Lower GI

Question 1

What is the pathophysiology of Hirschsprung’s disease?

Answer 1

Absence of ganglion cells in the myenteric plexus

Question 2

What condition is Hirschsprung’s disease associated with?

Answer 2

Down’s syndrome

Question 3

What would Hirschsprung’s disease appear as on barium imaging?

Answer 3

Dilated bowel then narrowed bowel where lacking ganglion cells and therefore not working

Question 4

What would you see on biopsy of bowel affected by Hirschsprung’s disease?

Answer 4

Hypertrophied nerve fibres but NO ganglia

Question 5

Treatment of Hirschsprung’s disease

Answer 5

Resect affected segment

Question 6

Where is volvulus most common in infants vs the elderly?

Answer 6

Small bowel (infants)
Sigmoid colon (elderly)

Question 7

What causes secretory diarrhoea?

Answer 7

Toxins (from infection)

Question 8

What causes exudative diarrhoea?

Answer 8

Invasion and mucosal damage (from infection)

Question 9

What causes pseudomembranous colitis?

Answer 9

Acute colitis with pseudomembrane formation

Caused by protein exotoxins of C.difficile after abx treatment

Question 10

What does pseudomembranous colitis look like on histology?

Answer 10

On sample: erythematous large bowl, pseudomembranes look like wet cornflakes (apparently)

On slide: looks like volcanic eruption of pus

Question 11

Management of pseudomembranous colitis

Answer 11

Vancomycin or metronidazole

Question 12

Where does ischaemic colitis/infarction typically occur in the bowel?

Answer 12

Usually occurs in segments in “watershed” zones, e.g. splenic flexure (SMA and IMA) and the rectosigmoid (IMA and internal iliac artery)

Question 13

Causes of bowel infarction (5 categories)

Answer 13

Arterial Occlusion: atheroma, thrombosis, embolism

Venous Occlusion: thrombus, hypercoagulable states

Small Vessel Disease: DM, cholesterol emboli, vasculitis

Low Flow States: CCF, haemorrhage, shock

Obstruction: hernia, intussusception, volvulus, adhesions

Question 14

Histological features of Crohn’s disease (intestinal)

Answer 14

• ‘Skip lesions’
• Transmural inflammation
• Non-caseating granulomas (slide pic with arrow)
• Sinus/fistula formation
• ‘Fat wrapping’
• Thick ‘rubber-hose’ like wall
• Narrow lumen
• ‘cobblestone mucosa’
• Linear ulcers
• Fissures
• Abscesses

Question 15

Histological features of Crohn’s disease (extra-intestinal)

Answer 15

Arthritis
Uveitis
Stomatitis/cheilitis
Skin lesions
•	Pyoderma gangrenosum
•	Erythema multiforme
•	Erythema nodosum

Question 16

Describe skip lesions (Crohn’s)

Answer 16

May have areas of healthy bowel in between lesions- pathology is not continuous along whole length of bowel

Question 17

What parts of the GI tract can be affected by Crohn’s?

Answer 17

ALL (mouth to anus)

Question 18

Is the pathology in UC continuous or interrupted?

Answer 18

Continuous

Question 19

Is the pathology in Crohn’s continuous or interrupted?

Answer 19

Interrupted

Question 20

Histological features of UC

Answer 20

May see mild ‘backwash ileitis’ and appendiceal involvement but small bowel and proximal GI tract not affected

Inflammation confined to mucosa (and submucosa) UNLIKE CROHN’S

Bowel wall normal thickness

Shallow ulcers

Crypt abscesses

Question 21

Extra-intestinal features of UC

Answer 21

• Arthritis
• Myositis
• Uveitis/iritis
• Erythema nodosum, pyoderma gangrenosum
• Primary Sclerosing Cholangitis (5.5% in pancolitis)

Question 22

Complications of UC

Answer 22

• Severe haemorrhage
• Toxic megacolon
• Adenocarcinoma (20-30 x risk)

Question 23

Types of lower GI tumours

Answer 23

Non-neoplastic polyps

Neoplastic epithelial lesions
– Adenoma
– Adenocarcinoma
– Carcinoid tumour

Mesenchymal lesions
– Stromal tumours
– Lipoma
– Sarcoma

Lymphoma

Question 24

Types of lower GI polyps

Answer 24

Polyps - Non-neoplastic
– (Hyperplastic)
– Inflammatory (“pseudo-polyps”)
– Hamartomatous (juvenile, Peutz Jeghers)

Polyps - Neoplastic
– Tubular adenoma
– Tubulovillous adenoma
– Villous adenoma

Question 25

Do hyperplastic polyps lead to cancer?

Answer 25

NO

Question 26

What do hyperplastic polyps look like on histology?

Answer 26

Wiggly outline

Question 27

What are the risk factors for a polyp becoming cancerous?

Answer 27

– Size of polyp (> 4 cm approx 45% have invasive malignancy)
– Proportion of villous component
– Degree of dysplastic change within polyp

Question 28

Which cancer are adenomas a precursor to?

Answer 28

Carcinoma

Question 29

Name the staging system for bowel cancer

Answer 29

Duke’s staging

Question 30

Most common type of bowel cancer

Answer 30

Adenocarcinoma (98%)

Question 31

At what age should a familial syndrome be considered in a patient with bowel cancer?

Answer 31

<50yrs

Question 32

Name 4 familial syndromes of bowel cancer

Answer 32

(Peutz Jeghers)

Familial adenomatous polyposis
– Gardner’s
– Turcot

Hereditary non polyposis colon cancer

Question 33

Mode of inheritance of FAP

Answer 33

Autosomal dominant

Question 34

Age of onset of FAP

Answer 34

25 yrs

Question 35

Minimum and average number of polyps in FAP

Answer 35

Minimum 100 polyps, average ~1,000 polyps

Question 36

Chromosome and gene implicated in FAP

Answer 36

Chromosome 5q21, APC tumour suppressor gene

Question 37

What distinguishes Gardner’s syndrome from FAP?

Answer 37

Same clinical, pathological, and etiologic features as FAP, with high Ca risk

Distinctive extra-intestinal manifestations:
– multiple osteomas of skull & mandible
– epidermoid cysts
– desmoid tumors
– dental caries, unerrupted supernumery teeth
– post-surgical mesenteric fibromatoses

Question 38

Mode of inheritance of HNPCC

Answer 38

Autosomal dominant

Question 39

Distinctive features of HNPCC

Answer 39

High frequency of carcinomas proximal to splenic flexure

Poorly differentiated and mucinous carcinoma more frequent

Multiple synchronous cancers

Presence of extracolonic cancers (endometrium, prostate, breast, stomach)