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Endocrine Assignment Hyperthyroid and Diabetes Mellitus Type I versus Type II By: Kristy, Marla, Meg and Carol (Group D) The thyroid gland is located in the neck, just below the larynx. It is responsible for producing hormones to regulate metabolic rates throughout the body (Huether, 2006). Thyroid Hormones (De Groot, 2008; Wikipedia, 2008) Secreted hormone Triiodthyronine (T3) Area where hormone is produced Thyroid Epithelial cell Hormone action Thyroxine (Tetraiodothyronine) (T4) Thyroid Epithelial cell Calcitonin Parafollicular Cell Very strong hormone Increases the basal metabolic rate and sensitivity to catecholamines. Affects protein synthesis Weaker hormone Increases the basal metabolic rate and sensitivity to catecholamines. Affects protein synthesis and often functions as a prohormone Construct bone Reduce blood Calcium Hyperthyroid is a condition where there is an elevated level of thyroid hormone (TH) within the body. There are basically two types of hyperthyroidism; primary hyperthyroidism and secondary hyperthyroidism. Primary hyperthyroidism is the most common. This is where the thyroid gland secrets more thyroxine (T4), triiodothyronine (T3) and calcitonin then what is needed by the body. Diseases like Graves’ disease, toxic multinodular goiter, solitary hyperfunctioning and follicullar thyroid carcinoma are considered primary hyperthyroid diseases. Secondary hyperthyroidism is a rare condition where the pituitary gland secrets increased amounts of TSH (thyroid stimulating hormone) because of pituitary adenomas. The increased circulating levels of thyroid hormone results in an increase in body metabolism, heat intolerance, and increased tissue sensitivity to sympathetic stimulation. (Jones & Huether, 2006). Discussion Question: What would you see for signs and symptoms of hyperthyroid? Most signs and symptoms are the same for all hyperthyroidisms; except infiltrative ophthalmopathy and dermopathy, which only occur in Graves disease (Merck Manual Professional, 2005). The signs and symptoms include the following, many of which are similar to those of adrenergic excess; such as nervousness, anxiety, irritability, tremors, palpitations, tachycardia, widened pulse pressure, hyperactivity, increased sweating with warm, moist skin, heat intolerance, fatigue, increased appetite, atrial fibrillation, weight loss, insomnia, muscle weakness, and frequent bowel movements (may or may not be diarrhea). Hypomenorrhea may also be present (Merck Manual Professional, 2005). Sudden weight loss due to an increased catabolism, the body is unable to meet metabolic needs (Jones & Huether, 2006). Tachycardia, irregular heartbeat, increased cardiac output and/or palpitations due to hypermetabolism and increased sensitivity to sympathetic stimulation (De Groot, 2008; Jones & Huether, 2006; Merck Manual Professional, 2005). It has been suggested that the changes in the cardiovascular system are secondary to increased demand for metabolites and to increased heat production. Dilatation of superficial capillaries for the dissipation of heat does cause increased blood flow and cardiac output. However, a direct action of thyroid hormone on the heart is also increased, since the sinus node has higher intrinsic activity. The isolated thyrotoxic heart beats faster than normal, and isolated papillary muscle from a thyrotoxic heart has a shortened contraction time. The heart shares in the general increase in respiratory quotient found in skeletal muscle. (De Groot, 2008; Merck Manual Professional, 2005). Hyperthyroidism is also associated with atrial fibrillation (Cappola, et al., 2006) Fatigue and muscle weakness due to sleep disturbances, increased metabolism, and energy expenditure resulting in feelings of exhaustion (Shoman, 2008). Dyspnea and decreased vital capacity due to weakness of respiratory muscles (Jones & Huether, 2006). Nervousness, anxiety, irritability, hand tremors, and insomnia possibly related to alterations in cerebral metabolism although this mechanism is not clearly understood (Jones & Huether, 2006). Changes in menstrual patterns, such as light or absent menstrual periods due to an increase in sex hormone-binding globulin or hypothalamic or pituitary alterations (Jones & Huether, 2006). Heat intolerance, sweating & increased sensitivity to heat due to the hyperdynamic circulatory state (Mayo Clinic, 2006). Changes in bowel patterns - frequent and less formed stools, nausea and abdominal pain due to increased glucose absorption, increase in cholesterol excretion in feces, and conversion of cholesterol to bile salts (Jones & Huether, 2006). Fecal and urinary calcium excretion is greatly augmented; rate of absorption from the gastrointestinal tract is accelerated. Increased frequency of normal bowel movements is common, and occasionally diarrhea occurs. Transit time is decreased, and fat absorption may be impaired to the point of steatorrhea if fat intake is excessive. (De Groot, 2008; Merck Manual Professional, 2005). Goiter - Hypertrophy of the thyroid gland due to increased activity of thyroid gland (Jones & Huether, 2006). Bruits over thyroid due to hyperactivity of thyroid gland (Jones & Huether, 2006). Hair loss and nails growing away from nail beds due to hyperdynamic circulatory state (Jones & Huether, 2006). Exophthalmous - Large and protruding eyes leading to decreased blinking due to overactivity of Muller muscle (Bermant, 2008; Jones & Huether, 2006). Ophthalmopathy - Infiltrative ocular changes due to inflammation of retro-orbital contents (Jones & Huether, 2006). Red, swollen skin with the texture of orange peels, usually on the shins and tops of the feet (Dermopathy) (De Groot, 2008; Merck Manual Professional, 2005). Discussion