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Unit 2 of 3 · B.Sc MLS Sem 4

Unit 2: Haemostasis and coagulation

Basic Haematological Techniques-II notes · PTU syllabus (BMLS402-18)

3 min read5 topics9 exam questions
On this page
  1. Unit summary
  2. Normal haemostatic mechanism
  3. Theories of blood coagulation
  4. Classification of coagulation factors
  5. Physiological properties of coagulation factors
  6. Natural anticoagulants and fibrinolysis
  7. Key terms
  8. Quick revision
  9. Important questions

Unit summary

Haemostasis stops bleeding through vessels, platelets and clotting factors working together. This unit covers the normal haemostatic mechanism, theories of blood coagulation, classification of coagulation factors and their physiological properties.

After this unit you can

  • Explain the stages of haemostasis
  • Explain the coagulation cascade and its modern cell-based model
  • Classify coagulation factors
  • Describe fibrinolysis and natural anticoagulants

PTU syllabus topics

  • Normal haemostatic mechanism and theories of blood coagulation
  • classification of coagulation factors
  • physiological properties of coagulation factors
ProcessThe coagulation cascade
  1. 1Intrinsic pathway

    Factors XII, XI, IX, VIII: tested by APTT

  2. 2Extrinsic pathway

    Tissue factor and factor VII: tested by PT

  3. 3Common pathway

    Factors X, V, II (prothrombin)

  4. 4Thrombin forms
  5. 5Fibrinogen to fibrin

    Stable clot with factor XIII

1

Topic 1

Normal haemostatic mechanism

ProcessHaemostasis
  1. 1Vascular phase

    Vasoconstriction of the injured vessel

  2. 2Primary haemostasis

    Platelets adhere to collagen through von Willebrand factor (GP Ib), activate, release ADP and thromboxane A2, aggregate through GP IIb/IIIa — platelet plug

  3. 3Secondary haemostasis

    Coagulation cascade forms fibrin to stabilise the plug

  4. 4Fibrinolysis

    Plasmin dissolves the clot as healing occurs

2

Topic 2

Theories of blood coagulation

  • Classical (Morawitz) theory: prothrombin → thrombin (with thromboplastin and calcium); thrombin converts fibrinogen → fibrin.
  • Cascade (waterfall) theory (Macfarlane; Davie and Ratnoff, 1964): a sequence of proenzymes activating one another.
ComparisonCoagulation pathways
Intrinsic pathway
Extrinsic pathway

Trigger

Contact with negatively charged surfaces — factor XII

Tissue factor (factor III) from damaged tissue

Factors

XII, XI, IX, VIII

VII

Test

APTT

PT

Common pathway

Factor X → Xa, with V and calcium converts prothrombin (II) → thrombin; fibrinogen (I) → fibrin; XIII cross-links fibrin

Same

  • Cell-based model (modern): initiation on tissue-factor-bearing cells (small amount of thrombin), amplification (activating platelets, V, VIII, XI) and propagation (large thrombin burst on platelet surfaces).
3

Topic 3

Classification of coagulation factors

ComparisonCoagulation factors
Name
Group

I

Fibrinogen

Fibrinogen group (also V, VIII, XIII) — consumed in clotting, absent from serum

II

Prothrombin

Vitamin K-dependent (II, VII, IX, X) — need calcium, adsorbed by barium sulphate

III

Tissue factor (thromboplastin)

—

IV

Calcium

—

V

Labile factor (proaccelerin)

Fibrinogen group; unstable on storage

VII

Stable factor

Vitamin K-dependent; shortest half-life (about 6 hours)

VIII

Antihaemophilic factor A

Fibrinogen group; labile; deficient in haemophilia A

IX

Christmas factor

Vitamin K-dependent; deficient in haemophilia B

X

Stuart–Prower factor

Vitamin K-dependent

XI

Plasma thromboplastin antecedent

Contact group

XII

Hageman factor

Contact group

XIII

Fibrin-stabilising factor

Cross-links fibrin

  • There is no factor VI (it was found to be activated factor V).
4

Topic 4

Physiological properties of coagulation factors

Key termsProperties
Site of synthesis
Mostly liver; VIII also endothelium
Vitamin K
Needed for γ-carboxylation of II, VII, IX, X — warfarin blocks it
Stability
V and VIII labile — plasma must be tested quickly or frozen
Serum vs plasma
Serum lacks fibrinogen, II, V, VIII
Calcium
Essential; citrate and EDTA bind it to prevent clotting
5

Topic 5

Natural anticoagulants and fibrinolysis

Key termsControl of clotting
Antithrombin
Inactivates thrombin and Xa; enhanced by heparin
Protein C and protein S
Inactivate Va and VIIIa
Tissue factor pathway inhibitor
Blocks TF–VIIa
Fibrinolysis
Plasminogen → plasmin (by tPA, urokinase) breaks fibrin into fibrin degradation products and D-dimer
  • D-dimer is raised in deep vein thrombosis, pulmonary embolism and DIC.

Key terms

Haemostasis
Process stopping bleeding
Platelet plug
Primary aggregate of platelets at injury
Tissue factor
Initiator of the extrinsic pathway
Vitamin K-dependent factors
II, VII, IX and X
Fibrinolysis
Breakdown of fibrin clots by plasmin

Quick revision

  • Vascular, platelet, coagulation, fibrinolytic phases; vWF, GP Ib, GP IIb/IIIa.
  • Classical and cascade theories; intrinsic, extrinsic, common pathways; cell-based model.
  • Factors I–XIII and groups; no factor VI.
  • Vitamin K, labile factors, serum vs plasma.
  • Antithrombin, protein C and S, TFPI; plasmin, D-dimer.

Important exam questions

Practice questions written to the PTU exam pattern for this unit's syllabus: short answers (Section A style) and long answers (Sections B and C style).

Short-answer questions

  1. Q1.What is primary haemostasis?
  2. Q2.Which factors are vitamin K-dependent?
  3. Q3.Which pathway does the PT test?
  4. Q4.What is the Christmas factor?
  5. Q5.Why is factor VI not used?
  6. Q6.What is D-dimer?

Long-answer questions

  1. Q1.Describe the normal haemostatic mechanism.
  2. Q2.Explain the coagulation cascade.
  3. Q3.Classify coagulation factors with their properties.

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