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PMCOL 200 > Adrenocorticosteroids > Flashcards

Adrenocorticosteroids Flashcards

1
Q

what hormone does the adrenal medulla produce?

A

adrenaline (catecholamine/aa hormone)

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2
Q

what type of hormones does the adrenal cortex produce?

A

steroid hormones (cholesterol-derived, lipid-soluble)

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3
Q

what are the 3 zones of the adrenal cortex? (out to in)

A

zona glomerulosa, zona fasciculata, zona reticularis

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4
Q

what zona secretes mineralocorticoids (aldosterone)?

A

zona glomerulosa (outer layer)

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5
Q

what zona secretes glucocorticoids (cortisol)?

A

zona fasciculata (middle)

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6
Q

what zona secretes androgens (DHEA)?

A

zona reticularis

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7
Q

what is the purpose of hormones secreted from the zona glomerulosa, fasciculata, and reticularis resp.?

A

glom: salt balance (salt)
fasc: metabolism and immunity (sugar)
ret: androgen/estrogen precursors (sex)

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8
Q

what does the HPA (hypothal-ant pit axis) stimulate for cortisol release?

A

zona fasciculata

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9
Q

what hormone stimulates steroid production/cortisol release from adrenal cortex?

A

adrenocorticotropic releasing hormone (ACTH)

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10
Q

where is ACTH released from?

A

anterior pituitary

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11
Q

when is ACTH released from the ant pit?

A

after meals, before waking (has circadian rhythm)

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12
Q

what hormone controls ACTH?

A

corticotropin-release hormone/factor (CRH/CRF)

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13
Q

where is CRH/CRF released from?

A

hypothalamus

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14
Q

how are steroid hormones stored?

A

are not stored, but synthesized and released when needed (ACTH triggers cortisol synthesis)

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15
Q

what does cortisol exert neg feedback on? (2)

A

CRH (hypo) and ACTH (ant pit)

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16
Q

t/f: cortisol cannot suppress synthesis of other stress signals (cytokines) that can stimulate cortisol HPA?

A

false, cortisol can suppress stress signals such as cytokines

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17
Q

what is the glucocorticoid response?

A

changes in stress response, catabolism, and immunosuppression in glucocorticoid target tissues from cortisol

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18
Q

where is renin secreted from?

A

juxtaglomerular apparatus (in kidney)

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19
Q

what does AT2 act on?

A

AT2 receptors in adrenal cortex to trigger aldosterone release

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20
Q

what is the mineralocorticoid response?

A

Na/H2O reabsorption and K excretion in kidney from aldosterone

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21
Q

what is the primary role of the RAAS system?

A

control of blood pressure and volume

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22
Q

what is the chaperone for the generalized cytoplasmic steroid hormone receptor?

A

Hsp90 (heat shock protein)

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23
Q

what is the effect of ligand binding to cytoplasmic receptors? (2)

A

Hsp dissociation, dimerization of steroid-receptor complex, transport into nucleus, influence of transcription in target genes

24
Q

what is the glucocorticoid response element (GRE)?

A

genes targeted by glucocorticoids (in complex w receptor and dimerized)

25
Q

what are 2 key gene products of GR binding?

A

lipocortin and COX-2

26
Q

what allows diff physl responses to glucocorticoids (GC response) and mineralocorticoids (MC response)?

A

diff receptors which target diff response elements

27
Q

what ratio does cortisol bind to glucocorticoid vs mineralocorticoid receptors?

A

1:1

28
Q

how do corticosteroids exhibit a spectrum of effects?

A

have diff affinities for either GC or MC receptor

29
Q

t/f: GC and MC receptors activate/repress transcription of diff genes

A

true

30
Q

what enzyme do glucocorticoid target tissues (adipose, muscle, liver) express? function?

A

11B-hydroxysteroid dehydrogenase, TYPE 1 (HSD1); converts cortisone (inactive) to cortisol (active)

31
Q

what does glucocorticoid target tissues having HSD1 suggest about cortisol specificity?

A

can be regulated by metabolism in target tissues (as well as affinity to receptor)

32
Q

what is the diff btwn prednisone vs prednisolone?

A

prednisone: not effective topically/inactive glucocorticoid
prednisolone: effective topically/active form of prednisone

33
Q

what is the best way to administer prednisone? why?

