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PATH30001 - Mechanisms of Disease > Lecture 15 - Ulcerative Colitis & Crohn's Disease > Flashcards

Lecture 15 - Ulcerative Colitis & Crohn's Disease Flashcards

1
Q

What are the various categories of ulcer-inflammatory conditions of the bowel?

A
  1. Infective
    • viral
    • bacterial
    • parasitic
  2. Non-infective
    • IBD (inflammatory bowel disease)
    • Enterocolitis
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2
Q

What are some viral causes of ulcer-inflammatory conditions of the bowel?

A

Rotavirus

Norovirus

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3
Q

What are some bacterial causes of ulcer-inflammatory conditions of the bowel?

A
  • E. coli

* Clostridium difficile

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4
Q

What are some parasitic causes of ulcer-inflammatory conditions of the bowel?

A
  • Giardia lamblia

* Schistosomiasis

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5
Q

What are the two major forms of IBD?

A

(Inflammatory bowel disease)
• Ulcerative colitis
• Crohn’s disease

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6
Q

Characterise IBD

A
  • Chronic inflammatory

* Ulcerative

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7
Q

What is the underlying cause of IBD?

A

Dysregulated & over-active immune response to microflora in the bowel

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8
Q

What are the clinical symptoms of IBD?

A
  • Rectal bleeding (in UC)
  • Diarrhoea
  • Abdominal pain
  • Fever
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9
Q

What is the defining feature of ulcerative colitis?

A

Involvement of the rectal mucosa

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10
Q

What are the systemic effects of UC?

A
  • Fever
  • Arthralgia
  • Inflammation of the eye
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11
Q

Describe the macroscopic changes to the rectal mucosa in UC

A
  • Shallow ulceration
  • Hyperaemic
  • Loss of haustra
  • Pseudopolyps
  • Narrowing of lumen
  • Shortening of colon
  • Granular mucosa
  • Diffusely inflamed
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12
Q

What is granular mucosa?

A
  • Roughened (not smooth) or sometimes reddish macroscopic appearance of the mucosa
  • Due to the inflammation
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13
Q

What does hyperaemic mean?

A

Increased blood flow

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14
Q

Explain Pseudopolyps

A
  • Mucosal bridges form initially
  • Later re-epithelialise as healing occurs
  • Resembles polyps
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15
Q

What are the microscopic changes in UC?

A
  • Goblet cell loss
  • Hyperplasia of epithelium
  • Neutrophil infiltration of crypts
  • Chronic inflammatory cells in lamina propria
  • Vascular congestion
  • Loss of epithelium; ulceration
  • Luminal pus
  • Distorted tubular architecture
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16
Q

Describe normal tubular architecture

A
  • Tubules extend completely across mucosa down to the muscularis mucosae
  • Parallel tubules
  • Uniformly spaced
  • Goblet cells present
  • Low levels of chronic inflammatory cells in lamina propria
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17
Q

What is the effect of loss of goblet cells?

A

Loss of mucin

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18
Q

Describe tubular architecture in UC

A
  • Distorted tubular architecture
  • Crypt abscesses
  • Inflamed tubules
  • Dense inflammatory infiltrate in LP
  • Eroded surface epithelium
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19
Q

Describe microscopic tissue features of UC remission

A
  • Tubular branching
  • Shortened tubules
  • Paneth cell metaplasia
  • Thickened muscularis mucosae
  • Epithelial dysplasia
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20
Q

Describe dysplasia in IBD

Describe the histological features

A
  • Abnormal cellular and architectural alterations
  • Confined to the mucosa by basement membrane
Cells show:
 • Loss of mucin
 • Nuclear enlargement
 • Nuclear pleomorphism
 • Loss of polarity; nucleus not in a defined position
 • Pseudostratification
 • Abnormal mitoses
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21
Q

What is pleomorphism?

A

Nuclear shape and size variation

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22
Q

What are the risk factors for developing malignancies in UC?

A
  • UC onset in childhood
  • Disease longer than 10 years in duration
  • Extent of pancolitis
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23
Q

What is pancolitis?

A

Extensive spread of UC throughout the large intestine to the ileocloacal junction

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24
Q

Describe the surveillance for malignancy in people with UC.

What happens if there is high grade dysplasia identified?

