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Z.Fiser > Fiser.21.Adrenal > Flashcards

Fiser.21.Adrenal Flashcards

1
Q

What is the vascular supply to the superior adrenal gland?

A

inferior phrenic artery

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2
Q

What is the vascular supply to the middle adrenal gland?

A

aorta

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3
Q

What is the vascular supply to the inferior adrenal gland?

A

renal artery

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4
Q

where does the left adrenal vein drain to?

A

left renal vein

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5
Q

where does the right adrenal vein drain to?

A

IVC

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6
Q

what are the two parts of the adrenal gland?

A

adrenal cortex and the adrenal medulla

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7
Q

what is the innervation of the adrenal cortex?

A

no innervation to the cortex

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8
Q

what is the innervation of the adrenal medulla?

A

innervated by the sympathetic splanchnic nerves

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9
Q

where do the lymphatics from the adrenals drain to?

A

subdiaphragmatic and renal LNs

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10
Q

describe the anatomy surrounding the anterior approach for left adrenalectomy

A

note the position of the phrenic vein in relationship to the left adrenal vein and tumor

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11
Q

describe the anatomy surrounding the anterior approach for right adrenalectomy

A

.

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12
Q

what is the HPA axis for cortisol?

A

CRH released by hypothalamus –> ACTH by apit –> cortisol by adrenal gland –> negative feedback

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13
Q

what percent of CT scans show an incidental adrenal mass?

A

1-2%

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14
Q

what percentage of adrenal incidentalomas are mets?

A

5%

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15
Q

what is the MCC of asymptomatic adrenal masses?

A

benign adenomas

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16
Q

what is the workup to r/o a functional adrenal mass?

A

urine metanephrines / VMA / catecholamines; urinary hydroxycorticosteroids, serum K with plasma renin and aldosterone levels

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17
Q

what is the workup to find a primary tumor if adrenal mets are suspected?

A

CXR, colonoscopy, and mammogram

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18
Q

what are four indications for adrenal mass resection?

A

ominous characteristics (non-homogenous); >4-6cm; functioning; or enlarging

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19
Q

how frequently do you need to image an incidentaloma to follow it as an outpatient?

A

repeat imaging every 3 months x 1 year; then yearly thereafter

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20
Q

what is the MCC of cancer mets to the adrenal? (top 4)

A

1 = lung CA, then breast CA, melanoma, renal CA

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21
Q

what is the workup for an asymptomatic adrenal mass in a patient with cancer history?

A

needs biopsy

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22
Q

how do you treat isolated mets to the adrenal gland?

A

adrenalectomy

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23
Q

what is the embryologic origin of the adrenal cortex?

A

mesoderm

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24
Q

what are the three layers of the adrenal cortex and what do they produce?

A

GFR = salt, sugar, sex; glomerulosa = aldosterone; fasciculata = glucocorticoids; reticularis = androgens / estrogens

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25
Q

what is the progression from cholesterol to the end products of the adrenal gland?

A

cholesterol –> progesterone –> androgens / cortisol / aldosterone

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26
Q

what two enzymes are present in all three zones of the adrenal cortex?

A

21-beta-hydroxylase and 11-beta-hydroxylase

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27
Q

where is corticotropin releasing hormone released from?

A

hypothalamus

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28
Q

after CRH is released by the hypothalamus, where does it go?

A

anterior pituitary gland

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29
Q

what hormone is released by the anterior pituitary gland to act on the adrenal cortex and what does it do?

A

anterior pituitary gland releases ACTH, which stimulates the adrenal cortex to release cortisol

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30
Q

when does cortisol have its diurnal peak?

A

at 4-6am

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31
Q

what are the 3 cardiovascular effects of cortisol?

A

inotropic, chronotropic, increases vascular resistance

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32
Q

what are the two metabolic effects of cortisol?

A

proteolysis and gluconeogenesis

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33
Q

what are the inflammatory effects of cortisol?

A

decreases inflammation

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34
Q

what are the effects of aldosterone in the kidney?

A

stimulates renal sodium resorption and secretion of potassium and hydrogen ion

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35
Q

name three stimuli for aldosterone secretion

A

angiotensin II, hyperkalemia, ACTH

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36
Q

what should you suspect with excess estrogen and androgen secretion by adrenals?

A

almost always cancer

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37
Q

what is the underlying pathophysiology of congenital adrenal hyperplasia?

A

enzyme defect in cortisol synthesis

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38
Q

what is the MC subtype of congenital adrenal hyperplasia and how often is it seen?

A

21-hydroxylase deficiency is the most common and seen in 90% of cases of CAH

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39
Q

what are the sx a/w 21-hydroxylase deficiency

A

precocious puberty in males and virilization in females

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40
Q

what is the underlying pathophysiology / chemical reaction causing sx with 21-hydroxylase deficiency

A

increased 17-OH-progesterone leads to increased production of testosterone

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41
Q

is 21-hydroxylase deficiency salt wasting or salt saving?

