Drug study

On
Corticosteroids

SUBMITTED TO:
RESPECTED
MRS.SMRITI ARORA MAAM
ASSISTANT PROFESSOR
RUFAIDA COLLEGE OF NURSING
JAMIA HAMDARD, DELHI.
SUBMITTED BY:
LIGY MARY THOMAS
MSC NURSING FIRST SEMESTER(2014-15)

INTRODUCTION

Corticosteroids are referred to glucocorticoids and mineralocorticoids.

Hydrocortisone (cortisol) is the principal glucocorticoid secreted by the zone fasciculate of the
adrenal cortex. Only cortisol has a feedback effect on the pituitary gland.
Cortisol has potent anti inflammatory activity and sodium retaining activity. Separation of these
two activities has led to the development of many drugs.
Corticosteroids are a class of steroid hormones that are produced in the adrenal cortex.
Corticosteroids are involved in a wide range of physiologic systems such as stress response,
immune response and regulation of inflammation, carbohydrate metabolism, protein catabolism,
blood electrolyte levels, and behavior.
Glucocorticoids such as cortisol control carbohydrate, fat and protein metabolism and are antiinflammatory by preventing phospholipids release, decreasing eosinophil action and a number of
other mechanisms.
Mineralocorticoids such as aldosterone control electrolyte and water levels, mainly by promoting
sodium retention in the kidney.
Common natural hormones
corticosterone (C21H30O4),
cortisone (C21H28O5, 17-hydroxy-11-dehydrocorticosterone)

BIOSYNTHESIS
The corticosteroids are synthesized from cholesterol within the adrenal cortex.
Most steroidogenic reactions are catalyzed by enzymes of the cytochrome P450 family. They are
located within the mitochondria and require adrenodoxin as a cofactor
Aldosterone and corticosterone share the first part of their biosynthetic pathway.
The last part is either mediated by the aldosterone synthase (for aldosterone) or by the 11hydroxylase (for corticosterone). These enzymes are nearly identical (they share 11hydroxylation and 18-hydroxylation functions).
Moreover, aldosterone synthase is found within the zona glomerulosa at the outer edge of the
adrenal cortex; 11-hydroxylase is found in the zona fasciculata and reticularis.

FIG 1: SYNTHESIS OF CORTICOSTEROIDS

CLASSES OF CORTICOSTEROIDS
Corticosteroids are generally grouped into four classes, based on chemical structure.
Allergic reactions to one member of a class typically indicate an intolerance of all members of the
class.
Coopman classification
This was named after S.Coopman who defined this classification in 1989
Group A Hydrocortisone type
o

(short to medium acting glucocorticoids) Hydrocortisone, Hydrocortisone acetate,

Cortisone acetate, Tixocortol pivalate, Prednisolone, Methylprednisolone, and
Prednisone.

Group B- Acetonides
o

Triamcinolone acetonide, Mometasone, Amcinonide, Budesonide, Desonide,

Fluocinonide, Fluocinolone acetonide, and Halcinonide.

Group C-Betamethasone type

Betamethasone, Betamethasone sodium phosphate, Dexamethasone, Dexamethasone

sodium phosphate, and Fluocortolone.

Group D-Esters
o

Hydrocortisone-17-butyrate , Betamethasone valerate , Betamethasone dipropionate ,

Prednicarbate , and Fluprednidene acetate

HISTORY
First known use was in 1944. Tadeusz Reichstein together with Edward Calvin Kendall and
Philip Showalter Hench were awarded the Nobel Prize for Physiology and Medicine in 1950 for
their work on hormones of the adrenal cortex, which culminated in the isolation of cortisone.
Corticosteroids have been used as drug treatment for some time.
Lewis Sarett of Merck & Co. was the first to synthesize cortisone, using a complicated 36-step
process that started with deoxycholic acid, which was extracted from ox bile.
The low efficiency of converting deoxycholic acid into cortisone led to a cost of US $200 per
gram. Russell Marker, at Syntex, discovered a much cheaper and more convenient starting
material, diosgenin from wild Mexican yams.
His conversion of diosgenin into progesterone by a four-step process now known as Marker
degradation was an important step in mass production of all steroidal hormones, including
cortisone and chemicals used in hormonal contraception.
In 1952, D.H. Peterson and H.C. Murray of Upjohn developed a process that used Rhizopus mold
to oxidize progesterone into a compound that was readily converted to cortisone.
The ability to cheaply synthesize large quantities of cortisone from the diosgenin in yams resulted
in a rapid drop in price to US $6 per gram, falling to $0.46 per gram by 1980. Percy Julian's
research also aided progress in the field.
The exact nature of cortisone's anti-inflammatory action remained a mystery for years after,
however, until the leukocyte adhesion cascade and the role of phospholipase A2 in the production
of prostaglandins and leukotrienes was fully understood in the early 1980s.
FUNCTIONS
Glucocorticoids affects metabolism of:

