Surg path thyroid.special

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Surg path thyroid.special

  1. 1. Thyroid Lesions Surgical Pathology OBJECTIVE: Identify the different thyroid lesions To Know the following : • Pathogenesis • Clinical Presentation • Gross & Microscopic • Prognosis/ Behavior • Staging • Treatment
  2. 2. Heterotropic Thyroid Tissue • Found anywhere along the course of the thyroiglossal duct ( Midline ) • Frequently Base of the tongue • Difficulty in swallowing • Respiratory obstruction • 70% with (+) gross lingual thyroid  Develop hypothyroidism after it’s removal
  3. 3. Heterotropic Thyroid Tissue
  4. 4. Thyroiditis 1. Acute Thyroiditis 2. Granulomatous Thyroiditis 3. Autoimmune Thyroiditis 4. Riedel’s Thyroiditis
  5. 5. Acute Thyroiditis  Infectious Nature – Bacterial > Viral  Neutrophilic infitrates + Thyroid Necrosis  Diagnosis : FNAB  Treatment – Medical with Drainage of Abscess – Fistulectomy
  6. 6. Granulomatous Thyroiditis de Quervain’s
  7. 7.  The immune response is not self- perpetuating, so the process is limited.  Viral antigen or thyroid antigen is released  Antigen w/in macrophages stimulates the formation of cytotoxic T lymphocytes, which then damage thyroid follicular cells. Granulomatous Thyroiditis de Quervain’s
  8. 8. DESCRIPTION  Middle age Women (3 to 5:1) M< W  30-40’s  Unknown Etiology  Believed to be a postviral inflammatory process
  9. 9. CLINICAL MANIFESTATION  Acute Symptoms  Sorethroat, Painful swallowing, Fever, Malaise  Marked Tenderness on the thyroid  Thyroid inflammation and hyperthyroidism are transient, usually diminishing in 2 to 6 weeks, even if the patient is not treated.
  10. 10. Transient Hperthyroidism is Due to:  Due to disruption of thyroid follicles and release of excessive thyroid hormone  Nearly all patients have high serum T4 and T3 and low serum TSH levels.  Radioactive iodine uptake is low because of suppression of TSH  Unlike hyperthyroid state  ( Graves ) – RAI uptake is INCREASED
  11. 11.  Later followed by  Transient, usually asymptomatic hypothyroidism lasting from 2 to 8 weeks,  Recovery is virtually always complete  Repaired by Fibrosis  Advanced Stage  Firm Thyroid gland Granulomatous Thyroiditis de Quervain’s
  12. 12. Morphology:  Assymetric gland enlargement : Usually 2x normal  On cut section, the involved areas are firm and yellow-white and stand out from the more rubbery, normal brown thyroid substance  Micro: Marked inflam + Giant cell Granulomas about damaged follicles
  13. 13. Granulomatous Thyroiditis de Quervain’s
  14. 14. Autoimmune Thyroiditis
  15. 15. Type Microscopic All show extensive lymphocytic infiltration of the glands with germinal centers Lymphocytic Thyroiditis Intervening follicles are relatively Normal Hashimoto’s Thyroiditis Follicles are lined by oncocytic cells Grave’s Disease Hyperplastic intervening follicles
  16. 16. Hashimoto’s Thyroiditis Struma Lymphocymatosa
  17. 17. DESCRIPTION:  Most common cause of hypothyroidism in areas of the world where iodine levels are sufficient.  Women Over 40y/o  W>M 10:1 to 20:1  Patients with Hashimoto disease are at increased risk for the development of B-cell lymphomas.
  18. 18.  Diffuse thyroid Enlargement ◦ Firm / Painless ◦ Tracheal & Esophageal Compression ◦ Not Adherent to surrounding structure  Initial  Mild Hyperthroidism ◦ High FT3, FT4, Low TSH , Low RAIU  Later  Hypothyroidism DESCRIPTION:
  19. 19. Pathogenesis: Both cellular and humoral factors contribute to thyroid injury This disease is believed to be caused primarily by a defect in T cells.
