Etiological and Functional Classification
Based on origin, enteropathies are divided into two large groups. Infectious enteropathy is most frequently encountered in clinical practice. Its development is triggered by pathogens such as Shigella, Salmonella, Yersinia, as well as various viruses and parasites.
Non-infectious disorders occur less frequently and are associated with:
- Alimentary causes (systematic unbalanced diet).
- Toxic effects (chronic alcohol abuse, smoking).
Depending on morphological changes in the small intestinal wall, the disease may occur with or without enterocyte dystrophy, be accompanied by partial villous atrophy, and localize predominantly in the ileum (ileitis).
From a functional perspective, the pathology is characterized by:
- Impaired membrane digestion (a classic example is disaccharidase deficiency).
- Disorders of absorption processes (malabsorption of water, electrolytes, vitamins, proteins, fats, carbohydrates, and iron).
- Disruption of intestinal motility (hyperkinetic or hypokinetic types of motor disorders develop).
Pathogenesis
The initial link in pathogenesis is always the disruption of the barrier function of a previously damaged intestinal wall. Following this, the core pathogenetic mechanisms unfold:
- There is a sharp decrease in the activity of both free enzymes and those bound to the enterocyte membrane. This inevitably leads to a severe disorder of membrane digestion.
- The proper function of transport channels is impaired, resulting in the blocked absorption of ions, water, and final hydrolysis products of nutrients.
The disease frequently becomes chronic due to the formation of vicious cycles. This is promoted by so-called aggravating factors: a decrease in the enzymatic activity of all digestive glands in the body, marked dysbiosis, systemic metabolic disorders, and a decline in the effectiveness of immune defense.
Intestinal Manifestations
Local symptoms directly depend on the localization of the inflammatory or dystrophic process.
- If the initial segment of the jejunum is affected, the pathology proceeds covertly with minimal intestinal manifestations.
- If the process involves the ileum, bile acid absorption is critically impaired. Accumulating in the intestinal lumen, bile acids actively stimulate the secretion of water, sodium, and chloride ions, and drastically enhance motility. The result of this mechanism is profuse diarrhea.
- With prolonged reflux ileitis, vitamin $B_{12}$ absorption is impaired, which predictably leads to the development of $B_{12}$-deficiency anemia.
Typical intestinal symptoms in enteropathies also include flatulence and steatorrhea (excess fat in the feces).
Extraintestinal Manifestations (Malabsorption Syndrome)
Systemic signs of the disease are caused by the development of malabsorption syndrome—a total impairment of nutrient absorption. This condition is accompanied by profound metabolic shifts.
Patients exhibit pronounced weight loss, frequently exceeding 20 kg. Trophic changes develop: the skin becomes dry, thinned, and flaky, hair loss begins, and nail plates thicken and become brittle. Protein deficiency leads to hypoproteinemia, resulting in peripheral edema.
Electrolyte malabsorption impacts the cardiovascular and nervous systems:
- Hypokalemia triggers cardiac arrhythmias and a predisposition to hypotensive reactions.
- Hypocalcemia causes paresthesias and specific spasms of small muscles. Striking markers include Chvostek's sign (local contraction of facial muscles upon a light tap just below the zygomatic arch) and Trousseau's sign (carpal spasm forming an "obstetrician's hand" when a blood pressure cuff is inflated on the upper arm).
The clinical picture is completed by a diverse range of symptoms due to total vitamin deficiency.