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Pharmacology Exam 3 > Ch.27: Corticosteroids (Vickroy) > Flashcards

Ch.27: Corticosteroids (Vickroy) Flashcards

1
Q

What are corticosteroids

A

group of natural and synthetic substances that mimic in-part or wholly the actions of the adrenal hormone cortisol
*widely used and misused

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2
Q

Are most therapeutic uses of corticosteroids based on glucocorticoid or mineralocorticoid actions?

A

glucocorticoid (affects hypothalamic-pituitary-adrenal (HPA) axis to affect metabolic processes in many cells)

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3
Q

What do mineralocorticoid receptors control?

A

electrolyte handling/water retention. Control sodium retention and potassium loss

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4
Q

major physiological effects of corticosteroids*

A
  • anti-inflamm.
  • immunosuppressive
  • metabolic changes (ie. metabolism)
  • electrolyte balance
  • CV homeostasis
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5
Q

low dose corticosteroids primarily affect:*

A

adrenal insufficiency

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6
Q

medium dose corticosteroids primarily cause:*

A

anti-inflamm.

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7
Q

high dose corticosteroids primarily cause:*

A

immunosuppression

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8
Q

Major clinical uses of corticosteroids (CCS)

A
  • allergy/anti-inflamm.
  • replacement therapy
  • metabolic therapy
  • immune suppression
  • cancer
  • circulatory shock
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9
Q

HPA axis

A

1) stressors stimulate hypothalamus to release CRH
2) CRH acts on pituitary gland to release ACTH
3) ACTH acts on adrenal glands to release cortisol
4) cortisol negatively feeds back to hypothalamus and pituitary gland
* exogenous glucocorticoids act like cortisol in this process to negatively feedback

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10
Q

examples of stressors

A
  • fear/pain/cold/injury
  • hemorrhage
  • major sx
  • severe infection
  • hypoglycemia
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11
Q

what 2 main classes of receptors mediate effects of CCS?

A

glucocorticoid and mineralocorticoid receptors

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12
Q

which usually requires a higher dose: pharmacological or physiologic dose?

A

pharmacological

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13
Q

How do glucocorticoids (GC) evoke their actions?

A
  • GENOMIC responses via cytosolics GCRs (slow)

- NON-GENOMIC responses via cytosolic or membrane-bound GCRs (fast)

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14
Q

main GC actions

A
  • inc. carb. metabolism
  • protein catabolism (aa shunted into gluconeogenesis)
  • mobilization of fatty acids from adipose
  • blockade of inflamm. cascade (higher doses)
  • altered electrolyte and water balance
  • CNS effects
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15
Q

how do GCs increase carb. metabolism?

A

inc. gluconeogenesis –> dec. cellular glucose use –> acute hyperglycemia

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16
Q

how do GCs block inflammatory cascade?

A
  • dec. vasoactive/chemoattractive factors
  • dec. lipolytic/proteolytic enzyme secretion
  • dec. leukocyte infiltration
  • dec. COX-2/NOS expression
17
Q

How do GCs alter electrolyte and water balance

A

by activation of mineralocorticoid receptors, Na is retained, K and Ca are lost. Intestinal Ca absorption decreases, ADH decreases –> PUPD

18
Q

adverse effects of GCs correlate with:**

A

DOSE and DURATION of treatment

19
Q

Main GC adverse effects

A
  • HPA axis suppression*
  • GI ulceration (especially if combined with an NSAID)*
  • muscle wasting
  • immunosuppression
  • hematopoietic changes
  • behavioral changes
  • diabetes
  • hypothyroidism
  • retarded growth
  • electrolyte imbalance
  • corneal ulceration
  • abortion
  • many effects overlap with NSAIDs.
20
Q

hematopoietic changes assoc. with GCs

A

increased platelets/neuts/RBC

decreased platelet aggregation/lymphos/monos/eos

21
Q

how to dampen HPA axis suppression effect of GCs

A

withdraw from GC tx SLOWLY

22
Q

GC –> urine glucose

A

inc.

23
Q

GC –> serum cholesterol

A

inc.

24
Q

GC –> serum K+

A

dec.

25
Q

GC –> thyroid function

A

dec.

26
Q

precautions for GC therapy*

A
  • NOT curative
  • use topicals to lessen negative systemic imbalances
  • use minimal dose
  • withdraw tx slowly
27
Q

GC contraindications

A
  • pre-existing infections
  • high dose in late pregnancy
  • diabetes
  • renal dz (due to fluid overload)
  • CHF (due to fluid overload)
  • young animals
  • GI ulcers/hypersecretory disorders
28
Q

4 types of administration routes for GCs

A

1) Topical (skin, eye, MM)
2) Inhaled (nasal mucosa, sinuses, bronchii, lungs)
3) Oral (include prednisone, prednisolone)
4) Systemic (IV, IM, SC, Intra-articular)

29
Q

Pharmacokinetics of GCs

A
  • actions last longer than drug lvls in plasma
  • hepatic metabolism
  • certain side chains delay metabolism and inc. duration of action
  • many systemic agents NOT bound to transcortin, which enhances cellular penetration
30
Q

Hydrocortisone

A

natural adrenal hormone that exhibits both gluco and mineralocorticoid activities*

  • admin. via all routes
  • anti-inflamm. at higher dose
  • downside: affects body’s fluid balance
  • used in SA and LA
31
Q

most widely used GC agent across species

A

dexamethasone

32
Q

dexamethasone (selectivity, dur. of action, potency, routes, species used in, side effects, etc.)

A
  • most widely used GC agent across species
  • GCR selective*
  • long-acting, synthetic
  • potent (30x more than cortisol)
  • anti-inflammatory with rapid onset*
  • routes: PO, IM, IV, topical
  • used a lot in cattle
  • can cause colonic perf. and laminitis in horses
33
Q

Triamcinolone

A
  • GCR selective*
  • intermediate duration of action
  • 4-5x more potent than cortisol
  • routes: PO, parenteral, topical, inhalation
34
Q

Prednisone/Prednisolone

A
  • mineralocorticoid selective*
  • synthetic
  • 4-5x more potent than cortisol
  • pred converts to prednisolone in liver
  • use PREDNISOLONE in cats/horses, not prednisone because they don’t convert it well in the liver
  • effects fluid balance
35
Q

Methyl-prednisolone**

A

-GCR selective
-synthetic
-lipid antioxidant action
-dur. of action formulation-dependent:
Sodium succinate: water soluble, rapid effect*
Acetate: insoluble, long acting*

36
Q

Order GCs in order of decreasing duration of action*

A

dexomethasone > triamcinolone > Prednisolone, Prednisone, Hydrocortisone

Pharmacology Exam 3 (11 decks)

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