2. • Cortisol, the endogenous glucocorticoid in the body, is produced
and secreted on the basis of feedback mechanisms of the
hypothalamus-pituitary-adrenal (HPA) axis.
• The adrenal cortex synthesizes and secretes the steroid hormones
that include mineralocorticoids and glucocorticoids and, to a
lesser extent, androgens.
• Exogenously administered adrenal cortex hormones
(corticosteroids) affect this feedback mechanism.
• Corticosteroids have a major role in the management of a variety
of disease processes. In primary or secondary adrenal cortex
insufficiency, they are used for replacement therapy.
INTRODUCTION
3. • Glucocorticoids have metabolic, anti-inflammatory, and growth-
suppressing effects.
• Cortisol is the “wake-up” hormone, and altered levels result in
changes in levels of awareness and sleep patterns.
• Central nervous system (CNS) effects also result in labile emotional
states, and high levels of cortisol are associated with decreased
recent memory recall.
• Glucocorticoids increase blood glucose concentration by stimulating
gluconeogenesis in the liver and by decreasing uptake of glucose
into muscle, lymphatic, and adipose cells.
• In extrahepatic tissues, they stimulate protein catabolism and inhibit
amino acid uptake and protein synthesis.
• Decreased proliferation of fibroblasts in connective tissue in
concert with the poor protein synthesis leads to poor wound healing
PHARMACODYNAMICS
4. • Glucocorticoids inhibit the immune and
inflammatory systems : BY
• depressing proliferation of T lymphocytes
- decreasing natural killer cell activity;
- reversing macrophage activity; and
- suppressing the synthesis, secretion, and actions of
chemical mediators involved in inflammatory and
immune responses.
• These chemical mediators include interleukins,
prostaglandins, leukotrienes, bradykinin, serotonin,
and histamine.
5. • Glucocorticoids also increase circulating
erythrocytes;
• increase appetite;
• promote fat deposits in the face and cervical areas,
• promote lipolysis in the extremities;
• increase uric acid excretion; and decrease serum
calcium levels,
(by inhibiting GI absorption of calcium and
phosphate)
6. • They also promote gastric acid secretion.
• In the urinary tract, glucocorticoids enhance
urinary excretion.
• Their feedback activity on the HPA axis
suppresses secretion and synthesis of
adrenocorticotropic hormone (ACTH) and
suppresses prostaglandin E production of
insulin-like growth hormone secretion so that
somatic growth is inhibited.
7. • Skeletal wasting also occurs and is most rapid during
the first 6 months of therapy. This osteoporotic
process is a result of stimulation of osteoclastic
activity and inhibition of osteoblastic activity.
• An additional factor in bone loss is the effect of
glucocorticoids on sex hormones, which results in
decreased circulating levels of anabolic hormones.
• Bone mineral density (BMD) rapidly declines
beginning within the first 3 months of
glucocorticoid therapy and peaks at 6 mths.
8. • they potentiate the effects of catecholamines, thyroid hormone,
and growth hormone on adipose tissue.
• Mineralocorticoids (predominantly aldosterone) are also secreted
by the adrenal cortex under the control of the reninangiotensin-
aldosterone system. The main role of aldosterone is to retain
sodium and water and excrete potassium.
• may be used as anti-inflammatory drugs.
• Prednisone, prednisolone, and fludrocortisone are synthetic steroids
with mixed cortisol and aldosterone activity but are used mainly for
their cortisol effects.
• Triamcinolone, dexamethasone, methylprednisolone, and
betamethasone are also synthetic compounds that have almost no
aldosterone activity and are used for their potent anti-inflammatory
activity.
S
9.
10. Absorption and Distribution
• Corticosteroids are all well absorbed from the upper jejunum.
• Those with IM formulations are well absorbed from IM
sites.
• Absorption is rapid for esters (sodium phosphates and
sodium succinate) and relatively slow for other derivatives
(acetates, acetonides, and tebutates).
• Absorption from local sites (e.g., intra-articular or
intrasynovial) is slower than from IM sites.
• Because onset, peak, and duration of action vary, these drugs
are classified into short-, intermediate-, and long-acting forms.
PHARMACOKINETICS
11. • Corticosteroids are reversibly bound to corticosteroid
binding proteins.
• They have significantly altered pharmacological effects
on patients with altered protein-binding capacities.
Pregnancy, for example, is a hyperproteinemic state in
which the total plasma level of steroid would be
elevated.
• All these drugs are widely distributed, cross the
placenta, and enter breast milk.
12. • The liver metabolizes hydrocortisone and this is the rate-
limiting step in its clearance.
• The metabolism and excretion of other corticosteroids
generally parallel those of hydrocortisone.
