3rd Year MBBS
Infection and Inflammation
Inflammatory Mediators, Morphologic Patterns and Outcomes of Inflammation
Connect the mediator response with tissue morphology, the possible outcomes of acute inflammation, and the consequences when inflammatory defense is inadequate or excessive.
1. THE TOPIC IN ONE CONNECTED FLOW
Inflammation begins when tissue injury or infection activates plasma protein systems and resident cells. Their mediators produce vascular and leukocyte responses, which determine the tissue pattern seen microscopically. The final result depends on whether the cause is removed, how much tissue is damaged, and whether the inflammatory response remains properly controlled.
effective mediator and leukocyte activity → removal of the cause → resolution or repair; defective activity → persistent infection and poor healing; excessive activity → collateral tissue injury.
2. KEY CLINICAL CONNECTIONS
Histamine → arteriolar dilatation + venular permeability → early redness and edema.
Bradykinin and PGE₂ → pain pathways → inflammatory tenderness.
C3b → microbial coating → easier phagocytosis.
C5a → leukocyte chemotaxis; C5b–C9 → membrane attack complex → microbial membrane injury.
Persistent fibrin → fibroblast and vessel ingrowth → organization → fibrosis.
Neutrophils + necrotic debris → pus → localized collection → abscess.