Graves' Disease: Difference between revisions
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== Definition/Description == | == Definition/Description == | ||
Graves’ is classified as an autoimmune disease that affects the thyroid gland. It causes goiters, hyperthyroidism, ophthalmopathy, and occasionally dermopathy. <ref name="Ginsberg">Ginsberg J. Diagnosis and Management of Graves’ Disease. Canadian Medical Associates Journal. 2003; 168(5):575-85.</ref> Graves' disease is known for increasing the thyroid stimulating hormone (TSH) which either raises the thyroxine (T4) levels (leading to [[Hyperthyroidism|hyperthyroidism]]) or, in approximately 10% of cases, an increase in triiodothyronine (T3) levels. The later is said to be a possible | Graves’ is classified as an autoimmune disease that affects the thyroid gland. It causes goiters, hyperthyroidism, ophthalmopathy, and occasionally dermopathy. <ref name="Ginsberg">Ginsberg J. Diagnosis and Management of Graves’ Disease. Canadian Medical Associates Journal. 2003; 168(5):575-85.</ref> Graves' disease is known for increasing the thyroid-stimulating hormone (TSH) which either raises the thyroxine (T4) levels (leading to [[Hyperthyroidism|hyperthyroidism]]) or, in approximately 10% of cases, an increase in triiodothyronine (T3) levels. The later is said to be a possible precursor to graves disease.<ref name="Ginsberg" /> <ref name="DD">Goodman C, Snyder T. Differential Diagnosis for Physical Therapists: Screening for Referral. St. Louis, Missouri: Saunders Elsevier, 2007.</ref><br> | ||
<br> | |||
''Manifestation of the Autoimmune Graves Disease <ref name="Ginsberg" />''<br> | ''Manifestation of the Autoimmune Graves Disease <ref name="Ginsberg" />''<br> | ||
| Line 18: | Line 16: | ||
Graves’ disease is more prevalent in the Caucasian race affecting more women than men, between the ages of 30 and 60.<ref name="DD" /><ref name="Heemminki">Hemminki K, Li X, Sundquist J, Sundquist K. The epidemiology of Graves’ disease: Evidence of a genetic and an environmental contribution. Journal of Autoimmunity 2010; 34:307-13.</ref> Graves’ disease accounts for 85% of all cases of hyperthyroidism. <ref name="Pathology">Goodman C, Fuller K. Pathology: Implications for the Physical Therapist. St. Louis, Missouri: Saunders Elsevier; 2009.</ref> | Graves’ disease is more prevalent in the Caucasian race affecting more women than men, between the ages of 30 and 60.<ref name="DD" /><ref name="Heemminki">Hemminki K, Li X, Sundquist J, Sundquist K. The epidemiology of Graves’ disease: Evidence of a genetic and an environmental contribution. Journal of Autoimmunity 2010; 34:307-13.</ref> Graves’ disease accounts for 85% of all cases of hyperthyroidism. <ref name="Pathology">Goodman C, Fuller K. Pathology: Implications for the Physical Therapist. St. Louis, Missouri: Saunders Elsevier; 2009.</ref> | ||
== Characteristics/Clinical Presentation == | == Characteristics/Clinical Presentation == | ||
Goiter, Exophthalmos, tremors, | Goiter, Exophthalmos, tremors, dermopathy, tachycardia with palpitations, heat intolerances, weight loss, increased deep tendon reflexes, weakness and muscle atrophy, increased cardiac output, myasthenia gravis, thin hair, warm moist skin, sensitivity to light, dysphasia, diarrhea, amenorrhea, polyuria, and many other presentations, some of which may not be as common and more subtle.<ref name="Pathology" /><br> | ||
<br> | |||
'''Most common diagnostic symptom<ref name="image 1">http://www.nlm.nih.gov/medlineplus/ency/imagepages/17067.htm</ref>''' | '''Most common diagnostic symptom<ref name="image 1">http://www.nlm.nih.gov/medlineplus/ency/imagepages/17067.htm</ref>''' | ||
[[Image:Wiki image 1.jpg|Image:Wiki_image_1.jpg]]< | == [[Image:Wiki image 1.jpg|Image:Wiki_image_1.jpg]] Associated Co-morbidities == | ||
Rheumatoid arthritis is one of the major associated autoimmune diseases along with Systematic lupus. There is an overall rise in incidence for a co-morbidity of any autoimmune diseases.<ref name="Boelaert">Boelaert K, Newby PR, Simmonds MJ, Holder RL, et al.Prevalence and relative risk of other autommune diseases in subjects with autoimmune thyroid disorders. American Journal of Medicine. 2010 Feb;123(2):183.</ref> Recommendation for further autoimmune disease screening may be warranted with the diagnosis of Graves' disease. | |||
