Download Endocrine Assignment Hyperthyroid and Diabetes Mellitus Type I

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
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_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.
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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