Thyroid disease for the primary care doctor

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Thyroid disease for the primary care doctor

  1. 1. Thyroid disease in primary care
  2. 2. Outline Thyroid anatomy and physiology Hypothyroidism Etiologies and work up Treatment Subclinical hypothyroidism Hyperthyroidism Role of the radioactive iodine uptake (RAIU) Etiologies and work up Treatment options Subclinical hypothyroidism Thyroid nodule Work up
  3. 3. Thyroid gland
  4. 4. Thyroid hormone physiology Most T4 and T3 bound to thyroxine binding globulin (TBG) in serum Unbound T4 (“free T4”) is active Very small changes in free T4 will affect TSH T4 is made exclusively in the thyroid
  5. 5. Hypothyroidism – clinical features Wt gain, high Goiter cholesterol Constipation Depression
  6. 6. Hypothyroidism - Etiologies Autoimmune: #1 cause in iodine sufficient areas Hashimoto’s (aka Chronic autoimmune thyroiditis) Iodine Deficiency is #1 cause worldwide Excess can also cause hypothyroidism Iatrogenic Drugs – Lithium, amiodarone Radioactive Iodine therapy / other radiation Transient (thyroiditis)
  7. 7. Antibodies in thyroid disease Group Anti TSHR Anti Tg Anti TPO General population 0 5-20 8-27 Graves’ disease 80-95 50-70 50-80 Autoimmune thyroiditis 10-20 80-90 90-100 Relatives of people with 0 30-40 30-50 autoimmune thyroiditis Type 1 diabetes 0 30-40 30-40 Pregnant women 0 About 14 About 14 TSHR: thyrotropin (TSH) receptor; Tg: thyroglobulin; TPO: thyroid peroxidase
  8. 8. Hashimoto’s thyroiditis Diagnosis Appropriate clinical setting (often goiter is present) Antibodies present Rule out Graves disease, cancer Biopsy shows lymphocytic infiltration of thyroid Disease course Usually painless (as compared to other thyroiditis) Initially may have transient hyperthyroidism Gradually progresses to overt hypothyroidism Usually permanently hypothyroid
  9. 9. Treatment – different formulations Generic name Composition Brand names Levothyroxine T4 Synthroid Levoxyl Euthyrox Levothroid Unithroid Liothyronine T3 Cytomel Liotrix 4:1 mixture T4 Thyrolar and T3 Thyroid USP Thyroid extract Armour thyroid of pork or beef S-P-T Thyrar Thyroid strong
  10. 10. Treatment – overt hypothyroidism Average replacement dose: 1.6 mcg/kg/day (~125 mcg a day) Initiate treatment with T4 – full dose in young Start low go slow in elderly (particularly those with CAD / angina) T3 has short half life and may cause swings between low and high T3 levels, causing varied symptoms Recheck TSH, T4 in 6 weeks, redose accordingly (T4 half life ~1 week) Continue until TSH returns to normal levels Monitor TSH q yearly once dose stable
  11. 11. T4 pearls Must be taken on an empty stomach Be consistent with brand names or generic formulations (different preparations act differently)
  12. 12. Subclinical hypothyroidism Mildly elevated TSH, normal T4 Often due to Hashimoto’s Usually progresses to overt hypothyroidism if left untreated Linked with atherosclerosis and increased risk of MI in elderly women1 May be related to dyslipidemias 1. Hak A et al. Ann Intern Med 2000 Feb 15;132(4):270-8
  13. 13. Txmt – subclinical hypothyroidism Pros Unrecognized vague symptoms may improve Possible correction of lipids may be cardio protective Will prevent progression to overt hypothyroidism Cons Expensive (medication and monitoring) May exacerbate angina or arrhythmia1 Benefit of treatment is not supported with data and is controversial 1. Chu JW et al. J Clin Endocrinol Metab 2001 Oct;86(10):4591-9.
