Etiology and Risk Factors
The development of chronic colitis is most often caused by the prolonged exposure of damaging factors to the mucosa of the large intestine. Pathophysiology identifies several key groups of etiologic factors:
- Intestinal Infections. These act as one of the main triggers. Bacterial pathogens include microorganisms causing shigellosis (dysentery), salmonellosis, and yersiniosis. Protozoan and parasitic infestations also play a major role: infections by Entamoeba, Giardia, Trichomonas, and Balantidium.
- Dietary Factors. Irregularities in dietary habits and nutrition inevitably affect the condition of the intestine. The risk increases with a monotonous diet (excess carbohydrates or proteins), vitamin deficiencies, regular consumption of spicy or hard-to-digest foods, and alcohol abuse.
- Congenital Enzymopathies. With a deficiency of specific enzymes (e.g., disaccharidase deficiency), food is not fully digested. Incomplete breakdown products directly irritate the intestinal mucosa, triggering inflammation.
- Intoxications. Toxic effects can be both external and internal:
- Exogenous intoxications occur during poisoning with heavy metal salts (lead, mercury), arsenic, and phosphorus.
- Endogenous intoxications develop against the background of systemic pathologies: uremia, liver failure, or hyperthyroidism.
- Iatrogenic (Drug-Induced) Factors. Uncontrolled and prolonged use of certain medications (laxatives, antibiotics, salicylates, digitalis preparations) can cause serious damage to the intestinal wall.
- Radiation Exposure. Massive X-ray irradiation or radiation therapy leads to the death of actively dividing intestinal epithelial cells.
- Ischemic Disorders. Blood circulation disorders in the mesenteric vessels cause tissue hypoxia. This factor is particularly relevant for elderly patients suffering from atherosclerosis.
Pathogenesis of Chronic Colitis
Long-term exposure to toxic, infectious, radiation, allergic, and other damaging factors triggers a complex cascade of pathological changes in the large intestine. The pathogenetic chain includes several sequential stages:
- Primary Mucosal Injury. A pronounced inflammatory-immunopathological injury of the intestinal wall tissues develops.
- Impairment of Principal Functions. Against the background of inflammation and dystrophy, organ function suffers: secretory, motor, and absorptive functions are suppressed or distorted.
- Damage to the Nervous Apparatus. The pathological process affects the innervation of the intestine. On the one hand, this leads to severe motility disorders, and on the other hand, it exacerbates trophic disturbances within the intestinal tissues themselves, creating a vicious cycle.
- Microbiological and Enzymatic Shifts. Due to changes in the intestinal environment, dysbiosis develops and secondary enzymopathy forms. Intestinal dyspepsia appears, which further disrupts digestive processes and the assimilation of essential nutrients.
- Systemic Body Reactions. The local process transitions to a systemic level: intestinal autoinfection and autointoxication develop. In response to tissue damage and the absorption of toxins, secondary immunopathological reactions are initiated.
Clinical Consequences
Although chronic colitis is a disease of the large intestine, its consequences affect the entire organism. The main clinical manifestation that completes the pathogenetic chain is malabsorption syndrome.
Due to the loss of absorptive function, dysbiosis, and accelerated (or spastic) motility, the body fails to receive adequate nutrients, vitamins, and trace elements. Combined with constant autointoxication and endogenous poisoning by decay products, this leads to emaciation, metabolic disorders, and a decrease in the patient's overall compensatory reserves.