Vitamins and Coenzymes — MCQs
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Which vitamin deficiency can cause rickets?
Thiamine deficiency in a chronic alcoholic can reduce energy production as a result of which of the following reasons?
Hypervitaminosis D may cause all of the following EXCEPT:
The deficiency of thiamine can be identified by measuring the red cell:
Which of the following is the synthetic vitamer of vitamin K?
Deficiency of which vitamin causes spinocerebellar ataxia?
The given condition is caused due to deficiency of which of the following?
A constellation of neuropathy, muscle weakness and wasting, cardiomegaly, edema, and ophthalmoplegia strongly suggests which of the following deficiencies?
Thiamine status of an individual can be detected by which of the following tests/enzymes in erythrocytes?
Collagen formation is affected in the deficiency of which vitamin?
Vitamins and Coenzymes Indian Medical PG Practice Questions and MCQs
Question 571: Which vitamin deficiency can cause rickets?
- A. Vitamin C
- B. Niacin
- C. Vitamin D (Correct Answer)
- D. Biotin
Explanation: **Explanation:** **Correct Answer: C. Vitamin D** Vitamin D (Calciferol) is essential for maintaining calcium and phosphate homeostasis. It promotes the intestinal absorption of calcium and phosphorus, which are critical for the mineralization of the bone matrix (osteoid). A deficiency in Vitamin D leads to inadequate mineralization. In children, where epiphyseal plates are still open, this results in **Rickets**, characterized by soft bones, skeletal deformities (like bow legs), and rachitic rosary. In adults, the same deficiency causes **Osteomalacia**. **Incorrect Options:** * **Vitamin C:** Deficiency leads to **Scurvy**. It is required for the hydroxylation of proline and lysine residues during collagen synthesis. Deficiency causes capillary fragility and gum bleeding, not primary mineralization defects. * **Niacin (B3):** Deficiency causes **Pellagra**, characterized by the "3 Ds": Dermatitis, Diarrhea, and Dementia. It is a precursor for NAD and NADP. * **Biotin (B7):** Serves as a coenzyme for carboxylation reactions (e.g., Pyruvate carboxylase). Deficiency is rare but typically presents with dermatitis, alopecia, and neurological symptoms, not bone pathology. **High-Yield Clinical Pearls for NEET-PG:** * **Active Form:** Calcitriol [1,25-(OH)₂D₃] is the most active form, synthesized in the kidney via the enzyme **1-alpha-hydroxylase**. * **Radiological Sign:** Look for "cupping and splaying" of metaphyses in Rickets. * **Biochemical Profile:** In Vitamin D deficiency, expect **Low Serum Calcium, Low Serum Phosphate, and Elevated Alkaline Phosphatase (ALP)**. Secondary Hyperparathyroidism is often present.
Question 572: Thiamine deficiency in a chronic alcoholic can reduce energy production as a result of which of the following reasons?
- A. It is required for the process of transamination
- B. It is a co-factor for oxidative reduction
- C. It is a co-enzyme for transketolase in the pentose phosphate pathway
- D. It is a co-enzyme for pyruvate dehydrogenase and a-ketoglutarate dehydrogenase in the TCA pathway (Correct Answer)
Explanation: **Explanation:** Thiamine (Vitamin B1) is converted into its active form, **Thiamine Pyrophosphate (TPP)**. TPP serves as an essential co-enzyme for several multi-enzyme complexes involved in carbohydrate metabolism. **Why Option D is Correct:** The primary reason for reduced energy production in thiamine deficiency is the impairment of the **Pyruvate Dehydrogenase (PDH)** and **$\alpha$-ketoglutarate dehydrogenase** complexes. * **PDH** converts Pyruvate to Acetyl-CoA, the entry point into the TCA cycle. * **$\alpha$-ketoglutarate dehydrogenase** is a rate-limiting step within the TCA cycle. When these enzymes are inhibited, the TCA cycle cannot function efficiently, leading to a drastic reduction in ATP production. This is particularly detrimental to high-energy-demand tissues like the brain and heart. **Analysis of Incorrect Options:** * **Option A:** Transamination requires **Pyridoxal Phosphate (Vitamin B6)**, not thiamine. * **Option B:** While TPP is involved in oxidative decarboxylation, "oxidative reduction" (Redox) is a broad term usually associated with NAD+ (B3) or FAD (B2). * **Option C:** While thiamine *is* a co-enzyme for transketolase, this pathway (HMP Shunt) is primarily for NADPH and ribose synthesis, not for the direct generation of ATP (energy). **High-Yield Clinical Pearls for NEET-PG:** * **Wernicke-Korsakoff Syndrome:** A classic triad of ataxia, ophthalmoplegia, and confusion seen in alcoholics due to thiamine deficiency. * **The "Glucose First" Rule:** Never give IV glucose to a malnourished/alcoholic patient before thiamine. Glucose loading precipitates Wernicke’s because it consumes the remaining thiamine stores to fuel the PDH reaction. * **Diagnostic Marker:** Erythrocyte transketolase activity is the most reliable biochemical test to diagnose thiamine deficiency.
