Immunology Flashcards
What type of shock can you get from gram neg and gram positive bacteria?
Gram neg (endotoxins LPS) septic shock Gram pos (superantigens) toxic shock (staph A) TSST-1 [super-absorbable tampons correlated with TSS]
define: septicemia, sepsis, septic shock and toxic shock
Septicemia: Life threatening bacterial infection of the blood stream (Gram -/+)
Sepsis: The presence of pathogenic organisms or their toxins in the blood or other tissues. Characterized by a systemic inflammatory response syndrome (SIRS).
Septic shock: Severe sepsis with hypotension despite fluid resuscitation.
Toxic shock: Subset of septic shock; the result of super antigens.
How is inflammation initiated in sepsis?
1 Endotoxin or LPS binding of Gram -
2 TLR4 and CD14 on Macrophage and NK
3 Release of cytokines like TNF alpha, IL-1, IL-6 (pro-inflammatory)
4 Activation of hypothalamus-Fever, tachycardia
4 Increase NO, prostaglandin, leukotriene activity in Endothelial cells leads to vasodilation
4 Damage to Endothelial cells
5 Cellular hypoxia (decreased vascular resistance)
6 lactic acidosis
7 Death
What’s the major difference between how septic and toxic shock?
How the bacteria are recognized
Septic Gram - PRR on phagocyte
Toxic Gram + HLA-TCR (binding them together leads to cross-linking activation; NOT processed into peptides)
What type of cells are activated in sepsis and toxic shock?
septic shock: NK and macrophage
Toxic shock: CD4 and macrophages (produce IL-2 unique b/c growth factor for T-cells) 10% T-cells get activated.
WHAT IS THE BIG PICTURE WITH SEPSIS AND TOXIC SHOCK?
Activation of immune system leading to increase in pro-inflammatory cytokines, inflammation, endothelial (and organ) damage, vascular leakage, decreased SVR and hypotension.
What is most responsible for the pathophysiology of septic shock?
The bodies inflammatory response rather than the infectious agent
Whose most susceptible to sepsis?
Immunocompromised
Organ transplant recipients
Patients with long term vascular access (i.e. dialysis)
What type of hypersensitivity is associated with anaphylatic shock? This is mediated by which Immunoglobulin? What effects does this have?
Type I
IgE binds to mast cells to stimulate the release of cytokines, breakdown of arachidonic acid, and granule exocytosis.
Bronchoconstriction, increased vascular permeability decrease SVR.
What effect does the release of cytokines, granules, and enzymatic products of arachidonic acid from mast cells, have on the body?
cytokines = inflammation
granules = vasoactive amines (histamine) lead to vasodilation, tissue damage from proteases
Arachidonic acid: breaks into PG (vasodilation), and Leukotrienes (smooth muscle contraction)
What effect does the histamine released from cardiac mast cells have on the heart?
Binds H1 receptor on vascular smooth muscle: decrease MAP, increase coronary flow
Binds H2 receptor on cardiac tissue: Induce arryhthmias, and AV blocks, and increases formation of thrombi
Release catecholamines-tachycardia and hypotension
