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EndoRepro 2 Exam 2 > Corticosteroids - Iszard > Flashcards

Corticosteroids - Iszard Flashcards

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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?

Study These Flashcards
A
  • decrease glucose uptake

- increase lipolysis

24
Q

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

Study These Flashcards
A

hyperglycemia

25
decreased activity/inhibition of 11b-dehydrogenase (11b-HSD2) results in what?
excessive activation of MR, mediated by cortisol
26
what are the known inhibitors of 11b-HSD2
- glycyrrhizin (licorice root) | - carbenoxolone
27
what do 11b-HSD2 inhibitors lead to?
- increase in Na and H2O retention - K loss = increase in BP
28
what is the duration of action of short-acting glucocorticoids?
8-12 hours
29
what is the DOA of intermediate acting glucocorticoids?
12-36 hours
30
what is the DOA of long-acting glucocorticoids?
36-72 hours
31
what is the MOA of prednisolone?
activation of GR alters gene transcription
32
what are the clinical applications of prednisolone?
many inflammatory conditions, organ transplantation, hematologic cancers
33
what are the pharmacokinetics of prednisolone?
duration of action is longer than pharmacokinetic half life of drug, owing to gene transcription effects
34
what are the toxicities, drug interactions of corticosteroids?
adrenal suppression, growth inhibition, muscle wasting, osteoporosis, salt retention, glucose intolerance, behavioral changes
35
what is the MOA of mifepristone?
pharmacologic antagonist of glucocorticoid and progesterone receptors
36
what are the clinical applications of mifepristone?
medical abortion, very rarely Cushings syndrome
37
what are the pharmacokinetics of mifepristone?
oral administration
38
what are the toxicities, drug interactions of mifepristone?
vaginal bleeding, abdominal pain, GI upset, diarrhea, HA
39
what is a class of steroid that influence salt and water balance?
mineralocorticoids | - primarily act on the kidney, where they cause Na and H2O retention and active excretion of K and H+
40
what is the primary mineralocorticoid?
aldosterone | - but progesterone and deoxycorticosterone have mineralocorticoid function
41
what is the MOA of fludrocortisone?
strong agonist at mineralocorticoid receptors and activation of glucocorticoid receptors
42
what is the clinical application of fludrocortisone?
adrenal insufficiency (Addison's disease)
43
what are the pharmacokinetics of fludrocortisone?
long duration of action
44
what are the toxicities, drug interactions of fludrocortisone?
salt and fluid retention, CHF, signs and symptoms of glucocorticoid excess
45
what is the MOA of spironolactone?
pharmacologic antagonist of mineralocorticoid receptor, weak antagonism of androgen receptos
46
what are the clinical applications of spironolactone?
aldosteronism from any cause, hypokalemia d/t diuretic effect, post MI
47
what are the pharmacokinetics of spironolactone?
slow onset and offset, duration 24-48 hrs
48
what are the toxicites, drug interactions of spironolactone?
hyperkalemia, gynecomastia, additive interaction with other K+ retaining drugs
49
what is the MOA of eplerenone?
mineralocorticoid receptor antagonism -> blocks the binding of aldosterone
50
what are the clinical applications of eplerenone?
indicated for the treatment of hypertension, to lower blood pressure - lowering BP reduces the risk of CV events
51
what are the pharmacokinetics of eplerenone?
eplerenone is cleared by CYP34A metabolism, with elimination half-life of 3-6 hours - steady state is reached within 2 days
52
what are the toxicities of eplerenone?
most common adverse reactions are hyperkalemia and increased creatinine
53
what is ketaconazole?
a synthesis inhibitor
54
what is the MOA of ketaconazole?
blocks fungal and mamalian CYP450 enzymes
55
what are the clinical applications of ketaconazole?
inhibits mammalian steroid hormone synthesis and fungal ergosterol synthesis
56
what are the pharmacokinestics of ketaconazole?
oral, topical administration
57
what are the toxicities and ketaconazole?
hepatic dysfunction, many drug-drug CYP450 interactions

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