Therapeutics of Corticosteroids Flashcards
what are some implications for clinical practice?
- DO. not administer CS unless absolutely indicated or more conservative measures have failed
- prescribe the lowest dose to achieve desired effects for the shortest duration possible
what is selection based on in corticosteroids?
primary indication
what types of mineralocorticoid do we select for anti-inflammatory repsonses?
minimal
what is the corticosteroid conversion?
hydrocortisone 20mg –> cortisone 25mg –> prednisone 5mg –> methylprednisolone 4mg –> dexamethasone 0.75mg
should patients on high dose glucocorticoid receive live vaccines?
NOOOOO
what is considered a high dose glucocorticoid?
- prednisone > or equal to 20mg/day (2mg/kg)
- used for 14 consecutive days or more
how is glucocorticoids related to Cushing’s syndrome?
- all forms of steroid with glucocorticoid are capable
- every mode of delivery is implicated
–> oral is most common
what are some clinical presentations of Chushing’s syndrome?
patients with cushing’s syndrome due to endogenous or exogenous glucocorticoid excess
1. moon face
2. redistribution of body fat
3. thick neck (buffalo hump)
4. muscle weakness
5. easy bruising
how do we know when to withdrawal a patient from a glucocorticoid?
- max desired benefit has been obtained
- inadequate benefit has been obtained
how do we taper corticosteroids?
- receive glucocorticoid dose equal to prednisone of 7.5 mg/day or greater for long term ( > 3 weeks)
–> STT can stop without taper <3 weeks - receive evening dose of prednisone 5 or greater > few weeks
- patients with cushingoid appearance
- end point: monitor patients signs and symptoms
how do we taper if someone is at risk for adrenal insufficiency?
- gradually taper prednisone 20 dose (equal) daily in AM
- change steroid to every other day
- stop steroid when equal physiologic dose is reached
what is considered a relatively stable taper and when do we use this?
- 10-20% of total daily dose
- longer duration - slower the withdrawal
what are CYP3A4 inducers?
phenytoin, rifampin, barbiturates, carbamazepine
how do we prevent hypocorticolism and development of adrenal insufficiency or adrenal crisis?
- HPA axis may take up to 1 year to recover after steroid d/c
- supplement with extra dose during period of physiologic stress
- evaluate risk for adrenal insufficiency
- avoid concurrent drugs that can induce steroid metabolism
how can we prevent hypercorticolism and development of cushing’s syndrome?
- give lowest dose and shortest duration
- avoid concurrent admin of drugs that inhibit steroid metabolism
what are CPY3A4 inhibitors?
protease inhibitors, antifungals
what is adrenal insufficiency?
inability of the adrenal gland to produce adequate amount of cortisol to regulate function in times of stress
what does a tertiary adrenal insufficiency mean and where is it at?
hypothalamus and exogenous steroid leads to suppression of HPA axis
what does a secondary adrenal insufficiency mean and where is it at?
pituitary and exogenous steroid leads to suppression of HPA axis
what does a primary adrenal insufficiency mean and where is it at?
adrenal gland and most common for Addison disease (70-90%)
what symptoms only occur in primary adrenal insufficiency?
salt cravings (22%), dehydration, hyperpigmentation of skin and mucous membranes (92%)
what is a clinical pearl for addisons disease?
looks great (tan) but feels awful think addison’s
what are the treatment strategies for dosing and spacing for chronic adrenal insufficiency?
- dose for short acting regimen
–> 2/3 dose in AM (6-8am)
–> 1/3 in afternoon (2 hors after lunch) - cortisol changes throughout the day so we want there to be cortisol all day and not just in the morning due to a half life of 12 hrs
when is fludrocortisone necessary with adrenal insufficiency?
when we have primary insufficiency due to destruction of adrenal and no aldosterone
what are the 5 S’s of adrenal crisis management?
steroids, salt, sugar, support, search
what are drug-drug interactions with induced steroid metabolism and ICS?
inducers: increase dose
what are drug-drug interactions with inhibit steroid metabolism and ICS?
dec. dose
what are monitoring parameters for over replacement ? (cushing)
weight gain, stretch marks, obesity, OP, HTN
what are monitoring parameters for under replacement? (addisons)
weight loss, fatique, nausea, myalgia, no energy
what is the appropriate replacement for steroid with secondary/ tertiary adrenal insufficiency?
until HPA axis is recovered; no long term
will replacement therapy lead to cushings syndrome?
no
what are some complications with prolonged corticosteroid therapy?
1, infections
2. myopathy
3. osteoporosis/ osteonecrosis
4. psych symptoms
5. fluid/ salt retention
6. metabolic changes
7. gastric ulcer
8. cataract
9. cardiovascular risk
what are therapeutic principles for corticosteroids?
- use only if pallative
- consider risk vs. benefits
- require frequent re-evaluation
- dose selection is trial and error
- single dose is likely no harm but few day therapy is unlikely harmful
- side effects are time and dose related
- abrupt cessation of prolong high dose leads to adrenal insufficiency (CONTRAINDICATED)
what is the therapeutic use for corticosteroids?
used in variety of conditions ranging from brain tumors to skin diseases
what are considered live vaccines?
measles, mumps, rubella (MMR), varicella, smallpox, rotavirus, yellow fever, live flu vaccine
