inflammation Flashcards
clinical signs of acute inflammation
calor, dolor, rubor, tumor (swelling, edema), functio laesa (loss of fxn)
duration of acute vs chronic inflammation
- acute: days to weeks
- chronic: weeks - months
specificity of acute vs chronic
- acute: nonspecific
- chronic: specific (where immune response activated)
inflammatory cells of acute vs chronic
- acute: neutrophils, macrophages
- chronic: lymphocytes, plasma cells, macrophages, fibroblasts
fluid exudation of acute vs chronic
- acute: yes
- chronic: no
tissue necrosis acute vs chronic
- acute: usually no
- chronic: yes (ongoing)
cardinal clinical signs acute vs chronic
- acute: redness, swelling, pain, fever
- chronic: no
fibrosis (collagen deposition) acute vs chronic
- acute: no
- chronic: yes
operative host responses acute vs chronic
- acute: plasma factors (complement, immunoglobulins, neutrophils, non-immune phago)
- chronic: immune response, phago, repair
systemic manifestation acute vs chronic
- acute: fever (high)
- chronic: weight loss, anemia, low grade fever
WBC count acute vs chronic
- acute: increase
- chronic: remain constant
vascular changes acute vs chronic
- acute: vasodilation, increased permeability
- chronic: new vessel formation (granulation tissue)
exudate
inflammatory extravascular fluid containing increased protein, cellular debris (pus, WBCs)
exudation
escape of fluid, proteins and blood cells from vascular system into interstitial tissue or body cavities
transudate
ultra filtrate of plasma resulting from hydrostatic imbalance across vascular endothelium, no protein
transudation
process of which transudate is pushed across the endothelium because of hydrostatic pressure diffs
pus
purulent inflamm exudate rich in leukocytes and parenchymal cell debris
edema
XS fluid in interstitial areas from exudate or transudate (within tissue)
effusion
escape of fluid from anatomical vessels by exudation/rupture (pleural effusion, middle ear effusion), within a cavity
changes in vascular flow in acute inflammation
- Initial transient vasoconstriction
- Vasodilation, causing increased blood flow ->redness and increased temp
- As blood flow increases, there is increased capillary pressure and permeability (results in net XS of fluid extravasated into interstitial tissues)
- vascular perm increased = edema
leukocyte extravasation
- margination : stimulus (injury) activates endothelial cells which display selectins (adhesion molecules) on activated endothelial cells
- rolling adhesion to endothelium (have integrins activated – adhesion receptors on leukocytes surfaces, which attach to endothelial cells)
- trasmigration across endothelium and migration through interstitial tissues toward chemotactic stimulus
chemotaxis
- occurs after leukocyte extravasation
- chemotactic agents for neutrophils include exogenous substances (bacterial products) as well as endogenous substances (complement, leukotrienes and cytokines) -> these activate leukocytes and cause them to release chemical mediators of inflammation
neutrophils
-can be exogenous (bacteria) or endogenous (complement, leukotrienes, and cytokines) substances
phagocytosis
- once leaks have assume at inflamm site, neutrophils and macrophages work to eliminate invading matter:
- recognition and attachment (opsonization, coat microbe with substance that increases efficiency of phago and IDs microbe as foreign)
- engulfment
- killing
what are arachidonic acid metabolites?
-powerful mediators of endothelial injury & tissue damage, synthesized by two types of enzymes:
i. leukotrienes (made by lipooxygenases): potent chemotaxic agent involved in vasoconstriction, bronchospasm, & vascular permeability
ii. prostaglandins (made by cyclooxygenases): pathogenesis of pain and fever
what are vasoactive amines?
- histamine and seratonin
- vasodilation and increased vascular permeability
histamine
mast cells (mediator released in response to physical injury, heat/cold, immune reactions
seratonin
basophils, platelets
complement system
20 component proteins found in plasma, function in innate and adaptive immunity, “complement cascade” affects multiple factors of acute inflammation: vascular permeability, vasodilation, leukocyte adhesion, chemotaxis, activation, phagocytosis
- C3 and C5 are most important
- acute inflammation
kinin system
- chemical mediator of acute inflamm
- creates vasoactive peptides from plasma proteins that increase vascular permeability, contraction of smooth muscle, dilation of blood vessels and pain (side note: bradykinin effects similar to histamine)
cytokines
proteins produced by many cell types (including lymphocytes and macrophages), regulate immune responses
- chem mediators of acute inflammation
- interleukin 1 and TNF
interleukin 1
produced by macrophages and monocytes; activates T cells and macrophages, promotes inflammation
-effects: fever, pain, vasodilation, enabling transmigration
TNF
cytotoxin from group of cytokines that cause cell death (adopt)
-derived from monocytes
nitric oxide
powerful vasodilator
oxygen derived free radicals
assist in killing foreign cells, unpaired electron (unstable, destructive)
-damages cell membranes of bacteria = lysis
outcomes of acute inflammation
- complete resolution (things return to normal)
- suppuration/abscess formation (walled off)
- repair (scarring)
- progress to chronic inflammation
granuloma
- aggregation of macrophages that form a particular pattern. May also occur with foreign bodies and insoluble immune particles.
- granulomatous inflammation: special type of chronic inflammation
common causes of granulomas
syphilis TB, sarcoidosis
lab diagnosis of inflammation - acute
- Examination of exudate (high protein levels and specific gravity), presence of neutrophils(bacterial) lymphocytes (viral),Biopsy of tissue, culture, gram-stain, antibody levels, complement level (looking for C3 and C5)
- CRP (c-reactive protein - acute)
- ESR (erythrocyte sed rate = non specific marker for inflamm = acute)
lab diagnosis of inflammation - chronic
-biopsy lesions, microbiologic cultures, immunologic studies, serologic studies for antibodies, skin tests for TB, fungus, serum autoantibody levels for autoimmune disease
primary intention
brings wound edges together to encourage healing, most efficient and results in least amount of scarring.
secondary intention
lesion is left open due to fear of infection, heals from inside out to prevent closing infection inside. Worst scaring but scar can be remodeled.
tertiary intention
(delayed primary closure)- delayed primary closure for 4-6 days due to some concern for infection.
phases of wound healing
- inflammation
- epithelization
- collagen synthesis
- scar maturation
inflammation
process by which body responds to local injury by attempting to contain and isolate injury, destroy pathogens, inactivate toxins and repair. Occurs within 3-24 hours after injury.
epithelization
Bridging to the wound with new epithelial cells, begins within about 12 hours from injury, new epithelial cells migrate from the wound edges. Wounds are sealed within 24-48 hours after injury
collagen synthesis
Fibroblasts and collagen aggregate around the wound to make new tissue and repair damaged areas, occurs within 4 days - 6 weeks after injury,
scar maturation
scar forms and remodels throughout the first year after the injury, takes a full year to come to final stage.
