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)
autoimmune gastritis steps
- autoimmune process against chief and parietal cells
- chronic inflamm of gastric body with loss of these cells
- achlorhydria (lack of HCl prod) + megaloblastic anemia (lack of IF)
why gastric antrum not affected by autoimmune gastritis
no chief or parietal cells there
complication of autoimmune gastritis with time
get atrophic mucosa (lacking parietal and chief cells, they are destroyed)
other complication of autoimmune gastritis
intestinal metaplasia
treatment of autoimmune gastritis
- NO CS (bad effects)
- B12 injection
autoimmune gastritis complications
- mucosal atrophy
- megaloblastic anemia (yrs after atrophy)
- intestinal metaplasia
- carcinoid tumors
- adenoCA
peptic ulcer disease def
breach beyond muscularis mucosa bc of imbalance in damaging and defensive forces of mucosa
peptic ulcer disease affects which regions the most (in order)
- duodenum
- stomach
- esophagus (GERD)
erosion vs peptic ulcer
peptic ulcer = below mucosa (beyond muscularis mucosa)
erosion = smaller damage limited to mucosa
defense mechanisms against peptic ulcers
- surface mucous
- bicarb
- epithelial regeneration
- prostaglandins (reduce acid secretion)
damaging forces causing peptic ulcers
- gastric acidity
- peptic enzymes
- H pylori
- NSAIDs
- bile reflux in stomach (for gastric ulcers)
- GERD (for cardia and lower esophagus ulcers)
macroscopic features of peptic ulcers (3)
- regularly shaped walls with margins at mucosa lvl (punched out ulcer)
- clean or sometimes hemorrhagic base
- gastric folds at edge of ulcer
- **no growth around. margins NOT elevated
complication of peptic ulcer
bleeding
most important peptic ulcer ddx and how to check that
ulcerated tumor (ulcerated adenoCA usually) -check with endoscopy and microscopy
how ulcerated tumor differs from peptic ulcer
- large
- irregular borders, thick and indurated
- elevated edges
- thick borders around the ulcer separate rugae from edge (ulcer = rugae touch edge)
- rough bottom, irregular, necrotic tissue
how ulcers form
damage to epith, it’s gone and clot presents in bottom of ulcer + edema bc of inflam nearby. edges not elevated. when epith gone, faster dev of ulcer
how tumor ulcerates
- tumor grows and becomes larger, center lacks blood supply and necroses
- necrosis spreads and necrotic tissue sheds (cavitary organ). LARGE ulcer ELEVATED edges
peptic ulcer vs ulcerated tumor consistency
peptic ulcer = soft (simply a part missing)
ulcerated tumor = hard (thickening bc of tumor) + enduration bc of desmoplasia
