Inflammation 1-3 🗸 Flashcards
Five causes of inflammation
infection
trauma
foreign bodies
immune reaction
necrosis
Vascular changes in response to injury
changes in blood flow and blood vessel caliber (vasodilation)
changes mediated by histamine and nitric oxide
results in calor and rubor
calor
heat of infected area
rubor
redness of inflammation
5 responses to injury
stasis
margination
rolling
adhesions
transendothelial migration
stasis
blood flow slows as a result of vasodilation
margination
slowed blood vessels allow WBCs to accumulate near the blood vessel wall (neutrophils are the main cell of acute inflammation)
rolling
selectins stimulate WBCs to roll along the cell wall
Adhesions
endothelial expression of cell adhesion molecules (ICAM and VCAM)
Adhesion molecules also expressed on WBCs - integrins and selectins
low affinity initially - affinity increased by proteoglycans + prostaglandins (VCAM and ICAM) and histamine + thrombin (selectins)
transendothelial migration
WBCs able to move through vascular endothelium (leaky)
caused by direct damage or endothelial contraction which is mediated by histamine, bradykinin, substance n and leukotrienes
pass through junctions, diapedesis, transcytosis
chemotaxis
Occurs after WBC has left the blood vessel
cells follow a chemical gradient and move along in
Phagocytosis (inflammation)
recognition and attachment happens first (aided by opsonins)
engulfment, then killing and degradation happens
two reactive species that help kill in phagocytosis and what produces them
oxygen - NADPH oxidase
nitrogen - nitric oxide species
causes of rubor and calor
increase perfusion
slow flow
increased permeability of vessels
tumour (swelling) caused by which vascular changes?
proteins exit the leaky blood vessels causing change in osmotic pressure
dolor (pain)
mediated by prostaglandins and bradykinin
functio laesa
loss of function
What is the outcome of acute inflammation dependant on?
site of injury (capacity for repair)
type of injury (severity, pathogenic organisms)
duration of injury
resolution of inflammation
complete restoration of tissue to normal after the removal of inflammatory components
erosions and abrasions
injury with basement membrane intact
heat rapidly with complete resolution
suppuration
formation of pus - neutrophils, bacteria, inflammatory debris
Empyema
space filled by pus and walled off
organisation in response to inflammation
scarring
What gives increased chances of organisation
lots of necrosis
lots of fibrin
poor blood supply
damage goes beyond the basement membrane
Chronic inflammation
characterised by lymphocytes and macrophages
when is chronic inflammation favoured?
suppuration, scarring
persistence of injury
infectious agent
type of injury - autoimmune, transplant rejection
granuloma
aggregate of epithelioid histiocytes (macrophages)
associated with foreign bodies - endogenous and exogenous
also associated with specific infections e.g. parasites, TB
Myocardial infarction causes…
hypoxia = no oxygen = no ATP therefore Na+/K+ ATPase fails and Ca2+ pump fails
Inflammation of the cells >20 minutes after MI
mild short-lived damage that doesn’t always result in tissue death, it is reversible
no microscopic changes to myocardium
Inflammation of the cells after 20 minutes after MI
cell death - results in necrosis
cell shrink and become red
Inflammation of the cells 24 hours after MI
cell contents leaked
complement cascade initiated
acute inflammation
necrosis - mostly coagulative
Inflammation of the cells 24-72 hours after MI
total loss of nuclei and striations
heavy neutrophilic infiltrate
Inflammation of the cells 3-7 after MI
heart is weakest - most vulnerable to cardiac rupture
Neutrophils fade away and are replaced by macrophages - chronic inflammation
Inflammation of the cells 2-6 weeks after MI
macrophages fade away, replaced by fibroblasts
fibroblasts lay down collagen - scarring (poor blood supply)
scarring means heart cant pump as well
nerve bundles may also be damaged
Inflammation of the cells 6+ weeks after MI
can’t date MI if took place longer then 6 weeks ago, only scar tissue left