Question 573: Hypervitaminosis D may cause all of the following EXCEPT:
- A. Remineralization of bone (Correct Answer)
- B. Deposition of calcium in arteries
- C. Renal calculi
- D. Loss of appetite
Explanation: **Explanation:** Vitamin D toxicity (Hypervitaminosis D) is characterized by excessive levels of 1,25-dihydroxyvitamin D, which leads to **hypercalcemia** and **hypercalciuria**. **Why "Remineralization of bone" is the correct answer:** Contrary to its physiological role in bone formation at normal levels, excessive Vitamin D stimulates high levels of **osteoclast activity**. This leads to increased bone resorption (demineralization), mobilizing calcium from the bones into the bloodstream. Therefore, hypervitaminosis D causes **demineralization**, not remineralization. **Analysis of Incorrect Options:** * **Deposition of calcium in arteries:** Hypercalcemia leads to **metastatic calcification**. Calcium deposits in soft tissues, including the media of arteries, heart, and lungs. * **Renal calculi:** Increased intestinal absorption and bone resorption lead to hypercalciuria (excess calcium in urine). This promotes the formation of calcium oxalate or calcium phosphate stones in the kidneys. * **Loss of appetite:** Anorexia (loss of appetite), nausea, and vomiting are early clinical symptoms of hypercalcemia affecting the gastrointestinal tract. **High-Yield NEET-PG Pearls:** * **Mechanism:** Vitamin D toxicity is usually due to over-supplementation, not sunlight, as the body degrades excess Vitamin D in the skin. * **Clinical Triad:** Hypercalcemia, Hypercalciuria, and Polyuria. * **Williams Syndrome:** A condition characterized by hypersensitivity to Vitamin D, leading to idiopathic infantile hypercalcemia. * **Treatment:** Immediate cessation of Vitamin D/Calcium intake, aggressive hydration, and administration of glucocorticoids (which decrease intestinal calcium absorption).
Question 574: The deficiency of thiamine can be identified by measuring the red cell:
- A. Transketolase (Correct Answer)
- B. Transaldolase
- C. Alpha ketoglutarate dehydrogenase
- D. Pyruvate dehydrogenase
Explanation: **Explanation:** Thiamine (Vitamin B1) serves as a vital cofactor in the form of **Thiamine Pyrophosphate (TPP)** for several key enzymes in carbohydrate metabolism. **Why Transketolase is the correct answer:** The erythrocyte (red cell) transketolase activation assay is the **gold standard** for diagnosing thiamine deficiency. Transketolase is an enzyme in the Pentose Phosphate Pathway (HMP Shunt) that requires TPP. In this diagnostic test, transketolase activity is measured before and after the addition of exogenous TPP. An increase in activity (>15-25%) indicates a biochemical thiamine deficiency. Red cells are used because they are easily accessible and reflect the body's overall thiamine status. **Why other options are incorrect:** * **B. Transaldolase:** Although it functions in the HMP shunt alongside transketolase, it is **not** TPP-dependent and thus cannot be used to measure thiamine levels. * **C & D. Alpha-ketoglutarate dehydrogenase and Pyruvate dehydrogenase:** Both are indeed TPP-dependent enzymes (part of the TCA cycle and link reaction). However, they are mitochondrial enzymes. Since mature red blood cells lack mitochondria, these enzymes cannot be measured in a red cell assay. **High-Yield Clinical Pearls for NEET-PG:** * **TPP-dependent enzymes (Mnemonic: APT):** **A**lpha-ketoglutarate dehydrogenase, **P**yruvate dehydrogenase, and **T**ransketolase (also Branched-chain ketoacid dehydrogenase). * **Clinical Deficiency:** Presents as **Beriberi** (Dry: polyneuritis; Wet: high-output heart failure) or **Wernicke-Korsakoff Syndrome** (Ataxia, Ophthalmoplegia, Confusion, and Confabulation). * **Rule of Thumb:** Always administer thiamine *before* glucose in malnourished/alcoholic patients to prevent precipitating Wernicke encephalopathy, as glucose oxidation consumes the remaining TPP.
