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Host system (Injury (Inflammation (Signs (REDNESS, 2., SWELLING, PAIN,…
Host system
Injury
An alteration in the body’s environment that causes tissue damage
Inflammation
The nonspecific response of the body to injury
Signs
REDNESS
2.
SWELLING
PAIN
LOSS OF NORMAL FUNCTION
reflexive vasoconstriction
vasodilation
increase blood flow hyperemia
redness/heat
permeable
Exudate into permeable tissue
swelling edema
Pain/swelling/ loss of function
dilutes pathogens decrease effectiveness
Blood more cellular viscous
decrease flow rate in circulation injured tissue
Margination
Movement WBC endothelial wall
Pavementing
2 more items...
Kinin prostaglandin release pressure sensory nerve
Pain
Acute
Cells
Neutrophils (PMNs)
Granular cytoplasm
Respond to chemotactic agents
Stem cell (marrow)
Lysosomal enzymes
Primary inflammation cell
Polymorphonucular
Plasma cells
Eosinophils
Mast cells
Derived from Stem cells
Chronic
Lymphocytes
Long lived
Mononuclear leukocytes from stem cells
B Lymphocyte
WBC defense against bac, virus, fungi
Antibodies
end binds B cell other to organism help kill it
Y shape protien
Immunoglobulins
IgM,
IgD
IgG
IgA
IgE
Coat bac for phagocytosis
Activate complement
Plasma Cell
Humoral immunity (antigen-antibody rnx)
T Lymphocte
WBC intensify response like B/ macrophage
pd cytokins interlukin further stimulate host
cytokins
protein secreted by cell affect behavior nearby cells
Monocytes (macrophages)
Nongranular cytoplasm
Chronic infection
Long lived
1 round nucleus
Macrophages in tissue
Phagocytosis
Present antigen to T-cell
Complement
Mediates vascular response by histamine release
Recruits phagocytic leukocytes (chemotaxis)
Opsonizes target phagocytic cells (recognizes & attaches targets)
serum factors facilitate phagocytosis (phagocytes attach to organisms by opsonins)
enhance phagocytosis by leukocytes (opsonization)
Damages target cells (or tissue) Called the complement cascade when activated
Chemical mediators
Lipoxygenase pathway
products leukotrienes
Cause adherence of PMNs to endothelial walls
chemotactic agents
Vasodilation & increased vascular permeability
Leukotrienes and prostaglandins are arachidonic acid metabolites
Derived from
WBC
Blood
Lysosomal enzymes
pathogenic organisms
Can start or amplify the inflammatory vascular response
Exogenous
Endogenous
Histamine (powerful vasodilator, mast cells
Kinins (vasodilator, bradykinins = pain!)
NSAID –aspirin mess with the kinins
Stimulates pd prostaglandins
May potentiate pain sensation in CNS
Fatty acids in tissue; are vasodilators increase permeability
cause CT change
Increase dilation
permability
induce pain
Arachadonic acid metabolites (from PMNs & macrophages – manufactured & not stored prostaglandins pain)
Cyclooxygenase (COX) Pathway
pd prostaglandins
capable of resorbing alveolar periodontitis
NSAIDs
inhibit cyclooxegenase suppressing prostaglandin synthesis
COX inhibitors
Mast Cell
CT cell from liver
contain heparin (anti-clotting polysaccharide)
contain histamine (mediator hypersensitivity dilates capillaries)
Eosinophils
granular leukocytes