NR507 Final Exam / NR 507 Week 8 Exam
Advanced Pathophysiology Questions and
Answers () (Complete Verified
Answers)
• Risk factors for Esophageal Stricture -✓✓Chronic untreated GERD
Repeated acid injury → fibrosis and narrowing
Barrett's esophagus increases risk
• Hiatal Hernia Treatment -✓✓Lifestyle modification (wt loss, elevate HOB, avoid large
meals, tight clothes, and trigger foods)
PPIs
Surgical repair if severe or refractory
• Pathophysiology of Appendicitis -✓✓Obstruction of appendix lumen (fecalith, lymphoid
hyperplasia)
Increased intraluminal pressure → ischemia → bacterial invasion → inflammation
• Symptoms of Appendicitis -✓✓Periumbilical pain → migrates to RLQ (McBurney's
point)
Nausea, vomiting
Low-grade fever
• Diagnosing Appendicitis -✓✓↑ WBC with left shift
↑ CRP
CT abdomen (gold standard)
• Risks for appendectomy in adults -✓✓Perforation risk increases with delayed
diagnosis
Higher complication rate than children
• Peptic ulcer disease (PUD) pathophysiology -✓✓Gastric acid and pepcin overwhelm
impaired mucosal defenses, distrupt bicarb barrier, reduce prostaglandin-mediated
protection + promote inflammation causing mucosal erosion and ulcer formation
• Risk factors for PUD -✓✓H. pylori
NSAIDs
Stress-related mucosal damage
• Gastric ulcers -✓✓Pain is worse w/ meals
Weight loss
Normal/low acid levels
,• Duodenal ulcers -✓✓Pain improves w/ meals
Weight gain
High acid levels
• Causes of gastric ulcers -✓✓Most commonly caused by H pylori, and NSAID. can also
be caused by stress, smoking, alcohol use, bile reflux, zollinger-ellison syndrome
• Signs and symptoms of duodenal ulcer -✓✓Epigastric pain relieved by food
frequent waking at night from pain
nausea
weight gain
gi bleed
• Pathophysiology of ulcerative colitis -✓✓Chronic continuous inflammation of colon and
rectum.
Mucosa and submucosa layers only, beginning in the rectum
Results from a dysregulated immune response to intestinal microbiota
• Risk factors for UC -✓✓Genetics
Immune dysregulation
Environmental factors
NON-SMOKERS OR FORMER SMOKERS have higher risk SMOKING IS
PROTECTIVE IN UC
• Risk factors for Crohns -✓✓Genetics
Immune Dysfunction
Environmental factors
Smoker
15-30 YRS
• Symptoms of UC -✓✓Chronic diarrhea
Bloody stools
Mucus in stool
Tenesmus
ABD pain
Urgency
Fatigue
Weight loss
• Pathophysiology of Crohn's disease -✓✓Chronic inflammatory bowl disease caused by
dysregulated immune activation resulting in transmural, segmental inflammation that
can affect ANY part of the GI tract from mouth to anus
, • Treatment of Crohn's disease -✓✓Anti-inflammatory meds like 5-aminosalicylates
(mesalamine)
Corticosteroids
Immunomodulators (azathioprine, meothorexate)
Biologic therapies (anti-TNF agents: infliximab, adalimumab)
Antibiotics if needed
Nutrition therapy!!!
• Nutrition Therapy for Crohns -✓✓High calorie
High protein diet
Vitamin + mineral supplementation
Enteral nutrition
• Pathophysiology of Non-alcoholic fatty liver disease -✓✓Insulin resistance → fat
accumulation in hepatocytes
Progresses to inflammation + fibrosis
• Pathophysiology of alcoholic cirrhosis -✓✓Chronic alcohol → hepatocyte injury →
fibrosis → nodular regeneration
• Diagnosing cirrhosis -✓✓Clinical assessment
Lab findings: ↑ AST & ↑ ALT , ↑ Alkaline phosphatase, ↑ total and direct bilirubin, ↑
PT/INR, ↓ Albumin, ↓ platelet count
Imaging: ultrasound is the first line
Liver biopsy: gold standard, confirms cirrhosis.
