Chronic inflammation Flashcards

1
Q

List the cell types involved in chronic inflammation

A

Lymphocytes
Macrophages
Plasma Cells

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2
Q

Major causes of chronic inflammation?

A

arising from acute inflammation

arising as a primary lesion (Primary skin lesions are those which develop as a direct result of the disease process.)

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3
Q

arising from acute inflammation

A
  • Large volume of damage
  • Inability to remove what caused acute inflammation before
  • Fails to resolve
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4
Q

arising as a primary lesion

A

No acute phase, only see chronic stages
Can be a result of:-

Auto-immunal disorder

material resistant to cellular digestion

Exogenous substances eg. Sutures (stitches, metal/ plastic e.g joint replacements, glass)

Endogenous subtances eg. Keratin, Hair, necrotic (dead) tissue, can’t be easily phagocytosed

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5
Q

What are some effects of chronic inflammation?

A
scarring and fibrosis (thickening and scarring of connective tissue, build up of scar tissue in an organ or tissue)
granuloma formation (cluster of immune cells
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6
Q

What is chronic inflammation?

A

body’s response to injury or infection
inflammation that features tissue or organ damage, (necrosis) loss of function ie leprosy- damage to cutaneous nerves so lose sensitivity
tends to be long term

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7
Q

Factors involved in promoting healing and repair?

A
Cleanliness
Apposition of edges
Sound nutrition
Metabolic stability and normality
Normal inflammatory and coagulation mechanisms
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8
Q

symptoms/ clinical presentations of chronic inflammation

A

often no specific ‘sore bit’
malaise (general feeling of illness/discomfort) and weight loss e.g tb- systemic effect

loss of function- autoimmune thyroiditis (functional gland destruction) hypothyroidism (doesn’t produce enough thyroid hormone
Chron’s disease (GI tract ulceration and fibrosis) pain, diarrhoea, gut obstruction
Leprosy (cutaneous nerve destruction) loss of sensation

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9
Q

Granulation tissue mechanism

A

capillaries grow into inflammatory mass
access of plasma proteins
macrophages from blood and tissue
fibroblasts lay down collagen to repair damaged tissue
- collagen replaces inflammatory exudate
- patches tissue defects, replaces dead or necrotic tissue
contracts and pulls together

the product of granulation tissue is fibrous tissue- a scar e.g small firm blemish on skin

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10
Q

Primary chronic inflammation:- autoimmune disease

A

autoimmune disease
self antibodies directed against own cell and tissue components- body attacks itself
damage or destroy organs, tissues, cells, cell components
thyroiditis, rheumatoid disease, sytemic lupus etc

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11
Q

examples of material resistant to digestion

A

mycobacteria (can cause tb)
brucella (bacteria from animals)
viruses

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12
Q

macrophage mechanisms

A

motile phagocyte move from blood
long lived
contain enzymes e.g lysozomes

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13
Q

effects of chronic inflammation

A

increase in lymphocytes, plasma cells, macrophages and fibroblasts
tissues or organ damage (necrosis) and loss of function
involves healing and repair- granulation tissue, scarring and fibrosis

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14
Q

role of Angiogenesis in healing and repair

A

angiogenesis is part of granulation tissue and repair
- it involves the formation of new blood vessels. Vascular endothelial growth factor (VEGF) is released by many hypoxic (tumour) cells, which stimulate proliferation. Enzyme secretion aids process.

Angiogenesis enables blood supply to enter damaged tissue

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15
Q

describe the sequence of events in healing and repair

A

injury, blood clot, acute inflammation, fibrin (forms the scab)
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- keratinocytes pushed up from layers of epidermis

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16
Q

What is pilonidal abscess?

A

hair shafts growing down into the skin- around about it you find inflammation etc. Very painful, curable though

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17
Q

Primary intention

A

when the dermal edges are close together- ie in apposition and produce a linear scar

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18
Q

secondary intention

A

larger wound - sides not in apposition
lots of granulation tissue in-growth so mass in the middle
a lot of blood clot too
more untidy scar

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19
Q

what factors help healing process

A

cleanliness
apposition of edges
sound nutrition- if you’re not properly nourished you don’t heal well as you don’t have a lot of energy required for healing process
corticosteroid therapy (a drug used for things like arthritis, lupus, asthma etc)
metabolic stability and normality
normal inflammatory and coagulation mechanisms

20
Q

Impaired wound healing

A

dirty, gaping wound, large haematoma
poorly nourished- lack of vitamins C, A
abnormal carbohydrate metabolism, diabetes (high glucose levels can make healing less possible as it interferes with process) etc
inhibition of angiogenesis

21
Q

what is haematoma

A

a solid swelling of blood in the tissue, outside of the blood vessels

22
Q

Fracture healing in bones general

A

same principles as healing at any site except you have to repair the bony structure as well as the soft tissue.

