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STEP Pharm II > Glucocorticoids, Mineralcorticoids, and Adrenocorticoid Antagonists > Flashcards

Glucocorticoids, Mineralcorticoids, and Adrenocorticoid Antagonists Flashcards

1
Q

What is the known ACTH analog?

A

Synthetic ACTH (AA 1-24) Cosyntropin (Cortrosyn)

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2
Q

What glucocorticoid analogs are on the market?

A

Cortisol=hydrocortisone (Cortef, Hydrocortone)Prednisone (Deltasone)Prednisolone (Delta- Cortef)Methlprednisolone (Medrol)Dexamethasone (Decadron)Budesonide Inhalation (Pulmicort)

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3
Q

What are the mineralcorticoid analogs?

A

Fludrocortisone (Florinef)

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4
Q

What arethe mineralcorticoid antagonists?

A

Spironolactone and Eplernone

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5
Q

What are some inhibitors of adrenocortical steroid synthesis or action?

A

Amingogluthemide (Cytadren)Ketoconazole (Nizoral)

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6
Q

What is ACTH made from?

A

proopiomelanocortin (POMC) (which is cleaved to form ACTH, MSH and endorphins)

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7
Q

Briefly describe the ACTH axis

A

Circadian rhythm and stress (sometimes in the form of immune factors like IL-1/2/6, TNFa)signal release of CRH from the hypothalamus, which stimulates release of ACTH from the anterior pituitary, and subsequent adrenal cortex hormone productionNOTE: It makes sense that inflammatory factors like IL-1 would stimulate ACTH and CRH given that cortisol inhibits their production via binding to white cells

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8
Q

Which is released from the adrenal cortex in large quantites, cortisol or aldosterone?

A

Cortisol is released at 10 mg/day and aldosterone is produced at 0.125 mg/day (100x difference).

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9
Q

What enzyme deactivates cortisol in cells where aldosterone acts to cortisone (kidney, colon, and salivary glands)?

A

11B-HSD type II (thus cortisol cannot bind to aldosterone receptors!)

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10
Q

In addition to direct effects, glucocorticoids also have permissive effects. What does this mean?

A

ex. epi and nor have minor effects on lipolysis in the absence of glucocorticoids, but much greater in their presence (this ex. is due to increased synthesis of lipases) due to upregulation of adrenergic receptors by cortisol

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11
Q

Do corticosteroids act quickly?

A

Most of the effects of steroid hormones are via upregulation of DNA transcription so they are delayed several hours. However, a few effects are immediate and are mediated by membrane receptors

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12
Q

What are the effects of glucocorticoids on blood glucose?

A

They protect the brain during starvation by keeping bloodglucose elevated via increased gluconeogenesis and glycogenolysis in the liver.Also, in the periphery glucosteroids decrease glucose uptake, increase proteolysis (to provide AAs for gluconeogenesis) and lipolysis (gycerol for gluconeogenesis)

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13
Q

How do glucocorticoids affect lipids?

A

In addition to promotinglipolysis, cortisol promotes redistribution of body fatandathey also have permissive effects on other agents such as GHand b-adrenergic receptor agonists(iso and nor)in increasing lipolysis in adipose tissue.

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14
Q

An excess of either glucocorticoids or mineralcorticoids will affect muscle how?

A

impair muscle function (primary aldosteronism causes muscle weakness via hypokalemia and glucocorticoids via increased proteolysis and Ca2+ loss)

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15
Q

How do glucocorticoids affect the brain?

A

It results in euphoria and feelings of well-being, high motor activity, insomnia, and restlessness(in addison’s disease, you might see apathy, depression, and irritability)

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16
Q

How do glucocorticoids affect the inflammatory process?

A

They are anti-inflammatory and inhibit:-phospholipase A2 action via lipocortin-production and release of cytokines (especially IL-1, IL-2, IL-6, and TNFa)-histamine and serotonin release

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17
Q

What is the half-life of cortisol,hydrocortisone, or cortisone acetate?

A

short (all of these can be given PO, IM, or IV)

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18
Q

What is the half-life of prednisone,prednisolone, or methylprednisolone?

A

intermediate (note prednisone can onlybe given PO, prednisolone IM and IV, and methlprednisolone IM, IV, and PO)

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19
Q

What are the long acting glucocorticoids?

A

Dexamethasone (IM, PO, topical, IV)and triamcinolone (PO, topical)

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20
Q

What are the AEs of glucocorticoid therapy?

A

-suppression of ACTH and TSH production from the pituitary (recovery can take weeks to months)-osteoporosis-induced diabetes-peptic ulcers-arousal and euphoria, followed by depression and insomnia commonly

21
Q

Other uses of glucocorticoid therapy in men?

A

can suppress gonadotroph secretion causing hypogonadism due to suppressed testosterone production

22
Q

Other glucocorticoid therapy in women?

A

can stop ovulation, or cause dysmenorrhea or dysfunctional uterine bleeding

23
Q

Other glucocorticoid therapy in children?

A

stunted linear growth (decreased GH and inhibition of IGF-1)

24
Q

How would acute adrenal insufficiency disorders of the adrenal gland or abrupt withdrawal of glucocorticoids be treated?