Question: Why do people "get" Type 1 vs. Type 2 diabetes mellitus? Type 1 Diabetes In type 1 diabetes there is wasting (atrophy) of the islet cells of the pancreas. As these are the cells responsible for insulin production, the result is either no insulin being produced at all or a severe deficiency of insulin production. Macrophages, T and B lymphocytes, and natural killer cells that are associated with protecting us from foreign invaders, are often present in type 1 diabetes. Stress, environmental factors, and genetics are thought to be contributing factors to the development of type 1 diabetes (Jones & Huether, 2006). Type 1 diabetes is not preventable (Canadian Diabetes Association, n.d.). There are two subsets of Type 1 Diabetes: immune & non-immune. In immune diabetes there is cell-mediated destruction of the pancreatic beta cells. This form of diabetes is thought to result from genetic-environmental factors. Between 10 and 13% of those with this type of diabetes have a parent or sibling with type 1 diabetes. For this kind of diabetes, the age at diagnosis peaks at about age 12 years (Jones & Huether, 2006). Autoantibodies against insulin (IAAs) are often found in these individuals. It is thought that these may be produced during the destruction of the islet and beta cells and that most likely this is due to an autoimmune process (Jones & Huether, 2006). Non-immune diabetes occurs as a result of another disease such as pancreatitis or in other cases it may be called idiopathic meaning that the cause is unknown. Idiopathic is also referred to as type 1B, type 1 diabetes and autoimmune type 1 diabetes is referred to as type 1A diabetes. (Jones & Huether, 2006). The key treatment for type 1 diabetes is insulin. Although usually given by injection, insulin by inhalation has also been used (CNN, 1999). More recently there has been success with islet cell transplants in treating type 1 diabetics whom meet specific criteria. Type 2 Diabetes Diabetes is the most common chronic disease in children. Type 2 diabetes is more common than type 1. For both children and adults, approximately one case is undiagnosed for each diagnosed case (Jones & Huether, 2006). The main abnormalities in the common forms of type 2 diabetes are decreased insulin secretion by beta cells and insulin resistance. With insulin resistance the body is unable to utilize insulin for glucose and lipid metabolism (Medical News Today, 2004). Obesity and once again genetics play a role in the development of type 2 diabetes. Included in type 2 diabetes are maturity-onset diabetes of youth (MODY) and gestational diabetes mellitus (GDM). (Jones & Huetehr, 2006). As Mrs. T has type 2 diabetes, her body’s ability to regulate blood sugar levels is not working correctly. Studies show that 80-90% of the people who are overweight (considered obese) develop type 2 diabetes (The Merck Manual Online Library, 2007). Type 2 diabetes is referred to as a progressive disease. Some people will require insulin to manage their disease in later stages (Canadian Diabetes Association, n.d.), some are able to control their diabetes through diet and exercise, and some require a little help from other antiglycemic medications. Mrs. T has some options for controlling her type 2 diabetes. References: Bermant, M. (2008). Eyelid Muscle Function and Anatomy Levator, Muller's, and Frontalis Muscles and Ptosis. Retrieved June 2, 2008 from http://www.plasticsurgery4u.com/procedure_folder/eyelid_recon_folder/eyelid_muscle _function.html Cable News Network. (1999, May, 1). Insulin inhaler may replace injections. Retrieved June 2, 2008 from http://www.cnn.com/HEALTH/9905/07/oral.insulin/ Canadian Diabetes Association. (n.d.) Insulin - Things you should know. Retrieved June 2, 2008 from http://www.diabetes.ca/Section_About/insulin.asp Canadian Diabetes Association. (n.d.). Type 1 diabetes: The basics. Retrieved June,2 2008 from http://www.diabetes.ca/Section_About/type1.asp Cappola, A. R., Fried, L. P., Arnold, A. M., Danese, M. D., Kuller, L. H., Burke, G. L., Tracy, R. P., & Ladenson, P. W. (2006). Thyroid status, cardiovascular risk, and mortality in older adults. The Journal of the American Medical Association, 295(9), 1033-41. De Groot, L. L. (2008). Graves' Disease and Manifestations of Thyrotoxicosis. Retrieved June 1, 2008 from http://www.thyroidmanager.org/chapter10/10-frame.htm Heuther, S. E. (2006). Mechanisms of hormonal regulation. In K. L. McCance & S. E. Huether (Eds.), Pathophysiology: The biologic basis for disease in adults and children (5th ed., pp. 655-680). St. Louis, MI: Elsevier Mosby. Jones, R. & Huether, S. (2006). Alterations of hormonal regulation. In K. L. McCance & S. E. Huether (Eds.), Pathophysiology: The biologic basis for disease in adults and children (5th ed., pp. 692-710). St. Louis, MI: Elsevier Mosby. Mayo Clinic. (2006). Hyperthyroidism (overactive thyroid gland). Retrieved May 19, 2008 from http://www.mayoclinic.com/health/hyperthyroidism/DS00344/DSECTION=2 Medical News Today. (2004, April, 21). What is the difference between type 1 and type 2 diabetes? Retrieved June 2, 2008 from http://www.medicalnewstoday.com/articles/7504.php Merck Manual Professional. (2005). Hyperthyroidism: Thyroid Disorders. Retrieved June 1, 2008 from http://www.merck.com/mmpe/sec12/ch152/ch152e.html The Merck Manual Online Library. (2007). Diabetes. Retrieved June 2, 2008 from http://www.merck.com/mmhe/sec13/ch165/ch165a.html?qt=diabets&alt=sh Shoman, M. (2008). Fatigue and exhaustion solutions: How to deal with tiredness related to hypothyroidism and hyperthyroidism. Retrieved June 2, 2008 from Thyroid-Info at http://www.thyroid-info.com/articles/tiredhelp.htm Wikipedia. (2008). Thyroid. Accessed June 1, 2008 from http://en.wikipedia.org/wiki/Thyroid_gland