Stomach

small group
2021
Jobs of the Stomach

• Store
• Mix/Grind/Meter
• Acidify and Sterilize
• Intrinsic Factor for B12 absorption
• Reduce Fe+++ to Fe++
• Initiate digestion
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 Response to A Meal
Antral Vagus
Receptive
Grinding
Relaxation

K+ H+
Amino Acids
ATP
pH -ase
Distension
Protein
(Dick’s
Burgers) + Kinase A
ACh
cAMP Ca++
+
+
ACh ACh Gastrin
Intr
in
Ner sic
ves GRP + +
ACh +
- - ACh
Histamine
Somatostatin
- Somatostatin -
+
ACh

3
 End of The Meal

K+ H+
Amino Acids ATP
pH -ase Prostaglandins
Distension
Protein -
- Kinase A

cAMP Ca++

Gastrin
H+
- +
- -
Histamine
Somatostatin
- Somatostatin
H+
+

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Two Most Common Causes of
Peptic Ulcer Disease
H. Pylori NSAIDS
 CC: 28 yo sees her PCP for ongoing mid-epigastric pain that has worsened

HPI: 10 year hx of moderate mid-epigastric pain. Typically occurs 1-2 hours after
eating. Pain wakes her from sleep. Relieved temporarily by food and antacids.
4 years ago, she stopped smoking and took 2-week course of H2 receptor
antagonist. She was H pylori positive and took 2-week course of PPI plus dual

Case 1 antibiotic therapy. She was symptom-free for 3 years.

1 year ago, she resumed smoking. Pain returned. She took H2 blocker for 2 months
with relief, but stopped the medicine, and her pain has returned.

PMH: only H pylori and dyspepsia as described above

SHx: recurrent smoker, now using 10-15/day
Meds: OTC antacids, no NSAIDs
NKDA
 What is your hypothesis as to her diagnosis?
The symptoms (periods of localized mid-epigastric pain, with relief by ingestion of food
or antacids, and recurrence with resumption of smoking) are typical of peptic ulcer
disease. The onset of symptoms in early adulthood, in the absence of NSAIDs, favor a
duodenal ulcer, rather than a gastric ulcer or chronic gastritis. Most peptic ulcers are
due to H Pylori infection or NSAID ingestion

To determine the exact location of an ulcer, endoscopy needs to be performed. Of

Case 1
note, 70% of PUD may be completely asymptomatic until the patient experiences
bleeding from the ulcer! The location of the ulcer may determine the symptoms but
using symptoms to guess the location of the ulcer is not very specific.
With a diagnosis of an ulcer, the cause needs to be determined. If it is due to H pylori,
patients need eradicative antibiotic treatment and then retesting for proof of
eradication. If it is NSAID-induced, NSAIDs need to be stopped, or if unable to,
medications to protect from the effects of NSAIDs.

All patients with PUD are put on a course of PPIs to promote healing.
A little more about H pylori
There are multiple ways to test for H pylori depending on the situation: serology, breath,
stool, and biopsies. Biopsy is the gold standard if patient has a complicated course, is
bleeding, or has a previous history of ulcer with recurrence of symptoms.

How does H. Pylori survive in an acidic environment?

H. Pylori prefers an alkaline environment and burrows in the alkaline mucous which coats the
stomach. It also makes urease which breaks down urea and liberates NH 3. NH3 traps
hydrogen ions resulting in a basic environment.

What are other risks of H. Pylori infection besides peptic ulcer?

H. Pylori infection can result in gastritis which over time can lead to atrophic gastritis with the
loss of parietal cells. This loss can lead to B-12 deficiency as the parietal cells secrete intrinsic
factor which is necessary for B-12 absorption. Chronic H. Pylori inflammation is associated
with an increase in gastric adenocarcinoma, and gastric lymphoma (MALT).

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 Smoking and PUD

By what mechanism does smoking contribute to her gastrointestinal

problems?

