Disorders of the Thyroid Gland


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  • Develops from the floor of the primitive pharynx during the 3rd week of gestation. The developing gland migrates along the thyroglossal duct to reach its final destination in the neck. This accounts for rare ectopic location of thyroid tissue at the base of the tongue. Also allows for thyroglossal duct cysts. Thyroid hormone synthesis begins around 11 weeks gestation.
  • Congenital hypothyroidism occurs in 1 in 4000 newborns and now a part of newborn screening in developed countries. Supplementation can prevent severe developmental abnormalities.
  • I disagree with dosing adjustments. I keep them on meds for 8 weeks, then recheck and titrate up from there every 6-8 weeks.
  • RAI= radioactive iodine
  • Hyperthyroidism-
  • Disorders of the Thyroid Gland

    1. 1. Disorders of the Thyroid Gland<br />Clinical Medicine I<br />Elizabeth Bunting, MS, PA-C<br />March 21, 2011<br />
    2. 2. Objectives<br />Describe the anatomy of the thyroid gland, with regard to its relationship to:<br />Other structures in the neck<br />The parathyroid glands<br />The major vessels<br />Embryologic development<br />Describe the regulation of thyroid metabolism, particularly:<br />The role of the thyroid gland in the hypothalamus-anterior pituitary-thyroid axis<br />The role of iodine within the gland in controlling thyroid function<br />
    3. 3. Objectives<br />Discuss the synthesis and secretion of thyroid hormone, describing:<br />The two principal thyroid hormones secreted<br />Their relative utilization within the body<br />How they are chemically related<br />Describe the action of the hormones, particularly:<br />The location of the receptors for thyroxine and triiodothyronine and their function<br />The hormonal effect on cellular metabolism and development<br />Define hyperthyroidism, list and describe the:<br />Associated pathophysiology<br />Common clinical presentations<br />Significant historical and physical exam findings<br />Diagnostic tests<br />Management<br />
    4. 4. Objectives<br />Define thyrotoxicosis, and describe its pathophysiology, clinical presentation, diagnostic work-up and management.<br />Define hypothyroidism, list and describe the:<br />Associated pathophysiology<br />Common presentations<br />Significant historical and physical exam findings<br />Diagnostic tests<br />Management<br />Define myxedema and myxedema coma, and describe their pathologic process, clinical presentation, diagnostic work-up and management.<br />Identify the different forms of thyroiditis and their distinguishing features and management<br />
    5. 5. Objectives<br />Describe the various therapies, such as:<br />Use of surgery, radioactive iodine, or anti-thyroid drugs for hyperfunction<br />Use of thyroid hormone for hypofunction<br />List and describe the types of thyroid cancer.<br />Explain the signs and symptoms, pathophysiology and epidemiology of thyroid cancer.<br />Discuss the diagnostic work-up and management of thyroid cancer.<br />Discuss the prognosis for each of the major types of thyroid cancer.<br />
    6. 6. Thyroid Anatomy<br />
    7. 7. Parathyroid Glands<br />
    8. 8. Embryonic Development of the Thyroid Gland and hormones<br />
    9. 9. Thyroid Physiology<br />
    10. 10. Thyroid Physiology<br />Makes <br />Thyrotropin Releasing Horomone<br />(TRH)<br />Hypothalmus<br />Anterior<br />Pituitary<br />Makes <br />Thyroid Stimulating Hormone (TSH) <br />Makes<br />T3(Triiodothyronine)<br />& T4 (Thyroxine)<br />Thyroid Gland<br />
    11. 11. Thyroid <br />Produces two related hormones<br />T3 – triiodothyronine<br />T4 – thyroxine<br />These hormones play a critical role in<br />Thermogenic homeostasis in adults<br />Metabolic homeostasis in adults<br />Cell differentiation during development<br />
    12. 12. Regulation of the Thyroid Axis<br />TSH is the most useful physiologic marker of thyroid hormone action<br />T3 and T4 are the dominant regulators of TSH production<br />TSH is released in a pulsatile manner and exhibits a diurnal rhythm<br />Highest levels at night<br />
    13. 13. <ul><li>Thyroid hormones T4 and T3 feed back to inhibit hypothalamic production of thyrotropin-releasing hormone (TRH) and pituitary production of thyroid-stimulating hormone (TSH).
