Colonic Pathology GSF 2011(1)

8/2/2019 Colonic Pathology GSF 2011(1)

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ColonicPathology


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Inflammatory

&

Neoplastic


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IDIOPATHIC CHRONIC

INFLAMMATORY BOWEL DISEASE

Crohns Disease&

Ulcerative Colitis


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CROHNS DISEASE

Common in North America and Northern

Europe

Prevalence from 30 to 100 per 100000

Family history common, relative risk for

a sibling is 13-36

Maximal incidence in young adults 15-30

yrs


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CROHNS DISEASE

Any portion of the GI tract can be affected but

pattern of anatomical involvement is important

Involvement of both terminal ileum and

caecum in 40-50%

In 20% of patients disease confined to the

colon

Discontinuous or skip lesions on

colonoscopy or barium studies are characteristic


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CROHNS DISEASE

Pathology (Macroscopic examination)

Involved bowel portions and associated

mesentery thickened and oedematousMucosal lesion typically begins as a

superficial ulcer

As disease advances ulcers enlarge, deepen

and eventually coalesce to form transverse and

longitudinal ulcers, giving cobblestone

appearance.


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CROHNS DISEASE


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CROHNS DISEASE


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CROHNS DISEASE

Histopathology

Transmural inflammation

Non-necrotising granulomas (40-60%)

Crypt abscesses

Ulcers may penetrate deeply forming fissures in

the muscularis propria leading to abscess and

fistula formationHealing of these penetrating lesions is

responsible for fibrosis and stricture formations


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CROHNS DISEASE


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CROHNS DISEASE

ComplicationsInflammatory adhesions, perforation, perirectal

disease (perianal fistulas and abscesses),

malabsorption, small bowel adenocarcinoma

Treatment

5-Aminosalycilic acid, steroids,

immunosuppressive drugs, monoclonalantibodies against TNF- (Infliximab), surgery


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ULCERATIVE COLITIS

Common in North America and Northern Europe.

Prevalence from 35 to 50 per 100000

Family history common, relative risk for a sibling

is 7-17. Maximal incidence in young adults 20-50

yrs., second peak 60-70 yrs


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ULCERATIVE COLITIS

HistologicallyCrypt abscesses with neutrophils within the

crypt, in the crypt wall and in the lamina

propriaCrypt architectural distortion, with gland

branching, shortening and loss of the normal

parallel arrangement of glands


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LAYERS OF THE LOWER GI TRACT


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Large Bowel


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ULCERATIVE COLITIS


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ULCERATIVE COLITIS


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ULCERATIVE COLITIS


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TOXIC MEGACOLON

High feverTachycardia

Diarrhoea

Paralysis of the motorfunction of the

transverse colon

Mortality up to 30%


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ULCERATIVE COLITIS

Complications

Toxic megacolon, perforation, massive haemorrhage,

colon cancer (correlation with colonic involvement and

duration of disease)

Treatment

5-ASA, steroids, immunosuppressive drugs, surgery


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Neoplastic


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Benign and Malignant

Intestinal polyps

Colorectal Polyps: definition, classificationand behaviour

Colorectal Cancer: location, risk factors,

screening, spread, staging, survival,complications


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INTRODUCTION

Terminology

Hyperplasia: increase in cell number bymitosis

Hypertrophy: increase in cell size without

cell division


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Terminology

Differentiation: cells develop specialised

function

Metaplasia: acquired form of altered

differentiation

Dysplasia: abnormal growth anddifferentiation of a

tissue often premalignant


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COLORECTAL POLYPS

Definition

Protruberant growthEpithelial (very common)

Mesenchymal (uncommon)

Benign or Malignant


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COLORECTAL POLYPS

Classification

1. INFLAMMATORY: pseudopolyps,

benign lymphoid polyps

2. HAMARTOMATOUS: juvenile polyp,

Peutz-Jegher

3. NEOPLASTIC: adenoma, adenocarcinoma

4. OTHERS: hyperplastic,

lipoma, leiomyoma


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INFLAMMATORY PSEUDOPOLYPS

Seen in ulcerative colitis and Crohns

diseaseMacroscopically: can look like

adenomas

Microscopically: inflammatory tissue,hyperplastic mucosa


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HAMARTOMATOUS POLYPS

Hamartoma:

Benign tumour-like lesion

Two or more differentiated tissue elements,

normally present in the organ


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HAMARTOMATOUS POLYPS

Juvenile Polyps: most common paediatric

GI polyps

Peutz-Jegher: GI polyps

pigmentations of oral

mucosa, lips, palms,

genitalia


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Juvenile polyp

Cystic glands with normal orinflamed epithelium

Germ line SMAD4 mutation

(18q21-22) (25-30%)Children mean age 8

80% in the rectum

Clinical manifestations: bleeding(up to 95%), prolapse


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Peutz-Jeghers Polyps (PJP)

