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Principles of Disease-Megan > Chronic Inflammation > Flashcards

Chronic Inflammation Flashcards

1
Q

What is chronic inflammation

A

Inflammation in which the cell population is especially: lymphocytes, plasma cells and macrophages
Tends to be long term

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2
Q

What does chronic inflammation tend to feature

A

Tissue or organ damage
Necrosis
Loss of function
Healing and repair (with granulation tissue, scarring and fibrosis)

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3
Q

What could chronic inflammation be due to

A

Following from ongoing acute inflammation

Arising as primary pathology

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4
Q

What are the clinical presentation of chronic inflammation

A

Often no specific area which is sore
Malaise (e.g. TB which can affect lung, lymph node, bone, kidney, skin causing a systemic effect)
Weight loss
Loss of function (e.g. autoimmune thyroiditis, a functional gland destruction, Crohn’s disease, a GI tract ulceration and fibrosis causing pain, diarrhoea and gut obstruction and Leprosy which is cutaneous nerve destruction causing loss of sensation)

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5
Q

How does acute inflammation lead to chronic inflammation

A

It follows on from where there is a large volume of damage and an inability to remove debris. When this fails to resolve the ongoing acute is insult

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6
Q

When chronic inflammation arises as a primary lesion what is seen

A

No preceding acute phase

Only chronic changes will be seen

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7
Q

What is organisation

A

An outcome of acute inflammation where granulation tissue is a characteristic which results in healing and repair and can lead to fibrosis and formation of a scar

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8
Q

What is the function of granulation tissue

A

Patches tissue defects
Replaces dead or necrotic tissue
Contracts and pulls together

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9
Q

What is the mechanism of action of granulation tissue

A 
Capillaries grow into inflammatory mass
Plasma proteins access 
Macrophages from blood and tissue
Fibroblasts lay down collagen to repair damaged tissue
Collagen replaces inflammatory exudate
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10
Q

What are the products of granulation tissue

A

Fibrous tissue - scar (small firm blemish on skin)
Fibrosis as a problem - adhesions between loops of bowel following peritonitis
Can progress to chronic inflammation

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11
Q

What cells are involved in primary chronic inflammation

A

Lymphocytes
Plasma cells
Macrophages
Fibrosis

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12
Q

What is primary chronic inflammation

A

An autoimmune disease where autoantibodies are directed against own cell and tissue components through autoantigens
It causes damage or destroy organs, tissues, cells and cell components and can result in thyroiditis, rheumatoid disease, pernicious anaemia (chief/parietal cells) and systemic lupus erythematosis (nuclear antigen)

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13
Q

What type of inflammation is common

A

Granulomatous

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14
Q

What could primary chronic inflammation be due to

A

Material resistant to digestion (e.g. mycobacteria, Brucella, viruses)
Cell wall resistant to enzymes
Exogenous substances (e.g. sutures, metal and plastic like joint replacements, mineral crystals, glass) which do not provoke an immune response
Endogenous substances (e.g. necrotic tissue, keratin, hair) which cannot be easily phagocytosed

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15
Q

What tissue components are involved in primary chronic inflammation

A

Granulation tissue

Collagen

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16
Q

What are lymphocytes

A

Cells which are part of the immune system

Small and round with lots of subtypes and functions

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17
Q

What are the main types of lymphocytes

A

T cells

B cells

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18
Q

What is the main function of lymphocytes

A

Immune response

Immune memory

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19
Q

What are plasma cells

A

Differentiated B cells that assist in antibody production and are intermediate in size

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20
Q

What mechanisms can B cells undertake

A

Differentiate into plasma cells to produce antibodies
Facilitate an immune response
Act with macrophages for the antigen presenting capacity
Have immune memory

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21
Q

What do T cells do

A

Produce cytokines
Produce interferons
Damage and kill (lyse) other cells
Destroy antigens

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22
Q

What do cytokines do

A

Attract and hold macrophages
Activate macrophages
Other cells (e.g. lymphocytes)
Affect permeability

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23
Q

What do interferons do

A

Antiviral effects

Attract and stimulate other cells

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24
Q

What do NK-cells do

A

Destroy antigens and cells using chemical mechanisms involving granule proteins

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25
Q

State the features of macrophages

A

Remove debris
Have a role in the immune system (APC)
Found in the bone marrow and blood tissues
Contain enzymes (e.g. lysozymes)

26
Q

What can macrophages be

A 
Monocyte
Histiocyte
Activated macrophage
Epithelioid cell
Giant cells
27
Q

What mechanisms are macrophages involved in

A

The motile phagocyte move from blood and live long
Can take over from neutrophils
Produce interferons and other chemicals to destroy or influence processes

28
Q

What are fibroblasts

A

Motile cells which are metabolically active and can make and assemble structural proteins (e.g. collagens various types)

