Haemostasis and coagulation Flashcards
Haemostasis
mechanism of forming a clot
thrombosis is pathological
clotting mechanisms
intrinsic: exposed collagen from injured blood vessel wall (test tube has anti-coagulants for when taking bloods
extrinsic: damaged tissue release thromboplastin
the amplification cascade
inactive X-> acitve X (thromboplastin, clotting factors (foreign surface))
prothrombin-> thrombin-> XIII (active X)
fibrinogen-> fibrin (thrombin) -> stable fibrin (XIII)
Fibrinogen can be used as
CV risk factor
smokers have it raised
pregnancy raised to reduce blood loss during birth
Platelets
non- nuclear cellular fragments
platelet adhesion
adheres to subendothelial surface on damage/ disease due to binding to von willebrand’s factor (a protein)
inactive factor X is a
serine protease
factor X is a
serine
adhesion causes a release of…
ADP signalling and thromboxane (signalling) promote aggregation
5-HT: vasoconstrictor NT
what happens when ADP receptors are activated
glycoprotein IIb-IIa expressed by platelets- enables crosslinking by vWF and fibrinogen-> mesh
clot consists of…
coagulated platelet factors and platelets
platelet plug promotes
coagulation reaction: -ve phospholipids or activated platelets adhered localise fibrin formation
Bleeding time
incisions to forearm with venous cuff
increased in platelet dysfunction and thrombocytopenia
Prothrombin time
INR
ttime for coagulation following addition of thromboplastin
see how long to use up
prolonged in abnormality of factors, liver disease and warfarin
liver disease (produces coagulation)
activated partial thromboplastin time (APTT)
examines intrinsic pathway, altered in changes of factors
when do you use INR
when prescribing warfarin
(healthy is 1)
maybe goes to 2,3
Thrombosis
unwanted blood clots
atherosclerosis
- Atherosclerosis arteries lined with cholesterol deposits
- Foam cells form beneath endothelium (cholesterol, macrophage) forms fatty streak- gets calcified- atheroma (narrowing artery)- plaque- when ruptures stimulate anti-inflammatory response- platelets form (clot in coronary artery- heart attack, cardiac muscle dies- VF) long term- develop heart failure
- Risk factors accelerate (male- being a female oestrogen tends to protect CV system, smoking, age) high bp- damages endothelium
AF
pacemakers around heart set up, random events to ventricles- irregular increase in hr
risk of clots in atria, if in LA-> thromboembolic stroke
risk of TIA- clot from heart to brain- resolves in 24hr
Rx: anticoagulant
Haemophilia
genetic- X chromosome
low or lacking factor VIII of clotting cascade
haemorrhage and prolonged bleeding
treat with factor VIII blood donors
or analogue of vasopressin (ADH) sprayed up nose increases VIII release
haemophilia B (Christmas disease)
deficiency factor IX- treated with prophylactic factor IX
Von Williebrand’s disease
hereditary lack or defect of vWF
impaired platelet reaction
increased bruising, nose bleeds, mucosal bleeding
Rx: vasopressin analogue, factor VIII or vWF
Liver disease
reduced synth of clotting time
thrombocytopenia
causes
reduced platelet number spontaneous skin bleeding- purpura idiopathic viral drug induced bruising toxins
Rx: drug induced- stop and treat with steroids to suppress IR
if unresponsive then splenectomy (spleen is site of platelet degradation)
