Vitamins and Coenzymes Practice Questions

Q: The following reaction occurs in which part of kidney?

Proximal convoluted tubule. **Proximal convoluted tubule** - The image shows the conversion of 25-hydroxycholecalciferol to **1,25 (OH)₂-D₃**, also known as calcitriol, via the enzyme **1α-hydroxylase**. - This critical hydroxylation reaction, occurring primarily in the **proximal convoluted tubule** cells of the kidney, produces the biologically active form of vitamin D. *Distal convoluted tubule* - The distal convoluted tubule is primarily involved in **fine-tuning** water and electrolyte reabsorption, influenced by hormones like aldosterone and antidiuretic hormone. - It does not contain the necessary enzymes, specifically **1α-hydroxylase**, for the final activation step of vitamin D. *Loop of Henle* - The loop of Henle's main function is to create a **medullary osmotic gradient** through countercurrent multiplication, crucial for concentrating urine. - It plays no significant role in the **hydroxylation of vitamin D** precursors. *Collecting duct* - The collecting duct is responsible for final adjustments to urine volume and concentration, largely under the influence of **antidiuretic hormone**. - It lacks the **enzymatic machinery** (1α-hydroxylase) required for the activation of vitamin D.

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

17-alpha-hydroxylase. ***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.

Q: Name the enzyme involved in this cycle:

Retinal isomerase. ***Retinal isomerase*** - This enzyme is crucial for the regeneration of **11-cis-retinal** from **all-trans-retinal** in the visual cycle. - It catalyzes the **isomerization** process, which is essential for rhodopsin to be reformed and ready to detect light again. *Retinol isomerase* - This term is a misnomer; the substrate that undergoes isomerization is retinal, not retinol. - While **retinol** is a precursor to retinal, it doesn't directly undergo the isomerization step that is vital for the visual cycle. *Transducin* - **Transducin** is a **G-protein** involved in signal transduction after light activates rhodopsin. - It binds to activated rhodopsin, triggering a cascade that ultimately leads to changes in membrane potential, but it is not an isomerase enzyme. *Gustducin* - **Gustducin** is a **G-protein** primarily involved in the **sensation of taste**, specifically bitter and sweet tastes. - It plays no role in the visual cycle or the isomerization of retinal.

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

2. ***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.

Q: The following lesion is seen in all of the following conditions except: (Recent NEET Pattern 2016-17)

Porphyria. ***Correct: Porphyria*** - **Porphyria** causes **photosensitive skin lesions** but does NOT cause pellagra or the **Casal's necklace** pattern shown in the image. - Porphyria results from defects in **heme synthesis**, leading to vesicles, bullae, and hyperpigmentation, particularly on sun-exposed areas. - The image depicts **Pellagra**, characterized by **photosensitive dermatosis** in a **Casal's necklace** distribution, caused by **niacin (vitamin B3) deficiency**. *Incorrect: Carcinoid syndrome* - **Carcinoid syndrome** can cause **pellagra** due to **tryptophan diversion** for excessive serotonin synthesis. - This leads to **niacin deficiency** and can present with the characteristic skin lesions shown in the image. - Classic features include flushing, diarrhea, and cardiac involvement. *Incorrect: Hartnup disease* - **Hartnup disease** is an **autosomal recessive disorder** with impaired absorption of neutral amino acids, including **tryptophan**. - Reduced tryptophan absorption leads to **secondary niacin deficiency**, causing pellagra-like symptoms. - Patients present with photosensitive dermatitis, cerebellar ataxia, and psychiatric manifestations. *Incorrect: Alcoholism* - **Chronic alcoholism** is a common cause of **pellagra** due to poor dietary intake, malabsorption, and impaired nutrient metabolism. - Alcoholics are at high risk for **niacin deficiency**, presenting with the **3 Ds**: dermatitis, diarrhea, and dementia. - The photosensitive rash in a Casal's necklace distribution is characteristic.

