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VenThrombPEShock
lecture 20 burns
| Question | Answer |
|---|---|
| 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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