Treatment of Thyroid and Diabetes

Diabetes and Thyroid

Diabetes

What is the mechanism of action of insulin and what are the differences in insulin therapy for Type I and Type II diabetes mellitus?

The pancreas secretes insulin, and it is used for the regulation of glucose from the blood into the cells. Insulin assists in lowering blood glucose by causing peripheral glucose uptake by skeletal muscle cells. The breakdown of fat, proteins, and manufacture of glucose is inhibited by insulin. Insulin will also increase protein synthesis and the conversion of excess glucose to fat. Patients suffering from diabetes are not able to produce enough insulin, and this leads to hyperglycemia. Insulin therapy for type I diabetes mellitus is aimed at increasing or providing insulin in the patient's body (Trauner, Richert, & Luddeke, 2013). For type II diabetes, insulin therapy is aimed at controlling blood sugar, increasing insulin levels, and lowering the patient's resistance to insulin. Patients suffering from type I diabetes produce very little insulin or cannot produce insulin. Insulin therapy increases their insulin levels. The insulin dosage will differ and change over time. This is due to many factors like weight, health conditions, activity level, what one eats, and work. Type II diabetes patients will eventually require insulin therapy, but the treatment goals are aimed at lowering their blood sugar levels. Insulin therapy is only used when their bodies become resistant to the produced insulin.

What is an incretin and how is it currently utilized for drug therapy in diabetes mellitus?

An incretin is a hormone that works to increase the secretion of insulin in a person's body. According to Kahn (2013) incretins are gastrointestinal hormones that cause a decrease in levels of blood glucose. It is believed that glucose in the digestive tract leads to feed forward mechanism that increases the secretion of insulin. This is done in anticipation of the rise in blood glucose levels that mostly occur after absorption of ingested carbohydrates. Incretin hormones include glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1. The use of incretin as a drug therapy for diabetes mellitus may provide a therapeutic solution. Glucagon-like peptide-1 (GLP-1) is a viable candidate for the management of type 2 diabetes mellitus. Stimulation of GLP-1 receptors is the best way to maintain high levels of GLP-1 in the patient. The receptors are stimulated by administration of GLP-1 agonists. Stimulating the receptors allows for the production of insulin in the body and the cells that destroy the insulin are hindered.

Metformin is a biguanide used for Type II diabetes mellitus. What is the mechanism of action? What are the indications and contraindications? Why does metformin not cause hypoglycemia? What is a potentially deadly adverse effect of biguanide therapy and how can this be avoided?

Metformin is an oral drug used as a first-line drug of choice for treating type 2 diabetes. The drug metformin prevents the liver from producing glucose, it improves the body's sensitivity to insulin, and reduces the quantity of sugar the intestines absorb. Metformin is used for treating a patient with type II diabetes. It lowers body weight, and does not cause hypoglycemia. For obese patients, it is recommended as a single drug therapy. Metformin is contraindicated for patients suffering from renal disease or anal dysfunction. Liver cirrhosis, hepatitis, alcoholism, and advanced cardiovascular disease. Metformin does not cause hypoglycemia because it diverts the glucose found in the gut wall to lactate using the anaerobic glycolysis pathway. Lactic acidosis is a deadly side effect of biguanide therapy. This condition occurs when there is inadequate clearance of lactic acid in the blood. This can be avoided by withdrawing the medication causing the condition.

Sulfonylureas are some of the first oral drugs used for Type II diabetes. Currently, the second generation of these drugs are preferred over the older ones. What is the mechanism of action of sulfonylureas? What are the side effects and precautions? Can these drugs be used with other classes of oral agents?

Sulfonylureas mechanism of action is causing the production of insulin from pancreatic beta cells that are still functioning. This assists in lowering blood glucose levels. Sulfonylureas also sensitize the beta cells to glucose, which assists in limiting glucose production in the liver. There is a possibility of sulfonylureas inducing hypoglycemia due to excess insulin release and production. They can also induce weight gain due to the increase in levels of insulin. Headache, abdominal upset, and hypersensitivity reaction are other side effects. Sulfonylureas should not be used during pregnancy or patients who are likely to get pregnant because they are potentially teratogenic. Sulfonylureas can be used safely with other oral drugs like metformin or glitazones.

Thyroid

Summarize the biosynthesis of the thyroid hormones

Biosynthesis of the thyroid hormones begins with the thyroid gland trapping iodine, which is essential for forming thyroid hormones. Iodine is found in soil and is contained in many foods. The gastrointestinal tract absorbs the iodine anion rapidly, and this is taken up by the thyroid gland. There is a specialized co transporter located at the basolateral membrane of the thyroid follicular cell. The cotransporter moves iodine anions in the follicular cell. There are other anions that might compete with the iodine anion for uptake by the thyroid. Iodine will leave the follicular cells and enter the follicle lumen across the apical membrane. Pendrin found on the apical membrane contributes to iodine anion secretion. As iodine anions are secreted into the follicle lumen, thyroglobulin is secreted by the follicular cells in the lumen. The thyroid hormones remain inactive while in the follicular lumen until they are hydrolyzed. Hydrolyzation results in the formation of T4 and T3 hormones.

What are the different roles of T3 and T4?

T3 is the most active and usable form of thyroid hormone. T3 is produced in tiny amounts based on what is needed, T4 is converted to T3 by the body when it needs T3 (Reinehr, 2010). The functions of the two hormones are similar, but they have differing roles. T4 is mainly used to regulate the heart's rhythm. An absence of T4 would lead to heart failure even if the person has a perfect heart. The main function of T3 is regulation of kidney rhythm. A person with a deficiency of T3 will manifest this symptoms bloating, loose bowels, fluid retention, colitis, weight gain, gas, and swelling of legs and ankles. The failure of the kidneys to filter blood properly, and flush out wastes and fluids leads to these symptoms.

How does the presentation of thyroid hyperfunction differ from hypofunction?