Acute inflammation Flashcards
why is inflammation important?
- which 2 common diseases is immune related?
recent concept that dieseases lik Asth and ather- immune related
inflammation essential in pathology
LO
inflammation
main categories
‘OR ‘ infection: can gave pus without infection
‘MOVEMENT’ = water first then cells move, always inside blood vessel towards outside blood vessel.
- acute (early), chronic (long) focus= acute
The cardinal signs of inflammation. how does occur?
inflammation is reaction to vascularised living tissue
- hot/red due to more blood flow
- swell= bc FLUID moves from inside blood vessel to outside in surr. region. e.g. transudate and exudate
- pain - FEEEL pain bc receptor recieves stimulus, resetting pain receptor (present in all tissues except brain (can’t feel pain)
Describe the 3 inflammatory cascade for
Injury
Infection
Foreign body
trigger/trauma/pathogen/ foriegn body (could even be sterile)= Acute inflammation. end result could be
good= healing
infection= pathogen enters wound-> chronic inflammation or healing acute inflammation= complex responses, either replace dying cells OR replacement by fibroblast and their secretions
where can inflammation NOt occur
cartilage, cornea,
Oedema:
Exudate:
Pus:
Purulent:
Suppuration:
oedema: excess water outside vessel
exudate: fluid has heaps protein
pus: exudate with heaps of WBC (neutrophils), water and debris of tissue cells
suppuration: formation of pus
purulent= pus
Acute inflammation – 3 events
always in order 1,2,3
- bigger capillaries
-more permeable (not everypart, only spec part)
-WBC comes out to tissue
process of inflammation and timeline
few hrs water increase
then neutrophils
then monos and macs
Exudation – how?
PCV= after capillaries, most fascinating part of microcirc bc transmigration and permeability changes here.
most capillaries are ‘dormant’ explain
passge bkood of dormant caps’OPEN’ under mediators from inflammation -> vaso dilation = OPEN
more blood goes through tissues
Carbon labelling of post-capillary venules
after histamine treatment
PCV artery
vein
capillary
do changes appear everywhere in capillaries when inflammation takes place?
demonstration that when inflammation trigg. PCV allows passage of fluid and later on cells. injected ink in study. after few mins of histamine injection. carbon ink only accumulated in PCV (not in capillaries, not vein and arteries.
Formation of the Exudate in Acute Inflammation
adhesion molecules heaps = makes it possible for free floating leokocytes adhere to endothelial cell= makes it possible for neutrophil to margination = stick on margin-> migrate -> exudate fluid
- dot lines= aim is to fight infection
- exudate could lead to tissue injury (pus)
why exudate?
- dilute toxin
- more flow to lymphatics = increase lymph drainage of loacal area
- Abs
- fibrin formed bc fibrinogen leaves
neutrophils move and responsible for destruction
exo vs transudate
bigger gaps in endothelial cell = exudate= high protein, follows transudate
transudate= leave vessel, low protein
changes in vasular flow
fluid passage
short lived
The acute inflammatory response is
STEREOTYPIC
3 classification of stress to cell
- introduces concept of sterotypic response= always same response.
always water first then neutrophils second. either leads to helaing or pus formation (destroys tissue)
Emigration of WBC – how?
- Leukocyte surface of endothelial cell (attach)
- other molecules expresson endothelial= firm adhesion
step 4: migration in response to small molecules which are chemoattractants. - leuks migrate by squeezing in endothelial
Selectins and their ligands
e.g. of molecules wer know.
dont need to memorise names on diagram
remember ‘SELECTIVE’ = later adhesion molecules
ndothelial molecules interacting with
leucocyte integrins
adhesion molecules for WBC to bind firm to endothelial
integrins= molecules on leuokocytes. single mutation in integrins can lead to integrin not so good leading to Leuk non adhesion / def= (kids defenseless).
mutation in molecules= high sensitivity to infections. if molecules not in proper form, migration does not occur so no vessels to defend us.
firm binding
Leucocyte-endothelial interactions:
different adhesion molecules at different steps
1. Primary
adhesion
spec change
- involved early on
integrins= later
poly vs mono cells
no need to kn
cells
neutrophils vs monocytes
lots of Neutrophils on margin of vessels then going out to do their job= phagocytose and kill by prod. ROS/enzymes/preoteinases etc
Abscesses
must be
Systemic Changes in Inflammation
many growth factors act on bone marrow to make more mediators
stimulate precursors to prod more WBC
abscess bigger= fever bc cytokines, IL-1/6 that overprod which reset the centres of hypothalamus whcih control temperature of body
- many proteins sec by liver= over prod or prod in lower amts= APP acute phase proteins= e.g. fibrinogen, completments, Igs, these proteins will be secreted in higher amts and detected in blood.
- malaise= sloppy tired mediated by cytokines, IL1, TNF, IL6 which can act on CNS and modify behaviour
Acute Phase Proteins (APPs)
- proteins needed for coagulation, repair vessels, defense, regulate proteinase inhibition, reg. metabolism.
positive: go up alot like, high amts
negative= lower amts during acute inflammatory reaction
Morphological types of acute inflammation
serous vs fibrinous
Sensitisation of pain receptors by
prod of mediators do more than open vessels (e.g. histanins, kinins) can influence small type C pain fibres (or pain fibres) which have pain receptors (in every tissue except brain), prostaglandens PgI2= mod fibres responsible for pian = reset sensitivity of receptors
instead of 1 AP
theres 5 times more on afferent fibres thats why we feel pain
Formation of pus
Outcomes of Acute Inflammation
Inflammation - an overview
questionnn
Appreciate the permeability changes in acute inflammation
Understand the process of leukocyte emigration
Discuss the anti-microbial activity of PMNs
Understand the role of cytokines and acute phase proteins during systemic inflammation
Identify the outcomes of acute inflammation
