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Physiology 3 Endocrine > Adrenal > Flashcards

Adrenal Flashcards

1
Q

the adrenals are a pair of glands weighing a total of about ____g, which are located one near each _____.

A

10g

kidney

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2
Q

each adrenal is actually ___ glands in one, the outer _____ that produces _____ and inner _____ that produces _____.

A 
2
outer adrenal cortex
steroid hormones (cortisol, androgens)
inner adrenal medulla
catecholamines (NE & E)
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3
Q

the adrenal cortex is around ____% of adrenal mass

A

90%

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4
Q

the adrenal medulla is around ____% of adrenal mass

A

10%

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5
Q

blood flowing through adrenal cortex drains into medullary ______, hence part of the blood supply supplying adrenal medulla is rich in _______.

what is the clinical significance of this? (what is the function)

A

medullary capillary sinusoids
corticosteroids (cortical steroids)

the corticosteroid-rich blood modulates or fine-tunes the ratio of E:NE released from the medulla such that elevated cortisol will increase the proportion of E

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6
Q

T/F: cortisol increases ratio of epinephrine secreted from adrenal medulla

A

TRUE

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7
Q

What are the 3 layers of the adrenal cortex and what does each produce? (superficial to deep)

A
  1. zona glomerulosa - aldosterone
  2. zona fasciculata - cortisol
  3. zona reticularis - cortisol & androgens (dehydroepiandosterone & androsternedione)
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8
Q

what are the 2 androgens that are produced in the zona reticularis of the adrenal cortex?

A

dehydroepiandosterone

androstenedione

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9
Q

T/F: you can live without the adrenal cortex (loss by disease or surgery)

A

FALSE - you will die within 1-2 weeks

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10
Q

What is the most likely cause of death from loss of the adrenal cortex by disease or surgery?

what happens when calorie intake is limited?

A

sodium depletion –> circulatory collapse

hypoglycemia

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11
Q

what are the 2 types of adrenocortical hormones? what does each produce? what is the function of each hormone produced?

A
  1. mineralocorticoids - aldosterone (Na/K+ balance)

2. glucocorticoids - cortisol (maintaining carbohydrate reserves)

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12
Q

T/F: the adrenal androgens have stronger effects than those of male testicular hormones (T, DHT) in puberty

A

FALSE - similar but weaker than male hormones

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13
Q

T/F: adrenal androgrens appear to be of importance in both sexes in mediating changes occurring in puberty

A

TRUE

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14
Q

How does the fetal adrenal compare with adult? what does it have?

A

fetal adrenal is bigger, for body size, than that of the adult

large steroidogenic “fetal zone”

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15
Q

The adrenal medulla embryologically arises from ____ and is innervated by neurons whose cell bodies reside in the _________. axons from these cells pass through the __________ to form ______ nerves.

A

neuroectoderm
spinal cord
paravertebral sympathetic ganglia
splanchnic nerves

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16
Q

The adrenal medulla stores _____g of catecholamines in _____ granules within ______ cells that stain with ______.

A

5-6g
secretory
chromaffin
chromium

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17
Q

the cells of the adrenal medulla are modified ____neurons

A

post-ganglionic

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18
Q

what do adrenal cortical hormones derive from?

A

cholesterol

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19
Q

what is the rate-limiting step in cortisol synthesis?

A

the first step: cholesterol –> pregnenolone

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20
Q

what is the role of StAR? (steroid acute regulatory protein)

A

stimulates transport of cholesterol from cytosol into the mitochondria where it can be acted on by enzyme –> pregnenolone

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21
Q

T/F: mineralocorticoid activity is predominantly associated with aldosterone and glucocorticoid activity with cortisol

A

TRUE

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22
Q

T/F: cortisol has both glucocorticoid and mineralocorticoid effect

A

TRUE

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23
Q

why doesn’t cortisol bind and influence mineralocorticoid receptors?

A

mineralocorticoid sensitive tissues contain Type II 11 beta-hydroxysteroid dehydrogenase (Type2 11beta-HSDH) that converts cortisol into cortisone, reducing mineralocorticoid effect

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24
Q

what is the role of Type II 11 beta-hydroxysteroid dehydrogenase

A

cortisol –> cortisone (reduce mineralocorticoid effect of cortisol)

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25
Q

steroid secretion represents _____ synthesis, since steroid hormones can’t be stored.

