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Systems: Alimentary AB > Pathology of Colon > Flashcards

Pathology of Colon Flashcards

1
Q

What type of role does the small bowel play?

A

Absorptive

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2
Q

What 2 types of role does the large bowel play?

A
  • Absorptive

- Secretory

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3
Q

What are the 3 sections of the small intestine?

A
  • Duodenum
  • Jejunum
  • Ileum
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4
Q

What are the different sections of the large intestine?

A
  • Caecum
  • Ascending colon
  • Transverse colon
  • Descending colon
  • Sigmoid colon (originates pelvic brim)
  • Rectum
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5
Q

What is the mucosa of the small intestine made up of?

A

Innumerable villi

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6
Q

What are the 3 types of cells in the small intestine?

A
  • Goblet cells
  • Columnar absorptive cells
  • Endocrine cells
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7
Q

How often are the cells in the small intestine renewed ?

A

4-6 days

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8
Q

What cells are found in the crypts of the large bowel?

A
  • Goblet cells
  • Endocrine cells
  • Stem cells
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9
Q

What are the surface cells of the large bowel?

A

Columnar absorptive cells

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10
Q

Describe the structure of the large bowel,

A
  • Flat: no villi

- Tubular crypts

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11
Q

What must the immune system balance in response to the large surface area of the GIT?

A

-Tolerance of harmless ingested substances against active defence reactions to potential microbial invaders

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12
Q

What does dysfunction of the intestinal immune system cause?

A
  • Chronic disease

- Life threatening acute conditions

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13
Q

What is small and large bowel peristalsis mediated by?

A

Intrinsic (myenteric plexus) and extrinsic (autonomic innervation) neural control

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14
Q

What is the myenteric plexus formed of?

A
  • Meissener’s plexus

- Auerbach plexus

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15
Q

Where is the Meissener’s plexus found?

A

Base of the submucosa

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16
Q

Where is the Auerbach plexus found?

A

Between the inner circular and outer longitudinal layers of the muscularis propria

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17
Q

Inflammatory bowel disease has pathological features of…

A
  • Ulcerative colitis
  • Crohn’s disease
  • Ischaemic colitis
  • Radiation colitis
  • Appendicitis
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18
Q

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 flora

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19
Q

What are the 2 main disease in idiopathic IBD?

A
  • Crohn’s disease

- Ulcerative colitis

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20
Q

Where can Crohn’s disease affect?

A

Any part of the GIT from the mouth to the anus

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21
Q

Where is ulcerative colitis limited to?

A

Colon

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22
Q

What role does genetics play in CD and UC?

A
  • 15% have affected 1st degree relatives
  • NOD2 gene mutation associated with CD
  • HLA associations with UC
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23
Q

What is the pathological cause of UC and CD?

A
  • Strong (exaggerated) immune response against normal flora with defects in the epithelial barrier function in genetically susceptible individuals
  • Defects in mucosal barrier could allow microbes access to mucosal lymphoid tissue triggering immune response
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24
Q

What is required for a diagnosis of IBD?

A
  • Clinical history
  • Radiographic examination
  • Pathological correlation
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25
Q

pANCA

A

Perinuclear antineutrophilic cytoplasmic antibody

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26
Q

What is the prevalence of UC?

A

-M=F

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27
Q

When does UC peak?

A
  • 20-30 years

- 70-80 years

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28
Q

What is the more common spread of UC?

A

Proximal

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29
Q

What other structure can also be involved in UC?

A

Appendix

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30
Q

What can occur with pancolitis?

A

Backwash ileitis

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31
Q

What is UC also associated with outside the colon?

A

Systemic manifestations

32
Q

What is the pathology of UC?

A
  • Large bowel only
  • Continues pattern of inflammation
  • Rectum to proximal
  • Pseudo polyps
  • Ulceration
  • Serosal surface minimal or no inflammation
33
Q

What is the histology of UC?

A
  • Mucosa shows inflammation
  • Cryptitis
  • Cryps abscesses
  • Architectural disarray of crypts
  • Mucosal atrophy
  • Ulceration into submucosa: pseudo polyps
  • Limited mainly to mucosa and submucosa
  • NO GRANULOMAS
  • Sub mucosal fibrosis
34
Q

How can dysplasia be graded?

A

High or low grade

35
Q

How does flat epithelial atypia become an invasive cancer?

A

Undergoes an adenomatous change

36
Q

Other than cancer what other complications are associated with UC?

A
  • Haemorrhage
  • Perforation
  • Toxic dilatation
37
Q

What is the prevalence of CD?

A

-F>M

38
Q

When do the peaks in CD occur?

A
  • 20-30 years

- 60-70 years

39
Q

What is the pathology of CD?

A
  • Granular serosa/ dull grey
  • Wrapping mesenteric fat
  • Mesentery thickened, oedematous and fibrotic
  • Wall thick, oedematous
  • Narrowing of lumen
  • Sharp demarcation of disease segments from adjacent normal tissue (skip lesions)
  • Ulcerations is like cobbles
40
Q

What is the histology of CD?

A
  • Cryptitis and crypt abscesses
  • Architectural distortion
  • Atrophy and crypt destruction
  • Deep ulceration
  • Transmural inflammation (chain of pearls)
  • NON-CASEATING GRANULOMAS
  • Fibrosis
  • Lymphangiectasia
  • Hypertrophy of mural nerves
  • Paneth cell metaplasia
41
Q

What are long term features of CD?