    14. 14. TSH stimulates thyroid gland production of T4 and T3</li></li></ul><li>Thyroid hormone synthesis, metabolism, and action<br /><ul><li>Iodide uptake is a critical first step in synthesis
    15. 15. Deficiency is prevalent in many mountainous regions globally and if present, may lead to goiter
    16. 16. If severe deficiency – hypothyroidism and cretinism
    17. 17. Recommended daily intake
    18. 18. 150 μg/d adults
    19. 19. 90-120 μg/d children</li></li></ul><li>Goiter<br />
    20. 20. Thyroid hormone synthesis, metabolism, and action<br /><ul><li>Iodide enters the thyroid and is used in production of both T3 and T4
    21. 21. T4 contains 4 iodine atoms
    22. 22. Removal of one of the iodine atoms leads to production of the potent hormone triiodothyronine (T3)</li></ul>T4 may be thought of as a precursor for the more potent T3<br />T4 is converted to T3 in the peripheral tissues<br />
    23. 23. Thyroid hormone synthesis, metabolism, and action<br /><ul><li>Hormones are released from the thyroid and the vast majority are protein bound and deposited in peripheral cells
    24. 24. Once in cells, hormones act as nuclear receptors
    25. 25. T3 99.7%
    26. 26. T4 99.98%
    27. 27. The unbound hormone is available to tissues
    28. 28. Serum concentrations
    29. 29. T3 0.14 μg/dL
    30. 30. T4 8 μg/dL</li></li></ul><li>Thyroid hormone synthesis, metabolism, and action<br />Laboratory evaluation of thyroid hormones<br />TSH – first thing you assess<br />Normal range 0.5-5 μU/ml<br />Normal result excludes a primary abnormality of function<br />Suppression = hyperthyroid<br />Elevated=hypothyroid<br />If abnormal TSH get<br />Free T4 <br />Normal 0.8-2.8 ng/dL<br />Elevated=hyperthyroid<br />Suppression=hypothyroid<br />
    31. 31. Thyroid hormone synthesis, metabolism, and action<br /><ul><li>Tests to determine the etiology of thyroid dysfunction
    32. 32. Anti-TPO – antithyroidperoxidase antibody
    33. 33. Used to detect autoimmune thyroid disease
    34. 34. Up to 80% of those with Graves’ disease have TPO antibodies
    35. 35. 90% of those with Hashimoto’s thyroiditis have TPO antibodies
    36. 36. Thyroid scanning and ultrasound
    37. 37. Nuclear imaging
    38. 38. Radioisotopes of iodine are selectively transported into the thyroid allowing for imaging
    39. 39. Ultrasound
    40. 40. Used in nodular thyroid disease
    41. 41. Can detect nodules >3mm
    42. 42. Also useful in eval of recurrent thyroid cancer</li></li></ul><li>Hypothyroid Disorders<br />
    43. 43. Hypothyroidism<br />Insufficiency in the amount of thyroid hormone in the body<br />PRIMARY HYPOTHYROIDISM: thyroid gland failure despite proper stimulation from the pituitary<br />SECONDARY HYPOTHYROIDISM: failure of the pituitary to produce TSH to stimulate the thyroid gland<br />TERTIARY HYPOTHYROIDISM: failure of the hypothalamus<br />
    44. 44. Primary Hypothyroidism<br />General Considerations<br />Common: affects 1% of the general population and 5% over the age of 60<br />Women > men 4:1 ratio<br />Mean age at diagnosis is 60 years<br />Prevalence increases with age<br />Thyroid hormone deficiency affects almost all body functions<br />
    45. 45. Primary Hypothyroidism<br /><ul><li>Causes
    46. 46. Iodine deficiency
    47. 47. most common cause worldwide
    48. 48. Autoimmune disease
    49. 49. Hashimoto’s thyroiditis
    50. 50. Iatrogenic
    51. 51. treatment of hyperthyroidism</li></ul>Trauma to thyroid/pituitary/hypothalamus<br />Radiation exposure<br />Severe infection<br />Neoplasia (pituitary tumor)<br />Drugs – glucocorticoids, phenobarbital, phenytoin, salicylates (large doses), fluorouracil, androgens, amiodarone, interferon<br />
    52. 52. Primary Hypothyroidism<br />Symptoms<br />Common manifestations<br />Weight gain<br />Fatigue, lethargy<br />Depression<br />Weakness<br />Dyspnea on Exertion<br />Arthralgias/myalgias<br />Muscle cramps<br />Paresthesias<br />Cold intolerance<br />Constipation<br />Dry skin, brittle hair and nails<br />Headache<br />Carpal Tunnel Syndrome<br />Menorrhagia<br />
