Gastrointestinal tract polyps

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Gastrointestinal tract polyps, also gastrointestinal polyps or GI polyps, are the bread & butter of a GI pathologists workload. Some of 'em are benign... some pre-malignant... some malignant... some weird. Most GI polyps are from the intestine, i.e. intestinal polyps.

Overview - there are four basic types:[1]

  • Hyperplastic - harmless, most common - 90% of all colonic polyps.[2]
  • Hamartomatous - weriod stuff, syndromic things.
  • Inflammatory - think inflammatory bowel disease, AKA pseudopolyps.
  • Adenomatous - premalignant, several types (see below).

Mnemonic: HHI-A.

Diagnostic variability for colorectal polyps is substantial among community pathologists.[3]

Basic approach

  1. Sessile (flat) or polypoid (spherical, possibly has a stalk)?
  2. Nuclear features of adenoma & loss of goblets (hyperchromatic nuclei, nuclei round vs. flat, loss of nuclear stratification)?
  3. Inflammation?
  4. Serrated architecture?

A set of decision trees for GI polyps

Decision tree - GI polyps

 
 
 
 
 
 
 
 
GI
polyp
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Polypoid
(Lollipop-like)
 
 
 
 
 
 
 
 
Sessile
(flat)
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Nuclear changes
 
 
 
No nuc. change
 
 
 
Serrated
 
Not serrated
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Polypoid adenoma
(below)
 
Serrated
 
Not serrated
 
SSA vs. HP
 
Normal vs. VA
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
HP
 
See misc.
polyps (below)
 
 
 
 
 
 
 
 

Notes:

  • Polypoid:
    • Stalk visible (lollipop handle visible) or epithelial surface on three sides (or more).
  • Sessile (flat):
    • "Line of muscularis mucosa" visible +/- test tube-like intestinal crypts.
  • Nuclear changes:
    • Nuclear enlargement (elongation), crowding/pseudostratification, hyperchromasia (more blue) - especially at the surface, i.e. adjacent to the lumen (as opposed to the base of the crypt).

Decision tree - polypoid adenoma

 
 
 
 
Polypoid adenoma
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Serrated
 
 
 
 
 
Non-serrated
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
TSA
 
Tubular arch.
 
Tubulovillous arch.
 
Villous arch.
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
TA
 
TVA
 
VA

Notes:[4]

  • TA, tubular component >75%.
  • VA, villous component >50%.


Decision tree - miscellaneous polyps

 
 
 
 
 
 
Misc. polyps
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Inflam.
 
 
 
 
 
No inflam.
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Benign
 
Inflam. p.
 
Hamart.
 
Benign
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
PJP
 
Juvenile
 
Other

Notes:


Hamartomatous polyps - basic DDx:

  • Juvenile polyp/Retention polyp -- DIES (dilated glands, incr. LP, eroded surface, stalk).
  • Peutz-Jeghers polyp (PJP) - frond-like with all mucosa components .

"Other" includes diagnoses which require history or tissue surround the polyp. These include the polyps seen in:

Tabular comparison of colonic polyps

Overview in two tables

Common colonic polyps

Type Key feature(s) Details Prevalence / prognosis Other DDx Image
Normal mucosa / no pathology test tubes in a rack-like morphology small nuclei, abundant goblet cells common / benign moderate inflammation is normal colonic spirochetes, cryptosporidiosis, microscopic colitis, CMV colitis Normal - low mag. (ohio-state.edu)
Hyperplastic polyp serrated at the surface abundant goblet cells, usu. left colon; no features of SSA common / benign may be syndromic, e.g. hyperplastic polyposis syndrome sessile serrated adenoma HP (WC)
Traditional adenoma nuclear hyperchromasia & pseudostratification / crowding at the luminal aspect decreased goblet cells, usu. polypoid - on a stalk, usu. left colon common / premalignant tubular adenoma, tubulovillous adenoma, villous adenoma traditional serrated adenoma, reactive changes (inflammation) TA - high mag. (WC), TA - low mag. (WC)

Less common

Type Key feature(s) Details Prevalence / prognosis Other DDx Image
Sessile serrated adenoma (SSA) basal crypt dilation & serration boot-shaped crypts, horizontal crypts, branching crypts uncommon / pre-malignant AKA sessile serrated polyp hyperplastic polyp SSA - low mag. (WC)
Traditional serrated adenoma (TSA) nuclear hyperchromasia & pseudostratification / crowding at the surface, serrated, villous-like architecture decreased goblet cells very rare / premalignant called "traditional" to differentiate from SSA traditional serrated adenoma (esp. villous adenoma) TSA - low mag. (WC), TSA - high mag. (WC)
Juvenile polyp (retention polyp) dilated glands, increased lamina propria eroded surface (due to trauma), stalk (polypoid), inflammation - common uncommon / benign if in isolation may be part of juvenile polyposis syndrome inflammatory pseudopolyp Gastric JP - low mag. (WC)
Inflammatory pseudopolyp inflammation, erosion/ulceration adjacent to polyp loss of mucosa adjacent to pseudopolyp uncommon / seen in IBD, increased risk of malignancy only seen in IBD; Dx implies IBD juvenile polyp Image
Peutz-Jeghers polyp (PJP) branching smooth muscle tree-like growth pattern very rare / syndromic; assoc. with cancer PJP not pre-malignant lesion in itself; see Peutz-Jeghers syndrome normal, classically in the small bowel PJP - low mag. (WC)

Common problems

Submucosal invasion

  • This may be difficult to assess histomorphologically; these one should show a friend.

Pseudoinvasion

See pseudoinvasion in colorectal adenomatous polyps.

