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EndoRepro 2 Exam 2 > Corticosteroids - Iszard > Flashcards

Corticosteroids - Iszard Flashcards

1
Q

in endocrine practice, when are corticosteroids given?

A
  • to establish the diagnosis and cause of Cushing’s syndrome
  • for the treatment of adrenal insufficiency using physiologic replacement doses
  • for the treatment of congenital adrenal hyperplasia, for which the dose and schedule may not be physiologic
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2
Q

what two groups of drugs are agonists or corticosteroids?

A
  • glucocorticoids (prednisone)

- mineralocorticoids (fludrocortisone)

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3
Q

what two groups of drugs are antagonists of corticosteroids?

A 
synthesis inhibitors (ketoconazole)
- receptor antagonists: glucocorticoid antagonists (mifepristone) and mineralocorticoid antagonists (spironolactone)
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4
Q

what two hormones bind the mineralocorticoid receptor with equal affinity?

A

aldosterone and cortisol

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5
Q

what does 11 b-dehydrogenase do?

A

converts active sterols (cortisol, corticosterone, prednisolone)
- to inert sterols (cortisone, 11-dehydrocorticosterone, prenisone)

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6
Q

what does 11 b-ketoreductase do?

A

converts inert sterols to active sterols

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7
Q

what are the short to medium acting (<12hrs) glucocorticoids?

A
  • hydrocortisone
  • cortisone
  • prednisolone
  • methylprednisolone
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8
Q

what is the 1 intermediate actine (12-36) glucocorticoid?

A

triamcinolone

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9
Q

what are the 2 long-acting (>36 hours) glucocorticoids?

A
  • betamethasone

- dexamethasone

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10
Q

what are the criteria for initiating glucocorticoid therapy in a medical emergency?

A
  • high doses can be administered for a few days with little risk
  • should not be given for more than a few days for these conditions
  • use must never replace or delay more specific primary therapies (abx for septic shock, etc)
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11
Q

what are the criteria for initiating chronic glucocorticoid therapy?

A
  • more consideration must be given to the evidence of therapy, in particular:
  • the dose
  • frequency
  • route of administration
  • the disease indexes to be monitored to assess therapeutic efficacy

NOTE: corticosteroids cannot be given chronically without the risk of adverse events

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12
Q

what are the common clinical applications: endocrine conditions

A
  • primary adrenal insufficiency (Addison’s disease)

- CAH

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13
Q

what is the treatment for primary adrenal insufficiency?

A

combination of glucocorticoid (hydrocortisone) and mineralocorticoid (fludrocortisone)

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14
Q

what is the treatment for CAH?

A

hydrocortisone + fludrocortisone

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15
Q

what are the common non-endocrine applications for glucocorticoids?

A
  • immunosuppression: following organ/bone marrow transplant, autoimmune disease (MS), hematologic cancers (leukemia)
  • inflammatory and allergic conditions: RA, IBD, asthma/COPD, allergic rhinitis, inflammatory dermatoses
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16
Q
  • decrease production of prostaglandings and leukotrienes
  • decreased production and increased apoptosis of immune cell types
  • decreased production of cytokines and their receptors
  • decreased transmigration of neutrophils and macrophages from blood into tissues
  • decreased expression of cell adhesion molecules
A

effects of glucocorticoids on immune system and inflammation

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17
Q

what are the consequences of glucocorticoids?

A
  • decreased inflammation and its manifestations
  • immune suppression
  • decreased allergic/hypersensitivity reactions
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18
Q

what are the metabolic effects of glucocorticoids on carbohydrate metabolism?

A
  • increase gluconeogenesis
  • increase glucose output
  • increase glycogen synthesis
  • decrease glucose uptake -> dvlpment of hyperglycemia
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19
Q

what are the metabolic effects of glucocorticoids on lipid metabolism?

A
  • increase lipolysis
  • increase FFA and glycerol into the gloconeogenic pathway
  • increase lipogenesis
  • increase fat deposition
  • change fat distribution
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20
Q

what are the metabolic effects of glucocorticoids on protein metabolism?

A
  • decreased AA uptake
  • decreased protein synthesis
  • dev of myopathy and muscle wasting
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21
Q

what are the anti-insulin actions of glucocorticoids in the liver?

A

increase gluconeogenesis

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22
Q

what are the anti-insulin actions of glucocorticoids in skeletal muscle?

A
  • decrease glucose intake
  • decrease glycogen synthetase
  • increase proteolysis
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23
Q

what are the anti-insulin actions of glucocorticoids in adipose tissue?

