Thyrotoxicosis are the clinical, physiologic and biochemical syndromes that result when tissues are exposed to, and respond to high levels of thyroid hormone. In most instances, thyrotoxicosis is due to hyperactivity of thyroid gland, or hyperthyroidism (hypermetabolism). Occasionally, thyrotoxicosis may be due to other causes such as excessive ingestion of thyroid hormone or secretion form ectopic sites. There are various forms of thyrotoxicosis and the most common is Graves' Disease.
Graves' disease, also known as Parry's or Basedow's disease or diffuse toxic goiter, is a disorder with three major manifestations: hyperthyroidism with diffuse goiter, ophthalmopathy, and dermopathy. They do not appear together. Indeed, one or two need never appear, and moreover, the three may run courses that are largely independent of one another.
It is the most common form of thyrotoxicosis. It affects as many as 1.9 per cent of the female population. The ratio of women to men is as high as 7:1. It reaches its peak incidence between the third and forth decades and the reason for the female predominance in this as in all thyroid diseases is unknown. Genetic factors play an important role, since there is an increased frequency haplotypes HLA-B8 and -DRw3 in Caucasian, HLA-Bw36 in Japanese, and HLA-Bw46 in Chinese patients with the disease.
Graves' disease is currently viewed as an autoimmune disease of unknown cause. Hyperthyroidism is its principal manifestation, yet TSH is suppressed and no intrinsic abnormalities in the gland have been identified.
In Graves' disease, T lymphocytes become sensitized to antigens within the thyroid gland and stimulate B lymphocytes to synthesize antibodies to these antigens. One such antibody is directed against the TSH receptor site in the thyroid cell membrane and has the capacity to stimulate the thyroid cell to increased growth and function.
The presence of these antibodies is positively correlated with active disease and with relapse of the disease. There is an underlying genetic predisposition, but it is nor clear what "triggers" the acute episodes. Some factors that may incite the immune response: pregnancy, particularly the postpartum period; iodine excess, particularly in areas of iodine deficiency; lithium therapy; viral or bacterial infections; glucocorticoid withdraw.
The etiology and pathogenesis of Graves' ophthalmopathy is not known. It may involve cytotoxic lymphocytes and cytotoxic antibodies sensitized to a common antigen in orbital fibroblasts, orbital muscle, and thyroid tissue, which would cause inflammation, resulting in proptosis of the globes. The pathogenesis of dermopathy may also involve this mechanism. Patients with exophthalmos and particularly those with dermopathy almost always have high titers of circulating TSH receptor antibodies, suggesting that these two clinical manifestations represent the most severe form of this disease.
Many symptoms of thyrotoxicosis suggest a state of catecholamine excess, but circulating levels of epinephrine are normal; thus, in Graves' disease, the body appears to be hyperactive to catecholamines and this may be due in part to a thyroid hormone-mediated increase in cardiac catecholamine receptors.
The thyroid gland id diffused enlarged, hypercellular, soft and vascular. There is a parenchymatous hypertrophy and hyperplasia. Usually there is little or no colloid present with lymphocytic infiltration and in some cases it is impossible to distinguish the microscopic picture from Hashimoto's thyroiditis. The disease is associated with generalized lymphoid hyperplasia and infiltration and occasionally with enlargement of the spleen and thymus. There may be degeneration of skeletal muscle fibers, enlargement of the heart, fatty infiltration or diffuse fibrosis of the liver, decalcification o the skeleton, and loss of body tissue.
The ophthalmopathy is characterized by and inflammatory infiltrate of the orbital contents. The dermopathy is characterized by thickening of the dermis, which is infiltrated with lymphocytes and with hydrophilic, metachromatically staining mucopolysaccarides.
The common clinical manifestations of hyperthyroidism are: palpitations, nervousness, easy fatigability, hyperkinesia, tremors, diarrhea, excessive sweating, intolerance to heat, preference for cold. There is often marked weight loss without loss of appetite. Proximal muscle weakness and loss of muscle mass may be so severe that the patient cannot rise from a chair without assistance. The patients often speaks very rapidly. The thyroid gland is diffused enlarged, and may be asymmetric or lobular. There may be a bruit over the thyroid that signifies that the patient is thyrotoxic. The patient often doesn't note the neck swelling and comes to the doctor because of the other signs and symptoms.
The eye signs of Graves' disease may be divided in two components: the spastic and the mechanical. The former includes the stare, lid lag, and lid retraction and accounts for the "frightened" facies. The mechanical component consists of proptosis of varying degree with ophthalmoplegia and congestive oculopathy characterized by chemosis, conjunctivitis, periorbital swelling, and the potential complications of corneal ulceration, optic neuritis, and optic atrophy. Exophthalmos(photo) may be unilateral early but usually progresses to bilateral involvement.
