Stomach Flashcards
Describe the epidemiology, pathophysiology, and treatment of H. pylori infection
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Identify the causes of gastritis
Infectious
lymphocytic
eosinophilic
gastritis assoc w/ systemic disease
Describe peptic ulcer disease pathogenesis
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Explain peptic ulcer disease treatment
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List the 5 most common types of gastric neoplasms
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Gastric emptying is slowed in response to:
- decrease in pH (acid)
- fatty acids and caloric density
- increase in osmolality
Autoimmune Atrophic Gastritis
- autoimm attack against parietal cells, IF
- Achlorhydria
- pernicious anemia (B12 low, IF absent)
- biopsies:atrophy, loss of parietal cells, intestinal metaplasia
- Risk of gastric carcinoid tumor
- Gastric cancer risk higher:
Infectious gastritis
Bacterial: H. pylori, syphilis, tuberculosis
Fungal: candidiasis, aspergillosis, histoplasmosis, mucormycosis
Parasitic: giardia, cryptospyridiosis, anisakiasis, strongyloidiasis
Viral: CMV
H. Pylori
- most common human bacterial infection
- infection lifelong for most
- 15% weight urease (Urea–>ammonia, neutralizaes H+)
- corkscrew into mucus
- CagA pathogenicity island/effector protein (injected into host cells, type IV secretion system; decreased cell ahdesions, assoc w/ ulcers DU and GU)
VacA of H. pylori
exotoxin, makes pores in membrane
inhibits T cells
Consequences of H. pylori
- PUD (1-10%)
- atrophic gastritis
- gastric cancer (0.1-3%)
- gastric lymphoma (
What does chronic gastritis look like?
mononuclear inflammatory (lymphocytes and plasma cells) cells within the lamina propria
What augments risk of progression from superficial gastritis to gastric atrophy and adenocarcinoma?
presence of genes like CAG island and vacA encoding virulence factors in H. pylori
H. pylori infection and duodenal ulcer
ANTRAL predominant infection–> acid secretion and DU (gastric metaplasia in duodenum; H. pylori colonize duodenum–> inflammation–> cell damage–> ulcer)
Acid secretion inversely correlates with severity of gastric BODY gastritis
Diagnosis of H. pylori
Endoscopy-Mucosal biopsy
- histology (prepyloric biopsy, high sens/spec)
- rapid urease test: sens 90%, spec 95%
No mucosal biopsy:
- blood antibody test (sens 85%, spec 79%; positive with prior infection)
- ***stool antigen test (sens/spec 95%)
- urea breath test-Ammonia (sens/spec 95%)
Treatment of H. pylori infection
Triple therapy:
PPI+clarithromycin+ amoxicillin 10-14 days
test for H pylori stool antigen
Rescue quadruple therapy: PPI+metronidazole + tetracycline + bismuth
When? PUD Gastric lymphoma FH of gastric carcinoma ?whenever diagnosed?
Other causes of gastritis
Non-H pylori infection uncommon
Immunosuppressed: CMV, candidiasis, aspergillosis, strongloides
Eosinophilic: can have ulceration early satiety, nausea, vomiting increased eos in the blood rare, cause unknown
thickened gastric folds
H pylori
Neoplasia
Menetrier’s Disease: VERY rare, inc mucus secretion, decreased acid, abd pain, wt loss, bleeding, hypoalbuminemia
lymphocytic infiltration
acid hypersecretory states (gastrinoma– ZE syndrome)
Gastropathies
(non inflammatory epithelial cell injury) -gastroduodenal inj in absence of signif inflammation: NSAIDs Ethanol Stress Ulceration Cocaine Bile Reflux
Ethanol Gastropathy
Similar to early NSAID type injury
Disrupts mucosa
Increased acid secretion
PUD with high concentration (>10%), high amounts of use, NSAID use
Gastric Protective Mechanisms
All are PG dependent: Mucous layer thickness Cell membrane hydrophobicity Bicarbonate secretion Mucosal blood flow Epithelial Cell migration/proliferation
NSAIDs and GI SE
COX-1 (constitutive): PG–> E2 protection of gastric mucosa, I2 hemostasis
COX2 (inducible): PG–> pain, inflammation, and fever
Sx: heartburn, n/v, abd pain
Mucosal lesion: 20% in 3 months
GI complications: eg perforated ulcers or GI bleeding
(ulcer goes into submucosa)
Peptic ulcer disease
Lifetime prevalence 5-10% Most asymptomatic Depends on H. pylori GU prevalence: male=female DU prevalence: male>female Increased incidence in COPD, cirrhosis, chronic renal failure, post-transplantation, smokers Decreasing incidence of non-NSAID ulcers
Assoc of H pylori with PUD
High prevalence of H. pylori in patients with PUD
H. pylori infection precedes ulcer
Cure of infection usually cures the ulcer
H. pylori proteins cause inflammation, apoptosis, disrupt cell adhesion…
Stress ulcers
ICU patients: CNS injury (Cushing’s ulcer) Burns (Curling’s ulcer) Prolonged mechanical ventilation >48h Coagulopathy
Fundus and body
Impaired mucosal protection
Increased acid secretion
Peptic ulcer complications
-Abdominal Pain
-Anemia
Fe deficiency from chronic blood loss
Acute bleeding
-Bleeding in 30%
-Acute bleed
Hematemesis-vomiting blood
Melena-black tarry malodorous stool
Perforation 5% lifetime
Gastric Outlet Obstruction-Duodenal Ulcer
Treatment of severe PUD
Acute Bleeding:
IV resuscitation–> restore intravascular volume
Acid suppression-PPI drip: Improves clotting
Endoscopy
Angiography-coils
Surgery
Perforation: Surgery
Treatment for PUD
PPI therapy:
Ulcer Healing 4-8 weeks
H. pylori test and treat
Confirm clearance if H.pylori positive
Risk factor avoidance
NSAIDs, Smoking
Chronic PPI if NSAID necessary-cardiac disease
Gastric polyps
Hyperplastic
found near gastritis-ulcer
rare malignant potential (>1cm)
Adenoma
Premalignant
FAP
Fundic gland polyps
chronic PPI use-benign
unrelated to H.pylori
Gastric adenocarcinoma
2nd most common cancer worldwide/2nd most common cause of cancer death
Gastric cancer treatment
Surgery
endoscopic removal for Stage O
Chemotherapy
Radiation therapy
GISTs
stromal tumor that is the most common mesenchymal tumor of the stomach (60%). Leiomyomas, etc. are NOT GISTs
Prognosis (worse) and treatment (Gleevec) different than other stromal tumors
cell of origin: interstitial cell of Cajal (pacemaker)
Positive for c-kit (CD117) mutation in transmembrane receptor tyrosine kinase (RTK)
10-30% malignant (intra-abdominal spread or liver)
Treated with surgery, imatinib (small molecule RTK inhibitor)
Gastric carcinoid
Neuroendocrine Tumor Annual 1:1,000,000 Found in fundus/body Autoimmune atrophic gastritis: -Hypochlorhydria elevated gastrin-->stimulates ECL cells antrectomy
ZE syndrome (gastrinoma) MEN1 -elevated gastrin-->stimulates ECL cells
Sporadic
More dangerous
MALT lymphoma
(mucosa assoc lymphoid tumor)
Low grade B-cell lymphomas arise in gastric MALT stimulated by H. pylori infection.
Eradication of H. pylori can sometimes induce regression of lymphoma
