Module 4 Pre-Quiz Review Lecture - Chapters 30, 31, & 33 (Spring 2024) PDF
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University of Nevada, Las Vegas
2024
Mary D. Bondmass
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This handout covers the pre-quiz review lecture for module 4, focusing on chapters 30, 31, and 33, which discuss pituitary drugs, thyroid and antithyroid drugs, and adrenal drugs. The material includes information on hormones, glands, and related drug therapies.
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3/28/2024 NURS 306 Module 4 Pre-quiz Review Lecture Chapters 30, 31, & 33...
3/28/2024 NURS 306 Module 4 Pre-quiz Review Lecture Chapters 30, 31, & 33 Mary D. Bondmass, Ph.D., RN, CNE Professor in Residence, School of Nursing University of Nevada Las Vegas [email protected] 702-285-3460 Maintenance of physiologic stability is the main goal of the endocrine system. The endocrine system must accomplish this task despite constant changes in the internal and external environments. Every cell and organ in the body comes under the influence of the endocrine system. It communicates with the nearly 50 million target cells in the body using a chemical “language” called hormones. Hormones are a large group of natural substances that cause highly specific physiologic effects in the cells of their target tissues. They are secreted into the bloodstream in response to the body’s needs and travel through the blood to their site of action—the target cell. The pituitary gland is made up of two distinct lobes—the anterior pituitary gland (adenohypophysis) and posterior pituitary gland (neurohypophysis). They are individually linked to and communicate with the hypothalamus, and each lobe secretes its own different set of hormones. The activity of the endocrine system is regulated by a system of surveillance and signaling usually dictated by the body’s ongoing needs. Hormone secretion is commonly regulated by a negative feedback loop. This is best explained using a fictional example: When gland X releases hormone X, this stimulates target cells to release hormone Y. When there is an excess of hormone Y, gland X senses this excess and decreases its release of hormone X. For decades, the pituitary gland was thought to be the master gland that regulated and controlled the other endocrine glands. However, evidence now suggests that the central nervous system (CNS), specifically the hypothalamus, controls the pituitary gland. The hypothalamus and pituitary gland are now viewed as functioning together as an integrated unit, with the primary direction coming from the hypothalamus. For this reason, these structures are now commonly referred to as the neuroendocrine system Chapter 30: Pituitary Drugs When you reach the end of this chapter, you will be able to do the following: 1. Describe the normal function of the anterior and posterior lobes of the pituitary gland and the impact of the pituitary gland on the human body. 2. Compare the various pituitary drugs with regard to their indications, mechanisms of action, dosages, routes of administration, adverse effects, cautions, contraindications, and drug interactions. 1 3/28/2024 A variety of drugs affect the pituitary gland. They are generally used as replacement drug therapy to make up for a hormone deficiency or as a diagnostic aid to determine the status of the patient’s hormonal functions. The currently identified anterior and posterior pituitary hormones and the drugs that mimic or antagonize their actions are listed in Table 30.1. The pituitary gland is made up of two distinct lobes—the anterior pituitary gland (adenohypophysis) and posterior pituitary gland (neurohypophysis). They are individually linked to and communicate with the hypothalamus, and each lobe secretes its own different set of hormones. These various hormones are listed in Box 30.1 and shown in Fig. 30.1. The anterior pituitary drugs discussed in this chapter are cosyntropin, somatropin, and octreotide; the posterior pituitary drugs discussed in this chapter are vasopressin and desmopressin. While you are expected to know a little about cosyntropin, and desmopressin, for the Module 4 quiz, your focus should be on somatropin, octreotide, and vasopressin. Patient Education General patient education for most patients (GPE) Do not use if there are known allergies or hypersenistiviy to drug or components of drug Read and follow instructions and use exactly as prescribed by your healthcare provider. Keep track of the number of doses used and ensure timely refills of your medication. Contact your healthcare provider if your symptoms do not improve or worsen, or if you experience any concerning side effects. Inform your healthcare provider about any other medications you are taking, including over-the-counter drugs and supplements, to prevent potential drug interactions. Educate the patient regarding potential side effects and proper administration techniques is essential for optimizing treatment outcomes. Patients should be closely monitored for adverse effects while any therapy, especially during prolonged treatment or in patients with comorbidities. 