Adrenal cortex: Hormones, physiology Flashcards
Glucocorticoids
- Synthesis
- Control of secretion
- Example
Synthesised by cells of the zona fascicularis
- 17a hydoxylase enzyme
- From cholesterol
Secretion stimulated by: - Stimulated by ACTH - Stress Inhibited by - Negative feedback
Example
- Cortisol
Mineralocorticoids
- Synthesis
- Control of secretion
- Example
Synthesised by cells of the glomerulosa
- 18-hydroxylase
- From cholesterol
Control of secretion
- RAAS control
Example
- Aldosterone
Adrenal androgens
- Synthesis
- Control of secretion
- Example
Synthesised by cells of the zone reticularis
- Using 17a-hydroxylase
- From cholesterol
Control of secretion
- regulated by ACTh release
Example
- Testosterone in very small amounts
Cortisol and ACTH diurnal variation
Cortisol levels peak after a delay, when there is an increase in ACTH initially
- Due to slow action of hormones
Cortisol and ACTH peak in the early morning.
Cortisol nadir is 2 hrs later than ACTH in the night.
- Negative feedback
Cortisol and stress
Stress from injury, trauma, psychological, hypoglycaemia, illness triggers CRH and ACTH release rapidly.
- High ACTH levels amplifies effects of cortisol.
Transport of corticosteroids [3]
Not water soluble—> Only 10% free.
75%—> Corticosteroid binding globulin/ transcortin.
15%—-> Bound to albumin
Transport of corticosteroids in pregnancy
CBG levels increase
- Causes increase in plasma cortisol
- Free cortisol level still stable.
Metabolism of steroid hormones
In the liver
- Glucuronidation to make water soluble
- Excreted in via kidney in urine.
Action of cortisol at normal levels
Inhibits insulin’s action of cellular glucose intake.
Promotes glycogenolysis.
Promotes hepatic gluconeogenesis by increasing amino acid uptake.
Lipolysis and fatty acid mobilisation.
- Potentiates GH and catecholamines.
Causes elation/ sedation.
Vasoconstriction
Action of XS cortisol levels
Fatty acid synthesis and deposition at
- Face
- Trunk
- Intrascapular region
Inhibits the uptake of amino acids in the periphery
- Inhibits skeletal muscle protein synthesis.
11-beta hydroxysteroid dehydrogenase
Enzyme that converts cortisol into cortisone.
- Does so in aldosterone sensitive tissue as cortisol can bind to mineralocorticoid receptors.
Immunological effects of corticosteroids.
Overall—> Suppresses the immune system.
- Allows function, despite injury/illness.
- Suppresses lymphoid tissue—> Reduced production of antibodies.
- Inhibits cellular function of immunological cells.
- Inhibits proteolytic enzymes that act as inflammatory mediators
- Inhibits phospholipase-A2—> inhibits prostaglandins formation.
Corticosteroids effects on injury/ Stress
Removes inflammation of injury, but does not help to redeem the underlying cause of injury.
- Inhibits tissue repair
Reduces inflammation reduces oedema
- Allows mobilisation of limbs
Sedation stimulated
- Relieves pain= more mobilisation of limbs.
Addison’s crisis
Hypoadrenalism
- Very low cortisol levels
Can occur when long-term treatment of corticosteroids is stopped abruptly.
- Cortex stops producing hormones.
- Fatal within 48 hrs.
Mineralocorticoid pharmacological uses
- Example
Replacement therapy
- e.g fludrocortisol
- Hypoaldosteronism treatment.
- Addison’s disease treatment
Aldosterone not used as it has a short plasma-half life.
NOT used as an immunosuppressant, does not have major immunological effects.
