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Unit 2 Phys II > L17-18: Adrenal gland > Flashcards

L17-18: Adrenal gland Flashcards

1
Q

Steroids produced by adrenal gland (cortex)

A

glucocorticoids
mineralocorticoids
androgens

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2
Q

Catecholamines produced by the adrenal gland (medulla)

A

epinephrine

norepinephrine

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3
Q

3 major arteries bring blood to the adrenal glands

A

superior, middle, and inferior suprarenal arteries

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4
Q

blood flow in the adrenal gland is a

A

sinusoid system

modulates activities of enzymes

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5
Q

Outermost layer of the adrenal cortex

A

zoma glomerulosa

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6
Q

middle layer of the adrenal cortex

A

zona fasciculata

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7
Q

deepest layer of the adrenal cortex

A

zona reticularis

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8
Q

zona glomerulosa produces

A

aldosterone

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9
Q

zona fascisculata produces

A

cortisol

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10
Q

zona reticularis produces

A

DHEA

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11
Q

Renal cortex produces

A

steroid hormones

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12
Q

renal medulla produces

A

catecholamines

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13
Q

an extension of, and under control of, the sympathetic nervous system

A

the medulla

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14
Q

medulla cells are called

A

chromaffin cells

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15
Q

regulation of aldosterone synthesis

A
  1. ACTH

2. RAAS

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16
Q

regulation of cortisol and adrenal androgens (DHEA) is under control of

A

ACTH

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17
Q

ACTH is released by

A

pituitary gland

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18
Q

Cortisol structure

A

21 carbons
ketone at C3
OH group at C11, C21

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19
Q

Aldosterone structure

A

21 carbons

Double bond a C18

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20
Q

DHEA stands for

A

dehydroepiandrosterone

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21
Q

DHEA/androstenedione structure

A

19 carbons
Doubt bond at C17
Lack C20, C21 (19 C total)

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22
Q

first, shared step of steroid hormone synthesis

A

conversion of cholesterol to pregnenolone

rate limiting

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23
Q

conversion of cholesterol to pregnenolone is catalyze by

A

desmolase

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24
Q

cholesterol is derived from

A

LDL (diet)
acetyl CoA (de novo)
Cholesterol esters from vesicles–> hydrolysis

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25
Q

Mediators of cholesterol mobilization

A

ACTH
Angiotensin II receptor
K+ channels

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26
Q

transporter of cholesterol to inner mitochondrial membrane

A

Steroidogenic acute regulatory protein (STaR)

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27
Q

desmolase is stimulated by

A

ACTH

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28
Q

drains adrenal blood flow

A

medullary vein

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29
Q

aldosterone is a

A

mineralocorticoid

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30
Q

cortisol is a

A

glucocorticoid

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31
Q

androstenedione is a

A

androgen

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32
Q

enzyme missing in zona glomerulosa

A

17 alpha hydroxylase

without it, only pathway is to synthesize aldosterone

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33
Q

17 alpha hydroxylase is necessary to synthesize

A

DHEA, androstenedione, cortisol

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34
Q

corticosterone is converted to aldosterone by

A

aldosterone synthase

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35
Q

aldosterone synthase activity is stimulated by

A

angiotensin II

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36
Q

secretagogues for aldosterone synthesis (3)

A
  1. ANG II
  2. Increase in plasma [K+]
  3. ACTH (weakly)
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37
Q

RAAS is stimulated by

A

Decrease in blood pressure

Decrease in ECF volume

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38
Q

Aldosterone binds to

A

Mineralocorticoid receptor 1 (MR1)

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39
Q

MR1 binds to

A

mineralcorticoid responsive element (MRE)

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40
Q

Aldosterone effects:

A
  1. Na+ reabsorption
  2. K+ secretion
  3. Net expansion of ECF
  4. H+ excretion
41
Q

Conn’s syndrome: primary hyperaldosteronism

A 
caused by a tumor
Hypernatremia, fluid retention, htn
Hypokalemia
Metabolic alkalosis
Low renin levels (htn)
42
Q

17 alpha-hydroxylase deficiency

A 
Glucocorticoids and steroids not produced
Increased 11-deoxycorticosterone, corticosterone: have mineralocorticoid function
low aldosterone (due to corticosterone excess)
low renin (htn)
43
Q

2 aldosterone precursors with mineralocorticoid function

A

11-deoxycorticosterone
corticosterone
if in excess, low aldosterone

44
Q

Inhibits renin secretion

A

htn

45
Q

Zona fasciculata lacks the enzymes

A

17, 20 lyase

Aldosterone synthase

46
Q

17, 20 lyase is necessary to

A

convert:
17-hydroxypregnenolone to DHEA
17-hydroxyprogesterone to androstenedione

47
Q

Cortisol negative feedback

A
  1. Directly inhibits CRH

2. Inhibits action of CRH on corticotrophs, decreasing ACTH release

48
Q

Corticotropin releasing hormone (CRH) is released during

A

stress

increases ACTH secretion

49
Q

do DHEA or Androstenedione have negative feedback loops on CRH or ACTH?

