NURSING
Page |1
Week 3 – GI
Most Likely / Most Important Diagnoses
May present with mild epigastric pain, and symptoms commonly
worsen after meals, although the pain is classically described as
"burning" and may be located in the substernal rather than
epigastric area.
Hematemesis in the setting of GERD-like symptoms is unusual
and represents an alarm symptom indicative of an upper GI bleed
GERD or tumor and warrants prompt GI referral for evaluation and upper
endoscopy.
Hematochezia and melena are not typically associated with
GERD.
Classic symptoms of heartburn and regurgitation
Likely to occur when gastric volume is increased (after large
meals)
Epigastric abdominal pain that improves with meals is the
hallmark of PUD. However, in some cases, symptoms of PUD
may worsen with meals.
NSAID use is associated with the development of PUD.
Hematemesis, if present, suggests more complicated disease
including bleeding ulcer and warrants urgent GI referral and
endoscopy.
Melena commonly occurs in the setting of an upper GI bleed
secondary to PUD or hemorrhagic gastritis (e.g. NSAID-gastritits).
Hematochezia only occurs in the setting of an upper GI bleed
Peptic ulcer
when massive (e.g. variceal rupture).
disease
Usually characterized by episodic or recurrent epigastric 'aching',
(PUD)
'gnawing', or 'hunger-like' pain or discomfort
Diagnosis with endoscopy and biopsy
Misc: Gastric ulcer pain may occur 5 to 15 minutes after eating
and remain until the stomach empties, which may be up to several
hours in duration, and the pain may otherwise be absent during
times of fasting. Pain from duodenal ulcers is often relieved by
eating, drinking milk, or taking antacids but may return anywhere
from 90 minutes to 4 hours after eating a meal. Both gastric and
duodenal ulcers may be associated with nausea and vomiting
occurring anytime shortly after eating to several hours later.
Gastritis Inflammation or irritation of the stomach lining often causing
sharp epigastric pain. This pain may be variably worsened or
improved with eating food.
Inflammatory forms of gastritis may be caused by chronic
, Page |2
infections such as H. pylori or acute infections such as viruses.
Non-inflammatory forms of 'gastritis' are more properly
histologically termed gastropathy. These may be caused by
chemical irritants to the stomach, including alcohol and NSAIDs.
Agents that Cause or Contribute to Peptic Ulcer Disease
Aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) are the
predominant pharmacologic agents that contribute to the development of PUD.
Classically, the elderly are at the highest attributable risk of ulceration and perforation
due to chronic NSAID use. Chronic NSAID use is a leading cause of morbidity in the
elderly.
Moderate to severe physiologic stress may lead to stress ulceration, predominantly in
patients in the intensive care unit (ICU).
Colonization of the stomach by H. pylori renders the underlying mucosa more
vulnerable to peptic acid damage by disrupting the mucous layer, liberating enzymes and
toxins, and adhering to the gastric epithelium. In addition, the body's immune response to
H. pylori incites an inflammatory reaction that contributes to tissue injury and leads to
chronic gastritis. In most individuals the chronic gastritis is asymptomatic and does not
progress. In some cases, however, altered gastric secretion coupled with tissue injury
leads to peptic ulcer disease. In other cases, gastritis progresses to mucosal atrophy,
intestinal metaplasia, and eventually gastric carcinoma. Rarely, persistent immune
stimulation of gastric lymphoid tissue can lead to gastric lymphoma.
COMPLICATIONS OF GERD AND PUD
GERD
Esophagitis develops when the mucosal defenses that normally counteract the effect of
injurious agents are overwhelmed by refluxed acid, pepsin, or bile.
Peptic strictures from fibrosis and constriction occur in about 10 percent of patients with
reflux esophagitis.
Replacement of the squamous epithelium of the esophagus by columnar epithelium
(Barrett's esophagus) may result from reflux esophagitis. Two to five percent of cases of
Barrett's esophagus may be further complicated by adenocarcinoma.
PUD
Hemorrhage or perforation into the peritoneal cavity or adjacent organs (causing
severe, persistent abdominal pain).
