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Endo/Repro 2 Final > Adrenal Corticosteroid Drugs > Flashcards

Adrenal Corticosteroid Drugs Flashcards

1
Q

Pharmacologic uses of [corticosteroids]

A
  1. Treat patients with [immunologic, inflammatory and allergic disorderd]
  2. Establish the diagnosis and cause of Cushings
  3. Tx adrenal insufficiency
  4. Tx CAH
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2
Q

What are adrenal corticosteroids?

A

Ligand-activated TF that modulate gene expression.

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3
Q

Aldosterone and Cortisol bind to MR receptor with ______ affinity

A

EQUAL

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4
Q

What are 3 active steroids?

A
  • 1. Cortisol
  • 2. Corticosterone
  • 3. Prednisolone
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5
Q

What are 3 inert steroids?

A
  1. Cortisone
  2. 11-dehydrocorticosterone
  3. Prednisone
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6
Q

What is required for an inert steroid => active?

A

11 B-HSD1

(11-ketoreductase)

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7
Q

What is required for an active steroid => inert?

A

11B-HSD2

(11B-dehydrogenase)

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8
Q

2 short- acting glucocorticoids (8-12 hours) and equivalent dose

A
  1. Hydrocortisone (Cortisol) = 20 mg
  2. Cortisone acetetate = 25 mg
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9
Q

Intermediate-acting glucocorticoids (12-36 hours) and equiv doses

A
  1. Prednisone = 5mg
  2. Prednisolone = 5mg
  3. Methylprednisolone = 4mg
  4. Triamcinolone = 4mg
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10
Q

Long-Acting (36 - 72 hours) Glucocorticoids

A
  1. Betamethasone = 0.75 mg
  2. Dexamethasone = 0.6 mg
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11
Q

Therapeutic effects of Glucocorticoids on [immune cells, tissues and organs]

A
  1. Immunosuppression
  2. Anti-inflammatory
  3. Anti-allergy
  4. Secondary Pain Relief (in addition to primary meds)
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12
Q

What factors influence the therapeutic and AE of Corticosteroids?

A
  1. Potency
  2. Pharmakokinetics
  3. Daily dose and timing
  4. Differnce in metabolism
  5. Duration of treatment
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13
Q

Corticosteroids are derived from _____

A

Cholesterol

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14
Q

How should [Corticosteroids] be given for medical emergencies?

A
  • High doses can be given for a FEW days with little risk, but no more than a few.
  • NEVER replace/ delay more specific primary treatments (ABX for septic shock).
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15
Q

How should Corticosteroids be given for Chronic Treatment?

A
  1. HIGHLY consider the evidence and how it should be used because it cannot be given chronically W/O adverse effects
    1. Dose/frequency
    2. Route of aministration
    3. Disease index to assess its therapeutic efficacy
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16
Q

Corticosteroids cannot be given chronically without _____

A

AE.

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17
Q

What are the guidlines for pharmocologic corticosteroid therapy?

A
  1. Give only if there is published evidence of therapetic benefit ONLY give after all other txs fail
  2. ID a specific therapetic objective and monitor the response to treatment. If none= stop taking
  3. Make sure take long enough to have a desired response, but no longer than necessary to have desired response.
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18
Q

When should you STOP taking corticosteroids?

A
  1. Objective therapeutic benefit is not observed
  2. Complications
  3. Max benefit is acheived
19
Q

Treatment for Primary Adrenal insufficiency (Addisons Disease) and Congenital Adrenal Hyperplasia

A

Hydrocortisone + Fludrocortisone

20
Q

When should corticosteroids be given for immunosuppresion?

A
  1. After organ/BM transplant
  2. AI disease
  3. Leukemia (Hematologic cancerS)
21
Q

When should corticosteroids be given for Inflammatory and Allergic conditions?

A
  1. RA
  2. IBD
  3. Asthma/COPD
  4. Allergic Rhinitis
  5. Skin disease (Psoriasis)/Hypersensitivity Reaction
22
Q

List 4 ways that glucocorticoids effect the immune system and inlammation

A
  1. ↓ production of prostaglandins, leukotrienes, cytokines and receptors
  2. ↓ production and ↑ apoptosis of immune cell types
  3. ↓ expression of cell adhesion molecules
  4. ↓ transmigration of neutrophils and macrophages from blood –> tissue
23
Q

What are consequences of Glucocorticoids?

A
  1. Immunosuprresion
  2. ↓ inflammation and consequences
  3. ↓ allergic/hypersensitivity reactions
24
Q

How do Glucocorticoids affect Carbohydrate Metabolism

A
  1. Has anti-insulin actions, causing hyperglycemia due to
    1. ↓ glucose uptake
    2. ↑ gluconeogenesis
    3. ↑ Glucose output
    4. ↑ glycogen synthesis
25
Q

How does glucocorticoids affect liver, skeletal muscle and adipose tissue?

