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
Three stages of granulation tissue
-Inflammatory
-Proliferative
-Renodeling stage
Granulation morphology
-Zone of necrotic debris and inflammation
-Zone of capillary sprouts and arches
-Zone of capillary and fibroblast proliferation
-Zone of mature CT
Macrophages in granulation tissue
-Remove debris
-Produce monokines involved in healing (PDGF, FGF, TGF b)
Endothelium in granulation tissue
-New vessels grow in response to angiogenic factors
-Provide nutrients to healing area
-Highly permeable and leak plasma and fluids to support healing
Fibroblasts in granulation
-Make collagen to fill the damaged area (induced by TGF b, FGF, EGF)
-Wound contraction (myofibroblasts)
WOund healing categories
-First intention
-Second intention
First intention healing
-Incisions
-Small defect and rapid healing
-Minimal scar
Second intention healin
-Excisional skin wounds
-Large defect and long healing
-Scar tissue
-Specialized tissue with damage may be lost
Factors affect healing
-Nutrition
-Age
-Presence of concurrent disease
-Persistence of damaging stimulus
-Size and location of damage
