Correct Answer: D. Bile duct obstruction
Bile duct obstruction causes vitamin K malabsorption due to impaired bile salt secretion into the intestine. Vitamin K is a fat-soluble vitamin requiring bile salts for emulsification and absorption in the terminal ileum. Without adequate bile flow, vitamin K cannot be absorbed, leading to deficiency of vitamin K–dependent clotting factors (II, VII, IX, X). Parenteral (intramuscular or intravenous) vitamin K bypasses the intestinal absorption pathway and directly replenishes hepatic stores, allowing the liver to synthesize these factors and correct the prolonged PT. This is the classic scenario where parenteral vitamin K is therapeutic. The key discriminator is that the liver is structurally and functionally intact—it can synthesize factors if given the cofactor. In bile duct obstruction (whether from stones, strictures, or malignancy), vitamin K repletion will restore coagulation within 12–24 hours. This is a standard Indian clinical presentation, particularly in patients with choledocholithiasis or pancreatic head tumors causing biliary obstruction.
Why the other options are wrong
A. Hepatitis A — Hepatitis A causes hepatocellular injury, not malabsorption. The liver itself is damaged and cannot synthesize clotting factors even if vitamin K is provided. Parenteral vitamin K will NOT correct the PT because the problem is loss of hepatic synthetic function, not vitamin K deficiency. Hepatitis A is acute and self-limited, but during the acute phase, PT prolongation reflects liver damage, not vitamin K lack. B. Pernicious anemia — Pernicious anemia is a vitamin B12 deficiency disorder due to lack of intrinsic factor, causing megaloblastic anemia and neurological complications. It has no direct relationship to vitamin K metabolism or coagulation. Parenteral vitamin K is irrelevant to B12 deficiency. This is an NBE distractor exploiting confusion between different parenteral vitamin therapies. C. Hemophilia B — Hemophilia B is a congenital deficiency of factor IX due to genetic mutation, not vitamin K deficiency. The liver cannot synthesize factor IX because the gene is defective. Parenteral vitamin K will not help because the problem is genetic, not nutritional. This is a trap for students who conflate factor IX deficiency (the stem) with hemophilia B without recognizing the acquired vs. congenital distinction.
High-Yield Facts
- Vitamin K–dependent factors: II, VII, IX, X (mnemonic: 2, 7, 9, 10 are even numbers or 'PIVKA' = Proteins Induced by Vitamin K Absence).
- Bile duct obstruction causes vitamin K malabsorption because bile salts are required for emulsification and absorption of this fat-soluble vitamin in the terminal ileum.
- Parenteral vitamin K (IM/IV) bypasses intestinal absorption and directly replenishes hepatic stores; effective only if the liver is structurally intact.
- PT corrects within 12–24 hours of parenteral vitamin K in malabsorption; if PT does not correct, suspect hepatocellular disease or DIC.
- Vitamin K deficiency causes prolonged PT with normal aPTT (factors II, VII, X are PT-dependent; factor IX is aPTT-dependent, but isolated IX deficiency is rare in acquired disease).
Mnemonics
PIVKA (Proteins Induced by Vitamin K Absence) Factors II, VII, IX, X are vitamin K–dependent. When K is absent, these factors are not carboxylated and become non-functional. Remember: Prothrombin (II), Intermediate (VII), Value (IX), Kinase (X)—or simply 2, 7, 9, 10. When Parenteral Vitamin K Works: LIVER INTACT Parenteral K helps only if the liver is structurally sound. In bile duct obstruction (malabsorption), liver is intact → K works. In hepatitis/cirrhosis (liver damage), liver is damaged → K fails. This is the clinical pearl that discriminates the correct answer.
NBE Trap
NBE pairs "Factor IX deficiency" in the stem with "Hemophilia B" in the options to trap students who assume any factor IX deficiency = hemophilia B, without recognizing that acquired vitamin K deficiency also causes factor IX deficiency. The key is distinguishing acquired (malabsorption) vs. congenital (genetic) deficiency.
Clinical Pearl
In Indian clinical practice, a patient with obstructive jaundice (pale stools, dark urine, pruritus) presenting with bleeding manifestations or prolonged PT should immediately raise suspicion for vitamin K deficiency. A single IM dose of vitamin K (10 mg) followed by PT reassessment at 24 hours is diagnostic and therapeutic—if PT corrects, malabsorption was the cause; if it persists, hepatocellular disease is likely.
_Reference: Harrison Ch. 139 (Coagulation Disorders); KD Tripathi Ch. 18 (Anticoagulants & Vitamin K); Robbins Ch. 4 (Hemostasis)_