== | There is also an increased risk of cancer in the thyroid nodules associated with Graves' disease and further ultrasonography imaging and/or biopsy may be needed for further testing if suspected malignancy.<ref name="Ginsberg" /><ref name="Pathology" /> | ||
Thyroid Storm: Caused by uncontrolled hyperthyroidism or other factors like traumatic injury or infection. Therapists should be aware of these signs and symptoms of Thyroid Storm: | |||
Thyroid Storm: Caused | |||
*Severe tachycardia with heart failure | *Severe tachycardia with heart failure | ||
*Hyperurthemia (up to 105 degrees) | *Hyperurthemia (up to 105 degrees) | ||
* | *Restlessness and agitation | ||
*Abdominal pain, nausea, and vomiting | *Abdominal pain, nausea, and vomiting | ||
*Possible coma | *Possible coma | ||
| Line 53: | Line 40: | ||
== Medications == | == Medications == | ||
'''Antithyroid drugs''' have the main effect of inhibition of thyroid hormones as well as a secondary purpose of reduction of thyrotropin-receptor antibodies and increasing | '''Antithyroid drugs''' have the main effect of inhibition of thyroid hormones as well as a secondary purpose of reduction of thyrotropin-receptor antibodies and increasing suppressor T-cells. These drugs are used mainly for controlling the thyroid in hopes to create euthyroid and have a remission period from Graves' Disease.<ref name="Franklyn">Franklyn J. The management of Hyperthyroidism. New England Journal of Medicine. 1994; 331(8):559.</ref> The three main medications are Methimazole, Carbimazole, and Propylthiouracil. The most preferred medication is methimazole, however, there are no significant differences among the antithyroid drugs in their success rates.<ref name="Cooper">Cooper D. Antithyroid drugs in the management of patients with Graves’ disease: An evidence based approach to therapeutic controversies. Journal of Clinical Endocrine and Metabolism. 2003; 88:3474-81.</ref> | ||
< | '''Beta Adrenergic- Antagonist Drugs '''are used for the treatment of symptoms such as tremors, anxiety, and palpitations. This medication is used as an adjunct therapy to other means of management for Grave's disease.<ref name="Cooper" /> | ||
''' | '''Inorganic Iodide '''is used only for short term reduction of thyroid hormones lasting effects from days to a few weeks.<ref name="Cooper" /> | ||
'''Radioiodine Therapy '''is becoming a more popular means of treatment which is used to destroy thyroid tissue with the ultimate goal of balanced thyroid hormones or [[Hypothyroidism|hypothyroidism]].<ref name="Cooper" /> | |||
'''Radioiodine Therapy '''is becoming a more popular means of treatment which is used to destroy thyroid tissue with the ultimate goal of balanced thyroid hormones or [[Hypothyroidism| | |||
== Diagnostic Tests/Lab Tests/Lab Values == | == Diagnostic Tests/Lab Tests/Lab Values == | ||
Thyroid blood serum tests are taken. A positive test result s in a decreased or normal TSH levels, elevated free thyroxine T4 for a diagnosis of | Thyroid blood serum tests are taken. A positive test result s in a decreased or normal TSH levels, elevated free thyroxine T4 for a diagnosis of hyperthyroidism. To specify graves disease Radioiodine uptake test is used.<ref name="Ginsberg" /> | ||
Thyroid stimulating Hormone Antibodies (TRAb) and thyroid peroxidase autoantibodies (TPOAb) may be found in most patients, but is not needed for specific diagnosis since most patients are diagnosed with blood serum tests and symptomology.<ref name="Fukushima">Fukushima H, Matsuo H, Imamura K, et al. Diagnosis and discrimination of autoimmune graves’ diseas nad Hashimoto’s disease using thyroid stimulation hormone receptor-containing recombinant proteoliposomes. Journal of Bioscience and Bioengineering. 2009. 108(6):551-56.</ref> | Thyroid-stimulating Hormone Antibodies (TRAb) and thyroid peroxidase autoantibodies (TPOAb) may be found in most patients, but is not needed for specific diagnosis since most patients are diagnosed with blood serum tests and symptomology.<ref name="Fukushima">Fukushima H, Matsuo H, Imamura K, et al. Diagnosis and discrimination of autoimmune graves’ diseas nad Hashimoto’s disease using thyroid stimulation hormone receptor-containing recombinant proteoliposomes. Journal of Bioscience and Bioengineering. 2009. 108(6):551-56.</ref> | ||
