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GI Block > Endo: Adrenal Disorders 1 > Flashcards

Endo: Adrenal Disorders 1 Flashcards

1
Q

What controls secretion of the different adrenal hormones?

A
  • Aldosterone secretion is regulated by angiotensin II
  • Cortisol and androgen secretion is regulated by ACTH
  • Norepi/epi are released in response to sympathetic stimulation
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2
Q

Describe the HPA axis, including negative feedback

A
  1. Hypothalamus releases CRH
  2. CRH stimulates the anterior pituitary to release ACTH
  3. ACTH stimulates adrenal gland to release cortisol and androgen

*Cortisol provides negative feedback onto hypothalamus and anterior pituitary

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3
Q

Name 2 stimulants for release of CRH from hypothalamus

A

Circadian rhythms

Stress

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4
Q

Where is the problem in primary and secondary adrenal insufficiency?

A
  • Primary: problem is in adrenal cortex
  • Secondary: problem is in pituitary or hypothalamus
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5
Q

Compare the levels of cortisol and aldosterone in primary and secondary adrenal insufficiency

A
  • Primary adrenal insufficiency: low cortisol and low aldosterone
  • Secondary adrenal insufficiency: low cortisol, normal aldosterone (ACTH is deficient but RAAS intact)
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6
Q

What is one infectious cause of primary adrenal insufficiency?

A

Tuberculosis

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7
Q

What is the most common cause of adrenal insufficiency?

A

Withdrawal of chronic glucocoticoids (secondary adrenal insufficiency)

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8
Q

Name 4 signs/labs unique to primary adrenal insufficiency

A
  • Salt craving
  • Vitiligo
  • Hyperpigmentation
  • Hyperkalemia
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9
Q

Name 3 electrolyte changes and one CBC change in adrenal insufficiency

A
  • Hyperkalemia (primary only)
  • Hyponatremia (primary only)
  • Hypoglycemia
  • Eosinophilia
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10
Q

What is the treatment for adrenal crisis?

A

IV Hydrocortisone

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11
Q

Why do patients with primary adrenl insuffiency have hyperkalemia and hyponatremia?

A

Lack of aldosterone (which normally stimulates kidneys to retain Na and secrete K)

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12
Q

Why do patients with primary adrenal insuffiency have hyperpigmentation

A

Increased synthesis of ACTH also produces excess Melanocyte Stimulating Hormone (POMC broken down into ACTH and MSH)

Primary has Pigmentation

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13
Q

What morning cortisol level is normal?

What diagnoses adrenal insufficiency?

A

Normal = 16-18

Adrenal Insufficiency = less than 5

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14
Q

Describe dynamic testing for adrenal insufficiency:

When is it used?

How does it work?

What question does it answer?

A
  • Perform this test when morning cortisol is less than normal (16-18)
  • Give synthetic ACTH (cosyntropin) and evaluate subsequent cortisol levels
  • Cortisol under 20 indicates primary adrenal insufficiency or chronic secondary adrenal insuff
  • This test answers: can your adrenals produce cortisol when stimulated?
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15
Q

Primary adrenal insufficiency

  • Baseline serum cortisol will be
  • Stimulated serum cortisol will be
  • Plasma ACTH will be
A

Primary adrenal insufficiency

  • Baseline serum cortisol will be less than 5
  • Stimulated serum cortisol will be less than 20
  • Plasma ACTH will be over 100
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16
Q

Secondary adrenal insufficiency

  • Baseline serum cortisol will be
  • Stimulated serum cortisol will be
  • Plasma ACTH will be
A

Secondary adrenal insufficiency

  • Baseline serum cortisol will be less than 5
  • Stimulated serum cortisol will be less than 20
  • Plasma ACTH will be low or normal
17
Q

Compare the treatment of primary and secondary adrenal insufficiency

A
  • Primary: give glucocorticoids and mineralocorticoids
  • Secondary: give glucocorticoids only
18
Q

What cells secrete renin?