A

de novo (synthesis from scratch)

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26
Q

T/F: catecholamines of adrenal medulla cannot be adequately stored

A

FALSE - stored in chromaffin cells

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27
Q

T/F: steroid hormones cross the membrane by going down their concentration gradient to enter circulation

A

TRUE - lipid soluble, so passively diffuse through membrane down their conc gradient

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28
Q

in circulation, what are steroid hormones bound to? (3)

A

transcortin (plasma binding protein)
CBG (corticosteroid binding globulin)
plasma albumin

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29
Q

most adrenal androgens travel in circulation bound to ______ and in the _____ form

A

albumin

sulfated

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30
Q

how does glucocorticoid binding of albumin differ from that of mineralocorticoids like aldosterone? % bound?
how does this binding affect the hormone effect (half life)?

A

glucocorticoids binding is favored over aldosterone

95% of glucocorticoids bound
60% of aldosterone bound

glucocorticoids have longer half life in plasma (90 minute vs 30 minutes for aldosterone) and has longer hormonal effect

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31
Q

how does half life and stability of DHEAS differ from that of glucocorticoids/mineralocorticoids?

A

DHEAS more stable
half life 10-20 hours (longest)
total plasma conc exceeds of other adrenal steroids in young adults

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32
Q

T/F: clearance of hormones is largely by renal/hepatic mechanisms

A

TRUE

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33
Q

compare b/w steroid hormones and peptide/amine hormones:

entry into cells
binding to what?
target

A

steroid entry: passive diffusion
peptide entry: don’t enter (work via secondary messengers at membrane)

steroid binding: cytoplasmic receptor proteins
peptide binding: plasma membrane receptors

steroid target: nucleus
peptide target: plasma membrane

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34
Q

what receptors do mineralocorticoids and glucocorticoids bind in cytosol? is there overlap?

A

mineralocorticoids bind type 1 receptors

glucocorticoids bind preferentially to type 2 receptors but can also bind to type 1 but usually intercepted in mineralocorticoid-sensitive tissues by type2beta11HSDH and inactivated

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35
Q

where are the greatest amounts of type 1 receptor for mineralocorticoids found?

A

kidney
colon
sweat/salivary glands

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36
Q

give the full mechanism in which steroid hormones affect gene trx

A

free steroid hormones diffuse through plasma membrane of cell

displace heat shock proteins (HSP90) which give up receptors that can now bind to ligand/hormone

HR complex enters nuclear membrane and binds to HRE (palindromic on DNA)

affected DNA sequence creates appropriate proteins for hormonal response

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37
Q

ACTH is derived from what pituitary prohormone?

it is required for the normal function of the zona ____ and zona ______. ACTH is the controlling factor for the synthesis/secretion of _____. in the absence of ACTH, the 2 zonas _____.

A

POMC

zone fasciculata and reticularis (where is secretes cortisol)
cortisol and androgens
atrophy

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38
Q

T/F: ACTH binds to only receptors in the zona fasciculata and zona reticularis of the adrenal cortex

A

FALSE - ACTH binds to receptors in all three layers of the adrenal cortex

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39
Q

in the zona glomerulosa, ACTH has a (major/minor) role in aldosterone production, although the prime regulator in this layer is _____.

A

minor

AngII

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40
Q

what layer of the adrenal cortex has necessary enzymes for DHEA production?

A

zona reticularis

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41
Q

how does ACTH stimulate the production of androgrens (steroid hormones)?

give the mechanism with all substrates and related enzymes

A

ACTH binds to receptor –> rise in intracellular cAMP
production of StAR protein that stimulates entry of cholesterol from cytosol to mitochondria –> cholesterol into pregnenolone

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42
Q

T/F: ACTH stimulation of steroid hormone secretion takes hours

A

1-2 minutes (peaking 15 minutes)

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43
Q

what controls the production of ACTH?

A

CRH (hypothalamic neuron)

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44
Q

T/F: ACTH has a circadian rhythm

A

TRUE

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45
Q

T/F: cortisol has a circadian rhythm

A

TRUE

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46
Q

How does ACTH secretion rates differ in the morning and evening?

A

peak rate in the morning before you wake up

steady decline in the evening hours

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47
Q

How does cortisol secretion rates differ in the morning and evening?

A

same as ACTH

peak rate in the morning (cortisol wakes you up)
steady decline in the evening hours

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48
Q

T/F: CRH and ACTH secretion is subject to negative feedback inhibition by cortisol

A

TRUE - long loop negative feedback

49
Q

T/F: circadian rhythm of ACTH appears to be the result of changes in the sensitivity of CRH secreting cells to cortisol

A

TRUE

50
Q

how does sensitivity of CRH to cortisol differ in the morning and evening?

