Thrombrosis & Aerterial thrombosis

Intro to Thrombrosis & Aerterial thrombosis

Haemostatis Over view

- Vessel Injury

- Vasoconstriction

- platelets roll and adhere ( bound exposed collagen by vWF and GPIB, release granules such as ADP and thromboxane A2 which

- aggregates platelets and activates them

(exposure of collagen releases TF which binds with cofactor 7. activated co factor 7 binds to TF which makes activated serine protease. Cleaves factor 10 to become activated factor 10 which binds to factor 5.

- COmplex is active and cleaves pro thrombin to make active thrombin) (extrinsic pathway)

Intrinsinc Amplification pathway is when much thrombin is made

- Thrombin cleaves fac 11, 8 and 5. activating them

Factor VIII is stabilised by vWF. activated VIII cleaves IXa which activates fac X. thrombin activates V which binds to give more V-X activated complex which cleaves prothrombin to create thrombin.

- Thrombin activates factor 11 whichadds to cycling activation of the IX pthway which binds to VIII

-          A lot of this occurs on the negatively charged platelet surface that ow attracts + coag facs from nlood

The activation of the coagulation Cascade forms a haemostatic Plug

Atherosclerosis

- the platelet aggregates together in the blood vessel

Venous Thrombosis

- is a coagulation issue

Haemostatis VS Thrombosis

Hameostasis

·       platelets activated and clot to prevent excessive blood loss

·       negatively regulated by intact endothelium via - inhibitors such as antithrombin, blood flow is constricted, fibrinolysis which breaks down fibrin etc

Thrombosis

·       Unwanted  formation of ablood clot called a THROMBUS . This blocks blood vessels.

·       Aerterial Thrombosis  is caused by vessel disease, this leads to Atherosclerotic (platelet aggregation in bloood vessel) rupture

·       TVenous thrombosis B due to slow blood flow and endothelal dysfunction or altered blood properties such as coagulation

--- In Artery ---

- Thicker vessel wall

- Artery has atherosclerotic plaque that can narrow the artery

-- In Vein --

- venous thrombosis

- not due to damage - altered properties of vessel wall, increases coagulation of blood.

- Spontaneous clots due to Coagulation Cascade trigger which forms fibrin Mesh.

INITIATION & PROGRESSION OF ATHEROSCLEROSIS

1. Begins w Fatty Streak - A deposit of low density lipoprotein carrying cholesterol UNDER endothelial layer.

·       immune cells enter site ti ckear fatty deposit

2. Macrophage becomes inflammatory cell to engulf it

·       occurs at site in vascular tree where lamina flow is disrupted. 

·       Undissolved stereaks become bigger, and T cels…