Term
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Definition
o Venous Stasis – slowed rate of blood flow; through immobility or compression o Vascular Injury – involves damage to vasculature favoring deposition of platelets/fibrin o Hypercoagulability – blood components are in favor of thrombosis to begin with |
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Term
why do we give heparin initially when starting warfarin in protein S deficient px? |
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Definition
Factors VII and X wane with warfarin therapy. You have tipped in favor however of coagulation during the first bit, X is still active |
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Term
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Definition
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Term
Protein C Def - prev, congenital?, warfarin effects? |
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Definition
o Prevalence – present in 1 in 200-500 individuals, 2-9% of individuals w/ venous thrombosis o Vs. Acquired – many diseases lead to acquired Protein C deficiency, so be wary of Dx congen. o Homozygous deficiency – neonatal purpura fulminans o Warfarin (Coumadin) – will lower protein C levels, so can’t Dx when on these drugs Warfarin hypercoagulability – warfarin dec. protein C faster than coagulants initially! |
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Term
what lowers protein S levels and thus confounds diagnosis of PSD? |
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Definition
o Oral contraceptives, pregnancy |
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Term
what lowers ATIII levels and thus confounds diagnosis of ATIIIDef? |
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Definition
chronic heparin therapy, or acute thrombosis |
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Term
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Definition
o aPTT test – heparin won’t prolong, since ATIII isn’t really there! Often how Dx is made… |
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Term
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Definition
o Action – binds & inhibits thrombin & Xa, along with IXa, XIa, XIIa o Severity – much more severe than protein C/S deficiencies; causes very early thromboses (teen) |
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Term
Review the Lecture Chart! |
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Definition
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Term
Pro-Coagulant Thrombophilias: name 6 |
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Definition
Factor V leiden, prothrombin 20210 mutation, fibrinolysis abnormality, hyperhomocysteinemia, dysfibrinogens, excessive clotting factor |
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Term
Factor V Leiden - mech, prevalence, thrombosis risk, contraceptives, effect of blood types/weight! |
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Definition
mutation in Factor V leading to resistance to protein C hypercoagulability o Protein C Resistance – protein C can no longer deactivate mutated factor V o Prevalence – only Caucasians o Thrombosis – 7x increase in risk with heterozygous mutation o Oral contraceptives – will magnify thrombosis risk o Some people will not have problems…O blood type matters – gives you less risk! 3X vs. 25.2! + weight => more risk! Metabolic syndrome! |
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Term
prothrombin 20210 mut - mech, prevalence |
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Definition
excessive prothrombin synthesis o Thrombosis – also increased risk o Prevalence – also only in Caucasians (some SE Asians too, likely result of trade routes) |
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Term
• Fibrinolysis Abnormality mech |
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Definition
– decreased levels of plasminogen or elevated plasminogen inhibitor (PAI-1) |
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Term
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Definition
associated with premature atherosclerosis, venous thromboembolism o Oxidative damage – elevated levels of homocysteine lead to vascular damage thrombosis o CAD – greater risk of CAD due to accelerated atherosclerosis o Methylene Tetrahydrofolate Reductase – elevated MTHFR leads to elevated homocysteine |
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Term
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Definition
fibrinogens polymerize too easily, or which lack cleavage sites thombosis |
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Term
Excessive Clotting Factor |
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Definition
most commonly too much Factor VIII hypercoagulability |
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Term
Tx for thrombophilic disorders |
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Definition
anticoag, lytic therapy, embolectomy, stenting, protein C concentrates, antithrombin III concentrates |
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Term
arterial vs. venous thrombus |
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Definition
• Arterial Thrombosis – atherosclerotic plaques, a “white thrombus” o Elevated – lipoproteins, factor VII, homocysteine, platelets, GpIIbIIIa gain-of-function • Venous Thrombosis – a “red thrombus” |
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Term
Lipoprotein (a) - what is it?, structure and function, role of ICAM-1, associated with ____ in men |
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Definition
• Lp(a) – modified LDL, serum levels are genetically determined • Structure – homologous to plasminogen interfere w/ fibrinolysis and interacts with macrophages to promote foam cell formation and deposition of cholesterol • ICAM-1 – enhanced expression leading to recruitment and binding of monocytes to vessel wall • Levels – associated w/ cerebrovascular disease in men |
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