Chapter 25

 Look at categories at beginning of chapter, these headings indicate important topics in the
chapter
 Corticosteroids:
o Produced and secrete based on feedback mechanism of hypothalamus-pituatary-
adrenal axis (HPA).
o Corticosteroids are exogenously administered adrenal cortex hormones, and affect this
feedback mechanism.
 Glucocorticoids: metabolic, anti-inflammatory and growth suppressing effects.
o Cortisol-wake up hormone, altered levels affect awareness and sleep patterns
o Increase blood sugar concentrations by stimulating gluconeogenesis in the liver and by
decreasing uptake of sugar into muscle, lymphatic and adipose tissues.
o Decreased proliferation of fibroblasts in connective tissue with poor protein synthesis
lead to poor wound healing.
o Inhibit inflammatory systems by:
 Decreasing proliferation of T-lymphocytes
 Decreasing natural killer cell activity
 Suppressing the synthesis, secretion and actions of chemical mediators
involved in inflammatory and immune responses.
 Be aware of information in figure 25-1
 Table 25-1: I suggest making some flash cards
o Know distinguishing features
 PO vs IM: what is different? Why would you pick one over the other?
o Know cortisone, hydrocortisone, methylprednisolone, prednisolone, prednisone
 Well absorbed from the upper jejunum.
 IM well absorbed at injection sites
 Have short-, intermediate, and long acting forms
 Reversibly bound to corticosteroid binding proteins.
o Altered protein binding capability will alter pharmacologic effects
 These drugs are widely distributed, cross the placenta and enter the breast milk.
 Liver metabolizes hydrocortisone, is a rate limiting step in clearance.
o Liver converts initial compounds into metabolites that are clinically active and
metabolized by liver for clearance.
o Renal clearance is increased when plasma levels are increased
 Precautions and contraindications:
o Contraindicated in presence of active, untreated infections
 May mask indications of infection, and new infections may appear during their
use
o May active latent TB
o Can cause HTN and increased water retention, increased excretion of potassium
o All glucocorticoids increase calcium excretion
 Problem for post menopausal women and others at risk for osteoporosis
o Alters liver’s glucose regulation, may have difficulty maintaining glycemic control
o Patient’s with peptic ulcer disease or ulcerative colitis, and stress have an increase
probability of GI bleeding and perforation.
o Corticosteroids cross the placenta and most are Category C
  ADR’S:
o Muscle and skin
 Can cause atrophy and thinning of skin, alopecia, poor healing, hirsutism.
 Also see muscle wasting
o Skeletal tissues:
 Osteoporosis develops in 11-20% in patients taking glucocorticoids for > 1 yr.
 Decreased BMD seen after 3 months of use
 BMD measured for all who plan for long term therapy
 American College of Rheumatologists recommend co-treatment with
bisphosphonate therapy based in risk assessment. (Fosamax or Actonel)
o Ocular tissues:
 Subcapsular cataracts and glaucoma, and possible damage to optic nerve
o GI system:
 Possible implication in induction of peptic ulcer disease
 Prophylaxis with PPI may be indicated based on risk
o CV System:
 HTN is a common adverse reaction
o CNS:
 Steroid psychosis: delirium, agitation, insomnia, mood swings and severe
depression
 Onset typically within 15-30 days
 Risk factors: females, high dose prednisone (>40 mg), family history of
psych disorder,
 If med cannot be stopped, psychotropic drugs are effective at relieving
symptoms
o Endocrine system:
 Prolonged therapy can lead to adrenal suppression
 Can increase blood sugar
 Amorrhea, post menopausal bleeding and other menstrual irregularities have
been seen
 Drug interactions:
o Additive hypokalemia can occur with other meds that also cause this ADR
o Increases risk for toxicity with digoxin
o Table 25-2
 Clinical Use and Dosing:
o Adrenocortical insufficiency
 Hydrocortisone
 Cortisone
o Inflammation
 Methylprednisolone,
o Immunosuppression
 Prednisone-short half life, low cost, easy to change dose, prednisolone
Table 25-3: cortisone, dexamethasone, hydrocortisone, methylprednisolone, prednisolone,
prednisone
Dosing principles:
1. Doses best taken by 9 am, as max activity of adrenal cortex is producing cortisol is between 2 am
and 8 am.
2. Initial dose depends on disease being treated. Monitor until acceptable response is obtained
3. Once acceptable response achieved, determine maintenance dose by decreasing dose in small
intervals until you obtain the lowest dose that maintains an adequate response.
4. Stop long term therapy gradually to prevent an adrenal insufficiency crisis
5. Most conditions that require chronic corticosteroid therapy can be well controlled on every
other day therapy, but must be initiated on every day therapy
6. Schedule for tapering and withdrawing is different.
a. Doses above 40 mg: dose reduce by 10 mg of prednisone every 1-3 weeks
b. Doses below 40 mg: reductions of 5 mg every 1-3 weeks.
c. At doses of 5-7.5 mg, can be switched to 1 mg tablets and weekly or biweekly reductions
can be done 1 mg at a time.

 Rational drug selection: Take into account the following

o Length of therapeutic activity
 Short, intermediate or long acting forms
 Short acting forms less likely to produce HPA suppression
 Long acting agents are preferred if the effects of high doses must be sustained
(increased intracranial pressure or organ transplant rejection)
o Relative potency
o Monitoring:
 Based on common ADR associated with use
 Weight gain, edema, HTN, potassium loss, protein catabolism,
 BMD testing for pts on long term therapy and increased risk for
osteoporosis
 Lab monitoring:
o Begins with initial assessment, serum electrolytes, glucose, CBC
o Long term therapy or high doses: stool for occult blood, serum
lipid analysis
o Slit lamp examination for those w/ increased risk of increased
ocular pressure, every 6 months for those on long term therapy
 Patient Education
o Administration: take as prescribed, do not double dose in case of missed doses
o DO NOT STOP without discussing with provider first
 ADR:
o Cause immunosuppression and may mask symptoms of infection.
o Avoid people who are sick
o Avoid vaccinations unless discussed first with provider
o Review possible/probably ADR’s
 Report: severe abdominal pain, tarry stools, unusual swelling, weight gain,
tiredness, bone pain, non-healing sores, visual disturbances and behavioral or
mood changes.
 Advise wearing a medical alert bracelet
 Lifestyle Management:
o A diet high in protein, potassium and calcium, and low in sodium and carbohydrates can
counteract some of the adverse reactions associated with corticosteroids.
o MVI with minerals, calcium, Vitamin D are appropriate
o Caloric management to prevent obesity should be discussed
o Alcohol should be avoided
o Osteoporosis risk can be reduced with calcium intake as well as regular exercise
o Stress management techniques are recommended because stress can be a source of
HPA stimulation.