Stress and Disease-8779877787878788.pptx

Stress and Disease.pptx

1. Stress & Diseases Presented by: Mental Health & Psychiatric Nursing Students Subject: Advanced Physiology and Pathophysiology ( MSN 302) Course: Masters of Science in Nursing Department: Mentel Health & Psychiatric Nursing College: Enam Nursing College

2. Group Members Nasrin Jahan Shirin Nahar Israt Jahan Shamima Nasrin Silviya Alam Mercy T. Barikder Maxim T. Barikder Mst NazminAkter Md. Masum Parves Dinia Mrong

3. Table of contents 01 03 02 04 Introduction Stress & Disease Historical Background General Concepts of Stress Psychoneuro - immunology ( PNI)

4. Table of contents 05 07 06 08 Stress Response: Central Nervous System Neuroendocrine Regulation ( HPA Axis) Stress & Immune System Stress, Personality, and Coping

5. Table of contents 09 10 Aging and Stress ( Stress-Age Syndrome) Conclusion

6. Learning Objectives Define stress and differentiate types of stress (acute, chronic, episodic, eustress). Define & Identify stressors. Summarize the evolution of stress research from ancient medicine to modern psychoneuroimmunology . Explain key concepts such as homeostasis, allostasis , and allostatic load. Explain CNS role in stress. Differentiate SAM vs HPA axis in stress response. Describe parasympathetic system’s balancing role in stress and inflammation.

7. Learning Objectives Recognize key mediators (cortisol, catecholamines , cytokines). Discuss effects of stress on health (cardiovascular, immune, metabolic, mental health). Compare personality types (A, B, C, D) in relation to stress vulnerability. Relate personality and coping styles to stress vulnerability. Outline stress and aging changes (Stress-Age Syndrome). Identify management strategies for stress (pharmacological & non-pharmacological).

8. Introduction to Stress & Disease Presented by : Nasrin Jahan Roll No. : 01

9. Introduction Pressure turns into stress when you feel unable to cope. People have different ways of reacting to stress, so a situation that feels stressful to one person may in fact be motivating to another . Stress can affect how you feel, how you think, how you behave and how your body works. Sleeping problems, sweating, loss of appetite and difficulty concentrating are common signs of stress.

10. Psychological Perception of Stress Stress begins with brain perception of a stressor . This triggers adaptational physiologic responses meant to support survival . When perceived demand exceeds adaptive capacity, stress → negative emotional and health outcomes.

11. Historical Background Of Stress and Diseases 02 Presented by : Shirin Nahar Roll No : 02

12. Historical Background Of Stress & Diseases The understanding of stress and its connection to diseases has evolved significantly over time, influenced by scientific, medical, and psychological discoveries. Below is a historical overview of key developments: The link between stress and disease has been recognized since ancient times. Early physicians like Hippocrates and Galen noted that emotions such as anger, fear, or grief could affect physical health .

13. Historical Background Of Stress & Diseases In the 17th–18th centuries , scientists began connecting stress with disorders like hypertension and nervous breakdowns . In the 20th century, Hans Selye (1936) introduced the concept of the “ General Adaptation Syndrome (GAS) ”, showing how the body responds to stress in three stages: alarm, resistance, and exhaustion . He demonstrated that chronic stress can weaken immunity and increase risk of diseases.

14. Historical Background Of Stress & Diseases 21st Century , epigenetics reveals how stress alters gene expression, increasing vulnerability to diseases (e.g., cancer, autoimmune disorders). Later research in psychoneuroimmunology showed how stress hormones (like cortisol) influence the immune system , making people more vulnerable to infections, cardiovascular disease, diabetes, and mental health disorders . Today , stress is recognized as a major risk factor for both physical and mental illnesses, including heart disease, stroke, anxiety, depression, and gastrointestinal problems.

15. General Concepts of Stress Presented by: Israt Jahan Roll No. : 03

16. Definition Stress is a state of strain, whether it is physical or psychological . ( Atkison , Berne & Woodworth ) Stress is defined as a constraining or impulsing force and as an effort or demand upon Physical or mental energy. ( Oxford Dictionary)

17. Types of Stress Acute Stress – Short-term, immediate reaction (e.g., exam stress). Chronic Stress – Long-term, ongoing stress (e.g., work pressure). Episodic Stress – Frequent acute stress episodes. Eustress – Positive stress that motivates.

18. What is a Stressor ? A stressor is any physical, psychological, social, environmental, or chemical factor that challenges an individual’s adaptive capacity and disrupts homeostasis, thereby triggering a stress response.

