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ABSITE 2022 > Chapter 21 - Adrenal > Flashcards

Chapter 21 - Adrenal Flashcards

1
Q

Arterial supply of the adrenal?

A

Superior adrenal (from inferior phrenic), middle adrenal (from aorta), inferior adrenal (from renal artery)

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2
Q

Venous drainage of adrenal?

A

Left adrenal to L. renal vein, R. adrenal to IVC

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3
Q

What % of CT scans show incidentaloma?

A

1-2%. Next steps: biochemical testing, determine if malignant characteristics, follow or cut out.

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4
Q

When is surgery indicated for incidentaloma?

A

Ominous characteristics (nonhomogenous, high signal intensity, w/o loss on opposed-phase imaging, >20 HU), >4-6cm, functioning, enlarging

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5
Q

How often do you need to follow an incidentaloma?

A

Q3 months for 1 year, then yearly

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6
Q

How do you work up an incidentaloma?

A

Even if benign looking, get workup. For aldosterone, check BP and serum K (if HTN or low K, get plasma renin and aldosterone). For pheo, check urine metanephrines/VMA/catecholamines. For cortisol secreting tumor, check urinary hydroxycorticosteroids. CXR, stool guiac and colonoscopy, mammogram.

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7
Q

What are common mets to the adrenal?

A

Lung CA (#1), breast, melanoma, renal

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8
Q

What do you do for a patient with cancer history and an asymptomatic adrenal mass?

A

Biopsy. Biopsy not indicated for much else.

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9
Q

Adrenal cortex layers and products?

A

GFR = salt, sugar, steroids; glomerulosa (aldosterone), fasciculata (glucocorticoids), reticularis (androgens/estrogen)

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10
Q

Adrenal medulla receives innervation from what?

A

Splanchnics

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11
Q

What causes the release of cortisol from the adrenal cortex?

A

CRH (hypothalamus) - ACTH (anterior pituitary) - release of cortisol

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12
Q

When does cortisol peak?

A

Diurnal, 4-6am

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13
Q

What are the effects of aldosterone?

A

Stimulates renal sodium resorption and secretion of K+, H+, and ammonia

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14
Q

What stimulates secretion of aldosterone?

A

Angiotensin II, hyperkalemia, ACTH

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15
Q

What 3 deficiencies cause congenital adrenal hyperplasia?

A

21-hydroxylase deficiency(90%), 11-hydroxylase deficiency, 17-hydroxylase deficiency

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16
Q

Characteristics of 21-hydroxylase deficiency?

A

Precocious puberty in males, virilization in females; inc. 17-OH progesterone leads to inc. production of testosterone; salt wasting causing hypotension

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17
Q

Treatment for congenital adrenal hyperplasia?

A

Cortisol, genitoplasty

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18
Q

Characteristics of 11-hydroxylase deficiency?

A

Precocious puberty in males, virilization in females; salt saving causing hypertension

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19
Q

Characteristics of 17-hydroxylase deficiency?

A

ambiguous genitalia in males at birth; salt saving

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20
Q

Symptoms of hyperaldosteronism (Conn’s syndrome)?

A

HTN w/o edema, hypokalmia. Weakness, polydipsia, polyuria.

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21
Q

Causes of primary hyperaldosteronism (low renin)?

A

Adenoma (80-90%), hyperplasia, ovarian tumor, cancer

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22
Q

Causes of secondary hyperaldosteronism (high renin)?

A

CHF, renal artery stenosis, liver failure, pregnancy, diuretics

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23
Q

How is the diagnosis of primary hyperaldosteronism made?

A

Urine aldosterone after salt load (will stay high; ie not suppressible); low serum K, high urine K, high serum Na, metabolic alkalosis; aldosterone:renin ratio >20. CT to determine location. If not definitive, get adrenal vein sample.

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24
Q

What is the NP-59 scintigraphy?

A

Shows hyper functioning adrenal tissue, differentiates adenoma from hyperplasia

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25
Q

Treatment for adenoma causing hyperaldosteronism?

A

Adrenalectomy

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26
Q

Treatment for hyperplasia causing hyperaldosteronism?

A

Medical tx 1st with spironalactone, ca-channel blocker, potassium

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27
Q

What is the #1 cause of hypocortisolism (Addison’s disease)?

