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Endocrine II midterm > Konorev DSA: Corticosteroids > Flashcards

Konorev DSA: Corticosteroids Flashcards

1
Q

What is the Mineralocorticoid we have to know?

A

Fludrocortisone

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2
Q

What are the glucocorticoids?

A
  • Hydrocortisone
  • Cortisone
  • Prednisone
  • Prednisolone
  • methypredisolone (those are short acting)
  • Tramcinolone is intermediate acting
  • Betametasone and Dexametasone are long acting
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3
Q

What are the Steroid synthesis inhibitors?

A
  • Aminoglutethimide
  • Ketoconazole
  • Metyrapone
  • Mitotane
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4
Q

What is the Glucocorticoid antagonist?

A

Mifepristone?

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5
Q

Aldosterone antagonists

A
  • Spironolactone

- Eplerenone

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6
Q

What are Mineralocorticoids induced by and what do they regulate?

A
  • induced by Ang II and K+

- regulate electrolyte, H2O balance and blood pressure

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7
Q

Glucocorticoids induction and what they regulate?

A
  • induced by ACTH

- Regulate metabolism and immunity

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8
Q

What are weak androgens converted to?

A
  • potent androgens in males

- estrogens in females

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9
Q

What carries steroid hormones?

A

Transcortin

  • high in preggo
  • low in liver disease
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10
Q

What is the role of the liver in pharmacokinetics or cortisol?

A
  • produces transcortin

- about 80% of cortisol is metabolized by the liver

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11
Q

When is the half-life of cortisol increased?

A
  • patients with liver diseases

- hypothyroid patients

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12
Q

MOA of adrenal corticosteroids

A
  • nuclear receptors
  • gene expression after lag period
  • -effects can last even after the agonist is gone
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13
Q

What are the target cells for Mineralocorticoids?

A
  • principal cells of collecting tubule and collecting duct

- other epithelial cells involved in electrolyte transport

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14
Q

What are the effects of activation of mineralocorticoid receptor in principal cells of collecting tubule and collecting duct?

A
  • increased eptihelial sodium channel (ENaC)
  • increased Na+/K+ pump
  • Retention of water and sodium, loss of potassium
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15
Q

Direct effects of mineralocorticoids on cardiovascular system

A
  • NADPH reductase—> oxidative stress
  • Collagen, TGFB –> fibrosis, cell senescence
  • IL-6, cell adhesion molecules —> inflammation
  • PAI-1–> inhibition of fibrinolysis, blood clotting
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16
Q

What does aldosterone excess directly cause?

A
  • cardiac fibrosis and hypertrophy

- vascular remodeling and inflammation

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17
Q

What is the transactivation mechansim of glucocorticoid effects?

A

-GR-ligand complex binds to GRE in gene promoters to activate gene expression

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18
Q

What is the transrepression mechanism of glucocorticoid effects?

A

-GR-ligand complex binds to other transcriptionfactor complexes to suppress their activation of gene transcription

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19
Q

What are glucocorticoid receptor isoforms?

A
  • encoded by the same gene
  • products of the alternative splicing
  • GRalpha is a protoypcal isoform
  • GRbeta lack 35 aa at C terminal- does not bind ligands and is inactive
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20
Q

What is GRbeta induced by?

A
  • TNF-alpha

- May be responsible for glucocorticoid resistance

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21
Q

What binds a mineralocorticoid receptor (MR) with equal affinity as cortisol?

A

aldosterone

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22
Q

What does 11B-HSD (hydroxysteroid dehydrogenase) type 2 do?

A
  • converts cortisol into inactive at MR cortisone

- makes tissues mineralocorticoid responsive for some reason

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23
Q

What is the result of decreased activity of 11B-HSD type 2?

A

excessive activation of MR mediated by cortisol

-causes hypertension and edema

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24
Q

What is that weird thing from candy that will decrease 11B-HSD type 2?

A

Glycyrrhizin

-because of this, it may cause hypertension

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25
Q

What do glucocorticoids do to carbohydrate metabolism?

A
  • increased gluconeogenesis (increased PEP carboxykinase)
  • increased glucose output into circulation (glucose-6-Phosphatase)
  • increased glycogen synthesis
  • decreased glucose uptake by muscle and adipose tissues (GLUT4)
26
Q

glucocorticoid effect on lipid metabolism

A
  • promote stimulation of hormone-sensitive lipase in adipose tissue–> increase lipolysis
  • incraese mobilization of FFA and glycerol into the gluconeogenic pathway
  • increase insulin secretion–> increased lipogenesis
  • Net increase in fat deposition
  • Change in fat distribution (shoulders neck face)
27
Q

glucocorticoid effect on protein metabolism

A
  • decreased aa uptake into cells
  • decreased ptn synth, negative nitrogen balance
  • mobilization of aas into the gluconeogenic pathway
  • skeletal muscle: suppressed protein synthesis will lead to the development of myopathy and muscle wasting
28
Q

What do the effects of glucorticoids on metabolism do to the actions of insulin?

A

ANTAGONIZE THEM!

29
Q

What do glucocorticoids do to the immune system?

A

suppresses it

30
Q

glucocorticoid effect on the cardiovascular system?

