Acute vs Chronic Stress Response & General Adaptation Syndrome

Overview

Focus: Differentiate acute vs. chronic (short- vs long-term) stress responses.
Framework: Selye’s General Adaptation Syndrome (GAS) with 3 stages: Alarm, Resistance, Exhaustion.
Primary hormones: Catecholamines (adrenaline/noradrenaline from adrenal medulla), Mineralocorticoids (aldosterone) & Glucocorticoids (cortisol from adrenal cortex).
Clinical importance: Unrelieved stress shifts body from adaptive to maladaptive states, leading to disease.

General Adaptation Syndrome (GAS) Review

Alarm: Immediate “fight-or-flight” response.
Resistance: Prolonged coping via adrenocortical hormones.
Exhaustion: Resources depleted, homeostasis collapses, disease develops.

Acute Stress Response (Alarm Stage)

Trigger: Sudden stressor.
Pathway: Hypothalamus → sympathetic nerve impulse → adrenal medulla releases catecholamines.
Effects: $ \uparrow HR$ , $ \uparrow BP$ , $ \uparrow\text{cardiac output}$ , Bronchiolar dilation, Hepatic & muscle glycogenolysis $ \rightarrow\uparrow [\text{glucose}]*\text{blood}$ (quick ATP), Peripheral vasoconstriction, Pupil dilation, Heightened alertness, Decreased GI motility.
Time scale: Seconds to minutes.

Chronic Stress Response (Resistance Stage)

Trigger: Continued/persistent stressor; ongoing sympathetic drive.
HPA axis sequence: Stressor → $ \uparrow$ CRH → Anterior pituitary secretes ACTH → ACTH stimulates adrenal cortex → aldosterone & cortisol.

Mineralocorticoid arm (Aldosterone)

Kidneys: $ \uparrow$ Na $^+$ reabsorption → water follows salt → $ \uparrow$ plasma volume.
Consequence: $ \uparrow Na^+{retention} \Rightarrow \uparrow H2O _{reabsorption} \Rightarrow \uparrow BV \Rightarrow \uparrow BP$ , increasing hypertension risk if prolonged.

Glucocorticoid arm (Cortisol)

Metabolic actions: Proteolysis & lipolysis → amino acids + fatty acids → hepatic gluconeogenesis → $ \uparrow$ blood glucose (slow, sustained energy).
Immune modulation: Acute is adaptive; Chronic leads to immunosuppression (infections, delayed healing).
Neural/psych effects: Altered neurotransmitters ( $ \downarrow$ serotonin) → anxiety, depression.

Transition to Exhaustion Phase

Occurs if stressor persists beyond adaptive limits.
Features: Resource depletion, persistent cortisol dysregulation, maladaptation, organ system damage, and disease onset.

Physiological & Pathological Consequences of Chronic Stress

Examples: CNS issues (memory/concentration loss, insomnia), Dermatological (pruritus, alopecia), Dental (periodontal disease), Cardiovascular (hypertension, atherosclerosis), Endocrine/Metabolic (hyperglycemia, diabetes risk), Immune (immunosuppression, autoimmune flares), GI (ulcers, altered motility), Reproductive issues.

Stress Management Strategies & Clinical Advocacy

Individualised: Nature walks, yoga, hobbies, mindfulness.
Role of health professional: Self-management, patient education for stress reduction, preventing progression to exhaustion.
Ethical dimension: Duty to mitigate chronic stress-related disease burden.

Key Takeaways & Exam Reminders

Memorise GAS stages & dominant hormones.
Acute = catecholamines, sympathetic; Chronic = cortisol + aldosterone, HPA axis.
Aldosterone → $ Na^+$ /water retention → $ \uparrow BP$ ; Cortisol → gluconeogenesis + immunosuppression.
Chronic stress leads to systemic pathologies (e.g., GI ulcer, hypertension, immunocompromise).
Include management/advocacy in case-based questions.