Autosomal dominantOccur throughout the GI tract

Small bowel more common than

large bowel

Intussusception and partial or

complete obstruction

Adenoma/Carcinoma in PJP

Carcinoma develops from

dysplastic foci (73% GI tract)


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NEOPLASTIC POLYPS

Definition

All are dysplastic

Disregulated proliferation

Failure to fully differentiate

Premalignant

Adenoma


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NEOPLASTIC POLYPS

Adenoma Classification

Tubular

Tubulovillous

Villous


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Tubular adenoma

Tubular growth


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Tubulo-villous adenomaMuscularis mucosa

Stalk

Villielongated crypts


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Villous adenoma

More than 75% villous
http://www.emedicine.com/cgi-bin/foxweb.exe/makezoom@/em/makezoom?picture=/websites/emedicine/med/images/Large/37073707villous-1.jpg&template=izoom2


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Flat/Depressed adenoma

High malignant potential

(even if small)

High incidence of severedysplasia

Associated with familial

colon cancer syndromes,HNPCC (50%) or FAP


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NEOPLASTIC POLYPS

Villosity (25-85%) of villous

adenomas may contain cancer

Size (30% of villous adenomas > 5cm

may contain cancer

Degree of dysplasia (severe)

Malignant potentialof adenomas is

proportional to:


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HYPERPLASTIC POLYP

Commonest in adults

Asymptomatic, any age but

increase in 60s and 70s, mostly

rectosigmoid< 5 mm, sessile nodule

Benign, no malignant potential

unless they are mixed (hyperplastic-adenomatous polyps, Serrated

Adenomas)


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Leiomyoma

Ileocaecal valve


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Leiomyomatous polyp

Rectum, as well as jejunum, ileum

Muscularis mucosa

Symptoms : anaemia, bleeding due to

ulceration, epigastric pain


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Colorectal Cancer


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Colorectal Cancer

Peaks at 75-80 years

Carcinoma colon F>M

Carcinoma rectum M>F

Location

Right colon 25%

Left colon 15%

Rectosigmoid 50%

i h i i


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Site Characteristics

Left ColonRight ColonPolypoid

Mass

Discomfort/anaemia

Anular,obstructing

Bleeding/mucus

Colicky painChange of bowel habit


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Screening

Colonoscopy: UC

FAP/HNPCC

Adenomatous Polyps

Faecal occult bloods (false positives)

Flexible sigmoidoscopy

Genetic testing


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Spread

Direct

Lymphatic

Vascular (liver, lungs, bones)


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Complications

Obstruction

PerforationBleeding

Pericolic abscess

Fistulae

Intussusception


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Survival

DUKEs staging 5 year survival

A

B

C (C1 and C2)

99%

75%

35%


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Tumour

T1:Tumour invades submucosa

T2:Tumour invades muscularis propria

T3:Tumour invades through the muscularis propria into the

subserosa, or into the pericolic or perirectal tissues

T4:Tumour directly invades other organs or structures,and/or perforates

Node

N0:No regional lymph node metastasis

N1:Metastasis in 1 to 3 regional lymph nodesN2:Metastasis in 4 or more regional lymph nodes

Metastasis

M0:No distant metastasis

M1:Distant metastasis present

TNM Staging System (Tumour, Node, Metastasis)


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Stage Groupings

Stage I:T1 N0 M0; T2 N0 M0

Cancer has begun to spread, but is still in the inner lining

Stage II:T3 N0 M0; T4 N0 M0

Cancer has spread to other organs near the colon or rectum. It has

not reached lymph nodes

Stage III:any T, N1-2, M0

Cancer has spread to lymph nodes, but has not been carried to

distant parts of the body

Stage IV:any T, any N, M1Cancer has been carried through the lymph system to distant parts

of the body. This is known as metastasis. The most likely organs to

experience metastasis from colorectal cancer are the lungs and liver


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CRC Survival

Stage grouping 5 year survivalI (Dukes A)

II (Dukes B)

III (Dukes C)

IV (Dukes D)

99%

75%

35%

5%

F ili l C l l C S d


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Familial Colorectal Cancer Syndrome

Dominant

Carcinoma developes younger

Right sided

Multiple

about 5% of casesabnormalities in 4 mismatch repair

genes (microsatellite instability)

HNPCC


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Identifying HNPCC

Amsterdam Criteria(all criteria must be met)

Three or more family members with colorectal cancer, at

least two of which must be first-degree relatives (e.g.

parent, sibling or child)

The disease affects family members from at least two

successive generations

One of the colorectal cancers must occur prior to age 50Familial Adenomatous Polyposis excluded

F ili l Ad P l i (FAP)


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Familial Adenomatous Polyposis (FAP)

Relatively rare condition

(approximately 1 in 8000 individuals)

Without intervention virtually all

people with this condition will

develop colon cancer

Characterised by multiple polyps

throughout the entire colon (up to

thousands) The polyps are not present at birth

but develop over time

Colonic Pathology GSF 2011(1)

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