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Miscellaneous > MCB Lecture 62 & 63 Tissue Injury, Chronic Inflammation > Flashcards

MCB Lecture 62 & 63 Tissue Injury, Chronic Inflammation Flashcards

0
Q

When can normal function be regained?

When is function not regained?

A

Normal function is regained when the tissue is regenerated, or if the scar is small

Function is lost when there is extensive fibrosis

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1
Q

What are the two outcomes of tissue injury?

A

Regeneration of tissue

Scarring, replacement by connective tissue

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2
Q

What are the requirements for regeneration?

A
  • The tissue must be made up of labile or stable cells

- Underlying structure of the organ must not be lost

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3
Q

When does scarring occur?

A

Scarring occur when the underlying tissue is lost, or when the cells are not capable of proliferation

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4
Q

Which compound regulates cell cycle?

A

Cyclins

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5
Q

When will a cell enter G0?

A

When growth factors are removed

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6
Q

What does FACS analysis tell us about the effect of removing growth factors from cells?

A

Normal: most cells in S phase, DNA content more than 1
Remove GF: cells enter Go, DNA content = 1
Apoptotic stumulus: cells die, DNA content less than 1

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7
Q

What are the three different classifications of cells based on proliferative capacity?

A

Labile
Stable
Permanent

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8
Q

What is labile tissue?

Eg. ?

A

These cells never enter Go and are always replicating
These tissues are capable of regeneration

For example: epithelium of skin and GIT, hematopoetic cells

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9
Q

What is stable tissue?

Eg. ?

A

This tissue leaves the cell cycle, but can re-enter if required to do so.

For example: parenchyma of most solid organs (liver, kidney), endothelium, smooth muscle

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10
Q

What is permanent tissue?

Eg. ?

A

These cells enter Go and cannot exit
These tissue can never be regenerated
These cells are do terminally differentiated

For example: neurons, cardiac and skeletal muscle

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11
Q

What changes occur in cells during proliferation?

A

Increase in cell size
Increase in mitosis
Protection against apoptosis

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12
Q

What are the triggers of proliferation? (3)

A
  • Growth factors
  • Hormones
  • Cytokines
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13
Q

What is the mechanism of growth factors causing proliferation?

A

Growth factors initiate a signal transduction pathway, leading to the transcription of genes such as cyclins that push the cell into the cell cycle.

  • prevent apoptosis
  • increase protein synthesis
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14
Q

What are the outcomes of growth factor signalling?

A

Migration
Angiogenesis
Proliferation
Differentiation

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15
Q

Which cytokine results in proliferation?

A

IL-2

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16
Q

What are the two basic classes of cells in an organ?

A

Parenchyma and stroma

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17
Q

What is parenchyma?

Give some examples

A

These are the function cells of an organ

Eg. Hepatocytes, myocytes, neurons

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18
Q

What is stroma?

What is it made up of?

A

The stroma is the support structure for the parenchyma

It is made up of connective tissue

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19
Q

What are the two forms of stroma?

A

Basement membrane

Interstitial matrix

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20
Q

Describe the possibility of tissue regeneration in the kidney

A

There is limited capacity for regeneration, and the underlying structure must be intact

The proximal ducts undergo hypertrophy and hyperplasia when the other kidney is removed

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21
Q

Describe tissue regeneration in the liver

A

The liver has good regenerative capacity if the underlying structure is maintained.

5-10% of the tissue may be regenerated in 4-6 weeks

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22
Q

What is steatosis?

A

This is when there are some fibrous hepatic nodules due to moderate alcohol intake. The nodules can be regenerated

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23
Q

What are the steps in repair by connective tissue?

