Etiology and Mechanisms of Development
The pathophysiology of gastroesophageal reflux disease is closely linked to impaired motor activity of the upper digestive tract. The pathogenesis is driven by two main causes leading to lower esophageal sphincter incompetence.
The first fundamental cause is a profound disruption of cholinergic innervation. Normal esophageal motility and sphincter tone are maintained by the coordinated action of the nervous system. In conditions such as encephalitis or neuritis, specific damage to neural structures occurs. The pathological process involves neuronal cell bodies as well as the trunks of the vagus nerve (nervus vagus). Furthermore, intramural nerve plexuses located directly within the wall of the digestive tube are damaged. Damage to these structures leads to dyscoordination of muscular contractions.
Another significant cause is a marked imbalance of bioactive substances regulating smooth muscle tone. In a healthy body, a strict equilibrium is maintained between stimulatory and relaxant molecules.
Bioactive substances that increase muscle tone include:
- Motilin
- Gastrin
- Substance P
Bioactive substances that decrease muscle tone include:
- Serotonin
- Secretin
- Vasoactive intestinal peptide (VIP)
- Somatostatin
- Dopamine
- Nitric oxide
Shifting the balance toward tone-reducing substances leads to pathological relaxation of the muscular apparatus and creates ideal conditions for the retrograde flow of food.
Pathogenesis of Impaired Food Passage
The consequence of the regulatory and innervation failures described above is the development of esophageal dysphagia. This pathological syndrome manifests as a marked slowing of food bolus transit through the digestive tube immediately following the act of swallowing. A persistent delay in the evacuation of swallowed food from the esophageal lumen into the gastric cavity occurs.
Impaired normal food transit inevitably affects the patient's overall nutritional status. Because the delivery of essential nutrients to the gastrointestinal tract is critically reduced and disrupted, the patient experiences progressive weight loss. The body begins to experience a deficit in energy and building blocks.
The central link in the disease pathogenesis is gastroesophageal reflux (GER) itself. From a physical standpoint, this phenomenon represents the retrograde (backward) flow of gastric contents into the esophageal lumen. When such reflux loses its rare, episodic nature, begins to recur frequently, and persists over a long period, a full-fledged pathological syndrome—GERD—is established.
Clinical Symptoms
The clinical picture of the disease develops as a result of the regular aggressive impact of gastric contents on the esophageal mucosa and respiratory structures. Characteristic symptoms include:
- Heartburn — the most typical and recognizable sign. The patient experiences an extremely unpleasant subjective burning sensation localized primarily in the epigastric region. This symptom occurs as a direct reaction to the reflux of acidic gastric contents into the esophagus.
- Belching — the uncontrolled release of small volumes of accumulated gas, and occasionally particles of undigested food, from the stomach back into the esophagus and oral cavity.
- Regurgitation (medical terminology: regurgitatio) — the involuntary reflux of part of the gastric contents not only into the mouth but also into the nasal passages. Notably, this phenomenon is frequently observed as a normal variant in newborns.
- Frequent food aspiration — a dangerous manifestation of the disease in which food masses and gastric contents enter the respiratory tract.