Correct Answer: C. Defective collagen formation
Scurvy is caused by vitamin C (ascorbic acid) deficiency, which is a cofactor for prolyl and lysyl hydroxylase enzymes. These enzymes catalyze hydroxylation of proline and lysine residues in procollagen, a critical step in collagen cross-linking and stabilization. Without adequate hydroxylation, collagen molecules cannot form stable triple helices and cannot be properly cross-linked, resulting in defective collagen that is mechanically weak and prone to degradation. This manifests clinically as bleeding gums (due to fragile gingival connective tissue), poor wound healing, easy bruisability (capillary fragility), perifollicular hemorrhages, and in severe cases, reopening of old scars. The bleeding occurs not from a coagulation defect but from structural failure of blood vessel walls and supporting connective tissue. In Indian populations, scurvy is occasionally seen in malnourished children, elderly individuals with poor dietary intake, and those with chronic malabsorption. The diagnosis is clinical (bleeding gums, perifollicular hemorrhages, anemia) and can be confirmed by low plasma ascorbic acid levels (<0.2 mg/dL). Treatment is vitamin C supplementation (100–200 mg daily), with rapid clinical improvement within days to weeks.
Why the other options are wrong
A. Increased keratinization of epithelium — This is wrong because vitamin C deficiency does NOT cause increased keratinization; rather, it causes defective collagen in the dermis, leading to fragile epithelial-dermal junction. Hyperkeratosis is seen in vitamin A deficiency (follicular hyperkeratosis), not scurvy. This option confuses the epithelial manifestations of different vitamin deficiencies and is a common NBE trap for students who conflate vitamin A and C deficiencies. B. Inhibition of clotting factors — This is wrong because scurvy does NOT impair the synthesis or function of clotting factors (which require vitamin K, not vitamin C). Prothrombin time and activated partial thromboplastin time are normal in scurvy. The bleeding in scurvy is due to structural weakness of blood vessel walls and connective tissue, not coagulopathy. This option represents a common misconception that all bleeding disorders are coagulation defects. D. Low calcium — This is wrong because scurvy is not caused by calcium deficiency, and calcium deficiency does not produce the characteristic bleeding gums and perifollicular hemorrhages of scurvy. Calcium deficiency causes hypocalcemia with tetany, paresthesias, and seizures. This option is a distractor that confuses micronutrient deficiencies and their distinct clinical presentations.
High-Yield Facts
- Vitamin C is a cofactor for prolyl and lysyl hydroxylase, which hydroxylate proline and lysine in procollagen to stabilize the collagen triple helix.
- Defective collagen in scurvy leads to fragile blood vessels, poor wound healing, and connective tissue breakdown—not a coagulation defect.
- Clinical signs of scurvy: bleeding gums, perifollicular hemorrhages, poor wound healing, easy bruisability, anemia (from chronic bleeding).
- Plasma ascorbic acid <0.2 mg/dL confirms scurvy; normal is 0.4–1.5 mg/dL.
- Treatment: vitamin C 100–200 mg daily orally; symptoms resolve within 1–2 weeks with proper supplementation.
Mnemonics
*C for Collagen Vitamin C → C*ollagen hydroxylation → defective collagen → bleeding gums, poor healing. Use this to remember that scurvy is fundamentally a collagen problem, not a coagulation problem.
NBE Trap
NBE pairs scurvy with bleeding to lure students into selecting a coagulation defect (clotting factors) or confusing it with vitamin A deficiency (keratinization). The key discriminator is that scurvy bleeding is due to structural collagen weakness, not impaired hemostasis.
Clinical Pearl
In Indian clinical practice, scurvy is occasionally encountered in malnourished elderly patients or those with chronic diarrhea (malabsorption). The rapid response to vitamin C supplementation (gum bleeding stops within days) is a bedside clue that distinguishes it from other bleeding disorders requiring investigation.
_Reference: Harper's Biochemistry Ch. 49 (Vitamins); KD Tripathi Pharmacology Ch. 61 (Vitamins); Robbins Pathology Ch. 9 (Environmental and Nutritional Pathology)_