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22 Cards in this Set
- Front
- Back
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Normal epithelium combats clotting via several factors. Name 3.
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1. Releases NO & prostacyclin - plt inhibitors
2. releasesTPA - activates plaminogen -> plasmin which breaks down fibrin(ogen) 3. Releases heparin like glycoaminosides 4. Degrades ADP(a platelet activator) by releasing ADPase |
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What are the 3 steps in platelet clot formation
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1. Adhesion
2. Activation 3. Aggregation |
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How does Adhesion of plt begin and what factors and receptors are involved
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Extracellular matrix (ECM) exposes vWF which allows for formation of ECM-vWF-(glycogen ib/!X/V)-Platelet complex
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What occurs during platelet activation (what do platelets release)
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Platelets release alpha granules (contain clotting and activation factors) and dense bodies (contain Ca, epi and other pro kinetic molecules)
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How does Heparin function
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It stimulates Anti-thrombin ~ 1000 fold. Anti-thrombin blocks thrombin(IIa) which is responsible for fibrinogen -> firbrin and amplification of other cascades
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Function of factor VII
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Binds to TF at site of injury and is activated to VIIa. This complex converts IX and X to their activated form
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Function of factor X/Xa.
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Factor Xa is localized to injury site and complexes with fVa. Xa/Va loacally catalyzes prothrombin -> thrombin
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How does thrombin affect the vWF/fVIII complex?
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It seperates them (this occurs locally at site of injury) which activates VIII which starts pro-clop loop
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What function does fIXa have?
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It bined to platelet to aid in plt activation
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What are the 3 major coagulation inhibiting mechanisms
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1. Serpins (Antithrombin, TFPI)
2. Heparin 3. anticoagulant proteases (protein C -> inactivates Va & VIIIa. Protein S -> accelerates action of protein C |
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Which factors are Vit K dependent
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VII, IX, X, prothrombin, protein C & protein S
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What factors can lead to vitamin K deficiency
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1. malnutrition
2. impaired intestinal absorbtion (obst jaundice, sprue) 3. compromised bacterial flora 2/2 antibiotics |
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How does liver disease affect clotting
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All factors except VIII are synthesized in liver. VII has the shortest half live
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What percentage of of pts on heparin will develop HIT
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5%
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Causes of thrombocytopenia (during pregnancy too
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1. HIT
2. During pregnancy (GI, preeclampsia, HELLP - hemolysis, incr lft, low plt) 3. splenic sequestration |
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Prolonged PT with nl PTT is indicative of
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fVII deficiency
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site of action, excretion, antidote and pre-procedure stop time of: Heparin
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1. Site: Antithrombin
2. Excetion: Hepatic 3. Antidote: protamine 4. Stop time: 6 hr |
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site of action, excretion, antidote and pre-procedure stop time of: LMWH
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1. Site: Antithrombin
2. Excetion: Renal 3. Antidote: protamine (partial) 4. Stop time: 12-24 hr |
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site of action, excretion, antidote and pre-procedure stop time of: Warfarin
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1. Site: Vit K dep factors
2. Excetion: Hepatic 3. Antidote: Vit K, rfVIIa, PCCS, Plasma 4. Stop time: 2-4 days |
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site of action, excretion, antidote and pre-procedure stop time of: Aspirin
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1. Site: Platelet COX-1
2. Excetion: Hepatic 3. Antidote: None 4. Stop time: 7 days |
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site of action, excretion, antidote and pre-procedure stop time of: Clopidigrel
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1. Site: Platelet ADP
2. Excetion: Hepatic 3. Antidote: None 4. Stop time: 5-7 days |
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site of action, excretion, antidote and pre-procedure stop time of: Abciximab
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1. Site: Platelet BPIIb-IIIa
2. Excetion: Renal 3. Antidote: None 4. Stop time: 72 hr |
