Coag U4 - Thrombotic Disorders Flashcards
thrombosis
inappropriate formation of a PLT or fibrin clot that obstructs a blood vessel
ischemia
loss of blood supply
necrosis
tissue death
thrombophilia
AKA hypercoagulability, predisposition to
thrombosis secondary to a condition
emboli
fragments of thrombi that move through the circulatory system and lodge in vasculature
pulmonary emboli (PE)
emboli that move through the heart and lodge in the arterial pulmonary vasculature
venous thromboembolism
prevalent in African Americans and women of childbearing age
symptoms of localized pain, sensation of heat, redness, edema
what are some examples of venous thrombosis?
PE and DVT
arterial thrombosis
activated PLTs, monocytes, and macrophages
embed fatty plaque within endothelial lining, suppress normal release of antithrombotic molecules (ex. NO, tissue factor) →
atherosclerotic plaque →
plaques rupture →
occlude arteries and trigger thrombotic events
what are some examples of arterial thrombosis?
MI and stroke
risk factors for thrombosis
age, immobilization, diet, pregnancy, smoking, inflammation, oral contraceptive use, hip/knee/prostate surgery
lupus anticoagulant
antiphospholipid antibody, the patient would clot which prolongs the result of PTT and therefore is more at risk for thrombosis
LAC testing
PTT – prolonged
mixing study – shortens prolonged PTT
DRVVT – ratio > 1.2
silica-based PTT – ratio < 1.2, difference of 8 seconds >
what are the 3 antiphospholipid antibodies?
LACs
ACL antibodies
anti-B2-GPI antibodies
APC resistance
factor V Leiden (R506Q) mutation gain of function renders factor V resistant to APC
prothrombin G20210A
mutation in prothrombin gene untranslated 3′ promoter region
moderate prothrombin activity elevation
factor V leiden (FVL)
a mutation in the factor V gene
substitutes glutamine for arginine at position 506 of the factor V molecule (FV R506Q)
what happens in FVL?
arginine substitution slows or resists APC hydrolysis
resistant factor Va remains active and raises production of thrombin, leading to thrombosis
AT deficiency
enhanced by heparin, inhibits serine proteases IIa, IXa, Xa, and XIa
PC deficiency
a serine protease that hydrolyzes factors Va and
VIIIa, requires protein S as a stabilizing cofactor
PS deficiency
a stabilizing cofactor for activated protein C, 40% free, 60% circulates bound to C4bBP
lipoprotein (a)
low-density lipoprotein that may predict
arterial thrombosis, contributes to thrombosis with antifibrinolytic property
CRP
calcium-dependent pentameric ligand-binding member of pentraxin family
made in the liver
chronic CRP concentrations of 1.5 mg/L or greater =
atherosclerosis, low-grade inflammation → increased risk of MI or stroke
FBG
increased fibrinogen = increased thrombosis
