Vitamin C and Collagen Synthesis — MCQs
The main function of Vitamin C in the body is
A patient presenting with bleeding gums and easy bruisability was diagnosed with scurvy. This condition results from a deficiency of which of the following?
How does vitamin C deficiency lead to scurvy?
Defect in Menkes disease:
Maximum concentration of vitamin A is found in which organ?
Which of the following is not typically associated with osteogenesis imperfecta?
Prolyl hydroxylase requires which cofactor?
A patient presents with annular, scaly plaques with perifollicular extension on the trunk. What is the most likely diagnosis?
Which of the following is absolutely essential for wound healing?
Which nutrient deficiency directly impairs hydroxylation during collagen synthesis?
Vitamin C and Collagen Synthesis Indian Medical PG Practice Questions and MCQs
Question 1: The main function of Vitamin C in the body is
- A. Cofactor for hydroxylation reactions in collagen synthesis (Correct Answer)
- B. Regulation of lipid synthesis
- C. Involvement as antioxidant
- D. Inhibition of cell growth
Explanation: ***Cofactor for hydroxylation reactions in collagen synthesis*** - Vitamin C (ascorbic acid) serves as an essential **cofactor** for **prolyl hydroxylase** and **lysyl hydroxylase** enzymes. - These enzymes catalyze the **hydroxylation of proline and lysine** residues in collagen, forming **hydroxyproline** and **hydroxylysine**. - This hydroxylation is crucial for the **stability and cross-linking** of collagen triple helix structure. - Deficiency leads to **scurvy**, characterized by defective collagen synthesis, bleeding gums, poor wound healing, and bone abnormalities. - This is the **primary and main function** of Vitamin C in the human body. *Involvement as antioxidant* - While Vitamin C does act as a **water-soluble antioxidant**, protecting cells from oxidative damage by free radicals, this is a **secondary function**. - It can donate electrons to neutralize reactive oxygen species and regenerate other antioxidants like Vitamin E. - This protective role is important but not the main function compared to its role in collagen synthesis. *Regulation of lipid synthesis* - Vitamin C is **not directly involved** in the primary pathways of lipid synthesis or metabolism. - It may play a minor role in **carnitine synthesis** (needed for fatty acid oxidation), but this is not a major function. - Other nutrients like B vitamins play more significant roles in lipid metabolism regulation. *Inhibition of cell growth* - Vitamin C does **not inhibit normal cell growth**; it is essential for cell health, differentiation, and tissue repair. - While high doses may have some anti-proliferative effects in certain cancer cell lines in vitro, this is not a physiological function in the healthy body.
Question 2: A patient presenting with bleeding gums and easy bruisability was diagnosed with scurvy. This condition results from a deficiency of which of the following?
- A. Inhibition of vitamin K
- B. Increased collagen breakdown
- C. Defective collagen synthesis
- D. Low vitamin C (Correct Answer)
Explanation: ***Low vitamin C*** - **Scurvy** is directly caused by a severe deficiency of **vitamin C (ascorbic acid)**. - Vitamin C is a cofactor for **prolyl hydroxylase** and **lysyl hydroxylase**, enzymes essential for **collagen synthesis**. - Its deficiency leads to defective collagen formation, resulting in weakened connective tissues and fragile capillaries, explaining the bleeding gums and easy bruising. *Inhibition of vitamin K* - **Vitamin K** is crucial for the synthesis of **blood clotting factors** (II, VII, IX, X). - Its inhibition (e.g., by warfarin) would lead to bleeding disorders but does not explain the characteristic connective tissue problems (poor wound healing, perifollicular hemorrhages) seen in scurvy. *Increased collagen breakdown* - Conditions like **Ehlers-Danlos syndrome** involve abnormal collagen structure leading to tissue fragility. - Scurvy is characterized by a problem in the *synthesis* rather than the increased *breakdown* of collagen. *Defective collagen synthesis* - While this describes the **pathophysiological mechanism** of scurvy, it is not the answer to what the patient is *deficient in*. - The question asks for the underlying **nutritional deficiency**, which is **vitamin C**—the root cause that leads to defective collagen synthesis.