Carbohydrate
Protein
Fat

Purine
Electrolytes

In addition, they affect the functional capacities of

Cardiovascular system
Central Nervous System
Skeletal System
Kidney

Protein and Carbohydrate metabolism

The term gluco means gluconeogenesis which is basically a catabolic process
Amino acids from muscle, liver synthesize glucose. A part of it is deposited as glucogen and the
remaining is released into the blood.
The nitrogen is excreted as urea and the explains the -ve nitrogen balance
Corticosteroids induce hyperglycemia in two ways
By producing more glucose from proteins and
By impairing peripheral utilization of glucose.
In Addisons disease, there is a decrease in the cortisol due to hypo function of the adrenal gland.
This will produce a decrease in the liver glycogen and decreased glycogen concentration of
muscle.
It will lead to hypersensitivity to insulin
Corticosteroid produce gluconeogenesis
Amino acid derived from muscle and bone matrix is converted to glucose and is accumulated in
fat depot.
Loss of amino acid from bone matrix causes calcium resorption which results in to increased
calcium excretion in urine.
Catabolic effects due to high dose of cortical or disease will lead to :
Osteoporosis
Wasting of muscle
Reduced mass of muscle
Increased blood sugar level
Decreased absorption of calcium from gut due to antagonism to Vitamin D.
Increase in blood glucose level increases insulin level as a temporary counter balance. If the
cortical level is in excess like in Cushings syndrome or cortisol has been given for prolonged
period, the beta cells get exhausted and results in diabetic like condition known as met diabetes or
steroid diabetes.
Fat Metabolism

Glucocorticoids in physiological concentration play a supportive role in mobilization of fat from

the peripheral fat depot by adrenaline and growth hormone.
This will mean that it plays a permissive role in the lipolytic or fatty acid releasing action of
adrenaline and growth hormone on the adipose tissue in inceasing the free fatty acid.
When large doses of corticosteroids are given for a longtime, there occurs a peculiar
redistribution of the fat in the body. It is drained from the extremities and deposited in the face, in
the neck and supraclavicular area.

Calcium Metabolism

Gluocorticoids antagonizes the action of vitamin D on the gut and reduces the absorption of
calcium.
By promoting breakdown of protein in the bone matrix, it brings about a secondary loss of
calcium from bone.
Calcium mobilized from bone is lost in urine.
When large doses of corticoids are given for long period they interfere with the development of
cartilage and inhibit linear growth in children.
Anabolic steroids and not Vitamin D antagonizes the catabolic effect of glucocorticoids.

Electrolyte and Water Metabolism

Main action on this metabolism is produced by mineral corticoids like aldosterone,

fludrocortisones and deoxycorticosterone which have potent sodium retaining activity in
exchange of potassium. In addition they also retain phosphate, bicarbonate and calcium.
However, main is sodium retention.
Cortisol and cortisone have some sodium-retaining activity. This becomes important only in
patients who are not able to tolerate additional sodium load.
Fluoro-corticoids do not possess sodium retaining activity and are used in such patients.

