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2. Foundations of Medicine PoD > Chronic Inflammation > Flashcards

Chronic Inflammation Flashcards

1
Q

Define chronic information

A
  • inflammation in which the cell population is especially: lymphocytes, plasma cells, macrophages
  • features tissue or organ damage, (necrosis), loss of function
  • healing and repair
    -granulation tissue
    -scarring and fibrosis
  • may follow from ongoing acute inflammation**
  • but also arises as primary pathology - no acute process
  • tends to be long-term
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2
Q

clinical presentations of chronic inflammation

examples also given but remember bold bits

A
  • malaise and weight loss
    -tuberculosis (lung, lymph node, bone, kidney, skin) - systemic effect
  • loss of function
    -autoimmune thyroiditis (functional gland destruction) - hypothyroidism
    -Crohn’s disease (GI tract ulceration and fibrosis) - pain, diarrhoea, gut obstruction
    -leprosy (cutaneous nerve destruction) - loss of sensation
  • No specific sore bit (unlike acute)
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3
Q

when do we see chronic inflammation: what causes it to occur

A
  • arising from acute inflammation
    -follows on from acute
    -large volume of damage
    -inability to remove debris
    -fails to resolve - ongoing acute insult
  • arising as a primary lesion
    -no preceding acute phase
    -only see chronic changes
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4
Q

angiogenesis

A
  • new vessels form- capillary buds
  • Vascular Endothelial Growth Factor (VEGF) released by hypoxic cells stimulates proliferation
  • enzyme secretion aids process
  • enable blood supply to enter damaged tissue
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5
Q

What outcome of acute inflammation is linked to chronic inflammation

A

Organisation: granulation tissue, angiogenesis, healing and repair, scar

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6
Q

granulation tissue mechanism of action (process)

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

helps us to restore normal function

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7
Q

Describe the overlap/interface between chronic and acute inflammation (briefly)

A

Mixture:
* exudate, neutrophils
* lymphocytes plasma cells, fibroblasts, fibrosis

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8
Q

pyogenic

A

pus?

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9
Q

what are the products of granulation tissue

A
  • fibrous tissue - scar, helpful
  • fibrosis as a problem (stick bits together when shouldn’t be)
  • chronic inflammation
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10
Q

primary chronic inflammation

factor/cause, explanation, example…

A
  • autoimmune disease
    -autoantibodies directed against own cell and tissue components - autoantigens. damage or destroy organs, tissues, cells, cell components (e.g.thyroiditis, rheumatoid disease, pernicious anaemia (chief/parietal cells), systemic lupus erythematosis (nuclear antigen))
  • lymphocytes, plasma cells, macrophages, fibrosis - immune response destroys tissue to which it was directed
  • material resistant to digestion
  • exogenous substances (foreign)
    -not provoke immune response
  • endogenous substances (necrotic tissue, keratin, hair -cannot easily be phagocytosed)
  • granulomatous inflammation common
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11
Q

pathogenesis of chronic inflammation: what cells and tissue components are involved?

5 cells, 2 tissue componenets…

A

Cells: lymphocytes, plasma cells, macrophages, fibroblasts + endothelial cells —> blood clotting/fibrin
Tissue Components: granulation tissue, collagen

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12
Q

B cells meachanism in immune/inflammatory system

essentially; B cell function

A
  • differentiate to plasma cells -antibodies
  • facilitate immune response
  • act with macrophages
    -antigen presenting capacity
  • immune memory
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13
Q

Role of T cells in immune/inflammatory response

A
  • Produce cytokines* (attract and hold macrophages, activate macrophages, other cells eg lymphocytes, permeability)*
  • T-cells produce interferons (antiviral effects, attract and stimulate other cells) helper?
  • damage and kill (lyse) other cells and destroy antigen - granule proteins
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14
Q

Summarise NK-cell mechanismsin immune system

A

Destroy antigens and cells:
* chemical mechanisms - granule proteins
* Innate immunity

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15
Q

Role of macrophages in immune/inflammatory reponse

A
  • removes debris
  • role in immune system - antigen presenting cell
  • monocyte, histiocyte, activated macrophage, epithelioid cell, giant cell

kills cells, removes dead cells, activates other immune cells

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16
Q

How do macrophages become involved in immune/inflammatory response

A
  • motile phagocyte so moves from blood
  • takes over from neutrophils
  • containse degrating enzymes (lysosomes) - kill
  • produces interferons and other chemicas (destroy/influence process)

interferons - recognise foreign body, signal to othher cells

17
Q

fibroblast function

A

Contribute to CT formation
Motile cell that cvcvan make and assemble structural proteins - collagens

