Path-Case 2
Terms
undefined, object
copy deck
- major cause of massive hematemesis
- acute gastritis
- how get acute gastritis
-
NSAID
alcohol - morphology of acute gastritis
-
The presence of PMNs above the BM (w/in surface epithelial & glandular layer ) is abnormal & signifies active inflammation)
-erosion - presentation of chronic gastritis
-
ASx
*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
-
PUD
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
Pangastritis:
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 - PUD
- 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"
- PUD
- how distinguish PUD ulcer from Gastric CA-intestinal type? (both have ulcer in duodenum)
-
PUD:
"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?
- NSAIDs
- 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
- stomach