lecture 20 burns
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| thrombus | show 🗑
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| clot | show 🗑
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| Virchow's triad | show 🗑
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| show | arteries, cardiac chambers
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| antiplt effects of endothelium | show 🗑
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| anticoagulant effects of endothelium | show 🗑
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| show | synthesis of tPA
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| show | stasis of blood or turbulent flow and hypercoagulability
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| show | 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
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| show | associated with endothelial injury and causes disruption of blood flow
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| show | CHF, bed rest/immobilization, obesity, preg, soft tissue or bone injury, systemic malignancies, etc
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| show |
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| show | plt/leukocyte/fibrin lamellae, distinguish a thrombus from a simple postmortem clot
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| show | dissolution
organization/recanalization
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| dissolution | show 🗑
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| show | "organizing" - fibroblasts, smooth muscle cells and endothelial cells migrate into fibrin-rich thrombus
"recanalization" - formation of new vessels within substance of thrombus
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| show | piece of thrombus that dislodged from thrombus and is travelling in the blood to distant sites
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| show | designates a massive PE
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| embolic occlusion of < than 30% of the pulmonary arterial tree, especially in a previously healthy pt | show 🗑
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| show | 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
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| show | gas, FB, fat emboli after trauma to long bones, tissue fragments like placenta, amniotic fluid and neoplastic cells
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| show | 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
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| show | costophrenic angle, usually on or near the pleural surface
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| show | severe hemodynamic and metabolic disturbance characterized by generalized decrease in perfusion of the microcirculation systemically
hypovolemic, cardiogenic and septic
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| show | shock as a result of failure of the pump for one of several reasons: massive PE, ventricular rupture, cardiac tamponade, MI, arrhythmias, etc
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| show | follows massive loss of volume from severe burns, hemorrhage, v/d. pt is clammy and cyanotic
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| septic shock | show 🗑
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| show | 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
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| show | acute hemorrhagic centrilobular necrosis b/c these hepatocytes are the last to receive blood from the portal triads ; "nutmeg" liver
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| result of shock in the kidney | show 🗑
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| show | 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
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