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Glucocorticoids Flashcards

(49 cards)

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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?

21
Q

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

22
Q

In which species is conversion of prednisone to prednisolone impaired?

23
Q

What is the glucocorticoid potency of short-acting glucocorticoids?

24
Q

What is the glucocorticoid potency of intermediate-acting glucocorticoids?

25
What is the glucocorticoid activity of long-acting glucocorticoids?
> 10
26
Which 2 configurations are important for corticosteroid activity?
1. 3-keto | 2. 4,5 delta
27
Which 2 configurations are important for glucocorticoid activity?
1. 11 beta-OH | 2. 17 alpha-OH
28
What is the purpose of 1,2-delta?
Strengthens 4,5-delta
29
What is the purpose of 16-OH, CH3?
Protects 17-OH
30
What is the purpose of 6-, 9-fluoro, 6-CH3?
Protect 11-OH and 4,5-delta
31
How would you administer a water soluble corticosteroid?
IV
32
How would you administer a water insoluble corticosteroid?
IM or SQ
33
Which two plasma proteins are involved in the binding of cortisol in the plasma?
1. Corticosteroid-binding globulin (CBG) | 2. Albumin
34
What are the adverse effects associated with glucocorticoids?
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
What are the 6 general contraindications for steroid use?
1. Late pregnancy 2. Burns 3. Diabetes mellitus 4. Corneal ulcer 5. Cardiac disorders 6. Uncontrolled infections
36
Dopamine (D2) receptors (increase or decrease) ACTH secretion?
Decrease
37
Primary hypoadrenocorticism = increased or decreased ACTH?
Increased ACTH
38
Secondary hypoadrenocorticism = increased or decreased ACTH?
Decreased ACTH
39
Can ACTH be used therapeutically?
No
40
Which of the following are reversible and which are irreversible: Ketoconazole, Trilostane, Selegiline, Mitotane.
Irreversible : Mitotane Reversible : Ketoconazole, Trilostane, Selegiline
41
Which layers of the adrenal cortex are affected by Mitotane?
Mitotane destroys (1) zona reticularis and (2) zona fasciculata
42
What are the 2 adverse effects associated with Mitotane?
1. Hypoadrenocorticism | 2. Hepatotoxicity
43
What is the mode of action of Trilostane?
Inhibits 3 beta-hydroxysteroid dehydrogenase (this enzyme forms the 3-keto group, and without that keto group, there is no corticosteroid activity)
44
What are the 2 adverse effects associated with Trilostane?
1. Adrenal gland necrosis (although rare) | 2. GI and reproductive disturbances (inhibits the synthesis of sex steroids)
45
What is the mode of action of Ketoconazole?
Inhibits steroidogenesis by inactivating cytochrome P450
46
What are the 3 adverse effects associated with Ketoconazole?
1. Hepatotoxicity 2. GI and reproductive disturbances 3. Drug interactions due to enzyme inhibition
47
What is the mode of action of Selegiline?
Inhibits ACTH secretion by increasing dopamine (dopamine decreases ACTH secretion)
48
What are the 4 D2-receptor agonists?
1. Bromocriptine 2. Cabergoline 3. Pergolide 4. Apomorphine
49
Which of the following is used to treat pituitary-dependent hyperadrenocorticism: Mitotane, Ketoconazole, Selegiline, or Trilostane?
Selegiline

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