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Y2 Pathology > Chronic inflammation and wound healing > Flashcards

Chronic inflammation and wound healing Flashcards

1
Q

Complete resolution of acute inflammation has what outcomes?

A
  • Return to normal vascular permeability
  • Drainage of proteins and fluid into lymphatics
  • Drainage into macrophages
  • Phagocytosis of degenerative neutrophils and necrotic debris
  • Disposal of macrophages
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2
Q

Under what specific conditions does chronic inflammation occur?

A
  • Persistent infections with e.g. parasites, fungi
  • Prolonged irritation
  • Cellular immune response, autoimmunity
  • Viral infections
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3
Q

Which cells are involved in active inflammation?

A
  • Macrophages
  • Lymphocytes
  • Plasma cells
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4
Q

Which cells characterise chronic inflammation?

A

Macrophages

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5
Q

Why do macrophages accumulate in chronic inflammation?

A
  • continued recruitment of monocytes
  • local proliferation of macrophages
  • immobilisation of macrophages by cyokines
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6
Q

What are the main essential roles of macrophages during chronic inflammation?

A
  • Phagocytosis
  • Antigen presentation (MHC II)
  • Secretory functions
  • Wound healing
  • Regulation of monocyte and granulocyte pools
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7
Q

What is a plasma cell?

A

An Ig producing differentiated B-cell

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8
Q

Out of neutrophils and macrophages, which is mitotically active?

A

Macrophages

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9
Q

Which cell type is terminally differentiated when arriving at the site of injury?

A

Neutrophils

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10
Q

What happens to macrophages when they arrive at the site of injury?

A

They differentiate into tissue macrophages, which get activated by inflammatory stimuli

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11
Q

Tissue destruction is induced by…?

A

Inflammatory cells

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12
Q

What are the main repair/regeneration steps?

A
  • connective tissue replacement of damaged tissue
  • proliferation of small blood vessels (angiogenesis)
  • fibrosis (scarring)
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13
Q

What does regeneration vs repair depend on?

A
  • how severe the injury is
  • whether there is damage to the basement membrane or not
  • type of tissue that is injured, some are better at regeneration
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14
Q

What are labile cells?

A

Continuously dividing cells due to a population of stem cells e.g. epidermis, GI tract

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15
Q

What are stable cells?

A

Quiescent cells (dormant, low levels of replication)
Proliferate in response to injury
e.g. liver hepatocytes

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16
Q

What are permanent cells?

A

Non-diving cells, cannot undergo mitosis

e.g. skeletal muscle cells

17
Q

What is the role of growth factors in regeneration and repair?

A

Work via receptors and initiate signalling pathways that influence the cell cycle
Cause proliferation of epithelial cell, parenchymal cells, and fibroblasts

18
Q

Define scarring

A

Deposition of collagen fibres as an attempt to replace lost tissue by fibroblasts

19
Q

When does scarring occur?

A

With tissue destruction including damage to both parenchymal cells and stromal framework

20
Q

Describe the formation of granulation tissue

A
  • begins from approx 24hrs after injury
  • fibrin is an essential framework
  • contains small new blood vessels and proliferating fibroblasts
  • inflammation still present
  • oedematous
21
Q

What are the main steps of angiogenesis?

A
  • Degradation of basement membrane
  • Migration of endothelial cells
  • Proliferation of endothelial cells
  • Recruitment of periendothelial cells
22
Q

What is VEGF?

A

Increase in vascular permeability which leads to an increased deposition of fibrinogen and fibronectin in EMC

23
Q

Which factors from inflammatory cells trigger fibroblast migration and proliferation?

A

GFs, IL-1, TNF

24
Q

What are the 5 main steps of scarring?

A
  • formation of granulation tissue
  • angiogenesis
  • migration and proliferation of fibroblasts
  • extracellular matrix deposition
  • tissue remodelling
25
Q

Tissue remodelling is mediated by?

A

MMPs (matrix metalloproteinases)

and their inhibitors TIMPs (tissue inhibitors of metalloproteinases)

26
Q

What is an abscess?

A

Suppurative (dominated by neutrophils) inflammation buried in a tissue or organ or a confined space, created by necrosis

27
Q

Describe the pathogenesis of an abscess formation

A
  • bacteria with a lower amount of hyaluronidase, cause a slower spread but induce a strong local reaction
  • necrosis of tissue occurs due to bacterial toxins and reduced perfusion
  • emigration of neutrophils -> phagocytosis of bacteria -> necrosis (liquefaction)
28
Q

What are the 3 layers of an abscess?

A

Inner - purulent exudate with liquefaction
Middle - immature cell-rich granulation tissue
Outer - mature, cell-poor, fibre rich granulation tissue

29
Q

Wound healing is a complex process which involves … ?

A
  • Induction of an acute inflammatory response
  • Regeneration of parenchymal cells
  • Migration and proliferation of parenchymal cells and connective tissue
  • ECM synthesis
  • Collagenisation and acquisition by wound strength
30
Q

Wound healing is stimulated by what factors?

A
  • Mediators of acute inflammation
  • Growth factors
  • Cell-ECM interactions
  • Angiogenesis and fibrosis
31
Q

What are the differences of healing by second intention to first intention?

A
  • More intense inflammatory reaction
  • Formation of a larger amount of granulation tissue
  • Wound contraction
32
Q

What features is scar tissue lacking?

A
  • Hair follicles
  • Sebaceous glands
  • Apocrine glands
33
Q

Which factors influence wound healing?

A 
Nutrition
Hormones
Infection
Wound size
Location of wound
Perfusion levels 
Foreign material

Y2 Pathology (33 decks)

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