Patho of Stomach [2] Flashcards
Epidemiology of H. Pylori infxn in children + adults
children: txnmissn is person to person: Oral-oral, fecal-oral
adult: age dep increase in prev., crowded living, SES during childhood
With H. Pylori infxns in children, if ingestion → acute gastritis with hypochlorhydia, which % resolves and which % progresses to chronic gastritis?
80% → chronic gastritis
20% → spontaneous clearance
infxn is lifelong for most
H. pylori is gram _____ and produces _____ which allows it to produce _____ to raise local pH, which can protect itself against ______.
negative rod
Urease
ammonia , stomach acid
Defense mech of H. pylori
- prod urease (prot fr. stom acid)
- burrow thru mucus layer + colonize epi
- virulence factors to avoid destruction + colonize + cause inflam response
- Injects CagA → inflammation cancer
- Secretes VacA → makes exotoxin that creates pores in membrane and inhibits T cells
Of the three phenotypic forms of H. pylori, what part of the stomach does H. pylori usually affect?
What characteristics can you see in these types of forms?
- mild, diffuse, chronic pan-gastritis
- unassociated w/ symptoms or disease states - antral infxn
- acid secretion and duodenal ulcer (DU) → gastric metaplasia in duodenum
- H. pylori colonization of duodenum → inflammation and cell dmg → ulcer - multifocal atrophic gastritis → low acid secretion → pt at risk for gastric ulceration + adenocarcinoma
Tx for H. pylori
triple therapy
PPI (Antibiotics work better in neutral pH) + amoxicillin + clarithromycin for 10-14 days
rescue quadruple therapy: same but add bismuth
Autoimmune atrophic gastritis
- what is it
- what does biopsy show
1 of the causes of gastritis
Autoimmune attack against parietal cells + IF →
achlorydia (lose acid production) + pernicious anemia (low B12)
- Biopsy shows atrophy, loss of parietal cells, intestinal metaplasia
- folds are gone + risk of gastric carcinoid tumor
Hypertrophic fold syndromes (→ gastritis) can be due to?
H. pylori Neoplasia Menetrier's disease Lymphocytic infiltration ZE syndrome
Menetrier’s disease
causes hypertrophic folds (thickened gastric folds)
very very rare
↓ acid, ↑ mucus secretion
abdominal pain, weight loss, bleeding, HYPOalbuminemia
No one sure what causes it
Noninflammatory epithelial cell injury
“The gastropathies”
NSAIDS Ethanol Stress ulcerations cocaine bile reflux
NSAIDS gastropathy
tx?
block COX1 → ↓ PG → ↓ protective factors Protective factors: - mucus layer thickness - cell membrane hydrophobicity - HCO3 secretion - mucosal blood flow - epithelial cell migration/proliferation
tx: PPIs and H2 r antagonists and misoprostol
Ethanol gastropathy + stress related
disrupt mucosa and increase acid secretion
Peptic ulcer disease
- prevalence?
- symptomatic vs asympto?
- risk factors
Disease of failed mucosal integrity (not excess acid/pepsin)
5-10%
GU is Male=Female
DU is male>female
Majority are asymptomatic
risk:
COPD, cirrhosis, CRF, post transplant, smokers
**H.pylori infxn! + NSAIDS predisposing factor
Presentation of PUD?
asymptomatic, but can have: burning epigastric pain that is relieved with food or antacids nocturnal pain relieved by antacids Intermittent pain Hematemesis Melena (black tarry stool)
PUD tx
speed up rate of healing and relieve ulcer symp.
PPI and H. pylori eradication
cornerstone of tx
- avoid NSAIDS and smoking
Stress ulcers commonly occur in which part of the stomach?
fundus, body
impaired mucosal protection, increased acid secretion
5 most common gastric neoplasm
- adenocarcinoma
- Gastric polys
- Stromal Tumors and GISTs
- Neuroendocrine tumors
- Lymphoma
Adenocarcinoma
- diffuse or intestinal?
- Which of these is associated with H.Pylori?
- prognosis?
- Surgical +endoscopy or chemo+radiation therapy?
Both
Diffuse is associated with signet-ring cells and excess mucin production
Intestinal: forms glands and is assoc. with atrophic gastritis, intestinal metaplasia, dysphagia
- both are assoc. with H. pylori
Prog depends on depth of invasion:
early = mucosa/sub
Late = penetrated muscular layer
Surgical or endoscopic if NO distant metastasis
(note: 2nd most common cancer world wide + 2nd most common cause of death from cancer world wide)
Types of gastric polyps
Hyperplastic (prolif of gastric foveolar cells)
- found near gastritis-ulcer
- rare malignant potential
Adenoma (dysplastic epi)
- premalignant
- FAP
Fundic gland polyps (dilated oxyntic glands)
- Chronic PPI use - benign
- unrelated to H. pylori
GISTs (a stromal tumor)
prognosis?
tx?
benign gastric tumors from supporting tissues (stromal tumors) that is the most common mesenchymal tumor of the stomach
- can be submucosal and subserosal, or both
Worse prognosis than other stromal tumors
tx: gleevac, surgery, imatinib
(leiomyomas and lipomas are NOT GISTs)
Cell of origin of GISTs
interstitial cells of Cajal
(+) for c-kit (CD117) mutation in RTK
10-30% malignant (remember it is worse prognosis than other stromal tumors?)
Gastric carcinoid
- found in which part of the stomach?
- cell origin?
- associated with?
fundus/body
Tumors of neuroendocrine cell origin
can be auotimmune atrophic gastritic, ZE syndrome, sporadic
Gastric lymphoma
- assoc with?
strong assoc. with H.Pylori → if not treated at low grade stage → high grade no longer treatable for antimicrobial, but need surgery
