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Clinical Med II > Exam 4 - Adrenal Disorders > Flashcards

Exam 4 - Adrenal Disorders Flashcards

1
Q

What are some clinical features of Cushing’s Syndrome?

A
  • Amenorrhea
  • Striae
  • Hyperpigmentation
  • Central obesity (“moon face”, “buffalo hump”)
  • HTN
  • Osteoporesis
  • Extremity muscle wasting
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2
Q

What type of etiology is 70% of all Cushing’s Syndrome?

Is Cortisol high or low?

Is ACTH high or low?

A

Cushing’s Disease = pituitary hypersecretion of ACTH

Cortisol is high

ACTH is high

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3
Q

What type of etiology is 20% of Cushing’s Syndrome?

Is Cortisol high or low?

Is ACTH high or low?

A

Iatrogenic or Factitious Cushing’s Syndrome (ACTH-independent) - administration of excessive synthetic glucocorticoid.

Cortisol is high

ACTH is low

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4
Q

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

A

24-hour urinary free cortisol excretion

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5
Q

What are the available first-line testing methods for Cushing’s Syndrome?

A
  • 24-hour urinary free cortisol excretion
  • Late-night salivary cortisol
  • Low-dose dexamethasone suppression test
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6
Q

What is an abnormal measurement for the Low-dose dexamethasone suppression test?

What does this raise suspicion for?

A

Elevated cortisol of > 5 mcg/dL

High suspicion for non-suppressible cortisol production from ACTH-independent etiology (adrenal adenoma)

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7
Q

What is the management of Cushing’s Syndrome?

A
  • Exogenous corticosteroids - taper to lowest therapeutic dose to control symptoms
  • Pituitary adenoma - transsphenoidal resection
  • Adrenal tumor - adrenalectomy
  • Adrenal hyperplasia - medical therapy
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8
Q

What is the 1st line medical management of Cushing’s Syndrome?

What can you add if this is ineffective?

A

Ketoconazole

If ineffective, add Metyrapone

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9
Q

What are the most common etiologies of Primary Hyperaldosteronism/Conn’s Syndrome?

A
  • Bilateral idiopathic adrenal hyperplasia (more common)

- Unilateral aldosterone-producing adenoma

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10
Q

What are some clinical features of Primary Hyperaldosteronism?

A
  • Hypertension*
  • Hypokalemia*
  • Muscle weakness
  • Paresthesias
  • Headache
  • Polyuria
  • Polydipsia
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11
Q

How is Primary Hyperaldosteronism diagnosed via labs?

A
  • Increased plasma aldosterone concentration (PAC)
  • Decreased plasma renin activity (PRA) or plasma renin concentration (PRC)
  • Spontaneous hypokalemia
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12
Q

How is Primary Hyperaldosteronism diagnosed via imaging?

A

CT abdomen to evaluate for adrenal adenoma or adrenal hyperplasia

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13
Q

What is the management for a unilateral adrenal adenoma?

A

Surgical removal

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14
Q

What is the management for bilateral idiopathic adrenal hyperplasia?

A

Spironolactone (1st line) - mineralocorticoid receptor antagonist
+ other antihypertensives

***Serum K+, Cr, and BP should be monitored frequently during the first 4-6 weeks of medical therapy

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15
Q

What disorder is due to decreased synthesis of ALL adrenocortical hormones (cortisol, aldosterone, androgens)?

A

Primary Adrenocortical Insufficiency: Addison’s Disease

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16
Q

What are clinical features associated with decreased aldosterone?

A

Hyperkalemia, hypotension, salt craving

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17
Q

What are clinical features associated with increased ACTH?

A

Hyperpigmentation

18
Q

What disorder is due to failure of the corticotrophs to adequately secrete ACTH?

A

Secondary Adrenocortical Insufficiency

19
Q

What disorder is due to insufficient corticotrophin-releasing hormone (CRH) from the hypothalmus?

A

Tertiary Adrenocortical Insufficiency

20
Q

What is different regarding the clinical features of Primary Adrenocortical Insufficiency compared to Secondary/Tertiary Adrenocortical Insufficiency?

A

In Secondary and Tertiary Adrenocortical Insufficiency, clinical features are related to cortisol and androgen deficiency. Aldosterone is normal and hyperpigmentation does not occur.

21
Q

What is the most common etiology of Primary Adrenocortical Insufficiency: Addison’s Disease?