A

Annual colonoscopy w/ biopsy after 7 years with the disease

Colectomy if there is high grade dysplasia / carcinoma identified

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25
Q

What are the complications of UC?

A 
Local complications
 • Bleeding
 • Malignancy
 • Perferations (if deep ulceration)
 • Toxic megacolon
  • Damage to bile ducts
  • Arthritis
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26
Q

Characterise Crohn’s disease very generally

A

Chronic inflammatory condition of the alimentary tract

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27
Q

Which regions can be affected in Crohn’s disease?

A

Potentially any part of the alimentary canal, but mostly:

Ileocolic: 45%
• distal small intestine
• proximal large intestine

Small bowel alone 33%

Colon alone 20%

28
Q

What are the clinical features of CD?

A
  • Fever, abdominal pain, diarrhoea
  • Fistula formation
  • Strictures
29
Q

What is a fistula?

A

Abnormal passage between two hollow organs

30
Q

What are strictures?

A

Abnormal narrowing of a passage

31
Q

What are the macroscopic features of CD?

A
  • Fistula formation
  • Aphthoid ulcers (small, discrete ulcers)
  • Strictured segments
  • Fat wrapping
  • Thickened, indurated wall of the intestine
  • Fissures (cleft ulcers)
  • Oedema → cobbled appearance
  • Enlarged LNs
  • ‘Skip lesions’
  • Serositis
32
Q

Describe fat wrapping

A

Extension of mesenteric fat around the intestine

‘creeps over the wall’ of the intestine

33
Q

What is ileitis?

A

Inflammation of the ileum

34
Q

What are some microscopic features of CD?

A
  • Ileitis (transmural inflammation)
  • Oedema
  • Granulomas; multinucleate giant cells
  • Pyloric gland metaplasia
35
Q 
Compare the macroscopic features of UC and CD:
 • Areas affected
 • Ileum
 • Ulceration
 • Fissuring
 • Serosa
 • Fat wrapping
 • Wall thickness
 • Shortening
 • Strictures
 • Fistulae
 • Pseudopolypsis
 • Anal lesions
 • Malignancy
 • Systemic complications
A

Areas affected: UC: continuous, CD: skip lesions

Ileum: UC: not involved, CD: commonly involved

Ulceration: present in both, UC: CD: cobble stone appearance

Fissuring: UC: - , CD: +

Serositis: UC: - , CD: +

Fat wrapping: UC: - , CD: +

Wall thickness: UC: normal, CD: oedematous, thick

Shortening: UC: due to muscle hypertrophy, CD: due to fibrosis

Strictures: UC: - , CD: +

Fistulae: UC: - , CD: +

Pseudopolypsis: UC: + , CD: -

Anal lesions: UC: - , CD: +

Malignancy: seen in both, but increased risk with UC

Systemic complications: similar in both: liver, eyes, skin, joints

36
Q

Describe ‘skip lesions’

A

Segmental lesions

• seen in CD: some areas are affected, with intervening normal regions

37
Q

What happens to the muscularis mucosae in UC?

A

Hypertrophy → shortening of colon

38
Q

Is malignancy common in UC and CD?

A

UC: 30-fold increased risk compared to general population
CD: 6-fold increased risk

39
Q

In what organs are systemic complications seen in UC and CD?

A
  • Joints
  • Eyes
  • Skin
  • Liver
40
Q 
Compare the macroscopic features of UC and CD:
 • Paneth cell metaplasia
 • Pyloric metaplasia
 • Granulomas
 • Fissures
 • Epithelial dysplasia
 • Anal lesions
A

Paneth cell metaplasia: UC: + , CD: -

Pyloric metaplasia: UC: - , CD: +

Granulomas: UC: - , CD: +

Fissures: UC: - , CD: +

Epithelial dysplasia: UC: in non-inflamed mucosa, CD: -

Anal lesions: CD: granulomas present

41
Q

What are the three things that can lead to IBD?

A
  • Presence of Luminal antigens
  • Genetic susceptibility
  • Environmental triggers
42
Q

What is the genetic basis of IBD?

