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Clinical Medicine 2 > Exam 4: Adrenal Gland > Flashcards

Exam 4: Adrenal Gland Flashcards

1
Q

What two classes of hormones does the adrenal gland produce?

A

Steroids and catecholamines

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2
Q

Where in the adrenal gland are catecholamines and peptides made?

A

Medulla

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3
Q

Where in the adrenal gland are mineralocorticoids (aldosterone (salt)) made?

A

The cortex, specifically zona glomerulosa

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4
Q

What does aldosterone do?

A

Regulates salt balance and blood volume

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5
Q

What controls the release of aldosterone?

A

AT II and serum potassium concentrations

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6
Q

Where in the adrenal gland are glucocorticoids produced?

A

Zona fasciculata

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7
Q

What does cortisol do?

A

Increases blood sugar and has many metabolic effects

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8
Q

What controls the release of cortisol?

A

ACTH, CRH

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9
Q

Where in the Adrenal Gland are androgens made?

A

The cortex, specifically the zone reticularis

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10
Q

What controls the release of androgens?

A

ACTH, CRH

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11
Q

What controls the release of catecholamines?

A

Preganglionic sympathetic neurons

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12
Q

Cortisol has negative feedback on what two things? This results in decreased production of what?

A

Cortisol has negative feedback on the hypothalamus, so it does not secrete CRH, and it has negative feedback on the anterior pituitary so it does not secrete ACTH

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13
Q

What are the functions of cortisol?

A

Stimulates gluconeogenesis, decreases glucose uptake by tissues, anti-inflammatory effects, reduces bone formation, increases proteolysis, decreases plasma Ca, and inhibits collagen formation

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14
Q

When are cortisol levels the highest?

A

The morning

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15
Q

What results from prolonged exposure to excess glucocorticoids and androgens?

A

Cushing’s syndrome

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16
Q

What are the clinical features of Cushing’s syndrome?

A

Amenorrhea, strifes, hyperpigmentation, central obesity, HTN, proximal muscle wasting, signs of androgen excess, and emotional lability

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17
Q

What are the two different types of cushings disease?

A

ACTH dependent (80%) and ACTH independent (20%)

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18
Q

What is the most common cause of Cushing’s syndrome?

A

Pituitary hypersecretion of ACTH, responsible for most cases of Cushing syndrome. This is known as cushings disease

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19
Q

What is the most common case of ACTH independent Cushing syndrome?

A

Latrogenic or fictitious Cushing’s syndrome

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20
Q

Is ACTH elevated or lowered in ACTH dependent Cushing’s syndrome?
What about ACTH independent?

A

Dependent: High
Independent: low

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21
Q

What is the gold standard for diagnosis of Cushing’s syndrome? What other tests can be done?

A

24 hour urinary free cortisol excretion is gold standard.

Late night salivary cortisol and low dose dexamethasone suppression test may also be used

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22
Q

What must you rule out when diagnosing Cushing’s syndrome?

A

You must exclude exogenous glucocorticoids

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23
Q

How is the lose dose dexamethasone suppression test performed?

A

1mg oral dose of dexamethasone at 11pm and serum cortisol levels are measured at 8am the following morning

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24
Q

What is an abnormal result in the low dose dexamethasone suppression test?

A

Elevated cortisol of >5mcg/dL is an abnormal result.

This is highly suspicious for non-suppressive cortisol production from ACTH independent etiology

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25
Q

What is the management of cushings disease caused by exogenous corticosteroids?

A

Taper to the lowest therapeutic dose to control symptoms

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26
Q

What is the management of Cushing’s syndrome caused by pituitary adenoma?

A

Transsphenoidal resection

27
Q

What is the management of Cushing’s syndrome caused by adrenal tumor?

A

Adrenalectomy

28
Q

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

A

Medial therapy is warranted

29
Q

What is the first line medical management of Cushing’s syndrome?

A

Ketoconazole (at higher doses, it inhibits steroidogensis)

30
Q

What drugs should you give for Cushing’s syndrome if ketoconazole was not effective?

A

Metyrapone

31
Q

What medication can be given for Cushing’s syndrome to achieve a “medical Adrenalectomy”?

A

Mitotane

32
Q

What are the functions of aldosterone?

A

Increase blood pressure, increase ECF volume, increase tubular reabsorption of sodium, promote excretion on potassium, and water retention

33
Q

What are the most common etiologies of primary hyperaldosteronism (Conns syndrome)?

A
  • Bilateral idiopathic adrenal hyperplasia is most common

- Unilateral aldosterone producing adenoma is second most common

34
Q

What are the clinical features of primary hyperaldosteronism?

A

HTN, hypokalemia, muscle weakness, paresthesias, HA, polyuria, and polydipsia

35
Q

How is primary hyperaldosteronism diagnosed?

