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Endocrine Fellowship Board Review > Adrenal > Flashcards

Adrenal Flashcards

1
Q

how long should adrenal nodules be followed radiographically

A

1-2 years

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2
Q

how often should adrenal nodules be followed biochemically

A

5 years

subclinical cushing’s is the most common cause of hormonally-active adrenal nodules

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3
Q

risk of adrenal mass becoming hormonally active durine 1,2,5 years

A

17%, 29%, 47%, respectively

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4
Q

what % of adrenal nodules are biochemically active

A

20%

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5
Q

cutoffs for 1mg dex suppression test

A

normal < 1.8
mild secretion 1.9 - 4.9
overt > 5.0

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6
Q

which adrenal nodule patients should be screened for hyperaldo

A

HTN, hypokalemia

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7
Q

why don’t we regularly screen for androgen/estrogen-producing adrenal nodules

A

very rare

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8
Q

imaging of choice for adrenal nodules

A

CT adrenal protocol

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9
Q

situations where MRI of adrenal nodules may be preferred

A

pregnancy
children
germline mutations
trying to limit radiation exposure

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10
Q

adrenal imaging to consider (besides CT/MRI)

A

FDG PET
MIBG (pheo/paraganglioma)
DOTATATE

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11
Q

what % of adrenal lesions < 4cm are ACC

A

2%

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12
Q

what % of adrenal lesions > 6cm are ACC

A

25%

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13
Q

precontrast HFU cutoff for non-malignant lesions

A

<10

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14
Q

indications for adrenal biopsy

A

hx of extraadrenal malignancy ONLY if it will change management
Infection
*MUST R/O PHEO FIRST
*biopsy cannot differentiate between cortical adenoma and ACC

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15
Q

most common causes of hyperaldosteronism

A

bilateral adrenal hyperplasia 60-65%

aldosterone-producing adenoma 30-40%

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16
Q

typical size of aldo-producing adenomas (APA)

A

< 2cm

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17
Q

only situation where AVS is not indicated for hyperaldosteronism

A

age < 35 with HTN/hypokalemia

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18
Q

AVS criteria for APA localization

A

ratio > 4:1 with cosyntropin

ratio > 2:1 without cosyntropin

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19
Q

perioperative management of pheo/paraganglioma

A

alpha blockade for 2 weeks
beta blockade if necessary
increase oral sodium/water intake

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20
Q

options for periperative alpha blockade for pheo/pgl

A

phenoxybenzamine 10mg BID
prazosin,doxazosin, terazosin
calcium channel blockers
titrate to low-normal blood pressure

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21
Q

which pheo/pgl patients need genetic screening for germline mutations?

A

ALL

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22
Q

what % of pheos are malignant

A

25%

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23
Q

postoperative monitoring of pheo/pgl patients

A

biochemical surveillance

25% of pheos are malignant

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24
Q

syndromes associated with pheo/pgl

A

VHL
neurofibromatosis
MEN 2A

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25
Q

typical recovery time of contralateral adrenal gland after adrenalectomy for cushing’s

A

6-18 months

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26
Q

what % of patients will have resolution of hypokalemia after adrenalectomy for APA

A

~100%

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27
Q

what % of patients will have significant improvement in BP after adrenalectomy for APA

A

~90%

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28
Q

what % of patients will be able to stop antihypertensive meds after adrenalectomy for APA

A

~30-60%

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29
Q

prevalence of nonclassical CAH in general population

A

1:1000

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30
Q

most common cause of cushing’s

A

exogenous steroids (iatrogenic)

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31
Q

cumulative effect of 40mg triamcinolone injection (Kenalog) is equivalent to how much hydrocortisone

A

1200mg

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32
Q

what to test for in cases of suspected exogenous glucocorticoid-associated cushings

A

urine synthetic glucocorticoid screen

33
Q

HTN, hypokalemia, but low aldo and renin levels

A

check 11-DOC, cortisol

possible 11B CAH

34
Q

newborn screen for CAH tests for which compound

A

17 OHP

35
Q

drugs which can precipitate pheo crisis

A 
D2 antagonists (metoclopromide (reglan), compazine)
IV glucocorticoids
glucagon
MAOIs
cosyntropin

IV contrast is OK’

36
Q

half-life of serum cortisol

A

30-60 min

37
Q

half life of serum cortisol

A

30-60 min

38
Q

half-life of DHEA-S

A

~24 hours

39
Q

DHEA-S value of what can rule out AI

A

> 100 mcg/dL

40
Q

endocrinopathies associated with Carney complex

A

PPNAD (primary pigmented adrenal nodules)
Adrenal Cushings (paradoxical increase in cortisol after 1mg DST)
Acromegaly

