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Endocrine > 379 Adrenal > Flashcards

379 Adrenal Flashcards

1
Q

three classes of corticosteroid hormones produced by the adrenal cortex

A

glucocorticoids, mineralocorticoids and adrenal androgen precursors

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2
Q

usual cause of hormone excess

A

neoplasia

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3
Q

weight of adrenal glands

A

6-11 g each

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4
Q

location of the adrenal glands

A

above the kidneys and have their own blood supply

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5
Q

embryonic origin of the adrenals

A

originate from the urogenital ridge and separate from the gonads and kidneys at the sixth week of gestation

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6
Q

play a crucial role in the development of the adrenal and regulate a multitude of adrenal genes involved in steroidogenesis

A

SF1 steroidogenic factor 1 and DAX1 dosage sensitive sex reversal gene 1

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7
Q

control the production of glucocorticoids and adrenal androgens

A

Hypothalamic-pituitary adrenal axis

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8
Q

regulates the mineralocorticoids

A

renin angiotensin aldosterone system

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9
Q

acts as the pivotal regular of the adrenal cortisol synthesis with additional short term effects on mineralocorticoid and adrenal androgen synthesis

A

ACTH

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10
Q

controls the pulsatile release of CRH and ACTH according to circadian rhythm

A

suprachiasmic nucleus of the hypothalamus

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11
Q

if cortisol production is driven by an ACTH producing pituitary adenoma, what is the effect of dexamethasone suppression tests

A

dexamethasone is ineffective at low doses but usually induced suppression at higher doses

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12
Q

if cortisol production is driven by an ectopic source, what is result of the dexamethasone suppression test

A

tumors are usually resistant to dexamethasone suppression

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13
Q

how to assess glucocorticoid deficiency

A

ACTH stimulation tests

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14
Q

how is the standard ACTH stimulation test done

A

0.25 mg IM or IV of cosyntropin is given and serum cortisol collection is done 0, 30 and 60 mins;

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15
Q

normal ACTH stimulation test result

A

cortisol more than 20 ug or more than 550 nmmol/L 30-60 min after cosyntropin stimulation

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16
Q

alternate test to check adrenal function

A

insulin tolerance test

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17
Q

how is the insulin tolerance test done

A

0.1 U/Kg IV regular insulin and then 0, 30, 60, 120 mins blood tests for glucose, cortisol, GH

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18
Q

normal response of the Insulin tolerance test

A

normal response is cortisol more than 20 ug/dL or GH more than 5.1 ug/L

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19
Q

side effect of insulin tolerance test

A

symptomatic hypoglycemia serum glucose of less than 40 mg/dL may be managed with oral or IV glucose

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20
Q

contraindication to insulin tolerance tests

A

coronary disease, cerebrovascular disease, seizure disorder

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21
Q

commonly accepted first line test to assess glucocorticoid deficiency

A

cosyntropin test

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22
Q

initiates the release of mineralocorticoids

A

renin from the juxtaglomerular cells in the kidney

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23
Q

hormone the enhances sodium retention and potassium excretion, increases arterial perfusion pressure, regulates renin release

A

aldosterone

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24
Q

True or false. HPA damage does not significantly impact the capacity of the adrenal to synthesize aldosterone

A

True.

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25
Q

Required for the initiation of steroidogenesis

A

ACTH stimulation

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26
Q

True or false. Adrenal steroidogenesis occurs in a zone specific fashion

A

True.

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27
Q

Zone of mineralocorticoid synthesis

A

zona glomerulosa

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28
Q

zone of glucocorticoid synthesis

A

zona fasciculata

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29
Q

zone of adrenal androgen synthesis

A

zona reticularis

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30
Q

required for all steroidogenic pathways

A

cholesterol

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31
Q

majority of steroidogenic enzymes

A

cytochrome P450

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32
Q

where are these steroidogenic enzymes located

A

mitochondrion, endoplasmic reticulum

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33
Q

majority of the DHEA form in the adrenal

A

it’s sulfate ester form, DHEAS

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34
Q

True or false. Cortisone also exerts glucocorticoid action but much weaker than cortisol itself.

A

True.

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35
Q

True or false. Free cortisol enter the cell directly not requiring active transport

A

True.

