Patho of Stomach [2]

Question 1

Epidemiology of H. Pylori infxn in children + adults

Answer 1

children: txnmissn is person to person: Oral-oral, fecal-oral
adult: age dep increase in prev., crowded living, SES during childhood

Question 2

With H. Pylori infxns in children, if ingestion → acute gastritis with hypochlorhydia, which % resolves and which % progresses to chronic gastritis?

Answer 2

80% → chronic gastritis
20% → spontaneous clearance

infxn is lifelong for most

Question 3

H. pylori is gram _____ and produces _____ which allows it to produce _____ to raise local pH, which can protect itself against ______.

Answer 3

negative rod
Urease
ammonia , stomach acid

Question 4

Defense mech of H. pylori

Answer 4

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

Question 5

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?

Answer 5

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

Question 6

Tx for H. pylori

Answer 6

triple therapy
PPI (Antibiotics work better in neutral pH) + amoxicillin + clarithromycin for 10-14 days

rescue quadruple therapy: same but add bismuth

Question 7

Autoimmune atrophic gastritis

• what is it
• what does biopsy show

Answer 7

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

Question 8

Hypertrophic fold syndromes (→ gastritis) can be due to?

Answer 8

H. pylori
Neoplasia
Menetrier's disease
Lymphocytic infiltration
ZE syndrome

Question 9

Menetrier’s disease

Answer 9

causes hypertrophic folds (thickened gastric folds)
very very rare
↓ acid, ↑ mucus secretion

abdominal pain, weight loss, bleeding, HYPOalbuminemia

No one sure what causes it

Question 10

Noninflammatory epithelial cell injury

“The gastropathies”

Answer 10

NSAIDS
Ethanol
Stress ulcerations
cocaine
bile reflux

Question 11

NSAIDS gastropathy

tx?

Answer 11

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

Question 12

Ethanol gastropathy + stress related

Answer 12

disrupt mucosa and increase acid secretion

Question 13

Peptic ulcer disease

• prevalence?
• symptomatic vs asympto?
• risk factors

Answer 13

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

Question 14

Presentation of PUD?

Answer 14

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)

Question 15

PUD tx

Answer 15

speed up rate of healing and relieve ulcer symp.

PPI and H. pylori eradication
cornerstone of tx
- avoid NSAIDS and smoking

Question 16

Stress ulcers commonly occur in which part of the stomach?

Answer 16

fundus, body

impaired mucosal protection, increased acid secretion

Question 17

5 most common gastric neoplasm

Answer 17

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

Question 18

Adenocarcinoma

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

Answer 18

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)

Question 19

Types of gastric polyps

Answer 19

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

Question 20

GISTs (a stromal tumor)
prognosis?
tx?

Answer 20

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)

Question 21

Cell of origin of GISTs

Answer 21

interstitial cells of Cajal
(+) for c-kit (CD117) mutation in RTK
10-30% malignant (remember it is worse prognosis than other stromal tumors?)

Question 22

Gastric carcinoid

• found in which part of the stomach?
• cell origin?
• associated with?

Answer 22

fundus/body
Tumors of neuroendocrine cell origin
can be auotimmune atrophic gastritic, ZE syndrome, sporadic

Question 23

Gastric lymphoma

- assoc with?

Answer 23

strong assoc. with H.Pylori → if not treated at low grade stage → high grade no longer treatable for antimicrobial, but need surgery