Corticosteroid Therapy

Corticosteroids are medications used for their anti-inflammatory and immunosuppressive effects to treat a broad range of conditions, including autoimmune diseases, asthma, rheumatoid arthritis, and inflammatory bowel disease; as well as preventing organ rejection in transplant recipients, and as a replacement in adrenal insufficiency. The two types of corticosteroids are glucocorticoids, like prednisone, and mineralocorticoids, like fludrocortisone. Okay, let’s start by reviewing the function of endogenous, or naturally occurring corticosteroids in the body, which come from the adrenal glands located on the top of each kidney. These glands secrete glucocorticoids such as cortisol, which is involved in the stress response, and metabolism of carbohydrates, fats, and proteins; and mineralocorticoids, like aldosterone, which play a role in fluid, sodium, and potassium balance, and blood pressure.
Now, the level of these corticosteroids in the body is regulated by the hypothalamic-pituitary-adrenal, or HPA axis. So, for example, stimuli like stress, pain, trauma, or low cortisol levels prompt the hypothalamus to release corticotropin hormone, or CRH, which tells the anterior pituitary gland to release adrenocorticotropic hormone, or ACTH.
ACTH will then travel to the adrenal cortex, stimulating it to release cortisol. Once cortisol reaches the needed level, this information is fed back to the hypothalamus, which stops secreting corticotropin, ultimately stopping the continued secretion of cortisol by the adrenals. This negative feedback mechanism keeps hormone activity within a normal range. Alright, prednisone impacts the inflammatory process by inhibiting the release of pro-inflammatory molecules such as prostaglandins, histamine, and interleukin-1, which results in a reduction of fever, swelling, warmth, redness, and pain.
Prednisone also suppresses the activation and migration of immune cells, increases glucose levels, suppresses protein synthesis, and mobilizes fat deposits.
On the other hand, fludrocortisone primarily acts on the kidney tubules to promote reabsorption of sodium and water, and excretion of potassium.
Now, most of the side effects of prednisone are related to high dosage or long-term use of glucocorticoids. These include iatrogenic Cushing syndrome, which can result in mood changes; weight gain, predominantly in the back between the shoulder blades and face; skin atrophy, hyperglycemia, and an increased risk of infections.
Long-term use of glucocorticoids may also cause peptic ulcer disease; osteoporosis and pathological fractures; immunosuppression; and ocular disorders like cataracts and glaucoma.
Since mineralocorticoids cause sodium and water reabsorption, patients taking fludrocortisone may experience fluid retention, edema, and hypertension. Other common side effects include hypokalemia and hyperglycemia.
Now, patients should not take prednisone if they have conditions that can be exacerbated by these medications, including cataracts, glaucoma, or peptic ulcer disease.
Both prednisone and fludrocortisone should not be used in patients with an active, serious infections due to their immunosuppressive effects; and they should be used with caution in patients with diabetes mellitus since corticosteroids increase glucose levels.
Nursing Considerations & Patient Education Now, when caring for a patient taking a corticosteroid, begin by assessing your patient’s current height, weight, and vital signs. Then review their most recent laboratory test results, including liver and renal function tests, glucose, and electrolytes, especially potassium and sodium. During care, monitor your patient closely for side effects, and evaluate for the effectiveness of treatment.