Adrenal Cortex: Glucocorticoid Flashcards

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1
Q

plasma profile of glucocorticoids

A

increased blood glucose, increased FFA, increased AA

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2
Q

what releases glucocorticoids

A

zona fasiculata

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3
Q

what hormones are released by the zona fasiculata

A

progesterone and cortisol

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4
Q

what makes progesterone into 17 hydroxyprogesterone

A

17a hydroxylase

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5
Q

what makes 17 hydroxyprogesterone into 11 deoxycortisol

A

21 beta hydroxylase

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6
Q

what makes deoxycortisol into cortisol

A

11 beta hydroxylase

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7
Q

what are the glucocorticoids

A

cortisol, cortisone, corticosterone

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8
Q

how does cortisol circulate

A

bound to transcortin and albumin

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9
Q

half life of glucocortisol

A

70min aka long

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10
Q

when are glucocorticoids released

A

in response to stress

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11
Q

major function of glucocorticoids

A

increase plasma glucose via gluconeogenesis

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12
Q

where are glucocorticoids metabolized

A

liver and kidney

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13
Q

what does cortisol do

A
  1. decrease bone formation, increase bone resorption
  2. decrease CT
  3. inhibit inflammatory and immune response
  4. maintain CO, increase arteriolar tone, decrease endothelial permeability
  5. facilitate maturation of the fetus
  6. increase glomerular filtration and free water clearance
  7. modulate emotional tone and wakefulness
  8. maintain muscle function, decrease muscle mass
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14
Q

when is cortisol released

A

increases with waking, possibly increased sensory input and visual processing

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15
Q

what chemical is on cortisol

A

hydroxy group on C11

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16
Q

cortisol to cortisone

A

11b hydroxysteroid dehydrogenase

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17
Q

what chemical is one cortisone

A

ketone on c11

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18
Q

regulation of cortisol

A

CRH–>AP–>ACTH–>adrenal cortex–>cortisol

negative feedback to AP and hypothalamus

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19
Q

how is ACTH released in the blood

A

CRH binds to Gs–>AC–>cAMP–>PKA–>P proteins–>POMC mRNA–>POMC–>ACTH, beta LPH into the blood

20
Q

how are the steroid enzymes released from adrenal gland

A

ACTH binds to adrenal gland Gs–>cAMP–>PKA–>p proteins–>mRNA–>steroidigenic enzymesto mito–>pregnenolone–>to SER–>back to mito–>glucocorticoids and androgens in blood

21
Q

what steroidogenic enzymes are made when ACTH binds

A

17 alpha and 21 beta hydroxylase

22
Q

what increases ACTH secretion

A
  1. decreased cortisol levels
  2. sleep wake transition
  3. stress, hypoglycemia, surgery, trauma
  4. psychiatric disturbances
  5. ADH
  6. alpha adrenergic agonists
  7. beta adrenergic antagonist
  8. serotonin
23
Q

what decreases ACTH secretion

A
  1. increased blood cortisol
  2. opioids
  3. somatostatin
24
Q

what is the diabetogenic effect of glucocorticoids

A

cortisol increases glucose production from non carb sources and increases glucose utilization

25
Q

action of insulin

A

decrease glycogenolysis, gluconeogenesis, ketogenesis and lipolysis

26
Q

action of glucagon and epinephrine

A

increase glycogenolysis, gluconeogenesis, ketogenesis, lipolysis

27
Q

what is the effect of glucocorticoids on AA production in the plasma

A

unbranched AA (alanine) are taken up into tissues faster than branched (leucine) and used more readily so there are increased numbers in the plasma

28
Q

what is the primary metabolic action of cortisol

A

gluconeogenesis

29
Q

what other actions does cortisol do

A

increased lipolysis, increased FFA and AA mobilization, decrease fat synthesis, inhibit glucose storage

30
Q

blood effect of glucocorticoids

A

increased FFA, increased ketone bodies, increased glucose, increase AA

31
Q

what does cortisol inhibit

A

cyclooxygenase (decreases prostaglandins, thromboxanes)

32
Q

what is cushings disease

A

excessive long term cortisol exposure

33
Q

sx of cushings

A

protein depletion, muscle weakness, fat redistribution into central obesity, increased glucose (may be confused with DM), increased Na retention, osteoporosis, suppressed immune system, insomnia

34
Q

normal response of dexamethasone suppression test

A

ACTH and cortisol will be depressed by low dose of dexamethasone

35
Q

what does the dexamethasone suppression test test

A

pathophysiology of anterior pituitary and adrenal

36
Q

ACTH secreting neoplasm of pituitary dexamethasone suppression test

A

low dose of dexamethasone will have little or no effect on ACTH and cortisol, high dose depress ACTH and cortisol

37
Q

ACTH secreting neoplasm of ectopic foci or cortisol secreting tumor of adrenal cortex dexamethasone suppression test

A

neither low or high dose will have any affect on ACTH or cortisol

38
Q

sx of adrenocortical insufficiency

A

weight loss, poor appetite, malaise, n/v, abdominal pain, fever, poor stress response, hypoglycemia, skin hyperpigmentation (addisons disease), low bp, vascular collapse, increased K

39
Q

what is cushings disease

A

hypercortisol, decreased ACTH if cortisol increased

40
Q

what is addisons disease

A

hypocortisol

41
Q

what is seen in 21b hydroxylase or 17a hydroxylase deficiency

A

increased ACTH because of decreased/absent cortisol

42
Q

plasma profile in primary addisons disease?

A

decreased cortisol, increased ACTH, and decreased plasma glucose

43
Q

plasma profile in cushings disease

A

ACTH, cortisol and plasma glucose all increased

secondary disorder

44
Q

plasma profile in 21 b hydroxylase deficiency

A

increased ACTH, decreased deoxycorticosterone, decreased aldosterone, decreased cortisol, increased dihydroepiandosterone (shunted toward adrenal androgens), increased urinary 17 ketosteroids

45
Q

plasma profile in 17 a hydroxylase deficiency

A

excess production of deoxycorticosterone and cortisone, causing high blood pressure.

cortisol and adrenal androgens (DHEA) are suppressed.

aldosterone indirectly suppressed bc high BP (inactivated RAAS)