Vitamins and Coenzymes Practice Questions

Q: Wernicke-Korsakoff's syndrome is due to the deficiency of:

Thiamine. ***Correct: Thiamine*** - **Wernicke-Korsakoff syndrome** is a severe neurological disorder caused by a profound deficiency of **thiamine (vitamin B1)**, most commonly seen in chronic alcoholics - **Thiamine** is crucial for **glucose metabolism** in the brain, and its deficiency leads to impaired neuronal function and brain damage - **Wernicke encephalopathy** presents acutely with confusion, ataxia, and ophthalmoplegia - **Korsakoff psychosis** represents the chronic phase with profound memory impairment and confabulation *Incorrect: Pyridoxine* - Deficiency of **pyridoxine (vitamin B6)** can cause peripheral neuropathy, seizures, and sideroblastic anemia, but is not the cause of Wernicke-Korsakoff syndrome - **Isoniazid** treatment is a common cause of pyridoxine deficiency *Incorrect: Riboflavin* - **Riboflavin (vitamin B2)** deficiency leads to cheilosis, angular stomatitis, glossitis, and seborrheic dermatitis, but is not associated with Wernicke-Korsakoff syndrome - It plays a vital role as a coenzyme (FAD, FMN) in various **redox reactions** *Incorrect: Vitamin B12* - Deficiency of **vitamin B12 (cobalamin)** causes megaloblastic anemia and subacute combined degeneration of the spinal cord, with distinct neurological symptoms different from Wernicke-Korsakoff syndrome - **Intrinsic factor** is necessary for its absorption in the terminal ileum

Q: Keshan's disease is due to deficiency of:

Selenium. **Selenium (Correct Answer)** - **Keshan disease** is an endemic cardiomyopathy characterized by multifocal myocyte necrosis, which has been directly linked to a severe dietary deficiency of **selenium**. - Selenium is an essential component of **glutathione peroxidase**, an enzyme critical for protecting cells against oxidative damage. - The disease is named after Keshan County in China where it was first identified in selenium-deficient regions. *Iron (Incorrect)* - **Iron deficiency** primarily leads to **anemia**, characterized by fatigue, pallor, and weakness due to insufficient hemoglobin production. - It does not directly cause the specific cardiomyopathy seen in Keshan disease. *Zinc (Incorrect)* - **Zinc deficiency** can cause a range of symptoms including impaired immune function, skin lesions (acrodermatitis enteropathica), hair loss, and growth retardation. - It is not associated with the cardiac manifestations of Keshan disease. *Copper (Incorrect)* - **Copper deficiency** can result in anemia, neutropenia, impaired immune function, and neurological dysfunction (Menkes disease). - While copper is important for various metalloenzymes, its deficiency does not cause Keshan disease.

Q: Hypocalcemia with hypophosphatemia is seen in:

Vitamin D deficiency rickets. ***Vitamin D deficiency rickets*** - **Vitamin D deficiency** impairs intestinal **calcium** and **phosphate** absorption, leading to both hypocalcemia and hypophosphatemia [1], [2]. - The body attempts to compensate by increasing parathyroid hormone (PTH) secretion, but the primary defect in vitamin D leads to low serum levels of both electrolytes [2], [3]. *Rhabdomyolysis* - **Rhabdomyolysis** primarily causes **hyperkalemia**, **hyperphosphatemia**, and **hypocalcemia** due to the release of intracellular contents from damaged muscle and calcium deposition in injured muscle. - While it causes hypocalcemia, it typically leads to **hyperphosphatemia**, not hypophosphatemia. *Crush injury* - Similar to rhabdomyolysis, **crush injury** involves massive muscle breakdown, leading to the release of intracellular components. - This typically results in **hyperkalemia**, **hyperphosphatemia**, and **hypocalcemia**, not hypophosphatemia. *Renal failure* - **Chronic renal failure** often leads to **hyperphosphatemia** due to impaired phosphate excretion and **hypocalcemia** due to reduced renal activation of vitamin D and impaired phosphate handling [2]. - While hypocalcemia is common, the presence of **hyperphosphatemia** differentiates it from vitamin D deficiency rickets [2], [3].

Q: Pseudo tumor cerebri is caused by?