The dermopathy consists of thickening of the skin(photo), particularly over the lower tibia. It is relatively rare and is usually associated with ophthalmopathy. The skin cannot be picked between the fingers. Body involvement, with subperiosteal bone formation and swelling is particularly evident in the metacarpal bones, but this is also rare. Amore common finding is separation of the fingernails from their beds, or onycholysis(photo).
Part 2 will consist of the clinical management of the patient with Graves' disease, including laboratory diagnosis, differential diagnosis, treatment and prognosis.
References
1 - Greenspan, FS in Greenspan, Basic and Clinical Endocrinology, 4th Edition
2 - Larsen, PR in Wyngaarden, Cecil Textbook of Medicine, 19th Edition
3 - Wartofsky, L in Isselbacher, Harrison's Principles of Internal Medicine, 13th Edition
4 - Dayan, CM, Chronic Autoimmune thyroiditis, NEJM Volume 335, number 2, 99-105
5 - Adlin, EV in NMS Medicine, 3rd Edition
Table Of Contents:
Alternative names
Definition
Causes, incidence, and risk factors
Prevention
Symptoms
Signs and tests
Treatment
Expectations (prognosis)
Complications
Calling your health care provider
Alternative names:
Definition:
Causes, incidence, and risk factors:
Prevention:
Symptoms:
Signs and tests:
Treatment:
Expectations (prognosis):
Complications:
Calling your health care provider:
What is Hyperthyroidism?
hyperthyroidism makes the body speed up. It occurs when there is too much thyroid hormone in the
blood ("hyper" means "too much"). Nearly 10 times more frequent in women, it affects about 2%
of all women in the United States.
THE THYROID CENTER There are several symptoms associated with hyperthyroidism. These include:
Diagnosis
A comprehensive history and physical examination should be performed by a physician with
particular attention to:
In addition to the examination, screening tests are often performed. Most types of hyperthyroidism
result in a below average Thyroid Stimulating Hormone (TSH) blood level. The recent
development of sensitive TSH is the single best screening test for hyperthyroidism. Other tests may
include:
Radioactive Iodine
Radioactive iodine is presently the treatment of choice for Graves' disease in the United States. This
treatment involves the ingestion of a radioactive iodine tablet which is then taken up by thyroid cells.
These overactive cells are damaged so that the thyroid can shrink in size and produce hormone at
normal levels.
There has been no effect on fertility, no increased incidence of congenital malformations, and no
increase in the risk of cancer in patients treated with radioactive iodine or in their offspring.
Radioactive iodine is not used during pregnancy because it may destroy the thyroid in the
developing fetus. Therefore, pregnancy should be postponed until about six months after
radioiodine therapy. In addition, radioactive iodine therapy should be deferred in women who are
breastfeeding because it appears in the milk.
Although it is safe treatment, most people become hypothyroid after radioactive iodine therapy and
therefore require lifelong thyroid hormone replacement therapy.
Antithyroid Drugs
The antithyroid drugs such as methimizole (Tapazole®) and propylthiouracil (PTU) may be
prescribed to suppress the production and release of thyroid hormones or to block thyroid hormone
activity throughout the body by inhibiting the use of iodine by the thyroid. These drugs are most
effective on patients with mild disease and small goiters. Disadvantages to antithyroid drugs
include:
While it was once a common treatment for Graves' disease in the past, thyroidectomy (thyroid
removal) is now uncommonly performed in the United States. If surgery is elected for a patient with
a toxic nodule, the surgeon removes the part of the thyroid which is dysfunctional and the thyroid
remnant usually resumes normal function. However, if the entire thyroid is over productive, as in
Graves' disease, the surgeon must remove most or all of the gland. In such cases, the patient must
then take thyroid hormone replacement pills for the rest of his or her life. Candidates for surgery
may include:
Occasionally drugs such as propanolol (Inderal®), atenolol (Tenormin®), metoprolol (Lopressor®),
nalodol (Corgard®) and Inderal-LA®(known as beta adrenergic blocking agents) are perscribed to
block the action of thyroid hormone on the heart. Although they do not reduce the hormone levels in
the blood, these drugs usually provide relief within hours. Unless the hyperthyroidism is caused by
thyroiditis, these drugs are used in conjunction with other treatments.
Graves' disease is an autoimmune disorder. It is caused by an abnormal protein, called thyroid
stimulating antibody. This antibody stimulates the thyroid gland to produce large amounts of thyroid
hormone in an uncontrolled manner. In normal people, the production of thyroid stimulating
antibody (and other abnormal antibodies) is prevented by a surveillance system. This system consists
of certain blood cells called suppressor and helper lymphocytes and Killer (K) cells, as well as other
constituents. The suppressor lymphocytes suppress unwanted lymphocytes.
Measurement of the thyroid stimulating antibody present in the blood of most patients with Graves'
disease is not usually necessary, in order to establish the diagnosis.
