Adrenal Hormones / Corticosteroids Flashcards

1
Q

Betamethasone

A

ketone based corticosteroid: cannot be broken down in body (good for Tx but bad for AE)

given IM to mom prior to birth for lung maturation

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2
Q

Cortisone

A

ketone based corticosteroid: cannot be broken down in body (good for Tx but bad for AE)

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3
Q

Dexamethasone

A

ketone based corticosteroid: cannot be broken down in body (good for Tx but bad for AE)

Stronger steroid = worse AE

Used to Diagnose Cushing’s Syndrome (pathological increase in cortisol)
- caused by too much glucocorticoid steroids, increased ACTH (cushing’s disease) or ACTH secreting tumors

Two Methods of Dexamethasone Suppression Test

  1. Low dose causes decrease in ACTH release in normal patients
  2. High Dose: decreased ACTH means pituitary producing too much ACTH and no suppression means tumor
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4
Q

Fludrocortisone

A

ketone based corticosteroid: cannot be broken down in body (good for Tx but bad for AE)

mineralocorticoid

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5
Q

Hydrocortisone

A

ketone based corticosteroid: cannot be broken down in body (good for Tx but bad for AE)

Tx: addison’s disease or any defect in CRH in HT
- maintain circadian rhythm to normal

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6
Q

Methylprednisolone

A

ketone based corticosteroid: cannot be broken down in body (good for Tx but bad for AE)

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7
Q

Prednisone

A

ketone based corticosteroid: cannot be broken down in body (good for Tx but bad for AE)

preferred in pregnancy because minimizes effects on fetus UNLESS FETUS IS TARGET

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8
Q

Triamcinolone

A

ketone based corticosteroid: cannot be broken down in body (good for Tx but bad for AE)

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9
Q

Loteprednol

A

Ester based corticosteroid: can be broken down in body

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10
Q

Adrenal Cortex

A

produces adrenocorticosteroids: glucocorticoids and mineralocorticoids + adrenal androgens

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11
Q

Adrenal Medulla

A

Epinephrine

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12
Q

Hypothalamus

A

produces Corticotropin-releasing hormone to stimulate anterior PG to release ACTH to stimulate cortex to produce cortisol, androgens, and aldosterone

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13
Q

Adrenocorticosteroids

  • types
  • clinical use ((5)
  • AE
A

bind to intracellular receptor

two types: glucocorticoids + mineralocorticoids

Therapeutic Uses:

  • Replacement Therapy
  • Dx Cushing Syndrome
  • Relief of Inflammatory Symptoms
  • Treatment of Allergies
  • Accelerate Lung Maturation

AE: decreased growth in children, osteoporosis, increase infection and impair wound healing, increased IOP, Cataracts (long-term use)

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14
Q

Glucocorticoids

A

receptors are widely distributed in body

cortisol is MAIN human glucocorticoid with diurnal variation and increased with stress

promotes normal metabolism, stimulates protein catabolism and lipolysis for glucose synthesis (increases resistance to stress by increasing glucose)

alters blood cell levels by decreasing WBC/macrophages and increasing RBC/platelets/Hb to DECREASE ability of body to fight infection

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15
Q

Mineralocorticoids

  • receptors
  • actions
  • increased by
A

receptors in secretory organs and brain

controls body’s water volume and electrolyte concentration (Aldosterone)
- increase sodium reabsorption in kidney and water retention (anti-diuretic)

secretion increased by ATII and Potassium

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16
Q

Metyrapone

A

inhibit cortisol synthesis

Inhibit Adrenocorticoid synthesis/Function

17
Q

Aminoglutheamide

A

blocks ALL steroid synthesis by blocking cholesterol from converting to pregnenolone

18
Q

Ketoconazole

A

at high doses will block enzymes responsible for steroid production

19
Q

Mifepristone

A

progesterone antagonist + blocks adrenocorticoid function/synthesis

20
Q

Spironolactone and Eplerenone

A

aldosterone receptors antagonist

21
Q

when to use corticosteroids? (7)

A

Iritis/Uveitis, Episcleritis, Inflammatory Keratitis and Corneal Infiltrates, Post-Op, Ocular Trauma, Adenoviral Infection

ANY INFLAMMATION

22
Q

when to NOT use corticosteroids?

A

Herpes Simplex Epithelial Keratitis

Bacterial or Fungal Infection

Large Corneal Epithelial Defects