== Etiology/Causes == | == Etiology/Causes == | ||
Graves' | Graves' Disease has both genetic causes, such as a lack of suppressor t-cells causing an increase in TSH receptor antibodies, and environmental causes which includes, but not limited to: stress, smoking, postpartum, and infections.<ref name="Ginsberg" /><ref name="Heemminki" /> | ||
== Systemic Involvement == | == Systemic Involvement == | ||
| Line 83: | Line 64: | ||
'''Dermopaty associated with Graves'<ref name="image 2">http://www.mayoclinic.com/health/medical/IM02348</ref>''' | '''Dermopaty associated with Graves'<ref name="image 2">http://www.mayoclinic.com/health/medical/IM02348</ref>''' | ||
[[Image:Gravesdermopathy.jpg|248x279px]] | [[Image:Gravesdermopathy.jpg|248x279px]]<br> | ||
=== Central Nervous System === | |||
* Tremor | |||
* Irritable | |||
* Labile emotions | |||
* Muscle weakness and myopathy | |||
* Increased DTR | |||
* Increased motor activity | |||
* Fatigue | |||
=== Cardiovascular === | |||
* Tachycardia | |||
* Palpitations | |||
* Repiratory muscle weakness | |||
* Increased RR and HR | |||
* Low blood pressure | |||
* Heart failure | |||
=== Integumentary === | |||
* Chronic periarthritis | |||
* Dilated capillaries | |||
* Heat intolerance | |||
* Brittle hair | |||
* Onycholysis | |||
* Pretibial myxedema | |||
=== Ocular === | |||
* Exophthalmos | |||
* Light sensitivity | |||
* Vision loss | |||
* Weak extraocular muscles | |||
=== Gastrointestinal === | |||
* Increased metabolism/weight loss | |||
* Increased peristalsis | |||
* Diarrhea | |||
* Dysphagia | |||
=== Genitourinary === | |||
* Polyuria | |||
* Amenorrhea | |||
* Female infertility | |||
* Miscarriage | |||
== Medical Management == | |||
The current best management of Graves' disease varies upon several factors of the individual receiving it. The options include partial/full removal of the thyroid gland, antithyroid drug therapy, and radioiodine therapy.<ref name="Franklyn" /><ref name="Koyuncu">Koyuncu A, AYdin C, Topcu O, et Al. Could thyroidectomy become the stansard treatment for Graves’ Disease? Surgery Today. 2010. 40:22-25.</ref> There are adjunct treatments for symptom management until euthyroid is achieved through medical management. | |||
Current clinical practice suggests that radioiodine therapy is the primary choice of treatment for Graves' disease, then either antithyroid drugs or surgery depending on the contraindications for one or the other.<ref name="Panareo">Panareo S, Rossi R, Fabbri S, et al. A practical method for the estimation of therapeutic activity in the treatment of Graves’ Disease hyperthyroidism. J of Nucl Med Mol Imaging. 2010. 54:1-9.</ref> | |||
Current clinical practice suggests that radioiodine therapy is the primary choice of treatment for Graves' disease, then either | |||
== Physical Therapy Management == | == Physical Therapy Management == | ||
Graves' disease is not directly managed by physical therapy but | Graves' disease is not directly managed by physical therapy but precautions and understanding of the disease are necessary when working with these patients. Deconditioning and muscle weakness are secondary ailments that is seen in this population and can be managed by a physical therapist.<ref name="Pathology" /> | ||
=== Perferred Practice Patterns<ref name="Pathology" /> === | |||
* Impaired Muscle performance | |||
* Impaired joint mobility, motor function, muscle performance, and range of motion associated with connective tissue dysfunction. | |||
* Impaired joint mobility, motor function, muscle performance, and range of motion associated with localized inflammation. | |||
* Impaired aerobic capacity/endurance associated with deconditioning | |||
Hyperthyroidism has key elements that will cause a decreased tolerance to physical activity. Therapists should be sensitive to patient complaints and symptoms to note an exacerbation if the patient is already diagnosed or be able to recognize symptoms in order to refer to a physician.<ref name="DD" /><br> | |||
=== Precautions for Graves Related Hyperthyroidism === | |||
*Decreased Cardiorespiratory function causing dyspnea on exertion and tachycardia | |||
*Decreased Cardiorespiratory function causing | |||
