9.1 Esophageal, Gastric & Peptic Ulcer Disorders

9.1 Esophageal, Gastric & Peptic Ulcer Disorders

High-Yield Overview: Upper gastrointestinal disorders present with overlapping symptoms such as dysphagia, chest pain, epigastric distress, and GI bleeding. Differentiating motor disorders from structural, inflammatory, or malignant etiologies requires systematic diagnostic algorithms—utilizing upper endoscopy (EGD) for mucosal evaluation and esophageal manometry for motor dysfunction.

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Esophageal Motility Disorders

Esophageal motility disorders result from impaired neuromuscular coordination of the esophageal body and lower esophageal sphincter (LES).

Achalasia

Achalasia is caused by the autoimmune or idiopathic degeneration of nitrinergic inhibitory ganglion cells in the myenteric (Auerbach) plexus. Loss of nitric oxide and vasoactive intestinal peptide (VIP) production leads to uninhibited smooth muscle contraction and failure of the LES to relax.

• Clinical Presentation: Progressive dysphagia to both solids AND liquids simultaneously, regurgitation of undigested food, nocturnal cough, heartburn, and unintentional weight loss.
• Diagnostic Evaluation:
  1. Barium Esophagram (Initial Screening): Shows distal esophageal narrowing with smooth tapering ("bird's-beak" sign) and proximal esophageal dilation with loss of normal peristalsis.
  2. Upper Endoscopy (EGD): Mandatory to exclude pseudoachalasia caused by esophageal adenocarcinoma or gastric cardia carcinoma invading the myenteric plexus.
  3. High-Resolution Esophageal Manometry (Gold Standard): Demonstrates incomplete LES relaxation (integrated relaxation pressure [IRP] >15 mmHg) and 100% aperistalsis in the distal esophagus.
• Management:
  • Low Surgical Risk Patients: Pneumatic balloon dilation, laparoscopic Heller myotomy with partial fundoplication, or Peroral Endoscopic Myotomy (POEM).
  • High Surgical Risk Patients: Endoscopic botulinum toxin injection into the LES, oral nitrates, or calcium channel blockers (diltiazem).

Diffuse Esophageal Spasm (DES) & Hypercontractile Esophagus

Diffuse Esophageal Spasm involves uncoordinated, non-peristaltic contractions of the distal esophagus with normal LES tone.

• Clinical Presentation: Episodic retrosternal chest pain mimicking angina pectoris, frequently precipitated by emotional stress, hot liquids, or extremely cold beverages. Transient dysphagia to solids and liquids.
• Diagnostics: Barium swallow demonstrates a "corkscrew" or "rosary bead" esophagus. Manometry reveals simultaneous, high-amplitude, non-peristaltic contractions in >20% of swallows with normal LES relaxation.
• Treatment: First-line therapy includes calcium channel blockers (e.g., diltiazem) and nitrates to promote smooth muscle relaxation. Tricyclic antidepressants (e.g., imipramine) reduce visceral hypersensitivity.

Systemic Sclerosis (Scleroderma) Esophagus

Scleroderma leads to smooth muscle atrophy and progressive fibrous replacement of the distal two-thirds of the esophagus.

• Features: Marked hypotensive LES (pressure <10 mmHg) and absence of distal peristalsis, causing severe, intractable GERD, erosive esophagitis, and peptic stricture formation.

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GERD, Barrett Esophagus & Adenocarcinoma

Gastroesophageal Reflux Disease (GERD)

GERD stems from transient lower esophageal sphincter relaxations (TLESRs) or decreased LES baseline tone.

• Alarm Features Requiring Immediate EGD:
  • Age >55 years with new-onset dyspepsia
  • Progressive dysphagia or odynophagia
  • Unintentional weight loss (>5% body weight)
  • Persistent vomiting or gastrointestinal bleeding (hematemesis, melena)
  • Unexplained iron deficiency anemia
• Empiric Management: In the absence of alarm features, patients receive an 8-week trial of once-daily proton pump inhibitors (PPIs) alongside lifestyle modifications (head elevation, avoiding late meals).

Barrett Esophagus & Esophageal Carcinoma

Barrett Esophagus represents intestinal metaplasia, where chronic acid exposure replaces normal stratified squamous epithelium with non-ciliated columnar epithelium containing goblet cells.