Ulcer scar healing or inflammation can impair gastric emptying leading to gastric outlet
obstruction syndrome.
Alarm Symptoms Warranting Referral to Gastroenterology for Endoscopy
Difficulty in swallowing. Dysphagia to solids suggests possible development
of peptic stricture. Rapidly progressive dysphagia potentially indicates
Dysphagia
adenocarcinoma. Dysphagia to liquids suggests development of a motility
disorder.
, Page |3
Initial onset
of upper GI
Increased chance of cancer.
symptoms
after age 50
May be associated with gastroparesis or gastric outlet obstruction (stricture
Early satiety
or cancer).
Vomiting blood, which suggests bleeding ulcer, mucosal erosions (erosive
Hematemesis gastritis/esophagitis), esophageal tear (Mallory-Weiss), or esophageal
varices.
Hematochezi Passing red blood with stool, which may indicate a rapidly bleeding ulcer or
a mucosal erosions.
Iron The presence of hematemesis, hematochezia, and/or iron deficiency anemia
deficiency may indicate possible bleeding from a peptic ulcer, mucosal erosions, or
anemia cancer.
Painful swallowing, which is associated with infections (e.g. candida),
Odynophagia
erosions, or cancer.
Recurrent
Suggestive of gastric outlet obstruction.
vomiting
Weight loss Associated with malignancy.
Treatment
GERD:
Self-directed trial of over-the-counter anti-secretory therapy, either a histamine-2 receptor
antagonist or a proton-pump inhibitor (PPI)
Lifestyle modifications.
PUD from H. pylori
"Triple therapy" for 10 to 14 days (70% to 85% eradication rate):
PPI standard dose twice daily (esomeprazole is dosed once daily)
Amoxicillin 1 g twice daily
Clarithromycin 500 mg twice daily
"Quadruple therapy" for 10 to 14 days (75% to 90% eradication rate):
PPI standard dose once or twice daily (OR ranitidine 150 mg twice daily)
Metronidazole 250 mg four times daily
Tetracycline 500 mg four times daily
Page |1
Week 3 – GI
Most Likely / Most Important Diagnoses
May present with mild epigastric pain, and symptoms commonly
worsen after meals, although the pain is classically described as
"burning" and may be located in the substernal rather than
epigastric area.
Hematemesis in the setting of GERD-like symptoms is unusual
and represents an alarm symptom indicative of an upper GI bleed
GERD or tumor and warrants prompt GI referral for evaluation and upper
endoscopy.
Hematochezia and melena are not typically associated with
GERD.
Classic symptoms of heartburn and regurgitation
Likely to occur when gastric volume is increased (after large
meals)
Epigastric abdominal pain that improves with meals is the
hallmark of PUD. However, in some cases, symptoms of PUD
may worsen with meals.
NSAID use is associated with the development of PUD.
Hematemesis, if present, suggests more complicated disease
including bleeding ulcer and warrants urgent GI referral and
endoscopy.
Melena commonly occurs in the setting of an upper GI bleed
secondary to PUD or hemorrhagic gastritis (e.g. NSAID-gastritits).
Hematochezia only occurs in the setting of an upper GI bleed
Peptic ulcer
when massive (e.g. variceal rupture).
disease
Usually characterized by episodic or recurrent epigastric 'aching',
(PUD)
'gnawing', or 'hunger-like' pain or discomfort
Diagnosis with endoscopy and biopsy
Misc: Gastric ulcer pain may occur 5 to 15 minutes after eating
and remain until the stomach empties, which may be up to several
hours in duration, and the pain may otherwise be absent during
times of fasting. Pain from duodenal ulcers is often relieved by
eating, drinking milk, or taking antacids but may return anywhere
from 90 minutes to 4 hours after eating a meal. Both gastric and
duodenal ulcers may be associated with nausea and vomiting
occurring anytime shortly after eating to several hours later.
Gastritis Inflammation or irritation of the stomach lining often causing
sharp epigastric pain. This pain may be variably worsened or
improved with eating food.
