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lecture 20 burns

thrombus solid intravascular mass formed during life from circulating blood elements; composed of mix of plts, leukocytes, RBCs and fibrin
clot masses of RBCs, plts, leukocytes and fibrin that form extravascularly after hemorrhage, in vitro or postmortem
Virchow's triad abnormality of endothelium interruption of blood flow (stasis) hypercoagulability
endothelial abnormalities are most important for thrombi that develop in the ____ & ______ arteries, cardiac chambers
antiplt effects of endothelium shielding plts from subendothelial EC matrix, inhibition of activated adhesion via prostacyclin and NO
anticoagulant effects of endothelium production of thrombomodulin & heparan sulfate and other anticoagulant glycoproteins
fibrinolytic effects of endothelium synthesis of tPA
the most 2 important causative factor for venous (and sometimes arterial) thrombi stasis of blood or turbulent flow and hypercoagulability
3 reasons why stasis promotes thrombogenesis 1) plts are brought into contact with endothelial surface 2) acivated coag factors reach high local factors 3) inflow of coag cascade factors is reduced
how atherosclerosis contributes to arterial thrombosis associated with endothelial injury and causes disruption of blood flow
examples of secondary hypercoagulable states (more important than primary or hereditary states) CHF, bed rest/immobilization, obesity, preg, soft tissue or bone injury, systemic malignancies, etc
initial plt aggregate then plt/leukocyte/fibrin meshwork = compeleted thrombus
lines of Zahn plt/leukocyte/fibrin lamellae, distinguish a thrombus from a simple postmortem clot
2 fates of thrombi dissolution organization/recanalization
dissolution fibrinolysis of fibrin matrix and complete resolution of thrombus
oragnization/recanalization "organizing" - fibroblasts, smooth muscle cells and endothelial cells migrate into fibrin-rich thrombus "recanalization" - formation of new vessels within substance of thrombus
thromboembolus piece of thrombus that dislodged from thrombus and is travelling in the blood to distant sites
embolic occlusion of > than 50-60% of the pulmonary arterial tree designates a massive PE
embolic occlusion of < than 30% of the pulmonary arterial tree, especially in a previously healthy pt classifies a minor PE
sequence of events leading to death after massive PE occlusion of PA, RV dilates b/c of increased workload, decreased filling of RA means less filling of LV, decreased LV output leads to systemic hypoperfusion including coronary arteries, kidneys and brain --> ischemia and infarcts
List various types of emboli. gas, FB, fat emboli after trauma to long bones, tissue fragments like placenta, amniotic fluid and neoplastic cells
pulmonary infarcts are usually a results of PEs especially in those with CHF, systemic hypotension or preexisting lung dz where bronchial circulation isn't enough to compensate for decrease inflow of blood from PAs
most typical area for pulmonary infarcts to occur costophrenic angle, usually on or near the pleural surface
definition of shock and examples of the 3 types severe hemodynamic and metabolic disturbance characterized by generalized decrease in perfusion of the microcirculation systemically hypovolemic, cardiogenic and septic
cardiogenic shock shock as a result of failure of the pump for one of several reasons: massive PE, ventricular rupture, cardiac tamponade, MI, arrhythmias, etc
hypovolemic shock follows massive loss of volume from severe burns, hemorrhage, v/d. pt is clammy and cyanotic
septic shock a result of overwhelming microbial infection, systemic vasodilation due to toxin-mediated processes leads to myocardial dysfunction and end organ hypoperfusion. pt is flushed and warm
result of shock in the heart subendocardium myocyte necrosis, decreased perfusion results in the tissue just beneath the endocardium dying first b/c it's the last to be perfused from the outside coronary arteries
result of shock in the liver acute hemorrhagic centrilobular necrosis b/c these hepatocytes are the last to receive blood from the portal triads ; "nutmeg" liver
result of shock in the kidney acute tubular necrosis associated with oliguria
DIC disseminated intravascular coagulation is a result of an insult to the systemic endothelium typically during septic shock; cytokine release favors procoagulation until all the factors and plts run out then hemorrhage is more likely
Created by: sirprakes



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