Gastrointestinal tract polyps
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
- Sessile (flat) or polypoid (spherical, possibly has a stalk)?
- Nuclear features of adenoma & loss of goblets (hyperchromatic nuclei, nuclei round vs. flat, loss of nuclear stratification)?
- Inflammation?
- 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:
- Juvenile polyps may have marked inflammation.
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
Early invasion
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
General
- Endoscopists go after anything that is polypoid... and that may be normal.
Normal colon
Microscopic
Features:
- Test tube like glands.
- Minimal palisading.
- Nuclei <3:1 = height:width.
- No nuclear pseudostratification.
- Deep part of crypt more hyperchromatic than superficial component.
Images:
- Normal colorectal mucosa (uwa.edu.au).[6]
- Colon (siumed.edu).
- Normal colon adjacent to a tubular adenoma (WC).
- Normal colorectal mucosa (maricopa.edu).
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Normal
COLON, 70 CM, BIOPSY: - COLORECTAL-TYPE MUCOSA WITHIN NORMAL LIMITS.
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.
Hyperplastic polyp
- The stomach lesion is dealt with in hyperplastic polyp of the stomach.
General
- Most common type of polyp:
- Approximately 90% of all colonic polyps.[2]
- Most common type of gastric polyp.[7]
- May be part of hyperplastic polyposis syndrome.[8]
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:
- WC:
- www:
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]
- Microvesicular serrated polyps (MVSPs).
- 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.
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COLONIC POLYP, 35 CM, BIOPSY: - HYPERPLASTIC POLYP.
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:
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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):
- Tubular adenoma - most common, lowest malignant potential.
- Tubulovillous adenoma.
- Villous adenoma - highest malignant potential.
- Sessile serrated adenomas:
- New kid on the block.
- Traditional serrated adenomas - nuclear features of 'traditional adenoma' + serrated architecture.
Notes:
- They are all considered pre-malignant, i.e. if you leave 'em in place they often develop into cancer.
- If multiple... think about familial adenomatous polyposis (FAP), attenuated FAP, MUTYH polyposis syndrome, serrated polyposis syndrome.
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
Microscopic
Features:[14]
- Glands surrounded by lamina propria.
- Hemosiderin.
- Lack of desmoplastic reaction.
Memory device LDH:
- Lamina propria.
- Desmoplasia lacking.
- Hemosiderin.
High-risk features in (colorectal) adenomatous polyps with carcinoma
Predictors of poor outcome with early submucosal invasion:[15]
- High tumour grade.
- Lymphovascular invasion.
- 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.
- If the microscope has a 22 mm eye piece and...
- Tumour bud = 1-4 cell(s); "high-grade budding" is >=10 tumour buds in a field of 0.385 mm2.[16]
- 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
- 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).
- Cigar-shaped (elongated) nucleus (usu. length:width > 3:1) - key feature.
- Loss/decrease of goblet cells (common).
- 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).
- Classically, adenomatous polyps have "reverse maturation":
- Ampullary adenomas often have less prominent pseudostratification and fine chromatin.
Images:
- WC:
- www:
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]
- VL 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 adenomas 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
- 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."
The Haggitt classification is margin call taken to the extreme. 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 a little scheme that is mostly useless. In the real world surgical pathology most polyps do not have a discernible neck or stalk.
Note:
- Dr. Haggitt is know for his tragic demise. He was shot by a resident that was about to be fired.[24]
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Negative for high-grade
COLONIC POLYP, SIGMOID COLON, BIOPSY: - TUBULAR ADENOMA, NEGATIVE FOR HIGH-GRADE DYSPLASIA.
Negative for high-grade - tubulovillous adenoma
COLONIC POLYP, SIGMOID COLON, BIOPSY: - TUBULOVILLOUS 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, NEGATIVE FOR HIGH-GRADE DYSPLASIA (IN 1/3 TISSUE FRAGMENTS).
Notes:
- "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.
- The phrase "negative for [...] malignancy" is also recommended in the Canadian consensus. This is not endorsed here, as one very frequently does not get submucosa. It is like reporting "negative for submucosal invasion" on gastric biopsies. Further, 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
- Colonic lesion.
