Inflammation and Repair Flashcards
Steps in LEUKOCYTE RECRUITMENT
MRATC
1. Margination
2.Rolling
3.Adhesion
4.Transmigration
5. Chemotaxis
The process of leukocyte ACCUMULATION at the PERIPHERY of the blood. vessels
Margination
TRANSIENT BINDING and DETACHMENT of leukocytes to the endothelium
Mediated by SELECTINS
Rolling
FRIM ADHESION of leukocytes to the endothelium
Mediated by INTEGRIN
Adhesion
The process of MIGRATION of 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
Type of inflammatory mediators that are normally SEQUESTERED in INTRACELLULAR GRANULES
Can be rapidly secreted by granule exocytosis or are synthesized de novo in response to a stimulus
CELL DERIVED MEDIATORS
histamine
serotonin
cytokines
arachidonic acid derivatives (prostaglandins and//leukotrienes)
Type of inflammatory mediators that are PRODUCED MAINLY in the LIVER
Present in the circulation as INACTIVE precursors that must be activated by PROTEOLYTIC cleavage to acquire their biologic properties
PLASMA DERIVED MEDIATORS
complement
coagulation system
kinin system
Vasoactive amine found in PLATELETS and NEUROENDOCRINE CELLS
Causes VASOCONSTRICTION
Serotonin
VASODILATION
PGI2 (Prostacyclin)
PGE1 (Prostaglandin)
PGE2 (Dinoprostone)
PGD2
VASOCONSTRICTION
TXA2
LTC4
LTD4
LTE4
INCREASED VASCULAR PERMEABILITY
LTC4
LTD4
LTE4
CHEMOTAXIS, LEUKOCYTE ADHESION
LTB4
Hydroxyeicosatetratenoic acid (HETE)
Most abundant complement
C3
Complement that acts as OPSONIN
C3b
ANAPHYLATOXINS
C3a, C4a, C5a
MEMBRANE ATTACK COMPLEX (MAC)
C5b
C6-C9
Deficiency of the ff complement-related protein causes HEREDITARY ANGIOEDEMA
C1 inhibitor deficiency
Deficiency of the ff complement protein increases susceptibility to INFECTIONS involving PYOGENIC BACTERIA
C3
Deficiency of the ff complement proteins increases susceptibility to IMMUNE COMPLEX MEDIATED DISEASE
C1q, C2 and C4
Deficiency of the ff complement protein increases susceptibility to NEISSERIA INFECTIONS
C5-C9
Main cells involved in CHRONIC INFLAMMATION
monocytes/macrophages
lymphocytes
Collections of ACTIVATED MACROPHAGES, some of which form MULTINUCLEATED GIANT CELLS often w/ T lymphocytes and sometimes associated w/ CENTRAL NECROSIS
Granuloma
2 kinds of cells seen in GRANULOMAS
Epithelioid cells
Giant cells
Precursor cell of epithelioid cells and giant cells
Macrophages
Type of tissue whose cells can READILY REGENERATE as long as the pool of stem cell is preserved
LABILE TISSUES
bone marrow
vaginal epithelium
Type of tissue whose cells are considered to be terminally differentiated and are NON-PROLIFERATIVE in POSTNATAL LIFE
PERMANENT TISSUES
neurons
cardiac muscle
Type of tissue whose cells are quiescent and have only minimal replicative activity in their normal state
Capable of PROLIFERATING IN RESPONSE TO INJURY OR LOSS OF TISSUE MASS
STABLE TISSUES
smooth muscles
endothelium
liver parenchyma
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 PERMANENT TISSUES
Connective Tissue Deposition
Steps in healing by CT deposition
- Angiogenesis
- Formation of granulation tissue
- Remodeling of the scar
Most notable growth factor in ANGIOGENESIS
VEGF
Most important CYTOKINE for synthesis and deposition of CT
TGF-B
Hallmark of REPAIR
Granulation tissue
Components of GRANULATION TISSUE
- Proliferation of FIBROBLASTS
- LOOSE CT
- Angiogenesis
- Inflammatory cells
Most important source of growth factors during repair
Macrophage
Factors that impede repair
infections
DM
vitamin C deficiency
glucocorticoids (-) TGF-B
pressure
poor perfusion
foreign bodies
location of injury
