Cortisol

Release

• release and synthesis stimulated by ACTH
• episodic release, 15-30 minutes after ACTH surge
• converted to metabolites, conjugated to glucuronides and excreted in urine

Actions

• permissive action rather than active
• stimulates protein degradation in preference to synthesis
  • excess of cortisol (Cushing's Syndrome) leads to excessive protein degradation, thinning of skin, atrophy of tissue
• stimulates gluconeogenesis in liver and reduced glucose uptake by other tissues
• stimulate lipolysis in extremities but laying down of fat in face and trunk
• required to maintain normal vascular integrity
• some antidiuretic action in kidney
• reduces inflammatory response
• modulates perception and emotion
• important in foetal maturation

Disorders

• deficiency of cortisol is Addison's Disease
  • either by lack of adrenal function or lack of ACTH stimulus
  • hypoglycemia through decreased gluconeogenesis and increased amino acid utilisation
  • insulin sensitivyt
  • weight loss
  • vasodilation/hypotension through effects on cappillary integrity and ECF volume
  • hypovolemia, hyponatremia, through increased sodium excretion
  • hyperkalemia through decreased potassium excretion
  • anemia
  • pigmentation
  • propensity toward autoimmune disease
• excess of cortisol is Cushing's Syndrome
  • redistibution of body fat to trunk and face
  • hyperglycemia through increased gluconeogenesis and decreased protein synthesis
  • insulin ressitance
  • decrease in protein structures if bone, skin, muscle
  • hyperlipemia through increased lipolysis
  • hypertension
  • hypervolemia and hypernatremia through increased sodium retention
  • decresead inflammatory response leading to increased susceptibility to infection
  • euphoria/depression
• acts in pituitary to inhibit ACTH secretion

14.4.2.1 Cortisol

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