Benign Gastric Disorders

Question 1

Describe morphology of H.pylori; what does it colonize?

Answer 1

Spiral shaped, microaerophilic, gram negative
bacteria
• Exclusively colonizes gastric type epithelium

Question 2

H. pylori is Noninvasive, but

Answer 2

stimulates inflammatory and immune responses

Question 3

What is the hallmark of H.pylori infection?

Answer 3

neutrophilic infiltration, along with lymphocytes, plasma cells, macrophages (chronic active gastritis)

Question 4

Virulence factors of H.pylori

Answer 4

cytotoxin associated gene A [CagA]) in some

strains cause more intense inflammation, damage, complications

Question 5

In EARLY stage H.pylori Gastritis, it is confined to_______ and will ihnibit D cell SST resulting in what?

Answer 5

confined to antrum

results in increased gastrin secration thus more acid

Question 6

Where are ulcers present in early stage H.pylori infection?

Answer 6

duodenal ulcers

Question 7

Chronic H. Pylori Gastritis: Late Stage
Goes to what area of stomach?
Inhibits what cell type to result in increased gastrin secration

Answer 7

Colonization and inflammation
expand to corpus/fundus
• Destruction of parietal cells
– Acid decreased → gastrin ↑

Question 8

Where do we see ulcers in LATE stage H.pylori infection

Answer 8

Gastric ulceration

Question 9

If H.pylori is eradicated, what happens to neutorphilic and lymphocytic infiltration?

Answer 9

If H. pylori eradicated:
– Neutrophilic infiltration resolves
– Lymphocytic infiltration may persist

Question 10

Epidemiology of H.Pylori

Answer 10

Infects ½ of world population
• Increased in developing countries
• Increased with crowding, poverty
• Increased with age (age < 12:10% vs age > 60: 50%)

Question 11

How and when is H.pylori aquired?

Answer 11

• Usually acquired in infancy/childhood
• Transmission like fecal/oral or oral/oral
• Acquisition 1%/year after childhood
• Declining in developed countries

Question 12

How do you Dx H.pylori infection

Answer 12

• Serology: Persists even after eradication (false positive)
• Endoscopic gastric mucosa biopsy
• Urea breath testing
• Stool antigen testing
• False negative with recent antibiotics or PPI therapy

Question 13

Adverse effects of H.pylori infection

Answer 13

• Peptic ulcer
• Enteric infections
• Malnutrition/iron & B12 deficiency
• Gastric neoplasia

Question 14

What type of gastric neoplasias

Answer 14

-Adenocarcinoma
– MALT lymphoma
– Carcinoid

Question 15

Adverse consequences of eradication of H.pylori

Answer 15

– GERD/adenocarcinoma of esophagus
– Weight gain?
– Atopic diseases?

Question 16

Inherited form associated with
immune response in the oxyntic
mucosa against parietal cells and
intrinsic factor (IF)

Answer 16

Autoimmune Gastritis

Question 17

In Autoimmune Gastritis; Inherited form associated with immune response in the oxyntic mucosa against

Answer 17

parietal cells and intrinsic factor (IF)

Question 18

Pt population we usually see autoimmune gastritis in?

What type of cells inflitrate the parietal cells?

Answer 18

• Three times more common in women
• Lymphocytic inflammation with
destruction of parietal cells
• Associated with other autoimmune
considers (Thyroid, celiac, Type I DM)

Question 19

Causes Achlorhydria (increased gastrin) and see reduced or absent IF

Answer 19

Atrophic metaplastic gastritis

Question 20

Consequences of Atrophic Metaplastic Gastritis

Answer 20

• Those of reduced acid secretion
• Pernicious anemia
• Gastric cancer
• Gastric carcinoid

Question 21

Inflammatory destruction of normal
mucosa with replacement by
metaplastic elements (commonly
intestinal type with goblet cells)

Answer 21

Atrophic metaplastic gastritis

Question 22

Difference between Type A and Type B atrophic metaplastic gastritis

Answer 22

Type A: body and fundus
– Autoimmune
• Type B: antrum (can extend proximally)
– H. pylori (may be absent at this stage)

