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Thyroid Overview

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    • 1. Thyroid Overview
    • 2. Objectives
      • Recognize the clinical findings of hypothyroidism.
      • Understand how to diagnose hypothyroidism: distinguish between Primary Hashimoto’s and Primary Subacute Hypothyroidism.
      • Understand the role of thyroid functional scans in the diagnosis of hypothyroidism.
      • Know the specific cellular activities that are overactive in Grave’s disease.
      • Understand how to diagnose Grave’s disease.
    • 3. Thyroid Hormone Physiology Review
      • Thyroid gland releases T4 and T3
      • Thyroid follicular cells uptake iodine.
      • Iodine oxidized & incorporated into MIT & DIT
      • Coupling of iodotyrosine with thyroglobuline forms T3 & T4.
      • Poteolysis of the thyroglbuline molecule releases MIRT, DIT, T3, T4 .
      • MIT and DIT are deiodinated and the liberated iodine is reused.
      • T4 & T3 (to a much lesser extent) released from thyroid.
      • TPO (thyroperoxidate) medicates thyroid hormone synthesis.
        • (mediates both: Oxidation of iodine; incorporation into tyrosyl resudues).
      • Thyroid hormones transported to carrier proteins. .04% of T4 is free; .4% of T3 is free; the free form is the biologically active form able to bind to thyroid receptors.
      • T3 has a much higher affinity for the thyroid receptor than T4.
      • The body regulates thyroid activity by converting T4 to T3 (by deiodinases).
      • Free thyroid hormone is transported through cell membrane by a carrier and binds to thyroid receptors (TR).
      • Thyroid function is regulated by the hypothalamic-pituitary-thyroid axis.
      • Synthesis of T4 and T3 regulated by TSH.
      • A negative feedback loop is present.
    • 4. Thyroid physiology
    • 5. Labs
      • Serum Total T4 ( Thyroxin) reflects thyroid hormone activity. Measures both free and bound T4 in healthy patients.
      • Serum Total T3 (Triiodothyronine) measures both free and bound T3 .
      • (TBG) is the major thyroid hormone binding proteins.
        • Other proteins with binding capacity: transthyretin (thyroxine-binding prealbumin) and albumin.
      • TSH is the only test that can detect small changes of thyroid hormone excess or deficiency.
      • Free Thyroid Hormone
        • (rarely ordered) Usually what is reported is an estimate of free T4 which is a calculated Free T4 Index (FT4 I)
    • 6. Labs
      • ╬ Serum TSH is the best SCREENING test for the diagnosis of hypothyroidism or hyperthyroidism in healthy ambulatory individuals.
      • TSH is the initial test done to assess thyroid function and the only test needed if it is normal.
    • 7. ╬ Possible Test Question
      • Which of the following is the best screening test for the diagnosis of hypothyroidism or hyperthyroidism in healthy ambulatory individuals.
      • Radioiodine I-123 uptake
      • Free T3
      • Free T4 Index
      • TSH (Correct answer)
      • TSH and functional scan
    • 8. Objective 1
      • Recognize the clinical findings of hypothroidism.
      • Understand how to diagnose hypothyroidism: distinguish between Primary Hashimoto’s and Primary Subacute Hypothyroidism.
      • Understand the role of thyroid functional scans in the diagnosis of hypothyroidism.
      • Know the specific cellular activities that are overactive in Grave’s disease.
      • Understand how to diagnose Grave’s disease.
    • 9. Clinical Findings of Hypothyroidism (part 1)
      • Skin:dry, rough, non-pitting edema in lower extremities (myxedema), coarse hair, hair loss (lateral aspects of eyebrows).
      • Ocular: swelling of eyelids.
      • CV: Bradycardia, impared contraction with reduced cardiac output, cardiomegaly, pericardial effusion, increased incidence of coronary atherosclerosis.
      • Pulmonary: Shortnes of breath and resp. failure with mexedema coma.
      • ENT: Husky voice due to infiltration of vocal cords, enlarged tongue with associated garbled voice and sleep apnea.