A
  • decrease glucose uptake

- increase lipolysis

24
Q

what do the anti-insulin effects of glucocorticoids lead to?

A

hyperglycemia

25
Q

decreased activity/inhibition of 11b-dehydrogenase (11b-HSD2) results in what?

A

excessive activation of MR, mediated by cortisol

26
Q

what are the known inhibitors of 11b-HSD2

A
  • glycyrrhizin (licorice root)

- carbenoxolone

27
Q

what do 11b-HSD2 inhibitors lead to?

A
  • increase in Na and H2O retention
  • K loss
    = increase in BP
28
Q

what is the duration of action of short-acting glucocorticoids?

A

8-12 hours

29
Q

what is the DOA of intermediate acting glucocorticoids?

A

12-36 hours

30
Q

what is the DOA of long-acting glucocorticoids?

A

36-72 hours

31
Q

what is the MOA of prednisolone?

A

activation of GR alters gene transcription

32
Q

what are the clinical applications of prednisolone?

A

many inflammatory conditions, organ transplantation, hematologic cancers

33
Q

what are the pharmacokinetics of prednisolone?

A

duration of action is longer than pharmacokinetic half life of drug, owing to gene transcription effects

34
Q

what are the toxicities, drug interactions of corticosteroids?

A

adrenal suppression, growth inhibition, muscle wasting, osteoporosis, salt retention, glucose intolerance, behavioral changes

35
Q

what is the MOA of mifepristone?

A

pharmacologic antagonist of glucocorticoid and progesterone receptors

36
Q

what are the clinical applications of mifepristone?

A

medical abortion, very rarely Cushings syndrome

37
Q

what are the pharmacokinetics of mifepristone?

A

oral administration

38
Q

what are the toxicities, drug interactions of mifepristone?

A

vaginal bleeding, abdominal pain, GI upset, diarrhea, HA

39
Q

what is a class of steroid that influence salt and water balance?

A

mineralocorticoids

- primarily act on the kidney, where they cause Na and H2O retention and active excretion of K and H+

40
Q

what is the primary mineralocorticoid?

A

aldosterone

- but progesterone and deoxycorticosterone have mineralocorticoid function

41
Q

what is the MOA of fludrocortisone?

A

strong agonist at mineralocorticoid receptors and activation of glucocorticoid receptors

42
Q

what is the clinical application of fludrocortisone?

A

adrenal insufficiency (Addison’s disease)

43
Q

what are the pharmacokinetics of fludrocortisone?

A

long duration of action

44
Q

what are the toxicities, drug interactions of fludrocortisone?

A

salt and fluid retention, CHF, signs and symptoms of glucocorticoid excess

45
Q

what is the MOA of spironolactone?

A

pharmacologic antagonist of mineralocorticoid receptor, weak antagonism of androgen receptos

46
Q

what are the clinical applications of spironolactone?

A

aldosteronism from any cause, hypokalemia d/t diuretic effect, post MI

47
Q

what are the pharmacokinetics of spironolactone?

A

slow onset and offset, duration 24-48 hrs

48
Q

what are the toxicites, drug interactions of spironolactone?

A

hyperkalemia, gynecomastia, additive interaction with other K+ retaining drugs

49
Q

what is the MOA of eplerenone?

A

mineralocorticoid receptor antagonism -> blocks the binding of aldosterone

50
Q

what are the clinical applications of eplerenone?

A

indicated for the treatment of hypertension, to lower blood pressure
- lowering BP reduces the risk of CV events

51
Q

what are the pharmacokinetics of eplerenone?

A

eplerenone is cleared by CYP34A metabolism, with elimination half-life of 3-6 hours
- steady state is reached within 2 days

52
Q

what are the toxicities of eplerenone?

A

most common adverse reactions are hyperkalemia and increased creatinine

53
Q

what is ketaconazole?

A

a synthesis inhibitor

54
Q

what is the MOA of ketaconazole?

A

blocks fungal and mamalian CYP450 enzymes

55
Q

what are the clinical applications of ketaconazole?

A

inhibits mammalian steroid hormone synthesis and fungal ergosterol synthesis

56
Q

what are the pharmacokinestics of ketaconazole?

A

oral, topical administration

57
Q

what are the toxicities and ketaconazole?

A

hepatic dysfunction, many drug-drug CYP450 interactions

EndoRepro 2 Exam 2 (10 decks)

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