2. Injury and Repair Flashcards
two major components of injury and repair
- vascular reaction
2. cellular reaction
components of acute inflammation
- increased blood flow to site (vasodilation via increases in hydrostatic pressure)
- changes in microvascular wall (vascular permeability)
- allows exudate (protein fluid) to leave to result in stasis (congestion with blood cells as relative proportion of cells to plasma increases…..thus more cells and less fluid in the vessel to make it easier for WBCs to grab onto the wall and get out into surrounding tissue and then also makes transmigration easier) - mechanisms - endothelial changes (rapid/reversible) and transcytosis; endothelial injury (direct and leukocyte mediated); angiogenesis (leaky until cells mature)
- activated leukocytes (exit microvasculature, accum at site of injury, activate at site of injury)
stimuli of acute inflammation
infec/toxins trauma physical/chemical injury necrosis foreign material (suture) immune reaction (and autoimmune) malignancy
leukocyte extravasation
- margination, rolling, adhesion
- transmigration (diapedesis)
- migration in intersitium
- chemotaxis
- activation
largely mediated by adhesion molecules:
- selectins, integrins
expression modulated by cytokines
leukocyte function
- regoc of targets
- phagocytosis
- release of leuk products (stimulate other WBCs, kill invasive organisms, attract other WBCs, change vascular permeability, etc
chemical mediators of inflammation produced by plasma or cells
plasma: pre-existing complement and kinins activated
cells: mediators sequestered until needed
chemical mediators of inflammation: vasoactive amines and plasma proteins
vasoactive amines: early release
- histamine
- serotonin
plasma proteins:
- complement
- kinin
- clotting
morphologic patterns of AI: effusion, fibinous inflammation, purulent inflammation, and ulcers
effusion: (blister) limited to an area
fibrinous inflamm: fibrinogen escapes vasculature & may scar (problem if trapped somewhere like the pericardium where there is no room)
purulent: formation of pus (neutrophils) eg abscess
ulcers: necrotic tissue sloughs, leaving tissue defect (skin, gut, oropharynx, etc)
major cell to describe cytology of acute vs chronic inflammation
acute: PMNs (neutrophils)
chronic: lymphocytes and plasma cells
causes of chronic inflammation
chronic infection, chronic exposure to toxin, autoimmunity
morphologic features of chronic inflammation?
mononuclear cell infiltrate (lymphocytes and plasma cells, macrophages, eosinophils, mast cells, few neutrophils)
tissue destruction
attempts at healing
granulomatous inflammation
subtype of chronic inflammation (response to foreign but indigestible material)
focus of macrophages (typically surrounded by lymphocytes)
foreign body granulomas (immunologically inert)
immune granulomas (cell mediated immune response to insoluble particles like heavy metal in the lung or infectious agents like TB)
sepsis is massive release of what?
cytokines (TNF, IL1)
defective inflammation
increased susceptibility to infections (chronic granulomatous disease)
prolonged infection/delayed wound healing (common in pts w/compromised blood flow like diabetics)
excessive inflammation: abn reaction like allergies or autoimmune OR protracted appropriate reaction like ongoing infection
can give rise to tissue injury (cirrhosis, ulceration), metaplasia, neoplasia
3 main types of tissues
normally dividing tissues with high rate of turnover (labile) like gut epith or renal tubular epith
normally very low turnover tissues with retained capacity for increased division (quiescent) like the liver
nondividing tissues like neurons or myocytes (some capacity, but super limited)