A

Genetic inheritance is more common in CD

Less common in UC

43
Q 
What are the effects of the following on UC and CD in terms of risk?
 • Smoking
 • Appendectomy
 • High sanitation in childhood
 • High intake of refined carbohydrates
 • Perinatal infection
 • Breast feeding
 • Oral contraceptive use
A

Smoking: UC: decreases, CD: increases
Appendectomy : UC: decreases, CD: 0
High sanitation in childhood : UC: 0, CD: increases
High intake of refined carbohydrates : UC: 0, CD: increases
Perinatal infection: UC: ? , CD: increases
Breast feeding: UC: decreases ? , CD: ?
Oral contraceptive use: UC: increases ? , CD: ?

44
Q

What are the different types of Th cell that can be stimulated?
How are the different types stimulated?

What are the various types associated with?

A

Different combination of cytokine release from APCs dictates the type of Th cell

Th1: cell mediated granulomas, CD

Th2: hypersensitivity, UC

Treg: tolerance

45
Q

How much bacteria are there in our gut?

A

2 kgs

Bacteria make up 50% of the dry weight of faeces

46
Q

Describe the muscle in the large intestine

A

The bands of longitudinal muscle
This allows some redundancy; if need be the large intestine can be lengthened
When tho muscle is contracted, haustra are formed.

47
Q

Why are pseudopolyps important?

A

They can lead to malignancies

48
Q

Describe wall thickness in UC and CD

A

UC: Normal thickness

CD: thickened

49
Q

At a tissue level, what is affected in UC?

Compare this with CD

A

UC: restricted to the mucosa.
Muscular propria and submucosa unaffected

CD: not restricted to the mucosa. All of the layers will be inflamed

50
Q

Compare intestinal narrowing in UC and CD

A

UC: due to muscularis mucosae hypertrophy
CD: due to fibrosis of the wall

51
Q

What is the significance of the nodules in the large bowel in UC?

A

This is the initial stage of dysplasia, and leads to malignancy

52
Q

What happens after 10 years of UC disease?

A

Rapidly increasing risk of malignancy

53
Q

What is toxic megacolon?

A

Dilation of the colon

due to inflammation of muscle layer

54
Q

Describe fissures

A

Complete thickness of tissue inflamed, spreading through to adjacent structures

55
Q

Describe fissuring ulcers

A

Very sharp, looks like a thorn that goes right through the wall.

Fibrin forms on outer surface, causing the neighbouring organs to stick to the inflamed organ
Inflammation spreads to this neighbouring tissue

56
Q

What is meant by transmural inflammation?

In which disorders is it seen?

A

Seen in CD, not UC

The entire extent of the wall thickness is inflamed

57
Q

What causes megacolon?

In which disorders is it seen?

A

Entire muscle axis inflamed

Seen in UC, not CD

58
Q

Which diseases exhibits ‘skip’ lesions?

A

CD

59
Q

What is the effect of serositis?

A

The inflamed organs sticks to neighbouring (healthy) organs

60
Q

What causes cobble stone areas?

Which disease is it seen in?

A

Lymphoedema
There is blockage of lymphatics, so that the tissue can no longer drain lymph

Seen in CD

61
Q

Which cytokine released by APCs leads to UC?

A

IL-4

Stimulates Th2

62
Q

Describe the response to gut microflora in normal cases.

Describe how this can be changed, leading to disease

A

Normal:
• peptidoglycan of bacteria stimulates TLR2
• NOD2 inhibits the intracellular transduction cascade
• No expression of IL-12
• No inflammation

Crohn's disease
 • Peptidoglycan stimulates TLR
 • Intracellular transduction cascade
 • Expression of IL-12
 • Chronic inflammation
 • Crohn's disease
63
Q

What is the role of M cells?

Where are they found?

A

They are found in Peyer’s patches, interspersed between the epithelial cells

Role:
• Translocate bacterial peptides from the luminal contents for exposure to APCs in the sub-epithelial dome

64
Q

What sort of response does one get when APCs release mainly IL-12?

A

Th1

65
Q

What sort of response does one get when APCs release mainly IL-10?

A

Treg

66
Q

What sort of response does one get when APCs release mainly IL-4?

A

Th2

67
Q

Describe how tolerance can break down in the gut mucosa

A
  • Excess secretion of IL-12
  • Increased Th1 response, decreased Treg
  • Pro-inflammatory; lymphoid & macrophage proliferation
  • Inhibition of apoptosis of lymphocytes
  • Crohn’s disease

PATH30001 - Mechanisms of Disease (34 decks)

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