Lower GI Flashcards

1
Q
  1. List some congenital disorders of the GI tract.
A

Atresia/stenosis
Duplication
Imperforate anus
Hirschsprung disease (MOST COMMON)

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2
Q
  1. What is Hirschsprung disease?
A

Caused by the absence of ganglion cells of the myenteric plexus results in failure of dilatation of the distal colon
Presents with constipation, abdominal distension, vomiting and overflow diarrhoea

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3
Q
  1. List some genetic associations of Hirschsprung disease.
A

Down syndrome

RET proto-oncogene Cr10

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4
Q
  1. How is Hirschsprung disease diagnosed?
A

Clinical impression
Full thickness rectal biopsy
Shows hypertrophied nerve fibres but no ganglia

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5
Q
  1. How is Hirschsprung disease treated?
A

Resection of affected (constricted) segment

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6
Q
  1. What is a volvulus?
A

twisting of a loop of bowel at the mesenteric base around a vascular pedicle

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7
Q
  1. Which part of the intestines tend to be affected by volvulus in children and the eldery?
A

Children – small bowel

Elderly – sigmoid colon

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8
Q
  1. Describe the pathophysiology of diverticular disease.
A

High intraluminal pressure (e.g. due to poor diet) leads to herniation of the bowel mucosa through weak points in the bowel wall (usually sites of entry of nutrient vessels)

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9
Q
  1. List some causes of acute colitis.
A

Infection
Drugs/toxins
Chemotherapy
Radiotherapy

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10
Q
  1. List the effects of infection on the colon.
A

Secretory diarrhoea (due to toxin)
Exudative diarrhoea (due to invasion and mucosal damage)
Severe tissue damage and perforation
Systemic illness

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11
Q
  1. What can cause pseudomembranous colitis?
A

Exotoxins by C. difficile

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12
Q
  1. How can C. difficile colitis be diagnosed?
A

Toxin stool assay

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13
Q
  1. How is pseudomembranous colitis treated?
A

Metronidazole or vancomycin

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14
Q
  1. Where in the intestines does ischaemic colitis tend to occur?
A

Watershed zones (e.g. splenic flexure, rectosigmoid)

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15
Q
  1. List some causes of ischaemic colitis.
A

Arterial occlusion (e.g. embolism)
Venous occlusion (e.g. thrombus)
Small vessel disease (e.g. diabetes mellitus)
Low flow states (e.g. CCF)
Obstruction (e.g. hernia, intussusception)

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16
Q
  1. List some characteristic features of Crohn’s disease.
A
Can occur anywhere from mouth to anus 
Skip lesions 
Transmural inflammation 
Non-caseating granulomas 
Sinus/fistula formation 
Mostly affects large bowel and terminal ileum 
Thick rubber hose-like wall 
Cobblestone mucosa 
Narrow lumen
17
Q
  1. List some extra-intestinal features of inflammatory bowel disease.
A

Arthritis
Uveitis
Stomatitis/cheilitis
Skin lesions (pyoderma gangrenosum, erythema multiforme, erythema nodosum)

18
Q
  1. List some characteristic features of ulcerative colitis.
A

Involves rectum and colon in a continuous fashion
May see backwash ileitis (involvement of the terminal ileum)
Inflammation is confined to the mucosa
Bowel wall is normal thickness

19
Q
  1. List some complications of ulcerative colitis.
A

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

20
Q
  1. Which liver condition is associated with UC?
A

Primary sclerosing cholangitis

21
Q
  1. List some types of neoplastic epithelial lesions that occur in the GI tract.
A

Adenoma
Adenocarcinoma
Carcinoid tumour

22
Q
  1. List some types of stromal lesions that occur in the GI tract.
A

Stromal tumours
Lipoma
Sarcoma
Other: lymphoma

23
Q
  1. List three types of non-neoplastic polyp.
A

Hyperplastic
Inflammatory (pseudopolyp)
Haemartomatous (juvenile, Peutz-Jeghers)

24
Q
  1. List three types of neoplastic polyp.
A

Tubular adenoma
Tubulovillous adenoma
Villous adenoma

25
Q
  1. What is an adenoma?
A

Excess epithelial proliferation with dysplasia

26
Q
  1. List some features of an adenoma that are associated with increased risk of becoming a carcinoma.
A

Size of polyp (> 4 cm = 45%)
Proportion of villous component
Degree of dysplastic change within a polyp

27
Q
  1. List some observations that have given rise to the adenoma-carcinoma sequence theory.
A

Areas with a high prevalence of adenomas have a high prevalence of carcinoma
Adenomas tend to appear 10 years before a carcinoma
Risk of cancer is proportional to the number of adenomas

28
Q
  1. List some familial syndromes that are characterised by intestinal polyps.
A

Peutz-Jegher’s syndrome
FAP (Gardner’s, Turcot)
HNPCC

29
Q
  1. Which gene is mutated in FAP?
A

APC gene – chromosome 5q21

30
Q
  1. What is Gardner’s syndrome?
A

Same features of FAP but with extra-intestinal manifestations: multiple osteomas of the skull and mandible, epidermoid cysts, desmoid tumours and supernumerary teeth

31
Q
  1. Where do carcinomas in HNPCC tend to occur?
A

Proximal to the splenic flexure

NOTE: poorly differentiated and mucinous cancers are more common. Polyps do not necessarily precede the cancer

32
Q
  1. Outline Dukes’ staging of colorectal cancer.
A

A – confined to bowel wall
B – through the bowel wall
C – lymph node metastases
D – distant metastases