Difference between revisions of "Esophagus"
(→Gastroesophageal reflux disease: +ref for long papillae) |
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#Inflammation, esp. eosinophils, lymphocytes with convoluted nuclei ("squiggle cells"). | #Inflammation, esp. eosinophils, lymphocytes with convoluted nuclei ("squiggle cells"). | ||
#+/-Spongiosis. | #+/-Spongiosis. | ||
#+/-Apoptotic cells.<ref name=pmid9926792>{{cite journal |author=Wetscher GJ, Schwelberger H, Unger A, ''et al.'' |title=Reflux-induced apoptosis of the esophageal mucosa is inhibited in Barrett's epithelium |journal=Am. J. Surg. |volume=176 |issue=6 |pages=569–73 |year=1998 |month=December |pmid=9926792 |doi= |url=}}</ref> | |||
Notes: | Notes: | ||
*Eosinophilic esophagitis is characterized by similar histomorphologic features -- key difference: more eosinophils. | *Eosinophilic esophagitis is characterized by similar histomorphologic features -- key difference: more eosinophils. | ||
*"Squiggle cells" may mimic neutrophils. | |||
==Eosinophilic esophagitis== | ==Eosinophilic esophagitis== |
Revision as of 18:53, 29 March 2011
Esophagus connects the pharynx to the stomach. It is afflicted by tumours on occasion. For some reason or another, it seems everyone at SMH gets a esophageal biopsy... yet patients at SB don't have esophagi.
Normal
General:
- Stratified squamous non-keratinized epithelium.
Normal (esophageal) squamous epithelium:
- Should "mature" to the surface like good stratified squamous epithelium does.
- No nuclei at luminal surface.
- Cells should become less hyperchromatic as you go toward the lumen.
- Mitoses should be rare and should NOT be above the basal layer.
- Inflammatory cells should be very rare.
Diagnoses
Common
- Normal.
- Metaplasia (Barrett's esophagus).
- Dysplasia.
- Adenocarcinoma.
Less common
- Squamous cell carcinoma.
- Eosinophilic esophagitis.
- Candidiasis.
- CMV esophagitis.
Tabular summary
Entity | Key feature | Other features | IHC/Special | Clinical | Image |
Normal | squamous epi. matures to surface | no inflammation, no atypia | - | - | [1] |
GERD | inflammation (eosinophils, lymphocytes) | elongated (epithelial) papillae, basal cell hyperplasia | incr. risk of Barrett's | ||
Eosinophilic esophagitis | abundant eosinophils | elongated (epithelial) papillae, basal cell hyperplasia, lymphocytes | unresponsive to PPIs | microscopic, endoscopic | |
Barrett's type change | goblet cells | no dysplasia | Alcian blue +ve | incr. risk of adenocarcinoma | [2] |
Dysplasia, low grade | nuclear crowding at surface | hyperchromasia, mild arch. complexity | incr. risk of carcinoma | ||
Dysplasia, high grade | cribriforming | marked nuc. crowding, hyperchromasia | marked incr. risk of carcinoma |
Indications
- Pyrosis = heartburn.[1]
Infection
Is a relatively common problem, especially in those that live at the margins (EtOH abusers) and immunosuppressed individuals (HIV/AIDS).
Useful stains
- PAS.
- Gram stain.
Overview
- Candida - worms.
- HPV - koilocytes.
- CMV - large nuclei.
- HIV - non-specific.
Candidiasis
Gross (endoscopic)
Features:
- White patches.
Microscopic
Features:
- Worm-like micro-organisms.
- Pseudohyphae (single cells).
- Thickness ~ 1/3-1/2 of squamous cell nucleus.
- Should be within (squamous) epithelium.
- On top of epithelium does not count,[2] i.e. it is likely an artifact.
Image: Esophageal candidiasis (WC).
Cytomegalovirus esophagitis
- AKA CMV esophagitis.
Clinical:
- Classically at the base of the ulcer; within endothelial cells.
Herpes esophagitis
General
Etiology:
- Herpes simplex virus.
Microscopic
Features (3 Ms):
- Moulding.
- Multinucleation.
- Margination of chromatin.
Images:
Human papilloma virus esophagitis
General:
- AKA HPV esophagitis.
Microscopic
Features:
- Koilocytes:
- Perinuclear clearing.
- Nuclear changes.
- Size similar (or larger) to those in the basal layer of the epithelium.
- Nuclear enlargement should be evident on low power, i.e. 25x. [7]
- Central location - nucleus should be smack in the middle of the cell.
Images:
Other
Gastroesophageal reflux disease
General
- Abbreviated GERD and GORD (gastro-oesophageal reflux disease).