      • GI: Reduced appetite, (increased weight is due to water retention), constipation, atrophic gastritis (50%), B12 malabsorption (12%).
      • CNS: severe brain damage in children born with hypothyroidism (cretinism) - the earlier the treatment the better the result. Reduced concentration, lethargy, coma, carpal tunnel. Slow relaxation phase of reflexes due to muscle dysfunction.
      • Muscles: Stiff, ache, elevated CPK and SGOT.
      • Anemia: mild normochromic normocitic is most common. Microcitic due to iron malabsorption; macrocitic due to B12 malabsorption.
    • 10. Clinical Findings of Hypothyroidism(part 2)
      • Renal: Glomerular filtration rate, renal plasma flow, tubular reabsorption are reduced (however - BUN and creatinine are normal); water excretion impaired.
      • Myxedema Coma: (decompensated hypothyroidism)
        • end stage of severe long-standing hypothyroidism,
        • mental obtundation is profound.
        • an endocrine emergencies as the mortality is over 50%.
        • usually accompanied by a subnormal temperature, bradycardia, and hypotension are present.
    • 11. Hypothyroidism
      • Epidemiology/pathophysiology;
      • 5 to 10% over 65
      • Causes:
      • *Defect within thyroid gland (Primary)
      • (accounts for ~98% of hypothyroidism)
      • *Deficiency of TSH (secondary)
      • *Deficiency of THR (tertiary or hypthalamic)
      • *Peripheral Tissue resistance to thyroid hormone
    • 12. Primary Hypothyroidism
    • 13. Labs
      • ╬ In primary hypothyroidism (99% of hypothyroidism) TSH is elevated.
      • TSH is one of the most sensitive tests in medicine.
    • 14. Labs
      • Order T4 after TSH if:
        • hypothalamic/pituitary disease is suspected
          • then a measure of free T4 (index or direct assay) is needed together with TSH.
        • significant alterations in binding proteins are expected,
          • then a measure of free T4 (index or direct assay) is needed together with TSH.
            • Clinical conditions associated with elevation in thyroid hormone binding proteins include active hepatitis, pregnancy, drugs (estrogen, raloxifene, tamoxifen, 5-fluorouracil, perphenazine, clofibrate, heroin and methadone), acute intermittent porphyria and hereditary TBG excess.
            • Clinical conditions associated with reduction in thyroid hormone binding proteins include cirrhosis, nephrotic syndrome, protein losing enteropathies, malnutrition, severe illness, drugs (androgens, glucocorticoids), and hereditary TBG deficiency.
    • 15. Primary Hypothyroidism
      • Types of primary hypothyroidism
        • Hashimoto’s thyroiditis
        • Subacute thyroiditis
        • Iatragenic
        • Drugs
        • Iodine deficiency
        • Dyshormonogenesis
        • Primary and Metastatic Tumor to the Thyroid (rare)
    • 16. Objective 2
      • Recognize the clinical findings of hypothroidism.
      • Understand how to diagnose hypothyroidism: distinguish between Primary Hashimoto’s and Primary Subacute Hypothyroidism.
      • Understand the role of thyroid functional scans in the diagnosis of hypothyroidism.
      • Know the specific cellular activities that are overactive in Grave’s disease.
      • Understand how to diagnose Grave’s disease.
    • 17. Primary Hypothyroidism
      • Types of primary hypothyroidism
      • *Hashimoto’s thyroiditis:
          • Most common cause of primary hypothyrodism.
          • Etiology: autoimmune destruction of the thyroid gland
          • ╬ TSH is elevated.
          • ╬ Anti-thyroglobuline and/or anti-TPO antibodies are present in most (90%) patients.
          • Autoimmune thyroiditis may coexist with other autoimmune diseases: pernicious anemia, RA, DM, “Burnt out” Grave’s disease.
