43. The Adrenal Gland Flashcards
What are the 3 types of hormone? Give an example for each.
What are the 3 receptor locations?
What 3 things can happen when an endocrine cell is stimulated?
Describe the divisions of the adrenal gland from out to in.
Peptide (insulin), amine (thyroxine), steroid (cortisol)
Cell surface, nucleus, cytoplasm
Increased hormone production, release of stored hormone, cell multiplication (e.g. organ/gland becomes larger)
Capsule, cortex (zona glomerulosa, zona fasciculata, zona reticularis), medulla
Describe the adrenal blood supply.
Adrenal glands help the body deal with stress - what are the 3 kinds of stress?
How do you produce multiple different hormones from the same organ? (Adrenal gland).
Enters through capsule, flows towards medulla. Medulla exposed to cortex hormones (which have effects e.g. steroid hormones upreg enzymes that lead to adrenaline prod in medulla). Every cell in adrenal gland no more than 1-2 cells away from blood supply.
Starvation, infection, severe volume loss
AG turns cholesterol into lots of different things - needs lots of enzymes and cofactors, diff ones expressed in diff areas of AG e.g. aldosterone in ZG only
What stimulates aldosterone release?
Why are there usually low aldosterone levels?
Cortisol and aldosterone both bind to the mineralocorticoid receptor, however there is more cortisol than aldosterone. How is excessive cortisol prevented from binding to the receptor?
What are the renal effects of aldosterone?
K and low BP. Also hemorrhage, Na+ loss, upright posture, decreased renal perfusion. (Hyperaldosteronism = high BP and low blood K)
Inhibited by Na excess
Converted to cortisone, which cant bind receptor.
Affects both principal (deals with Na) and intercalated (deals with H+) cells. Binds to receptors and upregulates processes: absorbs Na and secretes K -> thus causes low K
What 3 things could cause primary hyperaldosteronism?
How would it be diagnosed?
What is glucocorticoid remediable aldosteronism?
1) Conn’s syndrome: hypertension, supressed plasma renin activity, increased aldosterone secretion
2) Aldosterone producing adenoma
3) Bilateral adrenal hyperplasia
Aldosterone:renin (e.g. renin low b/c aldosterone high). Saline supression test. CT adrenal. Adrenal venous sampling.
Autosomal dominant disorder, increase in aldosterone secretion produced by ACTH no longer transient, a cause of primary hyperaldosteronism
How does liquorice affect aldosterone?
What is Liddle syndrome?
Syndrome of apparent mineralocorticoid excess: it inhibits cortisol -> cortisone so activates mineralocorticoid receptor -> hyperaldosteronism (hypertension, low K etc.)
ENaC are usually upregulated by aldosterone but in LS they’re upreg without aldosterone production, so looks like Conn’s syndrome (but only diff = low aldosterone levels)
Describe the production and regulation of glucocorticoids e.g. cortisol.
Describe the circadian rhythm of ACTH and cortisol secretion.
What is the glucocorticoid (cortisol) response to the following stresses:
a) starvation
b) infection
c) hypotension
[Pic - red = downreg, green = upreg]. Also downreg by steroids.
ACTH and cortisol highest before you wake and lowest when you go to bed.
a) tissue breakdown for fuel (e.g. muscle, fat, bone, protein)
b) immunosuppression
c) increase BP
What is Cushing’s syndrome? What are the causes?
How is it diagosed?
How is it treated?
Increased secretion of ACTH from the anterior pituitary -> excess cortisol. Causes: iatrogenic (e.g. excess steroid meds), corticotroph pituitary adenoma, ectopic ACTH secreting neuroendocrine tumour, cortisol secreting adrenal adenoma etc.
Overnight dexamethasone suppression test, 24hr urine free cortisol (measure when supposed to be high e.g. night). Imaging: MRI pituitary, CT adrenals etc.
If pituitary: transsphenoidal surgery, radiotherapy, gamma knife
If adrenal: adrenalectomy, ketoconazole/etomidate
What is Addison’s disease? What are the 2 main causes? And symptoms?
How is it diagnosed?
How is it treated?
Adrenal glands don’t produce enough steroid hormones. Main causes: autoimmune, TB. Symptoms: low BP, low glucose, low Na, high K. Hyperpigmentation, fatigue, weight loss. Opposite of Conn’s.
Low 9am cortisol (should be high), high ACTH, short aynacthen test
Replacement steroid (glucocorticoid = hydrocortisone, mineralocorticoid = fludrocortisone). Addisonian crisis = IV fluid resus, IM hydrocortisone.
What amino acid do amine hormones start from? What do they become?
Where are chromaffin cells found?
Describe alpha 1 and 2, and beta 1 and 2 adrenoceptors.
What are the symptoms of catecholamine excess?
Tyrosine -> L-DOPA -> DA -> NA -> adrenaline
Adrenal medulla, pre-aortic sympathetic chian, wall of urinary bladder etc. They secrete amine hormones IRT nervous stimulation.
A1: vasocontriction A2: presynaptic inhibitory B1: renin release and tachycardia B2: vaasodilation/lung bronchodilation (opposite to A1)
Hypertension, dyspnea, headache, palpitation, tremor, fatigue, weight loss etc.
What is a pheochromocytoma?
How is it diagnosed?
How is it treated?
What would happen if you treated a pt with pheochromocytoma with beta blockers alone?
Rare tumor of adrenal gland tissue, results in release of excess adrenaline and NA.
24hr urine metanephrines, plasma metanephrines, CT/MRI adrenals and abdomen, I123I-MIBG scintigraphy
Surgical resection pre-op alpha and beta blockers, if acute crisis = IV phentolamine, avoid opiates
Vasocontriction unbalanced by vasodilation so BP increase -> poss cause stroke
