Acute Inflammation 1 Flashcards
What are the cardinal signs of inflammation? (*)
rubor (redness), calor (heat), tutor (swelling), dolor (pain)
Inflammation results in
loss of function
What is the etiology of acute inflammation? (*)
- micro-organisms (bacteria, fungi, viruses, parasites) which cause infection)
- mechanical trauma/injury to tissue (includes sterile injury)
- chemical upset environment (pH, bile and urine which irritate peritoneum)
- extreme conditions (sunburn, frostbite, ionising radiation)
- dead tissue (irritation of cells near cell necrosis)
- hypersensitivity
What are the characteristics of inflammation process?
- series of events
- localised to affected tissue
- in microcirculation
- results in cardinal signs
What is microcirculation?
- capillary beds, fed by arterioles and drained by venules
- extracellular ‘space’ and fluid and molecules within it
- lymphatic channels and drainage
- Starling forces which control flow
- dynamic balance (hydrostatic/ colloid osmotic pressures)
What is the pathogenesis of acute inflammation?
- variations in vessel radius (flow)
- variations in vessel permeability (exudation)
- movement of neutrophils from the vessel to the extravascular space
How are the local changes in vessel radius and blood flow?
- transient (short lasting) arteriolar constriction
- local arteriolar dilatation
- relaxation of vessel smooth muscle (autonomic NS or mediator?
- > all this is the triple response (flush, flare, wheal)
Why does an increased radius induce an increased flow?
- Poiseuille’s law says flow is proportional to radius^4 (if radius increases, flow also does, drastically)
- increased arteriolar radius causes increased local tissue blood flow
What does increased flow induce?
redness and heat
Details about increased permeability
- localised vascular response
- involves microvascular bed
- helps endothelial leak (fluid and protein not held in vessel lumen, imbalance of Starling forces)
- locally produced chemical mediators
Effects of increased permeability
- net movement of plasma from capillaries to extravascular space
- exudation which produces exudates (fluid rich in protein, plasma, includes immunoglobulin and fibrinogen)
- fluid loss (increased viscosity)
- rate of flow slows (statis)
Effects of exudation
- oedema formed (accumulation of fluid in the extravascular space)
- swelling causes pain (+reduces function)
Effects of statis
change in flow characteristics
In a normal laminar flow, where are the erythrocytes and WBC (neutrophils) relative to each other?
the erythrocytes are on the outside and the neutrophils on the inside
Which is the most important WBC?
neutrophil polymorphonuclear leukocyte (= neutrophil = polymorph = NPL)
In a flow in inflammation, where are the erythrocytes and WBC (neutrophils) relative to each other?
RBD aggregate in the centre of the lumen (erythrocytes under rouleaux formation), neutrophils found near endothelium
What is neutrophil emigration called?
diapedesis
What the phases of neutrophil emigration?
- margination (neutrophils move to endothelial aspect of lumen)
- pavementing (neutrophils adhere to endothelium)
- emigration (neutrophils squeeze between endothelial cells, active process, to extravascular tissues)
What is the ideal outcome of acute inflammation? (inflammation resolved)
- inciting agent isolated & destroyed
- macrophages move in from the blood and phagocytose debris (then leave)
- epithelial surfaces regenerate
- inflammatory exudate filters away
- vascular changes return to normal
What are the benefits of acute inflammation? (*)
- rapid non specific response
- transient protection of inflamed area (cardinal signs and loss of function)
- neutrophils destroy organisms and denature antigen for macrophages
- plasma proteins localise process
- resolution and return to normal