19. Types of Stressors Physical/Biological Stressors: Trauma , injury, surgery Infection , fever, inflammation Noise , extreme temperatures, radiation Psychological Stressors Anxiety , fear, depression Work pressure, exams, performance demands Major life events (loss of loved one, divorce, job loss) Social Stressors Social isolation Discrimination, bullying, abuse Family conflict, strained relationships

20. Types of Stressors Environmental Stressors Overcrowding Pollution , toxins, allergens Natural disasters Chemical Stressors Drugs , alcohol, smoking Environmental toxins (e.g., heavy metals, pesticides ) Medications with side effects

21. Types of Stress Responses Reactive Response : physiologic reaction to psychological stressor Example : exam stress → ↑ heart rate, dry mouth Anticipatory Response : response in anticipation of stress Species-specific (predator threat ) Learned (conditioned memory programs)

22. Brain Regions Involved Hippocampus Amygdala Prefrontal Cortex PVN (Hypothalamus) HPA Axis

23. Homeostasis vs Allostasis Homeostasis The body maintains stable internal set points (e.g., temperature, blood glucose, pH). Goal: stability through constancy . Example: Body keeps blood pressure around a normal baseline. Allostasis The body achieves stability by changing set points in response to challenges . Goal: stability through change . Example: Under chronic stress, cortisol baseline shifts upward, heart rate and blood pressure remain higher than normal.

24. Allostatic Load The cumulative wear and tear on the body from repeated or chronic stress . Results from prolonged allostasis → when adaptive systems (HPA axis, autonomic, immune) are over-activated . Consequences : metabolic disorders, cardiovascular disease, immune suppression, mental health issues.

25. Psychoneuro -immunology Presented by: Shamima Nasrin Roll No. : 04

26. Psychoneuroimmunology Psychoneuroimmunology is a field of study that explores the intricate interactions between the mind, nervous system, and immune system.

27. Pathways of Stress Response Hypothalamic-Pituitary-Adrenal (HPA) axis → cortisol release Sympathetic-Adrenal-Medullary (SAM) system → catecholamines (epinephrine, norepinephrine ) Parasympathetic system → regulatory “brake ” Stress alters immune surveillance and inflammation

28. Mediators of Stress Glucocorticoids (Cortisol ) Catecholamines (Epinephrine, Norepinephrine ) Proinflammatory Cytokines ( IL-1, IL-6, TNF- α )

29. Effects of Stress on the Body The notes list the effects of stress on two systems: Immune System: Stress leads to a decrease in white blood cells (WBCs) and antibodies, resulting in slow wound healing . Cardiovascular System: Stress can cause an increase in blood pressure and raise the risk of heart disease.

30. Stress and Diseases Heart disease and hypertension Diabetes and obesity Gastrointestinal problems Cancer progression Depression and anxiety disorders Sleep Deprivation

31. Stress Response: Central Nervous System Presented by; Silviya Alam Roll No. : 05

32. What is Stress Response? The stress response is the body’s way of reacting to physical, emotional, or psychological challenges. In the central nervous system (CNS), it mainly involves the brain (especially hypothalamus and limbic system) and spinal cord, which coordinate with the autonomic nervous system and endocrine system.

33. Stress Response and CNS 1. Perception of Stress → Anticipatory response in the CNS 2. Limbic System → Motivation, emotion, cognition; stimulates endocrine response 3. Locus Ceruleus (LC) → Norepinephrine release; arousal, vigilance, anxiety 4. Sympathetic-Adrenal-Medullary (SAM) System → Fast response (Epinephrine, Norepinephrine) 5. Hypothalamic-Pituitary-Adrenal (HPA) Axis → Slower response (Cortisol release) 6. Physiologic & Behavioral Responses → Increased energy, coping, immune modulation

34. Sympathetic Nervous System & Stress Response Stress activates the SNS → stimulates catecholamine release (epinephrine & norepinephrine ). Source : Adrenal medulla ( chromaffin cells) + nerve endings . The effect of catecholamine is mediated through adrenergic receptors ( α1 , α2, β1, β2, β 3)

35. Parasympathetic System & Stress Acts as a counterbalance to the sympathetic nervous system (SNS). Helps determine adaptation vs maladaptation to stress . Parasympathetic activity opposes catecholamine (SNS) effects . Example : Slows heart rate (vagal tone ). Contributes to immune regulation and stress recovery. Proper stress response requires sympathetic–parasympathetic balance . Overactive SNS or underactive parasympathetic system → risk for maladaptation (e.g., chronic stress, inflammation, cardiovascular strain).

