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PHAR253 > Corticosteroids > Flashcards

Corticosteroids Flashcards

1
Q

Describe the sections of the adrenal glands and the hormones that each section is responsible for synthesizing.

A

adrenal cortex:
-fasciculata=glucocorticoids (cortisol)
-glomerulosa=mineralocorticoids (aldosterone)
-reticularis=sex hormones
adrenal medulla:
-epinephrine and norepinephrine
the adrenal glands sit on top of the kidneys

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2
Q

What are the primary functions of cortisol?

A

mediate the stress response
help regulate metabolism (fats, proteins, carbs)
help regulate the immune response
help regulate the inflammatory response
the body needs a good balance of cortisol to regulate the above

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3
Q

What is the trigger for cortisol release?

A

stress
it also helps restore hormone levels when stress resolves

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4
Q

What are the functions of cortisol during a short-term stress response?

A

increased blood pressure
increased heart rate
liver converts glycogen to glucose and releases it into the blood
dilates bronchioles
changed in blood flow (less to GI and reduced urine output)
increased metabolic rate

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5
Q

What are the functions of cortisol during a long-term stress response?

A

mineralocorticoids:
-retention of sodium and water by kidneys
-increased blood volume and blood pressure
glucocorticoids:
-proteins and fats broken down/converted to glucose
-increased blood glucose
-suppression of the immune system

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6
Q

How is production and secretion of cortisol regulated?

A

the hypothalamus-pituitary-adrenal (HPA) axis

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7
Q

Describe the cycle of cortisol release.

A
  1. stressors (hypoglycemia, low bp, surgery, fever, injury) causes the hypothalamus to release corticotropin-releasing hormone (CRH)
  2. CRH acts on pituitary gland to release adrenocorticotropic hormone (ACTH)
  3. ACTH acts on adrenal glands to release cortisol
    cortisol exhibits negative feedback on pituitary and hypothalamus
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8
Q

What is inflammation?

A

process whereby WBCs and other mediators protect against foreign substances
-serves several purposes initially
-may eventually become counterproductive

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9
Q

What are the possible outcomes of inflammation?

A

erythema
pruritis
edema

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10
Q

Describe the anti-inflammatory mechanism of cortisol.

A

altering cytokine release
blocking increased capillary permeability
less vasoactive substance release
inhibiting leukocyte and macrophage adhesion
interfering with phagocytosis
impedes each step of inflammatory process

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11
Q

Describe the immunosuppressive mechanism of cortisol.

A

altering cell function of specific genes
affecting the function of WBCs
inhibiting T-cell activation
inhibiting ILs, cytokines, gamma-interferon, and TNF-a synthesis

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12
Q

What are some of the “other” actions of corticosteroids?

A

anti-mitotic activity
anti-tumour effects
anti-emetic effects

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13
Q

Name a couple of disease states which use corticosteroids as therapy.

A

IBD
dermatitis
Addisons
leukemia
asthma
COPD
transplant
RA

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14
Q

Why might you want to use a local corticosteroid as opposed to a systemic corticosteroid?

A

less side effects when used locally

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15
Q

Ophthalmic and otic corticosteroids often come as a combo product with another class of medication, what is this class of medication?

A

antibiotics

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16
Q

What are some uses for ophthalmic/otic corticosteroids?

A

redness
swelling
itching
pain

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17
Q

What is the main issue with ophthalmic/otic corticosteroid drops?

A

correct delivery technique

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18
Q

What are the uses of nasal corticosteroids?

A

rhinitis
polyps
sinusitis

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19
Q

Which nasal corticosteroids can be found OTC?

A

fluticasone (FloNase)
triamcinolone (Nasacort)

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20
Q

What is the issue with nasal corticosteroids?

A

proper installation technique

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21
Q

What are some examples of different forms of inhaled corticosteroids?

A

nasal
metered-dose inhaler
dry powders for inhalation
combo products
nebulizers

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22
Q

What are the pros and cons of MDI?

A

pros: portability
cons: inhalation technique

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22
Q

What are the pros and cons of dry powders for inhalation?

A

pros:
-actuation
-portable
-show remaining doses
cons:
-powder deposition in mouth
-requires good lung function: age restrictions

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22
Q

What is the mainstay of asthma?

A

inhaled corticosteroids

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22
Q

What are the pros and cons of nebulizers?

A

pros:
-reasonable lung delivery when you cannot generate sufficient flow rate
-easy for infants (mask)
cons:
-time consuming (10-15min/dose)
-expensive
-non-portable equipment
-false sense of superiority

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23
Q

What are the different topical dosage forms of corticosteroids?

