pathology of the thyroid gland targon
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Pathology of the Thyroid Gland
Lt.col. R.TargonPhD medicine, professor
assistant
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Diseases of the Thyroid Gland
Congenital diseases
Inflammation Functional abnormality
Diffuse and Multinodular goiters
Neoplasia
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Anatomy
Intimate anatomical relationships
TG and recurrent laryngeal nerve TG and superior laryngeal nerve
TG and parathyroid glands
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Embriology
Originates from foramen ceacum at the base of the tongue
and descends into the neck, anterior to the hyoid bone, in front of the trachea.
The tract left behind ( thyreoglossal tract) may persist and form a cyst
(thyreoglossal cyst)
The cyst may form a cutaneous fistula (thyreoglossal fistula)
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Evaluation of Patients with Thyroid
Disease
Tests of Thyroid Function
Serum TSH
Total T4 and Total T3
Free T4 and Free T3
Thyroid Antibodies
Serum Thyroglobulin
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Evaluation of Patients with Thyroid
Disease
Thyroid Imaging
Radionuclide Imaging (iodine-123 (123I) and iodine-131 (131I))
Ultrasound
CT/MRI Scan
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Cases of midline swelling
Thyroid (patient with multinodular goitre)
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Cases of midline swelling
Thyreoglossal cyst
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Congenital Thyroid Diseases
Agenesis /Aplasia
Hypoplasia Accessory or aberrant thyroid glands
Thyroglossal duct cyst
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Thyroglossal Duct Cyst
Children
Failure of regression Neck, medial
Squamous or columnar lining
Complications: inflammation, sinus tracts
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Inflammation
Thyroiditis
Acute illness with pain
Infectious
Acute (Suppurative)
Chronic
Subacute or granulomatous (De Quervains)
Little inflammation with dysfunction
Subacute lymphocytic thyroiditis
Fibrous (Riedel) thyroiditis
Autoimmune
Hashimoto (lymphocytic) thyroiditis
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HASHIMOTO THYROIDITIS
Most common cause of hypothyroidism
Autoimmune, non-Mendelian inheritance
45-65 years, F:M = 10-20:1
Painless symmetrical enlargement (minimally ormoderately enlarged firm gland)
20% of patients present with hypothyroidism, and 5%present with hyperthyroidism (hashitoxicosis).
Risk of developing B-cell non-Hodgkins lymphoma Other concomitant autoimmune diseases
Endocrine and non-endocrine
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Hashimoto Thyroiditis
Pathogenesis
Immune systems reacts against a variety of thyroidantigens
Progressive depletion of thyroid epithelial cells which
are gradually replaced by mononuclear cells
fibrosis
Immune mechanisms may includes:
CD8+ cytotoxic T cell-mediated cell death
Cytokine-mediated cell death Binding of antithyroid antibodies antibody
dependent cell-mediated cytotoxicity
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Hashimoto Thyroiditis
Diffuse enlargement
Firm or rubbery
Pale, yellow-tan, firm
& somewhat nodular
cut surface
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Hashimoto Thyroiditis
Massivelymphoplasmcytic
infiltration with lymphoidfollicles formation
Destruction of thyroidfollicles
Remaining follicles are
small and many are linedby Hurthle cells
Increased interstitialconnective tissue
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Riedel's ThyroiditisRiedel's struma or invasive fibrous
thyroiditis predominates in women between the ages of 30 and 60
years
replacement of all or part of the thyroid parenchyma by
fibrous tissue, which also invades into adjacent tissues
"woody" thyroid gland with fixation to surrounding tissues
associated with other focal sclerosing syndromes,
including mediastinal, retroperitoneal, periorbital, andretro-orbital fibrosis, and sclerosing cholangitis, suggesting
that it may in fact be a primary fibrotic disorder.
