Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

33 Cards in this Set

  • Front
  • Back
major cause of massive hematemesis
acute gastritis
how get acute gastritis
morphology of acute gastritis
The presence of PMNs above the BM (w/in surface epithelial & glandular layer ) is abnormal & signifies active inflammation)

presentation of chronic gastritis
*no ulcers! (vs. PUD)
Et of chronic gastritis
1. Autoimmune
-Autoantibodies to components of parietal cells (i.e. H+,K+ ATPase & IF)
-affects body-fundus
-->achlorhydria (no gastric acid production)
-->can pernicious anemia

2. H pylori infxn-more common
-affects antrum
-normal gastrin levels
-hypochlorhydria<--parietal cell damage
Morph of chronic gastritis
lymphocytes & plasma cells present in the lamina propria
complication of chronic gastritis
gastric carcinoma
carcinoid tumor (autoimmune gastritis)
et of H. pylori
crowding, poor sanitation
H. pylori can cause:
chronic gastritis, PUD gastric carcinoma
gastric MALT lymphoma
pathogenesis of H. pylori infxn
H. pylori lies in the superficial mucus layer & among the microvilli of epi cells
(H. pylori does NOT invade the mucosa)
~ Cannot colonize areas w/ intestinal
Desc gastritis caused by H pylori
2 patterns of H. pylori induced gastritis:
Antral-type gastritis:
high acid
incr risk for duodenal ulcer (PUD)
low IL-1β production

low acid,
incr risk for adenocarcinoma, high IL-1β production
epigastric gnawing
pain worse at night & 1-3 hrs after meal
painr eleived by food and alkali
et of PUD
H pylori
chronic NSAID
pathologenesis of PUD
H pylori:
1. Although H.pylori does not invade, it induces an intense inflammatory response (incr production of pro-inflammatory cytokines)--chronically inflamed mucosa is more susecptible to acid injury
2. (urease, phospholipases, proteases, LPS)
3. H. pylori enhances gastric acid secretion & impairs duodenal bicarb
"punched out ulcer"
how distinguish PUD ulcer from Gastric CA-intestinal type? (both have ulcer in duodenum)
"punched out ulcer"
smooth and clean base
just 1 ulcer

Gastric carcinoma-intestinal type
not well demarcated
heaped up borders
>1 ulcer
morphology of PUD
4 layers: "NIGS" (superficial--base of ulcer-- to deep)
1. Necrotic debris
2. Inflam (PMNs)
3. Granulation tissue w/mononuclear infiltrate
4. Scar
in whom do we find gastric ulcers?
(gastric ulcers=stress ulcers)
critically ill pt
gastric ulcers are a complication of what?
where are ulcers in stress ulcers?
anywhere in stomach (vs. PUD: lesser curvature of stomach)
where are ulcers in PUD?
#1 duodenum
#2 antrum & lesser curvature of stomach
what can cause multiple stomach ulcers?
gastric ulcer
what determines clinical outcome of PUD?
ab to correct underlying condition (remember, pt pop is critically ill pts)
giant rugal folds
hypertrophic gastropathy AKA Menetrier Dz
cerebriform enlarged rugal folds
hypertrophic gastropathy AKA Menetrier Dz
what inc risk of gastric polyps?
chronic gastritis
what are the types of gastric polyps
hyperplastic (non-neo)
adenomatous (neo)
supraclavicular node
gastric CA
Virchow node
gastric CA
linitis plastica
=leather bottle

in gastric CA
Krukenberg tumor
=metastasis to bilateral ovaries

in gastric CA
gastric lymphoma
most are MALT, B cell
where is MC site of extra-nodal lymphoma