Patho of Stomach [2] Flashcards Preview

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Flashcards in Patho of Stomach [2] Deck (23):

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
ammonia , stomach acid


Defense mech of H. pylori

1. prod urease (prot fr. stom acid)
2. burrow thru mucus layer + colonize epi
3. 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?

1. mild, diffuse, chronic pan-gastritis
- unassociated w/ symptoms or disease states
2. antral infxn
- acid secretion and duodenal ulcer (DU) → gastric metaplasia in duodenum
- H. pylori colonization of duodenum → inflammation and cell dmg → ulcer
3. 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
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"

Stress ulcerations
bile reflux


NSAIDS gastropathy

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)

GU is Male=Female
DU is male>female
Majority are asymptomatic

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
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

1. adenocarcinoma
2. Gastric polys
3. Stromal Tumors and GISTs
4. Neuroendocrine tumors
5. Lymphoma


- diffuse or intestinal?
- Which of these is associated with H.Pylori?
- prognosis?
- Surgical +endoscopy or chemo+radiation therapy?

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

Fundic gland polyps (dilated oxyntic glands)
- Chronic PPI use - benign
- unrelated to H. pylori


GISTs (a stromal tumor)

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?

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