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Phase 2A Mehdi > Chronic Inflammation and Repair > Flashcards

Chronic Inflammation and Repair Flashcards

1
Q

What is Chronic inflammation

A

Prolonged tissue reaction to injury

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2
Q

What cells are dominantly found in chronic inflammation

A

Lymphocytes, Plasma cells and Macrophages

Neutrophil Polymorph is ACUTE

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3
Q

What are the causes of Chronic Inflammation

A

Primary (no acute response)
Transplant Rejection
Secondary/progression (from acute response)
Recurrent Acute Response

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4
Q

What type of inflammation tends to become chronic

A

Suppurative - A deep abscess cavity and delayed drainage allows more time for thicker fibrous walls that cannot fuse together.
The pus inside becomes organised by granulation tissue and is replaced then by a fibrous scar

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5
Q

what is an example of a chronic abscess

A

Osteomyelitis - bone abscess which cannot be targeted by macrophages

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6
Q

Why does indigestible material/necrotic bone support chronic inflammation

A

They are inert materials that are resistant to lysosomal enzymes

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7
Q

What are the most indigestible materials that give rise to Chronic inflammation

A

Foreign body materials- suture, glass, wood, metal

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8
Q

What type of inflammation do foreign body materials cause

A

Granulomatous Inflammation

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9
Q

What is Granulomatous Inflammation

A

causes

macrophages to form multinucleate giant cells called ‘foreign body giant cells’

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10
Q

What is Chronic Cholecystisis

A

Gallstones induce recurring acute inflammation which becomes Chronic

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11
Q

Describe the macroscopic appearance of Chronic inflammation

A
  • Chronic ulcer - Mucosa breach
  • Chronic abscess cavity - ie Osteomylitis
  • Thicker wall of hollow organ
  • Granulomatous Inflammation
  • Fibrosis
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12
Q

Describe the microscopic appearance of Chronic inflammation

A
  • Contains Lymphocytes/ plasma cells/ macrophages
  • macrophages can become multinucleate giants
  • New fibrous tissue (NO EXUDATION)
  • Tissue Necrosis
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13
Q

What is the paracrine stimulation of connective tissue proliferation

A

Angiogenesis -> Fibroblast Proliferation ->Collagen synthesis = Granulation tissue
This is regulated by Growth Factor that bind to specific receptors during proliferation

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14
Q

What Growth factors Regenerate epithelial cells

A

EGF

TGF-alpha

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15
Q

What are the 2 main lymphocytes in tissue infiltrate

A

B-Lymphocyte: Become plasma cells in antigen presence

T-Lymphocyte: Produce cytokines in antigen presence

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16
Q

How do macrophages move through tissues

A

By amoeboid motion in response to chemotactic stimuli

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17
Q

Do neutrophil polymorphs or macrophages live longer after ingesting micro-organisms

A

Macrophages live longer

Neutrophil only 3 days after ingesting

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18
Q

what mycobacteria can live inside macrophages

A

Mycobacterium tuberculosis

Mycobacterium leprae

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19
Q

what mycobacteria can live inside macrophages

A

Mycobacterium Tuberculosis

Mycobacterium Leprae

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20
Q

How do macrophages contribute to necrosis

A

In delayed-type hypersensitivity reactions, macrophage die and release lysosomal enzymes = large areas of necrosis

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21
Q

What are macrophages from inflamed tissue derived from

A

Reticuloendothelial system

-Adapted blood monocytes that have migrated from vessels

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22
Q

What does the reticuloendothelial system include

A

Haematopoetic stem cell -> monocyte ->

  • Macrophages
  • Osteoclasts
  • Tissue Histiocytes
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23
Q

What changes take place for a macrophage in an area of inflammation

A
  • Size increase
  • Protein synthesis
  • Mobility
  • Phagocytic activity
  • Lysozyme content
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24
Q

What cytokines does a macrophage produce

A 
Interferon-alpha
interferon-beta
IL-1
IL-6
IL-8
TNF-alpha
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25
Q

What is a granuloma

A

An aggregate of epithelioid histiocytes (can contain lymphocytes)

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26
Q

What is the most common cause of granulas

A

Tuberculosis

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27
Q

How can you identify tuberculosis with a stain

A

Bright Red with Ziehl-Neelsen

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28
Q

Describe the appearance Epithelioid Histiocytes

A
  • Large Nuclei
  • Eosinophilic cytoplasm
  • Elongated
  • Arranged in Clusters
  • Little phagocytic activity
  • Angiotensin Converting Enzyme
  • Levels of this enzyme can be a marker for systemic granulomatous disease
29
Q

Why does granuloma appearance alter

A
  • Caseous necrosis

- Histiocytes converted to multinucleate giant cells

30
Q

What is caseous necrosis

A

Tissue is soft and white like cheese

seen in tuberculosis

31
Q

What does the presence of granulomas and eosinophils indicate

A

The presence of parasitic infection (like worms)

32
Q

What induces granuloma formation

A

Beryllium

33
Q

When do Histiocytic giant cells form

A
  • Form where indigestible material accumulate
  • Form when foreign particles are too large for a single macrophage
  • Form when two or more macrophages engulf the same particle at the same time and fuse
34
Q

