Acute Inflammation Flashcards
What is acute inflammation and what is it’s aim?
Response of living tissue to injury in aim to minimise damage to tissue
5 clinical signs of acute inflammation?
Rubor, tumor, calor, dolor, loss of function
What are 5 causes of inflammation?
Microbial - e.g. bacterial Necrosis Hypersensitivity - e.g. hives Physical agents - e.g. heat Chemicals - e.g. acids
What is heat and redness caused by in inflammation?
Vasodilation
What are the vascular changes in inflammation (stage 1)
1) Transient vasoconstriction
2) Vasodilation - aim to increase b flow to bring inflame mediators
3) Increased permeability - exudate out (of protein rich fluid) - swelling also slows circulation
4) = Stasis in small blood vessels due to increased ratio of RBCs due to fluid leaving
What cell defines inflammation? What other cell after that?
Neutrophil
Macrophages
What happens during stage 3 of vascular changes Exudation of fluid and what effects does this have (3) ?
Protein rich fluid moves out of leaky capillaries into interstium. This
1) Delivers plasma proteins to the area of injury
2) Dilutes toxins
3) Increases lymphatic drainage (takes micro-organisms to phagocytes and antigens to immune system).
What is the hallmark of acute inflammation (2)?
Exudate of (oedemal) fluid Infiltration of inflammatory cells
What kind of plasma proteins are delivered to site of injury?
Immunoglobulins
Inflammatory mediators
Fibrinogen
(Acute phase proteins)
What is the definition of oedema?
Excess fluid in the interstitium
What is there a lot of in infection exudate?
Proteins
What kinds of proteins would you find in exudate?
Opsonins
Complement
Antibodies
Which chemical mediators increase blood flow (3)
Serotonin
Histamine
Prostaglandins
Which chemical mediators increase vascular permeability (4)
Serotonin
Histamine
Bradykinin
Leukotrienes
Which chemical mediators are important for neutrophil chemotaxis (3)?
C5a
LTB4
Bacterial peptides
What happens during stage 2 - Vasodilation in inflammation response vascular changes?
Vasodilators e.g. histamine, serotonin, prostaglandins increase blood flow, which increases the amount of fluid and leucocytes to the site of injury. Pressure in capillaries rise (increased hydrostatic pressure).
Venules become leaky
Blood stasis due to increased haematocrit with fluid beginning to move out into interstitium
Name an opsonin for phagocytosis in acute inflammation
C3b
What are the 7 stages of neutrophil migration, infiltration, and killing? What occurs in each?
1) Migration - to site of injury via chemotaxis - chemoattractants include c5a, LTB4, bacterial peptides
2) Activation - to a higher metabolic level
3) Margination - stasis causes neutrophils to line up at the edge of blood vessels along the endothelium (normally would be in centre of laminar flow)
4) Diapedesis through blood vessel wall
6) Recognition - attachment - recognise bacterium e.g. c3b opsonin and bind to bacterium
7) Phagocytosis
8) Killing - O2 dependent (free radicals) and O2 independent (enzymes)
How do neutrophils roll/diapedesis?
1) Digestion of basement membrane
2) Relaxation of interendothelial junctions
3) Extends pseudopod through vessel wall
Is bacterial endotoxin a chemoattractant? Is it a pyrogen?
Yes lipopolysaccharide is a chemoattractant
Yes a pyrogen too
What is different about an ‘activated’ neutrophil?
It is stickier than normal cells
What do neutrophils do in 4 easy steps?
Contact
Recognition - opsonins
Internalisation - phagolysosome
Degradation with lysosomal enzymes or free radicals
4 local complications of inflammation?
1) Damage to normal tissue
2) Loss of function
3) Loss of fluid (e.g. large burns)
4) Obstruction of tubes (e.g. bile duct)/compression of vital structures (TUMOR)
Give an example of a structure that could be compressed in inflammation? An example of a tube blocking? Loss of fluids?
Heart - cardiac tamponade
Tube - e.g. bile duct
Loss of fluids - e.g. burns
