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Endocrine Pharmacology > Glucocorticoids, Mineralocorticoids & Adrenocortical Antagonists > Flashcards

Glucocorticoids, Mineralocorticoids & Adrenocortical Antagonists Flashcards

1
Q

Adrenocortical Steroids Drug Types

A 
A. ACTH
B. Glucocorticoids
C. Mineralocorticoids
D. Mineralocorticoid antagonist
E. Inhibitors of adrenocortical steroids synthesis or action
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2
Q

ACTH Drugs

A
  1. Natural (animal) ACTH

2. Cosyntropin Synthetic ACTH (aa 1-24)

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3
Q

Glucocorticoids Drugs

A
  1. cortisol = hydrocortisone
  2. cortisone acetate
  3. prednisone
  4. prednisolone
  5. methylprednisolone
  6. dexamethasone
  7. betamethasone
  8. triamcinolone
  9. budesonide inhalalation
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4
Q

Mineralocorticoids Drugs

A
  1. Aldosterone

2. Fludrocortisone

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5
Q

Mineralocorticoid antagonist Drug

A

Spironolactone

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6
Q

Inhibitors of adrenocortical steroids synthesis or action Drugs

A
  1. aminoglutethimide

2. ketoconazole

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7
Q

ACTH (AdrenoCorticoTropic Hormone) is?

A

ACTH (corticotropin) is a peptide of 39 amino acids. It is synthesized as a part of a larger protein, proopiomelanocortin (POMC)

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8
Q

The cause of Cushing’s Syndrome is an?

A

Overproduction of ACTH by the anterior pituitary.

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9
Q

ACTH Mechanism of Action?

A

ACTH acts on the adrenal cortex by binding to a specific membrane receptor. The ACTH receptor is a G-protein coupled receptor. ACTH binding activates adenylate cyclase and increases intracellular cAMP.

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10
Q

The major clinical use of ACTH is?

A

In testing the integrity of the HPA axis to identify patients needing supplemental steroids.

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11
Q

Natural ACTH isolated from?

A

Animal glands

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12
Q

Synthetic ACTH?

A

(aa 1-24) called cosyntropin

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13
Q

Hypothalamic-Pituitary-Adrenal Axis (HPA) how to test?

A

Test of HPA axis: Measure cortisol, inject drug I.M. or I.V. measure cortisol at 30 to 60 min.). Cosyntropin is preferred because the animal product may contain high levels of vasopressin.

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14
Q

The main mineralocorticoid is?

A

Aldosterone

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15
Q

The main glucocorticoid is?

A

Hydrocortisone (same as cortisol).

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16
Q

Cortisol is released at?

A

10 mg/day

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17
Q

Aldosterone is produced at?

A

0.125 mg/day. (100X difference)

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18
Q

Adrenocortical Steroids Regulation?

A

Carbohydrate, protein and lipid metabolism.

Maintenance of fluid and electrolyte balance.

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19
Q

Adrenocortical Steroids Preservation of normal function of?

A

Cardiovascular system, immune system, kidney, skeletal muscle endocrine system and nervous system.

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20
Q

Adrenocortical Steroids Capacity to resist?

A

Stressful circumstances such as noxious stimuli and environmental changes.

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21
Q

Effects of Adrenocortical Steroids Permissive Effects Define?

A

Some effects of corticosteroids involve actions with other hormonal regulators that are called permissive effects.

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22
Q

Permissive Effects Only a small amount of glucocorticoid in needed to?

A

Greatly potentiate their lipolytic effects. Epinephrine and norepinephrine have minor effects on lipolysis in the absence of glucocorticoids.

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23
Q 
Corticoids are usually grouped according to
three criteria (3 major actions)?
A

– Effects of carbohydrate metabolism (glycogen deposition and gluconeogenesis)
– Antiinflammatory effects
– Relative potencies in Na+ retention

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24
Q

Most corticosteroid effects occur through?

A

Binding to nuclear receptors and either increase or decrease DNA transcription leading to changes in concentration of specific proteins.

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25
Q

Most corticosteroid effects are?

A

Delayed by several hours before corticosteroid therapy becomes manifest.

