Flashcards in 2. Acute inflammation - consequences (+ types of exudate) Deck (16)
Describe 4 possible local complications of acute inflammation.
1. Damage to normal tissue - secondary to neutrophil-produced ROS released in phagocytosis
2. Obstruction of tubes (e.g. bile duct, intestine), compression of vital structures (e.g. cardiac tamponade) or serositis - secondary to swelling from inflammatory exudate
3. Loss of fluid from a surface wound, e.g. burns (in tissue spaces, as fluid accumulates to tissue pressure increases until it reaches a level that prevents further exudation)
4. Pain and loss of function
Name 3 systemic effects of AI.
2. leucocytosis (increased WBC count)
3. acute phase response
What causes fever in AI?
1. 'Exogenous pyrogens' (esp. bacterial endotoxin) stimulate macrophages to produce 'endogenous pyrogens': cytokines such as TNFa and IL-1.
2. Cytokines cause increase in synthesis of prostaglandin E2 by anterior hypothalamus.
3. Prostaglandin E2 increases temp.
Why can fever be a useful AI response?
i) some bacteria can't survive at high temperatures (40-41 degrees)
ii) inflammation is more effective at higher temperatures
What causes leucocytosis in AI?
Macrophages and endothelial cells in injured tissues produce colony-stimulating factors (CSF)... stimulate bone marrow to produce more neutrophils.
What is the acute phase response?
Cytokine (IL-1, IL-6 and TNFa)-mediated change in the levels of some plasma proteins (within hrs of injury) as a result of liver changing its pattern of protein synthesis (decreased albumin, increased e.g CRP)
Causes decreased appetite, raised pulse rate and altered sleep patterns.
The acute phase response increases the synthesis of which proteins?
1. C-reaction protein (CRP) - opsonisation
2. fibrinogen - blood coagulation
3. C3 - complement
4. a1-antitrypsin - protease inhibitor
5. ceruloplasmin - free radical scavenger
6. haptoglobin - binds haemoglobin
What are the effects of bacterial products/inflammatory mediators spreading in the blood stream?
Inflammation/acute phase response occurs throughout body... shock = dramatic drop in BP due to widespread vasodilation and increase in vascular permeability with resultant fluid exudation.
What are the 4 possible results of acute inflammation?
1- complete resolution
2- continued acute inflammation with chronic inflammation - abscess
3- chronic inflammation and fibrous repair, probably with tissue regeneration
Describe the process of AI resolution.
1) Absence of mediators... normal vascular permeability returns... cessation of neutrophil emigration.
2) Exudate is reabsorbed into venules or is drained away in lymphatics.
3) Fibrin is degraded by plasmin and other proteases.
4) Neutrophils apoptose and are phagocytosed along with necrotic debris by macorphages.
5) If damaged parenchymal cells can regenerate, tissue returns to normal. If regeneration cannot occur or damage has been extensive, a fibrous scar forms.
How are chemical mediators removed upon resolution?
1- all mediators have short 1/2 lives
Mediators may be:
2- unstable, e.g. some arachidonic acid derivates (prostaglandins)
3- diluted in exudate, e.g. fibrin degradation products
4- inactivated by degradation, e.g. heparinase
5- bound by inhibitors, e.g. various anti-proteases
+ specific inhibitors of acute inflammatory changes
Name 4 different types of exudate.
2. haemorrhagic exudate
3. serous exudate
4. fibrinous exudate
What is pus and what does it indicate?
- Creamy/white exudate (as rich in neutrophils) from abscess.
- Typical of infections by chemotatic bacteria.
What is haemorrhagic exudate and what does it indicate?
- Appears bloody as many RBCs.
- Indicates significant vascular damage as well as inflammation - seen in destructive infections or when exudate is a result of infiltration by a malignant tumour.
What is serous exudate and what does it indicate?
- Clear as contain plasma proteins but few leucocytes - suggests there is no MO infection.
- Typically seen in blisters, e.g. after mild burn.