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DEMS: Unit III > Adrenal Gland Pharmacology > Flashcards

Adrenal Gland Pharmacology Flashcards

1
Q

Metabolic effects of glucocorticoids

A
  • Carbohydrates: ↑ gluconeogenesis, ↑ blood glucose, ↑ insulin
    • Excess = diabetes like state
  • Protein: ↓ protein synthesis, ↑ AA to glucose
    • Excess: muscle wasting, weakness, skin- connective tissue atrophy
  • Fat: ↑ lipolysis peripherally, ↑ FFA
    • Excess: ↑ lipogenesis (centrally via insulin) → centripetal obesity (moon facies and buffalo hump)
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2
Q

Drugs that must be activated @ liver

A
  • Ketone at carbon 11 means must be activated in liver
  • Hydrocortisone (Solu-Cortef®) → inactive until goes through liver
  • Prednisone → inactive until goes through liver where it is converted into Prednisolone
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3
Q

Drugs that are physiologically active as given

A
  • Drugs have Hydroxyl at Carbon 11 which means physiologically active.
  • Prednisolone has C1=C2 (double bond) which ↑ anti-inflammatory effects
  • Methylprednisolone (Solu-Medrol®) → has C1=C2 (double bond) + α-methyl group on C-6 which ↑ anti-inflammatory activity (5-6x stronger than cortisone)
  • Fludrocortisone has a fluorine at C-9 which ↑ mineralocorticoid activity
  • Dexamethasone has a fluorine at C-9 + α-methyl group on C-16: which ↑ anti-inflammatory effects 18x and essentially eliminates mineralocorticoid activity (of the fluorine group)
  • Triamcinolone is active and a topical/oral/injectable.
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4
Q

Tx of addison’s disease (acute and chronic)

A
  • Chronic: administer hydrocortisone with increased dose during stress.
    • Fludrocortisone is usually required for sufficient salt-retaining effect (unless mild case).
  • Acute (i.e. life threatening, immediate treatment): High IV cortisol dose until stable (correct fluid/electrolyte abnormalities).
    • Sometimes fludrocortisone needs after switch to lower oral cortisol dose
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5
Q

Tx of Cushing’s disease

A
  • Surgery is treatment of choice (pituitary/chest/abdomen).
  • Pharmacotherapy is adjunctive in refractory or inoperable cases = cortisol synthesis inhibitors.
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6
Q

Pharmacotherapy in Cushing’s disease/syndrome

A
  • ACTH Secretion Inhibitors
    • Cabergoline, Pasireotide
  • Cortisol Synthesis Inhibitors
    • Ketoconazole, Metyrapone, Etomidate
  • Adrenolytic Agents
    • Mitotane
  • Cortisol Receptor Blockers
    • Mifepristone
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7
Q

Tx of Primary Aldosteronism

A
  • Aldosterone antagonists (Spirinolactone + eplerenone)
  • hypertensive medications (Thiazide, CCB, ACE-I, ARBs)
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8
Q

Tx of Pheochromocytoma

A
  • Surgical removal of tumor but first need preoperative α blockade:
    • α-blockade: phenoxybenzamine: irreversible α1 + α2 antagonist
    • β-blockade: metoprolol always after adequate α-receptor blockade.
  • Then maybe Ca2+ blocker (nifedipine), then catecholamine synthesis inhibitor (metyrosine).
  • Then adrenalectomy - if inoperable or metastatic.
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9
Q

Tx of glucocorticoid insufficiency

A
  • Hydrocortisone
  • Prednisone
  • Dexamethasone
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10
Q

Tx of mineralcorticoid insuffiency

A

Fludrocortisone

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11
Q

Tx of Sex Steriod insuffieciency

A

DHEA

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12
Q

Hydrocortisone: GC v. MC vs. Anti-inflammatory actions & clinical uses

A
  • GC: MC: AI = 1:1:1
  • Uses
    • Acute (ER)
    • GC + MC replacement
    • Addison’s disease
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13
Q