A

salt wasting causing reduced sodium, increased potasssium, and hypotension

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42
Q

how do you treat 21-hydroxylase deficiency?

A

cortisol and genitoplasty

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43
Q

what are the sx a/w 11-hydroxylase deficiency?

A

precocious puberty in males or virilization in females

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44
Q

what chemical builds up in 11-hydroxylase deficiency?

A

increased 11 deoxycortisone

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45
Q

is 11-hydroxylase deficiency salt saving or salt wasting?

A

salt saving because deoxycortisone acts as a mineralocorticoid and causes hypertension

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46
Q

how do you treat 11-hydroxylase deficiency?

A

cortisol, genitoplasty

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47
Q

what hormone is built up in Conn’s syndrome?

A

aldosterone, (Conn’s syndrome = hyperaldosteronism)

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48
Q

what are the sx a/w Conn’s syndrome?

A

HTN 2/2 sodium retention without edema, hypokalemia, weakness, polydypsia, polyuria

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49
Q

what is the renin level associated with primary hyperaldosteronism?

A

renin level is low

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50
Q

what are the causes (and frequencies) of primary hyperaldosteronism?

A

adenoma (85%); adrenal hyperplasia (15%), ovarian tumors (rare); cancer (rare)

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51
Q

what is the renin level associated with secondary hyperaldosteronism?

A

renin level is high

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52
Q

which is more common: primary or secondary hyperaldosteronism?

A

secondary is more common

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53
Q

what are the 5 causes of secondary hyperaldosteronism?

A

renal artery stenosis, CHF, liver dz, diuretics, Bartter’s syndrome (renin-secreting tumor)

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54
Q

how do you diagnose primary hyperaldosteronism?

A

salt load suppression test –> best test, aldosterone will stay high; aldosterone:renin ratio > 20; plasma renin activity will be low

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55
Q

what are the BMP, UA, and ABG findings a/w primary hyperaldosteronism?

A

low serum potassium, high serum sodium, high urine K, metabolic alkalosis

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56
Q

why would you use NP-59 scintigraphy to localize source of primary hyperaldosteronism?

A

shows hyperfunctioning adrenal tissue, differentiates adenoma from hyperplasia, 90% accurate

57
Q

what two other localizing studies are available for primary hyperaldosternism besides the NP-59 scintigraphy?

A

MRI or adrenal vein sampling

58
Q

what two preoperative issues need to be controlled in primary hyperaldosteronism?

A

control HTN, K replacement

59
Q

how do you treat an adenoma causing primary hyperaldosteronism?

A

adrenalectomy

60
Q

how do you treat primary hyperaldosteronism 2/2 adrenal hyperplasia

A

seldom cured, medical therapy with spironolactone (inhibits aldosterone), CCBs, and potassium

61
Q

what are the adverse effects a/w bilateral resection with primary hyperaldosteronism 2/2 adrenal hyperplasia

A

increased morbidity with bilateral adrenalectomy

62
Q

why would bilateral adrenalectomy be indicated with primary hyperaldosteronism 2/2 adrenal hyperplasia?

A

refractory hypokalemia

63
Q

what medication will patients need postop s/p bilateral adrenalectomy for treatment of primary hyperaldosteronism 2/2 adrenal hyperplasia?

A

fludrocortisone

64
Q

What is the abnormality a/w Addison’s disease?

A

hypocortisolism / adrenal insufficiency

65
Q

what is the MCC of Addison’s disease?

A

withdrawal of exogenous steroids

66
Q

what is the MCC of primary Addison’s disease as well as five other causes?

A

1 cause = autoimmune disease; other causes include pituitary disease, adrenal infection, adrenal hemorrhage, adrenal mets, adrenal resection

67
Q

what are the effects of Addison’s disease on cortisol, ACTH, and aldosterone levels?

A

low cortisol, high ACTH, low aldosterone

68
Q

how do you diagnose Addison’s disease?

A

cosyntropin test: adminsiter ACTH, measure urine cortisol. Urine cortisol will remain low with hypocortisolism

69
Q

name five symptoms and two BMP findings a/w acute adrenal insufficiency?

A

hypotension; fever; lethargy; N/V; hypoglycemia; hyperkalemia

70
Q

how do you treat acute adrenal insuficiency?

A

dexamethasone, fluids, and administer cosyntropin test

71
Q

does dexamethasone interfere with the cosyntropin test?

A

nope

72
Q

name four sx and 2 BMP findings a/w chronic adrenal insufficiency

A

hyperpigmentation, weakness, weight loss, GI symptoms, hyperkalemia, hyponatremia

73
Q

how do you treat chronic adrenal insufficiency?