What are 2 stimulators for renin release?

A
  • Juxtaglomerular cells of kidney release renin
  • In response to
    • low renal perfusion
    • low sodium concentration in the distal tubule
19
Q

Describe the RAAS (5 steps)

A
  1. Renin released by JGA cells in response to decreased perfusion
  2. Renin cleaves Angiotensinogen (made in liver) into Angiotensin I
  3. Angiotensin I is cleaved into Angiotensin II by ACE in the lungs
  4. Angiotensin II stimulates aldosterone synthesis in adrenals
  5. Aldosterone causes Na reabsorption and K excretion in collecting duct principal cells
20
Q

Name 3 causes of primary hyperaldosteronism

Which is most common

A
  • Aldosterone-producing adenoma
    • most common
  • Bilateral adrenal hyperplasia
  • Glucocorticoid remediable hyperaldosteronism
21
Q

Describe the mechanism of glucocorticoid-remediable hyperaldosteronism.

What is the treatment?

A
  • Aldosterone synthase gene gets translocated next to 11beta hydroxylase
    • This causes aldosterone synthesis to be stimulated by ACTH
  • Tx: Glucocorticoids to shut down ACTH
22
Q

Name 4 labs indicative of hyperaldosteronism

A
  • Resistant hypertension
  • Hypokalemia
  • Hypernatremia
  • Metabolic alkalosis
23
Q

Describe 2 tests for primary hyperaldosteronism

A
  • Morning aldosterone/renin ratio greater than 20
  • Suppression test
    • Salt ingestion or give normal saline
    • Aldosterone should get suppressed below 5
    • Over 5 indicates primary hyperaldosteronism
24
Q

Why do we perform adrenal vein sampling in people with hyperaldosteronism over age 35?

A
  • Many older people have adrenal incidentalomas, so need to confirm that the mass seen on imaging is actually producing aldosterone (it may be unrelated)
25
Q

Treatment for primary hyperaldosteronism (2)

A
  • If unilateral adrenal adenoma -> surgery
  • If bilateral adrenal hyperplasia -> spironolactone
26
Q

Supraclaicular fat pad and purple striae indicate ________________

A

Supraclaicular fat pad and purple striae indicate Cushing’s syndrome (excess cortisol)

27
Q

Compare ACTH and cortisol levels in ACTH-secreting adenoma and ectopic ACTH tumor

A
  • ACTH-secreting adenoma
    • High ACTH, High Cortisol
  • Ectopic ACTH production
    • VERY high ACTH and cortisol
28
Q
A

High cortisol

Low ACTH (feedback mechanism is intact)

29
Q

Describe 3 tests that evaluate: does my patient have Cushing’s syndrome?

Which measure free v total cortisol?

A
  • 24 hr urinary free cortisol
  • Midnight salivary free cortisol
  • 1 mg DXM suppression test
    • measures total cortisol
30
Q

Describe the use of interior petrosal sinus sampling

A

Inferior petrosal sinus sampling of ACTH levels distinguish ectopic v pituitary sources of excess ACTH

  • Pituitary sources: ACTH will be higher in petrosal sinus than IVC
  • Ectopic soures: ACTH will be equal in petrosal sinuses and IVC
31
Q

What does the ACTH level tell us about the source hypercortisolemia?

A

High ACTH indicates that problem is not in adrenal gland

Low ACTH indicates that problem is the adrenal gland itself

32
Q

What is the use of an 8 mg DXM suppression test?

A

Distinguishes between hypercortisolemia due to pituitary adenoma and ectopic tissue (both secreting ACTH)

  • Pituitary ACTH-secreting adenoma will suppress by 50%
  • Ectopic ACTH source will not suppress at all
33
Q

What is first line tx of hypercortisolemia?

What is second line tx of hypercortisolemia? (4)

A
  • 1st line: Surgery
  • 2nd line: medical (cabergoline, octreotide, ketoconazole, mitotane)

GI Block (77 decks)

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