A

lotions
-least occlusive (useful for axilla, foot, groin, large, hairy areas)
creams
-medium occlusion, cosmetically most acceptable
gels
-non greasy, non occlusive can apply to face and hairy areas
ointments
-most occlusive, greasy, very dry areas

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24
Q

What are some factors that can impact the effectiveness of topical corticosteroids?

A

potency
moisture of skin (app following hydration=4-5x more absorp)
application technique
site (ex: elbow vs cheek)
skin condition

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25
Q

What are some dosage forms of corticosteroids which may be used rectally?

A

enemas
rectal ointment
rectal foam
suppositories
used for inflammation, itching, discomfort

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26
Q

True or false: a cream and ointment of a topical corticosteroid will have the same potency

A

false
ointment will be more potent

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27
Q

Which three topical corticosteroids represent low potency, mid potency, and high potency?

A

low: hydrocortisone
mid: betamethasone
high: clobetasol

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28
Q

When are intravenous steroids used?

A

when fast onset or high doses are required

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29
Q

Do intramuscular steroids provide fast pain relief?

A

no, delayed onset
provides depot effects-pain relief varies

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30
Q

Describe intra-articular steroids.

A

quicker onset and shorter duration vs IM
suppress endogenous cortisol levels within 24-48hrs
usual sites: hips, knees, ankles, shoulder, elbow, wrist

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31
Q

How frequently can a joint be injected with a corticosteroid?

A

no firm answer
typically 3-4x/yr

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32
Q

Describe the absorption of oral corticosteroids.

A

quick and rapid absorption from the gut
-oral doses are equivalent to IV

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33
Q

Which corticosteroid is available as an oral solution?

A

prednisolone

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34
Q

How much cortisol does our body produce per day? What is the equivalent dose of prednisone?

A

10-20mg/d
5mg of prednisone

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35
Q

What are the doses for the following intensities of prednisone therapy:
low dose or maintenance dose
moderate dose
high dose
massive dose

A

low dose or maintenance dose: 5-15mg/d
moderate dose: 0.5mg/kg/d
high dose: 1-3mg/kg/d
massive dose: 15-30mg/kg/d

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36
Q

What is the saying used to remember oral corticosteroids?

A

Care (cortisone)
Health (hydrocortisone)
Providers (prednisone)
Put (prednisolone)
Money (methylprednisolone)
in TD (triamcinolone, dexamethasone)
Bank (betamethasone)

37
Q

Describe cortisone based on anti-inflammatory potency, Na-retaining potency, t1/2, and equivalent dose.

A

anti-inflammatory potency: 0.8
Na-retaining potency: 1
t1/2: 8-12hrs
equivalent dose: 25mg

38
Q

Describe hydrocortisone based on anti-inflammatory potency, Na-retaining potency, t1/2, and equivalent dose.

A

anti-inflammatory potency: 1
Na-retaining potency: 1
t1/2: 8-12hrs
equivalent dose: 20mg

39
Q

Describe prednisone based on anti-inflammatory potency, Na-retaining potency, t1/2, and equivalent dose.

A

anti-inflammatory potency: 4
Na-retaining potency: 0.8
t1/2: 12-36hrs
equivalent dose: 5mg

40
Q

Describe prednisolone based on anti-inflammatory potency, Na-retaining potency, t1/2, and equivalent dose.

A

anti-inflammatory potency: 4
Na-retaining potency: 0.8
t1/2: 12-36hrs
equivalent dose: 5mg

41
Q

Describe methylprednisolone based on anti-inflammatory potency, Na-retaining potency, t1/2, and equivalent dose.

A

anti-inflammatory potency: 5
Na-retaining potency: 0.5
t1/2: 12-36hrs
equivalent dose: 4mg

42
Q

Describe triamcinolone based on anti-inflammatory potency, Na-retaining potency, t1/2, and equivalent dose.

A

anti-inflammatory potency: 5
Na-retaining potency: 0
t1/2: 12-36hrs
equivalent dose: 4mg

43
Q

Describe dexamethasone based on anti-inflammatory potency, Na-retaining potency, t1/2, and equivalent dose.

A

anti-inflammatory potency: 25
Na-retaining potency: 0
t1/2: 36-72hrs
equivalent dose: 0.75

44
Q

Describe betamethasone based on anti-inflammatory potency, Na-retaining potency, t1/2, and equivalent dose.

A

anti-inflammatory potency: 25
Na-retaining potency: 0
t1/2: 36-72hrs
equivalent dose: 0.75

45
Q

What is the relationship between anti-inflammatory potency and Na-retaining potency for oral corticosteroids?

