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Cells to systems > Lecture 12 - chronic inflammation and healing > Flashcards

Lecture 12 - chronic inflammation and healing Flashcards

1
Q

When does a chronic inflammation occur

A 
Occurs when acute inflammation fails to
resolve an insult:
– Foreign bodies
– Autoimmune disease
– Persistent infection
– Hypersensitivity/Allergic
disease
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2
Q

What are the 4 causes of chronic inflammation

A 
– Foreign bodies
– Autoimmune disease
– Persistent infection
– Hypersensitivity/Allergic
disease
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3
Q

What does peracute mean the time frame

A

(immediate) insult – minimal inflammation

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4
Q

What does acute mean in time frame

A

(<2 days) – acute inflammation

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5
Q

What does subacute mean in time frame

A

(2-7 days) – transitional period

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6
Q

What does Chronic mean in time frame

A

(7 days +) – chronic inflammation

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7
Q

What is the sequence of the name for each time frame

A
  • Peracute (immediate) – minimal inflammation
  • Acute (<2 days) – acute inflammation
  • Subacute (2-7 days) – transitional period
  • Chronic (7 days +) – chronic inflammation
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8
Q

What are the 3 features of chronic inflammation

A
  1. Changes in inflammatory cell population
  2. Inflammatory tissue damage
  3. Tissue healing
    – Regeneration, fibrosis and scar tissue formation
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9
Q

why does the celll type change in chronic inflammation

A

Represents induction of the ADAPTIVE immune response

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10
Q

What changes in cell type

A 
T lymphocytes
• Key cells of adaptive immune system
• Activated in response to specific
binding of antigen with T-cell receptor
• Proliferation of lymphocytes
• Produce cytokines to direct the
immune response
• No antigen recognition = minimal chronic
inflammation
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11
Q

What are the subtype of chronic inflammation

A 
Lymphocytic/Lymphoplasmacytic
Granulomatous
Eosinophilic
Often mixed, and may have neutrophil
component
– “Chronic-active” inflammation
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12
Q

What is another word for Lymphocytic inflammation

A

non-suppurative inflammation

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13
Q

What cells are responsible in lymphocytic inflammation

A
  • cytotoxic T cells
  • helper T cells (Th cells)
  • B cells
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14
Q

What is it called when plasma cells are present in a lymphocytic inflammation

A

Lymphoplasmacytic inflammation

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15
Q

What does perivascular mean

A

situated or occurring around a blood vessel.

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16
Q

What is common during lymphocytic inflammation

A

Perivascular distribution common
Sometimes form nodular aggregates
– Lymphoid follicles

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17
Q

What does lymphocytic inflammation commonly respond to?

A

cell-association antigen

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18
Q

What disease are usually prone to lymphocytic inflammation?

A 
• Auto-immune disease
– Type 1 diabetes
• Viral infections
– Rabies
– Viral hepatitis in humans
• Hypersensitivity diseases
– Inflammatory bowel disease
• Idiopathic???
– Lymphoplasmacytic stomatitis
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19
Q

What are the roles of macrophages

A

– Phagocytosis

– Direct inflammation and repair

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20
Q

What does phagocytosis do

A

• Digest and eliminate foreign agents
• Present antigen to T-cells (function as
antigen-presenting cell)

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21
Q

How does macrophage direct inflammation and repair

A

• Secrete cytokines such as interleukin 12
(IL-12) to promote inflammation
• Secrete cytokines such as TGF-β to
suppress inflammation and promote repair

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22
Q

What does macrophages respond to?

A

– Chronic infections (parasites, fungi,
mycobacteria)
– Foreign material

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23
Q

What is Macrophage-dominated inflammation called

A

GRANULOMATOUS INFLAMMATION

Sometimes also called histiocytic inflammation

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24
Q

What is clusters of macrophages called

A

GRANULOMAS

• Cells may fuse to form GIANT CELLS

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25
Q

What are the subtypes of granulomatous inflammation

A

– Pyogranuloma – central accumulation of neutrophils

– Caseating granuloma/necrogranuloma

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26
Q

What is Pyogranuloma

A

– central accumulation of neutrophils
▪ Seen with some foreign bodies, particularly with bacterial contamination
▪ Also with some infections (eg. Rhodococcus equi)

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27
Q

What is Caseating granuloma/necrogranuloma

A

▪ “Cheesy” centre composed of dead tissue

▪ Seen particularly with tuberculosis and some parasites

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28
Q

What do Granulomatous inflammation often form

A

discrete or coalescing
nodules in tissues
- Easy to mistake for NEOPLASIA

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29
Q

Do nodules develop in granulomatous disease?

A

no

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30
Q

What is eosinophilic inflammation

A

Primarily parasitic or allergic disease

31
Q

What does eosinophilic inflammation affected tissues often look like

A

green appearance

eosinophils are actually green!

32
Q

What do tissue damage result from?

A

– Damage by the original insult
– Release of inflammatory mediators
– Cellular phagocytosis or apoptosis
– Tissue death due to circulatory compromise (thrombosis)

33
Q

Do the body usually attempt to heal even in chronic inflammation?