• Cancer Risk: Increases the risk of esophageal adenocarcinoma by 30- to 40-fold (0.5% per year risk).
• Surveillance Protocol:
  • No Dysplasia: Surveillance EGD every 3 to 5 years.
  • Low-Grade Dysplasia: Endoscopic eradication therapy (radiofrequency ablation) or surveillance EGD every 6 to 12 months.
  • High-Grade Dysplasia: Endoscopic mucosal resection or radiofrequency ablation.

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Esophageal Perforation & Lacerations

Mallory-Weiss Syndrome

• Pathophysiology: Mucosa-only longitudinal laceration at the GE junction caused by a sudden increase in intra-abdominal and intra-gastric pressure (e.g., repetitive severe retching in alcohol use disorder or bulimia).
• Presentation: Painless hematemesis following violent vomiting.
• Management: 80-90% of bleeding stops spontaneously. Active bleeding is controlled via endoscopic thermal coagulation, epinephrine injection, or hemoclip placement.

Boerhaave Syndrome

• Pathophysiology: Transmural rupture of the distal esophagus secondary to sudden intraluminal pressure elevation during violent vomiting.
• Clinical Triad (Mackler Triad): Vomiting, sudden retrosternal/epigastric pain, and subcutaneous emphysema (crepitus over neck/chest; Hamman crunch on auscultation).
• Diagnostics: Water-soluble contrast esophagram (Gastrografin) is the preferred initial test. Barium contrast is strictly avoided due to risk of severe mediastinal fibrosis.
• Treatment: Broad-spectrum IV antibiotics, fluid resuscitation, and emergent surgical repair or endoscopic stenting within 24 hours.

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Peptic Ulcer Disease & Gastritis

Etiologies & Ulcer Differentiation

Peptic Ulcer Disease (PUD) results from mucosal defenses breaking down due to Helicobacter pylori infection, NSAID use, or hypersecretory states.

Diagnostic & Eradication Algorithm for H. pylori

                  Dyspepsia Symptoms Present
                              |
         +--------------------+--------------------+
         |                                         |
  Age >=55 OR Alarm Symptoms               Age <55 & No Alarm Symptoms
  (Dysphagia, Weight Loss, Anemia)                 |
         |                               Non-Invasive H. pylori Testing
  Perform EGD + Mucosal Biopsy           (Stool Antigen or Urea Breath Test)
         |                                         |
  +------+------+                               +--+--+
  |             |                               |     |
Positive     Negative                        Positive Negative
  |             |                               |     |
Treat        Treat                           Treat   Symptomatic
H. pylori    Etiology                        H. pylori PPI Therapy

• Eradication Regimens:
  • Clarithromycin Triple Therapy: PPI BID + Amoxicillin 1000 mg BID + Clarithromycin 500 mg BID for 14 days (use metronidazole 500 mg BID if penicillin-allergic).
  • Bismuth Quadruple Therapy (First-line if local clarithromycin resistance >15%): PPI BID + Bismuth subsalicylate 524 mg QID + Metronidazole 500 mg TID + Tetracycline 500 mg QID for 14 days.
  • Confirmation of Cure: Stool antigen test or urea breath test performed at least 4 weeks post-treatment and off PPI therapy for >=2 weeks.

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Gastric Neoplasms & Zollinger-Ellison Syndrome

Gastric Adenocarcinoma

1. Intestinal Type: Associated with H. pylori, chronic gastritis, nitrosamines, and blood type A. Forms bulky, ulcerated mass on curvature.
2. Diffuse Type: Associated with E-cadherin (CDH1) mutation. Features signet-ring cells and diffuse infiltration resulting in a thickened, rigid stomach wall (linitis plastica).

• Metastatic Signs: Virchow node (left supraclavicular), Sister Mary Joseph nodule (periumbilical), Krukenberg tumor (bilateral ovarian metastasis).

Zollinger-Ellison Syndrome (ZES)

Gastrin-secreting neuroendocrine tumor (gastrinoma) located in the duodenum or pancreas.

• Presentation: Refractory peptic ulcers extending past the duodenal bulb, accompanied by chronic watery diarrhea (acid inactivates pancreatic digestive enzymes).
• Screening: Fasting serum gastrin >1000 pg/mL.
• Confirmation: Secretin stimulation test (gastrin level increases >200 pg/mL after secretin administration). Associated with MEN1 syndrome in 30% of cases.