Thyroid Overview
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Thyroid Overview

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Thyroid Overview Thyroid Overview Presentation Transcript

  • Thyroid Overview
  • 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.
  • 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.
    View slide
  • Thyroid physiology View slide
  • 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)
  • 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.
  • ╬ 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
  • 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.
  • 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.
  • 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.
  • 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
  • Primary Hypothyroidism
  • Labs
    • ╬ In primary hypothyroidism (99% of hypothyroidism) TSH is elevated.
    • TSH is one of the most sensitive tests in medicine.
  • 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.
  • Primary Hypothyroidism
    • Types of primary hypothyroidism
      • Hashimoto’s thyroiditis
      • Subacute thyroiditis
      • Iatragenic
      • Drugs
      • Iodine deficiency
      • Dyshormonogenesis
      • Primary and Metastatic Tumor to the Thyroid (rare)
  • 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.
  • 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)
  • ╬ Lab summary - hypothyroidism
  • Primary Hypothyroidism
    • Types of primary hypothyroidism
      • Hashimoto’s thyroiditis:
    • *Subacute thyroiditis (hypothryroid phase):Aka: granulomatous, lymphocytic or postpartum thyroiditis . . . . . . . . . .
      • Iatragenic
      • Drugs
      • Iodine deficiency
      • Dyshormonogenesis
  • 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.
  • ╬ Lab summary - hypothyroidism
  • 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)
  • 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).
  • ╬ Lab summary - hypothyroidism
  • Tertiary Hypothryroidism
    • Due to hypothalamic disease:
      • sarcoidosis
      • tumors
      • radiation
  • Resistance to Thyroid Hormone
    • Peripheral resistance to thyroid hormone is very rare.
    • Beyond scope of this lecture.
  • 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).
  • 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).
  • 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.
  • 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.
  • 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
  • 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
  • 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.
  • . . . 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.
  • 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.
  • Hyperthyroidism: clinical findings
    • Weight loss
    • Heat intolerance
    • Insomnia
    • Sweating
    • Anxiety
    • Hyperkinesis
    • Dyspena
    • Palpitations
    • Atrial fibrilation
    • Irregular menses
    • Infertility
    • Increased frequency of bowel movements
    • Myalgia
  • 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
  • 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.
  • 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
  • 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.
  • 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
  • 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
  • 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
  • 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
  • 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.
  • 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.
    • 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.
  • . . . 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.
  • 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.
  • 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
  • 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).
  • 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).
  • 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.
  • 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).
  • 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.
  • TSH producing Pituitary Tumor
    • Very rare
    • TSH high; T4 T3 high
  • 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
  • Nuclear Imaging for thyrotoxicosis summary
  • 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 .
  • ╬ 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
    • ╬ 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).