SBM Unit 3: Coagulation cascade
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19 terms
Terms | Definitions |
|---|---|
 Ancistrodon rhodostoma | -Australian pit viper -venom is released into bloodstream -venom can cleave FPA & FPB, but cannot activate factor 13 -thrombi are formed, but rapidly disintegrate -individuals bitten by this snake are unable to form clots because platelets and fibrinogen are consumed in weak clots |
| Pseudonaja textilis | -Australian snake -venom contains factor 10a and modified factor 5 -modified factor 5 is resistant to degradation by PC + PS -modified factor 5 is able to activate factor 10 in absence of phospholipid membrane -modified factor 5 + factor 10a complex activates prothrombin and clots are formed -individuals bit by this snake rapidly clot -- DIC -- death |
| Sequence of hemostasis | 1. Neural vasoconstriction 2. Endothelium becomes activated: releases endothelin, P-selctin, and vWF (from Weibel-Palade bodies) 3. Platelets slow down and roll along endothelium, mediated by P-selectin 4. Platelets bind collagen, mediated by vWF 5. Concurrently, leukocytes roll along endothelium and release microparticles (containing tissue factor) |
| Weibel-Palade body | -storage granules of endothelial cells -contain vWF and P-selectin -release from endothelium trigger platelet and WBCs rolling adhesion/adhesion |
| Tissue factor | -transmembrane glycoprotein -present in the phopholipid bilayer of many cell types: endothelial cells, WBCS, platelets, etc. -tissue injury "decrypts" glycoprotein so that it can be released with microparticles -present in saliva |
| Discoverers of clotting factors and cascade | -Morowitz: clotting factors 1, 2, 3, & 4 (1905) -Ratnoff & Macfarlane: clotting cascade (1964) |
| Partial thromboplastin time | -normal: 30 to 40 seconds -add: silicate, phospholipids, and Ca -silicate activates factor 12 -detects deficiencies of factors 12, 11, 9, and 8 |
| Prothrombin time | -normal: 10 to 15 seconds -add: tissue factor and Ca -detects deficiencies of factor 7 |
| Common pathway | -factor 10 activated by extrinsic or intrinsic pathways -factor 10a + factor 5 activated prothrombin -thrombin activates fibrinogen -fibrin is cross-linked by thrombin-activated factor 13 |
| Tissue factor pathway inhibitor | -generated by intact endothelium to prevent spread of clot -binds to factor 10a and inhibits TF-factor 7a complex after a small amount of thrombin generated -why the intrinsic pathway must generate enough thrombin to form fibrin |
| Factor 11 | -part of the intrinsic pathway -binds to platelet GP IB-5-9 and is activated by thrombin -dimerizes and activates factor 9 -is inactivated by nexin 2 when it leaves the platelet GP -deficiency=Hemophilia C (mild bleeding disorder) |
| Fibrin | -structure: dimers of two triple helices (alpha, beta, and gamma) held together by diS bonds -central E domain and terminal D domain -at central E domain, fibrinopeptides A & B cap the alpha and beta chains -thrombin activation leads to cleavage of fibrinopeptides and exposure of E-domain "knobs" that fit into D-domains -factor 13 cross links via formation of amino-epsilon-(gamma-glutamyl) lysine bridge between D-domains |
| Coagulation inhibitors | generated by an intact endothelium to prevent clot from spreading -NO, PGI2, CD66 (ectoADPase) -ADAMTS13 protein -Tissue factor pathway inhibitor -Thrombomodulin -heparin-like proteoglycans |
| Physiologic anticoagulants | -Protein C -Protein S -Protein Z -Tissue factor pathway inhibitor -thrombomodulin -antithrombin |
| Antithrombin | -serine protease inhibitor (SERPIN) -inhibits thrombin and factors 10, 9, 11, 12, and TF-factor 7a -contains "bait" domain that binds thrombin -enhanced by heparin and heparin-like proteoglycans |
| Thrombomodulin | -released by intact endothelium -binds to thrombin to activate Protein C -Protein C binds to Protein S to inhibit factor 5 -PC + PS + factor 5 degrade factor 8 |
| Principle anti-coagulant mechanism | Endothelium |
| Critical factor for thrombus augmentation | Thrombin |
| First step in tissue repair | Clot lysis |
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