Test 2 Flashcards
hemostasis definition
the process of coagulation and lysis of clots in the body
four processes of hemostasis
- narrowing of blood vessels
- platelet activity
- activation of coagulation factors via intrinsic and extrinsic pathways
- fibrinolysis
excessive hemorrhage caused by
- delays in clot formation
- premature clot lysis
excessive thrombosis caused by
- inappropriate clot activation
- localization of the blood coagulation process
hyperreactivity of platelets leads to
arterial thrombosis
accelerated activity of the clotting system leads to
venous thrombosis
impaired coagulation caused by
- thrombocytopenia
- acquired coagulation disorders
- inherited factor deficiencies
activation of platelets steps
- adhesion
- aggregation
- fibrin formation
- clot retraction
platelet count panic values
<20
>1000
causes of thrombocytopenia
- decreased platelet production
- increased platelet destruction or consumption
- increased splenic sequestration
heparin induced thrombocytopenia (HIT)
- life threatening complication of exposure to heparin
- causes platelet activation that causes platelet consumption
- thrombosis risk is higher than bleeding risk
EDTA sensitivity (pseudothrombocytopenia)
- erroneous low platelet counts due to micro clumping of platelets in spite of anticoagulant in tube
- low platelet count without history of thrombocytopenia or bleeding episode*
- redraw specimen in tube with different anticoagulant
causes of thrombocytosis (high platelets)
- essential thrombocythemia (bone marrow over produces)
- reactive thrombocytosis
bleeding time
- measures the primary stage of hemostasis
- interaction of the platelet with the blood vessel wall and formation of hemostatic plug
platelet function analysis
-measures the time to form a platelet/RBC thrombus
platelet aggregation study
- gold standard for testing platelet response*
- measures if platelets aggregate, adhere, or release their granules
von Willebrands Type 1
- most common
- missing some VWF
- mild symptoms
von Willebrands Type 2
- defective VWF
- mild symptoms
von willebrands type 3
- limited or no VWF
- severe symptoms
von willebrand factor role
- VWF helps adhere platelets to exposed collagen in vessel walls
- VWF protects factor 8 from degradation by proteins C and S
von willebrands labs
- platelets = normal
- PTT = normal or increased
- VWF antigen = decreased
- factor 8 antigen = decreased
idiopathic thrombocytopenia purpura (ITP)
- unknown cause but usually follows viral illness in children
- platelets become bound to antibodies
ITP labs
- platelets = decreased
- bleeding time = increased
- PT/PTT = normal
ITP treatment
- splenectomy
- platelet transfusion for super low counts
thrombolytic thrombocytopenia purpura (TTP)
-small blood clots form throughout the body consuming large numbers of platelets
TTP pentad
- consumptive thrombocytopenia
- microangiopathic hemolytic anemia
- neurological
- fever
- renal dysfunction
TTP Labs
- platelets = decreased
- Hb = <10
- PT/PTT = normal
hemolytic uremic syndrome (HUS)
- rare disorder
- can occur with E. coli infection
HUS triad
- microangiopathic hemolytic anemia
- thrombocytopenia
- acute renal failure
HUS labs
- platelets = decreased
- PT, PTT = normal
- BUN/creatinine = elevated
HELLP
- Hemolysis
- Elevated Liver enzymes
- Low Platelet
- seen during pregnancy or within 48 hours post partum
HELLP labs
- platelets = lows
- microangiopathic blood smear
- PT, PTT = normal
- bilirubin/AST = elevated
extrinsic pathway factor
3, 7
intrinsic pathway factor
12, 11, 9, 8
thrombin time (TT)
- measures time needed for plasma to clot when thrombin is added
- can detect DIC
TT clinical implications
- increased = clots faster
- decreased = clots slower
activated partial thromboplastin time (PTT)
- screens for clotting disorders with deficiencies in the intrinsic pathway
- used to monitor unfractionated heparin therapy
heparin
- produces immediate anticoagulant effect by enhancing antithrombin
- neutralized by protamine in case of overdose
prothrombin time (PT)
- measure potential defect in extrinsic pathway
- dependent on vitamin K intake and absorption
- PV INR>3.6
- used to manage coumadin therapy
vitamin K dependent factors
- 2 (prothrombin)
- 7
- 4
- 10
- protein C & S
vitamin K deficiency causes
- drug therapy (coumadin, antibiotics)
- disease (malabsorption, biliary obstruction, malnutrition)
coumadin
- delays vitamin K formation interfering with dependent factors
- takes 48-72 hours to cause measurable change in PT/INR
protein C
- prevents thrombosis and enhances fibrinolysis
- inactivates factor 5 and 8
- protein C should be checked in conjunction with protein S
protein S
-enhances activities of protein C
antithrombin
-inhibits factor 10
factor V Leiden
- most common cause of hereditary hypercoagulopathy
- resistant to inactivation by protein C
DIC
-continuous generation of thrombin causes depletion of coagulation factors and platelets resulting in uncontrolled bleeding
DIC treatment
heparin
-blocks thrombin which blocks coagulation factor consumption