The symptoms and signs of Graves' hyperthyroidism are due to the effects of excess amounts of
thyroid hormone on body function and metabolism. Common symptoms include weight loss,
nervousness, irritability, intolerance to hot weather, excessive sweating, shakiness, and muscle
weakness. Other signs include a rapid pulse, loss of body fat and muscle bulk, thyroid enlargement
(goitre), fine tremors of the fingers and hot, moist, velvety skin.
About 50% of patients also have significant eye signs (Ophthalmopathy). The eyes, which bulge
from their sockets are red and watery and the lids are swollen. Quite often the eyes do not move
normally because the swollen eye muscles are unable to work precisely. The remaining 50% of
patients with Graves' hyperthyroidism may have slightly bulging eyes because of spasm of the
muscle of the lids, giving them a staring appearance.
Thyroid hormones have a wide variety of effects on the body and the symptoms and signs reflect
these. In simple terms, all the metabolic processes are "speeded up"; for example, the pulse rate is
rapid (over 100), bowel function is increased (diarrhea), and the sweat glands work excessively.
The nervous system is also stimulated so that the patient becomes irritable and nervous. Despite
increased appetite, the patient usually loses weight because food intake cannot keep up with the
increased breakdown of body proteins. The end result is a thin, hot, nervous patient with "poppy"
eyes and a goitre - a classical clinical situation quickly recognized by any medical practitioner who
has previously seen such a patient.
Because Graves' hyperthyroidism is caused by a genetically determined abnormality of the immune
system, the problem is complex and there is at present no specific treatment for the underlying
abnormality. Since the end result of this problem is an overstimulation of thyroid function, treatment
of the symptoms is quite easy - one can either surgically remove part of the thyroid gland
(thyroidectomy), destroy the thyroid cells with radioactive iodine, or block thyroid hormone
production with antithyroid drugs.
Although radioactive iodine is by far the simplest and most convenient treatment, its use in younger
adults and children has previously been a matter of concern because of the possible harmful effects
of radiation. Radioactive iodine has been used for over 40 years and there is no good evidence of
any harmful effects. Most thyroid specialists would recommend its use in all patients with Graves'
disease over the age of 20-25; some would use it in children as well.
Radioactive iodine is usually given in the form of a capsule. The dose is calculated from the size of
the goitre by performing a "Thyroid Uptake Test." Because radioactive iodine takes several weeks
to take its full effect, antithyroid tablets are also sometimes given until such time as the full effect
occurs.
Antithyroid drugs (of which Propylthiouracil and Methimazole are the only ones available in
Canada) are almost mandatory in children and adults under the age of 20-25. It may also be used at
any age so as to bring about remissions, or prior to ablation therapy. There are two main drawbacks
with this type of treatment:
In addition a very small percentage suffer side effects. Eventually, most patients require treatment
with either radioactive iodine or thyroidectomy. Another tablet that can be given to treat the
symptoms of hyperthyroidism is Propranolol. This drug blocks the effects of excess thyroid
hormones on the heart, blood vessels, and nervous system, but has no direct effect on the thyroid
gland.
Surgery is usually recommended for the 80% of patients under the age 20 who have a recurrence of
hyperthyroidism after antithyroid drugs. Thyroidectomy is also recommended for patients of any age
in whom the goitre is so big that it causes blockage of the windpipe (trachea) or food passage
(esophagus). In England and Europe, thyroidectomy is performed for Graves' disease much more
often than in Canada, largely because of experience and tradition. Thyroidectomy requires
admission to hospital for about 5 days and removal (by an experienced surgeon) of all but a small
portion of the gland.
After treatment with radioactive iodine or thyroidectomy, it is hoped that enough of the thyroid
gland remains to function normally. Occasionally, the gland becomes overactive again since the
abnormal stimulating antibody is still being produced by the lymphocytes. In other patients, there is
a strong tendency for the remaining thyroid gland to become underactive (hypothyroidism) - perhaps
80% of all patients with Graves' disease will eventually require lifelong thyroid hormone
replacement therapy. This is not considered a problem as long as the hypothyroidism is recognized
and treated. It is much more of a problem for patients to have a recurrence of hyperthyroidism
because of failure to remove enough gland or if too small dose of radioactive iodine is given. Indeed,
some specialists deliberately destroy the thyroid in order to prevent a recurrence of the
hyperthyroidism, and immediately treat with thyroid hormone in anticipation of hypothyroidism.
In Canada, Graves' disease accounts for at least 90% of all patients with hyperthyroidism.
Hyperthyroidism can also occur in older patients with long-standing nodular goitres.
Other uncommon causes of hyperthyroidism in Canada are painful (subacute) thyroiditis caused by
a viral infection of the thyroid gland in which the hyperthyroidism is due to leakage of thyroid
hormones from the swollen, damaged gland and "silent" thyroiditis, a similar condition but without
the painful swelling of the thyroid. Production of the printed version of this Health Guide was made possible through partial funding
assistance from Health Canada. The views expressed herein are solely those of the authors and do
not necessarily represent the official policy of Health Canada.Original published 1983. Revised November 1993. Graves' disease is an autoimmune disorder. It is caused by an abnormal protein, called thyroid
stimulating antibody. This antibody stimulates the thyroid gland to produce large amounts of thyroid
hormone in an uncontrolled manner. In normal people, the production of thyroid stimulating
antibody (and other abnormal antibodies) is prevented by a surveillance system. This system consists
of certain blood cells called suppressor and helper lymphocytes and Killer (K) cells, as well as other
constituents. The suppressor lymphocytes suppress unwanted lymphocytes.
