Contents 1 Learning Objectives 2 Esophagus 3 GERD 4 Barrett's Esophagus 5 Medications 6 EGD 7 Histology 8 Differentials 9 Patient communication 10 Misc/Additional Notes 11 Useful Resources

[edit] Learning Objectives

1. Describe the anatomy of the esophagus and the lower esophageal sphincter.

• The esophagus is 25cm in length (C6-T11) w/ diameter of 2cm.
• It is composed of the following layers:
  • Mucosa: non-keratinized, stratified squamous epi, lamina propia, muscularis mucosa
  • Submucosa
  • Muscularis externa: inner circular m. layer, outer longitudinal m. layer
    • Upper 1/3 = striated m.; middle 1/3 = striated + smooth m.; lower 1/3 = smooth m.
• There is NO SEROSA above the diaphragm → tumors spread faster
• The LES is 1in. above the gastroesophageal junction (GEJ), surrounded by the musculature of the diaphragm. It is a smooth m. thickening. Its opening is mediated by impulses in vagus n. branches: in absence of esophageal peristalsis → LES tightly closed → prevent reflux of gastric contents

2. Describe the histology of the normal esophagus and the changes that can occur with a change in esophageal pH.

• The normal esophagus has non-keratinized, stratified squamous epithelium. It contains a mucosal, submucosal, and muscularis externa layer. It does not have a serosal layer above the diaphragm.
• With decrease in esophageal pH, these cells undergo damage, leading to disruption of epithelial lining (ulcer) and bleeding in some instances. With chronic exposure to low pH, the squamous epithelial lining undergoes metaplastic change to become columnar, intestinal like epithelial cells, populated with goblet cells; these cells have more resistance to new acidic environment.

3. Describe the motility of the normal esophagus and its function. Discuss the role of esophageal motility in GERD.

• The esophagus moves food to stomach via peristalsis.
• Pharyngeal phase (of swallowing): < 1 s.
  • 1. Soft palate pulls upward → prevent reflux of food into nasopharynx & open narrow passage for food to move thru pharynx
  • 2. Vocal cords pull together & larynx moved forward & upward a/g epiglottis → prevent food from entering trachea & help open UES
  • 3. UES relaxes & muscles of pharynx contract strongly to force bolus deep into pharynx
  • 4. Peristaltic wave initiated, moves toward esophagus & forces food thru relaxed UES
• Esophageal phase (of swallowing): controlled mainly by swallowing center
  • After bolus passes UES, UES constricts
  • A peristaltic wave (1* peristalsis) begins just below UES; travels at 3-5cm/s
  • Bolus travels esophagus in < 10s.
  • After passing thru LES, LES constricts

If primary peristalsis is insufficient to clear debris from esophagus → 2* peristalsis initiated by esophageal distention: second wave begins above site of distention & moves downward

• As UES relaxes, LES also relaxes
• In GERD, problems arise whether it be
  • Lower resting tone, which increase reflux
  • TLESRs, which are short relaxations of LES indep. of swallowing
  • Impaired (prolonged) peristalsis

4. Define gastroesophageal reflux disease (GERD) and list factors for the development of this condition.

• GERD = collection of chronic symptoms or mucosal damage caused by reflux of gastric contents into esophagus
• Factors
  • LES incompetence
  • Very acidic gastric contents
  • Incompetent ENS
  • Vagotomy, other surgical procedures
  • Medications
  • Overeating
  • Smoking
  • Drinking

5. List and describe the mechanisms and triggers for the development of GERD symptoms.

• Regurg → LES incompetence, allows acid to travel from stomach
• Hearburn → Acid wearing away at epithelial lining of esophagus, ulcer
• Dysphagia: Obstruction caused by basal zone hyperplasia
• Odynophagia: Possibly due to bolus in contact w/ ulcer or obstruction due to BZH
• Cough: stim’n of esophageal-bronchial cough reflux

6. Describe the potential complications of GERD and its relation to esophageal cancer.

• Complications of chronic GERD may lead to Barrett’s esophagus (6-12% of cases). Barrett’s pts have 0.5% risk of developing adenocarcinoma of the esophagus (higher than general pop’n).

7. List the medical and surgical treatments for GERD.

• Lifestyle changes
  • Avoid precipitating foods: fatty, EtOH, caffeine, ?chocolate
  • Avoid recumbency for 3 hours postprandially
  • Elevate head of bed
  • Smoking cessation
  • Weight loss
• Antacids
• PPIs (proton pump inhibitor) - Omeprazole
• H2RAs (antihistamine) - Ranitidine
• Fundoplycation = wrap stomach around LES

8. Describe how H2 blocker and proton pump inhibitor medications change gastric acidity.

• H2 blocker competitively inhibit histamine binding to receptors of parietal cell. REDUCE basal, nocturnal & stimulus-induced gastric acid secretion.
• PPIs irreversibly binds & inhibits H+/K+ ATPase, thus inhibiting basal & stimulus-induced acid secretion. BLOCK final step of gastric acid production.

