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Yr2 GI Joe > Inflammatory bowel disease (colon pathology) > Flashcards

Inflammatory bowel disease (colon pathology) Flashcards

1
Q

What are the sections of the large bowel and how are they peritonised?

A

Caecum (retroperitoneal)

Ascending colon (Retroperitoneal)

Transverse colon (Intraperitoneal)

Descending colon (Retroperitoneal)

Sigmoid colon (Intraperitoneal)

Rectum (retroperitoneal)

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2
Q

What 3 cell types are most present in the small bowel?

A

Goblet cells

Columnar absorptive cells

Endocrine cells

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3
Q

What types of cells are found in crypts in the small intestine?

A

Stem cells Goblet cells Endocrine cells Paneth cells

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4
Q

How long does the process of cell renewal take in the small intestine?

A

4-6 days

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5
Q

How is the basic mucosal structure of the large bowel different to the small bowel?

A

Flat with no villi Tubular crypts On the surface, there is only columnar absorptive cells In the crypts, there are goblet cells, endocrine cells and stem cells (no cells of Paneth)

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6
Q

Neuromuscular control of the small/large bowel involves both intrinsic and extrinsic control What are these control mechanisms?

A

Intrinsic control is via the myenteric plexus Extrinsic control is through autonomic innervation

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7
Q

What are the 2 parts of the myenteric plexus?

A

Meissener’s plexus - around the base of the submucosa

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

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8
Q

What is idiopathic inflammatory bowel disease?

A

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

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9
Q

What are the 2 types of idiopathic inflammatory bowel diseases?

A

Ulcerative colitis

Crohn’s

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10
Q

Crohn’s disease and Ulcerative colitis are in many ways similar, but have a couple of key differences What is the difference between where they can be located?

A

Crohn’s can affect anywhere from the mouth to anus. Ulcerative colitis is limited only to the colon

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11
Q

Is family history important in Crohn’s patients?

A

Yes 15% have affected 1st degree relatives

Lifetime risk if either a parent or sibling is affected is 9%

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12
Q

What gene mutation is associated with Crohn’s disease?

A

NOD2

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13
Q

What gene mutations are associated with Ulcerative colitis?

A

HLA genes

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14
Q

What overall is believed to cause Crohn’s and Ulcerative colitis?

A

Strong immune response against normal flora with defects in the epithelial barrier function in genetically susceptible individuals

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15
Q

What is the role of intestinal flora in development of Crohn’s and UC?

A

No specific microbe has been identified

Defects in mucosal barrier could allow microbes access to mucosal lymphoid tissue triggering immune response

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16
Q

How are Inflammatory bowel diseases diagnosed?

A

Clinical history

Radiographic examination

Pathological correlation

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17
Q

What is pANCA, and why is useful in the diagnosis in some IBDs?

A

Perinuclear antineutrophilic cytoplasmic antibody (pANCA)

positive in 75% of UC patients BUT only 11% of CD patients (so not that useful for Crohn’s)

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18
Q

Describe the epidemiology of Ulcerative colitis

A

Male = Female frequency

More common in 20-30 and in 70-80 year olds

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19
Q

What are the types (by area) of ulcerative colitis?

A

Large bowel:

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20
Q

What is backwash ileitis?

A

Inflammation in the distal ileum thought to be due to “backwash” of cecal contents

(patients with pancolitis may develop this)

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21
Q

What is the prevalence of ‘Pancolitis’?

A

10% of UC patients

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22
Q

What other small part of the alimentary canal can be involved in UC?

A

Appendix

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23
Q

When does the large bowel look like in a patient with ulceratie colitis?

A

Continous pattern of inflammation from rectum proximally

Presence of Pseudoplyps and ulcers

24
Q

What are pseudopolyps?

A

Pseudopolyps are projecting masses of scar tissue that develop from granulation tissue during the healing phase in repeated cycle of ulceration

25
Q

How does Ulcerative colitis affect the mucosal surface of an affected area?

A

Inflammation obviously

Cryptitis, Dissaray of crypts, Crypt abscesses

Mucosal atrophy

26
Q

How does Ulcerative colitis affect the submucosal layer of the affected area?

A

Ulceration into submucosa- pseudopolyps

Limited mainly to mucosa and submucosa

NO granulomas

Submucosal fibrosis

27
Q

What is the link between Ulcerative colitis and cancer?

A

Increases risk of cancer

If pancolitis > 10years then increased risk of colon cancer by 20-30x

28
Q

What complications are associated with Ulcerative colitis?

A

Cancer

Haemorrhage

Perforation

Toxic dilatation

29
Q

Describe the epidemiology of Crohn’s disease

A

Females > males

Peaks 20-30 and 60-70 years old but can manifest at any age including children (@nick diston)

Most common in caucasians especially the Jewish

30
Q

Where is Crohn’s most likely to affect?

