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Neuroendocrine Exam 3 > Hypothalamic-Pituitary Relationships and Biofeedback Pt. II > Flashcards

Hypothalamic-Pituitary Relationships and Biofeedback Pt. II Flashcards

1
Q

what does the adrenal medulla secrete?

A

catecholamines- epinephrine and norepinephrine

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2
Q

What are the zones of the adrenal cortex from outer to inner?

A

zona glomerulosa, zona fasciculata, and zona reticularis

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3
Q

what does the zona glomerulosa secrete?

A

mineralocortcicoids (aldosterone)

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4
Q

what does the zona fasciculata secrete?

A

glucocorticoids (cortisol)

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5
Q

what does the zona reticularis secrete?

A

androgens

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6
Q

what stimulates the release of CRH from the hypothalamus?

A

stress and the circadian rhythm

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7
Q

what is the effect of cortisol on the immune system?

A

immunosuppression

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8
Q

what is the effect of cortisol on the liver?

A

gluconeogenesis

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9
Q

what is the effect of cortisol on the muscles?

A

protein catabolism

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10
Q

what is the effect of cortisol on adipose tissue?

A

lipolysis

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11
Q

cortisol has negative feedback loops where?

A

directly inhibits the anterior pituitary from secreting more ACTH, directly inhibits the hypothalamus from secreting more CRH, and also suppresses infection and inflammation

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12
Q

do androgens secreted by the zona reticularis have any feedback loops on the anterior pituitary or hypothalamus

A

NO ONLY CORTISOL DOES

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13
Q

when are the secretory rates of cortisol the highest?

A

in the early morning

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14
Q

what is the main stimulus for aldosterone secretion by the zona glomerulosa?

A

decreased Na+ or increased K+ in the blood or decreased blood pressure

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15
Q

if you have low BP/ low Na+ in the blood and high K+ in the blood what is stimulated?

A

the kidneys are stimulated to release renin

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16
Q

what does renin cause?

A

the conversion of angiotensinogen to angiotensin 1 (which is inactive)

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17
Q

what catalyzes the angiotensin 1 into its active form and what is the active form?

A

ACE and the active form is angiotensin II

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18
Q

what does angiotensin II do?

A

it acts on the zona glomerulosa to secrete aldosterone

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19
Q

what are the effects of aldosterone?

A

it causes BP to increase, Na+ levels in the blood to increase–> water and Na+ reabsorption

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20
Q

What are the signs of cushing’s syndrome?

A

truncal obesity, moon face, buffalo hump, easy bruising, HTN, acne

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21
Q

cushing’s syndrome is a result of what?

A

chronic excess of glucocorticoids

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22
Q

what is the low-dose dexamethasone supression test used for?

A

to test for Cushing’s syndrome

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23
Q

what would be a normal test finding of a low dose dexamethasone test?

A

low cortisol levels

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24
Q

what would be an abnormal test finding for a low dose dexamethasone test?

A

high/normal cortisol levels

25
Q

what would low levels of cortisol after a high dose of dexamethasone indicate?

A

cushing’s disease

26
Q

what is cushing’s disease?

A

an anterior pituitary tumor

27
Q

what would high levels/normal levels of cortisol and high levels of ACTH after a high dose of dexamethasone indicate?

A

an ectopic ACTH secreting tumor

28
Q

what would high/normal levels of cortisol and low levels of ACTH after a high dose of dexamethasone indicate?

A

adrenal cushing’s syndrome

29
Q

if there is long term treatment of exogenous glucocorticoids, what would happen?

A

the anterior pituitary would stop releasing ACTH and therefore the zona fasciculata would atrophy since it wasn’t being stimulated

30
Q

what are some examples of synthetic glucocorticoids?

A

prednisone, methylprednisone, and dexamethasone

31
Q

what is the term for excessive exogenous glucocorticoids?

A

Iatrogenic

32
Q

what would the levels look like for Iatrogenic cushing’s syndrome?

