NR507 Final Exam Study Guide
GERD (Gastroesophageal reflux disease): chronic condition
Subjective Assessment- can mimic cardiac chest pain, heartburn,
regurgitation, and dysphagia
Objective Assessment- in uncomplicated GERD this will be normal. In
severe cases there could be esophagitis.
Treatment- modify lifestyle, limit trigger foods (spicy, citrus, tomato,
caffeine, chocolate, alcohol), small frequent meals, don’t eat 2-3 hours
before bed, quit smoking, AVOID NSAIDS and Calcium channel blockers,
medications (PPI reduce gastric acid and promote healing) (H2 receptor
antagonists reduce gastric acid), The NP role is to evaluate the
effectiveness of intervention.
Warning Signs- dysphagia, age >50, odynophagia, nausea and vomiting,
weight loss, melena, and feeling full after little food
Lower Esophageal Sphincter (LES)- The LES is a ring of muscle located at the
junction of the esophagus and stomach. In GERD, the LES may have
reduced pressure or improper relaxation, allowing gastric acid to flow back
into the esophagus.
Hiatal Hernia- occurs when part of the stomach protrudes through the
diaphragm into the chest cavity. It can contribute to GERD by disrupting
the normal barrier between the esophagus and stomach.
Esophageal Motility Disorders (EMD)- Impaired esophageal peristalsis
(muscle contractions that propel food downward) and reduced esophageal
clearance can lead to the pooling of gastric acid in the esophagus.
Acidic Gastric Contents- Gastric acid, bile acids, and pepsin are the major
components of the gastric contents that reflux into the esophagus. These
substances can cause direct mucosal damage and trigger inflammation,
leading to the characteristic symptoms of GERD. This triggers GERD
Sample Questions:
o In managing GERD, the most appropriate medication regimen is a PPI
to reduce gastric acid, promote healing, and relieve symptoms.
o A patient prescribed a PPI returns for follow-up and reports break
through symptoms, what is the next action? To evaluate the
effectiveness and adherence to the treatment plan, inconsistent
timing can lead to breakthrough symptoms.
, o If PPI’s and lifestyle modifications are ineffective, what is the next
step? Endoscopy to directly visualize the issue.
Esophageal Stricture: narrowing of the esophagus. This condition can make
swallowing difficult or painful and may lead to complications if left untreated.
Causes- CHRONIC GERD, esophagitis (often due to GERD), injury (toxins,
thermal injury, and endoscopy damage), tumors, radiation, and infections
(fungal or bacterial infections).
Sample Questions:
o The most strongly associated risk factor is chronic GERD.
Symptoms- dysphagia, painful swallowing (odynophagia), regurgitation,
chest pain, unintentional weight loss, choking or gagging while eating
Appendicitis: an obstruction in the lumen of the appendix, which leads to
inflammation, infection, and possible perforation
Pathophysiology- luminal obstruction (typically caused by fecaliths),
preventing normal drainage of mucus and secretions, then increased
luminal pressure compresses blood vessels, compromising blood flow
(ischemia) as pressure rises leading to ischemia and necrosis, stagnant
bacteria (typically e. coli) is responded to by neutrophils causing
inflammation and pus formation, acute information shows edema, leads to
perforation (localized- abscess, generalized- peritonitis), then systemic
response
o Summary: obstruction- distention, ischemia- inflammation, necrosis-
perforation
Symptoms- periumbilical pain, right lower quadrant pain, fever and
leukocytosis, nausea and vomiting
Diagnosis: WBC >10,000, abdominal u/s, CT scan, and MRI (pregnant
women and children) to rule out non-appendiceal diseases.
Treatment: risks following an appendectomy 50- to 74-year-olds need a
colonoscopy due to increased risk of colon cancer.
Sample Questions:
o Which is most indicative of an inflamed appendix? Persistent/severe
localized pain (periumbilical or epigastric), with rebound tenderness.
o Which are signs and symptoms of appendicitis? Fever and chills due
to the inflammatory response.
o Prompt diagnosis and treatment (surgical removal) is crucial to
prevent perforation and sepsis.
