Unit I - Inflammation & Healing Flashcards
natural cycle of inflammatory process
cellular injury, acute inflammation, chronic inflammation with granuloma
*healing can occur at any stage
granuloma
inflammatory nodule
- granular, firm
- contains macrophages, epithelia cells and necrotic tissue
- persistent antigens
- surrounded by WBCs
- can lead to chronic inflammatory disease
dilution phase - 5 cardinal signs
- Redness (hyperemia -capillary dilation)
- Swelling (edema - increased capillary fluid permeability)
- Heat
- Pain
- Loss of function
dilution phase - process
starts with mast cells (degranulates), release pro inflammatory mediators, which initiate the inflammatory process, fluid exudate dilutes affected area, fibrin isolates the inflamed area
mast cell pro inflammatory mediators
vasoactive amines - cause vasodilation and increase vessel permeability
(histamine, serotonin, bradykinin)
pro inflammatory cytokines
signaling molecules that mobilize white blood cell communication
example of skin inflammation
Roasacea, nasal polyp
demolition phase
proliferation of white blood cells
most abundant WBCs are
neutrophils (PMNs)
diapedesis
process in which spaces between endothelial cells enlarge and neutrophils squeeze through
causes PMNs to migrate toward foreign body
chemotaxis
as PMNs proliferate, they must be transferred from the blood to the
ECF
WBC pavementation (margination) occurs because of loss of
laminar flow
allows things to get where they need to be (without it, could not fight off infection)
In laminar flow, most WBC (and RBC) are traveling in the area of highest velocity, i.e. the center of the blood vessel. As the velocity of blood flow decreases, more and more blood cells migrate to the edges of the blood vessel positioning them to marginate at the edges
As PMNs proliferate, they must be transferred from blood to ECF via Laminar flow; longest arrows in the center flow fastest, more to the periphery it is slower; difference in velocity causes the WBC to congregate at the center of the cell because that is where the blood is flowing fastest
phagocytosis
ingestion of foreign material (necrotic tissue, pathogens)
types of cytokines
eosinophil chemotactic factor (ECF), neutrophil chemotactic factor (NCT), tumor necrosis factor (TNF), platelet activating factor (PAF), interleukins
end result of phagocytosis (2 things)
colliquative necrosis with supportive drainage
suppuration - pus
after phagocytosis
fluid dilutes bad substance and fibrin in the plasmin limits the spread
acute inflammation (3 things)
- less than 2 weeks
- PMNs dominate/increase - “shift to the left” (70% to 90%)
- WBC count above normal (4000-8000 WBC)
chronic inflammation
- more than 2 weeks
- fatigue, weight loss, cognitive loss
- elevated monocytes and lymphocytes
- PMNs normalize/decrease - “shift to the right”
- mild leukocytosis or leukcytopenia
desirable effects of inflammation
- walls off an invading foreign body via fibrin in the exudate
- dilutes the concentration of the foreign body
- kills it with WBCs
undesirable effects of inflammation
- lassitude (fatigue)
- anorexia
- fever
- prostration
- acute phase response
acute phase proteins (synthesized by the liver)
25+
positive APPs: protein increases during acute phase response
negative APPs: protein decreases during acute phase response
**tests for inflammation with APPs (and what a positive test looks like)
increased erythrocyte sedimentation rate (ESR): attach to red blood cells, inc blood viscosity, look for inflammation
*POSITIVE TEST: blood separates faster than normal
type of healing - labile
(vegetative intermitotics)
- cells replace on periodic basis
ex: bone marrow, lining of GI tract, skin
type of healing - stable
(vegetative post-mitotics)
- cells replace only after injury
ex: liver
type of healing - permanent
(fixed post-mitotics)
- cells hypertrophy to take place of loss cells
ex: CNS, cardiac mx, kidney
regeneration/resolution of tissue injury
regrowth of original tissue (so must be irreversible injury)
NO destruction of tissue
(sunburn, cold)
replacement (2 kinds)
- replacement with different tissue (metaplasia) NO scar - barretts esophagus
- replacement with scar tissue: not functional and doesn’t perfuse blood well
repair healing - 2 ways
primary intention or secondary intention
primary intention
edges of a wound are in close approximation to each other
minimal scarring/loss of function
- bound by blood clot, inflammatory reaction and WBCs kill foreign bodies, fibroblasts/collagen and scar
- re-epithelialization must occur over an organized clot
secondary intention
wound edges NOT close together
takes much longer to heal, larger scar is formed, possible dysfunction
- collagen is different (may cause keloids)
keloid formation (hypertrophic scarring)
severe scarring due to deposition of type 3 collagen rather than type 1
redness
- capillary sphincter contracts
- blood flow decreases
- huge blood volume, low flow
(Rosacea)
swelling
- pro-inflammatory mediators (increase capillary permeability so it swells bc lots of fluid in it)
- increased hydrostatic pressure
- increased extracellular fluid
heat
increased blood volume in the area causes warmth
pain
- pressure on pain sensory endings
- increased acidity of extracellular fluid
- histamine, prostaglandins, bradykinin release
loss of function
due to all of the other symptoms
dystrophic calcification
common in bigger mx like quads
super infection forming gangrene
poor circulation impeding fast healing to injury, can lose limb
2 positive APPs to know:
CRP: binds to dead/dying cells
SAAP: recruits PMN’s and macrophages to sites with inflammation
negative APPs to know
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