HISTO: Lower GI Disease Flashcards

1
Q

What are the general effects of pathology of the large bowel?

A
  • Disturbance of normal function (diarrhoea, constipation)
  • Bleeding
  • Perforation/fistula formation
  • Obstruction
  • Systemic illness
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2
Q

Name 4 congenital disorders of the large bowel. What is the most common?

A
  1. · Atresia/stenosis (e.g. duodenal atresia)
  2. · Duplication
  3. · Imperforate anus
  4. · Hirschsprung’s Disease (MOST COMMON CONGENITAL ABNORMALITY)
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3
Q

What is the cause of Hirschsprung’s disease? Who is most affected? What other conditions/genetics is it associated with?

A
  • Caused by absence of ganglion cells of the myenteric plexus –> distal colon fails to dilate
  • 80% of cases occur in male babies
  • Associated with Down syndrome
  • Associated genetic abnormality: RET proto-oncogene Cr10
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4
Q

How does Hirschsprung’s disease present? How is it diagnosed and treated?

A

Presentation: constipation, abdominal distension, vomiting, overflow diarrhoea

Diagnosis

  • Clinical impression
  • Full thickness biopsy of affected segment
  • Hypertrophied nerve fibres but NO ganglia

Treatment

  • Resection of affected (constricted) segment
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5
Q

What are the types of mechanical disorders of the large bowel?

A
  1. Obstruction
  • · Adhesions
  • · Herniation
  • · Extrinsic mass
  • · Volvulus
  1. Diverticular disease
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6
Q

What is volvulus and which part of the bowel is affected in different age groups?

A
  • Complete twisting of a loop of bowel at the mesenteric base, around a vascular pedicle –> can lead to intestinal obstruction and infarction
  • Affects the small bowel in CHILDREN
  • Affects the sigmoid colon in the ELDERLY
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7
Q

What is the pathophysiology and complications of diverticular disease? Which side of the colon is most affected?

A

High intraluminal pressure leads to herniation of the bowel mucosa through weak points in the bowel wall (usually at points of entry of nutrient vessels)

90% occur in the left side of the colon

Complications

  • Pain
  • Diverticulitis
  • Perforation
  • Fistula (bowel, bladder, vagina)
  • Obstruction
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8
Q

What are the risk factors for diverticular disease?

A

High incidence in the WEST

Associated with a low fibre diet

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9
Q

What are the causes of acute colitis?

A

Acute Colitis

  • Infection (bacterial, viral, protozoal, fungal)
  • Drug/toxin (especially antibiotics)
  • Chemotherapy
  • Radiotherapy
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10
Q

What are the causes of chronic colitis?

A

Chronic Colitis

  • Crohn’s disease
  • Ulcerative colitis
  • TB
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11
Q

What are the effects of infection in the colon?

A

Effects of Infection in the Colon

  • Secretory diarrhoea (caused by toxin)
  • Exudative diarrhoea (invasion and mucosal damage)
  • Severe tissue damage and perforation
  • Systemic illness
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12
Q

What is shown? What are the causes?

A

Pseudomembraneous colitis

  • · Antibiotic-associated colitis
  • · Acute colitis with pseudomembrane formation
  • · Caused by protein exotoxins of C. difficile
  • · Characteristic microscopic appearance on biopsy
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13
Q

What is shown?

A

Pseudomembraneous colitis -

  • 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
  • C diff may be detected on a toxin stool assay
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14
Q
A
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15
Q

How do you treat pseudomembranous colitis?

A

Metronidazole or vancomycin

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16
Q

What is shown? Where does it usually occur?

A

Ischaemic colitis/infarction

  • Acute or chronic
  • Most common vascular disorder of the GI tract
  • Usually occurs in segments in watershed zones (e.g. splenic flexure and the rectosigmoid)
  • Extend can be mucosal, mural or transmural (leading to perforation)
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17
Q

What is the aetiology of ischaemic colitis?

A
  1. Arterial occlusion: atheroma, thrombosis, embolism
  2. Venous occlusion: thrombus, hypercoagulable states
  3. Small vessel disease: diabetes mellitus, cholesterol, vasculitis
  4. Low flow states: CCF, haemorrhage, shock
  5. Obstruction: hernia, intussusception, volvulus, adhesions
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18
Q

What is the aetiology of idiopathic chronic IBD?

A
  • Uncertain
  • Potential genetic predisposition
  • Possibly infectious contribution (e.g. Mycobacteria, Measles)
  • Possibly due to abnormal immunoreactivity
19
Q

What are the features of chronic IBD?

A
  • Diarrhoea with or without blood
  • Fever
  • Abdominal pain
  • Acute abdomen
  • Anaemia
  • Weight loss
  • Extra-intestinal manifestations
20
Q

What is shown? Who is most affected/what are the risks?

A

CROHN’S DISEASE

More common in Western populations; peak onset in early 20s; more common in White people; can affect the entire GI tract from mouth to anus

Description:

  • Skip lesions
  • Transmural inflammation
  • Non-caseating granulomas
  • Sinus/fistula formation
  • Most commonly affects the large bowel and terminal ileum
  • Fat wrapping of the bowel
  • Thick rubber-hose like wall
  • Narrow lumen
  • Cobblestone mucosa
  • Linear ulcers
  • Fissures
  • Abscesses
    *
21
Q

What are the extra intestinal features of Crohn’s disease?

