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VETM 443 Clin Pharm Tox > Glucocorticoids > Flashcards

Glucocorticoids Flashcards

1
Q

why is it rare to have spontaneous glucocorticoid deficiency without a concomitant mineralocorticoid deficiency

A

glucocorticoid production site, the zona fasciculata, is very close to mineralocorticoid production site, the zona glomerulosa

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2
Q

where are mineralocorticoids produced and what is an example this hormone type

A

zona glomerulosa of adrenal cortex; eg. aldosterone

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3
Q

where are glucocorticoids produced and what is an example this hormone type

A

zona fasciculata of adrenal cortex; cortisol, corticosterone, cortisone are examples

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4
Q

this hormone is released from the adrenal cortex in response to stress due to the action of the hypothalamic-pituitary-adrenal axis

A

cortisol

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5
Q

what is the effect of a LACK of aldosterone on calcium levels? how does this occur?

A

a lack of aldosterone decreases calcium excretion which can lead to hypercalcemia

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6
Q

what is the effect of aldosterone on blood pressure? how does this occur?

A

increased blood pressure: aldosterone causes retention of sodium and water by the kidney so increases blood volume, which increases blood pressure. also increases excretion of potassium by kidney into lumen in exchange for sodium uptake

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7
Q

name 7 effects of glucocorticoids

A

anti-inflammatory, immunosuppressive, vasoconstrictor/ positive ionotrope/ chronotrope, bronchodilator, catabolic (increased glucose production from amino acids), maintain fluid homeostasis, neuroprotective

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8
Q

which 2 effects of glucocorticoids only occur at supra physiological doses

A

anti-inflammatory and immunosuppressive effects

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9
Q

what do glucocorticoids inhibit

A

conversion of cell membrane phospholipids to arachidonic acid by phospholipase

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10
Q

why are the negative effects of NSAIDs also seen with glucocorticoids, but to a greater extent

A

glucocorticoids act earlier in the arachidonic acid pathway that NSAIDs, so there is no opportunity for glucocorticoids to be COX2 selective

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11
Q

what is the effect of a glucocorticoid deficiency on blood glucose

A

hypoglycemia (glucocorticoids increase blood glucose and antagonize insulin)

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12
Q

name 4 catabolic effects of glucocorticoids

A

promote lipolysis, promote gluconeogenesis, increase blood glucose and antagonize insulin, inhibit bone formation and promote bone loss

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13
Q

name 2 ways glucocorticoids maintain fluid homeostasis

A

mineralocorticoid activity to promote salt and water retention; inhibit LDH release leading to PU/PD

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14
Q

changes in WBC induced by glucocorticoids are consistent with what changes you would see on a CBC

A

consistent with stress leukogram changes

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15
Q

name 4 immunosuppressive effects of glucocorticoids

A

eosinopenia; lymphopenia; neutrophilia; reduced functionality of macrophages, monocytes, and eosinophils

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16
Q

what is the effect of a glucocorticoid deficiency on vasoconstriction

A

hypotension (glucocorticoids enhance vasoconstriction)

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17
Q

how do glucocorticoids lead to bronchodilation

A

increase beta-adrenergic receptor number and sensitivity, increasing effects of beta-2 agonists on bronchiolar smooth muscle

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18
Q

chronic glucocorticoid use increase the risk of this condition in cats, especially those with pre-existing disease, (hint: likely due to sodium/water retention in the kidney and resulting blood volume/hypertension)

A

congestive heart failure

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19
Q

how do glucocorticoids protect against hypoxic/ischemic brain damage

A

possibly by decreasing basal energy requirements of availability of energy substrates

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20
Q

name at least 5 effects of glucocorticoid deficiency

A

hypotension, hypoglycemia, anorexia, vomiting, diarrhea, weight loss, muscular weakness, increased susceptibility to stress, inability to maintain endothelial integrity and vascular tone, +/- hyponatremia, =/- polyuria

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21
Q

what is the difference between short-acting, intermediate-acting, and long-acting corticosteroids?

A

the glucocorticoids length of duration of action is based on the biological half-life of the parent compound (not the same as T1/2). short-acting formulations have a duration of action of under 12 hours, intermediate-acting 12-36 hours, and long-acting over 36 hours

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22
Q

how long do prednisone and prednisolone act for?

