CHAPTER 7. DIGESTIVE SYSTEM DISEASES

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GASTROESOPHAGEAL REFLUX DISEASE

Gastroesophageal reflux disease (GERD) is a chronic recurrent disease caused by spontaneous, regularly repeated reflux of gastric and/or duodenal contents into the esophagus, leading to damage to the lower part of esophagus.

The ratio of GERD in males to females of any age is 2-3:1. The frequency of reflux esophagitis detection in children with gastrointestinal tract diseases is from 8.7 to 17% (clinical guidelines).

Etiology and pathogenesis

GERD is a multifactorial disease, whose immediate cause is gastroesophageal reflux (GER). Two types of GER are distinguished.

• Acid reflux - decrease in esophageal pH to below 4.0 due to retrograde flow of acidic gastric contents into its cavity.

• Alkaline reflux - increase in esophageal pH to above 7.5 due to retrograde flow of duodenal contents (bile and pancreatic juice) into its cavity.

Predisposing and provoking factors for the development of GERD are shown in

table 7.1.

Table 7.1. Risk factors for developing gastroesophageal reflux disease

Predisposing factors

Provoking factors

School age (mostly senior) and male sex.

Family history of gastrointestinal diseases.

Organic lesions in gastroduodenal zone.

Autonomic dysregulation. Helminth parasite invasion. Foci of chronic infection. Obesity, etc.

Poor quality food and malnutrition Forced position of the body, leading to disturbance of esophageal-gastric motility and increase in intra-abdominal pressure (prolonged oblique position of the body, inadequate physical activity, driving a car, constipation, etc.)

Respiratory diseases (bronchial asthma, cystic fibrosis, recurrent bronchitis, etc.).

Medicines (anticholinergics, sedatives and hypnotics,

β-blockers, nitrates).

Smoking

The main condition for preventing GERD is normal functioning of the lower esophageal sphincter. Dysfunction of the lower esophageal sphincter develops via

the following mechanisms: primary decrease in sphincter pressure; an increase in the number and duration of episodes of transient relaxation of the sphincter, which can result in its transient relaxation, constant relaxation, temporary increase in intra-ab-dominal pressure; complete or partial destruction of the sphincter (for example, in case of hiatal hernia).

The pathogenesis of GERD, by analogy with the pathogenesis of peptic ulcer, can be represented as scales on which aggressive factors outweigh (ig. 7.1).