Which nursing actions should a nurse perform when caring for a patient with peptic ulcer disease

This NCLEX review will discuss Peptic Ulcer Disease (PUD).

As a nursing student, you must be familiar with peptic ulcer disease and how to care for patients who are experiencing this condition.

These type of questions may be found on NCLEX and definitely on nursing lecture exams.

Don’t forget to take the Peptic Ulcer Disease quiz.

You will learn the following from this NCLEX review:

• Definition of Peptic Ulcer Disease
• Types of PUD: Gastric and Duodenal Ulcers
• Stomach Anatomy
• Complications
• Signs and Symptoms
• How it is diagnosed
• Treatment
• Nursing Interventions
• Medications

Lecture on Peptic Ulcer Disease

NCLEX Review for Peptic Ulcer Disease

What is Peptic Ulcer Disease?

PUD is ulcer formation in the lining of the upper GI tract that affects mainly the mucosal lining of the stomach, duodenum or esophagus.

Three Types of Peptic Ulcers:

• Gastric Ulcers: located inside the stomach
• Duodenum Ulcer: located inside the duodenum which is the first part of the small intestine
• Esophageal Ulcer: located inside the lower part of the esophagus

*this lecture will concentrate on gastric and duodenum ulcers

How do these ulcers form? Acid production and breakdown of the defense system of the mucosal lining.

Anatomy of Stomach

Role of the stomach: liquefies the food by churning it and release acids and enzyme such as HCL (hydrochloric

acid) and pepsin to break down food.

Layers of the stomach:

Mucosa: top layer of the mucosa that releases mucous rich in bicarbonate that protects the lining from the stomach acid. It also contains gastric pits that contain the parietal, chief cells, and g-cells.

• Parietal cells: release hydrochloric acid along with intrinsic factor
• Chief cells: release pepsinogen which mixes with hydrochloric acid and becomes PEPSIN
• G-cells: release gastrin

Submucosa: made up of connective tissue, nerves, vessels

Muscularis externa (has 3 smooth muscle layers) : function is to perform peristalsis which pushes food down through the GI tract

Serosa: outer layer that has connective tissue that connects to surrounding organs

Pylorus: opening from the stomach to the first part of the small intestine (the duodenum). It is a muscular like structure that allows food to flow into the small intestine.

Duodenum: first part of the small intestine

Key Players in Peptic Ulcer Disease:

Result of PUD: The hydrochloric acid and pepsin in the stomach that normally works to digest food starts to erode the mucosal lining because the defense mechanisms of the stomach are disrupted or the amount of acid is excessive. In a sense, the stomach starts to digest itself.

The body tries to keep a fine balance between the amounts of stomach acid and defense mechanisms that protect the stomach from ulcer formation.

To function normally and prevent ulcers, the stomach has to have the good with the ugly because although they don’t really get along they need each other to perform digestion.

I like to break the key players into two teams. The GOOD team which is the defense system and the UGLY team which is the toxic system.

Good:

• the defense system of the stomach. The defense system protects the stomach lining so food can be digested. It takes a lot of effort to digest food so it can go through the lower GI tract.

Key Players in the Defense System:

• Bicarbonate (HCO3): coats the gastric layer and protects the cells from acids
• Prostaglandins: regulates perfusion to stomach, causes stomach cells to release mucous rich in bicarb, controls acid amounts via the parietal cells

*Anything that affects these “key players” increases the chances of ulcer formation…see the villains below.

Ugly:

• the toxic system of the stomach. It does the ugly/dirty work by breaking down the food…if the “good”/defense wasn’t in place the stomach in a sense would digest itself.

Key Players in the Toxic System:

• Hydrochloric acid via parietal cells
• Pepsin via chief cells

Villains: main causes of Peptic Ulcer Disease

• H. pylori: a bacterial infection (discussed more below)
• NSAIDs usage

So, what happens when acid penetrates the mucosa of the stomach? When the mucosal lining is damaged histamine is released and this is a catch 22 because it signals to the parietal cells to release more HCL…so you get even more toxic acid in the stomach which continues to erode the damaged area.

Causes of Peptic Ulcers:

• *Bacterial infection due to Helicobacter pylori (H. pylori):

Per CDC.gov: 90% of duodenal ulcers and up to 80% of gastric ulcers are caused by h. pylori (Helicobacter Pylori: Fact Sheet For Health Care Providers 1).