Question 3: How does vitamin C deficiency lead to scurvy?
- A. Defective collagen formation due to impaired synthesis (Correct Answer)
- B. Impaired immune response due to vitamin deficiencies
- C. Iron deficiency anemia
- D. Malabsorption of fat-soluble vitamins
Explanation: ***Defective collagen formation due to impaired synthesis*** - **Vitamin C** is a crucial cofactor for **prolyl hydroxylase** and **lysyl hydroxylase**, enzymes essential for the hydroxylation of proline and lysine residues in collagen. - Without proper hydroxylation, collagen molecules cannot form stable **triple helix structures**, leading to weakened connective tissues throughout the body, manifesting as scurvy. *Impaired immune response due to vitamin deficiencies* - While various vitamin deficiencies can impair the immune response, **scurvy's primary pathology** stems from defective collagen synthesis, not directly from immune system dysfunction. - Immune compromise might be a secondary effect in severe, prolonged scurvy, but it's not the **direct cause of the characteristic symptoms** like bleeding gums and poor wound healing. *Iron deficiency anemia* - **Vitamin C does enhance iron absorption** in the gut, so severe deficiency can indirectly contribute to **iron deficiency anemia**. - However, iron deficiency anemia is a *consequence* of prolonged scurvy, not the primary mechanism by which scurvy's defining symptoms occur. *Malabsorption of fat-soluble vitamins* - **Vitamin C** is a water-soluble vitamin and its deficiency does not directly cause malabsorption of **fat-soluble vitamins** (A, D, E, K). - Malabsorption of fat-soluble vitamins is typically linked to disorders of fat digestion or absorption, such as **pancreatic insufficiency** or **celiac disease**.
Question 4: Defect in Menkes disease:
- A. ATP7A (Copper-transporting ATPase) (Correct Answer)
- B. Prolyl oxidase
- C. Prolyl hydroxylase
- D. Lysyl oxidase
Explanation: ***ATP7A (Copper-transporting ATPase)*** - **Menkes disease** is an X-linked recessive disorder characterized by a defect in the **ATP7A gene**, which encodes a copper-transporting ATPase. - This defect leads to impaired intestinal absorption and cellular transport of copper, resulting in **copper deficiency** in various tissues despite adequate dietary intake. *Prolyl oxidase* - **Prolyl oxidase** is involved in proline metabolism, and defects are not associated with Menkes disease. - Deficiency of this enzyme is usually linked to hyperprolinemia. *Prolyl hydroxylase* - **Prolyl hydroxylase** is an enzyme critical for the hydroxylation of proline residues in collagen, a step essential for collagen stability. - While collagen synthesis requires copper (for lysyl oxidase), a direct defect in prolyl hydroxylase is not the cause of Menkes disease. *Lysyl oxidase* - **Lysyl oxidase** is a copper-dependent enzyme required for the cross-linking of collagen and elastin, contributing to connective tissue strength. - Although lysyl oxidase activity is reduced in Menkes disease due to copper deficiency, the primary defect is in the **ATP7A transporter**, not the lysyl oxidase enzyme itself.
Question 5: Maximum concentration of vitamin A is found in which organ?
- A. Liver (Correct Answer)
- B. Kidney
- C. Lung
- D. Heart
Explanation: ***Liver*** - The **liver** is the primary organ for **storage of vitamin A** (retinyl esters), accounting for 90% of the body's total vitamin A content. - **Hepatic stellate cells** within the liver are specialized for storing the majority of this fat-soluble vitamin. *Kidney* - The **kidney** plays a role in **vitamin D metabolism** and excretion, but not significant vitamin A storage. - While it helps regulate blood levels of various substances, it does not accumulate large quantities of vitamin A. *Lung* - The **lung** does not serve as a major storage site for **vitamin A**. - Its primary functions are related to **gas exchange**, not nutrient storage. *Heart* - The **heart** is responsible for **pumping blood** throughout the body and has minimal involvement in vitamin A storage. - It utilizes certain vitamins for its metabolic processes but does not act as a primary reservoir.
