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80 Cards in this Set
- Front
- Back
Thrombosis
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clot
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Embolus
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mass of clot free in blood
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Thromboemboli
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blockage of blood vessel
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Ischemic necrosis
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death due to lack of blood flow
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Infarct
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necrotic area
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Why are thrombus formations life threatening?
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Clots may dislodge/cause occlusion or infarct.
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Why are thrombi life-saving?
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1. Stop bleeding
2. Maintains homeostasis |
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What factors pre-dispose a patient to thrombosis?
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1. Injury to endothelium
2. Altered blood flow 3. Altered hemostatic systems 4. Proteins 5. Platelets |
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What are 5 therapeutic measures for thrombosis?
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1. Low dose heparin
2. Full dose coumadin 3. Aspirin 4. Stockings 5. Physical therapy |
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2 Inhibitors of Fibrinolysis
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-PAI-1
-a2-antiplasmin |
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4 Inhibitors of Coagulation
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-ATIII
-Protein C -Protein S -HC II |
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Activator of Fibrinolysis
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Plasmin activation
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Activator of Coagulation
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-Platelets
-Coag factors |
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8 Risk factors for Thrombosis
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-Age
-Pregnancy -Cancer -Smoking -Obesity -Immobility -Sepsis -Trauma |
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4 Challenges causing Thrombosis
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1. Injury
2. Pregnancy 3. Surgery 4. Medications |
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What general lab results accompany thrombosis?
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1. History
2. PT/PTT - normal to sl. low 3. NORMAL bleeding time 4. NORMAL platelet count |
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Why are thrombi life-saving?
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1. Stop bleeding
2. Maintains homeostasis |
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What factors pre-dispose a patient to thrombosis?
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1. Injury to endothelium
2. Altered blood flow 3. Altered hemostatic systems 4. Proteins 5. Platelets |
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What are 5 therapeutic measures for thrombosis?
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1. Low dose heparin
2. Full dose coumadin 3. Aspirin 4. Stockings 5. Physical therapy |
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2 Inhibitors of Fibrinolysis
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-PAI-1
-a2-antiplasmin |
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4 Inhibitors of Coagulation
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-ATIII
-Protein C -Protein S -HC II |
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Activator of Fibrinolysis
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Plasmin activation
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Activator of Coagulation
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-Platelets
-Coag factors |
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8 Risk factors for Thrombosis
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-Age
-Pregnancy -Cancer -Smoking -Obesity -Immobility -Sepsis -Trauma |
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4 Challenges causing Thrombosis
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1. Injury
2. Pregnancy 3. Surgery 4. Medications |
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What general lab results accompany thrombosis?
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1. History
2. PT/PTT - normal to sl. low 3. NORMAL bleeding time 4. NORMAL platelet count |
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What are the 4 more common hereditary disorders of hypercoagulation?
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1. Protein C defic.
2. Protein S defic. 3. ATIII defic. 4. APC resistance |
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What are the similar features of the four hereditary disorders?
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1. All autosomal dominant
2. All cause DVT |
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Which disorders have earliest onset?
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Proteins C/S - at birth in homozygotes
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Which disorders have earliest onset at adolescence?
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Proteins C/S - heterozygotes
ATIII - Heterozygotes |
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When does APC resistance become apparent in patients?
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Homozygotes - age 10-40
Heterozygotes - about 40 |
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Which disorder can cause:
-Superfic. thrombophlebitis -Purpura fulminans |
Super-thrmbophleb = Protein S
purpura fulminans = Protein C |
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What's the only difference btwn PRotein C/S disorders?
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-S causes pulmonary embolism and thrombophlebitis
-C causes purpura fulminans. -Homozygous C is fatal |
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What causes PRotein S deficiency?
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-Congenital - genetics
-Acquired - Vit K defic, Liver disease |
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Why does warfarin/coumadin therapy induce protein s/c deficiency?
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They have shorter t1/2's than other factors, so decrease faster; leaves patient at risk for thrombosis.
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-What does Factor V leiden deficiency cause?
-What causes it? |
-APC resistance
-Congenital - genetics |
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What is the main problem in APC resistance?
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-A point mutation of factor five; unable to be inactivated by APC.
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What 2 types of screening tests are used for APC resistance?
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1. Clot based - PT/APTT
2. Chromogenic |
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What test is used to confirm APCR?
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PCR on isolated DNA
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What are the 4 more common hereditary disorders of hypercoagulation?
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1. Protein C defic.
2. Protein S defic. 3. ATIII defic. 4. APC resistance |
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What are the similar features of the four hereditary disorders?
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1. All autosomal dominant
2. All cause DVT |
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Which disorders have earliest onset?
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Proteins C/S - at birth in homozygotes
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Which disorders have earliest onset at adolescence?