Smoking significantly reduces gastric blood flow, bicarbonate secretion

and mucous production. The alkaline mucous layer that covers the
stomach and duodenum is the most important protector against peptic
ulcer disease.
Case 1: Endoscopy
Normal Case 1

Endoscopic view of a duodenal ulcer in

the bulb, seen as an oval depression with a
clean, greyish base 10
Case 1: Gastric Biopsies

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Normal Case 1
Case 1: Gastric Biopsies (high power)

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H Pylori Virulence Factors
While the exact mechanism of how H. Pylori creates peptic ulcers in
not known there are multiple virulence factors which may facilitate
ulcer formation.
1. Recent studies suggest that H pylori will burrow into the cell
membrane and attach itself via adhesins. This damages the
membrane and make it more susceptible to attack by H+ ions.
2. H. Pylori makes several enzymes which can damage gastric mucosal
cells. These include lipases, proteases and mucinases which
degrades the mucous-bicarb layer -- the most important protective
mechanism of the stomach.
3. H. Pylori infection results in gastric inflammation with the liberation
of cytokines which can damage cells.
4. H. Pylori has urease which generates ammonia which is toxic to
cells.
5. Certain species of H. Pylori also make cytotoxins.
6. With antral H. Pylori infection the production of somatostatin is
decreased resulting in increased gastrin with increased gastric acid
output.

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 CC: 56 yo presents to ER after vomiting a cup of fresh blood and passing black
tarry like stools.

HPI: She has had intermittent heartburn for many years and self medicated
with antacids. Her heartburn is worse when she uses NSAIDs for her
osteoarthritis.
Case 2 PMH: as above, mild hypertension
SHx: physician, avid gardener, no tobacco, 5 glasses of wine/week
Meds: Mylanta daily, Advil 2-3 times a day for the past 2 weeks
NKDA

PE: Pt appears in moderate distress, pale, diaphoretic. 110 bpm, 95/60

Abd: moderate epigastric tenderness

Lab: Hct = 25% (normal is 40%)

 What is happening? What should your initial management be?
She is having an upper GI bleed. This is an urgent situation as she can bleed to death.
Immediately, we must address the patient’s impending state of shock and restore her
intravascular volume by starting an IV and rapidly infusing saline solution. Blood
should be drawn for typing and crossmatch as she will need transfusions.
Once her circulatory status is stabilized, an upper GI endoscopy should be performed
to find the lesion and stop the bleeding as is possible.
Case 2 How does NSAID use relate to her GI bleed?
NSAIDS are associated with GI bleeding; often the bleeding is the first symptom of an
NSAID-induced ulcer. The NSAID has a small local toxicity, but its major effect is due to
the inhibition of the protective prostaglandins in the mucosal layer. NSAIDs inhibit the
protective PGE2 secretion by blocking COX1. Chronic NSAID use can cause GI bleeding
even when administered via IV. The risk of GI bleeding is increased with concomitant
steroid use. The GI bleed can be worsened if the patient is on an anticoagulant. The
NSAID use itself may have some anticoagulant properties, also worsening the
problem. And last, patients with H pylori who use NSAIDs greatly increase their risk for
GI bleed (not simply additive risk, but synergistically increased risk) .

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Case 2
What is the differential diagnosis of an upper gastrointestinal hemorrhage?
Duodenal ulcer, gastric ulcer, erosive gastritis, severe peptic esophagitis and A-V
malformation (arterial-venous) are the most common. Esophageal or gastric varices can
rupture; these are more common in patients with cirrhosis. Benign or malignant masses
typically cause occult bleeding (oozing) more often than large acute GI bleeds.

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Case 2: Endoscopy

Normal Case 2

Right panel. shows a benign gastric ulcer. Note the large ulcer cavity, filled with yellowish exudate and a
blood clot, surrounded by swollen, inflamed antral mucosal folds. 17
Gastric Erosions and Ulcers
Superficial erosion Bleeding Ulcer

H+ Pepsin

The severity of gastric bleeding in acid-peptic disease is

determined by the depth of the mucosal penetration 18
Gastric Mucosal Defenses-very important
 Mucus and bicarbonate secretion:
Adherent, alkaline mucus gel impedes access of H+ and pepsin to the
epithelium; HCO3- neutralizes gastric acid especially next to the mucosa

 Prostaglandins & NO: enhance blood flow and secretion of mucus and HCO3-

 Resistance of gastric epithelium to acid: barrier to the reabsorption of

secreted H+

 Rapid renewal of epithelium: accelerated after injury & by gastrin and

prostaglandins
 Defenses impaired by: Smoking, alcohol, aspirin, NSAIDs, bile salts,
bacterial toxins and NH3. Smoking decreases gastric mucosal blood flow.
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 CC: 75 yo visits his doctor for decreased appetite

HPI: For 2 months, he has noticed early satiety of solid food. In addition, his
appetite has been decreasing. Now, with just a small amount of food, he feels
full. He has lost 15 lb in this time. He has no other complaints except fatigue.