6 Key Terms Hypothalamus The gland above and behind the pituitary gland and the optic chiasm. Both glands are suspended beneath the middle area of the bottom of the brain. The hypothalamus secretes the hormones vasopressin and oxytocin, which are stored in the posterior pituitary gland. The hypothalamus also secretes several hormone-releasing factors that stimulate the anterior pituitary gland to secrete a variety of hormones that control many bodily functions. Negative feedback loop A system in which the production of one hormone is controlled by the levels of a second hormone in a way that reduces the output of the first hormone. A gland produces a hormone that stimulates a second gland to produce a second hormone. In response to the increased levels of the second hormone, the source gland of the first hormone reduces production of that hormone until blood levels of the second hormone fall below a certain minimum level needed; then the cycle begins again. Neuroendocrine system The system that regulates the reactions to both internal and external stimuli and involves the integrated activities of the endocrine glands and nervous system. 2 3/28/2024 Somatropin Somatropin is a synthetic form of human growth hormone (HGH), which is responsible for stimulating growth, cell reproduction, and regeneration in humans. Mechanism of Action: Somatropin binds to growth hormone receptors on target cells, initiating signaling pathways that promote growth and metabolic effects, including protein synthesis, lipid metabolism, and carbohydrate metabolism. Indications: Somatropin is used to treat children and adults with growth hormone deficiency, resulting in short stature in children and metabolic disturbances in adults. It is also indicated for the treatment of short stature in girls with Turner syndrome, a chromosomal disorder characterized by short stature and other developmental abnormalities. Somatropin may be used to promote growth in children with chronic kidney disease who have short stature. Additionally, it is used in the treatment of children with Prader-Willi syndrome, a genetic disorder characterized by developmental delays, obesity, and short stature Counterindications: Somatropin is contraindicated in patients with active malignancy due to the potential risk of tumor growth. It should not be used in patients with acute critical illness due to the potential risk of complications and lack of efficacy. Somatropin (cont) Adverse effects: Somatropin therapy may rarely cause intracranial hypertension, presenting with symptoms such as headache, nausea, vomiting, and visual changes. Somatropin can increase blood glucose levels, leading to hyperglycemia or exacerbating existing diabetes mellitus. Injection Site Reactions: Pain, redness, and swelling at the injection site are common adverse effects of somatropin therapy. Peripheral edema may occur with somatropin treatment, particularly in adults. Somatropin may unmask or exacerbate preexisting hypothyroidism, necessitating thyroid function monitoring. Cautions: Caution is warranted when using somatropin in patients with intracranial lesions, such as pituitary tumors, due to the risk of increased intracranial pressure. Somatropin may affect glucose metabolism and insulin sensitivity, necessitating careful monitoring in patients with diabetes mellitus or impaired glucose tolerance. Long-term use of somatropin in children requires careful monitoring of skeletal growth and bone age to minimize the risk of accelerated bone maturation and potential adverse effects on final adult height. Drug Interactions Insulin and Oral Hypoglycemic Agents: Somatropin may potentiate the effects of insulin and oral hypoglycemic agents, requiring adjustments in dosage. Glucocorticoids: Concurrent use of glucocorticoids may antagonize the growth-promoting effects of somatropin. Thyroid Hormones: Thyroid hormone replacement therapy may potentiate the growth-promoting effects of somatropin. Octreotide Octreotide is a synthetic analog of the natural hormone somatostatin. Mechanism of Action: Exerts its pharmacological effects by binding to somatostatin receptors, particularly subtype 2 receptors (SST2). By doing so, it inhibits the release of various hormones such as growth hormone, insulin, glucagon, gastrin, and serotonin, among others. This leads to decreased secretion of these hormones and consequently helps in controlling symptoms associated with hormone hypersecretion syndromes. Indications: Primarily used to treat conditions such as acromegaly, severe diarrhea and flushing episodes associated with carcinoid syndrome, and certain types of tumors Counterindications: Individuals with a known hypersensitivity to octreotide or any of its components should avoid its use, and contraindicated in patients with acromegaly who have not responded adequately to surgical resection of the pituitary tumor. 