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36
Q

what drives aldosterone synthesis in the adrenal zona glomerulosa

A

aldosterone synthase (CYP11B2)

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37
Q

reflects a constellation of clinical features that result from chronic exposure glucocorticoids of any etiology

A

Cushing syndrome

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38
Q

what is Cushing’s disease

A

cushing syndrome caused by a pituitary corticotrope adenoma

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39
Q

True or false. Cushing’s syndrome is generally considered a rate disease

A

True.

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40
Q

True or false. Majority of Cushing syndrome is caused by ACTH producing corticotrope adenoma of the pituitary

A

True.

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41
Q

How many percent of Cushing syndrome is caused by adrenals

A

10%

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42
Q

Most common cause of Cushing’s syndrome

A

medical use of glucocorticoid for immunosuppresion or for the treatment of inflammatory disorders

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43
Q

mutation found in Cushings disease

A

deubiquitinase USP8

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44
Q

Causes predominant ectopic ACTH production

A

occult carcinoid tumors

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45
Q

rare notable cause of adrenal cortisol excess

A

macronodular adrenal hyperplasia

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46
Q

autosomal dominal multiple neoplasia associated with cardiac myxoma, hyperlentiginosis, Sertoli cell tumors, and PPNAD

A

Carney’s complex

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47
Q

rare cause of ACTH independent Cushing syndrome associated with polyostotic fibrous dysplasia, unilateral cafe au lait spots and precocious puberty

A

McCune Albright syndrome

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48
Q

most important features of cortisol excess

A

upregulation of gluconeogenesis, lipolysis, and protein catabolism

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49
Q

Algorithm for management of patients suspected with Cushings syndrome. Screening 24 hour urine?

A

24h urinary free cortisol excretion 3x above normal;

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50
Q

Algorithm for management of patients suspected with Cushings syndrome. Screening dexamethasone

A

dexamethasone overnight test with plasma cortisol more than 5 nmol/L at 8-9 Am after 1 mg dexamethasone at 11 PM

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51
Q

Algorithm for management of patients suspected with Cushings syndrome. Screening plasma cortisol

A

midnight plasma cortisol more than 130 nmol/L or midnight salivary cortisol more than 5 nmol/L

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52
Q

Algorithm for management of patients suspected with Cushings syndrome. Screening low DEXA

A

low dexa plasma cortisol more than 5 nmol/L after 0.5 mg dexamethasone q6hrs for 2 days

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53
Q

Algorithm for management of patients suspected with Cushings syndrome. Screening positive. What to do next?

A

Get plasma ACTH

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54
Q

Algorithm for management of patients suspected with Cushings syndrome. Screening positive. ACTH normal or high more than 15 pg/ml.

A

ACTH dependent Cushing

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55
Q

Algorithm for management of patients suspected with Cushings syndrome. Screening positive. ACTH supressed less than 15 pg/ml.

A

ACTH independent Cushing

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56
Q

Algorithm for management of patients suspected with Cushings syndrome. Screening positive. ACTH normal or high. What to do next?

A

MRI pituitary, CRH ttest, high dexa test

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57
Q

values for CRH test

A

ACTH increase more than 40% at 15-30 min plus cortisol increased more than 20% at 45-60 mins after CRH 100 ug IV

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58
Q

values for high DEX test

A

cortisol suppression more than 50% after q6hrs DEX for 2 days

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59
Q

Algorithm for management of patients suspected with Cushings syndrome. Screening positive. ACTH normal or high. CRH and high DEXX positive. What to do next?

A

Cushing disease. Transphenoidal pituitary surgery

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60
Q

Algorithm for management of patients suspected with Cushings syndrome. Screening positive. ACTH normal or high. CRH and high DEXA negative. What to do next?

A

Inferior petrosal sinus sampling (petrosal/peripheral ACTH ratio more than 2 at baseline, more than 3 at 2-5 mins after CRH 100 ug IV

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61
Q

Algorithm for management of patients suspected with Cushings syndrome. Screening positive. ACTH normal or high. CRH and high DEXA negative.Petrosal/Peripheral ACTH ratio more than 2. What to do?

