Vitamins and Coenzymes — MCQs

Vitamins and Coenzymes Indian Medical PG Practice Questions and MCQs

Question 251: Deficiency of vitamin C in an infant is best estimated by vitamin C level in which of the following?

A. Plasma
B. Urinary excretion
C. Buffy coat estimation (Correct Answer)
D. Adrenal cortical vitamin C estimation

Explanation: **Explanation:** The correct answer is **Buffy coat estimation**. Vitamin C (Ascorbic acid) is an essential water-soluble vitamin involved in collagen synthesis and antioxidant defense. In clinical practice, estimating the body's total vitamin C stores is crucial for diagnosing subclinical deficiency or scurvy. **1. Why Buffy Coat Estimation is Correct:** The buffy coat consists of leukocytes (white blood cells) and platelets. Leukocytes contain significantly higher concentrations of Vitamin C (nearly 20–40 times higher) compared to plasma. Because leukocytes have a longer half-life and maintain their vitamin C levels even when dietary intake fluctuates, they serve as the **most reliable index of total body stores**. A low buffy coat level is the "gold standard" for confirming chronic deficiency. **2. Why Other Options are Incorrect:** * **Plasma (Option A):** Plasma levels reflect **recent dietary intake** rather than total body stores. Levels can drop rapidly after a few days of poor intake, even if tissue stores are still adequate, leading to false-positive results for deficiency. * **Urinary Excretion (Option B):** Vitamin C is excreted in urine only when plasma levels exceed the renal threshold. It is a better indicator of **tissue saturation** (excess) rather than deficiency. * **Adrenal Cortical Estimation (Option D):** While the adrenal glands contain the highest concentration of Vitamin C in the body, this is not a clinically feasible or non-invasive method for estimation in an infant. **High-Yield Clinical Pearls for NEET-PG:** * **Biochemical Function:** Vitamin C is a co-factor for **Prolyl and Lysyl hydroxylase**, essential for the post-translational modification of collagen. * **Infantile Scurvy (Barlow’s Disease):** Typically presents with subperiosteal hemorrhage, "frog-leg" position, and Scorbutic rosary. * **Radiological Sign:** Look for the **Frankel line** (white line of dense calcification) and **Wimberger’s ring** (dense epiphysis) on X-rays.

Question 252: Which of the following conditions is NOT pyridoxine dependent?

A. Homocystinuria
B. Maple syrup urine disease (Correct Answer)
C. Oxaluria
D. Xanthinuria

Explanation: **Explanation:** The correct answer is **Maple Syrup Urine Disease (MSUD)**. This condition is caused by a deficiency in the **Branched-Chain Alpha-Keto Acid Dehydrogenase (BCKAD)** complex. This enzyme complex requires **Thiamine (Vitamin B1)** as a cofactor, along with Riboflavin (B2), Niacin (B3), Pantothenic acid (B5), and Lipoic acid. Therefore, MSUD is thiamine-dependent, not pyridoxine-dependent. **Analysis of other options:** * **Homocystinuria:** The most common form is due to a deficiency of **Cystathionine $\beta$-synthase**, which requires **Pyridoxal Phosphate (PLP/B6)** as a cofactor. A subset of patients responds to high doses of Vitamin B6. * **Oxaluria (Primary Hyperoxaluria Type 1):** This is caused by a deficiency of the liver-specific enzyme **AGT**. PLP is a mandatory cofactor for this enzyme; B6 supplementation helps reduce oxalate excretion by shifting glyoxylate metabolism away from oxalate production. * **Xanthurenic aciduria (Xanthinuria):** In the Kynurenine pathway of Tryptophan metabolism, the enzyme **Kynureninase** is highly sensitive to B6 deficiency. Lack of B6 leads to the accumulation of xanthurenic acid, which is excreted in the urine. **NEET-PG High-Yield Pearls:** * **PLP (B6) is a cofactor for:** All transamination reactions, decarboxylation (e.g., GABA, Histamine, Serotonin synthesis), and heme synthesis ($\delta$-ALA synthase). * **Sideroblastic Anemia:** Can be a manifestation of B6 deficiency due to impaired heme synthesis. * **Drug Interaction:** Isoniazid (INH) therapy for TB can induce B6 deficiency by forming a complex with pyridoxal, necessitating B6 supplementation to prevent peripheral neuropathy.

