Pathophysiology Notes

Page 1: Stress and Adaptation

  • Stress Response: A physiological state represented by a syndrome triggered by a stimulus demanding systemic change. It alters homeostatic balance and is a normal response to stressors.

    Components of Stress Response

    • Stressor: External or internal triggers.

    • Stress Response: The body's reaction, involving hormonal changes.

    • Pathophysiological Equilibrium: How chronic stress affects bodily functions.

  • Types of Stressors: Include both external stimuli and individual perceptions or psychological responses. Stress results in non-specific hormonal changes regardless of stressor type.

Adrenal Gland Structure

  • Capsule: Outermost protective layer, composed of fibrous tissue.

  • Adrenal Cortex: Accounts for 80-90% of the gland; composed of three zones:

    • Zona Glomerulosa

    • Zona Fasciculata

    • Zona Reticularis

  • Adrenal Medulla: Contains nerve tissue and makes up 10-20% of gland, functions as part of SNS.

Physiological Stress Response: HPA Axis

  • HPA Axis: Involves hypothalamus, pituitary gland, and adrenal cortex.

    • Responds uniformly to various stressors, activating the limbic system and central cortex leading to hypothalamic stimulation.

  • Acute Stress Feedback: Beneficial for fight-or-flight response, enhances alertness, cognitive function, and focus. However, can be detrimental, especially in patients like those with heart disease due to catecholamine surges.

  • Chronic Stress Feedback: In chronic conditions, feedback loops are impaired, preventing hypothalamus response to cortisol, resulting in continued secretion of CRH and ACTH.


Page 2: Short-term vs Prolonged Stress Response

  • Short-term Stress: Predominant catecholamine effects (e.g., epinephrine, norepinephrine).

  • Prolonged Stress: Corticosteroids take precedence, potentially leading to hypertension, vascular diseases, and sustained hyperglycemia.

Positive Consequences of Stress

  • Hypermetabolic state from processes like:

    • Lipolysis

    • Gluconeogenesis

    • Glycogenolysis

Negative Consequences of Prolonged Stress

  • Loss of muscle mass due to protein catabolism and gluconeogenesis.

  • Nitrogen depletion increases nitrogen excretion in urine.

  • Reduced immune response, specifically to T-cells leading to increased susceptibility to infections.

Measuring Stress Consequences

  • Biological Tests: Blood tests for hypoglycemia, adrenal function (aldosterone, cortisol, ACTH).

  • Psychosocial Assessments: Anxiety, mood, coping mechanisms through self-reported assessments.

Example Test: TSST

  • Trier Social Stress Test (TSST): Tests cortisol responses via a mock job interview, showing distinct cortisol spikes.


Page 3: Impact of Chronic Stress on Healing

  • Chronic stress linked to weaker vaccine responses and poorer wound healing.

  • High cortisol inhibits immune functions, increasing mortality risks by hampering the identification of pathogens and hence delaying wound healing.

Research Examples

  • Caregivers: Longer healing times compared to controls due to chronic stress.

  • Students: Healing times for cuts were significantly longer before exams than during vacation periods.

  • Hostility in Couples: Higher hostility correlates with slower healing rates.

Effects on the Brain

  • Hippocampus: Sensitive to glucocorticoids; chronic stress can damage this region, leading to cognitive difficulties.


Page 4: Clinical Implications of Stress

  • Classic symptoms: Sleep disturbances, insomnia, anxiety, muscle tension, GI issues (stomach upset, reflux, and bowel irregularities).

    Physical Health Impacts

    • Increased gastric acid due to cortisol can lead to ulcers.

    • Heart-related issues: hypertension, palpitations, chest pains, and pulmonary conditions.

Emotional and Behavioral Symptoms of Stress

  • Symptoms include anxiety, frustration, memory problems, lack of focus, and potential behavioral problems like addiction.

  • Stress also affects familial interactions, which can impact health teaching.

Clinical Interventions for Stress Management

  • Aim to eliminate stressors through medical treatments or environmental adjustments.

  • Managing stress response: healthy coping mechanisms, relaxation, and establishing priorities.

  • Preventative measures include stress management techniques and pain control.


Page 5: Non-Pharmacological Treatments for Stress

  • Techniques such as meditation, exercise, and biofeedback can reduce stress responses.

  • Factors Affecting Adaptation: Varies by individual circumstances and perceptions of stress.

  • Three Stages of Adaptation: Alarm, resistance/adaptation, exhaustion.


Page 6: Understanding Inflammation and Defense Mechanisms

  • Inflammation: Can be specific (immune) or non-specific, with innate responses present at birth and acquired responses developing over time.

Types of Defense Mechanisms

  • Natural Barriers: First line of defense including skin, mucous membranes, and their actions (e.g., sloughing, vomiting).

  • Inflammation: As a second line of defense and immunity as the final defense.


Page 7: Causes and Phases of Inflammation

  • Causes: Microbes, immune reactions, trauma, burns, etc.

  • Acute Inflammation: Fast response with defined phases resulting in localized healing.


Page 8: Cellular Response in Inflammation

  • Key cells: Neutrophils, Macrophages, and Eosinophils play various roles in inflammation.


Page 9: Role of Mast Cells and Mediators

  • Mast Cells: Release mediators that activate inflammatory responses through degranulation and mediator synthesis.


Page 10: Plasma Protein Systems in Inflammation

  • Activation of plasma proteins leads to a cascade effect, enhancing the inflammatory response.


Page 11: Inflammatory Mediators and Their Functions

  • Histamine: Causes vasodilation and increases vascular permeability.

  • Cytokines: Play a significant role in inflammation regulation.