Physio and Pharm Use of Adrenal Hormones Flashcards

1
Q

Definitions

  1. Corticosteroid
  2. Glucocorticoids
  3. Mineralocorticoids
A
  1. Both GCs and mineralocorticoids (hormones produced in the adrenal cortex)
  2. Relating to glucose metabolism (zona fasiculata)
  3. Mineral/electrolyte effects (zona glomerulosa)
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2
Q

Therapeutic uses of GCs

A

To establish the diagnosis and cause of Cushing’s syndrome
Treatment of adrenal insufficiency using physiologic replacement doses
Treatment of congenital adrenal hyperplasia
Pharmacologic doses for patients with inflammatory, allergic, and immunological disorders

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3
Q

Cortisol

  1. Inactive form
  2. Where is it activated
  3. Where it is inactivated
  4. What receptors does the active form bind
A
  1. Cortisone
  2. Liver
  3. Kidney and placenta
  4. Both GC and mineralocorticoid receptors
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4
Q

Prednisone

  1. Active form
  2. Where is it activated
  3. Where it is inactivated
  4. What receptors does the active form bind
A
  1. Prednisolone
  2. Liver
  3. Kidney and placenta
  4. GC&raquo_space;> mineralocorticoid receptors
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5
Q

4 drugs that increase hepatic steroid metabolism

A

Phenytoin
Barbiturates
Rifampin
Mitotane

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6
Q

Routes of admin of GCs

A
IV
IM
Intra-articular
Orally
Nasal spray
Topically
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7
Q

Primary adrenal insufficiency goals of treatment

A

Trying for physiological replacement

Want the diurnal variation

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8
Q

Classic 21 a-hydroxylase deficiency goals of treatment

A

Reduce the excessive CRH and ACTH to decrease production of adrenal-derived androgens

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9
Q

How does illness change GC administration?

A

3 times usual daily dose for 3 days if can take oral
IV or IM
Monitor because there are no hard and fast rules

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10
Q

Treatment for adrenal crisis

A

If no previous diagnosis (not on steroids), then give them dexamethasone
Known diagnosis = give regular steroids (HC)

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11
Q

Anti-inflammatory action

A

Primary anti-inflam mechanism: inhibit lipocortin-1 synthesis
Inhibit the 2 main inflammatory products prostaglandins and leukotrienes
Used in the treatment of disease caused by overactive immune systems (allergies, asthma, autoimmune diseases)

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12
Q

Budesonide

A

Topical used as an oral preparation
Extended release enhanced topical potency and limits systemic bioavailability
Used in IBD
Extensive first pass hepatic metabolism

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13
Q

Which GC is the most potent ACTH suppressor

A

Desamethasone

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14
Q

Complications of chronic GC use

A

HPA axis suppression (even after ACTH is restored, the hypoplastic adrenal glands may require a lot time to return to normal)
Cushing’s syndrome
Myopathy and osteoporosis

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15
Q

Why should potent topical GCs be avoided in children under 12?

A

Larger surface area to body weight ratio

Very sensitive to HPA suppression

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16
Q

Escape phenomenon

A

When the ECF expansion passes a certain point and Na is excreted
No edema in normal individuals with hyperaldosteronism

17
Q

Tapering GC use

A

First withdrawl GC for 24 hours or replace with equivalent dose of dexa
Perform 8 AM cortisol
Unless is clearly low or clearly normal, need ACTH stim test

18
Q

Fludrocortisone

A

Synthetic mineralocorticoid

Used in all patients with primary adrenal insufficiency or congenital adrenal hyperplasia