Steroids Flashcards

1
Q

Differentiate, broadly, Addison’s Disease from Cushing’s Disease

A

Addison’s: Underproduction of cortisol s/p adrenal insufficiency
Cushing’s: Overproduction of cortisol

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2
Q

How is synthetic ACTH used in current practice?

A

As a diagnostic agent only

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3
Q

What are the primary ways in which steroids differ from one another

A

Steroids differ in their potency and their lipophilicity

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4
Q

T/F: A steroid used in a joint injection should be highly lipophilic.

A

False: A hydrophilic steroid should be used so the steroid stays in the joint

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5
Q

What is the principle hormone secreted by the adrenal gland and how is it regulated?

A

Hydrocortisone: regulated by CRF from the hypothalamus and ACTH from the pituitary

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6
Q

How does the mechanism of glucocorticoids differ from most other medications we administer?

A

They both bind to membrane receptors and enter the cell nucleus to influence the activation and deactivation of genes on DNA which subsequently influences production of various proteins

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7
Q

What is the primary pharmacologic effect of administering steroid medications?

A

Suppression of DNA mediated synthesis of pro-inflammatory chemicals (LTs, PGs, cytokines, interleukins)

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8
Q

What is the general mechanism through which steroids cause adverse effects?

A

Through DNA activation of certain genes different from those that suppress inflammatory chemicals

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9
Q

Describe 7 AEs of steroids administration.

A

Hyperglycemia from gluconeogenesis and decreased use of glucose in the periphery
Catabolism and reduced anabolism
Osteoporosis with increased calcium excretion
Delayed growth in children
Fat deposition in the shoulders, face, and abdomen
Reduced healing
Suppress allergic responses and Ab production

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10
Q

T/F: IV administration of steroids has essentially the same onset of action as PO administration of the same drug.

A

True: Since steroids must enter the cell to have an effect, IV administration of the drug is not markedly faster than PO

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11
Q

In what patient populations do we need to be particularly cautious in using steroids?

A

Post-menopausal women s/p osteoporosis risk

Children s/p delayed growth

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12
Q

How are steroids dosed, generally?

A

Multiple dosing strategies - QD, QOD, short courses, etc.

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13
Q

Describe the term pulse therapy in relation to steroid administration.

A

High dose administration in very short courses (1 - 5 days)

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14
Q

If a person is instructed to take a steroid QD, what would be the best time for them to take their steroid?

A

In the morning because steroids are part of our wake-up cycle

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15
Q

What dose of steroids is required to suppress the HPA axis and decrease endogenous steroid production?

A

At least 20mg of prednisone or equivalent for at least 14 days

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16
Q

If a patient is on enough steroids to suppress their HPA axis, what will result from rapid withdrawal of the drug?

A

Acute adrenocortical insufficiency

17
Q

In patients on enough steroids to suppress their HPA axis, when might a clinician need to increase their dose?

A

During the course of stressful events (surgery for ex) - aka stress dose steroids

18
Q

What is the typical dose for stress dose steroids and what would the dose be for a minor procedure?

A

Typical: 50-100mg hydrocortisone IV

Minor procedure: 20mg hydrocortisone PO

19
Q

What is the minimum dose of topical or inhaled steroids needed to cause HPA axis suppression?

A

Topical and inhaled steroids do not usually cause HPA suppression regardless of dose

20
Q

Why should a person taking steroids wear a medical alert bracelet?

A

Tells providers to continue their steroid therapy if they are in an accident or other emergency

21
Q

Describe the dexamethasone suppression test.

A

Dex acts on the hypothalamus directly to suppress CRF. If adrenal production of hydrocortisone is subsequently reduced, it indicates an intact HPA axis. Used to diagnose Cushing’s disease.

22
Q

Describe the pharmacokinetics of hydrocortisone and state how it is available.

A

Naturally occuring hormone with an onset of action of about 1 hour
Highly bound to cortisol binding globulin - lowest in the morning
PO, IV, OTC topical formulations

23
Q

Describe the pharmacokinetics of prednisone and state how it is available.

A

Half life of 1-3 hours with biological effects in 2-8 hours
Lipophilic - high absorption in the gut
Primary PO agent used in the US - available IV as methylprednisolone

24
Q

List 8 common AEs associated with prednisone administration.

A
Osteopenia
Reduced gastric mucus production
Fat redistribution
Hyperglycemia
Depression and psychosis at high doses
Weight gain s/p Na retention and increased appetite
Hypokalemia
Immune suppression
25
Q

List some rare AEs associated with prednisone administration.

A

Avascular necrosis, tendon rupture, peptic ulcers, cataracts, menstrual disorders, thromboembolism

26
Q

What affect does steroid administration have on white blood cells?

A

Increase serum WBC count (aka demargination) because the WBCs become less sticky and not as many stick to the walls of the blood vessels

27
Q

What differentiates leukocytosis due to demargination from leukocytosis due to an infection?

A

Infection shows a left shift –> increase in immature WBCs called bands

28
Q

T/F: Patients on steroid therapy should not be given a vaccine.

A

False: use caution in live vaccines

There may be a blunted response to all vaccines but steroids are not a contraindication

29
Q

Describe a Medrol Dose Pack.

A

Twenty-one 4mg tabs - 6 tabs on the first day and take 1 less each subsequent day until the pack is finished (6 days).

30
Q

Define fluorinated steroids.

A

Steroids with something added to them to make them more potent.

31
Q

List the fluorinated steroids discussed in class.

A

Triamcinolone - joint injections and topical agents
Fludrocortisone - PO for Addison’s
Dexamethasone - most lipophilic steroid
Betamethasone - similar to dexamethasone

32
Q

List the inhaled steroid products discussed in class.

A

Beclomethasone, budesonide, fluticasone, mometasone, ciclesonide

33
Q

How are steroids used in pregnancy?

A

Use lowest possible dose and avoid fluorinated agents.

34
Q

What is the goal of treatment in Cushing’s disease?

A

Decrease the production of steroids

35
Q

List 5 medications used in Cushing’s disease.

A

Aminoglutethimide, Metyrapone, Ketoconazole, Finasteride, Dutasteride

36
Q

Describe the mechanism of action of finasteride and dutasteride.

A

5-alpha-reductase inhibitors –> they keep testosterone from getting converted to its more active metabolite.

37
Q

Describe the clinical uses (other than Cushing’s Disease) of finasteride and dutasteride.

A

Finasteride: male pattern baldness at low doses and BPH at high doses
Dutasteride: only for BPH –> twice as potent as finasteride