General Adaptation Syndrome

Mechanisms and pathways of the response

The development of the syndrome begins against the background of a generalized orienting reaction. When a pathogenic factor acts on the body, the central regulatory centers—the nervous and endocrine systems—are activated. They form functional systems that provide a response in three main directions:

• Behavioral (avoidance): the individual actively explores the environment to escape from the source of danger.
• Specific: the system directly responsible for combating the specific factor begins to work in an enhanced mode. This leads to hypertrophy of its structures and the formation of specific adaptation.
• Nonspecific: a classical stress reaction develops, ensuring the body's general resistance to any influences.

Stage I. Emergency (urgent) adaptation

The first phase is characterized by the maximum mobilization of all available reserves. It is based on a triad of regular changes:

1. Activation of exploratory behavior to gather information about the threat.
2. Hyperfunction of dominant systems (e.g., increased muscle work during physical exertion or oxygen transport during hypoxia).
3. Engagement of the nonspecific stress component (reaction of the heart, blood vessels, respiration, and immune system to any stimulus).

At the cellular level, hormones (adrenaline, noradrenaline, glucocorticoids, thyroid hormones) and local mediators (calcium ions, cytokines) are released. They activate protein kinases, triggering the breakdown of carbohydrates, fats, and proteins. Cell membranes are modified due to the intensification of free radical lipid peroxidation (LPO), which facilitates the transport of ions and substrates.

Important: due to a sharp increase in energy demand, relative blood supply insufficiency may occur. This is fraught with tissue necrosis and the development of "diseases of adaptation" (gastrointestinal ulcers, arterial hypertension, myocardial infarction, immunopathologies).

Stage II. Increased resistance

If the body successfully survives the first phase, the acute stress reaction subsides and stable adaptation is formed.

The main mechanism of this stage is the systemic structural trace of adaptation. The mass and number of structural elements in dominant systems increase (hyperplasia and hypertrophy), making their work powerful and reliable. Cross-adaptation often occurs—resistance not only to the primary stressor but also to other extreme factors.

However, the body's resources are limited. Energy and plastic materials are directed to hyperfunctioning organs at the expense of other tissues. This process is called the steal phenomenon.

Stage III. Exhaustion

This stage is not mandatory. It occurs if the extreme factor acts for too long, repeats multiple times, or resumes after a pause.

"Wear and tear" of specific defense systems occurs. Energy production decreases, rates of protein and nucleic acid synthesis drop, and structural restoration is disrupted. Weakened individuals and patients with severe chronic diseases are at risk. If the hypertrophied cells of dominant systems do not receive sufficient plastic supply, they die.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• The role of free radical lipid peroxidation (LPO) in cell membrane modification.
• Mechanisms of protein kinase activation by local function mobilizers.
• Pathogenesis of cell damage in pathological hypertrophy.
• Interaction of specific and nonspecific responses to an extreme factor.
• Formation of temporary connections and conditioned reflexes in the adaptation process.

Other topics in "Chapter 19. The Adaptive Process. Stress"

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.