36. Neuroendocrine Regulation: The Role of the HPA Axis in Stress and Disease 06 Presented by; Mercy T. Barikder Roll No. : 06

37. The neuroendocrine system plays a vital role in maintaining homeostasis by linking the central nervous system (CNS) and the endocrine system. One of the key components of this system is the hypothalamic-pituitary-adrenal (HPA) axis , which is primarily responsible for coordinating the body’s response to stress. Proper regulation of the HPA axis is essential for survival; however, dysregulation of this system is associated with a wide range of physiological and psychological disorders.

38. Structure and Function of the HPA Axis

39. The HPA Axis and the Stress Response Acute Stress Chronic Stress

40. HPA Axis Dysregulation & Diseases Psychiatric Disorders Depression: Often associated with hyperactivity of the HPA axis and elevated cortisol levels. Many patients exhibit impaired negative feedback regulation . Post-Traumatic Stress Disorder (PTSD): Characterized by low cortisol levels and enhanced negative feedback sensitivity, suggesting a unique form of HPA deregulation.

41. HPA Axis Dysregulation & Diseases Metabolic Disorders Chronic HPA activation contributes to insulin resistance , visceral obesity , and metabolic syndrome .

42. HPA Axis Dysregulation & Diseases Immune Disorders   Cortisol suppresses immune responses, making the body more susceptible to infections and slowing wound healing. Long-term exposure can also contribute to autoimmune diseases by altering cytokine balance. .

43. HPA Axis Dysregulation & Diseases Cardiovascular Disease Elevated cortisol levels are associated with hypertension , increased risk of myocardial infarction .

44. Mechanisms of Feedback Regulation Cortisol exerts its feedback effects primarily through glucocorticoid receptors (GRs) in the hypothalamus, pituitary, and hippocampus. These receptors help terminate the stress response when appropriate. Disruption in GR function is a hallmark of HPA axis dysfunction- Down regulation of GRs - common in depression, leading to poor feedback control and chronic cortisol elevation. U p regulation or hypersensitivity of GRs- may explain the enhanced feedback seen in PTSD.

45. Assessment of HPA Axis Function Salivary Cortisol Tests: Measure diurnal cortisol rhythm. Dexamethasone Suppression Test (DST): Assesses feedback sensitivity. ACTH Stimulation Test: Evaluates adrenal responsiveness.

46. Therapeutic Implications   Pharmacological Interventions   Antidepressants (e.g., SSRIs) help normalize HPA function . GR antagonists and CRH receptor antagonists are under investigation . Non-Pharmacological Approaches   Cognitive Behavioral Therapy (CBT) reduces perceived stress and may help restore normal HPA function .   Mindfulness-based stress reduction (MBSR) and physical activity are also effective in modulating the stress response.

47. Stress & Immune System Presented By: Maxim T. Barikder Roll No:07

48. Acute Stress & Immunity A short-term physiological and psychological response to an immediate perceived threat or challenge. Mediators : S ympathetic nervous system (SNS) H ypothalamic–pituitary–adrenal (HPA) axis.

49. Acute Stress & Immunity Active Stressors Brain identifies threat SNS – Adrenaline / Noradrenaline HPA Axis – Cortisol Immune cell mobilization Cortisol Regulates Inflammation Short-term: Boosted innate immunity

50. Acute Stress & Immunity Active Stressors Brain identifies threat SNS – Adrenaline / Noradrenaline HPA Axis – Cortisol Immune cell mobilization Cortisol Regulates Inflammation Short-term: Boosted innate immunity

51. Acute Stress & Immunity Active Stressors Brain identifies threat SNS – Adrenaline / Noradrenaline HPA Axis – Cortisol Immune cell mobilization Cortisol Regulates Inflammation Short-term: Boosted innate immunity

52. Chronic Stress & Immunity Chronic stress is the prolonged or repeated activation of the stress response system (HPA axis + sympathetic nervous system), lasting weeks to months (or longer). Unlike acute stress, which is short-term and adaptive, chronic stress becomes maladaptive and harmful to health.

