stomach

Question 1

Methods for liquid emptying, solid emptying and residual solids in stomach

Answer 1

Liquid emptying by tonic pressure gradient. Solid emptying by vagally-mediated contractions. Residual solids emptied during non-fed state by MMC every 90-120 minutes

Question 2

Factors that slow gastric emptying

Answer 2

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

Question 3

Causes of gastritis

Answer 3

infectious, lymphocytic, eosinophilic, associated with systemic dz

Question 4

Describe autoimmune atrophic gastritis, symptoms, and consequences

Answer 4

•Autoimmune attack against parietal cells. Causes achlorhydria, pernicious anemia (IF absent, B12 low). Biopsy shows: atrophy, loss of parietal clls and intestinal metaplasia. High risk for gastric carcinoid tumor risk

Question 5

Epidemiology of H Pylori

Answer 5

Most common human bacterial infection. Affects all mammals and >50% of world has it. Co-evolution.

Question 6

H Pylori method of infection

Answer 6

Gram negative rod, produces urease which makes ammonia to raise pH. Burrows in mucus layer and colonizes in gastric surface epithelium where it is neutral. Contains virulence factors that help avoid destruction by acid, colonize epithelium, damage epithelial cells and incite inflammation.

Question 7

H. Pylori effects on stomach

Answer 7

peptic ulcer (1-10%), atrophic gastritis, gastric cancer (0.1-3%), gastric lymphoma, most asymptomatic

Question 8

What proportion of H. Pylori infections turn into chronic gastritis

Answer 8

80% of those who develop acute gastritis with hypochlorhydria develop chronic gastritis. 20% have spontaneous clearance

Question 9

Histology of chronic gastritis

Answer 9

lymphocytes and plasma cells in lamina propria

Question 10

H Pylori progression

Answer 10

Helicobacter pylori colonization typically occurs during childhood and leads to superficial gastritis. The presence of genes such as the cag island and vacA that encode bacterial virulence factors augment the risk for progression to gastric atrophy, intestinal metaplasia, dysplasia and gastric adenocarcinoma

Question 11

Phenotypic types of H. pylori

Answer 11

1. Mild, diffuse chronic active superficial gastritis w/out Sx or disease states. 2. antral predominant gastritis, with relative sparing of the gastric body. Such individuals tend to have high levels of acid secretion and may develop duodenal ulcer. 3. Multifocal atrophic gastritis, with low acid secretions and risk for gastric ulceration or adenocarcinoma

Question 12

Diagnosis of H. Pylori

Answer 12

Endoscopy-mucosal biopsy, rapid urease test, blood antibody test, stool antigen test, urea breath test-ammonia

Question 13

H. Pylori histology

Answer 13

by infiltration of the gastric mucosa with neutrophils (active gastritis) and/or lymphocytes (chronic gastritis).

Question 14

H. pylori treatment

Answer 14

Triple therapy: PPI+clarithromycin+amoxicillin 10-14 days. Test for H.pylori-stool antigen. Rescue quadruple therapy: PPI+metronidazole+tetracycline+bismuth. Sequential therapy may be better than thriple therapy.

Question 15

Who should be tested for H. Pylori

Answer 15

Peptic ulcer disease, gastric lymphoma, history of gastric carcinoma

Question 16

Who is prone to non H pylori gastritis

Answer 16

immunocompromised- CMV, candidiasis, etc.

Question 17

lymphocytic gastritis appearance

Answer 17

normal gastric folds, mucosal nodularity with erosions, volcano-like (varioliform gastritis), or with giant gastric folds (hypertrophic lymphocytic gastritis).

Question 18

Lymphocytic gastritis cause

Answer 18

unknown

Question 19

lymphocytic gastritis symptoms

Answer 19

vague abdominal pain, anorexia, weight loss, occult bleeding, and hypoalbuminemia.