A

Cushing disease. Transphenoidal pituitary surgery

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62
Q

Algorithm for management of patients suspected with Cushings syndrome. Screening positive. ACTH normal or high. CRH and high DEXA equivocal. What to do next?

A

?

63
Q

Algorithm for management of patients suspected with Cushings syndrome. Screening positive. ACTH normal or high. CRH and high DEXA negative.Petrosal/Peripheral ACTH ratio negative. What to do?

A

Locate and remove ectopic ACTH source

64
Q

Algorithm for management of patients suspected with Cushings syndrome. Screening positive. ACTH supressed.

A

Unenhanced CT adrenal.

65
Q

Algorithm for management of patients suspected with Cushings syndrome. Screening positive. ACTH supressed. CT scan of adrenals, unilateral mass. What to do next?

A

Adrenal tumor workup

66
Q

Algorithm for management of patients suspected with Cushings syndrome. Screening positive. ACTH supressed. CT scan of adrenals, bilateral micro or macronodule adrenal hyperplasia. What to do next?

A

bilateral adrenalectomy

67
Q

Algorithm for management of patients suspected with Cushings syndrome. Screening positive. ACTH normal or high. CRH and high DEXA negative.Petrosal/Peripheral ACTH ratio negative. No ectopic ACTH source. What to do?

A

bilateral adrenalectomy

68
Q

can cause rapid inactivation of dexamethasone

A

concurrent intake of CYP3A4 inducing drugs such antiepileptics, rifampicin

69
Q

True or false. Concurrent intake of oral contraceptives that raise CBG and thus total cortical can cause failure to suppress after dexamethasone

A

True.

70
Q

How many weeks off estrogen can dexamethasone suppression test done?

A

4-6 weeks off estrogen

71
Q

investigation of choice for ACTH dependent cortisol excess

A

MRI

72
Q

What is the prognosis of overt Cushing syndrome

A

poor prognosis if left untreated

73
Q

treatment of choice of Cushing disease

A

selective removal of the pituitary corticotrope via endoscopic transphenoidal approach

74
Q

oral agents with established efficacy in Cushing syndrome

A

metyrapone and ketoconazole

75
Q

inhibits cortisol synthesis at the level of 11B hydroxylase

A

metyrapone

76
Q

inhibits early tels of steroidogenesis

A

ketoconazole

77
Q

dose of metyrapone

A

Metyrapone 500 mg TID max 6 g per day

78
Q

dose of ketoconazole

A

Ketoconazole 200 mg max 1200

79
Q

derivative of insecticide opDDD, is also effective in reducing cortisol

A

mitotane

80
Q

an agent that potently blocks 11B hydroxylase and aldosterone synthase

A

etomidate

81
Q

True or false. After successful removal of an ACTH or cortisol producing tumor, HPA axis will remain suppressed thus hydrocortisone replacement needs to be initiated at the time of surgery and slowly tapered following recovery to allow physiologic adaptation to normal cortisol levels

A

True.

82
Q

other name for aldosteroe producing adrenal adenoma

A

Conn’s syndrome

83
Q

most common cause of mineralocorticoid excess

A

primary aldosteronism

84
Q

clinical hallmark of mineralocorticoid excess

A

hypokalemic hypertension

85
Q

refers to patient with concurrent mild autonomous cortisol excess along with primary aldosteronism

A

Connshing syndrome

86
Q

accepted screening test for primary aldosteronism

A

concurrent measurement of plasma renin and aldosterone with subsequent calculation of the aldosterone renin ratio

87
Q

True or false. Serum potassium needs to be normalized prior to calculation the aldosterone renin ratio

A

True,

88
Q

should MR antagonist be stopped in screening for primary aldosteronism?