        • Subacute thyroiditis
        • Iatragenic
        • Drugs
        • Iodine deficiency
        • Dyshormonogenesis
        • Primary and Metastatic Tumor to the Thyroid (rare)
    • 18. ╬ Lab summary - hypothyroidism
    • 19. Primary Hypothyroidism
      • Types of primary hypothyroidism
        • Hashimoto’s thyroiditis:
      • *Subacute thyroiditis (hypothryroid phase):Aka: granulomatous, lymphocytic or postpartum thyroiditis . . . . . . . . . .
        • Iatragenic
        • Drugs
        • Iodine deficiency
        • Dyshormonogenesis
    • 20. Subacute thyroiditis-hypothyroid phase
      • Etiology: destruction of the thyroid gland
      • *(often due to upper respiratory illness).
      • *Destruction leads to release of thyroid hormone in circulation (rather than from an increase in synthesis of hormone).
      • Symptoms: depends on phase
      • Radioiodine I-123 uptake: low
      • Outcome:
      • 1. after thyrotoxic phase,
      • 2. subacute thyroiditis may progress to transient (6 - 12 months) hypothyroidism (90% are transient)
      • 3. return to euthyroidism
      • Supportive treatment only; no inhibitors of thyroid hormone synthesis are needed.
      • ╬ TSH is elevated; Anti-thyroglobuline and/or anti-TPO antibodies are not present.
      • It is important not to erroneously diagnose these patients with Hashimoto's and commit them to life-long thyroid hormone replacement therapy.
    • 21. ╬ Lab summary - hypothyroidism
    • 22. Primary Hypothyroidism
      • Types of primary hypothyroidism
        • Hashimoto’s thyroiditis:
        • Subacute thyroiditis:
      • *Iatragenic:
        • Post ablative following radioactive iodine administration or after thyroidectomy.
      • *Drugs:
        • Lithium, amiodarone (~40% iodine), high intake of iodine such as in seaweed or algae tablets from health food stores.
      • *Iodine deficiency:
        • in some less developed countries - goiter is present .
      • *Dyshormonogenesis:
        • Enzymatic defects in thyroid hormone biosynthesis lead to poor hormone secretion and development of goiter. This is a rare cause of hypothyroidism, especially in the adult patient. Failure of the thyroid gland to descend during embryogenenesis may also cause congenital hypothyroidism.
      • *Primary and Metastatic Tumor to the Thyroid (rare)
    • 23. Secondary Hypothyroidism
      • Adults:
        • Almost always due to pituitiary disease.
        • ╬ TSH is low or normal.
        • TSH may not be a biologically active as usual, but still detected in the TSH assay; TSH is called, “inappropriately normal.”
      • Selective TSH deficiency:
        • Very rare genetic cause of newborn hypothyroidism
        • May be seen in adults due to autoimmunity against thyrotrophs (cells that produce TSH).
    • 24. ╬ Lab summary - hypothyroidism
    • 25. Tertiary Hypothryroidism
      • Due to hypothalamic disease:
        • sarcoidosis
        • tumors
        • radiation
    • 26. Resistance to Thyroid Hormone
      • Peripheral resistance to thyroid hormone is very rare.
      • Beyond scope of this lecture.
    • 27. Functional Thyroid Imaging
      • Radioactive iodine (I-123), administered orally
      • the radioisotope and a scan (image) of the thyroid obtained 4 or 24 hours later.
      • I-123 is accumulated by thyroid follicular cell & incorporated into thyroglobulin (trapped and organified).
    • 28. Imaging
      • Radionuclide Imaging of the Thyroid
      • The radiotracer uptake is increased whenever thyroid under increased stimulus:
      • *Raised TSH
      • *Stimulating antibody of Grave’s disease
      • *When thyroid becomes autonomous (“hot” nodule or toxic multinodular goiter).
    • 29. Imaging
      • Radionuclide Imaging of the Thyroid
      • The radiotracer uptake is decreased whenever the thyroid is under decreased stimulus:
      • decreased TSH in hypopituitarism
      • exogenous thyroid hormone administration
      • when thyroid cells are damaged so that the uptake mechanism is defective
      • Hashimoto's thyroiditis:
      • autoimmune destruction of the thyroid gland;
      • Anti-thyroglobuline and/or anti-TPO antibodies are present in most (90%) patients
      • Subacute thyroiditis:
      • Destruction leads to release of thyroid hormone in circulation (rather than from an increase in synthesis of hormone).
