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GRAVES’ DISEASE AND IT’S
TREATMENTS
Supervised by Submitted by
Prem Prasad Dhiraj choudhary
(Associate professor) 0869PY131035
1
Introduction
2 Literature Review
3 Epidemiology
4 Etiology
5 Diagnosis
6 Pathophysiology
7 Treatment
8 Conclusion
9 References
Contents
LITERATURE REVIEW
 01.Burch HB, et al (2015) “Management of graves’
disease”Management of Graves disease includes treatment
with antithyroid drugs, RAI, or thyroidectomy. The optimal
approach depends on patient preference and specific patient
clinical features such as age, history of arrhythmia or
ischemic heart disease, size of goiter, and severity of
thyrotoxicosis. Physicians should be familiar with the
advantages and disadvantages of each therapy to best
counsel their patients.
 02.Streetman DD, et al (2003) ;Diagnosis and treatment of
disease”Julextensive experience with medical
management, controversy prevails regarding choosing
among the various drugs for treatment of Graves disease.
None of the treatment options, including antithyroid drugs,
radioiodine, and surgery, is ideal. Each has risks and
benefits, and selection should be tailored to the individual
patient.
Introduction
What is Graves’ Disease
It is an autoimmune condition that
affects thyroid function, causing
enlargement and overactivity
(hyperthyroidism) of the thyroid
SYMPTOMS
Tremor: in the hands
Whole body: excess sweating, excessive hunger,
fatigue, heat intolerance, high blood pressure, or
sweating
Heart: fast heart rate, irregular heart rate, or sensation
of an abnormal heartbeat
Eyes: abnormal protrusion of eyes, puffy eyes, or
watery eyes
Mood: anxiety or nervousness
Also common: absence of menstruation, diarrhea,
enlarged thyroid, graves' ophthalmopathy, hair loss,
insomnia, irritability, overactive thyroid, or weight loss
Ophthalmopathy Goiter Acropachy
Pretibial Myxedema
Symptoms
Epidemiology
 It occurs about 7.5 times more often in women than
men.
 Accounts for 60 to 80% of thyrotoxicosis.
 1 million cases per year in India
Etiology ( Causes)
 Caused by abnormal immune system response
that causes the thyroid gland to produce too
much thyroid hormone (hyperthyroidism)
Diagnosis Of Graves’ disease
 TSH , free T4 
 Thyroid auto antibodies
 Nuclear thyroid scintigraphy (I123)
B cells Plasma cells
Antbodies
immobilize antigen
immune system produces
auto antibodys called
thyroid stimulating
ammunoglobulin (TSI)
attech to thyroid cells
TSIs mimics the action of
the TSH
TSI binds to
TSH recepters
Thyroid gland is
stimulated to produce
excess amousnts of
thyroid hormones
This is where auto immune
disorder occurs
Pathophysiology of graves’ disease
Treatments of Graves’ disease
 Focused on treating hyperthyroidism by:
1. Medication
2. Surgery
3. Radioactive Iodine
Antithyroid drugs
Propylthiouracil (Safe In Pregnancy)
PTU also inhibits T4 to T3
conversion
Carbimazole, methimazole
Both inhibit thyroid peroxides
(beta blocker)
Adverse effects
 Rash
 Urticaria
 GI Symptoms
 Agranulocytes ( WBC)
Surgery
Expensive
Indications:
A large goiter (especially when compressing
the trachea)’
Suspicious nodules suspected cancer.
SE: Damage recurrent laryngeal nerve and
Hypoparathyoidism Hypocalcemia
RADIOACTIVE IODINE
Most cost effective
Best long term
management &
permanent cure
SE: Hypothyroidism
NATURAL TREATMENT FOR GRAVES DISEASE
 Manage Stress Levels
 Eat an Anti-inflammatory Diet
 Get Some Exercise
 Quit Smoking
 Lower Exposure to Environmental Toxins
 Treat Sensitivity of the Eyes and Skin
CONCLUSION
 Currant treatments for Graves’ disease is
effective but the ideal treatment is still not
available
 Some symptoms may be prevented with
proper diet, exercise and health care.
REFRENCES
 1.american thyroid association
 2.Brent, Gregory A. (Jun 12, 2008). "Clinical practice.
Graves' disease". The New England Journal of Medicine.
358 (24): 2594–2605. 2014).
 3.Nikiforov, Yuri E.; Biddinger, Paul W.; Nikiforova, Lester
D.R.; Biddinger, Paul W. (2012). Diagnostic pathology and
molecular genetics of the thyroid (2nd ed.). Philadelphia:
Wolters Kluwer Health/Lippincott Williams & Wilkins. p. 69
 4.Tomer Y, Davies T (1993). "Infection, thyroid disease, and
autoimmunity" (PDF). Endocr Rev. 14 (1): 107–20.
