Yr 2 - Clinical Pathology > Lower GI Pathology > Flashcards

Lower GI Pathology Flashcards

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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
Clinical presentation of Crohn's disease?
* 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
26
Complications of Crohn's disease?
* Toxic megacolon * Perforation * Fistula * Stricture (common) * Haemorrhage * Carcinoma * Short bowel syndrome (repeated resection - iatrogenic)
27
Most common location in GI tract of Crohn's disease?
**•Ileocolic 30 – 55 %** * Small bowel 25 – 35 % * Colonic 15 – 25 % * Peri-anal / ano-rectal 2 – 3 % * Gastro – duodenal 1 – 2 %
28
Do granulomas in the bowel wall suggest Crohn's disease or ulcerative colitis?
Crohn's disease
29
What are the hepatic manifestations of IBD?
* Fatty change & granulomas * PSC & bile duct carcinoma
30
What are the osteo-articular manifestations of IBD?
* Polyarthritis * Sacro-ileitis & Ankylosing Spondylitis
31
What are the muco-cutaneous manifestations of IBD?
* Oral ulcers * Pyoderma gangrenosum & erythema nodosum
32
What are the ocular manifestations of IBD?
Uveitis and retinitis
33
What are the systemic manifestations of IBD?
* Amyloidosis (due to chronic inflammation) * Thrombo-embolic disease
34
What are the risk factors for colorectal cancer (CRC) in ulcerative colitis?
**1.Early age of onset** **2.Duration of disease \> 8-10 years** **3.Total or extensive colitis** 4. PSC (inflammation of bile ducts) 5. Family History of CRC 6. Severity of inflammation ( pseudopolyps ) 7. Presence of dysplasia
35
Histological changes from ulcerative colitis to CRC?
Inflamed mucosa --\> low grade dysplasia --\> high grade dysplasia --\> colorectal cancer
36
Colitis surveillance for cancer risk:
37
What is ischaemic colitis?
* 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
Ischaemic colitis is usually multifactorial. What other diseases is it associated with?
Associated with other vascular diseases eg. hypertension, peripheral vascular disease, coronary artery disease, diabetes mellitus, chronic renal failure, IBS, COPD
39
What are the 3 clinical forms of ischaemic colitis?
1. Transient or “evanescent” ( \> 80% ) 2. Chronic segmental ulcerating ( ischaemic stricture ) 3. Acute fulminant & gangrenous ( 10-20% )
40
What is the most common form of ischaemic colitis?
Transient or 'evanescent'
41
Clinical features of ischaemic colitis?
* acute onset cramping abdominal pains * urge to defaecate * bloody diarrhoea / rectal bleeding
42
Recovery of ischaemic colitis?
* in majority symptoms improve within 48 hrs * complete recovery within 1 – 2 weeks * 20% require surgery for colonic infarction
43
What are the 3 major causes of mesenteric ischaemia (i.e. reduced blood supply to bowel)?
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
What can cause non-occlusive mesenteric ischaemia?
Low cardiac output with mesenteric vasoconstriction (“low flow state“) eg. MI, CCF, major surgery & trauma
45
Most common location of ischaemic colitis?
Left colon (rectum to splenic flexure)
46
Why is the splenic flexure particularly vulnerable to ischaemia?
Is a watershed area; in between supply of SMA and IMA
47
What are colorectal polyps?
* Mucosal protrusions in the colon * Solitary or multiple ( polyposis ) * Pedunculated, sessile or “flat” * Small or large
48
What is the difference between a sessile polyp and a pedunculated polyp?
**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
Classifications of colorectal polyps:
* Neoplastic, hamartomatous, inflammatory or reactive * Benign or Malignant * Epithelial or Mesenchymal
50
Different types of non-neoplastic polyps in the colo-rectum:
* 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
What is the most common colonic polyp?
Hyperplastic polyp
52
Where are hyperplastic polyps typically located?
located in rectum and sigmoid colon
53
Do hyperplastic polyps have malignant potential?
* 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
What is the most common type of colorectal polyp seen in children?
Juvenile polyp
55
Shape of juvenile polyps?
Often spherical and pedunculated
56
Where are juvenile polyps typically located?
Rectum and distal colon
57
Do juvenile polyps have malignant potential?
* Sporadic polyps have NO malignant potential * BUT --\> juvenile polyposis associated with increased risk of **colorectal** and **gastric** **cancer**
58
What is Peutz-Jeghers Syndrome?
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
Typical presentation of Peutz-Jeghers syndrome?
* 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
Benign vs malignant neoplastic polyps
61
What is the most common type of neoplastic polyp?
Adenoma (benign) --\> arising from epithelial lining of colon
62
Can benign colorectal adenomas progress to malignant?
Precursor of colorectal cancer (at least 80%)
63
How common are colorectal adenomas?
* Present 25% - 35% population \> 50 years * Multiple in 20 – 30 % patients
64
Macroscopic appearances of colorectal adenomas?
Pedunculated , sessile or “flat”
65
What factors suggest a high risk of malignant progression of colorectal adenomas?
* “flat” adenomas * Size ( most malignant polyps \> 10 mm ) * Villous & Tubulo-Villous * Severe ( high grade ) dysplasia * Lynch syndrome associated adenomas
66
Risk factors for colorectal cancer?
**•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
Which 2 genetic conditions predispose to colorectal cancer?
* FAP * HNPCC
68
What is FAP?
* 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
Inheritance of FAP?
Autosomal dominant
70
Colorectal cancer risk with FAP?
* 100 % lifetime risk of large bowel cancer (classical) * \< 100 % “attenuated” FAP
71
Treatment of FAP?
Remove large bowel in teen years
72
Inheritance of Lynch syndrome?
Autosomal dominant
73
Risk of colorectal cancer with Lynch?
50-70% lifetime risk of large bowel cancer
74
Mutation in what leads to Lynch?
Due to mutations in DNA mismatch repair genes
75
Which cancers does Lynch syndrome predispose you to?
Increased risk of endometrial, ovarian, gastric, small bowel, urinary tract and biliary tract cancer
76
Most common location of colorectal cancer?
2/3 develop in left colon between splenic flexure and colon
77
What is the most common type of colorectal cancer?
* Adenocarcinoma (\>95%) * Mucinous adenocarcinoma (10-20%)
78
Grading of colorectal cancers?
* Well differentiated 10 – 20 % * Moderately well differentiated 60 – 80 % * Poorly differentiated 10 – 20 %
79
Modes of spread of colorectal cancer?
* 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
Staging system of colorectal cancer?
TNM stage --\> describes extent of local and distant tumour spread
81
Yr 2 - Clinical Pathology
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