Abstract: . . .  neutrophils. slide w/ splenic infarct : result of arterial thrombotic occlusion (e.g. thromboembolus from a mitral valve , or local thrombosis due to sickle cell disease ). Yellow portion typical of necrotic tissue. slide w/ pulmonary embolus: in pulmonary artery, total infarction of upper lobe evident compared to other lobes. DISSEMINATED INTRAVASCULAR COAGULATION (DIC): Widespread thrombosis in the microcirculation with platelets and fibrin (few RBC) in capillaries. Activation of intrinsic . . .
. . .  called intermittent claudication, may be due to thrombus in fem or iliac ) Mural (the wall of): generally refers to heart ventricle, forms when a portion of wall is less kinetic (i.e. from scarring due to previous infarct.) Venous: 90% in leg veins (deep calf/femoral/popliteal/iliac) may be source of pulmonary embolism slide w/ coronary thrombus : Occlusion. Intima and media hard to distinguish and replaced by grey lipid material with cleft-like formations of cholesterol. Cholesterol looks . . .
. . .  due to sickle cell disease ). Yellow portion typical of necrotic tissue. slide w/ pulmonary embolus: in pulmonary artery, total infarction of upper lobe evident compared to other lobes. DISSEMINATED INTRAVASCULAR COAGULATION (DIC): Widespread thrombosis in the microcirculation with platelets and fibrin (few RBC) in capillaries. Activation of intrinsic pathway of coagulation. (Think sepsis or cancer) DIC mechanism : activation of intrinsic pathway Clinical findings: shock , respiratory . . .
. . .  Nomenclature : White thrombi: platelets, fibrin, scant RBCs Red thrombi: RBCs, tangled fibrin, attached to endothelium (bread and butter type) Occlusive: These are clinically threatening. May appear in coronary/cerebral/iliac/femoral (e.g. leg pain after relatively little exertion, a syndrome called intermittent claudication, may be due to thrombus in fem or iliac ) Mural (the wall of): generally refers to heart ventricle, forms when a portion of wall is less kinetic (i.e. from scarring due to . . .
. . .  TLR2 gram positive sepsis highly specific. (TLR4 KO mice do not develop shock even when injected with high levels of endotoxins) slide w/ nutmeg liver : massive amount of congestion Main culprit for low bp: NITRIC OXIDE 1. produced by endothelium and macrophages 2. NO Synthetase is induced in macrophages by numberous cytokines (iNOS) 3. deletion of cNOS (constitutive) from mice leads to systemic hypertension Mechanism : NO made by endothelial cells/macrophages diffuses through . . .
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