Inflammatory forms of gastritis may be caused by chronic
, Page |2
infections such as H. pylori or acute infections such as viruses.
Non-inflammatory forms of 'gastritis' are more properly
histologically termed gastropathy. These may be caused by
chemical irritants to the stomach, including alcohol and NSAIDs.
Agents that Cause or Contribute to Peptic Ulcer Disease
Aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) are the
predominant pharmacologic agents that contribute to the development of PUD.
Classically, the elderly are at the highest attributable risk of ulceration and perforation
due to chronic NSAID use. Chronic NSAID use is a leading cause of morbidity in the
elderly.
Moderate to severe physiologic stress may lead to stress ulceration, predominantly in
patients in the intensive care unit (ICU).
Colonization of the stomach by H. pylori renders the underlying mucosa more
vulnerable to peptic acid damage by disrupting the mucous layer, liberating enzymes and
toxins, and adhering to the gastric epithelium. In addition, the body's immune response to
H. pylori incites an inflammatory reaction that contributes to tissue injury and leads to
chronic gastritis. In most individuals the chronic gastritis is asymptomatic and does not
progress. In some cases, however, altered gastric secretion coupled with tissue injury
leads to peptic ulcer disease. In other cases, gastritis progresses to mucosal atrophy,
intestinal metaplasia, and eventually gastric carcinoma. Rarely, persistent immune
stimulation of gastric lymphoid tissue can lead to gastric lymphoma.
COMPLICATIONS OF GERD AND PUD
GERD
Esophagitis develops when the mucosal defenses that normally counteract the effect of
injurious agents are overwhelmed by refluxed acid, pepsin, or bile.
Peptic strictures from fibrosis and constriction occur in about 10 percent of patients with
reflux esophagitis.
Replacement of the squamous epithelium of the esophagus by columnar epithelium
(Barrett's esophagus) may result from reflux esophagitis. Two to five percent of cases of
Barrett's esophagus may be further complicated by adenocarcinoma.
PUD
Hemorrhage or perforation into the peritoneal cavity or adjacent organs (causing
severe, persistent abdominal pain).
Ulcer scar healing or inflammation can impair gastric emptying leading to gastric outlet
obstruction syndrome.
Alarm Symptoms Warranting Referral to Gastroenterology for Endoscopy
Difficulty in swallowing. Dysphagia to solids suggests possible development
of peptic stricture. Rapidly progressive dysphagia potentially indicates
Dysphagia
adenocarcinoma. Dysphagia to liquids suggests development of a motility
disorder.
, Page |3
Initial onset
of upper GI
Increased chance of cancer.
symptoms
after age 50
May be associated with gastroparesis or gastric outlet obstruction (stricture
Early satiety
or cancer).
Vomiting blood, which suggests bleeding ulcer, mucosal erosions (erosive
Hematemesis gastritis/esophagitis), esophageal tear (Mallory-Weiss), or esophageal
varices.
Hematochezi Passing red blood with stool, which may indicate a rapidly bleeding ulcer or
a mucosal erosions.
Iron The presence of hematemesis, hematochezia, and/or iron deficiency anemia
deficiency may indicate possible bleeding from a peptic ulcer, mucosal erosions, or
anemia cancer.
Painful swallowing, which is associated with infections (e.g. candida),
Odynophagia
erosions, or cancer.
Recurrent
Suggestive of gastric outlet obstruction.
vomiting
Weight loss Associated with malignancy.
Treatment
GERD:
Self-directed trial of over-the-counter anti-secretory therapy, either a histamine-2 receptor
antagonist or a proton-pump inhibitor (PPI)
Lifestyle modifications.
PUD from H. pylori
"Triple therapy" for 10 to 14 days (70% to 85% eradication rate):
PPI standard dose twice daily (esomeprazole is dosed once daily)
Amoxicillin 1 g twice daily
Clarithromycin 500 mg twice daily
"Quadruple therapy" for 10 to 14 days (75% to 90% eradication rate):
PPI standard dose once or twice daily (OR ranitidine 150 mg twice daily)
Metronidazole 250 mg four times daily
Tetracycline 500 mg four times daily