A
  1. Angiogenesis
  2. Migration and proliferation of fibroblasts
  3. ECM deposition by fibroblasts
  4. Remodeling
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24
When does repair by connective tissue occur?
If the tissue can not be regenerated, or if the underlying structure is lost
25
What is the aim of angiogenesis?
To bring the blood supply back to the damaged tissue
26
Describe the mechanism of angiogenesis
1. Vasodilation and increased permeability of the existing vasculature 2. Migration of endothelial cells 3. Proliferation of endothelium 4. Inhibition of proliferation and remodelling 5. Recruitment of peri endothelial cells
27
What are the features of the new vasculature produced in angiogenesis
Leaky, as the tight junctions haven't properly formed yet
28
Describe the migration and proliferation of fibroblasts during tissue regeneration
1. Macrophages and endothelium produce growth factors: PDGF and FGF-2 2. The growth factors stimulate recruitment and proliferation of fibroblasts
29
What is the function of fibroblasts in tissue regenerative by connective tissue?
To synthesise and secrete ECM, especially collagen
30
What are the stages of tissue repair?
Granulation tissue -> scar formation
31
Compare granulation tissue with scar tissue
Granulation: Proliferating fibroblasts Vascularised Loose ECM Scar tissue: Inactive fibroblasts A vascular Dense collagen and connective tissue
32
What is occurring during remodelling? | What does this result in?
- Switch from type III collagen to type I - Collagen is no longer degraded This results in increased tensile strength of the wound
33
What are the two types of cutaneous wound healing?
Healing by first intention | Haling by second intention
34
Describe what happens in healing by first intention in the first 24 hours
1. Scab formation | 2. Inflammation
35
What sort of wounds result in healing by first intention? | What are the features of these wounds?
Surgical wounds Paper cuts They are very clean, small wounds There is no necrotic tissue or inflammation
36
What are the features of healing by second intention?
Everything is larger: the wound, the clot, inflammation and granulation tissue
37
Describe wound contraction When does it occur?
This is when the some of the cells in gap the specialised granulation tissue contract like smooth muscle cells (myofibroblasts) This occurs in healing by the second intention Wound size reduced by 5-10% in 4-6 weeks
38
What are the aims of successful healing?
To regain function Rapidly resolve the injury Transient scar
39
What factors affect successful healing?
``` Nutrition Location of the scar Effect of contraction Persistence of foreign bodies Infection ```
40
What are some complications of healing that can occur?
Wound dehiscence Contraction Keloid formation
41
Describe wound dehiscence
This is when the wound opens us due to poor suturing, nutrition, mechanical forces or infection
42
What is keloid formation?
This is hypertrophy of the scar tissue, causing a raised mass of scar tissue due to excess collagen
43
What problems can occur with contractions of myofibroblasts ?
The limb contracts
44
What are the features of chronic inflammation? (Give histology cal features too)
Inflammation lasts weeks, to months to years Injury, inflammation and healing all occur at the same time - mononuclear cells - tissue damage - repair by fibroblasts - fibrosis
45
What are the two broad categories of cause of chronic inflammation?
Primary chronic inflammation Unresolved acute inflammation
46
How can acute inflammation lead to chronic inflammation?
Excessive cellular exudate Excessive necrosis Persistent causal agent
47
What are peptic ulcers? | What is it an example of ?
This is when there is damage to the epithelium of the stomach (infection or anti-inflammatory drug) that can't be resolved It is an example of acute infections persisting and causing chronic inflammation
48
Describe the histology of peptic ulcers
``` Epithelial interruption Necrotic debris (acellular) Non specific acute inflammation Granulation tissue Fibrosis ```
49
What is osteomyelitis? | What is it an example of?
This is when there is an unresolved infection in the bone (because the blood supply is poor) It is an example of unresolved acute infection turning into chronic infection
50
What is chronic choleystitis?
This is gall stones of the liver causing inflammation and thickening of the wall and chronic infection
51
What is primary chronic inflammation?
This is when the injury leads directly to chronic infection
52
What are the causes of primary chronic inflammation? (4)
1. Persistent infection 2. Immune mediated 3. Toxic agent 4. Primary granuloma
53
Which cells are involved in the chronic inflammatory response?
Macrophages Lymphocytes Other leukocytes
54
Describe the two types of macrophages and how each is activated
M1: classical activation: IFN-gamma and microbicidal products M2: alternate activation: cytokines: IL-4 and IL-13
55
What are the functions of macrophages in chronic inflammation?
M1: inflammation and killing M2: inhibition of inflammation and tissue repair
56
What is the role of lymphocytes in chronic inflammation?
