Coagulation and Thrombosis Oct16 M3 Flashcards
normal hemostasis def
blood clot formation to limit bleeding
thrombosis def
patho counterpart to hemostasis (blood clots in intact vessels)
3 elements controlling hemostasis and thrombosis
endothelial cells and vascular wall
platelets
coagulation cascade
4 steps of hemostasis
- arteriolar vasconstriction
- primary hemostasis (initial platelet plug)
- secondary hemostasis (stabilization of platelet plug)
- fibrinolysis and dissolution
vascular injury: endothelial cells release what
- endothelin: vasoconstriction
- procoagulative factors
way vessels constrict other than endothelin
neurogenic mechanism (SM reflex)
primary hemostasis: main component and 2 roles
platelets
- seal defects
- recruit and activate coagulation factors
3 steps of primary hemostasis
platetet adhesion, platelet activation, platetet aggregation
how platelet adhesion occurs
platelet bind to collagen by binding to vWF with receptor glycoprotein 1b
how vWF got on collagen and what collagen
collagen of ECM made available after endothelial cell injury. vWF bound to it
platelet activation def
platelets undergo irreversible shape change and secrete granules with calcium and Thromboxane A2
what calcium and thromboxane A2 secreted by platelets do
calcium is a cofactor for several coagulation factors
TxA2 activates other platelets
platelet aggregation def
binding to fibrinogen of nearby platelets with a R
normally synthesized anti-coagulation factors (by normal endothelium)
Prostaglandin PGI2 and NO
aspirin mode of action
inhibits COX 2, enzyme required to produce TxA2 and PG
secondary hemostasis def
coagulation cascade leading to stabilization of platelet plug
end result of coagulation cascade
activation of prothrombin into thrombin which cleaves fibrinogen into fibrin
fibrin roles (2)
- polymer to reinforce platelet plug
- activate more platelets
coagulation cascade def
successive series of enzymatic reactions where pro enzymes cleaved into enzymes
lab tests used to screen for coagulation disorders
PT, PTT, INR (normalization of PT)
some factors required for coagulation cascade
phospholipids, calcium, vitamin K
fibrinolysis def
breaking down fibrin platelet plug
fibrinolysis trigger
plasminogen activators activate plasminogen into plasmin, plasmin breaks down fibrin
Virchow’s triad on what controls thrombosis
Endothelial injury, abnormal blood flow, hypercoagulability
how abnormal blood flow can lead to thrombosis
turbulence in high flow regions: zones of low flow
thromboembolus def
thrombus fragile and breaks from vascular structure to propagate
embolus
any substance carried by blood
2 main types of thrombi
arterial and venous
arterial thrombi charact
zones of arterial turbulence, atherosclerotic plaque
venous thrombi charact
zones of stasis
thrombus on microscope
lines of Zahn (rainbow)
venous thrombi consequence
congestion, edema, embolisation (especially if above knee joint)
arterial thrombi consequence
tissue infarction by obstruction
Disseminated intravascular coagulation def
widespread thrombosis in microcirculation
Factors that influence infarct development
rate of occlusion, collaterol blood supplies, tissue susceptibility to ischemia, blood oxygenation
how infarcts classified
(colour)
red, white
red infarct charact
hemorrhagic: venous occlusion, when flow established after infarction, 2 circulations
white infarct charact
anemic infarct. (arterial occlusions in organs with end arterial circulation: heart, spleen, kidney)
lung what type of infarct and why
red bc 2 circulations
PE: cause in most cases
thrombi in large deep veins of the leg
how PE can be deadly
if blocks large pulmonary arteries
consequences of PE on pulm circulation
pulmonary hypertension, RHF, cor pulmonale, ischemia to downstream parenchyma
