Physiology of Adrenal Glands Flashcards

(62 cards)

1
Q

What is the origin of adrenal medulla?

A

Neuroectodermal origin

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2
Q

What does adrenal medulla secrete?

A

Catecholamines, epi and NE

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3
Q

What is the origin of adrenal cortex?

A

Mesodermal origin

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4
Q

Adrenal cortex releases hormones that are colelctively known as

A

corticosteroids

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5
Q

ZG will release

A

mineralocorticoids

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6
Q

ZF and ZR will release

A

glucocorticoids and androgens

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7
Q

ACTH will form due to processing the

A

POMC peptide

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8
Q

Alpha MSH is involved in

A

pigmentation of skin and appetite regulation

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9
Q

Beta endorphin is an endogenous opiate that can

A

inhibit pain sensitivity

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10
Q

Transcortin =

A

cortisol binding globulin

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11
Q

Most cortisol will bind to

A

CBG (cortisol binding globulin)

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12
Q

60% of aldosterone binds to

A

plasma proteins

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13
Q

Once adrenocortical hormones are released from plasma proteins, it will diffuse into

A

cells and bind to intracellular receptor

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14
Q

Steroid-receptor dimerization will occur and this complex will bind to

A

Glucocorticoid response elements (GRE)

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15
Q

Cortisol undergoes what type of release?

A

Pulsatile- highest in morning

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16
Q

Exogenous glucocorticoids are also given as

A

immunosuppressants

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17
Q

What is the rate limiting step in synthesis of corticosteroids?

A

Cholesterol desmolase

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18
Q

What can stimulate cholesterol desmolase?

A

ACTH

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19
Q

All adrenal cortex hormones are derived from what?

A

Cholesterol

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20
Q

Most of the cholesterol is received via

A

blood stream

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21
Q

Fasciculata/reticularis contains

A

17,20-lyase to make androgen

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22
Q

Gomerulosa contains _________ so that aldosterone can be made.

A

aldosterone synthase

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23
Q

Low-density lipoprotein receptor (LDLr) is located on the adrenal cells to facilitate

A

endocytosis of cholesterol

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24
Q

Adrenal androgens, DHEA and androstenedione, are produced in the fasciculata/reticularis and have

A

weak androgenic activity

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25
Zona fasciculata/reticularis are under control of
hypothalamic-pituitary axis
26
CRH is released by
paraventricular nuclei
27
CRH acts on corticotrophs via adenylyl cyclase/cAMP to
stimulate release of ACTH
28
Excess cortisol will _______ ACTH levels
decrease
29
Cortisol deficiency will _______ ACTH levels
increase
30
Chronic release of ACTH will have a ______ effect on the adrenal celsl and can induce hyperplasia
trophic
31
ZG does not produce
glucocorticoids
32
Why does ZG not produce glucocorticoids?
- Aldosterone synthase converts corticosterone to aldosterone - It lacks 17,alpha-hydrozylase and is unable to convert progesterone to cortisol
33
If there is a block at 21,β-hydroxylase or above, then
no mineralocorticoids will be produced
34
What factors can stimulate ACTH secretion?
- Stress, hypoglycemia, trauma, some drugs
35
What factors can inhibit ACTH secretion?
Somatostain, some drugs, increased blood cortisol levels
36
Cortisol will induce the synthesis of _______ which is an inhibitor of phospholipase A2
lipocortin
37
Cortisol inhibits the production of ______ and the proliferation of T lymphocytes
IL-2
38
Cortisol inhibits the release of ______ and _______ from mast cell and platelets
histamine and serotonin
39
What syndrome is the hypersecretion of cortisol?
Cushing's syndrome
40
Cushing's syndrome can be due to
chronic excess of glucocorticoids or from hypersecretion of cortisol from adrenal such as tumor
41
Excess cortisol can cause
hyperglycemia, increase in protein/lipid catabolsim, central obesity, poor wound healing, osteoporosis, hypertension
42
How is cushings treated?
Ketoconazole or metyrapone to block synthesis of glucocorticoids/adrenal androgens
43
Addisons is the loss of
adrenocorticol hormones
44
Addisons is commonly caused by
Auto immune destruction of adrenal cortex
45
Addisons is also known as
primary adrenocortical insufficiency
46
In addisons, there is a decrease in
all adrenocortical hormones
47
Loss of adrenocortical hormones will cause
hypoglycemia, hypotension, hyperkalemia, metabolic acidosis, weight loss
48
Why will pt with Addisons have hyperpigmentation?
Increase alpha MSH as a result of excess ACTH levels
49
ACTH, AngII, and increased extracellular potassium will all increase the release of
aldosterone
50
Aldosterone can be stimulated by
ACTH, low BP/volume through activation of RAAS and high plasma K
51
High extracellular K will act on adrenal cells to depolarize the cell membrane, which will do what?
Open VGCCs
52
Increases in intracellular calcium will activate
aldosterone synthase
53
Degradation of aldosterone occurs through
glucoronidation in liver
54
Once sodium and water are reabsorbed, this will increase arterial blood pressure. which will promote
pressure diuresis (loss of Na and water)
55
What is aldosterone escape?
The return of sodium and water back to normal once pressure diuresis is promoted?
56
What is Conn Syndrome?
Primary aldosteronism. Results from hypersecretion of aldosterone in absence of known stimulus
57
What is secondary aldosteronism?
Increased aldosterone secretion as a result of known stimulus (Increased AngII)
58
Slight expansion of volume will occur along with
sodium reabsorption, K+ secretion, and H+ secretion
59
Conn syndrome patient will be
hypertensive and arterial pH (metabolic alkalosis)
60
In Conn syndrome, what will happen to renin levels?
Will be decreased due to increase in ECF volume and increased renal perfusion pressure
61
What is treatment for Conn syndrome?
Administration of an aldosterone receptor antagonist followed by surgical removal of tumor
62
Adrenal adenoma can produce either
Cushing's syndrome or Conn Syndrome