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19 Cards in this Set
- Front
- Back
Hypercoagulable state
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Imbalanced hemostasis--> more procoagulant/clotting activity (or, less anticoagulant activity).
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Thrombosis
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Inappropriate formation of a plt. and/or fibrin clot that obstruct blood vessels known as thrombus (thrombi)--> ischemia & necrosis.
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Thrombophilia
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- Predisposition to thrombosis.
- Secondary to a congenital or acquired d/o. |
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Embolus
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- A piece of thrombotic material & travel through circulation.
- Lodging at a distant site, obstructing (embolism) blood flow--> ischemia & necrosis or cell death. |
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Thromboembolism
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Blockage that originates form a thrombus
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Etiology
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- Physical, bilogical, or chemical events that release prothrombotic mediators from damaged blood vessels (or, surpression of antithrombotic substances)
- Inappropriate/uncontrolled plt. activation - Uncontrolled triggering of the plasma coagulation sx. - Inadequate control of coagulaton &/or impaired fibrinolysis. |
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Venous thrombosis
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- Caused by coagulation sx imbalances.
- DVT, PE - 1:1000/year |
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Arterial thrombosis
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- Mechanism: atherosclerotic plaque formation in the vessel walls.
- Caused 80% of heart attack (myocardial infarct); 85% of strokes (cerebral infarct). |
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Acquired thrombosis
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Risk factors:
- Age, immobilization, oral contraceptives, pregnancy, smoking, inflammation. Associated w/ systemic dz: - MPD- ET, PV; cancer; leukemia- APL, AML--> DIC Double Hit: congenital + acquired--> synergistic effects |
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Thrombosis: Lab evaluation
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- Recommended to perform assays 14 days after anticoagulation therapy is d/c'd.
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Antiphospholipid (APL) antibodies.
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- Family of Ig that bind protein-PL complexes.
- Non-specific inhibitors: may bind a variety of protein- PL complex. |
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Lupus Anticoagulant (LA)
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- IgG immunoglobulins directed against several phospholipid protein complexes.
- Prolong the phospholipid dependent PTT rxn. |
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Test systems that are sensitive to LA & must fulfill the requirements.
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- Prolonged PL dependent clot formation (i.e. aPTT).
- Mixing study: failure to correct prolonged aPTT by mixing w/ normal PPP (plt poor plasma <10,000/uL). - Correction of the prolonged screen by addition of excess PL. - Exclusion of other coagulopathies. |
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Lupus Anticoagulant (LA) lab evaluation.
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- Mixing study is necessary: LA vs. specific inhibitors & factor deficiency
- 1st: perform thrombin time to r/o heparin as a cause of prolonged PTT. - If thrombin time w/in the normal limits (no heparin), Pt's PPP is mixed 1:1 w/ pooled normal plasma--> perform PTT. - If the result of the mixture w/in 10% of the pooled normal plasma= CORRECTION OCCURED= factor deficiency? - Next, incubate pt. PPP & pooled normal PPP for 1-2hrs at 37 Celsius. - Factor deficiency if PTT remains corrected. - Suspect LA if the initial 1:1 mixture remains uncorrected. - Confirmation analysis: new aliquot of pt. PPP is added to high PL rgt.--> shortening of PTT by at least 8 seconds= LA. - Possible presence of anti-factor antibody if the initial 1:1 mixture= normal & incubated mixture= uncorrected. |
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Dilute Russell's Viper Venom Time (dRVVT)
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- Sensitive to LA and Coumadin/Warfarin effect.
- dRVVT is neutralized by LA--> prolonged test. - High PL rgt. corrects the prolongation= confirm LA. |
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Antithrombin (AT) assay
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- Bind to heparin; inhibit thrombin, factors 10, 9, & 11.
- AT deficiency can be acquired (liver dz, prolonged heparin therapy, oral contraceptives, DIC) or congenital. |
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Protein C & S assays
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- Natural anticogualnt pathway
- Heterozygous deficiencies--> increased risk of recurrent DVT & PE. |
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Heparin Induced Thrombocytopenia (HIT).
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- Adverse effect of unfractioned heparin therapy.
- Also called HIT w/ thrombosis (HITT) - Detection of antibodies to the PF4-heparin complex. - Suspected when plt count <150 X 10^3/uL (or by 50% in pts w/ previous thrombocytopenia). - D/c heparin therapy & proceed w/ alternate anticoagulant. |
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HIT laboratory tests
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- Screening: kit & heparin induced antibody immunoassay
- Reference method: 14C serotonin release assay - Endothelial damage--> activated plts release serotonin (delta granules)--> vasoconstriction |