29.2 Introduction to the Esophagus and Stomach

Anatomy and Physiology of the Esophagus and Stomach

Esophagus and stomach structure and function, including sphincters

The esophagus is a muscular tube that connects the pharynx to the stomach. Its main job is transporting food (called a bolus) from the mouth to the stomach through wave-like muscle contractions called peristalsis. Two sphincters control what enters and exits the esophagus:

• Upper esophageal sphincter (UES) — prevents air from entering the esophagus during breathing. It relaxes during swallowing to let the bolus pass through.
• Lower esophageal sphincter (LES) — prevents stomach contents (acid, enzymes) from refluxing back into the esophagus. It relaxes during swallowing to let food enter the stomach.

The stomach is a J-shaped, muscular organ in the upper left abdomen. It serves three main functions: storing food, mechanically digesting it through churning, and chemically digesting it with acid and enzymes. It has four regions, each with a distinct role:

• Cardia — the area where the esophagus meets the stomach
• Fundus — the upper dome-shaped portion; primarily stores undigested food and gas
• Body — the large central region where most mixing and digestion occurs
• Pylorus — the lower portion connecting to the duodenum

The pyloric sphincter sits at the exit of the pylorus. It controls the passage of partially digested food, now called chyme, into the duodenum. By opening and closing in a regulated way, it controls the rate of gastric emptying so the small intestine isn't overwhelmed.

Common esophageal and stomach disorders

Gastroesophageal reflux disease (GERD) is a chronic condition where stomach contents repeatedly reflux into the esophagus, usually because the LES doesn't close properly.

• Symptoms: heartburn, regurgitation (backflow of stomach contents into the throat), and dysphagia (difficulty swallowing)
• Complications if untreated: esophagitis (inflammation of the esophageal lining), Barrett's esophagus (precancerous cellular changes), and esophageal strictures (narrowing from scar tissue)

Gastritis is inflammation of the stomach lining. Unlike GERD, the problem is in the stomach itself rather than the esophagus.

• Common causes: H. pylori bacterial infection, chronic NSAID use (e.g., ibuprofen), excessive alcohol intake, and severe physiological stress
• Symptoms: epigastric abdominal pain, nausea, vomiting, indigestion
• Complications: peptic ulcers (open sores in the stomach or duodenal lining) and, in chronic cases, increased risk of gastric cancer

Physiology of Digestion in the Stomach

Three phases of digestion and role of gastric acid secretion

Gastric digestion unfolds in three overlapping phases. Each phase has different triggers and different regulatory mechanisms, but they all influence how much acid and enzyme the stomach produces.

Phase 1: Cephalic Phase

This phase begins before food even reaches the stomach. The sight, smell, taste, or even thought of food triggers it.

1. Sensory input (sight, smell, thought of food) activates the brain.
2. The vagus nerve sends signals to the stomach.
3. These signals stimulate gastric acid secretion and increase gastric motility (contractions).

This is why your stomach may "growl" or you may start salivating when you smell something cooking. The cephalic phase accounts for roughly 20% of total gastric acid secretion for a meal.

Phase 2: Gastric Phase

This is the main phase of digestion, triggered when food actually arrives in the stomach.

• Mechanical digestion: strong stomach contractions mix and churn food, physically breaking it into smaller pieces.
• Chemical digestion: gastric glands secrete gastric juice containing several key components:
  • Hydrochloric acid ($HCl$) — creates the acidic environment (pH ~1.5–3.5) needed to denature proteins and activate pepsinogen
  • Pepsinogen — an inactive enzyme that $HCl$ converts into pepsin, which then breaks proteins down into smaller peptides
  • Intrinsic factor — a glycoprotein essential for vitamin $B_{12}$ absorption later in the ileum. Without it, patients develop pernicious anemia.

Acid secretion during this phase is regulated by the hormone gastrin (released from G cells in the pylorus) and continued vagus nerve stimulation. The gastric phase produces the largest volume of acid, roughly 60–70% of total secretion.

Phase 3: Intestinal Phase

This phase begins when chyme enters the duodenum. Its primary role is to slow things down and protect the small intestine from being overwhelmed by acid.

1. Chyme entering the duodenum triggers release of secretin and cholecystokinin (CCK).
2. These hormones stimulate pancreatic bicarbonate and enzyme secretion, plus gallbladder contraction to release bile.
3. Feedback mechanisms inhibit further gastric acid secretion and slow gastric emptying.

This negative feedback loop is clinically relevant: it explains why conditions that disrupt these signals (such as gastrinomas, which overproduce gastrin) can lead to excessive acid secretion and severe ulceration.