02 - Inflammation and Repair Flashcards
Response of vascularized tissues to infections and damaged tissues that brings cells and molecules of host defense from the circulation to the sites where they are needed, in order to eliminate the offending agents.
Inflammation
General steps of inflammatory response.
A. Recruitment of leukocytes
B. Regulation of response
C. Recognition of injurious agent
D. Removal of agent E. Resolution
Morphologic hallmarks of acute inflammation.
Vasodilation and accumulation of leukocytes and fluid in the extravascular tissue
Components of acute inflammation.
- Dilation of small vessels 2. Increased microvascular permeability 3. Emigration of leukocytes and their activation
Most notable mediator that produces vasodilation.
Histamine
Most common mechanism of increased microvascular permeability.
Endothelial cell contraction
Initial vascular response to injury.
Vasoconstriction
An ultrafiltrate of blood, which contains little protein, little or no cellular material, and low specific gravity as a result of osmotic or hydrostatic imbalance across the vessel wall without increase in vascular permeability.
Transudate
An extravascular fluid with high protein content; its presence implies an increased vascular permeability, triggered by tissue injury and ongoing inflammatory reaction.
Exudate
Steps in leukocyte recruitment.
A. Margination B. Rolling C. Adhesion D. Transmigration
The process of leukocyte accumulation at the periphery of blood vessels.
Margination
Molecules in the endothelium and leukocyte responsible for rolling.
P and E-selectins on endothelium with Sialyl-Lewis-X on leukocyte; Glycam-1, CD34 on endothelium with L-selectin on leukocyte
Molecules responsible for adhesion.
ICAM-1 on endothelium with CD11/CD18 integrins (aka, LFA-1, Mac-1) on leukocyte; VCAM-1 on endothelium with VLA-4 on leukocyte
The process of migration of the leukocytes through the endothelium.
Transmigration or diapedesis
Molecules in the endothelium responsible for transmigration.
PECAM-1/CD31
Process of leukocyte migration toward sites of infection or injury along a chemical gradient.
Chemotaxis
Exogenous chemoattractants.
Bacterial products (N-formylmethionine, lipids)
Endogenous chemoattractants.
IL-8, C5a, LTB4
Type of inflammatory mediators that are normally sequestered in intracellular granules and can be rapidly secreted by granule exocytosis or are synthesized de novo in response to a stimulus; examples: Histamine, Serotonin, Cytokines and Arachidonic acid derivatives
Cell-derived mediators
Type of mediators that are produced mainly in the liver and are present in the circulation as inactive precursors that must be activated by proteolytic cleavages to acquire their biologic properties; examples: Complement, coagulation and kinin systems
Plasma-derived mediators
Vasoactive amine that results in vasoconstriction; sources include platelets and neuroendocrine cells.
Serotonin
Most abundant complement.
C3
Complement that acts as an opsonin.
C3b
Anaphylatoxins.
C3a, C4a, C5a
Membrane attack complex.
C5b, C6-C9
Anti-inflammatory cytokines for regulation of the inflammatory response.
Lipoxin, TGF-_, IL-10
Inflammatory response of prolonged duration in which inflammation, tissue injury, and attempts at repair coexist, in varying combinations.
Chronic inflammation
Two kinds of cells seen in granulomas.
Epithelioid cells (activated macrophages with pink, granular cytoplasm, resembling epithelial cell) and giant cells
Type of tissue whose cells can readily regenerate as long as the pool of stem cells is preserved; examples: Bone Marrow, and Vaginal Epithelium
Labile tissues
Cells of theses tissues are quiescent and have only minimal replicative activity in their normal state; capable of proliferating in response to injury or loss of tissue mass; examples: Smooth muscles, Endothelium, and Liver Parenchyma
Stable tissues
Cells of these tissues are considered to be terminally differentiated and nonproliferative in postnatal life; examples: Neurons, Cardiac muscle
Permanent tissues
Type of repair that happens in labile and stable tissues; influenced by growth factors.
Regeneration
Type of repair that happens in chronic, severe inflammation, and in permanent tissues.
Connective tissue deposition
Steps in healing by connective tissue deposition.
A. Angiogenesis B. Formation of granulation tissue C. Remodeling of the scar
Most notable growth factor in angiogenesis.
VEGF
Most important cytokine for synthesis and deposition of connective tissue.
TGF-_
The pink, soft, granular tissue seen beneath the scab of a skin wound; hallmark of tissue healing; appears by 3-5 days.
Granulation tissue
Histologic findings of granulation tissue.
Proliferation of fibroblasts and new, thin-walled, delicate capillaries (angiogenesis) in a loose ECM, often with admixed inflammatory cells, mainly macrophages
