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46 Cards in this Set
- Front
- Back
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what are hormones made of?
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aminoacids or steriods & lipids.
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how do hormones move around without setting off a gamut of receptors?
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they don't circulate at high concentrations so that only tissues w/the most amount of receptor will appreciably respond; receptors are also controlled via expression; isolated systems; cell to cell diffusion; target cells can make chemicals that circulate & transform hormones into something even more attracted to them
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how are hormones carried through the body?
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in a free state or bound to protein
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how is thyroid hormone made?
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hypothalamus-> thyrotropin releasing hormone-> pituitary-> thyroid stimulating hormone-> thyroid-> T4, T3
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what does a normal pituitary do in response to a drop in thyroid hormone?
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increase secretion of thyroid stimulation hormone.
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what does a high TSH, w/low T4 signify?
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primary hypothyroidism.
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what does a high TSH, w/high T4 signify?
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secondary hyperthyroidism.
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what does a low TSH, w/high T4 signify?
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primary hyperthyroidism.
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what does a low TSH, w/low T4 signify?
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secondary hypothyroidism.
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what is a an IRMA sandwhich assay?
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jkljklk
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Name the 3 cortical layers of the adrenal gland.
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glomerulosa (aldosterone), fasciculata (cortisol/corticosterone), & reticularis (androgens)
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What happens when an enzyme pathway is defective for the synthesis of cortisol?
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ACTH increases-> adrenal gland becomes hyperplastic; the steriods in the pathway prior to the defect increase
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How is cortisol carried in the blood?
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bound to CBG or albumin; 10% is free
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how is cortisol released?
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CRH -> ACTH-> adrenal glands cortisol (androgen, aldosterone
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how can you assess adrenal cortical function?
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administer ACTH & then measure serum cortisol
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what inactivates cortisol to cortisone?
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many tissues reduce the 11-hydroxy group of cortisol
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how is aldosterone controlled?
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rising K+ levels can increase it; as well as the renin-angiotensin-aldosterone pathway; lung angio-tensin converting enzyme-> angiotensin II-> adrenals increased aldosterone synthesis
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what is in the adrenal medulla?
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postganglionic sympathetic neurons w/o axons; makes adrenaline & noradrenaline
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what happens w/a defective 21-hydroxylase?
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increased levels of 17-hydroxyprogesterone, 17-hydroxypregnenolone, & sex steriods
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What is primary adrenal insufficiency (aka Addison's disease)?
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adrenal cortical insufficiency that is do to to adrenal glands that don't make enough cortisol & aldosterone.
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What causes primary adrenal insufficiency?
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usually it's autoimmune, but can have other etiologies.
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How does primary adrenal insufficiency present?
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weight loss, muscle weakness, fatigue, hypotension, skin hyperpigmentation.
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How can you test for primary adrenal insufficiency?
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check for elevated ACTH & low aldosterone.
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What is secondary adrenal insufficiency?
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insufficiency is due to inadequate secretion of ACTH by pituitary.
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What causes secondary adrenal insufficiency?
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glucocorticoid tx, tumors/cysts, hemochromatosis, granulomas, POMC,...
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What labs do you use to test for secondary adrenal insufficiency?
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low ACTH
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When do you use a ACTH stimulation test?
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to distinguish b/w primary & secondary adrenal insufficiency. rise in cortisol suggests secondary adrenal insufficiency.
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When do you us a insulin-induced hypoglycemia test?
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only when you strongy suspect secondary adrenal insufficiency. their will be no response in these pts.
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What is metyrapone testing?
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meryrapone blocks 11beta-hydroxylase. this tests for integrity of the adrenal-pituitary axis. intact axis will increase ACTH & 11-deoxycortisol. any type of adrenal insufficiency will have low 11-deoxycortisol. ACTH is high in primary & low in secondary adrenal insufficiency.
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What is a 8am cortisol test?
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if plasma cortisol >15uL, then there's no adrenal insufficiency
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What is a paraganglioma?
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tumor in the sympathetic ganglia?
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How does pheochromocytoma present?
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palpitations, headache, & diaphoresis.
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What are the extra-adrenal locations for pheochromocytomas?
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sympathetic paraganglia, bladder, organ of Zuckerland.
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How do you screen for pheochromocytomas?
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24-hr urine for VMA & total metanephrines, measure free catecholamines; liquid chromatography.
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How do you localize a pheochromocytoma?
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T2-weighted MRI, CT, isotopic scan.
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What happens once a dx of phenochromocytoma is made?
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pt should be placed on alpha blockers until alpha blockade is achieved, then beta blockers until blockade, then surgery.
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What causes secondary hyperaldosteronism?
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messed up kidneys that make/don't make messed up renin. PRA levels are normal to elevated.
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What causes primary hyperaldosteronisn?
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messed up adrenal glands. PRA is suppressed. Conn's (adenoma)syndrome, bilateral cortical hyperplasia
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How do you tx Conn's syndrome?
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surgery.
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How do you tx bilateral cortical hyperplasia?
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spironolactone oe eplerenone.
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What is glucocorticoid-remediable hyperaldosteronism?
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translocation of ATCH promoter region that causes an increase in aldosterone synthesis (basically ATCH release=aldosterone release)
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How do you test for glucocorticoid-remediable hyperaldosteronism?
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use dexamethasone. if it helps the hypokalemia & hypertension, then you've clenched the case!
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What happens to aldosterone levels when people w/bilateral cortical hyperplasia sit upright?
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RAA axis responds normally w/an increase in aldosterone.
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What happens when people w/an aldosteronoma (Conn's)sit upright?
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aldosterone levels decrease due to renin suppression
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What are the 4 A's of aldosteronomas?
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1. atrociously high aldosterone
2. anomalous decline in postural aldosterone 3. awful hormone intermediates (18-hydroxycorticosterone) |
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What is the first test to exclude primary hyperaldosteronism.
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serum potassium level (4mEq/1 excludes).
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