Early invasion

See high risk features in (colorectal) adenomatous polyps with carcinoma.

Adenomatous vs. hyperplastic

Adenomatous polyps & hyperplastic polyps - a comparison (adapted from Li and Burgart[5]):

Attribute Hyperplastic polyp (HP) Sessile serrated adenoma (SSA) Traditional serrated adenoma (TSA) Traditional adenoma
-tubular adenoma
-tubulovillous adenoma
-villous adenoma
Classic location rectum/left colon right colon rectum/left colon rectum/left colon
Morphology polypoid flat (sessile) polypoid polypoid
Cytologic atypia
-Cigar nuclei
-Hyperchromasia
-Nuclear crowding		 absent absent present present
Location of worst atypia - - basal luminal
Cytoplasm eosinophilic prominent eosinophilia eosinophilic basophilic
Goblet cells abundant common less common less common
Luminal Serration present common present absent
SSA architecture
-Basal crypt serration
-Basal crypt dilation
-Horizonatal crypts
-Branched crypts		 absent present absent absent
Key feature(s) serrated luminal surf. & goblets abnorm. crypt arch. & sessile nuclear atypia & serrated nuclear atypia (luminal)
Image(s) low mag. low mag, low mag. low mag, very high mag. low mag., high mag.

Normal colonic mucosa:

  • Nuclei - round and basally located.
  • Abundant goblet cells.
  • Moderate inflammation.
  • Paneth cells - present in right colon.
  • Glands - straight, no branching; "test tube" shape.

Notes: Left colon refers to the sigmoid colon, descending colon and the distal half of the transverse colon; right colon refers to the cecum, ascending colon and proximal half of the transverse colon.

Normal

Normal colorectal mucosa

General

  • Endoscopists go after anything that is polypoid... and that may be normal.

Microscopic

Features:

  • Test tube like glands.
  • Minimal palisading.
    • Nuclei <3:1 = height:width.
  • No nuclear pseudostratification. †
  • Deep part of crypt is more hyperchromatic than superficial component - important.
    • The surface should be lighter staining than the deeper aspect, i.e. the deeper glands are dark blue and the superficial gland are light blue.

Note:

DDx (colorectal mucosa with minimal changes):

Images:

Sign out

Normal

COLON, 70 CM, BIOPSY:
- COLORECTAL-TYPE MUCOSA WITHIN NORMAL LIMITS.
Mucosa and submucosa
POLYP, SIGMOID COLON, BIOPSY:
- COLONIC MUCOSA AND SUBMUCOSA WITHIN NORMAL LIMITS.

Lymphoid nodule present

POLYP, ASCENDING COLON, BIOPSY:
- COLONIC MUCOSA AND SUBMUCOSA WITHIN NORMAL LIMITS WITH A MORPHOLOGICALLY BENIGN
LYMPHOID NODULE.

Note:

  • Lymphoid nodules manifest endoscopically as a small polypoid protuberances. It is worthwhile to report the presence of lymphoid nodules as they reassure the endoscopist that they probably sampled the abnormality they saw.

Suspected missed lesion

RECTOSIGMOID, BIOPSY:
- COLORECTAL-TYPE MUCOSA WITH A LYMPHOID AGGREGATE.
- NEGATIVE FOR ACTIVE COLITIS.
- NEGATIVE FOR DYSPLASIA AND NEGATIVE FOR MALIGNANCY -- SEE COMMENT.

COMMENT:
The clinical history is noted. This biopsy does not show neoplastic tissue; however, the
biopsy may not be representative of the lesion seen.

Levels were cut and these did not yield additional information. There are no changes to
suggest a chronic colitis.

Correlation with imaging may be useful. A re-biopsy is suggested.

Fecal material

General

  • Common.
  • Associated with poor bowel preparation.
  • Endoscopists go after anything that is polypoid and that may be nothing more than poo.

Microscopic

Features:

  • Plant material:
    • Yellow staining chicken wire-like material - may be linear.
      • Thick cell walls often without cytoplasm and usually without a nucleus.
  • Meat:
    • Eosinophilic honeycomb-like material without nuclei and without inflammation.
      • Essentially ischemic skeletal muscle without inflammation.
  • +/-Microorganisms.
  • +/-Inflammatory cells.

DDx:

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TRANSVERSE COLON, BIOPSY:
- FECAL MATERIAL.
- NO DEFINITE COLONIC MUCOSA IDENTIFIED.

Rectum

RECTUM, BIOPSY:
- FECAL MATERIAL.
- NO DEFINITE RECTAL MUCOSA IDENTIFIED.

Hyperplastic polyp

The stomach lesion is dealt with in hyperplastic polyp of the stomach.
  • Abbreviated HP.

General

Microscopic

Features:[2]

  • Irregular crypt architecture - tortuosity.
  • Serrated epithelial cells (at the surface of the gland) - only colorectal polyps - key feature.
    • Serrated appearance = saw-tooth appearance, epithelium has jagged edge.

Notes:

  • Significant negatives:
    • No nuclear atypia.
    • In the colon goblet cells should be present (as is usual).

DDx:

Images:

Subclassification

  • Usually not subclassified as there is no demonstrated prognostic significance;[8] the subtyping is an academic exercise.

HPs may be subclassified into two groups:[8]

  1. Microvesicular serrated polyps (MVSPs).
  2. Goblet cell serrated polyps (GCSPs).

Features of the HP subtypes:[8]

Subtype Histology Mutations Clinical relevance
Microvesicular microvesicles at the surface, serration
at the surface to the mid portion of glands 		BRAF V600E, CIMP possible sessile serrated adenoma precursor
Goblet cell superficial goblet cells, serration at
the surface 		KRAS unknown; probably benign

Notes:

  • CIMP = CpG island methylation phenotype.