Clinical:
- Treated with proton pump inhibitors (PPIs).
Microscopic
Features:
- Basal cell hyperplasia;[3] > 3 cells thick or >15% of epithelial thickness.
- Papillae elongated; papillae reach into the top 1/3 of the epithelial layer.[4]
- Inflammation, esp. eosinophils, lymphocytes with convoluted nuclei ("squiggle cells").
- +/-Spongiosis.
- +/-Apoptotic cells.[5]
Notes:
- Eosinophilic esophagitis is characterized by similar histomorphologic features -- key difference: more eosinophils.
- "Squiggle cells" may mimic neutrophils.
Eosinophilic esophagitis
General
Clinical:
Treatment:
- Avoid exacerbating antigens.
- Topical corticosteroids, e.g. fluticasone.
Biopsies:
- Should be taken from: upper, mid, lower and submitted in separate containers (eosinophilia present through-out-- to differentiate from GERD).
Associations:
Gross/endoscopic
Image: Trachealization - radiograph (nih.gov).
Microscopy
Features:[8]
- Mucosa with "abundant eosinophils".
- Basal cell hyperplasia.
- Papillae elongated.
Notes:
- Criteria for number of eosinophils/area is highly variable; there is a 23X fold variation in published values and only 11% of studies actually define an area (most studies, embarassing, only give the number of eosinophils per "HPF")![12]
- The group that published the article cited above did another one... [13]
- The most commonly reported cut points are 15, 20 and 24 eosinophils/HPF, without defining HPF.[12]
- The Foundation Series book[8] says: "> 20/HPF"; VL sees this definition as garbage, as "HPF" is not defined (see rant in the basics article).
- There is a consensus paper[14] that makes note of HPFitis... and then goes on to ignore to whole issue by defining EE as 15/HPF. It blows my mind that the people could so will fully blind and that the reviewers didn't understand this.
- Most resident microscopes at the Toronto teaching hospitals have 22 mm eye pieces and have for their highest magnification objective a 40X. De facto, this means most people in Toronto are using the Liacouras et al. definition.[15]
Image: Eosinophilic esophagitis (nih.gov).
Erosive esophagitis
DDx
- Infections.
- Crohn's disease.
- Pill esophagitis.
Work-up
- GMS.
- PAS.
- IHC for HSV, CMV.
Pill esophagitis
Classic causes:
- Alendronate (Fosamax) - for osteoporosis.
- Iron (can be demonstrated with Prussian blue stain).
- Doxycycline.
Preneoplastic
Barrett's esophagus
General
- Diagnosis is clinical.
- Pathologic correlate:
- Metaplastic transformation of stratified squamous epithelium to simple columnar epithelium with goblet cells.
- Pathologic correlate:
- Associated with chronic reflux.
Significance of Barrett's esophagus
- Increased risk of adenocarcinoma of the esophagus.
- Need on-going surveillance, i.e. long term follow-up/repeat esophagogastroduodenoscopy.
Microscopic
Features:
- Columnar epithelium.
- Goblets cells -- key feature.
Images:
Neoplastic
Dysplasia
Classification
- Indefinite for dysplasia.
- Low grade dysplasia.
- High grade dysplasia.
Management
Low grade dysplasia.
- Follow-up.
High grade dysplasia.
- Endoscopic mucosal resection.[16]
- Surgical resection.
Microscopy
Features:
- Nuclear changes.
- Nuclear hyperchromatism.
- Nuclear crowding.
- Cigar-shaped (ellipical) nuclei.
- Nuclear changes present at surface (not only in gland crypts).[17]
- If changes are present at the base but not at the luminal surface -- it "matures" and is not dysplasic.
Notes:
- Changes similar to those see in colorectal tubular adenomas.
- Presence of goblet cells is mildly reassuring its not dysplasia.[18]
Cancer
General
- Proximal esophagus: squamous cell carcinoma.
- Distal esophagus: adenocarcinoma arising from Barrett's esophagus.
Risks:
- EtOH.
- Barrett's esophagus.
- Smoking.
Squamous cell carcinoma
Like squamous cell carcinoma elsewhere.
Adenocarcinoma of the esophagus
General
- Often a prognosis poor - as diagnosed in a late stage.
- May be difficult to distinguish from adenocarcinoma of the stomach.
Tx
- Adenocarcinoma in situ (AIS) - may be treated with endoscopic mucosal resection & follow-up.[16]
- Surgery - esophagectomy.
Esophagus vs. stomach
The convention is it's esophageal if both of the following are true:[19]
- Epicenter of tumour is in the esophagus.
- Barrett's mucosa is present.
