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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
Mediators of cholesterol mobilization
ACTH Angiotensin II receptor K+ channels
26
transporter of cholesterol to inner mitochondrial membrane
Steroidogenic acute regulatory protein (STaR)
27
desmolase is stimulated by
ACTH
28
drains adrenal blood flow
medullary vein
29
aldosterone is a
mineralocorticoid
30
cortisol is a
glucocorticoid
31
androstenedione is a
androgen
32
enzyme missing in zona glomerulosa
17 alpha hydroxylase | **without it, only pathway is to synthesize aldosterone**
33
17 alpha hydroxylase is necessary to synthesize
DHEA, androstenedione, cortisol
34
corticosterone is converted to aldosterone by
aldosterone synthase
35
aldosterone synthase activity is stimulated by
angiotensin II
36
secretagogues for aldosterone synthesis (3)
1. ANG II 2. Increase in plasma [K+] 3. ACTH (weakly)
37
RAAS is stimulated by
Decrease in blood pressure | Decrease in ECF volume
38
Aldosterone binds to
Mineralocorticoid receptor 1 (MR1)
39
MR1 binds to
mineralcorticoid responsive element (MRE)
40
Aldosterone effects:
1. Na+ reabsorption 2. K+ secretion 3. Net expansion of ECF 4. H+ excretion
41
Conn's syndrome: primary hyperaldosteronism
``` caused by a tumor Hypernatremia, fluid retention, htn Hypokalemia Metabolic alkalosis Low renin levels (htn) ```
42
17 alpha-hydroxylase deficiency
``` Glucocorticoids and steroids not produced Increased 11-deoxycorticosterone, corticosterone: have mineralocorticoid function low aldosterone (due to corticosterone excess) low renin (htn) ```
43
2 aldosterone precursors with mineralocorticoid function
11-deoxycorticosterone corticosterone ***if in excess, low aldosterone***
44
Inhibits renin secretion
htn
45
Zona fasciculata lacks the enzymes
17, 20 lyase | Aldosterone synthase
46
17, 20 lyase is necessary to
convert: 17-hydroxypregnenolone to DHEA 17-hydroxyprogesterone to androstenedione
47
Cortisol negative feedback
1. Directly inhibits CRH | 2. Inhibits action of CRH on corticotrophs, decreasing ACTH release
48
Corticotropin releasing hormone (CRH) is released during
stress | increases ACTH secretion
49
do DHEA or Androstenedione have negative feedback loops on CRH or ACTH?
NO
50
only negative feedback loops for CRH or ACTH
Cortisol
51
ACTH is released in a
circadian/pulsatile pattern, mostly in morning | Cortisol and androgen levels reflect ACTH release
52
ACTH activity reflects
CRH secretion
53
overall metabolic effect of cortisol
increase blood glucose by enhancing gluconeogenesis | *essential for fasting and stress*
54
Cortisol increases 2 pathways
1. protein catabolism --> ammino acids | 2. lipolysis --> glycerol
55
Cortisol decreases
glucose uptake by tissues (glucose sparing)
56
Cardiovascular actions of cortisol
maintain normal BP | up-regulates alpha-1 receptor
57
Bone actions of cortisol
Decreases intestinal and renal calcium absorption | mobilizes calcium from bone, inhibits bone formation
58
excessive glucorticoids (or high blood cortisol) results in
bone loss
59
actions of cortisol on connective tissue/muscle
inhibits fibroblast proliferation, collagen formation skin thinning proteolysis in muscle: weakness
60
anti-inflammatory/immune actions of cortisol
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
Addison's disease: primary adrenocortical insufficiency
destruction of adrenal gland --> decreased synthesis of all adrenaocortical hormones
62
loss of cortisol (Addison's disease) (Secondary/Tertiary adrenocortical insufficiency)
hypoglycemia during stress weight loss muscle weakness
63
loss of aldosterone (Addison's disease)
hyperkalemia hypotension metabolic acidosis salt craving
64
loss of androgens (Addison's disease) (Secondary/Tertiary adrenocortical insufficiency)
in females, decreased pubic and axillary hair, decreased libido
65
other effects of Addison's disease
increased ACTH secretion --> alpha-MSH fragment--> hyperpigmentation of skin, nipples, knees, gums
66
ACTH is derived from
proopiomelanocortin (POMC)
67
POMC is cut into
gamma fragment beta endorphin: contains beta-MSH gamma liptropin ACTH: contains alpha-MSH
68
Secondary adrenocortical insufficiency
Failure of corticotrophs to secrete ACTH
69
Tertiary adrenocortical insufficiency
Insufficient CRH
70
In Secondary/Tertiary adrenocortical insufficiency
cortisol and androgen deficiency aldosterone levels normal (regulated by RAAS) no hyperpigmentation as low ACTH
71
Cushing's syndrome
``` primary adrenal hyperplasia: oversecretion of cortisol Low ACTH (negative feedback) ```
72
Cushing's disease
overactive anterior pituitary or ACTH-secreting cells in lung: excess ACTH same features as syndrome
73
Cushing's features
``` hyperglycemia increased proteolysis thin skin easy bruising muscle wasting central obesity moon face acne buffalo hump hypertension virilization ```
74
Zone reticularis lacks the enzyme
21 beta hydroxylase
75
21 beta hydroxylase is necessary for biosynthesis of
Cortisol | Aldosterone
76
DHEA in males
weak androgens, not important
77
DHEA in females
main source of androgens is the adrenal cortex | needed for pubic and axillary hair
78
Adrenal androgens are referred to as
17-ketosteroids | ketone at C17
79
21 beta hydroxylase deficiency
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
21 beta hydroxylase converts
1. progesterone to 11-deoxycorticosterone | 2. 17-hydroxyprogesterone to 11-deoxycortisol
81
when the clitoris enlarges and takes a penile form, it's called
Female pseudohermaphrodite/contra-sexual development
82
most stored catecholamines in granules are
epinephrine
83
rate limiting step of catecholamine synthesis
tyrosine hydroxylase
84
tyrosine hydroxylase converts
tyrosine to DOPA (dihydroxyphenlalanine) | in the cytosol
85
acute stimulation of the adrenal medulla
increased tyrosine hydroxylase *activity*
86
chronic stimulation of the adrenal medulla
increased *expression and concentration* of tyrosine hydroxylase
87
cortisol on the adrenal medulla
activates the last step of epinephrine synthesis | phenylethanolamine-N-methyltransferase
88
conversion of dopamine to norepinephrine occurs in
granules | dopamine, once produced, enters the granules
89
conversion of norepinephrine to epinephrine occurs in
cytosol
90
phenylethanolamine-N-methyltransferase
norepinephrine to epinephrine reaction | activated by cortisol
91
2 main enzymes to degrade catecholamines
1. Monoamine oxidase (MAO): mostly NE | 2. Catechol-0-methyltransferase (COMT): mostly epi
92
MAO is expressed in
neuronal cytoplasm
93
COMT is expressed in
heart, liver, kidney
94
excreted in urine, serves as an index for SNS activity
``` vanillylmandelic acid (VMA) product of Epi/NE breakdown ```
95
Medullary hypofunction occurs
post-adrenalectomy | no overt clinical difficulties
96
Medullary hyperfunction
pheochromatoma catecholamine secreting tumor 40s-50s, htn, rapid pulse, HA, chest pain, sweating, hyperglycemia, fatigue
97
Short term stress response
adrenal medulla: catecholamines
98
long term stress response
adrenal cortex: mineralocorticoids, glucocorticoids

Unit 2 Phys II (11 decks)

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