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
Q

What is the rate limiting step of catecholamine synthesis?

A

tyrosine – tyr hydroxylase –> L-DOPA

26
Q

What is the general formation of catecholamines and where does it occur?

A

in cytoplasm: Tyr –> DOPA –> dopamine

in granule: Dopamine –> NE

cytoplasm: NE –> epi -> to granule again for release

27
Q

What does VMAT do?

A

moves Epi into specialized storage vesicles for release

28
Q

How are chromaffin granules released?

A

via exocytosis after sympathetic stimulation

29
Q

How are catecholamines broken down?

A

NE/E –> thru MAO –> thru COMT –> VMA

*VMA measurement can determine catecholamine production

30
Q

What is MAO?

A

oxidizes stuff

breaks down catecholamines

used to treat neuropsychiatric disorders

31
Q

What is COMT?

A

methylates stuff

primary enzyme that inactivates catecholamines released from the adrenal gland

32
Q

What do you see in pheochromocytoma?

A

usually benign and unilateral adrenal tumor

excess catecholamines

symptoms wax and wane (high bp, headaches, sweating)