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Other Causes of Chronic Colitis

Disease General Description Pathogenesis Morphology Clinical features


Diversion colitis Occurs in the blind distal mucosal erythema and
colonic segment created friability with
after surgery diverts the lymphoplasmacytic
fecal stream to an ostomy inflammation
site
characteristic lymphoid
follicular hyperplasia
Microscopic colitis Endoscopic findings are There are two forms: Occurs typically in middle-
grossly normal, hence • Collagenous colitis: aged women
the designation dense submucosal band-
microscopic colitis like collagen with mixed chronic
inflammation in the lamina watery diarrhea and
propria. abdominal pain
• Lymphocytic colitis:
prominent intraepithelial
infiltrate of lymphocytes
without the band-like
collagen; it is
associated with
autoimmune diseases
and sprue.

Sigmoid Diverticulitis

Disease General Description Pathogenesis Morphology Clinical features


Sigmoid Diverticulitis Focal bowel wall Multiple flasklike Usually asymptomatic but
weakness (at sites of outpouchings that are may be associated
penetrating blood vessels) 0.5 to 1 cm in diameter with cramping, abdominal
allows mucosal discomfort, and
outpouching when there More common in the constipation
is increased intraluminal distal colon
pressure (e.g., with can result in pericolic
constipation and Occur where the abscesses, sinus tracts,
exaggerated peristaltic vasculature penetrates and peritonitis
contractions). the inner circular layer of
the muscularis propria at can cause fibrotic
Obstruction of diverticuli the taeniae coli. thickening and
leads to inflammation stricture formation
producing diverticulitis. The diverticulum wall is
lined by mucosa and
submucosa without
significant muscularis
propria, although the
muscularis between
diverticuli is
hypertrophic.

Polyps

 Masses that protrude into the gut lumen can be pedunculated or sessile and can be non-neoplastic or neoplastic.

Disease General Description Pathogenesis Morphology Clinical features


Non-neoplastic
Inflammatory polyps result from recurrent lamina propria
cycles of injury and fibromuscular hyperplasia,
healing mixed inflammatory
cell infiltrates, and
mucosal erosion and/or
hyperplasia
Hamartomatous polyps
 Juvenile polyps focal hamartomatous Mutations in typically single, large (1 to most occur in children
malformations SMAD4 and BMPR1A 3 cm), rounded, and younger than 5 years
of small intestine and genes involved in TGF-b pedunculated with and involve the rectum
colon mucosa signaling cystically dilated glands
and abundant lamina
propria.
 Juvenile rare autosomal dominant may require colectomy to increased
polyposis disorder characterized by limit bleeding due to polyp risk of colonic
syndrome up to 100 hamartomatous ulceration, and adenocarcinoma
polyps. pulmonary
arteriovenous
malformations are a
known extra-intestinal
manifestation.
 Peutz-Jeghers rare autosomal dominant heterozygous small bowel more than Hyperpigmented
syndrome syndrome (median age of loss-of-function mutation colon and stomach macules around the
onset is 11 years) in the LKB1/STK11 gene affected mouth, eyes, nostrils,
associated with multiple encoding buccal mucosa, palms,
gastrointestinal a kinase that regulates cell polyps are large, and gen-
hamartomatous polyps polarization and growth pedunculated, and ital and perianal regions
and mucocutaneuos lobulated with arborizing
hyperpigmentation smooth muscle increased risk of
surrounding normal several cancers
abundant glands including colon, pancreas,
breast, lung, gonads, and
can initiate uterus
intussusception

 Cowden loss-of-function mutations • Cowden syndrome:


syndrome and in PTEN,encoding a gastrointestinal polyps,
Bannayan- phosphatase that inhibits macrocephaly, and benign
Ruvalcaba-Riley signaling through the skin tumors; patients are
syndrome PI3K/AKT pathway. at increased risk of breast,
thyroid, and endometrial
cancers.
• Bannayan-Ruvalcaba-
Riley syndrome: patients
have similar
manifestations as for
Cowden syndrome, but
they also have mental
deficiency and
developmental delays,
while their risk
of malignancy is less.
 Cronkhite- rare non-hereditary Polyps histologically develops in individuals
Canada syndrome of unknown resemble juvenile polyps older than 50 years
syndrome etiology
cachexia, diarrhea, and
abdominal pain, as well as
nail atrophy, hair loss, and
skin pigmentation changes

despite nutritional
support, there is 50%
mortality.
Hyperplastic polyps result from decreased no malignant potential
epithelial turnover with
delayed shedding smaller than 5 mm and
are composed of well-
formed mature crowded
glands
Neoplastic polyps Colonic adenomas are Risk of malignancy is incidence of adenomas
benign polyp precursors to correlated to size (i.e,. approaches 50% by age
the majority of polyps more than 4 cm 50 years, but majority do
colorectal carcinomas have a 40% risk harboring not progress to
cancer) and severity of malignancy
dysplasia
most are clinically
range from 0.3 to 10 cm silent although large
and can be pedunculated specimens can cause
or sessile anemia

classified based on
architecture (tubular,
tubulovillous, and villous),
although these have little
clinical significance
• Sessile serrated
adenomas: full gland
length exhibits serrated
architecture; despite
malignant potential, they
do not have the
typical dysplastic
changes seen in other
adenomas.
• Intramucosal
carcinoma: occurs when
dysplastic cells invade the
lamina propria or
muscularis mucosa; little
metastatic potential
since colonic mucosa lack
lymphatic channels.
• Invasive
adenocarcinoma:
malignant and have
metastatic potential
because they have
crossed into submucosa
and can access
lymphatics.