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Clin Med II > Adrenal Disorders > Flashcards

Adrenal Disorders Flashcards

1
Q

What hormones are produced in the zona glomerulosa of the adrenal cortex and what is their function?

A

Mineralocorticoids (aldosterone); regulates salt balance and blood volume

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2
Q

What regulates the secretion of mineralocorticoids (aldosterone)?

A

Angiotensin II, serum K concentration

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3
Q

What hormones are produced in the zona fasciculata of the adrenal cortex and what is their function?

A

Glucocorticoids (cortisol); increases blood glucose, metabolic effects

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4
Q

What regulates the secretion of glucocorticoids (cortisol)?

A

ACTH, corticotropin-releasing hormone

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5
Q

What hormones are produced in the zona reticularis of the adrenal cortex and what is their function?

A

Androgens (DHEA); converted into testosterone, DHT and estradiol

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6
Q

What regulates the secretion of androgens (DHEA)?

A

ACTH, corticotropin-releasing hormone

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7
Q

What are the components of the hypothalamic-pituitary-adrenal cortex axis? (6 steps)

A

Hypothalamus → [CRH] → anterior pituitary → [ACTH] → adrenal cortex → [cortisol]

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8
Q

How does cortisol affect the anterior pituitary and hypothalamus?

A

Negative feedback

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9
Q

What 2 things does cortisol increase? (part of cortisol functions)

A

Stimulates gluconeogenesis (↑ blood glucose levels) and ↑ proteolysis in muscle

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10
Q

What 3 things does cortisol decrease? (part of cortisol functions)

A

↓ glucose uptake by tissues ↓ bone formation ↓ intestinal/ renal calcium absorption → ↓ plasma calcium

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11
Q

How does cortisol play a role in inflammation?

A

Anti-inflammatory effects

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12
Q

How does cortisol play a role in BP?

A

Maintains normal BP

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13
Q

Does cortisol inhibit or stimulate collagen formation?

A

Inhibits

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14
Q

When do levels of cortisol rise/peak/ fall? (circadian rhythm of cortisol)

A

Levels rise during sleep/ peak in AM & drop throughout the day

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15
Q

Pt presents with moon face and buffalo hump. What are you concerned for?

A

Cushing’s syndrome

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16
Q

Cushing’s is characterized as excess levels of what?

A

Glucocorticoid (cortisol) and androgens

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17
Q

Pt presents with amenorrhea, striae, hyperpigmentation, central obesity, osteoporosis, poor wound healing, HTN, depression, anxiety, and excess adrenal androgens causing hirsutism, acne, and increased libido. What condition do they have?

A

Cushing’s

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18
Q

Does ACTH dependent Cushing’s have high or low cortisol?

A

High (makes up about 80% of cases)

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19
Q

Does ACTH independent Cushing’s have high or low cortisol?

A

High (but low ACTH)

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20
Q

What is the primary etiology of ACTH dependent Cushing’s?

A

Cushing’s disease (pituitary hypersecretion)

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21
Q

Besides Cushing’s disease, what is the other most common etiology of ACTH dependent Cushing’s?

A

Ectopic secretion by non-pituitary tumor

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22
Q

What is the most common etiology of ACTH indepdent Cushing’s?

A

Latrogenic or factitious Cushing’s syndrome (administration of excessive synthetic glucocorticoid)

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23
Q

Would an adrenocortical adenoma/ carcinoma and pheochromocytoma cause ACTH dependent or ACTH independent Cushing’s?

A

ACTH independent

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24
Q

What is the gold standard for diagnosis of Cushing’s?

A

24 hour urinary free cortisol excretion

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25
Q

Exclusion of exogenous glucocorticoids, late night salivary cortisol, and low-dose dexamethasone suppression test are other diagnostic tests for what condition?

A

Cushing’s

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26
Q

What is an abnormal result for a low-dose dexamethasone suppression test?

A

Elevated cortisol of > 5 mcg/dL (suspicious for non-suppressible cortisol production from ACTH independent etiology)

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27
Q

When might you consider imaging (MRI, CXR, pelvic US, CT abdomen) in the diagnosis/ management of Cushing’s?

A

To rule out other causes

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28
Q

What is the treatment for Cushing’s caused by exogenous corticosteroids?

A

Taper to lowest therapeutic dose to control sxs

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29
Q

What is the treatment of Cushing’s caused by a pituitary adenoma?

A

Transsphenoidal resection

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30
Q

What is the treatment of Cushing’s caused by an adrenal tumor?

