Acute Inflammation Flashcards
triggers to acute inflammation (5)
pathogens(bacteria, viruses, parasites) physical agents( frost bites, radiation) chemical agents(chemical burns, irritants) mechanical injury (trauma, crush) foreign bodies( silica, swallowed bones)
purpose of inflammation (5)
- alert the body
- limit spread of infection
- protect injured site from becoming more infected
- eliminate dead cells
- create conditions required for healing
5 R’s
- recognition of injury
- recruitment of leucocytes
- removal of injurious agent
- regulation(closure of inflammatory response)
- resolution/ repair of affected tissue
local signs of inflammation (5)
redness swelling heat pain loss of function
what is pain due to
release of pain mediators
what is swelling due to
fluid accumulation in tissue due to increased permeability of vessels
what are the systemic changes in acute inflammation
pyrogens
synthesis of neutrophils
acute phase proteins
what are some examples of indogenous pyrogens
IL-1
TNF-a
what are exogenous pyrogens
microbial components
what is neurophilia
neutrophil synthesis
which protein does neurophilia occur by
G-CSF
examples of acute phase proteins
c-reactive protein
fibrinogen
complement
serum amyloid A protein (SAP)
where are acute phase proteins produced
liver
what is the acute phase protein production induced by
IL-6
IL-1
TNF-a
what will an increase in fibrinogen do
stacking of RBC’s (called rouleaux)
resulting in a faster sedimentation rate
3 vascular events
- vasodilation due to histamine+ serotonin
- inc blood flow to area(influx of WBC’s, O@, nutrients)
- blood vessel permeability increases
what is the fluid that has leaked out called
inflammatory exudate
4 different types of inflammatory exudate
purulent
fibrinous
serous
haemorrhagic
what is pus made of
dead cells
neutrophils
pus producing bacteria (pyogenic)
microbes
cellular events
- neutrophils- remove dead/ injured cells
- phago dead pathogens and tissue
- monocytes
- differentiate into macrophages
- phago
- release factors that promote tissue repair( TGF-B)
4 steps of neutrophil recruitment
- rolling selectins
- integrin activation by chemokines resulting in firm adhesion
- transmigration through endothelium
- chemotaxis to inflammed site
what does transient adhesion mean for leucocytes
detach and reattach as it rolls down endothelium
what do selectins do
mediate rolling of neutrophil
where are selectins expressed
activated endothelium
2 types of selectin
P-selectin- present in preformed granules
E-selectin- actively induced by IL-1 + TNF-a
what do selectins bind to
ligands on neutrophils (low affinity interaction)
- integrin activation by chemokines - what produces the chemokines
endothelium
- integrin activation by chemokines - what do the chemokines bind to
receptors on neutrophils
- integrin activation by chemokines - what does the binding of chemokines do
activation of integrin - move upto high affinity configuration
what are the integrin ligands called
ICAM-1
VCAM-1
what do neutrophils migrate through
interendothelial spaces
once in tissue, what do neutrophils follow
chemoattractant gradient towards site of infection
what are some chemoattractant molecules (released by macrophages/microbes)
IL-8
complement components(C5a)
bacterial components
what detect the neutrophils once in the tissue and release chemokines to alert rest of immune system
sentinel cells (dendritic, macrophages)
2 methods of pathogen destruction by neutrophils
release granule content (enzymes which are toxic),phagocytose
form nuetrophil extracellular traps (NET’s)
3 outcomes of acute inflammation
resolution
repair
chronic inflammation- abcess+pus+scarring
what does repair by replacement lead to
fibrosis- scarring
what is an abscess
mass of necrotic tissue caused by pyogenic bacteria
factors that favour resolution
minimal cell death
good regeneration ability
fast clearance
quick removal of dead tissue
factors that prevent healing
extensive injury poor vascular supply haemorrhage infection drugs- corticosteroids old age
