Secondary Hemostasis - How Your Blood Clots (Coagulation) - Hematology

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Secondary hemostasis, on the other hand, deals with converting fibrinogen into fibrin via the coagulation cascade to form a strong plug to stop bleeding.

Too little coagulation and you'll bleed. Too much coagulation and you will thrombose. Both extremes are bad.

Primary hemostasis is balanced on the dynamic harmonious antagonism between the smooth endothelium (that prefers laminar blood flow) and thrombocytes (which favor clotting and thrombosis).

Platelets are called thrombocytes "cells of thrombus".

The smooth endothelium is squamous epithelium that lines the blood and lymphatic vessels from the inside.

When platelets roll over the smooth endothelium, nothing happens.
But, once there is an injured endothelium, platelets adhere, activate and aggregate to form a temporary platelet plug (primary hemostasis).
Then, the coagulation factors are stimulated "thanks to subendothelial collagen, tissue thromboplastin and platelet factor 3), coagulation cascade ensues until fibrinogen is converted into fibrin fibers trapping the RBCs and forming a stronger thrombus (secondary hemostasis).

After that, fibrinolysis occur (thanks to tissue plasminogen activator or tPA) to destroy the clot and restore function and flow.

Hemostasis is defined as “cessation of blood bleeding”.

There are 2 types of hemostasis:
1. Primary hemostasis: formation of weak, temporary platelet plug (by platelets).
2. Secondary hemostasis: formation of stronger fibrin meshwork (by coagulation factors).

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To be able to answer exam questions, Try to think of primary hemostasis and secondary hemostasis as two separate entities. 1ry hemostasis involves platelets and 2ry hemostasis involves the coagulation cascade. If you like my videos, please consider leaving a tip at https://www.paypal.me/perfectionalis/
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