A

Adrenalectomy

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31
Q

What is the treatment of Cushing’s caused by adrenal hyperplasia, an inoperable tumor, or other malignancy?

A

Medical therapy

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32
Q

What is considered 1st line treatment for Cushing’s?

A

Ketoconazole

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33
Q

If Ketoconazole is ineffective in the treatment of Cushing’s, what might you add to the treatment regimen?

A

Metyrapone

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34
Q

What might you add to the treatment regimen of a pt with Cushing’s to achieve “medical adrenalectomy”?

A

Mitotane

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35
Q

What are the primary functions of aldosterone?

A

Increase BP and promote excretion of potassium (reabsorption of sodium)

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36
Q

What syndrome is excess aldosterone?

A

Conn’s

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37
Q

What is the most common etiology of Conn’s syndrome?

A

Bilateral idiopathic adrenal hyperplasia (60%)

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38
Q

What is the second most common etiology of Conn’s syndrome?

A

Unilateral aldosterone producing adenoma (APA) (30%)

39
Q

What are the primary sxs of Conn’s syndrome?

A

Hypertension and hypokalemia (others: muscle weakness, paresthesias, HA, polyuria, polydipsia)

40
Q

What 3 lab findings are diagnostic for Conn’s?

A
  1. Increased plasma aldosterone 2. Decreased plasma renin activity/ concentration 3. Spontaneous hypokalemia
41
Q

What is first line imaging for Conn’s used to evaluate for adrenal adenoma and adrenal hyperplasia?

A

CT abdomen

42
Q

If a pt presents with resistant HTN, what should you evaluate for?

A

Excess aldosterone

43
Q

What is the treatment of choice for Conn’s if the cause is a unilateral adrenal adenoma?

A

Surgical removal

44
Q

What is 1st line treatment for Conn’s if the cause if bilateral idiopathic adrenal hyperplasia?

A

Spironolactone (must monitor serum K, creatinine, and BP during first 4-6 weeks of therapy)

45
Q

Are cortisol levels high/ N/ or low for the following? Primary AI (Addison’s disease) Secondary AI Tertiary AI

46
Q

Are aldosterone levels high/ N/ or low for the following? Primary AI (Addison’s disease) Secondary AI Tertiary AI

47
Q

Are androgen levels high/ N/ or low for the following? Primary AI (Addison’s disease) Secondary AI Tertiary AI

48
Q

Are ACTH levels high/ N/ or low for the following? Primary AI (Addison’s disease) Secondary AI Tertiary AI

A

High, low, low

49
Q

Are CRH levels high/ N/ or low for the following? Primary AI (Addison’s disease) Secondary AI Tertiary AI

A

High, high, low

50
Q

What is primary adrenocortical insufficiency and synthesis of which adrenocortical hormones are decreased?

A

Addison’s, ALL are decreased

51
Q

Hypoglycemia, weight loss, and muscle weakness are indicative of decreased levels of what?

A

Cortisol (Addison’s)

52
Q

Decreased aldosterone causes what 2 sxs besides hyperkalemia and metabolic acidosis?

A

Hypotension and salt craving (Addison’s)

53
Q

Decreased libido and pubic hair in females is indicative of decreased levels of what?

A

Androgens (Addison’s)

54
Q

What primary sx will be caused by increased ACTH?

A

Hyperpigmentation (Addison’s)

55
Q

What is the most common etiology of Addison’s?

A

Autoimmune destruction of adrenal cortex

56
Q

S/p adrenalectomy, infection (TB, histo, cocci, HIV), hemorrhage/ infarction, CA/ mets can all be the cause of what condition?

A

Addison’s

57
Q

What are the primary sxs of Addison’s? (3)

A

Hyperpigmentation, salt craving, postural hypotension (also: muscle/joint pain, weight loss, hypoglycemia, depression, confusion, anxiety)

58
Q

What is the most common etiology of secondary AI?

A

Suppression of HPA axis by abrupt cessation of exogenous steroid

59
Q

Pituitary disease, endogenous steroid-producing tumor, and drugs that produce corticosteroids are all possible etiologies for what conditions?

A

Secondary/ tertiary AI

60
Q

What are the clinical features of secondary and tertiary AI related to?

A

Cortisol and androgen deficiency

61
Q

What are the 2 main differences between primary AI and secondary/ tertiary AI?

A

Aldosterone is normal and there is NO hyperpigmentation

62
Q

Failure of corticotrophs to adequately secrete ACTH is what type of AI?

