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Endocrine > Adrenal Physiology > Flashcards

Adrenal Physiology Flashcards

1
Q

True or false: the adrenal cortex and medulla are completely independent of one another

A

False–not completely, but mostly

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2
Q

What are the two major hormone types that are secreted by the adrenal glands?

A

Steroid hormones

Catecholamines

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3
Q

What are the steroid hormones that are secreted by the adrenal glands?

A

Glucocorticoids
Mineralocorticoids
Androgens

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4
Q

What are the catecholamines secreted by the adrenal glands?

A

Epi and NE

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5
Q

What part of the adrenal glands secretes aldosterone?

A

The zona glomerulosa

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6
Q

What controls the secretion of aldosterone?

A

Fluctuations in the extracellular levels of angiotensin II and K

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7
Q

What percent of the output of the adrenal cortex comes from the zona fasciculata and zona reticularis? What are the products of each of these areas?

A

75% and 10% respectively

Cortisol, corticosterone, and DHEA

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8
Q

Where are chromaffin cells located? What do they do? What regulates this?

A
  • Within the adrenal medulla
  • Synthesize and secrete epi and NE
  • ANS
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9
Q

When during the day are the highest cortisol levels?

A

In the morning, with a subsequent peak around 1300

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10
Q

What percent of glucocorticoid activity comes from cortisol?

A

95%

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11
Q

What is the signal for the release of CRH?

A

Diurnal patterns, stresses, and emotional stress

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12
Q

Where does CRH travel once released from the hypothalamus?

A

Down the hypophyseal portal venous plexus

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13
Q

What is the G protein that is activated once CRH reaches the pituitary? What does this cause?

A

Gs

Release of ACTH

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14
Q

What is ACTH a breakdown product of? What is the significance of this?

A

POMC

If ACTH levels are high, then melanocyte-stimulating hormone increases as well, which causes the hyperpigmentation of addison’s disease

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15
Q

What is the receptor that ACTH binds to? Where is this located, and what does this do?

A

MC2R

Surface of the adrenal cortex causing Gs activation, and cholesterol ester hydrolase

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16
Q

What are the enzymes that are activated in the adrenal cortex by ACTH binding? What do these do?

A

Cholesterol ester hydrolase–Elevates the availability of free cholesterol that feeds directly into the steroidogenesis pathways

StAR–increases cholesterol demolase

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17
Q

True or false: ACTH is released in a pulsatile fashion

A

True

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18
Q

How long does it take cortisol production to begin once ACTH binds?

A

15 minutes

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19
Q

How do glucocorticoids exert a negative feedback on the HPA axis?

A

Binding to the glucocorticoid receptor in the cytoplasm of both corticotroph cells in the pituitary and the CRH secreting cells of the hypothalamus

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20
Q

What are the intracellular events that occur when Glucocorticoid receptors are bound in the corticotrophs and hypothalamic CRH secreting cells? How fast is this, and what is the significance of this speed?

A

Translocate to the nucleus, where they modulate the expression of genes, and inhibit the synthesis of ACTH and CRH receptor

Slow, so does not account for the rapid feedback inhibition seen

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21
Q

What is the mechanism by which cortisol causes fast suppression of ACTH and CRH?

A

Unknown

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22
Q

When CRH binds to corticotrophs, is there a release of preformed ACTH, an increase in synthesis of ACTH, or both?

A

Both

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23
Q

ACTH causes hypertrophy of the adrenal glands. What is the significance of this?

A

Exogenous glucocorticoids will decrease size, whilst an ACTH secreting tumor will increase in size

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24
Q

Draw out the pathway

A

Pathway

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25
Q

What is the precursor molecule for all of the steroid hormones?

A

Cholesterol

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26
Q

What are the two source of cholesterol for steroid secreting cells?

A

LDL (80%)

De Novo synthesis (20%)

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27
Q

What is the first step in steroid synthesis from cholesterol?

A

Cholesterol desmolase (aka p450scc, or CYP11A1) cleaves cholesterol to pregnenolone

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28
Q

What is the protein that facilitates the transport of cholesterol into the mitochondria of steroid producing cells?

A

StAR protein

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29
Q

What is the rate limiting step of steroidogenesis?

A

Cholesterol cleavage to pregnenolone via cholesterol desmolase

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30
Q

Where in the cell does the conversion of pregnenolone to 17 hydroxypregnenolone take place?