Overview

The note focuses on differentiating acute versus chronic (short- vs long-term) stress responses, using Selye’s General Adaptation Syndrome (GAS) as a framework. This syndrome comprises three stages: Alarm, Resistance, and Exhaustion. Primary hormones involved include Catecholamines (adrenaline/noradrenaline from the adrenal medulla), Mineralocorticoids (aldosterone), and Glucocorticoids (cortisol from the adrenal cortex). Clinically, unrelieved stress can shift the body from an adaptive to a maladaptive state, leading to various diseases.

General Adaptation Syndrome (GAS) Review

GAS involves distinct stages: the Alarm stage is an immediate “fight-or-flight” response; the Resistance stage involves prolonged coping mechanisms via adrenocortical hormones; and the Exhaustion stage occurs when resources are depleted, homeostasis collapses, and disease develops.

Acute Stress Response (Alarm Stage)

An acute stress response is triggered by a sudden stressor. The pathway involves the Hypothalamus stimulating sympathetic nerve impulses, leading to the adrenal medulla releasing catecholamines. Effects include $\uparrow HR$ , $\uparrow BP$ , $\uparrow \text{cardiac output}$ , bronchiolar dilation, hepatic & muscle glycogenolysis resulting in $\uparrow [\text{glucose}]*\text{blood}$ for quick ATP, peripheral vasoconstriction, pupil dilation, heightened alertness, and decreased GI motility. This response typically occurs within seconds to minutes.

Chronic Stress Response (Resistance Stage)

Chronic stress is triggered by continued or persistent stressors, maintaining an ongoing sympathetic drive. The HPA axis sequence begins with a stressor leading to $\uparrow$ CRH, which prompts the Anterior pituitary to secrete ACTH. ACTH then stimulates the adrenal cortex to produce aldosterone and cortisol.

Mineralocorticoid arm (Aldosterone)

In the kidneys, aldosterone leads to $\uparrow$ Na $^+$ reabsorption, with water following salt, resulting in $\uparrow$ plasma volume. Consequently, $\uparrow Na^+ {retention} \Rightarrow \uparrow H 2O _{reabsorption} \Rightarrow \uparrow BV \Rightarrow \uparrow BP$ , which increases the risk of hypertension if prolonged.

Glucocorticoid arm (Cortisol)

Cortisol has several effects: metabolically, it induces proteolysis & lipolysis, yielding amino acids and fatty acids for hepatic gluconeogenesis, which leads to $\uparrow$ blood glucose for slow, sustained energy. While acute immune modulation is adaptive, chronic cortisol exposure results in immunosuppression, increasing susceptibility to infections and delaying healing. Neural/psychological effects include altered neurotransmitter levels (e.g., $\downarrow$ serotonin), contributing to anxiety and depression.

Transition to Exhaustion Phase

The exhaustion phase occurs if a stressor persists beyond the body's adaptive limits. This phase is characterized by resource depletion, persistent cortisol dysregulation, maladaptation, organ system damage, and the onset of various diseases.

Physiological & Pathological Consequences of Chronic Stress

Chronic stress can lead to numerous physiological and pathological consequences. Examples include CNS issues like memory and concentration loss, and insomnia; dermatological problems such as pruritus and alopecia; dental issues like periodontal disease; cardiovascular conditions including hypertension and atherosclerosis; endocrine/metabolic disorders like hyperglycemia and increased diabetes risk; immune system compromises, leading to immunosuppression and exacerbated autoimmune flares; GI issues such as ulcers and altered motility; and reproductive issues.

Stress Management Strategies & Clinical Advocacy

Stress management strategies are individualized and can include nature walks, yoga, hobbies, and mindfulness. Health professionals play a crucial role in promoting self-management and patient education for stress reduction, aiming to prevent progression to the exhaustion phase. Ethically, there is a duty to mitigate the burden of chronic stress-related diseases.

Key Takeaways & Exam Reminders

For exams, it is crucial to memorize the GAS stages and their dominant hormones. Remember that acute stress involves catecholamines and the sympathetic nervous system, while chronic stress involves cortisol and aldosterone via the HPA axis. Aldosterone leads to $Na^+$ /water retention and $\uparrow BP$ , while cortisol primarily causes gluconeogenesis and immunosuppression. Chronic stress often results in systemic pathologies such as GI ulcers, hypertension, and immunocompromise. Always remember to include management and advocacy in case-based questions.