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
State the features of macrophages
Remove debris Have a role in the immune system (APC) Found in the bone marrow and blood tissues Contain enzymes (e.g. lysozymes)
26
What can macrophages be
``` Monocyte Histiocyte Activated macrophage Epithelioid cell Giant cells ```
27
What mechanisms are macrophages involved in
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
What are fibroblasts
Motile cells which are metabolically active and can make and assemble structural proteins (e.g. collagens various types)
29
What is granulomatous inflammation characterised by
The presence of granulomas (granulomata) in tissues and organs
30
What stimulates granulomatous inflammation
Indigestible antigen (body cannot get rid of it) which causes many serious infectious and idiopathic (= no known cause) diseases
31
What are granulomas
Aggregates of epithelioid macrophages (epithelioid histioytes) in tissue
32
Describe the features of granulomas
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
What are giant cells
They are formed from the fusion of macrophages | They have a large cytoplasm with multiple nuclei (several types)
34
Where are the langhans type classically found
TB
35
Describe the features of langhans
Peripheral rim of nuclei | Large eosinophilic cytoplasm
36
When a foreign body enters the body what type of tissue is it associated with
``` Pyogenic granulation tissue Presents as: Acutely inflamed Neutrophils, pus Organisation Giant cells e.g. pilonidal abscess ```
37
Where is the nuclei in the warthin-finkeldy type
Central cluster of nuclei
38
Give examples of infectious granulomatous diseases that are relevant to global health
Tuberculosis – Mycobacterium tuberculosis Leprosy – Mycobacterium leprae Syphilis – Treponema pallidum
39
What is caseous nercrosis
Dead tissue surrounded by macrophages, giant cells, lymphocytes
40
Which drugs can be used to treat a patient with leprosy
Dapsone, rifampicin and clofazimine This combination kills the pathogen
41
Give example of non-infective granulomas
Rheumatoid disease Sarcoidosis Crohn’s disease
42
What is rheumatoid disease
A tissue specific auto-immune disease
43
What is crohn's disease
Chronic inflammatory bowel disease
44
How does wound healing occur
``` There is a: Phase of acute inflammation Granulation tissue formation Local angiogenesis – new vessels grow Fibrosis and scar formation ```
45
How does surgical wound healing occur
Healing by primary intention Minimal gap from blood clot Small amount of granulation tissue Small linear scar
46
How do larger defects heal
Healing by secondary intention Lots of granulation tissue ingrowth Contraction and scarring
47
Give an example when healing by primary intention occurs
Surgical wound healing
48
Give an example when healing by secondary intention occurs
For larger defects
49
Describe the sequence of events which occur for secondary intention healing
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
What helps a wound to heal
``` Cleanliness Apposition of edges (no haematoma) Sound nutrition Metabolic stability and normality Normal inflammatory and coagulation mechanisms Note local mediators ```
51
What prevents a wound from healing
Dirty, gaping wound, large haematoma Poorly nourished, lack of vitamins C, A Abnormal carbohydrate metabolism, diabetes, corticosteroid therapy Inhibition of angiogenesis
52
What are the features of fracture healing
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
Describe the sequence of events which occur in fracture healing
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
How do calluses form
Osteoblasts lay down woven bone Nodules of cartilage present Followed by bone remodelling
55
How does bone remodelling occur
Osteoclasts remove dead bone Progressive replacement of woven bone by lamellar bone Reformation of cortical and trabecular bone
56
Describe the process of angiogenesis
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
What does angiogensis and organisation in thrombosis do
Limits thrombus propagation | Reinstatement of flow
58
What does angiogenesis in malignant tumours have the potential for
Potential for therapeutic control
59
What does chronic inflammation have similarities with
Fibrosis and scarring in atherosclerosis
60
Name types of giant cells
Foreign body Langhans Silicone associated Warthin-Finkeldy
61
What is wound healing
Its a process of repair of tissue damage