Vitamin A excess. ***Vitamin A excess*** - **Hypervitaminosis A**, or excess vitamin A, is a known cause of **pseudotumor cerebri** (also called **idiopathic intracranial hypertension**). - This condition involves increased **intracranial pressure**, often without an obvious structural cause. *Vitamin B1 excess* - Excess intake of **vitamin B1 (thiamine)** is generally considered benign and is not known to cause pseudotumor cerebri. - Thiamine is a **water-soluble vitamin**, and excess amounts are typically excreted in urine. *Vitamin D excess* - **Vitamin D toxicity** primarily leads to **hypercalcemia**, which can cause kidney stones, bone pain, and gastrointestinal symptoms. - While it can have neurological effects due to hypercalcemia, it typically does not directly cause pseudotumor cerebri. *Vitamin E excess* - **Vitamin E excess** can interfere with **blood clotting** and may increase the risk of bleeding, especially in individuals taking anticoagulants. - There is no established link between hypervitaminosis E and the development of pseudotumor cerebri.

Q: Site of 25-hydroxylation of cholecalciferol

Liver. ***Liver*** - The **liver** is the site of **25-hydroxylation** of cholecalciferol (Vitamin D3) to form **25-hydroxycholecalciferol (calcidiol)**. - This reaction is catalyzed by **25-hydroxylase (CYP2R1)** in hepatocytes. - This is the **first step** in vitamin D activation; subsequent 1α-hydroxylation occurs in the **kidney** to form the active **calcitriol**. *Bone* - Bone is a **target organ** for active vitamin D (calcitriol) action, not a site of hydroxylation. - It responds to calcitriol for calcium homeostasis and bone remodeling. *Pancreas* - The pancreas has no role in vitamin D metabolism. - Its primary functions are digestive enzyme secretion and endocrine regulation (insulin, glucagon). *Heart* - The heart does not perform vitamin D hydroxylation. - While vitamin D receptors exist in cardiac tissue, the organ does not metabolize vitamin D.

Q: Secondary hyperparathyroidism due to Vit D deficiency shows :

Hypocalcemia. ***Hypocalcemia*** - **Vitamin D deficiency** leads to decreased intestinal absorption of calcium, causing **hypocalcemia** [3]. - This persistent **low serum calcium** is the primary stimulus for the parathyroid glands to increase PTH secretion, leading to secondary hyperparathyroidism [1], [2]. *Hypophosphatemia* - While PTH typically promotes phosphate excretion in the kidneys leading to hypophosphatemia, in **secondary hyperparathyroidism due to vitamin D deficiency**, the effect on phosphate can be variable [3]. - The goal of increased PTH is to raise calcium, and maintaining some level of phosphate is necessary for bone health and proper calcium regulation. Early or mild deficiency may not show significant hypophosphatemia. *Hypercalcemia* - **Hypercalcemia** is a characteristic feature of **primary hyperparathyroidism**, where the parathyroid glands autonomously overproduce PTH [1]. - In secondary hyperparathyroidism (due to vitamin D deficiency), the PTH is elevated in response to **low calcium**, and sustained significant hypercalcemia is not expected; in fact, the underlying problem is **hypocalcemia** [1]. *Hyperphosphatemia* - **PTH** generally acts to lower serum phosphate levels by promoting its renal excretion [2]. - Therefore, **hyperphosphatemia** is not typically observed in secondary hyperparathyroidism; rather, a more common finding would be normal or low phosphate due to the elevated PTH [3].

Q: Thiamine deficiency causes -

All of the options. ***All of the options*** - **Thiamine (vitamin B1)** is critical for nervous system, heart, and muscle function, as it is a coenzyme in carbohydrate metabolism [1], [2]. - Deficiency can manifest as **Wernicke-Korsakoff syndrome** (affecting the central nervous system), **beriberi** (affecting cardiovascular and peripheral nervous systems), or both [1]. *Peripheral neuropathy* - This is a hallmark of **dry beriberi**, leading to **symmetrical peripheral neuropathy** with muscle weakness and sensory loss [1]. - It results from the impaired function of peripheral nerves due to thiamine's role in myelin maintenance and nerve signal transmission [1]. *Ophthalmoplegia* - This symptom is characteristic of **Wernicke encephalopathy**, a severe neurological manifestation of thiamine deficiency. - It involves paralysis or weakness of the eye muscles, often accompanied by **nystagmus** and ataxia. *Cardiomyopathy* - This is a characteristic feature of **wet beriberi**, where thiamine deficiency impacts cardiac function due to decreased cellular energy production [1]. - It can lead to **high-output cardiac failure**, manifesting as edema and shortness of breath [1].

