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Gastrointestinal Pathology > Pathology of Colon > Flashcards

Pathology of Colon Flashcards

1
Q

Types of large bowel neoplasia

A 
Dysplasia 
- low grade
- high grade
Malignancy 
- colorectal carcinoma
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2
Q

Types of dysplasia of the large bowel

A

Adenoma (polyp)

  • tubular (90% occur in colon)
  • villous
  • tubulovillous
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3
Q

What % of dysplasias of the large colon are solitary?

A

50%

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4
Q

What is seen in low grade dysplasia of adenoma of the large colon?

A

Increased nuclear numbers
Increased nuclear size
Reduced mucin

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5
Q

What is seen in high grade dysplasia of adenoma of the large colon?

A

Carcinoma in situ
Crowded
Very irregular
Not yet invasive

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6
Q

What % of colorectal carcinomas are adenocarcinomas?

A

98%

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7
Q

Risk factors for colorectal carcinoma

A 
Lifestyle
Family history 
IBD 
Genetics
- FAP
- HNPCC
- Peutz-Jeghers
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8
Q

Presentation of right sided colorectal adenocarcinoma

A

Anaemia (altered blood PR)
Vague pain
Weakness
Obstruction

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9
Q

Presentation of left sided colorectal adenocarcinoma

A

Bleeding; fresh/altered blood PR
Altered bowel habit
Obstruction

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10
Q

Parts of the small bowel

A

Duodenum
Jejunum
Ileum

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11
Q

Parts of the large bowel

A 
Caecum 
Ascending colon 
Transverse colon 
Descending colon 
Sigmoid 
Rectum
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12
Q

Which parts of the large bowel are retroperitoneal?

A

Ascending colon

Descending colon

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13
Q

Where does the sigmoid originate?

A

Pelvic brim

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14
Q

3 types of cells in the small bowel

A

Goblet cells
Columnar absorptive cells
Endocrine cels

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15
Q

What is the mucosa of the small bowel?

A

Villi

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16
Q

Histology of small bowel

A 
Villi 
Goblet cells
Columnar absorptive cells
Endocrine cells
Crypts
Lamina propria, Muscularis mucosa, submucosa
Muscularis propria and subserosa
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17
Q

What type of crypts are found in the small bowel?

A

Stem
Goblet
Endocrine
Paneth

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18
Q

Histology of the large bowel

A 
Flat
No villi 
Tubular crypts 
Columnar absorptive cells on the surface
Crypts 
- goblet 
- endocrine
- stem
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19
Q

Cell turnover of the small bowel

A

4 - 6 days

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20
Q

Cell turnover of the large bowel

A

3 - 8 days

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21
Q

What controls large bowel peristalsis?

A

Intrinsic - myenteric plexus

Extrinsic - autonomic innervation

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22
Q

What makes up the myenteric plexus? Where are these found?

A

Meisseners plexus - base of the submucosa

Auerbach plexus - between the inner circular and outer longitudinal layers of the Muscularis propria

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23
Q

What does IBD have pathological features of?

A 
UC
CD
Ischaemic colitis
Radiation colitis
Appendicitis
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24
Q

Definition of idiopathic inflammatory bowel disease

A

Chronic inflammatory conditions resulting from inappropriate and persistent activation of the mucosal immune system driven by the presence of normal intraluminal flora

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25
Q

Two main disease of IBD

A

Ulcerative colitis

Crohn’s disease

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26
Q

What does IBD stand for?

A

Inflammatory bowel disease

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27
Q

Where can crohn’s disease affect?

A

Any part of the GI tract from mouth to anus

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28
Q

Where can UC affect?

A

Colon and rectum

29
Q

Which of the IBD diseases have extra intestinal manifestations?

A

Both CD and UC

30
Q

What % of patients with IBD have 1st degree relatives with IBD?

A

15%

31
Q

What is the lifetime risk of getting IBD if a sibling is affected?

A

9%

32
Q

What gene in particular is seen in association with CD?

A

NOD2 gene

33
Q

What associations are seen in UC?

A

HLA associations

34
Q

What % of patients is Panca +ve in IBD patients?

A

75% UC

11% CD

35
Q

Which gender gets UC more?

A

M = F

36
Q

What does Panca stand for?

A

Perinuclear antineutrophilic cytoplasmic antibody

37
Q

Peak ages for UC

A

20 - 30 years

70 - 80 years

38
Q

Where does UC more commonly spread?

A

Proximally

39
Q

What can also be involved in UC?