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26
Q

Some corticosteroid effects are?

A

Immediate and are mediated by membrane receptors.

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27
Q

Aldosterone and cortisol both bind to?

A

The mineralocorticoid receptor with equal affinity, but Cortisol is present in the circulation at much higher levels than aldosteone.

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28
Q

The enzyme 11β-hydroxysteroid dehydrogenase

type 2 converts?

A

Cortisol to cortisone in certain cells of the kidney, colon and salivary glands.

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29
Q

Cortisone does not bind to?

A

The mineralocorticoid receptor.

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30
Q

Glucocorticoids (cortisol) protect the brain during

starvation?

A

(even an overnight fast) by keeping blood glucose elevated. The mechanism is by increased gluconeogenesis and glycogenolysis in the liver. Also, in peripheral tissues, glucocorticoids.

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31
Q

Glucocorticoids (cortisol) Effects?

A 
Decrease glucose utilization.
Increase proteolysis (aa for gluconeogenesis)
Activate lipolysis (glycerol for gluconeogenesis and fatty acids for energy needed for glucose synthesis).
32
Q

Glucocorticoids oppose?

A

Insulin: Therefore: Glucocorticoid therapy can create major problems in diabetic patients.

33
Q

Two major effects of glucocorticoids on lipid

metabolism.

A

Restribution of body fat (seen in Cushing’s Syndrome and long-term glucocorticoid therapy).
Permissive effects on other agents such as growth hormone and β-adrenergic receptor agonists in increasing lipolysis in adipose tissue.

34
Q

Aldosterone is the most imporant?

A

Mineralocorticoid.

35
Q

Aldosterone acts on?

A

Distal tubules and collecting ducts of the kidney to increase reabsorption of Na+ and increase excretion of K+ and H+.

36
Q

Aldosterone has similar actions in the?

A

Colon, salivary glands and sweat glands.

37
Q

The overall effect of aldosterone is?

A

Increased extracellular fluid volume, hypokalemia and alkalosis.

38
Q

Aldosterone deficiency leads to?

A

Na+ loss, decreased extracellular fluid volume, hyponatremia, hyperkalemia and acidosis.

39
Q

Glucocorticoids also contribute to loss of?

A

Total body Ca2+ by multiple poorly understood mechanisms (gut and kidney)

40
Q

The most striking effects on the cardiovascular system are?

A

From mineralocorticoid actions to increase Na+ retention resulting in hypertension. These effects can lead to cerebral hemorrhage, stroke and hypertensive cardiomyopathy.

41
Q

Another major effect on the cardiovascualr system is

A

To enhance vascular reactivity to other substances (usually through increased synthesis of adrenergic receptors).

42
Q

Normal corticosteroid levels are required for?

A

Normal muscle function.

43
Q

Adrenocortical insufficiency (Addison’s disease) causes?

A

Diminished work capacity and fatigue. {Caused by decreased capacity of the circulatory system.}

44
Q

An excess of either glucorticoids or mineralocorticoids will?

A

Impair muscle function.

45
Q

Primary aldosteronism causes muscle weakness due to?

A

Hypokalemia.

46
Q

Glucocorticoid therapy can also lead to muscle weakness due to?

A

Muscle wasting (steroid myopathy) (increased proteolysis).

47
Q

Effects of Corticosteroids on the CNS are direct effects on?

A

Mood, behavior and brain excitability euphoria leading to a felling of well-­‐being, high motor activity, insomnia, restlessness.

48
Q

Addison’s disease effects on CNS?

A

Apathy, depression and irritability.

Some are frankly psychotic.

49
Q

Cushing’s syndrome effects on CNS?

A

High incidence of neuroses and psychoses.

50
Q

Effects of Corticosteroids on Blood Cells?

A

Increased hemoglobin and erythrocytes. Glucocorticoids also decrease eosinophils, monocytes and basophils (in a few hours after administration).
Glucocorticoids increase PMNs.

51
Q

Addison’s disease has a (blank) effect on lymphocytes?

A

Increases lymphocytes. Glucocorticoid therapy decrease lymphocytes.

52
Q

Glucorticoids suppress?

A

Inflammation caused by stress (mechanical, chemical, infectious and immunological).

