Inflammation Flashcards
stages of acute inflammation
fluidic
cellular
causes of acute inflammation (4)
infection - response to pathogen or toxins its produces
tissue necrosis - release cell contents
foreign bodies - either direct irritant effect or due to traumatic tissue injury
immune reactions - hypersensitivity, normal immune response damages own tissues
fluidic phase processes
immune cells mediator release (eg. cytokines) –>
vasodilation (slows blood, more time for immune cells to work) & increased vascular permeability (cells more able to move into the space where they are needed)
Inflammation Appearance
Pain
Redness - increased blood flow in the area
Heat
Swelling
Acute inflammation - chemical mediators
pre-formed - sit in granulocytes
- histamine - mast cells, vasodilation
- serotonin
- lysosomal enzymes
newly synthesized - produced at time of inflammation
- cytokines - lymphocytes and macrophages
- tumor necrosis factor and IL1 - main cytokines - t cells and mast cells
- nitric oxide
- prostaglandins - arachidonic acid
Liver factors
- factor XII - clotting factor
- complement
Dendritic cell function
antigen presenting cells
incited by innate immune system
mature to activate active immune system
innate - produce local cytokines
active - activate T-cells
systemic effects of acute inflammation
trigger brain to produce fever
trigger liver to produce acute phase proteins
trigger bone marrow to form WBCs
TNF slows heart - lowers output
thrombus formation
effects on skeletal muscle
platelet activation/aggregation
clotting factor release
thrombin - cleave fibrinogen to fibrin - pro inflammatory
fibrinogen - scaffolding for hemostatic plug (synthesised in liver)
Exudate types (4)
serous - clear, cell-poor - in spaces created by cell injury or into body cavities, not infected
catarrhal/mucoid - gelatinous/thick - in tissues where lots of goblet cells
fibrinous - sticky - caused by infectious microbes, in membranes of body cavities
suppurative/purulent - pus - neutrophils, usually bacteria causing liquefactive necrosis
neutrophil function in acute inflammation
first response cells - first 6-24 hours
rapid response to chemokines
short lived in tissue - undergo apoptosis
phagocytosis
recruit other cells
release antimicrobial agents
lobular nucleus and granular cytoplasm
termination of acute inflammation
when inciting agent is gone
due to:
- short life of neutrohphils and chemical mediators
- anti-inflammatory cytokines and arachidonic acid metabolites
- anti-inflammatory t-cells
- anti-inflammatory macrophages
chemotaxis
movement of an entity in response to a chemical stimulus
DAMPs
damage associated molecular pattern
produced by damaged tissue, recognised by macrophages and dendritic cells and presented to trigger cytokine release
PAMPs
pathogen associated molecular patterns
produced by microbes, recognised by macrophages and dendritic cells and presented to trigger cytokine release
cellular phase process
PAMPs/DAMPs –> cytokines –> mast cells –> inflammatory mediators released
chronic inflammation
occurs over a long time and/or fails to resolve
acute response fails to kill inciting agent
repeated episodes of acute inflammation
in response to specific pathogens
chronic inflammation mechanisms
agents that resist phagocytosis - eg bacteria that produce toxins that kill leucocytes
persistence after phagocytosis - mycobacteria - prevent lysosomal function, can’t fuse
isolation - hide within pus or other liquid
unresponsiveness - can’t be broken down, eg. plant materials, suture materials
immune disease - autoimmunity, leukocyte deficits
phagocytosis
leukocyte engulfs bacteria
forms phagocyte - pinched cell membrane containing pathogen
fuse with lysosome - phagolysosome
virulence factors of bacteria may block lysosome fusion
key inflammation cells
macrophages - phagocytosis
lymphocytes
fibroblasts - wall off infection or rebuild scaffolding of tissue
dendritic cells - present antigens
abscesses
form due to myeloperoxidase by neutrophils + cellular remnants of dead neutrophils –> pus
(rabbits, reptiles, birds, fish - no myeloperoxidase)
neutrophils in lumen
chronic - fibroblasts produce collagen and extracellular matrix proteins to wall off area
granulomatous inflammation
inciting agent not removed
mediated by macrophages
nodular or diffuse
histo - necrotic cellular debris, activated macrophages, multinucleated giant cells, lymphocytes
healing mechanisms (2)
regeneration - true healing and repair
- back to normal, no scar tissue
- repair damaged components
- proliferation of cells that have survived injury
- may involve tissue stem cells
connective (fibrous) tissue deposition
- when injured tissue can’t resolve completely or supporting tissue damaged
- scar tissue
- fibrosis - extensive deposition of collagen