29
Q

What is granulomatous inflammation characterised by

A

The presence of granulomas (granulomata) in tissues and organs

30
Q

What stimulates granulomatous inflammation

A

Indigestible antigen (body cannot get rid of it) which causes many serious infectious and idiopathic (= no known cause) diseases

31
Q

What are granulomas

A

Aggregates of epithelioid macrophages (epithelioid histioytes) in tissue

32
Q

Describe the features of granulomas

A

May contain giant cells
May surround dead material
May be surrounded by lymphocytes
Contain neutrophils, eosinophils (only specific types)
Response to indigestible antigen
Many are type IV Hypersensitivity reactions

33
Q

What are giant cells

A

They are formed from the fusion of macrophages

They have a large cytoplasm with multiple nuclei (several types)

34
Q

Where are the langhans type classically found

A

TB

35
Q

Describe the features of langhans

A

Peripheral rim of nuclei

Large eosinophilic cytoplasm

36
Q

When a foreign body enters the body what type of tissue is it associated with

A 
Pyogenic granulation tissue
Presents as:
Acutely inflamed 
Neutrophils, pus
Organisation
Giant cells
e.g. pilonidal abscess
37
Q

Where is the nuclei in the warthin-finkeldy type

A

Central cluster of nuclei

38
Q

Give examples of infectious granulomatous diseases that are relevant to global health

A

Tuberculosis – Mycobacterium tuberculosis
Leprosy – Mycobacterium leprae
Syphilis – Treponema pallidum

39
Q

What is caseous nercrosis

A

Dead tissue surrounded by macrophages, giant cells, lymphocytes

40
Q

Which drugs can be used to treat a patient with leprosy

A

Dapsone, rifampicin and clofazimine

This combination kills the pathogen

41
Q

Give example of non-infective granulomas

A

Rheumatoid disease
Sarcoidosis
Crohn’s disease

42
Q

What is rheumatoid disease

A

A tissue specific auto-immune disease

43
Q

What is crohn’s disease

A

Chronic inflammatory bowel disease

44
Q

How does wound healing occur

A 
There is a:
Phase of acute inflammation
Granulation tissue formation
Local angiogenesis – new vessels grow
Fibrosis and scar formation
45
Q

How does surgical wound healing occur

A

Healing by primary intention
Minimal gap from blood clot
Small amount of granulation tissue
Small linear scar

46
Q

How do larger defects heal

A

Healing by secondary intention
Lots of granulation tissue ingrowth
Contraction and scarring

47
Q

Give an example when healing by primary intention occurs

A

Surgical wound healing

48
Q

Give an example when healing by secondary intention occurs

A

For larger defects

49
Q

Describe the sequence of events which occur for secondary intention healing

A

Injury, blood clot, acute inflammation, fibrin
Many growth factors and cytokines involved
Granulation tissue growth - angiogenesis
Phagocytosis of fibrin
Myofibroblasts move in and lay down collagen
contraction of scar
Re-epithelialisation

50
Q

What helps a wound to heal

A 
Cleanliness
Apposition of edges (no haematoma)
Sound nutrition
Metabolic stability and normality
Normal inflammatory and coagulation mechanisms
Note local mediators
51
Q

What prevents a wound from healing

A

Dirty, gaping wound, large haematoma
Poorly nourished, lack of vitamins C, A
Abnormal carbohydrate metabolism, diabetes, corticosteroid therapy
Inhibition of angiogenesis

52
Q

What are the features of fracture healing

A

It’s the same principles as healing at any site
Modified by situation in bone
Have to repair bony structure as well as soft tissue

53
Q

Describe the sequence of events which occur in fracture healing

A

Trauma, fracture, haematoma
Bits of dead bone and soft tissue
Acute inflammation, organisation, granulation tissue, macrophages remove debris
Granulation tissue contains osteoblasts as well as fibroblasts

54
Q

How do calluses form

A

Osteoblasts lay down woven bone
Nodules of cartilage present
Followed by bone remodelling

55
Q

How does bone remodelling occur

A

Osteoclasts remove dead bone
Progressive replacement of woven bone by lamellar bone
Reformation of cortical and trabecular bone

56
Q

Describe the process of angiogenesis

A

New vessels form from capillary buds
Vascular Endothelial Growth Factor (VEGF) released by hypoxic cells stimulates proliferation
Enzyme secretion aids process
Enable blood supply to enter damaged tissue

57
Q

What does angiogensis and organisation in thrombosis do

A

Limits thrombus propagation

Reinstatement of flow

58
Q

What does angiogenesis in malignant tumours have the potential for

A

Potential for therapeutic control

59
Q

What does chronic inflammation have similarities with

A

Fibrosis and scarring in atherosclerosis

60
Q

Name types of giant cells

A

Foreign body
Langhans
Silicone associated
Warthin-Finkeldy

61
Q

What is wound healing

A

Its a process of repair of tissue damage

Principles of Disease-Megan (41 decks)

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