- More common in the right colon, i.e. ascending colon.
- May be seen in the context of serrated polyposis syndrome.
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).
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.
- The Stanford Surgical Pathology Criteria[25] require three adjacent crypts to be abnormal.
DDx:
- Hyperplastic polyp.
- Tubular adenoma - for SSA with dysplasia, TAs often less than 1 cm (uncommon for SSAs).
Images:
- SSA - low mag. (WC/Nephron).
- SSA - intermed. mag. (WC/Nephron).
- SSA - high mag. (WC/Nephron).
- SSA - low mag. (WC/Nephron).
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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
General
- May be a challenging diagnosis on a small biopsy.
Microscopic
Features:[26]
- Desmoplastic response - key feature.
- Spindle cells with large nuclei.
- Nuclei ~ size of a plasma cell.
- Eosinophilic cytoplasm.
- Spindle cells with large nuclei.
- Nuclear changes seen in adenomatous polyps.
- Enlarged.
- Chromatin hyperchromatic or vesicular.
- Round-shap or cigar-shaped and pseudostratified.
- Architectural changes - usually those of high-grade dysplasia:
- Cribriforming.
- Papillary tufting.
- Budding.
DDx:
- Pseudoinvasion - surrounded by lamina propria, desmoplasia lacking, hemosiderin-laden macrophages.
Note:
- Desmoplastic response is not predictive of submucosal invasion in pedunculated polyps.[27]
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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:[28]
There are two obscure hamartomatous polyp syndromes:[28]
- Bannayan-Riley-Ruvalcaba syndrome (BRBS).
- Devon polyposis syndrome (DPS).
Notes:
- BRBS is due to a PTEN mutation[29] (the same gene associated with Cowden's disease).
- DPS is reported in only one family that lives in Devon, UK.[30]
Juvenile polyp
- AKA retention polyp in adults.
General
May be part of a syndrome:
- Juvenile polyposis syndrome (JPS) - see JPS article for criteria.
- Cronkhite-Canada syndrome.
- Cowden syndrome.
Gross
- Mushroom-like shape.
Microscopic
- 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:
- Inflammatory polyp.
- Hyperplastic polyp of the stomach - less lamina propria, foveolar hyperplasia (long tortuous glands).
Images:
- Juvenile polyp (nature.com).
- Juvenile polyp of the stomach - very low mag. (WC)
- Juvenile polyp of the stomach - very low mag. (WC).
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
- Peutz-Jeghers syndrome is autosomal dominant.
- Altered gene: STK11.
Clinical
Features:[33]
- Melanocytic macules.
- Lips, buccal mucosa, and digits.
- Multiple Peutz-Jeghers polyps.
Increased risk of various neoplasms - primarily:
- Breast and gastrointestinal cancer.[34]
- Others tumours:[35]
- Granulosa cell tumour.
- Sertoli cell tumour - esp. with calcification.
Microscopic
- Frond-like polyp with all three components of mucosa:
- Muscosal epithelium (melanotic mucosa, goblet cells).
- Lamina propria.
- M. mucosae.
Notes:
- Frond = leaflike expansion.[36]
- The key is "thick" smooth muscle bundles - if one is lucky one sees branching.[37]
- "Thick" ~= thickness of muscularis mucosae.
- The key is "thick" smooth muscle bundles - if one is lucky one sees branching.[37]
Images:
- Peutz-Jeghers polyp - intestine (WC).
- Peutz-Jeghers polyp - stomach (WC).
- Peutz-Jeghers polyp (nature.com).
Cowden disease
- AKA Cowden syndrome.
General
Etiology:
- PTEN gene mutation.
Clinical features:[38]
- Hamartomatous polyps.
- Facial trichilemmomas (hair follicle root sheath epithelium tumour).
- Oral papillomas.
- Acral keratoses (peripheral keratoses).
Note:
- Lame mnemonic PATH:[39] Papilloma (oral), Acral keratosis, Trichilemmoma, Hamartomatous polyps.
Microscopic
Features:
- Hamartomatous polyp - features non-specific. (???)