A

morning: low sensitivity to cortisol, less negative feedback, high secretion rates of CRH, more basal ACTH and cortisol secretion
evening: higher sensitivity to cortisol, more negative feedback, decline in CRH, ACTH, cortisol levels

51
Q

T/F: Stress and ACTH override each other (antagonists)

A

FALSE - they both stimulate cortisol secretion, dont override if they have the same effect

52
Q

stressful stimuli lead to increases in CRH secretion, by neural pathways, overriding the ______

A

diurnal (circadian) rhythm

so like if its night time and ACTH and cortisol secretion rates are low, but you got mad stress, it don’t matter that its night time and your cortisol/ACTH levels gon go up

53
Q

T/F: acute stress will lead to establishment of new steady state of ACTH and cortisol production

A

FALSE - chronic stress

54
Q

what hormone is the “stress” hormone?

what are its main physiological purpose?

A

cortisol

maintain vital functions during periods of prolonged stress (physiological stress and sometimes psychological) and contain inflammatory response

55
Q

what does it mean that functions of cortisol are permissive?

A

cortisol doesn’t itself initiate changes but is required for the changes to be expressed fully

ex. cortisol is required for effect catecholamine response and it is the increased responsiveness of cells to catecholamines that allow the effects of cortisol to take place

56
Q

what happens in a cortisol deficit?

A

decrease cardiovascular responsiveness to catecholamines

reduced mobilization of fuel stores

increased vulnerability to stress

57
Q

what is the effect of cortisol on blood glucose?

what disease can this lead to?

A

increases blood glucose
oppose insulin
(body wants more sugar/energy for fight or flight)

diabetes

58
Q

what is the effect of cortisol on proteins?

A

promotes protein catabolism (breakdown) from muscles and CT to free the amino acids –> use in gluconeogenesis for sugar

stimulates production of gluconeogenic enzymes in liver

(don’t need to be making more muscle, need amino acids and sugar for energy)

59
Q

what is the effect of cortisol on use of glucose?

A

inhibits glucose transport into cells (EXCEPT THE BRAIN)

increases plasma glucose allowing body to use sugar/energy for survival

60
Q

T/F: cortisol administration will cause loss of action potentials and neuronal function

A

FALSE - cortisol inhibits glucose uptake by cells everywhere but the brain (glucose enters via GLUT1 channels)

61
Q

what is the effect of cortisol on protein synthesis?

A

decreases protein synthesis (promotes protein breakdown/catabolism) everywhere BUT THE LIVER

reduce uptake of amino acids into muscle cells

plasma amino acid levels increase

62
Q

what is the effect of cortisol on fat metabolism?

A

increases fat breakdown to liberate amino acids and glycerol for gluconeogenesis

HOWEVER, increases fat deposition on trunk and face

63
Q

why does fat metabolism response to cortisol vary?

A

different receptor responsivities to cortisol in different adipose tissues

64
Q

what is the effect of cortisol on CNS?

what happens in cortisol deficiency and excess?

A

feedback inhibition of CRH and ACTH in hypothalamus and adenohypophysis

affects perception

cortisol deficiency - accentuate (increase sensitivity) of taste, hearing, smell

cortisol excess - initial euphoria followed depression

65
Q

what is the effect of cortisol on cardiovascular?

what happens in cortisol deficiency?

A

required to maintain sensitivity of vasculature to catecholamines (NE/E)

deficiency - widespread vasodilation and hypotension

66
Q

what is the effect of cortisol on developmental effects?

A

cortisol has important role in maturation in fetal development

production of intestinal enzymes and pulmonary surfactant (giving corticosteroids to mother during late pregnancy with a potential premature baby can prevent RDS)

67
Q

what is the effect of cortisol on renal?

what happens with no cortisol?

A

CRH (produces ACTH –> cortisol) also produces ADH

no cortisol - increases secretion of CRH and ADH (no negative feedback), renal water absorption increases, can’t produce hypotonic urine (free water) even if the person has low osm

68
Q

what 2 factors count for water intoxication in cortisol deficient patients?

A
  1. increases secretion of CRH and ADH (no negative feedback), renal water absorption increases, can’t produce hypotonic urine (free water) even if the person has low osm
  2. hypotension in the absence of cortisol contributes to high plasma ADH levels
69
Q

what is the effect of cortisol on bones?

what happens with cortisol excess?