PMH: Hypothyroidism, well-controlled

SHx: retired policeman, widowed, no tobacco, 3 beers/week

Case 3 Meds: Thyroxine

NKDA

PE: Afeb, VSS

Abd: nontender, no masses palpated

Labs:
Hct: 34% (normal 45%) with microcytosis (small RBC)
Ferritin is low, Serum Iron is low
Stool hemoccult is positive (microscopic blood in the stool)

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 What is early satiety and what does it mean?
Early satiety is an uncomfortable sensation of gastric fullness after eating a small amount of
food. It implies that gastric emptying is impaired, or the wall of the stomach is no longer
compliant.
 
What are mechanisms of early satiety?
The mechanisms of early satiety relate to two things:
• an inability of the stomach to receptively relax – either due to a stiff stomach wall for
Case 3 some reason or due to lack of vagal innervation
• an inability of the stomach to empty – a common cause is gastroparesis secondary to
diabetes or a motor disorder. Or there could be a physical obstruction preventing the
stomach from emptying such as from an edematous pyloric channel ulcer or a tumor.
 
What is the differential diagnosis of early satiety?
Pyloric channel ulcer, diabetic gastroparesis, vagatomy or neurologic disease affecting the
vagus or enteric nervous system, gastric cancer – especially the form “Linitis Plastica”. 
 What do you make of his Iron deficiency anemia? What would be the mechanism if the patient was
found to be B-12 deficient?
His iron deficiency anemia has 2 causes:
• Blood loss: malignancies of the GI system very commonly cause oozing of blood into the system – not
enough to be noticeable in stool, but enough to drop the hematocrit and outpace the production of
RBCs. Testing for occult blood is a screen for GI cancers. BLOOD LOSS IS THE MOST COMMON CAUSE
OF IRON-DEFICIENCY ANEMIA.
Case 3 • Decreased absorption: iron absorption is very complex. Although absorption occurs in the duodenum,
the gastric acid is imperative for efficient absorption. The acid reduces ferric iron to ferrous iron which
can be absorbed. Iron absorption is reduced when taking PPIs, for instance, or when the stomach
cannot produce acid well (impaired parietal cells).
If the patient had B-12 deficiency you would know his parietal cells are impaired and no longer producing
intrinsic factor. Intrinsic factor is necessary for proper B-12 absorption. The impaired parietal cells are
commonly due to autoimmune atrophic gastritis or to H. Pylori infection.

How would you work this patient up and what is your presumptive diagnosis?
An older person with rapid weight loss has cancer until proven otherwise.
An imaging study of the stomach is the first step to revealing why he has weight loss, early satiety, occult
blood, and iron-deficiency anemia.
Case 3: Barium X-ray of stomach
Normal Case 3

Upper GI showing a rigid, non-distensible stomach, characteristic of linitus plastica due to gastric
adenocarcinoma infiltrating the stomach wall. 23
Case 3: Post-Mortum

Post-mortem specimen from the Thickened

patient with gastric wall
adenocarcinoma, illustrating
thickening and rigidity of the
gastric wall, due to tumor
infiltrating the muscle coats.

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“Bald” Tongue or Atrophic Glossitis
• Differential diagnosis includes:

• Nutritional deficiencies (iron, 

vitamin B12, folic acid)
• Dry mouth (sicca symptoms)
• Sjögren syndrome
• Oral Candida infection
• Protein-calorie malnutrition
• Celiac disease
• Lichen planus
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 B-12 Metabolism
Step 1: Ingest B12 (such as in liver or other meat
sources)
Step 2: B12 binds with Haptocorrin (also called R-
protein) from salivary glands. This protects the B12
from the stomach acid.
Step 3: Intrinsic Factor is secreted by parietal cells in
the stomach. It travels with the B12-Haptocorrin
complex but does not yet bind to the B12 in the
stomach.
Step 4: Pancreatic proteases cleave the B12 from
Haptocorrin in the duodenum and B12 now binds with
Intrinsic Factor
Step 5: B12-IF travels to the terminal ileum where the
B12-IF complex is absorbed. You need IF to absorb B12!
Step 6: B12 leaves IF and now binds with transport
proteins (transcobalamins) in these ilial enterocytes.
The bound B12 is carried through the portal vein to the
liver.
Steps 7: B12 may be stored in the liver or sent to
various places to be used as a co-enzyme. B12 is
important in making red blood cells and in nerve
maintenance.
Stomach Check List

Disease List Medication List

• Peptic ulcer disease • PPI’s
• NSAIDS • Anti-nausea medications
• H. Pylori
• Zollinger Ellison-Gastrinoma
• Gastric Adenocarcinoma
• Gastroparesis
• Hyperglycemia
• Diabetic Autonomic Neuropathy
• Idiopathic gastroparesis
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