      • When excess iodine "swamps" the radioactive tracer.
    • 30. Objective 3
      • Recognize the clinical findings of hypothroidism.
      • Understand how to diagnose hypothyroidism: distinguish between Primary Hashimoto’s and Primary Subacute Hypothyroidism.
      • Understand the role of thyroid functional scans in the diagnosis of hypothyroidism.
      • Know the specific cellular activities that are overactive in Grave’s disease.
      • Understand how to diagnose Grave’s disease.
    • 31. Imaging
      • ╬ Thyroid functional scans they are not helpful in the diagnosis of hypothyroidism and should not be used for this indication.
      • Hashimoto's thyroiditis :
      • autoimmune destruction of the thyroid gland;
      • Anti-thyroglobuline and/or anti-TPO antibodies are present in most (90%) patients.
      • DECREASED UPTAKE
      • Subacute thyroiditis:
      • Destruction leads to release of thyroid hormone in circulation (rather than from an increase in synthesis of hormone).
      • DECREASED UPTAKE
      • Thyroid functional scans are helpful in the differential diagnosis of hyperthyroidism and in determining the function of a thyroid nodule
    • 32. Imaging
      • ╬ Thyroid functional scans they are not helpful in the diagnosis of hypothyroidism and should not be used for this indication.
      • Hashimoto's thyroiditis :
      • DECREASED UPTAKE
      • Subacute thyroiditis:
      • DECREASED UPTAKE
    • 33. Other Thyroid Imaging
      • CT and MRI:
        • structural imaging modalities and provide no functional information.
        • NO role in the initial evaluation of thyroid dysfunction.
      • Ultrasound:
        • modality of choice for evaluation of thyroid structure (e.g. evaluation of thyroid nodules).
      • CT or MRI:
        • may be used to:
          • visualize a large substernal goiter
          • evaluate tracheal compression.
    • 34. . . . Hypothyroidism and pregnancy
      • Maternal hypothyroidism during pregnancy may lead to adverse fetal outcomes.
        • lower IQ as adolescents.
        • It is controversial whether all pregnant women should be screened for hypothyroidism.
        • Women with known hypothyroidism prior to pregnancy should have their dose of levothyroxine adjusted to maintain normal thyroid levels before conception and during pregnancy.
    • 35. Objective 4
      • Recognize the clinical findings of hypothroidism.
      • Understand how to diagnose hypothyroidism: distinguish between Primary Hashimoto’s and Primary Subacute Hypothyroidism.
      • Understand the role of thyroid functional scans in the diagnosis of hypothyroidism.
      • Know the specific cellular activities that are overactive in Grave’s disease.
      • Understand how to diagnose Grave’s disease.
    • 36. Hyperthyroidism: clinical findings
      • Weight loss
      • Heat intolerance
      • Insomnia
      • Sweating
      • Anxiety
      • Hyperkinesis
      • Dyspena
      • Palpitations
      • Atrial fibrilation
      • Irregular menses
      • Infertility
      • Increased frequency of bowel movements
      • Myalgia
    • 37. Hyperthyroidism - with low TSH
      • Grave’s Disease
      • Toxic Multinodular Goiter
      • Hyperthyroid phase of thyroiditis
      • Toxic Adenoma
      • Iodine-induced
      • Metastatic thyroid carcinoma, rare.
      • Excess beta-HCG from a molar pregnancy or choriocarcinoama
      • Ectopic/Exogenous, rare
    • 38. Grave’s Disease
      • 60-70% of all cases of hyperthyroidism.
      • 3% of population affected.
      • Female:Male ratio is 5:1 in 3rd or 4th decade.
    • 39. Graves Disease Findings
      • Weight loss
      • Heat intolerance
      • Insomnia
      • Sweating
      • Anxiety
      • Hyperkinesis
      • Dyspena
      • Palpitations
      • Atrial fibrilation
      • Irregular menses
      • Infertility
      • Increased frequency of bowel movements
      • Myalgia
      • Proximal Muscle weakenss
      • Eye findings:
      • *lid retraction
      • *lid lag
      • *stare
    • 40. Grave’s Disease
      • May be cyclic with exacerbations and remissions.
