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my presentation on grave disease differential diagnosis.pptx
- 1. Grave’s Disease (differentials) By – Dr. Anshul Moderator : Dr. Ashwani Sood
- 5. CAUSES Excessive TSH receptor stimulation Autonomous thyroid hormone secretion Destruction of thyroid follicles Extra thyroidal source of thyroid hormone Graves’ disease Multi-nodular goiter Autoimmune thyroiditis Factitious thyroiditis Chorionic Gonadotropin secreting tumors Toxic adenoma Sub acute thyroiditis Struma ovarii TSH secreting pituitary adenoma Acute thyroiditis Drug induced thyroiditis
- 6. Causes Frequency Graves’ disease ~70% Thyroiditis ~20% Toxic multinodular goiter ~5% Toxic adenoma ~5% Others < 1%
- 7. Grave’s disease •A/k/a Von Basedow’s disease •Accounts for 60-80% of thyrotoxicosis. •Incidence: 2% women, 1/10th in men •Peak incidence between 20 and 40 years of age. •Prevalence: depends on genetics and iodine consumption. •Have diffuse goiter and thyrotoxicosis.
- 8. Etiopathogenesis of Graves’ Disease • Genetic & Environmental factors play a role in triggering the autoimmune response •It is characterised by the presence of the serum antibodies against • TSH receptor (TSH-R) • Thyroid peroxidase (TPO) • Thyroglobulin (Tg)
- 11. GRAVES OPHTHALMOPATHY GRAVES DERMOPATHY GRAVES ACROPATHY Inflammatory disease caused by infiltration of orbital muscles leading to accumulation of glycosaminoglycans Accumulation of glycosaminoglycans in skin leading to dermopathy in <5% of GD patients Clubbing that occurs in <1% of GD patients Diamond triad
- 12. stellwag's sign-infrequent blinking Joffroy sign - absent crease in forehead on superior gaze
- 13. Numerous signs associated with Graves’ ophthalmopathy von Graefe's sign lid lag in down gaze Joffroy sign absent creases in the forehead on superior gaze Stellwag sign incomplete and infrequent blinking Möbius sign poor convergence Dalrymple's sign Upper lid retraction Kocher's sign eye globe lag in up gaze Vigouroux sign eyelid fullness Ballet sign restriction of extra ocular muscles Griffith sign Lower lid lag on down gaze Jellink's sign Increased pigmentation on the lids
- 16. Graves’ dermopathy (occurs in approximately 10% of patients with Graves’ disease) Myxedema (red, edematous skin) predominantly of hands and lower extremities Thyroid acropachy (soft tissue enlargement of fingers with clubbing) Alopecia or premature hair graying Vitiligo
- 18. Thyroiditis
- 20. Clinical presentation of thyroiditis In thyrotoxic phase of thyroiditis patient can present with symptoms of hyperthyroidism. Additional symptoms found in sub acute thyroiditis Neck pain radiating to ears Sore throat Malaise Myalgia
- 21. Subacute Thyroiditis Painful Firm to hard on palpation ESR >50 mm Painless Thyroiditis Look for h/o Post partum period Look for h/o Autoimmune disease Low to mod Anti TPO Ab FACTITIOUS THYROTOXICOSIS V/s Via proper history Serum Tg levels RAIU Fecal T4 ( i.c.o countering antibodies)
- 22. Toxic multinodular goiter (Plummer disease) Hyper functioning thyroid nodules that produce thyroid hormones in excess. Most commonly seen in the elderly. Patients present with tachyarrhythmias, weight loss, anxiety, and insomnia, atrial fibrillation or tachycardia . Weakness and wasting of muscles are common, the so-called apathetic or masked thyrotoxicosis.
- 23. Toxic adenoma Autonomously hyperfunctioning nodule that produces thyroid hormones in excess. Pathogenesis Toxic adenomas are true follicular adenomas Somatic point mutations in the TSHR gene, commonly in the third transmembrane loop. On ultrasound it appears as a single hypoechogenic nodule. Absence of infiltrative orbitopathy and myopathy, although cardiovascular manifestations may occur.
- 24. Iodine-Induced Thyrotoxicosis JOD-BASEDOW phenomenon It used to occur previously because of introduction of iodinated salt in iodine deficient areas. Now a days its mostly because of iodine contrast in CT.