• Induction of hepatic enzymes increases the metabolic
clearance of all corticosteroids.
• The liver converts cortisone to hydrocortisone, and
prednisone is converted to prednisolone.
• Approximately 1% of the daily dose of the drug is
excreted unchanged in urine.
METABOLISM AND EXCRETION
13.
14. • presence of active, untreated infections -may mask the
indications of infection, and new infections may appear
during their use.
• Corticosteroids may exacerbate systemic fungal
infections; therefore, corticosteroids are
contraindicated in patients with these infections.
• Corticosteroids may activate latent amebiasis or
tuberculosis.
PRECAUTIONS AND CONTRAINDICATIONS
15. • Patients positive for hepatitis B surface antigen.
• Patients with hypertension and cardiovascular
disorders (e.g., heart failure [HF])
(large doses of drugs with high relative mineralocorticoid potency
(e.g., cortisone and hydrocortisone) can cause elevated blood
pressure, salt and water retention, and increased excretion of
potassium)
• Used with caution in renal insufficiency, acute
glomerulonephritis, or chronic nephritis.
16. • Cautiously use in postmenopausal women and others
at risk for osteoporosis (patients with a lower body mass
index or parental history of hip fracture, smokers,
alcoholic drinks per day)-as corticosteroids increase
calcium excretion.
• Cautiously use in patients with diabetes mellitus- (may
have difficulty maintaining glycemic control because
corticosteroids alter the liver’s glucose regulation).
17. •
• atrophy and thinning of the skin,
• alopecia,
• acneiform eruptions,
• poor healing,
• purpura,
• striae,
• hirsutism,
• Desquamation of skin.
• Myopathy is also seen, with marked muscle wasting,
• Alteration in body fat is also noted truncal obesity,
• buffalo hump,
• moon face.
• Skeletal Tissues Osteoporosis develops.
• Skeletal fractures, mainly of the spine, ribs, and pelvis.
ADVERSE DRUG REACTIONS
18. • Eye-Prolonged use can cause cataracts, glaucoma with possible
damage to the optic nerve, and increased risk for secondary
ocular infections due to fungi or viruses.
• Gastrointestinal System -peptic ulcer disease.
• Cardiovascular System- Hypertension is a common adverse
reaction. This and other cardiovascular problems (e.g., fluid
and electrolyte disturbances).
• Central Nervous System -Delirium, agitation, insomnia,
mood swings, and severe depression .
The onset of symptoms is usually within 15 to 30 days
19. Endocrine System- Prolonged therapy with corticosteroids may
lead to adrenal suppression.
(To minimize this adverse reaction, the dose of corticosteroids
used for prolonged therapy should be tapered.)
-Amenorrhea
- Menstrual irregularities like Postmenopausal bleeding.
23. Assessment
History: Infections; renal or liver disease, hypothyroidism,
ulcerative colitis with impending perforation, diverticulitis, active
or latent peptic ulcer, inflammatory bowel disease, CHF,
hypertension, thromboembolic disorders, osteoporosis, seizure
disorders, diabetes mellitus; hepatic disease; lactation.
Physical: Weight, reflexes and grip strength, affect and orientation,
P, BP, peripheral perfusion, prominence of superficial veins,
adventitious sounds, serum electrolytes, blood glucose
NURSING RESPONSIBILITIES
24. • Monitor for the common adverse reactions associated with the use of
corticosteroids: weight gain, edema, hypertension, and indications of excessive
potassium loss and negative nitrogen balance associated with protein
catabolism.
• Carefully monitor the growth and development of children on prolonged
therapy.
• Laboratory monitoring begins with an initial assessment of serum electrolytes,
glucose, and CBC.
• For patients on long-term therapy or high doses, annual monitoring of these
parameters, as well as guaiac testing of stools and serum lipid analysis, is
appropriate.
• For patients at risk for or with indications of GI adverse reactions, upper GI
x-rays are desirable.
• Taper doses when discontinuing high-dose or long-term therapy to avoid
adrenal insufficiency.
NURSING RESPONSIBILITIES
25. • Do not give live virus vaccines with immunosuppressive doses
of corticosteroids.
• Do not stop taking the drug without consulting the health
care provider.
• Avoid exposure to infections.
• Report unusual weight gain, swelling of the extremities, muscle
weakness, black or tarry stools, fever, prolonged sore throat,
colds or other infections, worsening of the disorder for which
the drug is being taken.
• Assess the sign and symptom of Cushing syndrome-
(hypercortisolism)-fatty deposition at back(buffalo hump,
moon face), hirutism, menstrual abnormalities, delayed wound
healing, hyperglycemia, pendulous breast etc.
NURSING RESPONSIBILITIES
