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PA20.1-2 | Welcome to DIC & Vitamin K Deficiency
Learning Objectives
- Define disseminated intravascular coagulation (DIC) and explain the paradox of simultaneous thrombosis and haemorrhage.
- List the major triggers of DIC and link each to the pathogenetic mechanism of tissue factor release.
- Interpret the classic DIC laboratory panel: thrombocytopenia, prolonged PT and aPTT, low fibrinogen, elevated D-dimer/FDPs, and schistocytes.
- Distinguish acute DIC from chronic (compensated) DIC using clinical and laboratory criteria.
- Explain the role of vitamin K in γ-carboxylation of coagulation factors II, VII, IX, and X.
- List causes of vitamin K deficiency and predict the laboratory pattern (PT-first prolongation, normal fibrinogen and platelets).
- Construct a three-way differential comparison table distinguishing DIC, liver disease, and vitamin K deficiency.
INSTRUCTIONS
Haemostasis is a tightly regulated balance. In DIC that balance catastrophically tips both ways at once — the body clots and bleeds simultaneously. Understanding why requires you to trace the sequence from trigger → thrombin burst → factor consumption → secondary fibrinolysis. Vitamin K deficiency offers a clean counterpoint: the coagulation defect is selective, platelets are unaffected, and correction is straightforward. Together these two conditions form the backbone of the PA20.2 competency and appear repeatedly in clinical pathology examinations and clinical practice.
References
- Robbins & Kumar: Basic Pathology, 11th ed., Ch 4 (Haemodynamic Disorders) (textbook)
- Bancroft & Lakin: Theory and Practice of Histological Techniques, 8th ed. (textbook)
- Hoffbrand & Steensma: Essential Haematology, 8th ed., Ch 28 (textbook)
Version 2.0 | NMC CBUC 2024