A

decreased CRH, decreased ACTH, and decreased cortisol (the exogenous glucocorticoids mimic cortisol so there are symptoms like there is excessive amounts of cortisol when there really is not)

33
Q

what is the primary action of aldosterone?

A

renal sodium reabsorption

34
Q

why is addison disease often characterized by hyperpigmentation of the skin?

A

becasue addison disease leads to increased levels of ACTH and the ACTH contains the alpha-MSH fragment which leads to melanin synthesis

35
Q

what type of hormone is ACTH?

A

peptide hormone

36
Q

what is ACTH derived from?

A

POMC

37
Q

what are the lab levels for addison disease?

A

decreased Na+ in blood and increased K+ in blood

38
Q

if you have a primary adrenal insufficiency what would the levels of cortisol and aldosterone look like?

A

they would both be low

39
Q

if you have a secondary adrenal insufficiency what would the levels of cortisol and aldosterone look like?

A

the levels of cortisol would be low due to the low ACTH, but the aldosterone levels would be normal

40
Q

what are some causes of addison disease (primary adrenal insufficiency)

A

autoimmune disease, adrenal hemorrhage secondary to N. meningitidis, infection with tuberculosis or N. meningitidis

41
Q

what is primary hyperaldosteronism?

A

excessive release of aldosterone from the adrenal cortex

42
Q

what is conn’s syndrome?

A

it is an adenoma in the adrenal cortex (zona glomerulosa) that causes increased secretion of aldosterone

43
Q

what is secondary hyperaldosteronism?

A

excessive renin secretion by the juxtaglomerular cells in the kidney

44
Q

if you have ambiguous genitalia, hypertension, masculinization, and low potassium levels, what deficiency would you expect?

A

11-beta hydroxylase deficiency

45
Q

if you have ambiguous genitalia, hypotension, and masculinization, what deficiency would you expect?

A

21-Beta-hydroxylase deficiency

46
Q

if you have a 21-B hydroxylase deficiency what would the levels look like?

A

decreased cortisol, increased K+, decreased Na+ and increased renin

47
Q

if you have a 11-Beta-hydroxylase deficiency what would the levels look like?

A

increased Na+ levels, decreased K+ levels, decreased renin levels, decreased levels of cortisol

48
Q

an individual with an 11-B-hydroxylase deficiency would have hypertension due to what?

A

the accumulation of DOC, DOC can have mineralocorticoid activity

49
Q

what are you blocking with a 17-alpha hydroxylase deficiency?

A

cortisol production and androgen production–> so heavily leans on aldosterone production

50
Q

what are the symptoms of 17-alpha-hydroxylase deficiency?

A

hypertension and feminization

51
Q

the mineralocorticoid receptor is protected from activation by cortisol by what?

A

the enzyme 11B-HSD2

52
Q

all congenital adrenal enzyme deficiencies are characterized by what?

A

enlargement of both adrenal glands due to increased ACTH stimulation due to low levels of cortisol (adrenal hyperplasia)

53
Q

if a patient presents with hypertension, headaches, palpitations, and sweating, what might you suspect?

A

increased catecholamines from the adrenal medulla caused from a pheochromocytoma

54
Q

synthesis of catecholamines is under the control of what?

A

sympathetic activity and the CRH-ACTH-cortisol axis

55
Q

what effect does cortisol have on epinephrine?

A

cortisol upregulates PNMT enzyme which converts norepinephrine to epinephrine

56
Q

if there are high levels of metanephrine, what would you expect?

A

increased catecholamine production (epinephrine)

57
Q

if there are high levels of normetanephrine, what would you expect?

A

high levels of catecholamine production (norepinephrine)

58
Q

what converts catecholamines into their byproducts?

A

COMT

59
Q

epinephrine has a higher affinity for what receptor type?

A

B2

Neuroendocrine Exam 3 (19 decks)

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