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NE3 > hypothalamic pituitary relationshops 2 > Flashcards

hypothalamic pituitary relationshops 2 Flashcards

1
Q

name the regions of the adrenal medulla in order

A

Zona glomerulosa
zona fasciculata
zona reticularis

medulla

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2
Q

what class of hormone is aldosterone, what secretes it, what does it do?

A

mineralocorticoid

zona glomerulosa

regulates salt and volume homesotasis

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3
Q

what class of hormone is norepi and epi, what secretes it, what does it do?

A

catecholamine

medulla

respond to stress rapidly

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4
Q

what class of hormone is cortisol, what secretes it, what does it do?

A

glucocorticoid

zona reticularis

longer acting stress response

regulates glucose use, immune and inflammation

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5
Q

what class of hormone is DHEAS, what secretes it, what does it do?

A

steroid

zona fasciculata and reticularis

makes androgens

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6
Q

HPA axis is under negative feedback control of what?

A

cortisol

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7
Q

what causes CRH to be released?

what does it then cause to be released?

A

emotional stress, metabolic stress, physical stress

causes ACTH to be released from anterior pituitary

causes cortisol to be released

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8
Q

what are the actions of cortisol on organ systems?

A

immune suppression

gluconeogenesis in liver

protein catabolism in muscle

lipolysis in adipose tissue

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9
Q

how do circadian rhythms control cortisol?

A

cortisol high in the morning,

low in evening

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10
Q

what affect does aldosterone have?

A

water/na+ reabsorption by kidneys, BP goes up

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11
Q

how is aldosterone secretion regulated? list the steps

A

liver makes angiotensinogen

becomes angiotensin 1 via
renin (made in kidney due to low BP)

becomes angiotensin 2 due to ACE

goes to adrenal cortex

becomes aldosterone

targets kidney tubules

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12
Q

what effect does ACTH have on zona glomerulosa

A

increased secretion of aldosterone

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13
Q

what causes cushing syndrome(CS)? symptoms?

A

too much cortisol over time

truncal obesity
moon face
hump
osteoporosis
hirsutism
cognitive defects 
edema
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14
Q

what does the dexamethasone suppression test low dose show?

A

differentiates CS patients of any cause from patients who do not have CS

NO ACTH suppression shows CS

but doesnt show where ACTH is coming from

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15
Q

what does the dexamethasone suppression test high dose show?

when is it used

what does it show

A

distinguishes patients of CS caused by pituitary ACTH tumor and non pituitary ACTH tumor

used after diagnosis of CS is made

decrease in ACTH shows pituitary tumor
(feedback)

no change in ACTH shows ectopic tumor
(no feedback)

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16
Q

what does an excess of glucocorticoid do?

A

diabetogenic effect

visceral obesity

osteoporosis

thinning of skin, muscle atrophy

immunosuppression

water retention

decrease in growth

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17
Q

what is acth dependent cushing disease caused by?

A

acth secreting tumors (pituitary)

ectopic tumors

crh secreting tumors

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18
Q

what is acth independent cushing disease caused by?

A

adrenal carcinoma

adrenal adenoma

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19
Q

what is pseudo cushing syndrome?

A

major depression

anxiety

caused by illness or alcoholism rarely

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20
Q

what is the negative effect of exogenous glucocorticoids?

A

can atrophy adrenal cells that produce cortisol

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21
Q

whats the process by which aldosterone works?

A

combines with cytoplasmic receptor

initiates transcription in nucleus

new protein channels and pumps made

aldosterone induced proteins modulate channels and pumps

na reabsorption increased
k secretion decreased

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22
Q

where does ACTH come from? what does it make?

A

peptide from anterior pituitary, by POMC

makes cortisol

also MELANIN!

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23
Q

addisons disease causes what? by what?

A

hyperpigmentation, overproduction of ACTH

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24
Q

what is cosyntropin stimulation test used for?

A

detect adrenal gland insufficiency

cosyntropin in synthetic ACTH

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25
Q

what are the symptoms of a primary adrenal insufficiency?

A

adrenal gland not working

aldosterone and cortisol not produced

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26
Q

what are the symptoms of a secondary adrenal insufficiency?

A

aldosterone produced

cortisol not produced

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27
Q

what can cause primary adrenal insufficiency?

A

called addisons disease

can be autoimmune
can be hemhorrage
(waterhousefriedrichsen syndrome due to meningitidis)

infections such as tuberculosis

tumors going to adrenal gland

28
Q

how is adrenal insufficiency treated?

A

replacing hormones adrenal glands are not making

cortisol replaced with corticosteroid

aldosterone replaced by mineralocorticoid

29
Q

primary adrenal excess:

what happens to

plasma cortisol

CRH

ACTH

Hyperpigmentation

A

up

down

down

no hyper

30
Q

secondary pituitary excess:

what happens to

plasma cortisol

CRH

ACTH

Hyperpigmentation

A

up

down

up

yes hyper

31
Q

primary adrenal deficiency:

what happens to

plasma cortisol

CRH

ACTH

Hyperpigmentation

A

down

up

up

yes hyper

32
Q

secondary deficiency:

what happens to

plasma cortisol

CRH

ACTH

Hyperpigmentation

A

down

up

down

yes hyper

33
Q

steroid administration:

what happens to

plasma cortisol

CRH

ACTH

Hyperpigmentation

A

down (symptoms of excess)

down

down

no hyper

34
Q

what does primary hyperaldosteronism entail?

give an example

A

too much aldosterone from adreanl cortex

conns syndrome for example: adenoma of adrenal cortex

35
Q

what does secondary hyperaldosteronism entail?