A

1) increased plasma aldosterone concentration (PAC)
2) Decreased plasma renin activity (PRA) or plasma renin concentration (PRC)
3) Spontaneous hypokalemia

36
Q

What imaging can be obtained for primary hyperaldosteronism and why?

A

CT abdomen to evaluate for adrenal adenoma or adrenal hyperplasia

37
Q

If a patient being worked up for primary hyperaldosteronism does not have spontaneous hypokalemia, what must be done?

A

Confirmatory testing is required to establish diagnosis

38
Q

What is the management for a patient with primary hyperaldosteronism caused by a unilateral adrenal adenoma?

A

Surgical removal

39
Q

What is the management of a patient with primary hyperaldosteronism caused by bilateral idiopathic adrenal hyperplasia?

A
  • Mineralocorticoid receptor antagonist (Spironolactone is first line!!)
  • Antihypertensives
  • Monitor serum K, creatinine, and BP during first 4-6 weeks of therapy
40
Q

What disease results in decreased synthesis of all adrenocortical hormones, including cortisol, aldosterone, and androgens, however ACTH is high?

A

Primary adrenocortical insufficiency AKA Addison’s disease

41
Q

What causes secondary adrenocortical insufficiency?

A

Failure of the corticotrophs to adequately secrete ACTH

42
Q

What causes tertiary adrenocortical insuffiency?

A

Insufficient CRH from the hypothalamus

43
Q

What is the difference between primary adrenocortical insufficiency (AI) vs secondary and tertiary?

A

Secondary and tertiary AI clinical features are related to cortisol and androgen deficiency. Aldosterone is normal and hyperpigmentation does not occur

44
Q

What is the most common etiology of primary AI?

A

Autoimmune destruction of the adrenal cortex

45
Q

What is the most common cause of secondary AI?

A

Suppression of the HPA axis through abrupt cessation of exogenous steroids

46
Q

What is the one labs that is high in primary AI?

A

ACTH

47
Q

What lab is normal with secondary AI?

A

Aldosterone

48
Q

What lab is normal and what is lab is low in tertiary AI?

A

Aldosterone is normal and CRH is low

49
Q

What are the clinical features of primary AI?

A

Hyperpigmentation, salt craving, postural hypotension, depression/anxiety, and decreased pubic and axillary hair in females

50
Q

How is AI diagnosed?

A
  • Serum AM cortisol
  • cosyntropin (ACTH) stimulation test
  • ACTH, renin, and aldosterone
51
Q

What is an abnormal result of the cosyntropin stimulation test?

A

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

52
Q

What are the management options of AI?

A
  • Short acting glucocorticoids ( Hydrocortisone BID to TID)
  • Long acting glucocorticoids (dexamethasone, prednisone)
  • MIneralocorticoid (Fludrocortisone)
  • Consider oral DHEA replacement in women
53
Q

What is it called when a patient has a catecholamine secreting tumor that arises from chromaffin cells of the adrenal medulla?

A

Pheochromocytoma

54
Q

What is the clinical presentation of pheochromocytoma?

A

Classic triad: Episodic headache, tachycardia, and sweating

-paroxysmal HTN

55
Q

What are the most common etiologies of pheochromocytoma?

A
  • 60% are sporadic

- 40% are familial

56
Q

Are pheochromocytomas usually malignant or benign?

A

90% are benign

57
Q

What do most catecholamine secreting tumors arise from?

A

The adrenal medulla

58
Q

Patient presents with classic paroxysmal “attacks”, refractory HTN, and an abdominal mass. What should you suspect?

A

Pheochromocytoma

59
Q

How is pheochromocytoma diagnosed?

A
  • Plasma metanephrines
  • 24 hour urine catecholamines, metanephrines, and VMA
  • Clonidine suppression test
  • thyroid function tests
  • plasma epi and NE
60
Q

What imaging should be ordered to diagnose pheochromocytoma?

A

CT abdomen without contrast

61
Q

What is the management of pheochromocytoma?

A
  • Chemical sympathectomy stabilizes patient until surgery
  • Surgery is definitive
  • B blocker and alpha blocker
62
Q

What is it called when a patient has an adrenal mass lesion greater than 1cm in diameter, serendipitously discovered by radiologic exam?

A

Adrenal incidentaloma

63
Q

What is the management for an adrenal incidentaloma that has a negative work up, is likely benign, and is <2cm?

A

Repeat imaging at 6 months and repeat dexamethasone supression test every year for 4 years

64
Q

What is the management for an adrenal incidentaloma that has a negative work up, is likely benign, and is >2cm?

A

Consider surgical resection

Clinical Medicine 2 (22 decks)

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