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inflammation
response intended to:
eliminate initial cause of cell injury
remove damaged tissue
generate new tissue
endothelial hyperpermeabillity
reaction of vascularized tissues to injury
inflammatory mediators
tumor necrosis factor (alpha)
vascular endothelial growth factors (VEGF)
neutrophils
movement of fluid within cells or interstitial fluid
-itis
inflammation
cardinal signs of inflammation
rubor, tumor, calor, dolor, functio laesa
rubor
redness
tumor
swelling
calor
heat
dolor
pain
functio laesa
loss of function
acute inflammation
short duration (minutes to days)
exudation(secrete) of fluid and plasma, emigration of leukocytes(neutrophils) into tissues
what causes inflammation?
infections, trauma, immune reactions, physical agents, chemical agents, tissue necrosis from any cause
endothelial cells
barrier between circulating blood in vessels and surrounding tissues
what do endothelial cells produce?
antiplatelet and antithrombotic agents (maintains vessel patency)
vasodilators and vasoconstrictions regulate what?
blood flow
endothelial cells are involved in the formation of new blood vessels, this is called?
angiogenesis
platelets
involved in primary hemostasis
releases potent inflammatory mediators
increases vascular permeability
neutrophils
they are phagocytic leukocytes that arrive within 90 minutes
monocytes/ macrophages
phagocytic leukocyte that produce potent vasoactive mediators
vasoactive mediators
prostaglandins, leukotrienes, platelet activating factor, inflammatory cytokines
leukocytosis
increased white blood cells
bands
immature form of neutrophil
eosinophils
parasitic infection and allergic reactions
basophils
contains histamine
binding of IgE triggers release
mast cells
degranulation releases histamine, TNF, IL-16
TNF (tumor necrosis factor)
hypotension, tachycardia associated with sepsis
vasodilation
induced by histamine and nitric oxide mediators
vascular phase
vasodilation, erythema (redness), warmth, edema (swelling)
edema
increased osmotic pressure causes fluid to move into tissues ad produce swelling
cellular stage
margination, chemotaxis, leukocyte activation and phagocytosis, etc.
margination
cytokines cause endothelial cells to express adhesion molecules (leukocyte accumulation to the endothelium)
chemotaxis
chemokines direct trafficking of leukocytes
leukocyte activation and phagocytosis
monocytes, neutrophils and tissue macrophages activated
phagocytosis
engulf and degrade bacterial and cellular debris
what do metabolic burst pathways do?
generates toxic oxygen and nitrogen products that requires oxygen
this kills the microbe
histamine and prostaglandins have?
vasoactive and smooth muscle constricting properties
plasma proteases
activate complement system, clotting cascade, kinin system
chemotactic factors
chemokines
reactive molecules and cytokines are liberated from?
leukocytes
histamine
found in mast and basophil cells
involved IgE antibodies
what cells are first to be released?
mast and basophil cells
histamine causes what?
dilation of vessels, sneezing, runny nose, eye tearing, sinusitis, increased permeability
arachidonic acid metabolites
release leads to production of prostaglandins, induces inflammation, potentiate effects histamine
arachidonic acid metabolites promote?
platelet aggregation and vasoconstriction
platelet- activating factor
induces platelet aggregation and causes bronchospasm
plasma proteins
clotting, complement and kinin systems
clotting
endothelial adhesion, production of PAF
complement
increases vascular permeability, causes vasodilation, improves phagocytosis
kinin
releases bradykinin, increases permeability, contraction of smooth muscle
cytokines
TNF, IL-1 released in response to bacterial toxins, endotoxins, fever, lowers BP
nitric oxide
smooth muscle relaxation; compensatory mechanism that reduces inflammation
free radicals
released during phagocytic process
chronic inflammation
reaction that persists for a prolonged time (weeks to months) without resolution
etiologic agent examples
mycobacterium tuberculi (TB) and treponema pallidum (syphilis)
nonspecific inflammation
non-targeted response
granulomatous inflammation
chronic inflammation often causes a granuloma where there is massing of macrophages surrounded by lymphocytes (1-2 mm lesion)
tuberculosis
prototypical granulomatous chronic inflammatory disease
systemic manifestations of inflammation
acute-phase response, alterations in WBC count, fever, lymph node reaction
lymphadenitis
aka lymphadenopathy; the enlargement of lymph nodes caused by inflammatory processes
where do lymphocytes mature?
in the lymph node; become enlarged and tender during inflammatory process
tissue repair
response to injury in attempt to maintain normal body structure and function
regeneration
injured cells replaced with cells of the same type
replacement
leaves a permanent scar when replaced with connective tissue
body cells involved in tissue regeneration
labile, stable, permanent cells
labile
continue to divide and replicate throughout life, replacing cells that are continually being destroyed (epithelial cells)
what are cancer cells considered as?
labile cells because they are constantly dividing
stable
normally stop dividing when growth ceases; capable of regeneration when confronted with appropriate stimulus (liver and kidney cells)
permanent cells
cannot undergo mitotic division (nerve cells, cardiac muscle cells)
fibrous tissue repair
severe or persistent injury-repair cannot be accomplished with regeneration alone
occurs by replacement with connective (granulation) tissue (scars)
granulation tissue
glistening red, moist connective tissue
contains new capillaries (angiogenesis) and fibroblasts (fibrogenesis)
phases of wound healing
inflammatory phase, proliferative phase, wound contraction and remodeling phase
inflammatory phase
blood clot forms at time of injury
migration of phagocytic WBC to wound site
neutrophils arrive first to ingest and remove bacteria and cellular debris
macrophages arrive 24 hours later (ingest cellular debris)
hemostasis
constriction, platelet aggregation, increased permeability
proliferative phase
building of new tissue to fill wound space
fibroblasts and epithelialization
fibroblast
a connective tissue cell that synthesizes and secretes collagen and other substances needed for wound healing
what do fibroblasts produce?
growth factors that induce angiogenesis
epithelialization
final stage that forms new surface layer during the proliferative phase
remodeling phase
begins approx. 3 weeks (up to 12 months) after injury
fibrous scar developed (increase in tensile strength and shrinks to become less visible)
decreased vascularity
collagen synthesis by fibroblasts
carefully sutured wounds have approx. ___% of strength of unwounded skin
70%
primary intention of wound healing
clean laceration (edges are well approximated)
easily brought together, no missing tissue
secondary intention of wound healing
larger wounds that have greater loss of tissue and contamination
factors involved in wound healing
malnutrition, blood flow, oxygen delivery, impaired inflammatory and immune responses, infection, wound separation, foreign bodies, bite wounds
effects of age on wound healing
neonates, children, older adults
neonates and children
greater capacity for repair
may lack reserves needed to properly heal (electrolytes, temperature, rapid spread of infection)
sufficient calories needed
neonates and children have immature?
immune systems
increased water content means?
epidermis at risk
older adults
decreased in dermal thickness
decline in collagen content
loss of elasticity
vulnerable to chronic wounds
inspect areas for redness after how many minutes in older adults?
30 minutes and perform position changes
less than 6 hours pressure
ulceration
braden scale
scale used to predict patientโs risk of developing pressure injures
sensory perceptions, moisture, activity, mobility, nutrition, fraction shear