Describe the shape of Langerhans giant cells

A

Horseshoe arrangement - peripheral nuclei at one pole of the cell (seen in tuberculosis)

35
Q

Describe the shape of foreign body giant cells

A

Large cell with randomly scattered nuclei

36
Q

Describe the shape of Touton Giant cells

A

Central ring of nuclei

found when macrophages attempt to ingest lipids/xanthomas and dermatofibromas

37
Q

How is a yet inflammation a part of the CV system

A

Response too myocardial infarction and can cause cardiac rupture

38
Q

What inflammation has a role in Cancer

A

Chronic inflammation is involved in the initiation and propagation

39
Q

What inflammation has a role in myocardial fibrosis

A

Chronic inflammation

40
Q

How does inflammation play a role in atheroma formation

A
  • macrophages adhere to endothelium
  • migrate with t-cell into arterial intima
  • express cell adhesion molecules which pull other cells to the inflamed area
  • macrophage process lipids in plaques
41
Q

CNS tissue injury is a target of inflammation, what is the most common neurodegenerative disorder that chronic inflammation is a part of

A

Multiple sclerosis

42
Q

What is the difference between exudate and transudate

A

Exudate- high protein and increase vascular permeability

Transudate- low protein and normal permeability

43
Q

What are histiocytes

A

Monocytes become macrophages which can have specific names

Histiocytes are the other ones with no name

44
Q

What cells have good capacity to regenerate

A

Labile cells - surface epithelial are a common type because the layer must keep being replaced

45
Q

What cells tend to divide at a slow rate

A

Stable cell populations - hepatocytes and renal tubular cells are examples

46
Q

What cells have no effective regeneration

A

Permanent cells - Nerve cells and striated muscle cells

47
Q

What cells replaced cells that are lost through injury/normal ageing

A

Stem cells in labile and stable cell populations

48
Q

In stem cell mitosis, what are the two routes of the daughter cells

A
  • one differentiation pathway to become specialised

- one retention pathway to remain a stem cell

49
Q

Where are stem cells located

A
  • basal layer of epidermis
  • hair follicles
  • sebaceous glands
  • intestinal mucosa (bottom of crypts)
  • liver (between hepatocytes and bile ducts)
  • Bone marrow (hemopoietic stem cells)
50
Q

Describe labile cell healing

A

Loss of part of labile cell population
Remaining cells proliferate as a thin sheet (confluent layer) to cover defect
Cells stop proliferating via contact inhibition
Epidermis is rebuilt from the base up

51
Q

What is contact inhibition

A

The stimulus to proliferate cells is switched off - it controls growth and movement

52
Q

What is a confluent layer

A

A thin sheet of proliferated labile cells

53
Q

What is organisation

A

The repair of specialised tissue by the formation of a fibrous scar
It is a common consequence of pneumonia

54
Q

Describe organisation

A

Dead tissue is removed by macrophages/neutrophil polymorphs
Granulation tissue forms on top of fibrin
Granulation tissue contracts and collects collagen to form a scar

55
Q

When is granulation tissue needed

A

When specialised tissues are damaged sometimes they need repair because they cannot be regenerated

56
Q

How does granulation tissue come about

A

Capillary endothelial cells grow into vascular channels as loops arching the area
Fibroblasts divide and secrete collagen
Myofibroblasts are produced (fibroblasts + muscle filaments)
Myofibroblasts + capillary loops = granulation tissue

57
Q

Why is wound contraction important

A

It can reduce the tissue defect size by up to 80% to make it faster for repair

58
Q

How does wound contraction work

A

Myofibroblasts attach to each other and adjacent matric components to pull surrounding tissues inwards

59
Q

Why can wound contraction lead to problems

A

Stenosis/Stricture - if damage is circumferential around the lumen of a tube
Contracture - permanent shortening of muscle
Impaired mobility- cosmetic damage can cause considerable contraction

60
Q

How is an incised wound healed

A

First Intention

  • small cut blood vessels occluded by thrombosis
  • Fibrin binds the two sides of the wound
  • Coagulated blood forms a scab
  • Fibroblasts secrete collagen into the fibrin network
  • <10 days, suture/plaster can be removed
61
Q

When is healing by first intention used

A

Small wound

62
Q

When is healing by 2nd intention used

A

Tissue loss or failed first intention

63
Q

What can compromise healing by first intention

A

Infection

Local haemorrhage

64
Q

What does 2nd intention healing include

A

Phagocytosis- cell debris removal
Granulation tissue - fill in defects and lost specialised cells
Epithelial regeneration
Scarring

65
Q

What cell population are hepatocytes

A

Stable cell with great regeneration

66
Q

Other than hepatocytes where else can regeneration come from

A

Liver Progenitor cells

67
Q

What instance causes cirrhosis of the liver

A

When hepatocyte and liver architecture is damaged

68
Q

What cells regenerate

A 
Hepatocytes
Pneumocytes
Blood cells
Gut/Skin epithelium
Osteocytes
69
Q

What cells do not regenerate

A

Myocardial cells

Neurones

Phase 2A Mehdi (6 decks)

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