A
  • increased E and NE
  • increased HR and CO
  • elevated BP
31
Q

glucocorticoid effect on GI system?

A
  • decreased gastro-protective prostaglandins
  • decreased immune response against H. pylori
  • increase in gastric acid and pepsin secretion
32
Q

effect on CNS

A
  • insomnia
  • irritability
  • euphoria followed by depression
  • decreased sexual libido in males
33
Q

effect on bone growth

A
  • dereased blast activity
  • increased clast activity
  • growth retardation in children
  • osteoporosis, bone fractures
  • decreased intestinal and renal Ca2+ absorption
34
Q

effect on skin

A
  • low collagen
  • low fibroblast proliferation
  • low would healing, increased bruising
  • fragile and thin skin with stretch marks called striae
35
Q

Common clinical indication of adrenal corticosteroid drugs

A
  • replacement therapy
  • immunosupression
  • inflammatory and allergic conditions
36
Q

Adverse effects of Mineralocorticoids (Fludrocortisone)

A
  • retention of sodium and water, edema
  • HTN
  • increased preload and cardiac enlargement, development of congestive heart failure
  • K+ loss and alkalosis
37
Q

Adverse effects of Glucocorticoids

A

-can’t fight infections
-hyperglycemia
-striae, easy bruising
-muscle wasting
-HTN
-glaucoma
-cataracts
peptic ulcers
-psych disorders: euphoria, mania, anxiety
-Increased appetite and weight gain
-Osteoporosis
-retarded growth in children

38
Q

Dosing of adrenal corticosteroid drugs

A
  • use lowest dose for the shortest duration possible depending on the condition
  • reduce distribution of drugs into systemic circulation
  • give single daily doses in the morning
  • alternate day, short-course, pulse therapy administration
  • dose tapering
39
Q

What are some patient populations in which systemic glucocorticoids administration is problematic?

A
  • IC patients (AIDS)
  • Diabetics
  • Infections
  • pt’s w/ ulcers
  • pts w/ CV conditions
  • psych conditions
  • osteoporosis
  • children
40
Q

What are the inhibitors of adrenal corticosteroid action?

A
  • aminoglutethimide
  • ketoconazole
  • metyrapone
  • mitotane
  • mifepristone
  • spironolatctone
  • eplerenone
41
Q

MOA of aminoglutethimide?

A
  • blocks the conversion of cholesterol to pregnenolone

- reduces production of all steroid hormones

42
Q

Indications for aminoglutethimide?

A
  • was used for breast cancer

- adrenocortical cancer

43
Q

side effects of aminoglutethimide?

A
  • drowsiness

- GI upset

44
Q

MOA of Ketoconazole

A
  • P450 inhibition

- reduces synthesis of adrenal and sex hormones

45
Q

Indications of Ketoconazole

A
  • anitfungal drug
  • cushing’s syndrome
  • suppresses androgenic hair loss
  • prostate cancer
46
Q

side effects of Ketoconazole

A
  • Hepatotoxicity

- Gynecomastia in males

47
Q

MOA of Metyrapone

A
  • inhibition of steroid 11-hydroxylation

- relatively selectively suppresses formation of cortisol and corticosterone

48
Q

indications of metyrapone

A
  • cushings syndrome

* the only drug for this indication that can be used in pregnant women**

49
Q

side effects of metyrapone

A
  • accumulation of 11-deoxycortisol… increased aldosterone…. Na+ and H2O retention
  • same thing…. increased androgens…. hirsutism in women
  • GI upset
  • Dizziness
50
Q

MOA of Mitotane

A
  • Na+ ionofore, Ca2+ ionofore
  • Protein kinase C and adenylys cyclase inhibitor
  • non-selective cytotoxic action on adrenal cortex
51
Q

Indications for Mitotane

A

-Adrenal Carcinoma

52
Q

Side effects of Mitotane

A
  • depression, somnoloence
  • GI upset (diarrhea, nausea, vomiting
  • rashes
53
Q

MOA of Mifepristone

A
  • glucocorticoid receptor antagonist
  • stabilizes hsp90-GR complex in cytosol, prevents nuclear translocation of GR
  • Progesterone receptor antagonist
54
Q

Indication of Mifepristone

A
  • hypercortisolism in adult patients with endogenous Cushing’s syndrome
  • Anti-Progesterone action - used for medical termination of intrauterine pregnancy
55
Q

Side effects of Mifepristone

A
  • Dizziness
  • GI upset (anorexia, nausea, vomiting)
  • Fatigue
56
Q

Spironolactone MOA

A
  • Aldosterone receptor antagonist

- also an antagonist at androgen receptors

57
Q

Indications for Spironolactone

A
  • primary hyperaldosteronism
  • hirsutism in women
  • diuretic… used in treatment of HF and htn
58
Q

Side effects of Spironolactone

A
  • hyperkalemia
  • Gynecomastia and impotence in men
  • Menstrual abnormalities in women
59
Q

Eplerenone MOA

A
  • competitive antagonist of aldosterone at mineralocorticoid receptors
  • lower affinity for androgen receptors vs. spironolactone
60
Q

Indication of Eplerenone

A
  • HTN

- Heart failure

61
Q

Side effects of Eplerenone

A

-Hyperkalemia

Endocrine II midterm (13 decks)

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