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33 Cards in this Set

  • Front
  • Back
Fibrinolytic substance naturally released from endothelium?
tissue plasminogen activator (tPA)
Substance that binds and down-regulates thombin?
Normal properties of endothelium that prevent thrombi from forming (4)?
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
Virchow's Triad for developing thrombi (DVT)?
1)Stasis of blood

2)Vascular injury

3)Hypercoaguable state
States of hypercoagulability?
4)Advanced age
5)Drugs such as oral contraceptives
7)Heaprin induced thrombocytopenia (HIT)

Initiation of the clotting cascade?
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
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

T/F Pure or complete antithromin deficiency is incompatible with life?
Activated protein C (APC) acts on what?
Factor VIII and V
When to suspect problems with clotting?
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)
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
T/F Many people with congenital risk factors present in their 60s

Just b/c someone is older doesnt mean they cant have a congenital risk factor
2 Clinical presentations for the inherited coagulopathies are?
1)Neonatal Purpura Fulminans - homozygous deficiency of proteins C and S

2)Warfarin Skin Necrosis - v Factors II, VII, IX, X, protein C & S
What is the reason that pt initially put on Warfarin therapy becomes hypercoagulable at first?
Protein C (major anticoagulant) v b/f the cloting factors b/c it has a shorter half-life
One leg larger than other with heat, redness and pain?
Classic appearance of DVT
MC inherited coagulation risk factor is? Mechanism?
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"
2nd MC inherited coagulation risk factor in US Caucasians ? Mechanism?
Prothrombin 20210

Amino Acid base pair SUBSTITUTION

Does NOT have a screening or genetic test (have to do PCR)
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
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
How does thrombophilia (hypercoagulability) naturally increase
AGE (risk ^ from age 20-60)
T/F Most people who develop thrombi have only one big risk factor
F, each individual risk factor is weak, it is the combination of factors that is problematic
Lowering youru stress level = lowering what thrombosis risk factor?
Factor VIII
When can you not test for elevated Factor VIII?

Must test on outpatient basis
Activated protein C & S works by?
Blocking Factor Va (used for Factor Xa -> Prothrombin) & VIIIa (used for Prothrombin -> Thrombin)
Causes of more consumption of Protein C & S?
Surgery & DIC
Causes of less production of Protein C & S?
Liver disease & vitamin K deficiency (Warfarin)
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%

Lupus Anticoagulant works by?
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)
Only acquired hypercoagulability risk factor that may be treated?

Treated using what?

Vit B12, folate (B9), & B6
T/F Hyperhomocsteinemia and APLS are two things that cause BOTH venous AND arterial thrombosis
Condition where patient should NOT be tested for lupus or anti-thrombin measures?
when on Heparin (binds to antithrombin)
Only tests that can be interpreted when patients are on haprin/warfarin/spontaneous thrombosis?
Activated Protien C Resistance, anticardiolipin antibodies, Lupus anticoagulant, Prothrombin 20210 mutation
A person with a recent thrombosis may have what abnormalities (3)?
1) Consumes antithrombin & protein C/S

2) ^ Factor VIII

3) ^ homocysteine