      • Usually, ongoing destructive inflammation of thyroid gland.
      • Eventually leads to “burn out” form of the disease and resulting hypothyroidism.
      • Getting to hypothyroid state may take many years.
    • 41. Grave’s Disease
      • Familial predisposition
      • Overlap with automimmune Hashimoto’s thyroiditis and the associated:
        • Pernicious anemia
        • Myasthenia gravis
        • Vitiligo
        • Addisons disease
        • Type 1 Diabetes Mellitus
    • 42. Grave’s Disease
      • *Cause: circulating antibodies against various thyroid antigens.
        • The most important antibody:
          • The TSH receptor antibody (TSH-R Ab) is directed against the TSH receptor on the thyroid follicular cell membrane.
          • Other antibodies present:
            • Antibodies agains thyroid peroxidase (TPO)
            • Antibodies against thyroglobulin (TG
        • TSH-R Ab most often act as TSH receptor agonists.
          • increasing the activity of adenylate cyclase
          • increasing intracellular cyclic AMP levels
      • ╬ result in cellular overactivity:
              • increased iodine uptake
              • Increased thyroid hormone synthesis
              • Increased thyroid release
    • 43. Grave’s Disease
      • Cause: circulating antibodies against various thyroid antigens.
        • The most important antibody:
          • The TSH receptor antibody (TSH-R Ab) is directed against the TSH receptor on the thyroid follicular cell membrane.
          • Other antibodies present:
            • Antibodies agains thyroid peroxidase (TPO)
            • Antibodies against thyroglobulin (TG
        • * TSH-R Ab most often act as TSH receptor agonists.
          • increasing the activity of adenylate cyclase
          • increasing intracellular cyclic AMP levels
      • ╬ result in cellular overactivity:
              • increased iodine uptake
              • Increased thyroid hormone synthesis
              • Increased thyroid release
    • 44. Grave’s Disease
      • Cause: circulating antibodies against various thyroid antigens.
        • The most important antibody:
          • The TSH receptor antibody (TSH-R Ab) is directed against the TSH receptor on the thyroid follicular cell membrane.
          • Other antibodies present:
            • Antibodies agains thyroid peroxidase (TPO)
            • Antibodies against thyroglobulin (TG
        • TSH-R Ab most often act as TSH receptor agonists.
          • increasing the activity of adenylate cyclase
          • increasing intracellular cyclic AMP levels
      • ╬ result in cellular overactivity:
              • increased iodine uptake
              • Increased thyroid hormone synthesis
              • Increased thyroid release
    • 45. Objective 5
      • Recognize the clinical findings of hypothroidism.
      • Understand how to diagnose hypothyroidism: distinguish between Primary Hashimoto’s and Primary Subacute Hypothyroidism.
      • Understand the role of thyroid functional scans in the diagnosis of hypothyroidism.
      • Know the specific cellular activities that are overactive in Grave’s disease.
      • Understand how to diagnose Grave’s disease.
    • 46. Grave’s Disease
      • Labs
      • Increased T4 and T3
      • sometimes only T3 is elevated
      • Decreased TSH
      • ╬ IF TSH depressed, T3 T4 increased, & patient has Grave’s ophthalmopathy:
      • *lid retraction,
      • *stare,
      • *lid lag,
      • Then - your evaluation is finished; your diagnosis is made.
    • 47.
