Thrombosis/Embolism/Infarction/Shock

• 1. endothelial injury
• 2. alteration in blood flow
• 3. hypercoagulability

loss of barrier between blood and extracellular matrix, increased prothrombic activity caused by hemodynamic stress

• 1. turbulence induces endothelial dysfunction and activation
• 2. stasis causes platelets move to periphery of vessel lumen. This allows for concentration of clotting factors important in the formation of venous thrombi

• Inherited: Factor V Leiden mutation, prothrombin mutation, deficiencies of anticoagulant protein (antithrombin III)
• Aquired: prolonged bed rest, extensive tissue damage, cancer, pregnancy

produces a factor v that cannot be degraded by protein c

occur at sites of turbulence or endothelial cell injury. they have white appearance with distinct lines of Zahn and may be occlusive or mural. lodge in smaller arteries causing infarction.

non-bacterial thrombotic endocarditis: sterile thrombi on heart valve

dark red color with no clear lines of zahn. form in deep veins of the legs.

• 1. propagation (enlargement by fibrin/platelet deposition)
• 2. embolization (entire thrombus dislodges or piece breaks loose)
• 3. dissolution (lysis by fibrinolytic activity)
• 4. organization (deposition of collagen to replace fibrin and recanalization to reestablish flow)

depletion of coagulation factors and platelets via widespread activation of coagulation cascades. associated with widespread formation of microthrombi and risk of hemorrhage. conditions causing DIC include gram negative infection, obstetric complications, neoplasm, shock and massive injury.

solid, liquid, or gas carried from one point to another point in the vascular system

pulmonary arteries

• 1. no clinical manifestation (no ischemia due to double blood supply)
• 2. pulmonary hemorrhage and hematemesis due to ischemic injury without infarction
• 3. pulmonary infarction
• 4. sudden death due to large emboli obstructing a large pulmonary artery or straddling the bifurcation of the pulmonary arterial trunk (saddle embolus)
• 5. gradual obstruction that leads to pulmonary hypertension

embolus that arises in a systemic vein and crosses a communication from the venous side to the arterial side of circulation, usually through a patent foramen ovale or atrial septal defect.

origin is usually left atrium, left ventricle or ulcerated atherosclerotic plaque. can travel to any systemic artery.

• fat: fracture of large long bone or soft tissue injury
• air: decompression sickness
• amniotic fluid
• atherosclerotic

ischemic necrosis in an organ due to arterial obstruction

can be caused by venous occlusion, loose tissue, infarction followed by reflow of blood into the area

occurs with arterial occlusions in solid organs

• 1. wedge-shaped with point of wedge at site of arterial obstruction
• 2. infarcts usually followed by acute inflammation
• 3. infarcts in the brain result in liquefactive necrosis

systemic hypoperfusion of tissues

• 1. cardiogenic: loss of pumping capacity of the heart
• 2. hypovolemic: blood loss
• 3. septic: bacterial infection
• 4. anaphaylactic: IgE hypersensitivity
• 5. neurogenic: loss of vascular tone

• 1. vasodilation
• 2. hypotension
• 3. reduced myocardial contractility

LPS of Gm- binds to receptor on monocytes causing release of IL-1 and TNF, as well as secondary cytokines.

• 1. nonprogressive
• 2. progressive
• 3. irreversible

maintenance of tissue perfusion by tachycardia, renal conservation of water, redistrobution of blood to vital organs via peripheral vasoconstriction

inadequate perfusion with metabolic imbalances such as acidosis and increased lactic acid. acidosis reduces vasomotor response to sympathetic stimulation leading to pooling of blood and reduced perfusion. hypoxic injury to endothelium results in DIC.

tissue injury that cannot be reversed by reperfusion

• 1. Brain: ischemic necrosis of neurons in the brain
• 2. Heart: necrosis in the heart
• 3. Kidney: necrosis of tubular epithelial cells in the kidney (acute tubular necrosis)
• 4. Lungs: diffuse alveolar damage in the lungs due to endothelial injury (ARDS)
• 5. Adrenals: depletion of lipids in adrenal cortex
• 6. GI: mucosal hemorrhage and necrosis in the intestines
• 7. Liver: necrosis of the liver

• 1. tachycardia
• 2. tachypnea
• 3. hypotension
• 4. clammy skin
• 5. decreased urinary output
• 6. confusion
• 7. low blood pH (acidosis) and elevated lactic acid