53
Q

Glucorticoids enormous clinical utility in suppressing

inflammation makes them some?

A

Of the most often prescribed drugs.

54
Q

Glucocorticoids inhibit release of?

A

Arachidonic acid and its metabolites (prostaglandins and leukotrienes) through decreased expression of phospholipase-A2.

55
Q

Glucocorticoids inhibit production and release of?

A

Cytokines (especially IL-1, IL-6, and TNF-α). They inhibit histamine release.

56
Q

Glucorticoids Absorption?

A

Effective when given by mouth. Absorbed readily from intramuscular sites, conjunctival sac, skin, respiratory tract, and other local sites.

57
Q

Glucorticoids Transport

A

Circulating cortisol is 90% bound to proteins. Only
unbound corticosteroids can enter cells.
Two proteins account for binding - corticosteroid
binding protein (CBP, an α-globulin secreted by the
liver) and albumin. CBP has high affinity for binding,
but low capacity. Albumin has low affinity, but high capacity. CBP increases several-fold in pregnancy and during estrogen treatment.

58
Q

Cortisol or hydrocortisone
(Cortef, Hydrocortone)
Route
T½, relative

A

Oral, IM, IV

Short

59
Q

Cortisone acetate
(Cortone acetate)
Route
T½, relative

A

Oral, IM, IV

Short

60
Q

Prednisone (Deltasone)
Route
T½, relative

A

Oral

Intermediate

61
Q

Prednisolone (Delta-Cortef)
Route
T½, relative

A

IM, IV

Intermediate

62
Q

Methylprednisolone (Medrol)
Route
T½, relative

A

Oral, IM, IV

Intermediate

63
Q

Dexamethasone (Decadron)
Route
T½, relative

A

Oral, Topical, IM, IV

Long

64
Q

Betamethasone (Celestone)
Route
T½, relative

A

Oral, Topical

Long

65
Q

Triamcinolone (Aristocort)
Route
T½, relative

A

Oral, Topical

Long

66
Q

Side Effects of Glucocorticoid Therapy

A

Suppression of ACTH and TSH production from the
pituitary.
Osteoporosis
Chronic administration renders some individuals prone to diabetes.
Increased incidence of peptic ulcers. Perforated ulcers
go undetected.
CNS side effects - arousal and euphoria. Followed by depression, sleep disturbances.

67
Q

Side Effects of Glucocorticoid Therapy IN MEN

A

Glucocorticoids can suppress gonadotroph secretion which can cause hypogonadism due to decreased testosterone production.

68
Q

Side Effects of Glucocorticoid Therapy IN WOMEN

A

Glucocorticoids can stop ovulation, or cause dysmenorrhea or dysfunctional uterine bleeding.

69
Q

Side Effects of Glucocorticoid Therapy IN CHILDREN

A

Glucocorticoids may impair linear growth rate (decreased GH and inhibition of IGF-1 effects)

70
Q

Cessation after long term Glucocorticoid therapy has?

A

Very serious consequences, possibly fatal!

71
Q

Secretion of aldosterone by the adrenal gland is controlled by two mechanisms:

A

Renin-angiotensin system (angiotensin II stimulates aldosterone secretion)
Plasma potassium levels (High K+ increases secretion.)
ACTH mediated release is secondary to these two stimuli.

72
Q

Aldosterone Physiological Actions

A

Acts on the distal convoluted tubules in the kidney:

Promotes sodium reabsorption & Increases excretion of potassium & H+

73
Q

Side Effects of Aldosterone Therapy

A

Excessive salt and water retention.
Increased blood volume.
Congestive heart failure.

74
Q

Inhibitors of Synthesis and Action of Adrenocortical

Steroids

A

Aminoglutethimide

Ketoconazole

75
Q

Aminoglutethimide Mechanism?

A

Inhibits P450scc in synthetic pathway.

Inhibits overproduction of cortisol in Cushing’s syndrome.

76
Q

Ketoconazole Mechanism?

A

Antifungal agent.

Inhibits P45017α and P450scc to block cortisol in Cushing’s syndrome

Endocrine Pharmacology (5 decks)

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