,Hiatal Hernia: occur when part of the stomach pushes through the diaphragm
into the chest cavity. This is because of diaphragmatic weaknesses.
Symptoms- heartburn, chest pain, dysphagia, regurgitation, SOB, epigastric
pain
Risk Factors- obesity, pregnancy, frequent heavy lifting
Diagnosis- Barium Swallow (part of stomach visualized above diaphragm),
chest x ray, endoscopy, esophageal manometry
Treatment- depends on type and severity of symptoms, lose weight, eat
small frequent meals, wait 2-3 hours to lay down, elevate head of bed,
avoid food triggers, lose weight, and quit smoking
o Medications- antacids (tums), H2 receptor blockers (famotidine), PPI
(omeprazole), prokinetics (NOT COMMON) (metoclopramide)
o Surgery- hiatal hernia repair, gastropexy
Duodenal Ulcer
Pathophysiology- imbalance between aggressive (gastric acid and pepsin)
and the protective mechanisms of the duodenal mucosa. The imbalance
leads to erosion and ulceration of the mucosal lining typically in the first
portion (duodenal bulb).
o H. Pylori is the cause in 95 to 100% of the cases
o Gastric acid hypersecretion, impaired mucosal defense mechanisms,
and disruption of the balance between aggressive and defensive
factors
o Aggressive Factors- gastric acid, pepsin, H. pylori, NSAIDs
o Defensive Factors- mucus bicarbonate layer, prostaglandins, cellular
repair mechanisms
o Contributing Factors- NSAIDS, smoking, stress
Assessment- the goal is to identify the underlying cause and severity,
while assessing the potential complications. To do this we want a detailed
health history
Symptoms- epigastric pain (relieved by eating meals), dysphagia,
dyspepsia, vomiting, happens in the middle of the night
Complications- bleeding (black tarry stools), perforation (sudden severe
abdominal pain), obstruction
Risks- H. Pylori infection, NSAID use, smoking, alcohol consumption, stress,
or family history of PUD
, Physical Examination- anemia, dehydration, upper abdomen pain, rigidity
or guarding, rebound tenderness, absent bowel sounds, masses or
distention
Diagnosis- The gold standard is endoscopy to visualize and biopsy at the
same time, can also do a CBC, stool occult blood test, and renal function
tests
Treatment- dietary changes, smoking cessation, limit alcohol, avoid NSAIDS
o H. Pylori- triple therapy for 14 days (PPI, amoxicillin, and
clarithromycin)
Gastric Ulcer
Pathophysiology- involves imbalance between aggressive and protective
mechanisms, leading to erosion of stomach lining and ulcer formation in
the gastric mucosa, due to infection and NSAID overuse
Stages- hypersecretion, mucosal injury and inflammation, ulcer formation,
healing complications
Symptoms- pain after eating, nausea and vomiting, gastric bleeding,
anemia, bloating and indigestion
Risks- H. Pylori, NSAIDS, smoking, alcohol, stress, family history, age. These
risk factors are categorized as modifiable and non-modifiable
Sample Questions:
o In comparing gastric and duodenal ulcers which statement is most
accurate? H. pylori accounts for duodenal ulcer in 95-100% of the
cases.
o NSAIDS inhibit the activity of COX enzymes, reducing the production
of prostaglandins. Inhibition of prostaglandin synthesis by NSAIDS
compromise the protective mechanism and lead to mucosal damage
and increase risk for ulcer formation.
Peptic Ulcer Disease
A break or ulceration in the protective mucosal lining of the lower
esophagus, stomach, or duodenum. Least likely to occur in the large
intestine
o Erosion- superficial ulcerations that erode the mucosa but do not
penetrate the muscularis.
o Ulcer- True ulcers extend through the muscularis and damage blood
vessels causing hemorrhage and perforation of the GI wall
Pathophysiology- imbalance between the aggressive and protective
mechanisms
GERD (Gastroesophageal reflux disease): chronic condition
Subjective Assessment- can mimic cardiac chest pain, heartburn,
regurgitation, and dysphagia
Objective Assessment- in uncomplicated GERD this will be normal. In
severe cases there could be esophagitis.
