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FHB Exam 4: Endocrinology and Reproduction > Endocrine VII & VIII: HPA Axis & Adrenals > Flashcards

Endocrine VII & VIII: HPA Axis & Adrenals Flashcards

1
Q

What are functions that are NOT regulated by the HPA axis?

A

maintenance of water, sodium, potassium, and blood pressure (mineralocorticoids - aldosterone)

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2
Q

What does CRH regulate?

A

it is a central regulator of the HPA axis and stimulates the anterior pituitary (POMC and ACTH)

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3
Q

How are AVP and CRH synergistic?

A

ACTH release is amplified in the presence of AVP as opposed to CRH alone.

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4
Q

To which receptor does CRH bind to with the highest affinity?

A

CRH R1 in the anterior pituitary (CRH R2 binds w/ higher affinity to urocortin)

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5
Q

What is the precursor of ACTH?

A

POMC (CRH stimulates POMC gene expresion)

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6
Q

ACTH binds with high affinity to _______ and low affinity to _________.

A

MC2R (in adrenal cortex); MC1R (in skin)

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7
Q

Where do the adrenal cortex and medulla come from embryologically?

A
  • cortex from mesoderm

- medulla from neural crest

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8
Q

What do the adrenal cortex and adrenal medulla synthesize?

A
  • cortex synthesizes steroid hormones

- medulla synthesizes catecholamines

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9
Q

What are the 3 layers of the adrenal cortex, and what are they associated with producing?

A
  • zona glomerulosa (mineralocorticoids)
  • zona fasciculata (glucocorticoids - cortisol)
  • zona reticularis (weak androgens - DHEAS)
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10
Q

What is responsible for carrying glucocorticoids through the blood?

A

Corticosteroid Binding Globulin (CBG) - 90% of circulating cortisol is bound to it

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11
Q

How does estrogen affect CBG?

A

It increases CBG, resulting in less free cortisol. (on the other hand, shock and severe infection decrease CBG)

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12
Q

Does CBG have a higher binding affinity for cortisol or aldosterone?

A

cortisol (30-fold higher)

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13
Q

Which enzyme is important for increasing local cortisol concentrations?

A

11β-HSD1

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14
Q

Which receptor is ubiquitously expressed in most tissues, and what does this mean?

A

Glucocorticoid receptor, which means that almost all cells/tissues are targets for cortisol.

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15
Q

Is cortisol anabolic or catabolic? What is it in direct contrast to?

A

It is catabolic, and it is a potent counter-regulatory hormone to insulin.

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16
Q

What are the two types of adrenal insufficiency?

A

1) Primary - failure at adrenal (Addison’s Disease)

2) Secondary - failure to secrete CRH or ACTH (most common cause=sudden cessation of glucocorticoid therapy)

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17
Q

What is the most potent synthetic glucocorticoid analog?

A

dexamethasone (20x more potent than cortisol)

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18
Q

What is the difference between Cushing disease and Cushing syndrome?

A

Cushing disease is excessive cortisol secretion due to pituitary adenoma; Cushing syndrome is everything else (exact same presentation but NOT caused by a tumor)

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19
Q

What are the 3 enzymes that cortisol stimulates?

A

glucose-6-phosphatase, PEP carboxykinase, and tyrosine aminotransferase

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20
Q

Does cortisol promote or inhibit inflammation?

A

inhibits inflammation

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21
Q

What are the 2 means by which cortisol inhibits inflammation?

A

1) Increasing IkB transcription, which keeps NF-kB out of the nucleus
2) GR binding to NF-kB and preventing it from translocating into the nucleus

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22
Q

How does cortisol affect bone?

A

It inhibits intestinal calcium absorption and inhibits bone formation by decreasing IGF-I receptors. It also increases bone resorption by activating osteoclasts

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23
Q

How does cortisol affect the cardiovascular system?

A
  • stimulates RBC production
  • maintains responsiveness to catecholamine pressor effects (makes adrenergic receptors more sensitive to catecholamines)
  • maintains vascular integrity and reactivity
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24
Q

How does cortisol affect the CNS?

A
  • modulates emotional response (depression, anxiety, nervousness, panic, aggression)
  • impacts perception
  • potent negative feedback effect on CRH and ACTH release
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25
Q

When is glucocorticoid used during medical emergencies, and are there long-term side effects?

A

A high acute dose can be used to treat septic shock, severe asthma, and flare-ups of severe autoimmune diseases. There are typically no long-term side effects.

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26
Q

In which tissues is mineralocorticoid receptor (MR) expression high?

A

DT of kidney, colon, salivary ducts, sweat ducts

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27
Q

What is the main target of aldosterone?

A

kidneys! (stimulates Na+ and water reabsorption in the kidney and increases K+ secretion)

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28
Q

What stimulates RAAS?

A

decreased blood pressure stimulates renin release from the JGA of the kidney, which stimulates RAAS

29
Q

What are pheochromocytomas?

A

the “10% tumors” originating from chromaffin cells; result in catecholamine overproduction

30
Q

What are some of the extra-adrenal sites of pheochromocytomas?

A

-sympathetic nerve chain along spinal cord
-overlying the distal aorta
-within ureter
-within urinary bladder
(90% are in the adrenal glands, though)

31
Q

What is the difference between aldosterone and AVP in terms of osmoreglulation?