      • IF: TSH LOW; T3 T4 HIGH; EYE SIGNS; THEN, YOU DO NOT ORDER A SCAN. IF: TSH LOW; T3 T4 HIGH; EYE SIGNS; THEN, YOU DO NOT ORDER A SCAN. IF: TSH LOW;T3 T4 HIGH; EYE SIGNS; THEN, YOU DO NOT ORDER A SCAN. IF:TSH LOW; T3 T4 HIGH; EYE SIGNS; THEN, YOU DO NOT ORDER A SCAN. IF: TSH LOW; T3 T4 HIGH; EYESIGNS; THEN, YOU DO NOT ORDER A SCAN. IF: TSH LOW; T3 T4 HIGH; EYE SIGNS; THEN, YOU DO NOT ORDER A SCAN. IF: TSH LOW; T3 T4 HIGH; EYE SIGNS; THEN, YOU DO NOT ORDER A SCAN. IF: TSH LOW; T3 T4 HIGH; EYE SIGNS; THEN, YOU DO NOT ORDER A SCAN. IF: TSH LOW; T3 T4 HIGH; EYE SIGNS; THEN, YOU DO NOT ORDER A SCAN. IF: TSH LOW; T3 T4 HIGH; EYE SIGNS; THEN, YOU DO NOT ORDER A SCAN. IF: TSH LOW; T3 T4 HIGH; EYE SIGNS; THEN, YOU DO NOT ORDER A SCAN. IF: TSH LOW; T3 T4 HIGH; EYE SIGNS; THEN, YOU DO NOT ORDER A SCAN. IF: TSH LOW; T3 T4 HIGH; EYE SIGNS; THEN, YOU DO NOT ORDER A SCAN. IF: TSH LOW; T3 T4 HIGH; EYE SIGNS; THEN, YOU DO NOT ORDER A SCAN. IF: TSH LOW; T3 T4 HIGH; EYE SIGNS; THEN, YOU DO NOT ORDER A SCAN. IF: TSH LOW; T3 T4 HIGH; EYE SIGNS; THEN, YOU DO NOT ORDER A SCAN.
    • 48. . . . however . . .
      • IF TSH depressed, T3 T4 increased, & no ophthalmopathy:
      • Then get a Radioactive (I-123) scan:
      • Graves I-123 scan results will be:
      • elevated, diffuse, symmetric,
      • In Grave’s: I-123 uptake Thyroid autoantibodies may also be present:
      • anti-TPO (measured in clinical practice)
      • anti-TG
      • TSH-R Ab (not readily available)
      • In Graves: Orbital CT or MRI retro-orbital inflammation.
    • 49. Subacute Thyroiditis - hyperthyroid phase
      • Etiology: destruction of the thyroid gland
      • *(often due to upper respiratory illness).
      • *Destruction leads to release of thyroid hormone in circulation (rather than from an increase in synthesis of hormone).
      • Symptoms: same without Grave’s eye findings (in hyperthyroid phase.
      • Radioiodine I-123 uptake: low
      • Outcome:
      • after thyrotoxic phase,
      • subacute thyroiditis may progress to transient (6 - 12 months) hypothyroidism
      • Supportive treatment only; no inhibitors of thyroid hormone synthesis are needed.
    • 50. Compare: Graves vs Subacute Thyroiditis hyperthyroid phase ______________________________________________________________________________________________________________________________________________________________________________________________________________________________________________ Graves : Subacute Thyroiditis hyperthyroid phase
        • TSH-R Ab most often act as TSH receptor agonists
          • result in cellular overactivity:
            • Increased thyroid hormone synthesis.
            • Increased thyroid release
        • Etiology: destruction of the thyroid gland
          • Result in cellular underactivity
            • leads to release of thyroid hormone in circulation
            • (rather than from an increase in synthesis of hormone ).
      Radioiodine I-123 uptake: high Radioiodine I-123 uptake: low Eye signs: present Eye signs: not present
    • 51. Toxic Multinodular Goiter (MNG)
      • Frequency: 20-30% of hyperthyroid patients.
      • Pathophysiology: follicles - with some degree of autonomy - become large enough to increase overall hormone production. (Large doses of iodide can precipitate thyrotoxicosis in patients with non-toxic multinodular goiters).
    • 52. Toxic Multinodular Goiter (MNG)
      • Labs:
      • *TSH suppressed;
      • *T4 and T3 (high, normal, slightly elevated)
      • Radioiodine (I-123) scan:
      • *Areas of “hot” or “warm”
      • *With areas of “cold” uptake (corresponding to multiple nodules).
