Etiology and mechanisms of development
The pathophysiology of gastroesophageal reflux disease is closely related to impaired motor activity of the upper digestive tract. The pathogenesis is based on two main causes leading to failure of the sphincter mechanism.
The first fundamental cause is a profound impairment of cholinergic innervation. Normal esophageal motility and sphincter tone are ensured by the coordinated work of the nervous system. When pathologies such as encephalitis or neuritis develop, specific damage to neural structures occurs. The pathological process involves neuronal cell bodies as well as the trunks of the vagus nerve (nervus vagus). In addition, intramural nerve plexuses located directly within the thickness of the digestive tract wall are damaged. Damage to these structures leads to dyscoordination of muscle contractions.
The second significant cause is a pronounced imbalance of biologically active substances (BAS) that regulate smooth muscle tone. In a healthy body, a strict equilibrium is maintained between stimulator molecules and relaxant molecules.
Biologically active substances that increase muscle tone include:
- Motilin
- Gastrin
- Substance P
Biologically active 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 backflow of food.
Pathogenesis of food passage disorders
The consequence of the regulatory and innervation disruptions described above is the development of esophageal dysphagia. This pathological syndrome manifests as a pronounced slowing of the food bolus movement through the digestive tube immediately after the swallowing act is completed. A persistent delay in the evacuation of swallowed food from the esophageal lumen into the gastric cavity occurs.
The disruption of normal food transit inevitably affects the patient's general nutritional status. Due to the fact that the intake of essential nutrients into the gastrointestinal tract is critically reduced and impaired, the patient experiences progressive weight loss. The body begins to experience a deficit of energy and building blocks.
The central link in the pathogenesis of the disease is gastroesophageal reflux (GER) itself. From a physical point of view, this phenomenon represents retrograde—i.e., backflow—of gastric contents back into the esophageal lumen. When such reflux ceases to be a rare episodic phenomenon, begins to repeat frequently, and persists for a long time, a full-fledged pathological syndrome is formed — GERD.
Clinical symptoms
The clinical picture of the disease is formed as a result of the regular aggressive impact of gastric contents on the esophageal mucosa, as well as on the respiratory tract structures. Characteristic symptoms include the following manifestations:
- Heartburn is the most typical and recognizable sign. The patient experiences an extremely unpleasant subjective burning sensation localized predominantly in the epigastric region. This symptom occurs as a direct reaction to the reflux of acidic gastric contents into the esophagus.
- Belching is the uncontrolled release of small volumes of accumulated gases, and in some cases particles of undigested food, from the gastric cavity back into the esophagus and further into the oral cavity.
- Regurgitation (in medical terminology — regurgitatio) is the involuntary reflux of part of the stomach contents not only into the oral cavity but also into the nasal passages. It is worth noting that such a phenomenon is often observed as a normal variant in newborns.
- Frequent food aspiration is a dangerous manifestation of the disease in which food masses and gastric contents enter the respiratory tract.
Briefly: answers to topical questions
What complications can develop with a long-term course of GERD?
Complications of gastroesophageal reflux disease include:
- Bleeding — rare, predominantly seen in erosive and ulcerative esophagitis.
- Esophageal strictures — the outcome of severe inflammation leading to lumen narrowing; the main complaint is dysphagia.
- Barrett's esophagus (Columnar-Lined Oesophagus) — columnar cell metaplasia of the esophageal mucosa; the risk of development in patients with GERD is 10–15%. Long-term GERD is a risk factor for Barrett's esophagus.
- Esophageal adenocarcinoma — classified among GERD complications; the presence of columnar cell metaplasia increases the risk of developing adenocarcinoma by 30 times.
What instrumental diagnostic methods are used to confirm GERD?
To confirm the diagnosis of gastroesophageal reflux disease, endoscopic and functional methods are used:
- Esophagogastroduodenoscopy (EGD) — performed at the endoscopic stage; if visible signs of reflux esophagitis are present, a diagnosis of GERD is established. If there are no changes, the next diagnostic stage is indicated.
- 24-hour pH-impedance monitoring — performed when EGD is negative; it is the gold standard for detecting non-erosive reflux disease and allows the diagnosis of acidic, weakly acidic, and weakly alkaline refluxes.
- 24-hour pH monitoring — recommended for patients with suspected GERD in the absence of erosions or with grade A esophagitis, against the background of proton pump inhibitor withdrawal, to confirm or exclude the diagnosis.
Which drug groups are used for the medical treatment of GERD?
Medical treatment for gastroesophageal reflux disease includes main and additional drug groups.
Main groups:
- Proton pump inhibitors — drugs of choice for treating symptoms and existing erosive esophagitis.
- Potassium-competitive acid blockers (P-CABs).
- Alginates.
- Antacids.
- Prokinetics.
The choice of additional drugs depends on the GERD phenotype:
- Alginates — for symptom relief.
- Esophagoprotectors — to accelerate erosion epithelialization and protect the mucous membrane.
- H2-histamine receptor blockers — for relieving nighttime symptoms.
- Prokinetics — when gastric motor-evacuation function is slowed.
- Ursodeoxycholic acid preparations — for duodenogastroesophageal reflux.
To memorize tone-reducing substances (relaxants), use the phrase: "Segodnya Sekretno VIP Somatostatin Darit Oksid azota" (Serotonin, Secretin, VIP, Somatostatin, Dopamine, Nitric oxide).
Class and exam questions
What is the fundamental difference between GER and GERD?
Gastroesophageal reflux (GER) is the physical fact of stomach contents flowing back into the esophagus. GERD is an established pathological condition in which such reflux events recur frequently and persist for a long time.
Why might body weight decrease in reflux disease?
Progressive weight loss occurs due to the development of esophageal dysphagia. Slowing of food movement and delayed evacuation into the stomach lead to a critical impairment of nutrient intake into the gastrointestinal tract.
Which structures of the nervous system are affected in innervation disorders leading to GERD?
In neuritis and encephalitis, neuronal cell bodies, vagus nerve trunks, and intramural nerve plexuses of the digestive tract are damaged, leading to dyscoordination of motility.
What is regurgitation and for whom can it be a variant of normal?
Regurgitation is the involuntary reflux of gastric contents into the mouth and nasal passages. This phenomenon is frequently observed as normal in newborns.
What else to study on this topic
- Mechanisms of development of encephalitis and vagus nerve neuritis
- Physiological role of the intramural plexuses of the GI tract
- Pathogenesis of esophageal dysphagia at the cellular level
- Effect of acidic gastric contents on the esophageal epithelium
- Consequences of frequent food aspiration for the respiratory system
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