A
  • Small intestine malabsorption
  • Strictures
  • Fistulas and abscesses
  • Perforation
  • Increased risk of cancer
42
Q

Where can ischaemic lesions be restricted to?

A
  • Small intestine
  • Large intestine
  • Both
43
Q

Acute occlusion of which vessels can lead to infarction?

A
  • Celiac artery
  • Inferior mesenteric artery
  • Superior mesenteric artery
44
Q

Why may gradual occlusion of major supply vessels have little effect?

A

Anastomotic circulation

45
Q

What does occlusion od small end arteries lead to?

A

Lesions which are small and focal

46
Q

What conditions predispose for ischaemia?

A
  • Arterial thrombosis
  • Arterial embolism
  • Non-occlusive ischaemia
47
Q

What can cause arterial thrombosis ?

A
  • Severe atherosclerosis
  • Systemic vasculitis
  • Dissecting aneurysm
  • Hypercoaguable states
  • Oral contraceptives
48
Q

What can cause arterial embolisms?

A
  • Cardiac vegetations
  • Acute atheroembolism
  • Cholesterol ischaemia
49
Q

What can cause non-occlusive ischaemia?

A
  • Cardiac failure
  • Shock/dehydration
  • Vaso-constrictive drugs
50
Q

What is vulnerable to acute ischaemia?

A

Splenic flexure

51
Q

How does early intense congestion appear?

A
  • Dusky/purple/blue

- Lumen: sanguinous mucin

52
Q

What does arterial acute ischaemia look like?

A

There is sharp demarcation

53
Q

What does venous acute ischaemia look like?

A

Venous fade gradual

54
Q

What is the histology of acute ischaemia?

A
  • Oedema
  • Intestinal haemorrhages
  • Sloughing necrosis of mucosa-ghost outlines
  • Nuclei indistinct
  • Initial absence of inflammation
  • 1-4 days- bacteria- gangrene and perforation
  • Vascular dilatation
55
Q

What are the characteristics of chronic ischaemia?

A
  • Mucosal inflammation
  • Ulceration
  • Sub mucosal inflammation
  • Fibrosis
  • Stricture
56
Q

How does radiation colitis occur?

A
  • Abdominal irradiation can impair the normal proliferative activity of the small and large bowel epithelium
  • Usually rectum-pelvic radiotherapy
57
Q

What does the damage by radiation depend on?

A

Dose

58
Q

What does radiation target?

A

Actively dividing cells especially blood vessels and crypt epithelium

59
Q

What are the symptoms of radiation colitis?

A
  • Anorexia
  • Abdominal cramps
  • Diarrhoea
  • Malabsorption
60
Q

What does radiation colitis mimic?

A

IBD

61
Q

What is the histology of radiation colitis?

A
  • Bizarre cellular changes
  • Inflammation: crypt abscesses and eosinophils
  • Later arterial stenosis
  • Ulceration
  • Necrosis
  • Haemorrhage
  • Perforation
62
Q

What is the appendix essentially?

A
  • Bowel remnant which is a prominent lymphoid tissue that regresses with age
  • Undergoes fibrous obliteration
63
Q

How big is the appendix?

A

Approx 6-7cm

64
Q

Appendicitis

A

Acute inflammation of the appendix

65
Q

What causes appendicitis?

A

Obstruction eg. feocolith or enterobius vermicularis

66
Q

What does the increased intraluminal pressure associated with appendicitis lead to?

A

Ischaemia

67
Q

What is the histology of appendicitis?

A
  • Fibrinopurulent exudate
  • Perforation
  • Abscess
  • Acute suppurative inflammation in wall and pus in lumen
  • Acute gangrenous full thickness necrosis +/- perforation
68
Q

What is low grade dysplasia reasonably like?

A

Normal

69
Q

What is high grade dysplasia reasonably like?

A

Cancer

70
Q

What are the 3 different formations of adenomas (polyps) ?

A
  • Tubular
  • Villous
  • Tubulovillous
71
Q

Describe the histology of low grade dysplasia.

A
  • Increased nuclear no
  • Increased nuclear size
  • Reduced mucin
72
Q

Describe the histology of high grade dysplasia.

A
  • Carcinoma in situ
  • Crowded
  • Very irregular
  • Not yet invasive
73
Q

What are the risk factors for colorectal carcinomas such as adenocarcinomas?

A
  • Lifestyle
  • Family history
  • IBD
  • Genetics
74
Q

What genes can predispose you to CRC?

A
  • FAP
  • HNPCC
  • Peutz-Jeghers
75
Q

Describe right sided colorectal adenocarcinoma.

A
  • Exophytic/polypoid
  • Anaemia (altered blood PR)
  • Vague pain
  • Weakness
  • obstruction
76
Q

Describe left sided colorectal adenocarcinoma.

A
  • Annular (napkin ring lesion)
  • Bleeding (fresh/altered blood PR)
  • Altered bowel habit
  • Obstruction
77
Q

What determines the prognosis of CRC?

A
  • Tumour grade
  • TNM staging
  • Extramural venous invasion
  • Can it be resected?

Systems: Alimentary AB (37 decks)

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