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Thyroid Lesions
Surgical Pathology
OBJECTIVE:
Identify the different thyroid lesions
To Know the following :
• Pathogenesis
• Clinical Presentation
• Gross & Microscopic
• Prognosis/ Behavior
• Staging
• Treatment
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
Heterotropic
Thyroid
Tissue
Thyroiditis
1. Acute Thyroiditis
2. Granulomatous Thyroiditis
3. Autoimmune Thyroiditis
4. Riedel’s Thyroiditis
Acute Thyroiditis
 Infectious Nature – Bacterial > Viral
 Neutrophilic infitrates + Thyroid Necrosis
 Diagnosis : FNAB
 Treatment
– Medical with Drainage of Abscess
– Fistulectomy
Granulomatous
Thyroiditis
de Quervain’s
 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
DESCRIPTION
 Middle age Women (3 to 5:1) M< W
 30-40’s
 Unknown Etiology
 Believed to be a postviral inflammatory
process
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.
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
 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
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
Granulomatous Thyroiditis de
Quervain’s
Autoimmune
Thyroiditis
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
Hashimoto’s
Thyroiditis Struma
Lymphocymatosa
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.
 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:
Pathogenesis:
Both cellular and humoral
factors contribute to thyroid
injury
This disease is believed to be
caused primarily by a defect in
T cells.
(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
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
Surg path thyroid.special
Microscopic:
Small Atropic follicles
Lined by Hurthle cell
Extensive lymphos + germinal
center
Surg path thyroid.special
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
Riedel’s Thyroiditis
Fibrous Thyroiditis or
Invasive Thyroidits
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
Clinical :
Ill-Defined Mass
Profound Dyspnea
Extremely Firm Lesion 
Compress Trachea 
Slit like state
GROSS:
Microscopic :
Extensive fibrous tissue
Skeletal muscles are infiltrated
Patchy mononuclear
inflammation
Important Dxtic feature
Vasculitis (medium veins)
encased by fibrosis
MICROSCOPIC:
Therapy :
Steroid effective
Most Require Surgery
Incidence of Post-Op
Hypothyroidism is VeryLow
HYPERPLASTIC
THYROID DISORDER
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
GRAVES DISEASE
THYROID
Grave’s Disease
 Young Adult Females
 20-0 y/o
 Genetic factors – imp’t etiology
 HLA-B8 and DR3
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
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
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
Surg path thyroid.special
Surg path thyroid.special
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 )
TREATMENT
Antithyroid Drugs
Radioactive Iodine (ablation)
Subtotal Thyroidectomy
Thyroid remnant regenerates if
5g on each side is left
Preoperative Therapy
 Iodine
 Block Thyroglobulin secretion
 Cause involution of the epithelial cells
 Accumulation of colloid
Nodular Hyperplasia
THYROID
Nodular Hyperplasia
 Most Common Thyroid disease
 Some Cases Associated w/
Hashimoto’s
 Types of Simple Goiter ( Diffuse
NonToxic Goiter)
 Endemic Goiter
 Sporadic Goiter
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
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
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
Virtually All Longstanding Simple
Goiters convert to …
MULTINODULAR GOITER
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
GROSS
GROSS
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
MICROSCOPIC
Treatment
 Mild Asymptomatic  Require No
Tx
 Suppressive Medical Therapy with
Exogenous Thyroid Hormones
 Moderately Effective
 Bilateral Subtotal Thyroidectomy
 Disfugurement / Pressure
symptoms
Neoplasm of Thyroid
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
FOLLICULAR ADENOMA
DESCRIPTION
Benign encapsulated
Most Common Thyroid
Neoplasm
Usually Euthyroid w/ Cold
CT scan
Many (+) Elevated
Thyroglobulin
Few are toxic adenomas
Autonomous functioning
tumor
More Common in iodine
deficient regions
DESCRIPTION
GROSS:
 Almost Always Solitary
 Thin Capsule
 Signs of compression
 Degenerative changes
GROSS
GROSS
MANAGEMENT
 DDx
◦ Dominant Nodular Hyperplasia
◦ Minimally Invasive Follicular Ca
 Treatement
◦ Lobectomy
◦ Toxic Adenoma (warm nodules) 
Medical Tx – Less than Satisfactory
 Levothyroxine
MICROSCOPIC
MICROSCOPIC
Thyroid Carcinomas
 Papillary Ca – 75% to 85%
 Follicular Ca – 10% to 20%
 Medullary Ca – 5%
 Anaplastic Ca <5%
PAPILLARY CARCINOMA
THYROID
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
Increase incidence in
Hashimoto’s but vary widely
67% Localized thyroid
lesion
13% Thyroid & L.N lesion
20% L.N lesion
DESCRIPTION:
MORPHOLOGY-Gross
Variable size
Solid , whitish, firm,
clearly invasive
Papillary / Cystic
changes
GROSS:
Papillae
About half (+) PSammoma
Bodies
Ground glass Nuclei
◦ * Imp’t Clue to Dx
Scant mitosis
MORPHOLOGY- Microscopic
MICROSCOPIC
PAPILLARY Ca
Immunohistochemical Stain
High Molecular Weight Keratin
Reactivity to Thyroglobulin
S-100
Vimentin
Estrogen receptor
Variants:
Papillary Microcarcinoma
◦ Measuring < 1cm.
