Adrenal Gland Flashcards

1
Q

What is secreted in the different parts of the adrenal gland?

A

cortex = corticoids and androgens

medulla = catecholamines

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2
Q

In which CAH are sex hormones decreased?

A

defect in 17-alpha

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3
Q

How does the cortisol affect the liver, muscle, fat, and skin?

A

liver = increased gluconeogenesis

muscle = breakdown of protein

fat = lipolysis in extremeties, central fat deposition

skin = breakdown of collagen –> thin skin, easy bruising

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4
Q

How does cortisol affect the immune system, endocrine, and GI?

A

immune = depression

endocrine = insulin resistance, down regulates pituitary hormones

GI = interferes w/ Ca absorption –> risk of osteoporosis long-term

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5
Q

How is cortisol regulated by hypothalamus and pit?

A

CRH released from paraventricular nucleus of hypothalamus –> CRF1 receptor in pituitary –> ACTH –> cortisol

cortisol does negative feedback to both hypothalamus and ant pit

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6
Q

What is the ACTH molecule derived from and what is its significance to pigment?

A

derived from POMC –> ACTH in ant pit –> in non pituitary tissues, breaks down, contains MSH

MSH = melanocyte-stimulating hormone

excess ACTH –> hyperpigmentation

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7
Q

How do CRH and ACTH affect each other?

A

CRH –> ACTH

ACTH has negative feedback to CRH

CRH also inhibits itself

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8
Q

How do glucocorticoids specifically affect CRH and ACTH?

A

inhibit POMC transcription –> no ACTH

inhibit mRNA synthesis of CRH and ACTH

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9
Q

What is the difference btw a low and high dose DST?

A

low dose = determines whether a problem is present; normal = suppression of ACTH and cortisol

high dose = determines the source of the problem

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10
Q

What are the the results of high dose DST for pituitary cushing, adrenal cushing, and ectopic ACTH?

A

pituitary: supression of ACTH
adrenal: no suppression of cortisol
ectopic: no supression

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11
Q

What is the Cosyntropin stim test?

A

Admin ACTH –> see what happens

healthy = cortisol should increase

adrenal insuffiency = no response

dramatic increase in cortisol –> could be secondary adrenal insufficieny

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12
Q

What is the difference btw Cushing syndrome and Cushing Disease?

A

Cushing syndrome = umbrella term for high cortisol; non-pituitary cause

Cushing disease = pituitary tumor causing high cortisol

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13
Q

What would the results be of a low dose ONDST for cushing syndrome and disease?

A

syndrome = ACTH suppressed, cortisol not suppressed

disease = ACTH not suppressed, cortisol suppressed

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14
Q

What is Addison’s disease?

A

primary adrenal insufficiency

progressive destruction of adrenal gland

High ACTH but low cortisol

will fail cosyntropin stim test

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15
Q

What is secondary adrenal insufficiency?

A

usually a pituitary problem

sometimes too much steriods –> decreases ACTH

see low ACTH and low cortisol

On cosyntropin stim test: cortisol will rise dramatically

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16
Q

In what diseases would you see hyperpigmentation?

A

cushing disease (secondary cortisol excess)

Addison’s (primary adrenal insuficieny)

17
Q

How does Aldosterone affect the kidneys?

A

increases synthesis and activity of Na channels in apical membrane

Increases synthesis and activity of Na/K ATPase in the basolateral membrane of the distal tubule

overall = increased K excretion, increased sodium reabsorption

18
Q

What is Conn syndrome?

A

primary hyperaldosteronism = adrenal problem

usually neoplasm

see high BP and Na, low K

won’t change ACTH very much

low renin

19
Q

What is secondary hyperaldosteronism?

A

hypersecretion of renin by juxtaglomerular cells of kidney –> too much aldosterone

high BP and Na, low K

little change in ACTH

20
Q

What is hypoaldosteronism?

A

adrenal problem –> little aldosterone

low Na, high K

high renin (trying to raise aldosterone)

low BP

21
Q

What is secondary hypoaldosteronism?

A

Hyposecretion of renin –> not enough aldosterone

Low Na, high K

low BP

22
Q

How does ACTH affect cortisol and aldosterone?

A

affects cortisol much more

ACTH deficiency –> low cortisol, but little change in aldosterone

23
Q

What are the adrenal androgens and where are they from?

A

from zona reticularis –> DHEA and DHEAS –> precursors to sex hormones

rely on 3beta-HSD to exert activities

24
Q

How does the body stimulate catecholamine production?

A

Sympathetics –> ACh –> nicotinic receptors in adrenal medulla –> increased synthesis of tyrosine hydroxylase and activity of dopamine

25
What is the rate limiting step of catecholamine synthesis?
tyrosine -- tyr hydroxylase --\> L-DOPA
26
What is the general formation of catecholamines and where does it occur?
in cytoplasm: Tyr --\> DOPA --\> dopamine in granule: Dopamine --\> NE cytoplasm: NE --\> epi -\> to granule again for release
27
What does VMAT do?
moves Epi into specialized storage vesicles for release
28
How are chromaffin granules released?
via exocytosis after sympathetic stimulation
29
How are catecholamines broken down?
NE/E --\> thru MAO --\> thru COMT --\> VMA \*VMA measurement can determine catecholamine production
30
What is MAO?
oxidizes stuff breaks down catecholamines used to treat neuropsychiatric disorders
31
What is COMT?
methylates stuff primary enzyme that inactivates catecholamines released from the adrenal gland
32
What do you see in pheochromocytoma?
usually benign and unilateral adrenal tumor excess catecholamines symptoms wax and wane (high bp, headaches, sweating)