Acute Inflammation Flashcards
what is inflammation
vascular phase
- changes in blood flow
- accumulation of exudate
cellular phase
-delivery of neutrophils
what causes inflammation
trauma/ foreign body
microorganisms
hypersensitivity
other illnesses
what are the clinical signs of acute inflammation
rubor calor tumour dolor loss of function
vascular changes to blood flow
vasoconstriction (seconds)
vasodilation ( minutes)- heat and redness
increased permeability - fluid and cells can escape
what is starlings law
movement of fluid controlled by the balance of hydrostatic pressure and oncotic pressure
hydrostatic pressure- pressure exerted on a vessel wall by fluid- pushes fluid away
oncotic pressure- the pressure exerted by proteins- draws fluid towards
what is stasis
reduced flow through vessel
what is exudate
increased vascular permeability
protein rich fluid (delivers proteins to area of injury)
occurs in inflammation
delivers proteins
what is transudate
vascular permeability unchanged
fluid movement due to:
-increased capillary hydrostatic pressure
-reduced capillary oncotic pressure
occurs in
-heart failure
-hepatic failure
renal failure
how do neutrophils escape vessels
1) margination- movement from middle of blood vessel to periphery of blood vessel
2) rolling- stasis reduced flow of blood allow neutrophil to marginate
3) adhesion - they get tethered to one another
4) emigration ( diapedesis) - movement of neutrophil cell into interstitium through to the middle or between
what are selectins
expressed on activated endothelial cells
cells activated by chemical mediators
responsible for rolling
what are integrins
found on neutrophil surface
change from low affinity to high affinity state
responsible for adhesion
how do neutrophils move through the interstitium
chemotaxis
movement along an increasing chemical gradient of chemoattractants:
-bacterial peptides, inflammatory mediators
-rearragement of neutrophil cytoskeleton
what is opsoniation
when the C3b and Fb protein bind to the the C3b receptor on the neutrophil
systemic complications of inflammation
fever NSAIDs leucocytosis malaise reduced appetite altered sleep tachycardia Acute phase proteins: C-reactive protein release septic shock
what happens after acute inflammation
complete resolution
repair with connective tissue- fibrosis
progression to chronic inflammation- prolonged inflammation with repair
what causes appendicitis
blocked lumen- faecolith
accumulation of bacteria and exudate
increased pressure leads to perforation
what causes pneumonia
strepococcus pneumoniae
Haemophilus influenzae
signs and symptoms of pneumonia
shortness of breath
cough
sputum
fever
what causes bacterial meningitis
inflammation of meninges
Group B strepococcus
E coli
neisseria meningitides
signs and symptoms of meningitis
headache
neck stiffness
photophobia
altered mental state
FATAL
What is absess
accumulation of dead and dying neutrophils
associative liquefactive necrosis
cause compression of surrounding structures
pain
blockage of ducts
stages of pneumonia
congestion
red hepatisation
grey hepatisation
resolution
inherited angio-oedema
autosomal dominant recurrent attacks of swelling over regions in the body allergens can trigger swelling problem with C1 esterase inhibitor prolonged inflammation
chronic granulomatous disease
defects in phagcytes
this phagocytes are unable to produce radicals to allow oxidative damage in pathogens
corticosteriods given to reduce inflammation
antibiotics
alpha-1-antitrypsin deficiency
alpha-1-antitrypsin protects body tissues from damage by immune response against pathogens
increased risk of COPD, liver disease and panniculitis and swelling of vessels
shortness of breath
extensive cough
how is exudate formed
Tissue injury is followed by the release of vasoactive mediators.
These induce arterioles to dilate and capillary hydrostatic pressure therefore increases.
Inflammatory mediators also cause endothelial cells to contract and the walls of venules to become leaky.
Fluid and plasma proteins pass out into the extravascular space as a result of the increase in capillary hydrostatic pressure and the leaky vessel walls.
As plasma proteins have passed into the extravascular space the interstitial fluid colloid osmotic pressure increases and this holds the fluid in the extravascular space.
name some diseases in which a granuloma can be seen
- Tuberculosis
- Syphilis
- Leprosy
- Cat scratch disease
- Sarcoidosis
- Wegener’s granulomatosis
- Aspergillosis
what inflammatory mediators cause vasodilation
histamine
serotonin
prostaglandins
nitric oxide
which inflammatory mediators cause increased vascular permeability
histamine
bradykinin
leukotrienes
C3a and C5a
which inflammatory mediators are involved in chemotaxis
C5a
TNF-a
IL-1
bacterial peptide
which inflammatory mediators cause pain- increased nerve endings
bradykinin
substance P
prostaglandins
which inflammatory mediators cause fever
IL-1
IL-6
TNF-a