A

biologic half-life of 12-36 hours. they are intermediate acting corticosteroids (from Plumb’s)

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23
Q

are glucocorticoids such as prednisone and prednisolone more likely to cause adverse effect in the short term or in the long term

A

long term! there are many adverse effects associated with chronic use (from Plumb’s).

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24
Q

why should you NOT use prednisone in horses or cats

A

do not metabolize prednisone well. use prednisolone instead. (Plumb’s notes that it is poorly absorbed after oral use in horses and is not readily converted to prednisolone in cats)

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25
Q

all glucocorticoids used clinically are modifications of this basic steroid structure

A

cortisol

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26
Q

what structural changes are made to cortisol in different synthetic glucocorticoids

A

pharmacokinetics (residence in body, species differences in absorption), active vs inactive, affinity for GR receptor (affects potency) selectivity for GR and AR), interaction with GR (affects duration of activation)

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27
Q

when do the acetate and acetonide esters (types of glucocorticoid esters) have long-acting formulations

A

when parenteral

28
Q

what is the active metabolite of prednisone? how much more potent is the active metabolite?

A

prednisolone. 4x as potent

29
Q

is prednisone suitable for topical administration

A

no. not in any species.

30
Q

name 4 adverse effects of glucocorticoid drugs

A

stress leukogram, elevation in liver enzymes or steroid-induced hepatopathy, GI ulcers, PU/PD (not important to animal, but challenging for owner management), HPA axis suppression were all emphasized in class. also iatrogenic hyperadrenocorticism, polyphagia, poor wound healing, behaviour changes, muscel atrophy, hyperglycemias/insulin resistance, induction of parturition, possibly laminitis in horses.

31
Q

which glucocorticoids are most commonly used for anti-inflammatory and anti-allergic effects in large animals

A

prednisone (except in cats) or prednisolone (ok in cats) are most commonly used

32
Q

which glucocorticoid is most commonly used for anti-inflammatory and anti-allergic effects in large animal

A

dexamethasone most commonly used

33
Q

HPA acts suppression occurs in dogs after 2 weeks of glucocorticoid therapy. how can this suppression be reduced

A

alternate day therapy, although this would be inappropriate in replacement treatment programs. can taper withdrawal if have had chronic administrate

34
Q

can you co-administer an NSAID and steroid? why or why not?

A

no. GI lesions and renal abnormalities may occur

35
Q

name 4 diseases that often require treatment with glucocorticoids

A

atopic dermatitis, immune-mediated hemolytic anemia, lymphoma, equine or feline asthma

36
Q

name 4 contraindications for providing glucocorticoids

A

systemic fungal disease, laminitis in horses, concurrent infection, corneal ulcers

37
Q

there are many drug interactions, reported and theoretical, with prednisolone and prednisone. name 4 drugs with interactions

A

vaccines, especially live attenuated viral vaccines, rifampin, phenytoin, phenobarbital, NSAIDS, mitotane, ketoconazole, insulin, estrogens, ephedrine, potassium-wasting diuretics (furosemide, thazides), digoxin, cyclosporine, cyclophosphamide, aspirin (from Plumb’s)

38
Q

name 3 laboratory effects you might see after administering glucocorticoids such as prednisone and prednisolone

A

increase serum cholesterol levels, increase serum urine glucose levels, decrease serum potassium, suppress release of TSH and reduce T3 and T4 values, reactions to skin tests may be suppressed, false negative results of the nitro blue tetrazolium test for systemic bacterial infections (from Plumb’s)

39
Q

should you go read Plumb’s entries on prednisolone, prednisone, fluticasone, and dexamethasone

A

yes. we have to know detailed information about these drugs

40
Q

what glucocorticoid is used most commonly in vet med as an inhaled aerosol, often for treating feline asthma, chronic cough dogs, recurrent airway obstruction or inflammatory airway disease in horses

A

fluticasone (from Plumb’s)

41
Q

how is fluticasone metabolized

A

cytochrome P450 pathway to a metabolite with negligible pharmacologic activity (Plumb’s)

42
Q

when is fluticasone contraindicated

A

during acute bronchospasm or when patients are sensitive to it (Plumb’s)

43
Q

should you use fluticasone in pregnant animals? why or why not?