Blood
Glucocorticoids cause an increase in neutrophils and esonophils and decreases lymphocytes.
Long term and prolonged use increases erythrocytes and cause mild polycythemia and thus an
increase in coagulability.
In Cushings syndrome lymphocytosis and dissolution of lymphatic masses
In patients, with acute lymphoblastic leukemia, corticosteroids rapidly destroy lymphocytes. No
lymphocytes are seen in the normal persons.
Immune Response

In large doses gluco-corticoids cause involution of the thymus and lymph nodes as a result
lymphocyte count in blood goes down
Since lymphocytes are concerned with antibody production, glucocorticoids impair antibody
production.
In large doses it causes lysis of the T-cell, prevent homograft rejection and suppress cell mediated
hypersensitivity reactions.
Corticosteroid in doses of 40-60mg/ day modifies cell mediated immunity and does not suppress
the humoral antibody production by B lymphocytes.
Clinically, corticosteroids modify the course of many diseases in which immune responses are
believed to play a significant role. Although they do not modify the basic processes they suppress
the inflammatory response to injury.
Corticoids increase the susceptibility to a variety of bacterial, fungal, viral and parasitic super
infections. In such infections corticoids would cause the spread by inhibiting the protective
inflammatory reaction. Because inflammation is basically a protective reaction and its purpose is
to localize and destroy the irritant.

Anti-inflammatory Actions

Corticosteroids prevents and suppress the clinical features of inflammation (i.e. local heat,
redness, swelling and tenderness)
At tissue level they suppress the early phenomena (i.e. edema, fibrin deposition, capillary
dilatation, migration of phagocytes into inflamed area and phagocytosis) as well as the late
manifestations (i.e. capillary proliferation, fibroblastic proliferation, deposition of collagen) are
prevented.
But fibrous tissue once formed is not dissolved by corticosteroids.

Mechanism of anti-inflammatory action

Corticosteroids inhibit the recruitment of neutrophils and macrophages in affected area.

As a part of inflammatory response, the previously sensitized lymphocytes on meeting the
sensitizing antigen produce soluble factors called lymphokines.
One of this is called microphage migration inhibitory factor(MIF)
Migration inhibitory factor cause local accumulation of macrophages by inhibiting their mobility.
Corticosteroids block this effect of MIF on macrophages.
Corticosteroids inhibit the production of plasminogen activator by neutrophils thus inhibiting
conversion of plasminogen to plasmin. Plasmin helps the entry of neutrophils in to the area of
inflammation by hydrolysis of fibrin.
Glucocorticoids inhibit the release of arachidomic acid from phospholipids by inhibiting
phospholipase-A2 and therefore decrease the availability of prostaglandins and leukotreines which
play significant role in chemotaxis.

FIG 2: ANTI INFLAMMATORY ACTION OF CORTICOSTEROIDS

Cardiovascular System

Hypertension, salt and water retention can occur during the therapy but are uncommon with
fluoro-derivative corticosteroids
In shock, it is useful because they restore the sensitivity of arterioles to catecholamine

Central Nervous System

A critical level of corticosteroid is needed for normal activity of brain.
Deficiency and excess both affects the CNS activity
Apathy is a feature of Addisons disease and is corrected by corticosteroids
Large doses on Cushings syndrome produces mood elevation, euphoria, insomnia, restlessness
and even psychosis
Epilepsy may be aggravated.

PRINCIPLES OF THERAPEUTIC USES

In life threatening situations
Like pemphigus, acute leukemia, acute transplant rejection
Treatment is started with large doses and then adjusted
In diseases which are not life threatening
Like rheumatoid arthritis and others
Treatment is started with small dose and then gradually increased till desired effect has
been achieved.
Large dose
A dose more than 25 mg/day of cortisol or its equivalent of other corticosteroids.
Acute adrenal insufficiency
Results from abrupt withdrawal of large doses of corticosteroids
Insufficiency produces symptoms of dehydration, weakness, lethargy, hypotension,
shock, death.
Immediate treatment
Infusion of dextrose saline
Intravenous administration of Hydrocortisone (100mg 8 hourly) or its equivalent other
corticosteroids.
Congenital Adrenal Hyperplasia
This occurs due to genetic deficiency of enzyme beta hydrogenase needed for
biosynthesis corticosteroid causing reduced formation of cortisol.
Low level of cortisol produces a feedback stimulation o anterior pituitary.
Stimulation of the pituitary stimulates the release of adrenals and androgens.
This results in virulization.
Treatment includes:
Most suitable corticosteroid is Dexamethasone
It has high potency and longer duration of action with no or little sodium
retaining action

 A single dose of 1 mg at night is sufficient to inhibit corticotrophin release for 24

hours.