  20. 20. (1 ) They interact with B cells and stimulate the secretion of a variety of antithyroid antibodies, which may activate antibody- dependent cytotoxicity mechanisms Anti- Thyroglobulin & Thyroid peroxidase Anti-TSH receptor Anti- Iodine Transporter (2) Helper T cells may induce the formation of CD8+ cells, which can be cytotoxic to thyroid cells. (3) Cytokine –mediated cell death: CD4 T cell  IFN   macrophage recruit Activated T cells have two roles in the disease
  21. 21. Gross: ◦ Diffusely enlarged or Localized enlargement. ◦ The capsule is intact, and the gland is well demarcated from adjacent structures. ◦ The cut surface is pale, gray-tan, firm, and somewhat nodular
  22. 22. Microscopic: Small Atropic follicles Lined by Hurthle cell Extensive lymphos + germinal center
  23. 23. MANAGEMENT: Treatment : 1. No therapy 2. Subtotal Thyroidectomy 2o large lesions or pressure or confused as Ca.  Complications: ◦ Evolve Gradually  Malignant Lymphoma  Leukemia  Hurthle cell Ca
  24. 24. Riedel’s Thyroiditis Fibrous Thyroiditis or Invasive Thyroidits
  25. 25. Riedel’s Thyroiditis Fibrous Thyroiditis or Invasive Thyroidits Etremely rare Female Adults & Elderly Not Preceeded by : Acute Inflammatory condition Tenderness on thyroid Regional L.N. not involved
  26. 26. Clinical : Ill-Defined Mass Profound Dyspnea Extremely Firm Lesion  Compress Trachea  Slit like state
  27. 27. GROSS:
  28. 28. Microscopic : Extensive fibrous tissue Skeletal muscles are infiltrated Patchy mononuclear inflammation Important Dxtic feature Vasculitis (medium veins) encased by fibrosis
  29. 29. MICROSCOPIC:
  30. 30. Therapy : Steroid effective Most Require Surgery Incidence of Post-Op Hypothyroidism is VeryLow
  31. 31. HYPERPLASTIC THYROID DISORDER
  32. 32. Major Types of Hyperplastic Thyroid Disorder Type Mechanism Pathology Functional Status Dyshormogenetic Goiter Genetically Determined error in Thyroid hormone Nodular Less Freq- Diffuse hyperplasia Hypothyroid Grave’s Disease Autoimmune Diffuse Hyperplasia Hyperthyroid Endemic Goiter Iodine Deficiency Nodular Hyperplasia Usually- Euthyroid Sometimes- Hypo thyroid Sporadic Goiter Unknown Nodular Hyperplasia Usually- Euthyroid Sometimes- Hypothyroid Hyperthyroid
  33. 33. GRAVES DISEASE THYROID
  34. 34. Grave’s Disease  Young Adult Females  20-0 y/o  Genetic factors – imp’t etiology  HLA-B8 and DR3
  35. 35. Triad of Clinical Findings  Hyperthyroidism  Muscle Weakness , Weight Loss  Increase SNS  Infiltrative Ophthalmopathy  Exopthalmus  Localized, infiltrative dermopathy  Pretibial Edema – minority of cases  Shin area – scaly thickening and induration
  36. 36. Laboratory  Elevated free T3 T4  Increased RAI uptake in the presence of TSH < 0.1mU/L  Due to stimulation of follicles by TSI  Depressed TSH levels
  37. 37. MORPHOLOGY  Gross  Symmetric enlargement  Reddish , Succulent  Microscopic  Markedly Hyperplastic Follicles  Prominent Papillary formation  Some glands grow outside into the skeletalmuscle  1-9% incidence of malignant transformation
