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57 Cards in this Set
- Front
- Back
hemostasis definition
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prevention of blood loss
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hemostasis mechanisms
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1) vascular constriction 2) platlet plug 3) blood clot 4) growth of fibrous tissue
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trauma causes what reaction in vessel wall
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smooth muscle contraction
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mechanisms of smooth muscle contraction in vessel wall
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1) local myogenic spasm 2)local autacoid factors from platelets and injured tissues 3) nervous reflexes
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what are the nervoud impulses initiated by in vessel wall contraction
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pain nerve impulses from injured vessel or nearby tissues
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what is reponsible for most vasoconstiction of small vessels
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platlets releasing thromboxane A2
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size, number, and origin of platlets
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1-4 uL in diameter; 150,000-300,000 per uL; megakaryocytes in marrow
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active factors in platelet cytoplasm
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1) actin/myosin and thromosthnin 2) ER and golgi reminants 3) mitochondria 4)prostaglandin synthesis 5) fibrin stabilizing factor 6)growth factor
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platelet cell membrane
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glycoproteins on surface (repulses normal endothelium); phospholipids (activate stages of blood clotting process)
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platelet half life
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8-12 days (most removed by spleen)
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what happens to platelets when exposed to a damaged vascular surface
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swell, numerous pseudopods form, contractile proteins contract and release granules, become sticky and adhere to collagen or protein called con Willebrand factor, secrete lots of ADP, enzymes form thromboxane A (ADP and thromboxane activate other platelets)
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what occurs when platelet levels are diminished
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thousands of small hemmorrhagic areas develop under the skin and thoughout internal tissues
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how quickly does a blood clot form
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15-20 seconds if vascular wall trauma severe, 1-2 if minor
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how long until the blood clot retracts
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20 minutes to one hour (if not too large of a vessel or opening)
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2 potential fates of a blood clot
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1) invaded by fibroblasts 2) dissolve
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3 steps of clotting
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1) complex cascade resulting in prothrombin activator 2) Prothrombin catalyzed into thrombin (Ca++ needed) 3)thrombin converts fibrinogen to fibrin
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rate-limiting factor in blood coagulation
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usually formation of prothromin activator
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platlet involvemnt with prothrombin
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prothrombin attaches to platelet receptors bound to damaged tissue
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Prothrombin info (class, weight, concentration, origin)
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alpha2-globulin plasma protein; MW 68,700; 15 mg/dL; made in liver (vit K required)
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Fibrinogen info (weight, concentration, origin)
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MW 340,000 (large weight/size prevents leakage into interstitial fluids); 100-700 mg/dL plasma concentration; made in liver
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What can high capillary permeability cause
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fibrinogen leaks into interstitial fluids and clots form
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Thrombin action
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has weak proteolytic capabilities and removes 4 low MW peptides from fibrinogen creating fibrin monomer; activates fibrin-stabilizing factor; direct effect on prothrombin (positive feedback - also acts on factors responsible for prothrombin activator - factors 8-12)
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bonds of early fibrin monomers
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weak noncovalent hydrogen bonding (no cross-links)
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Fibrin-stbilizing factor origin, activation, and action
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in normal plasma globulins and released by platelets; thrombin activates; causes covalent bonds and cross-links between fibrin monomers
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blood clot definition
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meshwork of fibrin fibers running in all directions and entrapping blood cells, platelets, and plasma
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Why are platelets necessary for clot retraction
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attach to fibrin fibers and bond everything together; also release procoagulant substances including fibrin-stabilizing factor; have contractibility capability; Ca++ stored in platelets accelerate process
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Two pathways for prothrombin activator formation
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1) extrinsic pathway - trauma to vascular wall and tissues 2) intrinsic pathway - within blood itself
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Step 1 of extrinsic pathway
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Release of tissue factor aka tissue thromboplastin (phospholipids plus lipoprotein complex)
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Step 2 of extrinsic pathway
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activation of factor 10 by a complex of factor 7 and tissue factor in presence of Ca++
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Step 3 extrinsic pathway
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Factor 10a combines with tissue phospholipids and factor 5 ( V is not active until positive feedback) to form prothrombin activator (in presence of Ca++, converts prothrombin to thrombin)
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Step 1 intrinsic pathway
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blood trauma causes factor 12 activation and release of platelet phospholipids (including platelet factor 3)
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Step 2 of intrinsic pathway
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Factor 11 activated by 12 (requires kininogen and accelerated by prekallikrein)
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Step 3 intrinsic pathway
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Factor 9 activated by 11
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Step 4 intrinsic pathway
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Factor 10 activated by 9 with 8 and platelet phospholipids and platelet factor 3
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What facor is missing in hemophillia
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usually factor 8, sometimes (15%) factor 9
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Step 5 intrinsic pathway
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same as last step on extrinsic pathway: activated 10 combines with 5 and platelet/tissue phospholipids to form prothrombin activator
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How can blood be prevented from clotting when removed from a person
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keep Ca++ below threshold for clotting: add citrate ions (deionize) or oxalate ion (precipitate)
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What pathway is activated after blood vessel rupture
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both intrinsic via platelet/factor 7 interaction and extrinsic via tissue factor
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speed of extrinsic vs intrinsic pathway
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15 seconds vs 1-6 minutes
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What prevents clotting
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1)smooth endothelial walls 2)layer of glycocalyx on endothelium (mucopolysaccaride) repells clotting factors 3)thrombomodulin on endotheial membrane binds thrombin (activates protein C which inactivated factors 5 and 8)
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most important anticoagulants
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fibrin fibers and antithrombin III (aka antithrombin-heparin cofactor)
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how much thrombin do fibrin fibers absorb
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85-90%
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where is heparin found naturally in the body
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in capillaries, especially mast cells of lung and liver (receive venous blood from body, heparin prevents the growth of clots they may receive)
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Heparin action
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highly neg charge; combines with antithrombin III (increases effectiveness from 100 fold to 1000 fold; also removes factors 7,9, 10, and 11)
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plasmin (from plasma proteins as plasminogen)
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digests fibrin fibers and some other protein coagulants - fibrinogen, factors 5, 7, and 8, prothrombin
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plasmin activation
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tissue plasminogen activator (t-PA)
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vitamin K required for formation of what clotting factors
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prothrombin, protein C, and factors 7,9, and 10
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component of factor 8 deficient in hemophilia
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smaller component (most important for intrinsic pathway)
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component of factor 8 deficient in von Willebrand's diease
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loss of large component
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treatment for thrombocytopenia
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spleen removal
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cause of roughened endothelial surface
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arteriosclerosis, infection, or trauma
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treatment of thrombitic occusion
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genetically engineered t-PA (best within first hour of onset)
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occurance of thrombosis in bed ridden patients
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1 in 10
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disseminated intravascular coagulation
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clotting mechanism activated in widespread areas of circulation (common in septicemia)
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length of heparin effectiveness
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1.5-4 hours (broken down by heparinase)
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Coumarin (warfarin)
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decreases levels of prothrombin, factors 7, 9, and 10 (competes for vit K active sites))
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prothrombin time
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indication of prothrombin concentration in blood (normal about 12 s)
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