23
Q

common types of infectious granulomatous diseases

A

tb
leprosy
syphilis

24
Q

common types of non-infectious granulomatous diseases

A

rhematoid arthritis

chron’s

25
Q

common types of non-infectious granulomatous diseases

A

rhematoid arthritis

chron’s

26
Q

What is Granulomatous inflammation?

A

special type of chronic inflammation

presence of granulomas in tissues and organs

27
Q

What is Granulomatous inflammation?

A

special type of chronic inflammation

presence of granulomas in tissues and organs

28
Q

features of granuloma

A

aggregates of epitheloid (looks like epithelial cell but isn’t a cell) macrophages in tissue
may contain giant cells
may surround dead material
these contain neutrophils and eisonophils
many are type IV hypersensitivity

29
Q

Define epitheloid

A

looks like epithelial cell but isn’t

descriptive term

30
Q

giant cells

A

have large cytoplasm, multiple nuclei due to being formed from many macrophages fused together
don’t always need granulomas for them to be present

31
Q

langhans type?

A

a type of giant cell

identifiable from peripheral ring of nuclei

32
Q

langhans type?

A

a type of giant cell

identifiable from peripheral ring of nuclei

33
Q

what is foreign body granuloma?

A

any response to foreign material in the tissue
typically the nuclei are scattered willy nilly about the cytoplasm
- often becomes acutely inflamed, pus forms, neutrophils and giant cells are present

34
Q

How is Granulomatous inflammation stimulated?

A

by an indigestible antigen ie something the body can’t digest/ break down/ remove as it normally would

35
Q

sequence of events in bone fracture healing general

A

trauma, fracture, haematoma
then bits of dead bone and soft tissue
acute inflammation, organisation, granulation tissue, macrophages remove debris
granulation tissue contains osteoblasts as well as fibroblasts (can make new bone and fibrous tissue

36
Q

What is a severe problem associated with bone fractures?

A

you can lose a lot of blood

can be dangerous in elderly as if they break a bone they lose a good majority of their total blood volume.

37
Q

What happens almost instantaneously after fracture?

A

blood vessels are torn so blood starts to form underneath periosteum

38
Q

what happens after a few seconds/minutes after a fracture?

A

Haematoma formation- blood accumulates around fracture site and there’s major swelling and can be painful. Haematoma can cause the death of some cells ie bone and tissue.

39
Q

What happens a few days after fracture?

A

New blood vessels form (angiogenesis)
granulation tissue forms soft callus (mesh work of tissue) and fills in the gap and rejoins the fracture. Soft callus is fibrocartilaginous

40
Q

Which cells remove debris?

A

macrophages

41
Q

what is organisation?

A

an outcome of acute inflammation

involved in healing and repair- scar formation

42
Q

woven bone

A

Woven bone is characterized by haphazard organisation of collagen fibers and is mechanically weak. Woven bone is produced when osteoblasts produce osteoid rapidly

43
Q

what happens a few weeks after fracture?

A

bony callus formed

soft callus previously formed becomes bony callus

44
Q

what is woven bone later replaced by?

A
lamellar bone (spongy or trabecular) 
collagen fibers laid down with parallel alignment- making it strong
45
Q

Main differences between acute and chronic inflammation in terms of cells present, lesion and clinical examples?

A

acute
cells: at infection site- neutrophils, allergy- eisonophils, mast cells
lesion: rash, pus, abscess
clinical examples: abscesses (brain, skin), allergic reaction (anaphylaxis)

chronic
cells: macrophages, lymphocytes, plasma cells
lesion: rash, fibrosis, granuloma
clinical examples: autoimmune diseases like lupus, rheumatoid arthritic, cystic fibrosis