1 / 61

HYPERTHYROIDISM

HYPERTHYROIDISM. A Practical Approach to Dx. and Rx. Dr. R.V.S.N.Sarma., M.D., M.Sc., (Canada) Consultant Physician and Chest Specialist www.drsarma.in. Have patient seated on a stool / chair Inspect neck before & after swallowing Examine with neck in relaxed position

lila-bright
Download Presentation

HYPERTHYROIDISM

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. HYPERTHYROIDISM A Practical Approach to Dx. and Rx. Dr. R.V.S.N.Sarma., M.D., M.Sc., (Canada) Consultant Physician and Chest Specialist www.drsarma.in

  2. Have patient seated on a stool / chair Inspect neck before & after swallowing Examine with neck in relaxed position Palpate from behind the patient Remember the rule of finger tips Use the tips of fingers for palpation Palpate firmly down to trachea Pemberton’s sign for RSG Clinical Exam. of Thyroid

  3. Where to look for Thyroid ?

  4. Clinical Anatomy of Thyroid

  5. Clinical Exam of Thyroid

  6. Clinical Exam of Thyroid

  7. Clinical Exam of Thyroid

  8. Thyromegaly

  9. Hyperthyroidism • A hyper metabolic biochemical state • It is a multi system disease with • Elevated levels of FT4 or FT3 or both • What is thyrotoxicosis ? • What is hyperthyroidism ? • What are the various causes ? • How to differentiate the causes ? • What is the appropriate treatment ?

  10. Causes of Hyperthyroidism • Graves Disease – Diffuse Toxic Goiter • Plummer’s Disease – Toxic MNG • Toxic phase of Sub Acute Thyroiditis - SAT • Toxic Single Adenoma – STA • Pituitary Tumours – excess TSH • Molar pregnancy & Choriocarcinoma (↑↑ βHCG) • Metastatic thyroid cancers (functioning) • Struma Ovarii (Dermoid and Ovarian tumours) • Thyrotoxicosis Factitia ; INF, Amiodarone, SSRIs

  11. Graves Disease • The most common cause of thyrotoxicosis (50-60%). • Organ specific auto-immune disease • The most important autoantibody is • Thyroid Stimulating Immunoglobulin (TSI) or TSA • TSI acts as proxy to TSH and stimulates T4 and T3 • Anti thyro peroxidase (anti-TPO) antibodies • Anti thyro globulin (anti-TG) Anti Microsomal and other • Autoimmune diseases - Pernicious Anemia, T1DM • RA, Myasthenia Gravis, Vitiligo, Adrenal insufficiency.

  12. Graves Disease I 123 or TC 99m Normal v/s Graves

  13. Graves Disease

  14. Toxic Multinodular Goiter (TMG) • TMG is the next most common hyperthyroidism - 20% • More common in elderly individuals – long standing goiter • Lumpy bumpy thyroid gland • Milder manifestations (apathetic hyperthyroidism) • Mild elevation of FT4 and FT3 • Progresses slowly over time • Clinically multiple firm nodules (called Plummer’s disease) • Scintigraphy shows - hot and normal areas

  15. Toxic Multinodular Goiter (TMG)

  16. Toxic Multinodular Goiter (TMG)

  17. Sub Acute Thyroiditis (SAT) • SAT is the next most common hyperthyroidism – 15% • T4 and T3 are extremely elevated in this condition • Immune destruction of thyroid due to viral infection • Destructive release of preformed thyroid hormone • Thyroid gland is painful and tender on palpation • Nuclear Scintigraphy scan - no RIU in the gland • Treatment is NSAIDs and Corticosteroids

  18. Toxic Single Adenoma (TSA) • TSA is a single hyper functioning follicular thyroid adenoma. • Benign monoclonal tumor that usually is larger than 2.5 cm • It is the cause in 5% of patients who are thyrotoxic • Nuclear Scintigraphy scan shows only a single hot nodule • TSH is suppressed by excess of thyroxines • So the rest of the thyroid gland is suppressed

  19. Toxic Single Adenoma (TSA) Nucleotide Scintigraphy

  20. Age and Sex • Age • Graves disease 20 to 40 • Toxic MNG > 50 yrs • Toxic Single Adenoma 35 to 50 • Sub Acute Thyroiditis Any age • Sex M : F ratio • Graves Disease 1: 5 to 1:10 • Toxic MNG 1: 2 to 1: 4

  21. Nucleotide Scintigraphy

  22. Clinical Features • Those that occur with any type of thyrotoxicosis • Those that are specific to Graves disease • Non specific changes of hyper metabolism

  23. Common Symptoms • Nervousness • Anxiety • Increased perspiration • Heat intolerance • Tremor • Hyperactivity • Palpitations • Weight loss despite increased appetite • Reduction in menstrual flow or oligo-menorrhea

  24. Common Signs • Hyperactivity, Hyper kinesis • Sinus tachycardia or atrial arrhythmia, AF, CHF • Systolic hypertension, wide pulse pressure • Warm, moist, soft and smooth skin- warm handshake • Excessive perspiration, palmar erythema, Onycholysis • Lid lag and stare (sympathetic over activity) • Fine tremor of out stretched hands – format's sign • Large muscle weakness, Diarrhea, Gynecomastia

