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Pharm > Adrenal Steroids: Glucocorticoids > Flashcards

Adrenal Steroids: Glucocorticoids Flashcards

1
Q

What does the adrenal medulla secrete?

A

Epi

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2
Q

What does the adrenal cortex secrete?

A

Corticosteroids and Androgens

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3
Q

Corticosteroids include _______ and ______

A

Glucocorticoids, Mineralocorticoids

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4
Q

What are the functions of glucocorticoids?

A

Metabolic effects (mobilizes glucose), anti-inflammatory (SAIDs)

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5
Q

What is the function of mineralocorticoids?

A

Salt and water retention

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6
Q

Cortisol is a ______

A

Glucocorticoid
(and act at GC receptors)

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7
Q

Aldosterone is a _____

A

Mineralocorticoid
(and act at MC receptors)

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8
Q

What zone of the adrenal cortex secretes cortisol and androgens?

A

Zona fasciculata

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9
Q

The HPA axis is …

A

Hypothalamus (CRF) —> AP (ACTH) —> Adrenal Cortex (Cortisol)

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10
Q

Is cortisol stored?

A

No

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11
Q

Secretion of cortisol occurs in a diurnal rhythm, meaning ….

A

highest early in the AM
lowest in late afternoon

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12
Q

Cortisol is secreted in response to …

A

stress (physical, metabolic, mental)

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13
Q

mineralocorticoids (aldosterone) control ….

A

body fluid and electrolyte levels (sodium and water retention at the collecting duct of the renal nephron)

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14
Q

glucocorticoids have ______ and ______ effects

A

primary metabolic effects
CV effects

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15
Q

Glucocorticoids increase/decrease glucose?

A

increase

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16
Q

Glucocorticoids increase/decrease protein breakdown?

A

increase

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17
Q

Glucocorticoids increase/decrease CO?

A

increase
(also augments epi vasoconstriction)

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18
Q

cortisol is a __ _____ hormone

A

de novo

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19
Q

cortisol binds to ____ AND ____ receptors

A

GC and MC receptors

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20
Q

Aldosterone is regulated mainly by

A

RAAS

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21
Q

RAAS is activated by

A

Low BV, high K+

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22
Q

Aldosterone effects include:

A
  1. increase sodium and water retention
  2. increases K+ and H+ excretion
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23
Q

Cushing’s syndrome is

A

hypercortisolism
(moon face, buffalo hump, muscle wasting, bruise, easily, slow healing, osteoporosis, hypertension, diabetes, mental disturbances, infections)

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24
Q

Addison’s Diseases is

A

adrenal deficiency

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25
Q

cortisol is anabolic/catabolic hormone?

A

catabolic

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26
Q

fat redistribution is Cushing syndrome leads to …

A

buffalo hump

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27
Q

cortisol decreases body Ca2+ by

A

decreased GI absorption

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28
Q

cortisol alters ____ function

A

neuronal

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29
Q

cortisol ____ growth

A

inhibits

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30
Q

cortisol can induce fetal

A

lung surfactant

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31
Q

pharmacological doses of GC may cause sodium retention, CV issues, K+ and pH disturbances because

A

cortisol binds MC receptors

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32
Q

muscle wasting occurs in Cushing’s syndrome because

A

high cortisol breaks down protein

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33
Q

Addison’s Disease is adrenal deficiency and can cause

A

hyperpigmentation, weakness, weight loss, hypotension, depression, low glucose

34
Q

GC withdrawal can cause

A

adrenal deficiency

35
Q

adrenal hormones and many drug forms are/are not protein bound

A

are protein bound

36
Q

adrenal steroids are lipid soluble/insoluble

A

lipid soluble (free hormones/drug can cross cell membranes easily)

37
Q

adrenal steroid drugs activate ______ _____ _____ _____ receptors

A

intracellular nuclear transcription factors
(turn transcription of specific genes on or off)
(this takes time)

38
Q

cortisol is slowly/rapidly degraded?

A

RAPDILY

39
Q

adrenal steroid drugs impact metabolism by reduction of double bonds, conjugation and excreted by the

A

kidney

40
Q

adrenal steroid drugs can be modified to alter receptor ____

A

specificity
(anti-inflammatory drugs to eliminate MC-mediated adverse effects)
(there are a few highly MC-selective for endocrine and related uses)

41
Q

adrenal steroid drugs have structural modification that increase

A

potency, duration and receptor selectivity

42
Q

Cortisone is a prodrug of

A

hydrocortisone

43
Q

hydrocortisone has a shorter duration of action of about

A

8-12 hours
(therefore it is good for most endocrine replacement)

44
Q

hydrocortisone has activity and ____ and ____ receptors

A

GC and MC

45
Q

Due to significant MC receptors effects, hydrocortisone

A

is used as SAIDs for low level inflammation

46
Q

Prednisone (compared to hydrocortisone) has ____ metabolism, is _____ selective for GC vs. MC receptors and a _____ DOA