A

sER

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31
Q

What is the enzyme that converts 17-OH pregnenolone into 17-OH progesterone?

A

3beta hydroxysteroid dehydrogenase

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32
Q

What is the order of enzymes from cholesterol to the end of each of the synthesis pathways of mineralocorticoids and glucocorticoids? (3)

A

3beta
21
11

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33
Q

What prevents the formation of cortisol and androgens in the zona glomerulosa?

A

The zona glomerulosa does not contain 17-hydroxylase

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34
Q

What is the enzyme that converts corticosterone into aldosterone?

A

Aldosterone synthase (18 hydroxylase/dehydrogenase)

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35
Q

What is the first step of synthesis of androgens, starting with pregnenolone?

A

17-alpha-hydroxylase converts it to 17 hydroxypregnenolone

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36
Q

What happens to 17 hydroxypregnenolone in the zona glomerulosa?

A

Converted to DHEA by 17-alpha hydroxylase, which is then converted to androstenedione by 17-alpha-hydroxylase 17,20 lyase

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37
Q

What is the majority of cortisol in the plasma found as?

A

Bound to cortisol binding globulin (aka transcortin)

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38
Q

What percent of cortisol is bound to cortisol binding globulin? Albumin? Free?

A 
CBP = 40-70%
Albumin = 20-50%
Free = 10%
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39
Q

Where is the glucocorticoid receptor located on target cells? What type of receptor is this?

A

Nuclear hormone receptor that is free in the cytoplasm in complex with chaperone proteins

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40
Q

What happens when cortisol binds its receptor?

A

binding
causes a conformational change in GRs that allows them to disassociate from the chaperone proteins
and translocate to the nucleus where they homodimerize and bind to promoters or the intragenic
regions of glucocorticoid target genes

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41
Q

The genomic effects of GRs can occur within what time frame?

A

hours

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42
Q

What are the four main categories of glucocorticoid effects?

A
  1. Metabolic
  2. Anti-inflammatory
  3. Immunosuppressive
  4. Vascular reactivity
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43
Q

Glucocorticoids (cortisol) can increase the rate of gluconeogenesis by 6 to 10-fold by doing what?

A 
Increasing the
expression of
gluconeogenic enzymes
in the liver and
liberating amino acids
by causing the
degradation of muscle
and preventing new
protein synthesis
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44
Q

What is the effect of cortisol in fat cells?

A

Induces lipolysis

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45
Q

What is the effect of cortisol on amino acid and glucose uptake on non-hepatic cells?

A

Reduces

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46
Q

The overall effect of cortisol’s reducing non hepatic uptake of glucose and amino acid, and inducing lipolysis is to do what?

A

Shunt all products to the liver to increase gluconeogenesis and thus BG levels

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47
Q

What is the effect of cortisol on liver glycogen synthesis? How?

A

Increases by increasing expression and activity of hepatic glycogen synthase

48
Q

What is the enzyme that converts testosterone into DHT? What drug inhibits this enzyme?

A

5-alpha-reductase

Finasteride

49
Q

What is the enzyme that converts testosterone into estrogen? What is the drug that inhibits this enzyme?

A

Aromatase

Anastrozole

50
Q

What is the main regulated step of glucocorticoid synthesis? What chemical regulates this?

A

p450scc

ACTH increases the expression of this enzyme

51
Q

What is the order of enzymes that converts cholesterol to cortisol?

A

17
3beta
21
11

52
Q

How does cortisol get into the cell?

A

It’s lipophilic, therefore it passes through the lipid bilayer

53
Q

What particular part of the 17-alpha-hydroxylase enzyme converts 17 OH-pregnenolone into DHEA/androstenedione?

A

17-20 lyase

54
Q

What percent of testosterone comes from the adrenal glands in males?

A

Less than 5%

55
Q

What is the role of the adrenal androgens?

A

Maintaining normal axillary and pubic hair, as well as some metabolic actions

56
Q

When in a woman’s life are the androgens produced by the adrenal cortex particularly important?

A

Post menopausal

57
Q

What type of G protein is the melanocortin-2-receptor?

58
Q

What are the two ways in which ACTH increases the production of adrenal products?

A

Increases the expression/activity of:

  • p450ss
  • StAR protein
59
Q

What is the effect of cortisol on bones?

