Hem III and IV/Shock, Embolus, Necrosis Flashcards
What are the 3 main types of shock?
Cardiogenic shock, hypovolemic shock, and septic shock
What are the four main events in septic shock?
Vascular event (vasodilation, increased permeability)
Thrombotic (microvascular thrombosis, DIC)
Immunosuppressive (counter regulatory measure)
Metabolic (insulin resistance)
What produces the procoagulant state that can lead to thrombotic events in septic shock?
Endotoxins from the bacteria produce the procoagulant state
What causes adrenal insufficiency during shock?
Waterhouse-Friderichsen syndrome; it is adrenal hemorrhage and necrosis caused by DIC or endotoxin production from bacteria
What is disseminated intravascular coagulation (DIC)?
Concurrent microvascular thrombosis and fibrinolysis that occurs due to the procoagulant effects (from endotoxins of bacteria) and cytokines (TNF and IL-1) induce endothelial cells to make tissue factor leading to coagulation
What is the best screening test for DIC?
Elevated fibrin split products especially D-dimer
What is ARDS?
Adult respiratory distress syndrome. Combination of decreased cardiac output, vascular permeability and endothelial injury in the lungs.
What is the end result of septic shock (and what leads to mortality)?
End-organ damage
What are the 3 stages of shock?
- Nonprogressive phase where vital organ perfusion is maintained via reflex mechanisms
- Progressive stage where tissues are hypoperfused and acidosis sets in
- Irreversible stage where pronounced cell death is present
What is SIRS?
Systemic inflammatory response syndrome: nonspecific clinical response to either infection or noninfectious inflammatory process
What is bacteremia?
A blood infection without systemic response
What is acute tubular necrosis?
End-organ damage of the kidney, often due to shock
What is heparin-induced thrombocytopenia?
Platelet destruction due to heparin therapy; thrombosis results from destroyed platelets activating other platelets
How does fibrinolysis occur?
Tissue plasminogen activator converts plasminogen to plasmin, and plasmin cleaves fibrin and serum fibrinogen and blocks platelet aggregation
Why does cirrhosis of the liver lead to a disorder of fibrinolysis and plasmin overactivity?
Cirrhosis of the liver results in reduced production of alpha2-antiplasmin and thus overactivity of plasmin