18
Q

Summarise the outcome of chronic inflammation

A
  • ongoing tissue damage/destruction
  • insidious loss of function
  • cellular and stromal response (granulation tissue, angiogenesis)
  • fibrosis and scarring
  • granuloma formation
19
Q

adverse effects of tissue scarring

A

pain, tightness, itching, or difficulty moving - if internal that can be very bad

20
Q

effects of chhronic inflammation

(from goole)

A

Body’s inflammatory response can eventually start damaging healthy cells, tissues, and organs. Over time, this can lead to DNA damage, tissue death, and internal scarring. All of these are linked to the development of several diseases, including: cancer

21
Q

Major causes of chronic inflammation

A
  • autoimmune disorders
  • exposure to toxins
  • untreated acute inflammation
22
Q

explain granulomatous inflammation

A
  • characterised by presence of granulomas (granulomata) in tissues and organs
  • stimulated by indigestible antigen
    -body cannot get rid of it (important for global health)
  • many serious infectious and idiopathic (= no known cause) diseases
23
Q

Granulomas

A
  • aggregates of epithelioid macrophages in tissue
  • may contain giant cells
  • may surround dead material and be surrounded by lymphocytes
  • contain neutrophils, eosinophils
  • response to indigestible antigen
24
Q

what are many granulomas a result from (autoimmunity)

A

Type IV hypersensitivity reactions

25
Q

What are giant cells

A
  • granulomas comprise epithelioid histioytes (macrophages)
  • fusion of macrophages to form larger cells
  • large cytoplasm; multiple nuclei
  • not always granuloma for giant cells to be present
26
Q

what are foreign body types associated with and what is found there

A

Pyogenic granulation tissue - pus
acutely inflamed, neutrophils (pus), orginisation, giant cells

27
Q

Foreign body causing inflammation example

A

silicone: ruptured implants with vacuoles containing leaked silicone

28
Q

3 infectious granulomatous disease examples

A
  • tuberculosis - Mycobacterium tuberculosis
  • leprosy - Mycobacterium leprae
  • syphilis - Treponema pallidum
29
Q

caseous necrosis

A

dead tissue surrounded by macrophages, giant cells, lymphocytes - granulomas?

Tb common cause

30
Q

3 non-infective granulomas examples

A
  • rheumatoid disease - tissue specific auto-immune disease
  • sarcoidosis - classical clinical picture
  • Crohn’s disease - chronic inflammatory bowel disease
31
Q

Give brief overview of wound healing (from acute inflammation)

A

Process of repair to tissue damage
* phase of acute inflammation
* granulation tissue formation
* local angiogenesis (new vessel growth)
* fibrosis and scar formation

32
Q

sequence of events in wound healing

A
  1. injury, blood clot, acute inflammation, fibrin
  2. many growth factors and cytokines involved
  3. granulation tissue growth - angiogenesis
  4. phagocytosis of fibrin
  5. myofibroblasts move in and lay down collagen
  6. contraction of scar
  7. re-epithelialisation
33
Q

how does surgical wound healing compare to that of larger defects

A

only small amount of granulation tissue so not much contraction and scarring

34
Q

factors to favour wound healing

A

*cleanliness
*apposition of edges (no haematoma)
*sound nutrition
*metabolic stability and normality
*normal inflammatory and coagulation mechanisms
*note local mediators

35
Q

factors to impair wound healing

A

*dirty, gaping wound, large haematoma
*poorly nourished, lack of vitamins C, A
*abnormal CHO metabolism, diabetes, corticosteroid therapy
*inhibition of angiogenesis

36
Q

what is different about fracture healing compared to normal tissue healing

A

have to repair bony structure as well as soft tissue

37
Q

sequence of events 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

Callus formation:
* osteoblasts lay down woven bone
* nodules of cartilage present
* followed by bone remodelling
-osteoclasts remove dead bone
-progressive replacement of woven bone by lamellar bone
-reformation of cortical and trabecular bone

38
Q

role of angiogenesis in healing and repair

A

forming new blood vessels from preexisting vessels by invading the wound clot and organizing in to a microvascular network throughout the granulation tissue - provide nutrients and O2 to damaged/healing tissues

39
Q

factors to impair wound healing and repair

A

age/weight/sanitation etc.
Nutrients to wound/vasculature

maybe more, is Lo but had to google???

2. Foundations of Medicine PoD (28 decks)

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