General development mechanism and key systems
The development of the stress response begins with a triggering moment: exposure of the body to an extreme factor or deviation of homeostasis parameters from normal values. This is followed by a cascade of reactions:
- Nervous regulation: afferent impulse generation intensifies, and cortical and subcortical nerve centers are activated.
- Activation of effector systems: effects of the sympathetic nervous system (SNS) are enhanced, and endocrine glands are stimulated.
- Hormonal response: the concentration of corticosteroids, catecholamines, glucagon, and thyroid hormones sharply increases in the blood and tissues.
- Systemic effect: generalized organ hyperfunction occurs. At this stage, the maintenance of homeostasis is unstable.
For the rapid mobilization of protective, compensatory, and restorative mechanisms, the sympathoadrenal system (SAS) and the hypothalamic-pituitary-adrenal axis (HPA axis) are activated, with the latter playing a key role. The thyroid and pancreas are also involved. These non-specific mechanisms allow the body to escape the damaging factor, develop resistance, and maintain vital activity.
Alarm stage and metabolic support
Already at the first stage (the alarm stage), an active redistribution of resources—energy, plastic, and metabolic—begins. They are transported from unactivated tissues to dominant organs that implement specific adaptive reactions.
However, an excessively pronounced or prolonged alarm stage has a high pathogenic potential. The adaptive reaction can transform into a pathological process (disease) under the influence of the following risk factors:
- Hypercatecholaminemia.
- Excess glucocorticoids, mineralocorticoids, thyroid hormones, and other biologically active substances (BAS).
- Ischemia of individual organs and tissues.
With prolonged exposure to the stressor and excessive mobilization of metabolism, severe consequences develop: dystrophy, hypotrophy, erosions, ulcers, and necrosis. Typical localization of such lesions includes the gastrointestinal tract, kidneys, heart, and lymphoid tissue.
Resistance stage
The second stage of the stress response is aimed at developing increased resistance to a specific stressor exposure. During this period, organ function normalizes, metabolic intensity stabilizes, and hormone and metabolic substrate levels even out. As a result, homeostasis parameters are maintained within the normal range in a stable manner.
The morphofunctional basis of such resistance is the processes of hypertrophy and/or hyperplasia of structural elements. They affect tissues and organs that provide protection:
- Endocrine glands: pituitary gland, adrenal glands, thyroid gland.
- Visceral organs: heart, liver.
- Hematopoietic organs.
This ensures long-term specific adaptation of the body to the action of the stress agent.
Exhaustion stage
If the intensity of the stressor increases or its action lasts too long, compensatory and adaptive mechanisms become insufficient. A transition occurs to the third stage—the exhaustion stage.
It is characterized by deep disorder of nervous and humoral regulation mechanisms. Catabolic processes begin to dominate in tissues, and the functioning of systems and organs is impaired. The general outcome of this stage is a sharp decrease in the general resistance and adaptability of the body, leading to disruption of its normal vital activity.
Briefly: answers to topical questions
What is the mechanism of development of internal organ ischemia during the alarm stage?
During the alarm stage, sources confirm the following chain that can lead to ischemia of individual organs and tissues.
- Stressor/homeostasis deviation → increased afferent impulse generation and activation of cortical and subcortical nerve centers.
- Effector response → enhanced sympathetic effects and activation of endocrine glands.
- Hormonal response → increased content of corticosteroids, catecholamines, glucagon, and thyroid hormones in the blood and tissues.
- Hypercatecholaminemia causes vasospasm; for the kidneys, the chain is specified as: vasospasm → renal ischemia → nephron death.
An excessively pronounced or prolonged alarm stage may be accompanied by ischemia of individual organs and tissues and the transition of the adaptive reaction into a pathological process. Already at the alarm stage, the transport of energy, metabolic, and plastic resources from unactivated tissues and organs to dominant organs also occurs.
How do the function of the immune system and thymus change during the exhaustion stage?
During the exhaustion stage, sources confirm a general decrease in the body's resistance and adaptability against the background of disordered nervous and humoral regulation, dominance of catabolic processes, and impaired organ and system functions.
The following changes are confirmed for the immune system and thymus under stress:
- Thymus: accidental (rapid) involution develops as a reaction to stressful situations; the triggering mechanism is exposure to high doses of glucocorticoids.
- Thymic lymphoid cells: stress and steroid hormones are among the causes of their death; the thymus is sensitive to apoptosis-inducing factors.
- Immune system: glucocorticoids weaken cellular immunity, act as immunosuppressants in high doses, and suppress immune responses.
- Lymphoid tissue: glucocorticoids enhance protein catabolism.
Outcome for the exhaustion stage: a decrease in the general resistance and adaptability of the body.
To memorize the main stress hormones, use the abbreviation CCGT: Corticosteroids, Catecholamines, Glucagon, Thyroid hormones.
Class and exam questions
Which body systems play a key role in the development of the stress response?
For the rapid mobilization of adaptive mechanisms, the sympathoadrenal system, thyroid gland, and pancreas are activated. However, the key role in this process belongs to the hypothalamic-pituitary-adrenal axis (HPA axis).
What is the metabolic support during the alarm stage?
During the alarm stage, a large-scale redistribution of energy, metabolic, and plastic resources occurs. They are actively transported from unactivated tissues and organs to dominant organs, which are responsible for implementing specific adaptive reactions.
Why can prolonged stress lead to the development of disease?
An excessively prolonged alarm stage is accompanied by hypercatecholaminemia, excess corticosteroids, and tissue ischemia. This exhausts the body and causes dystrophic changes, hypotrophy, erosions, ulcers, and necrosis in the gastrointestinal tract, kidneys, heart, and lymphoid tissue.
What is the morphofunctional basis of the resistance stage?
Long-term adaptation is provided by processes of hypertrophy and hyperplasia of structural elements. These changes affect the endocrine glands (pituitary, adrenals, thyroid), visceral organs (heart, liver), and the hematopoietic system.
What else to study on this topic
- The role of the hypothalamic-pituitary-adrenal (HPA) axis in adaptation
- Mechanisms of redistribution of energy and plastic resources
- Pathogenic potential of stress: from hypercatecholaminemia to necrosis
- Morphofunctional changes in organs during the resistance stage
- Catabolic processes and regulatory disorders during the exhaustion stage
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