Prednisone: GC v. MC vs. Anti-inflammatory actions & clinical uses

A
  • GC: MC: AI = 4:1:4
  • Use
    • Steroid burst ==> GC + (less) MC
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14
Q

Methylprednisolone: GC v. MC vs. Anti-inflammatory actions & clinical uses

A
  • GC: MC: AI = 5:0:5
  • Use
    • steroid burst
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15
Q

Triamcinilone: GC v. MC vs. Anti-inflammatory actions & clinical uses

A
  • GC: MC: AI = 5:0:5
  • Use
    • Potent systemic agent with excellent topical activity.
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16
Q

Dexamethasone: GC v. MC vs. Anti-inflammatory actions & clinical uses

A
  • GC: MC: AI = 30:0:30
  • Use
    • Most potent α-inflammatory, used in cerebral edema, chemo-induced vomiting.
    • Greatest suppression of ACTH secretion
17
Q

Hydrocortisone: administration routes

A
  • Oral
  • Injectable
  • Topical
18
Q

Prednisone: administration routes

A

oral only

19
Q

Methylprednisolone: administration routes

A
  • Oral
  • Injectable
  • Parenteral
20
Q

Triamcinolone: administration routes

A
  • Topical (53)
  • Oral
  • Injectable
21
Q

Dexamethasone: administration routes

A
  • Oral
  • Injectable
  • Topical
22
Q

Salt-retaining activity of drug correlates to…

A

MC activity

23
Q

ACTH suppression of drug correlates to..

A

GC activity

24
Q

Corticosteroids that can be used topically

A
  • hydrocortisone
  • triamcinolone
  • dexamethason
25
Q

General dosing consideration for use of corticosteroids for anti-inflammatory use

A
  • REMEMBER: Mineralocorticoid side effects vary with agent
  • Dosage often by trial and error with re-evaluation
  • Consider seriousness of disease - minimal amount for desired effect - duration of therapy
  • Reduce dosage as soon as therapeutic objectives are obtained
26
Q

If using large doses of corticosteroids you should…

A
  • use shorter-acting agent with little MC
    • e.g. methylprednisolone
27
Q

Dosing consideration used to minimize adrenal suppression or adrenal insufficiency

A
  • Alternate day schedule à minimize adrenal suppression
    • Anti-inflammatory actions outlast HPA suppression
  • Terminate administration gradually (duration > 7-28 d)
    • Minimizes disease rebound and potential for symptoms of adrenal insufficiency (adrenal crisis)
28
Q

Potential toxicity of acute, short course, high dose

A
  • Mineralocorticoid effects: Salt and water retention ==> edema ==> increased blood pressure, hypokalemia
  • Glucocorticoid effects: Glucose intolerance in diabetics, mood changes (up or down), insomnia, GI upset
29
Q

Glucocorticoid effects of high dose sustained corticosteroid therapy

A
  • Iatrogenic Cushing’s syndrome
  • Hypothalamic-pituitary-adrenal axis suppression
  • Mood disturbance
  • impaired wound healing
  • increased susceptibility to infection
30
Q

Characteristics of iatrogenic cushing’s syndrome

A
  • hyperglycemia
  • protein wasting (muscle)
  • lipid deposition (weight gain)
  • ==> diabetes-like state
31
Q

Characteristics of HPA axis suppression

A
  • Can result in insufficient response to stress
  • More suppression with dexamethasone and betamethasone
  • Also may cause decrease in ACTH, GH, TSH, LH, sex steroids
32
Q

Possible consequences of large, chronic doses of corticosteroids

A
  • osteoporosis
  • posterior capsular cataracts
  • skin atrophy, loss of collagen support
  • growth retardation in children
  • peptic ulceration
33
Q

Short-medium acting corticosteroids

A
  • hydrocortisone
  • prednisone
  • methylprednisolone
34
Q

Intermediate-acting corticosteroids

A
  • tramicinolone
  • fluprednisolone
35
Q

Long-acting corticosteroids

A

dexamethasone

36
Q

Most common mineralcorticoid agent

A

fludrocortisone

DEMS: Unit III (24 decks)

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