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Yr 2 - Clinical Pathology > Lower GI Pathology > Flashcards

Lower GI Pathology Flashcards

1
Q

What are diverticula?

A

Protrusions of mucosa and submucosa from the bowel lining through the bowel wall into the surrounding fat

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2
Q

Most common site of diverticula?

A

Sigmoid colon

  • Located between mesenteric and anti-mesenteric taenia coli, or between two anti-mesenteric taenia coli
  • Less commonly extend into the proximal colon e.g. caecum in 15% of cases
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3
Q

What are taenia coli?

A
  • The taeniae coli are three separate longitudinal ribbons of smooth muscle on the outside of the ascending, transverse, descending and sigmoid colons
  • Generally, the colon wall distributes the three taeniae as two antimesenteric and one mesenteric linear muscular bands.
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4
Q

What are the 2 major types of diverticula?

A
  1. ‘True’/congenital diverticulum
  2. ‘False’/acquired/pseudo diverticulum
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5
Q

Difference between true vs false diverticulum?

A

True –> contain all layers of the bowel wall

False –> contains the mucosa and submucosa

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6
Q

Which type of diverticula is most common?

A

False/acquired/pseudo

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7
Q

What is acquired diverticula associated with?

A

DIET!:

  • Relationship with fibre content of diet
  • High fat and meat consumption risk factor
  • Less common in vegetarians

AGE:

  • Increases with age (rare under 40, around 50% over 90)
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8
Q

Pathogenesis of diverticula disease?

A
  • Increased intra-luminal pressure
    • Irregular, uncoordinated peristalsis
    • Overlapping (valve like) semi-circular areas of bowel wall –> closed compartments where pressure rises
  • Points of relative weakness in the bowel wall
    • Penetration by nutrient arteries between mesenteric and antimesenteric taenia coli – this is the point where the diverticuli will extend
    • Age related changes in connective tissue
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9
Q

Clinical presentation of diverticula?

A
  • 90-99% of people are asymptomatic
  • Cramping abdominal pain
  • Alternating constipation and diarrhoea
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10
Q

Potential acute complications of diverticula?

A
  • Diverticulitis/peridiverticular abscess (pain, fever, diarrhoea) –> most common complication
  • Perforation, can lead to peritonitis (surgical emergency)
  • Haemorrhage in 5% (ulceration erodes into artery/vein)
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11
Q

What is diverticulitis?

A

The infection/inflammation of diverticula

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12
Q

Potential chronic complications of diverticula?

A
  • Intestinal obstruction (strictures in 5-10%) –> due to repeated inflammation and repair through fibrosis
  • Fistula (urinary bladder, vagina) –> faecal material in urine/vagina
  • Diverticular colitis (segmental and granulomatous) –> lining mucosa of bowel inflamed, causing diarrhoea and bleeding
  • Polypoid prolapsing mucosal folds
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13
Q

Is there an increased risk of cancer in diverticula disease?

A

no

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14
Q

What is colitis?

A
  • Inflammation of the colon
  • sually mucosal inflammation but occasionally transmural (eg. crohns disease) or predominantly submucosal/muscular (eg. eosinophilic colitis)
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15
Q

Causes of acute colitis?

A
  • Acute infective colitis eg. campylobacter, shigella, salmonella, CMV
  • Antibiotic associated colitis (including PMC)
  • Drug induced colitis
  • Acute ischaemic colitis (transient or gangrenous)
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16
Q

2 major causes of chronic colitis?

A
  • Chronic idiopathic inflammatory bowel disease
  • Ischaemic colitis
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17
Q

What are the 2 major types of IBD?

A
  1. Ulcerative colitis
  2. Crohn’s disease
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18
Q

Peak age incidence of IBD?

A

20-40 years

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19
Q

Risk factors for IBD?

A
  • Cigarette smoking
    • Increases risk of Crohn’s disease
    • BUT decreases risk of ulcerative colitis (trialled nicotine medications)
  • Oral contraceptive
  • Childhood infections
  • Domestic hygiene
  • Appendicectomy (protective against UC)
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20
Q

How does cigarette smoking affect risk of Crohn’s disease vs ulcerative colitis?

A

Increases risk of Crohn’s disease BUT decreases risk of ulcerative colitis

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21
Q

Is IBD seen in the family?

A

Genetic component to both (but stronger in Crohn’s disease)

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22
Q

Clinical presentation of ulcerative colitis?

A
  • Diarrhoea ( > 66 % ) with urgency/tenesmus
  • Constipation ( 2 % )
  • Rectal bleeding ( > 90 % )
  • Abdominal pain ( 30 – 60 % )
  • Anorexia
  • Weight loss ( 15 – 40 % )
  • Anaemia
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23
Q

Complications of ulcerative colitis?

A
  • Toxic megacolon leading to perforation –> an acute form of colonic distension which can perforate and lead to peritonitis
  • Haemorrhage; ulceration of lining can erode into arteries and veins
  • Stricture (rare); is it malignant?
  • Carcinoma
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24
Q

Which parts of the GI tract does Crohn’s disease affect?

A

All levels from mouth to anus

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25
Q

Clinical presentation of Crohn’s disease?

