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Flashcards in Platelets and Coagulopathy Deck (41)
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4 components of haemostasis?

- endothelium
- platlets
- coagulation factos
- fibrinolytic factors


What are endothelial cells? What action do they have ?

- flattened cells lining blood vessels
- pro and anticoagulant properties
- normally anticoagulant - inhibit coagulation and platelet aggregation
- act as barrier to subendothelial collagen which is procoagulant


What is vWF produced by? Function?

- endothelial cells and platelets
- stored in Weibel Palade bodies
- Released early in haemostatic process
- responsible for platelet adhesion to collagen


Which reticular lines have the shortest half life? CLinical impliations?

- Neutrophils 6hrs
- Platelets ~1week
- RBC ~120d
> if BM affected, neutrophil numbers will be affected first, then platelets, then anaemia


What are platelets?

- small, discoid, ANUCLEAR cells
- megalokaryocyte (precursor in BM) breaks off to form platelets = thrombopoiesis
- mediated by thrombopoietin
- 3-5um pale basophilic with small red granules
- circulate for 5-9d most species


With generalised BM destruction what will be lost first?

- Neutrophils 6hrs t1/2


What is present on the outer membrane of platleets?

- receptors for ahesion and aggregation
> glycoproteins
- GP1b binds vWF
- GP IIbIIIa binds fibrinogen on adjacent platelets allwing aggregaion
* defects in receptors -> abnormal platelet function and clot formation*


What is contained within the platelets?

- cytoskeleton (actin and myosin allows for shape change)
- membrane bound granules
> alpha granules (red) - contain vWF, finbrinogen and factors V and VIII
> dense granules - contain ADP and calcium


What is primary hemostasis? 2*? What follows these?

1* = formation of 1* platlet plug
2* = activation of coagulation cascade and generation of insoluble fibrin which sabilises platlet plug
> Fibrinolysis - breakdown of fibrin and platelet plug


Outline steps of 1* haemosasis.

- damage endothelium exposes subendohelial collagen
- vWF released from damaged endothelium
- platelet adhesion occours
- platelets bind to collagen via receptor GPib and vWF from the endothelium
- once platelets adhered to collagen, undergo shape change and become spherical with filipodia
- additional receptors for vWF (GPIb) and fibrinogen (GPIIbIIIa) exposed


How does platelet aggregation occour?

- platelets bind fibrinogen via GPIIbIIIa
- fibrinogen generated from coagulation cascade
- released from platelets and found in plasma


What do platelets secrete?

- aggregating platelets degranulate
- ADP, fibrinogen, vWF
- TXA2 also released from platelet membrane
> increase platelet adhesion and aggregation
- also release factors V and VIII -> coagulation


What happens to the whole blood vessel whe damaged?

- vasoconstriction to v blood pressure and blood flow past the area


2* haemostasis

- involves activation of the coagulation cascade
- happens simultaneously with formation of platelet plug
- damage to endothelium releases tissue factor activating EXTRINSIC clotting pathway


What is the first and most important coagulation factors?

Tissue factor


What is the end point of the coagulation cascape?

- activate thrombin tha causes fibrinogen -> fibrin


What are coagulation factors?

- soluble enzymes (serine proteases) found in circulation
- each step of coagulation cascade converts one of these factors from inactive state (proenzyme) to its active state
- each step amplifies system
- > insoluble fibrin aim
- fibrin stablises 1* platelet plug


Do the intrinsic, extrinsic and common pathways exist in vivo?

no only in vitro


What is the intrsinc and extrinsic link -> common apthway factor?

factor 10 -> 10a


What is extrinsic system also known as? What does it do?

= Initiation
- most important in vivo
- tissue factor (TF) released from damaged tissue binds to and activates FVII in presence of calcium
- TF-FVII complex activates FX of common pathway and FIX of intrinsic pathway


What is he intrinsic pathway?

= Amplification pathway
- FXII activated by contat with negatively charged surface (cofactor HMWK)
- activated FXII cleaves and activates FXI which in turn activates FIX(calcium required)
- activated FIX activates FX of common pathway (calcium required)


Outline common pathway

- activation of factor X
- activated FX binds activated FV and calcium on platelet surface
- this converts prothrombin (FII) to thrombin (FIIa)
- thrombin converts fibrinogen (FI) to fibrin (FIa)
- fibrin crosslinked by activated FXIII


What are inhibitors of coagulation?

> antithrombin III
- inhibits thrombin and activated FX
- activity increased by heparin from endothelium
- protein C inactivates factors V and VIII
> fibrinolysis


Outline fibrinolysis

- enzymatic breakdown of fibrin by plasmin
- plasmin from plasminogen found in the platelet membrane and plasma
- plasmin degrades fibrinogen and fibrin to produce fibrin degradation products (FDPs)


What is coagulation?

2* haemostasis


How can platelets be evaluated in the lab?

> platelet conc (automated counts on EDTA)
- good accuracy for all species except cat, sheep and goat d/t overlap between RBC and platelet size
- platelet clumps can affect accuracy of counts d/t uneven distribution and overlap of size of clumps and RBCs
* very common in cats!!*


Which species must have a platelet count carried out from blood smear?

- cats
- CKC spaniels, often thrombocytopenic with giant platelets which may be counted as RBCs


What is thrombocytopenia? At what level may spontaneous haemorrhage occour?


What is thrombocytosis? Clinical relevance?

> 1000x10^9/L
^ risk thrombotic activity


What practical way can clotting times be evaluated?

> Buccal mucosal bleeding time (minutes)
- 1* haemostasis (evaluates platelet FUNCTION more than number and doesn't look at coagulation [2* clotting])
- spring loaded cassette