git lecture 3- tumors

8/10/2019 GIT Lecture 3- Tumors

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Dr. Marwan Qubaja / Pathology IIDr. Marwan Qubaja / Pathology II

GIT IIIGIT III -- Tumors of small and large intestinesTumors of small and large intestines11

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GIT III: Small and Large Intestines

Dr. Marwan Qubaja

Al-Quds University

Faculty of Medicine

Pathology Department

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Tumors of the SmallTumors of the Small

andand

Large IntestinesLarge Intestines


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Tumors of the Small and LargeTumors of the Small and Large

IntestinesIntestines Common site:Common site: Colorectal cancer

second to bronchogenic carcinoma among the cancer

killers

5% of population will develop colorectal cancer

40% of this population will die of the disease

Common type: adenocarcinomasadenocarcinomas ~ 70% of GImalignancies

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Tumors of the Small and Large IntestinesNon-neoplastic Polyps:

Hyperplastic polyps Hamartomatous polyps

o Juvenile polyps

o Peutz-Jeghers polyps

Inflammatory polyps

Lymphoid polyps

Neoplastic Epithelial Lesions:

Benign polyps

o Adenoma*

Malignant lesions

o Adenocarcinoma*

o Carcinoid tumor

o Anal zone carcinoma

Mesenchymal Lesions:

Gastrointestinal stromal tumors (benign or malignant)

Other benign lesions: Lipoma Neuroma Angioma

Kaposi sarcoma

Lymphoma


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PolypsPolyps

lesions arising from the epithelium of the mucosa

mass that protrudes into the lumenprotrudes into the lumen of the gut

Morphology:Morphology:

1.1. PedunculatedPedunculated or stalked polyp

2.2. SessileSessile, without a definable stalk

nonnon--neoplasticneoplasticpolyps:polyps:

due to abnormal mucosal maturation or inflammationinflammation

an example is the hyperplastichyperplastic polyppolyp

neoplasticneoplasticpolyps:polyps:

due epithelial proliferation and dysplasia termed adenomatous polyps or adenomasadenomas

are precursors of carcinoma

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Two types of adenoma:Two types of adenoma:

1. pedunculated

2. Sessile villous

Two forms of sessile polyp:Two forms of sessile polyp:

1. hyperplastic polyp

2. adenoma

Adenoma:Adenoma: neoplastic polypsneoplastic polyps


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PeutzPeutz--Jeghers polypsJeghers polyps

uncommon hamartomatoushamartomatous polypspolyps

Part of rare autosomal dominant PeutzPeutz--JeghersJeghers

syndromesyndrome

characterized by melanotic mucosal and cutaneouscutaneous

pigmentationpigmentation

associated with an increased risk of both intestinal and

extraintestinal malignancies.

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PeutzPeutz--JeghersJeghers

syndromesyndrome


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Adenomas:Adenomas: Neoplastic polypsNeoplastic polyps

Shape:Shape: pedunculatedpedunculated or sessilesessile, M = F

4 fold greater risk foradenomas among first-degree relatives

4 fold greater risk of colorectal carcinomarisk of colorectal carcinoma

result from epithelial proliferation and dysplasiaepithelial proliferation and dysplasia

Three subtypes:Three subtypes:

1.1. Tubular adenomasTubular adenomas: mostly tubular glands

2.2. Villous adenomas:Villous adenomas: villous projections

3.3. TubulovillousTubulovillousadenomas:adenomas: a mixture of the above

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Tubular adenomas:Tubular adenomas:

the most common

small and pedunculatedpedunculated

The lowest risk for cancerThe lowest risk for cancer

Tubulovillous adenomas:Tubulovillous adenomas:

5% to 10% of adenomas

Villous adenomas:Villous adenomas:

only 1% of adenomas

tend to be largelarge and sessilesessile

The highest risk for cancerThe highest risk for cancer


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Tubular adenomas

arise anywhere in the colon

50% in the rectosigmoid

% increasing with age

Varies from 0.3 cm to 2.5 cm

have stalks 1 to 2 cmstalks 1 to 2 cm long

and raspberry-like heads

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AA, Pedunculated tubular adenomaPedunculated tubular adenoma showing a fibrovascular stalk

covered by normal colonic mucosa and a head that contains abundant

dysplastic epithelial glands

BB, A small focus of adenomatous epithelium


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Villous adenomas:

up to 10 cm in diameter

cauliflowercauliflower--likelike masses projecting 1 to 3 cm

above the surrounding normal mucosa

invasive carcinoma is found in up to 40%invasive carcinoma is found in up to 40% of

these lesions

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Villous adenomaVillous adenoma is shown above the surface at the left, and

in cross section at the right. Note that this type of adenoma is

sessilesessile, rather than pedunculated, and larger than a tubularlarger than a tubular

adenomaadenoma


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AA, Sessile villous adenoma:Sessile villous adenoma: frond is lined by dysplastic epithelium

BB, Portion of a villous frond with dysplastic columnar epithelium on the leftand normal colonic columnar epithelium on the right

