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Endocrine 2-Unit 1 Pharm > Adrenal Corticosteroid Drugs (Konorev) > Flashcards

Adrenal Corticosteroid Drugs (Konorev) Flashcards

1
Q

Fludrocortisone is what type of drug?

A

Mineralocorticoid

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2
Q

Hydrocortisone, cortisone, prednisone, prednisolone, and methylprednisolone are what type of drugs?

A

Short-to-medium acting glucocorticoids (<12 hr)

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3
Q

Triamcinolone is what type of drug?

A

Intermediate acting glucocorticoid (12-36 hr)

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4
Q

Betametasone and dexametasone are what type of drugs?

A

Long acting (>36 hr) glucocorticoids

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5
Q

Aminoglutethimide, ketoconazole, metyrapone, and mitotane are what type of inhibitors?

A

Steroid synthesis inhibitors

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6
Q

Mifepristone is what type of drug?

A

Glucocorticoid antagonist

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7
Q

Spironolactone and eplerenone are what type of drugs?

A

Aldosterone antagonists

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8
Q

Mineralocorticoids are induced by __

Glucocorticoids are induced by __

A

Ang II and K+; regulate electrolyte, H2O balance and BP; Glomerulosa

ACTH; regulate metabolism and immunity; Fasciculata

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9
Q

This protein binds 90% of blood cortisol and 60% blood aldosterone. It is high during pregnancy, with estrogen administration, and in hyperthyroidism. It is low in liver disease

A

Transcortin or CBG

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10
Q

This enzyme converts cortisol —> cortisone

A

11 B-HSD2

This makes it mineralocorticoid responsive

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11
Q

These compounds inhibit 11 B-HSD type which results in excessive activation of MR mediated by cortisol. It can cause hypertension

A

Glycyrrhizin (active ingredient in licorice root extract)

Carbenoxolone (approved in UK to tx esophageal ulcers)

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12
Q

Inactivating mutations in ___ cause AME (Apparent Mineralocorticoid Excess) and presents as a form of severe juvenile HTN that is usuall transmitted as an autosomal recessive trait

A

11 B-HSD2

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13
Q

Target cell types of mineralocorticoids (Fludrocortisone)? Effect on gene expression in principal cells? Consequences?

A

Principal cells of collecting tubule and collecting duct

Increase ENaC on apical membrane, increase Na/K pump (basolateral)

Na retention, water retention, K loss

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14
Q

List the effect on gene expression for the following with mineralocorticoids:

NADPH reductase –> ____
Collagen, TGF-b–> ____
IL-6, cell adhesion molecules –> ____
PAI-1—> ____

A

Oxidative stress
Fibrosis, cell senescence
Inflammation
Inhibition of fibrinolysis, blood clotting

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15
Q

Aldosterone excess directly causes what in the heart and vasculature>

A

Cardiac fibrosis and hypertrophy
Vascular remodeling and inflammation

Use aldosterone antagonists in HTN and HF

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16
Q

Which glucocorticoids receptor isoform is prototypical? Which one does not bind ligands, is inactive, is induced by TNF-a, and may be responsible for glucocorticoid resistance?

A

GR-a

GR-B

17
Q

Metabolic effects of glucocorticoids on carbohydrate metabolism?

A
  • Increased gluconeogenesis (d/t increased PEP carboxykinase)
  • Increase glucose output into circulation (d/t increase G-6-Pase)
  • Increased glycogen synthesis (d/t increase glycogen synthase)
  • Decreased glucose uptake by muscle and adipose tissues (d/t decreased expression of GLUT4)
  • Development of hyperglycemia
18
Q

Metabolic effects of glucocorticoids on lipid metabolism?

A

Increase lipolysis
Increase mobilization of free FA and glycerol into the gluconeogenic pathway
Increased lipgenesis
Net increase in fat deposition
Change in fat distribution –> increased fat accumulation in the upper body (shoulders, neck, rounded face), thinning arms and legs

19
Q

Metabolic effects of glucocorticoids on protein metabolism?