Question 253: Barlow's syndrome is due to deficiency of which vitamin?

A. Vitamin E
B. Vitamin B6
C. Vitamin B1
D. Vitamin C (Correct Answer)

Explanation: **Explanation:** **Barlow’s syndrome** is the clinical term for **infantile scurvy**, which results from a deficiency of **Vitamin C (Ascorbic acid)**. Vitamin C is a critical cofactor for the enzymes *prolyl hydroxylase* and *lysyl hydroxylase*. These enzymes are responsible for the hydroxylation of proline and lysine residues during collagen synthesis. Without Vitamin C, defective collagen formation leads to weakened connective tissues, fragile blood vessels (causing subperiosteal hemorrhages), and impaired bone matrix formation. In infants, this manifests as painful limb swelling (pseudoparalysis) and a "scorbutic rosary" at the costochondral junctions. **Analysis of Incorrect Options:** * **Vitamin E:** Deficiency typically leads to hemolytic anemia, posterior column signs (ataxia, loss of proprioception), and retinal degeneration, but not bone or collagen defects. * **Vitamin B6 (Pyridoxine):** Deficiency causes peripheral neuropathy, sideroblastic anemia, and seborrheic dermatitis. It is also associated with isoniazid (INH) therapy. * **Vitamin B1 (Thiamine):** Deficiency leads to Beriberi (Dry or Wet) and Wernicke-Korsakoff syndrome, primarily affecting the cardiovascular and nervous systems. **High-Yield Clinical Pearls for NEET-PG:** * **Radiological Signs of Scurvy:** Look for **Frankel’s line** (dense zone of provisional calcification), **Wimberger’s ring** (sclerotic margin around epiphysis), and **Pelkan spurs**. * **Barlow’s Disease vs. Barlow’s Syndrome:** Do not confuse *Barlow’s Disease* (Infantile Scurvy) with *Barlow’s Syndrome* (Mitral Valve Prolapse), though in many medical entrance contexts, the term is used synonymously with Vitamin C deficiency. * Vitamin C also enhances **iron absorption** by maintaining it in the ferrous ($Fe^{2+}$) state.

Question 254: Magenta coloured tongue is seen in deficiency of which vitamin?

A. Niacin
B. Riboflavin (Correct Answer)
C. Vitamin B12
D. All of the above

Explanation: **Explanation:** The correct answer is **Riboflavin (Vitamin B2)**. **1. Why Riboflavin is correct:** Riboflavin is a precursor for the coenzymes **FMN** and **FAD**, which are essential for oxidation-reduction reactions. A deficiency of Vitamin B2 leads to a clinical constellation known as **Ariboflavinosis**. The hallmark sign is a **magenta-colored tongue**, which occurs due to inflammation (glossitis) and vascular changes in the lingual papillae. Other classic features include **cheilosis** (fissuring at the corners of the mouth), **angular stomatitis**, and **corneal neovascularization**. **2. Why other options are incorrect:** * **Niacin (B3):** Deficiency causes **Pellagra**, characterized by the 4 Ds (Dermatitis, Diarrhea, Dementia, and Death). The tongue in Pellagra is typically described as **"Beefy Red"** or "Scarlet," not magenta. * **Vitamin B12 (Cobalamin):** Deficiency leads to Megaloblastic anemia and Subacute Combined Degeneration of the spinal cord. The tongue appears **smooth, pale, and shiny** (Hunter’s glossitis or Atrophic glossitis) due to the loss of papillae. **3. NEET-PG High-Yield Pearls:** * **Riboflavin** is light-sensitive; phototherapy for neonatal jaundice can lead to its deficiency. * **Glutathione Reductase test:** The gold standard for diagnosing B2 deficiency is measuring the activity of erythrocyte glutathione reductase. * **Mnemonic for B2:** The "2s" — Vitamin **B2**, affects **2** C's (Cheilosis and Corneal vascularization), and results in a **Magenta** tongue (M is the 13th letter, 1+3=4, which is 2 squared). * **B3 vs. B2 Tongue:** Remember **B3 = Beefy Red**, **B2 = Magenta**.

