Gi Esophagus And Stomach Misc

Front 1

Parakeratosis in the esophageal biopsy suggests that you look for __

Back 1

Candida sp.

Front 2

In general, GE junction is about __ cm in women and __ cm in men, from the incisors

Back 2

Women: 35 cm
Men: 40 cm

Front 3

Cervical gastric heterotopia (aka___) is usually found at about ___ cm from incisors

Back 3

- inlet patch
- 15-20 cm
- typically oxyntic type mucosa, but can be transitional or cardiac type
- may see pancreatic tissue
- often inflamed
- may harbor H. pylori

Front 4

Plummer-Vinson syndrome is associated with an increased risk of __

Back 4

esophageal SCC in the postcricoid esophagus

Front 5

Achalasia

Back 5

most often primary (idiopathic)

Secondary:
- Chagas disease
- polio virus
- diabetic neuropathy
- amyloidosis

- incomplete relaxation of the LES, with increased resting tone

- 5% risk of esophageal SCC

Front 6

GERD: histologic findings

Back 6

- basal zone hyperplasia (>15-20% thickness of epithelium)
- elongation of vascular papillae (> 2/3 thickness of epithelium)
- typically mild inflammation w/ scattered Eos
- less commonly PMNs (more with more severe injury)
- may see balloon cells

Front 7

Barrett esophagus occurs in __% of pts with GERD

Back 7

10%

Front 8

GVHD in the esophagus

Back 8

- intraepithelial lymphocytosis
- basal vacuolar change
- epithelial apoptosis
- necrosis in severe disease
- could be bullous

Front 9

When evaluating an esophageal biopsy for possible GVHD, the most important additional consideration is __

Back 9

- infectious cause of esophagitis given that such patients are empirically treated with steroids

Front 10

Most patients with esoinophilic esophagitis have a clinical history of __

Back 10

- allergy
- asthma
- drug sensitivity
- peripheral eosinophilia
- increased IgE levels

Front 11

suggested Eos count for GERD vs EG

Back 11

< 8 Eos per hpf (GERD)
>24 Eos per hpf (EG)
in between requires clinicopathologic correlation

Important distinction: EG treated with steroids

Front 12

esophageal squamous papillomas are __ HPV related. Most occur in the __ eosphagus

Back 12

- usually NOT HPV relate
- distal esophagus

Front 13

pancreatic acinar cell metaplasia/heterotopia

Back 13

- typically in distal esophagus ( near GEJ)
- most are probably heterotopia rather than metaplasia

- incidental

Front 14

complete vs incomplete intestinal metaplasia

Back 14

- complete: mimics intestinal epithelium; see brush border, Paneth cells, absorptive cells - TYPICAL OF METAPLASIA OCCURING IN STOMACH

- incomplete: features of both intestinal and gastric epithelium (goblet cells mixed with foveolar-type cells) - TYPICAL OF BARRETT ESOPHAGUS

Front 15

The DDX with Barrett esophagus is with __

Back 15

gastric carditis
- requires endoscopic correlation

Front 16

American College of Gastroenterology guidelines for Barrett Esophagus F/up

Back 16

No dysplasia - two EGDs w/ bx - 3 year f/u

Low grade dysplasia - 1 year until no dysplasia

High grade dysplasia - expert consultation and repeat endoscopy to exclude carcinoma - f/u every 3 MONTHS

Front 17

About __% of high grade dysplasia in Barrett eso progress to adenocarcinoma in 5 yrs

Back 17

30-35%

Front 18

Barrett esophagus confers a __-fold risk of adenocarcinoma

Back 18

30-50 fold increase risk

Front 19

In Barrett eosphagus with HG dysplasia, __% are a/w adenocarcinoma

Back 19

40% - reason why esophagectomy was traditionally the therapy for HGD

Front 20

__% of pts wit Barret esophagus develop adenocarcinoma

Back 20

< 10%

Front 21

Adenocarcinoma typically occur in the __ third of the esophagus, while SCC occur in the __

Back 21

- Adenoca - distal third
- SCC - middle third

Front 22

Adenocarcinoma at the GEJ: if epicenter is in esophagus and Barrett mucosa is present, this suggest __

Back 22

esophageal origin

Front 23

Nonepidermolytic palmoplantar keratoderma (tylosis)

Back 23

- the only familial syndrome that predisposes to SCC of esophagus (95% risk of SCC by age 70)

- rare
- autosomal dominant
- hyperkeratosis of palms and soles and thickening of oral mucosa

Front 24

Esophageal SCC is linked to __ socioeconomic status

Back 24

low (not adenocarcinoma)

