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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
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.
Group B- Acetonides
o
Group D-Esters
o
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
Cardiovascular system
Central Nervous System
Skeletal System
Kidney
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.
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.
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
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.
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
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.
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,
Flunisolide
Fluticasone furoate
Fluticasone propionate
Triamcinolone acetonide
Beclomethasone dipropionate
Budesonide
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
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.
WEBSITES
www.wikipedia.org
www.slideshare.com