Peptic ulcer

Question 1

Definition

Answer 1

A term used to describe ulcerative disorders of the upper gastrointestinal tract i.e., esophagus, duodenum and jejunum but it mostly occurs in the duodenum.
Simply put, a peptic ulcer is the erosion of the mucosal lining of the GI tract.

Question 2

Mucosa

Answer 2

Top layer that releases mucus rich in bicarbonate that protects lining from acid & has gastric pits contains

• Parietal cells
• Chief cells
• G-cells

Question 3

Parietal cells

Answer 3

release HCL acid

Question 4

Chief cells

Answer 4

releases pepsinogen which forms pepsin

Question 5

G cells

Answer 5

releases gastrin

Question 6

Etiology

Answer 6

• Helicobacter Pylori ( H. pylori)
• Medications: NSAIDS
• Zollinger - Ellison Syndrome: tumor formation that over secrete gastrin; increases stomach acid

Question 7

Pathophysiology

Answer 7

The pathogenesis within peptic ulcers occur when the mechanisms that protect the mucosal layer of the stomach are destroyed which in turn allow the mucosa to be damaged by the corrosive effects of gastric acid (HCL) and pepsin secreted by parietal cells and chief cells. This destruction also occurs because of the activation of histamines which signals to parietal cells to produce more acids. The excessive acids and the lack of mucus leads to a vulnerable mucosa and the erosion of the mucosal layer resulting in an ulcer.

With H. pylori, this bacteria is spherical shaped and buries itself into the mucosal, releasing cytokines that induce inflammation and inflammation mediators. H. pylori also releases urease which breaks down urea into ammonia, neutralizing the acids so it could survive and therefore, damaging the mucosal further.

NSAIDs cause mucosal injury and inhibit prostaglandins which play an important role in regulating perfusion to the stomach and releasing bicarbonate which controls the amount of acid produced by the parietal cells.

Question 8

Clinical Manifestations (Gastric)

Answer 8

Food makes pain worse (1-2 hrs. after meal), pain (gnawing, aching), weight loss
Severe: vomit (coffee ground or bright red)

Question 9

Clinical manifestations (duodenal)

Answer 9

Food makes pain better (3-4 hrs. after meal), waking in the middle of the night w/ pain, pain gnawing, heart burn (acid reflux), normal weight

- Severe: tarry, watery, dark stools (melena), very pungent smell
- Frank (bright) red stools means it’s fresh blood
- Erosion of mucosa because of diarrhea

Question 10

Diagnostic tests

Answer 10

□ Physical examination – tenderness epigastric region, abdominal distension
□ Scope of the stomach, endoscopy (EGD
□ Upper GI series (pt. drink barium (radio pink solution) that will coat GI upper
□ CT scan w/ contract
□ H. pylori: blood test for antibodies, stool test
□ Stool for occult blood
□ Urea breath test

Question 11

Complications

Answer 11

• GI bleeding
  • tachycardia, hypotension, abdominal mass, dark, tarry stool, coffee ground emesis, pale
• Erodes a hole in lining (Perforation) which leads to peritonitis
  • Severe bloating, tachycardia, tachypnea, fever
• Obstruction @ pylorus from chronic ulceration
  • Vomiting, abdominal pain and bloating

Question 12

Nursing interventions

Answer 12

Assessing: Vital signs, abdomen

Monitoring: complications of peptic ulcer or surgery (gastric resection)

Tell patient to avoid spicy foods or acidic foots but to consume low fiber foods that are bland and easy to digest e.g.. white rice and bananas

Question 13

Dumping syndrome

Answer 13

This is when the stomach is unable to digest the foo efficiently so it enters the small intestines in this undigested form. It would be considered hypertonic and thus, fluid from the blood is pulled into the gut. It is categorized as early dumping or late dumping.

• EARLY dumping syndrome (15 - 30 mins)
  fluid shift cause small bowel distention, increased motility, heart tries to compensate,
  s+s. bloating, nausea, diarrhea, hypotension syncope
• LATE dumping (3 hrs.)
  food that entered too quickly sm. Intestine rich in carbs/ sugar which causes pancreas to release insulin = hypoglycemia
  s+s. sweating, weak, dizziness

Question 14

Pharmacological drugs

Answer 14

Antacid Medications help basic peptic ailments

Antacids (give alone): neutralize stomach acids e.g., Calcium carbonate

Mucosal healing (give on empty stomach): lines and adheres to ulcer site which protects it from acids e.g., Sucralfate

• H2 receptor blockers: Blocks histamine which causes parietal cells to decrease secretion of HCL e.g., end in tidine -> famotidine
• Bismuth subsalicylates: covers ulcers and helps kill bacteria, used w/ antibiotics or PPIs e.g., Pepto-Bismol
• Proton-Pump Inhibitors (PPIs): blocks the release of hydrogen ions by the proton pumps on parietal cells e.g., end in prazole -> omeprazole
• Antibiotics*: used to kill H. pylori e.g., amoxicillin, metronidazole
• Used in H. pylori treatment