inflamation Flashcards
what are the causes of acute inflammation (6)
micro organisms, mechanical, chemical, physical extremes, dead tissue, hyper sensitivity.
benefit of acute inflammation
protection of organism from itself
rapid response to non-specific insult
can return back to normal after process
how does dead tissue lead to inflammation
cell necrosis irritates adjacent tissue
what are the cardinal signs of inflammation
redness, heat, swelling, pain and loss of function
why is there a large flow change when the radius of a blood vessel changes
as flow is proportional to the (radius)^4 of the arterioles
why is there a large flow change when the radius of a blood vessel changes
as flow is proportional to the (radius)^4 of the arterioles
what is microcirculation
capillary beds fed by arterioles and drained by venules
extracellular space and fluid
lymphatic
transient arteriolar constriction
local change in blood flow, short time, protective (nail scratch experiment)
local arteriolar dilation
active hyperaemia
hyperaemia
increased blood flow through arterioles
final stage in local changes of blood vessels
relaxation of vessel smooth muscle
name the Triple Response
Flush, Flare, Wheal (mark left)
what changes occur in the inflammation of the lumen
margination - neutrophils move to edge of lumen
pavementing - neutrophils adhere to endothelium
emigration - squeeze between endothelia cells
what is laminar flow
when fluid flows in a single direction in parallel layers with NO DISTRUBTION
what do neutrophils become a part of after squeezing through endothelial cells
extravascular tissue
what is the ideal outcome of acute inflammation
inciting agent isolated and destroyed
macrophages move in from blood and phagocytose debris; then leave
epithelial surfaces regenerate
inflammatory exudate filters away
vascular changes return to normal - inflammation resolved
what are neutrophils
mobile phagocytes (WBCs) recognise foreign antigen
release granule contents
(release ENZYMES = PROTEASES)
phagocytose and destroy
what happens when neutrophils die
granules released
cell leftovers form pus (endogenous proteins)
what happens if pus extends into tissue
inflammation
what is an abscess
a collection of pus under pressure
what are the 2 types of abscess
single locule
multiloculated
how is a multiloculated abscess formed
when there is a break through the pyogenic membrane and forms new cavities
what is the pyogenic membrane
surrounds pus - messey membrane- no real structure
contains fibrin
what is a empyema, where are they found
pus in hollow viscus
gal blader, pleural cavity (surrounding lungs)
pyaemia
pus forming bacteria discharged into blood stream
What is granulation tissue
universal patch – repair kit for all damage
new capillaries, macrophages, fibroblasts and collagen
bacteraemia
bacteria in blood
septicaemia
growth of bacteria in blood
toxaemia
toxic products in blood
what is shock
the inability to perfuse tissue
what are the outcomes of septic shock
fatal
tissue hypoxia - cell death
haemorrhage
best what to get a positive outcome from septic shock
early detection and rapid intervention - intensive care
what is the formation of pus called
suppuration
what are the types of mediator molecules
inside cells
in plasma
released from cells
on endothelia cell surface membrane
what effects do mediators have
vasodilatation increased permeability neutrophil adhesion chemotaxis itch and pain
what are the 4 enzyme cascades in plasma
blood coagulation
fibrinolysis
kinin system
complement cascade
what are the blood coagulation pathways
clot fibrinogen in exudate - creates fibrin
fibrinolysis
breaks down fibrin, maintain blood supply
what is the kinin system
control pain - bradykinin
mediators result in..
positive and negative effects
dynamic balance
two formulas related to compensation of septic shock
BP = CO x SVR CO = SV x HR
SRV - systemic vascular resistance - the force opposing the heart to create BP
CO - cardiac output
what is leaked in exudate
fluid rich in protein - plasma
includes immunoglobulin and fibrinogen
what is the effect of exudation
oedema - accumulation if swelling tissue = causes pain and reduces function
what are the benefits of acute inflammation
protect damaged area
rapid response
histamine is release by what in response to what
release by MAST CELLS in response to LOCAL INJURY (IgE)
what are cytokines and chemokines
signalling molecules
chemotaxis= get cells to move to site of inflammation
what dose nitric oxide do
NO = smooth muscle relaxation, anti-platelet, regulate leukocyte recruitment to inflammatory focus
what two pathways are involved in inflammatory cytokine production
MAPK (protein kinase)
NF–kB (kappa kappa B)
what dose the complement cascade do
ties immune system with inflammation
what are the outcomes of acute inflammation
resolution = everything back to normal
suppuration - pus
organisation - granulation tissue = scar
dissemination = septic
chronic inflammation