  14. 14. “Guidelines” Recommendations1 (2004 clinical consensus group): Initiate treatment with T4 if TSH >10 Goal TSH is to return to normal levels Consider treatment also if pt pregnant, has ovulatory problems, having behavioral problems 1. Sirks MI et al. JAMA 2004 Jan 14;291(2):228-38
  15. 15. Special considerations Surgical patients Urgent surgeries should not be postponed If NPO no need for IV thyroid hormone until ~1 week Pregnant patients Thyroid needs go up (fetus, T4 clearing, incr TBG) TSH must be measured once every trimester
  16. 16. Screening for hypothyroidism NHANES III1 ~13,000 people had thyroid function tests 4.6% found to have hypothyroidism (0.3 overt, 4.3 subclinical) Q 5-year screening in everyone found to be NOT cost effective2 Recommendations of various groups conflict Only screening in elderly is somewhat recommended Insurance companies will not pay for screening TSH in asymptomatic patient 1. Hollowell JG et al. J Clin Endocrinol Metab 2002 Feb;87(2):489-99 2. Danese MD et al. JAMA 1996 Jul 24-31;276(4):285-92.
  17. 17. Hypothyroidism – flowsheet review High TSH Check fT4 Low free T4 Normal free T4 (subclinical hypothyroidism) Check TPO, TG, TSHR Ab + TPO antibody - TPO antibody Probable Hashimoto’s ?pregnant, ovulatory dysfunction, hyperlipidemia, behavior problem, goiter? Yes to any of above No Yearly follow up Start T4 therapy If TSH becomes >10
  18. 18. Outline Thyroid anatomy and physiology Hypothyroidism Etiologies and work up Treatment Subclinical hypothyroidism Hyperthyroidism Role of the radioactive iodine uptake (RAIU) Etiologies and work up Treatment options Subclinical hypothyroidism Thyroid nodule Work up
  19. 19. Hyperthyroidism – clinical features Bone thinning Goiter Weight loss Atrial fibrillation
  20. 20. Radioactive Iodine Uptake (RAIU) Radioactive iodine given to patient to ingest Detector placed over thyroid in 24h % of dose taken up reported No pretty pictures! NOT THE SAME AS RADIONUCLIDE THYROID SCAN
  21. 21. RAIU High RAIU Thyroid is making a lot of thyroid hormone (requiring uptake of large amounts of iodine) Low RAIU Thyroid gland is not making extra hormone Thyroid saturated with iodine
  22. 22. Etiologies of hyperthyroidism HIGH RAIU LOW RAIU Graves Disease Thyroiditis: Inflammation of #1 cause of hyperthyroidism thyroid causes release of Toxic (“hot”) nodules: preformed thyroid hormone #2 cause Exogenous thyroid hormone Hyperplasia of follicular cells, Iodine excess: independent of TSH regulation Uncommon; usually from Tumors: medications (IV contrast, Germ cell tumors, amiodarone) choriocarcinoma, hydatidiform moles stimulate TSH receptor
  23. 23. Graves’ Disease Autoimmune disease Assoc with thyroid autoantibodies 5x more common in women, usually 30-50 y/o TSH receptor stimulating IgG Clinical triad: Goiter (70% of cases) Opthalmopathy Dermopathy (pretibial myxedema)
  24. 24. Antibodies in thyroid disease Group Anti TSHR Anti Tg Anti TPO General population 0 5-20 8-27 Graves’ disease 80-95 50-70 50-80 Autoimmune thyroiditis 10-20 80-90 90-100 Relatives of people with 0 30-40 30-50 autoimmune thyroiditis Type 1 diabetes 0 30-40 30-40 Pregnant women 0 About 14 About 14 TSHR: thyrotropin (TSH) receptor; Tg: thyroglobulin; TPO: thyroid peroxidase
  25. 25. Thyroiditis -Wide spectrum of diseases that overlap with each other -Usually cause transient hyperthyroidism hypothyroidism resolution within 8-10 weeks PAINFUL PAINLESS Subacute granulomatous (aka de Hashimoto’s Quervains) Usually leads to permanent Pain radiates to the ear hypothyroidism Infectious: viral or bacterial Silent (aka “painless” aka subacute lymphocytic) Viral much more common, usually after URI Variant of Hashimoto’s Radiation Postpartum 7-10 d after starting radioactive Drug induced iodine treatment IFN alfa, IL-2 Amiodarone Lithium Fibrous (aka Riedel’s) Adjacent tissue invasion causes neck pain
  26. 26. Amiodarone and thyroid disease 37% iodine Half life is 100 days RAIU is always low (thyroid is always saturated with iodine already) Hyperthyroidism Thyroiditis (unclear mechanism) Iodine excess can cause hyperthyroidism Hypothyroidism Iodine excess can cause hypothyroidism Blocks T4 to T3 conversion Check TSH before starting, q3 months when on medication
