Difference between revisions of "Gastrointestinal tract polyps"
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Increased risk of various neoplasms - primarily: | Increased risk of various neoplasms - primarily: | ||
*Breast and gastrointestinal cancer.<ref name=pmid20581245>{{cite journal |author=Beggs AD, Latchford AR, Vasen HF, ''et al.'' |title=Peutz-Jeghers syndrome: a systematic review and recommendations for management |journal=Gut |volume=59 |issue=7 |pages=975–86 |year=2010 |month=July |pmid=20581245 |doi=10.1136/gut.2009.198499 |url=}}</ref> | *Breast and gastrointestinal cancer.<ref name=pmid20581245>{{cite journal |author=Beggs AD, Latchford AR, Vasen HF, ''et al.'' |title=Peutz-Jeghers syndrome: a systematic review and recommendations for management |journal=Gut |volume=59 |issue=7 |pages=975–86 |year=2010 |month=July |pmid=20581245 |doi=10.1136/gut.2009.198499 |url=}}</ref> | ||
*Others tumours:<ref>URL: [http://www.ncbi.nlm.nih.gov/omim/175200 http://www.ncbi.nlm.nih.gov/omim/175200]. Accessed on: 22 December 2010.</ref> | |||
**[[Granulosa cell tumour]]. | |||
**[[Sertoli cell tumour]] - esp. with calcification. | |||
===Microscopy=== | ===Microscopy=== | ||
Revision as of 21:42, 22 December 2010
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.
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?
Decision tree for GI polyps
Decision tree - GI polyps
| GI polyp | |||||||||||||||||||||||||||||||||||||||
| Polypoid (Lollipop-like) | Sessile (flat) | ||||||||||||||||||||||||||||||||||||||
| Nuclear features | No nuc. change | Serrated | Not serrated | ||||||||||||||||||||||||||||||||||||
| Polypoid a. | 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.
Decision tree - polypoid adenoma
| Polypoid adenoma | |||||||||||||||||||||||||||||||
| Serrated | Non-serrated | ||||||||||||||||||||||||||||||
| TSA | Tubular arch. | Tubulovillous arch. | Villous arch. | ||||||||||||||||||||||||||||
| TA | TVA | VA | |||||||||||||||||||||||||||||
Notes:[3]
- 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 .
Tabular comparison of colonic polyps
Adenomatous polyps & hyperplastic polyps - a comparison (adapted from Li and Burgart[4]):
| Hyperplastic polyp (HPP) | 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 |
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.
Hyperplastic polyp
General
- Most common colonic polyp (90% of all colonic polyps[2]).
Microscopy
Features:[2]
- Irregular crypt architecture - tortuosity.
- Serrated epithelial cells (at the surface of the gland).
- Serrated appearance = saw-tooth appearance, epithelium has jagged edge.
- Significant negatives:
- No nuclear atypia.
- Goblet cells should be present (as is usual in the colon).
Images:
Adenomatous polys
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, some people doubt their existance.
- Traditional serrated adenomas - nuclear features of 'traditional adenoma' + serrated architecture.
They are all considered pre-malignant, i.e. if you leave 'em in place they often develop into cancer.
Management of (intestinal) polyps
Follow-up interval for polyps (colonoscopy interval):[5]
- 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 (any of the following):[5]
- Tubulovillous.
- Villous.
- High grade dysplasia.
- Size >= 1 cm.
Mnemonic: GAS = grade (high), architecture (tubulovillous, villous), size (>1 cm).
Traditional adenoma
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":
Typing
Subclassified as:[6]
- Tubular (most common), tubular component >75%.
- Villous (least common ~= 1% of (traditional) adenomas), villous component >50%.
- Tubulovillous (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%.
Notes:[6]
- Most villous adenomas are sessile, i.e. flat.[7]
- 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.
- There are different definitions for tubular adenoma, tubulovillous adenoma, and villous adenomas.[7]
- Health Organization (WHO) criteria: villous adenomas >80% villous architecture.
Grading
Most institutions grade adenomas into:[8]
- Low grade.
- Near normal glandular architecture.
- Goblet cells present.
- High grade.
- Have "architectural complexity", i.e. cribriform glands, branching glands.
- Lamina propria invasion.
- Sheets of cells -- no longer resemble glands.
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.
Micrograph:
- Tubular adenoma negative for high grade dysplasia - high mag. - wikimedia.org.
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:[9][10]
- 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.[11]
Sessile serrated adenomas
General
- Colonic lesion.
- More common in the right colon, i.e. ascending colon.
Epidemiology
- Thought to lead to colorectal cancer through a different pathway that most tumours in the left colon/rectum.
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.
Micrographs:
Hamartomatous polyps (overview)
Numerous types of hamartomatous polyps exist:
- Peutz-Jeghers syndrome.
- Juvenile polyposis syndrome.
- Cowden's disease.
There are several obscure/very rare types not listed above.
Further reading: Gastrointestinal & Liver Pathology.[12]
Juvenile polyp
General
- Referred to retension polyps in non-juveniles.
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:
- Nuclear changes may be like those seen in adenomatous polyps.
- IHC can be used as an adjunct (p53, Ki-67).
- p53 mutations in dysplastic epithelium -- negative stain (normal).
Images:
- Juvenile polyp (nature.com).
- Juvenile polyp of the stomach - very low mag. (WC)
- Juvenile polyp of the stomach - very low mag. (WC).
DDx:
- Inflammatory polyp.
Peutz-Jeghers polyp
General
Epidemiology
- Peutz-Jeghers syndrome is autosomal dominant.
- Altered gene: STK11.
Clinical
Features:[15]
- Melanocytic macules.
- Lips, buccal mucosa, and digits.
- Multiple Peutz-Jeghers polyps
Increased risk of various neoplasms - primarily:
- Breast and gastrointestinal cancer.[16]
- Others tumours:[17]
- Granulosa cell tumour.
- Sertoli cell tumour - esp. with calcification.
Microscopy
- Frond-like polyp with all three components of mucosa:
- Muscosal epithelium (melanotic mucosa, goblet cells).
- Lamina propria.
- M. mucosae.
Image:
Cowden disease
Etiology
- PTEN gene mutation.
Clinical features:[18]
- Hamartomatous polyps.
- Facial trichilemmomas (hair follicle root sheath epithelium tumour).
- Oral papillomas.
- Acral keratoses (peripheral keratoses).
Cronkhite-Canada syndrome
- Abbreviated CCS.
General
Clinical features:[19]
- Hamartomatous polyps.
- Ectodermal abnormalities (nail atrophy, skin pigment, alopecia).
Microscopic
Features:
- Polyps have same morphology as juvenile polyp/retension polyp.
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.
- ↑ 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.
- ↑ 5.0 5.1 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.
- ↑ 6.0 6.1 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.
- ↑ 7.0 7.1 http://emedicine.medscape.com/article/170283-overview
- ↑ http://www.pathologyoutlines.com/colontumor.html#adenoma
- ↑ http://www.ganfyd.org/index.php?title=Haggitt_classification
- ↑ 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.
- ↑ 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.
- ↑ 13.0 13.1 13.2 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.
- ↑ 14.0 14.1 14.2 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.
- ↑ 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.
- ↑ 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.