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 agent
inflammation
the initial response to infections and tissue damage
acute inflammation
Inflammatory response of prolonged duration in which inflammation, tissue injury, and attempts at repair coexist, in varying combinations
chronic inflammation
Restoration of tissue architecture and function after and injury
tissue repair
cellular infiltrate in acute inflammation
mainly neutrophils
cellular infiltrate in chronic inflammation
monocytes/ macrophages, lymphocytes
severe and progressive tissue injury, fibrosis
a. chronic inflammation
b. acute inflammation
chronic
Usually mild and self limited tissue injury and fibrosis
a. chronic inflammation
b. acute inflammation
acute inflammation
prominent local and systemic signs
a. chronic inflammation
b. acute inflammation
acute
less local and systemic signs
a. chronic inflammation
b. acute inflammation
chronic
components of acute inflammation
- Dilation of small vessels
- Increased microvascular permeability
- Emigration of leukocytes and their activation
initial vascular response to injury
vasoconstriction
Most notable mediator that produces vasodilation; stored in mast cells, platelets, and basophils
histamine
Most common mechanism of increased microvascular permeability in acute inflammation
Endothelial cell contraction
what cells produce histamine in inflammation
mast cells
platelets
basophils
Morphologic hallmarks of acute inflammation
Vasodilation
- Accumulation of leukocytes and fluid in the extravascular tissue
outcomes of acute inflammation
- Resolution
- Pus formation (abscess)
- Healing by fibrosis
- Progression to chronic inflammation
Steps in leukocyte recruitment
A. Margination
B. Rolling
C. Adhesion
D. Transmigration
E. Chemotaxis
The process of leukocyte accumulation at the periphery of blood vessels
margination
Transient binding and detachment of leukocytes to the endothelium, mediated by selectins
rolling
Firm adhesion of leukocytes to the endothelium, mediated by integrins
adhesion
The process of migration of the leukocytes through the endothelium, mediated by PECAM-1/CD31
Transmigration or Diapedesis
Process of leukocyte migration toward sites of infection or injury along a chemical gradient, mediated by exogenous or endogenous substances
chemotaxis
what mediates rolling
selectins
what mediates adhesion
integrins
what mediates transmigration or diapedesis
PECAM-1 / CD31
Vasoactive amine found in platelets and neuroendocrine cells; causes vasoconstriction
Serotonin
Type of inflammatory mediators that are produced mainly in the liver, and are present in the circulation as inactive precursors that must be activated by proteolytic cleavage to acquire their biologic properties;
Plasma-derived mediators
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 (Prostaglandins and Leukotrienes)
Cell-derived mediators
PGI2 (prostacyclin)
a. vasodilation
b. vasoconstriction
c. increased vascular permeability
d. chemotaxis, leukocyte adhesion
a.
PGE1
a. vasodilation
b. vasoconstriction
c. increased vascular permeability
d. chemotaxis, leukocyte adhesion
a.
PGE2
a. vasodilation
b. vasoconstriction
c. increased vascular permeability
d. chemotaxis, leukocyte adhesion
a
PGD2
a. vasodilation
b. vasoconstriction
c. increased vascular permeability
d. chemotaxis, leukocyte adhesion
a
LTC4
a. vasodilation
b. vasoconstriction
c. increased vascular permeability
d. chemotaxis, leukocyte adhesion
c
D4
a. vasodilation
b. vasoconstriction
c. increased vascular permeability
d. chemotaxis, leukocyte adhesion
c,b
E4
a. vasodilation
b. vasoconstriction
c. increased vascular permeability
d. chemotaxis, leukocyte adhesion
c,b
TXA2
a. vasodilation
b. vasoconstriction
c. increased vascular permeability
d. chemotaxis, leukocyte adhesion
b
LTC4
a. vasodilation
b. vasoconstriction
c. increased vascular permeability
d. chemotaxis, leukocyte adhesion
b.
D4
a. vasodilation
b. vasoconstriction
c. increased vascular permeability
d. chemotaxis, leukocyte adhesion
b,c
E4
a. vasodilation
b. vasoconstriction
c. increased vascular permeability
d. chemotaxis, leukocyte adhesion
b,c
LTB4
a. vasodilation
b. vasoconstriction
c. increased vascular permeability
d. chemotaxis, leukocyte adhesion
d
Hydroxyeicosatetraenoic acid (HETE)
a. vasodilation
b. vasoconstriction
c. increased vascular permeability
d. chemotaxis, leukocyte adhesion
d.
most abundant complement
C3
complement that acts as an opsonin
C3b
anaphylatoxins
C3a, C4a, C5a
membrane attack complex
C5b
C6-c9
Deficiency of the following complement-related protein causes hereditary angioedema
C1 inhibitor deficiency
Deficiency of the following complement protein increases susceptibility to infections involving pyogenic bacteria
C3
Deficiency of the following complement proteins increases susceptibility to immune complex-mediated disease
C1q, C2, C4
Deficiency of the following complement proteins increases susceptibility to Neisseria infections
C5-C9
Main cells involved in chronic inflammation
macrophages
lymphocytes
Collections of activated macrophages; some of which form multinucleated giant cells, often with T lymphocytes, and sometimes associated with central necrosis
granuloma
Two kinds of cells seen in granulomas
- Epithelioid cells
2. Giant cells
Type of tissue whose cells can readily regenerate as long as the pool of stem cells is preserved
labile tissues
Type of tissue whose cells are quiescent and have only minimal replicative activity in their normal state
stable tissues
Type of tissue whose cells are considered to be terminally differentiated and are non-proliferative in postnatal life
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
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-β
Hallmark of repair
Granulation tissue
Components of granulation tissue
- Proliferation of fibroblasts
- Loose connective tissue
- Angiogenesis
- Inflammatory cells