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Endocrine Week 2 > Adrenal Physiology > Flashcards

Adrenal Physiology Flashcards

1
Q

Where are the adrenal glands located?

A

in the retroperitoneal cavity above each kidney. These glands receive the most blood flow per unit weight of any organ

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2
Q

Where does the adrenal medulla derive from?

A

neuroectodermal tissue

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3
Q

Where does the adrenal cortex derive from?

A

mesoderm

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4
Q

When does the adrenal cortex differentiate in gestation?

A

week 8. However, this is a fetal adrenal cortex and soon after birth it involutes, and is replaced by the three-layered adult adrenal cortex

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5
Q

What hormones does the adrenal cortex secrete?

A

glucocorticoids, mineralcorticoids, and androgens

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6
Q

What hormones do the zone reticularis and fasciculata secrete? zona glomerulosa?

A

glucocorticoids (cortisol and corticosterone) and adrenal androgens (DHEA, and DHEA sulfate). NOTE: the zone reticularis develops postnatally (by 3 yo)

The zona glomerulosa secretes mineralcorticoids (aldosterone) and has abundant smooth ER

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7
Q

What is the blood supply to the adrenal gland?

A

Each gland is supplied by the superior, middle and inferior suprarenal arteries, which arise from the inferior phrenic artery, abdominal aorta and renal artery respectively. The blood reaches the outer surface of the gland before entering and supplying each layer. When the blood reaches the adrenal’s center, it flows into the medullary vein. The medullary veins emerge from the hilum of each gland before forming the suprarenal veins, which join the inferior vena cava on the right side and the left renal vein on the left.

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8
Q

Describe the portal system of the adrenal glands

A

Blood enters the cortex via the capsular artery and enters a capillary system in the Z.G., which drains to the corticol sinusoid in the Z.F., the venous capillary plexus in the Z.R. while a concurrently corticol arteriolr branches from the capsular artery and drains to the medullary arteriole. The medullary arteriole then joins the venous capillary plexus near the medulla and drains to the medullary vein

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9
Q
A
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10
Q

How are the adrenal cortex hormones made?

A

all from cholesterol delivered via blood or made de novo which then use layer-specific enzymes to produce specific hormones

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11
Q

What is the first step in adrenal cortex hormone synthesis?

A

conversion of cholesterol to pregnenolone using cytochrome P450 side-chain cleavage via cholesterol desmolase (requires adrenodoxin reductase, NADPH, and O2)

NOTE: ALL layers of the cortex contain cholesterol desmolase (stimulated by ACTH)

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12
Q

What two things can happen to pregnenolone?

A

3B-hydroxysteroid dehydrogenase can form progesterone OR

17a-hydroxylase can form 17-hydroxy-pregnenolone

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13
Q

What can happen to progesterone?

A

21-hydroylase can turn it to 11-deoxy-corticosterone OR

converted to 17-hydroxyl-progesterone via 17a-hydroxylase

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14
Q

How is 11-deoxy-corticosterone transformed to aldosterone?

A

via 11B hydroxylase first to corticosterone and then

via aldosterone synthase (via a corticosterone intermediate) to aldosterone

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15
Q

What can happen to 17-hydroxy-pregnenolone?

A

3B-hydroxysteroid dehydrogenase can convert it to 17-hydroxyprogesterone OR

DHEA can be form (no enzyme)

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16
Q

What can happen to 17-hydroxyl-progesterone?

A

21-hydroxylase can convert it to 11-deoxy-cortisol OR

non-enzymatic conversion to androsterone (which then makes androgens testosterone and estradiol) NOTE: in males, adrenal androgens are of little significance since the testes produce their own testosterone but they are important in females

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17
Q

How is 11-deoxy-cortisol converted to cortisol?

A

11B-hydroxylase

NOTE: Cortisol is not absolutely necessary to sustain life is corticosterone can be made (i.e. in an isolated 17a hydroxylase deficiency)

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18
Q

What drugs inhibit glucocorticoid synthesis?

A

Metyrapone (11B-hydroxylase) and ketoconazole (cholesterol desmolase and other)

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19
Q

What regulates the secretion of ACTH?

A

CRH from the paraventricular nuclei in the hypothalamus acts on corticotrophs of the anterior pituitary via Gs mechanisms

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20
Q

How is the zona glomerulosa controlled?