◦ Common incidental finding
◦ 1/3 assoc w/ cervical mets
◦ Distant mets Exceptionally Rare
◦ Excellent Prognosis
VARIANTS:
Variants :
Encapsulated Variant
◦Totally surrounded by
capsule
◦Incidence of distant mets/
tumor death is Nearly Zero
◦Still assoc. with nodal mets
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
Tall/ Columnar Variant
◦Tend to affect Older Patients
more often than conventional
◦ More Aggressive
Variant:
 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 :
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
Prognosis :
 Prognosis
◦ General Excellent Prognosis
 Prognosis decreases with:
◦ Age Male
◦ Tall Variant Size
◦ Multicentricity Distant Mets
◦ Reactivity EMA , LeuMI
◦ Aneuploidy
Factors that NOT generally
correlate w/ Prognosis
◦ Proportion of papillae to follicles
◦ Psammoma bdies
◦ Cervical node Mets
◦ Fibrosis
Prognosis :
THYROID
Follicular Carcinoma
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
 Metastasis Usually Blood Borne
 Lungs & Bones
 Confirmed by (+) Thyroglobulin stain
 Prognosis:
 Minimally Invasive
 Clearly Invasive  architecture & Cytologic
differentiation
DESCRIPTION :
IMMUNOCHEMISTRY
 Immunohistochemical
Reactivity for Thyroglobulin & Low M.W.
Kerain
 Oncogene ras point mutation is higher
in follicular than papillary
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%
MICROSCOPIC
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
MEDULLARY
CARCINOMA
THYROID
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
MEDULLARY CARCINOMA
 Invades locally and
metastasize
 Metastasis common in
Sporadic and MEA III
MORPHOLOGY :
 Gross:
◦ Solid, firm, non-encapsulated
but relatively well-
circumscribed
MORPHOLOGY
MORPHOLOGY:
MICROSCOPIC:
◦ Solid proliferation of round to
polygonal cells
◦ Granular amphophilic
cytoplasm
◦ Medium nucleus
◦ Highly vascular stroma
◦ Coarse calcification
MEDULLARY CARCINOMA
Treatment
 Total Thyroidectomy + Cervical
Lympadenectomy
 5 year survival rate about 35%
 Not particularly responsive to RAI ,
external radiation or chemotx
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
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
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
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
STAGING OF THYROID TUMORS
for Undifferentiated Tumor
 ALL CASES ARE STAGE IV
STAGE IV ANY T ANY N ANY M
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
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
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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  • 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. 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
  • 4. Thyroiditis 1. Acute Thyroiditis 2. Granulomatous Thyroiditis 3. Autoimmune Thyroiditis 4. Riedel’s Thyroiditis
  • 5. Acute Thyroiditis  Infectious Nature – Bacterial > Viral  Neutrophilic infitrates + Thyroid Necrosis  Diagnosis : FNAB  Treatment – Medical with Drainage of Abscess – Fistulectomy
  • 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. DESCRIPTION  Middle age Women (3 to 5:1) M< W  30-40’s  Unknown Etiology  Believed to be a postviral inflammatory process
  • 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. 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.  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. 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
  • 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
  • 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.  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. 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. (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. 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
  • 23. Microscopic: Small Atropic follicles Lined by Hurthle cell Extensive lymphos + germinal center
  • 25. 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
  • 27. 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
  • 28. Clinical : Ill-Defined Mass Profound Dyspnea Extremely Firm Lesion  Compress Trachea  Slit like state
  • 30. Microscopic : Extensive fibrous tissue Skeletal muscles are infiltrated Patchy mononuclear inflammation Important Dxtic feature Vasculitis (medium veins) encased by fibrosis
  • 32. Therapy : Steroid effective Most Require Surgery Incidence of Post-Op Hypothyroidism is VeryLow
