Graves' Disease: Difference between revisions

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== 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 supressor T-cells. These drugs are used mainly for controlling the thyroid in hopes to create a stable thyroid and have a remission period rom 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 perferred 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><br>  
'''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 supressor T-cells. These drugs are used mainly for controlling the thyroid in hopes to create euthyroid and have a remission period rom 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 perferred 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><br>  


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'''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|hypothyriodism]].<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|hypothyriodism]].<ref name="Cooper" />


== Diagnostic Tests/Lab Tests/Lab Values  ==
== Diagnostic Tests/Lab Tests/Lab Values  ==

Revision as of 04:28, 2 April 2011

 

Welcome to PT 635 Pathophysiology of Complex Patient Problems This is a wiki created by and for the students in the School of Physical Therapy at Bellarmine University in Louisville KY. Please do not edit unless you are involved in this project, but please come back in the near future to check out new information!!

Original Editors - Erin Shinkle from Bellarmine University's Pathophysiology of Complex Patient Problems project.

Lead Editors - Your name will be added here if you are a lead editor on this page.  Read more.

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 precurser to graves disease.[1] [2]


Manifestation of the Autoimmune Graves Disease [1]

File:22ff1.gif

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, dermopaty, 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]

Rhuematoid arthritis is one of the major associated autoimmune diseases along with Systematic lupus. There is an overall raise in incidence for a co-morbidity of any autoimmune diseases.[6] Recommendation for futher autoimmune disease screening may be warrented 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 from 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)
  • Reselessness 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 supressor T-cells. These drugs are used mainly for controlling the thyroid in hopes to create euthyroid and have a remission period rom Graves' Disease.[7] The three main medications are Methimazole, Carbimazole, and Propylthiouracil. The most perferred medication is methimazole, however, there are no significant differences among the antithyroid drugs in their success rates.[8]


Beta Adrenergic- Antagonist Drugs is used for treatment of symptoms such as tremors, anxiety, and palpitations. This medication is used as an adjunct therapy to other means of management for Graves 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 hypothyriodism.[8]

Diagnostic Tests/Lab Tests/Lab Values[edit | edit source]

Thyroid blood serum testsare taken A positive test results include a decreased or normal TSH levels, elevated free thyroxine t4 diagnosis of hyperthyriodism. 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]

Has both genetic causes, lack of suppressor t-cells causing increase in TSH receptor antibodies, and environmental causes which includes, but not limited to the following: stress, smoking, post pardum, 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]

File:Gravesdermopathy.jpg


Systemic involvement of hyperthyroid symptoms in Graves' Disease. [4]

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 (current best evidence)
[edit | edit source]

The current best management of Graves' disease varies upon several factors of the individual recieving it. The options include partial and full removal of thyroid gland, antithyroid drug therapy, and radioiodine therapy.[7][11]  There are adjunct treatments for symptom management until euthyroid is acheived through medical management.


Current clinical practice suggests that radioiodine therapy is the primary choice of treatment for Graves' disease, then either antithyriod 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 percautions and understanding of the disease is 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]

4C: Impaired Muscle performance

4D: Impaired joint mobility, motor function, muscle performance, and range of motion associated with connective tissue dysfunction.

4E: impaired joint mobility, motor function, muscle performance, and range of motion associated with localized inflammation.

6B: Impaired aerobic coapcity/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 patient is already diagnosed or be able to recognize symptoms in order to refer to physician.[2]


Percautions for Graves Related Hyperthyroidism

  • Decreased Cardiorespiratory function causing dypsnea 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]



Therapist should have a base knowledge and understanding of the medication and or surgeries that these patients have undergone. The reasons are as follows:

  1. Medications can fluxuate the thyroid hormones to either send patient into Hypothyroidism or Hyperthyroidism. It is imparative to watch for symptoms or patient complaints that may indicate a fluxuation and refer patient back to their endocrinologist since these two extremes will vary tolerance for physical activity.[2][4]
  2.  If patient has recently had surgery or radioiodine treatment it is possible that you will see hypothyroidism.[7]
  3. If patient is on Beta blockers for management tremors, anxiety, and palpitations during 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 rate of percieved exertion.[4]


Percautions/Symptoms related to hypothyroidism (if patient on medication or post surgical) [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

Alternative/Holistic Management (current best evidence)[edit | edit source]