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Proteins C/S - heterozygotes
ATIII - Heterozygotes |
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When does APC resistance become apparent in patients?
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Homozygotes - age 10-40
Heterozygotes - about 40 |
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Which disorder can cause:
-Superfic. thrombophlebitis -Purpura fulminans |
Super-thrmbophleb = Protein S
purpura fulminans = Protein C |
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What's the only difference btwn PRotein C/S disorders?
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-S causes pulmonary embolism and thrombophlebitis
-C causes purpura fulminans. -Homozygous C is fatal |
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What causes PRotein S deficiency?
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-Congenital - genetics
-Acquired - Vit K defic, Liver disease |
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Why does warfarin/coumadin therapy induce protein s/c deficiency?
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They have shorter t1/2's than other factors, so decrease faster; leaves patient at risk for thrombosis.
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-What does Factor V leiden deficiency cause?
-What causes it? |
-APC resistance
-Congenital - genetics |
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What is the main problem in APC resistance?
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-A point mutation of factor five; unable to be inactivated by APC.
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What 2 types of screening tests are used for APC resistance?
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1. Clot based - PT/APTT
2. Chromogenic |
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What test is used to confirm APCR?
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PCR on isolated DNA
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What is the principle of the aPTT for Fx V leiden?
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-Fx V deficient plasma + Pt.
-If prolonged, Fx V is ok -If not, Fx V is resistant. |
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What type of APCR is more common; hetero or homozygous?
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Homozygous - 50-100%
Hetero = 5-10% |
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What are 7 results of Thrombosis?
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1. Deep vein thrombosis
2. pulmonary embolism 3. recurrent pregnancy loss 4. Myocardial infarct 5. CVA 6. Phlebitis 7. Post-op thrombosis |
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What are the 3 main lab criteria for diagnosing LA?
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-Abnormal PT
-Prolonged PTT that doesn't correct -Pos drVVT |
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What is the LA basically?
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An Antiphospholipid Antibody.
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What are non-lupus causes of anticardiolipin antibody?
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-malignacies
-immune thrombocytopenic purpura -infections -chlorpromazine/procainamide |
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What are the 2 more common causes of deep vein thrombosis?
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-LA - 8-14%
-Factor V Leiden 40-50% -Protein S = 5% -PC/ATIII = 3% |
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why are the pt/ptt prolonged in LA states?
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-They inhibit clotting in vitro by attacking actin; but not in vivo.
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What are 3 types of tests for LA?
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1. Increased phospholipid (sta-clot)
2. Decreased phospholipid 3. Specific Elisas for IgG/M |
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What is the basic principle of the StaClot procedure?
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1. 2 tubes incubated; one w/ hexagonal phase phospholipid.
2. Run aPTT on both; the HPE will neutralize LA if present 3. Compare clotting times. |
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What tests specifically detect LA's?
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-LA screen
-LA confirm |
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What is the reagent in LA tests?
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Dilute Russell's viper venom
(DRVVT) |
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What is the principle of the DRVVT LA-screen?
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-Viper venom activates Fx X
-Bypasses VII/factors above 9/8 in intrinsic. -Specific b/c less affected by factor deficiencies or inhibitors. |
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What happens in the LA confirm?
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-More procoag phospholipid is put in to neutralize LA.
-Polybrene also added for heparin resistance. |
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Why would heparin interfere with LA testing?
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Of course the PPT would be prolonged and uncorrected.
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What's another name for inhibitor assays?
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mixing studies
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what is the principle of mixing studies?
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-mix suspect plasma w/ PPP.
-If it doesnt correct, or is prolonged after incubation, confirm w/ factor assays. |
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NAME THE:
-Increased phospholipid test -Decreased phospholipid test |
Incr = StaClot
Decr = LA COnfirm |
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So when do we test for inhibitors?
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When PT/PTT are prolonged by:
-LA -other factor inhibitors -heparin |
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If PT AND aPTT are abnormal and uncorrectable:
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contamination, probly heparin
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What 3 therapeutic agents given to patients with LA?
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-Heparin
-Coumadin -LMWH if pregnant |
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What 2 miscellaneous thrombotic disorders must i know?
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1. Hyperhomocysteinemia
2. Prothrombin mutations |
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What causes hyperhomocystin?
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-Vascular toxin
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What should i remember about prothrombin mutations?
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-Test with PCR
-Lifelong Warfarin therapy |
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If not a factor disorder or circulating anticoagulant, what can alter fibrinolysis?
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1. Plasminogen deficiency
2. Dysfibrinogenemia 3. Increased PAI-1 |
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what is PAI-1?
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Tissue plasminogen activator inhibitor - keeps the activation of plasminogen in check.
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What causes plasminogen deficiency?
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Autosomoal dominant inheritance.
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How is plasminogen deficiency tested for?
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Functional antigen assay
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