Microscopic
Features:
- Adenocarcinoma:
- Cell clusters that form glands.
- Nuclear atypia of malignancy:
- Size variation.
- Shape variation.
- Staining variation.
- Mitoses common.
Images:
Grading
Graded like other adenocarcinoma:[19]
- >95 % of tumour in glandular arrangement = well-differentiated.
- 95-50% of tumour in glandular arrangement= moderately-differentiated.
- <50% of tumour in glandular arrangment = poorly-differentiated.
IHC
Adenocarcinoma:
- CK7 +ve, CK20 +ve.
Weird stuff
- Inflammatory polyp - assoc. trauma/previous intervention.
- Giant fibrovascular polyp - loose connective tissue covered with squamous epithelium.
- Granular cell tumour.
- Squamous papilloma - koilocytes.
- Heterotopic gastric mucosa ("inlet patch") - benign appearing gastric mucosa.
Granular cell tumour
Microscopic
Features:
- Abundant eosinophilic granular cytoplasm key feature.
- Granules:
- Size: 1-3 micrometers.
- Poorly demarcated.
- Granules:
- Usu. bland (cytologically non-malignant) nuclei.
Images:
See also
References
- ↑ URL: http://dictionary.reference.com/browse/pyrosis. Accessed on: 21 June 2010.
- ↑ ALS. 4 October 2010.
- ↑ Steiner, SJ.; Kernek, KM.; Fitzgerald, JF. (May 2006). "Severity of basal cell hyperplasia differs in reflux versus eosinophilic esophagitis.". J Pediatr Gastroenterol Nutr 42 (5): 506-9. doi:10.1097/01.mpg.0000221906.06899.1b. PMID 16707971.
- ↑ 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. 804. ISBN 0-7216-0187-1.
- ↑ Wetscher GJ, Schwelberger H, Unger A, et al. (December 1998). "Reflux-induced apoptosis of the esophageal mucosa is inhibited in Barrett's epithelium". Am. J. Surg. 176 (6): 569–73. PMID 9926792.
- ↑ 6.0 6.1 6.2 PMID 19596009.
- ↑ URL: http://www.medicinenet.com/eosinophilic_esophagitis/page2.htm#tocc. Accessed on: 1 December 2009.
- ↑ 8.0 8.1 8.2 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. 19. ISBN 978-0443066573.
- ↑ Leslie C, Mews C, Charles A, Ravikumara M (April 2010). "Celiac disease and eosinophilic esophagitis: a true association". J. Pediatr. Gastroenterol. Nutr. 50 (4): 397–9. doi:10.1097/MPG.0b013e3181a70af4. PMID 19841598.
- ↑ Al-Hussaini, AA.; Semaan, T.; El Hag, IA.. "Esophageal trachealization: a feature of eosinophilic esophagitis.". Saudi J Gastroenterol 15 (3): 193-5. doi:10.4103/1319-3767.54747. PMID 19636182.
- ↑ URL: http://www.ajronline.org/cgi/reprint/164/4/900.pdf. Accessed on: 4 October 2010.
- ↑ 12.0 12.1 Dellon ES, Aderoju A, Woosley JT, Sandler RS, Shaheen NJ (October 2007). "Variability in diagnostic criteria for eosinophilic esophagitis: a systematic review". Am. J. Gastroenterol. 102 (10): 2300–13. doi:10.1111/j.1572-0241.2007.01396.x. PMID 17617209.
- ↑ PMID 19830560.
- ↑ Furuta GT, Liacouras CA, Collins MH, et al. (October 2007). "Eosinophilic esophagitis in children and adults: a systematic review and consensus recommendations for diagnosis and treatment". Gastroenterology 133 (4): 1342–63. doi:10.1053/j.gastro.2007.08.017. PMID 17919504.
- ↑ Liacouras CA, Spergel JM, Ruchelli E, et al. (December 2005). "Eosinophilic esophagitis: a 10-year experience in 381 children". Clin. Gastroenterol. Hepatol. 3 (12): 1198–206. PMID 16361045.
- ↑ 16.0 16.1 Sampliner RE (March 2009). "Endoscopic Therapy for Barrett's Esophagus". Clin. Gastroenterol. Hepatol.. doi:10.1016/j.cgh.2009.03.011. PMID 19306943.
- ↑ GAG. January 2009.
- ↑ GAG. January 2009.
- ↑ 19.0 19.1 Humphrey, Peter A; Dehner, Louis P; Pfeifer, John D (2008). The Washington Manual of Surgical Pathology (1st ed.). Lippincott Williams & Wilkins. pp. 168. ISBN 978-0781765275.