A

as anti-inflammatory potency increases, Na-retaining potency decreases
ex: cortisone has highest Na-retaining potency and betamethasone has highest anti-inflammatory potency

46
Q

What are the adverse effects of ophthalmic corticosteroids?

A

stinging, redness
tearing, burning
secondary infection
more serious: glaucoma, cataracts

47
Q

What are the adverse effects of oral inhaled steroids?

A

thrush (rinse mouth)
hoarseness
dry mouth
difficulty swallowing
dysphoria

48
Q

What are the adverse effects of nasal corticosteroids?

A

rhinorrhea
burning
sneezing
bloody nose (point away from septum)

49
Q

What are the adverse effects of topical corticosteroids?

A

burning
irritation
skin atrophy
tachyphylaxis
telangiectasia

50
Q

List the many systemic complications of corticosteroids.

A

euphoria
insomnia/restlessness
buffalo hump
moon face
hypertension
thinning of skin
increased abdominal fat
easy bruising
poor wound healing
muscle wasting
benign intracranial hypertension
cataracts

51
Q

How do the CNS effects of corticosteroids manifest?

A

acute:
-euphoria
-insomnia
-restlessness
-memory impairment
chronic:
-altered mood: depression, mania,
adverse effects are dose related

52
Q

Describe cataracts as an adverse effect of corticosteroids.

A

caused by systemic and topical steroids (topical>)
long term steroid users should have routine eye exams
risk factors: daily dose, cumulative dose, duration, age

53
Q

Describe glaucoma as an adverse effect of corticosteroids.

A

caused by systemic and topical steroids (topical>)
risk factors: pre-existing POAG, diabetes, family hx, RA
occurs within weeks

54
Q

Is steroid-induced cataracts or glaucoma reversible upon steroid d/c?

A

cataracts: no
glaucoma: yes

55
Q

Describe Cushingoid features as an adverse effect of corticosteroids.

A

hypercortisolism alters normal fat distribution
-fat redistribution from periphery to trunk
manifests as centripetal obesity
-moon face, buffalo hump, protuberant abdomen
can occur in first couple months dose and duration dependent

56
Q

Describe GI adverse effects of corticosteroids.

A

GI upset (take with food)
dyspepsia
increased risk of PUD with an NSAID

57
Q

Describe glucose intolerance as an adverse effect of corticosteroids.

A

steroids induce gluconeogenesis and decrease tissue utilization of glucose
dose related and BG increases are normally mild
increased BG can occur in those with or without DM
elevated BG may persists for months upon d/c

58
Q

True or false: sodium and water retention from corticosteroids typically resolves upon d/c

A

true

59
Q

Which potency of steroids are likely to cause increased appetite?

A

high potency
-increased appetite can be used therapeutically

60
Q

Describe growth retardation as an adverse effect of corticosteroids.

A

all corticosteroids can affect growth patterns; dose dependent
more pronounced with oral therapy
decreasing osteoblasts, GH secretion, inhibiting insulin receptors

61
Q

What is the body’s main stress system?

A

the HPA axis
-releases cortisol to activate a response to stress

62
Q

Describe normal functioning of the HPA-axis.

A

normal secretion: 10-20mg/d of cortisol
cortisol highest at 7-8m (decreases throughout day)
increased release during periods of acute stress

63
Q

What is the effect on the HPA-axis from corticosteroids?

A

negative feedback on CRH and ACTH=suppression of HPA-axis
-body cant produce more cortisol in times of need

64
Q

If HPA-axis suppression is present, what will happen if steroids are abruptly d/c or the patient becomes severely ill?

A

opposite of high cortisol:
-hypotension
-hypoglycemia
-weight loss
-confusion
-flu like symptoms

65
Q

What are the factors that may predict the occurrence of HPA-axis suppression?

A

dose
duration
type of steroid
route of admin
time of admin
interval

66
Q

True or false: the minimum dose/interval/duration of corticosteroids required to cause HPA-axis suppression is easy to predict

A

false
hard to predict

67
Q

How long does it take the HPA-axis to return to normal when someone has discontinued chronic steroid use?

A

weeks to > 1 year

68
Q

At what dose of prednisone does HPA-axis suppression invariably occur with long term use?

A

> 15mg/d
variable with 5-15mg/d

69
Q

At what dose of prednisone is HPA-axis suppression unlikely to occur during short term use?

A

15-40mg/d x 5-7d
maybe: 1mg/kg/d x 2wks or 15-40mg/kg/d x 1-4wks

70
Q

Who should be screened for HPA-axis suppression?

