactone to ascorbic acid in the final oxidation step.

Question 734: Which vitamin is required for glycogen phosphorylase?

A. Lipoic acid
B. TPP
C. PLP (Correct Answer)
D. Riboflavin

Explanation: ***PLP*** - **Pyridoxal phosphate (PLP)**, a derivative of vitamin **B6**, acts as a crucial coenzyme for **glycogen phosphorylase**. - It participates in the **phosphorolysis of α-1,4 glycosidic bonds** to release glucose-1-phosphate from glycogen. *Lipoic acid* - **Lipoic acid** is a coenzyme primarily involved in **oxidative decarboxylation** reactions, such as those catalyzed by pyruvate dehydrogenase and α-ketoglutarate dehydrogenase. - It plays no direct role as a coenzyme for **glycogen phosphorylase**. *TPP* - **Thiamine pyrophosphate (TPP)**, a derivative of vitamin **B1**, is essential for enzymes like **pyruvate dehydrogenase** and **α-ketoglutarate dehydrogenase**. - It is involved in transferring aldehyde groups, not in the phosphorolysis of glycogen. *Riboflavin* - **Riboflavin (vitamin B2)** is a precursor for **flavin adenine dinucleotide (FAD)** and **flavin mononucleotide (FMN)**, which are crucial for redox reactions in intermediary metabolism. - It is not a direct coenzyme for **glycogen phosphorylase**.

Question 735: How does vitamin C deficiency lead to scurvy?

A. Defective collagen formation due to impaired synthesis (Correct Answer)
B. Impaired immune response due to vitamin deficiencies
C. Iron deficiency anemia
D. Malabsorption of fat-soluble vitamins

Explanation: ***Defective collagen formation due to impaired synthesis*** - **Vitamin C** is a crucial cofactor for **prolyl hydroxylase** and **lysyl hydroxylase**, enzymes essential for the hydroxylation of proline and lysine residues in collagen. - Without proper hydroxylation, collagen molecules cannot form stable **triple helix structures**, leading to weakened connective tissues throughout the body, manifesting as scurvy. *Impaired immune response due to vitamin deficiencies* - While various vitamin deficiencies can impair the immune response, **scurvy's primary pathology** stems from defective collagen synthesis, not directly from immune system dysfunction. - Immune compromise might be a secondary effect in severe, prolonged scurvy, but it's not the **direct cause of the characteristic symptoms** like bleeding gums and poor wound healing. *Iron deficiency anemia* - **Vitamin C does enhance iron absorption** in the gut, so severe deficiency can indirectly contribute to **iron deficiency anemia**. - However, iron deficiency anemia is a *consequence* of prolonged scurvy, not the primary mechanism by which scurvy's defining symptoms occur. *Malabsorption of fat-soluble vitamins* - **Vitamin C** is a water-soluble vitamin and its deficiency does not directly cause malabsorption of **fat-soluble vitamins** (A, D, E, K). - Malabsorption of fat-soluble vitamins is typically linked to disorders of fat digestion or absorption, such as **pancreatic insufficiency** or **celiac disease**.

Question 736: Which nutrient deficiency directly impairs hydroxylation during collagen synthesis?

A. A. Vitamin D
B. B. Copper
C. C. Vitamin E
D. D. Vitamin C (Correct Answer)

Explanation: ***Vitamin C*** - **Vitamin C** (ascorbic acid) is a crucial **cofactor** for the enzymes **prolyl hydroxylase** and **lysyl hydroxylase**, which are essential for **collagen cross-linking and stability**. - Its deficiency leads to **scurvy**, characterized by weakened connective tissue, impaired wound healing, and fragile blood vessels due to **defective collagen synthesis**. *Vitamin D* - **Vitamin D** is primarily involved in **calcium and phosphate homeostasis**, which are vital for bone mineralization. - Its deficiency can lead to **rickets** in children and **osteomalacia** in adults, conditions of weakened bones, but not directly to collagen defects. *Copper* - **Copper** is a cofactor for **lysyl oxidase**, an enzyme that cross-links collagen and elastin, contributing to the tensile strength of connective tissues. - While copper deficiency can affect collagen structure, **Vitamin C deficiency** has a more direct and severe impact on the initial synthesis and hydroxylation steps of collagen, making it the primary answer for collagen defects. *Vitamin E* - **Vitamin E** is a fat-soluble antioxidant that protects cell membranes from **oxidative damage**. - Its deficiency is associated with neurological symptoms and hemolytic anemia but does not directly cause defects in **collagen synthesis or structure**.

Question 737: Which vitamin deficiency leads to Wernicke-Korsakoff syndrome?

A. Vitamin B6
B. Riboflavin
C. Niacin
D. Thiamine (Correct Answer)

Explanation: ***Thiamine*** - Wernicke-Korsakoff syndrome is primarily caused by **thiamine (Vitamin B1) deficiency**, often seen in individuals with chronic alcohol abuse due to poor nutrition and impaired absorption. - **Thiamine** is crucial for **glucose metabolism** in the brain, and its deficiency leads to neuronal damage in specific brain regions. *Vitamin B6* - **Vitamin B6 (pyridoxine)** deficiency can cause neuropathy, dermatitis, and seizures, but it is not directly responsible for Wernicke-Korsakoff syndrome. - While sometimes seen in alcoholics, B6 deficiency manifests differently from the classic Wernicke-Korsakoff triad of confusion, ataxia, and ophthalmoplegia. *Riboflavin* - **Riboflavin (Vitamin B2)** deficiency leads to symptoms like cheilosis, glossitis, and angular stomatitis. - It does not directly cause the neurological and cognitive impairments characteristic of Wernicke-Korsakoff syndrome. *Niacin* - **Niacin (Vitamin B3)** deficiency causes **pellagra**, characterized by the 3 D's: dermatitis, diarrhea, and dementia. - Although it involves neurological symptoms, the specific presentation of pellagra is distinct from Wernicke-Korsakoff syndrome.

