Adrenal Flashcards
how long should adrenal nodules be followed radiographically
1-2 years
how often should adrenal nodules be followed biochemically
5 years
subclinical cushing’s is the most common cause of hormonally-active adrenal nodules
risk of adrenal mass becoming hormonally active durine 1,2,5 years
17%, 29%, 47%, respectively
what % of adrenal nodules are biochemically active
20%
cutoffs for 1mg dex suppression test
normal < 1.8
mild secretion 1.9 - 4.9
overt > 5.0
which adrenal nodule patients should be screened for hyperaldo
HTN, hypokalemia
why don’t we regularly screen for androgen/estrogen-producing adrenal nodules
very rare
imaging of choice for adrenal nodules
CT adrenal protocol
situations where MRI of adrenal nodules may be preferred
pregnancy
children
germline mutations
trying to limit radiation exposure
adrenal imaging to consider (besides CT/MRI)
FDG PET
MIBG (pheo/paraganglioma)
DOTATATE
what % of adrenal lesions < 4cm are ACC
2%
what % of adrenal lesions > 6cm are ACC
25%
precontrast HFU cutoff for non-malignant lesions
<10
indications for adrenal biopsy
hx of extraadrenal malignancy ONLY if it will change management
Infection
*MUST R/O PHEO FIRST
*biopsy cannot differentiate between cortical adenoma and ACC
most common causes of hyperaldosteronism
bilateral adrenal hyperplasia 60-65%
aldosterone-producing adenoma 30-40%
typical size of aldo-producing adenomas (APA)
< 2cm
only situation where AVS is not indicated for hyperaldosteronism
age < 35 with HTN/hypokalemia
AVS criteria for APA localization
ratio > 4:1 with cosyntropin
ratio > 2:1 without cosyntropin
perioperative management of pheo/paraganglioma
alpha blockade for 2 weeks
beta blockade if necessary
increase oral sodium/water intake
options for periperative alpha blockade for pheo/pgl
phenoxybenzamine 10mg BID
prazosin,doxazosin, terazosin
calcium channel blockers
titrate to low-normal blood pressure
which pheo/pgl patients need genetic screening for germline mutations?
ALL
what % of pheos are malignant
25%
postoperative monitoring of pheo/pgl patients
biochemical surveillance
25% of pheos are malignant
syndromes associated with pheo/pgl
VHL
neurofibromatosis
MEN 2A
typical recovery time of contralateral adrenal gland after adrenalectomy for cushing’s
6-18 months
what % of patients will have resolution of hypokalemia after adrenalectomy for APA
~100%
what % of patients will have significant improvement in BP after adrenalectomy for APA
~90%
what % of patients will be able to stop antihypertensive meds after adrenalectomy for APA
~30-60%
prevalence of nonclassical CAH in general population
1:1000
most common cause of cushing’s
exogenous steroids (iatrogenic)
cumulative effect of 40mg triamcinolone injection (Kenalog) is equivalent to how much hydrocortisone
1200mg
what to test for in cases of suspected exogenous glucocorticoid-associated cushings
urine synthetic glucocorticoid screen
HTN, hypokalemia, but low aldo and renin levels
check 11-DOC, cortisol
possible 11B CAH
newborn screen for CAH tests for which compound
17 OHP
drugs which can precipitate pheo crisis
D2 antagonists (metoclopromide (reglan), compazine) IV glucocorticoids glucagon MAOIs cosyntropin
IV contrast is OK’
half-life of serum cortisol
30-60 min
half life of serum cortisol
30-60 min
half-life of DHEA-S
~24 hours
DHEA-S value of what can rule out AI
> 100 mcg/dL
endocrinopathies associated with Carney complex
PPNAD (primary pigmented adrenal nodules)
Adrenal Cushings (paradoxical increase in cortisol after 1mg DST)
Acromegaly
most sensitive test for detecting cushings disease recurrence
late night salivary cortisol
most common cause of true cushing’s syndrome in pregnancy
adrenal adenomas
most common cause of true cushing’s in adults
pituitary
normal glucocorticoid physiology during pregnancy
increased cortisol binding globulin increased serum cortisol increased salivary cortisol increase urinary cortisol ACTH/CRH production by the placenta
diagnosis of cushing’s in pregnancy
UFC > 4x upper limit of normal
Salivary 3-4X upper limit of normal
1mg DST not used
Can use 8mg DST to determine source if hypercortisolism is present
treatment of cushing’s in pregnancy
surgery (2nd trimester)
metyrapone
Do NOT use mitotane.