A

with caution. unknown if drug enters maternal milk and has teratogenic effects in lab animals (Plumb’s)

44
Q

should you give prednisone or prednisolone to pregnant animals

A

with caution: can enter milk, can cause unwanted effects in offspring, can induce parturition especially in large animals in late stage pregnancy (Plumb’s)

45
Q

name a drug interaction with fluticasone

A

use caution with drugs that inhibit CYP 3A4 isoenzymes such as ketoconazole (Plumb’s)

46
Q

what are potential routes of administration for glucocorticoid drugs

A

IV, IM, SQ, oral, local (e.g intra-articular), inhaled, topical (skin, ears, eyes). note that prednisone cannot be given topically and that local administration will reduce systemic effects

47
Q

what are some similarities and differences between adrenal-dependent and pituitary-dependent hyperadrenocorticism?

A

similarities: symptoms are related to excess of glucocorticoids, involves increased endogenous secretion. adrenal-dependent: more common type in large dogs, increased cortisol, adrenal neoplasia. pituitary-dependent: more common type in small dogs and horses, increased ACTH, adenomas.

48
Q

what are the treatment target organs of hyperadenocorticism

A

pituitary (to suppress ACTH release), adrenal gland (suppress cortisol release)

49
Q

what are 2 other names for hyperadrenocorticism

A

Cushing’s or in horses, PPID (pituitary pars intermedia dysfunction)

50
Q

where does trilostane target in the hyperadrenocorticism pathway? what organ?

A

competitively inhibits the conversion of pregnenolone to progesterone, targeting the adrenal gland

51
Q

where does mitotane target in the hyperadrenocorticism pathway? what organ?

A

inhibits conversion of cholesterol to pregnolone by inhibiting cytochrome P450 enzymes, as well as inhibiting conversion of prenenolone to progesterone. targets adrenal gland

52
Q

trilostane and mitotane adverse effects are generally associated with what? name 5 adverse effects

A

hypoadrenocorticism. lethargy, vomiting, diarrhea, inappetence, weakness

53
Q

what is the mechanism of action for selegiline in hyperadrenocorticism therapy? what organ does it target?

A

dopamine agonist, causes feedback inhibition of ACTH from pituitary. also a monoamine oxidase inhibitor. targets pituitary

54
Q

what is the mechanism of action for pergolide mesylate in hyperadrenocorticism therapy? what organ does it target?

A

acts as dopamine agonist and inhibits production of POMC-derived hormones. targets pituitary

55
Q

what drug is used to treat hyperadrenocorticism in dogs, but is only effective in 20% of patients, so would likely be used in dogs unable to tolerate trilostane or mitotane

A

selegiline

56
Q

what is the standard treatment drug for pituitary pars intermedia dysfunction (PPID) in horses

A

pergolide mesylate

57
Q

what are symptoms of hypoadrenocorticism or Addison’s disease

A

lethargy, vomiting, diarrhea, inappetence, weakness, PU/PD, electrolyte abnormalities

58
Q

what is hypoadrenocorticism or Addison’s disease?

A

usually an autoimmune disease in dogs that causes both mineralocorticoid and glucocorticoid deficiency

59
Q

should you treat hypoadrenocorticism with a mineralocorticoid or glucocorticoid first

A

mineralocorticoid first and add glucocorticoid if needed

60
Q

oops! you gave your patient iatrogenic hypoadrenocorticism. why did this happen?

A

usually result of HPA axis inhibition due to glucocorticoid treatment and occurs when chronic glucose therapy is stopped to quickly

61
Q

how can you prevent iatrogenic hypoadrenocorticism

A

if ending chronic glucocorticoid therapy, TAPER glucocorticoids

62
Q

what drug(s) is used for glucocorticoid replacement for hypoadrenocorticism?

A

dexamethasone for acute crisis (rapid onset of action and less reactivity with cortisol assays so can be gives before testing in emergency), then prednisone or prednisolone

63
Q

what drug is used for mineralocorticoid replacement in repository form (injection lasting 25 days) as the standard treatment for dog hypoadrenocorticism

A

DOCP, deoxycorticosterone pivalate

64
Q

what hypoadrenocorticism drug has both mineralocorticoid and glucocorticoid activity and requires daily oral dosing

A

fludrocortisone acetate

65
Q

how long is the half life of dexamethodone compared to its biological activity

A

half life is only 2-5 hours in dogs, but biologic activity can be over 48 hours (Plumb’s)

66
Q

can dexamethasone be used alone for treatment of adrenal insufficiency

A

generally no. it has a negligible mineralocorticoid effects (Plumb’s)

67
Q

is dexamethasone considered long-acting or short-acting

A

long-acting (Plumb’s)

VETM 443 Clin Pharm Tox (18 decks)

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