A

Yesregardless of whether insult resolved

– Usually ineffective without resolution of insult

34
Q

What is the 2 major pathways of healing

A

– Regeneration

– Repair

35
Q

What is an exmaple of tissue that have specialized healing mechanisms

A

bone

36
Q

What is regeneration

A

Replacement of damaged tissue with the original

cell type

37
Q

What is regeneration depend on

A
  • Viability of original cells
  • Type of tissue
  • Preservation of connective tissue scaffold
38
Q

What are the regeneration cell types

A

Labile cells
Stable cells
Permanent cells

39
Q

What is the function of labile cell

A

Undergo constant turnover and can regenerate
completely from germinal cells
– Epidermis of skin, intestinal epithelium, bone marrow

40
Q

Where do labile usually be at

A

Epidermis of skin, intestinal epithelium, bone marrow

41
Q

What is the function of stable cell

A

Normally quiescent (ie. not dividing), but have the
ability to regenerate if required
– Hepatocytes, osteocytes, renal tubular epithelium

42
Q

Where do stable cell usually located at

A

Hepatocytes, osteocytes, renal tubular epithelium

43
Q

What is the function of permanent cells

A 
– Considered terminally
differentiated
– Do not regenerate
– Neurons, cardiac
muscle
44
Q

Where is permanent cell located at

A

Neurons, cardiac

muscle

45
Q

Do permanent cell regenerate

A

no

46
Q

How is tissue repaired

A 
• Replacement of damaged
tissue by fibrous connective
tissue (scar tissue)
– Also referred to as fibrosis
• Restores structure at expense
of function
• Occurs in competition with
regeneration
47
Q

How does repair occur?

A

• Defect is initially filled by formation of granulation tissue
– Fragile, vascular connective tissue
– COMPLETELY DIFFERENT FROM GRANULOMA

48
Q

What is the inflammatory phase of repairing tissue

A

• Clearance of damaged tissue debris
– Neutrophils and macrophages
• Replaced by fibrin coagulum

49
Q

what is the proligerative phase of repairing tissue

A

– Production of granulation tissue
– Angiogenesis
• Fibroplasia

50
Q

What is Angiogenesis for in proliferative phase

A

• Provides oxygen and nutrients for healing
• Hypoxia in damaged tissue stimulates release of
growth factors (eg. VEGF, FGFs, Angiopoietins) to
promote blood vessel development

51
Q

What is angiogenesis

A

Angiogenesis is the formation of new blood vessels. This process involves the migration, growth, and differentiation of endothelial cells, which line the inside wall of blood vessels.

52
Q

What is frbroplasia

A

– Production of collagen stroma
– Migration of fibroblasts and deposition of immature
type 3 collagen
– Occurs under influence of growth factors (PDGF,
FGFs, TGF-β)

53
Q

What is fibroplasia growth influenced by?

A

occurs under influence of growth factors (PDGF,

FGFs, TGF-β)

54
Q

What is the Maturation phase and scar

formation of repairing tissue

A 
• Reorganization of collagen
and change in collagen type
(Type 1)
– Type 1 collagen stronger
– Organized parallel with lines of
tension
• Contraction of connective
tissue
• Maturation and regression of
vasculature
55
Q

What is the intention of primary healing

A

restoring to intact skin after fibrin is grown on the surface

56
Q

What is the intention of secondary healing

A

for bigger wound

57
Q

What is the steps of primary intention heal

A
  1. Wound edges joined by fibrin plug
    (24hrs)
  2. regrowth of basel layer of epidermis (days)
  3. Lysis of fibrin and re-epithelialisation (1week)
  4. Restoration of intact skin (weeks)
58
Q

What is the difference between primary and secondary intention healing

A
  • More inflammation
  • More granulation tissue
  • More fibrosis/scarring
  • PROLONGED HEALING
59
Q

What is the steps in secondary intention healing

A
  1. Large defect filled by fibrin clot (2-3 days)
  2. New blood vessels and fibroblast (granulation tissue) grow from the demis into fibrin
  3. Collagen laid down by granulation tissue fibroblasts to restore integrity (2-4 weeks)
  4. Maturation of collagen achieves structural integrity and allows regrowth of epidermis
60
Q

What factors influence healing?

A
  • Infection
  • Foreign material
  • Nutrition
  • Movement/pressure
  • Vascular/Oxygen supply
  • Hormones
  • Concurrent disease
  • Age
61
Q

What are some abnormal healing?

A
  • Proud flesh

* Keloid

62
Q

What is keloid

A

– Formation of excessive scar tissue during healing

– Rare in animals, people of African descent predisposed

63
Q

What is proud flesh

A

– Formation of excessive granulation tissue that delays healing
– Common in horses

64
Q

What animal commonly have proud flesh

A

horse

65
Q

What are the consequences of scar tissue

A
  • Strictures
  • Adhesions
  • Restricted movement
66
Q

What is strictures

A

– Scar contracture causing narrowing of hollow organ

67
Q

What is adhesions of scars

A

– Formation of fibrous tissue attachments between adjacent organs

68
Q

Why does scar restrict movement

A

– Contraction of scar tissue around joints and tendons can prevent normal
movement

69
Q

What directs inflammation?

A

T lymphocyte

70
Q

What can T cell differentiate into after getting signalled by a antigen presenting cell

A
  • Th1 cell, Further differentiate into macrophage recuitment and igG antibody production
  • Th2 cell, further differentiate into eosinophil recruitment and igE antibody production
  • Cytotoxic T cell
71
Q

What disease are usually prone to lymphocytic inflammation?

A

auto-immune disease

-type 1 diabetes

72
Q

Do granulomatous alway lead to granulomatous inflammation

A

no, example of it is johne’ disease granulomatous enteritis

73
Q

What is one difference between regeneration and repair?

A

Repair doesnt restore the function, but just the structure

74
Q

What is angiogenesis stimulated by?

A

hypoxia

Cells to systems (25 decks)

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