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Metabolic Endocrinology > Adrenal Gland > Flashcards

Adrenal Gland Flashcards

1
Q

what are the two sections making up the adrenal gland

A

adrenal cortex (90%) and inner medulla (10%)

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2
Q

what are the 3 zones making up the adrenal cortex

A

zona glomerulosa
zona fasciculata
zona reticulosa

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3
Q

which hormone is produced by the zona glomerulosa

A

aldosterone

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4
Q

which hormone is produced by the zona fasiculata

A

cortisol and corticosterone

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5
Q

which hormones are produced by the zona reticulosa

A

sex steroids - androgens mainly which are precursors for testosterone

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6
Q

which hormone are produced by the medulla

A

catecholamines (epinephrine and norepinephrine)

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7
Q

humans produce less corticosterone than poultry, but they are produced as intermediates fro synthesis of ______

A

aldosterone

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8
Q

what is the main glucocorticoid produced by large mammals

A

cortisol

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9
Q

what is the main glucocorticoid produced by rodents and birds

A

corticosterone

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10
Q

what type of cells make up the medulla

A

modified neurons

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11
Q

what is the first step of steroidogenesis common to all steroids

A

the formation of pregnenolone from cholesterol

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12
Q

what is a rate limiting step of steroidogenesis

A

uptake of cholesterol regulated by StAR

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13
Q

which enzyme regulate uptake of cholesterol

A

StAR protein [steroid acute regulatory protein]

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14
Q

what stimulates the production of StAR

A

tropic hormones such as ACTH in the adrenal gland and gonadotropics in gonads will bind to GPCR and induce StAR gene through cAMP

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15
Q

where does steroidogenesis occur

A

in the mitochondria

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16
Q

what is the action of P450scc and which gene encodes this enzyme?

A

P450scc is encoded by CYP11A1 and cleaves the side chan of cholesterol to produce prgnenolone

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17
Q

which enzyme converts pregnenolone to progesterone

A

HSD3B2

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18
Q

which enzyme converts 11-deoxycorticosterone -> corticosterone -> 18OH-corticosterone -> Aldosterone

A

CYP11B2

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19
Q

which enzyme converts pregnenolone to 17OH-pregnenolone

A

CYP17A1

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20
Q

which enzyme converts 17OH-pregnenolone to 17OH-progesterone

A

HSD3B2

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21
Q

which enzymes convert cortisol to cortisone and vice versa

A

HSD11B2

HSD11B1

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22
Q

which enzymes do the cells found in zona glomerulosa require to produce aldosterone

A 
CYP11A1
HSD3B2 
CYP21A2
CYP11B1
CYP11B2
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23
Q

which enzymes do the cells found in zona reticularis require to produce testosterone

A

CYP11A1
CYP17A1
HSD3B2
HSD17B

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24
Q

which enzymes do the cells found in zona fasciculata require to produce cortisol/cortisone

A 
CYP11A1
CYP17A1
HSD3B2
CYP21A2
CYP11B1
HSD11B2 and HSD11B1
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25
Q

tissues that produce steroids are ______ because producing steroids is _____

A

metabolically active

energetic demanding

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26
Q

what is the main source of cholesterol used for steroidogensis

A

circulatory LDL

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27
Q

cortisol can be covered to inactive ____ by the ____ and other target cells

A

cortisone

liver

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28
Q

what is the pathways of cortisol secretion

A

diurnal rhythm and stressors (hypoglycemia, hypotension, fever, trauma) will stimulate the hypothalamus which will release CRH which acts on the pituitary
Pituitary will release ACTH which acts on cells found in zona fasciculata in adrenals -> cortisol secretion

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29
Q

what is the feedback regulation of cortisol

A

negative feedback on hypothalamus and pituitary

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30
Q

what are the effects of cortisol on metabolism

A

increases: GLUCONEOGENESIS in liver , glycogenolysis, proteolysis, lipolysis [glucocorticoid involved in glucose metabolism and energy]

