Physiology of Stress – Critical Care & Emergency Nursing

Vocabulary flashcards summarizing essential terms, hormones, pathways, and phenomena related to the physiologic stress response in critically ill patients.

Stress

A perceived or anticipated threat that disrupts homeostasis and exceeds an individual’s capacity to meet demands.

Homeostasis

The body’s tendency to maintain a stable internal environment.

Hypothalamic-Pituitary-Adrenal (HPA) Axis

Neuroendocrine pathway in which the hypothalamus releases CRH, the pituitary secretes ACTH, and the adrenal cortex produces cortisol during stress.

Autonomic Nervous System (ANS)

Involuntary nervous system composed of sympathetic and parasympathetic branches that regulates visceral functions.

Sympathetic Nervous System (SNS)

ANS branch that mediates the fight-or-flight response via rapid catecholamine release.

Parasympathetic Nervous System (PNS)

ANS branch that counterbalances the SNS and promotes rest-and-digest activities.

Catecholamines (CAs)

Stress hormones (epinephrine, norepinephrine) released from adrenal medulla and sympathetic nerves.

Epinephrine

Catecholamine acting on α and β receptors; increases cardiac output, causes vasodilation, and raises blood glucose.

Norepinephrine

Catecholamine acting primarily on α receptors; raises blood pressure, dilates pupils, and causes piloerection.

Corticotropin-Releasing Hormone (CRH)

Hypothalamic hormone that initiates HPA activation by stimulating ACTH release.

Adrenocorticotropic Hormone (ACTH)

Anterior pituitary hormone that prompts the adrenal cortex to secrete cortisol.

Cortisol

Glucocorticoid that elevates blood glucose, modulates metabolism, and exerts anti-inflammatory effects; chronic excess leads to pathology.

General Adaptation Syndrome (GAS)

Selye’s three-phase response to stress: alarm, resistance, and exhaustion.

Alarm Phase

First GAS stage; SNS and HPA activation release catecholamines and cortisol (fight-or-flight).

Resistance Phase

Second GAS stage; continued hormone release allows adaptation but decreases immune activity.

Exhaustion Phase

Final GAS stage; physiologic resources depleted, leading to allostatic overload and disease risk.

Allostasis

Achievement of stability through change by activating adaptive physiological mechanisms.

Allostatic Load

Cumulative wear and tear from repeated allostatic responses to stressors.

Allostatic Overload

Pathologic state when chronic activation of stress systems produces illness and disease.

Metabolic Syndrome

Cluster of metabolic abnormalities (obesity, insulin resistance, dyslipidemia, hypertension) linked to chronic cortisol excess.

Neuropeptide Y (NPY)

Peptide co-released with norepinephrine that augments vasoconstriction and stress responses.

Inflammatory Cytokines

Signaling proteins (e.g., IL-1β, IL-6, TNF-α) elevated by stress, promoting inflammation.

T-Helper 1 (Th1) Cells

Lymphocytes mediating cellular immunity; activity decreases during chronic stress.

T-Helper 2 (Th2) Cells

Lymphocytes mediating humoral immunity; activity increases with stress, fostering autoimmunity.

Growth Hormone (GH)

Anterior pituitary hormone that counters insulin, supports tissue repair, and rises during acute stress.

Antidiuretic Hormone (ADH)

Posterior pituitary hormone that conserves water to maintain circulating volume under stress.

Aldosterone

Mineralocorticoid that promotes sodium and water retention via the renin-angiotensin-aldosterone system.

Endorphins

Endogenous opioids that modulate pain and down-regulate stress pathways during stress.

Enkephalins

Endogenous opioids similar to endorphins that blunt the stress response.

Chronic Stress

Prolonged exposure to stressors leading to sustained HPA/SNS activation and health consequences.

Acute Stress

Short-term stress that triggers rapid adaptive responses beneficial for immediate survival.

Telomere Erosion

Shortening of chromosome end-caps accelerated by chronic stress, indicative of biological aging.

Renin-Angiotensin-Aldosterone System (RAAS)

Hormonal cascade that increases blood pressure and volume; activated alongside stress hormones.

Lipolysis

Breakdown of triglycerides into free fatty acids, stimulated by catecholamines and cortisol.

Gluconeogenesis

Hepatic production of glucose from non-carbohydrate sources, driven by cortisol and epinephrine.

Hyperglycemia

Elevated blood glucose common during stress due to cortisol and epinephrine effects.

Immunosuppression

Reduced immune function occurring with chronic cortisol and catecholamine exposure.

Adaptive Behavior

Coping actions that effectively reduce stress and promote health.

Maladaptive Behavior

Coping actions that worsen stress effects or health outcomes.

Capillary Permeability (Third Spacing)

Albumin leakage into interstitium during stress, causing edema and hypovolemia.

Cardiac Output

Volume of blood the heart pumps per minute; increased by catecholamines during stress.

Hyperosmolarity

High serum solute concentration resulting from stress-induced hyperglycemia and diuresis.

Microthrombi

Small clots that may form during stress due to increased platelet aggregation.

Burnout

State of emotional, physical, and mental exhaustion from chronic workplace stress.

Social Isolation

Lack of social connections that serves as a chronic psychosocial stressor.