A

Autoimmune destruction of the adrenal cortex

22
Q

What is the most common etiology of Secondary Adrenocortical Insufficiency?

A

Suppression of the HPA axis through abrupt cessation of exogenous steroid

23
Q

The following clinical features are associated with what disorder?

  • Cortisol: Low
  • Aldosterone: Low
  • Androgens: Low
  • ACTH: High
  • CRH: High
A

Primary Adrenocortical Insufficiency: Addison’s Disease

24
Q

The following clinical features are associated with what disorder?

  • Cortisol: Low
  • Aldosterone: Normal
  • Androgens: Low
  • ACTH: Low
  • CRH: High
A

Secondary Adrenocortical Insufficiency

25
Q

The following clinical features are associated with what disorder?

  • Cortisol: Low
  • Aldosterone: Normal
  • Androgens: Low
  • ACTH: Low
  • CRH: Low
A

Tertiary Adrenocortical Insufficiency

26
Q

The following clinical features are associated with what disorder?

  • Hyperpigmentation of the skin
  • Salt craving
  • Postural hypotension
  • Decreased pubic hair and axillary hair in females
  • Weight loss
  • Hypoglycemia
A

Primary Adrenocortical Insufficiency: Addison’s Disease

27
Q

How can adrenal insufficiency be diagnosed?

A
  • Serum AM Cortisol

- Cosyntropin (ACTH) Stimulation Test

28
Q

What is the Cosyntropin (ACTH) Stimulation Test?

What constitutes an abnormal result?

A

Evaluates the ability of the adrenal gland to respond to ACTH

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

29
Q

What is the management for adrenal insufficiency?

A
  • Short-acting glucocorticoids* (hydrocortisone BID to TID)
  • Long-acting glucocorticoids (dexamethasone, prednisone if non-compliant with short-acting)
  • Mineralocorticoid (fludrocortisone)
  • Consider oral DHEA replacement in women
30
Q

What is the classic triad associated with pheochromocytoma? What other symptom is it associated with?

A

Episodic headache, tachycardia, and sweating

Also associated with paroxysmal HTN

31
Q

When should you suspect pheochromocytoma?

A
  • Paroxysmal “attacks”
  • Refractory HTN or onset < 20 years old
  • Abdominal mass
  • Family hx
  • Incidentally discovered adrenal mass
32
Q

What three tests are important to obtain in the initial workup for pheochromocytoma?

A
  • Plasma metanephrines
  • 24-hour urine catecholamines, metanephrines, VMA
  • Clonidine Suppression Test
33
Q

Once biochemical diagnosis of pheochromocytoma is made, what should the next step be and why?

A

CT scan of the abdomen without contrast as the majority of pheochromocytoma cases are due to a tumor of the adrenal medulla

34
Q

What is the management for pheochromocytoma?

A
  • “Chemical Sympathectomy” to stabilize patient until surgical excision
  • Alpha-blocker (phenoxybenzamine) and beta blocker (propranolol)
  • Surgery is definite
35
Q

What is an adrenal mass lesion that is greater than 1 cm in diameter, discovered by radiologic examination?

A

Adrenal Incidentaloma

36
Q

What is the diagnostic workup of Adrenal Incidentaloma?

A
  • Rule out pheochromocytoma and subclinical Cushing’s Syndrome in all patients
  • Rule out primary hyperaldosteronism if HTN
  • Do not biopsy if known primary malignancy elsewhere or biochemical evidence of pheo
37
Q

What is the management for Adrenal Incidentaloma if the workup is negative and likely benign and < 2 cm?

A

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

38
Q

What is the management for Adrenal Incidentaloma if the workup is negative and likely benign and > 2 cm?

A

Consider surgical resection

39
Q

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

What disorder is an abnormal results associated with?

A

Cortisol ELEVATED after administration of dexamethasone 9 hours earlier.

Cushing’s Syndrome (non-suppressible cortisol production from ACTH-independent etiology)

40
Q

What is an abnormal result in the Cosyntropin Stimulation test?

What disorder is an abnormal results associated with?

A

Cortisol DOES NOT increase after administration of ACTH.

Addison’s Disease

41
Q

What is an abnormal result in the clonidine suppresion test?

What disorder is an abnormal results associated with?

A

Catecholamine production is NOT reduced after administration of clonidine.

Pheochromocytoma

Clinical Med II (17 decks)

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