Question 255: Xanthine oxidase is associated with which co-factor?

A. Zinc
B. Copper
C. Selenium
D. Molybdenum (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Molybdenum** **Concept:** Xanthine oxidase (XO) is a complex metalloenzyme that plays a critical role in the catabolism of purines. It catalyzes the oxidation of hypoxanthine to xanthine and xanthine to **uric acid**. The enzyme requires **Molybdenum** (in the form of a molybdopterin cofactor), **Iron** (Fe-S clusters), and **FAD** to function. Molybdenum is essential for the oxygen atom transfer during the hydroxylation of the substrate. **Why other options are incorrect:** * **Zinc:** Associated with enzymes like Carbonic anhydrase, Alcohol dehydrogenase, Carboxypeptidase, and DNA polymerase. * **Copper:** A cofactor for Cytochrome c oxidase, Tyrosinase, Lysyl oxidase, and Superoxide dismutase (cytosolic). * **Selenium:** Essential for **Glutathione peroxidase** (antioxidant defense) and Deiodinase (thyroid hormone metabolism). **High-Yield Clinical Pearls for NEET-PG:** * **Gout Connection:** **Allopurinol**, the drug of choice for chronic gout, is a suicide inhibitor of Xanthine oxidase. It reduces the production of uric acid. * **Molybdenum-dependent enzymes:** Apart from Xanthine oxidase, Molybdenum is also a cofactor for **Sulfite oxidase** and **Aldehyde oxidase**. * **Genetic Deficiency:** Rare hereditary deficiency of Xanthine oxidase leads to **Xanthinuria**, characterized by low serum uric acid levels and potential xanthine stones in the urinary tract. * **Free Radical Production:** Xanthine oxidase is a significant source of Superoxide ($O_2^-$) radicals, especially during reperfusion injury following ischemia.

Question 256: Megaloblastic anaemia occurs due to which of the following deficiencies?

A. Iron deficiency
B. Folate deficiency (Correct Answer)
C. Vitamin C deficiency
D. Protein deficiency

Explanation: **Explanation:** **Megaloblastic anemia** is a type of macrocytic anemia characterized by the presence of large, nucleated red blood cell precursors (megaloblasts) in the bone marrow. The underlying mechanism is **impaired DNA synthesis** while RNA and protein synthesis remain intact, leading to "nuclear-cytoplasmic asynchrony." **Why Folate deficiency is correct:** Folate (Vitamin B9) is essential for the synthesis of **thymidine**, one of the four bases in DNA. Specifically, tetrahydrofolate (THF) acts as a one-carbon donor in the conversion of dUMP to dTMP. When folate is deficient, DNA replication is hindered, causing cells to grow in size without dividing, resulting in macrocytosis and megaloblastic changes. (Note: Vitamin B12 deficiency also causes megaloblastic anemia via the "folate trap" mechanism). **Why other options are incorrect:** * **Iron deficiency:** Causes **microcytic hypochromic anemia** due to impaired hemoglobin synthesis. * **Vitamin C deficiency:** Leads to **Scurvy**. While Vitamin C aids iron absorption, its primary deficiency does not characteristically cause megaloblastic anemia. * **Protein deficiency:** Associated with **Kwashiorkor**, which typically presents with normocytic anemia due to overall reduced erythropoiesis. **NEET-PG High-Yield Pearls:** 1. **The Folate Trap:** B12 deficiency leads to a functional folate deficiency because folate becomes "trapped" as N5-methyl THF, which cannot be converted back to the active THF form. 2. **Diagnostic Marker:** Hypersegmented neutrophils (≥ 5 lobes) on a peripheral smear are the earliest sign of megaloblastic anemia. 3. **Differentiating B12 vs. Folate:** B12 deficiency presents with **neurological symptoms** (Subacute Combined Degeneration of the spinal cord) and elevated **Methylmalonic Acid (MMA)** levels, whereas folate deficiency does not.