    53. 53. Primary Hypothyroidism<br />Symptoms<br />Less common<br />Decreased appetite and weight loss<br />hoarseness<br />Decreased sense of taste and smell<br />Deminished auditory acuity<br />Signs <br />Bradycardia<br />Diastolic hypertension<br />Thin, brittle nails, hair<br />Peripheral edema<br />Puffy face and eyelids (myxedema)<br />Skin pallor or yellowing (carotenemia)<br />Delayed DTR<br />Goiter<br />
    54. 54. Primary Hypothyroidism<br />Diagnostic findings<br /> TSH<br /> Free T4<br />Treatment<br />Treat the underlying cause if possible<br />Thyroid replacement with T4<br />Levothyroxine (Synthroid) <br />Adults <60 years without evidence of heart disease<br />Start with 25-75 μg qd<br />Repeat TSH in 6 weeks<br />Adjust dosage by 25 μg every 1-3 weeks based on TSH<br />Goal – symptom relief and TSH in lower half of reference range<br />
    55. 55. Primary Hypothyroidism<br />Treatment<br />Adults >60 years or patients with known cardiac disease<br />Start with 25-50 μg qd<br />Medication increases cardiac contractility and oxygen demand and don’t want to precipitate an MI<br />Repeat TSH in 6 weeks<br />Adjust dosage by 25 μg every 1-3 weeks based on TSH<br />Goal – symptom relief and TSH in lower half of reference range<br />
    56. 56. Primary Hypothyroidism<br />Treatment<br />Average daily replacement dose is usually 1.7μg/kg body weight (typically 100-150 μg)<br />Once full replacement is achieved and TSH levels are stable you can extend f/u visits to 6 months and then yearly<br />Take Levothyroxine (Synthroid) at least 4 hours between antacids, vitamins, seizure meds, food, lovastatin, sertraline – these medications affect T4 absorption or clearance<br />
    57. 57. Myxedema<br /><ul><li>Severe hypothyroidism
    58. 58. Signs and symptoms
    59. 59. Severe Fatigue
    60. 60. Weakness
    61. 61. Cardiac enlargement (myxedema heart)
    62. 62. Pericardial effusions
    63. 63. Psychosis (myxedema madness)
    64. 64. Hypothermia
    65. 65. Stupor or myxedema coma
    66. 66. Hypoventilation, leading to hypoxia and hypercapnia
    67. 67. Pituitary enlargement due to hyperplasia of TSH secreting cells</li></li></ul><li>Myxedema<br />Diagnostic studies<br />T4 low<br />TSH is increased<br />Hyponatremia<br />Hypoglycemia<br />Anemia<br />Hypotension<br />
    68. 68. Myxedema<br />Treatment<br />High mortality rate even with treatment<br />Thyroid hormone replacement (initially IV then switch to oral)<br />Levothyroxine 500μg IV bolus<br />Continue orally at 50-100 μg/day<br />
    69. 69. Myxedema Coma<br />Medical emergency<br />Often induced by underlying infection: cardiac, respiratory, or CNS system illness, cold exposure or drug use<br />Multiple organ abnormalities and progressive mental deterioration<br />Very rare, but has high mortality rate<br />Most commonly results from stressful situations (e.g. trauma, surgery, burns, infection)<br />Can occur because of coexisting disease states (e.g. diabetes, MI, fluid and electrolyte abnormalities)<br />Can be precipitated by certain medications<br />
    70. 70. Myxedema Coma<br />Treatment<br />IV thyroid hormone replacement<br />Treat underlying infection, if present<br />Monitor TSH<br />Monitor glucose and sodium levels<br />Warming if hypothermia (blankets only)<br />Prognosis<br />Mortality rate of 30 – 60%<br />Poor prognosis if advanced age, bradycardia and persistent hypothermia<br />
    71. 71. Cretinism<br />Congenital hypothyroidism<br />Etiology<br />1 in 4000 live births<br />Pathology<br />Hypoplasia or aplasia of the thyroid gland<br />OR failure of the gland to migrate into normal anatomic location<br />OR ineffective hormone due to enzyme deficiency<br />
    72. 72. Cretinism<br />Clinical features<br />Sluggishness<br />Pale, gray, cool or mottled skin<br />Nonpitting myxedema<br />Constipation<br />Large tongue<br />Poor muscle tone<br />Mental retardation<br />Dry, brittle hair<br />