A

NO

50
Q

only negative feedback loops for CRH or ACTH

A

Cortisol

51
Q

ACTH is released in a

A

circadian/pulsatile pattern, mostly in morning

Cortisol and androgen levels reflect ACTH release

52
Q

ACTH activity reflects

A

CRH secretion

53
Q

overall metabolic effect of cortisol

A

increase blood glucose by enhancing gluconeogenesis

essential for fasting and stress

54
Q

Cortisol increases 2 pathways

A
  1. protein catabolism –> ammino acids

2. lipolysis –> glycerol

55
Q

Cortisol decreases

A

glucose uptake by tissues (glucose sparing)

56
Q

Cardiovascular actions of cortisol

A

maintain normal BP

up-regulates alpha-1 receptor

57
Q

Bone actions of cortisol

A

Decreases intestinal and renal calcium absorption

mobilizes calcium from bone, inhibits bone formation

58
Q

excessive glucorticoids (or high blood cortisol) results in

A

bone loss

59
Q

actions of cortisol on connective tissue/muscle

A

inhibits fibroblast proliferation, collagen formation
skin thinning
proteolysis in muscle: weakness

60
Q

anti-inflammatory/immune actions of cortisol

A

induces synthesis of lipocortin: inhibits phospholipase 2: decreased prostaglandins and leukotrienes

inhibits production of IL-2

Inhibits release of histamine and serotonin from mast cells

61
Q

Addison’s disease: primary adrenocortical insufficiency

A

destruction of adrenal gland –> decreased synthesis of all adrenaocortical hormones

62
Q

loss of cortisol (Addison’s disease) (Secondary/Tertiary adrenocortical insufficiency)

A

hypoglycemia during stress
weight loss
muscle weakness

63
Q

loss of aldosterone (Addison’s disease)

A

hyperkalemia
hypotension
metabolic acidosis
salt craving

64
Q

loss of androgens (Addison’s disease) (Secondary/Tertiary adrenocortical insufficiency)

A

in females, decreased pubic and axillary hair, decreased libido

65
Q

other effects of Addison’s disease

A

increased ACTH secretion –> alpha-MSH fragment–> hyperpigmentation of skin, nipples, knees, gums

66
Q

ACTH is derived from

A

proopiomelanocortin (POMC)

67
Q

POMC is cut into

A

gamma fragment
beta endorphin: contains beta-MSH
gamma liptropin
ACTH: contains alpha-MSH

68
Q

Secondary adrenocortical insufficiency

A

Failure of corticotrophs to secrete ACTH

69
Q

Tertiary adrenocortical insufficiency

A

Insufficient CRH

70
Q

In Secondary/Tertiary adrenocortical insufficiency

A

cortisol and androgen deficiency
aldosterone levels normal (regulated by RAAS)
no hyperpigmentation as low ACTH

71
Q

Cushing’s syndrome

A 
primary adrenal hyperplasia: oversecretion of cortisol
Low ACTH (negative feedback)
72
Q

Cushing’s disease

A

overactive anterior pituitary or ACTH-secreting cells in lung: excess ACTH
same features as syndrome

73
Q

Cushing’s features

A 
hyperglycemia
increased proteolysis
thin skin
easy bruising
muscle wasting
central obesity
moon face
acne 
buffalo hump
hypertension
virilization
74
Q

Zone reticularis lacks the enzyme

A

21 beta hydroxylase

75
Q

21 beta hydroxylase is necessary for biosynthesis of

A

Cortisol

Aldosterone

76
Q

DHEA in males

A

weak androgens, not important

77
Q

DHEA in females

A

main source of androgens is the adrenal cortex

needed for pubic and axillary hair

78
Q

Adrenal androgens are referred to as

A

17-ketosteroids

ketone at C17

79
Q

21 beta hydroxylase deficiency

A

no cortisol or aldosterone, increased androstenedione
masculization in utero of female genitalia (androgenital syndrome)
increased 17-ketosteroids in urine
high ACTH: trophic effects (lack of feedback control)

80
Q

21 beta hydroxylase converts

A
  1. progesterone to 11-deoxycorticosterone

2. 17-hydroxyprogesterone to 11-deoxycortisol

81
Q

when the clitoris enlarges and takes a penile form, it’s called

A

Female pseudohermaphrodite/contra-sexual development

82
Q

most stored catecholamines in granules are

A

epinephrine

83
Q

rate limiting step of catecholamine synthesis

A

tyrosine hydroxylase

84
Q

tyrosine hydroxylase converts

A

tyrosine to DOPA (dihydroxyphenlalanine)

in the cytosol

85
Q

acute stimulation of the adrenal medulla

A

increased tyrosine hydroxylase activity

86
Q

chronic stimulation of the adrenal medulla

A

increased expression and concentration of tyrosine hydroxylase

87
Q

cortisol on the adrenal medulla

A

activates the last step of epinephrine synthesis

phenylethanolamine-N-methyltransferase

88
Q

conversion of dopamine to norepinephrine occurs in

A

granules

dopamine, once produced, enters the granules

89
Q

conversion of norepinephrine to epinephrine occurs in

A

cytosol

90
Q

phenylethanolamine-N-methyltransferase

A

norepinephrine to epinephrine reaction

activated by cortisol

91
Q

2 main enzymes to degrade catecholamines

A
  1. Monoamine oxidase (MAO): mostly NE

2. Catechol-0-methyltransferase (COMT): mostly epi

92
Q

MAO is expressed in

A

neuronal cytoplasm

93
Q

COMT is expressed in

A

heart, liver, kidney

94
Q

excreted in urine, serves as an index for SNS activity

A 
vanillylmandelic acid (VMA)
product of Epi/NE breakdown
95
Q

Medullary hypofunction occurs

A

post-adrenalectomy

no overt clinical difficulties

96
Q

Medullary hyperfunction

A

pheochromatoma
catecholamine secreting tumor
40s-50s, htn, rapid pulse, HA, chest pain, sweating, hyperglycemia, fatigue

97
Q

Short term stress response

A

adrenal medulla: catecholamines

98
Q

long term stress response

A

adrenal cortex: mineralocorticoids, glucocorticoids

Unit 2 Phys II (11 decks)

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