• Pathophysiology of ascites development in liver cirrhosis -✓✓Portal hypertension →
splanchnic vasodilation → reduced effective arterial volume → neurohormonal
activation → renal sodium and water retention → ↓ oncotic pressure and accumulation
of fluid in the peritoneal cavity
• Physical symptoms due to ascites associated with cirrhosis -✓✓Abd distention +
discomfort/pain
Abd taut + shiny
Dyspnea
Orthopnea
Decreased exercise tolerance
Early satiety
Nausea
Decreased appetite
Peripheral edema
Umbilical changes
• Treatment goals of patients who have ascites due to cirrhosis -✓✓Sodium restriction
Diuretics (spironolactone)
Advanced Pathophysiology Questions and
Answers () (Complete Verified
Answers)
• Risk factors for Esophageal Stricture -✓✓Chronic untreated GERD
Repeated acid injury → fibrosis and narrowing
Barrett's esophagus increases risk
• Hiatal Hernia Treatment -✓✓Lifestyle modification (wt loss, elevate HOB, avoid large
meals, tight clothes, and trigger foods)
PPIs
Surgical repair if severe or refractory
• Pathophysiology of Appendicitis -✓✓Obstruction of appendix lumen (fecalith, lymphoid
hyperplasia)
Increased intraluminal pressure → ischemia → bacterial invasion → inflammation
• Symptoms of Appendicitis -✓✓Periumbilical pain → migrates to RLQ (McBurney's
point)
Nausea, vomiting
Low-grade fever
• Diagnosing Appendicitis -✓✓↑ WBC with left shift
↑ CRP
CT abdomen (gold standard)
• Risks for appendectomy in adults -✓✓Perforation risk increases with delayed
diagnosis
Higher complication rate than children
• Peptic ulcer disease (PUD) pathophysiology -✓✓Gastric acid and pepcin overwhelm
impaired mucosal defenses, distrupt bicarb barrier, reduce prostaglandin-mediated
protection + promote inflammation causing mucosal erosion and ulcer formation
• Risk factors for PUD -✓✓H. pylori
NSAIDs
Stress-related mucosal damage
• Gastric ulcers -✓✓Pain is worse w/ meals
Weight loss
Normal/low acid levels
,• Duodenal ulcers -✓✓Pain improves w/ meals
Weight gain
High acid levels
• Causes of gastric ulcers -✓✓Most commonly caused by H pylori, and NSAID. can also
be caused by stress, smoking, alcohol use, bile reflux, zollinger-ellison syndrome
• Signs and symptoms of duodenal ulcer -✓✓Epigastric pain relieved by food
frequent waking at night from pain
nausea
weight gain
gi bleed
• Pathophysiology of ulcerative colitis -✓✓Chronic continuous inflammation of colon and
rectum.
Mucosa and submucosa layers only, beginning in the rectum
Results from a dysregulated immune response to intestinal microbiota
• Risk factors for UC -✓✓Genetics
Immune dysregulation
Environmental factors
NON-SMOKERS OR FORMER SMOKERS have higher risk SMOKING IS
PROTECTIVE IN UC
• Risk factors for Crohns -✓✓Genetics
Immune Dysfunction
Environmental factors
Smoker
15-30 YRS
• Symptoms of UC -✓✓Chronic diarrhea
Bloody stools
Mucus in stool
Tenesmus
ABD pain
Urgency
Fatigue
Weight loss
• Pathophysiology of Crohn's disease -✓✓Chronic inflammatory bowl disease caused by
dysregulated immune activation resulting in transmural, segmental inflammation that
can affect ANY part of the GI tract from mouth to anus
, • Treatment of Crohn's disease -✓✓Anti-inflammatory meds like 5-aminosalicylates
(mesalamine)
Corticosteroids
Immunomodulators (azathioprine, meothorexate)
Biologic therapies (anti-TNF agents: infliximab, adalimumab)
Antibiotics if needed
Nutrition therapy!!!
• Nutrition Therapy for Crohns -✓✓High calorie
High protein diet
Vitamin + mineral supplementation
Enteral nutrition
• Pathophysiology of Non-alcoholic fatty liver disease -✓✓Insulin resistance → fat
accumulation in hepatocytes
Progresses to inflammation + fibrosis
• Pathophysiology of alcoholic cirrhosis -✓✓Chronic alcohol → hepatocyte injury →
fibrosis → nodular regeneration
• Diagnosing cirrhosis -✓✓Clinical assessment
Lab findings: ↑ AST & ↑ ALT , ↑ Alkaline phosphatase, ↑ total and direct bilirubin, ↑
PT/INR, ↓ Albumin, ↓ platelet count
Imaging: ultrasound is the first line
Liver biopsy: gold standard, confirms cirrhosis.
• Pathophysiology of ascites development in liver cirrhosis -✓✓Portal hypertension →
splanchnic vasodilation → reduced effective arterial volume → neurohormonal
activation → renal sodium and water retention → ↓ oncotic pressure and accumulation
of fluid in the peritoneal cavity
• Physical symptoms due to ascites associated with cirrhosis -✓✓Abd distention +
discomfort/pain
Abd taut + shiny
Dyspnea
Orthopnea
Decreased exercise tolerance
Early satiety
Nausea
Decreased appetite
Peripheral edema
Umbilical changes
• Treatment goals of patients who have ascites due to cirrhosis -✓✓Sodium restriction
Diuretics (spironolactone)