Question 257: A 45-year-old diabetic patient presents with hypertriglyceridemia and elevated LDL. Which of the following vitamins can be indicated in this patient?

A. Thiamine
B. Riboflavin
C. Niacin (Correct Answer)
D. Pantothenic acid

Explanation: **Explanation:** **Correct Option: C (Niacin/Vitamin B3)** Niacin, specifically in the form of nicotinic acid, is used pharmacologically to treat dyslipidemia. It acts by inhibiting the enzyme **hormone-sensitive lipase** in adipose tissue, which reduces the breakdown of triglycerides into free fatty acids (FFAs). Since fewer FFAs reach the liver, there is a decreased synthesis of VLDL, which subsequently leads to **lower levels of LDL and triglycerides**. Additionally, Niacin is the most potent vitamin for **increasing HDL levels** by inhibiting the hepatic uptake of Apolipoprotein A-I. **Why other options are incorrect:** * **A. Thiamine (B1):** Primarily acts as a coenzyme for oxidative decarboxylation (e.g., Pyruvate Dehydrogenase). Deficiency leads to Beriberi or Wernicke-Korsakoff syndrome, but it has no lipid-lowering properties. * **B. Riboflavin (B2):** Precursor for FAD and FMN, involved in redox reactions. It does not influence plasma lipid profiles. * **D. Pantothenic acid (B5):** A constituent of Coenzyme A (CoA). While CoA is essential for fatty acid metabolism, B5 supplementation is not a clinical treatment for hyperlipidemia. **High-Yield NEET-PG Pearls:** * **Side Effects:** The most common side effect of Niacin is **cutaneous flushing**, mediated by Prostaglandin D2/E2 (can be prevented by Aspirin). * **Metabolic Risks:** Niacin can cause **hyperuricemia** (precipitating gout) and **hyperglycemia** (use with caution in diabetics, though still indicated for severe dyslipidemia). * **Key Enzyme:** Niacin inhibits **Diacylglycerol acyltransferase-2 (DGAT-2)** in the liver, further reducing triglyceride synthesis.

Question 258: Increase in pyruvate and lactate levels is seen in which of the following vitamin deficiencies?

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

Explanation: **Explanation:** The correct answer is **Thiamine (Vitamin B1)**. Thiamine, in its active form **Thiamine Pyrophosphate (TPP)**, serves as an essential coenzyme for the **Pyruvate Dehydrogenase (PDH) complex**. This enzyme complex is responsible for the oxidative decarboxylation of pyruvate into Acetyl-CoA, which then enters the TCA cycle. When thiamine is deficient, the PDH complex cannot function. Consequently, pyruvate cannot be converted to Acetyl-CoA and instead follows an alternative metabolic pathway: it is reduced to **Lactic Acid** by lactate dehydrogenase. This leads to an accumulation of both pyruvate and lactate in the blood, often resulting in lactic acidosis. TPP is also a cofactor for $\alpha$-ketoglutarate dehydrogenase and branched-chain $\alpha$-ketoacid dehydrogenase. **Why other options are incorrect:** * **Pyridoxine (B6):** Primarily involved in transamination and decarboxylation of amino acids (e.g., ALT, AST). Its deficiency leads to sideroblastic anemia or peripheral neuropathy, not elevated lactate. * **Niacin (B3):** While NAD is a cofactor for PDH, niacin deficiency (Pellagra) is classically characterized by the "4 Ds": Dermatitis, Diarrhea, Dementia, and Death. * **Vitamin C:** Acts as an antioxidant and a cofactor for prolyl hydroxylase (collagen synthesis). Deficiency leads to Scurvy. **High-Yield Clinical Pearls for NEET-PG:** * **Wernicke-Korsakoff Syndrome:** Classically seen in alcoholics due to thiamine deficiency; characterized by ataxia, ophthalmoplegia, and confusion. * **Beriberi:** "Dry" (peripheral neuropathy) vs. "Wet" (high-output heart failure with edema). * **Diagnostic Test:** Thiamine status is best assessed by measuring **Erythrocyte Transketolase activity** (another TPP-dependent enzyme). * **Clinical Caution:** Always administer thiamine *before* glucose in malnourished patients to prevent precipitating Wernicke encephalopathy, as glucose loading further depletes remaining thiamine stores via the PDH reaction.

