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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
What is a granuloma
An aggregate of epithelioid histiocytes (can contain lymphocytes)
26
What is the most common cause of granulas
Tuberculosis
27
How can you identify tuberculosis with a stain
Bright Red with Ziehl-Neelsen
28
Describe the appearance Epithelioid Histiocytes
- 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
Why does granuloma appearance alter
- Caseous necrosis | - Histiocytes converted to multinucleate giant cells
30
What is caseous necrosis
Tissue is soft and white like cheese | seen in tuberculosis
31
What does the presence of granulomas and eosinophils indicate
The presence of parasitic infection (like worms)
32
What induces granuloma formation
Beryllium
33
When do Histiocytic giant cells form
- 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
Describe the shape of Langerhans giant cells
Horseshoe arrangement - peripheral nuclei at one pole of the cell (seen in tuberculosis)
35
Describe the shape of foreign body giant cells
Large cell with randomly scattered nuclei
36
Describe the shape of Touton Giant cells
Central ring of nuclei | found when macrophages attempt to ingest lipids/xanthomas and dermatofibromas
37
How is a yet inflammation a part of the CV system
Response too myocardial infarction and can cause cardiac rupture
38
What inflammation has a role in Cancer
Chronic inflammation is involved in the initiation and propagation
39
What inflammation has a role in myocardial fibrosis
Chronic inflammation
40
How does inflammation play a role in atheroma formation
- 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
CNS tissue injury is a target of inflammation, what is the most common neurodegenerative disorder that chronic inflammation is a part of
Multiple sclerosis
42
What is the difference between exudate and transudate
Exudate- high protein and increase vascular permeability | Transudate- low protein and normal permeability
43
What are histiocytes
Monocytes become macrophages which can have specific names | Histiocytes are the other ones with no name
44
What cells have good capacity to regenerate
Labile cells - surface epithelial are a common type because the layer must keep being replaced
45
What cells tend to divide at a slow rate
Stable cell populations - hepatocytes and renal tubular cells are examples
46
What cells have no effective regeneration
Permanent cells - Nerve cells and striated muscle cells
47
What cells replaced cells that are lost through injury/normal ageing
Stem cells in labile and stable cell populations
48
In stem cell mitosis, what are the two routes of the daughter cells
- one differentiation pathway to become specialised | - one retention pathway to remain a stem cell
49
Where are stem cells located
- 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
Describe labile cell healing
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
What is contact inhibition
The stimulus to proliferate cells is switched off - it controls growth and movement
52
What is a confluent layer
A thin sheet of proliferated labile cells
53
What is organisation
The repair of specialised tissue by the formation of a fibrous scar It is a common consequence of pneumonia
54
Describe organisation
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
When is granulation tissue needed
When specialised tissues are damaged sometimes they need repair because they cannot be regenerated
56
How does granulation tissue come about
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
Why is wound contraction important
It can reduce the tissue defect size by up to 80% to make it faster for repair
58
How does wound contraction work
Myofibroblasts attach to each other and adjacent matric components to pull surrounding tissues inwards
59
Why can wound contraction lead to problems
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
How is an incised wound healed
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
When is healing by first intention used
Small wound
62
When is healing by 2nd intention used
Tissue loss or failed first intention
63
What can compromise healing by first intention
Infection | Local haemorrhage
64
What does 2nd intention healing include
Phagocytosis- cell debris removal Granulation tissue - fill in defects and lost specialised cells Epithelial regeneration Scarring
65
What cell population are hepatocytes
Stable cell with great regeneration
66
Other than hepatocytes where else can regeneration come from
Liver Progenitor cells
67
What instance causes cirrhosis of the liver
When hepatocyte and liver architecture is damaged
68
What cells regenerate
``` Hepatocytes Pneumocytes Blood cells Gut/Skin epithelium Osteocytes ```
69
What cells do not regenerate
Myocardial cells | Neurones

Phase 2A Mehdi (6 decks)

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