  38. 38. PATHOGENESIS  TSH is NOT involved in pathogenesis  IgG against TSH receptor  TSI IMMUNOGLOBULIN  TBII THYROTROPIN-BINDING INHIBITOR IMMUNOGLOBULIN  Increased Incidence after Irradiation to neck lesions  Also caused by Amiodarone – associated Thyrotoxicosis ( 37% iodine )
  39. 39. TREATMENT Antithyroid Drugs Radioactive Iodine (ablation) Subtotal Thyroidectomy Thyroid remnant regenerates if 5g on each side is left
  40. 40. Preoperative Therapy  Iodine  Block Thyroglobulin secretion  Cause involution of the epithelial cells  Accumulation of colloid
  41. 41. Nodular Hyperplasia THYROID
  42. 42. Nodular Hyperplasia  Most Common Thyroid disease  Some Cases Associated w/ Hashimoto’s  Types of Simple Goiter ( Diffuse NonToxic Goiter)  Endemic Goiter  Sporadic Goiter
  43. 43. Endemic Goiter  Due to low Iodine  Lead to Decreased synthesis of Thyroid Hormones  Compensatory Increase TSH secretion  Goiter Initially  Hyperactive thyroid Later  Follicular atrophy  Goitrous Hypothyroidism
  44. 44. Sporadic (Nodular) Goiter  Less frequent than endemic  Female Preponderance Puberty or Young adult  Pathogenesis- Unknown  Features Mild Dietary Deficiency of iodine Slight Hormonal Impairment Increase Renal Clearance of iodide
  45. 45. Simple Goiter Gross  Diffusely enlarged thyroid gland  Rarely exceeds 100-150 grams Clinical Manifestation  Euthyroid – majority  Mass effect  T3,T4 normal  TSH usually elevated or upper range
  46. 46. Virtually All Longstanding Simple Goiters convert to … MULTINODULAR GOITER
  47. 47. Gross- Multinodular Goiter  Thyroid enlarged & Distorted shape- Asymmetrical  May weigh > 2000grams  Capsule Stretch out  Multiple nodules on cutting w/ partial or complete capsule  Hges/ calcification/ cystic degeneration
  48. 48. GROSS
  49. 49. GROSS
  50. 50. Microscopic  Nodular hyperplasia w/ papillary formation  Granulomatous rxn to ruptured follicles  Variable follicular size  No compression of adjacent parenchyma  Nodules are polyclonal by cytogenetic studies
  51. 51. MICROSCOPIC
  52. 52. Treatment  Mild Asymptomatic  Require No Tx  Suppressive Medical Therapy with Exogenous Thyroid Hormones  Moderately Effective  Bilateral Subtotal Thyroidectomy  Disfugurement / Pressure symptoms
  53. 53. Neoplasm of Thyroid
  54. 54. Clues to nature of given nodule Solitary nodules tend to be Neoplastic than are multiple nodules  Nodules in young patients are likely Neoplastic than in older patients  Nodules in males are more likely neoplastic than females  History of radiation to Head/Neck is associated with Increased incidence of Thyroid Malignancy  Hot Nodules in scan are more likely Benign
  55. 55. FOLLICULAR ADENOMA
  56. 56. DESCRIPTION Benign encapsulated Most Common Thyroid Neoplasm Usually Euthyroid w/ Cold CT scan Many (+) Elevated Thyroglobulin
  57. 57. Few are toxic adenomas Autonomous functioning tumor More Common in iodine deficient regions DESCRIPTION
  58. 58. GROSS:  Almost Always Solitary  Thin Capsule  Signs of compression  Degenerative changes
  59. 59. GROSS
  60. 60. GROSS
  61. 61. MANAGEMENT  DDx ◦ Dominant Nodular Hyperplasia ◦ Minimally Invasive Follicular Ca  Treatement ◦ Lobectomy ◦ Toxic Adenoma (warm nodules)  Medical Tx – Less than Satisfactory  Levothyroxine
