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Bloc E - GI & Metabolism > Feb15 M3-Pathology Upper GI-non-neoplastic > Flashcards

Feb15 M3-Pathology Upper GI-non-neoplastic Flashcards

1
Q

esophagus epithelium

A

stratified squamous

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2
Q

normal maturation of esophagus epith vs squamous cell CA in situ

A

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

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3
Q

causes of esophagitis

A
  • GERD (is the most common)
  • infectious
  • radiation
  • Crohn’s
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4
Q

causes of GERD

A
  • abnormal LES tonus
  • hiatus hernia
  • diabetic neuropathy (LES problem)
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5
Q

GERD symptoms

A

heartburn, dysphagia
endoscopy: erythma. severe = erosions, ulcers.
complication = stricture, Barrett’s esophagus

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6
Q

GERD on histo

A

-less cell maturation (darker mucosa bc not more cytoplasm): bc less time for that, turnover increased bc cells lost at increased frequency

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7
Q

GERD details on histo

A
  • thickened basal cell layer
  • elongated LP papillae
  • intraepith eosinophils
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8
Q

eosinophilic esophagitis symptoms and diff with GERD

A
  • same as GERD (heartburn, dysphagia, pain)
  • allergic process
  • can span entire esophagus
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9
Q

eosinophilic esophagitis on histo

A

same as GERD but 10x more eosinophils

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10
Q

GERD vs EE rx

A 
GERD = PPI
EE = CS
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11
Q

herpes esophagitis causes and endoscopy findings

A
  • HSV1 and HSV2 infection
  • bc of immunosuppression (AIDS, transplant, malignancy)
  • endoscopy = vesicles followed by ulcers
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12
Q

herpes esophagitis on histo

A
  • major changes in squamous epith cells
  • inflam (histiocytes, neutrophils and plasma cells)
  • ground glass viral inclusions
  • multinucleation
  • nuclear molding
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13
Q

Barrett’s esophagus def + important thing

A

(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)

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14
Q

BE endoscopy what and why

A

what: mucosa is salmon-pink and velvety (as opposed to normal whitish)
why: follow up for dev of dysplasia, adenoCA

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15
Q

BE why happens + charact on histo

A

columnar epith metaplasia bc has goblet cells (mucous) and also absorptive type cells. (mucous = better adapt to injury)

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16
Q

BE LP capillaries charact

A

covered by single layer of epith cells so look bright red (RBC clear)
normal mucosa = caps covered with multilayer epith cells

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17
Q

BE what’s normal

A

preserved bottom-top polarity. bottom = nucleus prominent. top = cytoplasm prominent

18
Q

low-grade dysplasia from BE charact

A

-lack of polarity and maturation (less cyto)
-nuclear enlargement
-nuclear stratification
GLANDULAR epithelium

19
Q

3 important cell types in normal gastric oxyntic mucosa

A
  • 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
20
Q

most common gastritis and charact

A

H pylori. attaches to mucosal epith

symptoms: none or dyspepsia (discomfort) or epigastric pain

21
Q

complications of H pylori

A
  • gastric atrophy
  • intestinal metaplasia
  • peptic ulcer
  • gastric cancer
  • lymphoma
22
Q

stains for H pylori

A
  • gemsa stain: see it attached to columnar cells of gastric foveolar epith
  • immunostain: Ab to H pylori: attached to surface of columnar cells
23
Q

chronic active gastritis secondary to H pylori: most important things based on the name

A

chronic = plasma cells in LP

active (to not say acute bc is not acute) = neutrophils infiltrating LP and glands

24
Q

intestinal metaplasia in chronic gastritis: why happens + problem

A
  • patches of intestinal metaplasia with goblet cells bc are more resistant to H pylori colonization
  • precursor of dysplasia (followed by cancer)
25
Q

autoimmune gastritis steps

A
  1. autoimmune process against chief and parietal cells
  2. chronic inflamm of gastric body with loss of these cells
  3. achlorhydria (lack of HCl prod) + megaloblastic anemia (lack of IF)
26
Q

why gastric antrum not affected by autoimmune gastritis

A

no chief or parietal cells there

27
Q

complication of autoimmune gastritis with time

A

get atrophic mucosa (lacking parietal and chief cells, they are destroyed)

28
Q

other complication of autoimmune gastritis

A

intestinal metaplasia

29
Q

treatment of autoimmune gastritis

A
  • NO CS (bad effects)

- B12 injection

30
Q

autoimmune gastritis complications

A
  • mucosal atrophy
  • megaloblastic anemia (yrs after atrophy)
  • intestinal metaplasia
  • carcinoid tumors
  • adenoCA
31
Q

peptic ulcer disease def

A

breach beyond muscularis mucosa bc of imbalance in damaging and defensive forces of mucosa

32
Q

peptic ulcer disease affects which regions the most (in order)

A
  1. duodenum
  2. stomach
  3. esophagus (GERD)
33
Q

erosion vs peptic ulcer

A

peptic ulcer = below mucosa (beyond muscularis mucosa)

erosion = smaller damage limited to mucosa

34
Q

defense mechanisms against peptic ulcers

A
  • surface mucous
  • bicarb
  • epithelial regeneration
  • prostaglandins (reduce acid secretion)
35
Q

damaging forces causing peptic ulcers

A
  • gastric acidity
  • peptic enzymes
  • H pylori
  • NSAIDs
  • bile reflux in stomach (for gastric ulcers)
  • GERD (for cardia and lower esophagus ulcers)
36
Q

macroscopic features of peptic ulcers (3)

A
  • 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
37
Q

complication of peptic ulcer

A

bleeding

38
Q

most important peptic ulcer ddx and how to check that

A 
ulcerated tumor (ulcerated adenoCA usually)
-check with endoscopy and microscopy
39
Q

how ulcerated tumor differs from peptic ulcer

A
  • 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
40
Q

how ulcers form

A

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

41
Q

how tumor ulcerates

A
  • tumor grows and becomes larger, center lacks blood supply and necroses
  • necrosis spreads and necrotic tissue sheds (cavitary organ). LARGE ulcer ELEVATED edges
42
Q

peptic ulcer vs ulcerated tumor consistency

A

peptic ulcer = soft (simply a part missing)

ulcerated tumor = hard (thickening bc of tumor) + enduration bc of desmoplasia

Bloc E - GI & Metabolism (58 decks)

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