A

Yes for at least 4 weeks prior to ARR testing

89
Q

when is ARR screening positive

A

if ARR more than 750 pmol/L per ng/ml per hour with concurrently high normal or increased aldosterone

90
Q

how is the saline test done

A

2L of physiologic saline administered for 4 hr period then serum aldosterone is suppressed to less than 140 nmol/L or 5 ng/dL

91
Q

What does a positive saline test mean

A

autonomous mineralocorticoid excess

92
Q

how is oral sodium loading test done

A

300 nmol NaCl/day for 3 days

93
Q

alternative to sodium test

A

fludrocortisone suppression test 0.1 mg q6hrs with 30 nmmol NaCl q8hrs for 4 days

94
Q

disadvantage of using fludrocoritsone plus Nacl

A

risk of profound hypokalemia and incrased hypertension

95
Q

next step after the diagnosis of hyperaldosteronism is established

A

use adrenal imaging to further assess the cause

96
Q

imaging of choice in primary aldosteronism as it provides excellent visualization of adrenal morphology

A

Fine cut CT scanning of the adrenal region

97
Q

when is adrenal venous sampling done

A

only be carried out in surgical candidate with either no obvious lesion on CT or evidence of unilateral lesion in patients with more than 40

98
Q

how is lateralization in primary aldosteronism confirmed

A

aldoserone/cortisol ratio 2x higher on the affected side

99
Q

cortisol gradient between vena cava and each adrenal vein on adrenal venous sampling

A

cortisol gradient more than 3

100
Q

which is adrenal vein is more difficult to cannulate

A

right adrenal vein

101
Q

how to avoid postsurgery hypoaldosteronism

A

MER antagonist spironolactone 12.5 to 50 mg BID and titrated up to maximum of 400 mg/day to control blood pressure and normalize potassium

102
Q

most selective MR antagonist

A

Eplerenone 25 mg BID titrated up to 200 mg/ day

103
Q

another drug useful in primary aldosteronism, a sodium channel blocker

A

Amiloride 5-10 mg BID

104
Q

Clinical suspicion of mineralocorticoid excess

A

severe hypertension despite 3 agents; hypokalemia, adrenal mass or family history of early onsent hypertension or cerebrovascular events at less than 40 years old

105
Q

Screening for mineralocorticoid excess

A

ARR on current BP medications and hypokalemia corrected

106
Q

what is a positive ARR screen

A

ARR more than 750 pmol:ng/ml and aldosterone more than 450

107
Q

confirmation of diagnosis of mineralocorticoid excess

A

saline infusion, oral sodium loading, fludrocortisone suppression

108
Q

what to do if both renin and aldosterone suppressed

A

24 hr urinary steroid profile

109
Q

True or false. Majority of adrenal nodules are endocrine inactive adrenocortical adenomas

A

True,

110
Q

True or false. Adrenocortical carcinoma is considered a highly malignant tumor

A

True,

111
Q

True or false. FNA is not indicated in ACC

A

True,

112
Q

Why is FNA not indicated in Adrenocortical adenoma

A

cytology and also histopathology of a core biopsy cannot differentiate between benign and malignant primary adrenal masses; FNA violates th tumor capsule and may even cause needle canal metastasis

113
Q

most common histopathologic classification of ACC

A

Weiss score

114
Q

Mixed excess production of several corticosteroid classes by an adrenal tumor is generally indicative of malignancy

A

True.

115
Q

FNA of a pheochromocytoma can cause a life threatening hypertensive crisis

A

True.

116
Q

Algorithm for the management of patient with incidentally discovered adrenal mass. Screening tests?

A

plasma metanephrines or 24 hr urine for metanephrine excretion, 24 hr urine for free cortisol, plasma ACTH, dexamethasone 1 mg overnight test, plasma aldosterone and plasma renin in patients with hypertension and or hypokalemia, if tumor more than 4 cm serum 17B hydroxyprogesterone and DHEAS

117
Q

when should serum 17B hydoxyprogesterone and DHEAS taken

A

patients with incidental adrenal mass of more than 4 cm

118
Q

How many dexamethasone 1 mg overnight tests for a positive result

A

at least 2 out of 4 tests

119
Q

high sensitive for the detection of malignancy and can be used to detect small metastases or local recurrence that may not be obvious on CT

A

18 FDG PET

120
Q

Most common metastasis in ACC

A

liver and lung

121
Q

most important prognostic histopathologic parameter in ACC

A

Ki67 proliferation index

122
Q

Meaning of Ki67 proliferation index in ACC

A

less than 10%slow to moderate growth velocity and Ki67 more than 10% means poor prognosis including high risk or recurrence and rapid progression