Non Endocrine Uses

Rheumatoid arthritis
Corticosteroids are used when non steroidal anti inflammatory drugs and other drugs
have failed
And when multiple joints are affected with pain, swelling and severely progressive
disability.
If only 1-2 large bones are involved it is administered locally as intra articular injection.

FIG 3: INTRA ARTICULAR INJECTION

Bronchial asthma
Beclomethasone is widely used corticosteroid by inhalation.
But in acute, severe and sustained episode i.e. status asthmaticus systemic therapy of a
bronchodilator with corticosteroid is needed

FIG 4: INHALED CORTICOSTEROIDS

Shock
Very high doses of corticosteroid like 300mg cortisol or its equivalent as a minimum
daily dose is used I.V. in septic shock and hypovolemic shock i.e. in circulatory collapse
unresponsive to pressor amines.
Allergic reactions
Life saving drug in anaphylactic shock is adrenaline.
Corticosteroid is given as an adjunct
In blood transfusion reactions
Cerebral edema
Valuable in reducing cerebral edema due to head injury, encephalitis, malignant diseases
etc.
Only fluoro-derivative corticosteroids should be used which does not cause sodium and
water retention
Allergic disorders
In hay fever, allergic rhinitis, allergic conjunctivitis, atopic and contact dermatitis.
Ulcerative colitis
Used both topically by retention enema (30mg) for local effect on colon and
systematically, oral or I.V. especially in acute attack
Collagen diseases
It is characterized by defect in connective tissue protein (collagen) in joints, organs and
deep tissue skin layer. Examples of such diseases are lupus erythematous.
Corticosteroids suppress the disease and relieve symptoms.
Leukemia
Most effective in causing rapid improvement in acute leukemia
In acute lymphocytic leukemia of children, corticosteroids reduce white blood count,
control toxemia and fever.
Antimetabolites has slow onset of action and therefore it is started with corticosteroids till
steroid is withdrawn.

TOXICITY AND SIDE EFFECTS

Lowers Glucose Tolerance

Corticosteroids decrease the glucose tolerance due to its effect on carbohydrate
metabolism.
Borderline diabetes may be aggravated
Precaution is the adjustment of diet may be needed
Myopathy
Long term use of corticosteroids (high dose) leads to muscle wasting due to muscle
deamination leading to muscle weakness.
It specially affects arms, legs, shoulders and pelvic muscle.
Precaution is to take high protein diet
Peptic ulcer
Very common side effect
Increases the gastric acidity
Corticosteroids can aggravate the pre-existing peptic ulcer and may even cause
perforation.
Patient should be advised not to take corticosteroids on empty stomach. Patient with
history of hyperacidity should take antacids routinely with corticosteroids.

Increased susceptibility to infections

Corticosteroids impair resistance to infection
Aggravation of tuberculosis has been most widely cited
Vigorous effective chemotherapy if it has to be given together.
Hypokalaemia and sodium retention
Corticosteroids with mineral corticoid activity produce loss of potassium leading to
muscular weakness and hypokalaemia alkalosis.
Use fluoro derivative or supplement by giving potassium chloride
Sodium retention may increase blood pressure. In extreme cases edema and congestive
heart failure may develop.
Fluoro-derivative or supplement with a diuretic.
Behavioral
Mental disturbance may occur. Nervousness, euphoria, insomnia and mood fluctuation.
A serious paranoid state or depression with risk of suicide
It may cause psychopathies of manic depression and schizophrenia especially in patients
with history of depression.

CONTRAINDICATION

Peptic ulcer
Infections
Hypertension with CHF
Psychosis
Glaucoma

DURATION OF ACTION
Short acting (12 hours or less)
Hydrocortisone
Cortisone
Intermediate acting (12-24hours)
Prednisolone
Prednisone
Methyl prednisolone
Triamcinolone
Long acting
Betamethasone
Dexamethasone
ROUTES OF ADMINISTRATION
Topical steroids
For use topically on the skin, eye, and mucous membranes.
Topical corticosteroids are divided in potency classes I to IV,

FIG 5: TOPICAL CORTICOSTEROIDS

Inhaled steroids
For use to treat the nasal mucosa, sinuses, bronchi, and lungs. This group includes:

Flunisolide
Fluticasone furoate
Fluticasone propionate
Triamcinolone acetonide
Beclomethasone dipropionate
Budesonide

There is also a combination preparation containing fluticasone propionate and

salmeterol xinafoate (a long-acting bronchodilator). It is approved for children
over 12 years old.

