acute and chronic inflammation, hypersensitivity 08 20 14 Flashcards
cellular infiltrate in acute vs chronic inflammation
acute: mostly neutrophils
chronic: monocytes and macrophages, lymphocytes
tissue injury in acute vs chronic inflam
acute: mild, self-limited
chronic: usually severe and progressive
local and systemic signs in acute vs chronic inflam
acute: prominent
chronic: may be subtle
stimuli for acute inflam
infections
physical trauma
physical and chemical agents (burns, frostbite, irradiation, chemicals)
tissue necrosis
foreign bodies
hypersensitivity rxns (environmental substances and self antigens)
How are antigens recognized?
Toll-like receptors (once activated, stimulate TNF release)
Inflammasome (activates caspase-1, activating IL-1, which causes leukocyte recruitment)
diff btwn toll like receptor and inflammasome
toll like recognizeds extracellular microbes
inflammasome recongizes parts of dead cells and some microbes
vasodilatation caused by
histamine and nitric oxide
increased vascular permeability caused by
histamine, bradykinin
endothelial cell injury (burns, etc)
bradykinin causes
vasodilatation
increasedy vascular permeability
pain
diff btwn transudate and exudate
transudate is when there’s fluid movement across the capillary wall
exudate is protein and fluid that leak out across capillary wall due to inflammation
edema
excess fluid in interstitium or serosal cavities
transudate definition
hypocellular and low protein content
non-inflammatory extravascular fluid, ultrafiltrate of plasma, low SPECIFIC GRAVITY <1.012
excudate def
cellular and protein rich
inflammatory extravascular fluid
high specific gravity >1.020
caused by change in normal blood vessel permeability
pus definition
purulent exudate rich in leukocytes
steps in leukocyte recruitment to injury site
margination rolling adhesion transmigration chemotaxis
role of selectins in inflammation
help with rolling and loose attacment to endothelial cells
present on endothelial cells, platelets, leukocytes
role of integrins in inflammation
stable attachment of leukocytes to endothelium
what drives transmigration in inflammation
chemokine CD31 (PECAM1) on leukocytes and endothelial cells
list chemotactic factors to help leukocytes migrate to injury site
bacterial products
chemokines
complement
leukotrienes
whend does leukocyte activation occur
what activates leukocytes
after recruitment of leukocyte to site of injury
what activates leukocyte? microbes, necrotic tissue, mediators
how do leukocytes that do phagocytosis recognize microbe?
specific surface receptors on leukocyte or
opsonins (igG, complement proteins, lectins)
how do leukocytes deal with injury?
killing-within phagolysosome, ROS
secreting enzymes into extracellular space (releasing enzymes like elastase that degrade microbes and dead tissue)
what are the principal mediators of inflammation
histamine, NO histamine, bradykinin IL-1, TNF, bacterial products IL-1, TNF bradykinin ROS, NO
how can defects in leukocyte fxn come about?
acquired:
defect in leukocyte production
defect in adhesion to endothelium and chemotaxis
defect in pahgocytososis and microbicidal activity
less common:
genetic causes
why is chronic inflam not good
can lead to fibrosis/scarring and loss of fxn
list morphologic patterns of acute inflam
serous
fibrinous
suppurative
ulcer
serous inflam
mildest form of acute inflam
outpouring of thin fluid that is protein-poor from plasma or serosal cavity linings
ex of serous inflam
peritoneal, pleural, pericardial EFFUSIONS (congestive heart failure, fluid overload)-effusions are defined as fluid in a serous cavity
skin blister from burn, viral infection , or trauma (fluid from traumatized epithelium or leaky endothelium)
fibrinous inflam
more severe injury
larger vascular leaks, passage of fibrinogen through leak, fibrinogen converted to FIBRIN
affects linings like pericardium, pleura, peritoneum, meninges
could resolve or become scarring
ex of fibrinous inflam
fibrinous pericarditis from uremia, transmural myocardial infarct, acute rheumatic fever
fribrnous pleuritis overlying pulmonary infarct
fibrinous peritonitis from ascites
suppurative (purulent) inflam
large numbers of neutrophils present along with necrotic cells, edema fluid, and bacteria…usually becomes liquefied into PUS
occurs with infections; some bacteria more likely to produce this rxn (called pyogenic bacteria-like Staph)
ABSCESS: central area of necrotic tissue surrounded by preserved neutrophils, dilated vessels, and fibroblastic proliferation
ex of suppurative (purulent) inflam
acute appendicitis, acute brnchopneumonia, acute meningitis
ulcer
local defect caused by necrotic cells and sloughing of necrotic and inflammatory tissue
surface of organ or tissue
ex of ulcers
peptic ulcer skin ulceration (in circulatory deficiencies)
what causes chronic inflammation
persistent infections
prolonged exposure to toxic agents
immune-mediated inflammatory diseases (autoimmune diseases)
macrophages in acute vs chronic inflam
in acute: monocytes becomes the tissue macrophages and participate in acute inflam
in chronic: macrophages persist because of continuous release of dead cells and microbes and stimulation by cytokines from activated T cells
morphologic features of chronic inflam
mononuclear cell infiltrate-macrophages, lymphocytes, plasma cells
chronic inflam produces
angiogenesis, mononuclear cell infiltrate, fibrosis
acute inflam can produce
resolution, pus, or fibrosis
granulomatous inflam
distinctive pattern of chronic inflam (prominent macrophages/histiocytes w/ epithelioid apperance)
multinucleated giant cells-giant cell formation induced by INF-gamma
develop as a result of specific infec, foreign bodies, immune rxn against self antigen
collar of lymphocytes, plasma cells
surrounding fibrosis
systemic effects of inflam
fever
elevated plasma levels of acute-phase proteins
leukocytosis
how does fever occur?
pyrogens (LPS or IL1, TNF)
prostaglandins (specifically PGE2)-stimulate hypothalamus
what is the action of acute-phase proteins made by liver?
they bind to microbe wall aiding in elimination
types of leukocytosis and what they say about underlying cause of inflam
neutrophilia-bacterial infec–left shift
lymphocytosis-viral infec
eosinophilia-allergies, asthma, parasites
leukopenia-typhoid, rickettsiae, some protozoans