A

Withdrawal of exogenous steroids

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28
Q

What is the #1 primary disease causing hypocortisolism?

A

Autoimmune disease

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29
Q

Hormone/electrolyte aberrations with hypocortisolism?

A

Low cortisol and aldosterone; low serum Na, high serum K.

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30
Q

Symptoms of acute adrenal insufficiency?

A

Hypotension, fever, lethargy, abdominal pian, low glucose, depressed mental status, nausea/vomiting, high K+.

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31
Q

Treatment of adrenal insufficiency?

A

Dexamethasone, fluids, ACTH stim test

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32
Q

Most common cause of hypercortisolism (Cushing’s syndrome)?

A

Iatrogenic

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33
Q

How is the diagnosis of hypercortisolism made?

A

1st: 24h urine cortisol (most sensitive).
2nd: low dose overnight dexamethason suppression test (test urine to see if the cortisol has been suppressed - if low, Cushing’s disease, if high, go to 3).
3rd: serum ACTH (if high, ectopic ACTH or pituitary tumor and go to 4, if low ACTH, pt has cortisol-secreting tumor).
4th: serum ACTH high - high dose overnight dexamethasone suppression test (positive = pituitary, negative = ectopic).
5th: CRH test - pituitary adenomas will increase ACTH, ectopic producers will have no change in ACTH; MRI useful, NP-59 to localize and differentiate from hyperplasia.

34
Q

1 noniatrogenic cause of Cushing’s syndrome?

A

Pituitary adenoma (70-80%)

35
Q

Test findings with pituitary adenoma?

A

Cortisol should be suppressed with either low- or high-dose dexamethasone suppression test

36
Q

Treatment of pituitary adenoma?

A

Transsphenoidal resection; unresectable or residual tumors treated with XRT. (Hypercortisolism w/ high ACTH suppressible w/ high dose)

37
Q

2 noniatrogenic cause of Cushing’s syndrome?

A

Ectopic ACTH - most commonly from small cell lung cancer

38
Q

Test findings with ectopic ACTH?

A

Hypercortisolism w/ elevated ACTH. Cortisol is NOT suppressed with either low-or high-dose dexamethasone suppression test.

39
Q

Treatment of ectopic ACTH secreting tumor?

A

Resection of primary if possible; medical suppression or bilateral adrenalectomy for inoperable lesions

40
Q

3 noniatrogenic cause of Cushing’s syndrome?

A

Adrenal adenoma

41
Q

Test findings with adrenal adenoma causing Cushing’s?

A

Low ACTH, unregulated steroid production; does not suppress

42
Q

Treatment for adrenal hyperplasia?

A

Bilateral adrenalectomy

43
Q

Medical therapy for ectopic ACTH production or adrenocortical cancer (ACC) with residual or metastatic disease after resection?

A

Ketoconazole/metyrapone (inhibit steroid fomation), aminoglutethimide (inhibits cholesterol conversion), Op-DDD (adrenal-lytic, used for metastatic disease)

44
Q

Postoperative care of bilateral adrenalectomies includes what?

A

Steroids

45
Q

Age distribution of adrenocortical carcinoma?

A

Bimodal (before age 5, in the 5th decade)

46
Q

% of adrenocortical carcinomas that are functional?

A

50% cortisol, aldosterone, sex steroids

47
Q

Symptoms seen in children with adrenocortical carcinoma?

A

90% with virilization (precocious puberty in boys, virilization in females)

48
Q

Symptoms of adrenocortical carcinoma?

A

Abdominal pain, weight loss, weakness

49
Q

Treatment of adrenocortical carcinoma?

A

Radical adrenalectomy; mitotane for residual or recurrent disease

50
Q

Survival rate of adrenocortical carcinoma?

A

20% 5-year survival

51
Q

What is the adrenal medulla derived from?

A

Ectoderm neural crest cells

52
Q

Steps of catecholamine production?

A

Tyrosine –> dopa –> dopamine –> norepinephrine –> epinephrine

53
Q

What is the rate-limiting step in catecholamine production?

A

Tyrosine hydroxylase (tyrosine to dopa)

54
Q

What enzyme converts norepi to epi (requires methylation)?

