Vitamins and Coenzymes — MCQs

Vitamins and Coenzymes Indian Medical PG Practice Questions and MCQs

Question 691: A child presents with a history of fractures, multiple petechiae, perifollicular hemorrhages, and gum bleeding. Which of the following enzyme defects is involved?

A. Tyrosinase
B. Prolyl hydroxylase (Correct Answer)
C. Alkaline phosphatase
D. Lysyl oxidase

Explanation: ***Prolyl hydroxylase*** - **Vitamin C (Ascorbic acid)** is a necessary cofactor for Prolyl hydroxylase and Lysyl hydroxylase, which are essential for the hydroxylation of proline and lysine residues in procollagen. - Deficiency of Vitamin C leads to inactivation of this enzyme, resulting in unstable and defective **collagen** that causes vascular fragility (leading to petechiae and gum bleeding) and impaired bone matrix (resulting in fractures). *Lysyl oxidase* - **Lysyl oxidase** is required for the crucial cross-linking of collagen and elastin fibers, a process that relies on **copper**, not Vitamin C, as a main cofactor. - A defect in this enzyme primarily causes syndromes like certain types of **Ehlers-Danlos Syndrome** (Type V) or features associated with **Menkes disease**. *Tyrosinase* - **Tyrosinase** is the key enzyme in the biosynthesis of **melanin** from tyrosine. - A defect in Tyrosinase causes various forms of **Albinism**, characterized by lack of pigmentation in the skin, hair, and eyes, which is unrelated to the described hemorrhagic and skeletal findings. *Alkaline phosphatase* - **Alkaline phosphatase (ALP)** plays a vital role in bone mineralization by hydrolyzing pyrophosphate, preventing its inhibitory effect on calcification. - While important for bone health, ALP deficiency causes **Hypophosphatasia**, and it is not directly involved in the pathogenesis of structural collagen defects seen in **Scurvy**.

Question 692: What is correct about the vitamin shown below?

A. γ-carboxylation of glycine residues to clotting factor 2,7, 9 and 10
B. γ-carboxylation of glutathione residues to clotting factor 2,7, 9 and 10
C. γ-carboxylation of aspartic acid residues to clotting factor 2,7, 9 and 10
D. γ-carboxylation of glutamic acid residues to clotting factor 2,7, 9 and 10 (Correct Answer)

Explanation: ***γ-carboxylation of glutamic acid residues to clotting factor 2,7, 9 and 10*** - The image depicts **gamma-glutamyl carboxylase** catalyzing the carboxylation of a glutamic acid residue to form gamma-carboxyglutamate. - This vitamin K-dependent modification is essential for the activation of **clotting factors II, VII, IX, and X**, which are proteins involved in blood coagulation. *γ-carboxylation of glycine residues to clotting factor 2,7, 9 and 10* - **Glycine** residues do not undergo gamma-carboxylation in the context of vitamin K-dependent protein modification. - The specific amino acid residue involved in this carboxylation is **glutamic acid**, not glycine. *γ-carboxylation of glutathione residues to clotting factor 2,7, 9 and 10* - **Glutathione** is a tripeptide (glutamate-cysteine-glycine) and is not a residue within a larger clotting factor protein that undergoes gamma-carboxylation. - Gamma-carboxylation is specific to **glutamic acid residues** within particular proteins, not glutathione. *γ-carboxylation of aspartic acid residues to clotting factor 2,7,9 and 10* - While **aspartic acid** is an acidic amino acid, it is not the specific residue that undergoes vitamin K-dependent gamma-carboxylation. - The reaction specifically targets the **gamma-carbon of glutamic acid residues**.

Question 693: Which enzyme marked as $X$ is missing in synthesis of vitamin $D_{3}$ ?