Question 575: Which of the following is the synthetic vitamer of vitamin K?
- A. Phylloquinone
- B. Menaquinone
- C. Menadione (Correct Answer)
- D. All of the above
Explanation: **Explanation:** Vitamin K exists in several forms, categorized based on their source and chemical structure. The correct answer is **Menadione (Vitamin K3)** because it is the only **synthetic, water-soluble** form of Vitamin K. Unlike natural forms, it lacks the long isoprenoid side chain, making it a provitamin that must be alkylated in the liver to become biologically active (menaquinone-4). **Analysis of Options:** * **Phylloquinone (Vitamin K1):** This is the **natural** form of Vitamin K synthesized by **plants**. It is the primary dietary source (found in green leafy vegetables) and is fat-soluble. * **Menaquinone (Vitamin K2):** This is the **natural** form synthesized by **intestinal bacterial flora**. It is also fat-soluble and plays a significant role in bone metabolism. * **Menadione (Vitamin K3):** As a synthetic compound, it was previously used for supplementation but is now restricted in clinical practice for neonates due to its potential to cause oxidative stress. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Action:** Vitamin K acts as a coenzyme for **$\gamma$-glutamyl carboxylase**, which converts glutamic acid residues to $\gamma$-carboxyglutamate (Gla) on clotting factors **II, VII, IX, and X**, as well as Proteins C and S. * **Warfarin Connection:** Warfarin inhibits **Vitamin K Epoxide Reductase (VKOR)**, preventing the regeneration of active Vitamin K (hydroquinone). * **Toxicity Warning:** Menadione (K3) can cause **hemolytic anemia, hyperbilirubinemia, and kernicterus** in infants because it reacts with sulfhydryl groups like glutathione, leading to oxidative damage to RBC membranes. * **Newborn Prophylaxis:** Since Vitamin K does not cross the placenta well and breast milk is a poor source, newborns receive an injection of **Phylloquinone (K1)** to prevent Hemorrhagic Disease of the Newborn.
Question 576: Deficiency of which vitamin causes spinocerebellar ataxia?
- A. Vitamin B12
- B. Vitamin E (Correct Answer)
- C. Vitamin C
- D. Vitamin A
Explanation: **Explanation:** **Vitamin E (Tocopherol)** is a potent lipid-soluble antioxidant that protects cell membranes from oxidative damage. The nervous system is particularly vulnerable to oxidative stress. Deficiency leads to a clinical syndrome characterized by **spinocerebellar ataxia**, loss of vibratory and position sense (posterior column involvement), and absent deep tendon reflexes. This occurs because Vitamin E is essential for maintaining the integrity of the axons in the spinal cord (specifically the spinocerebellar tracts and dorsal columns). **Analysis of Options:** * **Vitamin B12 (Cobalamin):** Deficiency causes **Subacute Combined Degeneration (SCD)** of the spinal cord. While it involves the posterior columns and lateral corticospinal tracts, the classic presentation is megaloblastic anemia and "pins and needles" sensations, rather than pure spinocerebellar ataxia. * **Vitamin C (Ascorbic Acid):** Deficiency leads to **Scurvy**, characterized by defective collagen synthesis, capillary fragility (petechiae, bruising), and bleeding gums. It does not cause primary neurological degeneration. * **Vitamin A (Retinol):** Deficiency primarily affects vision (night blindness, xerophthalmia) and epithelial integrity (Bitot’s spots, follicular hyperkeratosis). **High-Yield Clinical Pearls for NEET-PG:** * **Mimicry:** Vitamin E deficiency presents almost identically to **Friedreich’s Ataxia**. * **Hemolysis:** In addition to neurological symptoms, Vitamin E deficiency can cause **hemolytic anemia** due to increased oxidative fragility of RBC membranes. * **Risk Factors:** It is most commonly seen in patients with fat malabsorption syndromes (e.g., Cystic Fibrosis, Abetalipoproteinemia, or Chronic Cholestasis). * **Key Tracts involved:** Spinocerebellar tract (ataxia) and Dorsal columns (loss of proprioception).
