Acute Inflammation 1 Flashcards

1
Q

What are the cardinal signs of inflammation? (*)

A

rubor (redness), calor (heat), tutor (swelling), dolor (pain)

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2
Q

Inflammation results in

A

loss of function

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3
Q

What is the etiology of acute inflammation? (*)

A
  • 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
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4
Q

What are the characteristics of inflammation process?

A
  • series of events
  • localised to affected tissue
  • in microcirculation
  • results in cardinal signs
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5
Q

What is microcirculation?

A
  • 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)
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6
Q

What is the pathogenesis of acute inflammation?

A
  • variations in vessel radius (flow)
  • variations in vessel permeability (exudation)
  • movement of neutrophils from the vessel to the extravascular space
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7
Q

How are the local changes in vessel radius and blood flow?

A
  • 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)
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8
Q

Why does an increased radius induce an increased flow?

A
  • 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
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9
Q

What does increased flow induce?

A

redness and heat

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10
Q

Details about increased permeability

A
  • 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
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11
Q

Effects of increased permeability

A
  • 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)
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12
Q

Effects of exudation

A
  • oedema formed (accumulation of fluid in the extravascular space)
  • swelling causes pain (+reduces function)
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13
Q

Effects of statis

A

change in flow characteristics

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14
Q

In a normal laminar flow, where are the erythrocytes and WBC (neutrophils) relative to each other?

A

the erythrocytes are on the outside and the neutrophils on the inside

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15
Q

Which is the most important WBC?

A

neutrophil polymorphonuclear leukocyte (= neutrophil = polymorph = NPL)

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16
Q

In a flow in inflammation, where are the erythrocytes and WBC (neutrophils) relative to each other?

A

RBD aggregate in the centre of the lumen (erythrocytes under rouleaux formation), neutrophils found near endothelium

17
Q

What is neutrophil emigration called?

A

diapedesis

18
Q

What the phases of neutrophil emigration?

A
  • margination (neutrophils move to endothelial aspect of lumen)
  • pavementing (neutrophils adhere to endothelium)
  • emigration (neutrophils squeeze between endothelial cells, active process, to extravascular tissues)
19
Q

What is the ideal outcome of acute inflammation? (inflammation resolved)

A
  • 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
20
Q

What are the benefits of acute inflammation? (*)

A
  • 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