*Palpitations/Atrial Fibrillation (therefore therapist should be monitoring vital signs and symptoms) | *Palpitations/Atrial Fibrillation (therefore therapist should be monitoring vital signs and symptoms) | ||
*Decreased efficiency of oxygen uptake in peripheral musculature | *Decreased efficiency of oxygen uptake in peripheral musculature | ||
| Line 153: | Line 135: | ||
All of these are reversible with the management of thyroid hormones and acheivement of Euthyroid. <ref name="DD" /><ref name="Mercuro">Mercuro G, Panzuto MG, Bina A, et al. Cardiac function, physical exercise Capacity, and quality of Life during long term thyrotropin-suppressive therapy with Levothyroxine: Effect of individual Dose Tailoring. J of Clinical endocrinology and metabolism. 2000 85: 159-164.</ref> | All of these are reversible with the management of thyroid hormones and acheivement of Euthyroid. <ref name="DD" /><ref name="Mercuro">Mercuro G, Panzuto MG, Bina A, et al. Cardiac function, physical exercise Capacity, and quality of Life during long term thyrotropin-suppressive therapy with Levothyroxine: Effect of individual Dose Tailoring. J of Clinical endocrinology and metabolism. 2000 85: 159-164.</ref> | ||
The therapist should have a base knowledge and understanding of the medication and or surgeries that these patients have undergone. The reasons are as follows: | |||
#Medications can fluctuate the thyroid hormones to either send the patient into Hypothyroidism or Hyperthyroidism. It is imperative to watch for symptoms or patient complaints that may indicate a fluctuation and refer the patient back to their endocrinologist since these two extremes will vary tolerance for physical activity.<ref name="DD" /><ref name="Pathology" /> | |||
# If a patient has recently had surgery or radioiodine treatment it is possible that you will see hypothyroidism.<ref name="Franklyn" /> | |||
#If a patient is on Beta-blockers for management tremors, anxiety, and palpitations during the exacerbation period, the therapist must be aware fo the physiological effects this can have on a patient during physical therapy.<ref name="Franklyn" />Therefore, a better measurement of vitals is the rate of perceived exertion.<ref name="Pathology" /><br> | |||
=== Precautions/Symptoms Related to Hypothyroidism === | |||
If the patient is on medication or is post-surgical there are certain things that need to be taken into consideration: <ref name="Pathology" /> | |||
*Excessive fatigue and apathy | |||
*Excessive fatigue and apathy | |||
*Sensitivity to cold | *Sensitivity to cold | ||
*Weight gain/ dry brittle hair/ and other | *Weight gain/ dry brittle hair/ and other | ||
*Decreased cardiac output, low pulse and poor circulation | *Decreased cardiac output, low pulse and poor circulation | ||
*Ataxia, intention tremor, and nystagmus | *Ataxia, intention tremor, and nystagmus | ||
== Differential Diagnosis == | == Differential Diagnosis == | ||
*Hyperthyroidism | *[[Hyperthyroidism]] | ||
*Thyroid Storm | *[[Thyroid Storm (Thyroid Crisis)|Thyroid Storm]] | ||
*Hyperparathyroidism | *[[Hyperparathyroidism]] | ||
* | *[[Thyroid Cancer|Thyroid cancer]] | ||
*Myasthenia gravis | *[[Myasthenia Gravis|Myasthenia gravis]] | ||
*Psychological disorders (anxiety, panic attacks, or mood disorders) | *Psychological disorders (anxiety, panic attacks, or mood disorders) | ||
*Atrial | *[[Atrial Fibrillation]] | ||
*Congestive Heart Failure | *Congestive Heart Failure | ||
<ref name="DD" /><ref name="Pathology" /><ref name="Fukushima" /> | |||
== Resources == | == Resources == | ||
* [http://www.ngdf.org/ National Graves' Disease Foundation] | |||
National Graves' Disease Foundation | * [http://thyroid.org/ American Thyroid Association (ATA)] | ||
* [http://www.aace.com/ American Association of Clinical Endocrinologists (AACE)] | |||
* [http://www.endo-society.org/ The Endocrine Society] | |||
* [http://www.hormone.org/ The Hormone Foundation] | |||
* [http://www.aarda.org/ American Autoimmune Related Diseases Associations (AARDA)] | |||
== References == | == References == | ||
<references /> | <references /> | ||
Revision as of 18:19, 1 January 2020
Original Editors - Erin Shinkle from Bellarmine University's Pathophysiology of Complex Patient Problems project.