    73. 73. Cretinism<br />Diagnostic studies<br />Low T4<br />Elevated TSH<br />Delayed skeletal maturation on x-rays<br />Treatment – thyroid hormone replacement<br />Prevention<br />Neonatal screening within 60 days of birth<br />Improved prognosis with therapy started in first 2 months of life<br />
    74. 74. Hyperthyroid Disorders<br />
    75. 75. Hyperthyroidism<br />Etiology<br />Grave’s disease – most common<br />Toxic multinodular goiter and thyroid adenomas<br />Subacute (de Quervain) Thyroiditis<br />Exogenous thyroid hormone<br />Struma Ovarii (ovarian teratoma)<br />No goiter<br />Pituitary tumor secreting TSH<br />Secondary hyperthyroidism<br />Normal or increased TSH with diffuse goiter and elevated T4<br />Medication induced Amioderone<br />
    76. 76. Grave’s disease<br />Epidemiology <br />Accounts for 60-80% of thyrotoxicosis<br />Females > males at 8:1<br />Typically occurs between ages 20-40<br />Pathology<br />Grave’s disease is an autoimmune disorder<br />Involves the formation of autoantibodies that bind to the TSH receptors in the thyroid and stimulate gland hyperfunction<br />Characterized by an increase synthesis and release of thyroid hormones<br />Gland is typically enlarged<br />Familial tendency (HLA-B8 and HLA-DR3)<br />
    77. 77. Grave’s disease<br />Symptoms<br />Descending order of frequency<br />Hyperactivity, irritability, dysphoria<br />Heat intolerance, increased sweating<br />Palpitations<br />Fatigue, weakness<br />Weight loss (increased appetite)<br />Diarrhea<br />Polyuria<br />Oligomenorrhea, loss of libido<br />
    78. 78. Grave’s disease<br />Signs<br />Descending order of frequency<br />Tachycardia; A fib in the elderly, PACs<br />Tremor<br />Goiter may be present (absence of goiter does not rule out hyperthyroidism)<br />Skin warm, moist<br />Muscle weakness, proximal myopathy<br />Exophthalmos, proptosis, lid lag with downward gaze (von Graefe sign) or retraction (Dalrymaple sign), staring appearance (Kicher sign)<br />Thyroid dermopathy – pretibialmyxedema<br />Hyperreflexia<br />Thyroid acropachy (digital clubbing) rare<br />Hypokalemic periodic paralysis<br />
    79. 79. Grave’s disease<br />Diagnostic studies<br /> TSH<br /> T3 and T4 both total and free<br />Anti-TPO positive in up to 80%<br />TSH receptor antibody (TRaB) positive in 65%<br />Imaging<br />Thyroid RAI uptake and scan<br />High in Grave’s Disease and toxic nodular goiter<br />MRI of orbits if eye concerns<br />
    80. 80. Grave’s disease<br />Management<br />Clinical features generally worsen without treatment<br />Treat by <br />reducing thyroid hormone synthesis, using antithyroid drugs –propylthiouracil (PTU), methimazole<br />Reducing the amount of thyroid tissue with radioiodine treatment (RAI)<br />Causes progressive destruction of thyroid cells<br />Reducing the amount of thyroid tissue with thyroidectomy<br />If not responding to medical treatment<br />Large goiters<br />Beta-blockers (propanolol) for symptoms during early treatment with antithyroid drugs and radioiodine tx<br />
    81. 81. Thyroid Storm<br />Rare <br />Life-threatening emergency<br />Exacerbation of hyperthyroidism/ thyrotoxicosis<br />Usually precipitated by stress (surgery, infection, delivery, trauma)<br />High mortality rate 30% even with treatment – cardiac failure, arrhythmia, or hyperthermia<br />Pathology – same as hyperthyroidism with addition of stressor as above<br />
    82. 82. Definitions<br />Hypothyroidism: hypoactive thyroid gland<br />Hyperthyroidism: hyperactive thyroid gland<br />Thyrotoxicosis: excessive thyroid hormone<br />Thyroid storm: the life threatening result of excessive thyroid hormone and physical stress<br />Myxedema: Severe result of lack of thyroid hormone<br />
    83. 83. Thyroid Storm<br />Clinical features<br />Exaggerated signs and symptoms of hyperthyroidism<br />High fever<br />Marked delirium<br />Severe tachycardia<br />Seizures<br />Nausea, vomiting and diarrhea<br />Dehydration<br />Coma<br />Jaundice <br />Death <br />