  25. Specific to Graves Disease • Diffuse painless and firm enlargement of thyroid gland • Thyroid bruit is audible with the bell of stethoscope • Ophthalmopathy – Eye manifestations – 50% of cases • Sand in eyes, periorbital edema, conjunctival edema (chemosis), poor lid closure, extraocular muscle dysfunction, diplopia, pain on eye movements and proptosis. • Dermoacropathy – Skin/limb manifestations – 20% of cases • Deposition of glycosamino glycans in the dermis of the lower leg – non pitting edema, associated with erythema and thickening of the skin, without pain or pruritus - called (pre tibial myxedema)

  26. Clinical Presentations

  27. MNG and Graves Huge Toxic MNG Diffuse Graves Thyroid

  28. Higher grades of Goiter (Diffuse) Graves Toxic MNG

  29. Grade IV Toxic MNG Huge Toxic MNG Huge Toxic MNG

  30. Thyroid Ophthalmopathy Proptosis Lid lag

  31. Ophthalmopathy in Graves Periorbital edema and chemosis

  32. Ophthalmopathy in Graves Occular muscle palsy Laka Laka Laka

  33. Severe Exophthalmia

  34. Thyroid Dermopathy Pink and skin coloured papules, plaques on the shin

  35. Graves with Acropathy Graves Goiter Acropathy

  36. Thyroid Acropathy Clubbing and Osteoarthropathy

  37. Onycholysis

  38. Non specific changes • Hyperglycemia, Glycosuria • Osteoporosis and hypercalcemia • ↓ LDL and Total Cholesterols • Atrial fibrillation, LVH, ↑ LV EF • Hyper dynamic circulatory state • High output heart failure • H/o excess Iodine, amiodarone, contrast dyes

  39. Nine Square Approach PRIMARY HYPERTHYROID LOW NORMAL HIGH FREE THYROXINE or FT4 LOW NORMAL HIGH THYROID STIMULATING HORMONE - TSH

  40. Nine Square Approach SUB CLINICAL HYPERTHYROID LOW NORMAL HIGH FREE THYROXINE or FT4 LOW NORMAL HIGH THYROID STIMULATING HORMONE - TSH

  41. Diagnosis • Typical clinical presentation • Markedly suppressed TSH (<0.05 µIU/mL) • Elevated FT4 and FT3 (Markedly in Graves) • Thyroid antibodies – by Elisa – anti-TPO, TSI • ECG to demonstrate cardiac manifestations • Nuclear Scintigraphy to differentiate the causes

  42. Algorithm for Hyperthyroidism Measure TSH and FT4  TSH, FT4 N  TSH,  FT4 N TSH, FT4 N  TSH,  FT4 FNAC, N Scan Primary (T4) Thyrotoxicosis Pituitary Adenoma Measure FT3 High T3 Toxicosis Features of Grave’s Normal Sub-clinical Hyper Yes No  RAIU Low RAIU F/u in 6-12 wks Rx. Grave’s www.drsarma.in Sub Acute Thyroiditis, I2, ↑ Thyroxine Single Adenoma, MNG

  43. Treatment Options • Symptom relief medications • Anti Thyroid Drugs – ATD • Methimazole, Carbimazole • Propylthiouracil (PTU) • Radio Active Iodine treatment – RAI Rx. • Thyroidectomy – Subtotal or Total • NSAIDs and Corticosteroids – for SAT

  44. Symptom Relief • Rehydration is the first step • β – blockers to decrease the sympathetic excess • Propranalol, Atenelol, Metoprolol • Rate limiting CCBs if β – blockers contraindicated • Treatment of CHF, Arrhythmias • Calcium supplementation • SSKI or Lugol solution for ↓ vascularity of the gland

  45. Anti Thyroid Drugs (ATD)

  46. How long to give ATD ? • Reduction of thyroid hormones takes 2-8 weeks • Check TSH and FT4 every 4 to 6 weeks • In Graves, many go into remission after 12-18 months • In such pts ATD may be discontinued and followed up • 40% experience recurrence in 1 yr. Re treat for 3 yrs. • Treatment is not life long. Graves seldom needs surgery • MNG and Toxic Adenoma will not get cured by ATD. • For them ATD is not the best. Treat with RAI.

  47. Radio Active Iodine (RAI Rx.) • In women who are not pregnant • In cases of Toxic MNG and TSA • Graves disease not remitting with ATD • RAI Rx is the best treatment of hyperthyroidism in adults • The effect is less rapid than ATD or Thyroidectomy • It is effective, safe, and does not require hospitalization. • Given orally as a single dose in a capsule or liquid form. • Very few adverse effects as no other tissue absorbs RAI

  48. Radio Active Iodine (RAI Rx.) • I123 is used for Nuclear Scintigraphy (Dx.) • I131 is given for RAI Rx. (6 to 8 milliCuries) • Goal is to make the patient hypothyroid • No effects such as Thyroid Ca or other malignancies • Never given for children and pregnant/ lactating women • Not recommended with patients of severe Ophthalmopathy • Not advisable in chronic smokers

  49. Surgical Treatment • Subtotal Thyroidectomy, Total Thyroidectomy • Hemi Thyroidectomy with contra-lateral subtotal • ATD and RAI Rx are very efficacious and easy – so • Surgical treatment is reserved for MNG with • Severe hyperthyroidism in children • Pregnant women who can’t tolerate ATD • Large goiters with severe Ophthalmopathy • Large MNGs with pressure symptoms • Who require quick normalization of thyroid function

  50. Preoperative Preparation • ATD to reduce hyper function before surgery • βeta blockers to titrate pulse rate to 80/min • SSKI 1 to 2 drops bid for 14 days • This will reduce thyroid blood flow • And there by reduce per operative bleeding • Recurrent laryngeal nerve damage • Hypo parathyroidism are complications

More Related