Top Contributors - Erin Shinkle, Elaine Lonnemann, Lucinda hampton, Admin, Kim Jackson, WikiSysop, Wendy Walker and Andeela Hafeez
Definition/Description[edit | edit source]
Graves’ is classified as an autoimmune disease that affects the thyroid gland. It causes goiters, hyperthyroidism, ophthalmopathy, and occasionally dermopathy. [1] Graves' disease is known for increasing the thyroid-stimulating hormone (TSH) which either raises the thyroxine (T4) levels (leading to hyperthyroidism) or, in approximately 10% of cases, an increase in triiodothyronine (T3) levels. The later is said to be a possible precursor to graves disease.[1] [2]
Manifestation of the Autoimmune Graves Disease [1]
Prevalence[edit | edit source]
Graves’ disease is more prevalent in the Caucasian race affecting more women than men, between the ages of 30 and 60.[2][3] Graves’ disease accounts for 85% of all cases of hyperthyroidism. [4]
Characteristics/Clinical Presentation[edit | edit source]
Goiter, Exophthalmos, tremors, dermopathy, tachycardia with palpitations, heat intolerances, weight loss, increased deep tendon reflexes, weakness and muscle atrophy, increased cardiac output, myasthenia gravis, thin hair, warm moist skin, sensitivity to light, dysphasia, diarrhea, amenorrhea, polyuria, and many other presentations, some of which may not be as common and more subtle.[4]
Most common diagnostic symptom[5]
Image:Wiki_image_1.jpg Associated Co-morbidities[edit | edit source]
Rheumatoid arthritis is one of the major associated autoimmune diseases along with Systematic lupus. There is an overall rise in incidence for a co-morbidity of any autoimmune diseases.[6] Recommendation for further autoimmune disease screening may be warranted with the diagnosis of Graves' disease.
There is also an increased risk of cancer in the thyroid nodules associated with Graves' disease and further ultrasonography imaging and/or biopsy may be needed for further testing if suspected malignancy.[1][4]
Thyroid Storm: Caused by uncontrolled hyperthyroidism or other factors like traumatic injury or infection. Therapists should be aware of these signs and symptoms of Thyroid Storm:
- Severe tachycardia with heart failure
- Hyperurthemia (up to 105 degrees)
- Restlessness and agitation
- Abdominal pain, nausea, and vomiting
- Possible coma
Immediate referral is necessary.[2]
Medications[edit | edit source]
Antithyroid drugs have the main effect of inhibition of thyroid hormones as well as a secondary purpose of reduction of thyrotropin-receptor antibodies and increasing suppressor T-cells. These drugs are used mainly for controlling the thyroid in hopes to create euthyroid and have a remission period from Graves' Disease.[7] The three main medications are Methimazole, Carbimazole, and Propylthiouracil. The most preferred medication is methimazole, however, there are no significant differences among the antithyroid drugs in their success rates.[8]
Beta Adrenergic- Antagonist Drugs are used for the treatment of symptoms such as tremors, anxiety, and palpitations. This medication is used as an adjunct therapy to other means of management for Grave's disease.[8]
Inorganic Iodide is used only for short term reduction of thyroid hormones lasting effects from days to a few weeks.[8]