Question 20

eosinophilic gastritis symptoms, findings

Answer 20

ulceration, early satiety, nausea, vomiting. Increased eos in blood. Cause is unknown

Question 21

causes of thickened gastric folds

Answer 21

H pylori, neoplasia, menetriers disease, lymphocytic infiltration, acid hypersecretion (zollinger-ellision syndrome)

Question 22

What is Menetriers disease

Answer 22

rare- increased mucus production and decreased acid causes abd pain, weight loss, bleeding and hypoalbuminemia

Question 23

list gastropathies

Answer 23

Gastroduodenal injury in the absence of significant inflammation: NSAIDs, Ethanol, Stress, Ulceration,
Cocaine, Bile RefluxGastroduodenal injury in the absence of significant inflammation: NSAIDs, Ethanol, Stress, Ulceration,
Cocaine, Bile Reflux

Question 24

ethanol gastropathy

Answer 24

disrupts mucosa, subepithelial hemorrhage, increases acid secretion. Peptic ulcer disease can occur with high concentration, high amounts of use and/or NSAID use

Question 25

Gastric protective mechanisms

Answer 25

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

Question 26

NSAIDs MOA

Answer 26

Block COX-1: blocks prostaglandins which normally protect gastric mucosa and cause hemostasis. Block COX-2: blocks prostaglandins which cause pain, inflammation and fever

Question 27

GI side effects associated with NSAIDs

Answer 27

Heartburn, nausea, vomiting, and abdominal pain. Mucosal lesions in 20% over 3 months. GI complications include erosions, perforated ulcers or GI bleeding. Gastric ulcers most common but duodenal ulcers can occur.

Question 28

compare erosion vs ulcer

Answer 28

erosion only extends into mucosa. Ulcer is lesion greater than 5mm in diameter with depth that breaches the muscularis mucosa

Question 29

treatment of NSAID induced ulcers

Answer 29

PPIs. H2 receptor antagonists may heal duodenal ulcers but are less effective with gastric ulcers. Misoprostol also used but causes diarrhea

Question 30

Prevention of NSAID induced ulcers

Answer 30

Only recommended if prior history. H2-receptor antagonists in standard ulcer healing doses will effectively prevent the formation of NSAID-induced duodenal ulcers but not gastric ulcers. More potent H2 receptor antagonists or proton pump inhibitors will prevent gastric ulcers as well. Misoprostol, reduces the development of NSAID-induced gastric ulcers

Question 31

Why are COX-2 specific NSAIDs not commonly used

Answer 31

increase risk of MI

Question 32

Cause of peptic ulcer disease

Answer 32

Primarily a disease of failed gastroduodenal mucosal integrity, not of excess acid/pepsin secretion. H pylori (causes inflammation, apoptosis and disrupts cell adhesion) and NSAIDs are major contributors

Question 33

Causes of stress ulcers

Answer 33

CNS injury (Cushing’s ulcer), Burns (Curling’s ulcer), Prolonged mechanical ventilation >48h, Coagulopathy. These can all lead to impaired mucosal protection and increased acid secretion.

Question 34

Peptic ulcer complications

Answer 34

abd pain, anemia, bleeding, hematemesis, melena, perforation (into liver or pancreas, not peritoneum), gastric outlet obstruction-duodenal ulcer

Question 35

Treatment of severe peptic ulcer disease

Answer 35

IV fluids, PPI drip to suppress acid and improve clotting, endoscopy, angiography, surgery to fix perforation and bleeding. Treat H pylori if present

Question 36

5 most common gastric neoplasms

Answer 36

polyps, adenocarcinoma, stromal tumors, neuro-endocrine tumors, lymphoma

Question 37

compare hyperplastic, adenoma and fundic gland polyps

Answer 37

hyperplastic: rare malignant potential, found near gastritis-ulcer. Adenoma: premalignant, seen in FAP. Fundic gland: found in chronic PPI use- benign.

Question 38

Which kind of cancer does H pylor predispose to

Answer 38

H pylori > gastric atrophy > intestinal metaplasia > dysplasia > gastric adenocarcinoma

Question 39

gastric stromal tumors

Answer 39

Benign gastric tumors arising from the supporting tissues (stromal tumors) include leiomyomas and lipomas. Malignant stromal tumors include leiomyosarcoma or liposarcoma.

Question 40

GISTs

Answer 40

Most common mesenchymal tumor of stomach. Originate from interstitial cell of Cajal. Prognosis is bad and treatment is Gleevec (diff than other stromal tumors).

Question 41

Gastric carcinoid tumor description and causes

Answer 41

neuroendocrine tumor, found in fundus/body. Caused by autoimmune atrophic gastritis (hypochlorhydria and elevated gastrin stimulates ECL cells), ZE syndrome (elevated gastrin stimulates ECL cells), or sporadic (more dangerous)

Question 42

MALT lymphoma causes

Answer 42

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