3 3/28/2024 Octreotide (cont) Adverse effects: GI effect are the most common, including nausea, vomiting, abdominal discomfort, flatulence, and diarrhea are common adverse effects of octreotide. Hypoglycemia or hyperglycemia may occur due to alterations in insulin and glucagon secretion. Injection site pain, erythema, and swelling at the injection site are common with subcutaneous administration. Bradycardia, arrhythmias, and conduction abnormalities may occur, particularly with high doses or in patients with underlying cardiac conditions, and may increase the risk of gallstone formation or exacerbate symptoms in patients with preexisting gallstones. Cautions: Octreotide may affect glucose metabolism and can cause hypoglycemia or hyperglycemia, necessitating careful monitoring in diabetic patients. Patients with a history of gallstones may experience exacerbation of symptoms due to reduced gallbladder contractility with octreotide use. Octreotide can affect thyroid function tests, so thyroid function should be monitored regularly in patients receiving long-term therapy. Dose adjustments may be necessary in patients with renal impairment. Octreotide may cause bradycardia and conduction abnormalities, particularly in patients with preexisting cardiac conditions. Drug Interactions: May potentiate the effects of insulin and oral hypoglycemic agents, may increase blood levels of cyclosporine, and for patients taking beta-blockers, octreotide may increase the risk of bradycardia and conduction abnormalities. Beta-Blockers with concurrant use Vasopressin Vasopressin, also known as antidiuretic hormone (ADH), is a hormone naturally produced in the hypothalamus and released from the posterior pituitary gland. It plays a crucial role in regulating water balance and blood pressure in the body. Synthetic forms of vasopressin are used in medicine for various indications. Mechanism of Action: Vasopressin acts primarily on V1 and V2 receptors in the body: Activation of V1 receptors on vascular smooth muscle leads to vasoconstriction, which increases peripheral vascular resistance and elevates blood pressure. Activation of V2 receptors in the renal collecting ducts enhances water reabsorption, reducing urine output and helping to maintain fluid balance. Indications: Hemodynamic Support: Vasopressin is used as a vasopressor agent in the management of hypotension, especially in septic shock or other forms of distributive shock. Diabetes Insipidus: In cases of central diabetes insipidus (due to deficient vasopressin secretion), vasopressin or its analogs are used to replace the deficient hormone and reduce polyuria and polydipsia. Gastrointestinal Bleeding: Vasopressin may be used as an adjunctive therapy to control acute variceal bleeding by causing vasoconstriction in the splanchnic circulation. Counterindications: Individuals with a known hypersensitivity to vasopressin or its analogs should avoid its use, and caution should be used in patients with coronary artery disease due to the potential for exacerbating myocardial ischemia. Vasopressin (cont) Adverse effects: Cardiovascular Effects: Hypertension, peripheral ischemia, myocardial ischemia, and arrhythmias may occur due to excessive vasoconstriction. Hyponatremia: Vasopressin-induced water retention can lead to dilutional hyponatremia, especially in patients with impaired renal function. Gastrointestinal Effects: Nausea, vomiting, and abdominal cramps may occur, particularly with higher doses. Allergic Reactions: Hypersensitivity reactions, including anaphylaxis, have been reported with vasopressin administration. Cautions: Used with caution in patients with cardiovascular disease, including hypertension and heart failure (can exacerbate these conditions), in patients with hyponatremia, as vasopressin administration can further decrease serum sodium levels, and dose adjustments may be necessary in patients with renal impairment due to the risk of fluid retention and electrolyte disturbances Drug Interactions Concurrent use of vasopressin with other vasopressor agents, (e.g., such as norepinephrine or epinephrine), may potentiate the hypertensive effects and increase the risk of adverse cardiovascular events, and vasopressin may enhance the renal effects of lithium, potentially leading to lithium toxicity. 4 3/28/2024 Chapter 31: Thyroid and Antithyroid Drugs When you reach the end of this chapter, you will be able to the following: 1. Briefly discuss the normal anatomy and physiology of the thyroid gland. 