Stress Response Notes PDF

**Stress Response** **Describe the Contribution of the Sympathetic Nervous System (SNS) and the Hypothalamic-Pituitary-Adrenal (HPA) Axis to the Stress Response** **Overview of Stress Response** - The stress response occurs when an individual perceives or anticipates a threat, triggering tw...

**Stress Response** **Describe the Contribution of the Sympathetic Nervous System (SNS) and the Hypothalamic-Pituitary-Adrenal (HPA) Axis to the Stress Response** **Overview of Stress Response** - The stress response occurs when an individual perceives or anticipates a threat, triggering two major systems: - **Sympathetic Nervous System (SNS)** - **Hypothalamic-Pituitary-Adrenal (HPA) Axis** Together, they initiate and maintain the **"fight or flight"** response to mobilize energy and resources needed to combat the stressor. **1. Sympathetic Nervous System (SNS)** - The SNS is part of the **autonomic nervous system (ANS)** and plays a key role in **immediate, short-term stress responses**. **Activation Process:** 1. **Perception of threat:** The brain (amygdala and hypothalamus) perceives the threat. 2. **Signal transmission:** Hypothalamus sends signals via the spinal cord to the adrenal medulla. 3. **Release of catecholamines:** - **Epinephrine (adrenaline)** and **norepinephrine (noradrenaline)** are released from the **adrenal medulla**. - These catecholamines initiate the \"fight-or-flight\" response. **Effects of Catecholamines:** - Increased heart rate and cardiac output (enhances oxygen delivery to muscles) - Dilation of airways to increase oxygen uptake - Breakdown of glycogen into glucose (for quick energy) - Redirection of blood flow from non-essential systems (e.g., digestive) to muscles and brain - Increased sweating (to cool the body) **Adrenergic Receptors:** - **α-adrenergic receptors:** Mostly cause vasoconstriction and blood pressure regulation. - **β-adrenergic receptors:** Enhance heart rate, lung capacity, and muscle function. **2. Hypothalamic-Pituitary-Adrenal (HPA) Axis** - The HPA axis is responsible for the **longer-term stress response** by releasing hormones that affect metabolism, immune function, and energy regulation. **Activation Process:** 1. **Hypothalamus activation:** Perceived stress triggers the hypothalamus to release **corticotropin-releasing hormone (CRH)**. 2. **Pituitary gland stimulation:** CRH stimulates the anterior pituitary to release **adrenocorticotropic hormone (ACTH)**. 3. **Adrenal cortex activation:** ACTH stimulates the adrenal cortex to release **cortisol** into the bloodstream. **Role of Cortisol:** - Mobilizes energy by promoting gluconeogenesis (formation of glucose from non-carbohydrate sources like amino acids) - Suppresses non-essential functions (e.g., digestion, reproduction) - Inhibits the immune system to prevent overactivation - Maintains blood pressure by enhancing the effects of catecholamines **Chronic Effects of Cortisol:** - Prolonged cortisol secretion can lead to: - **Fat accumulation** in the abdomen and trunk - **Suppressed immune function**, increasing susceptibility to infection - **Impaired memory** and hippocampal function - **Increased inflammation** due to downregulation of glucocorticoid receptors (GR), promoting proinflammatory cytokine production. **Interplay Between SNS and HPA Axis** - The SNS and HPA axis work in tandem: - The **SNS** deals with immediate, short-term stress responses by activating the body for **\"fight-or-flight.\"** - The **HPA axis** helps regulate the longer-term stress response by maintaining energy availability and modulating other body systems to adapt to prolonged stress. **Clinical Implications** - **Acute Stress:** Activation of both systems is adaptive, allowing individuals to quickly respond to dangers. - **Chronic Stress:** Continuous activation can contribute to: - **Mental illnesses** such as anxiety, depression, and PTSD - **Metabolic disorders** (e.g., diabetes due to elevated blood glucose) - **Cardiovascular disease** due to prolonged sympathetic activation and hypertension. **Explain How Chronic Activation of the Stress Response Can Facilitate Mental Illness Development** **1. The Stress Response Mechanism** - The stress response is activated when an individual perceives or anticipates a threat, engaging major physiological systems: - **Hypothalamic-pituitary-adrenal (HPA) axis** - **Sympathetic Nervous System (SNS)** - **Immune system**. **2. Acute Stress vs. Chronic Stress** - **Acute stress** (short-term) is beneficial as it helps the body respond to immediate challenges. - **Chronic stress** occurs when the body remains in a prolonged state of heightened alertness, leading to negative effects such as: - **Elevated cortisol levels** - **Persistent activation of the SNS** - **Increased proinflammatory cytokine production (e.g., IL-1β, IL-6, TNF-α)**. **3. Pathophysiological Effects of Chronic Stress on Mental Health** - **Overactivation of HPA Axis:** - Continuous activation leads to **excessive cortisol secretion**, resulting in: - Immune system suppression - **Hippocampal damage**, impairing memory and emotional regulation - Disrupted negative feedback in cortisol regulation. - **Proinflammatory State:** - Chronic stress reduces the efficacy of glucocorticoid receptors, limiting cortisol's anti-inflammatory role. - Persistent inflammation (via IL-1β, IL-6, and TNF-α) is associated with **depression, anxiety, and neurodegeneration**. **4. Effects on Brain Regions and Neurotransmitter Systems** - **Hippocampus:** - Chronic stress **reduces hippocampal volume**, impairing short-term memory and emotional regulation, contributing to **depression and PTSD**. - **Amygdala:** - Hyperactivation leads to **heightened fear responses and emotional dysregulation**, seen in **anxiety disorders**. - **Prefrontal Cortex:** - Impaired function disrupts **decision-making and emotional regulation**, common in **major depressive disorder (MDD)** and **PTSD**. - **Neurotransmitter Dysregulation:** - Chronic stress decreases **serotonin** and **norepinephrine**, contributing to mood disorders. - Increased cortisol affects **dopamine signaling**, leading to motivational and reward system disruptions, which are implicated in **depression and addiction**. **5. Specific Mental Disorders Associated with Chronic Stress** - **Major Depressive Disorder:** - Linked to prolonged HPA activation, decreased serotonin, and hippocampal atrophy. - Elevated proinflammatory cytokines further exacerbate symptoms. - **Anxiety Disorders:** - Overactivity of the amygdala and disruptions in GABA receptor signaling. - Chronic stress sensitizes the **autonomic nervous system**, leading to heightened fear responses. - **Post-traumatic Stress Disorder (PTSD):** - Reduced hippocampal volume and hyperactive amygdala responses contribute to **intrusive thoughts and hypervigilance**. - Dysregulated prefrontal cortex fails to inhibit inappropriate fear responses. - **Substance Use Disorders:** - Chronic stress downregulates prefrontal cortex control over impulses, leading to **dysregulated dopamine and glutamate signaling**, promoting addiction. **6. Clinical Implications** - Understanding how chronic stress contributes to mental illness highlights the need for: - Early **stress management interventions** (e.g., mindfulness, CBT) - **Pharmacological treatments** targeting neurotransmitter systems and HPA regulation - **Anti-inflammatory treatments** to address the chronic inflammatory state seen in depression and PTSD. These notes synthesize the connection between prolonged stress response activation and the pathogenesis of mental illnesses using key physiological mechanisms.