A
  • Diarrhoea ( may be bloody )
  • Colicky abdominal pain
  • Palpable abdominal mass
  • Weight loss / failure to thrive
  • Anorexia
  • Fever
  • Oral ulcers
  • Peri – anal disease (don’t see this in ulcerative colitis)
  • Anaemia
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26
Q

Complications of Crohn’s disease?

A
  • Toxic megacolon
  • Perforation
  • Fistula
  • Stricture (common)
  • Haemorrhage
  • Carcinoma
  • Short bowel syndrome (repeated resection - iatrogenic)
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27
Q

Most common location in GI tract of Crohn’s disease?

A

•Ileocolic 30 – 55 %

  • Small bowel 25 – 35 %
  • Colonic 15 – 25 %
  • Peri-anal / ano-rectal 2 – 3 %
  • Gastro – duodenal 1 – 2 %
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28
Q

Do granulomas in the bowel wall suggest Crohn’s disease or ulcerative colitis?

A

Crohn’s disease

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29
Q

What are the hepatic manifestations of IBD?

A
  • Fatty change & granulomas
  • PSC & bile duct carcinoma
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30
Q

What are the osteo-articular manifestations of IBD?

A
  • Polyarthritis
  • Sacro-ileitis & Ankylosing Spondylitis
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31
Q

What are the muco-cutaneous manifestations of IBD?

A
  • Oral ulcers
  • Pyoderma gangrenosum & erythema nodosum
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32
Q

What are the ocular manifestations of IBD?

A

Uveitis and retinitis

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33
Q

What are the systemic manifestations of IBD?

A
  • Amyloidosis (due to chronic inflammation)
  • Thrombo-embolic disease
34
Q

What are the risk factors for colorectal cancer (CRC) in ulcerative colitis?

A

1.Early age of onset

2.Duration of disease > 8-10 years

3.Total or extensive colitis

  1. PSC (inflammation of bile ducts)
  2. Family History of CRC
  3. Severity of inflammation ( pseudopolyps )
  4. Presence of dysplasia
35
Q

Histological changes from ulcerative colitis to CRC?

A

Inflamed mucosa –> low grade dysplasia –> high grade dysplasia –> colorectal cancer

36
Q

Colitis surveillance for cancer risk:

A
37
Q

What is ischaemic colitis?

A
  • Colonic injury secondary to an acute, intermittent or chronic reduction in blood flow
    • May be occlusive or non-occlusive (NOMI)
      • Complete occlusion of vessel, narrowing of vessel or hypotension
38
Q

Ischaemic colitis is usually multifactorial. What other diseases is it associated with?

A

Associated with other vascular diseases eg. hypertension, peripheral vascular disease, coronary artery disease, diabetes mellitus, chronic renal failure, IBS, COPD

39
Q

What are the 3 clinical forms of ischaemic colitis?

A
  1. Transient or “evanescent” ( > 80% )
  2. Chronic segmental ulcerating ( ischaemic stricture )
  3. Acute fulminant & gangrenous ( 10-20% )
40
Q

What is the most common form of ischaemic colitis?

A

Transient or ‘evanescent’

41
Q

Clinical features of ischaemic colitis?

A
  • acute onset cramping abdominal pains
  • urge to defaecate
  • bloody diarrhoea / rectal bleeding
42
Q

Recovery of ischaemic colitis?

A
  • in majority symptoms improve within 48 hrs
  • complete recovery within 1 – 2 weeks
  • 20% require surgery for colonic infarction
43
Q

What are the 3 major causes of mesenteric ischaemia (i.e. reduced blood supply to bowel)?

A
  1. Arterial embolism (40-50%) especially cardiac e.g. MI, AF, endocarditis
  2. Arterial thrombosis (25-30%) especially SMA origin
  3. Non-occlusive mesenteric ischaemia (20%)
44
Q

What can cause non-occlusive mesenteric ischaemia?

A

Low cardiac output with mesenteric vasoconstriction (“low flow state“) eg. MI, CCF, major surgery & trauma

45
Q

Most common location of ischaemic colitis?

A

Left colon (rectum to splenic flexure)

46
Q

Why is the splenic flexure particularly vulnerable to ischaemia?

A

Is a watershed area; in between supply of SMA and IMA

47
Q

What are colorectal polyps?

A
  • Mucosal protrusions in the colon
  • Solitary or multiple ( polyposis )
  • Pedunculated, sessile or “flat”
  • Small or large
48
Q

What is the difference between a sessile polyp and a pedunculated polyp?

A

Sessile polyps: Sit on the surface of the mucous membrane. They are flat or dome-shaped and do not have a stalk.

Pedunculated polyps: Raised, mushroom-like growths that are attached to the surface of the mucous membrane by a long, thin stalk (peduncle)

49
Q

Classifications of colorectal polyps:

A
  • Neoplastic, hamartomatous, inflammatory or reactive
  • Benign or Malignant
  • Epithelial or Mesenchymal
50
Q

Different types of non-neoplastic polyps in the colo-rectum:

A
  • Hyperplastic polyps
  • Hamartomatous polyps
  • Peutz-jeghers polyps
  • Juvenile polyps
  • Polyps related to mucosal prolapse
  • Post-inflammatory polyps (“pseudopolyps”)
  • Inflammatory fibroid polyp
  • Benign lymphoid polyp
51
Q

What is the most common colonic polyp?