    84. 84. Thyroid Storm<br />Diagnostic studies<br />Highly elevated T3 and T4<br />EKG may show sinus tachycardia, a-fib or flutter<br />Management<br />Aggressive use of and large dose of propylthiouracil (PTU)<br />Oral or IV Ipodate Sodium(decreases thyroid hormone production) with Iodide given 1 hour later as Lugol solution<br />Propranolol given (cautiously if heart failure)<br />Glucocorticoids (inhibits peripheral conversion of T4 to T3<br />
    85. 85. Toxic Multinodular Goiter<br />Multiple thyroid nodules that range in morphology from hypercellular regions to cystic areas filled with colloid<br />Women > men<br />Clinical presentation<br />Subclinical hyperthyroidism or mild thyrotoxicosis<br />Usually elderly<br />A fib, tachycardia<br />Nervousness, tremor<br />Weight loss<br />Recent exposure to iodine, from contrast dyes or other sources, may precipitate or exacerbate thyrotoxicosis<br />
    86. 86. Toxic Multinodular Goiter<br />Diagnostic testing<br />T3 and T4 with T3 elevated to a higher degree<br /> TSH<br />Thyroid scan shows heterogeneous uptake with multiple regions of increased and decreased uptake<br />Treatment<br />Management is challenging<br />Antithyroid drugs in combination with beta blockers<br />However this treatment often stimulates the growth of the goiter<br />Radioiodine can be used to treat areas of autonomy<br />Surgery provides definitive treatment<br />
    87. 87. Thyroiditis<br />Classifications<br />Acute thyroiditis (Suppurativethyroiditis)<br />Subacutethyroiditis<br />Painless or silent thyroiditis<br />Hashimoto’s thyroiditis (Chronic lymphocytic thyroiditis)<br />Riedel thyroiditis<br />
    88. 88. Thyroiditis<br />Acute thyroiditis<br />Rare<br />Due to suppurative infection of the thyroid<br />Typically occurs in children or young adults<br />Signs and symptoms<br />Thyroid pain often referred to throat or ears<br />Small, tender goiter that may be asymmetric<br />Fever, dysphagia and erythema over the thyroid<br />Laboratory<br /> ESR<br /> WBC<br />Normal thyroid function<br />
    89. 89. Thyroiditis<br /><ul><li>Diagnostic testing</li></ul>FNA biopsy shows infiltration by PMN leukocytes<br />Culture of the sample can identify the organism<br /><ul><li>Treatment</li></ul>Antibiotics guided by culture<br />Surgery may be needed to drain abscess<br />
    90. 90. De Quervain’sThyroiditis<br />AKA SubacuteThyroiditis, granulomatousthyroiditis, giant cell thyroiditis<br />Etiology – probably viral, may be preceded by viral URI<br />Symptoms can mimic pharyngitis<br />Peak incidence occurs between 30-50<br />Women>men 3:1 ratio<br />
    91. 91. De Quervain’sThyroiditis<br />Pathology<br />Enlargement and patchy inflammatory infiltrate of thyroid<br />During initial phase of follicular destruction, there is release of thyroid hormones, leading to increased circulating T3 and T4 and suppression of TSH<br />After several weeks, the thyroid is depleted of stored thyroid hormone and a phase of hypothyroidism typically occurs, with low free T3 and T4 and moderately increased TSH levels<br />Finally thyroid hormone and TSH levels return to normal as disease subsides<br />Thyrotoxicosis hypothyroidism NL thyroid function<br /> lasts several weeks lasts 4-6 months returns within 12 months<br /> (develops in 50%)<br />
    92. 92. De Quervain’sThyroiditis<br />Clinical features<br />Often complain of sore throat<br />Exquisitely tender thyroid with small goiter (one or both lobes may be affected)<br />Pain is often referred to jaw or ear<br />Sometimes fever<br />Malaise and URI symptoms may precede the thyroid-related features<br />There may be signs of thyrotoxicosis or hypothyroidism, depending on the phase of the illness<br />
    93. 93. De Quervain’sThyroiditis<br />Diagnostic studies<br />Lymphocytosis on CBC <br />Elevated ESR<br />Thyroid function tests evolve through 3 distinct phases over about 6 months<br />Thyrotoxic phase - T3 and T4 elevated, TSH suppressed<br />Hypothyroid phase<br />Recovery phase<br />Negative antibody tests<br />Low thyroid radioiodine uptake (RAIU)<br />