A

Appendix

40
Q

Features of UC

A

Large bowel only
Continuous pattern of inflammation
Rectum to proximal

41
Q

Pathology of UC

A

Pseudopolyps
Ulceration
Serosal surface minimal or no inflammation

42
Q

Histology of UC

A 
Mucosa inflamed
Cryptitis
Crypt abscesses 
Architectrual disarray of crypts 
Mucosal atrophy 
Ulceration into submucosa-pseudopolyps
Limited mainly to mucosa and submucosa
NO granulomas
Submucosal fibrosis
43
Q

Risk of developing cancer if have pancolitis >10 years

A

20-30x higher risk

44
Q

Complications of UC

A

Cancer
Haemorrhage
Perforation
Toxic dilatation

45
Q

Where can CD affect?

A

Any level of GIT from mouth to anus

46
Q

Which gender gets CD more?

A

F > M

47
Q

Peak ages of crohn’s disease

A

20 - 30

60 - 70

48
Q

Where does crohns disease affect?

A

40% small intestine
30% colon
30% small and large intestine

49
Q

Pathology of CD

A

Granular serosa/dull grey
Wrapping mesenteric fat
Mesentery - thickened, oedematous and fibrotic
Wall thick and oedematous
Narrowing of lumen
Sharp demarcation of disease segments from adjacent normal tissue “skip lesions”
Ulceration - “cobblestone”

50
Q

Histology of CD

A 
Cryptitis
Crypt abscess
Architectural distortion 
Deep ulceration 
Transmural inflammation - chain of pearls
Non caseating granulomas
Fibrosis
Lymphagiectasia
Hypertrophy of mural nerves
Paneth cell metaplasia 
Islands of macrophages all grouped together 
Bowel tries to heal itself - fibrosis
51
Q

Long term features of CD

A 
Small intestine malabsorption 
Strictures
Fistulas
Abscesses 
Perforation 
Increased risk of cancer - 5x
52
Q

What can lead to infarction of the bowel? What is this called?

A 
Acute occlusion of 1 of the 3 major supply vessels leads to infarction 
- coeliac 
- inferior mesenteric
- superior mesenteric 
Ischaemic enteritis
53
Q

Why can gradual occlusion in the bowel have little effect?

A

Anastomotic circulation

54
Q

Predisposing conditions for ischaemia of the bowel

A 
Arterial thrombosis
- severe atherosclerosis
- systemic vasculitis eg. PAN, HSP
- Dissecting aneurysm 
- Hypercoagulable stress
- Oral contraceptives
Arterial embolism 
- cardiac vegetations 
- acute atheroembolism 
- cholesterol embolism 
Non occlusion 
- cardiac failure 
- shock / dehydration 
- vasoconstrictive drugs e.g. propranolol
55
Q

Histology of acute ischaemia of the bowel

A

Oedema
Interstitial haemorrhages
Sloughing necrosis of mucosa-ghost outlines
Nuclei indistinct
Initial absence of inflammation
1 - 4 days; bacteria - gangrene perforation
Vascular dilatation

56
Q

Histology of chronic ischaemia of the bowel

A 
Mucosal inflammation 
Ulceration 
Submucosal inflammation 
Fibrosis 
Stricture
57
Q

Definition of radiation colitis

A

Abdominal irradiation can impair the normal proliferate activity of the small and large bowel epithelium

58
Q

Where does radiation colitis usually effect and why?

A

Usually rectum

Pelvic radiotherapy

59
Q

What does the damage of radiation colitis depend on?

A

The dose

60
Q

Symptoms of radiation colitis

A

Anorexia
Abdominal cramps
Diarrhoea
Malabsorption

61
Q

What can chronic radiation colitis mimic?

A

IBD

62
Q

Histology of radiation colitis

A 
Bizarre cellular changes
Inflammation
- crypt abscesses and eosinophils
Later arterial stenosis
Ulceration 
Necrosis
Haemorrhage 
Perforation
63
Q

How often does the GI system turn over?

A

Once a week

64
Q

What is the appendicitis a remnant of?

A

Possible bowel remnant

65
Q

How big is the appendix?

A

Average 6 - 7cm

66
Q

What is the appendix?

A

Prominent lymphoid tissue that regresses with age

67
Q

Causes of appendicitis

A 
Obstruction e.g. feocolith (faecal stone)
Enterobius vermicularis (worms)
Infection
68
Q

Pathology of appendicitis

A

Increased intraluminal pressure

  • ischaemia
  • still proliferating so increases the pressure which leads to ischaemia as reduced blood flow
69
Q

Histology of appendicitis

A

Macro
- fibrinopurulent exudate, perforation, abscess
Micro
- acute suppurative inflammation in wall and pus in lumen
- Acute gangrenous - full thickness necrosis +/- perforation

Gastrointestinal Pathology (26 decks)

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