Dysphagia

Role of chewing and prerequisites for disorders

The digestive process begins in the oral cavity, and its disorders often precede deeper pathologies. Key factors here include pain syndromes arising from inflammation (stomatitis, gingivitis, glossitis, periodontitis). An important role is played by dental arch defects (missing or absent teeth), as well as pathologies of the temporomandibular joint and masticatory muscles, including bone fractures, atrophy, or muscle hypertonus.

Behavioral habits are also worth noting: eating on the run or reading at the table leads to insufficient chewing. As a result, poorly chewed food causes mechanical damage to the gastric mucosa, provokes disruptions in its secretion and motility, and causes general digestive disorders in the stomach and intestines.

Etiology of dysphagia and aphagia

The causes of dysphagia (or its extreme form — aphagia) are quite diverse. In clinical practice, the following groups of factors are most commonly distinguished:

• Pain syndrome: inflammation, ulceration of the oral mucosa, as well as trauma and skull bone fractures.
• Masticatory apparatus lesions: arthritis and arthrosis of the temporomandibular joints, paresis, paralysis, and hypo- or hypertonus of the masticatory muscles.
• Neurological deficits: damage to the neurons of the swallowing center and conduction pathways (especially against the background of cerebrovascular disorders). This also includes impaired afferent and efferent innervation during inflammation or damage to the branches of the cranial nerves: vagus (n. vagus), trigeminal (n. trigeminus), and glossopharyngeal (n. glossopharyngeus).
• Local structural changes: the presence of scars, neoplasms, or ulcers directly in the pharynx and esophagus.
• Psychogenic factors: severe stress or hysterical episodes can provoke the development of aphagia.

Consequences of swallowing disorders

The inability to swallow food normally triggers a cascade of severe complications:

1. Malnutrition: food does not enter the stomach in sufficient volume, leading to systemic digestive disorders and emaciation.
2. Food aspiration: the entry of food masses into the respiratory tract provokes bronchospasm, bronchitis, aspiration pneumonia, and even lung abscess.
3. Asphyxia: massive food entry into the respiratory tract (which often happens in unconscious patients or during emergence from anesthesia) leads to suffocation.

Esophageal dysfunction

This is a standard form of digestive system pathology characterized by impeded food movement through the esophagus, problems with its passage into the stomach, and reflux (backflow of gastric contents). Most often, disruptions occur at the level of the upper and lower (cardiac) sphincters.

Among the main causes of dysfunction are:

• Neurogenic disorders: encephalitis, pathological stress, mental disorders, as well as dystrophic and destructive changes in the neurons of the vagus nerve and intramural plexuses. Normally, vagal influences enhance peristalsis. Plexus neurons can either activate contraction via cholinergic muscarinic M₂-receptors or inhibit it via nicotinic and muscarinic M₁-receptors.
• Humoral shifts: excessive effects of nitric oxide (NO) or vasoactive intestinal peptide (VIP).
• Sclerotic wall changes: scarring after extensive erosions and ulcers, chemical and thermal burns, as well as systemic diseases (dermatomyositis, generalized scleroderma).
• Spasms: local or diffuse esophagospasm occurring during neuroses or attempts to swallow too large a piece of solid food.

Main forms of esophageal pathology

Key consequences and forms of dysfunction are:

• Achalasia (from Greek a — absence and chalasis — relaxation) is a state of prolonged spasm of the esophageal body wall muscles and its lower sphincter. Peristalsis ceases, the sphincter does not relax sufficiently, thereby impairing the passage of food into the stomach.
• Diffuse esophageal spasm — contraction of muscle fibers in all areas of the wall. Important difference from achalasia: in diffuse spasm, the tone of the lower esophageal sphincter remains normal.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Pathology of the temporomandibular joint and masticatory apparatus and its effect on digestion
• Mechanisms of neurogenic regulation of esophageal motility (role of M₁ and M₂ receptors)
• Humoral factors of esophageal dysfunction (effects of VIP and NO)
• Sclerotic changes of the esophageal wall in systemic diseases (scleroderma, dermatomyositis)
• Consequences of mechanical damage to the gastric mucosa

Other topics in "Chapter 24. Typical Forms of Digestive System Pathology"

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.