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Surg path thyroid.special
- 1. Thyroid Lesions Surgical Pathology OBJECTIVE: Identifythe different thyroid lesions To Know the following : • Pathogenesis • Clinical Presentation • Gross & Microscopic • Prognosis/ Behavior • Staging • Treatment
- 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.
- 4. Thyroiditis 1. Acute Thyroiditis 2.Granulomatous Thyroiditis 3. Autoimmune Thyroiditis 4. Riedel’s Thyroiditis
- 5. Acute Thyroiditis InfectiousNature – Bacterial > Viral Neutrophilic infitrates + Thyroid Necrosis Diagnosis : FNAB Treatment – Medical with Drainage of Abscess – Fistulectomy
- 6.
- 7. The immuneresponse 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. DESCRIPTION Middle ageWomen (3 to 5:1) M< W 30-40’s Unknown Etiology Believed to be a postviral inflammatory process
- 9. CLINICAL MANIFESTATION AcuteSymptoms 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. Transient Hperthyroidism is Dueto: 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. Later followedby 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. Morphology: Assymetric glandenlargement : 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.
- 14.
- 15. Type Microscopic All showextensive 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.
- 17. DESCRIPTION: Most commoncause 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. Diffuse thyroidEnlargement ◦ Firm / Painless ◦ Tracheal & Esophageal Compression ◦ Not Adherent to surrounding structure Initial Mild Hyperthroidism ◦ High FT3, FT4, Low TSH , Low RAIU Later Hypothyroidism DESCRIPTION:
- 19. Pathogenesis: Both cellular andhumoral factors contribute to thyroid injury This disease is believed to be caused primarily by a defect in T cells.
- 20. (1 ) Theyinteract 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. Gross: ◦ Diffusely enlargedor 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
- 23. Microscopic: Small Atropic follicles Linedby Hurthle cell Extensive lymphos + germinal center
- 25. MANAGEMENT: Treatment : 1. Notherapy 2. Subtotal Thyroidectomy 2o large lesions or pressure or confused as Ca. Complications: ◦ Evolve Gradually Malignant Lymphoma Leukemia Hurthle cell Ca
- 26. Riedel’s Thyroiditis Fibrous Thyroiditisor Invasive Thyroidits
- 27. Riedel’s Thyroiditis Fibrous Thyroiditisor Invasive Thyroidits Etremely rare Female Adults & Elderly Not Preceeded by : Acute Inflammatory condition Tenderness on thyroid Regional L.N. not involved
- 28. Clinical : Ill-Defined Mass ProfoundDyspnea Extremely Firm Lesion Compress Trachea Slit like state
- 29.
- 30. Microscopic : Extensive fibroustissue Skeletal muscles are infiltrated Patchy mononuclear inflammation Important Dxtic feature Vasculitis (medium veins) encased by fibrosis
- 31.
- 32. Therapy : Steroid effective MostRequire Surgery Incidence of Post-Op Hypothyroidism is VeryLow
- 33.
- 34. Major Types ofHyperplastic 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
- 35.
- 36. Grave’s Disease YoungAdult Females 20-0 y/o Genetic factors – imp’t etiology HLA-B8 and DR3
- 37. Triad of ClinicalFindings Hyperthyroidism Muscle Weakness , Weight Loss Increase SNS Infiltrative Ophthalmopathy Exopthalmus Localized, infiltrative dermopathy Pretibial Edema – minority of cases Shin area – scaly thickening and induration
- 38. Laboratory Elevated freeT3 T4 Increased RAI uptake in the presence of TSH < 0.1mU/L Due to stimulation of follicles by TSI Depressed TSH levels
- 39. MORPHOLOGY Gross Symmetricenlargement Reddish , Succulent Microscopic Markedly Hyperplastic Follicles Prominent Papillary formation Some glands grow outside into the skeletalmuscle 1-9% incidence of malignant transformation
- 42. PATHOGENESIS TSH isNOT 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 )
- 43. TREATMENT Antithyroid Drugs Radioactive Iodine(ablation) Subtotal Thyroidectomy Thyroid remnant regenerates if 5g on each side is left
- 44. Preoperative Therapy Iodine Block Thyroglobulin secretion Cause involution of the epithelial cells Accumulation of colloid
- 45.
- 46. Nodular Hyperplasia MostCommon Thyroid disease Some Cases Associated w/ Hashimoto’s Types of Simple Goiter ( Diffuse NonToxic Goiter) Endemic Goiter Sporadic Goiter
- 47. Endemic Goiter Dueto low Iodine Lead to Decreased synthesis of Thyroid Hormones Compensatory Increase TSH secretion Goiter Initially Hyperactive thyroid Later Follicular atrophy Goitrous Hypothyroidism
- 48. 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
- 49. Simple Goiter Gross Diffuselyenlarged thyroid gland Rarely exceeds 100-150 grams Clinical Manifestation Euthyroid – majority Mass effect T3,T4 normal TSH usually elevated or upper range
- 50. Virtually All LongstandingSimple Goiters convert to … MULTINODULAR GOITER
- 51. 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
- 52.
- 53.
- 54. Microscopic Nodular hyperplasiaw/ papillary formation Granulomatous rxn to ruptured follicles Variable follicular size No compression of adjacent parenchyma Nodules are polyclonal by cytogenetic studies
- 55.