Sign out

COLONIC POLYP, 35 CM, BIOPSY: 
- HYPERPLASTIC POLYP.

COLONIC POLYP, SIGMOID COLON, BIOPSY: 
- HYPERPLASTIC POLYP.

POLYP, RECTUM, BIOPSY: 
- HYPERPLASTIC POLYP.
Numerous hyperplastic polyps
COLONIC POLYP(S), BIOPSY: 
- HYPERPLASTIC POLYP, SEE COMMENT.  

COMMENT: 
Eight pieces of tissue were received.  On microscopy eight pieces of tissue 
are identified and all eight (individually) have the diagnostic features of a
hyperplastic polyp.  If these fragments all represent individual polyps and more
polyps of this type are present in the individual, it raises the possibility of 
a serrated polyposis syndrome.

Micro

Goblet cell type

The sections show colonic-type mucosa with superficial serrations rich in goblet cells. There are no serrations in the crypt base and there is no crypt base dilation. No dysplasia is present.

Generic

The sections show colonic-type mucosa with superficial serrations. There are no serrations in the crypt base and there is no crypt base dilation. No dysplasia is present.

Inflammatory pseudopolyp

  • AKA inflammatory polyp.

General

  • Not a true polyp.
  • The label inflammatory pseudopolyp = inflammatory bowel disease (IBD).
    • If there is no history of IBD... reconsider the diagnosis.

Microscopic

Features:

  • Polypoid shape.
  • Inflammation - esp. neutrophils - key feature.

Negatives:

  • No nuclear atypia.
    • May have focal nuclear hyperchromasia and nuclear enlargement.
  • No dilated glands.

DDx:

Images:

Sign out

SIGMOID COLON POLYP, PERI-DIVERTICULAR, BIOPSY:
- INFLAMMATORY PSEUDOPOLYP.

Micro

The sections show a fragment of colorectal mucosa with focal ulceration, acute inflammation and a well-vascularized stroma with plump stromal cells. Occasional stromal cells have nuclear hyperchromasia.

Adenomatous polyps

Overview

Several types of adenomatous polyps are recognized:

  • Traditional adenomas (have three subtypes):
    1. Tubular adenoma - most common, lowest malignant potential.
    2. Tubulovillous adenoma.
    3. Villous adenoma - highest malignant potential.
  • Sessile serrated adenomas:
    • New kid on the block.
  • Traditional serrated adenomas - nuclear features of 'traditional adenoma' + serrated architecture.

Notes:

Management of (adenomatous colonic) polyps

Follow-up interval for polyps (colonoscopy interval):[9]

  • Normal follow-up (includes presence of hyperplastic polyps): ~10 years.
  • 1-2 low risk (adenomatous) polyps: 5-10 years.
  • 3-10 low risk polyps or a high risk polyp: 3 years.
  • >10 low risk polyps: <3 years.
  • Inadequately removed polyps: <6 months.

Classified as high risk polyp (any of the following):[9]

  • Tubulovillous.
  • Villous.
  • High grade dysplasia.
  • Size >= 1 cm.

Mnemonic: GAS = grade (high), architecture (tubulovillous, villous), size (>1 cm).

Note:

  • High risk polyp, as defined above, is also called advanced adenoma;[10] however, it should be noted that there are different definitions for advanced adenoma (e.g. Winawer & Zauber[11] include early invasive tumours). Thus, it is best to avoid the term.

Pseudoinvasion in colorectal adenomatous polyps

  • AKA pseudoinvasion.

General

  • Mimic of invasion.
  • Pedunculated polyps.[12]
  • Left-sided lesions, esp. sigmoid colon.[13]

Microscopic

Features - classic:[14]

  1. Dysplastic glands surrounded by lamina propria.
  2. Hemosiderin.
  3. Lack of desmoplastic reaction.
  • +/-Cystic spaces with rounded contours without cells floating in them.

Memory device (classic features) LDH:

  • Lamina propria.
  • Desmoplasia lacking.
  • Hemosiderin.

DDx:

High-risk features in (colorectal) adenomatous polyps with carcinoma

Predictors of poor outcome with early submucosal invasion:[15]

  1. High tumour grade.
  2. Lymphovascular invasion.
  3. High-grade tumour budding.
    • Tumour bud = 1-4 cell(s); "high-grade budding" is >=10 tumour buds in a field of 0.385 mm2.[16]
      • If the microscope has a 22 mm eye piece and...
        • A 20x objective, the field is approximately 0.950 mm2 -- to match the area/bud -- it would be 24.68 buds/0.950 mm2.
        • A 40x objective, the field is approximately 0.238 mm2 -- to match the area/bud -- it would be 6.17 buds/0.238 mm2.
  4. Extensive submucosal invasion.
    • >= 4 mm width or >= 2 mm depth.

If none of the above factors is present the risk of lymph node metastasis is < 1%. The presence of one risk factor increases the risk to ~20%. If multiple risk factors are present the chance of lymph node metastases is greater than 35%.[15]

Traditional adenoma

Includes tubular adenoma, tubulovillous adenoma, and villous adenoma.

General

  • Most common group of adenomas in GI tract.

Microscopic

  1. Nuclear changes at the surface (of the mucosa) - key feature.
    • Cigar-shaped (elongated) nucleus (usu. length:width > 3:1) - key feature.
      • Normal nuclei are round.
    • Nuclear crowding/pseudostratification - key feature.
    • Nuclear hyperchromasia (more blue).
    • +/-Loss of nuclear polarity (nuclei no longer on basement membrane).
  2. Loss/decrease of goblet cells (common).
  3. Cytoplasmic hyperchromasia.

