Edema- fluid in interstitial space Thorax- pleural Pericardium pericardial Peritoneum-ascites Anasarca-generalized Transudate due to hydrodynamic derangement (watery)

Exudate-- inflammation with various things Edema can be fatal Brain sulci are filled by swelling (sign of edema) Pulmonary- like drowning Uncle herniation- midbrain pushed through magnum stop breathing Hyperemia- increased blood through vessels Red tissue with oxygenation Congestion- passive process due to outflow Red-blue due to deoxygenated Very correlated with edema Acute and chronic Chronic in lungs can be seen as reddish brown pigments (hemosiderin- thicker and refractory) Nutmeg liver- brown in liver with pale (congestion) Sinusoids are backed up ACUTE IS redder Chronic was more purple Hemorrhage- extravasation of blood outside vessels Hematoma- inside bruise Petechiae- small Purpura- med Ecchymoses-large Epidural hematoma- blood on top of dura (sig trauma, middle meningeal artery) Subdural hematoma- elderly (minor trauma, usually dont even hit head) slow bleed Hemopericardium heart sac so full of blood cant see heart Acceleration/deacceleration injury- aorta tears slightly from heart and leaks into sac Mediastinum is wide Hemorrhage- volume, rate, location Hemostasis-hemostatic plug at vascular rinjury Thrombosis- inappropriate formation of clot in vascular system

Vascular wall, platelets, coagulation Endothelium Intact endothelium platelets keep moving ; ECM helps make thrombi Anticoagulant properties- heparin like, thrombomodulin (prevent clotting) Fibrinolytic- synthesize plasminogen activator fibrinolysis Prothrombotic- von willebrand- bind platelets to collagen; tissue factor extrinsic; plasminogen inhibitors Platelets Adhesion by won willebrand Secretion by alpha and delta granules Aggregation-adp and thromboxane a2 for primary plug; thrombin causes more aggregation makes fibrin cementing platelets into place PT monitor coumadin Ptt monitor heparin (check acute thrombosis/embolism) Thrombosis- endothelial injury, alteration in blood flow, hypercoagubility Endothelial injury ECM exposure Infarction, atherosclerosis, inflammation Turbulence and stasis Disrupts flow of platelets, clotting factors concentrate, clotting factor inhibitors are blocked, Atherlosclerosis, aneurysm, infarction Hypercoaguability- factor v gene mutation (leyden); prothrombin gene mutation Acquired- bed rest/sitting; cancer, thrombocytopenia; antiphoslipid syndrome; the pill Disseminate intravascular coagulation Sudden thrombi in circulation; rapid consumption of platelets; fibrinolytic mechanism causing bleeding; burns, septic shock etc Thrombus- blood layers out of fibring and plate cells (lines of zahn) Mural thrombi- ventricular wall Arterial thrombi- coronary, cerebral, femoral Venous LEGS Premortem morphology: (firm, adherenet, lines of zahn) Post mortem: soft, not adherent, red bottom, yellow top Fibrinolytic pathways can break up thrombi, if fibrin is polymerized they dont dissolve Therapeutic agents acute phase If they remain they become Organized: ingrowth of endothelial cells, fibroblasts, smooth muscle, Vascular channel formation in thrombus, incorporated into wall Embolism- mass carried in blood (thombus stuck) Most are due to thrombus

Pulmonary thromboembolism- 95% in leg veins; 80% small and incorporated into vasculature; Symptomatic in CHF affecting bronchial circulation infarction; large emboli death when occluding/blocking pulmonary circulation Arterial thromboembolism- cardiac mural thrombi/valvular vegetations; lower extremities, brain, intestines, kidney; cause inrfarction Infarction- necrosis secondary to compromise Usually a thrombus, and arterial Sometimes plaque/spasm Affected by: vascular supply, occulusion, vulnerability, oxygen content Wedge shaped Poorly defined and hemmorhagic at first Get hyperemic rim Coagulative necrosis scar tissue Brain will result in caviation