lOMoARcPSD|62982272
NR507 Final Exam Studyguide
Advanced Pathophysiology (Chamberlain University)
Scan to open on Studocu
Studocu is not sponsored or endorsed by any college or university
Downloaded by elizabeth moses ()
, lOMoARcPSD|62982272
NR507 – Advanced Pathophysiology
Exam Study Guide – Final Study Guide
Exam Format: Cumulative
Question Type: Multiple Choice
Number of Questions: 100
Time Allotted: 120 minutes
Testing Timeframe: The final exam will only be available starting on Wednesday Week 8 at
12:01 am MT until Saturday Week 8 at 11:59 pm MT.
1. Exam Coverage
Content Areas:
Week 5: Gastrointestinal and Neurobiological Pathologies
Week 6: Endocrine Pathologies
Week 7: CNS Sensory and Motor Pathologies
Week 8: Brain and Dermatological Pathologies
2. Key Concepts to Study
Gastrointestinal pathologies:
Pathophysiology of GERD
involves several mechanisms that allow the contents of the stomach
especially acid and digestive enzymes like pepsin) to reflux into the esophagus
leading to mucosal injury and symptoms like heartburn and regurgitation.
Signs and symptoms of GERD
Heartburn
Burning sensation in the chest (retrosternal)
Often worse after meals or when lying down
Improves with antacids
Regurgitation
Sour or bitter-tasting fluid in the throat or mouth
Especially when bending over or lying flat
Dysphagia (difficulty swallowing)
May indicate esophageal inflammation or stricture formation
Chest pain
Non-cardiac in nature
Burning or squeezing, often mistaken for angina
Atypical s/s
Chronic cough
Hoarseness or voice changes
Sore throat or frequent throat clearing
Asthma-like symptoms or worsening of asthma
Laryngitis
Downloaded by elizabeth moses ()
, lOMoARcPSD|62982272
Dental erosion (due to acid exposure)
Globus sensation (feeling of a lump in the throat)
Pharmacologic management of GERD
PPI – 1st Line -omeprazole
Inhibit H⁺/K⁺-ATPase in gastric parietal cells → suppress gastric acid secretion.
Taken 30–60 min before meals (best before breakfast)
Superior to H2 blockers for healing erosive esophagitis
Typically used for 4–8 weeks; long-term use if symptoms persist
or in severe cases
H2 Receptor Agonists – famotidine
Block H2 receptors on parietal cells → ↓ acid secretion
For mild or intermittent symptoms
Less effective than PPIs for healing esophagitis
Can be used at bedtime for nocturnal symptoms (often in
combination with daytime PPI)
Antacids
Neutralizes gastric acid -Calcium carbonate (tums)
Short acting
Alginates (gavison) use with antacids
Forms gel raft – helps prevent reflux
Prokinetic Agents
Increases tone and improves gastric emptying
Used with PPIs in some cases
Risk factors for esophageal stricture
Chronic GERD (most common)
Esophagitis
Esophageal surgery or radiation
Ingestion of corrosive substances -caustic ingestion – alkali and acid burns
Prolonged NG tube
Hiatal hernia
Medications -pill induced esophagitis (potassium chloride, NSAIDs)
Smoking and alcohol
Hiatal hernia treatment
depends on the type, severity of symptoms, and the presence of complications
sliding hernia
most common
stomach and JE junction slide into esophagus
commonly associated with GERD
Downloaded by elizabeth moses ()
, lOMoARcPSD|62982272
paraoesophageal hernia
part of stomach herniates beside esophagus
risk of strangulation or obstruction
Treatment
Control symptoms/prevent complications
Lifestyle modifications
Weight loss
Smaller meals
Avoid lying down after meals
Elevate HOB
Avoid trigger foods -spicy, fatty, caffeine, chocolate, alcohol
Smoking cessation
Pharmacological Therapy – PPI, H2 antagonists, antacids, prokinetics
Surgical Interventions
Laparoscopic paraoesophageal fundoplication – most common
Pathophysiology of appendicitis
inflammation of the vermiform appendix, usually caused by obstruction of the
appendiceal lumen. It is a surgical emergency and one of the most common causes of
acute abdominal pain.