A

corticosteroids

74
Q

what is the hormonal disturbance seen with Cushing’s syndrome?

A

hypercortisolism

75
Q

what is the MCC of Cushing’s syndrome?

A

most commonly iatrogenic

76
Q

what is the first diagnostic test you perform when evaluating for Cushing’s syndrome?

A

24 hour urine cortisol and ACTH

77
Q

How do you interpret a patient being evaluated for Cushing’s syndrome with 24 hour urine with low ACTH and elevated cortisol?

A

patient has a cortisol-secreting lesion (adrenal adenoma or adrenal hyperplasia)

78
Q

How do you interpret a patient being evaluated for Cushing’s syndrome with 24 hour urine with elevated ACTH and elevated cortisol? What is the next step in dx?

A

pt has a pituitary adenoma or an ectopic source of ACTH. Next step is to perform a high-dose dexamethasone suppression test.

79
Q

what cancer can be an ectopic source of ACTH?

A

small cell lung CA

80
Q

How do you interpret a patient with Cushing’s syndrome with suppressed urine cortisol after the high-dose dexamethasone suppression test?

A

pituitary adenoma

81
Q

How do you interpret a patient with Cushing’s syndrome with elevated/unchanged urine cortisol after the high-dose dexamethasone suppression test?

A

ectopic producer of ACTH

82
Q

why is NP-59 scintigraphy useful in Cushing’s syndrome?

A

can localize tumors and differentiate adrenal adenomas from hyperplasia

83
Q

What is Cushing’s disease?

A

pituitary adenoma

84
Q

what is the #1 cause of non-iatrogenic Cushing’s disease and with what frequency?

A

80% of non-iatrogenic cases of Cushing’s syndrome 2/2 Cushing’s disease (pituitary adenoma)

85
Q

what are the findings in Cushing’s disease with low- and high-dose dexamethasone suppression test?

A

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

86
Q

is Cushing’s disease usually 2/2 macroadenomas or microadenomas?

A

microadenomas

87
Q

what are two diagnostic maneuvers to figure out the laterality of Cushing’s disease?

A

petrosal venous sampling or MRI

88
Q

how do you treat Cushing’s disease?

A

most tumors removed with transsphenoidal approach; unresectable or residual tumor tx with XRT

89
Q

what is the #2 non-iatrogenic cause of Cushing’s disease?

A

ectopic ACTH

90
Q

what is the MCC of ectopic ACTH?

A

small cell lung CA

91
Q

what are the findings with the low and high-dose dexamethasone suppression test with ectopic ACTH?

A

cortisol is not suppressed with either low or high-dose dexamethasone suppression test

92
Q

what imaging can be used to help localize source of ectopic ACTH?

A

CT chest/abdomen

93
Q

what is the treatment for ectopic ACTH?

A

resection of primary tumor if possible; medical suppression for inoperable lesions

94
Q

what is the #3 cause of non-iatrogenic Cushing’s syndrome?

A

adrenal adenoma

95
Q

what are the ACTH findings with adrenal adenoma?

A

low ACTH with elevated cortisol, its unregulated steroid production

96
Q

what is the treatment for adrenal adenoma?

A

adrenalectomy

97
Q

what are the first and second-line treatments for adrenal hyperplasia?

A

metyrapone (blocks cortisol synthesis) and aminoglutethimide (inhibits steroid production); bilateral adrenalectomy if medical tx fails

98
Q

what are two indications for bilateral adrenalectomy in the setting of Cushing’s syndrome?

A

1) patients with ectopic ACTH from a tumor that is unresectable (would need to be a slow growing tumor-this is rare); or 2) ACTH from pituitary adenoma that cannot be found

99
Q

what medication do you need to provide after bilateral adrenalectomy for Cushing’s syndrome

A

steroids postop

100
Q

what age groups and sex are most likely to present with adrenocortical carcinoma?

A

bimodal distribution (before age 5 and in the 5th decade); more common in females

101
Q

what symptoms are seen in children with adrenocortical carcinoma?

A

90% show virilization - precocious puberty in boys, virilization in girls; abdominal pain; weight loss; weakness

102
Q

what symptoms are seen in adults with adrenocortical carcinoma?

A

rare cause of Cushing’s syndrome; feminization in men, masculinization in women; abdominal pain; weight loss; weakness

103
Q

what percentage of patients with adrenocortical carcinoma have advanced disease at the time of diagnosis?

A

80%

104
Q

what is the treatment for adrenocortical carcinoma?

A

radical adrenalectomy

105
Q

what is the role of debulking in treatment of adrenocortical carcinoma?

A

debulking helps symptoms and prolongs survival

106
Q

what is the role of mitotane in the treatment of adrenocortical carcinoma?