FIG 6: INHALED CORTICOSTEROIDS

Oral forms
Such as prednisone and prednisolone.

FIG 7: ORAL CORTICOSTEROIDS

Systemic forms
Available in injectables for intravenous and parenteral routes.

FIG 8: INJECTABLE CORTICOSTEROID

1. HYDROCORTISONE
Therapeutic Action
Enters target cells and binds to cytoplasmic receptors; initiates many complex reactions that are
responsible for its anti- inflammatory, immunosuppressive (glucocorticoid) and salt retaining
(mineral corticoid) actions.
Indication
Replacement therapy in adrenal cortical insufficiency
Allergic states-severe or incapacitating allergic conditions
Hypercalcemic associated with cancer
Short term inflammatory and allergic disorders such as rheumatoid arthritis, collagen
diseases, dermatologic diseases, status asthmaticus and autoimmune disorders
Hematologic disorders- thrombocytopenic purpura, erythroblastopenia
Trichinosis with neurologic or myocardial involvement
Ulcerative colitis, acute exacerbation and palliation in some leukemia and lymphomas

 Intra articular or soft tissue administration: arthritis, psoriatic plaques

Retention enema: for ulcerative colitis
Topical preparations: minor skin irritations and rashes due to seborrhic dermatitis and
psoriasis
Dermatological preparation: to relieve inflammatory and pruritic manifestations
Ophthalmic diseases: acute and chronic severe allergy or inflammatory conditions.
Contraindication
Systemic administration
Contraindicated with allergy to any component of the drug, fungal infections,
amoebiasis, hepatitis B, and immunosuppressant.
Use cautiously with kidney disease, liver disease, cirrhosis, hypothyroidism,
ulcerative colitis, diverticulitis, recent GI surgery, active or latent peptic ulcer,
inflammatory bowel disease, hypertension, heart failure, convulsive disorders,
metastatic carcinoma.

Retention enemas, intrathecal foam

Contraindicated with systemic fungal infections, recent intestinal surgery,
extensive fistulas
Topical dermatologic preparation
Contraindicated with fungal, tubercular, herpes simplex skin infections, varicella.
Dosages
Individualize dosage based on severity and response rather than on formulae.
Oral (hydrocortisone cypionate): 20-240 mg/day in single or divided doses.
IM, IV (hydrocortisone sodium succinate): 100-150 mg initially, then reduce
dose based on condition and response but give no less than 25mg/day.
Retention enema (hydrocortisone): 100mg nightly for 21 days.
Intrathecal foam (hydrocortisone acetate): 1 applicator daily or bid for 2-3 weeks
and second day thereafter.
Topical dermatologic preparation: apply sparingly to affected area bid-qid.
Adverse effects
Systemic
CNS: Vertigo, headache, parasthesia, insomnia, seizures, psychosis
CV: Hypotension, shock, hypertension and heart failure, thrombophlebitis, cardiac
arrhythmias secondary to electrolyte disturbances
Dermatologic: thin, fragile skin, purpura, ecchymoses
EENT: Cataracts, glaucoma.
Endocrine: growth retardation, decreased carbohydrate tolerance and diabetes mellitus.
GI: Peptic ulcer, pancreatitis, abdominal distension, nausea, vomiting, increased appetite
and weight gain.
Hematologic: Hypocalcaemia, hypokalaemia, increased blood sugar
Hypersensitivity: Anaphylactoid or hypersensitivity reactions.
Musculoskeletal: Muscle weakness, steroid Myopathy, and loss of muscle mass,
osteoporosis
Adverse effects related to specific routes of administration
IM repository injections: Atrophy at injection site
Intra-articular: Osteonecrosis, tendon rupture, infection

Intralesional therapy, head and neck: blindness

Intraspinal: meningitis, adhesive arachnoiditis
Intrathecal administration: Arachnoiditis
Retention enema: local pain, rectal bleeding, systemic absorption and adverse effects.
Topical dermatologic ointments, creams, sprays: local burning, irritation, skin atrophy.