Question 577: The given condition is caused due to deficiency of which of the following?
- A. Niacin
- B. Iron
- C. Zinc (Correct Answer)
- D. Selenium
Explanation: ***Zinc*** - **Acrodermatitis enteropathica** is the pathognomonic skin manifestation of **zinc deficiency**, presenting with perioral, perianal, and acral dermatitis. - Zinc is essential for **wound healing**, **immune function**, and maintaining skin integrity, particularly in rapidly dividing cells. *Niacin* - **Niacin deficiency** causes **pellagra** with the "4 Ds": dermatitis, diarrhea, dementia, and death. - The dermatitis in pellagra typically presents as **photosensitive** skin lesions in sun-exposed areas, not the perioral/perianal pattern seen here. *Iron* - **Iron deficiency** primarily causes **microcytic anemia** with symptoms like fatigue, pallor, and koilonychia (spoon nails). - Iron deficiency does not typically cause the characteristic **acrodermatitis enteropathica** skin pattern observed in this condition. *Selenium* - **Selenium deficiency** can cause **Keshan disease** (cardiomyopathy) and **Kashin-Beck disease** (osteoarthropathy). - Selenium deficiency does not produce the distinctive **perioral and perianal dermatitis** that characterizes zinc deficiency.
Question 578: A constellation of neuropathy, muscle weakness and wasting, cardiomegaly, edema, and ophthalmoplegia strongly suggests which of the following deficiencies?
- A. Cobalamin deficiency
- B. Thiamine deficiency (Correct Answer)
- C. Niacin deficiency
- D. Riboflavin deficiency
Explanation: **Explanation:** The clinical presentation described is a classic manifestation of **Thiamine (Vitamin B1) deficiency**, which presents in two major forms: **Dry Beriberi** and **Wet Beriberi**, often accompanied by **Wernicke-Korsakoff Syndrome**. 1. **Why Thiamine is correct:** Thiamine pyrophosphate (TPP) is a vital cofactor for enzymes like pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase. Deficiency leads to ATP depletion, affecting high-energy tissues: * **Dry Beriberi:** Characterized by peripheral neuropathy, muscle wasting, and weakness. * **Wet Beriberi:** Involves the cardiovascular system, leading to high-output heart failure, **cardiomegaly**, and **edema**. * **Wernicke Encephalopathy:** Presents with the triad of **ophthalmoplegia** (eye muscle paralysis), ataxia, and confusion. 2. **Why other options are incorrect:** * **Cobalamin (B12):** Deficiency causes Subacute Combined Degeneration of the spinal cord (SCD) and megaloblastic anemia, but not cardiomegaly or acute ophthalmoplegia. * **Niacin (B3):** Deficiency leads to **Pellagra**, characterized by the 3 Ds: Dermatitis, Diarrhea, and Dementia. * **Riboflavin (B2):** Deficiency presents with Cheilosis, glossitis, and corneal neovascularization (the "2 Cs" of B2). **High-Yield NEET-PG Pearls:** * **Enzyme Marker:** Erythrocyte **transketolase** activity (decreased in thiamine deficiency) is the gold standard for diagnosis. * **Wernicke’s Triad:** Confusion, Ataxia, Ophthalmoplegia. * **Korsakoff Syndrome:** Irreversible amnesia and **confabulation** (making up stories) due to damage to the mammillary bodies. * **Clinical Rule:** Always administer thiamine *before* glucose in malnourished/alcoholic patients to prevent precipitating Wernicke encephalopathy.
