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unit 6: physiology > adrenal gland (10) > Flashcards

adrenal gland (10) Flashcards

1
Q

is the total loss of the adrenal cortex life threatening? what about of the adrenal medulla?

A

life threatening for the loosing cortex, not medulla

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2
Q

what 2 zones produce glucocorticoids & androgen?

A

zona fasciculata & zona reticularis

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3
Q

what 4 hormones are secreted from the adrenal medulla?

A

epi, norepi, dopa and domapine

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4
Q

what is the precursor for all the adrenal cortex hormones?

A

cholesterol

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5
Q

what step is the rate limiter hormone synthesis?

A

cholesterol–> pregnenolone

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6
Q

what enzyme is needed for the synethesis of DHEA and androgen?

A

17,20 desmolase

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7
Q

why can’t the zona glomerulsa layer only make aldosterone?

A

because it lacks the 17-a-hydroxylase enzyme but still has aldosterone synthase

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8
Q

what limits the secretion of aldosterone by the adrenal gland?

A

it is limited by the rate at which the glomerulosa cells can synthesis the hormone

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9
Q

what are the 3 ways that aldosterone can be found in the serum>

A

free in plasma 37%
bound to CBG
bound to albumin

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10
Q

what is the function of aldosterone?

A

stimulate kidney to reabsorb sodium & water and enhance K secretion
Does this by increasing the transcription of sodium-potassium pump and expression of apical sodium channels

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11
Q

describe the form of cortisol in the plasma?

A

90% bound to cortisol binding protein (CBP)
7% bound to albumin
3% circulates “free”

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12
Q

what is cortisol’s effect on ACTH and CRH?

A

downregulates them

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13
Q

what is cortisol’s effect on POMC gene transcription?

A

cortisol inhibits it

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14
Q

what 3 tissue types in the body respond the most to cortisol?

A

liver
skeletal muscle
adipose tissue

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15
Q

list the metabolic effects of cortisol

A
  • Stimulates gluconeogenesis
  • Enhance protein breakdown in muscle cells to
  • Stimulates lipolysis in adipose tissue
  • Decreases osteoblastic activity in trabecular bone and interferes with Ca++ absorption in the gut
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16
Q

describe the anti-inflammatory effects of cortisol

A
  • Inhibits production of cytokines
  • Inhibits production of chemo-attractant molecules
  • Stabilize lysosomal enzymes
  • Contributes to vasoconstriction & decrease capillary permeability
  • Inhibits histamine release from mast cells
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17
Q

describe the immunosuppressive effects of cortisol

A
  • COX1 and COX2 are inhibited
  • Inhibits histamine release from mast cells
  • IL2 and its receptors are inhibited by cortisol
  • Inhibits both cellular & humoral cell immunity
  • Inhibits hypersensitivity reactions (esp. cell mediated)
  • Decrease lymphocyte proliferation
18
Q

what is considered the most important regulator of cortisol synthesis?

A

ACTH

19
Q

what type of receptor does ACTH bind to in the adrenal gland?

A

a melanocortin-2-receptor

20
Q

where is ACTH released from?

A

anterior pituitary

21
Q

describe the mechanism of how CRH stimulates the release of ACTH

A

CRH binds to CRH receptor on a coricotroph cell→activates camp→PKA→ causes calcium influx→results in exocytosis of presynthesized ACTH

22
Q

in the anterior pituitary, what does the processing of POMC give rise to?

A

ACTH and b-lipotrophin

23
Q

what is the effect of cortisol on CRH secretion?

A

cortisol decreases the mRNA and peptide levels of CRH and inhibits the release of presynthezied CRH

24
Q

when are cortisol levels in the blood the highest? the lowest?

A

highest in the early morning. lowest in the evening

25
Q

what does major stress do to cortisol levels?

A

enhance CRH secretion→enhanced ACTH secretion→increase cortisol

26
Q

what does depression do to cortisol levels? hypoglycemia?

A

both increase cortisol levels

27
Q

what is the most common form of a congenital adrenal hyperplasia

A

21-a-hydroxylase deficiency

28
Q

what are the effects of 21-a-hydroxylase deficiency?

A
  • “salt loosing” & dehydration & hypotension from decreased Aldosterone synthesis
  • hypoglycemia & increased size of adrenal gland from decreased cortisol feedback
  • increased androgen production so ambiguous genitalia in females and males go through early puberty
29
Q

how do you diagnose 21-a-hydroxylase deficiency?

A

there will be elevation of 17-hydroxyprogesterone before & after ACTH stimulating test
-also diagnosis should be confirmed with molecular genetic analysis of CYP21 gene

30
Q

what hormones are affected in a 17-a-hydroxylase?

A

reduced cortisol and androgen levels

aldosterone levels will be normal or increased

31
Q

how come in a 17-a-hydroxylase deficiency you dont get hyperglycemia?

A

you still have activecorticosterone

it has a much weaker effect than cortisol, but still some effect

32
Q

what is the name of the syndrome caused by too much cortisol activity?

A

cushing syndrome

33
Q

list 3 things that could cause cushing’s syndrome

A
  1. This can occur if patient uses too much exogenous glucocorticoids
    (Prolonged use of immunosuppresants- ex prednisone)
  2. ACTH producing hormones
  3. Adrenal tumors
34
Q

what is the difference between cushing syndrome and cushings disease?

A

disease- only caused by ACTH producing tumors

syndrome- multitude of causes

35
Q

in cushing syndrome, what is the affect on androgens?

A

there is too much androgen

36
Q

why is “moonface” seen in patients with cushing’s syndrome?

A

because cortisol promotes fat deposition in the face

37
Q

what is dexamthesone?

A

it is a potent synthetic form of glucocorticoid that is used in a diagnostic test for cushings?

38
Q

if a patient has high cortisol and low ATCH after a dexamethaone test, what does this mean?

A

adrenal tumor

39
Q

if a patient has high cortisol and high ATCH after a dexamethaone test, what does this mean?

A

ACTH producing hormone

40
Q

what is addison’s disease?

A

hypoadrenal function

41
Q

what are the two most commons of addison’s disease?

A

autoimmune disease or TB infection

42
Q

what does the lack of aldosterone in addison’s disease lead to?

A

hypotension and hyperkalemia

unit 6: physiology (13 decks)

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