[edit] Esophagus

• Structure

Striated upper third, smooth lower third, mixed middle third Mucosa layer, submucosa, muscular layer, lacking serosal layer except on the lowest part (clinically important for holding stitches)

• • How does an intubation work?
    • What is the relationship of the trachea to the esophagus and the relationship of the epiglottis to the trachea
    • What do you see when you do an endotracheal intubation?
  • Where is the upper esophageal sphincter?

A 3cm segment in the proximal esophagus at the level of the cricopharyngeus muscle Robbins Path, ASR

• • Where is the lower esophageal sphincter?

The distal 1-2cm of the esophagus, just superior to the gastroesophageal junction Johnson GI Physio, ASR

• • Where is the diaphragm?
• Physiology

Swallowing – can control the initial part of swallowing, the following events are involuntary, controlled mainly by vagus nerve (via myenteric plexes) or reflex control.

[edit] GERD

• Symptoms

Mucosal damage caused by abnormal reflux of gastric contents Angina Dysphagia Bleeding, ulcer Histo: increased eosinophils and neutrophils increased basal layer proliferation for protection, Elongation of papilla to increase stability

• • Why does he cough

Reflux can go into pharynx or larynx causing irritation Recurrent pulmonary aspiration can cause pneumonia or asthma

• What causes it?
  • Is the peristalsis of the esophagus affected?

Can be a factor (sluggish peristalsis), when reflux materials are inadequately removed

• • Is H. pylori a factor?

Doesn’t cause GERD, but inhibit H+ pumps in stomach, so if cured, GERD may worsen

• • Is there a hereditary factor?

Some familial link, occurs more often in some families

• • Are there certain foods that affect it more?

Foods that increase acid secretion can be a problem Calcium channel blockers also make GERD worse

Is it associated with obesity? Increase gastric pressure, increase occurrence of GERD

• Treatments

Surgery: stomach may be wrapped around bottom of the esophagus (fundalplication)

• Longer term effects/progression of disease
  • How long does GERD persist before it progresses to Barrett's?

The longer it lasts, the higher the odds of developing it

• • How long does it typically persist as Barret's before it continues on to cancer?

Rapidly increasing dysphagia and weight loss could mean adenocarcinoma

[edit] Barrett's Esophagus

• Structure

Goblet cells, change to intestinal-like cells, but do not absorb like intestine

• Physiology

Distal squamous mucosa of the esophagus is replaced with metaplastic columnar epithelium; appears to be the result of alteration of the differentiation program of stem cells in the esophageal tract. Cells are not true absorptive enterocytes but rather intestinal mucin-secreting intestinal cells intermixed with columnar cells exhibiting secretory and absorptive features, a phenotype not observed elsewhere in the GI tract.

source: Robbins Path ASR

• • How long is it usually?

18-25 cm in adults (source: Lange GI Physiology; ASR)

• Long term effects

Barrett esophagus occurs in app. 10% of people with GERD and is the single most important risk factor for esophageal adenocarcinoma.

Dysplastic changes are indicative of pending adenocarcinoma

0.5% increased risk of developing carcinoma

• Symptoms
  • If he has Barrett's, will he still feel burning?
  • Do you have to have an ulcer to have Barrett's
• Diagnostic tests

pH test probes for 24 hours, good but not very sensitive

Barium swallow: allows visualization of sphincters, hiatal hernia

Clinical response to acid suppression (screening test to determine extent of esophageal damage from reflux) – if symptoms go away with acid suppression, EGD is not required, if they persist, damage extent is worrisome, and further investigation is necessary

EGD and biopsy to find dysplasia Esophageal momometry to test sphincters

• Risk factors
  • overeating, smoking, drinking coffee?
  • What are the mechanisms for how overeating, coffe, smoking, and drinking affect the esophagus?

Nictotine reduces amount of saliva produced, saliva is required to clear esophagous

Caffeine may reduce LES tone, increases H+

• Treatment

[edit] Medications

• Antacids
  • effects of long-term antacid use

Can worsen GERD by preventing gastric emptying Can weaken bone tissue by preventing uptake of phosphate

• Ranitidine

Blocks histamine which prevents H+ secretion from parietal cells Aids repair and protection Can be taken orally Can reduce 90% of acid secretion

• Omeprazole

Proton pump inhibitor Can block 100% of acid production

[edit] EGD

• How is it done?
• What are they looking at?
  • What would you see in a normal EGD?
• What is causing the salmon color?

[edit] Histology

• What do you expect to see in the esophageal-gastric junction?
  • Normally
  • Pathologically

[edit] Differentials

• Chest pain
  • How does the patient describe the chest pain

[edit] Patient communication

• How to explain "modifying lifestyle" to patient

[edit] Misc/Additional Notes

Put anything else we may have left out, relevant or otherwise, down here.

[edit] Useful Resources