Notes:

  • Nuclear changes deep to the surface are non-neoplastic if normal appearing mucosa (with small round nuclei) is superficial to it; mucosa that is more blue and atypical deep and less blue without nuclear atypia at the surface is said to be "maturing".
    • Classically, adenomatous polyps have "reverse maturation":
      • The surface is more hyperchromatic (more blue).
      • The base is more mature (more globlet cells, no nuclear changes -- less blue).
  • Ampullary adenomas often have less prominent pseudostratification and fine chromatin.

Images:

Typing

Subclassified as:[18]

  • Tubular adenoma (most common), tubular component >75%.
  • Villous adenoma (least common ~= 1% of (traditional) adenomas), villous component >50%.
  • Tubulovillous adenoma (uncommon ~5-10% of (traditional) adenomas), villous component >=25% & <=50%.

In other words:

  • Tubular T/V >75% / <25%; Tubulovillous T/V <=75%-50% / 25%-<50%; Villous T/V <=50% / >50%.

Note 1:[18]

  • Most villous adenomas are sessile, i.e. flat.[19]
  • Tubular adenomas tend to be pedunculated, i.e. have a stalk.
  • Villous adenomas have a worse prognosis and warrant closer follow-up.
  • One needs only to remember the criteria for tubular adenomas and villous adenomas, as tubulovillous adenomas are what is left over.
    • Tubular adenomas >75% tubular, Villous adenoma >=50% villous.
  • Historically, there were different definitions for tubular adenoma, tubulovillous adenoma, and villous adenomas.[19]
    • Health Organization (WHO) criteria: villous adenomas >80% villous architecture.

Note 2:

  • There is no formal definition of "villous" architecture.[20]
    • Onlinepathology suggests: slender finger-like projections with length-to-width ratio greater than 4.

Note 3:

  • The term tubular adenoma is used in different contexts; it should not be confused with Sertoli cell nodule (AKA testicular tubular adenoma).

Grading

Adenomas are usually graded with a two-tier system:[21]

Feature Low grade dysplasia (LGD) High grade dysplasia (HGD) Importance
Architecture tubular, minimal focal gland fusion acceptable any of the following: (gland) cribriforming, glandular budding, intraluminal papillary tufting, sheeting (of epithelium), lamina propria invasion † key feature
Cytology usu. no features of HGD any of the following: loss of nuclear stratification, enlarged nuclei, loss of cell polarity, prominent nucleoli, open (clear) chromatin supportive feature, not sufficient alone for HGD

Low power colour can be suggestive of HGD:

Feature Low grade High grade
Colour light blue dark blue

Note:

  • † In the colon, unlike other areas of the GI tract, invasive carcinoma is defined by neoplastic cells through the muscularis mucosae. In all other places, e.g. small bowel, invasive carcinoma is defined by neoplastic cells through the basement membrane.

Image:

Margins

Main article: Surgical margins
  • Some pathologists believe it is impossible to determine margins in polypectomies.
  • Others comment on what they see and then disclaim based on limitations with something like "... margin clear in plane of section."

Haggitt classification

The Haggitt classification is a staging scheme. Surgeons may ask about it 'cause a guy (who probably didn't do a lot of pathology) put it in a widely read surgery textbook. In short:[22][23]

  • 0 - intramucosal carcinoma.
  • 1 - in submucosa but in head of polyp.
  • 2 - neck of polyp.
  • 3 - stalk of polyp.
  • 4 - submucosa of the bowel wall but above muscularis propria.

It is mostly useless; most polyps do not have a discernible neck or stalk.

Note:

  • Dr. Haggitt is known for GI pathology and his tragic demise.[24] He was shot by a resident that was about to be fired.[25][26]

Sign out

Negative for high-grade

COLONIC POLYP, SIGMOID COLON, BIOPSY: 
- TUBULAR ADENOMA.
- NEGATIVE FOR HIGH-GRADE DYSPLASIA.

Tubulovillous adenoma - negative for high-grade

COLONIC POLYP, SIGMOID COLON, BIOPSY: 
- TUBULOVILLOUS ADENOMA.
- NEGATIVE FOR HIGH-GRADE DYSPLASIA.

Villous adenoma - negative for high-grade

COLONIC POLYP, DESCENDING COLON, BIOPSY: 
- VILLOUS ADENOMA.
- NEGATIVE FOR HIGH-GRADE DYSPLASIA.

Focal high-grade

COLONIC POLYP, TRANSVERSE COLON, BIOPSY:
- TUBULAR ADENOMA WITH FOCAL HIGH-GRADE DYSPLASIA.

High-grade

COLONIC POLYP, SIGMOID COLON, BIOPSY: 
- TUBULAR ADENOMA WITH HIGH-GRADE DYSPLASIA.

Assessment of invasion

SIGMOID LESION, 25 CM, BIOPSY: 
- TUBULAR ADENOMA.
- NEGATIVE FOR HIGH-GRADE DYSPLASIA, SEE COMMENT.  

COMMENT: 
No definite submucosa is present; thus, the presence or absence of invasion cannot be assessed.

Fragment counting

COLONIC POLYP, TRANSVERSE COLON, BIOPSY:
- TUBULAR ADENOMA (IN 1/3 TISSUE FRAGMENTS).
- NEGATIVE FOR HIGH-GRADE DYSPLASIA.