Question 259: Which of the following vitamins deficiency occurs exclusively in carnivores?

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

Explanation: ### Explanation **Correct Option: D (Vitamin C)** The question highlights a unique evolutionary and physiological trait regarding Vitamin C (Ascorbic acid) synthesis. Most mammals possess the enzyme **L-gulonolactone oxidase**, which allows them to synthesize Vitamin C from glucose via the uronic acid pathway. However, humans, higher primates, guinea pigs, and **obligate carnivores** (such as cats) have lost the gene for this enzyme. In the context of this specific question, while humans are omnivores, among the choices provided, Vitamin C is the only nutrient whose deficiency is a significant risk in carnivores if they do not consume fresh organ meats (like liver), as they cannot synthesize it endogenously. In medical exams, this "exclusive" deficiency often refers to the lack of endogenous synthesis in specific species groups. **Analysis of Incorrect Options:** * **A. Thiamine (B1):** Deficiency (Beriberi/Wernicke-Korsakoff) is primarily seen in humans consuming polished rice or chronic alcoholics. It is found in both plant (husk) and animal sources. * **B. Niacin (B3):** Deficiency (Pellagra) is classically associated with populations consuming maize/corn-based diets (low tryptophan). It is synthesized from tryptophan in most species. * **C. Cobalamine (B12):** This is synthesized exclusively by microorganisms. It is found only in animal products; therefore, deficiency occurs in **strict vegetarians (vegans)**, not carnivores. **High-Yield Clinical Pearls for NEET-PG:** * **Enzyme Defect:** Humans lack **L-gulonolactone oxidase**, making Vitamin C an essential dietary requirement. * **Biochemical Function:** Vitamin C is a co-factor for **prolyl and lysyl hydroxylase**, essential for collagen synthesis (post-translational modification). * **Scurvy Signs:** Perifollicular hemorrhages, corkscrew hair, swollen/bleeding gums, and impaired wound healing. * **Iron Absorption:** Vitamin C facilitates the absorption of non-heme iron by reducing $Fe^{3+}$ (ferric) to $Fe^{2+}$ (ferrous) state.

Question 260: Dermatitis and alopecia are due to deficiency of which micronutrient?

A. Zinc (Correct Answer)
B. Molybdenum
C. Magnesium
D. Calcium

Explanation: **Explanation:** **Zinc** is an essential trace element that serves as a cofactor for over 300 enzymes, including those involved in DNA synthesis, protein metabolism, and cell division. It is particularly crucial for rapidly dividing cells like those in the skin and hair follicles. * **Why Zinc is correct:** Zinc deficiency leads to impaired keratinization and wound healing. The classic clinical triad of zinc deficiency includes **acrodermatitis enteropathica** (periorificial and acral dermatitis), **alopecia**, and **diarrhea**. It is also associated with growth retardation, hypogonadism, and impaired night vision (as it is a cofactor for retinol dehydrogenase). **Analysis of Incorrect Options:** * **Molybdenum:** This is a cofactor for enzymes like xanthine oxidase and sulfite oxidase. Deficiency is extremely rare but typically presents with neurological symptoms and lens dislocation, not dermatological issues. * **Magnesium:** Primarily involved in neuromuscular transmission and ATP-dependent enzymatic reactions. Deficiency (hypomagnesemia) leads to neuromuscular irritability, tetany, and arrhythmias. * **Calcium:** Essential for bone mineralization, blood coagulation, and muscle contraction. Deficiency leads to rickets/osteomalacia and tetany. **High-Yield Clinical Pearls for NEET-PG:** * **Acrodermatitis Enteropathica:** An autosomal recessive disorder causing impaired intestinal zinc absorption. * **Zinc & Wound Healing:** Zinc is a cofactor for **Matrix Metalloproteinases (MMPs)**, which are essential for collagen remodeling. * **Diagnosis:** Low serum alkaline phosphatase levels can sometimes be a clue to zinc deficiency, as the enzyme is zinc-dependent.

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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