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?

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
what does major stress do to cortisol levels?
enhance CRH secretion→enhanced ACTH secretion→increase cortisol
26
what does depression do to cortisol levels? hypoglycemia?
both increase cortisol levels
27
what is the most common form of a congenital adrenal hyperplasia
21-a-hydroxylase deficiency
28
what are the effects of 21-a-hydroxylase deficiency?
- “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
how do you diagnose 21-a-hydroxylase deficiency?
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
what hormones are affected in a 17-a-hydroxylase?
reduced cortisol and androgen levels | aldosterone levels will be normal or increased
31
how come in a 17-a-hydroxylase deficiency you dont get hyperglycemia?
you still have activecorticosterone | it has a much weaker effect than cortisol, but still some effect
32
what is the name of the syndrome caused by too much cortisol activity?
cushing syndrome
33
list 3 things that could cause cushing's syndrome
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
what is the difference between cushing syndrome and cushings disease?
disease- only caused by ACTH producing tumors | syndrome- multitude of causes
35
in cushing syndrome, what is the affect on androgens?
there is too much androgen
36
why is "moonface" seen in patients with cushing's syndrome?
because cortisol promotes fat deposition in the face
37
what is dexamthesone?
it is a potent synthetic form of glucocorticoid that is used in a diagnostic test for cushings?
38
if a patient has high cortisol and low ATCH after a dexamethaone test, what does this mean?
adrenal tumor
39
if a patient has high cortisol and high ATCH after a dexamethaone test, what does this mean?
ACTH producing hormone
40
what is addison's disease?
hypoadrenal function
41
what are the two most commons of addison's disease?
autoimmune disease or TB infection
42
what does the lack of aldosterone in addison's disease lead to?
hypotension and hyperkalemia