The adrenal gland Flashcards
Vasculature of adrenal glands, veins and arteries
Right adrenal gland drains into IVC. Left drains into renal vein. Both have many arteries but only one vein.
Adrenal medulla
Chromaffin cells secrete catecholamines - eg adrenaline, epinenphrine
Adrenal cortex
Secretes corticostreroids - eg aldosterone, cortisol , little bit of sex steroids
Layers of adrenal cortex outer to inner
Zona glomerulosa
Zona fasciculata
Zona reticularis
what are steroids
molecules coming from cholesterol
Aldosterone pathway
Cholesterol -
(3hydroxysteroid dehydrogenase) progesterone - (21hydroxylase) 11-deoxycorticosterone - (11) corticosterone - (18) aldosterone
Cortisol pathway
Cholesterol - (3hydroxysteroid dehydrodgenase) progesterone - (17hydroxylase) 17 - OH progesterone - (21) 11-deoxycortisol - (11) cortisol
Aldosterone method of action
To maintain blood pressure
Stiumlates Na+ reabsorption in distal convoluted tubule and cortical collecting duct in kidney (and sweat glands, gastric glands, colon)
Stimulates K+ and H+ secretion in distal convoluted tubule and cortical collecting duct.
Regulation of aldesterone
Juxtaglomerular apparatus detects low blood pressure, make renin (usually inhibited by high BP).
Renin converts angiotensinogen to angiotensin 1 converted by angiotensin converting enzyme ACE to angiotensin 2
Causes vasoconstriction but most importantly stimulates aldesterone production from Zona glomerulosa of adrenal cortex.
Physiological effects of cortisol
peripheral protein catabolism hepatic gluconeogenesis increased blood glucose concentration fat metabolism enhanced effect of glucagon and catecholamines increase BP
Addisons’s disease - Primary adrenal failure. Summary is
Autoimmune destruction of adrenal cortex. Tuberculosis organisms eats it.
Cortisol and aldesterone deficiency, salt loss, low BP eventual death
Addison’s disease symptoms
Darkening of skin - hyperpigmentation Severe fatigue Unintentional weight loss Low BP Vomiting Diarrhoea
Why do addison’s patients have hyperpigmentation?
POMC, pro-opio-melanocortin is a large precursor protein which is cleaved to form ACTH and MSH and endorphins.
Adrenal failure, no cortisol leads to no inhibition of ACTH production, more produced, more MSH as a byproduct.
Treatment of Addison’s disease
Rehydrate with normal saline
Dextrose to prevent hypoglycemia
Cushing’s syndrome symptoms
Lose protein in muscles, weak - myopathy thin skin centripetal obesity Mental changes - depression High blood pressure Diabetes Osteoporosis Stretch marks.
Cushing’s syndrome causes
too much cortisol Taking steroids orally pituitary dependent cuhsing's disease ectopic ACTH (lung cancer) adrenal adenoma or carcinoma
Precursor for Adrenaline and Noradrenaline synthesis
Tyrosine
Storage of catecholamines, binding of Adrenaline and Noradrenaline in blood
stored in cytoplasmic granules and released in response to ACh from preganglionic sympathetic neurones. Adrenaline and Noradrenaline bind to albumin
Degradation of adrenaline and noradrenaline
monoamine oxidase and catechol-O-methyl transferase
Static blood tests
test in morning - many hormones secreted according to circadian rhythm
only a snapshot hormone release is pulsatile, may have just missed a pulse.
Dynamic blood tests
suppression test - too much hormone
stimulation test - too little hormone
Troubleshooting test results
Have conditions changed?
Look at pre-test probability
Logistics of test - wrong patient?
Repeat test