These bacteria are spiral-shaped which helps them  invade the GI mucosa.

How can h. pylori live in the acidic conditions of the stomach?  Because it secretes urease and this breakdown UREA which produces ammonia to neutralize the acid. In addition, the ammonia causes more damage to the mucosal lining.

It is most likely spread from consuming something contaminated with h. pylori via fecal to oral or oral to oral.

• *NSAIDs (long term usage):

Think of how NSAIDS work: they work to decrease the production of prostaglandins.

Prostaglandins cause us to feel pain, inflammation, fever etc. Remember the stomach uses prostaglandins to keep the stomach protected by promoting the stomach cells to release mucous rich in bicarb, regulates acid amount via parietal cells, and perfusion to stomach. NSAIDs inhibit them from working.

Therefore, if a patient takes NSAIDs for a long period of time the defense system of the stomach is broken down….hence risk for ulcer formation.

• Zollinger-Ellison Syndrome: tumor formation that causes increased release of gastrin which increases stomach acid production.

*most common

Other factors that can increase susceptibility: smoking, alcohol, genetics, NOTE: stress and certain foods do not causes ulcers but can irritate them and prolong their healing.

Treatment for PUD:

• Medications: proton pump inhibitors, antibiotics, Histamine receptor blockers, antacids, bismuth subsalicylates
• Severe cases due to chronic ulcer formation:
  • Surgery:
    • Vagotomy: cutting parts of the vagus nerve to prevent it from stimulating the gut to produce hydrochloric acid
    • Pyloroplasty: performed when there is scarring to the pylorus (specifically from chronic duodenal ulcers) that can cause an obstruction in the opening of the duodenum from the stomach so GI contents can NOT flow into the small intestine.
    • Gastric resection: (various types) removal of the diseased parts of the stomach
      • Watch for dumping syndrome post-opt: stomach is not able to regulate the movement of food due to the removal of sections of the stomach (usually the pyloric valve and duodenum) so it enters into the small intestine too fast before the stomach can finish digesting it. The food will act hypertonically and cause water from the blood to enter jejunum (see more below).

Diagnosed:

For ulcers from H. Pylori:

• Blood or stool test
• UREA breath test: patient will ingest a urea tablet and if h. pylori is present it will break down urea into ammonia and carbon dioxide. Breath samples will be analyzed for abnormally high carbon dioxide levels.

Scope of the stomach (EGD)

Upper GI series: patient will drink barium which will coat the stomach and  x-rays will be taken to assess for ulcers

CT scan of the abdomen with contrast

Complications of Peptic Ulcer Disease

GI bleeding, formation of holes in the stomach at the site of ulceration which is perforation and this can lead to peritonitis, bowel blockage in the pylorus due to chronic ulceration from a duodenal ulcer, and increased risk of GI cancer

Signs and Symptoms of PUD

Mainly: Indigestion and Epigastric pain….described as burning, dull, or gnawing pain
Gastric Ulcers

• Food makes pain worst (pain 1-2 hours minutes after eating)
• Report of pain dull and aching
• Weight loss
• Severe: vomit blood more common

Duodenal Ulcers

• Pain happens when stomach empty…food makes it BETTER (pain 3-4 hours after eating)
• Wake in middle of night with pain
• Report of pain gnawing
• Weight normal
• Severe: tarry, dark stool from GI bleeding

Nursing Interventions for Peptic Ulcer Disease

Goals: assessing, monitor, educate, and administering meds per physician’s order

Assessing:

• Bowel sounds: hyper/hypoactive or absent, palpation for tenderness, inspect for bloating or mass, assess vital signs
• Ask patient when do you experience stomach pain? Does eating help it or make it worst? Do you awake with pain in the middle of the night?
• Assess medical history: taking what medications? NSAIDS, salicylates, corticosteroids, anticoagulant…make ulcer worst), any history of being diagnosed with h. pylori or any one in your family have it, smoking , drinking  alcohol or caffeine products (prevents ulcer from healing and can exacerbate ulcers)

