Peptic Ulcer Disease

Peptic ulcer flows from GERD

Acid Environment
HCl acid secretion by gastric parietal cells:
Mucosal barrier allows H20, electrolytes, glucose to pass though but acid cannot,
protecting lining of GI tract.
Impaired barrier back diffusion of acid occurs: HCL enters mucosa and damages
tissue  cell destruction and inflammation
Gastric ulcer --- pain worst 30-60 min after or with eating. Relieved with vomiting
Duodenal ulcer --- pain on empty stomach and at night --- relieved by food and antacid

Agents that destroy mucosal barrier

Helicobacter pylori (H-pylori)…culprit causing this disease
Unknown route of transmission
Generates ammonia  chronic inflammation  mucosa vulnerable to other noxious
substances
Secretes urease which protects it from acid destruction…it kind of make a little
bubble around it, to prevent itself from being destroyed by the acid

Agents that destroy mucosal barrier…the barrier is now damage and more susceptible
to further destruction by noxious substance
ASA…aspirin
Inhibits synthesis of mucous and causes abnormal permeability

Corticosteroids
Decreases rate of mucous cell renewal…once the cell are destroyed, it delays or

inhibit the renewal of the new cells

Increased vagal stimulation…stress causes increase in vagal stimulation (stimulation of
the vagus nerve)
Increased secretion of HCl altered mucosal barrier

Caffeine
Stimulates gastric acid secretion

Cigarette smoking
Delays mucosal healing

Theory: Causes decreased pancreatic secretion of HCO3 (base)  decreased pH in

duodenum (more acid there)

Diagnostic tests
Urea Breath Test…most common (done in GI lab)
No PPIs or H2RAs for 2 weeks prior
No antibiotics for 30 days prior
NPO after midnight
Pt. swallow a Capsule containing radioactive urea that will be broken down by H.
Pylori into C02 & nitrogen
Exhale into a collection bag; Positive test will identify carbon-dioxide with
radioactive isotope
Barium contrast xray…upper or lower GI (this is case upper GI)
Endoscopy…go down with a scope and visualize any abnormalities and ulcer
formation…they can also take a tissue sample looking for cellular changes and H-pylori

Treatment: Medications
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Antibiotic therapy...in combination with PPI
2 or more meds to decrease resistance to meds…one antibiotic increase the risk of
drug resistance (combination of PPI or H2RA and some type on antibiotic regimen)
Examples:
1. Amoxicillin & Clarithromycin (Biaxin)
2. Metronidazole (Flagyl) & Tetracycline

Complications

Hemorrhage
Most common
Erosion of tissue through a blood vessel
o Signs/ Symptoms…bright red blood (in stool or vomit), hypovolemic
leading to shock, changes in LOC from decrease perfusion, decrease BP,
increase HR, abdominal pain, decrease urine output, SOB, cool, clammy
o Treatment: Fluid, backup circulation blood volume…start IV, surgery
(large amount of blood), hemoglobin & hematocrit (HgB…if below 8 the
dr. will decide to transfuse…1-2 units of packed RBCs), NG tube (NPO,
try to get out any blood that’s in there)
Perforation
Most lethal

- In the picture we have a perforated ulcer in the stomach, stomach contents leaking
out into the peritoneal cavity
o Signs/ Symptoms: Peritonitis, sudden onset abdominal pain (patient with
history of peptic ulcer disease)
 Patient is at risk for…sepsis, septic shock r/t bacteria getting into
the blood stream from perforation, leading to peritonitis
 Rigid board-like abdomen (severe abdominal pain)
 Infectious process, elevated temperature, WBCs will go up
o Treatment: Broad spectrum antibiotic (three different types), surgery
emergency(fix hole), IV and NG tube to suction (to suck out any acid from
the stomach contents)
Gastric Outlet Obstruction

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 Here scar tissues form at the gastric outlet – the area where the stomach empties into
the duodenum. Scar tissue forms d/t repeated exposure to the acid and areas of
inflammation. Narrowing of the outlet. Edema occurs because of the swelling and scar
tissue. Sometimes it can completely block the content. Stomach contents can’t get out
to the duodenum.
o Signs/ Symptoms: Vomiting, abdominal pain, bloating, feeling of fullness
o Treatment: Pylori-plasty (removes scar tissue) or balloon dilation (open
up pyloric so food can get through), and NG tube to suction (remove all
gastric contents in the stomach before they vomit it). Note in NG tube:
[Patient NPO when NG tube. Mouth is dry. No saliva stimulation] Provide
skin care to the nare (lubrication) and oral care every 2 hours.