Notes

  1. "Negative for high-grade dysplasia and malignancy" is recommended in the Canadian consensus.[21] The reasoning for the first part is: "with low-grade dysplasia" may lead to over treatment by physicians that are not aware that all (traditional) adenomas have low-grade dysplasia.
  2. The phrase "negative for [...] malignancy" is also recommended in the Canadian consensus. This is not endorsed by onlinepathology, as one very frequently does not get submucosa. It is like reporting "negative for muscularis propria invasion" on a urinary bladder biopsy without muscularis propria. Further, the guidelines are inconsistent in that they do not advise "negative for dysplasia and malignancy" for SSAs. If there is clinical suspicion of an invasive malignancy, it is useful to comment that no submucosa is present.

Micro

Tubular-tubulovillous interface

The sections shows colorectal-type mucosa with a tubule-forming epithelium that has cellular pseudostratification and enlarged hyperchromatic nuclei, from the crypt base to the luminal aspect (dysplasia).

No cribriforming of glands, epithelial budding or intraluminal papillary tufting is identified. Goblet cells are present in the dysplastic epithelium. Dysplastic nuclei have an ellipsoid-shape and basally stratified.

A small number of rare finger-like epithelial projections (villi) are noted; however these appear to comprise less than 20% of the sampled tissue. It is possible that the villous component is higher, due to sampling error; thus, this could represent a tubulovillous adenoma.

Tubulovillous adenoma

The sections shows colorectal-type mucosa with a tubule-forming and villous-forming epithelium that has cellular pseudostratification and enlarged hyperchromatic nuclei, from the crypt base to the luminal aspect (dysplasia).

No cribriforming of glands, epithelial budding or intraluminal papillary tufting is identified. Goblet cells are rare in the dysplastic epithelium. Dysplastic nuclei have an ellipsoid-shape and basally stratified.

The villous component is over 25% of the lesion but less than 50% of the lesion.

Traditional serrated adenoma

General

  • Very rare.

Microscopic

Features:

  • Serrated.
  • Nuclear atypia (as in tubular adenoma).
  • Villous architecture.

DDx:

Images:

Sessile serrated adenoma

  • Often abbreviated SSA.
  • AKA sessile serrated polyp, abbreviated SSP.
  • AKA sessile serrated lesion.
  • AKA sessile serrated adenoma/polyp, abbreviated SSA/P.

General

Epidemiology:

  • Thought to lead to colorectal cancer through a different pathway that most tumours in the left colon/rectum.
  • Microvesicular hyperplastic polyps are hypothesized to be the the precursor of SSAs.[8]

Microscopic

Features:

  • Serrated.
  • Crypt dilation at base - a key feature - very common.
    • "Boot"-shape or "L"-shaped glands.
  • Crypt branching.
  • Horizontal crypts (crypts that run along the muscular mucosae).

Minimal extent:

  • Onlinepathology likes the German Society of Pathology proposal: at least two different crypts -- crypts do not have to be adjacent.[27][28]
  • An expert panel lead by Rex states that one unequivocally altered crypt should prompt calling SSA.[29]
  • The Stanford Surgical Pathology Criteria note that the WHO requires three adjacent crypts to be abnormal.[27][30]

Notes:

  • Typically do not have nuclear atypia, i.e. no nuclear crowding, no nuclear hyperchromasia, no cigar-shaped nuclei.
    • SSAs with nuclear atypia may be referred to as advanced sessile serrated adenomas.

DDx:

Images:

Sign out

COLONIC POLYP, ASCENDING COLON, BIOPSY: 
- SESSILE SERRATED ADENOMA.
- NEGATIVE FOR DYSPLASIA.

COLONIC POLYP, ASCENDING COLON, BIOPSY: 
- SESSILE SERRATED ADENOMA WITH DYSPLASIA.

Note:

  • The above exactly mirrors the Canadian consensus.[21]

Malignant polyps

Colorectal adenocarcinoma

Main article: Colorectal adenocarcinoma

General

  • Diagnosis may be a challenging on a small biopsy.

Clinical

Invasion can be predicted based on endoscopic findings:

Microscopic

One of the two following:

  1. Usual morphology - features:[34]
    • Nuclear changes seen in adenomatous polyps - malignant-appearing cells.
      • Enlarged nuclei.
      • Chromatin hyperchromatic or vesicular.
      • Round-shape or cigar-shaped and pseudostratified.
    • Architectural changes - usually those of high-grade dysplasia:
      • Cribriforming.
      • Papillary tufting.
      • Budding.
      • Sheeting.
    • Deep involvement - one of the two following - key feature:
      1. Malignant-appearing cells in the submucosa.
        • Pseudoinvasion must be excluded.
      2. Desmoplastic response.
        • Spindle cells with:
          • Large nuclei (nucleus ~ size of a plasma cell).
          • Eosinophilic cytoplasm.
  2. Signet ring cells.

DDx:

Note:

  • Desmoplastic response is not predictive of submucosal invasion in pedunculated polyps.[35]

Image:

Sign out

RECTOSIGMOID TUMOUR, BIOPSY:
- INVASIVE ADENOCARCINOMA, MODERATELY DIFFERENTIATED.

Micro

The sections shows colorectal-type mucosa with a tubule-forming epithelium that has cellular pseudostratification and enlarged hyperchromatic nuclei, from the crypt base to the luminal aspect (dysplasia).

There is cribriforming of glands and epithelial budding. Plump spindle cells with eosinophilic cytoplasm surround the abnormal epithelium (desmoplastic stroma). No definite submucosa is identified; the diagnosis is based on the stromal desmoplasia.

Hamartomatous polyps

Overview

There are three well known hamartomatous polyp syndromes:[36]

There are two obscure hamartomatous polyp syndromes:[36]

  • Bannayan-Riley-Ruvalcaba syndrome (BRBS).
  • Devon polyposis syndrome (DPS).