A

Increases resorption

60
Q

How does cortisol decrease inflammation/the immune response? (3)

A

-decreasing the synthesis and
release of a precursor to prostaglandins and leukotrienes
-decreasing the permeability of capillaries
-decreasing the production of platelet activating factor and nitric oxide

61
Q

How does cortisol regulate BP?

A

maintaining responsiveness of vascular smooth muscle to the

catecholamines by increasing alpha receptor

62
Q

What is a major reason to give premature infants cortisol?

A

Increases lung maturation

63
Q

What is the effect of cortisol on RBC production?

64
Q

What is the effect of cortisol on appetite?

65
Q

How does Cushing’s syndrome cause DM II?

A

Chronically increased BG levels, and decreased sensitization of cells to insulin

66
Q

Why is it that giving pressors to a patient with adrenal insufficiency will not cause as large of an increase in BP as a normal pt?

A

Loss of alpha receptors that are usually maintained by cortisol

67
Q

What is the main mineralocorticoid produced by the body?

A

Aldosterone

68
Q

What are the cellular effects of aldosterone binding its receptor?

A

Once the MR is bound and
activated by aldosterone, it stimulates the expression of the amiloride sensitive epithelial sodium channel (ENaC) and the basolateral Na+, K+-ATPase pump

69
Q

What, generally, are the renal effects of aldosterone?

A

Increase in the reabsorption of Na and water, and secretion of K in the collecting ducts of the kidney tubule

70
Q

MRs and GRs have a high degree of homology. What is the significance of this?

A

Blood levels of cortisol are at least 100-fold greater than aldosterone. Therefore, if no other factors existed, aldosterone would have little utility, as MRs would be continuously regulated by cortisol

71
Q

MRs and GRs have a high degree of homology, and cortisol has a much, much higher concentration in the blood than aldosterone. How do the aldosterone target cells prevent their regulation by cortisol?

A

aldosterone target cells express the type 2
isoform of 11β-hydroxysteroid dehydrogenase (11β-HSD2), which converts active cortisol into inactive
cortisone, while not acting on aldosterone

72
Q

What happens to aldosterone regulation with Cushing’s?

A

11β-HSD2 is overwhelmed, causing cortisol to stimulate Mineralocorticoid receptors, leading to increases in BP, Na, water and hypokalemia

73
Q

Aldosterone synthesis and
release from the adrenal
zona glomerulosa is primarily
regulated by what?

A

angiotensin II (ANG II) and extracellular K+

74
Q

What triggers angiotensin release? What cells release this, and what are its effects?

A

Decreases in blood volume trigger the juxtaglomerular cells to secrete renin

Renin cleaves angiotensinogen to ANG I

75
Q

What are the steps of the renin-angiotensin system?

A

Renin released by juxtaglomerular cells cleaves angiotensinogen to ANG I, which is then converted by ACE to ANG II

76
Q

What are the effects of ANG II?

A
  • Induces the synthesis and secretion of aldosterone

- Causes vasoconstriction

77
Q

What is the half-life and breakdown product of ANG II?

A

less than 1 min

ANG III (which still maintains some physiological effects)

78
Q

What happens when ANG II binds to AT receptor on the plasma membrane of the adrenal glomerulosa cells? What type of G protein?

A

Gq, causes the release of aldosterone

79
Q

What is the relative strength of the adrenal androgens (DHEA and androstenedione)?

A

Weak (i.e., they bind to the androgen receptor with

a lower affinity than testosterone)

80
Q

What is the major cell type in the adrenal medulla? How are these cells stimulated to release catecholamines?

A

Chromaffin cells

Function like ANS–ACh stimulates them to release and synthesize catecholamines

81
Q

What is percent of the adrenal medulla’s secretions are epi/NE?

A 
Epi = 80%
NE = 20%
82
Q

What is the enzyme located in the cytoplasm of chromaffin cells that converts NE to epi? What can increase the expression/activity of this enzyme?

A

phenylethanolamine-N-methyltransferase (PNMT)

Cortisol increases the expression

83
Q

How is it that cortisol deficiencies can lead to catecholamine deficiencies?

A

Loss of PMNT expression (converts NE to Epi) if there is no cortisol

84
Q

What happens to epi/NE that leaks out of the secretory vesicles of chromaffin cells?

A

Continuously metabolized by COMT

85
Q

What are the breakdown products of epi/NE?

A

Epi - metanephrine

NE - normetanephrine

86
Q

Do 11-deoxycorticosterone (DOC) and corticosterone have mineralocorticoid activity?