Nursing considerations
Assessment

History: Infections, kidney disease, liver disease, hypothyroidism, ulcerative colitis with
impending perforation, diverticulitis, recent GI surgery, inflammatory bowel disease,
hypertension, heart failure, thrombophlebitis, osteoporosis, metastatic carcinoma.
Physical: Weight, ophthalmic examination, blood pressure, respiration, auscultation,
adventitious sounds, peripheral perfusion, liver palpation, chest X ray, serum electrolytes,
urinalysis, serum cholesterol.

Interventions
Give daily before 9 am to mimic normal peak diurnal corticosteroid levels.
Space multiple doses evenly throughout day
Do not give IM injections if patient has thrombocytopenic purpura
Rotate sites of IM repository injections to avoid local atrophy.
Use minimal doses for minimal duration to minimize adverse effects.
Taper doses when discontinuing high dose or long term therapy.
Arrange for increased dosage when patient is subject to unusual stress
Ensure that adequate amount of calcium is taken if prolonged administration of steroids.
Use alternate-day maintenance therapy with short acting corticosteroids whenever
possible.
Do not give live virus vaccines with immunosuppressive doses of hydrocortisone.
Provide antacids between meals to help avoid peptic ulcer.
Avoid prolonged use, especially near eyes, in genital and rectal areas, on face, and in skin
creases.
Teaching points
To take drug exactly as prescribed. Do not stop taking this drug without notifying the
health care provider, slowly taper drug to avoid problems.
Dosage reductions may create adrenal insufficiency. Report any fatigue, nausea,
vomiting, anorexia, muscle wasting, weight loss, dizziness or low blood sugar.
Take with meals if GI upset occurs.
Frequent follow-up visits to the health care provider needed to monitor the drug response
and adjust dosage.
Wear a medical alert ID if using a long term therapy.
May experience side effects: increase in appetite, weight gain, heartburn, indigestion,
muscle weakness, fatigue, poor wound healing.
Maintain normal bowel function with proper diet, adequate fluids intake, and regular
exercise when on anorectal preparations.

2. PREDNISONE

Therapeutic action
Enters target cells and binds to intracellular corticosteroid receptors, initiating many complex
reactions that are responsible for its anti-inflammatory and immunosuppressive effects.
Indications
Replacement therapy in adrenal cortical insufficiency
Hypercalcemia associated with cancer
Short term management of various inflammatory and allergic disorders such as
rheumatoid arthritis, collagen diseases, status asthmaticus and autoimmune disorders
Hematologic disorders: Thrombocytopenia purpura, erythroblastopenia.
Ulcerative colitis and palliation in some leukemia and lymphomas.

Contraindication
Contraindicated with infections, especially tuberculosis, fungal infection, amoebiasis,
varicella, antibiotic resistant infections.
Use cautiously with renal disorders, liver disease, ulcerative colitis, hypertension,
osteoporosis, heart failure, diabetes mellitus.
Dosage
Physiologic replacement: 0.05-2mg/kg/day PO or 4-5 mg/m2/day PO in equal divide doses every
12 hour.
Other indications: Individualize dosage depending on the severity of condition and the patients
response rather than by strict adherence to formulae that correct adult doses for age or body
weight.
Adverse effects:
CNS: Vertigo, headache, seizures, psychosis, cataracts, insomnia, depression, glaucoma.
CV: Hypotension, shock, hypertension, thromboembolism, fat embolism, cardiac
arrhythmias.
Electrolyte imbalance: Sodium and fluid retention, hypokalaemia, hypocalcaemia.
Endocrine: growth retardation, decreased carbohydrate tolerance, diabetes mellitus,
increased blood sugar.
GI: Nausea, vomiting, abdominal distension, pancreatitis
Hypersensitivity: Hypersensitivity or anaphylactoid reactions
Musculoskeletal: Muscle weakness, steroid Myopathy, loss of muscle mass,
osteoporosis.
Nursing considerations:
Assessment
History: Infections, renal or liver disease, hypothyroidism, ulcerative colitis,
diverticulitis, inflammatory bowel disease, hypertension, heart failure, osteoporosis,
hepatic disease, and diabetes mellitus.

 Physical: Weight, reflexes and grip strength, adventitious sounds, blood glucose, serum
electrolytes.

