Feb15 M3-Pathology Upper GI-non-neoplastic Flashcards
esophagus epithelium
stratified squamous
normal maturation of esophagus epith vs squamous cell CA in situ
normal: proliferative layer at the bottom. progress to surface and acquire more cytoplasm, nucleus smaller
squamous cell CA in situ: cytoplasm doesn’t get bigger, nuclei don’t get smaller
causes of esophagitis
- GERD (is the most common)
- infectious
- radiation
- Crohn’s
causes of GERD
- abnormal LES tonus
- hiatus hernia
- diabetic neuropathy (LES problem)
GERD symptoms
heartburn, dysphagia
endoscopy: erythma. severe = erosions, ulcers.
complication = stricture, Barrett’s esophagus
GERD on histo
-less cell maturation (darker mucosa bc not more cytoplasm): bc less time for that, turnover increased bc cells lost at increased frequency
GERD details on histo
- thickened basal cell layer
- elongated LP papillae
- intraepith eosinophils
eosinophilic esophagitis symptoms and diff with GERD
- same as GERD (heartburn, dysphagia, pain)
- allergic process
- can span entire esophagus
eosinophilic esophagitis on histo
same as GERD but 10x more eosinophils
GERD vs EE rx
GERD = PPI EE = CS
herpes esophagitis causes and endoscopy findings
- HSV1 and HSV2 infection
- bc of immunosuppression (AIDS, transplant, malignancy)
- endoscopy = vesicles followed by ulcers
herpes esophagitis on histo
- major changes in squamous epith cells
- inflam (histiocytes, neutrophils and plasma cells)
- ground glass viral inclusions
- multinucleation
- nuclear molding
Barrett’s esophagus def + important thing
(not esophagitis) replacement for normal mucosa with intestinal columnar-type epithelium. caused by prolonged GERD
*** higher risk of esophageal adenoCA (BE to dysplasia to adenoCA)
BE endoscopy what and why
what: mucosa is salmon-pink and velvety (as opposed to normal whitish)
why: follow up for dev of dysplasia, adenoCA
BE why happens + charact on histo
columnar epith metaplasia bc has goblet cells (mucous) and also absorptive type cells. (mucous = better adapt to injury)
BE LP capillaries charact
covered by single layer of epith cells so look bright red (RBC clear)
normal mucosa = caps covered with multilayer epith cells
BE what’s normal
preserved bottom-top polarity. bottom = nucleus prominent. top = cytoplasm prominent
low-grade dysplasia from BE charact
-lack of polarity and maturation (less cyto)
-nuclear enlargement
-nuclear stratification
GLANDULAR epithelium
3 important cell types in normal gastric oxyntic mucosa
- mucous secreting cells (pale)
- parietal cells (HCl and IF): bright red, lot of mt
- chief cells (pepsinogen): rough ER, lot of ribosomes, look blue
- normal LP shows NO INFLAM cells
most common gastritis and charact
H pylori. attaches to mucosal epith
symptoms: none or dyspepsia (discomfort) or epigastric pain
complications of H pylori
- gastric atrophy
- intestinal metaplasia
- peptic ulcer
- gastric cancer
- lymphoma
stains for H pylori
- gemsa stain: see it attached to columnar cells of gastric foveolar epith
- immunostain: Ab to H pylori: attached to surface of columnar cells
chronic active gastritis secondary to H pylori: most important things based on the name
chronic = plasma cells in LP
active (to not say acute bc is not acute) = neutrophils infiltrating LP and glands
intestinal metaplasia in chronic gastritis: why happens + problem
- patches of intestinal metaplasia with goblet cells bc are more resistant to H pylori colonization
- precursor of dysplasia (followed by cancer)