Outcomes of acute inflammation Flashcards

1
Q

what are systemic manifestations of acute inflammation?

A
  • fever
  • malaise (general discomfort & illness)
  • loss of appetite
  • nausea
  • haemotological changes (increased erythrocytes sedimentation rate, leukocytosis)
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2
Q

what are outcomes of inflammation?

A
  • resolution
  • suppuration
  • scarring or fibrosis
  • chronic inflammation
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3
Q

what is resolution outcome?

A
  • everything back to normal

ideal conditions:
= good regenerative capacity
= minimal tissue damage/cell death
= quick elimination

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4
Q

what is suppuration outcome?

A

= formation of pus - mix of dead & alive neutrophils, debris, bacteria etc

  • if walled off = can form abscess (pocket of pus)
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5
Q

what is organisation/fibrosis/scarring outcome?

A
  • secondary healing - formation of granulation tissue (scar forming)
  • can occur when substantial amounts of tissue loss or large amounts of fibrin
    -new capillaries lead to more macrophages lead to proliferation of fibroblasts -> fibrosis/scarring
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6
Q

what is primary intention of skin healing?

A

2 edges of wound brought together, fibrin joins edges (weakly) - overtime, epidermal regrowth & collagen synthesis makes stronger join

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7
Q

what is secondary intention of skin healing?

A

tissue defect filled in by granulation tissue, can’t bring edges together so epithelial regrowth over the surface & fibrous scar forms & contracts over time

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8
Q

describe (simply) bone healing

A

initial haematoma/inflammatory response →callous formation (not particularly strong but holds together) → replaced eventually by stronger lamellar bone

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9
Q

how does liver heal?

A
  • Loss of hepatocytes without damage to architecture = Can get complete healing
  • Loss of hepatocytes plus damage to architecture = Fibrous scarring / nodules
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10
Q

how does kidney heal?

A
  • Epithelium can regenerate, architecture can’t
  • Similar to liver
  • Loss of tubular epithelium only can regenerate/repopulate cells
  • Destruction of glomerulus or damage to interstitium usually results in scarring / impaired function
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11
Q

how does smooth muscle heal?

A
  • vascular smooth muscle cells can regenerate
  • Other smooth muscle cells … not so much
  • Damaged muscle is replaced by scar tissue (makes less movement)
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12
Q

how does neural tissue heal?

A
  • CNS doesn’t repair well
  • peripheral nerves may regrow but recovery is variable
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13
Q

how does acute inflammation progress to chronic inflammation?

A
  • if causative agent NOT removed
  • cellular exudate starts to change -> from neutrophils to lymphocytes, plasma cells & macrophages

*chronic inflammation CAN sometimes occur as primary

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14
Q

what is most common type of acute inflammation to progress to chronic?

A

suppurative - most likely to fail
= collection of pus, abscess formation and walling off with granulation & fibrous tissue

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15
Q

what can favour progression from acute to chronic inflammation?

A

presence of foreign material
- the material cannot be digested/broken down
- often provokes granulomatous inflammation/foreign body giant cells

occurring cycle of acute inflammation then healing

*most acute inflammation resolves

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16
Q

what are macroscopic signs of chronic inflammation?

A
  • chronic ulcer
  • chronic abscess cavity
  • fibrosis/thickening of tissue
17
Q

what are the cells of chronic inflammation and what do they look like?

A

lymphocytes (small purple dots- circle)
plasma cells (fried egg)
macrophages (bigger blobby ones- like big fried eggs)
eosinophils (tomatoes with sunglasses on - due to bilobed nucleus)

18
Q

what are cytokines function?

A

small proteins which enhance cell mediated immunity & enhance antibody response

examples
=cell signalling (IL’s, TNF alpha) promoting chemotaxis (chemokines)
= antiviral defences (interferon’s) promote apoptosis

19
Q

what is a granuloma?

A

=organized collection of immune cells that form in response to persistent stimuli that the body is unable to eliminate

= made of collection of histiocytes (monocytes -macrophages & dendritic cells)

20
Q

what is involved in granulomatous inflammation and what are associated conditions?

A
  • involves formation of giant cells by macrophages colliding
    lots of associated conditions e.g. foreign body reactions, infections (tuberculosis), sarcoidosis= unkown chronic disease (systemic disease), crohns disease
21
Q

how do giant cells form?

A

when macrophages collide when more than 1 tries to eat same particle so end up with huge multi-nucleated cell

22
Q

what are types of giant cell and what does nuclei look like in each one?

A

foreign body type - nuclei randomly scattered

langhans - often seen in TB, horseshoe nuclei

touton type - lipid breakdown & xanthomas, neat little circles of nuclei

=they’re all multi-nucleated