53. Chronic Stress & Immunity

54. Th1 cells Vs. Th2 cells Feature Th1 Cells Th2 Cells Primary Function Cell-mediated immunity Humoral immunity Cytokine Profile IFN- γ, TNF, IL-2 IL-4, IL-5, IL-10, IL-13 Pathogens Intracellular bacteria, viruses, cancer Parasites, allergens Inflammation Pro-inflammatory Anti-inflammatory, promotes IgE Cell Activation Macrophages, cytotoxic T cells B cells, eosinophils

55. Chronic Stress & Immunity

56. Chronic stress & Immunity Active Stressors Brain identifies threat SNS – Adrenaline / Noradrenaline HPA Axis – Cortisol Immune cell mobilization Cortisol Regulates Inflammation Repeated/prolonged: Immunosuppression

57. Innate vs Adaptive Immunity in Chronic Stress Aspect Innate Immunity (Chronic Stress) Adaptive Immunity (Chronic Stress) Cells affected NK cells ↓, macrophages ↓ Th1 ↓, Th2 ↑, B cells ↑ Effect on defense Poor viral/tumor defense Weak pathogen control, ↑ antibodies Cytokines ↑ IL-6, TNF- α, CRP (chronic inflammation) ↓ IFN-γ, IL-2 (Th1), ↑ IL-4, IL-10 (Th2) Clinical impact More infections, chronic inflammation ↑ Allergies, asthma, autoimmunity

58. Disease links: Chronic inflammation is a central driver of many stress-related conditions: Cardiovascular disease: atherosclerosis, hypertension. Metabolic disease: insulin resistance, type 2 diabetes, obesity. Neuropsychiatric disease: depression, anxiety, cognitive decline. Autoimmune disorders: rheumatoid arthritis, lupus, multiple sclerosis

59. Stress & Immune System

60. Stress, Personality, & Coping Presented By: Mst Nazmin Akter Roll No: 09

61. Stress does not affect all individuals in the same manner. The degree of physiological and psychological impact depends largely on personality traits and coping mechanisms.

62. Personality & Stress Vulnerability Type A Personality: Highly competitive, ambitious, impatient, and time-conscious individuals. They are more prone to stress-related illnesses, particularly cardiovascular diseases such as hypertension, myocardial infarction, and coronary artery disease. Their heightened sympathetic activity and chronic hyperarousal contribute to pathology. Type B Personality: Relaxed, patient, and less competitive individuals. They experience less stress reactivity and have a lower incidence of stress-induced diseases. Type C Personality: Passive, suppressive, and conflict-avoiding individuals. They often internalize emotions, which predisposes them to depression and possibly immune-related disorders.

63. Personality & Stress Vulnerability Type D Personality (“Distressed Personality”): Characterized by negative affectivity and social inhibition. These individuals have a higher risk of psychological disorders, chronic stress, and poor health outcomes. Neuroticism and Emotional Instability: People high in neuroticism are more vulnerable to stress, anxiety, and somatic complaints. Resilient Personality: Optimistic, emotionally stable, and solution-oriented individuals are able to buffer stress effectively, leading to better physical and mental health outcomes

64. Coping Mechanisms

65. Coping Mechanisms Coping refers to the strategies an individual employs to manage stress. These strategies are broadly classified as: Problem-Focused Coping: Directly addressing the source of stress to eliminate or reduce it. Examples : developing time-management skills, problem-solving, seeking practical help. Associated with long-term positive outcomes and better adjustment.

66. Coping Mechanisms Emotion-Focused Coping: Aimed at regulating emotional responses rather than altering the stressor itself. Examples : relaxation techniques, meditation, prayer, journaling, and social support seeking. Useful when stressors are beyond one’s control (e.g., loss, terminal illness).

67. Coping Mechanisms Adaptive (Healthy) Coping: Regular physical exercise, mindfulness, supportive relationships, positive reframing, and acceptance. Maladaptive ( Unhealthy) Coping: Substance abuse, denial, aggression, avoidance, and withdrawal. These often worsen the stress response and lead to physical or psychiatric morbidity .

68. Interaction Between Stress, Personality, & Coping Individuals with hostile, competitive, or pessimistic personalities tend to engage in maladaptive coping, resulting in higher disease risk. Resilient individuals often select problem-focused or adaptive coping strategies, which mitigate the harmful physiological effects of chronic stress. Research in psychoneuroimmunology shows that effective coping enhances immune response, whereas maladaptive coping suppresses immunity and increases vulnerability to infections and chronic disease.

69. Aging & Stress (Stress-Age Syndrome ) Presented By: Dinia Mrong Roll No: 10

70. Aging significantly alters the body’s ability to respond to stress. The concept of Stress-Age Syndrome describes the cumulative physiological, immunological, and psychological consequences of stress in the elderly population .