Weird stuff
Cronkhite-Canada syndrome
- Abbreviated CCS.
General
Clinical features:[40]
- Hamartomatous polyps.
- Ectodermal abnormalities (nail atrophy, skin pigment, alopecia).
Microscopic
Features:
- Polyps have same morphology as juvenile polyp/retension polyp.
- Crypt dilation and edema in non-polypoid mucosa[41] - key feature.
Images:
Ganglioneuroma
General
- May be part of MEN 2B.
Microscopic
Features - see ganglioneuroma:
- Ganglion cells - key feature.
- Large cells with a round nucleus and a prominent nucleolus.
Images:
- Ganglioneuroma - intermed. mag. (WC).
- Ganglioneuroma - high mag. (WC).
- Ganlioneuroma - very high mag. (WC).
Inflammatory myoglandular polyp
General
- Controversial - probably not a distinct pathologic entity.[42]
- Rare, benign, non-neoplastic.[43]
- Large bowel, usually rectosigmoid.
Microscopic
Features:[44]
- Granulation tissue within the lamina propria.
- Lamina propria smooth muscle.
- Irregular gland architecture:
- Cystic dilatation.
- Tortuosity.
DDx:[42]
- Mucosal prolapse syndrome.
- Polypoid prolaping mucosal fold in diverticular disease.
- Inflammatory cloacogenic polyp.
- Inflammatory cap polyp.
Image:
See also
References
- ↑ 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.
- ↑ 2.0 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ URL: http://www.lab.anhb.uwa.edu.au/mb140/CorePages/GIT/git.htm. Accessed on: 18 October 2012.
- ↑ 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.
- ↑ 8.0 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.
- ↑ 9.0 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.
- ↑ 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.
- ↑ 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.
- ↑ 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/.
- ↑ 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.
- ↑ 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/.
- ↑ 15.0 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.
- ↑ 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.
- ↑ URL: http://daveproject.org/colon-cancer-prevention-flat-lesion-and-endoscopic-mucosal-resection/2011-06-10/. Accessed on: 24 August 2012.
- ↑ 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.
- ↑ 19.0 19.1 URL: http://emedicine.medscape.com/article/170283-overview.
- ↑ R. Riddell. 12 August 2011.
- ↑ 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.
- ↑ URL: http://www.ganfyd.org/index.php?title=Haggitt_classification. Accessed on: 19 March 2011.
- ↑ 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.
- ↑ Two die in UW medical school shooting. seattlepi.com. URL: http://www.seattlepi.com/local/pathweb.shtml. Accessed on: April 23, 2009.
- ↑ URL: http://surgpathcriteria.stanford.edu/gitumors/sessile-serrated-polyp-adenoma/. Accessed on: 26 September 2012.
- ↑ 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.
- ↑ 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.
- ↑ 28.0 28.1 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.
- ↑ Online 'Mendelian Inheritance in Man' (OMIM) 153480
- ↑ 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.
- ↑ 31.0 31.1 31.2 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.
- ↑ 32.0 32.1 32.2 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.
- ↑ URL: http://www.ncbi.nlm.nih.gov/omim/175200. Accessed on: 13 July 2010.
- ↑ 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.
- ↑ URL: http://www.ncbi.nlm.nih.gov/omim/175200. Accessed on: 22 December 2010.
- ↑ URL: http://dictionary.reference.com/browse/frond. Accessed on: 26 July 2011.
- ↑ C. Streutker. 26 July 2011.
- ↑ 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.
- ↑ URL: http://www.pathologyexpert.com/boards/onlinefiles/syndromes.htm. Accessed on: 6 December 2011.
- ↑ 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.
- ↑ 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.
- ↑ 42.0 42.1 Bhathal, PS.; Chetty, R.; Slavin, JL. (Aug 1993). "Myoglandular polyps.". Am J Surg Pathol 17 (8): 852-3. PMID 8338196.
- ↑ 43.0 43.1 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/.
- ↑ 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.
External links
- Serrated polyps quiz (unibas.ch) - nice quiz... though it is annoying that one has to click on the images to enlarge 'em.