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What is fibrous repair? In which populations does it occur? Briefly describe the process

-The replacement of functional tissue with scar tissue
-Permanent cell lines eg myocytes
-Blood clot forms -> granulation tissue as infiltrated by macrophages and fibroblasts -> fibroblasts produce collagen and ECM. Angiogenesis occurs. Cell population falls and collagen increases -> fibrous scar


Briefly describe the process of angiogenesis

-Proteolysis of endothelial basement membrane of existing vessel
-Proliferation and migration of endothelial cells which arrnage themselves into a new vessel following a designated tip cell
-Remodelling and stablisation of new vessel making sure it connects with venous system


What are the constituents of ECM?



What is healing by primary or secondary intention?

-Primary intention = apposed edges with minimal clotting. Epidermis regenerates with minimal contraction
-Secondary intention = large wounds or ulcers -> Epidermis has to regenerate from base up forming a scab. more granulation tissue and fibrous repair -> contraction to make edges meet


Briefly explain what happens in a minor cut in successful haemostasis

-BVs contract to limit blood flow -> Platelets become activated by extrinsic pathway and adhere to the damaged vessel wall and each other and set off a cascade activating other platelets to form a platelet plug and stop the bleeding -> primary haemostatic plug -> more platelets adhere and fibrinogen is converted to fibrin by thrombin causing cross linking of platelets making a stable secondary haemodynamic plug


Name some endogenous proteins which help control the coagulation cascade to prevent thrombosis

-Anti-thrombin III, Protein C and S


What is fibrinolysis? Name an endogenous mediator and how this process is used clinically

-The breakdown of fibrin to control excessive clotting
-tPA (alteplase) or streptokinase


What is thrombosis? What causes it to occur? What is Virchows traid?

-Inappropriate clot formation inside a blood vessel
-Inappropriate activation of the clotting cascade
-Abnormal BVs (atheroma, hypertension, toxins), abnomal consituents (OCP, smoking, surgery, blood disorders) and abnormal flow (stasis, AF, CCF, valvular disease). 2/3 needed for thrombosis


What are the possible outcomes of thrombosis?

-Propagation -> progressive spreas
-Organisation -> lumen remains obstructed but turned to granulation tissue


What is an embolism?

-Blockage of a BV by part of a thrombus which has broken off from a different site (doesnt have to be thrombus)


Give some factors which predispose to DVT



Describe the intrinsic and extrinsic pathways

-Intrinsic is activated by endothelial damage which initiates the formation of the primary complex which becomes activated. Activated FXIIa activates FXI which activates FIX. FIXa activates FX which activates prothrombin which activates fibrinogen
-Extrinsic is activated by damage to the BV allwing FVII to be exposed to TF causing its activation -> FVIIa activates FX which activates prothrombin which activates fibrinogen