Measurement of the thyroid stimulating antibody present in the blood of most patients with Graves'
disease is not usually necessary, in order to establish the diagnosis.
The symptoms and signs of Graves' hyperthyroidism are due to the effects of excess amounts of
thyroid hormone on body function and metabolism. Common symptoms include weight loss,
nervousness, irritability, intolerance to hot weather, excessive sweating, shakiness, and muscle
weakness. Other signs include a rapid pulse, loss of body fat and muscle bulk, thyroid enlargement
(goitre), fine tremors of the fingers and hot, moist, velvety skin.
About 50% of patients also have significant eye signs (Ophthalmopathy). The eyes, which bulge
from their sockets are red and watery and the lids are swollen. Quite often the eyes do not move
normally because the swollen eye muscles are unable to work precisely. The remaining 50% of
patients with Graves' hyperthyroidism may have slightly bulging eyes because of spasm of the
muscle of the lids, giving them a staring appearance.
Thyroid hormones have a wide variety of effects on the body and the symptoms and signs reflect
these. In simple terms, all the metabolic processes are "speeded up"; for example, the pulse rate is
rapid (over 100), bowel function is increased (diarrhea), and the sweat glands work excessively.
The nervous system is also stimulated so that the patient becomes irritable and nervous. Despite
increased appetite, the patient usually loses weight because food intake cannot keep up with the
increased breakdown of body proteins. The end result is a thin, hot, nervous patient with "poppy"
eyes and a goitre - a classical clinical situation quickly recognized by any medical practitioner who
has previously seen such a patient.
Because Graves' hyperthyroidism is caused by a genetically determined abnormality of the immune
system, the problem is complex and there is at present no specific treatment for the underlying
abnormality. Since the end result of this problem is an overstimulation of thyroid function, treatment
of the symptoms is quite easy - one can either surgically remove part of the thyroid gland
(thyroidectomy), destroy the thyroid cells with radioactive iodine, or block thyroid hormone
production with antithyroid drugs.
Although radioactive iodine is by far the simplest and most convenient treatment, its use in younger
adults and children has previously been a matter of concern because of the possible harmful effects
of radiation. Radioactive iodine has been used for over 40 years and there is no good evidence of
any harmful effects. Most thyroid specialists would recommend its use in all patients with Graves'
disease over the age of 20-25; some would use it in children as well.
Radioactive iodine is usually given in the form of a capsule. The dose is calculated from the size of
the goitre by performing a "Thyroid Uptake Test." Because radioactive iodine takes several weeks
to take its full effect, antithyroid tablets are also sometimes given until such time as the full effect
occurs.
Antithyroid drugs (of which Propylthiouracil and Methimazole are the only ones available in
Canada) are almost mandatory in children and adults under the age of 20-25. It may also be used at
any age so as to bring about remissions, or prior to ablation therapy. There are two main drawbacks
with this type of treatment:
In addition a very small percentage suffer side effects. Eventually, most patients require treatment
with either radioactive iodine or thyroidectomy. Another tablet that can be given to treat the
symptoms of hyperthyroidism is Propranolol. This drug blocks the effects of excess thyroid
hormones on the heart, blood vessels, and nervous system, but has no direct effect on the thyroid
gland.
Surgery is usually recommended for the 80% of patients under the age 20 who have a recurrence of
hyperthyroidism after antithyroid drugs. Thyroidectomy is also recommended for patients of any age
in whom the goitre is so big that it causes blockage of the windpipe (trachea) or food passage
(esophagus). In England and Europe, thyroidectomy is performed for Graves' disease much more
often than in Canada, largely because of experience and tradition. Thyroidectomy requires
admission to hospital for about 5 days and removal (by an experienced surgeon) of all but a small
portion of the gland.
After treatment with radioactive iodine or thyroidectomy, it is hoped that enough of the thyroid
gland remains to function normally. Occasionally, the gland becomes overactive again since the
abnormal stimulating antibody is still being produced by the lymphocytes. In other patients, there is
a strong tendency for the remaining thyroid gland to become underactive (hypothyroidism) - perhaps
80% of all patients with Graves' disease will eventually require lifelong thyroid hormone
replacement therapy. This is not considered a problem as long as the hypothyroidism is recognized
and treated. It is much more of a problem for patients to have a recurrence of hyperthyroidism
because of failure to remove enough gland or if too small dose of radioactive iodine is given. Indeed,
some specialists deliberately destroy the thyroid in order to prevent a recurrence of the
hyperthyroidism, and immediately treat with thyroid hormone in anticipation of hypothyroidism.