A

PNMT, found only in the adrenal medulla (only medulla tumors can secrete epinephrine)

55
Q

What is the only tumor that will produce epinephrine?

A

Adrenal pheochromocytomas (ectopic will not)

56
Q

What enzyme converts norepi to normetanephrine and epi to metanephrine?

A

Monoamine oxidase (MAO)

57
Q

Where is extra-adrenal neural crest tissue found?

A

In the retroperitoneum, organ of Zuckerkandl

58
Q

What do pheochromocytomas arise from?

A

Chromaffin cells; arise from sympathetic ganglia or ectopic neural crest cells

59
Q

What is the 10% rule with pheos?

A

10% malignant, bilateral, in children, familial, extra-adrenal

60
Q

What syndromes are pheos associated with?

A

MEN IIa, MEN IIb, von Recklinghausen’s disease, tuberous sclerosis, VHL, Sturge-Weber disease

61
Q

Which side has more pheos?

A

Right side

62
Q

Are extra-adrenal tumors more likely malignant or benign?

A

Malignant

63
Q

Symptoms of pheos?

A

HTN (episodic), headache, diaphoresis, palpitations

64
Q

How is the diagnosis of pheo made?

A

Urine mtanephrines and plasma VMA (VMA most sensitive), CT or MRI to localize, MIBG scan (norepi analogue) to localize if CT/MRI not definitive. FDG-PET only if suspicious for metastasis.

65
Q

Is venography used for pheos?

A

NO, can cause hypertensive crisis

66
Q

Preoperative treatment of pheos?

A

Volume replacement, alpha-blockers (phenoxybenzamine), then beta-blocker if pt has tachycardia or arrhythmias

67
Q

What causes hypertensive crisis with pheos?

A

Unopposed alpha stimulation; can be precipitated by beta blockers given before alpha blockers; can cause heart failure in patients with cardiomyopathy

68
Q

Treatment of pheo?

A

Resection, check for other tumors, ligate adrenal veins to avoid spilling catecholamines; debulking if unresectable; metyrosine (inhibits tyrosine hydroxylase)

69
Q

What are frequent post op conditions following pheo resection?

A

Persistent hypertension, hypotension, hypoglycemia, bronchospasm, arrhythmias, intracerebral hemorrhage, CHF, MI

70
Q

What are extra-adrenal sites of pheos?

A

Vertebral bodies, bladder, aortic bifurcation (organ of Zuckerkandl)

71
Q

Where is the organ of Zuckerkandl?

A

Inferior aorta near bifurcation

72
Q

What can falsely elevate VMA?

A

Coffee, tea, fruits, vanilla, iodine contrast, labetalol, alpha- and beta-blockers

73
Q

What are ganglioneuromas?

A

Rare, benign, asymptomatic tumor of neural crest origin in the adrenal medulla or sympathetic chain

74
Q

Indications for unilateral adrenalectomy?

A

Aldosteronoma, cortisol-secreting adenoma, unilateral pheo, virilizing or feminizing tumor, nonfunctioning tumor (>4-5cm, carcinoma, solitary unilateral mets)

75
Q

Indications for bilateral adrenalectomy?

A

Bilateral pheos, Cushing’s caused by bilateral nodular adrenal hyperplasia or ectopic ACTH-producing tumor unresponsive to primary therapy

76
Q

Biochemical diagnosis of pheo?

A

Plasma fractionated metanephrines and/or 24h urine catecholamines and metanephrines. Confirm one with the other.

77
Q

Biochemical diagnosis of aldosteronoma?

A

Plasma aldosterone concentration and plasma renin activity, then determine ratio; urinary aldosterone and potassium on high-salt diet.

78
Q

Biochemical diagnosis of Cushing’s disease from cortical adenoma?

A

24h urine free cortisol; overnight low-dose DMST; plasma ACTH

79
Q

Biochemical diagnosis of adrenal cortical carcinoma?

A

24h urine cortisol, plasma DHEA level

80
Q

Biochemical diagnosis of incidentaloma?

A

Low-dose DMST, plasma fractionated metanephrines/urine catecholamines; plasma aldosterone concentration and plasma renin activity if hypertensive or hypokalemic

ABSITE 2022 (50 decks)

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