Adrenal - basic Flashcards
What are the layers of the adrenal gland capsule (outside to inside)
Zona glomerulosa
Zona fasciculata
Zona reticularis
Describe the nerve supply at the medulla of the adrenal gland
ACh acts on nicotinic receptors
What does the zona glomerulosa produce and why?
Mineralocorticoids (like aldosterone) because it lacks the 17-a-hydroxylase enzyme and so therefore can’t make glucocorticoids and adrenal steroids
What enzyme is missing from the zona glomerulosa
17-a-hydroxylase, so cannot make glucocorticoids or adrenal steroids
What does the zona fasciculata produce and why?
Glucocorticoids (cortisol) because it lacks the aldosterone synthase enzyme and so cannot make mineralocorticoids.
What enzyme is missing from the zona fasciculata/reticularis?
Aldosterone synthase, so cannot make mineralocorticoids
Which substance is ACTH derived from
pro-opiomelanocortin
Describe the regulation of the synthesis of cortisol
Corticotropin releasing hormone (CRH) is released from the hypothalamus, which causes corticotrophs in the ant. pituitary to release ACTH. ACTH stimulates the zona fasciculata to synthesise and release cortisol.
Cortisol then feeds back to the corticotrophs in the ant. pituitary to reduce the release of ACTH and on the hypothalamus to reduce the release of CRG
What type of receptor does ACTH act on in the synthesis of steroid hormones? What happens in the cell?
GPCR (MCR2, melanocortin 2 receptor), increasing adenylyl cyclase which leads to an increase in cAMP levels.
PKA is activated which activates cholesteryl ester hydroxylase (CEH) which liberates cholesterol from lipid droplets.
Cholesterol 20,22-hydroxylase (desmolase) is the first enzyme in the pathway and is also stimulated. This is the rate limiting step.
What enzyme catylses the rate limiting step of the production of steroid hormones in the adrenal gland?
Cholesterol 20,22-hydroxylase (desmolase); first enzyme in the pathway.
What are the metabolic effects of glucocorticoids?
Decrease in cell uptake and use of glucose
increased gluconeogenesis (leads to hyperglycaemia)
decreased protein synthesis
increased protein breakdown (muscle wasting)
decreased Ca2+ absorption in gut
increased Ca2+ secretion in the kidney
decreased activity of osteoblasts
increased activity of osteoclats (osteoporosis)
(hyperglycaemia, muscle wasting, Ca2+ removed, osteoporosis)
What are the anti-inflammatory effects of glucocorticoids?
Early phase: reduced redness, pain, heat + swelling
Late phase: reduced wound healing, repair + proliferation
Generally: decreased expression of COX2, cytokine production and complement in plasma, NO release, histamine and IgG production.
What are the effects of glucocorticoids on water and electrolytes?
Increased Na retention
increased K excretion
increased water retention
What type of receptor does cortisol have the highest affinity for? How is this managed?
Cortisol has a higher affinity for mineralocorticoid receptors than glucocorticoid receptor.
Therefore cortisol in converted into an inactive cortisone by 11-B-hydroxysteroid dehydrogenase (11 B-HSD)
What are some of the adverse effects of glucocorticoids
supression of response to infection supression of endogenous glucocorticoid production metabolic effects osteoporosis iatrogenic cushings syndrome