Treatment- modify lifestyle, limit trigger foods (spicy, citrus, tomato,
caffeine, chocolate, alcohol), small frequent meals, don’t eat 2-3 hours
before bed, quit smoking, AVOID NSAIDS and Calcium channel blockers,
medications (PPI reduce gastric acid and promote healing) (H2 receptor
antagonists reduce gastric acid), The NP role is to evaluate the
effectiveness of intervention.
Warning Signs- dysphagia, age >50, odynophagia, nausea and vomiting,
weight loss, melena, and feeling full after little food
Lower Esophageal Sphincter (LES)- The LES is a ring of muscle located at the
junction of the esophagus and stomach. In GERD, the LES may have
reduced pressure or improper relaxation, allowing gastric acid to flow back
into the esophagus.
Hiatal Hernia- occurs when part of the stomach protrudes through the
diaphragm into the chest cavity. It can contribute to GERD by disrupting
the normal barrier between the esophagus and stomach.
Esophageal Motility Disorders (EMD)- Impaired esophageal peristalsis
(muscle contractions that propel food downward) and reduced esophageal
clearance can lead to the pooling of gastric acid in the esophagus.
Acidic Gastric Contents- Gastric acid, bile acids, and pepsin are the major
components of the gastric contents that reflux into the esophagus. These
substances can cause direct mucosal damage and trigger inflammation,
leading to the characteristic symptoms of GERD. This triggers GERD
Sample Questions:
o In managing GERD, the most appropriate medication regimen is a PPI
to reduce gastric acid, promote healing, and relieve symptoms.
o A patient prescribed a PPI returns for follow-up and reports break
through symptoms, what is the next action? To evaluate the
effectiveness and adherence to the treatment plan, inconsistent
timing can lead to breakthrough symptoms.
, o If PPI’s and lifestyle modifications are ineffective, what is the next
step? Endoscopy to directly visualize the issue.
Esophageal Stricture: narrowing of the esophagus. This condition can make
swallowing difficult or painful and may lead to complications if left untreated.
Causes- CHRONIC GERD, esophagitis (often due to GERD), injury (toxins,
thermal injury, and endoscopy damage), tumors, radiation, and infections
(fungal or bacterial infections).
Sample Questions:
o The most strongly associated risk factor is chronic GERD.
Symptoms- dysphagia, painful swallowing (odynophagia), regurgitation,
chest pain, unintentional weight loss, choking or gagging while eating
Appendicitis: an obstruction in the lumen of the appendix, which leads to
inflammation, infection, and possible perforation
Pathophysiology- luminal obstruction (typically caused by fecaliths),
preventing normal drainage of mucus and secretions, then increased
luminal pressure compresses blood vessels, compromising blood flow
(ischemia) as pressure rises leading to ischemia and necrosis, stagnant
bacteria (typically e. coli) is responded to by neutrophils causing
inflammation and pus formation, acute information shows edema, leads to
perforation (localized- abscess, generalized- peritonitis), then systemic
response
o Summary: obstruction- distention, ischemia- inflammation, necrosis-
perforation
Symptoms- periumbilical pain, right lower quadrant pain, fever and
leukocytosis, nausea and vomiting
Diagnosis: WBC >10,000, abdominal u/s, CT scan, and MRI (pregnant
women and children) to rule out non-appendiceal diseases.
Treatment: risks following an appendectomy 50- to 74-year-olds need a
colonoscopy due to increased risk of colon cancer.
Sample Questions:
o Which is most indicative of an inflamed appendix? Persistent/severe
localized pain (periumbilical or epigastric), with rebound tenderness.
o Which are signs and symptoms of appendicitis? Fever and chills due
to the inflammatory response.
o Prompt diagnosis and treatment (surgical removal) is crucial to
prevent perforation and sepsis.