A

promotes bone breakdown

excess - enhance osteoclastic activity (breakdown) –> osteoporosis

70
Q

what is the effect of cortisol on immunity?

what are the mechanisms in which it affects immunity?

A

contains inflammatory response (decrease immunity)

  • stabilize lysosomal membranes (prevent release of degradative enzymes)
  • decrease capillary permeability
  • depress phagocyte activity
  • suppress synthesis of IL-1
  • inhibit production of eicosanoids (prostaglandins, leukotrienes)
  • depress release of histamine from mast cells in lung
  • reduce allergic responses
71
Q

how can cortisol be beneficial and detrimental on immune system?

A

benefits - can reduce swelling/tissue damage in auto-immune diseases like rheumatoid arthritis

cons - can allow resurgence of latent infections

72
Q

what is the effect of pharmacological administration of glucocorticoids (cortisol)?

A

prolonged administration of cortisol leads to feedback inhibition of ACTh production, atrophy of dependent adrenal cells (zona fasciculata and reticularis), reduce ability for body to endogenously create cortisol

withdrawal from meds needs to be GRADUAL DECLINE of meds

73
Q

how is cortisol eliminated in body?

A

free plasma cortisol filtered in kidney –> reduced to tetrahydrocortisol and conjugated with glucuronic acid –> excreted in urine as glucuronide metabolites

74
Q

what is the difference in which cortisol and androgens are excreted in urine?

A

androgens - sulfated form in urine

cortisol - reduced to tetrahydrocortisol and conjugated with glucuronic acid –> excreted in urine as glucuronide metabolites

75
Q

adrenal androgens are produced in ___ quantities in fetus and are very important during _______.

A

large

fetal development

76
Q

how does adrenal androgen production levels differ during fetal development?

A

large in fetus
postnatal production is low
rises during pre-pubertal period (adrenarche)
contributes to events after puberty (onset of axillary and pubic hair growth, secretion from axillary sebaceous glands)

77
Q

define adrenarche

A

pre-puberty

development of zona reticularis, early stage of sexual maturation

78
Q

in adult females, the adrenals are a major source of ____ and after conversion into _____ in the periphery, contribute to stimulation of axillary and pubic hair growth. some _____ is also converted in the periphery to estrogen. this is a major source of _____ in post-menopausal women whose ____ are no longer active. there is some evidence that ___ levels have an influence on libido in women.

A 
estrogen
testosterone
androstenedione
estrogen 
ovaries 
DHEA
79
Q

in adult males, DHEA is insignificant in comparison to _____, produced in the testes AND _____ produced from testosterone.

A

testosterone

dihydrotestosterone

80
Q

what is the aim of dietary DHEA supplementation?

A

reverse the effects of aging

81
Q

what controls adrenal androgen production?

A

ACTH

82
Q

how is free DHEA excreted in urine?

A

free DHEA-S in plasma is filtered in kidney and excreted in urine in the sulfated form

83
Q

where in the adrenal cortex is aldosterone formed?

A

zona glomerulosa

84
Q

what is the primary function of aldosterone?
its production is under the control of what? (3)
what happens in its absence? can cortisol save the body?

A

Na+ reabsorption in distal nephron and secretion of K+

AngII, plasma K+, ACTH (less extent)

disrupt fluid and ion balance, but if sufficient cortisol is present, cortisol’s mineralocorticoid effects can prevent progressive fluid loss

85
Q

how is AngII produced?

A

rising levels of renin

86
Q

renin is a _____ produced by _____ of the ______. it is stimulated by _____ at the AA or by ____ stimulation via renal nerve

A 
protease
granular cells
JGA
fall in perfusion pressure 
SNS
87
Q

how does AngII stimulate aldosterone production at zona glomerulosa?

A

via receptor mediated increase in IP3 –> increases StAR (cholesterol into mito)

88
Q

T/F: aldosterone levels are increased by elevated estrogen

A

TRUE - during pregnancy

estrogen-stimulated increase in angiotensinogen production in liver

89
Q

aldosterone increases the activity of ____ in the basolateral membrane of target cells and also increasing rate of ___ entry on the luminal surface through added ____ channels.

A

Na+-K+-ATPase
sodium
sodium

90
Q

in addition to the distal nephron, where else are mineralocorticoid receptors found? (aldosterone receptors)

A

where sodium is excreted

ex. sweat/salivary glands and colon

91
Q

what are the ratios of storage of…
E:NE
ATP:catecholamines
ATP:E:NE

A

E:NE –> 5:1
ATP:catecholamines –> 1:4
ATP:E:NE –> 1:20:4

92
Q

5:1 is the ratio of what?