A

It requires ACTH to produce aldosterone, but otherwise is under control of the renin system

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21
Q

How is cortisol released? What pattern? When?

A

It is released in a pulsatile manner, averaging about 10 bursts/24 hr with the highest rates occurring just before awakening (e.g. 8 am) and the lowest around midnight

NOTE: androgens and ACTH are secreted in similar patterns

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22
Q

How does cortisol regulate ACTH and CRH?

A

Feedback on both

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23
Q

What are the immediate effects of ACTH on the adrenal cortex?

A

stimulates transfer of stored cholesterol to the mitochondria to activate cholesterol desmolase

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24
Q

The diurnal pattern that drives CRH secretion can be abolished by what?

A

coma, blindness, or constant exposure to either light or dark

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25
Q

What isa dexamethasone suppression test?

A

dexamethasone is a synthetic glucocorticoid that mimics cortisol actions including stimulating negative feedback on ACTH secretion. Thus, the response to a low dose of dexamethasone should be .

This can be used to test whether hypercorticolism is due to an ACTH-secreting tumor (will not see decreased ACTH and cortisol with low dose, but will with a higher dose)) or a cortisol-secreting tumor (will not see decreased ACTH and cortisol with low or high dose)

26
Q

What other things stimuate ACTH secretion?

A

decreased cortisol levels

stress, hypoglycemia, trauma

ADH or Serotonin

a-adrenergic agonists or B-adrenergic antagonists

27
Q

What other things inhibit ACTH secretion?

A

opiods and somatostatin

28
Q

When are aldosterone levels highest? Lowest?

A

Same as other adrenal cortex hormones in that it is diurnal, and highest right before awakening and lowest around midnight

29
Q

How is aldosterone regulated?

A

angio II increases the synthesis and secretion of aldosterone by stimulating cholesterol desmolase and aldosterone synthase via Gq protein binding to AT1 receptors in the zona glomerulosa.

This occurs in response to a decrease in ECF volume causing decreased renal perfusion

30
Q

What does aldosterone do?

A

stimulates Na+ reabsorption by the kidneys to help restore ECF Na+ content and ECF volume AND

reduces serum K+ and H+

31
Q

How else can aldosterone be stimulated to be released? Inhibited?

A

increased serum K+ depolarizes adrenal cells and opens Ca2+ channels causing aldosterone to release

Inhibited: ANP

32
Q

How do adrenal cortical steroids work on a mechanistic basis?

A

They are steroid hormones so they induce transcription and protein synthesis.

33
Q

What are the actions of glucocorticoids?

A
  • increase gluconeogenesis, proteolysis, and lipolysis
  • decrease glucose utilization and insulin sensitivity
  • inhibit inflammatory and immune response
  • enhance vascular responsiveness to cateholamines and maintains fluid volume/BP
  • inhibit bone formation
  • increase GFR
  • decrease REM sleep, modulates emotion
34
Q

How does cortisol promote a diabetogenic state?

A

It causes protein and fat catabolism, thereby providing additional AAs and glycerol to the liver for gluconeogenesis AND decreases glucose utilization and insulin sensitivity

Thus, an effect of hypocortisolism is hypoglycemia (Addison’s disease, etc.)

35
Q

How does cortisol interfere with inflammatory responses?

A

1) induces lipocortin, an inhibitor or phospholipase A2
2) inhibits production of Il-2 and thus T cell proliferation
3) inhibits histamine and serotonin release from mast cells and platelets

36
Q

How does cortisol upregulate responsiveness to catecholamines?

A

upregulating a1 receptors (stimulates vasoconstriction)

Thus, hypotension is a symptom of hypocortisolism

37
Q

How does cortisol increase GFR?

A

causes vasodilation of affarent arterioles

38
Q

How/where does aldosterone cause Na+ reabsorption and K+ secretion? H+ secretion?

A

Na+ reabsorption and K+ secretion- principal cells (PT) via increasing apical ENaC channels

H+ secretion- a-intercalated cells by increasing H+ ATPase apical proton pumps

Thus, symptoms of hypercortisolism are HTN, hypokalemia, and metabolic alkalosis

39
Q

The affinity of mineralcorticoid receptors for aldosterone is jsut as high for what?

A

cortisol.

40
Q

Why doesnt more cortisol bind to mineralcorticoid receptors than aldosterone considering similar receptor specificity and that circulating levels of aldosterone are much lower than cortisol?