 5.Menconi, F; Marcocci, C; Marinò, M (2014). "Diagnosis
and classification of Graves' disease.". Autoimmunity
reviews. 13 (4-5): 398–402.
 6.Umena S, Takano T, Iijima T, Hidaka Y, Yagoro A, Takai S,
et al. A case of repeated painless thyroiditis followed by
Graves’ disease. Endocr J
 7. Stocker DJ, Foster SS, Solomon BL, Shriver CD, Burch HB. Thyroid canceryield in
patients with Graves’ disease selected for surgery on the basis of coldscintiscan defects.
Thyroid 2002;12:305-11
 8.page 157 in:Elizabeth D Agabegi; Agabegi, Steven S. (2008). Step-Up to Medicine
(Step-Up Series). Hagerstwon, MD: Lippincott Williams & Wilkins.
 9.Bunevicius, R; Prange AJ, Jr (2006). "Psychiatric manifestations of Graves'
hyperthyroidism: pathophysiology and treatment options.". CNS Drugs. 20 (11): 897–
909.
 10.Yeung SJ. Graves disease. Pathophysiology. Medcape. November 18, 2015.
https://emedicine.medscape.com/article/120619-overview#a5. Accessed March 8, 2016.
 11. Yeung SJ. Graves disease treatment & management. November 18, 2015.
https://emedicine.medscape.com/article/120619-treatment. Accessed March 8, 2016.
 12. Marcocci C, Chiovato L, Mariotti S, Pinchera A: Changes of circula.1ing thyroid
autoantibody levels during and after therapy with methimazole in patients with Graves'
disease. J Endocrinol Invest 5:13, 1982.
 13. Pinchera A, Liberti P, Martino E, Fenzi GF, Grasso L, Rovis I, Baschieri L: Effects of
antithyroid therapy on the long acting thyroid stimulator and the antithyroglobulin
antibodies. J Clin Endocrinol Metab 29:231, 1969.
 14. Barbosa, J., Wong, E. & Doe, R.P. (1972) Ophthalmopathy of Graves’disease:
outcome after treatment with radioactive iodine, surgery or antithyroid drugs. Archives of
Internal Medicine, 130, 111–113.
 15. Vestergaard, H. & Laurberg, P.(1989) Radioiodine and aggravationof
ophthalmopathy. Lancet, 8 , 653 – 647.

More Related Content

Graves' disease

  • 1. GRAVES’ DISEASE AND IT’S TREATMENTS Supervised by Submitted by Prem Prasad Dhiraj choudhary (Associate professor) 0869PY131035
  • 2. 1 Introduction 2 Literature Review 3 Epidemiology 4 Etiology 5 Diagnosis 6 Pathophysiology 7 Treatment 8 Conclusion 9 References Contents
  • 3. LITERATURE REVIEW  01.Burch HB, et al (2015) “Management of graves’ disease”Management of Graves disease includes treatment with antithyroid drugs, RAI, or thyroidectomy. The optimal approach depends on patient preference and specific patient clinical features such as age, history of arrhythmia or ischemic heart disease, size of goiter, and severity of thyrotoxicosis. Physicians should be familiar with the advantages and disadvantages of each therapy to best counsel their patients.  02.Streetman DD, et al (2003) ;Diagnosis and treatment of disease”Julextensive experience with medical management, controversy prevails regarding choosing among the various drugs for treatment of Graves disease. None of the treatment options, including antithyroid drugs, radioiodine, and surgery, is ideal. Each has risks and benefits, and selection should be tailored to the individual patient.
