Lower GI

Question 1

What are some of the congenital dosorders of the lower GI tract?

Answer 1

1. Failure of development of lumen: atresia (=no connection/ no communication of 2 parts of bowel) /stenosis
2. Duplication

Question 2

What site does Hirschsprung’s diasese originate from?

What is the patholgoy?

Answer 2

Starts in the rectum which fails to dilate + spreds more proximally (during surgery: resection with frozen sections)

Absence of ganglion cells in the submucosal and myenteric plexuses (picture pointing to ganglions, would be abscent in hhirschsprung’s)

Question 3

What is the main site of volvuli in children and adults?

Answer 3

Volvulus = Complete twisting of a loop of bowel at mesenteric base around vascular pedicle

Small bowel (infants)
Sigmoid colon (elderly)

Question 4

What are the main causes of acute colitis?

Answer 4

• Infection
• Drug/toxin (especially antibiotic)
• Chemotherapy
• Radiation

Question 5

What are the main causes of chronic colitis?

Answer 5

Crohn’s
Ulcerative colitis
TB

Question 6

What are the main pathogens causing infectious colitis?
(go over mmost common)

Answer 6

• Viral e.g. CMV (partiuclarl in immunsoupressed / with IBD), Norovirus, Adenovirus
• Bacterial - most common)e. g. Salmonella, Campylobacter, C-diff
• Protozoal e.g. Entamoeba hystolytica
• Fungal e.g. candida

Question 7

What is pseudomembranous colitis?

How is it diagnosed?

Answer 7

Antibiotic associated colitis
–> then caues acute colitis with pseudomembrane formation (pseudomembrane = infalmmatory protein exotoxins formed by C-diff )

Caused by protein exotoxins of Clostridiumdifficile –> detection ofC-diff toxin makes diagnosis

Question 8

What is the usual inflammation seen in patients with Ischaemic colitits?

Answer 8

Depending on the degree of ischaemia,can be:
Mucosal, mural, transmural (perforation)

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

Question 9

What are the pathological/histological feature of Crohn’s disease?

Answer 9

• Whole of GI tract can be affected (mouth to anus)
• ‘Skip lesions’
• Cobble.stone appearance (because normal parts of mucosa shine through)
• Transmural inflammation –>
• Fissure/ sinus/fistula formation
• Non-caseating granulomas

Question 10

What are some of the common extra-intestinal manifestations of Crohn’s disease?

Answer 10

Arthritis
Uveitis
Stomatitis/cheilitis

Skin lesions

• Pyoderma gangrenosum
• Erythema multiforme
• Erythema nodosum

Question 11

What are the pathological/histological feature of UC?

Answer 11

• Involves rectum and colon in continuous fashion
• May see mild ‘backwash ileitis’ and appendiceal involvement but small bowel and proximal GI tract not affected.
• Inflammation confined to mucosa
• Bowel wall normal thickness
• Shallow ulcers

Question 12

What are the mmain complications of UC?

Answer 12

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

Question 13

What are some of the extra-intesinal features of UC?

Answer 13

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

Question 14

What are the 2 different types of polyps that occur in the bowel?

Answer 14

1.non-neoplastic
–> hyperplastic and Sessile Serrated Lesions (SSL risk factor for adenomas as they may show dysplasia)
–> Inflammatory and Hamaromaous (e.g. Peutz Jeghers)

2. Neoplastic
–> Tubular adenoma
–> tubulovillous adenoma
–> villous adenoma

Question 15

What is a Sessile Serrated Lesion in the lower GI tract?

Answer 15

Non-neoplastic polyp that shows

• Hyperplastic polyp with architectural abnormalities
• May show dysplasia (borderline neoplastic)

Question 16

What is the definition and epidemiology of lower GI adenomas?

Answer 16

Excess epithelial proliferation + dysplasia

20-30% prevalence before age 40
40-50% prev. after age 60

Question 17

What are the different types of Neoplastic polyps (Adenoma) in the lower GI tract?

Answer 17

-> Tubular adenoma
–> tubulovillous adenoma
–> villous adenoma

Question 18

What are the histological characteistics of a tubular adeonoma?

Answer 18

Flat surface
Glands

Question 19

What are the characteristics of a villous adenoma?

Answer 19

Villous surface –> irregular surface

Question 20

What are the characteristics of tubulo-villous adenoma?

Answer 20

some mixed components

Question 21

What characteristics in a single adenoma incrase the risk that it might be a carcinoma/ progress?

Answer 21

Size (>1cm)
Proportion of villous component (high)
Degree of dysplasia (high)

Question 22

Explain the adenoma carcinoma sequence in the development of colon cancer

Answer 22

multiple factors/ evidence that it is likely that carcinomas derive from adenomas

Question 23

Name some familial syndromes that pre-dispose to development of colon cancer?

Answer 23

• Hereditary non polyposis colon cancer –> mutation in DNA repair)

Familial adenomatous polyposis
* Gardner’s
* Turcot

Question 24

What are the characteristics of FAP?

(Epidemiology, genetic mutation, prognosis )

Answer 24

Autosomal dominant - average onset is 25 years old
Mutation in APC tumour suppressor gene (on chromosme 5q21)

Causing: Adenomatous polyps, mostly colorectal

• Minimum 100 polyps, average ~1,000 polyps
• virtually 100% will develop cancer within 10 to 15 years –> prophylactic excision of colon
• 5% periampullary Ca

Question 25

What is Gardner's syndorme and Turcot syndrome?

Answer 25

FAP + extra-intestinal symptoms Gardner: osteomas desmoid tumors Turcot: Brain

Question 26

What is Lynch syndrome? What is the pathophysiology + inheritence pattern?

Answer 26

Lynch syndrome = Hereditary Non-polyposis Colorectal Cancer (HNPCC) * Autosomal dominant mutation in t least 1 of 4 DNA mismatch repair genes involved --> not in itself oncogenic, but become cancerous because oncogenic umutations don't get repaired * May have polyps --> usually develop colorectal cancer at early age (in splenic flexure) * Other extra-colonic cancers: endometrium, prostate, breast, stomach * 3-5% of all colorectal cancers due to * Numerous DNA replication errors

Question 27

What is the most common colon cancer? What is the epidemiology + risk factors

Answer 27

98% colorectral carcinoma Peak incidence : 60-79 years If < 50yrs consider familial syndrome Western population Generic risk factors * IBD * adenoma * low fibre-diet, lack of exercise

Question 28

What is the new staging system of colorectal carcinoma

Answer 28

Now only normla TNM stageing used