  62. 62. MICROSCOPIC
  63. 63. MICROSCOPIC
  64. 64. Thyroid Carcinomas  Papillary Ca – 75% to 85%  Follicular Ca – 10% to 20%  Medullary Ca – 5%  Anaplastic Ca <5%
  65. 65. PAPILLARY CARCINOMA THYROID
  66. 66. DESCRIPTION: Most common type of thyroid Malignancy Any age, Usually 40 y/o Account for >90% of thyroid malignancy in children 5-10% has History of Irradiation to Head/Neck
  67. 67. Increase incidence in Hashimoto’s but vary widely 67% Localized thyroid lesion 13% Thyroid & L.N lesion 20% L.N lesion DESCRIPTION:
  68. 68. MORPHOLOGY-Gross Variable size Solid , whitish, firm, clearly invasive Papillary / Cystic changes
  69. 69. GROSS:
  70. 70. Papillae About half (+) PSammoma Bodies Ground glass Nuclei ◦ * Imp’t Clue to Dx Scant mitosis MORPHOLOGY- Microscopic
  71. 71. MICROSCOPIC
  72. 72. PAPILLARY Ca
  73. 73. Immunohistochemical Stain High Molecular Weight Keratin Reactivity to Thyroglobulin S-100 Vimentin Estrogen receptor
  74. 74. Variants: Papillary Microcarcinoma ◦ Measuring < 1cm. ◦ Common incidental finding ◦ 1/3 assoc w/ cervical mets ◦ Distant mets Exceptionally Rare ◦ Excellent Prognosis
  75. 75. VARIANTS:
  76. 76. Variants : Encapsulated Variant ◦Totally surrounded by capsule ◦Incidence of distant mets/ tumor death is Nearly Zero ◦Still assoc. with nodal mets
  77. 77. Variant: Diffuse Sclerosing Variant Bilateral dense sclerosis + severe lympho infiltrates & Psammoma Clincally mistaken for Hashimo to’s Nodal Mets nearly all (+) Lung mets commo n Disease free survival rate is LOWER than conventi onal papillary
  78. 78. Tall/ Columnar Variant ◦Tend to affect Older Patients more often than conventional ◦ More Aggressive Variant:
  79. 79.  Follicular Variant ◦ Composed almost entirely of follicles ◦ Ground glass nuclei ◦ Scalloped edges ◦ Behavior similar to conventional papillary Ca  High Nodal Mets  Mets usually exhinit papillary type Variants :
  80. 80. Spread & Metastasis :  ¼ show extension to tissues of the neck  Lymphatic mets > Blood  Cervical mets ◦ Very Common ◦ Usually young patient ◦ May be the !st sign  Lungs ◦ most common Blood Mets ◦ CT scan
  81. 81. Prognosis :  Prognosis ◦ General Excellent Prognosis  Prognosis decreases with: ◦ Age Male ◦ Tall Variant Size ◦ Multicentricity Distant Mets ◦ Reactivity EMA , LeuMI ◦ Aneuploidy
  82. 82. Factors that NOT generally correlate w/ Prognosis ◦ Proportion of papillae to follicles ◦ Psammoma bdies ◦ Cervical node Mets ◦ Fibrosis Prognosis :
  83. 83. THYROID Follicular Carcinoma
  84. 84. DESCRIPTION :  Malignant tumor exhibiting follicular cell differentiation  Women Usually >50y/o  Diagnosis : (+) Capsular or Vascular Invasion  Psammoma Bodies are Absent  Almosy Always Solitary, Never Occult lesion
  85. 85.  Metastasis Usually Blood Borne  Lungs & Bones  Confirmed by (+) Thyroglobulin stain  Prognosis:  Minimally Invasive  Clearly Invasive  architecture & Cytologic differentiation DESCRIPTION :
  86. 86. IMMUNOCHEMISTRY  Immunohistochemical Reactivity for Thyroglobulin & Low M.W. Kerain  Oncogene ras point mutation is higher in follicular than papillary
