Histo: Lower GI Disease Flashcards

1
Q

List some congenital disorders of the GI tract.

A
  • Atresia/stenosis (e.g. duodenal atresia)
  • Duplication
  • Imperforate anus
  • Hirschsprung disease (MOST COMMON)
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2
Q

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

Epidemiology of hirschsprung disease

A

80% of cases occur in male babies

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4
Q

List some genetic associations of Hirschsprung disease.

A
  • Down syndrome
  • RET proto-oncogene Cr10
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5
Q

How is Hirschsprung disease diagnosed?

A
  • Clinical impression
  • Full thickness rectal biopsy
  • Shows hypertrophied nerve fibres but NO ganglia
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6
Q

How is Hirschsprung disease treated?

A

Resection of affected (constricted) segment

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7
Q

Types of GI Mechanical Disorders

A
  • Obstruction
    o Adhesions
    o Herniation
    o Extrinsic mass
    o Volvulus
  • Diverticular disease
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8
Q

What is a volvulus?

A

Complete Twisting of a loop of bowel at the mesenteric base around a vascular pedicle

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9
Q

What can Volvulus lead to?

A

intestinal obstruction and infarction

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10
Q

Which part of the intestines tend to be affected by volvulus in children and the elderly?

A

Children - small bowel

Elderly - sigmoid colon

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11
Q

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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12
Q

What is diverticulular disease associated with?

A
  • High incidence in the WEST
  • Associated with a low fibre diet
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13
Q

90% of diverticular disease occur on what side of the colon?

A

left side of the colon

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14
Q

List some causes of acute colitis.

A

*Infection (bacterial, viral, protozoal, fungal)
*Drug/toxin (especially antibiotics)
*Chemotherapy
*Radiotherapy

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15
Q

List some causes of chronic gastritis?

A

*Chronic Colitis
*Crohn’s disease *Ulcerative colitis
*TB

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16
Q

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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17
Q

What can cause pseudomembranous colitis?

A

*Antibiotic-associated colitis
*Acute colitis with pseudomembrane formation
*Caused by protein exotoxins of C. difficile

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18
Q

What is the Characteristic microscopic appearance of pseudomembranous colitis on biopsy?

A

Looks a bit like volcanoes exploding onto the surface

The bits on the surface are the necrotic pseudomembranous regions full of pus and inflammatory cells

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19
Q

How can C. difficile colitis be diagnosed?

A

Toxin stool assay

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20
Q

How is pseudomembranous colitis treated?

A

Metronidazole or vancomycin

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21
Q

Where in the intestines does ischaemic colitis tend to occur?

A

Occurs in segments In Watershed zones (e.g. splenic flexure, rectosigmoid)

22
Q

Types of ischaemic colitis /infarction

A

Acute or chronic

23
Q

Most common vascular disorder of the GI tract

A

Ischaemic colitis/infarction

24
Q

Where can ischaemic colitis extend?

A

Extend can be mucosal, mural or transmural (leading to perforation)

25
Q

List some causes of ischaemic colitis.

A

o Arterial occlusion: atheroma, thrombosis, embolism
o Venous occlusion: thrombus, hypercoagulable states
o Small vessel disease: diabetes mellitus, cholesterol, vasculitis
o Low flow states: CCF, haemorrhage, shock
o Obstruction: hernia, intussusception, volvulus, adhesions

26
Q

What is the aetiology of Idiopathic Chronic Inflammatory Bowel Disease

A
  • Aetiology
    o Uncertain
    o Potential genetic predisposition
    o Possibly infectious contribution (e.g. Mycobacteria, Measles)
    o Possibly due to abnormal immunoreactivity
27
Q

Clinical features of Idiopathic Chronic Inflammatory Bowel Disease

A

o Diarrhoea with or without blood
o Fever
o Abdominal pain
o Acute abdomen
o Anaemia
o Weight loss
o Extra-intestinal manifestations

28
Q

Crohns epidemiology

A

o More common in Western populations
o Peak onset in early 20s
o More common in White people

29
Q

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
  • fat wrapping of the bowel
  • Thick rubber hose-like wall
  • Cobbelstone mucosa
  • Narrow lumen
  • linear ulcers
    *fissures
    *abcesses
30
Q

List some extra-intestinal features of inflammatory bowel disease.

A
  • Arthritis
  • Uveitis
  • Stomatitis/cheilitis
  • Skin lesions (pyoderma gangrenosum, erythema multiforme, erythema nodosum)
31
Q

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)
  • o May see appendiceal involvement
    o Small bowel and proximal GI tract is not affected
  • Inflammation is confined to the mucosa
  • Bowel wall is normal thickness
    o Shallow ulcers
32
Q

List some complications of ulcerative colitis.

A
  • Severe haemorrhage
  • Toxic megacolon
  • Adenocarcinoma (20-30x increased risk)
33
Q

Extra-intestinal Manifestations of ulcerative colitis?

A
  • Arthritis
  • Myositis
  • Uveitis/iritis
  • Erythema nodosum, pyoderma gangrenosum
  • Primary sclerosing cholangitis
34
Q

Which liver condition is associated with UC?

A

Primary sclerosing cholangitis

35
Q

List some types of neoplastic epithelial lesions that occur in the GI tract.

A
  • Adenoma
  • Adenocarcinoma
  • Carcinoid tumour
36
Q

List some types of stromal lesions that occur in the GI tract.

A
  • Stromal tumours
  • Lipoma
  • Sarcoma
  • Other: lymphoma
37
Q

List three types of non-neoplastic polyp.

A
  • Hyperplastic
  • Inflammatory (pseudopolyp)
  • Haemartomatous (juvenile, Peutz-Jeghers)
38
Q

List three types of neoplastic polyp.

A
  • Tubular adenoma
  • Tubulovillous adenoma
  • Villous adenoma
39
Q

What is an adenoma?

A
  • Excess epithelial proliferation with dysplasia
  • NOTE: there are three types - tubular, tubulovillous and villous
40
Q

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

A
  • Size of polyp (>4cm = 45%)
  • Proportion of villous component
  • Degree of dysplastic change within a polyp
41
Q

List some observations that have given rise to 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
42
Q

List some familial syndromes that are characterised by intestinal polyps.

A
  • Peutz-Jegher’s dynrome
  • FAP (Gardner’s, Turcot)
  • HNPCC
43
Q

What is the inheritance pattern of FAP?

A

Autosomal dominant

44
Q

Which gene is mutated in FAP?

A

APC gene - chromosome 5q21

NOTE: almost 100% will develop cancer in 10-15 years

45
Q

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

46
Q

What is the inheritance pattern of HNPCC?

A

Autosomal dominant

47
Q

Which gene mutation is associated with HNPCC?

A

1 of 4 DNA mismatch repair genes is mutated

48
Q

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.

49
Q

Outline Dukes’ staging of colorectal cancer.

A

A - confined to bowel wall

B - through the bowel wall

C - lymph node metastases

D - distant metastases

50
Q

General effects of pathology in the large bowel

A

• Disturbance of normal function (diarrhoea, constipation)
• Bleeding
• Perforation/fistula formation
• Obstruction
• Systemic illness

51
Q

Epidemiology of Ulcerative colitis

A

o Slightly more common than Crohn’s disease
o Peak age 20-25 years
o More common in White people