They make antibody and kill infected cells
57
Describe the vicious circle of T cell and macrophage activation
M1 activates lymphocytes by presenting antigen and releasing stimulatory cytokines T cells stimulate macrophages by releasing IFN-gamma and IL-4 and IL-13
58
What are the macroscopic morphologies of chronic inflammation?
``` Chronic ulcers - peptic ulcer Chronic abscess cavities - bacterial abscesses in the lung Thickened wall - chronic choleystitis Granulomatous - sarcoidosis Fibrosis - Asbestosis of lung ```
59
What are the two classes of morphology of chronic inflammation?
Diffuse | Granulomatous
60
Describe the structure of diffuse chronic inflammation Give an example
No granuloma Eg. Asbestosis
61
Describe the Pathogenesis of asbestosis
1. Asbestos fibres are inhaled and penetrate deep into the lung 2. Diffuse pulmonary interstitial fibrosis forms 3. Contraction of the walls leads to enlarged air spaced and honey combed effect 4. Walls of visceral pleura are thick and fibrous
62
What are other types of diffuse chronic inflammation?
``` Chronic bronchitis Bronchiectisis Ulcerative colitis Rheumatoid arthritic Atherosclerosis Peptic ulcers ```
63
What is the structure of granulomatous chronic inflammation? Give the structure of this feature
Possible zone of necrosis (caseating or non caseating) Epithelioid cells Lymphocytes Macrophages Multi nucleates giant cells Collagen and fibroblasts around the outside
64
What are the different types of granulomatous lesions?
Immune mediated (caseating, non-caseating) Foreign body
65
What causes the immune mediated granulomas? Describe the structure of the granuloma
Caused by a nonfiction such as tuberculosis The granuloma has caseous necrotic tissue in the centre
66
What is an example of something causing non-caseating granuloma? What is the structure of the granuloma?
Sarcoidosis Cause unknown No necrotic tissue in the granuloma Non horseshoe arrangement of nuclei in the giant cells
67
Where do non-caseating granulomas occur?
They occur in many different organs throughout the body, but cause the most harm in the lungs
68
Describe the steps leading to foreign body mediated granuloma
1. Inert, foreign material enters (talc, silica, splinter, prosthesis) 2. Too large to be phagocytosed 3. Granuloma forms to barricade it off to prevent further damage
69
What are the sequelae of chronic inflammation? (4) | Give example of diseases for each
``` Contraction of fibrous tissue - chronic rheumatic fever Loss of parenchyma and thus function - cirrhosis of the liver Metaplasia - smoking Neoplasia - hepatocellular carcinoma (in the liver) ```
70
Describe what happens in healing by the first intention over the next 3 days
1. Mitoses under the scab 2. Neutrophils are replaced by macrophages, which clear the debris 3. Granulation tissue forms: fibroblasts make ECM , angiogenesis
71
Describe what happens over the next few weeks in healing by first intention
1. Scarring - fibroblasts inactive - vasculature decreases - type 1 -> type 3 collagen ( strong wound) - oedema drains - epithelium has been regenerated
72
What type of morphology of chronic inflammation is chronic bronchitis? What causes it?
Diffuse Cigarette smoke and pollutants - exogenous toxins
73
What type of morphology of chronic inflammation are peptic ulcers? What causes it?
Diffuse, chronic ulcers Caused by persistent infection of helicobacter pylori
74
What type of morphology of chronic inflammation is ulcerative colitis? What causes it?
Diffuse Autoimmune, inappropriate immune response
75
What type of morphology of chronic inflammation is rheumatoid arthritis?
Diffuse, immune complexes in joints Type III hypersensitivity
76
What type of morphology of chronic inflammation is sarcoidosis?
Granulomatous (non-caseating)
77
What type of morphology of chronic inflammation is asbestosis?
Diffuse, fibrous thickening of visceral pleura
78
What type of morphology of chronic inflammation is tuberculosis? What causes it?
Granulomatous; caseating granuloma in lungs Persistent infection of mycobacterium tuberculosis in. Alveolar macrophages
79
What type of morphology of chronic inflammation is foreign body?
Granulomatous, non necrotic
80
What type of morphology of chronic inflammation is atherosclerosis? What causes it?
Diffuse Caused by an endogenous toxin
81
What type of morphology of chronic inflammation is chronic choleystitis?
Diffuse, thickening of wall of gall bladder
82
Which different CD4+ t lymphocytes have a role in chronic inflammation? Differentiate between their different roles
Th1: classically activate macrophages by secreting IFN-gamma Th2: secrete IL-4 IL-5 IL-13 for alternate macrophage activation Allergic inflammation, protection against helminthic parasites Th17: secrete IL-17 for leukocyte recruitment
83
What is a tubercle?
It is the lesion in mycobacterium tuberculosis chronic inflammation
84
What is chronic rheumatic fever?
This happens after a strep infection --> type II hypersensitivity. This causes fibrosis of the mitral valves. The thick fibrous tissue contracts --> stenosis

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