PrednisonePrepared by: Abdulaziz Thaer Aziz, RN

Email: Abd_abuthaer@yahoo.com

Directed by: Dr. Heba Khader, Ph.D., Pharmacist

Steroid Hormones and Cancer• Tumors that are steroid sensitive may be either:

Hormone-responsive

Tumor regresses following

treatment with a specific hormone

Hormone treatment mostly

given for pattiative

In few cases use cytotoxic effect of glucocorticoids on

lymphomas

Hormone-dependent

Remove hormonal stimulus causes

tumor regression

Surgery: orchiectomy for

patients with advance prostate

cancer

Drugs: antiestrogentamoxifen is used to

prevent estrogen stimulation of breast

cancer cells

• Prednisone is an oral, naturally-occurring corticosteroid

produced in the body by the cortex of adrenal glands. It

mimics the action of cortisol (hydrocortisone) with less

mineralocorticoid activity than cortisol.

• Corticosteroids have many effects on the body, but the

most common are used for their potent anti-

inflammatory effects on immune system (arthritis,

colitis and asthma).

• It was observed that patients with cushing syndrome

have lymphocytopenia and decreased lymphoid mass.

This result from corticosteroid action on lymphocyte

formation and distribution, that is, movement of these

cells from the circulation to lymphoid tissue.

Mechanism of Action

• Prednisone itself is inactive and must first be preduced to

predinsolone by 11-β-hydroxysteroid dehydrogenase. The

steroid binds to a receptor that triggers the production of specific

protein.

• Glucocorticoids are naturally occurring hormones that prevent

or suppress inflammation and immune responses when

administered at pharmacological doses. At a molecular level,

unbound glucocorticoids readily cross cell membranes and bind

with high affinity to specific cytoplasmic receptors. This binding

induces a response by modifying transcription and, ultimately

protein synthesis to achieve the steroid's intended action.

Mechanism of Action• Such actions may include: inhibition of leukocyte infiltration at the site

of inflammation, interference in the function of mediators of

inflammatory response, and suppression of humeral immune

responses. Some of the net effects include reduction in edema or scar

tissue, as well as a general suppression in immune response. The

degree of clinical effect is normally related to the dose administered.

• The anti-inflammatory actions of corticosteroids are thought to involve

phospholipase A2 inhibitory proteins, collectively called lipocortins.

Lipocortins, in turn, control the biosynthesis of potent mediators of

inflammation such as prostaglandins and leukotrienes by inhibiting the

release of the precursor molecule arachidonic acid. Likewise, the

numerous adverse effects related to corticosteroid use are usually

related to the dose administered and the duration of therapy.

• Resistance is associated with an absence of

the receptor protein or a mutation that

lowers receptor affinity for the hormone.

However, some resistant cells appear to

have functional receptors, but some

subsequent step(s) is affected.

Pharmacokinetics• Prednisone is rapidly absorbed across the GI membrane

following oral administration. Peak effects can be observed after

1-2 hours. The circulating drug binds extensively to the plasma

proteins albumin and transcortin, with only the unbound portion

of a dose active.

• Systemic prednisone is quickly distributed into the kidneys,

intestines, skin, liver and muscle. Corticosteroids distribute into

the breast milk and cross the placenta. Prednisone is metabolized

by the liver by microsomal oxidizing enzymes to the active

metabolite prednisolone (caution with hepatic dysfunction ),

which is then further metabolized to inactive compounds.

• These inactive metabolites, as well as a small portion of

unchanged drug, are excreted in the urine.

Indications• Remission of acute lymphocytic leukemia

• Chronic lymphocytic leukemia

• Hodgkin's and non-Hodgkin's lymphomas

• Mycosis fungoides

• Congenital adrenal hyperplasia

• Replacement therapy for primary adrenocortical insufficiency (Addison's disease)

• Replacement therapy for secondary or tertiary adrenocortical insufficiency (defect either in CRF production by hypothalamus or corticotropinproduction by pituitary)

• Relief of inflammatory symptoms

• Treatment of allergies

• thrombocytopenia

• Nervous system: acute exacerbations of multiple sclerosis

• Edematous state: to induce a diuresis or remission of proteinuria in the nephrotic syndrome

Mycosis fungoides: A type of non-Hodgkin lymphoma that first

appears on the skin and can spread to the lymph nodes or other organs

such as the spleen, liver, or lungs.

Withdrawal• Withdrawal from the drugs can be a serous problem, because if

the patient Withdrawal from these drugs can be a serious

problem because, if the patient has experienced hypothalamic-

pituitary-adrenal-suppression, abrupt removal of the

corticosteroids causes an acute adrenal insufficiency syndrome

that can be lethal.

• This risk, coupled with the possibility of psychological

dependence on the drug and the fact that withdrawal might

cause an exacerbation of the disease, means the dose must be

tapered according to the individual, possibly through trial and

error. The patient must be monitored carefully.

Prednisone: Nursing Diagnoses and Outcomes

• Excess Fluid Volume related to sodium and water retention secondary to corticosteroid therapy• Desired outcome: The patient will

relate causative factors and methods of preventing edema and exhibit decreased peripheral and sacral edema.

• Risk for Infection or Risk for Injury related to anti-inflammatory, immunosuppressive, dermatologic, and metabolic effects of chronic corticosteroid therapy• Desired outcome: The patient

will demonstrate knowledge of risk factors associated with potential for infection or injury and will practice appropriate precautions for prevention.

• Imbalanced nutrition: More than Body Requirements related to increased appetite secondary to corticosteroid medications• Desired outcome: The

patient will maintain a healthy weight, discuss current nutritional needs, and discuss the effects of exercise on weight control.

• Altered Body Image related

to cushingoid characteristics

or physical changes

secondary to glucocorticoid

therapy

• Desired outcome: The

patient will verbalize and

demonstrate acceptance

of appearance, verbalize

and demonstrate healthy

adaptation and coping

skills.

Prednisone: Planning and Interventions

• Maximizing therapeutic effects

• The most opportune time for administration of daily doses or

alternate-day doses of glucocorticoids is early in the morning.

• Minimizing adverse effects

• Monitor the patient, especially the surgical patient, carefully for

signs of infection.

• Administration can lead to peptic ulcer disease.

Prednisone: Teaching, Assessment, and Evaluations

• Patient and family education

• Discuss taking the drug exactly as prescribed.

• Discuss not stopping the drug abruptly.

• Emphasize the importance of patients’ notifying all health care

providers about glucocorticoid therapy.

• Ongoing assessment and evaluation

• Monitor for therapeutic drug response, adverse drug reactions, and

indications of drug toxicity.