innate immunity
non-specific immunity –> natural barriers and inflammation
inflammatory response
adaptive immunity
targets specific microbes (antigens) that have breached surface barriers
develops after exposure to specific antigen
full immune response
purpose of inflammation
minimize the effects of injury by rapidly diluting, destroying, or neutralizing the harmful agent
allows new tissue to be generated
protective effect
causes of inflammation
direct physical damage ischemia/infarction allergic reaction extremes of heat or cold infection
inflammation process
cell injury –> damaged cell releases inflammatory mediators into ISF and blood)
- acute inflammation (local response) –> vascular stage; cellular stage
- systemic response (fever,, malaise, headache, anorexia)
leukocytes
neutrophils
basophils
eosinophils
lymphocytes
T-lympho (cell-mediated)
B-lympho (anti-bodies)
monocytes (phagocytosis; travel in BVs)
macrophages (mature monocyte; phagocytosis; remove debris)
5 cardinal signs of inflammation
redness warmth swelling loss of function pain
vascular response
- vasodilation
2. increased capillary permeability
vasodilation importance
hyperemia = increase in blood flow to the injured tissue (getting more WBC to injured area to help with resolution)
vasodilation –> redness and warmth
capillary permeability importance
more permeability = need to get WBC from capillary into injured tissue; fluid into ISF can also dilute toxin
plasma proteins enter interstitial space –> fluid in IS space increases –> swelling; loss of function
mediators: later stages of inflammation
mast cells activate membrane phospholipids –> arachidonic acid
AA –> leukotrienes (lipooxygenase) or prostaglandins/thromboxanes (cyclooxygenase)
L = increased capillary permeability
PG = vasodilation and increased capillary permeability
cellular response
changes in endothelium; WBCs move into area of injury or infection
stages of cellular response
- margination and adhesion of WBCs to endothelium (vessel wall near injured tissue)
- diapedesis (migrate through endothelium; go through capillary bed)
- chemotaxis –> neutrophils attracted to area of inflammation
- phagocytosis (removal of debris/antigen)
cause of fever
pyrogens (interleukin-1)
act on hypothalamus
purpose
body temp higher –> impairs growth of bacteria, viruses, and pathogens
patterns
varying depending on what is causing the fever (can give clues to what is causing it)
intermittent, remittent, sustained, recurrent
course of a fever
- release of pyrogens in circulation
- hypothalamic control reset –> high
- body response = increase body temp (shiver, vasoconstriction, increased HR/BMR, curl up body)
- body reaches new temperature (feel warm)
- remove pyrogens –> resets hypothalamus to normal
- body response –> increase heat LOSS (sweating, vasodilation, lethargy, extend body)
complications of inflammation
- infection
2. skeletal muscle spasm
chronic inflammation common characteristics
Less swelling and exudate
Presence of more macrophages, fibroblasts, lymphocytes
Continued tissue destruction
More fibrous scar tissue
Granuloma may develop around foreign object
ASA and NSAIDS
inhibit cyclooxygenase –> less production of PG –> limiting cap. permeability –> decreased swelling and vasodilation
local effects –> reduces warmth and redness in inflammed tissue
systemic effects –> decrease fever and reduce pain
acetaminophen
systematic effects
reduces PGs –> fever and pain management
glucocorticoids
inhibit arachidonic acid –> decrease in leukotrienes AND PG (decreased vasodilation and cap. permeability)
prolonged use: decrease bone density; decrease WBC activity (prone to infection)