Question 6: Which of the following is not typically associated with osteogenesis imperfecta?
- A. Blue sclera
- B. Lax ligament
- C. Bilateral Hip dislocation (Correct Answer)
- D. Osteoporosis
Explanation: ***Bilateral Hip dislocation*** - While hip dislocations can occur in severe cases due to bone fragility, **bilateral hip dislocation** is not a characteristic or typical primary association with osteogenesis imperfecta. - The underlying issue is primarily **bone fragility** leading to fractures, not inherent joint instability or malformation causing bilateral dislocation. *Blue sclera* - **Blue sclera** is a classic sign of osteogenesis imperfecta, caused by the thinness of the sclera allowing the underlying choroid vessels to show through. - This is due to a defect in **Type I collagen** synthesis, which affects not only bones but also other connective tissues including the sclera. *Lax ligament* - **Lax ligaments** are common in osteogenesis imperfecta due to the generalized **connective tissue defect**, particularly involving Type I collagen. - This can contribute to joint instability, *hypermobility*, and an increased risk of sprains. *Osteoporosis* - **Osteoporosis** with reduced bone mineral density is a hallmark feature of osteogenesis imperfecta, leading to **fragile bones** and recurrent fractures. - The genetic defect in **Type I collagen** impairs bone matrix formation, resulting in weak and brittle bones.
Question 7: Prolyl hydroxylase requires which cofactor?
- A. Vitamin C (Correct Answer)
- B. Iron (Fe²⁺)
- C. Molybdenum
- D. Vitamin K1
Explanation: ***Vitamin C*** - **Prolyl hydroxylase** is an enzyme critical for the hydroxylation of proline residues during **collagen synthesis**. - **Vitamin C** (ascorbic acid) acts as an essential **cofactor**, reducing the ferric iron of the enzyme back to its ferrous state after each catalytic cycle, enabling continued activity. - The enzyme requires both **iron (Fe²⁺)** as a metal cofactor and **vitamin C** to maintain the iron in its reduced state. *Iron (Fe²⁺)* - While **iron** is indeed required by prolyl hydroxylase as a **metal cofactor**, the question asks for the cofactor, which specifically refers to **vitamin C**. - Iron functions as part of the enzyme's active site, but vitamin C is the reducing agent that keeps iron functional. - Vitamin C deficiency (scurvy) leads to defective collagen synthesis despite adequate iron. *Molybdenum* - **Molybdenum** is a cofactor for several human enzymes, including **xanthine oxidase** and **sulfite oxidase**. - However, it plays no direct role in the activity of prolyl hydroxylase. *Vitamin K1* - **Vitamin K1** is a crucial cofactor for **gamma-glutamyl carboxylase**, an enzyme involved in the carboxylation of glutamic acid residues in clotting factors. - It is not involved in the hydroxylation of proline by prolyl hydroxylase.
Question 8: A patient presents with annular, scaly plaques with perifollicular extension on the trunk. What is the most likely diagnosis?