A

Slower metabolism (more potent)
Partially selective for GC R
Longer DOA (18-36 hours), 1/d admin, convenience/compliance)

47
Q

Dexamethasone is ____ GC selective

A

HIGHLY
(with minimum MC activity)

48
Q

Dexamethasone DOA is

A

36-54 hours

49
Q

Dexamethasone is very potent and therefore works at ____ doses

A

low

50
Q

Dexamethasone is important for

A

very strong anti-inflammatory effects, powerful SAID reserved for severeinflammation

51
Q

Hydrocortisone < prednisone < dexamethasone

A

increasing selectivity for GC receptors, slower metabolism/increase potency, increased DOA

52
Q

Fludrocortisone use

A

Endocrine diseases when MC replacement/action is the goal
Adrenal failure, 21-hydroxylase deficiency

53
Q

Fludrocortisone has increased potency and selectivity for what kind of receptor?

A

MC

54
Q

Fludrocortisone is orally effective with

A

1/d admin

55
Q

In terms of DOA and selectivity, Hydrocortisone is

A

short-acting
non-selective

56
Q

In terms of DOA and selectivity, prednisone is

A

intermediate-acting
partially GC selecting

57
Q

In terms of DOA and selectivity, Dexamethasone is

A

long-acting
highly GC selective

58
Q

Spironolactone is a MC

A

antagonist

59
Q

Spironolactone uses:

A

K+ sparing diuretic
aldosterone-secreting tumors
endocrine disorders with excess MCs

60
Q

Glucocorticoid Preparations are:

A
  1. orally effective, good for long-term replacement
  2. water-soluble for parenteral use
  3. poorly soluble suspension, sustained effect when given IM
  4. local administration to avoid systemic toxicity (i.e. inhalers, nasal sprays, ointments, ophthalmic prep, enemas)
61
Q

What are the most powerful anti-inflammatory drugs?

A

GCs

62
Q

why are GCs not the first choice as an anti-inflammatory drug?

A

toxicities

63
Q

GCs decrease redness and swelling via

A

vasoconstriction, decreased vascular permeability, decreased histamine release

64
Q

GCs decrease fever and pain via

A

inhibit AA metabolism, decreases prostaglandin/leukotrienes from inflammatory cells and decrease COX2 expression

65
Q

What are the WBC effects of GCs?

A

decrease all except increased circulating neutrophils

66
Q

What are the cytokines and other mediators effects of GCs?

A

decrease cytokines, change in tissue degrading enzymes (collagenase)

67
Q

What are the anti-inflammatory and immunosuppressive uses of GCs?

A
  1. arthritis, bursitis
  2. skin diseases (i.e. dermatitis)
  3. collagen vascular disease (i.e. lupus)
  4. hypersensitivity, allergic reaction
  5. asthma
68
Q

In terms of drug choice, hydrocortisone is used in:

A

many OTC preps

69
Q

In terms of drug choice, prednisone

A

has a longer DOA

70
Q

In terms of drug choice, dexamethasone is used

A

if very high doses are needed

71
Q

Side effects/toxicities of GC drugs include ____ and ____ receptors toxicities

A

MC and GC

72
Q

MC receptors toxicities include

A

high Na+, low K+, alkalosis, edema, HTN

73
Q

GC receptor toxicities include:

A
  1. poor wound healing
    (due to decreased fibrin, collagen)
  2. increased risk of infection
    (due to immune suppression)
  3. decreased response to stress
    (due to feedback suppression of HPA axis)

Also: muscle wasting, weakness, skin thinning, easy brushing, fat redistribution, trunk obesity, osteoporosis, activation of peptic ulcer, diabetes/insulin resistance, weight gain, inhibition of growth in children, euphoria, insomnia, restlessness, psychosis, cataracts, glaucoma

74
Q

contraindications of GC drug use include

A

CV disease, diabetes, ulcer, infections, osteoporosis, glaucoma … etc.

75
Q

short term high dose therapy of GC is

A

safe

76
Q

long term low dose therapy of GC is

A

safe

77
Q

long term high dose GC therapy can be

A

very toxic

78
Q

GC steroid therapy is generally only palliative meaning …

A

GCs do NOT treat underlying disease

79
Q

Pros and Cons of GC use in terms of underlying disease

A

Pros: GCs may prevent irreversible tissue damage due to inflammation
Cons: GCs may WORSEN underlying disease

80
Q

Clinical strategies to limit toxicities of GC drugs include

A

use as last resort, lowest dose for shortest amount of time, reduce but maybe not eliminate symptoms, local administration, alternative day therapy, 2/3 dose AM and 1/3 dose PM to mimic normal diurnal rhythm and minimize HPA axis suppression

81
Q

anti-inflammatory effect and toxic effects are mediated by the same/different GC receptor?

A

SAME

Pharm (6 decks)

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