Radioiodine Therapy is becoming a more popular means of treatment which is used to destroy thyroid tissue with the ultimate goal of balanced thyroid hormones or hypothyroidism.[8]
Diagnostic Tests/Lab Tests/Lab Values[edit | edit source]
Thyroid blood serum tests are taken. A positive test result s in a decreased or normal TSH levels, elevated free thyroxine T4 for a diagnosis of hyperthyroidism. To specify graves disease Radioiodine uptake test is used.[1]
Thyroid-stimulating Hormone Antibodies (TRAb) and thyroid peroxidase autoantibodies (TPOAb) may be found in most patients, but is not needed for specific diagnosis since most patients are diagnosed with blood serum tests and symptomology.[9]
Etiology/Causes[edit | edit source]
Graves' Disease has both genetic causes, such as a lack of suppressor t-cells causing an increase in TSH receptor antibodies, and environmental causes which includes, but not limited to: stress, smoking, postpartum, and infections.[1][3]
Systemic Involvement[edit | edit source]
Graves' Disease is a systemic autoimmune disease that effect the eyes (as seen above with Exophthalmos), skin, and thyroid gland (which regulates the body on multiple levels).[2][4]
Dermopaty associated with Graves'[10]
Central Nervous System[edit | edit source]
- Tremor
- Irritable
- Labile emotions
- Muscle weakness and myopathy
- Increased DTR
- Increased motor activity
- Fatigue
Cardiovascular[edit | edit source]
- Tachycardia
- Palpitations
- Repiratory muscle weakness
- Increased RR and HR
- Low blood pressure
- Heart failure
Integumentary[edit | edit source]
- Chronic periarthritis
- Dilated capillaries
- Heat intolerance
- Brittle hair
- Onycholysis
- Pretibial myxedema
Ocular[edit | edit source]
- Exophthalmos
- Light sensitivity
- Vision loss
- Weak extraocular muscles
Gastrointestinal[edit | edit source]
- Increased metabolism/weight loss
- Increased peristalsis
- Diarrhea
- Dysphagia
Genitourinary[edit | edit source]
- Polyuria
- Amenorrhea
- Female infertility
- Miscarriage
Medical Management[edit | edit source]
The current best management of Graves' disease varies upon several factors of the individual receiving it. The options include partial/full removal of the thyroid gland, antithyroid drug therapy, and radioiodine therapy.[7][11] There are adjunct treatments for symptom management until euthyroid is achieved through medical management.
Current clinical practice suggests that radioiodine therapy is the primary choice of treatment for Graves' disease, then either antithyroid drugs or surgery depending on the contraindications for one or the other.[12]
Physical Therapy Management [edit | edit source]
Graves' disease is not directly managed by physical therapy but precautions and understanding of the disease are necessary when working with these patients. Deconditioning and muscle weakness are secondary ailments that is seen in this population and can be managed by a physical therapist.[4]
Perferred Practice Patterns[4][edit | edit source]
- Impaired Muscle performance
- Impaired joint mobility, motor function, muscle performance, and range of motion associated with connective tissue dysfunction.
- Impaired joint mobility, motor function, muscle performance, and range of motion associated with localized inflammation.