Surgical interventions
Bilroth I
Removal of 2/3 of the stomach
Anastamosis of remaining stomach to duodenum. The antrum part of the stomach is
removed (most common site where ulcers are formed), connecting the duodenum
back to the stomach
Also called Gastroduodenostomy

Surgical interventions
Bilroth II (more common) – extensive surgery
Removal of 2/3 of the stomach
Anastamosis of remaining stomach to jejunum…by passing the duodenum,
connecting rite to the jejunum
Also called Gastrojejunostomy

Surgical interventions
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Vagotomy
Severing the vagus nerve to interrupt innervation to the stomach
Vagus nerve causes stimulation of HCl acid (decreasing the stimulation)
Can be done with Bilroth I or Bilroth II procedures

Pyloroplasty…use if pt. has gastric obstruction

Surgical elimination of the pyloric sphincter to facilitate the easy passage of contents from the
stomach to the duodenum
Increases gastric emptying
Post-op Care after Bilroth I and Bilroth II:
NG tube to suction: Make sure NG tube is patent. Suction is working. All contents are being removed
so they are not accumulating in the stomach causing pressure on the suture line. First 24 hrs, because
the surgical site is right in the stomach, it is normal for the drainage to be red in color; About 36-48
hours, expect drainage is yellowish green or like a bile color. If Patient NG dislodge or accidentally
pulls the NG tube, CALL THE SURGEON. When RN put the tube in, there is a possibility that you
(RN) could hit the tube up in the suture line. If you disrupt that suture lines, patient can have
PERFORATION. Gastric contents would go into the peritoneal cavity from the GI tract, patient could
have abscess form, and peritonitis.

Surgical interventions: Complications

Pernicious Anemia
Because 2/3 of the stomach was removed, these cause decrease of the parietal cells of the
stomach also.
R/T loss of intrinsic factor which is produced by parietal cells of the stomach. Intrinsic factor is
required to absorb Vit B12. Patient will need vitamin B12 injection for the rest of their life.
Dumping syndrome
After surgery, stomach has no control of the amount of gastric chyme entering the intestine so a
bolus of hyperosmolar chyme enters/dumping the intestine. Very common for a patient that had
Bilroth I or II end up with dumping syndrome. After a year the body will start to adjust and they
don’t have as many signs and symptoms
Bowel releases large
Hyperosmolar food bolus
enters of hypertonic fluid Fluid shift: Decrease
stomach and intestine into intestinal lumen in plasma volume

Distention of
Bowel lumen Urge to defecate;
diarrhea
Clinical Manifestations: Weakness,
sweating, palpitations, dizziness,
abdominal cramping, epigastric Onset: within 15-30 minutes of eating
fullness, nausea Duration: till 1 hour after eating
Goal: Slow rapid passage of food into intestine; slow signs and symptoms
1. Rest period after eating, usually 30min after meal. We want the patient to LAY DOWN (want to slow
it down, working against gravity. Sitting up gravity will dump it down even faster. Laying down will
be hard for the food to be dumped, they will also elevate their head if they have reflux)
2. Small, frequent meals to prevent OVER DISTENTION OF STOMACH
3. Avoid drinking fluids with meals. Give fluid separately - BEFORE OR AFTER to prevent over
distend their stomach
4. Eat dry foods…help prevent postprandial hypoglycemia
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5. Low carbohydrate. NOT refined sugars.
Postprandial Hypoglycemia
 Prevention: Dietary modifications for Dumping syndrome
 Interventions to slow down:
 Try to delay huge amount of food dumped into the intestine from the stomach
 Small frequent feeding
 Low carbohydrate food. Limit high carbohydrate.

High carbohydrate
food enters stomach Hyperglycemia
and intestine
Secondary Hypoglycemia

Excessive insulin
release

S/S: Treatment: Fast-acting carbohydrate

Sweating, weakness, Prevention: Dietary modifications for
Confusion, palpitations, Dumping syndrome
Tachycardia, anxiety

Bile Reflux Gastritis

Alkaline gastritis (related to bile)
No more pyloric sphinter to keep bile into duodenum

Bile reflux into Bile salts damage gastric mucosa

stomach in absence
of pylorus

Ulcer formation

Sign and symptoms:

constant epigastric
distress after meals; Treatment:
vomiting Questran AC or with meals
Cholestyramine binds with bile salts