A

mitotane is an adrenal-lytic for residual, recurrent, or metastatic disease

107
Q

what is the 5-year survival rate for adrenocortical carcinoma?

A

20%

108
Q

what is the embryological origin of the adrenal medulla?

A

from ectoderm neural crest cells

109
Q

what are the five steps of catecholamine production starting with tyrosine

A

tyrosine –> dopa –> dopamine –> norepinephrine –> epinephrine

110
Q

what is the enzyme that catalyzes the rate limiting step in catecholamine production?

A

tyrosinehydroxylase catalyzes tyrosine –> dopa

111
Q

what is the enzyme that converts norepinephrine to epinephrine and where is it located?

A

PNMT (phenylethanolamine N-methyltransferase) located only in the adrenal medulla (exclusive producers of epinephrine)

112
Q

what is the only tumor that will produce epinephrine?

A

adrenal pheochromocytoma

113
Q

what is the function of monamine oxidase? (3)

A

breaks down catecholamines; converts norepinephrine to normetanephrine; epinephrine to metanephrine

114
Q

what is the byproduct of the 3 reactions catalyzed by monoamine oxidase?

A

vanillylmandelic acid (VMA)

115
Q

where are there extra-adrenal rests of neural crest tissue?

A

usually in the retroperitoneum, most notably in the organ of Zuckerkandl at the aortic bifurcation

116
Q

what is the cell type that makes up pheochromocytomas?

A

chromaffin cells, arise from sympathetic ganglia or ectopic neural crest cells

117
Q

how rare and fast-growing are pheochromocytomas?

A

rare and slow-growing

118
Q

what is the 10% rule of pheochromocytomas (5)

A

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

119
Q

name 5 disease syndromes a/w pheochromocytomas

A

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

120
Q

what side do pheos tend to present on?

A

right-sided predominance

121
Q

are extra-adrenal tumors more likely to be benign or malignant

A

more likely to be malignant

122
Q

what are the S/Sx a/w pheochromocytoma

A

episodic HTN; headache; diaphoresis; palpitations

123
Q

how do you dx pheochromocytoma?

A

urine metanephrines & VMA (VMA most sensitive); clonidine suppression test: tumor does not respond and keeps catecholamines elevated

124
Q

how do you image pheochromocytoma that is not seen on CT/MRI?

A

MIBG scan (norepinephrine analogue) can help identify location if having trouble finding tumor with CT/MRI

125
Q

why should you avoid venography in pheochromocytoma?

A

can cause hypertensive crisis

126
Q

what three meds need to be given preoperatively in patients with pheochromocytoma and in what order?

A

1) volume replacement; 2) alpha blocker first (phenoxybenzamine) to avoid hypertensive crisis; then 3) beta blocker if patient has tachycardia or arrhythmias

127
Q

why does the order of supplying antihypertensives to a patient with pheochromocytoma matter?

A

need to give alpha blocker before beta blocker because unopposed alpha stimulation can lead to stroke, hypertensive crisis, and heart failure

128
Q

how do you treat pheochromocytoma and what do you need to do before manipulating the tumor?

A

treat with adrenalectomy, ligate adrenal veins first to avoid spilling catecholamines

129
Q

what is the role of debulking in treating patients with pheochromocytoma?

A

debulking helps symptoms in patients with unresectabe disease

130
Q

what is the role of metyrosine in treating pheochromocytoma?

A

inhibits tyrosine hydroxylase causing reduced synthesis of catecholamines

131
Q

what three meds need to be ready at the time of surgery for pheochromocytoma?

A

sodium nitroprusside (Nipride); phenlyephrine (Neosynephrine); and antiarrhythmic agents (ex: amiodarone)

132
Q

what are 9 postop complications after adrenalectomy for pheochromocytoma?

A

persistent HTN, hypotension, hypoglycemia, bronchospasm, arrhythmias, intracerebral hemorrhage, CHF, MI

133
Q

name other sites of pheochromocytomas (4)

A

vertebral bodies, opposite adrenal gland, bladder, aortic bifurcation

134
Q

what is the most common site of extramedullary tissue with pheochromocytomas?

A

organ of Zuckerkandl (inferior aorta near bifurcation)

135
Q

name 8 causes of falsely elevated VMA

A

coffee, tea, fruits, vanilla, iodine contrast, labetalol, alpha blockers, beta blockers

136
Q

name two cancers caused by extra-medullary tissue

A

medullary cancer of the thyroid and extra-adrenal pheochromocytoma

137
Q

what is a ganglioneuroma (cell of origin) and where is it located?

A

rare, benign, asymptomatic neural crest tumor in the adrenal medulla or sympathetic chain

138
Q

how do you treat ganglioneuroma

A

resection

Z.Fiser (22 decks)

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