adrenal glands Flashcards
describe how the adrenal glands develop?
- urogenital ridge has the adrenogonadal primordium
- primordial germ cells invade the adrenogonadal primordium
- splits off into adrenal and gonadal primordium
- Adrenal part gets invaded with neural crest cells which develop into nervous tissue
- gets surrounded by capsule of mesenchymal cells
- Starts to differentiate the cortex in the embryo into the definitive and fetal zone
what are the 3 cortical zones of the adrenal glands? what do they each make?
- ZG – make aldosterone. Not a continuous layer
- ZF – makes glucocorticoids. Main one is cortisol
- ZR – makes adrenal androgens
where is the adrenal artery?
on the outside of the adrenal glands
what layer of the adrenals are closest to the blood vessels?
ZF
describe the passage of blood through the adrenal glands
- Delivers blood to the plexus of blood vessels under the capsule
- Blood flows through the capsule, ZG, ZF, ZR to the medulla
what kind of blood does the medulla receive?
blood with high levels of hormones
why does the adrenal gland have a lot of fat?
bc it makes cortisol which is fat
what are the types of stress?
starvation, infection and severe volume loss
what enzyme is found in the ZG and what gene is associated with this?
ZG is characterised by aldosterone synthase
CYP11B2 is the gene for the aldosterone synthase enzyme
what enzyme is found in the ZF?what gene is associated with this?
• ZF is characterised by CY11B1 (beta hydroxylase)
what is aldosterone release stimulated by?
potassium and low BP
what stimulates renin release?
sodium loss, haemorrhage, upright posture and decreased renal perfusion
describe how the RAA system works?
renin release is stimulated
• Increases AT1 AT2
• Angiotensin 2 causes vasoconstriction. Also increases aldosterone production
• AT2 binds to AT receptors on the ZG cells to increase aldosterone secretion
• Aldosterone causes vasoconstriction increased BP
• Affects kidney to increase total body fluid volume reduces K+
what effect do aldosterone and cortisol have on inflammation?
- Aldosterone = pro-inflammatory
* Cortisol = anti-inflammatory
what binds to the mineralcorticoid receptor? which binds more
aldosterone and cortisol
cortisol binds more
what stops only cortisol binding to the MCR?
cortisol –> cortisone by an enzyme called 11BHSD-2– stops cortisol binding to receptor instead of aldosterone
what are the 2 main cells involved in the renal effects of aldosterone?
o Principal cell (DCT) – needed in salt and water balance
o intercalated cell – acid-base balance
what is the effect of high aldosterone in principal cells?
- If aldosterone binds to the MCR, it activates all processes for reabsorbing Na+ and secreting K+
- Upregulates the sodium/potassium pump for energy and inserts more ENAC channels into the luminal membrane for Na+ absorption.
- For electroneutrality you have to secrete K+ and absorb Cl- along w the Na+
- High aldosterone = loss of K+ and Na+ reabsorption
what is the effect of aldosterone on the intercalated cell?
- Aldosterone upregulates;
- H+/K+ exchanger and a H+ ATPase –> loss of H+ ions fall in acid levels alkalotic state
- High BP Aldosterone = loss potassium = metabolic alkalosis
what happens in Conn’s syndrome?
o Hypertension
o Suppressed plasma renin activity
o Increased aldosterone secretion
what causes primary hyperaldosteronism?
- conn’s syndrome
- aldosterone producing adenoma
- bilateral adrenal hyperplasia
how do you diagnose hyperaldosteronism?
aldosterone:renin ratio saline suppression test CT adrenal adrenal venous sampling metomidate PET
what are symptoms of syndrome of apparent mineralocorticoid excess and what causes it?
• Glycorisic acid inhibits 11BHSD-2 – increases cortisol levels in contact with the MCR low K+, metabolic alkalosis and high BP from liquorice toxicity
what happens in Liddle syndrome?
- Import more ENAC channels into the luminal membrane of the collecting duct increased Na+ absorption
- Leads to: hypertension, hypokalaemia and metabolic alkalosis