A

renal cells require the presence of 11B-hydroxysteroid dehydrogenase (11B-HSD1), which converts cortisol to cortisterone, which has low affinity.

More cortisol is found in bound state than aldosterone and thus cant bind, and

Aldosterone dissociates from the mineralcorticoid receptor 5x slower than the glucocorticoids

41
Q

How is cortisol carried in blood?

A

cortisol binds to carrier proteins like CBG (cortisol binding globulin) and tetrahydrocortisol (90% bound, 10% free). The free form is the only available one for function

42
Q

What is the half-life of cortisol?

A

70-90min

43
Q

How is cortisol metabolized and eliminated?

A

mostly via conversion to cortisterone via 11B-HSD2 some in the liver and mostly in the kidneys which are released in urine as 17-hydroxycorticosteroids

NOTE: 11B-HSD1 converts cortisterone to cortisol and is found in the kidney and adipose

44
Q

How is aldosterone metabolized?

A

in the liver to tetrahydroglucuronide and excreted in urine (1% intact, 40% as tetraglucuronide)

45
Q

What is the half-life of aldosterone?

A

15-20 min (poor protein binding)

46
Q

Note about steroid receptors

A

They bind in the cytosol (thyroid is the only one that binds in the nucleus) and the response is SLOW

47
Q

What are the results of a 21-hydroxylase deficiency?

A

decreased cortisol AND aldosterone synthesis causing hypoglycemia, Na+ loss and

increased sex hormones leading to virilization

48
Q

What are the results of a 11B-hydroxylase deficiency?

A

excess mineralcorticoid activity via 11-deoxycorticosterone (not aldosterone!),

decreased cortisol production

increased androgens

49
Q

What are the results of a 11B-hydroxysteroid dehydrogenase type II deficiency?

A

decreased cortisol conversion to cortisterone leading to excess mineralcorticoid activity

Commonly due to licorice toxicity

50
Q
A
51
Q

What is the bulk of the secretions of the adrenal medulla?

A

epinephrine (80%) and nor (20%) (from a tyrosine precursor)

52
Q

What causes release of epi and nor granules?

A

increases in Ach cause a rise in intracellular Ca2+ in chromaffin cells

53
Q

What is the half-life of catecholamines?

A

2 min

54
Q

How are epi and nor eliminated?

A

They are acted on by MAO to form 3,4-dihydrophenylglycol or COMT to form metanephrine or norpmetanephrine, which are all then acted upon by the opposite enzymes (COMT or MAO) in the liver/kidney to form vanillylmandelic acid (VMA) which is eliminated in urine

55
Q

Which catecholamines bind to a-adrenergic receptors?

A

epi > nor> iso

56
Q

Which catecholamines bind to b-adrenergic receptors?

A

iso > nor >epi

57
Q

What are the effects of a-adrenergic binding?

A
  • vasoconstriction
  • piloerection
  • iris dilation
  • intestinal relaxation and sphincter contraction
  • bronchoconstriction
  • cardiac contractility
  • hepatic glucose production and decreased insulin release
58
Q

What are the effects of b-adrenergic binding?

A

vasodilation

cardioacceleration and increased myocardial strength (B1)

uterus relaxation

bronchodilation (B2)

glycogenolysis and lipolysis (B3)

increased glucagon and renin release

59
Q

Chronic exposure of adrenergic receptors to catecholamines results in what?

A

receptor downregulation and degradation

60
Q

Chronic exposure of adrenergic receptors to glucocorticoids and thyroid hormones results in what?

A

receptor upregulation

61
Q

What is a Metyrapone stimulation test?

A

Metyrapone inhibits 11B-hydroxylase which inhibits cortisol production. In a normal patient, giving Metyrapone should cause an acute reduction in serum cortisol, increased ACTH, and increased 11-deoxycortisol

If adrenally deficieny, you will see an acute reduction in serum cortisol, increased ACTH, but no change in 11-deoxycortisol

62
Q

What is a CRH stimulation test?

A

Differentiates between a pituitary source (i.e. Cushing disease) and an ectopic source of ACTH. In Cushing disease, CRH administration increases plasma ACTH and cortisol and in pts. with ectopic ACTH-producing tumors, you see no change in cortisol levels

Endocrine Week 2 (15 decks)

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