A

too much renin secreted by kidney

36
Q

what does hypoaldosteronism entail?

A

destruction of adrenal cortex

defects in making aldosterone

inadequate stimulation to make aldosterone

37
Q

addisons disease causes what?

how is it treated

A

hypotension, hyponatremia

steroid replacement therapy for life

38
Q

primary hyperaldosteronism causes what?

how is it treated

A

hypertension, hypokalemia, low plasma renin

solved with surgery or spironolactone

39
Q

how do we test PAC-PRA ration to detect primary hyperaldosteronism?

A

PAC-PRA ration greater than 20

PAC greater or equal to 15

test for primary aldosteronism

40
Q

describe how aldosterone is made by adrenal cortex?

A

zona glomerulosa

cholesterol
to
pregnenolone
to 
progesterone (3b hydroxysterois dehydrogenase)
to
11-deocycorticosterone (21b hydroxylase)
to
corticosterone (11b hydroxyalase)
to 
aldosterone
41
Q

describe how cortisol is made by adrenal cortex?

A

zona fasciculata and reticularis

cholesterol
to
pregnenolone
to 
progesterone (3b hydroxysterois dehydrogenase)
to
17OH progesterone (17a hydroxylase)
to
11 deoxycortisol (21b hydroxyalase)
to 
cortisol (11b hydroxylase)
42
Q

describe how androgens is made by adrenal cortex?

A

zona fasciculata and reticularis

cholesterol

to
17OH pregnenolone (17a hydroxylase)
to

androgens

43
Q

what prevents activation of mineralocortoid receptor by cortisol?

A

enzyme 11b-HSD2

44
Q

what are all congenital adrenal enzyme deficiencies marked by?

A

bot adrenal glands are enlarged due to high acth

not enough cortisol to stop it

45
Q

17 a deficiency, what happens to:

mineralocorticoids

cortisol

sex hormones

blood pressure

K+

labs

other presentations

A

up

down

down

up

down

down androstenedione

lack of sexual development

46
Q

21 b deficiency, what happens to:

mineralocorticoids

cortisol

sex hormones

blood pressure

K+

labs

other presentations

A

down

down

up

down

up

up renin, up 17 hydroxyprogesterone

salt wasting, precocious puberty

47
Q

11b deficiency, what happens to:

mineralocorticoids

cortisol

sex hormones

blood pressure

K+

labs

other presentations

A

down aldosterone, up DOC

down

up

up

down

down renin

viriliation

48
Q

what is a pheochromocytoma, what happens?

A

adrenal gland tumor, too much ep and norepi released
activate a and b adrenergic receptors

causes hypertension

49
Q

what are the catecholamine, what do they respond to?

what do they influence

A

epi and nor epi

respond to stress such as hypoglycemia or exercise

influences metabolism and cardiac output

50
Q

what controls synthesis of catecholamines?

how is it upregulated?

A

sympathetic activity and CRH-ACTH-Cortisol Axis

upregulated by cortisol via PNMT

51
Q

what signals catecholamine release from adrenal medulla?

A

AcH

52
Q

whats the rate limiting step of norepi and epi production?

A

tyrosine hydroxylase, tyrosine to dopa

53
Q

name the steps of norepi production?

A 
tyrosine to dopa, 
to
DA 
to
chromaffin granule

norepi diffuses out

54
Q

how is epi made from norepi?

A

norepi diffuses out of granule,

made into E via PNMT

E goes back to granule via VMAT

55
Q

how are E stored?

A

in chromaffin granules with ATP, Ca and proteins

as chromogranins

56
Q

what tumors do circulating chromogranins signal?

A

paragangliomas

57
Q

what breaks down catecholamines

A

COMT mostly

58
Q

what signals total catecholamine production?

A

catecholamines, metanephrines, VMA

59
Q

pheochromocytoma is signalled by what?

A

elevated levels of catecholamines and byproducts

60
Q

a receptors and b3 receptors respond better to what?

what do they do

A

NE

a: increase vascular smooth muscle constriction
b3: increase hepatic glucose output , lipolysis

61
Q

b1 receptors respond better to what?

what do they do

A

both norepi and epi

increase cardiac output

62
Q

b2 receptors respond better to what?

what do they do

A

epi

decrease contraction of blood vessels

63
Q

what mediates long term stress response?

what happens?

A

mineralocorticoids
-blood pressure rise, kidneys retain water

glucocorticoids

  • immune system repressed
  • blood glucose rises, protein and fats broken down
64
Q

what mediates short term stress response?

what happens?

A

catecholamines

  • heart rate rises
  • blood pressure rises
  • bronchioles dilate
  • metabolic rate increases
  • liver makes glucose
65
Q

what does epinephrine do?

A 
up glycogenolysis
up gluconeogenesis
up lipolysis
up calorigenesis
down glucose use 
up insuln and gucagon
up cardiac contractlity
up heart rate
up arterior dilation
up muscle relaxation
66
Q

what does norepi do?

A 
up gluconeogensis
up glycogenolysis
down insulin
up cardiac contractility
up artery vasoconstriction 
up sphincter contraction
up platelet aggregation

NE3 (15 decks)

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