Lecture 2 - Acute Inflammation Flashcards
define acute inflammation
the response of living tissue to injury initiated to limit the tissue damage
what causes acute inflammation?
microbial infections hypersensitivity reactions physical agents chemicals tissue necrosis
what are the macroscopic features of acute inflammation?
calor rubor tumour dolor loss of function
what are the microscopic features of acute inflammation?
vasodilation gaps form in endothelium exudation margination and emigration macrophages and lymphocytes
how is vasodilation brought about in ai?
small adjacent blood vessels dilate with increased blood flow
how are endothelium gaps brought about in ai?
endothelial cells swell and retract - no longer completed intact internal lining
how is exudation brought about in ai?
vessels become leaky - water, salts, small plasma proteins leak out
how is margination and emigration brought about in ai?
circulating neutrophils adhere to swollen endothelial cells (m)
neutrophils migrate through vessel basement membrane (e)
how are macrophages and lymphocytes brought about in ai?
migrate in a similar way to neutrophils
what are the chemical mediators of vasodilation?
histamine
prostaglandins
c3a
c5a
what are the chemical mediators of vascular permeability?
histamine, prostaglandins, kinins
what are the chemical mediators of emigration of leukocytes?
leukotrienes
il-8
c5a
what do neutrophils do?
phagocytose microorganisms by making contact, recognising and internalising them - phagosomes then fuse with lysosomesmove to the site of injury by chemotaxiscan release toxic metabolites and enzymes when activated
what is the acute phase response?
decreased apptite
raised heart rate
altered sleep pattern
changes in plasma concentration of acute plasma proteins
give examples of acute phase proteins
c reactive proteins
fibrinogen
alpha1 antitrypsin
what causes fever?
endogenous pyrogens, il-1, tnf alpha and prostaglandin are produced
what are the possible results of ai?
complete resolution
continued ai with ci (abscess)
ci and fibrous repair, probably with tissue regeneration
death
how does resolution come about?
all mediators have short half lives and can be inactivated by degradation, dilution in exudate or inhibition
gradually all changes of ai reverse and vascular changes stop
potential for damaged tissue to regenerate if tissue architecture is intact
what are possible complications of ai?
swelling - blockage of tubes
exudate - compression
loss of fluid
pain and loss of function
describe a skin blister
caused by heat, sunlight, chemicals
pain and profuse exudate
collection of fluid strips of overlying epithelium
few inflammatory cells giving clear exudate
resolution or scarring
describe an abscess
solid tissues
inflammatory exudate forces tissues apart
liquefactive necrosis in centre
may cause high pressure causing pain
may cause tissue damage and squash adjacent structures
describe pericarditis
inflammation of serous cavity
pericardium becomes inflamed and increases pressure on heart
give examples of disoders of ai
alpha 1 antitrypsin deficiency
inherited complement deficiencies
defects in neutrophil function
defects in neutrophil numbers
what is hereditary angio oedema?
caused by deficiency of c1 inhibitor
c1 is a complement protein that cleaves c2 and c4 to form c3
c1 inhibitor inhibits c1 and bradykinin
uninhibited bradykinin increases permeability of endothelia causing oedema
treated with c1 inhibitor infusion or fresh frozen plasma
what is alpa 1 antitrypsin deficiency?
alpha 1 antitrypsin inhibits elastase
without the inhibition elastase breaks down lung/liver tissue
causes emphysema and liver sclerosis
what is chronic granulomatous disease?
recessive sex linked
immune phagocytes cant form ros
cant kill some bacteria without ros
granulomas formed in an attempt to contain the bacteria