In Canada, Graves' disease accounts for at least 90% of all patients with hyperthyroidism.
Hyperthyroidism can also occur in older patients with long-standing nodular goitres.
Other uncommon causes of hyperthyroidism in Canada are painful (subacute) thyroiditis caused by
a viral infection of the thyroid gland in which the hyperthyroidism is due to leakage of thyroid
hormones from the swollen, damaged gland and "silent" thyroiditis, a similar condition but without
the painful swelling of the thyroid. Production of the printed version of this Health Guide was made possible through partial funding
assistance from Health Canada. The views expressed herein are solely those of the authors and do
not necessarily represent the official policy of Health Canada.Original published 1983. Revised November 1993. Graves' eye disease, like Graves' hyperthyroidism and Hashimoto's thyroiditis, is an autoimmune
disorder. It is caused by the reaction of antibodies and certain white blood cells called lymphocytes,
with proteins in eye muscle and the connective tissue and fat around the eyeball. This condition must
be distinguished from the mild eye signs of "poppy" eyes and spasm of the eye lids which occur in
most hyperthyroid patients due to an effect of excessive thyroid hormones.
The characteristic features of Graves' eye disease are symptoms of inflammation of the eye tissues.
The eyes are painful, red and watery - particularly in sunshine or wind. The covering of the eye is
inflamed and swollen.
The lids and tissues around the eyes are swollen with fluid. The eyeballs bulge out of their sockets.
Because of eye muscle movement, the eyes are unable to move normally and there may be blurred
or double vision.
On examination, it can be seen that the eyes are pushed out of their sockets. This can be measured
using an instrument called an "exophthalomometer."
There are no tests presently available to confirm the diagnosis of Graves' eye disease although good
progress is being made in Canada in the development of a simple antibody test to measure the
proteins in the blood which cause the eye disease. Such a test would be useful in patients with
Graves' hyperthyroidism to identify those who may be likely to develop the eye disease.
The eye changes tend to "burn out" within a period of about 24 months and, in most cases, there is a
satisfactory end result even without any treatment. The double vision and the bulginess usually do
not disappear completely. Many patients are worried by the cosmetic appearance of their swollen,
bulgy eyes, whereas others, with less severe defects, are inconvenienced by their inability to read
clearly because of double vision. The impact of the eye disease also depends on the age, sex, and
occupation of the patient.
Unfortunately, there is no satisfactory treatment. Because hyperthyroidism seems to influence the
eye disease, it is very important to treat the hyperthyroidism quickly and effectively but to avoid
hypothyroidism, which also harms the eyes. In most patients, the eyes tend to get somewhat better
when the thyroid abnormality has been treated.
In a few patients, the condition progresses regardless of what is done to the thyroid gland. These
patients must be treated with strong drugs such as steroids or immunosuppressive drugs to prevent
the unlikely occurrence of optic nerve swelling and blindness. If these measures do not work within
a few days, it may be necessary to relieve pressure in the orbit by removing part of the tissue either
by operation or by treating the eyes with X-rays. Both treatments very quickly reduce the pressure
on the eyeball and the surrounding orbital tissues and prevent permanent optic nerve damage or
glaucoma.
Once treated, or when the eyes have "burnt out" without treatment, the eye inflammation rarely
reoccurs and treatment need not be continued. Patients who have not had thyroid disease previously
must be examined on a regular basis in case they develop thyroid disease. Patients with eye disease
who have had their hyperthyroidism treated previously should also be examined at regular intervals
to make certain that thyroid function remains normal since recurrence of hyperthyroidism, or
development of hypothyroidism, may cause the eye disease to flare up. Production of the printed version of this Health Guide was made possible through partial funding
assistance from Health Canada. The views expressed herein are solely those of the authors and do
not necessarily represent the official policy of Health Canada.Original published 1983. Revised April 1992. Table Of Contents: Alternative names: Definition: Causes, incidence, and risk factors: Prevention: Symptoms: Late symptoms:
Signs and tests: Additional laboratory abnormalities may include:
Treatment: Expectations (prognosis): Complications: Other complications include:
Calling your health care provider: Table Of Contents: Alternative names: Definition: Table Of Contents: Alternative names: Definition: Causes, incidence, and risk factors: Prevention: Symptoms:
Signs and tests: This disease may also alter the following test results:
Treatment: Expectations (prognosis): Complications:
Calling your health care provider: Table Of Contents: Alternative names: Definition: Causes, incidence, and risk factors: Prevention: Symptoms:
Signs and tests: Treatment: Expectations (prognosis): Complications:
Calling your health care provider: Definitions (from Stedman's Concise Medical Dictionary)
bosselated - Marked by numerous bosses or rounded protuberances.
