Coag issues Flashcards
what is von willebrand dis
- auto dom cauing lack of VWF
- most common bleeding disorder
- vWF enhances platelet agg and adhesion
3 main clinical feat
- cut and mucosal bleeds
- mennorhagia
- GI bleeds
Dx findings
prolonged bleed times, normal platelets PTT may be up
Tx of VWD
- DDVAP - causes endothelial excretion of VWF
- factor 7 concentrates
- avoid aspirin/NSAIDS
what is hemophlia A
X linked
- def. in factor 8
- amount of bleed depends on how much factor
5 features of hemo A
- hemarthrosis
- knees most common
- can cause destruciton - intracranial bleeds
- intramuscular hematoma
- retroperitoneal hematoma
- hematuria or hematospermia
Dx of hemo A
- long PTT
2. low factor 8 levels
what does PT (INR) and PTT measure
PT and INR - extrinsic and common
PTT - intrinsic and common
Tx of hemo A
- arthrosis
- analgesia
- immobilize - clotting factor replacement
- factor replacement
- not FFP and cryoprecipitate - DDVAP can help
what is hemo B
X linked
- loss of factor 9
otherwise the same as A
what is DIC
abnormal activation of caog leading to microthrombi throughout the system
- comsumes platelets, fibrin, and coag factors
- fibrinolytic mech are activated so get bleeding and thrombosis at same time
causes of DIC
- infections
- most common, esp gr neg sepsis - obstetric complications
- major tissue injury
- malig. - lung, pancreas, prostate, GI, myelocytic leukemia
- shock
clin features of DIC
- bleeding tendency
- espcialyl when acute - thrombosis
- can get infarcts
Dx of DIC
increased - PT, PTT, INR, bleed times, D-dimer
decreased - platelets, fibrinogen
Tx of DIC
manage issue causing
support
- FFP
- platelet transfusions
what is coagulopathy of liver disease
- clotting factors made by liver
- must be severe disease
feat. of coagulopathy of liver disease
- long bleeds
2. prolinger PTT and INR
Tx of liver
- FFP
- vit K
- platelet tranfusion
7 inherited hypercoaguable states
- antithrombin def.
- antiphosphlipd antibody syndrome
- protein C def. (inhibs facotr 5 and 7)
- proteint S def
- factor 5 leiden
- protein C can’t inactivate 5 - prothrombin gene mutation
- hyperhomocystenemia
MOA of heparin
potentiates the action of antithrombin to inhibit clotting factors 2a and 10a
- longer INR
- half life of 1 hour
MOA of LMWH
inhibit 10a
- can’t be meaured by PT or INR
- easier than heparin
- SC and less SE
MOA of warfarin
vit K antagonist
- loses 10, 9, 7, 2 and C and S