    • 53. Toxic Ademoma
      • 3-5% of thyrotoxicosis
      • Cause:
      • * a single hyperfunctioning follicular thyroid adenoma
          • ~50% have an activating mutation in the TSH receptor causing overproduction of thyroid hormone in the monoclonal tumor
      • Excess thyroid hormone is produced;
      • Reduces TSH;
      • Remainder of thyroid gland remains quiet
      • Radiodine I-123 scan:
      • *One “hot” nodule;
      • *Remainder of gland is suppressed.
    • 54. Iodine-induced Thyrotoxicosis
      • Administering iodine may cause thyrotoxicosis in patients with:
      • *iodine deficiency (endemic) goiter
      • *Multinodular goiter (with areas of autonomy or an Autonomous nodule)
      • Pathogenesis: ? Perhaps loss of normal adaptation of thyroid to iodine excess. (Usually mild and remits after stopping the iodine therapy).
    • 55. Troma Ovarii
      • Ectopic thyroid tissue
        • Dermoid tumors
        • Ovarian teratoma
      • Radioiodide scan of neck: decreased uptake
      • Radioiodid scan of pelvic area: shows increased uptake
      • Tx: remove tumor.
    • 56. TSH producing Pituitary Tumor
      • Very rare
      • TSH high; T4 T3 high
    • 57. Other causes of thyrotoxicosis
      • Metastatic Thyroid Carcinoma
      • Molar Hydatiform Pregnancy and Choriocardinoma
      • Thyrotoxicosis Factitia: serrupticious ingestion of thyroid hormone. Seen in psychiatric patients, medical professionals, or people wanting to lose weight.
      • Decreased:
        • TSH
        • Radioiodid I-123 uptake
        • secretion of thyroglobulin
    • 58. Nuclear Imaging for thyrotoxicosis summary
    • 59. OBJECTIVES
      • Understand how to diagnose hypothyroidism: distinguish between Primary Hashimoto’s and Primary Subacute Hypothyroidism.
      • Understand the role of thyroid functional scans in the diagnosis of hypothyroidism.
      • Recognize the clinical findings of hypothroidism.
      • Know the specific cellular activities that are overactive in Grave’s disease.
      • Understand how to diagnose Grave’s disease .
    • 60. ╬ Possible Test Question
      • Which of the following is the best screening test for the diagnosis of hypothyroidism or hyperthyroidism in healthy ambulatory individuals.
      • Radioiodine I-123 uptake
      • Free T3
      • Free T4 Index
      • TSH (Correct answer)
      • TSH and functional scan
    • 61.
    • 62.
      • ╬ In primary hypothyroidism (99% of hypothyroidism) TSH is elevated.
      • ╬ Serum TSH is the best SCREENING test for the diagnosis of hypothyroidism or hyperthyroidism in healthy ambulatory individuals.
      • ╬ Thyroid functional scans they are not helpful in the diagnosis of hypothyroidism and should not be used for this indication.
      • Hashimoto’s thyroiditis:
          • ╬ TSH is elevated.
          • ╬ Anti-thyroglobuline and/or anti-TPO antibodies are present in most (90%) patients.
      • Subacute thyroiditis - hypothyroid phase:
          • ╬ TSH is elevated.
          • ╬ Anti-thyroglobuline and/or anti-TPO antibodies are NOT present.
          • Radioiodine I-123 uptake: low (may order in hyperthyroid phase)
      • ╬ RECOGNIZE THE CLINICAL FINDINGS OF HYPOTHYROIDISM (TOO MANY TO LIST).
      • ╬ C ellular overactivities of Grave’s disease: increased iodine uptake, Increased thyroid hormone synthesis, Increased thyroid release (as a result of the TSH receptor agonist, TSH-R Ab).
      • ╬ IF TSH depressed, T3 T4 increased, Grave’s ophthalmopathy (lid retraction, stare, lid lag) are present, then - your evaluation is finished; your diagnosis is made. (You do not need a functional scan for the diagnosis).