Graves' disease - 1.) toxic goiter characterized by diffuse hyperplasia of the thyroid gland, a form
of hyperthyroidism; exophthalmos is a common, but not invariable, concomitant; 2.) thyroid
dysfunction and all or any of its clinical associations; 3.) an organ-specific autoimmune disease of
the thyroid gland. See: thyrotoxicosis, Hashimoto's thyroiditis, goiter, myxedema. Syn: Basedow's
disease, ophthalmic hyperthyroidism, Parry's disease.
proptosis - Protrusion of one or both eyeballs; can be congenital and familial, or due to pathology,
such as a retro-orbital tumor (usually unilateral) or thyroid disease (usually bilateral).
Syn:exophthalmos.
chemosis - Edema of the bulbar conjunctiva, forming a swelling around the cornea.
thyrotoxicosis - The state produced by excessive quantities of endogenous or exogenous thyroid
hormone.
hyperhidrosis - Excessive or profuse sweating. Syn: hyperephidrosis, hyperidrosis, polyhidrosis,
polyidrosis, sudorrhea.
onycholysis - Loosening of the nails, beginning at the free border, and usually incomplete.
polycythemia - An increase above the normal in the number of red cells in the blood. Syn:
erythrocythemia.
myxedema - Hypothyroidism characterized by a relatively hard edema of subcutaneous tissue, with
increased content of proteoglycans in the fluid; characterized by somnolence, slow mentation,
dryness and loss of hair, increased fluid in body cavities such as the pericardial sac, subnormal
temperature, hoarseness, muscle weakness, and slow return of a muscle to the neutral position after
a tendon jerk; usually caused by removal or loss of functioning thyroid tissue.
acropachy - Thickening of peripheral tissues; seen most often in hypothyroidism and hypertrophic
pulmonary osteoarthropathy. Diagnosis of Thyroid Diseases
Richland College When diagnosing hyperthyroidism, vital signs are checked, temperature, pulse rate of
breathing, and blood pressure show an increased heart rate. The thyroid is enlarged.
Serum TSH is decreased, serum T3, T4 and thyroid resin uptake are elevated.
Hyperthyroidism can alter the results of the vitamin B-12, visual field, radioactive iodine
uptake, triglycerides and cholesterol test. It can also alter glucose levels. Hypothyroidism
Some diagnostic evaluations are that T3 and T4 levels are low, and TSH levels and serum
cholesterol levels are elevated. ECG shows sinus bradycardia, low voltage QRS complex
and flat or inverted T waves. Some abnormalities that may occur are that liver enzymes
and serum prolactin are increased. Serum sodium and blood glucose are low. A CBC
shows anemia.
Looking at a persons medical history may help. A high birth weight of over 8 lb. may
suggest a low functioning thyroid. Frequent ear infections, colds, pneumonia or other
infections can suggest a low functioning thyroid. Girls with menstrual irregularities and
painful periods during puberty also suggest a low functioning thyroid. Headaches, sinus
infections, visual disturbances, difficulty in swallowing, heat palpitations, indigestion,
diarrhea, constipation, infertility and persons requiring 12 or more hours of sleep
sometimes suggests hypothyroidism. Subacute Thyroiditis
Diagnosis can be made if there are low levels of TSH, radioactive uptake of iodine is low,
serum T3 and T4 levels are elevated, and erythrocyte sedimentation rate is increased. Hashimoto's Thyroiditis
In Hashimoto's thyroiditis, the basal metabolic rate is low, T3 and T4 levels may be
normal, but becomes subnormal as the disease progresses, TSH levels are elevated,
antithyroglobulin antibodies and antimicrosomal antibodies are always present, and high
levels of thyroglobulin binding proteins are usually present. Hashimoto's thyroiditis may
alter the results of the radioactive iodine uptake test, blood differential, and
antimitochondrial antibody tests.
Columbia-Presbyterian Medical Center
Hyperthyroidism is the result of an overactive thyroid, producing excess thyroid hormone. There are
several types of hyperthyroidism, each associated with a different particular cause, which include:
Symptoms
Treatment and Management
Other Treatments
Health Guides on Thyroid Disease #6
Graves' Hyperthyroidism
(Thyrotoxicosis)
Graves' disease is named after the Irish physician who described several cases in the London
Medical Journal in 1835. It was actually first described by Parry a few years earlier. In Europe the
disease is known as Basedow's disease. In all countries it is also known as "thyrotoxicosis". Graves'
disease, by far the most common cause of hyperthyroidism in Canada, affects perhaps one in every
100 people. It appears to be becoming even more common. The disease is an inherited disorder,
although not every member of the afflicted families will suffer this condition. It is more common in
females than in males.
Thyroid Stimulating Antibody
Clinical Features
Treatment
Radioactive Iodine
Antithyroid Drugs
Thyroidectomy
Other Causes Of Hyperthyroidism
A printed version of this Health Guide is available to health care professionals and the public. For
more information call the National Office or contact your local chapter.
Copyright © 1996 Thyroid Foundation of Canada/La Fondation canadienne de la Thyroïde.
