Graves' Disease

 

Introduction[edit | edit source]

Photograph showing a classic finding of Graves' Disease, proptosis and lid retraction.

Graves' disease is the most common cause of hyperthyroidism. It is a disorder with systemic manifestations that primarily affect heart, skeletal muscle, eyes, skin, bone, and liver. Failure to diagnose Graves' disease can predispose thyroid storm which carries high morbidity and mortality[1].

Graves' disease is an autoimmune disease which primarily affects the thyroid gland. It may also affect multiple other organs including eyes and skin. It is the most common cause of hyperthyroidism[1].

Epidemiology[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]

Etiology[edit | edit source]

Like all autoimmune diseases, it occurs more commonly in patients with a positive family history. It is precipitated by environmental factors eg stress, smoking, infection, iodine exposure, and postpartum, as well as after highly active antiretroviral therapy (HAART) due to immune reconstitution.[1]

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]

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.[5] 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.[6][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.[6]

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]

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

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:

  1. 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]
  2.  If a patient has recently had surgery or radioiodine treatment it is possible that you will see hypothyroidism.[7]
  3. 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]

[2][4][9]

Resources[edit | edit source]

References[edit | edit source]

  1. 1.0 1.1 1.2 Pokhrel B, Bhusal K. Graves disease. StatPearls [Internet]. 2021 Jul 21.Available: https://www.ncbi.nlm.nih.gov/books/NBK448195/(accessed 23.2.2022)
  2. 2.0 2.1 2.2 2.3 2.4 2.5 2.6 Goodman C, Snyder T. Differential Diagnosis for Physical Therapists: Screening for Referral. St. Louis, Missouri: Saunders Elsevier, 2007.
  3. 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. 4.0 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.
  5. 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.
  6. 6.0 6.1 Ginsberg J. Diagnosis and Management of Graves’ Disease. Canadian Medical Associates Journal. 2003; 168(5):575-85.
  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.