15.10 Adrenal Cortex Flashcards

1
Q

adrenal cortex is composed of what three layers?

A

glomerulosa, fasciciulata, reticularis

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2
Q

glomerulosa produces

A

mineralcorticoids (e.g., aldo)

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3
Q

fasiculata produces

A

glucocorticoids (e.g., cortisol)

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4
Q

reticularis produces

A

sex steroids (e.g., testosterone)

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5
Q

What is Cushing syndrome?

A

Excess cortisol (hypercotisolism)

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6
Q

why does Cushing cause muscle weakness with thin extremities?

A

cortisol breaks down muscle producing amino acids for gluconeogenesis

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7
Q

why does cushion cause moon facies + buffalo hump + truncal obesity?

A

cortisol –> high glucose –> high insulin –> increased storage of fat

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8
Q

why does cushing cause HTN?

A

cortisol upregulates alpha1 recepots on arterioles

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9
Q

why does cushing cause osteoporosis?

A

inhibits osteoblasts, GI ca2+ abs, sex steroids;

increases bone resorption & urine ca2+ loss

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10
Q

why does cushing cause immunosuppression?

A

cortisol inhibits PLA2, IL2, and hist release from mast cells

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11
Q

why does cushing cause abdominal striae

A

impaired synthesis of collagen with thinning of skin

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12
Q

6 clinical manifestations of cushing

A
  1. muscle weakness w/ thin extremities
  2. moon facies, buffalo hump, truncal obesity
  3. abdominal striae
  4. HTN
  5. osteoporosis
  6. immunosuppression
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13
Q

how to diagnose cushing

A

24-hr urine cortisol levels

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14
Q

4 causes of cushing

A
  1. exogenous corticosteroids
  2. primary adrenal adenoma, hyperplasia or CA
  3. ACTH-secreting pituitary adenoma
  4. paraneoplastic ACTH secretion (small cell)
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15
Q

exogenous corticosteroids –>

A

bilateral adrenal atrophy bc steroids suppress ACTH secretion (negative feedback)

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16
Q

primary adrenal adenoma, hyperplasia, or carcinoma

A

unilateral adrenal atrophy (of the uninvolved gland)

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17
Q

ACTH-secreting pituitary adenoma

A

bilateral adrenal hyperplasia

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18
Q

what could you use to distinguish ACTH secreting pituitary adenoma and paraneoplastic ACTH secretion? (NB: both would result in bilateral hyperplasia)

A

High-dose dexamethasone

19
Q

high-dose dexamethasone effect on ACTH production by a pituitary adenoma?

A

DECREASES it (so decreases cortisol)

20
Q

high-dose dexamethasone effect on ectopic ATCH production by a small cell lung carcinoma?

A

NO EFFECT (so cortisol stays high)

21
Q

what is conn syndrome?

A

hyperaldosteronism - excess aldosterone

22
Q

conn syndrome presentation

A

HTN due to sodium retention (maybe - aldo escape with ANP?), hypokalemia, metabolic alkalosis

23
Q

effect of increased aldo

A

increased sodium reabsorption and K+ secretion by principal cells and increased H+ secretion by alpha-intercalated cells

24
Q

most common cause of primary hyperaldosteronism

A

sporadic adrenal hyperplasia (adrenal adenoma and carcinoma are less common)

25
Q

hormone levels in primary hyperaldosteronism

A
high aldo
low renin (high BP down regulates via negative feedback)
26
Q

seen with activation of the RAS system (e.g. by renovascular hypertension or CHF)

A

secondary hyperaldosteronism

27
Q

hormone levels in secondary hyperaldosteronism

A

high aldo

high renin

28
Q

excess sex steroids with hyperplasia of both adrenal glands

A

congenital adrenal hyperplasia

29
Q

most common cause of congenital adrenal hyperplasia

A

21-hydroxylase deficiency

30
Q

21-hydroxylase is required for the production of what?

A

aldosterone and corticosteroids

31
Q

21-hydroxylase deficiency causes steroidogensis to be shunted towards

A

sex steroid prodcution

32
Q

cortisol levels in 21 hydroxylase deficiency

A

low cortisol –> increased ACTH secretion (loss of negative feedback) –> bilateral adrenal hyperplasia

33
Q

electrolytes and volume status in congenital adrenal hyperplasia

A

hyponatremia,
hyperkalemia,
hypovolemia

34
Q

lack of cortisol in 21 hydroxylase deficiency presents how?

A

life-threatening hypotension

35
Q

congenital adrenal hyperplasia clinical presentation

A

clitoral enlargement in females or precocious puberty in males due to excess androgens

36
Q

how would you treat congenital adrenal hyperplasia?

A

cortisol to suppress ACTH

37
Q

lack of adrenal hormones is called

A

adrenal insufficiency

38
Q

characterized by hemorrhagic necrosis of the adrenal glands, classically due to DIC in young children with N meningitis infection; lack of cortisol exacerbates hypotension, often leading to death

A

Waterhouse-Friderichsen syndrome

39
Q

chronic adrenal insufficiency due to progressive destruction of the adrenal glands

A

Addison’s dz

40
Q

causes of addison disease

A
  1. AI (west)
  2. TB (developed)
  3. lung cancer, which loves to metastasize to the adrenals
41
Q

electrolyte and volume abnormalities in addison

A

hyponatremia, hyperkalemia

hypovolemia, hypotension

42
Q

why do you seen hyperpigmentation in addison?

A

increased ACTH by productions stimulate melanocytic production of pigment

43
Q

clinical symptoms of addison

A

hyponatremia + hyperkalemia
hypotension + hypovolemia
hyperpigmentation
weakness, vomiting, diarrhea