2. Discuss the various functions of the thyroid gland and related hormones. 3. Describe the differences in the diseases resulting from the hyposecretion and hypersecretion of thyroid gland hormones. 4. Identify the various drugs used to treat the hyposecretion (hypothyroidism) and hypersecretion (hyperthyroidism). 5. Discuss the mechanisms of action, indications, dosages, routes of administration, contraindications, cautions, drug interactions, and adverse effects of the various drugs used to treat hypothyroidism and hyperthyroidism. Key Terms Euthyroid Referring to normal thyroid function. Hyperthyroidism A condition characterized by excessive production of the thyroid hormones. A severe form of this disorder is called thyrotoxicosis. Hypothyroidism A condition characterized by diminished production of the thyroid hormones. Thyroid-stimulating hormone (TSH) An endogenous substance secreted by the pituitary gland that controls the release of thyroid gland hormones and which is necessary for the growth and function of the thyroid gland (also called thyrotropin). Thyroxine (T4) The principle thyroid hormone that influences the metabolic rate. Triiodothyronine (T3) A secondary thyroid hormone that also affects body metabolism. Levothyroxine Levothyroxine is a synthetic form of thyroxine (T4), a thyroid hormone produced by the thyroid gland. It acts as a replacement for deficient or absent endogenous thyroxine Mechanism of Action: Once absorbed, levothyroxine is converted into triiodothyronine (T3) in peripheral tissues, where it exerts its effects by binding to thyroid hormone receptors in the nucleus of target cells. Thyroid hormones regulate metabolism, growth, and development in the body. Indications: Levothyroxine is the primary treatment for hypothyroidism, a condition characterized by insufficient thyroid hormone production. Used as hormone replacement therapy in patients who have undergone thyroidectomy or radioactive iodine therapy for thyroid cancer. May be to shrink goiters associated with hypothyroidism. Sometimes used in thyroid suppression tests to assess the function of the thyroid gland. Counterindications: Levothyroxine is contraindicated in patients with acute myocardial infarction and thyrotoxicosis unless hypothyroidism is also present, and in individuals with a known hypersensitivity to levothyroxine or any of its components should avoid its use. 5 3/28/2024 Levothyroxine (cont) Adverse effects: Adverse cardiovascular effects of levothyroxine may include tachycardia, palpitations, hypertension, and angina, particularly in patients with underlying cardiovascular disease. , tremors, nervousness, and insomnia are among the central nervous system adverse effects associated with levothyroxine. Gastrointestinal adverse effects (diarrhea, vomiting, & abdominal cramps may occur), particularly with excessive doses. Prolonged use at excessive doses may increase the risk of osteoporosis and bone fractures. Excessive doses can lead to symptoms of hyperthyroidism, including weight loss, heat intolerance, and excessive sweating. Cautions: Caution is warranted in patients with a history of cardiovascular disease, as levothyroxine can exacerbate cardiac symptoms. Can affect glucose metabolism and may require adjustments in insulin or oral antidiabetic medication dosages in patients with diabetes mellitus. Levothyroxine should be used cautiously in patients with adrenal insufficiency, as it can precipitate adrenal crisis Elderly patients may be more sensitive to the effects of levothyroxine and may require lower initial doses. Drug Interactions Antacids & calcium supplements may impair the absorption when taken concurrently (should be taken at least four hours apart from these agents; iron supplements may reduce the absorption of levothyroxine; should be taken at least four hours apart from iron supplements: bBile acid sequestrants (Cholestyramine and Colestipol) can decrease the absorption of levothyroxine; may increase the metabolism of warfarin, leading to decreased anticoagulant effects. Propylthiouracil Propylthiouracil (PTU) is an antithyroid medication used in the treatment of hyperthyroidism. Mechanism of Action: The primary mechanism of action involves inhibiting the synthesis of thyroid hormones, thyroxine (T4), and triiodothyronine (T3), by interfering with the enzyme thyroid peroxidase. By blocking the iodination of tyrosine residues and coupling reactions in the thyroid gland, PTU reduces the production of thyroid hormones, thereby lowering their levels in the bloodstream. Indications: Propylthiouracil is used to manage hyperthyroidism, including Graves' disease and toxic nodular goiter. It may also be used in the management of thyrotoxic crisis (thyroid storm), a life-threatening complication of severe hyperthyroidism. Counterindications: Propylthiouracil is contraindicated in individuals with a known