Q: The bony deformity of 'pigeon chest' in children occurs due to deficiency of:

Vitamin D. ***Vitamin D*** - A deficiency in **Vitamin D** leads to **rickets** in children, impairing proper bone mineralization. - This softening of bones can cause skeletal deformities, including **pigeon chest** (pectus carinatum), where the sternum protrudes forward. *Vitamin K* - **Vitamin K** is crucial for **blood clotting** by synthesizing coagulation factors. - Its deficiency primarily leads to bleeding disorders, not skeletal deformities like pigeon chest. *Vitamin A* - **Vitamin A** is essential for **vision**, immune function, and cellular growth. - A deficiency can cause **night blindness** and impaired immunity, but it is not directly linked to bone deformities. *Vitamin E* - **Vitamin E** is a powerful **antioxidant** that protects cells from damage. - While essential for neurological function and immunity, its deficiency does not cause skeletal abnormalities such as pigeon chest.

Q: 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?

Corn. ***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**.

Q: In hyperemesis gravidarum, Wernicke's encephalopathy is seen due to the deficiency of

vitamin B1. ***vitamin B1*** - **Wernicke's encephalopathy** is directly caused by a severe deficiency of **thiamine (vitamin B1)**. - In **hyperemesis gravidarum**, persistent vomiting leads to inadequate intake and absorption of this vital vitamin. *vitamin B6* - Deficiency of **vitamin B6 (pyridoxine)** can cause peripheral neuropathy, glossitis, and dermatitis. - While important for many metabolic processes, its deficiency is not directly linked to Wernicke's encephalopathy. *vitamin B12* - **Vitamin B12 (cobalamin)** deficiency primarily results in megaloblastic anemia and subacute combined degeneration of the spinal cord. - It does not cause the specific neurological triad of Wernicke's encephalopathy. *vitamin B9* - Deficiency of **vitamin B9 (folate)** leads to megaloblastic anemia and is crucial for neural tube development. - It is not associated with the pathogenesis of Wernicke's encephalopathy.

Q: 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 ?

Both 1 and 2. ***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 1

What is correct about the vitamin shown below?

Accepted Answer

γ-carboxylation of glutamic acid residues to clotting factor 2,7, 9 and 10

Answer

γ-carboxylation of glycine residues to clotting factor 2,7, 9 and 10

Answer

γ-carboxylation of glutathione residues to clotting factor 2,7, 9 and 10

Answer

γ-carboxylation of aspartic acid residues to clotting factor 2,7, 9 and 10

Question 2

The following reaction occurs in which part of kidney?

Accepted Answer

Proximal convoluted tubule

Answer

Distal convoluted tubule

Answer

Loop of Henle

Answer

Collecting duct

Question 3

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

Accepted Answer

17-alpha-hydroxylase

Answer

3-beta-hydroxylase

Answer

21-hydroxylase

Answer

24-hydroxylase

Question 4

Name the enzyme involved in this cycle:

Accepted Answer

Retinal isomerase

Answer

Retinol isomerase

Answer

Transducin

Answer

Gustducin

Question 5

Which of the following reactions is responsible for folate trap?

Accepted Answer

2

Answer

1

Answer

3

Answer

All of the above

Question 6

The following lesion is seen in all of the following conditions except: (Recent NEET Pattern 2016-17)

Accepted Answer

Porphyria

Answer

Carcinoid syndrome

Answer

Hartnup disease

Answer

Alcoholism

Question 7

The bony deformity of 'pigeon chest' in children occurs due to deficiency of:

Accepted Answer

Vitamin D

Answer

Vitamin K

Answer

Vitamin A

Answer

Vitamin E

Question 8

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?

Accepted Answer

Corn

Answer

Wheat

Answer

Fish

Answer

Rice

Question 9

In hyperemesis gravidarum, Wernicke's encephalopathy is seen due to the deficiency of

Accepted Answer

vitamin B1

Answer

vitamin B6

Answer

vitamin B12

Answer

vitamin B9

Question 10

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 ?

Accepted Answer

Both 1 and 2

Answer

1 only

Answer

2 only

Answer

Neither 1 nor 2

Vitamins and Coenzymes — MCQs

Vitamins and Coenzymes — MCQs

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