Online cases from Yaah's attending (they gud)

[LADoc00]

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http://southbaypath.org/2006Monterey/2006 Spring Conference Cases.htm

Post your answers here....
Ive only looked at case 1: hint _____ esophagitis.

This is a graded excercise.

 

[Pingu]

1. Eosinophilic Esophagitis

3. Mucinous Cystadenocarcinoma-the desmoplastic stroma and glandular spaces tip it over to carcinoma vs. adenoma

15. Gastric adenoma- FAP and always look at the surface epithelium for gastric adenomas

16. Celiac Sprue- Increased # of intraepithelial lymphocytes

 

[Pingu]

9. Pseudoinvasion with an adenomatous polyp

 

[yaah]

We actually heard about a couple of these cases the other day. The appendiceal mucinous things are best called "mucinous neoplasms" by him and then you go from there based on other features.

Case #8 is not really diagnosable. This is an example of "could be Crohns could be UC" and is probably best classified as indeterminate because of the normal TI, patchy disease which looks like UC when it is there, and other clinical features.

#13 is one of his favorite cases - ischemia is notoriously focal and you can argue that foci at the extreme edges of those biopsies are consistent with it.

Not sure about some of those stomach cases. I think you are right about #15, the polyps were probably FGP which were not pictured.

Those two colon cases with the focal cryptitis I don't know what to make out of. They always make sense when I see cases with him but in actuality I have only had two weeks on the GI path service thus far in my training...

I am frankly stunned there is no GIST case there so he can go off about mitotic counts and how unhelpful they are.

 

[Pingu]

I thought one of them was collagenous colitis but I wasn't sure...with LaDoc grading its always best to be a mite restrained. 🙂

 

[djmd]

5 is Intestinal metaplasia ie Barrett's
6 is 5+ Dysplasia (can see it well enough to go beyond just Dsyplasia, prob LG)

16 is intra-epi lymphs, but architecure is normal. Don't call it Sprue. Finding can be seen in H.Pylori, prob included glutin sensitive enteropathyin DDx, as they will have done the test for it anyways.

14 looks like Colorectal Ca. I'd look at closely to r/o some reactive inflamed mimic but.. at that power, CA.

12 could be lymphocytic colitis, but I dont know why the circled a focus of polys in the deep crypt. Focal Active, bowel prep?
How we doing so far LADoc?

 

[Pingu]

I'm going to go out on a limb and call #7 collagenous colitis. I've been thinking about it all night and although I would like a trichrome, I really think it is collagenous.

 

[torero]

1. Eosinophilic esophagitis
2. Autoimmune gastritis
3. Mucinous Tumor of the appenxix
4. a. DALM – recommend colectomy
b. TA with high grade dysplasia – continue surveillance
c. TA with high grade dysplasia – continue surveillance
5. Intestinal metaplasia c/w Barrets; no dysplasia identified
6. Intestinal metaplasia c/w Barrets; extensive low grade dysplasia identified
7. Lymphocytic colitis
8. Chronic colitis with moderate activity consistent with chronic
inflammatory bowel disease of undetermined type
9. TA with “misplaced” glands aka pesudoinvasion
10. Chronic gastritis with minute granuloma, probably secondary to crypt
rupture
11. Body-type gastric mucosa with acute erosive gastritis (see note)
Note: these changes could be secondary to NSAID, steroids or ETOH
12. Chronic colitis with mild activity and no architectural changes (see note)
Note: The differential diagnosis includes lymphocytic colitis or
changes secondary to drugs
13. Colonic mucosa with chronic inflammation; no definite evidence of
ischemia is identified.
(note -not for clinicians to see- there is some weak evidence of
ischemia, but not compelling enough to make a firm dx)
14. Colonic mucosa with high grade dysplasia; invasive carcinoma is not
identified in this biopsy material
15. Gastric adenoma
16. Non-specific duodenitis. No evidence of celiac disease identified

I wonder why they didn’t include a case of sessile serrated adenoma – something everyone is now talking about in GI path…

 

[greennature]

1. reflux esophagitis
2. Intestinal metaplasia
3. Cystadenocarcinoma
4. Serrated adenoma
5. Barretts
6. Adenocarcinoma in situ
7. Lymphocytic colitis
8.Chronic active colitis consistent with IBD
9. stalk effect or pseudoinvasion
10. active colitis with granuloma around ruptured gland
11.adenocarcinoma in situ
12. ?
13. Chronic ischemic changes
14. Carcinoma in situ
15. Tubular adenoma
16. Celiac disease

 

[LADoc00]

Henry Appleman= THE MAN. That guy is totally whacky, he was the hit.