A

Slightly, but yes

87
Q

How does elevated [K] lead to the secretion of aldosterone?

A

Depolarizes the glomerulosa cells by increasing Ca levels

88
Q

What causes renin release?

A

Decrease perfusion of juxtaglomerular cells

89
Q

Where is angiotensinogen found?

A

Circulating in the plasma

90
Q

Are ACE inhibitors K sparing? Why or why not?

A

Yes, because blocking of ANG lower aldosterone production, which would normally excrete K in exchange for Na and water

91
Q

What are the peripheral effect of aldosterone?

A

Prevents Na lost in sweat

Prevents loss of Na in stools

92
Q

What are the enzymes that activate and deactivate cortisone/cortisol respectively?

A

11-beta-HSD1 activates

11-beta-HSD2 deactivates

93
Q

What are the tissues that have 11-beta-HSD2?

A

Kidney
Colon
Salivary glands

94
Q

What are the tissues that have 11-beta-HSD1?

A

Liver
Brain
Lung
Adipose tissue

95
Q

What is “Apparent mineralocorticoid excess” (AME)?

A

rare genetic mutation causing an inactivation of 11-beta-HSD2

This translates into an apparent mineralocorticoid excess d/t cortisol stimulation of MR receptors

96
Q

What is congenital adrenal hyperplasia

A

Genetic defect in adrenal steroid biosynthetic enzymes, leading to reduced cortisol levels, and an increase in ACTH

97
Q

What is the half-life of catecholamines?

A

0.5-2 minutes

98
Q

What happens when catecholamines enter into their target cells?

A

Metabolized into vanillylmandelic acid (VMA) by MAO and COMT

99
Q

What is the normal proportion of urine catecholamines? (3)

A

50% metanephrines
35% VMA
10% conjugated catecholamines

100
Q

What is Cushing’s disease?

A

ACTH secreting pituitary tumor

101
Q

How does ACTH increase the synthesis of androgens?

A

binding to MC2Rs on the adrenal cortex

102
Q

How does Cushing’s lead to HTN?

A

Saturation of 11-beta-HSD2

103
Q

What is the most commonly affected enzyme in the cortisol synthesis pathway? What happens when this enzyme is defective/deficient?

A

21-hydroxylase
Cholesterol is shunted down the androgen pathway

Low cortisol = increased ACTH secretion

104
Q

What is the effect of 21-hydroxylase deficiency in newborn females?

A

masculinization of genitalia d/t overproduction of adrenal androgens

105
Q

What happens with 17-alpha-hydroxylase deficiency?

A

Deficiency in adrenal glucocorticoids and androgens, and an excess in aldosterone. This leads to HTN and hypokalemia

106
Q

What happens with 11-beta-hydroxylase deficiency? How is this different from 21-alpha-hydroxylase deficiency?

A

Loss of aldosterone and cortisol, but increased adrenal androgen synthesis. However, there is not salt-wasting and low BP d/t the activity of DOC–there is actually HTN

107
Q

What is the usual presentation of 17-alpha-hydroxylase deficiency in males and females?

A

Ambiguous genitalia in males

Lack of secondary sex characteristics in females

108
Q

Name the disease:

  • High mineralocorticoids
  • Low [K]
  • Low cortisol
  • Low androgens
  • HTN
A

17-alpha-hydroxylase deficiency

109
Q

Name the disease:

  • Low mineralocorticoids
  • High [K]
  • Low cortisol
  • High androgens
  • Low BP
A

21-alpha hydroxylase deficiency

110
Q

Increased levels of 17-OH-Progesterone is characteristics of what disease?

A

21-alpha hydroxylase deficiency

111
Q

Name the disease:

  • Low mineralocorticoids
  • Low [K]
  • Low cortisol
  • High androgens
  • HTN
  • Increased DOC
A

11-beta-hydroxylase

112
Q

How do you differentiate pituitary hypersecretion of ACTH vs ectopic ACTH production?

A

Dexamethasone will suppress pituitary ACTH production

113
Q

What is the cofactor for DOPA production of Y-hydroxylase?

114
Q

What is the enzyme that converts epi into metanephrine, and NE into Normetanephrine?

115
Q

What is the enzyme that converts NE and epi into Dihydroxymandelic acid, which is then converted to VMA by COMT?

116
Q

Which has a greater Alpha receptor stimulation: NE or epi?

Endocrine (32 decks)

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