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Pharmacology > Glucocorticoids > Flashcards

Glucocorticoids Flashcards

1
Q

What is the effect on glucocorticoids on plasma glucose levels?

A

Increased plasma glucose due to increased gluconeogenesis

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2
Q

What is a negative consequence of the increased plasma glucose?

A

Diabetes mellitus

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3
Q

How do glucocorticoids effect glycogenolysis?

A

They don’t!

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4
Q

What is the effect of glucocorticoids on protein metabolism?

A

Increased protein breakdown –> increased amino acids

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5
Q

What are the effects of glucocorticoids on lipid metabolism?

A
  1. Increase in bile production

2. Increase in fat redistribution

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6
Q

What are the effects of mineralocorticoids on electrolyte and water balance?

A

Increase Na+ and HCO3- retention while decreasing retention of H+, Cl-, and K+

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7
Q

How do glucocorticoids cause PU/PD?

A

Decreased ADH secretion

Glucocorticoids increase C.V. –> increase GFR –> increase Na+ and H2O excretion

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8
Q

How do glucocorticoids cause osteoporosis?

A

Decrease gut absorption and renal reabsorption of Ca2+ –> decreased plasma Ca2+ –> increased PTH –> increased bone resorption

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9
Q

What is the effect of glucocorticoids on osteoblasts?

A

Increases apoptosis of osteoblasts

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10
Q

What is the effect of glucocorticoids on osteoclasts?

A

Increases the life span of osteoclasts

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11
Q

Glucocorticoids (increase or decrease) excitation?

A

Increase

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12
Q

Mineralocorticoids (increase or decrease) excitation?

A

Decrease

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13
Q

What are the 2 major cardiovascular effects of glucocorticoids and mineralocorticoids?

A
  1. Increased vasomotor response

2. Increased myocardial contraction

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14
Q

How do mineralocorticoids effect blood pressure?

A

Increase blood pressure by increasing Na+ in ECF

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15
Q

How do mineralocorticoids increase myocardial contractility?

A

Decrease of K+ in ECF leads to increase in myocardial Ca2+

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16
Q

Mineralocorticoids induce hypokalemia. Hypokalemia + digitalis = ___?___

A

Cardiac arrhythmia

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17
Q

Glucocorticoids and mineralocorticoids both increase vasomotor response and myocardial contractions. How do glucocorticoids do this?

A

Increase epi, NE –> increase expression of alpha-1 and beta adrenergic receptors –> increase angiotensinogen –> increase ACE –> decrease bradykinin –> vasoconstriction –> decreases capillary permeability –> decreases edema

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18
Q

Describe the effects of glucocorticoids on the following: RBCs, neutrophils, eosinophils, lymphocytes, WBCs, platelets, lymph nodes, thymus.

A

RBCs - increased

Neutrophils - increased

Eosinophils - decreased

Lymphocytes - decreased

WBCs - decreased function

Platelets - increased

Lymph node - decreased in size

Thymus - decreased in size

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19
Q

What is the T1/2 of short acting corticosteroids?

A
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20
Q

What is the T1/2 of intermediate acting corticosteroids?

A

12-36 hours

21
Q

What is the T1/2 of long-acting corticosteroids?

A

36-72 hours

22
Q

In which species is conversion of prednisone to prednisolone impaired?

A

Cats

Horses

23
Q

What is the glucocorticoid potency of short-acting glucocorticoids?

A
24
Q

What is the glucocorticoid potency of intermediate-acting glucocorticoids?

A

4-5

25
Q

What is the glucocorticoid activity of long-acting glucocorticoids?

A

> 10

26
Q

Which 2 configurations are important for corticosteroid activity?

A
  1. 3-keto

2. 4,5 delta

27
Q

Which 2 configurations are important for glucocorticoid activity?

A
  1. 11 beta-OH

2. 17 alpha-OH

28
Q

What is the purpose of 1,2-delta?

A

Strengthens 4,5-delta

29
Q

What is the purpose of 16-OH, CH3?

A

Protects 17-OH

30
Q

What is the purpose of 6-, 9-fluoro, 6-CH3?

A

Protect 11-OH and 4,5-delta

31
Q

How would you administer a water soluble corticosteroid?

A

IV

32
Q

How would you administer a water insoluble corticosteroid?

A

IM or SQ

33
Q

Which two plasma proteins are involved in the binding of cortisol in the plasma?

A
  1. Corticosteroid-binding globulin (CBG)

2. Albumin

34
Q

What are the adverse effects associated with glucocorticoids?

A
  1. Decreased wound healing
  2. Increased susceptibility to infection
  3. Thrombosis
  4. Myopahty
  5. Osteoporosis
  6. GI ulcers
  7. Hepatotoxicity
  8. Diabetes
  9. Glaucoma
  10. CHF in cats
  11. Laminitis
  12. Abortion
35
Q

What are the 6 general contraindications for steroid use?

A
  1. Late pregnancy
  2. Burns
  3. Diabetes mellitus
  4. Corneal ulcer
  5. Cardiac disorders
  6. Uncontrolled infections
36
Q

Dopamine (D2) receptors (increase or decrease) ACTH secretion?

A

Decrease

37
Q

Primary hypoadrenocorticism = increased or decreased ACTH?

A

Increased ACTH

38
Q

Secondary hypoadrenocorticism = increased or decreased ACTH?

A

Decreased ACTH

39
Q

Can ACTH be used therapeutically?

A

No

40
Q

Which of the following are reversible and which are irreversible: Ketoconazole, Trilostane, Selegiline, Mitotane.

A

Irreversible : Mitotane

Reversible : Ketoconazole, Trilostane, Selegiline

41
Q

Which layers of the adrenal cortex are affected by Mitotane?

A

Mitotane destroys (1) zona reticularis and (2) zona fasciculata

42
Q

What are the 2 adverse effects associated with Mitotane?

A
  1. Hypoadrenocorticism

2. Hepatotoxicity

43
Q

What is the mode of action of Trilostane?

A

Inhibits 3 beta-hydroxysteroid dehydrogenase (this enzyme forms the 3-keto group, and without that keto group, there is no corticosteroid activity)

44
Q

What are the 2 adverse effects associated with Trilostane?

A
  1. Adrenal gland necrosis (although rare)

2. GI and reproductive disturbances (inhibits the synthesis of sex steroids)

45
Q

What is the mode of action of Ketoconazole?

A

Inhibits steroidogenesis by inactivating cytochrome P450

46
Q

What are the 3 adverse effects associated with Ketoconazole?

A
  1. Hepatotoxicity
  2. GI and reproductive disturbances
  3. Drug interactions due to enzyme inhibition
47
Q

What is the mode of action of Selegiline?

A

Inhibits ACTH secretion by increasing dopamine (dopamine decreases ACTH secretion)

48
Q

What are the 4 D2-receptor agonists?

A
  1. Bromocriptine
  2. Cabergoline
  3. Pergolide
  4. Apomorphine
49
Q

Which of the following is used to treat pituitary-dependent hyperadrenocorticism: Mitotane, Ketoconazole, Selegiline, or Trilostane?

A

Selegiline

Pharmacology (21 decks)

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