    94. 94. De Quervain’sThyroiditis<br />Treatment<br />ASA or NSAIDS typically sufficient to control symptoms<br />May use beta blockers for symptoms during thyrotoxicosis phase<br />Thyroid hormone during hypothyroid stage may be needed<br />RAI can be used to cause prompt fall of T3 and improve thyrotoxic symptoms<br />Monitor thyroid function every 2-4 weeks using TSH and free T4<br />
    95. 95. Painless Thyroiditis<br />Autoimmune thyroiditis<br />Categories<br />Sporadic<br />Occurs in patients with underlying autoimmune thyroid disease<br />Postpartum<br />Occurs in 7.2% of women 3-6 months after pregnancy<br />3 times more common in women with type 1 diabetes<br />70% chance of recurrence with subsequent pregnancies<br />
    96. 96. Painless Thyroiditis<br />Clinical features<br />Clinical course similar to subacute thyroiditis except there is little to no thyroid tenderness<br />Thyrotoxicosis stage lasting 2-4 weeks followed by hypothyroid stage for 4-12 weeks, and then resolution<br />Labs<br />Positive anti-TPO<br />Normal ESR<br />Management<br />Initial stage usually mild<br />Can use propranolol for symptoms if needed<br />Second stage – thyroxine replacement – use only for 6-9 months as recovery is the rule<br />
    97. 97. Hashimoto’s Thyroiditis<br />Chronic lymphocytic thyroiditis due to autoimmunity<br />Epidemiology<br />Women > men 6:1 ratio<br />14.3% of Caucasians<br />10.9% of Hispanics<br />5.3% of Blacks<br />Mean age at diagnosis is 60 years<br />Prevalence increases with age<br />Tends to be familial<br />
    98. 98. Hashimoto’s Thyroiditis<br />Most common type of thyroid disorder in the US<br />Pathology<br />Immune mediated destruction of thyroid parenchyma<br />B-lymphocytes invade the thyroid gland which leads to follicular atrophy and then fibrosis<br />Initially may have hyperthyroidism due to passive release of stored thyroid hormone<br />Detectable levels of anithyroid antibodies – anti-TPO or antithyroglobulin antibodies or both<br />Only a small subset of individuals with elevated antithyroid antibody levels ever develop thyroid dysfunction<br />Found in 3% of men and 13% of women<br />
    99. 99. Hashimoto’s Thyroiditis<br />May be associated with other autoimmune diseases<br />Type I diabetes, Addison’s disease, pernicious anemia<br />Signs and symptoms<br />May be hyperthyroid, euthyroid or hypothyroid<br />Thyroid gland may be diffusely enlarged (goiter), firm or rubbery, usually nontender<br />Surface of thyroid may be irregular or nodular<br />Slow progression to hypothyroidism over years<br />Patients often present with signs and symptoms of hypothyroidism<br />Dry skin, decreased sweating, thinning of skin, myxedema, puffy face and eyelids, nonpittingpretibial edema, dry/brittle hair, depression<br />Thyroid is diffusely enlarged, firm, and finely nodular<br />
    100. 100. Hashimoto’s Thyroiditis<br />Diagnostic studies<br />Thyroid function tests<br />Hyperthyroid phase<br /> Free T4 levels higher than T3 due to it being the greater stored hormone<br />Because T4 is less active than T3 the hyperthyroid symptoms are less severe than in other thyroiditis conditions<br />TSH<br />Hypothyroid state<br />Free T4 <br />TSH<br />Positive antithyroid antibodies<br />Anti-TPO in 90%<br />Antithyroglobulin antibodies in 40%<br />
    101. 101. Hashimoto’s Thyroiditis<br />Imaging<br />Ultrasound shows diffuse heterogeneous density and hyperechogenicity<br />FNA for nodules<br />Doppler may be needed to distinguish between Graves Disease and Hashimoto’s<br />Treatment <br />Thyroxine hormone replacement <br />If hypothyroid<br />Or if euthyroid with goiter present<br />Will shrink the goiter by 30% in most cases over 6 months<br />