hypersensitivity to the medication. PTU should not be used in patients with severe liver impairment due to the risk of hepatic failure. Propylthiouracil (cont) Adverse effects: PTU can rarely cause liver damage, presenting as elevated liver enzymes, hepatitis, or fulminant hepatic failure. Patients should be monitored for signs of liver dysfunction, including jaundice, abdominal pain, and dark urine. There is a risk of agranulocytosis, a severe drop in white blood cell count, with PTU therapy. Patients should be monitored for signs of infection, such as fever and sore throat, and regular blood cell counts should be performed. Skin rash, pruritus, and urticaria are common adverse effects of PTU therapy. Joint and muscle pain may occur as side effects of PTU treatment. Nausea, vomiting, and gastrointestinal upset may occur with PTU use. Cautions: Caution is advised when using PTU in patients with mild to moderate liver dysfunction, as it can rarely cause hepatotoxicity. PTU may be used cautiously during pregnancy, particularly in the first trimester when it is preferred over methimazole due to a lower risk of causing congenital malformations. However, the risks and benefits should be carefully considered, and close monitoring of thyroid function is necessary. PTU is excreted in breast milk, so caution is advised when used in breastfeeding women. Drug Interactions PTU may potentiate the effects of anticoagulants, increasing the risk of bleeding. Close monitoring of coagulation parameters is recommended. Concurrent use of PTU with theophylline may increase theophylline levels, necessitating dose adjustments and monitoring for signs of toxicity. PTU may interfere with the metabolism of warfarin, leading to fluctuations in INR (International Normalized Ratio). 6 3/28/2024 Chapter 33: Adrenal Drugs When you reach the end of this chapter, you will be able to the following: 1. Discuss the normal anatomy, physiology, and related functions of the adrenal glands, including specific hormones released from the glands. 2. Briefly compare the hormones secreted by the adrenal medulla with those secreted by the adrenal cortex. 3. Compare the glucocorticoids and mineralocorticoids with regard to their basic properties, roles in normal physiologic functioning, diseases that alter them, and their use in pharmacotherapy. 4. Contrast Cushing’s syndrome, Addison’s disease, and addisonian crisis. 5. Contrast the mechanisms of action, indications, dosages, routes of administration, cautions, contraindications, drug interactions, and adverse effects of glucocorticoids, mineralocorticoids, and antiadrenal drugs. Key Terms Addison’s disease A chronic disease associated with the hyposecretion of corticosteroids. Adrenal cortex The outer portion of the adrenal gland. Adrenal crisis An acute, life-threatening state of profound adrenocortical insufficiency requiring immediate medical management. It is characterized by glucocorticoid deficiency, a drop in extracellular fluid volume, hyponatremia, and hyperkalemia. Adrenal crisis is also referred to as addisonian crisis. Adrenal medulla The inner portion of the adrenal gland. Aldosterone A mineralocorticoid hormone produced by the adrenal cortex that acts on the renal tubule to regulate sodium and potassium balance in the blood. Cortex The general anatomic term for the outer layers of a body organ or other structure. Corticosteroids Any of the natural or synthetic adrenocortical hormones; those produced by the cortex of the adrenal gland (adrenocorticosteroids). Cushing’s syndrome A metabolic disorder characterized by abnormally increased secretion of the corticosteroids. Key Terms (cont) Epinephrine An endogenous hormone secreted into the bloodstream by the adrenal medulla; also a synthetic drug that is an adrenergic vasoconstrictor and increases cardiac output. Glucocorticoids A major group of corticosteroid hormones that regulate carbohydrate, protein, and lipid metabolism and inhibit the release of adrenocorticotropic hormone (ACTH). Hypothalamic-pituitary-adrenal (HPA) axis A negative feedback system involved in regulating the release of corticotropin-releasing hormone by the hypothalamus, ACTH (corticotropin) by the pituitary gland, and corticosteroids by the adrenal glands. Suppression of the hypothalamic-pituitary-adrenal axis may lead to Addison’s disease and possible adrenal crisis or addisonian crisis. This suppression results from chronic disease or exogenous sources, such as long-term glucocorticoid therapy. Medulla An anatomic term for the most interior portions of an organ or structure. Mineralocorticoids A major group of corticosteroid hormones that regulate electrolyte and water balance; in humans the primary mineralocorticoid is aldosterone. Norepinephrine An adrenergic hormone, secreted by the adrenal medulla, that increases blood pressure by causing vasoconstriction but does not appreciably affect cardiac output; it is the immediate metabolic precursor to epinephrine. 