3️⃣ Chemical mediators of acute inflammation Flashcards
(13 cards)
Which cells produce preformed mediators?
Mast cells, basophils, platelets store histamine in granules.
What are plasma-derived mediator systems?
Complement cascade, kinin system, coagulation cascade, fibrinolytic system—circulate as zymogens activated locally.
List advantages of plasma-derived mediators.
Inactive precursors reduce systemic toxicity, localized activation, amplification cascades, cross-talk between pathways.
What triggers histamine release?
Physical injury, IgE cross-linking, C3a/C5a, cytokines.
What are histamine’s actions?
Arteriolar vasodilation and increased venular permeability via endothelial cell contraction.
What are the three main classes of eicosanoids?
Prostaglandins, leukotrienes, and lipoxins, derived from arachidonic acid.
What are prostaglandins’ roles in inflammation?
Vasodilation, increased permeability, pain sensitization (hyperalgesia), fever induction.
What are leukotrienes’ roles?
Chemotaxis (LTB₄), increased vascular permeability (LTC₄, LTD₄, LTE₄), bronchoconstriction.
What is the role of lipoxins?
Anti-inflammatory: inhibit neutrophil adhesion and chemotaxis, promote resolution.
Which cytokines mediate the acute phase response?
IL-1, IL-6, and TNF-α induce hepatic synthesis of acute phase proteins (CRP, SAA, fibrinogen).
How do prostaglandins mediate fever?
They reset hypothalamic thermoregulatory center to a higher set-point, via PGE₂.
What changes constitute the acute phase response?
Fever, leukocytosis (neutrophilia/lymphocytosis/eosinophilia), elevated acute-phase proteins, anorexia, malaise, tachycardia.
Describe key events in septic shock.
Microbial products induce massive TNF/IL-1 release, leading to DIC, distributive shock (vasodilation, increased leakage), organ failure.
