Vitamins and Coenzymes Practice Questions

Q: Which of the following conditions is NOT pyridoxine dependent?

Maple syrup urine disease. **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.

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

Vitamin C. **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.

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

Riboflavin. **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**.

Q: Xanthine oxidase is associated with which co-factor?

Molybdenum. ### 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.

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

Folate deficiency. **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.

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

Niacin. **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.

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

Zinc. **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.

Question 1

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

Accepted Answer

Buffy coat estimation

Answer

Plasma

Answer

Urinary excretion

Answer

Adrenal cortical vitamin C estimation

Question 2

Which of the following conditions is NOT pyridoxine dependent?

Accepted Answer

Maple syrup urine disease

Answer

Homocystinuria

Answer

Oxaluria

Answer

Xanthinuria

Question 3

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

Accepted Answer

Vitamin C

Answer

Vitamin E

Answer

Vitamin B6

Answer

Vitamin B1

Question 4

Magenta coloured tongue is seen in deficiency of which vitamin?

Accepted Answer

Riboflavin

Answer

Niacin

Answer

Vitamin B12

Answer

All of the above

Question 5

Xanthine oxidase is associated with which co-factor?

Accepted Answer

Molybdenum

Answer

Zinc

Answer

Copper

Answer

Selenium

Question 6

Megaloblastic anaemia occurs due to which of the following deficiencies?

Accepted Answer

Folate deficiency

Answer

Iron deficiency

Answer

Vitamin C deficiency

Answer

Protein deficiency

Question 7

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

Accepted Answer

Niacin

Answer

Thiamine

Answer

Riboflavin

Answer

Pantothenic acid

Question 8

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

Accepted Answer

Thiamine

Answer

Pyridoxine

Answer

Niacin

Answer

Vitamin C

Question 9

Which of the following vitamins deficiency occurs exclusively in carnivores?

Accepted Answer

Vitamin C

Answer

Thiamine

Answer

Niacin

Answer

Cobalamine

Question 10

Dermatitis and alopecia are due to deficiency of which micronutrient?

Accepted Answer

Zinc

Answer

Molybdenum

Answer

Magnesium

Answer

Calcium

Vitamins and Coenzymes — MCQs

Vitamins and Coenzymes — MCQs

On this page

Practice by Chapter

Want unlimited practice?