7 3/28/2024 Fludrocortisone Fludrocortisone is a synthetic mineralocorticoid that primarily acts by increasing renal sodium reabsorption and potassium excretion. Mechanism of Action: Exerts its effects by binding to mineralocorticoid receptors in the distal tubules and collecting ducts of the kidneys, promoting sodium retention and water reabsorption. Indications: Primary Adrenocortical Insufficiency (Addison's Disease): Fludrocortisone is often used as replacement therapy in patients with primary adrenocortical insufficiency to restore mineralocorticoid activity. Salt-Wasting Adrenogenital Syndrome: It can be used in the management of salt-wasting adrenogenital syndrome, a rare condition characterized by impaired adrenal steroidogenesis leading to electrolyte imbalances. Counterindications: Individuals with a known hypersensitivity to fludrocortisone or any of its components should avoid its use, and in patients with systemic fungal infections (unless they are already receiving appropriate antifungal therapy). Adverse effects: fludrocortisone (cont) Fludrocortisone can lead to fluid retention, edema, and hypertension due to its mineralocorticoid effects; excessive sodium retention and potassium excretion can result in hypokalemia (which may lead to muscle weakness, cardiac arrhythmias, and other complications); drug-induced sodium retention can contribute to hypertension, particularly in susceptible individuals; may exacerbate glucose intolerance or diabetes mellitus (necessitating careful monitoring of blood glucose levels in diabetic patients); at high doses may increase the risk of osteoporosis and bone fractures; chronic administration can suppress the hypothalamic-pituitary-adrenal (HPA) axis, leading to adrenal insufficiency upon abrupt withdrawal;GI disturbances such as nausea, vomiting, and abdominal pain may occur, and psych issues, especially at higher doses; mood swings, depression, and insomnia, have been reported with corticosteroid therapy, although they are less common with mineralocorticoids like fludrocortisone. Cautions: Used with caution in patients with preexisting cardiovascular disease (may exacerbate hypertension and fluid retention; may be necessary in patients with renal impairment to avoid excessive sodium retention and potassium loss with higher doses; metabolism may be impaired in patients with hepatic dysfunction; corticosteroids, including fludrocortisone, may mask signs of infection or exacerbation of existing infections; should be used with caution in pregnant or breastfeeding women, weighing the potential benefits against the risks to the fetus or infant. Drug Interactions Antihypertensive agents, nonsteroidal anti-inflammatory Drugs (NSAIDs) (on concomitant use of NSAIDs may increase the risk of gastrointestinal bleeding and ulceration): concurrent use of diuretics may exacerbate electrolyte imbalances, particularly hypokalemia; Potassium-sparing diuretics (may potentiate the potassium-sparing effects of other diuretics, increasing the risk of hyperkalemia); estrogen-containing medications may potentiate the mineralocorticoid effects of fludrocortisone, leading to fluid retention and hypertension. Methylprednisolone Methylprednisolone is a synthetic glucocorticoid (class of steroid hormones produced by the adrenal glands that play a crucial role in regulating various physiological processes in the body, including metabolism, immune response, and stress response). Mechanism of Action: Exerts its effects by binding to glucocorticoid receptors present in the cytoplasm of cells. Upon binding, the glucocorticoid-receptor complex translocates into the nucleus and modulates gene transcription (this leads to a wide range of anti-inflammatory, immunosuppressive, and metabolic effects). Indications: Used to manage a variety of inflammatory conditions, including rheumatoid arthritis, asthma exacerbations, inflammatory bowel disease, and dermatologic conditions. Used to treat allergic reactions, such as severe allergic rhinitis or contact dermatitis. Indicated as an immunosuppressive agent in autoimmune disorders such as systemic lupus erythematosus and autoimmune hepatitis. Used in the treatment of acute exacerbations of asthma and as maintenance therapy in chronic asthma. Counterindications: For patients with systemic fungal infections unless they are receiving concurrent appropriate antifungal therapy, and for individuals with a known hypersensitivity to methylprednisolone or any of its components should avoid its use. 8 3/28/2024 Adverse effects: Methylprednisolone (cont) Prolonged use can suppress the natural production of cortisol by the adrenal glands, leading to adrenal insufficiency upon discontinuation. Methylprednisolone can increase susceptibility