- 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)

Stomach Flashcards by Aubrae Anne

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

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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

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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:

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Infectious gastritis

Bacterial: H. pylori, syphilis, tuberculosis

Fungal: candidiasis, aspergillosis, histoplasmosis, mucormycosis

Parasitic: giardia, cryptospyridiosis, anisakiasis, strongyloidiasis

Viral: CMV

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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)

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VacA of H. pylori

exotoxin, makes pores in membrane

inhibits T cells

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Consequences of H. pylori

PUD (1-10%)
atrophic gastritis
gastric cancer (0.1-3%)
gastric lymphoma (

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What does chronic gastritis look like?

mononuclear inflammatory (lymphocytes and plasma cells) cells within the lamina propria

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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

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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

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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%)

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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