A. 3-beta-hydroxylase
B. 17-alpha-hydroxylase (Correct Answer)
C. 21-hydroxylase
D. 24-hydroxylase

Explanation: ***17-alpha-hydroxylase*** - The diagram illustrates the synthesis of **vitamin D3**, which involves hydroxylation steps at positions C-25 in the liver and C-1 in the kidneys. These are catalyzed by **25-hydroxylase** and **1-alpha-hydroxylase**, respectively. - **17-alpha-hydroxylase** is involved in the synthesis of steroid hormones (like cortisol, androgens, and estrogens) from cholesterol, not in the synthesis or metabolism of vitamin D3; therefore, its absence would not be relevant to vitamin D synthesis. *3-beta-hydroxylase* - **3-beta-hydroxysteroid dehydrogenase** is crucial for the synthesis of all steroid hormones, converting delta-5-3-hydroxysteroids to delta-4-3-ketosteroids. - Its presence is essential for **steroidogenesis**, but it does not play a direct role in the specific hydroxylation steps for vitamin D activation. *21-hydroxylase* - **21-hydroxylase** is an enzyme involved in the synthesis of steroid hormones such as cortisol and aldosterone from progesterone and 17-hydroxyprogesterone. - Deficiency of this enzyme leads to **congenital adrenal hyperplasia**, a condition unrelated to vitamin D metabolism. *24-hydroxylase* - **24-hydroxylase** is responsible for the inactivation of vitamin D metabolites by adding a hydroxyl group at position C-24, leading to degradation. - This enzyme is part of the **catabolic pathway** to regulate vitamin D levels, rather than being a missing enzyme in the primary synthesis of active vitamin D.

Question 694: Which of the following reactions is responsible for folate trap?

A. 1
B. 2 (Correct Answer)
C. 3
D. All of the above

Explanation: ***Option 2*** - Reaction 2, catalyzed by **methionine synthase**, is directly responsible for the **folate trap**. - This enzyme uses **5-methyl-THF** (methyl-tetrahydrofolate) as a methyl donor to convert homocysteine to methionine, with **vitamin B12** (methylcobalamin) as a coenzyme. - In **vitamin B12 deficiency**, methionine synthase cannot function, preventing 5-methyl-THF from being converted back to THF. - This causes accumulation of folate in the "trapped" 5-methyl-THF form, which cannot be used for other essential reactions requiring THF (such as DNA synthesis). *Option 1* - Reaction 1 and Reaction 2 are likely **parts of the same methionine synthase reaction**, not separate reactions. - The complete reaction involves: 5-methyl-THF donates its methyl group → vitamin B12 (forming methylcobalamin) → methyl group transfers to homocysteine → forming methionine and regenerating THF. - While this step is part of the overall mechanism, the key point is that **impairment of this cycle due to B12 deficiency** causes the trap, which is most accurately attributed to the methionine synthase reaction as a whole (Reaction 2). *Option 3* - Reaction 3 represents downstream metabolism of methionine, such as formation of **S-adenosylmethionine (SAM)** or transsulfuration pathways. - These reactions are not directly involved in the interconversion of folate forms or the mechanism of the folate trap. *All of the above* - The folate trap specifically refers to the inability to regenerate THF from 5-methyl-THF due to impaired **methionine synthase activity** (Reaction 2) in **vitamin B12 deficiency**. - Only Reaction 2 is directly responsible for this phenomenon.

Question 695: A patient presents with recurrent oral lesions and eye redness as shown in the images below. The patient also complains of chronic diarrhea and abdominal discomfort. Which test is recommended for this patient?

A. Anti-endothelial cell antibodies
B. Anti-endomysial antibodies (Correct Answer)
C. RBC glutathione reductase levels
D. Serum methylmalonic acid levels

Explanation: ***Anti-endomysial antibodies*** - The image on the left shows **aphthous stomatitis**, and the one on the right shows **conjunctivitis** with dilated vessels. These two findings, along with other potential symptoms (e.g., GI, arthritis), could indicate **celiac disease**. - **Anti-endomysial antibodies** are highly specific for **celiac disease**, which can manifest with extraintestinal symptoms including recurrent aphthous stomatitis and, less commonly, ocular symptoms. *Anti-endothelial cell antibodies* - These antibodies are associated with **vasculitis** and other autoimmune conditions that primarily affect blood vessels. - While some vasculitides can cause ocular inflammation and oral lesions, they don't typically present with the specific combination and appearance of symptoms seen here. *RBC glutathione reductase levels* - This test measures the activity of the enzyme **glutathione reductase** in red blood cells. - It is primarily used to assess **riboflavin (vitamin B2) deficiency** and has no direct relevance to the conditions suggested by the visual findings. *Serum methylmalonic acid levels* - Elevated **serum methylmalonic acid (MMA)** levels are a sensitive indicator of **vitamin B12 deficiency**. - While vitamin B12 deficiency can cause glossitis (inflammation of the tongue), it doesn't typically cause aphthous stomatitis or conjunctivitis.

