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Endocrine Physiology > Glucocorticoids > Flashcards

Glucocorticoids Flashcards

1
Q

where is cortisol produced?

A

adrenal cortex- fasciulate and reticularis

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2
Q

which is produced more: cortisol or aldo?

A

cortisol 100x more than aldo

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3
Q

what is the blood concentration of cortisol? how does it travel

A

.4 uM- 96% bound to corticosteroid binding globulin

free cortisol is biologically active

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4
Q

what is the defining chemical feature of cortisol?

A

OH at 11th position

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5
Q

where is aldosterone produced

A

glomerulosa (outer most cortex)

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6
Q

what is the precursor for all adrenocortical hormones?

A

cholesterol

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7
Q

what is the first step in converting the adrenocortical hormone precursor into either aldo or cortisol?

A

cholesterol desmolase (p450) converts it into pregnenolone

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8
Q

what are the actions of 21B-hydroxylase

A

converts 17-hydroxyprogesterone towards cortisol

converts progesterone towards aldo

also a p450 enzyme

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9
Q

21B-hydroxylase deficiency

A

results in excess androgens and accelerated development of secondary sexual characteristics.
w/o negative feedback of cortisol, increased ACTH secretion

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10
Q

where does cortisol feedback?

A

negative on pit (inhibit ATCH) and hypo (inhibit CRH)

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11
Q

congenital adrenal hyperplasia

A

ACTH acts as a growth factor on the adrenal gland. in deficiencies such as 21B-hydroxylase, w/o negative feedback from cortisol, unregulated ACTH causes excess adrenal growth

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12
Q

how does ACTH exert its effects on the adrenal glands

A

ACTH receptor is MC2R- Gs protein that increases cAMP, which releases IP3 and DAG to activate PKC, which increases steroid response immediately, and a tropic growth effect over the long term

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13
Q

how does cortisol exert its effects?

A

receptor- GR- cytoplasmic receptor

cortisol diffuses through cell and binds receptor, causing it to translocate into nucleus, altering protein transcription

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14
Q

where are cortisol receptors found?

A

entire body

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15
Q

what is the timeline of cortisol effects?

A

slow- related to changes in transcription

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16
Q

what are the effects of cortisol on the body?

A
  • raises blood sugar by stimulating gluconeogensis and glycogenolysis
  • increases circulating lipids via lipolysis
  • inhibits peripheral glucose uptake
  • redistribution of body fat to trunk
  • increases effects of vascular pressors by increasing AVP receptors
  • initiate muscle breakdown for protein
  • anti-inflammatory and immunosuppressive actions (decrease in cytokine production)
  • decreases bone mass and impairs wound healing by increasing osteoclast number and decreasing fibroblast protein synthesis

-CNS effects-
insomnia, hyperactivity, increase appetite, impairs memory

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17
Q

how are cortisols effects related to insulin?

A

they antagonize each other

18
Q

what is the main stimulus for cortisol release?

A

stress- caused by trauma, emotional situations, and changes in blood sugar or blood volume

19
Q

what are the differences between primary, secondary, and tertiary adrenal deficiencies

A

1 d/t destruction of adrenal cortex (Addisons)
2 inadequate ACTH secretions
3 inadequate CRH secretion

20
Q

why is hyperpigmentation seen in Addisons

A

MSH comes from the same precursor as ACTH, which is continuously stimulated b/c of a lack of cortisol

21
Q

what are the symptoms of Addisons

A 
hyperpigmentation
weakness/fatigue
hypotension
weight loss
naseau/vomitting
loss of appetite
fasting hypoglycemia
muscle/joint pain
22
Q

what is Cushing syndrome?

A

hypercortisolism- 2 types

ACTH dependent- ACTH or CRH hypersecretion

ACTH independent- adrenal tumor or medicated

23
Q

what are the symptoms of Cushings syndrome?

A 
trunal obesity
moon face
buffalo hump
abdominal striae
osteoporosis
hypertension
brusing
poor wound healing
glucose intolerance/diabetes
psychosis
infections
hirusitism
24
Q

what is the major minerlocorticoids?

A

aldosterone

25
Q

aldosterone has no specific binding protein

A

ok

26
Q

what are plasma concentrations of aldo

A

.1 nM

27
Q

what is aldos half life?

A

30 min

28
Q

what are the effects of aldosterone

A

Na reabsorption, K secretion

regulates ECFV and blood pressure

29
Q

where is aldosterone synthase found

A

zona glomerulosa- converts corticosterone into aldo

30
Q

what are the non renal aldosterone effects?

A
  1. reabsorb Na in colon (important in neonates)
  2. reabsorb Na from sweat glands
  3. increase taste bud sensitivity to salt and increase salt appetite
31
Q

what are the aldo effects on the kidney?

A

DT and CD= increase Na absorption, increase K secretion, increase H secretion

32
Q

what are the main regulators of aldo?

A

RAS system- renin secreted from kidney d/t low BP causes conversion of Ang2, which activates Aldo
{K} in blood stream

33
Q

what is the MOH of the aldo receptor?

A

binds to mineralcorticoid receptor in the cytoplasm, translocates to nucleus and minds to mineralcorticoid response elements and effects transcription

34
Q

11HSD2

A

mineralcorticoid receptor has same affinity for cortisol and aldo. to compensate for this, 11HSD2 converts cortisol into inactive cortisone in locations where aldo must work

35
Q

how does cortisone cream work?

A

high levels of cortisone force the rxn with 11HSD2 back to cortisol

36
Q

11HSD2 deficiencies

A

apparent mineralcorticoid excess-

can’t outcompete cortisol, so cortisol binds in high amounts.

results in high BP, high Na, low K, low renin, low aldo, high cortisol/cortisone ratio

37
Q

what is the effect of licorice on cortisol?

A

inhibits 11HSD2 and causes hypertension

38
Q

hypoaldosteronism

A

low BP, low Na, high K

Addisons is a combined mineralocorticoid and glucocorticoid deficiency b/c of adrenal cortex destruction

39
Q

what is isolated mineralocorticoid deficiency d/t

A

aldosterone synthase defect

40
Q

pseudohypoaldosteronism

A

rare disorder where defects exist in Na channels in the CD or the MR-

causes hyperaldosterone but Na secretion and salt wasting

41
Q

hyperaldosteronism

A

high BP, high Na, low K

primary- usually caused by cancer in adrenal gland. can also be cauesed by adrenal hyperplasia

secondary- d/t edema in congestive heart failure, liver cirrhosis, or nephrotic syndrome which causes low effective blood volume d/t excess sweating.

Endocrine Physiology (5 decks)

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