Inflammation Flashcards
5 steps of inflammatory response
recognition recruitment removal regulation resolution
signs of inflammation
dolor calor rubor tumor functio laesa (loss of function)
acute inflammation
minutes or hours
mainly neutrophils
usually mild
prominent
chronic inflammation
days
monocytes/macrophages and lymphocytes
often severe and progressive
less prominent; subtle
monocyte
large cell with a nucleus that does not fill cell space
lymphocyte
cell with a nucleus that mostly fills cell space
stimuli for acute inflammation
infection, trauma, necrosis, foreign bodies, immune reactions
vascular reaction (acute inflammation)
increased vasodilation and vascular permeability
cell response (acute reaction)
emigration of leukocytes from the circulation and accumulation at the focus of injury followed by activation of leukocytes
pattern recognition receptors
receptors that sense infectious pathogens and substances
inflammasome
a cytoplasmic complex that identifies products of damaged cells and activated capsase-1
hydrostatic pressure
pressure due to the water molecules being pushed slightly close together by the heart beating
higher at arterial end of the capillaries
oncotic pressure
large amounts of protein in the blood exerts an osmotic pressure that pulls water into the blood
constant pressure
edema
accumulation of free fluid in interstitial spaces increased hydrostatic pressure loss of plasma protein increased capillary permeability lymphatic obstruction
major mediator of vessel changes
histamine
difference between mast cell and basophil
mast cell is a lot bigger
basophil has smaller nucleus and a ton of granulocytes
how do leukocytes get to the site of inflammation?
- margination and rolling
- adhesion
- transmigration
- chemotaxis
first cell to respond to inflammation
neutrophil (6-24 hrs), then monocyte
how do leukocytes destroy a pathogen
- recognition and attachment to pathogen (pattern recognition receptors, opsonins, cytokine receptors)
- engulfment of pathogen (when opsonins are sensed)
- killing and degradation of pathogen
classical pathway
activated by antibody immune complexes
non classical pathway
activated by LPS
cyclooxygenase
will turn arachidonic acid into prostaglandins, prostacyclins, and thromboxanes
prostaglandins
inflammation, clotting, thermoregulation
prostacyclins
vasodilation, inhibit platelet activation, reduces clotting
thrombaxanes
platelet activation and stickiness
lipoxygenase
will turn arachidonic acid into leukotrienes
leukotrienes
causes most of the inflammation in asthma and allergic rhinitis
smooth muscle contraction in the trachea
where do anti inflammatory steroids act?
phospholipase A2 - turns membrane phospholipid to arachidonic acid
where does aspirin act?
cox
how can omega 3s help inflammation?
block the actions of arachidonic acid metabolites by competitively binding
inhibit cox; activate resolvins (anti inflammatory)
cell derived mediators for acute inflammation
performed granules (histamine and serotinin) newly synthesized molecules (aa, ROS, PAF, cytokines, NO)
plasma protein mediators for acute inflammation
complement activation
factor 7 activation
morphology of acute inflammation
serous, fibrinous, purulent, abcess
serous inflammation
watery, fluid filled space
burns and viral infections
fibrinous inflammation
fibrinous exudate
more serious for prolonged injuries/inflammation that increase blood flow
purulent inflammation
purulent exudate
infection with a specific pathogen (pyogenic)
abscess
focal collection of pus with a necrotic region surrounded by neutrophils
can be replaced with CT (scar)
ulcer
local defect on the surface of the tissue from necrosis and shedding
mucosa and skin
stimuli for chronic inflammation
persistent infections
immune mediated inflammatory diseases
prolonged exposure to toxic agents
metabolic inflammation
cell mediators for chronic inflammation
microbes (LPS) and IFN-gamma for classic activation - M1
cytokines other than IFN gamma for alternative activation
classic activation (chronic)
microbial actions
inflammation
alternative activation (chronic)
tissue repair, fibrosis
anti inflammatory actions
cd4 T cell
promotes inflammation by secreting cytokines
cd4 T cell mediation
cd4 cell will release 3 subsets of cytokines, one being IFN gamma which will activate M1 and will release M1 cytokines
positive feedback
causes of a granuloma
persistent t cell response
certain immune mediated diseases
sarcoidosis (non caseating)
noncaseating granulomas
shaumann bodies - calcium and protein
asteroid bodies - stellate inclusion
risk factors of noncaseating granulomas
below the age of 40
black is more susceptible than white
can affect lungs, heart, skin, spleen
amyloidosis
aggregation of misfolded proteins
alzheimers is most common form
risk factors of ammyloidosis
older aged males more than females family history kidney dialysis can affect heart, kidneys, liver, spleen, nervous sys
systemic effects of chronic inflammation
fever, acute phase proteins, leukocytosis
diet and inflammation (pathway)
SFA, LPS, TNF can all activate TLR4 which is activated as an innflammatory pathway
TLR4 will activate ceramine which will lead to insulin resistance (lipotoxicity)
t/f. foods that increase insulin also increase sfa in the blood
true
problematic waist to hip ratios
men - more than 1
women - more than .8
which type of body fat is pro inflammatory
visceral
two types of tissue repair
regeneration
scar formation
labile tissues
cells are always proliferating
bone marrow, skin, gi tract, oral mucosa
stable tissues
cells usually in resting phase, can proliferate if necessary
liver, kidney, pancreas
permanent tissues
cells are totally out of cell cycle
neurons, cardiac muscle
incision wound
longer than they are deep
stab wound
deeper than they are long
puncture wound
caused by shapr point, not sharp edge
chopping wounnd
combination of blunt and sharp characteristics
first intention
healing incision wounds
regeneration
second intention
healing wider wounds
scar
two sections of ECM to repair
basement membrane
interstitial matrix
fuctions of ecm
mmechanical support
control of cell proliferation
scaffolding for tissue renewal
establishment of tissue microenviornments
steps for scar formation
angiogenesis
migration and proliferation (granulation tissue)
remodeling - scar
factors that influence tissue repair (6)
infection, nutrition, gucocorticoids, poor perfusion, foreign bodies, location
