Heartburn and gastroesophageal reflux
Heartburn is traditionally described as a specific burning sensation localized in the lower esophagus. The pathophysiology of this symptom is based on impaired barrier function of the sphincter apparatus.
The key triggering factor is a pathological decrease in the tone of the cardiac sphincter of the stomach (also known as the lower esophageal sphincter). Normally, this sphincter prevents the backflow of food. However, when its tone drops, conditions are created for the development of gastroesophageal reflux. This process is the uncontrolled backflow of acidic contents from the stomach cavity back into the esophageal lumen. It is the contact of the acidic environment with the mucous membrane that generates the characteristic burning sensation.
Nausea as a precursor
In pathological physiology, nausea is defined as an extremely unpleasant, yet completely painless subjective sensation. As a rule, this condition acts as a direct precursor to the impending act of vomiting.
From the perspective of neurophysiological processes, the mechanism of nausea is based on subthreshold excitation of the neurons in the vomiting center. This means that a stimulating signal is already entering the central nervous system, but its strength is not yet sufficient to cross the excitability threshold and trigger a full motor reflex.
Physiology and mechanism of the act of vomiting
Vomiting is classified as a complex involuntary reflex act. Externally, it manifests as the forceful expulsion of the contents of the stomach (and in some cases, the intestine) outward. The ejection of masses occurs sequentially through the esophagus, pharyngeal structures, and the oral cavity.
The central link controlling this process is the activation of neurons in the vomiting center of the medulla oblongata. The physiology of the act itself represents a strictly coordinated chain of combined phenomena:
- A sharp increase in antiperistalsis of the gastric wall (movement of contraction waves in the reverse direction).
- Simultaneous powerful contraction of the diaphragm muscles and abdominal wall musculature, which creates high pressure.
- Obligatory relaxation of the muscles of the cardiac region of the stomach and the esophagus to ensure the unobstructed exit of masses.
Pathogenic and protective significance of vomiting
When assessing the significance of vomiting for the body, two diametrically opposed aspects are distinguished:
- Protective effect: vomiting acts as an emergency mechanism for expelling various toxic substances and accidentally swallowed foreign bodies from the stomach, preventing their further movement down the tract.
- Pathogenic significance: during the process of vomiting, the body inevitably loses significant volumes of fluid, vital ions, and nutrients.
The clinical significance of these losses increases manifold and becomes critical in prolonged and/or repeated vomiting, which requires close medical attention.
Briefly: answers to topical questions
What factors and substances cause a pathological decrease in the tone of the cardiac sphincter?
A pathological decrease in tone / dysfunction of the cardiac (lower esophageal) sphincter is associated with the following factors:
- systemic diseases, primarily systemic sclerosis (atrophy of the cardia muscles);
- acquired weakness of the lower esophageal sphincter;
- pregnancy;
- vagotomy;
- peptic ulcer disease;
- any mechanical disorders of the closing sphincter;
- administration of drugs that reduce sphincter tone: anticholinergics, sedatives, hypnotics, beta-blockers, nitrates.
Which receptor zones and afferent pathways stimulate the vomiting center?
Activation of the vomiting center in the medulla oblongata occurs through several stimulation pathways:
- chemoreceptors of the trigger zone on the floor of the fourth ventricle — respond to chemical substances in the blood or cerebrospinal fluid;
- peripheral stimulation — receptors of the pharynx and gastric mucosa;
- vestibular apparatus — during motion sickness.
According to the receptor map of sources: the trigger zone contains D2-dopamine and 5-HT3-serotonin receptors; the vestibular nuclei contain M1-cholinergic and H1-histamine receptors; the visceral afferent system from the pharynx and stomach contains 5-HT3 receptors.
To memorize the physiology of vomiting, use the three-step rule: "Antiperistalsis — Tension — Relaxation". First, the stomach pushes the masses backward (antiperistalsis), then the diaphragm and abdominal wall press from the outside (tension), and the cardiac region and esophagus open the path (relaxation).
Class and exam questions
What is the main cause of heartburn?
The basis is a decrease in the tone of the lower esophageal (cardiac) sphincter, which makes the backflow of acidic stomach contents into the esophagus possible — gastroesophageal reflux.
How does nausea differ from vomiting in terms of neurophysiology?
Nausea occurs during subthreshold excitation of the vomiting center. When the excitation reaches the threshold, a full reflex act of vomiting is triggered.
Which muscles ensure the expulsion of contents during vomiting?
Expulsion occurs due to increased antiperistalsis of the stomach itself, as well as a powerful simultaneous contraction of the abdominal wall muscles and the diaphragm.
In what cases does vomiting become dangerous for the patient?
Vomiting acquires pronounced pathogenic significance during a prolonged or recurrent course, as it leads to critical loss of fluid, ions, and nutrients by the body.
What else to study on this topic
- Consequences of fluid and ion loss during repeated vomiting
- Mechanisms and differences of duodenogastric reflux
- Pathophysiology of dysphagia and regurgitation
- The role of the medulla oblongata in the formation of protective reflexes
- Disorders of intestinal motor function and antiperistalsis
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