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Adenomas:Adenomas: Clinical FeaturesClinical Features

small adenomas are usually asymptomaticasymptomatic

overt or occult rectal bleedingrectal bleeding

hypoproteinemiahypoproteinemia or hypokalemiahypokalemia

Treatment:Treatment:

all adenomas, regardless of their location, are to be

considered potentially malignant

Surgical excision


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Familial Adenomatous Polyposis (Familial Adenomatous Polyposis (FAPFAP))

uncommon autosomalautosomal dominantdominant disorders

risk of colonic cancer is almost 100%risk of colonic cancer is almost 100% by midlife

usually 500 to 2500 colonic adenomas

> 100 adenoma> 100 adenoma is required for the diagnosis

may be present anywhere in the GTI

Most polyps are tubular adenomastubular adenomas

Treatment:Treatment: prophylactic colectomy

Gardner syndrome:Gardner syndrome: osteomas and soft tissue tumor with FAP

TurcotTurcotsyndrome:syndrome: gliomas with FAP

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Familial adenomatous polyposisFamilial adenomatous polyposis


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Colorectal CarcinomaColorectal Carcinoma

~ 98% are adenocarcinomasadenocarcinomas

peak incidence is 60 to 70 years of age

Males > females

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Risk factors:Risk factors:

Adenomatous polypsAdenomatous polyps

FAPFAP

Ulcerative colitisUlcerative colitis

Family history of colorectal carcinomaFamily history of colorectal carcinoma

low fiber and high fat dietlow fiber and high fat diet

Protective effect by NSAIDs


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Morphologic and Molecular Progression in Neoplasm:

Neoplastic transformation is a progressive process involving

multiple hits or genetic changes

hyperplasiahyperplasia

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Molecular model for the evolution of colorectal

cancers through the adenoma-carcinoma

sequence

In colon

cancer:

APCAPC

inactivation is

an importantfirst step in

oncogenesis


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25% are in the cecum or ascending colon25% are in the cecum or ascending colon

25% in the rectum and distal sigmoid25% in the rectum and distal sigmoid

25% are in the descending colon and25% are in the descending colon and

proximal sigmoidproximal sigmoid

25% are scattered elsewhere25% are scattered elsewhere


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Carcinomas in the proximal colon:Carcinomas in the proximal colon:

tend to be polypoid, exophyticexophytic masses

obstruction is uncommon

Colorectal CarcinomaColorectal Carcinoma-- MorphologyMorphology


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CarcinomasCarcinomas in the distal colon:in the distal colon:

tend to be annular encircling

lesions

produce napkin-ring

constrictions of the bowel

cause narrowing of the lumen

The arrows identify separate

mucosal polyps

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Colorectal CarcinomaColorectal Carcinoma-- Clinical FeaturesClinical Features

Asymptomatic

Cecal and right colonic cancers:

FatigueFatigue and iron deficiency anemiaanemia

LeftLeft--sided lesionssided lesions:

produce occult bleeding

changes in bowel habitchanges in bowel habit

left lower quadrant discomfort

Metastasis sites are:Metastasis sites are:

regional lymph nodes

liver, lungs, and bones

serosal membrane of the peritoneal cavity


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TNM STAGING OF COLON CANCERSTumor (T)

0 = none evident

is = in situ (limited to mucosa)

1 = invasion of submucosa

2 = invasion of muscularis propria

3 = invasion of subserosa or pericolic fat

4 = invasion of contiguous structures

Lymph Nodes (N)

0 = none evident

1 = 1 to 3 positive pericolic nodes

2 = 4 or more positive pericolic nodes

3 = any positive node along a named blood vessel

Distant Metastasis (M)

0 = none evident

1 = any distant metastasis

5-Year Survival Rates

Tl = 97%

T2 = 90%

T3 = 78%

T4 = 63%

Any T; N1; M0 = 66%

Any T; N2; M0 = 37%

Any T; N3; M0 = data not available

Any Ml = 4%

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Digital rectal examination

Fecal testing for occult blood loss

Barium enema

BiopsyBiopsy by sigmoidoscopy, and colonoscopy

CT

Serum markers: CEACEA

Molecular detection of APCdetection of APC mutations in epithelial cells

isolated from stools

Colorectal CarcinomaColorectal Carcinoma-- DiagnosisDiagnosis


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Small Intestinal NeoplasmsSmall Intestinal Neoplasms

~ 3% to 6% of gastrointestinal tumors

Mostly benign tumors:Mostly benign tumors:

stromal tumors of smooth muscle origin

Adenomas

Lipomas

Malignant:Malignant:

Adenocarcinomas

Carcinoids (50%)

Lymphoma

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develops from enterochromaffin cellsenterochromaffin cells

The appendix is the most common site

rectal and appendiceal carcinoids almost

never metastasize

associated with carcinoid syndrome (1%)

arise from elaboration of serotonin

Carcinoid TumorsCarcinoid Tumors


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Multiple protruding tumors are present at the ileocecal

junction

Carcinoid TumorsCarcinoid Tumors

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Clinical Features of Carcinoid Syndrome

Vasomotor disturbances

Cutaneous flushes and apparent cyanosis (most patients)

Intestinal hypermotility

Diarrhea, cramps, nausea, vomiting (most patients)

Asthmatic bronchoconstrictive attacks

Cough, wheezing, dyspnea (about one third of patients)

Hepatomegaly

Nodular, related to hepatic metastases (some cases)

Niacin deficiency (due to shunting of niacin to serotonin synthesis)

Systemic fibrosis

Cardiac involvement

Pulmonic and tricuspid valve thickening and stenosis

Endocardial fibrosis, principally in right ventricle (bronchial carcinoids affectthe left side)

Retroperitoneal and pelvic fibrosis

Collagenous pleural and intimal aortic plaques

git lecture 3- tumors

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