A

E:NE

93
Q

1:4 is the ratio of what?

A

ATP:catecholamines

94
Q

give the mechanism of catecholamine biosynthesis

A 
tyrosine --> DOPA --> dopamine 
dopamine enters chromaffin cell
dopamine --> NE 
NE leaves chromaffin cell
NE --> E via PNMT
E enters chromaffin cell

NE and E both in chromaffin cell until used

95
Q

how is chromaffin exocytosis stimulated?

A

binding of Ach (sympathetic cholinergic stimulation) to chromaffin cells –> rise in intracellular calcium levels –> exocytosis

96
Q

T/F: chromaffin cell exocytosis of catecholamines is associated with an increase in intracellular cAMP levels

A

FALSE - intracellular calcium levels

97
Q

what % of catecholamines are free in circulation and what % of catecholamines are loosely associated with albumin?

A

50% bound, 50% free in circulation

98
Q

T/F: catecholamines are slowly cleared from circulation

A

FALSE - rapidly cleared, half life of 10-15 seconds, very unstable

90% of catecholamines go through vasculature in one go

99
Q

compare response time of medullary catecholamines to cortical corticosteroids

A

catecholamines - rapid response time, fast turn-over

corticosteroids - slower, longer lasting effects of hormone

100
Q

what are the two ways catecholamines are uptaken by cells?

A
  1. neuronal - repackaged for reuse or degraded by neuronal cytosolic enzyme MAO (coupled with sulfate or glucuronic acid –> urine)
  2. non-neuronal - inactivated enzymatically by MAO and catecholamine-O-methyl transferase (COMT)
101
Q

what is a non-invasive way of monitoring circulating hormone levels? for corticosteroids

A

measure urinary concentrations of its degradation products

  1. neuronal - repackaged for reuse or degraded by neuronal cytosolic enzyme MAO (coupled with sulfate or glucuronic acid –> urine)
102
Q

compare the effects of catecholamines (NE and E) on the different types of plasma membrane receptors (alpha, beta1, beta2)

A

NE and E have similar effects on B1 receptors

NE - potent A agonist, little effect on B2
E - stronger A agonist, potent B2 agonist

103
Q

the fetal zone of the adrenal gland produces what androgen?

A

DHEA

104
Q

T/F: the zona glomerulosa is one of the few places of adrenal gland that produces aldosterone

A

FALSE - its the ONLY place in adrenal gland that produces aldosterone

105
Q

T/F: the zona reticularis primarily secretes weak androgens

A

FALSE - strong androgens

106
Q

what serves as a primary source of cholesterol to adrenals?

A

LDL

107
Q

T/F: DHEA and Androstenedione are downstream metabolites of pregnenolone

A

TRUE

108
Q

What are 2 examples of androgens?

A

DHEA

androstenedione

109
Q

out of cortisol, aldosterone, DHEA, DHEA-S, and androstenedione –> which has the highest secretion rate?

A

cortisol or DHEA

110
Q

out of cortisol, aldosterone, DHEA, DHEA-S, and androstenedione –> which has the highest plasma conc?

A

DHEA-S

111
Q

T/F: StAR is rate limiting

A

TRUE

112
Q

T/F: high excess cortisol doses can reduce mass of lymphoid tissue like spleen, thymus, lymph nodes

A

TRUE

113
Q

what is cushing’s syndrome?

A

hyperadrenocorticism

too much cortisol –> fat builds in face and trunk

114
Q

what is addison’s disease?

A

hypocortisolism

too little cortisol

115
Q

how does congenital adrenal hyperplasia (CAH) differ b/w females and males?

A

males - leads to adrenogenital syndrome
no change in external genitalia, early development of secondary sex characteristics, accelerated masculinisation

females - may cause pseudohermaphroditism
external genitalia masculinisation, child may be mistaken for male

116
Q

T/F: AngII is rapidly metabolized

A

TRUE

117
Q

T/F: adrenal medulla is more nerve than gland

A

FALSE - ductless gland, more gland

118
Q

what are the two types of chromaffin cells and what do they store?

A

A - 80%, small granules, EPINEPHRINE

N - 20%, large granules, NOREPINEPHRINE

119
Q

epinephrine especially effects B2 receptors

what organ has a rich distribution of B2?

A

liver

Physiology 3 Endocrine (9 decks)

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