Acute vs chronic inflammation Flashcards
General features of acute inflammation
-Short time frame
-See cardinal signs
-Neutrophils and fibrin dominate
-Return to normal, see tissue fibrosis, or progress to chronic inflammation
General features of chronic inflammation
-Long time frame
-Cardinal signs are not prominent
-Macrophages and lymphocytes predominate
-Cell mediated immunity important
-Ongoing with or without progression or resolve with tissue damage and fibrosis
Development of chronic inflammation
Persistence of the agent or material that incited inflammation. Acute response was unable to resolve inflammatory stimulus. Can be due to resistant agent or low resistance of the host
Vascular events of chronic
-Mediators of acute vascular changes are degraded
-Emigration shifts to macrophages and lymphocytes
Cells involved in chronic inflammation
-Monocytes
-Lymphocytes
-NK cells
-Fibroblasts
-Endothelium
Cells derived from macrophages
-Epithelioid macrophages-Larger and have secretory role
-Giant cell-Fuse macrophage and epithelioid cell, phagocytic and secretory
Mediators of chronic inflammation
-Lymphokines
-Monokines
The ideal resolution
-Stimuli removed
-Mediators removed
-Vessels return to normal
-Inflammatory debris removed
-Normal cells repopulate
-Tissue return to normal
Not ideal resolution
-Stimuli not removed
-Tissue does not return to normal (irreversible) usually due to collagen
Healing
Initiated at time of injury
Mechanisms of healing
-Regeneration-Return to normal
-Replacement- replaced by fibrous connective tissue (new homeostasis acheived)
Regeneration occurs with what cells
-Labile and stable cells not permanent cells (neurons, cardiac myocytes)
Criteria for regeneration to occur
-Stromal integrity- need ECM architecture of the tissue
-Regenerative capacity of the injured cells
Granulations
Mechanism used to replace irreversibly damaged tissue
Granulation tissue
Transient fibrovascular tissue grows into site of irreversible damage. Minimize size of damage and replace with collagen
