Thrombopilia/Hypercoag States Flashcards
most important part of virchow’s traid for arteries
vessel injury
Virchow’s Triad
blood vessel wall damage
altered blood flow( stasis)
altered blood composition (hypercoag)
most important part of virchow’s tria for veins
stasis, hypercoag
treatment of hyperhomocysteinemia
vitamins will bring down homocysteine levels but not decrease the risk of thrombosus
4 types of antiphospholipid antibody diseases
lupus anticoagulant
anti bII/Gp1
anti-prothrombin
anti-cardiolipin
how does lupus anticoagulant work
prevents binding of prothrombinase complex to phospholipid surface
lab studies
prolongs PTT and sometimes (but not commonly) PT
effects of lupus anticoagulant
in vitro- prolongs clotting time
in vivo- triggers thrombosis (by unknown mech in both arterial and venous)
activated protein C resistance
due to g–>a in factor 5 which renders factor 5a resistant to inactivation by activated protein C
ways to acquire APCR
pregnancy cancer thalidomide uses in multiple myeloma oral contraceptives lupus anticoagulants
Factor V Leiden
heterozygotes 5-8% caucasians, asymptomatic in majority, mild risk factor for venous thrombosus, homozygotes have a much higher risk
where does factor V affect?
venous circulation, little to no risk for arterial circulation
prothrombin G20210A
G–>A point mutation in 3’ untranslated region of prothrombin gene
same manifestation as factor V leiden
hereditary protein c deficiency genetics
autosomal dominant
homos lethal in utero
venous not arterial thrombosis
job of protein C
with cofactor protein S, inactivates factors V and VIII
lab tests for protein C deficiency
screen activity level–>if low screen for antigen–>if low, type 1, if normal, type 2
how is protein S different from protein C?
longer half life
protein S deficiency genetics
normally lethal as homozygous- autosomal dominant
Type 1 Protein S deficiency
functional activity low
free antigen low
total antigen low
type II protein S deficiency
functional activity low
free antigen normal
total antigen normal
type III protein S deficiency
functional activity low
free antigen low
total antigen normal
hereditary antithrombin def genetics
autosomal dom
homos die
when does antithrombin deficiency present
usually before agre 50, typically <35
why is antithrombin deficiency different?
more severe than thrombophilia
why does factor V leiden persist in population
higher sperm count in males, less bleeding in childbirth–>gene persists
