haemostasis Flashcards
describe the actions of haemostasis after an artery is severed
- artery contracts and pressure decreases downstream
- primary haemostat plug forms out of platelets= v fragile and temporary (1min)
- secondary haemostat plug forms and firkin stabilises it (30 mins)
components that platelets are activated by
collagen surfaces
ADP (released by platelets and damaged RBC)
thromboxane (aggregates platelets)
thrombin (informs which clotting factors are activated)
action of platelets once activated
- stick to vWF on endothelial membrane
- aggregate other platelets to form a plug and bound by fibrinogen to form secondary plug
- change shape to stick spiny spheres
- factors excreted which aid growth of platelet plug e.g ADP or thomboxne
action of aspirin
it irreversibly acetylates an enzyme of prostogladin synthesis meaning platelets can’t produce thromboxane reducing coagulation
what does the intrinsic pathway of the clotting cascade involve
triggered by damaged blood vessel. contained in the blood. involves factors I, II, IX, X, XI, and XII
what des extrinsic pathway involve
trauma to extravascular cells. triggered by thromboplastin outside blood. involves factors I, II, VII, and X
learn clotting cascade
:)
cofactors needed by the clotting cascade
ca2+ and phospholipids act as cofactors for enzymes in these reaction
ALSO vit k required for synthesis of protein S and C (anticoagulants)
role of vascular wall in coagulation
contracts when vessel damage sub endothelium traps platelets also balances coagulation by secreting protein C= anticoagulant plasminogen activator = fibrinolysis vWF= clotting
factors opposing clot
antithrombin III
protein C
protein S
also oppose it by dilution of clotting factors
if missing any of these leads to thrombosis
describe clot retraction
platelets die = cling to fibrin and pull on actin and myosin filaments together.
describe fibrinolysis
- plasminogen (inactive precursor circulating blood made in liver) is activated by tea (tissue plasminogen activator)
= PLASMIN - plasmin is an enzyme used by macrophages to break down fibrin
- increase in FDP (breakdown product of fibrin which is found very high in thrombosis
- eventually clot is replaced by granulation tissue and leaves a scar
how is fibrinolysis activated
activated by clotting cascade. fibrin increases activity of plasminogen activators. fibrinolytic activity drops after surgery increasing risk of DVT
what are streptokinase and urokinase and side effects
streptokinase (from streptococcus) and urokinase (from urea) are also plasminogen activators.
side effects of these drugs = bleeding e.g nose bleeds.
used to break down clots
what is haemophilia and effects
have platelets but lack clotting factors so can’t produce fibrin
easy bruising, haemorrhage after surgery and trauma.
may develop harm-arthritis from minor injuries
petechiae is also seen
what is haemophilia A
factor VIII deficiency - X linked and therefore affects males. treated by infusion of engineered factor VIII
what is haemophilia B
reduction in factor IX = prolonged APTT. treated by infusion of engineered factor IX
what is vonwillerbrands disease
reduced FVIII- leads to bleeding e.g nose bleeds, bruising,prlonged bleeding after trauma.
skin and mucosal associated bleeding - gums, bruising and epistaxis
what is DIC
disseminated intravascular coagluation - activator of clotting which gets into blood forming clots. no disease in itself always occurs as a complication e.g sepsis or trauma
treatment of DIC
treat underlying cause of DIC
if lots of bleeding because factors/ platelets have been consumed require transfusion
sometimes anticoagulant e.g herapin is needed
causes of DIC
gangrene, renal failure, respiratory distress, haemorrhage
signs of DIC
increased FDP’s e.g Ddimers in the blood as the fibrinolytic system is activated and damage to RBC as the move past thrombi
screening tests
PT- measure extrinsic pathway (time to make prothrombin)
APPT- measures intrinsic common pathway - time to make partial thromboplastin
thrombin time
fibrinogen