A

orally (vs topically); first metabolism/tissue enzymes activate it to prednisolone

34
Q

why does cortisol have weak mineralocorticoid effects in vivo if it activates GR and MR?

A

mineralocorticoid target tissues (kidney cells) express 11B-hydroxysteroid dehydrogenase, TYPE 2 (HSB2) that converts cortisol to cortisone (inactivates it)

35
Q

what does licorice contain? effect?

A

inhibitor to HSB2 which allows cortisol (glucocorticoid) to affect aldosterone (mineralocorticoid) target tissues (kidneys) and cause high BP (Na/H2O retention)

36
Q

what is apparent mineralocorticoid excess disease? effect?

A

mutations in HSB2 gene which decr its activity and incr activation of MR in kidneys by cortisol (GC), incr BP

37
Q

how do glucocorticoids (cortisol) incr circulating glucose levels? (2)

A

incr gluconeogenesis and release from liver, inhibits insulin in muscle and adipose (prevents glucose uptake

38
Q

how do glucocorticoids (cortisol) affect fat/lipid balance?

A

incr lipolysis in limbs but fat deposition in viscera/trunk area (“skinny fat”)

39
Q

what is the overall catabolic effect of cortisol?

A

loss of muscle and bone mass in limbs

40
Q

what are the 2 inflammatory mechanisms affected by glucocorticoids (cortisol)?

A

inhibits phospholipase A2/arachidonic acid synthesis and inhibits cyclo-oxygenase 2 (COX-2)/prostanoid synthesis

41
Q

what are 2 actions of COX-2?

A

inflammatory mediator that plays an early step in metabolism of arachidonic acid into prostanoids

42
Q

how do glucocorticoids inhibit COX-2?

A

suppress COX-2 gene transcription (long-term) - don’t directly inhibit COX-2/receptor

43
Q

what are lipocortins/annexins?

A

family of proteins that have “annexin repeats”

44
Q

how does annexin A-1 (gene) exhibit anti-inflammatory effects? (2)

A

prevents WBC infiltration into tissues and suppresses phospholipase A2 activity (prevents arachidonic acid/prostanoid synth)

45
Q

what induces expression of lipocortin/annexin A-1?

A

glucocorticoid receptor activation

46
Q

what is Addison’s disease?

A

chronic adrenocortical insufficiency, decr glucocorticoid (cortisol) and mineralocorticoid (aldosterone) synthesis

47
Q

what are 4 symptoms of Addison’s disease?

A

fatigue, salt and sugar imbalances, skin discolouration

48
Q

how is Addison’s disease treated?

A

GC/MC supplements (hydrocortisone)

49
Q

what is Cushing’s syndrome?

A

adrenal overactivity leading to excessive cortisol

50
Q

what are 4 potential causes of Cushing’s syndrome?

A

adrenal tumour (cortisol producing), pituitary tumour (ACTH producing), drug-induced (chronic GC treatment), ectopic tumour (ACTH producing)

51
Q

what are 3 symptoms of Cushing’s syndrome?

A

round face/fatty trunk, muscle loss, osteoporosis (protein and bone catabolism)

52
Q

what is a potential treatment for Cushing’s syndrome?

A

resection of adrenal/pituitary tumour and adjustment of cortisol levels

53
Q

what are 8 possible therapeutic purposes for glucocorticoids?

A

anti-inflammatory/immunosuppressant, allergic rxns, eye inflammation, pain/scarring reduction, GI disease (IBS), hematological disorders (leukemia, myeloma), asthma, organ transplant (avoid rejection)

54
Q

what symptoms may occur if GC supplements are stopped abruptly?

A

Addison-like symptoms/’Addisonian’ crisis: hypoglycemia, hyperkalemia, hyponatremia (low Na), low BP

55
Q

what causes Addison-like symptoms/’Addisonian’ crisis when GC supplements are stopped abruptly?

A

negative feedback from GC supplememnts suprresses CRH and ACTH, therefore decr levels wo/ GC causes decr cortisol levels and side effects

56
Q

what is a way to prevent side effects when stopping long-term GC use?

A

tapering (dont stop abruptly)

57
Q

what 9 side effects of GC treatment?

A

hyperglycemia, opportunistic/latent infections, osteoporosis, muscle wasting, slow wound healing, ulcerations, hypertension, psychosis, ‘Cushingoid’ (fat redistribution)

PMCOL 200 (27 decks)

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