hemostasis Flashcards
3 key components of normal hemostasis
vascular endothelium
platelets
clotting factors
define normal hemostasis
physiologic process by which blood vessel lining cells, platelets, and coagulation factors in blood work together to stop bleeding
define coagulation
process by which liquid blood converted to solid clot.
3 requirements for optimal function of normal hemostasis
- normal blood tempp
- normal pH
- normal calcium concentration.
process of primary hemostasis
- exposed subendothelial cells. vWF sees and spreads like glue . vWF adheres and sticks to platelet via gp1b. = platellet adhesion
- platelet secretion -platelet secretes contents to attract more platelets
- platelet aggregation - via gp2b3a platelet binds fibrinogen to form blood clot
lab eval of primary hemostasis
platelets: number, size morphology, special platelet function tests, medication history
vWF = factor level & fxn
secondary hemostasis.
extrinsic 7–> 10 -> 5 -> 2 ->1
intrinsic 12 -> 11 -> 9_>(cofacotr 8) -> 10 -> 5 -> 2-> 1
after 1 - crosslinked qith 13.
activation of factor 2 AKA thrombin = key. converts fibrinogen to fibrin = stable clot formed.
factor 7 - extrinsic factor. quickly turns off pathway after beginning activation.
thrombin activates facotrs 11, 8, 5, in pathway. so factor 12 isnt really necessary for coagulation.
lab eval of secondary hemostasis
PTT = assess intrinsic pathway - activate factor 12 in lab.
PT = measure extrinsic pathway
converted to INR - international normalization ratio.
detecting clot formation in vivo = optical density, electromechanical.
define fibrinolysis
normal process that breaks down/lyses clot away in time.
plasminogen – activated to plasmin breaks down fibrin.
lab evaluation
test fibrinogen, d-dimers, other special tests
bleeding disorders
acquired or hereditray.
acquired more frequent.
categories? platelet, VWF, factor deficiencies
cause of acquired: meds, alcohol ,liver/kidney failure,
hereditary - primary hemostasis defect
cause
clinical presentation
causes: VWF disease; platelet dysfunction
clincial presentation: muco-cutaneous bleeding: nose bleeds, heavy periods.
secondary hemostasis defects
cause
clinical presentation
cause: low coagulation factors
x-linked - hemophilia A (deficient factor 8)
hemophilia B - deficient factor 9.
autosomal recessive - hemophilia C.
clinical presentation: deep tissue hematoma - bleeding in joints/muscles.
vWF disease
low or abnormal
autosomal dominant.
most common hereditary disorder.
presents: muco-cutanesous. usually mild or asymptomatic
hereditary platelet disorders
present w muco-cutaneous bleeding.
treatment = platelet transfusion.
- bernard-soulier: autosomal recessive, gp1b deficiency. no platelet adhesion. = severe bleeding
glanzmann’s thrombasthenia: autosomal recessive, gp2b3a deficiency. no platelet aggregation or binding to fibrinogen. = severe bleeding
platelet granule abnormalities/secretion defects = no granules to be secreted. cant recruit/activate other platelets to amplify platelet adhesion