Question 738: A patient is diagnosed with scurvy. This condition is due to a deficiency in which vitamin?

A. Vitamin A
B. Vitamin C (Correct Answer)
C. Vitamin D
D. Vitamin E

Explanation: ***Vitamin C*** - **Scurvy** is directly caused by a prolonged and severe deficiency of **Vitamin C (ascorbic acid)**. - Vitamin C is essential for **collagen synthesis**, and its deficiency leads to impaired wound healing, fragile blood vessels, and gum disease, which are hallmarks of scurvy. *Vitamin A* - Deficiency in Vitamin A primarily causes **vision problems**, such as night blindness, and can lead to xerophthalmia, but not scurvy. - It plays a crucial role in **immune function** and cell growth, distinguishing its role from collagen synthesis. *Vitamin D* - A deficiency in Vitamin D is associated with **rickets** in children and **osteomalacia** in adults, conditions primarily affecting bone mineralization. - It is vital for **calcium and phosphate absorption**, which is unrelated to the collagen defects seen in scurvy. *Vitamin E* - Deficiency in Vitamin E is rare and can lead to **neurological symptoms** like ataxia and peripheral neuropathy. - It acts as a **powerful antioxidant**, protecting cells from oxidative damage, which is a different metabolic pathway than Vitamin C's role in collagen.

Question 739: Which of the following vitamins is essential for the carboxylation of glutamate residues in blood clotting factors?

A. Vitamin A
B. Vitamin D
C. Vitamin E
D. Vitamin K (Correct Answer)

Explanation: ***Vitamin K*** - **Vitamin K** is a crucial cofactor for the enzyme **gamma-glutamyl carboxylase**. - This enzyme catalyzes the **carboxylation of specific glutamate residues** in clotting factors II, VII, IX, and X, which is essential for their activation. *Vitamin A* - **Vitamin A** (retinol) is primarily involved in **vision**, immune function, and cell growth/differentiation. - It does not play a direct role in the post-translational modification of blood clotting factors. *Vitamin D* - **Vitamin D** is essential for **calcium and phosphate homeostasis**, bone mineralization, and immune regulation. - It has no known function in the carboxylation of glutamate residues for blood coagulation. *Vitamin E* - **Vitamin E** (tocopherol) functions as a potent **antioxidant**, protecting cell membranes from oxidative damage. - It is not directly involved in the synthesis or activation of blood clotting factors by carboxylation.

Question 740: What is the effect of biotin deficiency on acetyl-CoA carboxylase activity?

A. No change in pyruvate carboxylase activity
B. Decreased acetyl-CoA carboxylase activity (Correct Answer)
C. Increased propionyl-CoA carboxylase activity
D. Impaired fatty acid synthesis

Explanation: ***Decreased acetyl-CoA carboxylase activity*** - Biotin is an essential **cofactor** for carboxylase enzymes, including acetyl-CoA carboxylase. - Biotin deficiency directly impairs the function of **acetyl-CoA carboxylase**, leading to decreased enzyme activity. - This is the **most direct answer** to what happens to acetyl-CoA carboxylase activity specifically. *No change in pyruvate carboxylase activity* - Pyruvate carboxylase also requires **biotin** as a cofactor for its activity. - Biotin deficiency would similarly lead to **decreased pyruvate carboxylase activity**, not no change. *Increased propionyl-CoA carboxylase activity* - Propionyl-CoA carboxylase is another biotin-dependent enzyme. - Biotin deficiency would result in **decreased**, not increased, propionyl-CoA carboxylase activity. *Impaired fatty acid synthesis* - While this statement is **true**, it describes a downstream **metabolic consequence** of decreased acetyl-CoA carboxylase activity. - Acetyl-CoA carboxylase catalyzes the rate-limiting step of fatty acid synthesis (acetyl-CoA → malonyl-CoA). - The question specifically asks about the **effect on the enzyme activity itself**, making "Decreased acetyl-CoA carboxylase activity" the more direct and precise answer.

Practice by Chapter

Fat-Soluble Vitamins: A, D, E, K

Practice Questions

Vitamin A and Vision

Practice Questions

Vitamin D and Calcium Metabolism

Practice Questions

Vitamin E and Antioxidant Functions

Practice Questions

Vitamin K and Blood Coagulation

Practice Questions

Water-Soluble Vitamins: B Complex and C

Practice Questions

Thiamine (B1) and Pyruvate Dehydrogenase

Practice Questions

Riboflavin (B2) and Flavin Coenzymes

Practice Questions

Niacin and NAD/NADP

Practice Questions

Vitamin B6 and Transamination

Practice Questions

Folate and Vitamin B12 in One-Carbon Metabolism

Practice Questions

Vitamin C and Collagen Synthesis

Practice Questions

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