  87. 87. PROGNOSIS  Minimally Invasive  Grossly encapsulated  Solid, Fleshy  Full thickness capsular invasion and expand like mushroom  Vascular Invasion Venous invasion w/in capsule Must contain one or more clusters of tumor attched to the wall  Mets <5%
  88. 88. MICROSCOPIC
  89. 89. PROGNOSIS  Widely Invasive Widespread invasion of blood vessel and/or Adjacent thyroid tissue Often lacks encapsulation Mets is more common Skeletal muscle mets  shoulder girdle, sternum, skull, iliac bone
  90. 90. MEDULLARY CARCINOMA THYROID
  91. 91. DESCRIPTION :  Composed of C ( parafolliculaar ) cells  Mostly located in Midportion or Upper Half of the gland  Immunohistochemical stain ◦ Reactive Keratin, Calcitonin CEA, NSE ◦ ACTH, Cakcitonin gene related peptide ◦ Generally Negative for Thyroglobulin
  92. 92. MEDULLARY CARCINOMA  Invades locally and metastasize  Metastasis common in Sporadic and MEA III
  93. 93. MORPHOLOGY :  Gross: ◦ Solid, firm, non-encapsulated but relatively well- circumscribed
  94. 94. MORPHOLOGY
  95. 95. MORPHOLOGY:
  96. 96. MICROSCOPIC: ◦ Solid proliferation of round to polygonal cells ◦ Granular amphophilic cytoplasm ◦ Medium nucleus ◦ Highly vascular stroma ◦ Coarse calcification
  97. 97. MEDULLARY CARCINOMA Treatment  Total Thyroidectomy + Cervical Lympadenectomy  5 year survival rate about 35%  Not particularly responsive to RAI , external radiation or chemotx
  98. 98. PROGNOSIS: Good Prognostic factor  Young age, female, familial , confined lesion Poor Prognostic factor  Sporadic cases ( older age affected )  High mitosis  Small cell type  Poor Staining for Calcitonin & Increased Reactivity for CEA Calcitonin production related to differentiation
  99. 99. STAGING OF THYROID TUMORS for Papillary & Follicular  UNDER 45 YEARS OLD STAGE I ANY T ANY N M0 STAGE II ANY T ANY N M1
  100. 100. STAGING OF THYROID TUMORS for Papillary & Follicular  45 YEARS OLD AND OVER STAGE I T1N0M0 STAGE II T2N0M0 T3N0M0 STAGE IIII T4N0M0 ANY T , N1 , M0 STAGE IV ANY T , ANY N M1
  101. 101. STAGING OF THYROID TUMORS for Medullary STAGE I T1 N0 M0 STAGE II T2 T3 T4 N0 M0 STAGE III ANY T N1 M0 STAGE IV ANY T ANY N M1
  102. 102. STAGING OF THYROID TUMORS for Undifferentiated Tumor  ALL CASES ARE STAGE IV STAGE IV ANY T ANY N ANY M
  103. 103. STAGING OF THYROID TUMORS  PRIMARY TUMOR-Solitary or Multifocal  Measure the largest for classfication TX Primary tumor cannot be assesses TO No evidence of primary tumor T1 Tumor 1 cm or less in greatest dimension limited to the thyroid T2 Tumor > 1cm but not more than 4cm T3 Tumor > 4cm in greatest dimension limited to the thyroid T4 Tumor of any size extending beyond the thyroid capsule
  104. 104. STAGING OF THYROID TUMORS  LYMPH NODE – Regional nodes are the Cervical and Upper Mediastinal LN NX Regional LN cannot be assesses N0 No regional LN metastasis N1 Regional LN metastasis N1a Metastasis in Ipsilateral Cervical LN N1b Metastasis in Bilateral , Midline, or Contralateral Cervical or Mediastinal LN
  105. 105. STAGING OF THYROID TUMORS  DISTANT METASTASIS MX Presence of Distant Metastasis cannot be Assesed M0 No distant metastasis M1 Distant metastasis

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