Q: Dementia is produced by deficiency of vitamin

Thiamine. thiamine - **Thiamine deficiency** (Vitamin B1) can lead to **Wernicke-Korsakoff syndrome**, a severe neurological disorder characterized by **ataxia**, **ophthalmoplegia**, and **confusion**, [1], [2] which can progress to **dementia** and memory loss (Korsakoff psychosis) [2]. - This is particularly common in individuals with **chronic alcoholism** due to poor nutrition and impaired thiamine absorption [4]. *Pyridoxine* - **Pyridoxine deficiency** (Vitamin B6) can cause **peripheral neuropathy**, **anemia**, and **seizures**, but it is not typically associated with dementia as a primary symptom. - While essential for neurotransmitter synthesis, its deficiency does not directly lead to the neurocognitive decline seen in dementia. *Vitamin D* - **Vitamin D deficiency** is associated with various health issues, including **bone demineralization** (osteoporosis), muscle weakness, and, in severe cases, rickets or osteomalacia. - While some studies suggest a potential link between low vitamin D and cognitive decline, it is not a direct cause of dementia in the same way thiamine deficiency is. *Vitamin A* - **Vitamin A deficiency** can lead to **night blindness**, **xerophthalmia**, and impaired immune function [3]. - While crucial for vision and immune health, its deficiency is not a direct cause of dementia.

Q: A 30-year-old highly health conscious woman has been ingesting vitamins and health foods. She is complaining of hair loss, double vision and headache. Her liver function tests are abnormal. She may be suffering from

Hypervitaminosis A. ***Hypervitaminosis A*** - Chronic intake of excessive amounts of **vitamin A** can lead to symptoms such as **hair loss**, **double vision (diplopia)**, and **headache**. - **Liver function abnormalities** are a common feature of hypervitaminosis A due to the liver's role in vitamin A storage and metabolism. *vitamin E deficiency* - **Vitamin E deficiency** typically manifests with neurological symptoms like **ataxia**, **peripheral neuropathy**, and **muscle weakness**, given its role as an antioxidant. - It is not associated with the constellation of symptoms presented, especially **hair loss**, **double vision**, **headache**, and **liver dysfunction**. *Hypervitaminosis D* - **Hypervitaminosis D** primarily leads to **hypercalcemia**, presenting with symptoms such as **nausea**, **vomiting**, **polyuria**, and **kidney stones**. - It does not typically cause **hair loss**, **double vision**, or direct effects on **liver function** in the way described. *Vitamin C deficiency* - **Vitamin C deficiency** (scurvy) is characterized by symptoms like **gingival bleeding**, **petechiae**, **poor wound healing**, and **fatigue**. - These symptoms are distinctly different from the **neurological and hepatic manifestations** seen in the patient.

Question 1

Wernicke-Korsakoff's syndrome is due to the deficiency of:

Accepted Answer

Thiamine

Answer

Pyridoxine

Answer

Riboflavin

Answer

Vitamin B12

Question 2

Vitamin K leads to?

Accepted Answer

γ-carboxylation of glutamic acid residues in clotting factors II, VII, IX, and X

Answer

β-carboxylation of glutamic acid residues in clotting factors II, VII, IX, and X

Answer

α-carboxylation of aspartic acid residues in clotting factors II, VII, IX, and X

Answer

γ-carboxylation of aspartic acid residues in clotting factors II, VII, IX, and X

Question 3

Keshan's disease is due to deficiency of:

Accepted Answer

Selenium

Answer

Iron

Answer

Zinc

Answer

Copper

Question 4

Hypocalcemia with hypophosphatemia is seen in:

Accepted Answer

Vitamin D deficiency rickets

Answer

Rhabdomyolysis

Answer

Crush injury

Answer

Renal failure

Question 5

Pseudo tumor cerebri is caused by?

Accepted Answer

Vitamin A excess

Answer

Vitamin B1 excess

Answer

Vitamin D excess

Answer

Vitamin E excess

Question 6

Site of 25-hydroxylation of cholecalciferol

Accepted Answer

Liver

Answer

Bone

Answer

Pancreas

Answer

Heart

Question 7

Secondary hyperparathyroidism due to Vit D deficiency shows :

Accepted Answer

Hypocalcemia

Answer

Hypophosphatemia

Answer

Hypercalcemia

Answer

Hyperphosphatemia

Question 8

Thiamine deficiency causes -

Accepted Answer

All of the options

Answer

Peripheral neuropathy

Answer

Ophthalmoplegia

Answer

Cardiomyopathy

Question 9

Dementia is produced by deficiency of vitamin

Accepted Answer

Thiamine

Answer

Pyridoxine

Answer

Vitamin D

Answer

Vitamin A

Question 10

A 30-year-old highly health conscious woman has been ingesting vitamins and health foods. She is complaining of hair loss, double vision and headache. Her liver function tests are abnormal. She may be suffering from

Accepted Answer

Hypervitaminosis A

Answer

Vitamin E deficiency

Answer

Hypervitaminosis D

Answer

Vitamin C deficiency

Vitamins and Coenzymes — MCQs

Vitamins and Coenzymes — MCQs

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