Only use ketoconazole for emergencies (potentially teratogenic)
treatment of cushing’s in pregnancy
surgery (2nd trimester)
metyrapone
Do NOT use mitotane.
Only use ketoconazole for emergencies (potentially teratogenic)
best test to determine etiology of ACTH-dependent cushings (ie pituitary vs ectopic)
IPSS
% of DM pts with underlying Cushing’s
~2-3%
CBC findings in pheo/paraganglioma
elevated hgb/hct (volume contraction)
DHEA-S level that should prompt concern for adrenal tumor
> 700mcg/dL
differential diagnosis of hyperandrogenism and amenorrhea
hyperprolactinemia nonclassical CAH Cushings Hypothyroidism PCOS
causes of “pseudocushings”
obesity
depression
alcoholism
DHEA-S level in adrenal cushing’s
low
half-life of DHEA-S
16 hours
classic presentation of hyperaldosteronism
hypertension
hypokalemia
metabolic alkalosis
most common causes of primary hyperaldosteronism
bilateral adrenal hyperplasia (IHA)
aldosterone-producing adenoma
pathogenesis of glucocorticoid-remedial aldosteronism
genetic defect in which aldosterone is ACTH-dependent
who should be screened for hyperaldosteronism
pts with: HTN and spontaneous hypokalemia Hypokalemia on low-dose diuretic Refractory HTN on 3+ meds HTN and adrenal incidentaloma HTN with OSA HTN with +fam hx for hyperaldo HTN and afib
HTN, suppressed renin, aldo < 5
low renin HTN (think cushings, CAH, 11-DOC)
HTN, suppressed renin, aldo 5-15
equivocal; proceed to saline/salt suppresion
HTN, suppressed renin, aldo > 15, hypokalemia
confirmed hyperaldo; no salt/saline suppression needed
next step after biochemical confirmation of hyperaldosteronism
CT adrenals
which hyperaldo patients can proceed to surgery without AVS
confirmed biochemical hyperaldo, unilateral adrenal nodule >1cm, age < 35 years old. Everyone else gets AVS
medical treatment options for primary hyperaldosteronism
spironolactone
eplerenone (no gynecomastia)
+/0 amiloride
mechanism of action of amiloride
ENaC inhibitor in renal collecting system (slows Na influx and thus reduces activity of Na/K ATP-ase)
what to counsel hyperaldo patients regarding daily salt intake
low sodium diet. high sodium diet transports more sodium to renal collecting tubules, which increases plasma volume and worsens hypokalemia
hyperaldosteronism with large adrenal mass
adrenocortical carcinoma
size of most aldosterone-producing adenomas
< 2cm, hypodense
first step in interpretation of AVS
check adrenal vein:IVC cortisol ratio to determine proper catheter placement
AVS ratio that suggests unilateral adenoma
ratio of of the aldo/cortisol ratio > 4 (with cosyntropin)
reason for using aldo/cortisol ratios in AVS interpretation
it corrects for venous admixture in the L adrenal venous system from the phrenic vein
possible suppression tests for suspected hyperaldosteronism
oral salt loading
saline suppression
fludrocortisone suppression
captopril challenge
what to do if hypotension after unilateral adrenalectomy for hyperaldosteronism
fludrocortisone. contralateral adrenal usually kicks in within a day or two
what can aldosterone-producing adenomas co-secrete
cortisol. check DST
what can happen to GFR after starting spironolactone/eplerenone for hyperaldo
decrease in GFR (pts with hyperaldo are hyperfiltrating, which increases GFR)
treatment goals of mineralocorticoid receptor antagonist in primary hyperaldosteronism
normalize: blood pressure potassium renin **can increase spironolactone to whatever dose is necessary to achieve these goals
which is a more potent inhibitor of mineralocorticoid receptor, spironolactone or eplerenone
spironolactone
initial imaging test of choice for suspected pheo
abdominal CT
