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DEMS: Unit III > Adrenal Pharmacology > Flashcards

Adrenal Pharmacology Flashcards

1
Q

General Uses of GC

A

Anti-inflammatory (GC only)
Immunosuppressive (GC only)
Physiologic replacement (Both GC & MC)

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2
Q

Tx of adrenal insufficiency (Addision’s)

A 
-Chronic: 
Cortisol (GC replacement)
fludrocortisone (MC replacement)
DHEA (sex steroid replacement in women) 
-Acute (adrenal crisis: hyponatermia &hyperkalmeia): IV cortisol (IF PREVIOUS Dx) or dexamethasone(w/out previous Dx)
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3
Q

Cushing’s Tx Hypercortisolism

A
  • If due to tumor: remove it
  • ACTH secretion inhibitors (Cabergoline & Pasireotide)
  • Cortisol Synthesis inhibitors (Ketoconazole, Metyrapone, etomidate)
  • Cortisol receptor anatgonist: Mifepristone
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4
Q

Congenital Adrenal Hyperplasia Mutations

A

-21 hydroxylase def: inc. androgens & dec MC=hypotension
-17alpha hydroxylase: no androgens, inc MC=HTN
-11beta hydrooxylase: inc androgens & inc MC=HTN
Cortisol almost always absent=inc ACTH (no suppression)

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5
Q

Preop management of pheochromocytoma

A
  • First give: alpha blockers (phenoxybenzamine, pazosine, Terazosin, Doxazosin)
  • Then Give: Beta Blockers (metoprolol)
  • CCB (alone i.e. nifedipine)
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6
Q

Anti-inflammatory effects of GC

A
  • inhibits Phospholipase A2 (no arachidonic acid)

- Inhibits COX2 (down regulation of PG, Tx, LT, LX: all eicosanoids)

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7
Q

Immunpsuppressive effects of GC

A
  1. Suppress T-cell activation
  2. Suppress cytokine production
  3. Prevent mast cell and eosinophil from releasing mediators (His, PG, LT)
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8
Q

Overall effect of GC

A
  • Reduced vasodilation
  • Decreased fluid exudation
  • Decreased accumulation/activation of immune cells
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9
Q

11beta-HSD1

A
  • Found in Liver
  • Activating (Ketone->OH)
  • Not present in fetus
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10
Q

11beta-HSD2

A
  • Found in Kidney
  • Inactivating (OH->Ketone): protects kidney from unreg MC activity.
  • Present in Placenta
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11
Q

Metabolic effects of Cortisol (physiologic)

A
  • Increase gluconeogenesis (Increase blood Glu)
  • Lower protein synthesis (Increase AA to Glu)
  • Increase lipolysis (Increase FFA)
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12
Q

effects of Aldosterone (physiologic)

A
  • Increase Na+ reabsorption at kidney (Increase blood volume and BP)
  • loosely coupled to K+ and H+ secretion
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13
Q

SE of Excess GC use

A
  • Diabetes like state
  • Muscle wasting. skin-connective tissue atrophy
  • increase central lipogenesis (insulin action): Centripetal obesity (moon facies, buffalo hump)
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14
Q

SE of MC use

A

Known as “salt retaining” effects

  • Increased Na+:increase BP
  • Increased water: edema
  • Increased K+ and H+ secretion: hypokalemia and metabolic alkalosis
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15
Q

Adverse Effects of high, sustained GC therapy

A

-Iatrogenic Cushing’s syndrome (too much GC,
get extreme GC side effects)
-HPA axis suppression (insuff response to
stress)
-Mood disturbance (initial euphoria, then
psychic letdown when dose reduced;
insomnia)
-Impaired wound healing (due to catabolism
of collagen/fibroblasts)
-Increased susceptibility to infection

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16
Q

Adverse effects seen w/ very large doses of GC

A
  • Osteoporosis (risk dec by bisphosphonates)
  • Posterior capsular cataracts (esp in children receiving prolonge asthma treatment)
  • Skin atrophy/loss of collagen support
  • Growth retardation in kids
  • peptic ulcers
17
Q

Oral GC agents

A
  • pro-drug: prednisone, cortisone
  • has ketone at carbon 11
  • must be metabolized to active OH
18
Q

Topical GC agents

A

cortisol (hydrocortisone) is already

active

19
Q

IV GC agents

A

prednisolone=activated

prednisone

20
Q

Hydrocortisone (cortisol)

A
  • Physiologic replacement (equal GC/MC activity) and in emergencies
  • oral and parenteral
21
Q

Prednisone

A
  • Most common oral agent
  • Activated to prednisolone via 1st poss in liver
  • no topical effect
  • GC:MC activity is 13:1
22
Q

Can you separate MC actions from GCC actions?

A

yes (dexamethasone), but can NOT separate anti-inflammatory from GCC actions & can NOT separate anti-inflammatory from immunosuppressive actions

23
Q

Tx of primary aldosteronism (APA)

A

Preop (aldosterone antagonists)

  • Spironolactone
  • Eplerenone
24
Q

Tx of primary aldosteronism (IHA)

A

Aldosterone antognists PLUS BP meds (CCB, ACEI, ARB)

25
Q

Congenital Adrenal Hyperplasia

A
  • Cortisol synthesis is diminished leads to increased ACTH (loss of GC feedback inhibition) leads to adrenal hyperplasia
  • Can be accompanied by excess or deficiency of adrenal mineralocorticoids or androgens
26
Q

GC anti-inflammatory use dosing considerations

A
  • Reduce dosage as soon as therapeutic objectives are obtained
  • Large doses: use shorter-acting agent with little MC
  • Alternate day schedule: minimize adrenal suppression
  • Anti-inflammatory actions outlast HPA suppression
  • Terminate administration gradually (duration > 7-28 d) to minimize disease rebound and symptoms of adrenal insufficiency (adrenal crisis)
27
Q

Methylprednisone

A

Best if want parenteral admin (solu-medrol) but can use orally
-no better than oral prednisone in acute asthma
minimal MC action

28
Q

Triamcinolone

A

Potent systemic agent w/ excellent topical activity

NO MC activity

29
Q

Dexamethosone

A

Most potent anti-inflammatory (activated)
used in adults (hydrocortisone in kids)
-used in cerebral edema, chemo-induced vomiting
Minimal MC action
greatest suppression of ACTH secretion @ pituitary.

DEMS: Unit III (21 decks)

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