Abstract: . . .  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 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 like lens-like empty spaces with surrounding grew material from . . .
. . .  (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 pathway of coagulation. (Think sepsis or cancer) DIC mechanism : activation of intrinsic pathway Clinical findings: shock , respiratory distress, CNS depression, heart/renal failure Pathophysiology . . .
. . .  (several cm): extravasated blood in extravascular space (as opposed to congestion in which the blood remains in the vasculature) Hemothorax: hemotoma in thoracic cavity Hemopericardium : in pericardium Hemoperitoneum : in peritoneum Petechiae : pinpoint hemorrhages (1-2 mm) [are not blanched with pressure] associated with disseminated intravascular condition (DIC) because of widespread clotting and fibrinolysis that goes on in small vessels Purpura : larger (1 cm) Ecchymoses : larger (a few cm) and blotchy (eg: what third year med students produce when they first attempt to draw blood) Significance of hemorrhage . . .
. . .  - Toll-like receptors (TLR) are the actual signaling receptors -> activate Nf kappaB to initiate massive cytokine synthesis (positive feedback loop) *potential therapeutic target* - TLR4 gram negative shock, 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 . . .
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