GI POLYP

Introduction
• Polyps are most common in the colo-rectal region
but may occur in the esophagus, stomach, or
small intestine.
• Most polyps begin as small elevations of the
mucosa as sessile.
• As sessile polyps enlarge, proliferation of cells
adjacent to the mass and the effects of traction
on the luminal protrusion, may combine to create
a stalk.
• Polyps with stalks are termed pedunculated.
 Classification
• Intestinal polyps can be classified as
nonneoplastic or neoplastic in nature.
• The most common neoplastic polyp is the
adenoma, which has the potential to progress
to cancer.
• The nonneoplastic polyps can be further
classified as inflammatory, hamartomatous, or
hyperplastic.
 Hyperplastic polyp
• Sixth and seventh decades of life.
• Result from decreased epithelial cell turnover and
delayed shedding of surface epithelial cells, leading to
a “piling up” of goblet cells and absorptive cells.
• No malignant potential.
• It must be distinguished from sessile serrated
adenomas, that are histologically similar but have
malignant potential.
• Epithelial hyperplasia can occur as a nonspecific
reaction adjacent to or overlying any mass or
inflammatory lesion and, therefore, can be a clue to
the presence of an adjacent, clinically important lesion.
 Morphology
• Most commonly found in the left colon and are
typically less than 5 mm in diameter, single or
multiple, smooth.
• Histologically, hyperplastic polyps are composed
of mature goblet and absorptive cells.
• The delayed shedding of these cells leads to
crowding that creates the serrated surface
architecture that is the morphologic hallmark of
these lesions .
• Serration is typically restricted to the upper third,
or less, of the crypt
 Inflammatory Polyps
• Polyps that form as part of the solitary rectal ulcer
syndrome are examples of purely inflammatory lesions.
• Clinical triad of rectal bleeding, mucus discharge, and an
inflammatory lesion of the anterior rectal wall.
• Imapaired anorectal sphincter, leading to pressure of
rectum causing abrasion.
• An inflammatory polyp results from chronic cycles of
injury and healing.
• The distinctive histologic features of a typical inflammatory
polyp include mixed inflammatory infiltrates, erosion, and
epithelial hyperplasia together with lamina propria
fibromuscular hyperplasia
A.The dilated glands, proliferative epithelium, superficial erosions, and inflammatory
infiltrate are typical of an inflammatory polyp. However, the smooth muscle hyperplasia
within the lamina propria suggests that mucosal prolapse has also occurred. B, Epithelial
hyperplasia. C, Granulation tissue-like capillary proliferation within the lamina propria
caused by repeated erosion
 Hamartomatous Polyps
• Hamartomatous polyps occur sporadically or as
components of various genetically determined or
acquired syndromes.
• Hamartomatous polyp syndromes are caused by
germline mutations in tumor suppressor genes or
protooncogenes.
• Some of these syndromes are associated with
increased cancer risk, either within the polyps or at
other intestinal or extra-intestinal sites.
• Thus, in some hamartomatous polyp syndromes, the
polyps can be considered to be pre-malignant,
neoplastic lesions, much like adenomas.
 Juvenile Polyps

• Juvenile polyps are focal malformations of the epithelium and lamina propria.
• These may be sporadic or syndromic, but the morphology of the two forms is often
indistinguishable.
• Children younger than 5 years of age.
• Most juvenile polyps are located in the rectum and typically present with rectal
bleeding.
• Sporadic juvenile polyps are usually solitary lesions and may also be referred to as
retention polyps. In contrast, individuals with the autosomal dominant syndrome
of juvenile polyposis have from 3 to as many as 100 hamartomatous polyps and
may require colectomy to limit the chronic and sometimes severe hemorrhage
associated with polyp ulceration.
• A minority of patients also have polyps in the stomach and small bowel that can
undergo malignant transformation.
• Pulmonary arteriovenous malformations and other congenital malformations are
recognized extraintestinal manifestation of juvenile polyposis.
• SMAD 4 gene.
• Less than 3 cm in diameter.
