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57 Cards in this Set

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