  • 4. Introduction What is Graves’ Disease It is an autoimmune condition that affects thyroid function, causing enlargement and overactivity (hyperthyroidism) of the thyroid
  • 5. SYMPTOMS Tremor: in the hands Whole body: excess sweating, excessive hunger, fatigue, heat intolerance, high blood pressure, or sweating Heart: fast heart rate, irregular heart rate, or sensation of an abnormal heartbeat Eyes: abnormal protrusion of eyes, puffy eyes, or watery eyes Mood: anxiety or nervousness Also common: absence of menstruation, diarrhea, enlarged thyroid, graves' ophthalmopathy, hair loss, insomnia, irritability, overactive thyroid, or weight loss
  • 7. Epidemiology  It occurs about 7.5 times more often in women than men.  Accounts for 60 to 80% of thyrotoxicosis.  1 million cases per year in India
  • 8. Etiology ( Causes)  Caused by abnormal immune system response that causes the thyroid gland to produce too much thyroid hormone (hyperthyroidism)
  • 9. Diagnosis Of Graves’ disease  TSH , free T4   Thyroid auto antibodies  Nuclear thyroid scintigraphy (I123)
  • 10. B cells Plasma cells Antbodies immobilize antigen immune system produces auto antibodys called thyroid stimulating ammunoglobulin (TSI) attech to thyroid cells TSIs mimics the action of the TSH TSI binds to TSH recepters Thyroid gland is stimulated to produce excess amousnts of thyroid hormones This is where auto immune disorder occurs Pathophysiology of graves’ disease
  • 11. Treatments of Graves’ disease  Focused on treating hyperthyroidism by: 1. Medication 2. Surgery 3. Radioactive Iodine
  • 12. Antithyroid drugs Propylthiouracil (Safe In Pregnancy) PTU also inhibits T4 to T3 conversion Carbimazole, methimazole Both inhibit thyroid peroxides (beta blocker)
  • 13. Adverse effects  Rash  Urticaria  GI Symptoms  Agranulocytes ( WBC)
  • 14. Surgery Expensive Indications: A large goiter (especially when compressing the trachea)’ Suspicious nodules suspected cancer. SE: Damage recurrent laryngeal nerve and Hypoparathyoidism Hypocalcemia
  • 15. RADIOACTIVE IODINE Most cost effective Best long term management & permanent cure SE: Hypothyroidism
  • 16. NATURAL TREATMENT FOR GRAVES DISEASE  Manage Stress Levels  Eat an Anti-inflammatory Diet  Get Some Exercise  Quit Smoking  Lower Exposure to Environmental Toxins  Treat Sensitivity of the Eyes and Skin
  • 17. CONCLUSION  Currant treatments for Graves’ disease is effective but the ideal treatment is still not available  Some symptoms may be prevented with proper diet, exercise and health care.
  • 18. REFRENCES  1.american thyroid association  2.Brent, Gregory A. (Jun 12, 2008). "Clinical practice. Graves' disease". The New England Journal of Medicine. 358 (24): 2594–2605. 2014).  3.Nikiforov, Yuri E.; Biddinger, Paul W.; Nikiforova, Lester D.R.; Biddinger, Paul W. (2012). Diagnostic pathology and molecular genetics of the thyroid (2nd ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. p. 69  4.Tomer Y, Davies T (1993). "Infection, thyroid disease, and autoimmunity" (PDF). Endocr Rev. 14 (1): 107–20.  5.Menconi, F; Marcocci, C; Marinò, M (2014). "Diagnosis and classification of Graves' disease.". Autoimmunity reviews. 13 (4-5): 398–402.  6.Umena S, Takano T, Iijima T, Hidaka Y, Yagoro A, Takai S, et al. A case of repeated painless thyroiditis followed by Graves’ disease. Endocr J
  • 19.  7. Stocker DJ, Foster SS, Solomon BL, Shriver CD, Burch HB. Thyroid canceryield in patients with Graves’ disease selected for surgery on the basis of coldscintiscan defects. Thyroid 2002;12:305-11  8.page 157 in:Elizabeth D Agabegi; Agabegi, Steven S. (2008). Step-Up to Medicine (Step-Up Series). Hagerstwon, MD: Lippincott Williams & Wilkins.  9.Bunevicius, R; Prange AJ, Jr (2006). "Psychiatric manifestations of Graves' hyperthyroidism: pathophysiology and treatment options.". CNS Drugs. 20 (11): 897– 909.  10.Yeung SJ. Graves disease. Pathophysiology. Medcape. November 18, 2015. https://emedicine.medscape.com/article/120619-overview#a5. Accessed March 8, 2016.  11. Yeung SJ. Graves disease treatment & management. November 18, 2015. https://emedicine.medscape.com/article/120619-treatment. Accessed March 8, 2016.  12. Marcocci C, Chiovato L, Mariotti S, Pinchera A: Changes of circula.1ing thyroid autoantibody levels during and after therapy with methimazole in patients with Graves' disease. J Endocrinol Invest 5:13, 1982.  13. Pinchera A, Liberti P, Martino E, Fenzi GF, Grasso L, Rovis I, Baschieri L: Effects of antithyroid therapy on the long acting thyroid stimulator and the antithyroglobulin antibodies. J Clin Endocrinol Metab 29:231, 1969.  14. Barbosa, J., Wong, E. & Doe, R.P. (1972) Ophthalmopathy of Graves’disease: outcome after treatment with radioactive iodine, surgery or antithyroid drugs. Archives of Internal Medicine, 130, 111–113.  15. Vestergaard, H. & Laurberg, P.(1989) Radioiodine and aggravationof ophthalmopathy. Lancet, 8 , 653 – 647.