Luminal obstruction – primary trigger
Caused by:
Fecalith (hard stool)
Lymphoid hyperplasia
Foreign body
Worms
tumors
Mucus secretion continues behind obstruction
Leads to increased luminal pressure
Causes obstruction
Bacterial overgrowth and inflammation
Most common – e coli
Ischemia and wall necrosis
Impairs arterial blood flow, leading to ischemia
Perforation
Localized or general peritonitis
Possible complications
Perforations
Abscess
Sepsis
Appendiceal mass
Portal pylephlebitis (rare)
Downloaded by elizabeth moses ()
NR507 Final Exam Studyguide
Advanced Pathophysiology (Chamberlain University)
Scan to open on Studocu
Studocu is not sponsored or endorsed by any college or university
Downloaded by elizabeth moses ()
, lOMoARcPSD|62982272
NR507 – Advanced Pathophysiology
Exam Study Guide – Final Study Guide
Exam Format: Cumulative
Question Type: Multiple Choice
Number of Questions: 100
Time Allotted: 120 minutes
Testing Timeframe: The final exam will only be available starting on Wednesday Week 8 at
12:01 am MT until Saturday Week 8 at 11:59 pm MT.
1. Exam Coverage
Content Areas:
Week 5: Gastrointestinal and Neurobiological Pathologies
Week 6: Endocrine Pathologies
Week 7: CNS Sensory and Motor Pathologies
Week 8: Brain and Dermatological Pathologies
2. Key Concepts to Study
Gastrointestinal pathologies:
Pathophysiology of GERD
involves several mechanisms that allow the contents of the stomach
especially acid and digestive enzymes like pepsin) to reflux into the esophagus
leading to mucosal injury and symptoms like heartburn and regurgitation.
Signs and symptoms of GERD
Heartburn
Burning sensation in the chest (retrosternal)
Often worse after meals or when lying down
Improves with antacids
Regurgitation
Sour or bitter-tasting fluid in the throat or mouth
Especially when bending over or lying flat
Dysphagia (difficulty swallowing)
May indicate esophageal inflammation or stricture formation
Chest pain
Non-cardiac in nature
Burning or squeezing, often mistaken for angina
Atypical s/s
Chronic cough
Hoarseness or voice changes
Sore throat or frequent throat clearing
Asthma-like symptoms or worsening of asthma
Laryngitis
Downloaded by elizabeth moses ()
, lOMoARcPSD|62982272
Dental erosion (due to acid exposure)
Globus sensation (feeling of a lump in the throat)
Pharmacologic management of GERD
PPI – 1st Line -omeprazole
Inhibit H⁺/K⁺-ATPase in gastric parietal cells → suppress gastric acid secretion.
Taken 30–60 min before meals (best before breakfast)
Superior to H2 blockers for healing erosive esophagitis
Typically used for 4–8 weeks; long-term use if symptoms persist
or in severe cases
H2 Receptor Agonists – famotidine
Block H2 receptors on parietal cells → ↓ acid secretion
For mild or intermittent symptoms
Less effective than PPIs for healing esophagitis
Can be used at bedtime for nocturnal symptoms (often in
combination with daytime PPI)
Antacids
Neutralizes gastric acid -Calcium carbonate (tums)
Short acting
Alginates (gavison) use with antacids
Forms gel raft – helps prevent reflux
Prokinetic Agents
Increases tone and improves gastric emptying
Used with PPIs in some cases
Risk factors for esophageal stricture
Chronic GERD (most common)
Esophagitis
Esophageal surgery or radiation
Ingestion of corrosive substances -caustic ingestion – alkali and acid burns
Prolonged NG tube
Hiatal hernia
Medications -pill induced esophagitis (potassium chloride, NSAIDs)
Smoking and alcohol
Hiatal hernia treatment
depends on the type, severity of symptoms, and the presence of complications
sliding hernia
most common
stomach and JE junction slide into esophagus
commonly associated with GERD
Downloaded by elizabeth moses ()
, lOMoARcPSD|62982272
paraoesophageal hernia
part of stomach herniates beside esophagus
risk of strangulation or obstruction
Treatment
Control symptoms/prevent complications
Lifestyle modifications
Weight loss
Smaller meals
Avoid lying down after meals
Elevate HOB
Avoid trigger foods -spicy, fatty, caffeine, chocolate, alcohol
Smoking cessation
Pharmacological Therapy – PPI, H2 antagonists, antacids, prokinetics
Surgical Interventions
Laparoscopic paraoesophageal fundoplication – most common
Pathophysiology of appendicitis
inflammation of the vermiform appendix, usually caused by obstruction of the
appendiceal lumen. It is a surgical emergency and one of the most common causes of
acute abdominal pain.
Luminal obstruction – primary trigger
Caused by:
Fecalith (hard stool)
Lymphoid hyperplasia
Foreign body
Worms
tumors
Mucus secretion continues behind obstruction
Leads to increased luminal pressure
Causes obstruction
Bacterial overgrowth and inflammation
Most common – e coli
Ischemia and wall necrosis
Impairs arterial blood flow, leading to ischemia
Perforation
Localized or general peritonitis
Possible complications
Perforations
Abscess
Sepsis
Appendiceal mass
Portal pylephlebitis (rare)
Downloaded by elizabeth moses ()