Question 696: A 36 year old man presents with decreased appetite, mouth soreness, diarrhoea and irritability. On examination he has a bright red tongue with a pigmented scaly rash around the neck. Which one of the following food items in his diet has a bearing on his disease?

A. Wheat
B. Fish
C. Corn (Correct Answer)
D. Rice

Explanation: ***Corn*** - A diet heavily reliant on **corn** (maize) as a staple lacking proper fortification or preparation can lead to **niacin (Vitamin B3) deficiency**, historically common in regions where corn was the primary dietary component. - The symptoms described—**decreased appetite, mouth soreness, diarrhea, irritability, bright red tongue (glossitis)**, and a **pigmented scaly rash around the neck (Casal's necklace)**—are classic manifestations of **pellagra**, a disease caused by niacin deficiency. *Wheat* - While wheat is a common dietary staple, it is not typically associated with classic pellagra symptoms like **Casal's necklace** or severe **glossitis** that point specifically to niacin deficiency. - Wheat-related issues usually involve **celiac disease** (gluten intolerance) or other sensitivities, presenting with different gastrointestinal and dermatological profiles. *Fish* - Fish is a good source of various nutrients, including some B vitamins, and is generally not associated with causing nutritional deficiencies like pellagra. - No symptoms described are typically linked to a diet rich in fish or lack thereof in a way that points to the given presentation. *Rice* - Rice can be a staple food, but a diet predominantly of polished rice can lead to **thiamine (Vitamin B1) deficiency** causing **beriberi**, which presents differently (e.g., neuropathy, heart failure). - It does not cause the characteristic dermatological signs of pellagra like **Casal's necklace**.

Question 697: Consider the following statements : 1. The deficiency of thiamine leads to the accumulation of pyruvic and lactic acids in the body. 2. Riboflavin deficiency impairs the optimal utilization of pyridoxine. Which of the statements given above is/are correct ?

A. Both 1 and 2 (Correct Answer)
B. 1 only
C. 2 only
D. Neither 1 nor 2

Explanation: ***Both 1 and 2*** - **Statement 1 is correct**: Thiamine (vitamin B1) as **thiamine pyrophosphate (TPP)** is an essential coenzyme for the **pyruvate dehydrogenase complex** and **α-ketoglutarate dehydrogenase**. Deficiency blocks pyruvate conversion to acetyl-CoA, causing accumulation of **pyruvic acid** and its reduction product **lactic acid**, leading to metabolic acidosis seen in **beriberi** and **Wernicke-Korsakoff syndrome**. - **Statement 2 is correct**: Riboflavin (vitamin B2) as **FMN** serves as a cofactor for **pyridoxine 5'-phosphate oxidase**, the enzyme that converts pyridoxine 5'-phosphate and pyridoxamine 5'-phosphate to the active form **pyridoxal 5'-phosphate (PLP)**. Riboflavin deficiency impairs this conversion, leading to **functional vitamin B6 deficiency** even with adequate dietary pyridoxine intake. *1 only* - This option is incorrect because it ignores the well-established biochemical relationship between riboflavin and pyridoxine metabolism. Both statements are factually accurate. *2 only* - This option is incorrect because statement 1 is definitively correct. Thiamine deficiency is a classic cause of **pyruvic and lactic acid accumulation** due to impaired oxidative decarboxylation. *Neither 1 nor 2* - This option is incorrect as both statements are medically and biochemically accurate, reflecting established vitamin interdependencies and metabolic pathways.

Question 698: Among the following, which has the highest quantity of retinol (Vitamin A) activity per 100 g of fruit?

