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RE Pharm > Iszard- Adrenal Corticosteroid Drugs > Flashcards

Iszard- Adrenal Corticosteroid Drugs Flashcards

1
Q

What are non endocrine uses of corticosteroids?

A

A. Inflammation
B. Allergic disorders
C. Immunological disorders (immune suppression)

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2
Q

What are endocrine uses of corticosteroids?

A

A. Establish the diagnosis and cause of Cushing’s Syndrome

B. Treatment of adrenal insufficiency using physiologic replacement doses

C. Treatment of congenital adrenal hyperplasia for which the dose and
schedule may not be physiologic

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3
Q

What are corticosteroid agonists?(2)

A
  1. Glucocorticoids - Prednisone

2. Mineralocorticoids - fludrocortisone

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4
Q

What are the corticosteroid receptor antagonists? (2)

A
  1. Glucocorticoid antagonists-mifepristone

2. Mineralocorticoid antagonists (spironolactone)

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5
Q

What are the corticosteroid synthesis inhibitors?(1)

A

Ketoconazole

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6
Q

What is the replacement therapy for primary adrenal insufficiency (Addison’s disease)?

A

glucocorticoid (hydrocortisone)+mineralcorticoid (fludrocortisone)

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7
Q

What is the treatment for Congenital Adrenal Hyperplasia?

A

Hydrocortisone+fludrocortisone

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8
Q

How long should corticosteroids be given?

A

Emergency-> give high does for a few days with little risk

Chronic therapy–> more risks

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9
Q

What are the effects of corticosteroids steroids on the immune sx? (5)

A
  1. Decrease production of prostaglandins and leukotrienes
  2. Decreased production and increased apoptosis of immune cell types
  3. Decreased production of cytokines and their receptors
  4. Decreased transmigration of neutrophils and macrophages from blood into tissues
  5. Decreased expression of cell adhesion molecules
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10
Q

What are the consequences of corticosteroids on the immune sx? (3)

A
  1. Decreased inflammation and its manifestations

2, Immune suppression

  1. Decreased allergic/hypersensitivity reactions
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11
Q

What are the effects of glucocorticoids on carbohydrate metabolism?

A
  • increased Gluconeogenesis
  • increaed Glucose Output
  • increased GlycogenSynthesis
  • Decreased Glucose Uptake. –>Development of Hyperglycemia
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12
Q

What are the effects of glucocorticoids on protein metabolism?

A
  • Decreased AA Uptake
  • Decreased Protein Synthesis
  • Dev. Of Myopathy and Muscle Wasting
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13
Q

What are the effects of glucocorticoids on lipid metabolism?

A

-increasedFFA & Glycerol into the gluconeogenic pathway

  • increased Lipogenesis
  • increased Fat Deposition
  • change in Fat Distribution
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14
Q

Glucocorticoid administration can be problematic in what patients? (8)

A
  1. Immunocompromised patients (HIV/AIDS)
  2. Diabetics
  3. Patients with infections
  4. Patients with peptic ulcers
  5. Patients with cardiovascular conditions(HTN, CHF, Angina)
  6. Patients with psychiatric conditions
  7. Patients with osteoporosis
    (postmenopausal women)
  8. Children
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15
Q

Decreased activity of what enzyme results in excessive activation of MR by cortisol causing an increase in blood pressure

A

11β-HSD2

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16
Q

What inhibits 11β-HSD2? (2)

A
  1. Glycyrrhizin (Licorice root extract)

2. Carbenoxolone (UK approved for Rx-esophageal ulcers)

17
Q

Glucocorticoids act as anti-insulins to cause what?

A

Hyperglycemia

  1. increase gluconeogenesis in liver
  2. increase proteolysis in skeletal muscle
  3. Increase lipolysis in adipose tissue
18
Q

What are the short to medium acting glucocorticoids?

A
  1. Hydrocortisone (cortisol)
  2. Cortisone

<12 hours

19
Q

What are the Intermediate-Acting glucocorticoids?

A
  1. Prednisone
  2. Prednisolone
  3. Methylprednisolone
  4. Triamcinolone

12-36 hours

20
Q

What are the long acting corticosteroids?

A
  1. Betamethasone
  2. Dexamethasone

> 36 hours

21
Q

How should corticosteroids be dosed?

A
  1. lowest dose for the shortest duration possible
  2. try to avoid systemic circulation –> topical/inhaled routes
  3. alternate days
  4. single does in AP
22
Q

What can treat cancer of the adrenal glands (adrenal cortical carcinoma)?

A

Mitotane

23
Q

What is Prednisolone MOA?

A
  • Activation of GR alters gene transcription

- used in Many Inflammatory conditions, organ transplantation, hematologic cancers

24
Q

What is Mifepristone MOA?

A

Pharmacologic antagonist of glucocorticoid and progesterone receptors

25
Q

What is clinical application of mifepristone?

A

Medical abortion and very rarely for Cushing’s Syndrome

  • oral administration
  • can cause vaginal bleeding and abdominal pain
26
Q

What do mineralocorticoids do?

A

influence salt and water balance.

27
Q

Where do mineralocorticoids act? What is the main effect?

A

primarily act on the kidney, where they cause sodium and water retention and
active excretion of potassium and protons.

28
Q

What are the mineralcorticoids?

A
  • aldosterone
  • progesterone
  • deoxycorticosterone
29
Q

What is The MOA of Fludrocortisone?

A

Strong agonist at mineralocorticoid receptors and activation of glucocorticoid receptors

30
Q

What is clinical application of Fludrocortisone?

A

Adrenal insufficiency

- long duration of action

31
Q

What medication is used in the diagnosis of adrenal insufficiency and occasionally in the treatment of Cushing’s syndrome (hypercortisolism)?

A

Metyrapone

32
Q

Where is MOA of spironolactone?

A

mineralocorticoid receptor, weak antagonism of androgen receptors

33
Q

What is clinical use of Spironolactone?

A

ldosteronism from any cause, hypokalemia due to diuretic effect, post myocardial infarction

34
Q

What is the MOA of Epierenone?

A

Mineralocorticoid Receptor Antagonism» blocks the binding of aldosterone

35
Q

What is clinical use of eplerenone?

A
  • hypertension, to lower blood pressure.

- Lowering blood pressure reduces the risk of fatal and nonfatal cardiovascular (CV) events, primarily strokes and MI.

36
Q

Whare is MOA of Ketaconazole?

A

Blocks fungal and mammalian CYP450 enzymes

  • used to inhibit mammalian steroid hormone synthesis and fungal ergosterol synthesis

RE Pharm (3 decks)

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