A

Hyperplastic polyp

52
Q

Where are hyperplastic polyps typically located?

A

located in rectum and sigmoid colon

53
Q

Do hyperplastic polyps have malignant potential?

A
  • Small distal HPs have NO malignant potential
  • Some large right sided “hyperplastic polyps” (sessile serrated lesions) may give rise to microsatellite unstable carcinoma (10 – 15 % all colorectal cancer)
54
Q

What is the most common type of colorectal polyp seen in children?

A

Juvenile polyp

55
Q

Shape of juvenile polyps?

A

Often spherical and pedunculated

56
Q

Where are juvenile polyps typically located?

A

Rectum and distal colon

57
Q

Do juvenile polyps have malignant potential?

A
  • Sporadic polyps have NO malignant potential
  • BUT –> juvenile polyposis associated with increased risk of colorectal and gastric cancer
58
Q

What is Peutz-Jeghers Syndrome?

A

Peutz–Jeghers syndrome is an autosomal dominant disorder characterised by the development of benign hamartomatous polyps in the gastrointestinal tract and hyperpigmented macules on the lips and oral mucosa (melanosis).

59
Q

Typical presentation of Peutz-Jeghers syndrome?

A
  • Present clinically in teens or 20s
  • Abdominal pain (intussusception), gastro-intestinal bleeding & anaemia
  • Increased risk of cancer
  • Multiple gastro-intestinal tract polyps (predominantly small bowel)
  • Muco-cutaneous pigmentation
    • 1 – 5mm macules peri-oral , lips , buccal mucosa , fingers and toes
60
Q

Benign vs malignant neoplastic polyps

A
61
Q

What is the most common type of neoplastic polyp?

A

Adenoma (benign) –> arising from epithelial lining of colon

62
Q

Can benign colorectal adenomas progress to malignant?

A

Precursor of colorectal cancer (at least 80%)

63
Q

How common are colorectal adenomas?

A
  • Present 25% - 35% population > 50 years
  • Multiple in 20 – 30 % patients
64
Q

Macroscopic appearances of colorectal adenomas?

A

Pedunculated , sessile or “flat”

65
Q

What factors suggest a high risk of malignant progression of colorectal adenomas?

A
  • “flat” adenomas
  • Size ( most malignant polyps > 10 mm )
  • Villous & Tubulo-Villous
  • Severe ( high grade ) dysplasia
  • Lynch syndrome associated adenomas
66
Q

Risk factors for colorectal cancer?

A

•Diet

•Dietary fibre (protective), fat, red meat, folate (protective), calcium

  • Obesity / Physical Activity
  • Alcohol
  • NSAIDs & Aspirin ( protective )
  • HRT and oral contraceptives
  • Schistosomiasis
  • Pelvic radiation
  • Ulcerative colitis and Crohns disease
67
Q

Which 2 genetic conditions predispose to colorectal cancer?

A
  • FAP
  • HNPCC
68
Q

What is FAP?

A
  • An inherited disorder characterised by increased risk of cancer of the large intestine (colon) and rectum
  • Due to a mutation in the APC tumour suppressor gene
  • Associated with multiple benign adenomatous polyps in the colon
69
Q

Inheritance of FAP?

A

Autosomal dominant

70
Q

Colorectal cancer risk with FAP?

A
  • 100 % lifetime risk of large bowel cancer (classical)
  • < 100 % “attenuated” FAP
71
Q

Treatment of FAP?

A

Remove large bowel in teen years

72
Q

Inheritance of Lynch syndrome?

A

Autosomal dominant

73
Q

Risk of colorectal cancer with Lynch?

A

50-70% lifetime risk of large bowel cancer

74
Q

Mutation in what leads to Lynch?

A

Due to mutations in DNA mismatch repair genes

75
Q

Which cancers does Lynch syndrome predispose you to?

A

Increased risk of endometrial, ovarian, gastric, small bowel, urinary tract and biliary tract cancer

76
Q

Most common location of colorectal cancer?

A

2/3 develop in left colon between splenic flexure and colon

77
Q

What is the most common type of colorectal cancer?

A
  • Adenocarcinoma (>95%)
    • Mucinous adenocarcinoma (10-20%)
78
Q

Grading of colorectal cancers?

A
  • Well differentiated 10 – 20 %
  • Moderately well differentiated 60 – 80 %
  • Poorly differentiated 10 – 20 %
79
Q

Modes of spread of colorectal cancer?

A
  • Direct invasion of adjacent tissues
  • Lymphatic metastasis (lymph nodes)
  • Haematogenous metastasis (liver & lung)
  • Transcoelomic (peritoneal) metastasis
  • Iatrogenic spread eg. needle track recurrence, port site recurrence
80
Q

Staging system of colorectal cancer?

A

TNM stage –> describes extent of local and distant tumour spread

81
Q
A

Yr 2 - Clinical Pathology (80 decks)

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