- 56. Treatment Mild Asymptomatic Require No Tx Suppressive Medical Therapy with Exogenous Thyroid Hormones Moderately Effective Bilateral Subtotal Thyroidectomy Disfugurement / Pressure symptoms
- 57.
- 58. Clues to natureof 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
- 59.
- 60. DESCRIPTION Benign encapsulated Most CommonThyroid Neoplasm Usually Euthyroid w/ Cold CT scan Many (+) Elevated Thyroglobulin
- 61. Few are toxicadenomas Autonomous functioning tumor More Common in iodine deficient regions DESCRIPTION
- 62. GROSS: Almost AlwaysSolitary Thin Capsule Signs of compression Degenerative changes
- 63.
- 64.
- 65. MANAGEMENT DDx ◦ DominantNodular Hyperplasia ◦ Minimally Invasive Follicular Ca Treatement ◦ Lobectomy ◦ Toxic Adenoma (warm nodules) Medical Tx – Less than Satisfactory Levothyroxine
- 66.
- 67.
- 68. Thyroid Carcinomas PapillaryCa – 75% to 85% Follicular Ca – 10% to 20% Medullary Ca – 5% Anaplastic Ca <5%
- 69.
- 70. DESCRIPTION: Most common typeof 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
- 71. Increase incidence in Hashimoto’sbut vary widely 67% Localized thyroid lesion 13% Thyroid & L.N lesion 20% L.N lesion DESCRIPTION:
- 72. MORPHOLOGY-Gross Variable size Solid ,whitish, firm, clearly invasive Papillary / Cystic changes
- 73.
- 74. Papillae About half (+)PSammoma Bodies Ground glass Nuclei ◦ * Imp’t Clue to Dx Scant mitosis MORPHOLOGY- Microscopic
- 75.
- 76.
- 77. Immunohistochemical Stain High MolecularWeight Keratin Reactivity to Thyroglobulin S-100 Vimentin Estrogen receptor
- 78. Variants: Papillary Microcarcinoma ◦ Measuring< 1cm. ◦ Common incidental finding ◦ 1/3 assoc w/ cervical mets ◦ Distant mets Exceptionally Rare ◦ Excellent Prognosis
- 79.
- 80. Variants : Encapsulated Variant ◦Totallysurrounded by capsule ◦Incidence of distant mets/ tumor death is Nearly Zero ◦Still assoc. with nodal mets
- 81. 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
- 82. Tall/ Columnar Variant ◦Tendto affect Older Patients more often than conventional ◦ More Aggressive Variant:
- 83. 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 :
- 84. 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
- 85. Prognosis : Prognosis ◦General Excellent Prognosis Prognosis decreases with: ◦ Age Male ◦ Tall Variant Size ◦ Multicentricity Distant Mets ◦ Reactivity EMA , LeuMI ◦ Aneuploidy
- 86. Factors that NOTgenerally correlate w/ Prognosis ◦ Proportion of papillae to follicles ◦ Psammoma bdies ◦ Cervical node Mets ◦ Fibrosis Prognosis :
- 87.
- 88. DESCRIPTION : Malignanttumor exhibiting follicular cell differentiation Women Usually >50y/o Diagnosis : (+) Capsular or Vascular Invasion Psammoma Bodies are Absent Almosy Always Solitary, Never Occult lesion
- 89. Metastasis UsuallyBlood Borne Lungs & Bones Confirmed by (+) Thyroglobulin stain Prognosis: Minimally Invasive Clearly Invasive architecture & Cytologic differentiation DESCRIPTION :
- 90. IMMUNOCHEMISTRY Immunohistochemical Reactivity forThyroglobulin & Low M.W. Kerain Oncogene ras point mutation is higher in follicular than papillary
- 91. 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%
- 92.
- 93. PROGNOSIS Widely Invasive Widespreadinvasion of blood vessel and/or Adjacent thyroid tissue Often lacks encapsulation Mets is more common Skeletal muscle mets shoulder girdle, sternum, skull, iliac bone
- 94.
- 95. DESCRIPTION : Composedof 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
- 96. MEDULLARY CARCINOMA Invadeslocally and metastasize Metastasis common in Sporadic and MEA III
- 97. MORPHOLOGY : Gross: ◦Solid, firm, non-encapsulated but relatively well- circumscribed
- 98.
- 99.
- 100. MICROSCOPIC: ◦ Solid proliferationof round to polygonal cells ◦ Granular amphophilic cytoplasm ◦ Medium nucleus ◦ Highly vascular stroma ◦ Coarse calcification
- 101. MEDULLARY CARCINOMA Treatment TotalThyroidectomy + Cervical Lympadenectomy 5 year survival rate about 35% Not particularly responsive to RAI , external radiation or chemotx
- 102. 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
- 103. STAGING OF THYROIDTUMORS for Papillary & Follicular UNDER 45 YEARS OLD STAGE I ANY T ANY N M0 STAGE II ANY T ANY N M1
- 104. STAGING OF THYROIDTUMORS 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
- 105. STAGING OF THYROIDTUMORS 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
- 106. STAGING OF THYROIDTUMORS for Undifferentiated Tumor ALL CASES ARE STAGE IV STAGE IV ANY T ANY N ANY M
- 107. STAGING OF THYROIDTUMORS 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
- 108. STAGING OF THYROIDTUMORS 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
- 109. STAGING OF THYROIDTUMORS DISTANT METASTASIS MX Presence of Distant Metastasis cannot be Assesed M0 No distant metastasis M1 Distant metastasis