"Ahnjeonbaekho-tang (AJBHT), an herbal remedy for Graves’ disease, consists of eight medicinal herbs, including Pueraria thunbergiana and Scutellaria baicalensis, which are the main herbs regulating thyroid hormone.  Puerariathunbergiana contains isoflavones, such as daidzein,daidzein, puerarin, and puerarin xyloside. The main componentsof Scutellaria baicalensis are baicalein, baicalin,chrysin, oroxylin, wogonin, and wogonoside.  Among these components, daidzein and baicalein are known to have antithyroid effects. Recently, we reported that AJBHT treatment can improve clinical symptoms and decrease levelsof thyroid hormone in Graves’ disease patients who have sideeffects from antithyroid drugs..." - This holistic approach was done in a clinical trial for treatment of Graves' disease. Although the trial revealed a decrease in both T3 and T4 thyroid hormones and an increase in Thyroid stimulating hormone, this is only one clinical trail and is not suffiecient evidence to support the use of AJBHT. [14]


Bugleweed and Lemonbalm: In combination with lemonbalm this plant is said to decrease thyroidd stimulating hormones and T4 levels. Bungleweed, along with lemonbalm help block the graves disease causing antibodies from binding to the thyroid gland.[15][16]          

Bugleweed Picture[17]                                                       Lemonbalm Picture[18] 

File:Bugleweed-1.jpg             File:Lemon-Balm-2z.jpg 


As with many other alternative therapies, these methods have limited clinical evidence to support the use of these herbs for Graves' Disease.

Differential Diagnosis[edit | edit source]

  • Hyperthyroidism
  • Thyroid Storm
  • Hyperparathyroidism
  • Tyroid cancer
  • Myasthenia gravis
  • Psychological disorders (anxiety, panic attacks, or mood disorders)
  • Atrial Fibrilation
  • Congestive Heart Failure

[2][4][9]

Case Reports/ Case Studies[edit | edit source]

add links to case studies here (case studies should be added on new pages using the case study template)

Related Articles (from Pubmed)[edit | edit source]

Failed to load RSS feed from http://eutils.ncbi.nlm.nih.gov/entrez/eutils/erss.cgi?rss_guid=129mA77YOoVgFoCXx_rkYBbrw3zdVAHK4wr_5RPyB-clEKnMnJ|charset=UTF-8|short|max=10: Error parsing XML for RSS

Resources
[edit | edit source]

National Graves' Disease Foundation

      http://www.ngdf.org/


American Thyroid Association (ATA)

       http://thyroid.org/

American Association of Clinical Endocrinologists (AACE)

       http://www.aace.com/

The Endocrine Society

       http://www.endo-society.org/

The Hormone Foundation

        http://www.hormone.org/

American Autoimmune Related Diseases Associations (AARDA)

         http://www.aarda.org/



References[edit | edit source]

see adding references tutorial.

  1. 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. 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. 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. 4.00 4.01 4.02 4.03 4.04 4.05 4.06 4.07 4.08 4.09 4.10 Goodman C, Fuller K. Pathology: Implications for the Physical Therapist. St. Louis, Missouri: Saunders Elsevier; 2009.
  5. http://www.nlm.nih.gov/medlineplus/ency/imagepages/17067.htm
  6. 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. 7.0 7.1 7.2 7.3 Franklyn J. The management of Hyperthyroidism. New England Journal of Medicine. 1994; 331(8):559.
  8. 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. 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.
  10. http://www.mayoclinic.com/health/medical/IM02348
  11. Koyuncu A, AYdin C, Topcu O, et Al. Could thyroidectomy become the stansard treatment for Graves’ Disease? Surgery Today. 2010. 40:22-25.
  12. 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.
  13. 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.
  14. Lee BC, Kang SI, Ahn YM, et al. An alternative therapy for Graves’ disease: Clinical Effects and Mechanisms of an Herbal Remedy. Biol. Pharm. Bull. 2008. 31(4) 583—587.
  15. UofMhealth. Bugleweed. http://www.uofmhealth.org/health-library/hn-2055003#hn-2055003-uses. (accessed 29 Mar 2011).
  16. UofMhealth. Lemon balm. http://www.uofmhealth.org/health-library/hn-2121004#hn-2121004-uses. (accessed 29 Mar 2011).
  17. http://home.howstuffworks.com/bugleweed.htm
  18. http://destinyhealth4u4evercatherineshanahan.blogspot.com/2010/06/my-5-top-mood-boosters.html