Notes:

  • BRBS is due to a PTEN mutation[37] (the same gene associated with Cowden's disease).
  • DPS is reported in only one family that lives in Devon, UK.[38]

Juvenile polyp

  • AKA retention polyp in adults.

General

May be part of a syndrome:

Gross

  • Mushroom-like shape.

Microscopic

Features:[39][40]

  • Eroded, smooth or lobulated surface.
  • Pedunculated.
  • Increased lamina propria (LP) +/- edema.
  • Cystically dilated gland.
  • Often inflammed.

Mnemonic DIES = dilated glands, increased LP & inflammation of the LP, eroded/smooth surface, stalk.

Notes:

  • May have nuclear changes like those seen in adenomatous polyps.

DDx:

Images:

IHC

  • Usually none.

Notes:

  • IHC can be used if it is suspected to have dysplasia (p53, Ki-67).
    • p53 mutations in dysplastic epithelium -- negative stain (normal).

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RECTOSIGMOID POLYP, BIOPSY: 
- RETENTION POLYP.

Peutz-Jeghers polyp

General

Epidemiology

Features:[39][40]

Clinical

Features:[41]

  • Melanocytic macules.
    • Lips, buccal mucosa, and digits.
    • Multiple Peutz-Jeghers polyps.

Increased risk of various neoplasms - primarily:

Microscopic

Features:[39][40]

  • Frond-like polyp with all three components of mucosa:
    1. Muscosal epithelium (melanotic mucosa, goblet cells).
    2. Lamina propria.
    3. M. mucosae.

Notes:

  • Frond = leaflike expansion.[44]
    • The key is "thick" smooth muscle bundles - if one is lucky one sees branching.[45]
      • "Thick" ~= thickness of muscularis mucosae.

Images:

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Duodenum

POLYPS, DUODENUM, EXCISION:
- PEUTZ-JEGHERS POLYPS (x2) WITH BRUNNER'S GLANDS.
- NEGATIVE FOR DYSPLASIA AND NEGATIVE FOR MALIGNANCY.

Colon

 POLYP, COLON (40 CM), EXCISION:
- PEUTZ-JEGHERS POLYP.
- NEGATIVE FOR DYSPLASIA AND NEGATIVE FOR MALIGNANCY.

Cowden disease

Main article: Cowden syndrome
  • AKA Cowden syndrome.

General

Etiology:

  • PTEN gene mutation.

Clinical features:[46]

  • Hamartomatous polyps.
  • Facial trichilemmomas (hair follicle root sheath epithelium tumour).
  • Oral papillomas.
  • Acral keratoses (peripheral keratoses).

Note:

  • Lame mnemonic PATH:[47] Papilloma (oral), Acral keratosis, Trichilemmoma, Hamartomatous polyps.

Microscopic

Features:

  • Hamartomatous polyp - features non-specific. (???)

Weird stuff

Cronkhite-Canada syndrome

  • Abbreviated CCS.

General

Clinical features:[48]

  • Hamartomatous polyps.
  • Ectodermal abnormalities (nail atrophy, skin pigment, alopecia).

Microscopic

Features:

  • Polyps have same morphology as juvenile polyps/retension polyps.
  • Crypt dilation and edema in non-polypoid mucosa[49] - key feature.

DDx:

Images:

Ganglioneuroma

Main article: Ganglioneuroma

General

Microscopic

Features - see ganglioneuroma:

  • Ganglion cells - key feature.
    • Large cells with a round nucleus and a prominent nucleolus.

Images:

Inflammatory myoglandular polyp

General

  • Controversial - probably not a distinct pathologic entity.[50]
  • Rare, benign, non-neoplastic.[51]
  • Large bowel, usually rectosigmoid.

Microscopic

Features:[52]

  1. Granulation tissue within the lamina propria.
  2. Lamina propria smooth muscle.
  3. Irregular gland architecture:
    • Cystic dilatation.
    • Tortuosity.

DDx:[50]

Image:

