1.2.2 Inflammation, DIC and Shock Flashcards
Stage in which compensatory physiologic mechanisms may allow survival (reversible)
Non-progressive stage
What causes bleeding associated with DIC?
Central event is the activation of the intrinsic or extrinsic clotting cascade within the vascular compartment by tissue injury. Platelets and clotting factors are consumed by massive intravascular coagulation, often in the capillary beds.
What is this an image of?
Diffuse alveolar damage - so called shock lung
What is significant about Waterhouse-Friderichson syndrome?
infarcted adrenal glands due to DIC. Need to used corticosteroids because fluid and pressors will not be enough
What is the arrow pointing to?
Schistocytes which are caused by the fibrin meshwork fragmenting normal RBCs
What is hypovolemic shock?
results from low cardiac output due to low blood volume; bleeding
What is shock?
a state in which diminished cardiac output or reduced effective circulating blood volume impairs tissue perfusion and leads to cellular hypoxia
Capillary bed perfused, sphincters controlled, AV shunts controlled, minimal hypoxia and drop of pH across capillary beds are characteristic of what stage?
Normal stage
What is the importance of factor XII (Hageman’s Factor)
Microbial components can activate coagulation in affected tissues directly through factor XII
What is the role of PDGF as a tissue mediator?
Secreted by activated platelets and macrophages. Induces vascular remodeling and smooth muscle cell migration. Stimulates fibroblast growth and collagen synthesis
What is this?
Nutmeg liver - centri-lobular congestion
What are some roles of inflammatory responses in septic shock?
TNF, IL-1, and other cytokines will trigger downstream events leading to a hyper inflammatory state
What is this an image of?
Waterhouse-Friderichson syndrome (NEEDS CORTICOSTEROIDS!)
Arteriolar vasodilation (pooling of blood), increased capillary hydrostatic pressure, decreased function of vital organ, and severe metabolic lactic acidosis are characteristics of what stage?
Irreversible stage
What is the role of organ dysfunction in septic shock?
Systemic hypotension, interstitial edema, and small vessel thrombosis all decrease the delivery of oxygen and nutrients to tissues
Stage in which increasing tissue hypoxia and beginning of lactic acidosis due to anaerobic metabolism in the tissues
Progressive
Peripheral vasoconstriction, AV shunts open (redistributing blood to heart and brain), decreased pH across capillary beds, hemodilution (interstitial fluid moves into vascular spaces) are characteristics of what stage?
Reversible or non-progressive stage
What is the role of EGF as a tissue mediator?
Stimulates cell growth via tyrosine kinases
What is the role of induction of a pro-coagulative state in septic shock?
Sepsis alters the expression of many factors to favor coagulation by decrease of endothelial anti-coagulant factors. Can lead to DIC
What is the role of FGF as a tissue mediator?
Stimulates angiogenesis
What is the role of endothelial activation in septic shock?
activation leads to widespread leakage and tissue edema which has deleterious effects on nutrient delivery and waste removal
What is this an image of?
Nutmeg Liver - from passive congestion, this was a result of right-sided heart failure
What is the arrow pointing to?
Fibrin thrombi in the glomerulus caused by DIC
Decreased blood volume, maximum peripheral vasoconstriction, lactic acidosis, decreased capillary perfusion, sludging and clotting begin are characteristics of what stage?
Progressive stage
Stage that even if the hemodynamic defects are corrected tissue survival is not possible
Irreversible
What is the arrow pointing to?
Microthrombi in the glomerulus caused by DIC.
What percent of patients survive hypovolemic shock?
90% survival with appropriate management
Anaerobic metabolism in tissues leads to what?
Lactic acidosis
What is the role of TGF-beta as a tissue mediator?
Angiogenesis, fibrosis, and cell cycle arrest
What is this an image of?
Shock liver, with cell dropout - prolonged hypoxia produces “cell dropout” (necrosis) of hepatocytes. Liver enzymes would be moderately increased
What percent of patients survive septic or cadiogenic shock?
50-80% range
How to manage septic shock?
pressors (dopamine) and IV fluid to manage until the underlying cause is discovered
What is cardiogenic shock?
results from low cardiac output due to myocardial pump failure
What is the role of VEGF as a tissue mediator?
Stimulates angiogenesis
What is systemic inflammation shock?
inflammatory mediators lead to vascular leakage and blood pooling
What is the presentation of DIC in the clinic?
Massive bleeding