A

Decreased AA uptake into cells
Decreased protein synthesis, - nitrogren balance
Mobilization of AAs into gluconeogenic pathway
Skeletal muscle: suppressed protein synthesis wil lead to development of myopathy and muscle wasting

20
Q

The effects of glucocorticoids on the immune system and inflammation occurs due to transrepression of ___

A

NF-kB and AP-1 which leads too…

  • decreased PLA2 and COX2 –> decreased production of PGs and LTs
  • decreased production and increased apoptosis of immune cell types
  • decreased production of cytokines (TNF-a, IL1, IFNy) and their receptors
  • decreased expression of cell adhesion molecules
  • decreased transmigration of neutrophils and macrophages from blood into tissues
21
Q

What are some common clinical applications for adrenal corticosteroid drugs for endocrine conditions?

A

Acute and chronic adrenal insufficiency

Congential adrenal hyperplasia (21a-hydroxylase deficiency)

22
Q

List some non-endocrine conditions for the use of adrenal corticosteroids

A

Immunosuppression–> following organ or HSC transplant; autoimmune disease; hematological disorders

Inflammatory and allergic conditions –> RA, IBD, asthma and COPD, allergic rhinits, skin diseases, hypersensitivity rxns

23
Q

Adverse effects of mineralocorticoids?

A

Retention of Na and water, edema
HTN
Increased preload and cardiac enlargement, development of CHF
K loss and alkalosis (muscle spasms and tetany)

24
Q

Adverse effects of glucocorticoids?

A 
Suppressed ability to fight infx, opportunistic infx
Hyperglycemia
Skin: striae, easy bruising
Muscle wasting, steroid myopathy
HTN
Steroid-induced glaucoma
Cataracts
Peptic ulcers
Psych disorders
Osteoporosis
Retarded growth in children
25
Q

Aminoglutethimide:

MOA?
Indications?
Side effects?

A

MOA: blocks conversion of cholesterol to pregnenolone; reduces production of all steroid hormones

Indications: adrenocortical cancer

Side effects: drowsiness, GI upset

26
Q

Ketoconazole:

MOA?
Indications?
Side effects?

A

MOA: P450 inhibition, reduces synthesis of adrenal and sex hormones

Indications: antifungal drug, Cushing’s syndrome, suppresses androgenic hair loss, prostate CA

Side effects: hepatotoxicity, gynecomastia in males

27
Q

Metyrapone:

MOA?
Indications?
Side effects?

A

MOA: Inhibition of steroid 11-hydroxylation; relatively selectively suppresses formation of cortisol and corticosterone

Indications: Cushings syndrome (can be used in pregnant women)

Side effects: accumulation of 11-deoxycortisol –> increased aldosterone –> Na and H2O retention
-accumulation of 11-deoxycortisol –> increased androgens –> hirsutism in women
GI upset and dizziness

28
Q

Mitotane:

MOA?
Indications?
Side effects?

A

MOA: Na ionofore, Ca ionofore; Protein kinase C and AC inhibitor; Non-selective cytotoxic action on adrenal cortex

Indications: adrenal carcinoma

Side effects: depression, somnolence; GI upset; rashes

29
Q

Mifepristone:

MOA?
Indications?
Side effects?

A

MOA: glucocorticoid receptor antagonist; stabilizes hsp90-GR complex in cytosol, prevents nuclear translocation of GR; Progesterone receptor antagonist

Indications: hypercortisolism in adult pts with endogenous Cushing’s syndrome; anti-progesterone action-used for medical termination of intrauterine pregnancy

Side effects: dizziness, GI upset, Fatigue

30
Q

Spironolactone:

MOA?
Indications?
Side effects?

A

MOA: aldosterone receptor antagonist; also antagonist at androgen receptors

Indications: primary hyperaldosteronism; hirsutism in women; diuretic-used in tx of HF and HTN

Side effects: Hyper-K, gynecomastia and impotence in men, menstrual abnormalities in women

31
Q

Eplerenone:

MOA?
Indications?
Side effects?

A

MOA: competitive antagonist of aldosterone at mineralocorticoid receptors; lower affinity for androgen receptors vs spironolactone

Indications: HTN; HF

Side effects: Hyper-K

Endocrine 2-Unit 1 Pharm (5 decks)

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