  27. 27. Treatment – Graves’ Disease Beta blocker to help autonomic symptoms 3 options to treat thyroid – radioactive iodine, surgery, or medications 1 trial comparing 3 methods, each were equally effective in normalizing TSH within 6 weeks1 Radioactive Iodine (I131) Most popular treatment in US (less popular in Europe / Japan) Doses sufficient to cure hyperthyroidism usually lead to permanent hypothyroidism within 12 weeks (3% a year) Surgery (remove thyroid) Unpopular for Grave’s Disease; recommended if large goiter 1. Torring O et al. J Clin Endocrinol Metab 1996 Aug;81(8):2986-93
  28. 28. Treatment – Graves’ Disease Medication - thionamides (Propylthiouracil or Methimazole) Inhibit iodine processing by thyroid PTU also blocks T4 to T3 conversion (give for prethyroidectomy prophylaxis if needed) Often used for symptom relief prior to surgery or radioactive iodine Methimazole is preferred (fewer side effects, ease of dosing) except for pregnant patients (harmful to fetus) and pre surgical prophylaxis 30% people can achieve long term remission
  29. 29. Treatment – Toxic nodular disease Radioactive iodine Extremely effective and localizes to nodules Patients often do NOT become hypothyroid Surgery Indicated if large goiter is present, recommended if co existing cold nodules present Medications Rarely achieve remission with these alone (unlike Graves) Usually used to achieve euthyroid state before more definitive therapy
  30. 30. Subclinical hyperthyroidism Low TSH, normal T4 and T3 Same etiologies of overt hyperthyroidism (endogenous causes) Progression to overt hyperthyroidism is uncommon (4% a year)1 Also caused by too high of a T4 dose (exogenous) Clinical manifestations similar to overt hyperthyroidism Higher risk for AFib (13% of patients in one study as opposed to 14% of patients with overt hyperthyroidism and 2% of euthyroid pt’s)2 Decreased LDL Decreased bone density 1. Sandrock D et al. Acta Endocrinol (Copenh) 1993 Jan;128(1):51-5 2. Auer J et al. Am Heart J 2001 Nov;142(5):838-42.
  31. 31. Txmt – subclinical hyperthyroidism Little data to guide treatment Recommendations1 (2004 clinical consensus group): High risk patients (elderly or post menopausal not on HRT) If TSH <0.1, evaluate and treat If 0.1 to 0.5, treat if bone density is low or thyroid radionuclide scan has focal hot area; observe if all studies are negative Low risk patients If TSH <0.1, consider treatment if bone density low or thyroid radionuclide scan has hot area If TSH 0.1 to 0.5, monitor 1. Surks MI et al. JAMA 2004 Jan 14;291(2):228-38
  32. 32. Low TSH Hyperthyroidism – flowsheet review Check free T4 Elevated Normal (subclinical hyperthyroidism) Risk stratify RAIU High risk pt High RAIU Low RAIU Low risk pt (elderly, post -Graves’ -Thyroiditis menopausal) -Toxic nodule(s) -Iodine excess -Tumor (rare) -Amiodarone Consider treatment if Treat if TSH TSH <0.1 with <0.1, consider bone disease; treatment if <0.5 otherwise with bone dz monitor yearly Treat underlying Treat (medication vs cause I131 vs surgery)
  33. 33. Outline Thyroid anatomy and physiology Hypothyroidism Etiologies and work up Treatment Subclinical hypothyroidism Hyperthyroidism Role of the radioactive iodine uptake (RAIU) Etiologies and work up Treatment options Subclinical hypothyroidism Thyroid nodule Work up
  34. 34. Work up of thyroid nodule FNA and biopsy as initial test of thyroid nodules Some patients with larger benign FNA’s may receive T4 to try to shrink nodule
  35. 35. Radionuclide thyroid scans HOT COLD
  36. 36. Take home points Screening for hypothyroidism is controversial Considered q5 years especially in the elderly Name brand vs generic thyroid hormone replacement can be different Check TSH ~4-6 weeks after changing doses #1 cause of hypothyroidism = Hashimoto’s #1 cause of hyperthyroidism = Graves Low RAIU = thyroiditis and iodine excess (e.g. amiodarone) Treat subclinical thyroid disease when appropriate!

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