- 25. AIT 1 AIT 2 Underlying thyroid disease Yes No Onset after starting Amiodarone ~ 3 months ~ 30 months Thyroid antibodies Present in Graves’ Usually absent Vascularity High Low RAIU Low/normal/high Suppressed Treatment Antithyroid drugs Oral prednisone Amiodarone continuation No Possible
- 26. Hamburger Thyrotoxicosis • It is an unusual exogenous thyrotoxicosis occurred in mid west US in 1985. • The source was the inclusion of large quantities of bovine thyroid in ground beef preparations. • When slaughtering practices changed, this condition disappeared. • Such possibility although remote, should be considered in case of epidemic exogenous thyrotoxicosis.
- 27. Miscellaneous Thyrotoxicosis Factitia - Occurs on thyroid medication but mostly occurs when patients take thyroid hormone superstitiously . HCG secreting tumor - tumors like choriocarcinoma, trophoblastic tumor and hydatidiform mole produce HCG which is weak TSH agonist. S.TSH – suppressed and RAIU% - Elevated. Metastatic thyroid carcinoma rarely cause hyperthyroidism mostly follicular carcinoma Struma ovarii - benign rare ovarian teratoma with functioning thyroid tissue.
- 28. Hashitomotos Disease Usually presents as hypothyroidism But 5 % develop thyrotoxicosis K/A HASHITOXICOSIS Considered as overlap of Grave’s and Hashimoto’s disease RAIU is RAISED during this phase. Scan shows diffuse increased uptake. Treatment = Radioiodine.
- 29. Investigations - TFT TSH level Most sensitive test for hyperthyroidism. Suppressed TSH level and elevated peripheral hormone level confirms suspected Thyrotoxicosis. Free T₄ level Total T₃ or free T₃ levels
- 30. Investigations
- 31. Other laboratory tests TSH receptor antibodies test High titers of TSH receptor antibodies support a diagnosis of Graves’ disease. Third-generation TSH receptor antibody tests are 98% sensitive and 99% specific for Graves’ disease. Thyroid peroxidase antibodies test High titers support thyroiditis as a cause of thyrotoxicosis. Thyroglobulin test Circulating thyroglobulin level is elevated in all forms of thyroiditis and suppressed in factitious thyrotoxicosis.
- 32. USG neck To measure the increased blood flow and vascularity of the thyroid gland. To look for increased size. To look for nodules in the thyroid gland.
- 35. RAIU For differential diagnosis of Thyrotoxicosis Normal Range of % RAIU TIME 1-6% 2 hours 6-18% 24 hours
- 41. Thank YOU
- 44. Hallmarks of the disease were palpitation, goiter, and exophthalmos, called the Merseburg triad after the hometown of von Basedow (Merseburg,Germany).
Editor's Notes
- GO is likely to be active at CAS values of >3/7 or >4/10 Clinical Activity Score(CAS) (amended by EUGOGO) 1 point is given for the presence of each of the parameters assessed. The sum of all points defines clinical activity: 3/7 is active ophthalmoplegia at first examination and 4/10 in successive examinations.
- The serum T4 and T3 concentrations may be only marginally increased, and a suppressed TSH may be the major abnormality. The total RAIU is only slightly increased or within the normal range unless following iodine exposure. Radioiodine I-131 is the usual therapy for toxic nodules because the radiation is delivered selectively to the hyper functioning tissue sparing suppressed extra nodular tissues.
- The iodine induces thyroiditis and thyrotoxicosis; RAIU % is suppressed. Sometimes iodine can induce subclinical graves or Toxic MNG; RAIU % elevated.
- Free T₄ level is high in most cases of overt hyperthyroidism. Free T₄ level falls within reference range in subclinical hyperthyroidism. Free T₄ assay is preferred to total T₄ because of the prevalence of binding protein alterations that impact measurement. Total T₃ or free T₃ levels T₃ is the more bioactive thyroid hormone and is converted from T₄ in several organs (eg, liver, kidneys). T₃ level is often elevated to a greater extent than T₄ level in severe hyperthyroidism. T₃ level falls within reference range in subclinical hyperthyroidism. Total T₃ measurement is preferable to free T₃ measurement because the latter is less widely validated.
- 2 HR – 1- 6 % 24 HR – 6 – 18%