41
Q

most sensitive test for detecting cushings disease recurrence

A

late night salivary cortisol

42
Q

most common cause of true cushing’s syndrome in pregnancy

A

adrenal adenomas

43
Q

most common cause of true cushing’s in adults

A

pituitary

44
Q

normal glucocorticoid physiology during pregnancy

A 
increased cortisol binding globulin
increased serum cortisol
increased salivary cortisol
increase urinary cortisol
ACTH/CRH production by the placenta
45
Q

diagnosis of cushing’s in pregnancy

A

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

46
Q

treatment of cushing’s in pregnancy

A

surgery (2nd trimester)
metyrapone

Do NOT use mitotane.
Only use ketoconazole for emergencies (potentially teratogenic)

47
Q

treatment of cushing’s in pregnancy

A

surgery (2nd trimester)
metyrapone

Do NOT use mitotane.
Only use ketoconazole for emergencies (potentially teratogenic)

48
Q

best test to determine etiology of ACTH-dependent cushings (ie pituitary vs ectopic)

A

IPSS

49
Q

% of DM pts with underlying Cushing’s

A

~2-3%

50
Q

CBC findings in pheo/paraganglioma

A

elevated hgb/hct (volume contraction)

51
Q

DHEA-S level that should prompt concern for adrenal tumor

A

> 700mcg/dL

52
Q

differential diagnosis of hyperandrogenism and amenorrhea

A 
hyperprolactinemia
nonclassical CAH
Cushings
Hypothyroidism
PCOS
53
Q

causes of “pseudocushings”

A

obesity
depression
alcoholism

54
Q

DHEA-S level in adrenal cushing’s

A

low

55
Q

half-life of DHEA-S

A

16 hours

56
Q

classic presentation of hyperaldosteronism

A

hypertension
hypokalemia
metabolic alkalosis

57
Q

most common causes of primary hyperaldosteronism

A

bilateral adrenal hyperplasia (IHA)

aldosterone-producing adenoma

58
Q

pathogenesis of glucocorticoid-remedial aldosteronism

A

genetic defect in which aldosterone is ACTH-dependent

59
Q

who should be screened for hyperaldosteronism

A 
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
60
Q

HTN, suppressed renin, aldo < 5

A

low renin HTN (think cushings, CAH, 11-DOC)

61
Q

HTN, suppressed renin, aldo 5-15

A

equivocal; proceed to saline/salt suppresion

62
Q

HTN, suppressed renin, aldo > 15, hypokalemia

A

confirmed hyperaldo; no salt/saline suppression needed

63
Q

next step after biochemical confirmation of hyperaldosteronism

A

CT adrenals

64
Q

which hyperaldo patients can proceed to surgery without AVS

A

confirmed biochemical hyperaldo, unilateral adrenal nodule >1cm, age < 35 years old. Everyone else gets AVS

65
Q

medical treatment options for primary hyperaldosteronism

A

spironolactone
eplerenone (no gynecomastia)
+/0 amiloride

66
Q

mechanism of action of amiloride

A

ENaC inhibitor in renal collecting system (slows Na influx and thus reduces activity of Na/K ATP-ase)

67
Q

what to counsel hyperaldo patients regarding daily salt intake

A

low sodium diet. high sodium diet transports more sodium to renal collecting tubules, which increases plasma volume and worsens hypokalemia

68
Q

hyperaldosteronism with large adrenal mass

A

adrenocortical carcinoma

69
Q

size of most aldosterone-producing adenomas

A

< 2cm, hypodense

70
Q

first step in interpretation of AVS

A

check adrenal vein:IVC cortisol ratio to determine proper catheter placement

71
Q

AVS ratio that suggests unilateral adenoma

A

ratio of of the aldo/cortisol ratio > 4 (with cosyntropin)

72
Q

reason for using aldo/cortisol ratios in AVS interpretation

A

it corrects for venous admixture in the L adrenal venous system from the phrenic vein

73
Q

possible suppression tests for suspected hyperaldosteronism

A

oral salt loading
saline suppression
fludrocortisone suppression
captopril challenge

74
Q

what to do if hypotension after unilateral adrenalectomy for hyperaldosteronism

A

fludrocortisone. contralateral adrenal usually kicks in within a day or two

75
Q

what can aldosterone-producing adenomas co-secrete

A

cortisol. check DST

76
Q

what can happen to GFR after starting spironolactone/eplerenone for hyperaldo

A

decrease in GFR (pts with hyperaldo are hyperfiltrating, which increases GFR)

77
Q

treatment goals of mineralocorticoid receptor antagonist in primary hyperaldosteronism

A 
normalize:
blood pressure
potassium
renin
**can increase spironolactone to whatever dose is necessary to achieve these goals
78
Q

which is a more potent inhibitor of mineralocorticoid receptor, spironolactone or eplerenone

A

spironolactone

79
Q

initial imaging test of choice for suspected pheo

A

abdominal CT

Endocrine Fellowship Board Review (11 decks)

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