,Hiatal Hernia: occur when part of the stomach pushes through the diaphragm
into the chest cavity. This is because of diaphragmatic weaknesses.
Symptoms- heartburn, chest pain, dysphagia, regurgitation, SOB, epigastric
pain
Risk Factors- obesity, pregnancy, frequent heavy lifting
Diagnosis- Barium Swallow (part of stomach visualized above diaphragm),
chest x ray, endoscopy, esophageal manometry
Treatment- depends on type and severity of symptoms, lose weight, eat
small frequent meals, wait 2-3 hours to lay down, elevate head of bed,
avoid food triggers, lose weight, and quit smoking
o Medications- antacids (tums), H2 receptor blockers (famotidine), PPI
(omeprazole), prokinetics (NOT COMMON) (metoclopramide)
o Surgery- hiatal hernia repair, gastropexy
Duodenal Ulcer
Pathophysiology- imbalance between aggressive (gastric acid and pepsin)
and the protective mechanisms of the duodenal mucosa. The imbalance
leads to erosion and ulceration of the mucosal lining typically in the first
portion (duodenal bulb).
o H. Pylori is the cause in 95 to 100% of the cases
o Gastric acid hypersecretion, impaired mucosal defense mechanisms,
and disruption of the balance between aggressive and defensive
factors
o Aggressive Factors- gastric acid, pepsin, H. pylori, NSAIDs
o Defensive Factors- mucus bicarbonate layer, prostaglandins, cellular
repair mechanisms
o Contributing Factors- NSAIDS, smoking, stress
Assessment- the goal is to identify the underlying cause and severity,
while assessing the potential complications. To do this we want a detailed
health history
Symptoms- epigastric pain (relieved by eating meals), dysphagia,
dyspepsia, vomiting, happens in the middle of the night
Complications- bleeding (black tarry stools), perforation (sudden severe
abdominal pain), obstruction
Risks- H. Pylori infection, NSAID use, smoking, alcohol consumption, stress,
or family history of PUD
, Physical Examination- anemia, dehydration, upper abdomen pain, rigidity
or guarding, rebound tenderness, absent bowel sounds, masses or
distention
Diagnosis- The gold standard is endoscopy to visualize and biopsy at the
same time, can also do a CBC, stool occult blood test, and renal function
tests
Treatment- dietary changes, smoking cessation, limit alcohol, avoid NSAIDS
o H. Pylori- triple therapy for 14 days (PPI, amoxicillin, and
clarithromycin)
Gastric Ulcer
Pathophysiology- involves imbalance between aggressive and protective
mechanisms, leading to erosion of stomach lining and ulcer formation in
the gastric mucosa, due to infection and NSAID overuse
Stages- hypersecretion, mucosal injury and inflammation, ulcer formation,
healing complications
Symptoms- pain after eating, nausea and vomiting, gastric bleeding,
anemia, bloating and indigestion
Risks- H. Pylori, NSAIDS, smoking, alcohol, stress, family history, age. These
risk factors are categorized as modifiable and non-modifiable
Sample Questions:
o In comparing gastric and duodenal ulcers which statement is most
accurate? H. pylori accounts for duodenal ulcer in 95-100% of the
cases.
o NSAIDS inhibit the activity of COX enzymes, reducing the production
of prostaglandins. Inhibition of prostaglandin synthesis by NSAIDS
compromise the protective mechanism and lead to mucosal damage
and increase risk for ulcer formation.
Peptic Ulcer Disease
A break or ulceration in the protective mucosal lining of the lower
esophagus, stomach, or duodenum. Least likely to occur in the large
intestine
o Erosion- superficial ulcerations that erode the mucosa but do not
penetrate the muscularis.
o Ulcer- True ulcers extend through the muscularis and damage blood
vessels causing hemorrhage and perforation of the GI wall
Pathophysiology- imbalance between the aggressive and protective
mechanisms