Front 25

Squamous epithelial dysplasia in the esophagus is __ alone

Back 25

uncommonly
- worrisome for invasvie carcinoma

Front 26

Reactive gastropathy

Back 26

- epithelial mucin loss
- smooth muscle stranding in lamina propria
- corkscrew contour to the antral glands (foveolar hyperplasia)
- lamina propria edema
- vascular ectasia
- minimal active and chronic inflammation

two main associations: bile reflux and NSAIDs

Front 27

gastric mucosal calcinosis

Back 27

- incidental finding
- typically in tips of the foveolae
- typically seen in renal failure patients taking antacids (likely result of overall abd calcium metabolism in these patients)

Front 28

duodenal ulcers that often accompany H. pylori gastritis are secondary to __

Back 28

- H. pylori infection damages the D cells in the antrum
- D cell secrete somatostatin, which keeps gastrin secretion in check
- loss of D cells leads to increase gastrin secretion and excess acid production leading to duodenal ulcers

Front 29

metaplastic atrophic gastritis occurs in two types

Back 29

- autoimmune (AMAG)
- environmental

Front 30

AMAG is due to __

Back 30

-autoAb against parietal cells and intrinsic factor

- pernicious anemia/ B12 def

Front 31

AMAG - IHC that my be useful

Back 31

- gastrin - to rule out bx of true antrum vs. antralized metaplastic fundic mucosa

Front 32

In AMAG, endocrince cell hyperplasia in the body of the stomach occurs due to __

Back 32

- loss of parietal cells and acid secretion leads to increased gastrin production from G cells in antrum
- gastrin levels increase w/ corresponding increase in acid secretion
- endocrine cells in the gastric body and fundus become hyperplastic secondary to gastrin
- the endocrine cell hyperplasia is highlighted by chromogranin

Front 33

in AMAG, a bx of the antrum may show

Back 33

- reactive gastropathy, but usually no metaplasia

Front 34

in AMAG, the metaplasia in the body can be _ or __

Back 34

- pseudopyloric (antral)
- intestinal

Front 35

Early AMAG, before complete loss of parietal cells is recognized by

Back 35

- deep or diffuse lymphoplasmacytic infiltrate w/in lamina propria w/ foci of gland infiltration and damage
- epithelial metaplasia
- parietal cell pseudohypertrophy
- ECL cell hyperplasia (liner or nodular)

Front 36

Environmental metaplastic atrohic gastritis

Back 36

- formeraly type B gastritis or multifocal atrophic gastritis

- main cause - H. pylori
- other causes:
- excessive salt, smoked foods, nitrites, paucity of green vegetables and fruits, nitrosamines

KEY: it is most marked in the antrum!!

- first appears as multiple foci in the transition zone between body and antrum at the lesser curvature
- over time, entire antrum is affected and the body is SPARED, HOWEVER, after many years the body is affected but they retain enough parietal cell mass that pernicious anemia does not occur; serum gastrin is normal

Front 37

GAVE (gastric antral vascular ectasia), aka ___

Back 37

watermelon stomach
- often presents with iron def due to chronic bleeding
- may be a/w CREST syndrome, scleroderma, chronic liver disease

- foveolar hyperplasia
- dilated mucosal capillaries
- focal thrombi
- fibromuscular hypertrophy

Changes suggestive of prolapse component

Resemble reactive gastropathy, but there are fibrin thrombi and vascular ectasia

Resembles portal gastropathy with the vascular ectasia but there are fibrin thrombi

Front 38

Dieulafoy lesion (aka__)

Back 38

Caliber-persistent artery
- gastric bleed (recurrent often massive bleeding, typically with hematemesis and melena)

- should be in DDX of patient with massive upper GI bleed and no endoscopically identifiable source

- typically located at proximal fundus at lesser curvature

Front 39

Gastric bleed

Back 39

- GAVE
- Dieulafoy lesion
- varices
- ulcer
- malignancy

Front 40

focal chronic gastritis could be seen in

Back 40

Crohn disease
- small foci of inflammation separated of foci of more normal mucoas
- +/- granulomas

Front 41

Menetrier disease

Back 41

syndrome of hypertrophic gastric folds, oxyntic gland loss (achlorohydria), and protein loss

- CANNOT DX ON MUCOASL BX W/O CLINICAL ENDOSCOPIC FINDINGS
- histologically, looks like a hyperplastic polyp!!
- hyperplastic foveolar epithelium, arranged in a disorderly fashion, w/ loss of parietal cells body or fundus

- present with hypoproteinemia due to loss across the abnormal gastric mucosal barrier; peripheral edema

- adults and children affected
- adutls: chronic course
- children: self-limited course and CMV implicated