Home Page | Health Guides Index | Next Health Guide
Health Guides on Thyroid Disease #6
Graves' Hyperthyroidism (Thyrotoxicosis)
Graves' disease is named after the Irish physician who described several cases in the London
Medical Journal in 1835. It was actually first described by Parry a few years earlier. In Europe the
disease is known as Basedow's disease. In all countries it is also known as "thyrotoxicosis". Graves'
disease, by far the most common cause of hyperthyroidism in Canada, affects perhaps one in every
100 people. It appears to be becoming even more common. The disease is an inherited disorder,
although not every member of the afflicted families will suffer this condition. It is more common in
females than in males.
Thyroid Stimulating Antibody
Clinical Features
Treatment
Radioactive Iodine
Antithyroid Drugs
Thyroidectomy
Other Causes Of Hyperthyroidism
A printed version of this Health Guide is available to health care professionals and the public. For
more information call the National Office or contact your local chapter.
Copyright © 1996 Thyroid Foundation of Canada/La Fondation canadienne de la Thyroïde.
Home Page | Health Guides Index | Next Health Guide
Health Guides on Thyroid Disease #7
Graves' Eye Disease (Ophthalmopathy)
Graves' eye disease is an eye condition which occurs in about 50% of patients who currently have,
or have had, Graves' hyperthyroidism. However, approximately 10% of patients who have this eye
disorder never develop hyperthyroidism. The reasons for the association of hyperthyroidism with the
eye disease are unknown.
Clinical Features
Laboratory Tests
Natural History
Treatment
Long Term Management
A printed version of this Health Guide is available to health care professionals and the public. For
more information call the National Office or contact your local chapter.
Copyright © 1996 Thyroid Foundation of Canada/La Fondation canadienne de la Thyroïde.
Alternative names
Definition
Causes, incidence, and risk factors
Prevention
Symptoms
Signs and tests
Treatment
Expectations (prognosis)
Complications
Calling your health care provider
A condition of decreased activity of the thyroid gland, an organ of the endocrine system, caused by
disease of the gland.
The thyroid gland is an important organ of the endocrine system, located in the front of the neck just
below the larynx. The thyroid gland secretes the hormones thyroxine (T4), triiodothyronine (T3),
and calcitonin, which control body metabolism and regulate calcium balance. The secretion of T3
and T4 by the thyroid is controlled by an endocrine feedback system involving the pituitary gland
and the hypothalamus in the brain. Calcitonin is regulated by the amount of calcium in the blood
and acts in conjunction with the parathyroid gland to control calcium levels.
Since the thyroid gland is regulated by the pituitary gland and the hypothalamus, some thyroid
disorders may result not only from defects in the gland itself, but also from disruption of the control
system. However, the causes of primary hypothyroidism are conditions that affect the gland itself
rather than its control mechanisms. These conditions may include diseases of the thyroid gland such
as Hashimoto's disease, iodine therapy for hyperthyroidism, thyroid surgery, X-ray treatment of the
neck, certain medications such as lithium, or the cause may be unknown.
Primary hypothyroidism may cause a variety of symptoms and may affect all body functions. The
body's normal rate of functioning slows causing mental and physical sluggishness. The symptoms
may vary from mild to severe. The most severe form is called myxedema which is a medical
emergency. Risk factors include being over 50 years old, being female, obesity, thyroid surgery, and
X-ray or radiation treatments to the neck. The incidence is 9 out of 1000 people.
In many cases, the condition is not preventable. Awareness of risk may allow early diagnosis and treatment.
Early symptoms:
A physical examination reveals an enlarged thyroid gland by palpation, and delayed muscle reflexes.
Vital signs (temperature, pulse, rate of breathing, blood pressure) reveal a slow heart rate, low blood
pressure and low temperature.
A chest X-ray reveals an enlarged heart.
Laboratory tests to determine thyroid function include:
The purpose of treatment is to replace the deficient thyroid hormone. Levothyroxine is the most
commonly used medication, but others are available. The lowest dose effective in relieving
symptoms is given. Life-long therapy is indicated as relapses will occur if therapy is interrupted.
Medication must be continued even when symptoms subside.
After replacement therapy has begun, report any symptoms of increased thyroid activity
(hyperthyroidism), such as restlessness, rapid weight loss, and sweating.
A high-fiber, low-calorie diet and moderate activity will help relieve constipation and promote
weight loss.
Myxedema coma is treated by intravenous thyroid replacement and steroid therapy. Supportive
therapy of oxygen, assisted ventilation, fluid replacement, and intensive care nursing may be indicated.
With early treatment, return to the normal state is usual. However, relapses will occur if the
medication is not continued. Myxedema coma can result in death.
Myxedema coma, the most severe form of hypothyroidism, is rare. It may be caused by an infection,
illness, exposure to cold or certain medications. Symptoms and signs of myxedema coma include:
Call your health care provider if signs of myxedema are present, or if chest pain or rapid heart beat occur.