71. Neuroendocrine Alterations HPA Axis Dysregulation : With aging, cortisol secretion becomes prolonged and less tightly regulated. Chronic hypercortisolemia contributes to impaired glucose metabolism, memory decline, and hippocampal atrophy. Sympathetic Nervous System Changes: Older adults show reduced β- adrenergic responsiveness, yet experience prolonged sympathetic activation during stress. This imbalance leads to hypertension, arrhythmias, and impaired cardiovascular adaptability. Reduced Catecholamine Clearance: Results in exaggerated cardiovascular responses and increased vascular stiffness.

72. Immune Senescence and Stress Aging naturally reduces immune efficiency ( immune-senescence ). Chronic stress accelerates this decline by increasing pro-inflammatory cytokines (IL-6, TNF-α), leading to a state of “inflammation.” Stress impairs T-cell mediated immunity, increasing susceptibility to infections, malignancies, and autoimmune disorders in elderly individuals.

73. Clinical Consequences of Stress-Age Syndrome Cardiovascular System: Increased prevalence of hypertension, ischemic heart disease, and stroke . Metabolic Effects: Elevated risk of type 2 diabetes mellitus, obesity, and metabolic syndrome due to chronic cortisol elevation. Musculoskeletal System: Accelerated bone loss (osteoporosis), sarcopenia (muscle wasting), and frailty.

74. Clinical Consequences of Stress-Age Syndrome Cognitive Decline: Stress exacerbates neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease by damaging hippocampal neurons . Psychiatric Outcomes: Depression, anxiety, sleep disorders, and decreased coping capacity become more pronounced with age

75. Psychological and Social Dimensions Elderly individuals face additional stressors: bereavement, retirement, financial insecurity, and social isolation. Loss of social roles and autonomy further intensifies psychological stress, often leading to depression and reduced quality of life

76. Management and Prevention Non-Pharmacological Interventions: Regular exercise, yoga, meditation, and mindfulness-based stress reduction improve both psychological well-being and physical health. Strong social support networks and community engagement protect against loneliness and depression. Pharmacological Considerations: Careful management of comorbidities and minimization of polypharmacy is essential, as drug interactions may exacerbate stress-related complications. Holistic Care Approach: Elderly stress management should integrate medical, psychological, and social strategies tailored to individual needs

77. Conclusion

78. Conclusion Stress has a profound impact on both physical and mental health, contributing to conditions such as cardiovascular disease, diabetes, gastrointestinal problems, anxiety, and depression. Chronic stress disrupts the body’s neuroendocrine and immune systems, making individuals more vulnerable to illness. For nurses, recognizing and managing stress is crucial not only for patient care but also for their own well-being.

79. Conclusion Effective strategies such as mindfulness, relaxation techniques, cognitive-behavioral approaches, and strong social support can help reduce stress and improve outcomes. For MSN students, understanding the biopsychosocial connection between stress and illness enhances holistic, patient-centered care and promotes resilience in practice. Ultimately, addressing stress is vital for preventing disease, improving recovery, and ensuring both patient and provider health.

80. R eferences   McCance , K. L., & Huether , S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). Elsevier. 323-340 Herman , J. P., et al. (2016). Regulation of the hypothalamic-pituitary-adrenocortical stress response. Comprehensive Physiology, 6(2), 603–621. McEwen, B. S. (2007). Physiology and neurobiology of stress and adaptation. The American Journal of Psychiatry, 164(10), 1512–1520. Smith, S. M., & Vale, W. W. (2006). The role of the hypothalamic-pituitary-adrenal axis in neuroendocrine responses to stress. Dialogues in Clinical Neuroscience, 8(4), 383–395. Whitworth, J. A., Williamson, P. M., Mangos, G., & Kelly, J. J. (2005). Cardiovascular consequences of cortisol excess. Vascular Health and Risk Management , 1(4), 291–299 .

81. Quiz Stress & Disease

82. Who introduced the concept of the General Adaptation Syndrome (GAS)? Walter Cannon Hans Selye Sigmund Freud Hippocrates

83. Which of the following best defines allostasis ? a) Stability through constancy b) Return to baseline after stress c) Stability through change d) Physiological wear and tear

84. Which brain region is most involved in fear and emotional memory in stress? Hippocampus Prefrontal cortex Amygdala Cerebellum

85. The end product of the HPA axis stress response is: a) Epinephrine b) Cortisol c) Acetylcholine d) Norepinephrine

86. Acute stress typically: Suppresses innate immunity Enhances innate immunity Has no effect on immune response Increases autoimmune activity immediately

87. Thank You