• Typically pedunculated, smooth-surfaced,
reddish lesions with characteristic cystic
spaces on cutting.
• Microscopically these cysts are dilated and
filled with mucin and inflammatory debris.
• Lamina propria expanded by mixed
inflammatory infiltrates.
 Peutz-Jeghers Syndrome
• Autosomal dominant syndrome.
• Median age of 11 years with multiple GI hamartomatous
polyps and mucocutaneous hyperpigmentation involving
buccal mucosa as well.
• Peutz-Jeghers syndrome is associated with a markedly
increased risk of several malignancies.
• Lifetime risk is approximately 40% for these, and regular
surveillance is recommended beginning at birth, for sex
cord tumors of the testes; late childhood for gastric and
small intestinal cancers; and the second and third decades
of life for colon, pancreatic, breast, lung, ovarian, and
uterine cancers.
• Germline mutation in SKT11 gene.
• The polyps of Peutz-Jeghers syndrome are most
common in the small intestine.
• Grossly, the polyps are large and pedunculated with a
lobulated contour.
• Histologic examination demonstrates a characteristic
arborizing network of connective tissue, smooth
muscle, lamina propria, and glands lined by normal-
appearing intestinal epithelium.
• The arborization and presence of smooth muscle
intermixed with lamina propria are helpful in
distinguishing polyps of Peutz-Jeghers syndrome from
juvenile polyps.
 Neoplastic Polyps
• Any neoplastic mass lesion in the GI tract may
produce a mucosal protrusion, or polyp.
• This includes adenocarcinomas,
neuroendocrine (carcinoid) tumors, stromal
tumors, lymphomas, and even metastatic
cancers from distant sites.
• The most common neoplastic polyps are
colonic adenomas, which are precursors to the
majority of colorectal adenocarcinomas.
• Adenomas are intraepithelial neoplasms that
range from small, often pedunculated, polyps
to large sessile lesions.
• Male predominance.
• Precursor to carcinoma
• Regular surviellance (colonoscopy)
 Morphology
• Size: 0.3 to 10 cm in diameter .
• Pedunculated or sessile, with velvety surface.
• Histologically, the hallmark of epithelial dysplasia
is nuclear hyperchromasia, elongation, and
stratification.
• Cellular feature: Prominent nucleoli, eosinophilic
cytoplasm, and a reduction in the number of
goblet cells.
• Pedunculated adenomas have slender
fibromuscular stalks containing prominent blood
vessels derived from the submucosa.
• Adenomas can be classified as tubular,
tubulovillous, or villous based on their
architecture.
 Adenomatous Polyposis
• Familial adenomatous polyposis (FAP) is an
autosomal dominant disorder in which
patients develop numerous colorectal
adenomas as teenagers.
• It is caused by mutations of the adenomatous
polyposis coli, or APC gene.
• At least 100 polyps are necessary for a
diagnosis of classic FAP.
• Colorectal adenocarcinoma develops in 100%
of untreated FAP patients, often before age 30
and nearly always by age 50.
• As a result, prophylactic colectomy is the
standard therapy for individuals carrying APC
mutations.
• Colectomy prevents colorectal cancer, but
patients remain at risk for neoplasia at other
sites.
 Hereditary Non-Polyposis
Colorectal Cancer
• Hereditary non-polyposis colorectal cancer
(HNPCC) or Lynch syndrome, was originally
described based on familial clustering of
cancers at several sites including the
colorectum, endometrium, stomach, ovary,
ureters, brain, small bowel, hepatobiliary
tract, pancreas, and skin.
• HNPCC is thought to account for 2% to 4% of all
colorectal cancers.
• Colon cancers in HNPCC patients tend to occur at
younger ages than sporadic colon cancers and are
often located in the right colon.
• HNPCC is caused by inherited mutations in genes that
encode proteins responsible for the detection, excision,
and repair of errors that occur during DNA replication.
• There are at least five such mismatch repair genes, but
majority of patients with HNPCC have mutations in
MSH2 or MLH1.