123
Q

most common cause of primary adrenal insufficiency

A

autoimmune adrenalitis

124
Q

consequence of dysfunction of the hypothalamic pituitary component of HPA axis

A

secondary adrenal insufficiency

125
Q

clinical features of primary adrenal insufficiency

A

loss of both glucocorticoid and mineralocorticoid section

126
Q

other name of primary adrenal insufficiency

A

Addison’s disease

127
Q

Differentiate primary from secondary adrenal insufficiency

A

secondary adrenal insufficiency only glucocorticoid deficiency is present as the adrenal itself is still intact and still amenable to regulation by RAA system

128
Q

distinguishing feature of primary adrenal insufficiency

A

hyperpigmentation, which is caused by excess ACTH stimulation of melnocytes

129
Q

where is hyperpigmentation most pronounced in skin primary adrenal insufficiency

A

in skin areas exposed to increased friction or shear stress and is increased by sunlight

130
Q

characteristic biochemical feature in primary adrenal insufficiency

A

hyponatremia

131
Q

differentiate primary from secondary adrenal insufficiency as to skin pigmentation

A

primary adrenal insufficiency: hyperpigmentation; secondary adrenal insufficiency: alabaster due to lack of ACTH stimulation

132
Q

how is adrenal insufficiency established

A

short cosyntropin test with cortisol levels less than 450-500 nmol/L (16-18 ug/dL) sampled 30-60 min after ACTH stimulation

133
Q

what is the next step once adrenal insufficiency is confirmed

A

measurement of plasma ACTH

134
Q

initial management of acute adrenal insufficiency

A

immediate rehydration with saline infusion at rate of 1 L/h with continuous cardiac monitoring

135
Q

how is glucocorticoid replacement done in acute adrenal insufficiency

A

Hydrocortisone 100 mg bolus IV then 200 mg hydrocortisone over 24 hrs

136
Q

when can mineralocorticoid replacement in acute adrenal insuffiency done

A

when daily hydrocortisone dose has been reduced to less than 50 mg because higher of hydrocortisone provide sufficient stimulation of mineralocorticoid receptors

137
Q

how glucocorticoid replacement done in chronic adrenal insufficiency

A

replace physiologic daily cortisol production by oral administration of 15-25 mg hydrocortisone in two or three divided doses

138
Q

True or false. Pregnancy may require an increase in hydrocortisone dose by 50% during the last trimester

A

True.

139
Q

True or false. In all patients, at least one half of the daily dose should be administered in the morning

A

True.

140
Q

why are long acting glucocorticoids such as prednisolone or dexamethasone not preferred

A

they result in increased glucocorticoid exposure

141
Q

equipotency for 1 mg hydrocortisone

A

1.6 mg cortisone acetate, 0.2 mg prednisolone, 0.25 mg prednisone, 0.025 mg dexamethasone

142
Q

Diagnosis. Low normal ACTH, normal renin, normal aldosterone

A

secondary adrenal insufficiency

143
Q

Diagnosis. High ACTH, high renin, low aldosterone

A

primary adrenal insufficiency

144
Q

treatment of primary adrenal insufficiency

A

mineralocorticoid and glucocorticoid replacement

145
Q

treatment of secondary adrenal insufficiency

A

glucocorticoid replacement

146
Q

True or false. All patients with adrenal insufficiency need to be instructed about the requirement for stress related glucocorticoid dose adjustment

A

True. Doubling dose in case of intercurrent illness or stress

147
Q

how is mineralocorticoid replacement done in primary adrenal insufficiency

A

Fludrocortisone 100-150 ug

148
Q

equivalent of 40 mg hydrocortisone

A

100 ug fludrocortisone

149
Q

True or false. Fludrocortisone should be increased to by 50-100 ug during the summer and during pregnancy

A

True,

150
Q

True or false. Pregnancy has antimineralocorticoid activity from progesterone

A

True

151
Q

caused by mutation in genes encoding steroigenic enzymes involve in glucocorticoid synthesis

A

congenital adrenal hyperplasia

152
Q

most prevalent cause of CAH

A

mutations in CYP21A2

153
Q

useful marker for overtreatment in CAH

A

17OHP

Endocrine (15 decks)

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