jessica3l33's version from 2015-04-27 17:17

Section 1

Question Answer
what happens in secondary hemostasistransforms circulating blood into insoluble gel, fibrinogen converted to fibrin
nonwettableminimal interaction between endothelial cells and blood
vascular system structuremade of basement membrane or subendothelium, ,submembraneus tissue
vascular system functionsvasoconstriction, diversion of clood flow, initiation of platlete activation, initiation of coagulation
prostacyclininhibits platlet aggregation
ADPpromotes platlet aggregation
tissue thromboplastintissue factor that initiates fibrin formation
von willebrand factorfacilitates platlet adhesionby binding endothelium to platlet membrane receptor glycoprotein Ib
Factor Vactivates prothrombin in coagulation system
thrombomodulininhibits thrombin
plasminogen activatorsinitiate fibrinolysis
heparin sulfatehelps activate antithrombin
three platlet zonesperipheral, sol-gel, organelle
peripheral zonestimulus receptor and transmitter region
glycocalyxsurface coat of glycoproteins that functions in ABO blood group specificity, tissue compatibility, platelet antigenicity, transmission receptors
GpIbreceptor for coagulation protein von willebrand factor
Gp III/IIIafibrinogen recptor
platlet aggregating agentsADP, thrombin, epinephrine, and serotonin
PF3platlet thromboplastin
PF4anti heparin
arachidonic acidprecursor to thromboxane A2 platelet aggregating agent
open canicular systempassageway to link internal environment to surface
submembraneous regionspecialized microfilaments that helps to maintain normal shape of platlets
sol-gel zonecytoskeleton and contractile region
most numerous organelles granules
TEMtransmission electron microscopy
Dense bodies containADP, ATP, calcium catecholamines, serotonin
DTS storage site for calcium site of thromboxane and prostaglandin synthesis
number of mitochondria per platlet10-60
what is the AAA reaction?adhere, activate, aggregate
describe mechanism of aggregationcalcium, fibrinogen, GpIIb/IIIa
asprin effectseffeccts enzyme cyclo oxygenase and ultimately impairs platlet aggregation
prostacyclin synthesis generatesPGI2
PGI2potent inhibitor of aggregation and is a vasodilator
reactions of secondary hemostasisprothrombin-->thrombin, fibrinogen-->fibrin

Section 2

Question Answer
Hereditary hemorrhagic Talengiectasia,family history of bleeding and purple legions, genetic mutation of 9q, diagnosis is by family history
Henoch schonlein purpuravascular damage from deposition of immune complexes, viral or bacterial infection in children
senile purpuadegernerating skin inadequately supports blood vessels
scurvyvitamin C deficiency, needed for collagen synthesis
immune thromboctopeniaimmune mediated plpatlet destruction, affects children, resolves spontaneously
chronic ITPmostly occurs in young women 25-50 y/o, can cause heavy periods and nosebleeds, autoimmune condition
secondary immune throbocytopeniaassociated with HIV, after blood transfusion
Thrombotic thrombocytopenic purpurarare, severe hemolysis, microangiopathic severe anemia, platlet thrombi in small vessesl
Hemolytic uremic syndromesimilar to TTP but in children, microangiopathic hemolytic anemia, thrombocytopenia, renal failure
Disseminated intravascular coagulationplatlets become trapped in fibrin clots
heparin can causethrombocytopenia
splenomegalytrapping too many platlets in the spleen
von willebrand diseaseimpaired platlet adhesion, can be corrected by adding ristocetin

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