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46 Cards in this Set

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