P- Stomach Flashcards
What are the 4 layers of the stomach?
- mucosa
- submucosa
- muscle layer
- Serosa (this is what the esophagus lacks, making it easier to tear)
How does the mucosa of the fundus/body of the stomach differ from that of the antrum?
Fundus/Body
- shallow gastric pits
- tubular glands with parietal (HCl) and chief (pepsinogen) cells and mucus cells
Antrum
- longer gastric pits
- shorter, branched glands with G (gastrin) cells
How does mucosa in the body region of the stomach protect itself from autodigestion?
Its surface is covered in mucus secreted by the foveolar epitheleal cells that line it
What cells are found in the glands in the body of the stomach and what does each secrete?
Gastric glands are oxyntic and are composed of:
- parietal cells -HCl (intermixed with foveolar cells
- Chief cells - proteolytic enzyme pepsin (pepsinogen) at the bottom of the gland
What cells are found in the glands in the antrum of the stomach. What do they produce?
G cells are endocrine cells that make gastrin.
Gastrin promotes secretion of pepsin from the chief cells and acid from the parietal cells in the body of the stomach
What is gastritis?
What is the cause of MOST gastritis?
inflammation, irritation, and/or erosion/ulceration of the mucosa of the stomach.
H. pylori is the cause of most gastritis but other causes are irritation due to:
- alcohol use
- chronic vomit
- stress
- meds (aspirin/NSAIDs)
- bile reflux from duodenum
- pernicious anemia
What are the most common symptoms of gastritis?
What can occur if the irritation leads to erosions/ulcers?
- nausea
- abdominal bloating
- hiccups
- heartburn, epigastric pain
With erosions/ulcers:
- hematemesis- vomiting blood (“coffee ground emetesis”)
- melena - black tarry stool
What is the main histological finding of chronic gastritis (regardless of cause)?
Chronic inflammatory cells (lymphocytes and plasma cells) in the lamina propria of the mucosa.
This inflammation can lead to the destruction of parietal cells/glandular atrophy and development of intestinal metaplasia.
When the etiology of gastritis is H. pylori, the tissue damage is usually associated with what?
- Active (neutrophils, PMNs, acute)
- Chronic (lymphocytes, plasma cells)
T and B cells respond to H. pylori and this is followed by neutrophilic infiltration of the gastric epithelium to phagocytize the bacteria.
There will be dense lymphoid follicles with germinal centers (like those seen in lymph nodes)
You do a biopsy of a stomach and notice neutrophilic infiltrate in the mucosa. There are also lymphoid follicles with germinal centers. What is the likely cause of the problem?
H. pylori
When the etiology of gastritis is autoimmune, what will the tissue damage show?
How does this differ from H. pylori?
- destroyed parietal cells
- glandular atropy
- lymphocyte infiltrate in the mucosa/lamina propria
- intestinal metaplasia
All 4 of those are also seen with H. pylori, however, there are NO neutrophils with autoimmune and there are neutrophils with H. pylori
Describe the structure of H. pylori.
It is a helix-shaped, G- curved rod
How does H. pylori colonize the gastric mucosa?
- H. pylori uses flagella to burrow into the mucus to get close to the epithelial cell layer
mucus is constantly being produced and removed on the luminal side.
- H. pylori avoids being carried into the lumen via chemotaxis. It senses the pH gradient and swims away from acidic content
- It produces adhesins to attach to the membrane associated lipids on the epithelial cell surface
- It produces urease which turns urea into ammonia. It accepts an H+ to become ammonium lower the pH around it to promote survival ***
The survival of H. pylori in the acidic stomach is dependent on urease activity
Why is H. pylori toxic to epithelial cells of the stomach destroying the mucosa and causing mucosal cell death?
- Mucosal damage - mucinase in H. pylori
- Mucosal cell death - ammonia, cytotoxin A
- Inflammation - gastric acid, proteases, leukocyte chemotaxis
H. pylori-associated chronic gastritis progresses by one of two topographic patterns. What are they?
- Diffuse antral gastritis
2. multi-focal atrophic gastritis
Describe diffuse antral gastritis.
What is the histology?
What disease is it associated with?
H. pylori causes chronic gastritis with activity in the antrum only.
This is associated with peptic ulcers.
Describe multifocal atrophic gastritis.
What is the histology?
What disease is associated with it?
H. pylori causes chronic gastritis that involves the body AND antrum.
Histologically there is:
1. glandular atropy
2. replacement of glands by intestinal-type epithelium (intestinal metaplasia)
This is associated with gastric carcinoma and ulcers.
What are the 2 non-invasive and 1 invasive test for H. pylori?
- serological tests for antibodies (s/s 85%)
- urea breath test (s/s >90%)
- EGD for biopsy and the tissue is used for Rapid Urease Test (RUT) or histology (>90%)
How does RUT work?
It is called the CLOTest.
EGD is used to biopsy. Some tissue is plated on agar.
Urea is added and if it changes to red than that means urease was present (a sign of H. pylori)
What is the incidence of H. pylori in the US? Why does the incidence have to be determined indirectly?
It is 0.5% of the susceptible population become infected each year and has been decreasing over time.
It is determined indirectly because acute H. pylori infections invariable pass undetected
What is treatment for H. pylori?
Triple therapy:
1. bismuth, metronidazole, tetracyline
or
- PPI, metronidazole, clarithromycin
Basically you need acid suppressant and antibiotic
How do PPIs help treat H. pylori?
They increase gastric pH which can enhance tissue concentration/efficiency of antimicrobials
What are the major complications of H. pylori induced chronic gastritis?
- gastric/duodenal ulcers
- gastric adenocarcinoma
- gastric lymphoma (MALT)
MOST remain asymptomatic
What is the inheritance pattern of autoimmune chronic gastritis?
What is it characterized by?
AD disorder that is characterized by autoantibodies against:
- parietal cell H/K ATPase
- parietal cell intrinsic factor.
What are the changes seem over time with autoimmune chronic gastritis?
- Autoimmune destruction of the parietal cells leads to decreased acid production and hypochorhydria. It also leads to gastrin overproduction.
- Inadequate IF leads to vit B12 malabsorption and pernicious anemia (megaloblastic)
Why is autoimmune chronic gastritis limited to the body and fundus?
Because that is where parietal cells are and the autoantibodies are directed against parietal cells