A
  1. Liver: ↑ gluconeogenesis
  2. Skeletal muscle (3)
    1. ↓ glucose uptake
    2. ↓ glycogen synthetase
    3. ↑ proteolysis
  3. Fat:
    1. ↓ glucose uptake
    2. ↑ lipolysis
26
Q

When treating DB patients with corticosteroids, what additional medication should you consider?

A

Pramlintide + insulin: anti-DB med that can help to control blood sugar

27
Q

↓ activity/ inhibition of 11B HSD2 (11β-hydroxysteroid-dehydrogenase) = ________

A

↑ active cortisol => ↑ binding onto MR

28
Q

What are known inhibitors of 11β-hydroxysteroid-dehydrogenase type 2?

A
    • Glycyrrhizin (licorice root extract)
    • Carbenoxolone (UK med to tx esophageal ulcers)
29
Q

What is the downstream effect following inhibition of 11β-hydroxysteroid-dehydrogenase type 2 by substances such as glycyrrhizin (licorice root extract)?

A
  1. ↑ (+) of MR receptor by cortisol
  2. ↑ Na/H20 retention; ↑ K+ loss
  3. ↑ BP
30
Q

Which patients should we be cautious in adrenal corticosteroids?

A
  1. Immunocompromised (HIV/AIDS)
  2. DB
  3. Pts with infection, peptic ulcers, CV diseases, psychiatric condition
  4. Post-menopausal women with osteoporosis
  5. Children
31
Q

AE with of corticosteroids occur with _______ and can cause _____

A

Prolonged use of high doses

Cushing disease

32
Q

How do we dose adrenocorticoid drugs?

A
  1. Lowest concentration for shortest time possible
  2. Try to avoid putting into systemic circulation: use topical or inhalation routes
  3. Give single dose in the morning (AM)
  4. Alternate day, short-course therapy
  5. Dose tapering to allow HPA axis to recovery when reach theraptic benefit
33
Q

When dose-tapering off of glucocorticoids, what is important?

A

Measure the integrity of the HPA axis with

1. Morning serum cortisol

2. ACTH test

3. CRH test

34
Q

Drug used to treat adrenal cortical carcinoma (cancer in adrenal glands)

A

Mitotane

35
Q

Which drug has the strongest anti-inflammatory activity, relatie hydrocortisone? Weakest?

A

Strongest = dexamethasone and betamethasone

Weakest= cortisone acetate (0.8)

36
Q

Prednisolone

MOA:

Clinical applications:

Pharmokinetics:

AE:

A
  • Glucorticoid AGO => + GR => alter gene transcription
  • Inflammatory conditions, organ transplant, hematologic cancers
  • Duration of activity is longer than 1/2 life bc it affects gene transciption
  • Adrenal suppresion
37
Q

Mifepristone

  • MOA:
  • Clinical applications:
  • Pharmokinetics:
  • AE:
A
  • Glucocorticoid/progesterone R ANT
  • Abortions (and rarely Cushings)
  • Taken orally
  • Vaginal bleeding
38
Q

Fludrocortisone

  • MOA:
  • Clinical applications:
  • Pharmokinetics:
  • AE:
A
  • Mineralocorticoid***/glucocortioid AGO
  • Adrenal Insuffiency (Addisons disease)
  • LONG duration of action
  • AE (3)
    • Na+/H20 retention,
    • CHF
    • Signs of Glucocorticoid excess
39
Q

2 Mineralcorticoid-R ANT

A

1. Spironolactone

2. Eplerenone

40
Q

Spironolactone

  • MOA:
  • Clinical applications:
  • Pharmokinetics:
  • AE:
A
  • Mineralcorticoid ANT; weak androgen R ANT
  • Treats
    1. Aldosteronism,
    2. Hypokalemia due to diuretic effect,
    3. Post-MI
  • Slow onset and offset (lasts 24-48 hrs)
  • AE
    1. ​Hyperkalemia
    2. Gynecomastia
    3. Ineration with other K+ retaining drugs
41
Q

Eplerenone

MOA:

Clinical applications:

Pharmokinetics:

AE:

A
  • Mineralcorticoid R ANT
  • Treats HTN to lower BP.
  • Short half life (3-6 hours) bc broken down by CYP3A4
  • AE
    1. Hyperkalemia
    2. ↑ Cr
42
Q

What is the Corticosteroid Synthesis Inhibitor?

A

Ketoconazole

43
Q

Ketoconazole

  • MOA
  • Clinical Applications
  • Pharmacokinetics
  • AE
A
  • Blocks corticosteroid synthesis by blocking fungal/mammilian CYP450
  • Prevents steroid hormone and funal ergosterol synthesis
  • Taken oral or topically
  • Many drug-drug CYP450 interactions

Endo/Repro 2 Final (11 decks)

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