See also

References

  1. ↑ Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, Mo: Elsevier Saunders. pp. 856. ISBN 0-7216-0187-1.
  2. ↑ 2.0 2.1 2.2 Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, Mo: Elsevier Saunders. pp. 858. ISBN 0-7216-0187-1.
  3. ↑ Rex, DK.; Alikhan, M.; Cummings, O.; Ulbright, TM. (Oct 1999). "Accuracy of pathologic interpretation of colorectal polyps by general pathologists in community practice.". Gastrointest Endosc 50 (4): 468-74. PMID 10502165.
  4. ↑ Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, Mo: Elsevier Saunders. pp. 860. ISBN 0-7216-0187-1.
  5. ↑ Li SC, Burgart L (March 2007). "Histopathology of serrated adenoma, its variants, and differentiation from conventional adenomatous and hyperplastic polyps". Arch. Pathol. Lab. Med. 131 (3): 440-5. PMID 17516746. http://journals.allenpress.com/jrnlserv/?request=get-abstract&issn=0003-9985&volume=131&page=440.
  6. ↑ URL: http://www.lab.anhb.uwa.edu.au/mb140/CorePages/GIT/git.htm. Accessed on: 18 October 2012.
  7. ↑ Jain, R.; Chetty, R. (Sep 2009). "Gastric hyperplastic polyps: a review.". Dig Dis Sci 54 (9): 1839-46. doi:10.1007/s10620-008-0572-8. PMID 19037727.
  8. ↑ 8.0 8.1 8.2 8.3 8.4 Huang, CS.; Farraye, FA.; Yang, S.; O'Brien, MJ. (Feb 2011). "The clinical significance of serrated polyps.". Am J Gastroenterol 106 (2): 229-40; quiz 241. doi:10.1038/ajg.2010.429. PMID 21045813.
  9. ↑ 9.0 9.1 Levine JS, Ahnen DJ (December 2006). "Clinical practice. Adenomatous polyps of the colon". N. Engl. J. Med. 355 (24): 2551–7. doi:10.1056/NEJMcp063038. PMID 17167138. http://content.nejm.org/cgi/reprint/355/24/2551.pdf.
  10. ↑ Laiyemo, AO.; Murphy, G.; Albert, PS.; Sansbury, LB.; Wang, Z.; Cross, AJ.; Marcus, PM.; Caan, B. et al. (Mar 2008). "Postpolypectomy colonoscopy surveillance guidelines: predictive accuracy for advanced adenoma at 4 years.". Ann Intern Med 148 (6): 419-26. PMID 18347350.
  11. ↑ Winawer, SJ.; Zauber, AG. (Jan 2002). "The advanced adenoma as the primary target of screening.". Gastrointest Endosc Clin N Am 12 (1): 1-9, v. PMID 11916153.
  12. ↑ Byun, TJ.; Han, DS.; Ahn, SB.; Cho, HS.; Eun, CS.; Jeon, YC.; Sohn, JH.; Oh, YH. (Jun 2009). "Pseudoinvasion in an adenomatous polyp of the colon mimicking invasive colon cancer.". Gut Liver 3 (2): 130-3. doi:10.5009/gnl.2009.3.2.130. PMC PMC2852693. PMID 20431736. https://www.ncbi.nlm.nih.gov/pmc/articles/PMCPMC2852693/.
  13. ↑ Odze, Robert D.; Goldblum, John R. (2009). Surgical pathology of the GI tract, liver, biliary tract and pancreas (2nd ed.). Saunders. pp. 512. ISBN 978-1416040590.
  14. ↑ Muto, T.; Bussey, HJ.; Morson, BC. (Jan 1973). "Pseudo-carcinomatous invasion in adenomatous polyps of the colon and rectum.". J Clin Pathol 26 (1): 25-31. PMC 477644. PMID 4540378. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC477644/.
  15. ↑ 15.0 15.1 Ueno, H.; Mochizuki, H.; Hashiguchi, Y.; Shimazaki, H.; Aida, S.; Hase, K.; Matsukuma, S.; Kanai, T. et al. (Aug 2004). "Risk factors for an adverse outcome in early invasive colorectal carcinoma.". Gastroenterology 127 (2): 385-94. PMID 15300569.
  16. ↑ Ueno, H.; Murphy, J.; Jass, JR.; Mochizuki, H.; Talbot, IC. (Feb 2002). "Tumour 'budding' as an index to estimate the potential of aggressiveness in rectal cancer.". Histopathology 40 (2): 127-32. PMID 11952856.
  17. ↑ URL: http://daveproject.org/colon-cancer-prevention-flat-lesion-and-endoscopic-mucosal-resection/2011-06-10/. Accessed on: 24 August 2012.
  18. ↑ 18.0 18.1 Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, Mo: Elsevier Saunders. pp. 860. ISBN 0-7216-0187-1.
  19. ↑ 19.0 19.1 URL: http://emedicine.medscape.com/article/170283-overview.
  20. ↑ R. Riddell. 12 August 2011.
  21. ↑ 21.0 21.1 21.2 Driman, DK.; Marcus, VA.; Hilsden, RJ; Owen, DA (2012). "Pathologic reporting of colorectal polyps: pan-Canadian consensus guidelines". Canadian Journal of Pathology 4 (3): 81-90.
  22. ↑ URL: http://www.ganfyd.org/index.php?title=Haggitt_classification. Accessed on: 19 March 2011.
  23. ↑ Haggitt, RC.; Glotzbach, RE.; Soffer, EE.; Wruble, LD. (Aug 1985). "Prognostic factors in colorectal carcinomas arising in adenomas: implications for lesions removed by endoscopic polypectomy.". Gastroenterology 89 (2): 328-36. PMID 4007423.
  24. ↑ Rodger C. Haggitt Endowed Chair in Gastroenterology. URL: http://depts.washington.edu/givemed/prof-chair/endowments/rodger-haggitt/. Accessed on: February 2, 2013.
  25. ↑ Two die in UW medical school shooting. seattlepi.com. URL: http://community.seattletimes.nwsource.com/archive/?date=20000629&slug=4029355. Accessed on: 4 February 2013.
  26. ↑ URL: http://www.washington.edu/alumni/columns/sept00/choices.html. Accessed on: 4 February 2013.
  27. ↑ 27.0 27.1 Ensari, A.; Bilezikçi, B.; Carneiro, F.; Doğusoy, GB.; Driessen, A.; Dursun, A.; Flejou, JF.; Geboes, K. et al. (Nov 2012). "Serrated polyps of the colon: how reproducible is their classification?". Virchows Arch 461 (5): 495-504. doi:10.1007/s00428-012-1319-7. PMID 23052370.
