Pathogenesis of digestive system diseases

Secondary mechanisms of GI damage

The gastrointestinal tract often suffers not only from direct impacts, but also indirectly due to pathologies of other body systems. The primary source of digestive problems can be the circulatory system, kidneys, liver, or endocrine apparatus.

• Liver: In liver failure, bile production is critically impaired. Without it, adequate digestion and assimilation of food are impossible, ultimately leading to digestive disorders up to malabsorption syndrome.
• Kidneys: If the kidneys fail to cope with their function (renal failure), the body triggers compensatory mechanisms. Urea and other metabolites begin to be actively excreted through the intestinal mucosa. The consequence of this is direct toxic damage to the mucosa by metabolic products.
• Endocrine glands: Tumors of the adrenal cortex (corticosteromas) release huge doses of glucocorticoids and mineralocorticoids into the blood. This hormonal shock provokes the appearance of steroid ulcers on the mucous membrane of the stomach and/or intestine.

Regulatory disorders and risk factors

Normal digestive function depends on a delicate balance of stimulating and inhibitory signals. Pathogenic factors cause a deficiency or excess of these influences at various levels:

1. General regulatory systems (central nervous system, systemic hormonal background).
2. Local systems, which include the enteric nervous and enteroneuroendocrine networks.

The main pathogenetic link here is the disruption of the neurohumoral control mechanisms of the GI tract. Damage is realized through an imbalance of biologically active substances (peptides, prostaglandins, biogenic amines, specific hormones) and distortion of autonomic neurogenic effects (sympathetic or parasympathetic influences).

Certain conditions facilitate the realization of the action of causal agents:

• Hereditary predisposition: Familial tendency to peptic ulcers of the stomach and duodenum has been proven. There is also a clear correlation of the incidence with genetic markers, for example, with a specific blood group of the patient.
• Impaired reactivity of the organism: Digestive system diseases often develop against the background of hyperreactive states. Classic examples are general sensitization of the organism or prolonged emotional overstrain (chronic stress).
• General risk factors: The patient's sex is of great importance. Thus, peptic ulcer disease of the stomach and duodenum is statistically diagnosed much more frequently in young males.

Classification of digestive disorders

Globally, all disorders of the gastrointestinal tract can be divided according to the stages of the digestive process. The following pathologies are distinguished:

1. Taste.
2. Appetite.
3. Digestion in the oral cavity.
4. Swallowing and movement of food through the esophagus.
5. Digestion in the stomach.
6. Digestion in the intestine.

These functional failures underlie specific clinical forms and syndromes: colitis, enteritis, irritable bowel syndrome, peptic ulcer disease of the stomach and duodenum, as well as malabsorption syndrome.

Pathology of the gustatory analyzer

Taste disorders are a prime example of a malfunction at the very first stage of digestion. Typical forms include:

• Ageusia (from Greek geusis — taste) — complete loss of taste sensations.
• Hypogeusia — pathological decrease in sensitivity.
• Hypergeusia — excessive, heightened sensations.
• Parageusia — qualitatively inadequate taste perception.
• Dysgeusia — perverted taste sensations.

These disorders arise due to organic lesions or functional defects at one of the three levels of the analyzer:

1. Receptor level: Alteration of receptor sensitivity itself (hypersensitization or hyposensitization) due to chemical and thermal burns, mechanical damage to the oral cavity, or local inflammation (stomatitis, glossitis).
2. Conduction level: Blockade of impulse transmission from receptors to centers along nerve trunks. It occurs in neuritis, ruptures, damage, or neurodystrophy of the glossopharyngeal and lingual nerves, as well as in alteration of the thalamus area.
3. Central level: Damage to neurons of the cortical analyzer against the background of encephalitis, hemorrhages, severe neuroses, and neuropsychiatric disorders.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Mechanisms of malabsorption syndrome development
• Pathogenesis of peptic ulcer disease of the stomach and duodenum
• The role of the enteric nervous system in local GI regulation
• Effect of the sympathetic and parasympathetic systems on bowel motility
• Etiology and pathogenesis of irritable bowel syndrome

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

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