I had to do a total double take tho when he said clinicians DONT care about high grade dysplasia in a tubular adenoma(or tubular vs. tubulovillous etc, he said they are treated the same if completely excised)....Im not so sure about that, but he is the man. UMich definitely has some pimpage going on.

 

[yaah]

Well, clinicians here don't care. As he says, he doesn't report things if they don't care. He is kind of a minimalist in many ways. It's like how they report a lot of colon biopsies as "no significant abnormality" even if are small foci of acute inflammation, etc. They also don't subclassify the colon adenomas other than "adenoma" unless it is a serrated polyp. Villous, Tubular, Tubulovillous are all just "adenoma."

Definitely whacky though. During signout he occasionally breaks into songs about diarrhea.

 

[torero]

The problem with high-grade dysplasia in colonic adenomas is that most of the time what you receive is not a nice, well oriented polyp, but fragments of adenoma, and cannot tell if it’s completely excised or not. So most of the time you end up saying “-Fragments of TA with high-grade dysplasia (see note). Note: completeness of excision cannot be assessed because stalk/base is not visualized microscopically.” With this report they usually go back and try to excise the area endoscopically.

Dysplasia in the esophagus (in the setting of Barretts) is a whole different ballgame, tho. Reporting low versus high-grade dysplasia makes a HUGE difference. With low grade dysplasia they’ll just rebiopsy in 6 months. A diagnosis of high-grade dysplasia will trigger an esophagectomy. And you better be sure the dysplasia is high-grade (lack of surface maturation, gland fusion, loss of nuclear polarity) because the finding of low-grade dysplasia/reactive changes only in an esophagectomy specimen will probably trigger a visit to the court!

GI path = 👍 , Yaah. Have you considered fellowship training with Dr. Appelman?

 

[yaah]

The problem with high-grade dysplasia in colonic adenomas is that most of the time what you receive is not a nice, well oriented polyp, but fragments of adenoma, and cannot tell if it's completely excised or not. So most of the time you end up saying "-Fragments of TA with high-grade dysplasia (see note). Note: completeness of excision cannot be assessed because stalk/base is not visualized microscopically." With this report they usually go back and try to excise the area endoscopically.

The deal with this here is that they trust clinicians. If someone has a adenomas, they get rescoped in a certain time limit. If it is a large adenoma or suspicious clinically, they get followed up at closer intervals or get resected anyway. So telling them it is high grade dysplasia doesn't really affect their management. The only time they comment on margins/stalk here is when there is invasive CA and they comment on whether it involves the stalk.

Dysplasia in the esophagus (in the setting of Barretts) is a whole different ballgame, tho. Reporting low versus high-grade dysplasia makes a HUGE difference. With low grade dysplasia they'll just rebiopsy in 6 months. A diagnosis of high-grade dysplasia will trigger an esophagectomy. And you better be sure the dysplasia is high-grade (lack of surface maturation, gland fusion, loss of nuclear polarity) because the finding of low-grade dysplasia/reactive changes only in an esophagectomy specimen will probably trigger a visit to the court!

I believe it is still recommended that all barrett's dysplasia cases be reviewed by a subspecialist. There is a lot of gray area. There are 3 excellent GI pathologists here, and on every case of Barrett's they get with dysplasia they pass the case around and all record their dx separately, and very rarely do they agree (although usually it is 2:1 in favor of one dx).

GI path = 👍 , Yaah. Have you considered fellowship training with Dr. Appelman?

I have considered it. Will probably do GU instead though. The thing is, doing regular residency here is almost the equivalent of a GI path fellowship. They are all great teachers.

 

[LADoc00]

I think GU>>GI, at least the way most GI docs currently practice: The reasoning at least for me is that most GI procedures take place on the hospital grounds typically in an outpatient/same day surgery center type facility. Now, most pathology groups have exclusive contracts with the hospital that usually (should) include this center meaning regardless, GI docs must send their stuff to you. Urologists tho perform needle bx's in their office, where they have the choice to send specimens to you or to a national lab. You have to compete for their biz, making a GU cred more marketable than GI. I think a GI fellowship will be more useful but a GU fellowship (with emphasis on prostate) will bank you more $$$ in the end.