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33 Cards in this Set
- Front
- Back
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Fibrinolytic substance naturally released from endothelium?
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tissue plasminogen activator (tPA)
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Substance that binds and down-regulates thombin?
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Thrombomodulin
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Normal properties of endothelium that prevent thrombi from forming (4)?
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1) Antiplatelet agonist proteins - prostacyclins, NO, ATPase
2)Heparin-like molecules 3)Thrombomodulin - actuas on the acdtivated protein C system (APC) 4)tPA - fibrinolytic that cleaves the clot |
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Virchow's Triad for developing thrombi (DVT)?
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1)Stasis of blood
2)Vascular injury 3)Hypercoaguable state |
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States of hypercoagulability?
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1)Pregnancy
2)Obesity 3)Immobilization 4)Advanced age 5)Drugs such as oral contraceptives 6)Trauma 7)Heaprin induced thrombocytopenia (HIT) With excdeption of HIT, THERE ARE NO TESTS TO DEMONSTRATE THE HYPERCOAGULABLE CONDITION |
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Initiation of the clotting cascade?
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Vacular wall injury exposing Fibroblast (FB) & Tissue factor (TF)
TF pairs with Factor VIIa to start cascade TF Pathway Inhibitior quickly gets rid of the complex of TF and VIIa |
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What does Antithrombin bind to to control/prevent thombosis?
What is the anticoagulant that binds to antithrombin? |
Antithrombin binds factor Xa and Thrombin
Antithrombin doesnt make the pt anticoagulated but it's absence makes pt's pro-coagulative Heparin |
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T/F Pure or complete antithromin deficiency is incompatible with life?
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T
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Activated protein C (APC) acts on what?
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Factor VIII and V
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When to suspect problems with clotting?
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1)Venous thrombosis at a young age (<45-50 YO)
2)Spontaneous/unexplained thrombosis 3)Recurrent episodes of thrombosis 4)Thrombosis @ unusual sites (axillary vein) |
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Venous thrombosis mostly related to ____ deposition
Arterial thrombi (MI, stroke) mostly related to _____ |
venous = fibrin deposition
arterial = platelets; this is why aspirin used to treat arterial thrombi |
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T/F Many people with congenital risk factors present in their 60s
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T
Just b/c someone is older doesnt mean they cant have a congenital risk factor |
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2 Clinical presentations for the inherited coagulopathies are?
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1)Neonatal Purpura Fulminans - homozygous deficiency of proteins C and S
2)Warfarin Skin Necrosis - v Factors II, VII, IX, X, protein C & S |
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What is the reason that pt initially put on Warfarin therapy becomes hypercoagulable at first?
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Protein C (major anticoagulant) v b/f the cloting factors b/c it has a shorter half-life
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One leg larger than other with heat, redness and pain?
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Classic appearance of DVT
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MC inherited coagulation risk factor is? Mechanism?
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Factor V Leiden
one amino acid SUBSTITUTION Prevents prote`in C from inactivating factor V, leaving active factor V and thus generating more thrombin (AA 506 resists inactivation by APC) Recall Factor V works with factor X to cleave prothrombin into thrombin (=more fibrin) Test using screening test called "activated protein C resistance test" |
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2nd MC inherited coagulation risk factor in US Caucasians ? Mechanism?
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Prothrombin 20210
Amino Acid base pair SUBSTITUTION Does NOT have a screening or genetic test (have to do PCR) |
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Risk for developeing thrombis for Factor V Leiden (hetero & homo)?
Prothrombin 20210? |
Factor V Leiden hetero = 3x normal
Factor V Leiden homo = 18x normal Prothrombin 20210 = 2-5x normal |
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What is the worst deficieny (compatible with life) in terms of causing a thrombis?
What are the chances of developing thrombis? |
Heterozygous state of ANTITHROMBIN deficiency (remember homo is not compatible with life)
60% by 60 years of age |
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How does thrombophilia (hypercoagulability) naturally increase
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AGE (risk ^ from age 20-60)
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T/F Most people who develop thrombi have only one big risk factor
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F, each individual risk factor is weak, it is the combination of factors that is problematic
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Lowering youru stress level = lowering what thrombosis risk factor?
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Factor VIII
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When can you not test for elevated Factor VIII?
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in the HOSPITAL SETTING (STRESS)
Must test on outpatient basis |
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Activated protein C & S works by?
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Blocking Factor Va (used for Factor Xa -> Prothrombin) & VIIIa (used for Prothrombin -> Thrombin)
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Causes of more consumption of Protein C & S?
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Surgery & DIC
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Causes of less production of Protein C & S?
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Liver disease & vitamin K deficiency (Warfarin)
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One of the MC acquired hypercoagulability states is called? Name the two different Ab's?
Diagnose syndrome by? |
Antiphospholipid syndrome (APLS)
1)Lupus Anticoagulant (*no specific test*) 2)Anticardiolipin antibodies (*more specific test*) Diagnose APLS by manifestations in one or both of above Ab tests for 12 WEEKS if thrombus occurs, then chance of reoccurence is 11% MUST BE ON LIFE LONG COUMADIN |
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Lupus Anticoagulant works by?
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using igG autoantibodys that bind to protein phospholipid comlexes in plasma, delaying the clotting time -> predisposing to thrombosis
Misleading name because it is neither limited to people with lupus nor does it cause bleeding (it causes thrombosis) |
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Only acquired hypercoagulability risk factor that may be treated?
Treated using what? |
Hyperhomocysteinemia
Vit B12, folate (B9), & B6 |
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T/F Hyperhomocsteinemia and APLS are two things that cause BOTH venous AND arterial thrombosis
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T
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Condition where patient should NOT be tested for lupus or anti-thrombin measures?
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when on Heparin (binds to antithrombin)
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Only tests that can be interpreted when patients are on haprin/warfarin/spontaneous thrombosis?
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Activated Protien C Resistance, anticardiolipin antibodies, Lupus anticoagulant, Prothrombin 20210 mutation
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A person with a recent thrombosis may have what abnormalities (3)?
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1) Consumes antithrombin & protein C/S
2) ^ Factor VIII 3) ^ homocysteine |
