Essay On Hyperthyroidism
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Mechanism of action for propylthiouracil
Propylthiouracil is used to treat hyperthyroidism. It is applied taken orally, and it is used to reduce the overreaction of the thyroid glands. The mechanism of action for Propylthiouracil is similar to methimazole. The major cause of hyperthyroidism is Grave’s disease. Thyroid glands secretes two hormones, triiodothyronine (T3) and thyroxide (T4). Overproduction of these hormones leads to the hyperthyroidism condition. These hormones are formed by the combination of protein thyroglobulin and iodine, which are activated by the enzyme peroxidase. Propylthiouracil (PTU) inhibits the enzyme peroxidase and iodine from interacting. Thus, it prevents the formation of hormones T3 and T4 (Briggs, Freeman & Yaffe, 2011).
Pharmacological effects of Propylthiouracil
Propylthiouracil increases the effects of oral blood thinners such as warfarin. Thus, if there should be changes in the warfarin dosage for patients prescribed propylthiouracil. Moreover, if the patient carries on with the warfarin dosage, there should be close monitoring of the patient. Further, PTU reduces the role of beta-blockers. Hyperthyroidism leads to the reduction of beta-blockers. Thus, PTU retains the hyperthyroidism condition and the production of beta-blockers returns to normal (Braverman, Cooper, Werner & Ingbar, 2013).
Place in Therapy
Propylthiouracil is recommended for patients with Grave’s disease, toxic multinodular goiter and hyperthyroidism. However, these patients should either be intolerant to methimazole or patients who cannot get radioactive iodine therapy and surgery (Briggs, Freeman & Yaffe, 2011).
Nevertheless, the drug is prohibited to any patient who has hypersensitivity towards the drug or any of its components. This is because the drug can easily lead to liver toxicity, agranulocytosis and hypothyroidism (Braverman, Cooper, Werner & Ingbar, 2013).
Mechanisms of action for methimazole
Methimazole is also used to treat Grave’s hyperthyroisim. The mode of action for methimazole is quite similar to that of PTU. Methimazole mainly prevents the synthesis of the thyroid hormone produced by the thyroid gland. Further, methimazole also has immunomodulatory and antioxidant effects on immune cells or thyrocytes. The drug cures Grave’s hyperthyroidism by decreasing antithyroid antibodies titers. The drug is not protein bound. Thus, the distribution of the drug is minimal since it is actively concentrated in the thyroid glands. Methimazole is iodinated once in the body, and degraded in the thyroid gland. The circulation of methimazole is excreted renally, after being metabolized in the liver (Farrell, & Golan, 2008).
Pharmacological effects of methimazole
Methimazole can cause various side effects such as anorexia, lethargy and vomiting. Further, methimazole is not advisable for patients with hypertensive reaction towards the drug. The drug can cause hives, swollen, throat, tongue and face in an allergic reaction. Moreover, methimazole increases the risk of bleeding. Therefore, patients who have been on methimazole therapy should not go on surgery while still on prescription (Farrell & Golan, 2008).
Place in therapy
Methimazole is preffered to PTU because it has less severe consequences. Long-term methimazole therapy is better than surgery because it reduces the level of complications brought about by surgery. For instance, hyperthyroidism surgery can lead to postsurgical hypoparathyroidism and hypothryroidism (Antony, 2012).
Mechanisms of action for Iodide
Iodide is used together with sodium (sodium iodide) to treat thyroid carcinomas and hyperthyroidism. The mechanism of action for this drug mainly entails reducing the uptake of iodide. The reduction in the uptake of iodine reduces the production of thyroid hormones by the thyroid gland (Antony, 2012).
Pharmacological effects of iodide
Iodide has side effects such as vomiting and diarrhea. Further, iodide should not be prescribed to patients who are pregnant or breastfeeding. Consequently, the use of iodide to treat hyperthyroidism is limited to thyroid malignancies that depend on iodide uptake. Further, the use of this therapy can cause thyroiditis and enlargement of the thyroid gland. Therefore, there should be beta-blocker therapy before prescription of sodium iodide. Iodide should not be used on patients with hypersensitivity towards the drug (Heymann, 2008).
Place in therapy
Iodide is used to treat hyperthyroidism and thyroid carcinoma. Iodide therapy should be prescribed on patients after a clinical assessment. The clinical assessment should evaluate the patients history, laboratory tests and physical assessments on the patient. This is done in order to assess if there are any barriers to thyroid iodine uptake or conditions that may alter the effectiveness of the drug (Heymann, 2008).
Mechanisms of action for Radio Active Iodine
Radioactive iodine is available in tablets. The drug works by destroying tissues in the thyroid gland through radioactivity. It can act by destroying part or the whole thyroid gland. This depends on the aim of the therapy. The drug only affects thyroid gland cells. Therefore, the radiation does not risk other parts of the body. Patients undergoing this therapy are advised to drinks a lot of fluids to ease release of the radioactive iodine through urine (Frandsen, Pennington & Abrams, 2014).
Pharmacological effects of Radioactive Iodine
The use of radioactive iodine therapy can lead to hypothyroidism. This is mainly because the therapy kills excessive amount of thyroid cells. Thus, this leads to the body producing sustainable thyroid hormones (Antony, 2012).
Further, the therapy can lead to nausea and swollen salivary glands. Consequently, some patients complain of metallic taste. Further, the therapy is not advisable for pregnant women or women who are preparing to get pregnant (Antony, 2012).
Place in Therapy
Radioactive iodine is mainly used to treat hyperthyroidism. Approximately 90 percent of patients who take this treatment require only a single dose to cure their hyperthyroidism. however, the effects of the treatment are felt after a month (Frandsen, Pennington & Abrams, 2014).
Briggs, G. G., Freeman, R. K., & Yaffe, S. J. (2011). Drugs in pregnancy and lactation: A reference guide to fetal and neonatal risk. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins.
Braverman, L. E., Cooper, D. S., Werner, S. C., & Ingbar, S. H. (2013). Werner & Ingbar's the thyroid: A fundamental and clinical text. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins Health.
Farrell, S. E., & Golan, D. E. (2008). Principles of pharmacology. Philadelphia: Wolters Kluwer Health/ Lippincott Williams & Wilkins.
Anthony, P. K. (2012). Pharmacology secrets. Philadelphia, Pa: Hanley & Belfus.
Heymann, W. R. (2008). Thyroid disorders with cutaneous manifestations. London: Springer.
Frandsen, G., Pennington, S. S., & Abrams, A. C. (2014). Abrams' clinical drug therapy: Rationales for nursing practice. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins.