Acute Inflammation Flashcards
What is acute inflammation?
The response of living tissue to injury. It limited damage, is stereotyped, innate, short duration and immediate.
What are the clinical signs of acute inflammation?
Rubor, tumor, dolor, calor, loss of function.
What causes inflammation?
Trauma, micro-organism, hypersensitivity and other illnesses.
Describe vascular phase- changes in blood flow.
Vasoconstriction (seconds) -> vasodilation (minutes): heat and redness -> increased permeability: fluid and cells can escape.
Describe vasodilation, increased vessel permeability and fluid movement in AI.
Vasodilation: increased capillary hydrostatic pressure. Increased vessel permeability: plasma proteins move into interstitium, increased interstitial oncotic pressure, fluid movement: out of vessel into interstitium: oedema (tumor).
Describe exudate.
Increased vascular permeability, protein rich fluid, occurs in inflammation.
Describe transudate.
Vascular permeability unchanged, fluid movement due to: increased capillary hydrostatic pressure, reduced capillary oncotic pressure. Occurs in heart failure.
How is vascular phase effective?
Interstitial fluid dilutes toxins, exudate delivers proteins and fluid drains to lymph nodes where antigens are delivered.
How do neutrophils escape vessels?
Margination -> rolling -> adhesion -> emigration (diapedesis)
Describe selectins.
Expressed on activated endothelial cells, cells activated by chemical mediators, they’re responsible for ‘adhesion’.
Describe 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.
What do neutrophils do?
Phagocytosis- phagosome fuses with lysosome, produce secondary phagolysosomes, also release inflammatory mediators.
How do neutrophils recognise what to phagocytose?
Opsonisation: toxin covered in C3b and Fc, receptors for C3b and Fc on neutrophil surface.
How is the cellular phase effective?
Removal of pathogens and necrotic tissue, release of inflammatory mediators.
Describe inflammatory mediators.
Chemical messengers control and co-ordinate the inflammatory response, they originate from activated inflammatory cells, platelets, endothelial cells and toxins.
Local vs Systemic AI.
Local- specific to one area. Systemic- the whole body.
Examples of local complications.
Swelling: compression of tubes e.g. airways, bile duct. Exudate: compression of organs, e.g. cardiac tamponade. Loss of fluid e.g. burns. Pain: muscle atrophy.
Examples of systemic complications.
Fever: some inflammatory mediators are pyrogens, they act on the hypothalamus to alter temperature e.g. prostaglandins. Leucocytosis: increased production of white cells, inflammatory mediators act on bone marrow. Septic shock: huge release of chemical mediators, widespread vasodilation, hypotension, tachycardia, multi-organ failure -> can be fatal.
What happens after acute inflammation?
- Complete resolution. 2. Repair with connective tissue (fibrosis). 3. Progression to chronic inflammation.