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31
Q

what are the effects of cortisol on cardiovascular system

A

increases myocardial contractility, cardiac output, catecholamine pressor effect

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32
Q

cortisone cannot be converted back to cortisol. true or false

A

false, cortisone can be converted to active form cortisol through HSD11B1

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33
Q

how is cortisol production activated

A

ACTH activates cortisol production from cholesterol via G-protein/cAMP signaling pathway and through enzymatic cascade

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34
Q

secretion of cortisol is ____

A

pulsatile

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35
Q

what is a diurnal rhythm

A

when the concentration of plasma hormones is highest in the morning

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36
Q

why is there a higher level of cortisol early in the morning?

A

the average level increases due to the summation of more frequency pulses of ACTH

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37
Q

how is circulating cortisol transported

A

transported by corticosteroid binding globulin CBG=transcortin or albumin

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38
Q

___ cortisol is protected from inactivation by the ____

A

bound cortisol

liver

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39
Q

which enzyme converts cortisol to cortisone

A

HSD11B2

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40
Q

why is it important to be able to convert cortisol into its inactive form cortisone

A

cortisol levels are much higher than aldosterone concentrations. This high concentration of cortisol can cause it to bind to mineralocorticoid receptors NR3C2 which can cause aldosterone-like symptoms such as hypertension, hypokalemia, low renin, and low aldosterone levels . Therefore aldosterone responsive cells have to be able to inactive cortisol to be able to respond specifically to aldosterone

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41
Q

which receptors is the glucocorticoid receptor

A

NR3C1

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42
Q

which glucocorticoid receptor isoform has a negative feedback on the other isoform

A

GR beta inhibits GR alpha

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43
Q

the metabolic effect of cortisol are generally opposite to ____ and similar to ____

A

opposite to insulin but similar to GH

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44
Q

in muscle cells, adipocytes and lymphocytes, cortisol has a ____ effect and in liver it has a ____ effect

A

catabolic

anabolic in liver

45
Q

the overall effect of cortisol on liver is ____. how so?

A

anabolic: increased enzyme activity, gluconeogenesis, glycogen synthesis, glycogen storage

46
Q

cortisol increases ____ despite the increase in ____

A

increases blood glucose despite the increase in glycogen storage

47
Q

how does cortisol have an anti-inflammatory property

A

cortisol inhibits the immune response by decreasing the number of lymphocytes and antibody production -> anti-inflammatory

48
Q

mechanism of action of hydrocortisone cream

A

used as topical anti-inflammmatory treatment because skin has HSDB1 which activates cortisone into cortisol

49
Q

what are the 3 mechanisms used by glucocorticoid receptors to inhibit inflmmation

A
  1. with coactivators C-fos/C-jun activated inhibitor I-kappa-B) of the immune response transcription factor NFkB
  2. GR-cortisol binds and inhibits nuclear migration of NFkB
  3. GR competes with NFkB for other interacting transcription factors (eg. CREB)
50
Q

what is the main transcription factor of pathay o inflammation

A

NFkB

51
Q

what are the main effects of cortisol

A

anti-inflammatory and glucose metabolism

52
Q

what is Cushing’s syndrome and what causes it

A

overproduction of cortisol due to:

  • CRH producing tumor
  • ACTH producing tumor
  • lack of feedback control of cortisol
  • cortisol producing adrenal tumor
  • iatrogenic [most common cause, resulting from chronic glucocorticoid therapy]
53
Q

what are the symptoms of Cushing’s syndrome

A
  • diabetes (increased gluconeogeneiss)
  • muscle wasting (protein catabolism)
  • increased and redistribution of adipose tissue
  • susceptibility to infection (decreased immune cells/reponse)
  • sodium retention and hypertension -> apparent mineralocorticoid excess AME
  • low ACTH in primary hypercortisolism
54
Q

what is Addison disease

A

adrenal hypofunction, most commonly due to destruction of the adrenal gland by an autoimmune response

