Final Exam Study Guide (In-Depth)
Week 5 – Gastrointestinal & Neurobiological
Pathologies
Gastroesophageal Reflux Disease (GERD)
Pathophysiology
● Transient lower esophageal sphincter (LES) relaxations and/or hypotensive LES →
reflux of gastric contents → esophagitis (acid + pepsin + bile salts).
● Risk amplifiers: hiatal hernia, delayed gastric emptying, obesity (↑ intra-abdominal
pressure), pregnancy, ETOH, nicotine, chocolate, caffeine, certain meds (CCBs,
nitrates, anticholinergics, theophylline).
Clinical
● Heartburn (post-prandial, supine), regurgitation, sour taste, chronic
cough/hoarseness, dysphagia (stricture). Alarm: dysphagia, odynophagia, weight
loss, GI bleed, anemia.
Complications
● Erosive esophagitis → stricture (fibrosis/narrowing).
● Barrett’s esophagus (intestinal metaplasia) → ↑ risk adenocarcinoma.
Diagnosis
● Typical symptoms → empiric PPI trial.
● Alarm features or refractory → EGD ± biopsy. Ambulatory pH impedance if unclear.
Management
, ● Lifestyle: weight loss (highest impact), elevate HOB, avoid late meals, triggers.
● Pharmacologic: PPIs > H2RAs; add alginate antacids PRN.
● Refractory/complicated: EGD; surgical options (Nissen fundoplication) esp. with large
hiatal hernia.
Exam Pearls
● Long-standing GERD → progressive solid food dysphagia = peptic stricture.
● Chronic GERD + intestinal metaplasia on biopsy = Barrett’s.
Hiatal Hernia
Types: Sliding (95%) vs Paraesophageal.
Tx: Treat GERD; surgery for paraesophageal (risk of strangulation) or refractory symptoms.
Appendicitis
Pathophysiology: Lumen obstruction (fecalith/lymphoid hyperplasia) → venous congestion
→ ischemia → bacterial overgrowth → transmural inflammation → perforation.
Clinical: Periumbilical → RLQ pain (McBurney), anorexia, N/V, low-grade fever;
psoas/obturator/Rovsing signs.
Labs/Imaging: Leukocytosis with left shift; CRP ↑. Adult diagnosis: CT abd/pelvis with
contrast (US in children/pregnancy).
Risks in adults: perforation, abscess, ileus; peri-op: wound infection, adhesions.
Peptic Ulcer Disease (PUD)
Mechanisms
● H. pylori (↑ gastrin, ↓ somatostatin; cytotoxins; mucosal inflammation).
● NSAIDs (↓ prostaglandins → ↓ mucus/bicarbonate, ↓ mucosal blood flow).
● Hypersecretory states (Zollinger–Ellison).
Risk Factors: H. pylori, NSAIDs, steroids + NSAIDs, smoking, severe illness (stress ulcers),
prior PUD, chronic ETOH.