Nursing considerations for corticosteroids and immunosuppressants
Nursing considerations for corticosteroids and immunosuppressants ( 3 Questions)
A nurse is administering methylprednisolone (Medrol), a glucocorticoid, to a client who has multiple sclerosis. What are some of the expected pharmacologic effects of methylprednisolone in this condition? (Select all that apply)
Option A is incorrect because methylprednisolone does not promote sodium reabsorption and potassium excretion in the kidney, increasing blood volume and blood pressure. This is the effect of mineralocorticoids such as aldosterone, which regulate the fluid and electrolyte balance in the body. Methylprednisolone has a low affinity for mineralocorticoid receptors and does not have significant mineralocorticoid activity¹².
Methylprednisolone is a synthetic glucocorticoid that reduces inflammation, pain, fever, and allergic reactions by inhibiting the synthesis of prostaglandins and leukotrienes¹². Prostaglandins and leukotrienes are lipid-derived inflammatory mediators that are involved in various inflammatory and allergic conditions such as asthma, rheumatoid arthritis, and anaphylaxis. Methylprednisolone inhibits their synthesis by blocking the enzyme cyclooxygenase (COX) and lipoxygenase (LOX), respectively. Methylprednisolone also influences the carbohydrate, protein, and fat metabolism in various tissues, increasing blood glucose and suppressing immune response¹². Methylprednisolone modulates the expression of genes involved in immune regulation, apoptosis, and cell differentiation by interacting with glucocorticoid receptors.
Option C is incorrect because methylprednisolone does not regulate the secretion of adrenocorticotropic hormone (ACTH) from the anterior pituitary gland, maintaining the feedback loop of cortisol production. This is the effect of endogenous glucocorticoids such as cortisol, which are produced by the adrenal cortex in response to ACTH stimulation. Methylprednisolone suppresses the secretion of ACTH from the pituitary gland by negative feedback inhibition, which can lead to adrenal insufficiency if methylprednisolone is discontinued abruptly¹².
Multiple sclerosis is a chronic autoimmune disease that affects the central nervous system, causing inflammation, demyelination, and axonal damage³. Methylprednisolone is used to treat acute relapses of multiple sclerosis by reducing the inflammation and edema in the brain and spinal cord³. Methylprednisolone may also have some neuroprotective effects by inhibiting the production of reactive oxygen species and nitric oxide, which can cause oxidative stress and neuronal injury³.
Methylprednisolone is a synthetic glucocorticoid that reduces inflammation, pain, fever, and allergic reactions by inhibiting the synthesis of prostaglandins and leukotrienes¹². Prostaglandins and leukotrienes are lipid-derived inflammatory mediators that are involved in various inflammatory and allergic conditions such as asthma, rheumatoid arthritis, and anaphylaxis. Methylprednisolone inhibits their synthesis by blocking the enzyme cyclooxygenase (COX) and lipoxygenase (LOX), respectively. Methylprednisolone also influences the carbohydrate, protein, and fat metabolism in various tissues, increasing blood glucose and suppressing immune response¹². Methylprednisolone modulates the expression of genes involved in immune regulation, apoptosis, and cell differentiation by interacting with glucocorticoid receptors.
Multiple sclerosis is a chronic autoimmune disease that affects the central nervous system, causing inflammation, demyelination, and axonal damage³. Methylprednisolone is used to treat acute relapses of multiple sclerosis by reducing the inflammation and edema in the brain and spinal cord³. Methylprednisolone may also have some neuroprotective effects by inhibiting the production of reactive oxygen species and nitric oxide, which can cause oxidative stress and neuronal injury³.
The other options are incorrect because:
Option A is incorrect because methylprednisolone does not promote sodium reabsorption and potassium excretion in the kidney, increasing blood volume and blood pressure. This is the effect of mineralocorticoids such as aldosterone, which regulate the fluid and electrolyte balance in the body. Methylprednisolone has a low affinity for mineralocorticoid receptors and does not have significant mineralocorticoid activity¹².
Option C is incorrect because methylprednisolone does not regulate the secretion of adrenocorticotropic hormone (ACTH) from the anterior pituitary gland, maintaining the feedback loop of cortisol production. This is the effect of endogenous glucocorticoids such as cortisol, which are produced by the adrenal cortex in response to ACTH stimulation. Methylprednisolone suppresses the secretion of ACTH from the pituitary gland by negative feedback inhibition, which can lead to adrenal insufficiency if methylprednisolone is discontinued abruptly¹².