55
Q

if the adrenal glands are not functioning, what are the consequences

A
  • very low or absence of cortisol

- very low of absence of aldosterone

56
Q

what is the main function of zona glomerulosa

A

produces aldosterone: recovery of sodium in the kidney and enhances potassium secretion into the urine adjusting extra-cellular fluid and blood volume

  • regulation of fluid volume
  • water absorption
  • sodium/potassium homeostasis
  • sodium transport
57
Q

what structure present in the arterioles regulate how much blood goes into the capillaries

A

precapillary sphincters

58
Q

the _________ is a major determinant of the BP in the arteries and controls the distribution of the blood supply to tissues

A

diameter of arterioles

59
Q

which factors positively regulate the sodium appetite

A
  • aldosterone

- angiotensin 2

60
Q

which factors negatively regulate the sodium appetite

A

increased sodium concentration of blood plasma, post-ingestive signals from the gut sensed via the vagus nerve, circulating and CNS peptide hormones/neuromodulators

61
Q

thirst and sodium appetite effectively adjust BP and blood volume. true or false

A

false, thrust is much more robust in terms of effectively adjusting BP and blood volume than sodium appetite

62
Q

_____ cells detect sodium levels in kidney tubule

A

macula densa cells

63
Q

______ cells near afferent arterioles detect BP

A

juxtaglomerular cells

64
Q

Pericytes near afferent arterioles produce ____

A

renin

65
Q

Renin synthesis and secretion is simulated by _____ and ____

A

macula dense cells and juxtaglomerular cells

66
Q

explain the renin-angiotensin-aldosterone system

A
  • renin from afferent arterioles in kidney converts angiotensinogen from liver to angiotensin 1
  • angiotensin converting enzyme from endothelial cells of lungs converts angiotensin 1 to a angiotensin 2
  • angiotensin 2 stimulates aldosterone secretion by zona glomerulosa
  • angiotensin 2 increases sodium absorption and potassium excretion and water retention
67
Q

angiotensin 2 is inactivated to angiotensin 3 by _____

A

aminopeptidase A

68
Q

the posterior pituitary releases ____ which also stimulates water resorption in kidney

A

AVP/ADH antidiuretic hormone

69
Q

aldosterone adds ____ on distal tubule side of kidney to achieve water absorption

A

aquaporins

70
Q

aldosterone activates ____ on distal tubule side of kidney to excrete potassium

A

ROMK and BK channels

71
Q

aldosterone activates ____ on distal tubule side of kidney to absorb sodium

A

ENaC

72
Q

aldosterone acts mainly on ____ and ____ for sodium retention and potassium excretion

A

distal tubules and collecting ducts of the kidney

73
Q

what is the net effect of aldosterone

A

rise in plasma volume and hence blood pressure

74
Q

what is Conn’s disease

A

hyperaldosteronism due to hypersecretion of aldosterone usually caused by adrenal hyperplasia or tumor

75
Q

what are the consequences of hyperaldosteronism

A
  • excess excretion of potassium and H+ [serum alkalosis and neuropathy - hypokalemia]
  • increased water retention
  • increased sodium reabsorption
  • increased blood pressure
76
Q

what causes hypoaldosteronism and what are the symptoms

A

impaired function of aldosterone or deficiency of aldosterone production

  • low sodium (hyponatremia)
  • too much potassium (hyperkalemia)
  • metabolic acidosis
  • low BP
77
Q

what is the function natriuretic peptides

A

ANP and BNP peptides that increase the excretion of water and sodium thereby decreasing blood volume and blood pressure

78
Q

which cells produce natriuretic peptides

A

heart muscle cells

79
Q

where are the natriuretic peptide receptors located

A

located in the glomeruli, medullary collecting ducts of the kidney, zona glomerulosa fo the adrenal cortex and in peripheral arterioles

80
Q

mode of action of natriuretic peptides

A

they can inhibit renin production in kidney which will reduce angiotensin and aldosterone production + increase GFR causing excretion of sodium [natriuresis] => decreased blood volume and decrease BP

