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Endocrinology > Adrenals > Flashcards

Adrenals Flashcards

1
Q

Starting from the outside, what are the layers of the adrenal gland?

A

capsule, zona glomerulosa, zona fasciculata, zona reticulata, medulla

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2
Q

What area of the adrenal gland is NOT under control of ACTH?

A
  • Zona Glomerulosa: Mineralicorticoids (Ex: Aldosterone)

- under Angiotensin II control ([K+])

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3
Q

What are the Adrenal products secreted via ACTH stimulation?

A

Zona Fasciculata: Glucocorticoids (Cortisol)

Zona Reticulata: Adrogens (DHEA androstenedione)

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4
Q

What are the products of the Zona Reticulata?

A

Androgens (DHEA, androstenedione)

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5
Q

What is the only steroid hormone that is not protein-bound in the blood?

A

DHEA (it is sulfated)

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6
Q

Cyp450scc (CypIIa; aka Desmolase) is an enzyme that does what?

A

Converts Cholesterol into Pregnenolone

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7
Q

All of the Congenital Adrenal Hyperplasias exhibit what 2 signs?

A

Lo cortisol, thus Hi ACTH (which grows the adrenal)

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8
Q

Having a congenital 17a-hydroxylase (cyp17) deficiency will effectively ‘turn off’ what areas?

A
  • turn off the zona fasciculata, reticularis

- turn of the Gonads too! (testes/ovaries)

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9
Q

Having a congenital 21-hydroxylase deficiency will effectively ‘turn-off’ what areas?

A

-turn off zona glomerulosa and zona fasciculata

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10
Q

Having a congenital 11B-hydroxylase deficiency will effectively ‘turn off’ what areas?

A

-turn off zona glomerulosa and zona fasciculata

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11
Q

Primary Adrenal Insufficiency involves what gland and messenger?

A
  • Crappy cortex

- lo cortisol leads to hi POMC/ACTH

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12
Q

What are 4 causes of Primary Adrenal Insufficiency in order of occurrence?

A 
#1: autoimmune adrenalitis
#2: Infectious adrenalitis (TB, fungal, HIV related, lung mets)
#3: Adrenal hemorrhage (post-meningococcal)
#4: Adrenomyeloneuropathy (X linked, men)
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13
Q

What are some common signs and symptoms of PAI/Addison disease?

A
  • weakness, fatigue, anorexia/wt loss

- hypoNa, hyperK, acidosis, hyperpigmentation

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14
Q

Cushing’s syndrome is an excess of what?

A

cortisol

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15
Q

Describe a typical patient with Cushing’s

A
  • Fat (buffalo hump, moon face, truncal obesity)
  • Weak (atrophied mm, lo immune, osteoporosis)
  • Hypertensive
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16
Q

Why are Cushing’s pts fat?

A
  • cortisol will increase BLOOD GLUCOSE

- this leads to hi insulin, which increases adipose uptake

17
Q

Why are Cushing’s pts weak?

A
  • cortisol encourages protein catabolism (muscles, bones, joints)
  • inhibits Phospholipase A2, IL-2, and histamine
18
Q

Why are Cushing’s pts hypertensive?

A
  • cortisol has a permissive effect on catecholamines

- excess cortisol=excess alpha1 receptors

19
Q

Describe the top 4 causes of Cushing’s syndrome.

A
  • exogenous corticosteroids
  • primary adrenal adenoma
  • secondary ACTH pituitary adenoma
  • paraneoplastic ACTH (Ex: small cell lung carcinoma)
20
Q

What two tests are run if hi cortisol is expected?

A
  • lo dose dexamethasone (should suppress cortisol; tells if have hi cortisol)
  • hi dose dexamethasone (tells us where its from)
21
Q

Hyperaldosteronism classically presents with what 2 signs?

A

-hypokalemia, metabolic alkalosis, HTN

22
Q

Describe primary and secondary causes for hyperaldosteronism.

A
  • Primary: most often adrenal adenoma (Conn’s)

- Secondary: overactivation of RAA system (ex: renal artery stenosis/fibromuscular dysplasia)

23
Q

What is the clinical difference between 11B-hydroxylase and 21-hydroxylase deficiencies?

A
  • 11B-OH: less aldosterone deficiency signs (allows for production of 11-DOC, which is a mild version of aldosterone)
  • 21-OH: will show aldosterone and cortisol deficiency signs
24
Q

Describe the connection between Meningococcal infection and adrenals.

A

Waterhouse-Friedrichsen syndrome

  • Neisseria meningitidis infection
  • presents with DIC
  • then bilateral adrenal necrosis/insufficiency
  • result: lo cortisol and big hypotension
25
Q

What area of cancer loves to metastasize to the adrenals?

A

Lung cancers

26
Q

Pheochromocytomas present with what triad?

A

headache, diaphoresis, palpitations

27
Q

Describe the treatment of a pheochromocytoma.

A
  • first: Give phenoxybenzamine (irreversible alpha blocker)

- second: excise the adrenal gland

28
Q

What ectopic area classically presents with a pheochromocytoma?

A

Bladder wall (episodic HTN when you piss)

29
Q

Name 3 big pathological associations of pheochromocytoma.

A
  • MEN 2A and 2B
  • VHL disease (cerebellum+renal cell CA)
  • NF1
30
Q

Secondary adrenal insufficiency is characterized by what key physiologic difference?

A

A decrease in ACTH from anterior pituitary

31
Q

How does SAI differ from PAI/Addison’s in presentation?

A
  • NO hyperpigmentation

- NO hypoNa and hyperK

32
Q

Describe the function of the cortisol-cortisone shunt.

A
  • @hi levels, cortisol can hit mineralicorticoid receptors too.
  • Kidneys have 11B-HSD2; converts cortisol to cortisone
  • Liver has 11B-HSD1; converts cortisone back into cortisol
33
Q

AME (apparent mineralicorticoid excess) syndrome is what?

A
  • 11B-HSD2 deficiency
  • symptoms identical to hyperaldosteronism
  • can be induced by licorice

Endocrinology (7 decks)

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