Question 23

Define Gastritis

Answer 23

inflammation associated mucosal injury

• Infectious, autoimmune

Question 24

Define Gastropathy

Answer 24

epithelial cell damage and regeneration with minimal or no associated inflammation
• Bile, alcohol, aspirin, NSAIDs, ischemia

Question 25

inflammation associated mucosal injury | • Infectious, autoimmune

Answer 25

Gastritis

Question 26

epithelial cell damage and regeneration with minimal or no associated inflammation • Bile, alcohol, aspirin, NSAIDs, ischemia

Answer 26

Gastropathy

Question 27

Affects of NSAIDS on stomach

Answer 27

* Trapped in epithelial cells * Uncoupling of oxidative phosphorylation * Reduced energy production * Increased cell permeability * Rapid cell death and superficial mucosal injury

Question 28

What is a systemic effect of NSAIDS

Answer 28

• Inhibit COX-1 prostaglandin | synthesis,

Question 29

What is the result of inhibited COX-1 prostaglandin synthesis from NSAIDS?

Answer 29

``` REDUCES: • Mucosal blood flow and oxygen delivery • Mucin, bicarbonate, and phospholipid secretion • Epithelial cell proliferation and migration ```

Question 30

destructive breach of mucosa that extends below muscularis mucosa

Answer 30

ulcer

Question 31

destruction superficial to muscularis mucosa

Answer 31

erosion

Question 32

Prevalance and risk factors of peptic ulcer disease

Answer 32

• Prevalence of 2% – Risk increases with age, smoking • H. pylori associated decreasing

Question 33

NSAID/aspirin and peptic ulcer disease correlation

Answer 33

``` • Among NSAID/aspirin users – 50% develop erosions – 25% of chronic users develop PUD – 2-4% have complications, resulting in 100,000 hospitalizations each year in U.S. ```

Question 34

Three most common causes of Peptic ulcer disease

Answer 34

– Aspirin/NSAIDs – Helicobacter pylori – Surreptitious/unaware NSAID use

Question 35

Risk Factors for NSAID/ASA | PUD and Complications

Answer 35

* Age > 65 * Dose and duration of therapy * Prior PUD/complication * Concurrent use of: • Aspirin/another NSAID * Glucocorticoids• Anticoagulants,• Clopidogrel * Selective serotonin reuptake inhibitors

Question 36

Less common causes of Peptic ulcer diesease

Answer 36

``` – Gastric malignancy • Adenocarcinoma • Lymphoma – Viral infection (Herpes/CMV) – Bisphosphonates – Anastomotic ulceration (gastric bypass) – Stress ulceration ```

Question 37

Rare causes of Peptic ulcer disease

Answer 37

``` – Zollenger-Ellison syndrome – Other hypersecretory states – Crohn’s disease – Mesenteric ischemia (incl. cocaine) – Radiation therapy – Treponema pallidum – Hepatic artery infusion of 5-fluorouracil ```

Question 38

Complications of peptic ulcer disease

Answer 38

* Acute GI hemorrhage * Chronic GI blood loss/iron deficiency anemia * Perforation/peritonitis/pancreatitis * Gastric outlet obstruction * Gastrointestinal fistula * Malabsorption/malnutrition/weight loss * Iatrogenic complications

Question 39

Difference and simularity between symptoms in Duodental ulcer vs gastric ulcer

Answer 39

``` Chronic dyspeptic epigastric pain – DU: 2-3 hours after meals/night – GU: worse with meals – Waxes/wanes over weeks • Nausea • Anorexia/weight loss ```

Question 40

Acute pain in pt with peptic ulcer is concerning because?

Answer 40

may be d/t perforation

Question 41

Below are symptoms of? • Hematemesis (loss of 25% of total blood volume) • Melena, red blood per rectum (loss of 33% blood volume) • Recurrent post-prandial vomiting(obstruction) • Diarrhea (fistula) • May have no symptoms

Answer 41

Peptic ulcer disease