Monitoring: for complications of peptic ulcer disease or surgery

• GI bleeding: pale skin, mucous membranes, increased HR and decreased BP, bloating or mass in abdomen, dark/tarry stool, vomiting blood that is red or dark like coffee ground (seen this and it looks just like it)….collecting occult blood in stool per MD order
• Perforation/Peritonitis: severe abdominal pain with bloating, vomiting, fever, increase HR and respirations
• Obstruction in pylorus: due to scarring for ulceration….cause vomiting, abdominal pain, bloating
• Dumping Syndrome: if surgery for treatment of PUD, especially gastric resection.
  • What is dumping syndrome? Parts of the stomach have been removed. The stomach is not able to regulate the movement of food due to the removal of sections of the stomach (usually the pyloric valve and duodenum) so it enters into the small intestine too fast before the stomach can finish digesting it. The food will act hypertonically and cause water from the blood to enter jejunum.
    • Early dumping (happens 15-30 minutes after eating): fluid shifts and this causes small bowel distention and increased bowel motility. The patient will have: nausea, bloating, and diarrhea.
    • In addition, from the quick shifting of fluid the heart tries to compensate so the patient may experience hypotension, syncope, dizzy.
    • Late dumping (3 hours after eating): the food that has entered into the small intestine is high in carbs/sugars (body was unable to break it down because it entered into the small intestine too early). This will cause the pancreas to release insulin. The patient will experience signs and symptoms of hypoglycemia like sweating, weak, dizzy.

Note: patients can have both or just one type of dumping

Patient education on how to decrease signs and symptoms:

• eat many small meals rather than 3 large ones
• lie down for 30 minutes after eating
• eat without drinking fluids….wait 30 minutes after meals and then consume liquids
• avoid sugary food and drinks
• eat food high in protein, fiber, and low-carbs

DIET for Ulcers:

Avoid spicy, acidic foods(tomato/citric juices/fruits), foods with caffeine, chocolate, soft drinks , fried foods, alcohol

Consume a low-fiber diet that is bland and eat to digest, eat white rice, bananas etc.

Medications

• Proton-pump inhibitors
• Histamine-receptor blockers
• Bismuth Subsalicylates
• Mucosal healing
• Antacids
• Antibiotics

Antacid Medications Help Basic Peptic Aliments

Antacids: neutralizes the stomach acid

• Types: Magnesium Hydroxide, Calcium Carbonate…these are chewed thoroughly and then swallowed
• Interferes with MANY drugs: antibiotics, mucosal healing, H2 blockers so always give alone and allow for 1-2 hours before administering other medications

Mucosal healing: Sucralfate “Carafate” lines the stomach and adheres to the ulcer site and protects it from acids and enzymes. Take on empty stomach…hour before eating….don’t give at same time as antacids or H2 blockers

*Histamine-receptor blockers: H2 blockers “Ranitidine HCL “Zantac” or Famotidine “Pepcid”

• End in “tidine”
• How do they work? They block histamine. When histamine is released it causes the parietal cells to release HCL but this response will be blocked so gastric acid secretion will be decreased.

Avoid giving at the same time with antacids or Carafate. Instead give 30-45 minutes apart.

*Bismuth Subsalicylates: Pepto-Bismol….used for h.pylori infections by covering the site of the ulcer and keeps the stomach acid away. It is used with antibiotics, PPIs, or H2 blockers for treatment.

*Proton-pump Inhibitors (PPIs):  decreases stomach acid and help the protect stomach lining

• *used with h.pylori infection along with antibiotics
• Types: “Omeprazole “Prilosec” or Pantoprazole “Protonix”…drugs
• end in “prazole”
• How do they work? Attaches to the “proton pump” on the parietal cells which is the hydrogen/potassium (H+, K+) ATPase enzyme and blocks the release of hydrogen ions. These ions would mixed with the chloride ions and form gastric acid but this is blocked so there is decrease in gastric acid.

*Antibiotics: used if h. pylori is causing the ulcer formation: various regime ordered by physician. They are used with PPIs or bismuth subsalicylate or H2 blockers

• Types: Clarithromycin (Biaxin), Metronidazole (Flagyl), Tetracycline, Amoxicillin (Amoxil)

*used to treat h. pylori infections

More NCLEX review

References:

1. “Definition & Facts For Peptic Ulcers (Stomach Ulcers) | NIDDK”. National Institute of Diabetes and Digestive and Kidney Diseases. N.p., 2014. Web. 28 Mar. 2017.
2. “Dumping Syndrome | NIDDK”. National Institute of Diabetes and Digestive and Kidney Diseases. N.p., 2013. Web. 28 Mar. 2017.
3. Helicobacter Pylori: Fact Sheet For Health Care Providers. 1st ed. Centers for Disease Control and Prevention, 1998. Web. 29 Mar. 2017.