NR 507 Final Exam Comprehensive Review: Key Concepts and
Disorders| Questions and Verified Answers | 100% Correct
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
o Diagnosis: EGD(GOLD STANDARD), lab tests (CBC, stool, serum urea and e-), H/ pylori
testing, abd. Ultrasound, CT (emergency)
o Treatment: Meds and lifestyle mods
• Ulcerative Colitis- Distruption of intestinal mucosal barrier, epithelial cell dysfunction, loss of goblet
cells, and chronic inflammation and ulcerations
o Characterized as continuous inflammation that starts in rectum and continues up through
the cecum
o A colectomy is considered a curative procedure.
o S/S: diarrhea, abdominal pain and cramping, rectal bleeding, urgency to defecate, fatigue,
fever, anemia, colon cancer
o Treatment: Amniosalicylate (Sulfasalazine)
• Crohn’s Disease- Cobble Stone appearance in imaging
o Genetic predisposition
o Immune dysregulation: immune response to intestinal microbiota leading to chronic
inflammation and tissue damage
o Environmental factors: infections, smoking, diet
o Disruption of intestinal barrier: leads to increased permeability, bacterial invasion, and
further immune activation
o Transmural inflammation: leads to complications like strictures, fistulas, and abscesses.
o S/S: abdominal pain, diarrhea, wt. loss, fatigue, fever, rectal bleeding, colon CA
o Treatment: FODMAP Diet, smoking cessation, steroids, immunosuppressants, anti -TNF-alpha,
antiintegrins, and IL inhibitors (for the most severe form)
• Cirrhosis: the late stage of liver scarring (fibrosis) caused by long term liver damage
o Can cause: nodule formation, vascular changes (Portal HTN, splenomegaly, varices), liver
dysfunction (decreased albumin, clotting), and complications (hepatocellular CA, portal
HTN).
o Portal HTN: increased resistance to blood flow, formation of collateral circulation
▪ Complications: variceal bleeding, ascites, splenomegaly, hepatic encephalopathy,
hepatorenal syndrome
o S/S: fatigue, wt loss, abdominal discomfort, N/V, jaundice, spider angiomas (dilated
capillaries), palmar erythema, bruising/bleeding, caput meduse (dilated veins around
umbilicus), hepatic encephalopathy (confusion, tremors), peripheral neuropathy, ascites,
hepatomegaly, splenomegaly, variceal bleeding, melena stool, bloody vomit, gynecomastia,
testicular atrophy, amenorrhea, Vit. Deficiencies (thiamine, folate, B12), muscle wasting,
hypoalbuminemia.
o Diagnosis: elevated liver enzymes and bilirubin, low albumin, prolonged PT INR,
thrombocytopenia, elevated GGT, CT, fibroscan, ultrasound
▪ Liver biopsy is performed to confirm dx when there are not enough clinical symptoms
o Treatment: relieve discomfort as there is NO CURE
• Hepatic Encephalopathy
o Early/Mild S/S: cognitive changes behavioral changes and neuromuscular changes like
memory changes sleep disturbances and subtle personality changes
o Moderate symptoms: cognitive impairment, like confusion, disorientation drowsiness, and
lethargy, behavioral symptoms, like agitation, and neuromuscular abnormalities, like
unsteady gait and asterixis
• Alcoholic Fatty Liver Disease: caused by excessive alcohol consumption
• Non-Alcoholic Fatty Liver Disease: caused by obesity, T2DM, poor diet
o Insulin resistance= fat influx in liver.
• Major Depressive Disorder (MDD)
o Neurotransmitter imbalance: serotonin, norepinephrine, and dopamine
o Neuroendocrine dysregulation-abnormalities in the hypothalamic-pituitary-adrenal axis
causing elevated cortisol levels
o Chronic inflammation
Disorders| Questions and Verified Answers | 100% Correct
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
o Diagnosis: EGD(GOLD STANDARD), lab tests (CBC, stool, serum urea and e-), H/ pylori
testing, abd. Ultrasound, CT (emergency)
o Treatment: Meds and lifestyle mods
• Ulcerative Colitis- Distruption of intestinal mucosal barrier, epithelial cell dysfunction, loss of goblet
cells, and chronic inflammation and ulcerations
o Characterized as continuous inflammation that starts in rectum and continues up through
the cecum
o A colectomy is considered a curative procedure.
o S/S: diarrhea, abdominal pain and cramping, rectal bleeding, urgency to defecate, fatigue,
fever, anemia, colon cancer
o Treatment: Amniosalicylate (Sulfasalazine)
• Crohn’s Disease- Cobble Stone appearance in imaging
o Genetic predisposition
o Immune dysregulation: immune response to intestinal microbiota leading to chronic
inflammation and tissue damage
o Environmental factors: infections, smoking, diet
o Disruption of intestinal barrier: leads to increased permeability, bacterial invasion, and
further immune activation
o Transmural inflammation: leads to complications like strictures, fistulas, and abscesses.
o S/S: abdominal pain, diarrhea, wt. loss, fatigue, fever, rectal bleeding, colon CA
o Treatment: FODMAP Diet, smoking cessation, steroids, immunosuppressants, anti -TNF-alpha,
antiintegrins, and IL inhibitors (for the most severe form)
• Cirrhosis: the late stage of liver scarring (fibrosis) caused by long term liver damage
o Can cause: nodule formation, vascular changes (Portal HTN, splenomegaly, varices), liver
dysfunction (decreased albumin, clotting), and complications (hepatocellular CA, portal
HTN).
o Portal HTN: increased resistance to blood flow, formation of collateral circulation
▪ Complications: variceal bleeding, ascites, splenomegaly, hepatic encephalopathy,
hepatorenal syndrome
o S/S: fatigue, wt loss, abdominal discomfort, N/V, jaundice, spider angiomas (dilated
capillaries), palmar erythema, bruising/bleeding, caput meduse (dilated veins around
umbilicus), hepatic encephalopathy (confusion, tremors), peripheral neuropathy, ascites,
hepatomegaly, splenomegaly, variceal bleeding, melena stool, bloody vomit, gynecomastia,
testicular atrophy, amenorrhea, Vit. Deficiencies (thiamine, folate, B12), muscle wasting,
hypoalbuminemia.
o Diagnosis: elevated liver enzymes and bilirubin, low albumin, prolonged PT INR,
thrombocytopenia, elevated GGT, CT, fibroscan, ultrasound
▪ Liver biopsy is performed to confirm dx when there are not enough clinical symptoms
o Treatment: relieve discomfort as there is NO CURE
• Hepatic Encephalopathy
o Early/Mild S/S: cognitive changes behavioral changes and neuromuscular changes like
memory changes sleep disturbances and subtle personality changes
o Moderate symptoms: cognitive impairment, like confusion, disorientation drowsiness, and
lethargy, behavioral symptoms, like agitation, and neuromuscular abnormalities, like
unsteady gait and asterixis
• Alcoholic Fatty Liver Disease: caused by excessive alcohol consumption
• Non-Alcoholic Fatty Liver Disease: caused by obesity, T2DM, poor diet
o Insulin resistance= fat influx in liver.
• Major Depressive Disorder (MDD)
o Neurotransmitter imbalance: serotonin, norepinephrine, and dopamine
o Neuroendocrine dysregulation-abnormalities in the hypothalamic-pituitary-adrenal axis
causing elevated cortisol levels
o Chronic inflammation