A

IV isotonic NaCl + 5% glucose + corticosteroids (after a dexamethasone test) orIV hydrocortisone (cortisol)

25
Q

How would chronic adrenal insufficiency disorders (e.g. Addison’s)with less severe symptomsbe treated?

A

daily hydrocortisone or cortisone acetate (2/3 dose in morning and 1/3 evening)or dexamethasone or prednisone-add additional mineralcorticoid therapy if needed–(fludrocortisone acetate)

26
Q

What glucocorticoid has been used for rheumatic disorders?

A

PO prednisone usually (and renal diseases)

27
Q

How would you treat allergic disease?

A

anaphylaxis requires immediate epiLong term:antihistamines for moderate symptomsIV methylprednisolone for sevre symptomsIntranasal steroids for allergic rhinitis (fluticasone)

28
Q

Other uses of glucocorticoids?

A

-ocular diseases (dexamethasone)-skin diseases (hydrocortisone)-GI disease (Chronic UCand CD)-hydrocortisone, prednisone, and budesonide (high first pass effect)-hepatic disease (prednisone, prednisolone)-lymphocytic leukemia and lymphoma-asthma (budesonide inhalation suspension)

29
Q

In general, the most used systemic steroids in practice are what?

A

hydrocortisone, methylprednisolone, and dexamethasone

30
Q

What are the AEs ofspironolactone?

A

anti-androgen effects (gynecomastia) and can cause decreased spermatogenesisNOTE: Eplerenone is similar to spiro but is much more specific for the mineralcorticoid receptor and has little or no anti-androgen effect

31
Q

AEs ofaldosterone therapy (fludrocortisone)?

A

-excessive salt and water retention-increased BP and CHF

32
Q

How is ketoconazole used for tx in Cushing’s syndrome?

A

inhibits P450scc (desmolase)to P45017a to block cortisol production (blocks all steroid hormone synthesis)

33
Q

Other uses of keto?

A

adrenal carcinoma, breast and prostate cancer, and hirsutism

34
Q

AEs of keto?

A

adrenal insufficiencysevere hepatotoxicity

35
Q

How can aminoglutethimide (Cytadren) used for treatment of Cushing’s disease?

A

It inhibits P450scc (converts cholesterol to pregnenolone)and inhibits all steroid production

36
Q

How can the AEs of steroid use be minimalized?

A

-local application (for example aerosols for asthma)-alternative day therapy (to reduce pitutiary suppression)-tapering the dose soona fter achieving a therapeutic response

37
Q

What is Flucticazone (Flonac)?

A

a glucocorticoid that has recently gonegeneric (December 2015) and has since been associated with inflammatory rxns because its insolubleand a new emulsifying substance is being used which is causing the rxn

38
Q

What things are released from POMC when it is broken down?

A

ACTH, a-MSH, y-MSH, CLIP, y-lipotrophin, B-endorphin

39
Q

What is themajor clinical use of ACTH?

A

is in testing the integrity of the HPA axis to identify patients needing supplemental steroids.•Test of HPA axis: Measure cortisol, inject drug I.M. or I.V. measure cortisol at 30 to 60 min.) Use a synthetic ACTH called Cosyntropin

40
Q

Effects of steroids

A

•Regulation in carbohydrate, protein and lipid metabolism•Maintenance of fluid and electrolyte balance•Preservation of normal function of cardiovascular system, immune system, kidney, skeletal muscle endocrine system and nervous system•Capacity to resist stressful circumstances such as noxious stimuli and environmental changes

41
Q

Effects of Aldosterone on CV system

A

•The most striking effects on the cardiovascular system are from mineralocorticoid actions to increase Na+ retention resulting in hypertension.•These effects can lead to cerebral hemorrhage, stroke and hypertensive cardiomyopathy.•Another major effect is to enhance vascular reactivity to other substances (usually through increased synthesis of adrenergic receptors).

42
Q

How do glucocorticoids affect blood cells?

A

Glucocorticoids increasehemoglobin and erythrocytes.•Addison’s disease increases lymphocytes. Glucocorticoid therapy decrease lymphocytes.•Glucocorticoids also decrease eosinophils, monocytes and basophils (in a few hours after administration).•Glucocorticoids increase polymorphonuclear leukocytes.

43
Q

How are steroids typically given?

A

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

44
Q

How does cortisol circulate?

A

•Circulating cortisol is 90% bound to proteins. Only unbound corticosteroids can enter cells.

45
Q

What proteins are the main binders of cortisol in blood?

A

•Two proteins account for binding - corticosteroid binding protein (CBP, an a-globulin secreted by the liver) and albumin.CBP has high affinity for binding, but low capacity, whileAlbumin has low affinity, but high capacity.

46
Q

What situations might you see increased levels of CBP?

A

CBP increases several-fold in pregnancy and during estrogen treatment.

47
Q

Which steroids have no mineralcorticoid activity?

A

The long-acting glucocrticoids, dexamethasone and betamethasone (these are also the most potent)

48
Q

How would you treatCongenital adrenal hyperplasia (agenetic disorder lacking enzymes to produce cortisol or aldosterone or both-results in increased ACTH secretion for lack of feedback)

A

Hydrocortisone with or without fludrocortisone acetate

STEP Pharm II (42 decks)

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