  • 34. 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
  • 36. Grave’s Disease  Young Adult Females  20-0 y/o  Genetic factors – imp’t etiology  HLA-B8 and DR3
  • 37. 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
  • 38. 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
  • 39. 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
  • 42. 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 )
  • 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
  • 46. Nodular Hyperplasia  Most Common Thyroid disease  Some Cases Associated w/ Hashimoto’s  Types of Simple Goiter ( Diffuse NonToxic Goiter)  Endemic Goiter  Sporadic Goiter
  • 47. 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
  • 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  Diffusely enlarged 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 Longstanding Simple 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. GROSS
  • 53. GROSS
  • 54. 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
  • 56. Treatment  Mild Asymptomatic  Require No Tx  Suppressive Medical Therapy with Exogenous Thyroid Hormones  Moderately Effective  Bilateral Subtotal Thyroidectomy  Disfugurement / Pressure symptoms
  • 58. 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
  • 60. DESCRIPTION Benign encapsulated Most Common Thyroid Neoplasm Usually Euthyroid w/ Cold CT scan Many (+) Elevated Thyroglobulin
  • 61. Few are toxic adenomas Autonomous functioning tumor More Common in iodine deficient regions DESCRIPTION
  • 62. GROSS:  Almost Always Solitary  Thin Capsule  Signs of compression  Degenerative changes
  • 63. GROSS
  • 64. GROSS
  • 65. MANAGEMENT  DDx ◦ Dominant Nodular Hyperplasia ◦ Minimally Invasive Follicular Ca  Treatement ◦ Lobectomy ◦ Toxic Adenoma (warm nodules)  Medical Tx – Less than Satisfactory  Levothyroxine
  • 68. Thyroid Carcinomas  Papillary Ca – 75% to 85%  Follicular Ca – 10% to 20%  Medullary Ca – 5%  Anaplastic Ca <5%
  • 70. 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
  • 71. Increase incidence in Hashimoto’s but 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
  • 74. Papillae About half (+) PSammoma Bodies Ground glass Nuclei ◦ * Imp’t Clue to Dx Scant mitosis MORPHOLOGY- Microscopic
  • 77. Immunohistochemical Stain High Molecular Weight 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
  • 80. Variants : Encapsulated Variant ◦Totally surrounded 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 ◦Tend to 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 NOT generally correlate w/ Prognosis ◦ Proportion of papillae to follicles ◦ Psammoma bdies ◦ Cervical node Mets ◦ Fibrosis Prognosis :
  • 88. 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
  • 89.  Metastasis Usually Blood Borne  Lungs & Bones  Confirmed by (+) Thyroglobulin stain  Prognosis:  Minimally Invasive  Clearly Invasive  architecture & Cytologic differentiation DESCRIPTION :
  • 90. IMMUNOCHEMISTRY  Immunohistochemical Reactivity for Thyroglobulin & 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%
  • 93. 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
  • 95. 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
  • 96. MEDULLARY CARCINOMA  Invades locally and metastasize  Metastasis common in Sporadic and MEA III
  • 97. MORPHOLOGY :  Gross: ◦ Solid, firm, non-encapsulated but relatively well- circumscribed
  • 100. MICROSCOPIC: ◦ Solid proliferation of round to polygonal cells ◦ Granular amphophilic cytoplasm ◦ Medium nucleus ◦ Highly vascular stroma ◦ Coarse calcification
  • 101. MEDULLARY CARCINOMA Treatment  Total Thyroidectomy + 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 THYROID TUMORS for Papillary & Follicular  UNDER 45 YEARS OLD STAGE I ANY T ANY N M0 STAGE II ANY T ANY N M1
  • 104. 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
  • 105. 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
  • 106. STAGING OF THYROID TUMORS for Undifferentiated Tumor  ALL CASES ARE STAGE IV STAGE IV ANY T ANY N ANY M
  • 107. 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
  • 108. 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
  • 109. STAGING OF THYROID TUMORS  DISTANT METASTASIS MX Presence of Distant Metastasis cannot be Assesed M0 No distant metastasis M1 Distant metastasis