NR 507 Final Review
Advanced Pathophysiology (Chamberlain University)
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Final Review
GERD- Lower Esophageal Sphincter (LES) dysfunction.
o S/S: Heartburn (burning in chest), regurgitations, dysphagia, and chest pain.
o Treatment: lifestyle modifications-HOB elevated, avoid citrus, alcohol, caffeine, carbonation,
avoid eating before bedtime, smoking cessation as it weakens the sphincter.
o Medications: Antacids, if it doesn’t improve, EGD.
o NP roe in GERD management is to evaluate the effectiveness of treatment.
o Warning signs of GERD: age over 50, dysphagia, odynophagia (pain on swallowing), N/V, wt
loss, melena, feeling full after little food.
Esophageal Stricture- chronic inflammation and the development of scar tissue that thickens the
wall of the esophagus.
o Risk factors: GERD, esophagitis, radiation therapy, ingestion of caustic substances like
strong acids or bases, and tumors.
o S/S: dysphasia, sensation of food sticking to the throat, pain when swallowing, food
regurgitation, unintentional weight loss.
o Diagnosis: Barium swallow or EGD.
o Treatment: Meds to reduce inflammation, dilation of stricture, and addressing underlying
cause.
Appendicitis- involves obstruction of the lumen or the opening of the appendix which leads to a
cascade of events resulting in inflammation, infection, and, if untreated, potential perforation.
o Patho: luminal obstruction -> increased luminal pressure -> compromised blood flow
(ischemia) -> bacterial overgrowth (E. coli) -> acute inflammation (pus formation) ->
Perforation
o S/S: Periumbilical pain, RLQ pain, fever and leukocytosis, N/V
o Diagnosis: WBC > 10,000 and increased neutrophils and CRP, abd. ultrasound, CT scan, MRI
o Treatment: appendectomy
Risk is colon CA among those aged 50-74 y/o
Hiatal Hernia- Major risk factor for GERD.
o Diaphragmatic weakness
o Factors: aging, obesity, pregnancy, increased intra-abdominal pressure (chronic coughing or
Valsalva maneuver), structural abnormalities of diaphragm
o Treatment: lifestyle modification, eating small and frequent meals, meds (antacids, PPI;s,
prokinetic agents), surgery to repair (usually w/ severe S/S).
Duodenal Ulcer- Most common peptic ulcer
o Usually caused by H. pylori 95-100% of the time (bacteria that stimulates gastrin secretion
leading to gastric acid hypersecretion)
o Disruption of the balance between aggressive and defensive factors:
Aggressive: Gastric acid, pepsin, H. pylori, NSAIDS
Defensive: Mucus-bicarbonate layer, prostaglandins, cellular repair mechanisms
o S/S: Pain begins 30min-2hrs after eating when the stomach is empty, not unusual for pain to
occur in the middle of the PM and disappear by AM.
o Exam findings: anemia, dehydrated, pain in upper abd., guarding, rigidity, distention
o Pain is usually relieved by ingestion of food or antacids.
o Diagnosis: EGD (Gold standard), H. pylori testing, imaging studies
o Treatment: lifestyle mods, meds, treat H. pylori if that’s the reason
Gastric Ulcer- Pain is relieved w/ food
o Risk factors: h. pylori, NSAIDS, smoking, alcohol, stress, fam hx, obesity, age >65
Peptic Ulcer Disease (PUD)- a break or ulceration in the protective mucosal lining of the lower
esophagus, stomach, or duodenum.
o Least likely to occur in the Large Intestine
o Erosion- superficial ulcers, don’t penetrate
o Ulcer- damages blood vessels
o S/S: epigastric pain 1-3 hrs after eating, pain relieved by eating
o Zollinger-Ellison syndrome causes increased risk of peptic ulcers d/t increase in gastric acid
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