A. Papaya
B. Tomato
C. Ripe Mango (Correct Answer)
D. Orange

Explanation: ***Ripe Mango*** - **Ripe mangoes** are an excellent source of **beta-carotene**, which the body converts into **retinol (Vitamin A)**. - They contain approximately **1,262 µg retinol activity equivalents (RAE)** per 100 g, which is significantly higher than the other options listed. - While fruits contain provitamin A carotenoids rather than preformed retinol, mangoes provide the highest **Vitamin A activity** among these choices. *Papaya* - While papaya does contain **beta-carotene**, its concentration is much lower (approximately **47 µg RAE/100 g**). - It is a good source of Vitamin C and other antioxidants, but not the leading source of Vitamin A among these fruits. *Tomato* - Tomatoes are rich in **lycopene**, another carotenoid, but it is not converted to **retinol** as beta-carotene is. - They have low overall **Vitamin A activity** (approximately **42 µg RAE/100 g**) compared to mangoes. *Orange* - Oranges are primarily known for their high content of **Vitamin C** and are poor sources of **Vitamin A**. - Their Vitamin A activity is minimal (approximately **11 µg RAE/100 g**), with primary carotenoids being **beta-cryptoxanthin** and **zeaxanthin**, which contribute less to Vitamin A activity.

Question 699: Match List-I with List-II and select the correct answer using the code given below the Lists:

A. A→3 B→2 C→1 D→4
B. A→1 B→4 C→2 D→3
C. A→4 B→2 C→1 D→3
D. A→3 B→1 C→2 D→4 (Correct Answer)

Explanation: ***A→3 B→1 C→2 D→4*** - **Thiamine (Vitamin B1)** deficiency can lead to **beriberi**, which often manifests as **wet beriberi** characterized by **high-output cardiac failure**, edema, and peripheral neuropathy. - **Niacin (Vitamin B3)** deficiency causes **pellagra**, a disease classically presenting with the "4 Ds": **dermatitis**, diarrhea, dementia, and death. - **Retinol (Vitamin A)** deficiency is primarily known for causing **xerophthalmia**, which includes early signs like **night blindness** and later stages like Bitot's spots (foamy keratin debris on the conjunctiva) and keratomalacia. - **Cholecalciferol (Vitamin D)** deficiency leads to **rickets in children**, characterized by impaired bone mineralization causing skeletal deformities such as a **rachitic rosary** (enlargement of the costochondral junctions). *A→3 B→2 C→1 D→4* - This option incorrectly matches Niacin with Bitot's spots (Vitamin A deficiency) and Retinol with Dermatitis (Niacin deficiency). - The correct associations are Thiamine with cardiac failure, Niacin with dermatitis, Retinol with Bitot's spots, and Cholecalciferol with rachitic rosary. *A→1 B→4 C→2 D→3* - This option incorrectly matches Thiamine with dermatitis, Niacin with rachitic rosary, and Cholecalciferol with cardiac failure. - Each of these pairings contradicts the established clinical manifestations of the respective vitamin deficiencies. *A→4 B→2 C→1 D→3* - This option incorrectly associates Thiamine with rachitic rosary, Niacin with Bitot's spots, and Retinol with dermatitis. - The symptoms listed are characteristic of different vitamin deficiencies than those incorrectly matched in this choice.

Question 700: Which one of the following vitamins given as a supplement during the peri-conceptional period to a woman can help prevent the neural tube defects in the baby ?

A. Riboflavin
B. Folic acid (Correct Answer)
C. Thiamine
D. Vitamin B12

Explanation: ***Folic acid*** - **Folic acid** (vitamin B9) supplementation is crucial during the **peri-conceptional period** to prevent neural tube defects. - Adequate folic acid intake helps in the proper development and closure of the **neural tube** in the embryo, which forms the brain and spinal cord. *Riboflavin* - **Riboflavin** (vitamin B2) is essential for energy metabolism and cellular growth but has no direct, established role in preventing neural tube defects. - Deficiency can lead to **ariboflavinosis**, characterized by skin lesions, but not directly linked to neural tube malformations. *Thiamine* - **Thiamine** (vitamin B1) is vital for carbohydrate metabolism and nerve function. - Its deficiency causes **beriberi** and neurological problems in adults, but it does not directly prevent neural tube defects. *Vitamin B12* - **Vitamin B12** (cobalamin) is important for DNA synthesis and nerve function, and it works closely with folate. - While B12 deficiency can lead to megaloblastic anemia and neurological issues, **folic acid** is the primary vitamin for preventing neural tube defects.

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

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free