1.8 Immunology of Shock

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  1. What is septicemia?
    • Life threatening bacterial infection of the blood stream
    • Gr+ or Gr- bacteria
  2. What is sepsis?
    • Presence of pathogenic organisms or their toxins in the blood or other tissues
    • Characterized by a systemic inflammatory response which can progress to circulatory system dysfunction, multiple organ failure, and death
  3. What is septic shock?
    Severe sepsis with hypotension despite adequate fluid resuscitation
  4. What is toxic shock?
    Subset of septic shock produced by organisms which produce super-antigens
  5. What is anaphylatic shock?
    • Type 1 hypersensitivity
    • Circulatory collapse
    • Respiratory difficulties
    • IgE mediated
  6. What is the microorganism most likely involved in the initiation of septic shock?
    • Bacteria
    • Gr(-) endotoxin - LPS
    • Gr(+) exotoxin - superantigen
    • Virus - influenza, varicella
    • Fungi - Candida spp
    • Protozoa

    • E. Coli
    • Pseudomonas aeruginosa
    • Staph Aureus
    • Strep pyogens and agalactiae
    • And others
  7. What is the mechanism by which endotoxins can result in the pathophysiology of shock?
    • Gr- Bacteria¬†
    • Binds to CD14 and TLR
    • Activates Macrophages and NK cells
    • Induce synthesis of TNF-a and IL-1B
    • Responsible for Septic Shock
  8. What is the mechanism by which superantigens can result in the pathophysiology of shock?
    • Gr+ Bacteria
    • Bind to HLA II and TCR
    • Activate macrophages and CD4+ T cells
    • Induce synthesis of TNF-a, IL-1B, IL-2, and IFN-y
    • Responsible for Toxic Shock Syndrome
  9. What is the pathophysiology of anaphylactic shock, including sensitization, mast cell activation, and degranulation, and mediator activities?
    • Allergen cross-links IgE on mast cells through Fce receptors
    • (Cross linking causes degranulation, breakdown of Arachidonic Acid, Synthesis and secretion of cytokines)
    • Mediators released
    • Bronchoconstirction, mucus secretion, diminished cardiac contractility, increased vascular permeability, vasoconstriction of arteries
  10. What do endotoxins bind to?
    CD14 and TLR
  11. What does Endotoxins (LPS) activate?
    Macrophages and NK cells
  12. What does Endotoxin (LPS) induce synthesis of?
    TNF-a and IL-1B
  13. What is Endotoxin (LPS) responsible of causing?
    Septic Shock
  14. What type of bacteria produces Endotoxin (LPS)?
    Gr (-) Bacteria
  15. What type of bacteria produces Superantigen (Exotoxin)?
    Gr (+) Bacteria
  16. What does Superantigens bind to and is it at the antigen binding site?
    • HLA II and TCR
    • No
  17. What does Superantigens (Exotoxin) activate?
    Macrophages and CD4+ T Cells
  18. What does Superantigen (Exotoxin) induce synthesis of?
    TNF-a, IL-1B, IL-2, and IFN-y
  19. What is Superantigen (Exotoxin) responsible of causing?
    Toxic Shock Syndrome
  20. What diseases are Superantigens implicated in?
    • Food Poisoning
    • Erythematous skin reaction
    • Fever
    • Toxic Shock Syndrome
  21. What does Superantigens cross link with?
    MHC II and TCR V-B regions
  22. Are superantigens processed by APC?
  23. What do activated APC and T cells release and what do they affect?
    • Release inflammatory cytokines and other mediators
    • Affects endothelial cells
  24. Who are most susceptible to sepsis?
    • Individuals w/ compromised immune response
    • Organ transplant recipients
    • Patients w/ long term vascular access
  25. What does Nitric Oxide do?
    Increases vasodilation
  26. What does Leukotrienes and Prostaglandins do?
    Increase vasodilation
  27. What does Bradykinin do?
    Increase capillary permeability
  28. What does disseminated intravascular coagulation do?
    Formation of clots
  29. Where are Cardiac Mast Cells found and what receptors do they possess and what binds to them?
    • Present in and around cardiac vessels
    • Has Fce receptors which bind IgE
  30. What can degranulate Cardiac Mast Cells?
    • Antigen and other stimuli
    • C3a and C5a, substance P, eosinophilic cationic proteins
    • Muscle relaxants, contrast media
  31. What do histamine bind to on vascular smooth muscle and what is the effect?
    • H1 Receptors
    • Rapid decrease in mean aortic pressure
    • Increase in coronary blood flow
  32. What do histamine bind to on cardiac tissue and what is the effect?
    • H2 Receptors
    • Induces arrhythmias and AV conduction blocks
    • Induces tissue factor which activates factor X leading to formation of thrombi
  33. What does histamine induce release of and what are the effects?
    • Catecholamines
    • Hypotension
    • Tachycardia
  34. What are CV effects of eicosanoids (Leukotrienes, Prosteoglycans)?
    • Induce increased coronary vascular resistance
    • Decreases contractile function
  35. What are CV effects of platelet activation factor (PAF)?
    • Decreases coronary blood flow
    • Depresses myocardial contractility
    • Recruits neutrophils and eosinophils
    • Activates platelets
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1.8 Immunology of Shock
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