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25 Cards in this Set

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arterial thrombosis most frequently caused by
vascular dz (atherosclerosis)
Lupus Anticoagulants (LA)
paradoxically prolong IN VITRO coagulation tests while producting a risk for thrombophilia IN VIVO
mech of DIC
secondary mechanism of dz that results in intravascular generation of thrombin and plasmin that exceed their natural inhibitors
acquired/genetic risk factors assoc w/arterial atherosclerosis
1. hyperhomocysteinemia
2. HIT
3. lupus anticoagulants
pathogenesis of arterial thrombosis
1. arterial atheosclerosis (like vessel wall abnormality)
2. platelet activation
(like hypercoagulability)
3. rheology of blood flow (shear stress)
(like venous stasis)
what is the final event in MI
thrombosis
what genes cause VTE?
VTE is multicausal and multigenetic
Virchow's Triad
1. endothelial/vessel wall abnormality
2. venous stasis
3. intrinsic hypercoagulability of blood
what are examples of intrinsic hypercoagulability
-pregnancy
-anti-phospholipid Ab (lupus anticoagulant or anticardiolipin Ab)
-estrogen (oral contraceptives, hormone replacement therapy)
antiphospholipid AB syndrome
prsence of antiphospholipid antibodies (LAC or ACA)in assoc w/
a. arterial/venous thrombosis
b. recurrent fetal wastage
c. thrombocytopenia
what are examples of antiphospholipid antibodies?
lupus anticoagulants
lupus anticoagulants
-prolong the aPTT in an inhibitor pattern (mixing studies do not correct)
-neutralized by xs lipid (phospholipid) or platelets
Acquired risk factors for VTE
1. lupus anticoagulants/antiphospholipid Ab
2. HIT
3. DIC
4. TTP/HUS
5. Myeloproliferative/bone marrow D/O
6. nephrotic syndrome (hypercoagulability results from loss of natural anticoagulant proteins such as AT; assoc w/renal vein thrombosis)
ex of myeloproliferative/bone marrow D/O
1.polycythemia vera
2.essential thrombocytopenia
3.Paroxysmal nocturnal hemoglobinuria
paroxysmal nocturnal hemoglobinuria
stem cell D/O w/complement-dependent destruction of RBC's assoc w/increased risk of DVT
inherited risk factors for VTE
1. AT deficiency
2. Protein C deficiency
3. Protein S deficiency
4. Factor V Leiden
5. Prothrombin 20210A
Factor V Leiden
MC inherited risk factor for VTE;
point mutation (arg 506) eliminates protein C cleavage site in Factor 5A-->resistnace to Activated protein C-->Protein C can't terminate coag
Risk factors for VTE that can be genetic or acquired
1. Hyperhomocysteinemia (homozygous cystathionine synthetase deficiency)
2. elevated Factor 8 levels (assoc w/inflammatory states)
3. dysfibrinogenemias
complications of VTE
1. post-phlebitic syndrome
2. pulmonary insufficiency/embolus
anticoagulants
Hirudin
Argatroban
mechanism of HIT
heparin generates Ab that recognizes platelet factor 4PF4-heparin complex-->Fc dependent platelet activation and destruction
Tx for HIT
-stop heparin Tx and instead use hirudin and argotroban
pathogenesis of TTP/HUS
endothelial injury triggers the diffuse deposition of platetlet and fibrin
-->fragmentation of RBC's
Myeloproliferative/BM
1.polycythemia
2.essential thrombocytopenia
3.paroxysmal nocturnal hemoglobinuria
what constitutes severe HIT?
severe is greater than 50% reduction in platelet counts, usually "late" (5-14 days)