- Impaired aerobic capacity/endurance associated with deconditioning
Hyperthyroidism has key elements that will cause a decreased tolerance to physical activity. Therapists should be sensitive to patient complaints and symptoms to note an exacerbation if the patient is already diagnosed or be able to recognize symptoms in order to refer to a physician.[2]
Precautions for Graves Related Hyperthyroidism[edit | edit source]
- Decreased Cardiorespiratory function causing dyspnea on exertion and tachycardia
- Palpitations/Atrial Fibrillation (therefore therapist should be monitoring vital signs and symptoms)
- Decreased efficiency of oxygen uptake in peripheral musculature
- Heat intolerance is seen in Grave's disease
- Myopathies and proximal muscle weakness
All of these are reversible with the management of thyroid hormones and acheivement of Euthyroid. [2][13]
The therapist should have a base knowledge and understanding of the medication and or surgeries that these patients have undergone. The reasons are as follows:
- Medications can fluctuate the thyroid hormones to either send the patient into Hypothyroidism or Hyperthyroidism. It is imperative to watch for symptoms or patient complaints that may indicate a fluctuation and refer the patient back to their endocrinologist since these two extremes will vary tolerance for physical activity.[2][4]
- If a patient has recently had surgery or radioiodine treatment it is possible that you will see hypothyroidism.[7]
- If a patient is on Beta-blockers for management tremors, anxiety, and palpitations during the exacerbation period, the therapist must be aware fo the physiological effects this can have on a patient during physical therapy.[7]Therefore, a better measurement of vitals is the rate of perceived exertion.[4]
Precautions/Symptoms Related to Hypothyroidism[edit | edit source]
If the patient is on medication or is post-surgical there are certain things that need to be taken into consideration: [4]
- Excessive fatigue and apathy
- Sensitivity to cold
- Weight gain/ dry brittle hair/ and other
- Decreased cardiac output, low pulse and poor circulation
- Ataxia, intention tremor, and nystagmus
Differential Diagnosis[edit | edit source]
- Hyperthyroidism
- Thyroid Storm
- Hyperparathyroidism
- Thyroid cancer
- Myasthenia gravis
- Psychological disorders (anxiety, panic attacks, or mood disorders)
- Atrial Fibrillation
- Congestive Heart Failure
Resources[edit | edit source]
- National Graves' Disease Foundation
- American Thyroid Association (ATA)
- American Association of Clinical Endocrinologists (AACE)
- The Endocrine Society
- The Hormone Foundation
- American Autoimmune Related Diseases Associations (AARDA)
References[edit | edit source]
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 Ginsberg J. Diagnosis and Management of Graves’ Disease. Canadian Medical Associates Journal. 2003; 168(5):575-85.
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 Goodman C, Snyder T. Differential Diagnosis for Physical Therapists: Screening for Referral. St. Louis, Missouri: Saunders Elsevier, 2007.
- ↑ 3.0 3.1 Hemminki K, Li X, Sundquist J, Sundquist K. The epidemiology of Graves’ disease: Evidence of a genetic and an environmental contribution. Journal of Autoimmunity 2010; 34:307-13.
- ↑ 4.0 4.1 4.2 4.3 4.4 4.5 4.6 4.7 4.8 4.9 Goodman C, Fuller K. Pathology: Implications for the Physical Therapist. St. Louis, Missouri: Saunders Elsevier; 2009.
- ↑ http://www.nlm.nih.gov/medlineplus/ency/imagepages/17067.htm
- ↑ Boelaert K, Newby PR, Simmonds MJ, Holder RL, et al.Prevalence and relative risk of other autommune diseases in subjects with autoimmune thyroid disorders. American Journal of Medicine. 2010 Feb;123(2):183.
- ↑ 7.0 7.1 7.2 7.3 Franklyn J. The management of Hyperthyroidism. New England Journal of Medicine. 1994; 331(8):559.
- ↑ 8.0 8.1 8.2 8.3 Cooper D. Antithyroid drugs in the management of patients with Graves’ disease: An evidence based approach to therapeutic controversies. Journal of Clinical Endocrine and Metabolism. 2003; 88:3474-81.
- ↑ 9.0 9.1 Fukushima H, Matsuo H, Imamura K, et al. Diagnosis and discrimination of autoimmune graves’ diseas nad Hashimoto’s disease using thyroid stimulation hormone receptor-containing recombinant proteoliposomes. Journal of Bioscience and Bioengineering. 2009. 108(6):551-56.
- ↑ http://www.mayoclinic.com/health/medical/IM02348
- ↑ Koyuncu A, AYdin C, Topcu O, et Al. Could thyroidectomy become the stansard treatment for Graves’ Disease? Surgery Today. 2010. 40:22-25.
- ↑ Panareo S, Rossi R, Fabbri S, et al. A practical method for the estimation of therapeutic activity in the treatment of Graves’ Disease hyperthyroidism. J of Nucl Med Mol Imaging. 2010. 54:1-9.
- ↑ Mercuro G, Panzuto MG, Bina A, et al. Cardiac function, physical exercise Capacity, and quality of Life during long term thyrotropin-suppressive therapy with Levothyroxine: Effect of individual Dose Tailoring. J of Clinical endocrinology and metabolism. 2000 85: 159-164.