Question 579: Thiamine status of an individual can be detected by which of the following tests/enzymes in erythrocytes?
- A. Transaldolase
- B. Glucose-6-phosphatase
- C. Transketolase (Correct Answer)
- D. Enolase
Explanation: **Explanation:** **Thiamine (Vitamin B1)** serves as a vital cofactor in the form of **Thiamine Pyrophosphate (TPP)** for several key enzymes in carbohydrate metabolism. The assessment of thiamine status is clinically performed by measuring the activity of **Erythrocyte Transketolase (ETKA)**. 1. **Why Transketolase is Correct:** Transketolase is a key enzyme in the **Hexose Monophosphate (HMP) Shunt** (Pentose Phosphate Pathway) that requires TPP as a coenzyme. In a laboratory setting, the activity of transketolase in a patient's red blood cells is measured before and after the addition of TPP. An increase in enzyme activity (TPP effect) of >15-25% indicates a functional thiamine deficiency. 2. **Analysis of Incorrect Options:** * **Transaldolase:** While also part of the HMP shunt, it does **not** require TPP or any other cofactor for its action. * **Glucose-6-phosphatase:** This enzyme is involved in gluconeogenesis and glycogenolysis (converting G6P to glucose). It is primarily found in the liver and kidneys, not erythrocytes, and is not thiamine-dependent. * **Enolase:** An enzyme of the glycolytic pathway that converts 2-phosphoglycerate to phosphoenolpyruvate. It requires **Magnesium (Mg²⁺)** and is inhibited by fluoride, but it does not require thiamine. **High-Yield Clinical Pearls for NEET-PG:** * **TPP-dependent enzymes:** "**A**ptitude **T**est for **K**rebs" — **A**lpha-ketoglutarate dehydrogenase, **T**ransketolase, and **P**yruvate dehydrogenase (also Branched-chain ketoacid dehydrogenase). * **Clinical Deficiency:** Thiamine deficiency leads to **Beriberi** (Dry: polyneuritis; Wet: high-output heart failure) and **Wernicke-Korsakoff Syndrome** (triad of ophthalmoplegia, ataxia, and confusion), commonly seen in chronic alcoholics. * **Gold Standard:** While ETKA is the functional test, direct measurement of thiamine diphosphate in whole blood using HPLC is now considered the most sensitive diagnostic method.
Question 580: Collagen formation is affected in the deficiency of which vitamin?
- A. Vitamin A
- B. Vitamin C (Correct Answer)
- C. Vitamin B2
- D. Vitamin D
Explanation: **Explanation:** **Vitamin C (Ascorbic Acid)** is the correct answer because it serves as a vital co-factor for the post-translational modification of collagen. Specifically, it is required by the enzymes **prolyl hydroxylase** and **lysyl hydroxylase**. These enzymes hydroxylate proline and lysine residues in the pro-alpha chains of collagen. This hydroxylation is essential for: 1. **Hydrogen bond formation:** Which stabilizes the triple helix structure of collagen. 2. **Cross-linking:** Which provides tensile strength to the connective tissue. In the absence of Vitamin C, the collagen produced is under-hydroxylated and unstable, leading to the clinical manifestation of **Scurvy** (characterized by capillary fragility, bruising, and poor wound healing). **Why other options are incorrect:** * **Vitamin A:** Primarily involved in vision (rhodopsin cycle), epithelial cell differentiation, and immune function. * **Vitamin B2 (Riboflavin):** Functions as a precursor for FAD and FMN, which are essential for redox reactions in the TCA cycle and Electron Transport Chain. * **Vitamin D:** Regulates calcium and phosphate metabolism and is essential for bone mineralization (deficiency leads to Rickets or Osteomalacia), but it does not directly mediate collagen synthesis. **High-Yield Clinical Pearls for NEET-PG:** * **Enzyme Mechanism:** Vitamin C keeps the iron cofactor of hydroxylase enzymes in the reduced **ferrous (Fe²⁺) state**. * **Scurvy Symptoms:** "Corkscrew hair," perifollicular hemorrhages, and swollen, bleeding gums. * **Wound Healing:** Collagen is the primary protein involved in the proliferative phase of wound healing; thus, Vitamin C deficiency significantly delays recovery.
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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