Pathogenesis at the cellular level
Damage is rooted in the disruption of neurohumoral regulation mechanisms resulting from deviations in homeostasis parameters. Four main pathogenetic chains leading to cell death or dysfunction are distinguished:
- Imbalance of biologically active substances (BAS). Leads to the inefficient consumption of oxygen and metabolic substrates, creating an acute deficiency of them in tissues.
- Cellular hyperfunction. Working to the point of exhaustion inevitably ends in the development of dystrophy and dysplasia.
- Calcium overload. An excess of calcium ions inside the cell triggers the calcium triad of structural damage.
- Catabolism explosion. Excessive activation of hydrolases, free radicals, and lipid peroxidation (LPO) destroys cell membranes, enzymes, and nucleic acids.
The result of these processes is a global disruption of plastic processes and vital activity of the entire organism.
Biochemical shifts and mobilization of reserves
Pathogenic changes are closely associated with an endocrine storm. The concentration of catecholamines, glucocorticoids, antidiuretic hormone (ADH), and somatotropic hormone (STH) in the blood rises sharply.
At the cellular level, this hormonal cocktail provokes hyperactivity of lipases and phospholipases, as well as the mass generation of reactive oxygen species. As a result, lipid components of membranes and associated enzyme complexes are damaged, and transmembrane processes collapse.
High levels of stress hormones cause excessive mobilization of proteins, fats, and carbohydrates. This process has a dual nature:
- Adaptive effect: emergency provision of substrates to dominant functional systems.
- Pathogenic effect: during a prolonged reaction, reserves are depleted, leading to dystrophy and necrosis in both hyperfunctioning and "resting" tissues.
Centralization of blood circulation and immune failure
During pronounced, prolonged, or repeated stress, the body sacrifices the periphery to save vital centers. The phenomenon of blood flow redistribution develops: perfusion of the heart and brain increases, while the skin, kidneys, and gastrointestinal tract (GIT) suffer from ischemia. It is this hypoperfusion that causes the appearance of so-called "stress ulcers" and erosions.
Chronic stress also strikes the immune surveillance system. Its efficiency drops, while the synthesis of nucleic acids and proteins is activated. Such a combination—weakening of genetic control plus active gene expression—creates a favorable ground for the activation of oncogenes and the development of tumor processes.
Two scenarios: adaptation or pathology
Depending on the biological significance, strength, and duration of exposure, the stress response can follow one of two paths:
- Adaptive reaction. Occurs during moderate exposure. Homeostasis is maintained, and the body acquires a state of increased resistance. Cross-nonspecific adaptation is formed—resistance increases not only to the initial stressor but also to other aggressive factors. This principle is used for artificial conditioning (metered physical exercise, hypobaric hypoxia, autohemotherapy, temperature exposures).
- Pathogenic reaction. Develops under excessively strong, frequent, or prolonged exposure, when the body is unable to maintain homeostasis parameters. Adaptation fails, which manifests as severe life-support disorders, the development of extreme states (shock, collapse, coma), and the risk of transition to the terminal stage.
Briefly: answers to topical questions
What specific processes comprise the calcium triad of cell structure damage?
Sources indicate that an excess of Ca2+ ions causes the activation of cytoplasmic enzymes, which includes three processes:
- Activation of lytic ATPase — splitting of ATP leads to a decrease in energy reserves and disruption of cationic pumps;
- Activation of phospholipases — splitting of phospholipids in the cytoplasmic and mitochondrial membranes disrupts their function;
- Activation of proteases — destruction of cytoskeleton proteins.
This leads to the transition of reversible changes into irreversible cell damage.
What three stages of the general adaptation syndrome are distinguished during prolonged stress?
Three stages are distinguished in the stress response:
- Alarm stage.
- Resistance stage.
- Exhaustion stage.
To quickly recall the target organs suffering from ischemia during the centralization of blood circulation, use the abbreviation KGI: Kidneys, Gastrointestinal tract, Integument (skin).
Class and exam questions
Why do gastric ulcers occur during severe stress?
Due to the phenomenon of blood flow redistribution. Blood is directed to the heart and brain, while hypoperfusion and ischemia occur in the gastrointestinal tract, leading to the formation of erosions and "stress ulcers".
What is the dual effect of substance mobilization during stress?
On the one hand, mobilization provides energy and substrates to actively working systems (adaptation). On the other hand, during a prolonged reaction, reserves are depleted, leading to tissue dystrophy and necrosis.
How is chronic stress linked to the risk of tumor development?
Prolonged stress reduces the efficiency of immune surveillance. Against the background of stress-induced activation of protein and nucleic acid synthesis, this creates ideal conditions for the expression of oncogenes.
What else to study on this topic
- Mechanisms of neurohumoral regulation in the stress response
- Calcium triad of cell damage
- Free-radical lipid peroxidation (LPO)
- The phenomenon of cross-nonspecific adaptation
- Extreme and terminal states upon adaptation failure
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