Pathology
Haemorrhagic Disorders
Haemorrhagic disorders for MBBS and NEET-PG: normal haemostasis, ITP, haemophilia, von Willebrand disease and DIC with their laboratory findings, mapped to NMC codes PA21.1 to PA21.5.
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Haemorrhagic Disorders
Haemorrhagic disorders for MBBS and NEET-PG: normal haemostasis, ITP, haemophilia, von Willebrand disease and DIC with their laboratory findings, mapped to NMC codes PA21.1 to PA21.5.
This chapter covers disorders of bleeding. It describes normal haemostasis, then separates platelet and vascular disorders from coagulation factor disorders, and details immune thrombocytopenic purpura, the haemophilias, von Willebrand disease and disseminated intravascular coagulation with their laboratory findings.
High-yield: Haemorrhagic Disorders
- Haemostasis has three stages: vascular constriction, primary platelet plug formation and the coagulation cascade forming fibrin.
- Platelet (primary haemostasis) disorders cause mucocutaneous bleeding, petechiae and purpura.
- Coagulation factor (secondary haemostasis) disorders cause deep bleeding into joints and muscles and delayed bleeding.
- The prothrombin time assesses the extrinsic and common pathways; the activated partial thromboplastin time assesses the intrinsic and common pathways.
- Immune thrombocytopenic purpura is an autoimmune destruction of platelets, with a low platelet count but a normal or raised marrow megakaryocyte number.
- Haemophilia A is an X-linked deficiency of factor VIII and prolongs the activated partial thromboplastin time with a normal prothrombin time.
- Haemophilia B (Christmas disease) is an X-linked deficiency of factor IX.
- Von Willebrand disease is the most common inherited bleeding disorder and causes a prolonged bleeding time with reduced factor VIII.
- Disseminated intravascular coagulation is widespread activation of coagulation that consumes platelets and clotting factors.
- In DIC the platelets are low, prothrombin time and activated partial thromboplastin time are prolonged, fibrinogen is low and D-dimer is high.
- Schistocytes on the blood film reflect the microangiopathic haemolysis of DIC.
- Vitamin K deficiency reduces factors II, VII, IX and X and prolongs the prothrombin time.
- Thrombotic thrombocytopenic purpura is caused by deficiency of the ADAMTS13 protease and features a pentad including fever and neurological signs.
- Bleeding time and platelet count assess primary haemostasis, while the prothrombin time and activated partial thromboplastin time assess the coagulation pathways.
Platelet versus coagulation bleeding
- **Platelet or vascular:** Mucocutaneous bleeding, petechiae and purpura; prolonged bleeding time.
- **Coagulation factor:** Deep bleeds into joints and muscles; delayed bleeding; prolonged PT or aPTT.
- **Haemophilia A:** Factor VIII deficiency; prolonged aPTT, normal PT.
- **DIC:** Low platelets, prolonged PT and aPTT, low fibrinogen, high D-dimer.
NMC competencies in this chapter
- **PA21.1:** Normal haemostasis
- **PA21.2:** Aetiology, pathogenesis and pathology of vascular and platelet disorders including ITP and haemophilias
- **PA21.3:** Differentiate platelet from clotting disorders
- **PA21.4:** Disseminated intravascular coagulation: laboratory findings and diagnosis
- **PA21.5:** Vitamin K deficiency: laboratory findings and diagnosis
Frequently Asked Questions
How do platelet and coagulation bleeding differ?
Platelet disorders cause superficial mucocutaneous bleeding with petechiae and purpura, while coagulation factor disorders cause deep, delayed bleeding into joints and muscles.
What are the laboratory findings in DIC?
Low platelets, prolonged prothrombin and activated partial thromboplastin times, low fibrinogen and raised D-dimer, often with schistocytes on the film.
What deficiency causes haemophilia A?
An X-linked deficiency of factor VIII, which prolongs the activated partial thromboplastin time while the prothrombin time stays normal.
Why does vitamin K deficiency cause bleeding?
Because vitamin K is needed to activate clotting factors II, VII, IX and X, so its deficiency prolongs the prothrombin time and impairs coagulation.
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