to infections due to its immunosuppressive effects. Methylprednisolone can exacerbate glucose intolerance and predispose patients to hyperglycemia or diabetes mellitus. Long-term use of methylprednisolone can increase the risk of osteoporosis and bone fractures. Hypertension: Methylprednisolone can cause sodium and water retention, leading to hypertension. Gastrointestinal adverse effects such as gastritis, peptic ulcers, and gastrointestinal bleeding may occur with methylprednisolone use Methylprednisolone can cause psychiatric disturbances, including mood swings, agitation, and insomnia. Cautions: Methylprednisolone should be used cautiously in patients with diabetes mellitus, in patients with a history of cardiovascular disease, infections (can mask signs of infection, making diagnosis and treatment challenging) and us with caution in patients with existing infections, in patients with glaucoma, as it can increase intraocular pressure, and dose adjustments may be necessary in patients with hepatic impairment due to altered pharmacokinetics. Drug Interactions Anticoagulants (can potentiate the effects) and NSAIDs ( increasing risk of bleeding and ulceration), and cyclosporine (may increae blood levels). Additionally, Methylprednisolone can reduce the effectiveness of vaccines and increase the risk of vaccine-related adverse effects. Live vaccines should be avoided during treatment with methylprednisolone. Prednisolone Prednisolone is a synthetic corticosteroid that acts similarly to endogenous glucocorticoids (corticosteroids are a class of steroid hormones that are structurally similar to cortisol, the primary glucocorticoid hormone produced by the adrenal glands). Mechanism of Action: Binds to glucocorticoid receptors, forming a complex that translocates into the nucleus of target cells. This complex modulates gene transcription, resulting in a wide range of anti-inflammatory, immunosuppressive, and metabolic effects. Indications: Used to manage various inflammatory conditions, including rheumatoid arthritis, asthma exacerbations, inflammatory bowel disease, dermatologic conditions, and allergic reactions. Used as an immunosuppressive agent in autoimmune disorders such as systemic lupus erythematosus, autoimmune hepatitis, and vasculitis. Indicated in the treatment of acute exacerbations of asthma and chronic obstructive pulmonary disease (COPD). Often used as part of immunosuppressive regimens in organ transplantation to prevent rejection. Contraindications: Individuals with a known hypersensitivity to prednisolone or any of its components should avoid its use, and prednisolone is contraindicated in patients with systemic fungal infections unless they are receiving concurrent appropriate antifungal therapy. Adverse effects: Prednisone(cont) Prolonged use of prednisolone can suppress the natural production of cortisol by the adrenal glands, leading to adrenal insufficiency upon discontinuation. Prednisolone can increase susceptibility to infections due to its immunosuppressive effects. Prednisolone can exacerbate glucose intolerance and predispose patients to hyperglycemia or diabetes mellitus. Long-term use of prednisolone can increase the risk of osteoporosis and bone fractures. Prednisolone can cause sodium and water retention, leading to hypertension. Gastrointestinal adverse effects such as gastritis, peptic ulcers, and gastrointestinal bleeding may occur with prednisolone use. Prednisolone can cause psychiatric disturbances, including mood swings, agitation, and insomnia. Cautions: should be used cautiously in patients with diabetes mellitus, as it can worsen glucose intolerance; patients with a history of cardiovascular disease (can exacerbate hypertension and heart failure); Corticosteroids can mask signs of infection, making diagnosis and treatment challenging (caution also in patients with existing infections); in patients with glaucoma, as it can increase intraocular pressure; and dose adjustments may be necessary in patients with hepatic impairment due to altered pharmacokinetics Drug Interactions: Prednisolone can potentiate the effects of anticoagulants, increasing the risk of bleeding; concurrent use of prednisolone with NSAIDs may increase the risk of gastrointestinal bleeding and ulceration; may increase blood levels of cyclosporine; can reduce the effectiveness of vaccines and increase the risk of vaccine-related adverse effects. Live vaccines should be avoided during treatment with prednisolone. 9 3/28/2024 Module 4 Quiz Chapter 30 - 33: Review Drugs Profiles octreotide, p. 478 acarbose, p. 505 somatropin, p. 479 glipizide, p. 505 vasopressin, p. 479 liraglutide, p. 507 levothyroxine, p. 485 metformin, p. 505 propylthiouracil, p. 487 pioglitazone, p. 505 fludrocortisone, p. 522 repaglinide, p. 505 methylprednisolone, p. 523 sitagliptin, p. 505 prednisone, p. 522 10