  28. ↑ Aust, DE.; Baretton, GB. (Sep 2010). "Serrated polyps of the colon and rectum (hyperplastic polyps, sessile serrated adenomas, traditional serrated adenomas, and mixed polyps)-proposal for diagnostic criteria.". Virchows Arch 457 (3): 291-7. doi:10.1007/s00428-010-0945-1. PMID 20617338.
  29. ↑ Rex, DK.; Ahnen, DJ.; Baron, JA.; Batts, KP.; Burke, CA.; Burt, RW.; Goldblum, JR.; Guillem, JG. et al. (Sep 2012). "Serrated lesions of the colorectum: review and recommendations from an expert panel.". Am J Gastroenterol 107 (9): 1315-29; quiz 1314, 1330. doi:10.1038/ajg.2012.161. PMID 22710576.
  30. ↑ URL: http://surgpathcriteria.stanford.edu/gitumors/sessile-serrated-polyp-adenoma/. Accessed on: 26 September 2012.
  31. ↑ Onishi, T.; Tamura, S.; Kuratani, Y.; Onishi, S.; Yasuda, N. (2008). "Evaluation of the depth score of type V pit patterns in crypt orifices of colorectal neoplastic lesions.". J Gastroenterol 43 (4): 291-7. doi:10.1007/s00535-008-2161-1. PMID 18458845.
  32. ↑ Uno, Y.; Munakata, A.. "The non-lifting sign of invasive colon cancer.". Gastrointest Endosc 40 (4): 485-9. PMID 7926542.
  33. ↑ Ishiguro, A.; Uno, Y.; Ishiguro, Y.; Munakata, A.; Morita, T. (Sep 1999). "Correlation of lifting versus non-lifting and microscopic depth of invasion in early colorectal cancer.". Gastrointest Endosc 50 (3): 329-33. doi:10.1053/ge.1999.v50.98591. PMID 10462651.
  34. ↑ Kimura, R.; Fujimori, T.; Ichikawa, K.; Ajioka, Y.; Ueno, H.; Ohkura, Y.; Kashida, H.; Togashi, K. et al. (Aug 2012). "Desmoplastic reaction in biopsy specimens of early colorectal cancer: a Japanese prospective multicenter study.". Pathol Int 62 (8): 525-31. doi:10.1111/j.1440-1827.2012.02840.x. PMID 22827760.
  35. ↑ Hirose, M.; Fukui, H.; Igarashi, Y.; Fujimori, Y.; Katake, Y.; Sekikawa, A.; Ichikawa, K.; Tomita, S. et al. (Dec 2010). "Detection of desmoplastic reaction in biopsy specimens is useful for predicting the depth of invasion of early colorectal cancer: a Japanese collaborative study.". J Gastroenterol 45 (12): 1212-8. doi:10.1007/s00535-010-0288-3. PMID 20665053.
  36. ↑ 36.0 36.1 Iacobuzio-Donahue, Christine A.; Montgomery, Elizabeth A. (2005). Gastrointestinal and Liver Pathology: A Volume in the Foundations in Diagnostic Pathology Series (1st ed.). Churchill Livingstone. pp. 345. ISBN 978-0443066573.
  37. ↑ Online 'Mendelian Inheritance in Man' (OMIM) 153480
  38. ↑ Allibone, RO.; Nanson, JK.; Anthony, PP. (Jul 1992). "Multiple and recurrent inflammatory fibroid polyps in a Devon family ('Devon polyposis syndrome'): an update.". Gut 33 (7): 1004-5. PMID 1644320.
  39. ↑ 39.0 39.1 39.2 Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, Mo: Elsevier Saunders. pp. 859. ISBN 0-7216-0187-1.
  40. ↑ 40.0 40.1 40.2 Bronner, MP. (Apr 2003). "Gastrointestinal inherited polyposis syndromes.". Mod Pathol 16 (4): 359-65. doi:10.1097/01.MP.0000062992.54036.E4. PMID 12692201. http://www.nature.com/modpathol/journal/v16/n4/full/3880773a.html.
  41. ↑ URL: http://www.ncbi.nlm.nih.gov/omim/175200. Accessed on: 13 July 2010.
  42. ↑ Beggs AD, Latchford AR, Vasen HF, et al. (July 2010). "Peutz-Jeghers syndrome: a systematic review and recommendations for management". Gut 59 (7): 975–86. doi:10.1136/gut.2009.198499. PMID 20581245.
  43. ↑ URL: http://www.ncbi.nlm.nih.gov/omim/175200. Accessed on: 22 December 2010.
  44. ↑ URL: http://dictionary.reference.com/browse/frond. Accessed on: 26 July 2011.
  45. ↑ C. Streutker. 26 July 2011.
  46. ↑ Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, Mo: Elsevier Saunders. pp. 858-9. ISBN 0-7216-0187-1.
  47. ↑ URL: http://www.pathologyexpert.com/boards/onlinefiles/syndromes.htm. Accessed on: 6 December 2011.
  48. ↑ Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, Mo: Elsevier Saunders. pp. 858-9. ISBN 0-7216-0187-1.
  49. ↑ Mitchell, Richard; Kumar, Vinay; Fausto, Nelson; Abbas, Abul K.; Aster, Jon (2011). Pocket Companion to Robbins & Cotran Pathologic Basis of Disease (8th ed.). Elsevier Saunders. pp. 430. ISBN 978-1416054542.
  50. ↑ 50.0 50.1 Bhathal, PS.; Chetty, R.; Slavin, JL. (Aug 1993). "Myoglandular polyps.". Am J Surg Pathol 17 (8): 852-3. PMID 8338196.
  51. ↑ 51.0 51.1 Meniconi, RL.; Caronna, R.; Benedetti, M.; Fanello, G.; Ciardi, A.; Schiratti, M.; Papini, F.; Farelli, F. et al. (2010). "Inflammatory myoglandular polyp of the cecum: case report and review of literature.". BMC Gastroenterol 10: 10. doi:10.1186/1471-230X-10-10. PMC 2828397. PMID 20102635. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2828397/.
  52. ↑ Nakamura, S.; Kino, I.; Akagi, T. (Aug 1992). "Inflammatory myoglandular polyps of the colon and rectum. A clinicopathological study of 32 pedunculated polyps, distinct from other types of polyps.". Am J Surg Pathol 16 (8): 772-9. PMID 1309176.

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