    102. 102. Riedel Thyroiditis<br />AKA Invasive fibrous thyroiditis, Riedel struma, woody thyroiditis, ligneous thyroiditis, invasive thyroiditis<br />Generally a manifestation of multifocal systemic fibrosis syndrome<br />Causes hypothyroidism and sometimes hypoparathyroidism<br />RARE<br />Generally found in middle-aged or elderly women<br />Signs and symptoms:<br />Thyroid enlargement is asymmetrical and stony, hard and adherent to neck structures<br />
    103. 103. Riedel Thyroiditis<br />Signs and symptoms cont’d:<br />Compression of the thyroid causes dysphagia, dyspnea, pain and hoarseness<br />Fibrosis happens in other areas of the body as well<br />Treatment<br />Tamoxifen can provide remission in 3-6 months<br />Short term corticosteroids can help with compression<br />Surgical decompression may be needed<br />
    104. 104. Thyroid Nodules<br />Must consider cancer<br />Pathology<br />Adenomas, cysts, colloid nodules (most common nodules), localized thyroiditis, and cancer (mostly papillary and follicular)<br />Clinical features<br />Most are asymptomatic<br />May have hyper- or hypothyroidism<br />
    105. 105. Thyroid Nodules<br />Clinical features<br />Suspect cancer if rapid growth, fixed in place with no movement on swallowing, hx of neck radiation, male sex, extremes of age<br />Diagnostic studies<br />TSH and free T4<br />Fine needle aspiration and cytology<br />Ultrasound <br />
    106. 106. Thyroid Nodules<br />Management<br />MUST exclude malignancy<br />Treatment according to specific diagnosis<br />If malignant, surgery followed by thyroid radioiodine ablation<br />
    107. 107. Thyroid Cancers<br />Epidemiology<br />Most common malignancy of the endocrine system<br />Uncommon, diagnosed in less than 1% of the population<br />Women > men 3:1 ratio <br />Male sex associated with worse prognosis<br />Incidence increases with age<br />Classification<br />Papillary carcinoma (most common)<br />Follicular<br />Medullary<br />Anaplastic (most aggressive)<br />
    108. 108. Thyroid Cancers<br />Risk Factors of thyroid cancer in pt with a thyroid nodule<br />History of head and neck irradiation<br />Age <20 or >45<br />Bilateral disease<br />Large nodule size, >4cm<br />New or enlarging neck mass<br />Male sex<br />Nodule fixed to adjacent surfaces<br />Genetic factors, especially medullary which has familial predisposition<br />
    109. 109. Thyroid Cancers<br />Signs and symptoms<br />Palpable, firm, nontender nodule in the thyroid<br />Most are asymptomatic<br />Possible hoarseness<br />Possible neck pain<br />Possible cervical LAD<br />Only 5% of palpable thyroid nodules are malignant<br />Thyroid function tests are usually normal<br />
    110. 110. Thyroid Cancers<br />Diagnostic studies<br />Serum calcitonin and CEA levels may be elevated in medullary cancer<br />Usually seen as a “cold” nodule on radioactive iodine thyroid scan<br />Ultrasound shows solid, well-formed nodule/s and can detect metastases in the neck<br />FNA needed<br />CT scan – used to detect metastases<br />MRI and PET scans- distant mets<br />
    111. 111. Thyroid Cancers<br />Treatment<br />Surgical excision with near-total thyroidectomy with post-surgical radioablation of the remnant thyroid tissue<br />Most tumors are still TSH responsive, TSH suppression is a mainstay of treatment<br />Goal is TSH range 01.-0.5 IU/L<br />Chemo used if mets are present<br />
    112. 112. Thyroid Cancers<br />PapillaryFollicularMedullaryAnaplastic<br />Incidence MOST 2nd MOST Uncommon LEAST<br /> COMMON COMMON COMMON<br />Av. Age 42 50 50 57<br />Females 70% 72% 56% 2%<br />Deaths 6% 24% 33% 98%<br />I uptake + ++++ 0 0<br />Degree of + ++-+++ +-++++ ++++++++<br />Malignancy<br />
    113. 113. Any Questions???<br />
    114. 114. References<br />Jennifer Forbes, MHS, PA-C: many slides are hers from last year<br />CMDT<br />Harrison’s Principles of Internal Medicine<br />Images:<br />www.riversideonline.com/.../DS00396.cfm<br />ehp.niehs.nih.gov/.../howdeshell-full.html<br />healthfiles.net/disease/toxic-nodular-goiter/<br />www.missionfoto.com/images/fall03/goiter.html<br />