High-yield map
Key points before the detail
- 01
Primary haemostasis is platelet centred; secondary haemostasis stabilises the plug with fibrin.
- 02
Tissue factor with factor VII is a major physiological initiator of coagulation.
- 03
Thrombin is a central amplifier: it makes fibrin and activates platelets and multiple coagulation factors.
- 04
Antithrombin, protein C/S and tissue-factor pathway inhibitor restrain clotting, while tPA-driven plasmin breaks down fibrin.
Primary haemostasis
Vessel injury exposes subendothelial matrix and von Willebrand factor. Platelets adhere, activate, change shape and release mediators that recruit additional platelets. Activated glycoprotein IIb/IIIa receptors bind fibrinogen and link platelets into an aggregate. This plug forms rapidly but is mechanically strengthened by fibrin.
Secondary haemostasis and thrombin
Exposure of tissue factor activates factor VII and initiates generation of factor Xa and small amounts of thrombin. Thrombin then amplifies the system by activating platelets and cofactors and by converting fibrinogen into fibrin. Factor XIII cross-links fibrin to stabilise the clot.
Natural anticoagulant checks
| System | Main effect |
|---|---|
| Antithrombin | Inhibits thrombin and several activated serine proteases, especially factor Xa. |
| Protein C and protein S | Activated protein C inactivates factors Va and VIIIa with protein S as a cofactor. |
| TFPI | Limits tissue-factor/factor VIIa pathway activity. |
| Intact endothelium | Provides antiplatelet, anticoagulant and fibrinolytic signals. |
Fibrinolysis
Endothelial tissue plasminogen activator converts plasminogen to plasmin on the fibrin surface. Plasmin cleaves fibrin into degradation products, including D-dimer when cross-linked fibrin is broken down. Fibrinolysis is regulated so that the clot can be remodelled without uncontrolled systemic proteolysis.
How physiology maps to common tests
| Test | What it samples |
|---|---|
| Platelet count | Quantity, not platelet function. |
| PT/INR | Especially tissue-factor/extrinsic and common-pathway factor activity; strongly affected by vitamin-K antagonism. |
| APTT | Contact/intrinsic and common-pathway factor activity; affected by unfractionated heparin among other causes. |
| Fibrinogen | Availability of the soluble precursor needed for fibrin formation. |
| D-dimer | Evidence that cross-linked fibrin has formed and been degraded; sensitive in selected contexts but not specific for thrombosis. |
Active recall
Close the notes and answer these
Try each question from memory before revealing the answer. These public prompts are a small preview of the integrated retrieval system inside SurgAtlas.
01What is the difference between primary and secondary haemostasis?
Primary haemostasis forms a platelet plug; secondary haemostasis generates fibrin that stabilises that plug.
02Why is thrombin central to coagulation?
It converts fibrinogen to fibrin and amplifies coagulation through platelet and factor activation.
03What enzyme directly breaks down fibrin?
Plasmin, generated from plasminogen.
Sources & editorial basis
References & editorial basis
- SurgAtlas production chapter — Applied Physiology — Haemostasis & Coagulation. Primary source for this public lesson. Stable physiological principles have been condensed from the corresponding SurgAtlas production teaching.
- Hoffbrand’s Essential Haematology. Reference for stable haemostatic physiology and laboratory principles.
This lesson is derived from the corresponding SurgAtlas production teaching material. Where the source makes current management or guideline claims, the public lesson uses the cited contemporary guidance. It is written for education and examination preparation, not as patient-specific clinical advice.
Editorial details
Medical Doctor (MD) · MRCS Part A · Physician · Surgical Educator
SurgAtlas is an educational resource. For patient care, verify current national guidance, local antimicrobial and transfusion policies, specialty pathways and individual patient factors.
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