63
Q

Insufficient CRH from the hypothalamus is what type of AI?

64
Q

What are the 2 best diagnostic methods for AI?

A

Serum AM cortisol (low) and Cosyntropin (ACTH) stimulation test (can also use serum ACTH, renin, aldosterone)

65
Q

What test evaluates for the ability of the adrenal gland to respond to ACTH and what should happen?

A

Cosyntropin (ACTH) stimulation test, should produce cortisol

66
Q

What is considered an abnormal result for a Cosyntropin (ACTH) stimulation test?

A

Cortisol fails to increase by 7mg/dL above baseline OR to > 18 mcg/dL

67
Q

If on Cosyntropin (ACTH) stimulation test you note an exaggerated and prolonged ACTH response, should you be concerned for secondary or tertiary AI?

68
Q

If on Cosyntropin (ACTH) stimulation test you note an absent or subnormal ACTH response, should you be concerned for secondary or tertiary AI?

69
Q

What is the management for AI? (4)

A

Short-acting glucocorticoids, long-acting glucocorticoids (if non-compliant w/ short-acting), Mineralocorticoid, oral DHEA replacement (women)

70
Q

What short-acting glucocorticoids are used in the treatment of AI?

A

Hydrocortisone BID to TID

71
Q

What long-acting glucocorticoids are used in the treatment of AI? (if non-compliant w/ short-acting)

A

Dexamethasone, prednisone

72
Q

What mineralocorticoid is used in the treatment of AI?

A

Fludrocortisone

73
Q

What is defined as a catecholamine-secreting tumor that arises from chromaffin cells of adrenal medulla?

A

Pheochromocytoma (rare)

74
Q

Do you see excess or low catecholamines with a pheochromocytoma?

75
Q

MEN2 syndrome can be a possible familial cause of what?

A

Pheochromocytoma (40%)

76
Q

Are pheochromocytomas more commonly benign or malignant?

A

90% benign

77
Q

Paraanglioma can be the cause of what?

A

Pheochromocytoma

78
Q

What is the classic triad of sxs associated with a pheochromocytoma?

A

Episodic HA, tachycardia, sweating (associated w/ paroxysmal HTN)

79
Q

what instances should you suspect a possible pheochromocytoma? (3)

A

Paroxysmal “attacks”, refractory HTN (or onset < 20 yo), family history (also: abd/ adrenal mass, other diagnoses (MEN2, NF))

80
Q

What 3 labs are included in the initial workup for a possible pheochromocytoma?

A

Plasma metanephrines, 24-hour urine (catecholamines, metanephrines, VMA), Clonidine Suppression Test (can also order plasma epi/ NE)

81
Q

What imaging would you order after a lab dx of pheochromocytoma has been made?

A

CT abdomen w/o contrast

82
Q

What is the 1st line management for pheochromocytoma?

A

“Chemical sympathectomy” to stabilize until surgery (which is definitive)

83
Q

What pharmacologic treatment might be used for the management of a pheochromocytoma?

A

Pure alpha-blocker (phenoxybenzamine) and beta-blocker (propranolol)

84
Q

An adrenal mass lesion > 1 cm in diameter and serendipitously discovered by imaging but RARE is what?

A

Adrenal incidentaloma

85
Q

What is included in the workup of ALL pts with possible adrenal incidentaloma?

A

R/o pheochromocytoma and subclinical Cushing’s Syndrome

86
Q

What is included in the workup of pts with HTN at presentation with possible adrenal incidentaloma?

A

R/o primary aldosteronism

87
Q

What is included in the workup of pts with a hx of a primary malignanct elsewhere with possible adrenal incidentaloma?

A

DO NOT biopsy if biochemical evidence of pheo or if known widespread metastatic disease

88
Q

What is the management for possible adrenal incidentaloma if workup is negative + likely benign + < 2cm? (2)

A

Repeat imaging @ 6 months, repeat dexamethasone suppression test annually x 4 years

89
Q

What is the management for possible adrenal incidentaloma if workup is negative + likely benign + > 2cm?

A

Consider surgical resection

90
Q

What is dexamethasone?

A

Potent glucocorticoid

91
Q

What disease does the following correspond to?

A

Cushing’s syndrome

92
Q

What disease does the following test/ abnormal results correspond to?

A

Addison’s disease

93
Q

What disease does the following test/ abnormal results correspond to?

A

Pheochromocytoma

Clin Med II (12 decks)

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