81
Q

androgens are precursors for _____

A

testosterone

82
Q

sex steroids are mainly synthesized in the ____ and regulated by

A

gonads regulated by gonadotropins

83
Q

which are the female sex steroids

A

estrogen and progesterone

84
Q

which is the male sex steroid

A

androgen

85
Q

the zona reticularis contributes to the production of ____ and _____ regulated by _____ and _____

A

DHEAS and androstenedione regulate by ACTH and hypothalamic CrH

86
Q

while aldosterone production by glomerulosa is less under the influence of _____ and more under the influence of _____, zona fasciculata and reticularis are mainly regulated by _____ and ____

A

ACTH
angiotensin
CRH and ACTH

87
Q

what is CAH and what causes it

A

congenital adrenal hyperplasia which is caused by deficiency of CYP21A2 in zona glomerulosa and fasciculata causing reduced aldosterone and cortisol but excessive androgen production in zona reticularis causing masculinization of genitalia

88
Q

which cells make up the adrenal medulla

A

Chromaffin cells

89
Q

what are chromatin cells

A

modified postganglionic sympathetic neurons

90
Q

how do chromaffin cells release catecholamines

A

preganglionic neurons release acetylcholine to stimulate the chromaffin cells to release catecholamines

91
Q

what is the role of catecholamines

A

they coordinate fight-or-flight response to alarm by increasing blood pressure and cardiac output and dilating pupils

92
Q

catecholamines are synthesized from ____

A

tyrosine

93
Q

what is the rate limiting step of catecholamine synthesis

A

tyrosine into Dopa through tyrosine hydroxylase

94
Q

epinephrine (catecholamine) synthesis is under the influence of ____

A

cortisol

95
Q

which enzyme is stimulated by cortisol in epinephrine synthesis [norepinephrine to epinephrine]

A

phenylethanolamine N-methyltrasnferase PNMT

96
Q

which are the 2 catecholamines that are released by medulla and their proportions

A
  • 80% are epinephrine

- 20% norepinephrine

97
Q

how are catecholamines degraded

A

inactivated by monoamine oxidase MAO and COMT pathways into vanillylmandelic acid VMA which is excreted

98
Q

the adrenal medulla secretes catecholamines and other hormones including ____

A

met-enkephalin and leu-enkephalin which are related to endorphins

99
Q

function of enkephalins

A

block neurotransmitters like morphine

act as an endogenous analgesic [runners overcoming pain and being euphoric]

100
Q

the ____ nervous system activates the adrenal medulla in a fight-or-flight response releasing _____

A

sympathetic nervous system

releasing norepinephrine and epinephrine

101
Q

effect of epinephrine

A
  • rapidly metabolizes fatty acids as the primary fuel for muscle action: increases muscle glycogenolysis, mobilizes glucose for the brain by increasing hepatic glycogenolysis and gluconeogenesis, preserves glucose for CNS by decreasing insulin release leading to reduced glucose uptake by muscle/adipose, increases cardiac output
102
Q

effect of norepinephrine

A

elicits réponses of the CV system - increased blood flow and decreased insulin secretion

103
Q

which are the adrenergic receptor and what do they bind

A

alpha and beta1 bind epinephrine and norepineprhine

beta2 bind primarily epinephrine

104
Q

____ activates beta2 receptors and dilates bronchioles - relief od asthma

A

salbutamol

105
Q

which of epinephrine and norepinephrine has a greater effect on cardiac stimulation leading to greater cardiac output?

A

epinephrine

106
Q

which of epinephrine and norepinephrine has a greater effect on constriction of blood vessels leading to increased peripheral resistance -> increased arterial pressure

A

norepinephrine

107
Q

which of epinephrine and norepinephrine has a greater effect on increasing metabolism

A

epinephrine

108
Q

what are the effects of cortisol suppression on adrenal medulla

A

epinephrine deficiency

Metabolic Endocrinology (10 decks)

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