A
  • Arthritis
  • Uveitis
  • Stomatitis/cheilitis
  • Skin lesions
    • Pyoderma gangrenosum
    • Erythema multiforme
    • Erythema nodosum
22
Q

What is shown? Who is most affected/what are the risk factors?

A

ULCERATIVE COLITIS

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

Description:

  • Involves the rectum and colon in a contiguous fashion
  • May see mild backwash ileitis (where the terminal ileum also gets inflamed)
  • May see appendiceal involvement
  • Small bowel and proximal GI tract is not affected
  • Inflammation is confined to the mucosa
  • Bowel wall is normal thickness
  • Shallow ulcers
23
Q

What are the complications of UC?

A

Severe haemorrhage

Toxic megacolon

Adenocarcinoma (20-30 x increased risk)

24
Q

What are the extra-intestinal complications of UC?

A

Arthritis

Myositis

Uveitis/iritis

Erythema nodosum, pyoderma gangrenosum

Primary sclerosing cholangitis

25
Q

List the tumours of the colon and rectum.

A

Non-neoplastic polyps

Neoplastic epithelial lesions

  • Adenoma
  • Adenocarcinoma
  • Carcinoid tumour

Mesenchymal lesions

  • Stromal tumours
  • Lipoma
  • Sarcoma

Lymphoma

26
Q

What is this?

A

Type of non-neoplastic polym - hyperplastic

27
Q

What are the types of polyps?

A

Non-neoplastic polyps

  • Hyperplastic
  • Inflammatory (pseudopolyps)
  • Hamartomatous (juvenile, Peutz-Jeghers)

Neoplastic Polyps

  • Tubular adenoma
  • Tubulovillous adenoma
  • Villous adenoma
28
Q

What is this? What are the three types? Who is most affected?

A

Excess epithelial proliferation with dysplasia (this is abnormal growth that is moving towards cancer)

40-50% prevalence > 60 years

THREE types:

  • Tubular
  • Villous
  • Tubulovillous
29
Q

What is this?

A

tubular adenoma

30
Q

What is this?

A

Villous adenoma

31
Q

What are the risk factors for cancer from a polyp?

A

Size of polyp (> 4 cm = 45% invasive risk)

Proportion of villous component

Degree of dysplastic change within a polyp

32
Q

What are the reasons for adenoma-carcinoma sequence?

A
  • Areas that have a high prevalence of adenomas also have a high prevalence of carcinomas
  • The distribution within the colon is similar
  • Adenomas tend to appear about 10 years before carcinoma
  • Residual adenomas may be found near a carcinoma
  • Risk of cancer is proportions to the number of adenomas
  • Screening and removal of adenoma reduces the risk of cancer
33
Q

What are the symptoms of adenoma?

A

Aymptomatic or may bleed and cause anaemia

34
Q

Name 3 familial syndromes characterised by polyps.

A

Peutz-Jeghers syndrome

Familial adenomatous polyposis (FAP)

  • Gardner’s
  • Turcot

Hereditary non-polyposis colorectal cancer (HNPCC)

35
Q

What genetics causes FAP? What is the age of onset? What is the risk of cancer?

A

Autosomal DOMINANT

Genetics: APC tumour suppressor gene on chromosome 5q21

Average age of onset is 25 years

Characterised by large numbers of adenomatous polyps (mostly colorectal)

Minimum 100 polyps

Virtually 100% will develop cancer within 10-15 years

36
Q
A
37
Q

What is Gardner’s syndrome? What are the extra-intestinal manifestations?

A

Same clinical, pathological and aetiological features of FAP with high cancer risk

There are distinctive extra-intestinal manifestations:

  • Multiple osteomas of the skull and mandible
  • Epidermoid cysts
  • Desmoid tumours
  • Dental caries, unerrupted supernumerary teeth
  • Post-surgical mesenteric fibromatoses
38
Q

What is HNPCC? What are the genetics? What type of cancers are most common here and where are they usually found? What may NOT be found?

A
  • Uncommon autosomal DOMINANT condition
  • 3-5% of colorectal cancers
  • 1 of 4 DNA mismatch repair genes are mutated
  • Numerous DNA replication errors
  • Onset of colorectal cancer at an early age
  • High frequency of carcinomas proximal to the splenic flexure
  • Poorly differentiated and mucinous carcinoma are more frequent
  • Multiple synchronous cancers
  • Presence of extra-colonic cancers (e.g. endometrium, prostate, breast, stomach)
  • NOTE: you do NOT necessarily get polyps in this condition
39
Q

What is shown?

A

Dark purple is bad

Colorectal carcinoma

40
Q

What type are most colorectal carcinomas?

A

98% are adenocarcinomas

41
Q

What are the risk factors for colorectal adenocarcinoma?

A
  • Age 60-80 years (if < 50 years consider familial syndrome)
  • More common in Western populations
  • Diet (low fibre, high fat)
  • Lack of exercise
  • Obesity
  • Familial
  • Chronic inflammatory bowel disease
42
Q

What are the symptoms of colorectal carcinoma?

A
  • Bleeding
  • Change in bowel habit
  • Anaemia
  • Weight loss
  • Pain
  • Fistula
43
Q

What is grade? How are colorectal carcinomas staged?

A

Grade = extent of differentiation

Dukes’ Staging

  • A = confined to bowel wall
  • B = through bowel wall
  • C = lymph node metastases
  • D = distant metastases

TNM staging is used now

44
Q

Why is staging of colorectal carcinoma important?

A

The staging determines the (1) treatment and also gives an idea of (2) prognosis