A
  • Aldosterone: primary regulator of EC volume, stimulates Na+ and water reabsorption in kidney, leading to incr. ECF volume and BP (target=sodium)
  • AVP: primary regulator of free water balance, stimulates distal nephron water permeability, leading to incr. water retention and decr. plasma osmolality (target=water)
32
Q

What happens to cortisol in the kidney?

A

it is normally converted to inactive cortisone by 11β-HSD2 (ensures that MR is not over-stimulated by both aldosterone AND cortisol)

33
Q

What is an inhibitor of 11β-HSD2?

A

certain drugs, like carbenoxolone, which will result in excess MR activation; licorice can also inhibit this enzyme and cause increased sodium and water retention

34
Q

What is the main function of the zona reticularis?

A

produces weak androgens, like DHEA-S

35
Q

What is the importance of the DHEAS metabolite, androstendione?

A

it is a precursor for the more potent androgen, testosterone, and for estrogens

36
Q

About 50% of total androgen precursors in adult male ________ come from _______.

A

prostate; adrenal cortex

37
Q

What is the primary source of androgens and estrogens in post-menopausal women?

A

zona reticularis of adrenal cortex

38
Q

What is the first step in conversion of cholesterol to hormones in all zones of the adrenal cortex?

A

cholesterol –> pregnenolone via CYP11A1 (aka, desmolase)

39
Q

Which enzyme converts pregnenolone (P5) to progesterone?

A

3β-HSD

40
Q

Where is 17α-hydroxylase made?

A

in the zona fasciculata and zona reticularis

41
Q

Which enzyme converts progesterone to 17(OH) progesterone?

A

17α-hydroxylase

42
Q

Which enzyme converts 17(OH) progesterone to 11-deoxycortisol?

A

21α-hydroxylase

43
Q

Which enzyme converts 11-deoxycortisol to cortisol?

A

11α-hydroxylase

44
Q

CAH is due to a deficiency in which enzyme?

A

21α-hydroxylase, resulting in excess DHEA, no mineralocorticoids, and no glucocorticoids

45
Q

What are some of the clinical indications of CAH?

A

virilization (masculinization), ambiguous genitalia at birth, sodium loss

46
Q

What are the top 2 most common causes of CAH?

A 
#1: 21α-hydroxylase deficiency 
#2: 11α-hydroxylase deficiency
47
Q

What are the 3 main targets of epinephrine?

A

muscle, liver, fat

48
Q

Which receptors does epi work through?

A

adrenergic receptors (both alpha and beta)

49
Q

What can be used clinically to detect tumors producing epi or norepi?

A

urinary VMA (vanillylmandelic acid), as it is a breakdown product of epi and norepi

50
Q

What are some of the enzymes that mediate catecholamine clearance?

A

COMT and MAO

51
Q

10% of pheochromocytomas are:

A
  • malignant
  • bilateral
  • in children
  • familial
  • recur
  • associated with MEN syndromes
  • present with a stroke
  • extra-adrenal
52
Q

Epinephrine directly inhibits _______.

A

insulin (this is because we want mobilization of glucose stores under stress; not storage)

53
Q

What are the key players of the HPA axis?

A
  • Hypothalamus: CRH
  • Pituitary: ACTH
  • Adrenal: Cortisol
54
Q

Where is corticotropin-releasing hormone made?

A

PVN of hypothalamus

55
Q

Is CRH pulsatile?

A

Yes! It results in episodic release of ACTH.

56
Q

What does cortisol bind to?

A

glucocorticoid receptors (GR) on target cells (almost EVERY cell in the body is a target for cortisol!)

57
Q

What are steroidogenic cells characterized by histologically?

A

large lipid droplets

58
Q

How does ACTH affect cholesterol in the body?

A

It is involved with steroid biosynthesis by stimulating conversion of cholesterol to pregnenolone.

59
Q

What is the major second messenger activated when ACTH binds to MC2R receptor?

A

cAMP, which induces immediate, subsequent, and long-term effects

60
Q

How does cortisol affect muscle?

A

It increases transcription of the E3 ubiquitin ligases, MuRF-1, stimulating proteolysis. It simultaneously inhibits amino acid uptake and AkT phosphorylation, resulting in decreased protein synthesis.

61
Q

How does glucocorticoid deficiency affect BP?

A

results in hypotension, as cortisol helps to maintain vascular integrity and reactivity

62
Q

How does prolonged glucocorticoid therapy affect the HPA axis?

A

It shuts it down. High levels of cortisol exert negative feedback on CRH and ACTH. Prolonged shut-down of HPA axis leads to atrophy of zona fasciculata and inability to synthesize endogenous glucocorticoids.

63
Q

What synthetic glucocorticoid has the most potent mineralocorticoid effect?

A

fludrocortisone (125x more potent than cortisol)

64
Q

What synthetic glucocorticoid has NO mineralocorticoid effect?

A

dexamethasone

65
Q

What is the primary and secondary effect of mineralocorticoids?

A
  • primary: Na+ retention by kidney

- secondary: water retention

66
Q

What is 11-deoxycortisone?

A

a precursor of aldosterone that also has mineralocorticoid action

67
Q

What are the functions of angiotensin II?

A

It is a vasoconstrictor and stimulates aldosterone.

68
Q

What makes a weak androgen “weak”?

A

low binding affinity for androgen receptors (AR)

69
Q

Which enzyme does the drug carbenoxolone (along w/ licorice) inhibit?

A

11β-HSD2 (so, both result in excess MR activation leading to incr. Na+ and water retention)

FHB Exam 4: Endocrinology and Reproduction (14 decks)

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