- A. Psoriasis
- B. Lichen planus
- C. Tinea (Correct Answer)
- D. Pityriasis versicolor
Explanation: ***Tinea*** - **Tinea corporis** classically presents with **annular, scaly plaques with central clearing** and an active, raised border. - On hairy areas or with follicular involvement, dermatophyte infections show **perifollicular extension** as the fungus invades hair follicles. - The **annular morphology with scale** is pathognomonic for dermatophyte infection, confirmed by **KOH preparation** showing septate hyphae. - Common sites include trunk, limbs, and any body area with hair follicles. *Psoriasis* - Presents with **well-demarcated, erythematous plaques** with **silvery-white scales**, typically on extensor surfaces (elbows, knees, scalp). - **Follicular psoriasis** is rare and shows **pinpoint follicular papules**, not annular plaques with perifollicular extension. - Auspitz sign (pinpoint bleeding on scale removal) helps differentiate from tinea. *Lichen planus* - Characterized by **pruritic, polygonal, purple, planar papules** (the "6 Ps"). - **Lichen planopilaris** (follicular variant) causes **scarring alopecia** with follicular hyperkeratosis, not annular scaly plaques. - Wickham striae may be visible on mucosal surfaces. *Pityriasis versicolor* - Caused by **Malassezia species**, presents as **hypo- or hyperpigmented macules** with fine scale on trunk and upper arms. - **Follicular variant** (pityriasis folliculorum) shows discrete follicular papules, NOT annular plaques. - "Spaghetti and meatballs" appearance on KOH prep (short hyphae and spores) differentiates from dermatophytes.
Question 9: Which of the following is absolutely essential for wound healing?
- A. Balanced diet
- B. Vitamin C (Correct Answer)
- C. Vitamin D
- D. Carbohydrates
Explanation: ***Vit C*** - **Vitamin C** is absolutely essential for wound healing because it is a crucial cofactor for **collagen synthesis**, specifically for the hydroxylation of proline and lysine residues. - Without adequate vitamin C, strong, stable **collagen fibers** cannot be formed, leading to impaired wound tensile strength and delayed healing. *Balanced diet* - While a **balanced diet** provides overall nutritional support for wound healing, it is a general principle, not a single, absolutely essential nutrient in the same way **Vitamin C** is for a specific biochemical process. - A balanced diet incorporates many components, but specifically points to **Vitamin C's** role makes it more specific and thereby the correct answer. *Vit D* - **Vitamin D** plays a role in bone health and immune function but is not directly involved in the **collagen synthesis** or immediate structural integrity of new tissue formation in wound healing to the same critical extent as Vitamin C. - Its effects on wound healing are more indirect, through modulation of inflammation and cell proliferation, rather than being an "absolutely essential" direct component of the healing process. *Carbohydrates* - **Carbohydrates** are important for providing energy for cellular activities during wound healing. - However, they are not directly involved in the **structural integrity** or **collagen formation** of the healing tissue itself, unlike Vitamin C.
Question 10: Which nutrient deficiency directly impairs hydroxylation during collagen synthesis?
- A. A. Vitamin D
- B. B. Copper
- C. C. Vitamin E
- D. D. Vitamin C (Correct Answer)
Explanation: ***Vitamin C*** - **Vitamin C** (ascorbic acid) is a crucial **cofactor** for the enzymes **prolyl hydroxylase** and **lysyl hydroxylase**, which are essential for **collagen cross-linking and stability**. - Its deficiency leads to **scurvy**, characterized by weakened connective tissue, impaired wound healing, and fragile blood vessels due to **defective collagen synthesis**. *Vitamin D* - **Vitamin D** is primarily involved in **calcium and phosphate homeostasis**, which are vital for bone mineralization. - Its deficiency can lead to **rickets** in children and **osteomalacia** in adults, conditions of weakened bones, but not directly to collagen defects. *Copper* - **Copper** is a cofactor for **lysyl oxidase**, an enzyme that cross-links collagen and elastin, contributing to the tensile strength of connective tissues. - While copper deficiency can affect collagen structure, **Vitamin C deficiency** has a more direct and severe impact on the initial synthesis and hydroxylation steps of collagen, making it the primary answer for collagen defects. *Vitamin E* - **Vitamin E** is a fat-soluble antioxidant that protects cell membranes from **oxidative damage**. - Its deficiency is associated with neurological symptoms and hemolytic anemia but does not directly cause defects in **collagen synthesis or structure**.
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