Interventions
Administer once-a-day doses before 9am to mimic normal peak corticosteroid blood
levels.
Increase dosage when patient is subject to stress.
Taper doses when discontinuing high-dose or long-term therapy to avoid adrenal
insufficiency.
Do not give live virus vaccines with immunosuppressive doses of corticosteroids.
Teaching points
Do not stop taking the drug without consulting the health provider taking once daily
doses at about 9 am
Avoid exposure to infections
Report unusual weight gain, swelling of the extremities, muscle weakness, prolonged
sore throat, and fever.
3. PREDNISOLONE
Therapeutic action
Enters target cells and binds to intracellular corticosteroid receptors, thereby initiating many
complex reactions that are responsible for its anti-inflammatory and immune suppressive effects.
Indication
Systemic
Hypercalcemic associated with cancer
Short term management of various inflammatory and allergic disorders such as
rheumatoid arthritis, collagen disease, dermatologic disease and autoimmune disorders.
Hematologic disorders: Thrombocytopenia purpura, erythroblastopenia
Ulcerative colitis and palliation in some leukemias and lymphomas
Trichinosis with neurologic or myocardial involvement.
Prednisolone has weaker mineralcorticosteroid activity than hydrocortisone and is not
used in physiologic replacement therapy.
Contraindication
Contraindicated with infections
Use cautiously with renal or liver disease, hypothyroidism, ulcerative colitis,
diverticulitis, active or latent peptic ulcer, heart failure, hypertension, osteoporosis,
diabetes mellitus, seizure disorders.
Dosages
Individualize dosage depending on severity of condition and patients response rather than by
strict adherence to formulae that correct adult doses for age or weight. Carefully observe growth
and development in infants and children on prolonged therapy.
Oral suspension

0.14-2mg/kg/day PO in three to four divided doses.

Nephrotic syndrome: 60mg/m2/day PO in three divide doses for 4 weeks. Then single doses for 4
weeks. Alternatively, 40mg/m2/day PO.
Adverse effects
CNS: vertigo, headache, paresthesias, insomnia, psychosis, seizures, increased IOP.
CV: Hypotension, shock, thromboembolism, thrombophlebitis, fat embolism.
Electrolyte imbalance: Hypokalaemia, hypocalcaemia.
Endocrine: growth retardation, decreased carbohydrate intolerance, increased blood
sugar, diabetes mellitus.
GI: Peptic ulcer, pancreatitis, abdominal distension, nausea, vomiting, increased appetite,
weight gain.
Musculoskeletal: muscle weakness, steroid Myopathy, loss of muscle mass,
osteoporosis, spontaneous fractures.
Nursing considerations
Assessment:
History: Infections, renal or liver disease, hypothyroidism, diverticulitis, seizure
disorder, osteoporosis, diabetes mellitus, hypertension, inflammatory bowel disease, heart
failure.
Physical: Weight, affect and orientation, pulse, respiration, peripheral perfusion,
adventitious sounds, blood glucose, serum electrolytes.
Interventions:
Administer once a day doses before 9am mimic normal peak corticosteroid blood levels.
Increase dosage when patient is subject to stress.
Have patient place orally disintegrating tablet in mouth, let dissolve, and then swallow.
Taper doses when discontinuing high dose or long term therapy to avoid adrenal
insufficiency.
Do not give live virus vaccines with immunosuppressive doses of corticosteroids.
Teaching points:

Take once a day daily doses before 9am, if using orally dissolving tablet, place in mouth,
let dissolve and then swallow.
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, cods or other infections.

SUMMARY
The corticosteroid are the class of steroid hormones produced in the adrenal cortex involved in a wide
range of physiologic systems such as stress, immune response, protein and carbohydrate metabolism,
blood electrolyte levels exhibiting common side effects on the central nervous system, gastrointestinal
tract.

CONCLUSION
The corticosteroids are the steroid synthesized by the cholesterol within the adrenal cortex.
Glucocorticosteroids and mineralocorticoids are the two main types of steroids used. These are effective
in a long term therapies but have to cautiously used due its adverse effects

BIBLIOGRAPHY

Amy.M.Karch, Lippincotts Nursing Drug Guide, 2011, Lippincott Williams & Wilkins
Publications, pg no 36-40, 608-611, 990-994.
H.H. Siddiqui, Essentials of Medical Pharmacology, First Edition, Globalmedik Publishers, 2010,
pg no.377-385.

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