Stomach

Question 1

Describe the epidemiology, pathophysiology, and treatment of H. pylori infection

Answer 1

f

Question 2

Identify the causes of gastritis

Answer 2

Infectious
lymphocytic
eosinophilic
gastritis assoc w/ systemic disease

Question 3

Describe peptic ulcer disease pathogenesis

Answer 3

f

Question 4

Explain peptic ulcer disease treatment

Answer 4

f

Question 5

List the 5 most common types of gastric neoplasms

Answer 5

f

Question 6

Gastric emptying is slowed in response to:

Answer 6

• decrease in pH (acid)
• fatty acids and caloric density
• increase in osmolality

Question 7

Autoimmune Atrophic Gastritis

Answer 7

• 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:

Question 8

Infectious gastritis

Answer 8

Bacterial: H. pylori, syphilis, tuberculosis

Fungal: candidiasis, aspergillosis, histoplasmosis, mucormycosis

Parasitic: giardia, cryptospyridiosis, anisakiasis, strongyloidiasis

Viral: CMV

Question 9

H. Pylori

Answer 9

• 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)

Question 10

VacA of H. pylori

Answer 10

exotoxin, makes pores in membrane

inhibits T cells

Question 11

Consequences of H. pylori

Answer 11

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

Question 12

What does chronic gastritis look like?

Answer 12

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

Question 13

What augments risk of progression from superficial gastritis to gastric atrophy and adenocarcinoma?

Answer 13

presence of genes like CAG island and vacA encoding virulence factors in H. pylori

Question 14

H. pylori infection and duodenal ulcer

Answer 14

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

Question 15

Diagnosis of H. pylori

Answer 15

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%)

Question 16

Treatment of H. pylori infection

Answer 16

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?

Question 17

Other causes of gastritis

Answer 17

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

Question 18

thickened gastric folds

Answer 18

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)

Question 19

Gastropathies

Answer 19

(non inflammatory epithelial cell injury)
-gastroduodenal inj in absence of signif inflammation:
NSAIDs
Ethanol
Stress 
Ulceration
Cocaine
Bile Reflux

Question 20

Ethanol Gastropathy

Answer 20

Similar to early NSAID type injury
Disrupts mucosa
Increased acid secretion

PUD with high concentration (>10%), high amounts of use, NSAID use

Question 21

Gastric Protective Mechanisms

Answer 21

All are PG dependent:
Mucous layer thickness
Cell membrane hydrophobicity
Bicarbonate secretion
Mucosal blood flow
Epithelial Cell migration/proliferation

Question 22

NSAIDs and GI SE

Answer 22

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)

Question 23

Peptic ulcer disease

Answer 23

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

Question 24

Assoc of H pylori with PUD

Answer 24

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…

Question 25

Stress ulcers

Answer 25

``` 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

Question 26

Peptic ulcer complications

Answer 26

-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

Question 27

Treatment of severe PUD

Answer 27

Acute Bleeding: IV resuscitation--> restore intravascular volume Acid suppression-PPI drip: Improves clotting Endoscopy Angiography-coils Surgery Perforation: Surgery

Question 28

Treatment for PUD

Answer 28

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

Question 29

Gastric polyps

Answer 29

Hyperplastic found near gastritis-ulcer rare malignant potential (>1cm) Adenoma Premalignant FAP Fundic gland polyps chronic PPI use-benign unrelated to H.pylori

Question 30

Gastric adenocarcinoma

Answer 30

2nd most common cancer worldwide/2nd most common cause of cancer death

Question 31

Gastric cancer treatment

Answer 31

Surgery endoscopic removal for Stage O Chemotherapy Radiation therapy

Question 32

GISTs

Answer 32

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)

Question 33

Gastric carcinoid

Answer 33

``` 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

Question 34

MALT lymphoma | (mucosa assoc lymphoid tumor)

Answer 34

Low grade B-cell lymphomas arise in gastric MALT stimulated by H. pylori infection. Eradication of H. pylori can sometimes induce regression of lymphoma