adrenal glands and physiological responsess

• Stress


  A stress response can be elicited by stimuli ('stressors') that disrupt, or threaten to disrupt homeostasis
• Types of stressors


  • Physical (trauma, surgery, intense temps)
  • Chemical (toxins, reduced oxygen supply)
  • Physiological (heavy exercise, pain)
  • Psychological (anxiety, fear, grief)
  • Social (personal conflicts, change in lifestyle)

  
• "the nonspecific response of the body to any demand made upon it"
• Each stressor can cause specific reactions (e.g. oedema in the case of a broken leg, gastrointestinal upset in response to food poisoning)
• There will also be non specific reactions of the whole organism (e.g. increased output of adrenal cortical steroids) which are not dependent on the nature of the stimulus
• Hans Selye's General Adaptation Syndrome

  1. Alarm reaction

  2. Resistance stage

  3. Exhaustion
• Revised General Adaptation Syndrome

  1. Alarm reaction

  2. Resistance stage

  3. Allostatic overload
• Alarm reaction


  Immediate (acute) 'fight-or-flight' response. Higher brain centres informed to send signals in attempt to restore stability (allostasis)
• Alarm reaction


  • This response varies depending on the biological sex and the nature and severity of the stressor
• Resistance stage


  As stressor persists defence and adaptation strategies are optimized and sustained
• Allostatic overload


  Stress mediators can have both protective and damaging effects. Thus chronic problems can arise due to the stress mediators themselves rather than the exhaustion of defence mechanisms per se
• Adrenal glands


  Essential for life. 4 distinct zones but often acts as one functional unit to cope with stress

  
• Adrenal gland regions


  • Medulla
  • Zona reticularis
  • Zona fasciculata
  • Zona glomerulosa

  
• Adrenal gland hormones


  • Catecholamines (adrenaline & noradrenaline)
  • Androgens (DHEA)
  • Glucocorticoids (cortisol)
  • Mineralocorticoids (aldosterone)

  
• Adrenal medulla


  Central region of adrenal gland is a modified sympathetic ganglion. Sympathetic stimulation → chromaffin cells release catecholamines into the blood

  
• Adrenaline


  A 'neurohormone'. Chromaffin cells are modified postganglionic sympathetic neurons

  
• Acute stress response


  1. Adrenal medulla releases catecholamines (adrenaline and noradrenaline)

  2. Short term effects (e.g. increased heart rate, blood pressure, glycogenolysis, bronchodilation, altered blood flow pattern, increased metabolic rate)

  
• Longer term stress response


  1. Hypothalamic-Pituitary-Adrenal (HPA) axis activated

  2. Adrenal cortex releases glucocorticoids (cortisol) and mineralocorticoids (aldosterone)

  3. Effects (e.g. increased gluconeogenesis, proteolysis, lipolysis, reduced immune function, increased sodium/water retention, increased blood volume and pressure)

  
• Cortisol secretion has a circadian diurnal rhythm and also increases in response to stressors
• Actions of cortisol


  Primary role is to increase blood glucose at the expense of fats and protein (stimulates gluconeogenesis, inhibits glucose uptake, inhibits protein synthesis, stimulates protein degradation, facilitates lipolysis)
• Cortisol is antagonistic to actions of insulin - long term it induces insulin resistance. It is permissive for the actions of glucagon and growth hormone
• If wounded or facing a life-threatening situation, the metabolic actions of cortisol help protect the brain from malnutrition during an extended fasting period and provide building blocks for tissue repair
• Ration


  Increases in response to stress
• Cortisol secretion pattern


  • Lipolysis
  • Gluconeogenesis
  • Proteolysis

  
• Tissues affected by cortisol


  • Muscles
  • Liver
  • Adipose
• Primary role of cortisol

  To increase blood glucose at the expense of fats and protein
• Actions of cortisol


  1. Stimulates hepatic gluconeogenesis

  2. Inhibits glucose uptake in tissues (except brain and liver)

  3. Inhibits protein synthesis and stimulates protein degradation

  4. Facilitates lipolysis
• Cortisol


  Is antagonistic to actions of insulin - long term it induces insulin resistance
• Cortisol

  Is permissive for the actions of glucagon and growth hormone
• If wounded or facing a life-threatening situation, the metabolic response to stress is to forego eating, protect the brain from malnutrition during an extended fasting period, and provide a supply of building blocks for tissue repair of injuries
• How cortisol increases sensitivity to adrenaline, noradrenaline and angiotensin II


  1. Increases synthesis of hormone receptors

  2. Increases synthesis of catecholamines and Na/K ATPase pumps

  3. Decreases synthesis of nitric oxide

  
• Cortisol is 'permissive' for the actions of adrenaline, noradrenaline and angiotensin II


  It contributes to the maintenance of cardiac contractility, vascular tone and blood pressure
• Therapeutic utility of cortisol in allergies, autoimmune diseases and transplantation


  • Decreases formation of prostaglandins and leukotrienes
  • Inhibits the accumulation of macrophages and neutrophils
  • Stabilizes lysosomal membranes
  • Decreases production of T cells and B cell proliferation
  • Reduces fever
• Cortisol


  Inhibits bone formation, stimulates bone resorption
• Cortisol


  Alters mood and behaviour, affects memory and learning, stimulates red blood cell production, stimulates gastric acid secretion
• Aldosterone increases the reabsorption of sodium whilst increasing the excretion of potassium
• Major regulators of the Renin-Angiotensin-Aldosterone System (RAAS)


  • ACTH (HPA axis)
  • ACE (produced in lung and kidney endothelium)

  
• Summary of hormonal response to stress


  1. Hypothalamus releases CRH

  2. Anterior pituitary releases ACTH

  3. Adrenal cortex releases cortisol

  4. Adrenal medulla releases adrenaline

  5. Endocrine pancreas decreases insulin and increases glucagon

  6. Arteriolar smooth muscle causes vasoconstriction

  7. Kidney decreases blood flow and increases renin, angiotensin II and aldosterone

  
• Phaeochromocytoma


  Adrenal medulla tumour causing excess catecholamine (adrenaline & noradrenaline) secretion

  
• Conn's syndrome


  Primary: Small, aldosterone-secreting tumour of the zona glomerulosa

  Secondary: RAAS too active due to low renal blood flow