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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-
  • Transcript

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

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