Abstract: . . .  leading to thrombosis . Page 4 Thrombi 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 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 other plaque material. Also see fibrosis. slide w/ MI : gross appearance of heart with acute myocardial infarct coagulative necrosis . Color looks like tiger skin pale and yellow (necrotic) areas juxtaposed to normal beefy red areas. Under high power: myocytes with absent nuclei and deep red color, surrounded . . .
. . .  acute myocardial infarct coagulative necrosis . Color looks like tiger skin pale and yellow (necrotic) areas juxtaposed to normal beefy red areas. Under high power: myocytes with absent nuclei and deep red color, surrounded by 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 pathway of coagulation. (Think sepsis or cancer) DIC mechanism : activation of intrinsic pathway Clinical findings: shock , respiratory distress, CNS depression, heart/renal failure Pathophysiology : rapid consumption of fibrinogen, platelets, prothombin, factors V, VIII, X, and at same time generation of fibrin split products D-DIMERS (important diagnostic entity produced by plasmin. slide w/ DIC : capillary with platelets and fibrin Enter Dr. Marcantonio: PART II SEPTIC SHOCK (often see DIC in this . . .
--2695,2,674,2859,13474