Call your health care provider if restlessness, rapid weight loss, excessive sweating, or other
symptoms occur after beginning thyroid replacement.
Alternative names
Definition
A gland of internal secretion located in the base of the neck on both sides of the lower part of the
larynx and upper part of the trachea.
For information about a specific type of thyroid disease see one of the following documents:
Alternative names
Definition
Causes, incidence, and risk factors
Prevention
Symptoms
Signs and tests
Treatment
Expectations (prognosis)
Complications
Calling your health care provider
Basedow's disease; diffuse thyrotoxic goiter
A disease associated with overactivity of the thyroid gland (hyperthyroidism).
Located in the front of the neck just below the larynx, the thyroid gland is an important organ of the
endocrine system. The thyroid gland secretes the hormones thyroxine (T4), triiodothyronine (T3),
and calcitonin ,which control body metabolism and regulate calcium balance. The secretion of T3
and T4 by the thyroid is controlled by an endocrine feedback system involving the pituitary gland
and the hypothalamus in the brain. Calcitonin is regulated by the amount of calcium in the blood
and acts in conjunction with the parathyroid gland to control calcium levels. Since the thyroid gland
is regulated by the pituitary gland and the hypothalamus, thyroid disorders may result not only from
defects in the gland itself, but also from disruption of the control system. Thyroid disorders caused
by overproduction of thyroid hormones are called hyperthyroidism, and underproduction of these
hormones is known as hypothyroidism.
Graves' disease is one of most common causes of hyperthyroidism. The production of thyroid
hormone is increased resulting in an enlarged thyroid gland and many changes within the body. The
cause of the disease is unknown but may be related to a genetic or immune system disorder. Other
disorders of the endocrine system may be present in people with Graves' disease. The symptoms of
hyperthyroidism are present and, in addition, the eyeballs may protrude (exophthalmos) causing
irritation and tearing. Risk factors are being female over 20 years old, although the disorder may
occur at any age. The incidence is 5 out of 10,000 people.
The cause is unknown; therefore prevention is unknown.
Physical examination shows an increased heart rate. Examination of the neck may show thyroid
enlargement or goiter.
The purpose of treatment is to control the overactivity of the thyroid gland. Beta-blockers
(Propranolol) are used to treat symptoms of rapid heart rate, sweating, and anxiety until the
hyperthyroidism is controlled. Hyperthyroidism is treated with antithyroid medications, radioactive
iodine, or surgery to remove a portion of the thyroid gland.
The eye problems of Graves' disease usually resolve with treatment of the underlying disorder.
Sometimes prednisone is required for severe inflammation. Taping the eyes closed at night to
prevent drying is sometimes indicated. Sunglasses and eyedrops may lessen irritation of the eyes.
Rarely, surgical decompression of the orbit may be required.
For most people, Graves' disease responds well to treatment, but lifelong observation by a health
care professional is important because of possible serious complications associated with the disease.
Thyroid surgery can result in hypothyroidism. Side effects may be caused by antithyroid
medications.
Call for an appointment with your health care provider if eye problems, or general symptoms worsen
or do not improve with treatment.
Call your health care provider if rapid heart rate, chest pain, difficulty breathing, or other new
symptoms appear.
Alternative names
Definition
Causes, incidence, and risk factors
Prevention
Symptoms
Signs and tests
Treatment
Expectations (prognosis)
Complications
Calling your health care provider
An aggressive form of cancer of the thyroid gland.
Anaplastic carcinoma of the thyroid is one of the most rapidly growing and invasive types of thyroid
cancer. It occurs in people over 60 years and may cause obstruction of the trachea. The cause is
unknown, but radiation may be a contributing factor. Thyroid function tests are usually normal.
Risk factors are radiation therapy to the head or neck and age greater than 60 years old. Other types
of thyroid cancer are papillary carcinoma, follicular carcinoma, medullary carcinoma, thyroid
lymphoma, and metastatic thyroid cancer. Anaplastic carcinoma accounts for about 1% of all
thyroid cancers. The incidence is 3 out of 10,000 people.
unknown
A physical examination shows single or multiple nodules of the thyroid.
Treatment of this type of cancer is with surgery to remove the tumor, or radiation therapy, or both.
Surgical risks involve inadvertent removal of the parathyroid glands or resection (partial excision)
of nerve tissue of the larynx which leads to serious complications.
The stress of illness can often be helped by joining a support group where members share common
experiences and problems. See cancer - support group.
One variety of this cancer, the giant cell type, carries an expected life span of less than 6 months.
The small cell variety may have a prognosis (expected life span) of up to 5 years after diagnosis.
Call your health care provider if there is persistent hoarseness, changing voice, cough, or coughing
up blood.
Picture:
P0629.pctThyroid cancer, CT scan
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Student Projects for Biol. 2402 - Anatomy & Physiology
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Last Updated on February 11, 1999 by Dr.D.HAMMOUDI