A

those who take oral corticosteroids for > 2 consecutive weeks or > 3 cumulative weeks during the previous 6 months
no clear guidance on when to perform HPA-axis testing

71
Q

What are the symptoms of mild adrenal insufficiency?

A

they are non descript
therefore anyone with unexplained symptoms after steroid withdrawal should be tested for HPA-axis suppression

72
Q

What kind of infections do oral corticosteroids increase a patients susceptibility to?

A

viral infections (varicella zoster)
bacterial infections (cellulitis)
fungal infections (candida)

73
Q

What are the doses of prednisone that are unlikely to increase a patients susceptibility to infection?

A

<10mg/d or cumulative dose <700mg

74
Q

Describe the dermatological adverse effects of corticosteroids.

A

acne
bruising
thin skin (reversible)
striae (irreversible)
impaired wound healing
steroids inhibit epidermal cell division and DNA synthesis

75
Q

What are the effects of corticosteroids on bone?

A

protein catabolism
osteoblast inhibition
GH inhibition
decreased Ca absorption and decreased renal Ca absorption

76
Q

When does bone loss occur with corticosteroids?

A

most rapidly in first 3 months
-peaks at 6 months
-systemic therapy for > 2-3 months=major risk factor
-risk increased with doses as low as 2.5-7.5mg/d
-30-50% will develop osteoporosis with chronic treatment

77
Q

Which patients on corticosteroid therapy should undergo a risk assessment for fracture?

A

patients on >2.5mg/d for >3 months

78
Q

What is osteonecrosis? What can increase the risk of osteonecrosis?

A

death of bone tissue due to impaired blood supply
increased risk with high dose and duration of steroids

79
Q

How does corticosteroid induced osteonecrosis manifest?

A

joint pain and decreased ROM
symptoms develop after a few months to a few years

80
Q

Describe myopathy as an adverse effect of corticosteroids.

A

due to decreased protein synthesis in muscle
more common with prolonged courses of high dose (prednisone doses >10mg/d)
characterized by arm and leg weakness after weeks-months of use

81
Q

What are the long term side effects of corticosteroids in kids?

A

weight gain
growth retardation
Cushingoid features
infection: most serious AE

82
Q

What are the adverse effects of corticosteroids in kids during short courses of therapy?

A

vomiting
mood changes
sleep disturbances
serious AEs are uncommon

83
Q

True or false: short-term therapy of corticosteroids mitigates the risk of adverse effects

A

false

84
Q

Which patients are treated with corticosteroids for COVID-19? Which steroid is used and what is the dose?

A

hospitalized patients requiring O2
-improve clinical outcomes and decrease mortality
dexamethasone 6mg OD up to 10 days

85
Q

What are the guidelines for corticosteroid dosing?

A

there are no set guidelines
-goal is to bring inflammation or immunologic reactions under control with minimal effective dose (MED)
-dose depends on situation & clinical experience
-initial dosing: OD or BID
-maintenance dosing: OD

86
Q

After how many weeks of corticosteroid usage should we consider that the patients will require a taper?

A

> 3 weeks

87
Q

What are some examples of tapering regimens?

A

decrease daily dose by set amounts q few days/weeks
-decrease depends on starting point
decrease daily dose by a percentage per week

88
Q

How do we transition someone on corticosteroids from a divided dose to once daily dosing?

A

<2 weeks: convert ASAP
-ex: prednisone 5mg BID–>10mg OD
>2 weeks: convert over a 2 week period

89
Q

What are some situations where you may see EOD of corticosteroids?

A

chronic administration is necessary
children requiring maintenance dosing

90
Q

Which steroids are ideal for EOD?

A

short-intermediating duration of action
-minimizes accumulation which could negate EOD benefits

91
Q

Describe how to convert a patient to EOD.

A
  1. determine MED (taper daily dose by 2.5-5mg/week until MED)
  2. optimal EOD is 2.5-3x the MED
  3. alternate the new calculated dose with MED
  4. taper the MED dose by 5mg/week until removed
  5. taper current dose by 5mg/week to achieve a new MED
92
Q

What are some examples where stress dosing of corticosteroids may be required?

A

moderate illness
major surgery

93
Q

What is steroid pulse therapy?

A

the administration of short-term, high-dose, IV or po steroids in various situations where rapid remission of serious conditions is required

94
Q

What are the advantages and disadvantages of steroid pulse therapy?

A

advantages:
-more rapid control of condition
-help avoid AEs by avoiding prolonged steroid therapy
disadvantages:
-certain AEs may be more likely and significant

PHAR253 (16 decks)

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