A

40% Small intestine (especially the end of the SI)

30% SI and LI

30% Colon

31
Q

What is the difference between Crohn’s and UC in terms of the layers of the Gut tube affected?

A

In UC - Only the mucosa and sometimes the Sub mucosa are affected

In Crohn’s - All 4 layers of gut tube inflammed

32
Q

What specific type of inflammation is present in Crohn’s and not in UC?

A

Crohn’s features non-caseating Granulomas

UC does not have Granulomas

33
Q

Describe the pathological appearance of Crohn’s

A

Alternating ‘skip lesions’ with Thickened, oedematous wall and ‘cobblestone ulceration’

Affected areas may feature:

structuring

Granular serosa / dull grey

Wrapping mesenteric fat

Mesentry- thickened, oedematous and fibrotic (more fibrosis than UC)

34
Q

What are the main histological features of Crohn’s affected tissue?

A

Cryptitis & crypt abscesses

Architectural distortion

Crypt atrophy/destruction

*Non-caseating granulomas*

*Transmural inflammation* - ‘chain of pearls’

Fibrosis

Lymphangiectasia (dilation of lymph vessels)

Hypertrophy of mural nerves

Paneth cell metaplasia

35
Q

What main histological differences are specific to Crohn’s and not UC?

A

NC Granulomas

Transmural inflammation (C of P)

Lymphangiectasia

Hypertrophy of mural nerves

36
Q

What are the long term effects of crohn’s on the affected area?

A

Malabsorption of SI (if affected)

Stricture / narrowing

Fistulas, abscess formation & perforation

Increased risk of cancer

37
Q

The wall appearance in Crohn’s is ______ whereas in Ulcerative colitis it is _______

A

Crohn’s = thickened

UC = Thinner

38
Q

Ischaemic enteritis can affect what parts of the digestive tract?

A

Small or large intestine (or both)

39
Q

Ishcaemic enteritis can lead to infarction if there is acute occlusion of what arteries?

A

Coeliac

Superior mesenteric

Inferior mesenteric

(these are the 3 major supply vessels)

40
Q

Why would gradual occlusion of the supply vessels (such as the coeliac artery) be unlikely to cause ischaemia?

A

Anastomotic circulation means there are alternative routes for arterial supply

41
Q

How common is mesenteric venous occlusion compared to arterial occlusion of the gut?

A

Less common

42
Q

What layers of the gut tube would be affected in a major vessel occlusion?

A

Ischaemic enteritis through major vessel occlusion would cause transmural injury (all layers)

43
Q

What types of conditions would predispose someone to ischaemic enteritis?

A

Arterial thrombosis (atherosclerosis, hypercoagulable states, oral contraceptives etc)

Arterial embolism (atheroembolisms, vegatations etc)

Non-occlusive ischaemia (cardiac failure, shock etc)

(full list on ppt)

44
Q

How would acute ischaemia appear histologically?

A

Oedema

Interstitial haemorrhages

Sloughing necrosis of mucosa-ghost outlines

Nuclei indistinct

Initial absence of inflammation

1-4 days – bacteria-gangrene and perforation

Vascular dilatation

45
Q

What are the main patholical effects of chronic ischaemia?

A

Mucosal and Submucosal inflammation

Ulceration and Fibrosis

Strictures

46
Q

Why does radiation cause inflammation of the colon?

A

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

Dividing cells are especially at risk of damage

47
Q

What area of the digestive tract most commonly gets radiation colitis and why?

A

Rectum - due to pelvic radiotherapy

48
Q

What are the symptoms of radiation colitis?

A

Anorexia

Abdominal cramps

Diarrhoea

Malabsorption

Chronic RC has similar symptoms of IBD

49
Q

What histological changes are seen in radiation colitis?

A

Inflammation - crypt abscesses and EOSINOPHILS

Arterial stenosis (late)

Ulceration, necrosis, haemorrhage, perforation

50
Q

What is the difference between the appendix in young and old people?

A

In young people there is prominent lymphoid tissue

This regresses with age

51
Q

What causes appendicits?

A

Obstruction:

  • Pinworm (Enterobius vermicularis)
  • Feocolith (stones made of hardened faeces)
52
Q

Appendicits can cause increased intralumenal pressure

What can this lead to?

A

Local ischaemia

53
Q

What macroscopic features are present in appendicitis?

A

fibrinopurulent exudate

perforation

abscess

54
Q

What microscopic features are present in appendicits?

A

Acute suppurative inflammation in wall and pus in lumen

Acute gangrenous-full thickness necrosis +/- perforation

55
Q
A

Yr2 GI Joe (28 decks)

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