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Functional Abnormality
Hyperfunction
in level of hormone toxic effects
Due to: Diffuse hyperplasia
Hyperfunctioning multinodular goiter
Hyperfunctioning adenoma
Subacute lymphocytic thyroiditis
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Functional Abnormality
Hypofunction
in level of hormone impair development in infants
and slowing of physical and mental ability in adults
Due to:
Postablation
Surgery
Radiation
Autoimmune thyroiditis
Drugs
Dyshormonogenetic
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Graves Disease
Most common cause of endogenous hyperthyroidism
Autoimmune disease with genetic susceptibility associated withHLA-B8 and DR3 Female:Male = 5:1 Peak incidence between the ages 40 and 60 years
Characterized by hyperthyroidism, symptoms of increased
adrenergic stimulation include palpitations, nervousness, fatigue,emotional lability, hyperkinesis, and tremors Diffuse enlargement with audible bruit Ophthalmopathy with exophthalmos: Wide,staring gaze (fixed look) Lid lag, (von Graefe's sign) Spasm of the upper eyelid revealing the sclera above the
corneoscleral limbus (Dalrymple's sign) Dermopathy (Pretibial myxedema) Gynecomastia levels of free T4 & T3and levels of TSH in blood uptake of radioactive iodine
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Graves Disease
Ophthalmopathy with exophthalmos
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Graves Disease
Ophthalmopathy with exophthalmos
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Graves Disease
Dermopathy (Pretibial myxedema)
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Graves Disease
Autoimmune disease with breakdown of helper-T-cell tolerance
Excessive production of TWO thyroid autoantibodies:
1) Thyroid-stimulating antibody (TSAb) &2) Growth-stimulating antibody (GSAb)
Antibodies bind to the TSH receptor of the follicular cell
Stimulation of the cell resulting in:
Increased levels of thyroid hormones &
Hyperplasia of the thyroid gland
Hyperthyroidism and Thyroid gland enlargement
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Graves Disease
Symmetrical
enlargement of
thyroid gland
Cut-surface is
homogenous, soft and
appear meaty
Hyperplasia andhypertrophy of
follicular cells
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Diffuse & Multinodular goiters
Latin gutteria, struma
Reflects impaired synthesis of thyroid hormone
most often caused by iodine deficiency
Impairment leads to compensatory in TSHlevels hypertrophy and hyperplasia of follicular
cells gross enlargement of gland
Euthyroid metabolic state
Degree of enlargement is proportional to level and
duration
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Diffuse nontoxic goiter
Diffuse non-toxic (simple) goiter
colloid goiter
Endemic
sporadic (dyshormonogenetic)
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Endemic Goiter
Low iodine content in drinking water & food(Himalayas, Alps, Andes, areas far from the
sea) Prevalence decreasing due to prophylactic
iodination of salt
Iodine deficiency causes decreased hormonelevels & consequent elevation in TSH
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Sporadic Goiter
Commonest type of goiter
Euthyroid, but may be hypo- or hyper-
Mostly idiopathic, but RARELY, may be causedby:
Drugs used in Rx of hyperthyroidism
Goitrogens e.g. cauliflower, cabbage, cassava
Suboptimal iodine intake
Hereditary enzymatic defects
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Multinodular goiter Recurrent episodes of hyperplasia and involution
leads to irregular enlargement
All long standing diffuse endemic and sporadic goitermay eventually convert to multinodular goiter
Causes most extreme enlargement and may bemistaken for neoplasm
May arise due to variable response of follicular cellsto external stimuli such as trophic hormones
With uneven follicular hyperplasia, generation ofnew follicles and uneven accumulation of colloid rupture of follicle and vessels hemorrhage, scarring& calcification nodularity
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Multinodular Goiter
Asymmetric
enlargement
Multinodular
Haemorrhage
Calcification
Fibrosis
Cystic degeneration
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Multinodular Goiter
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Multinodular Goiter
Numerous follicles
varying in size
Recent haemorrhage
Haemosiderin
Calcification
Cystic degeneration
+/- dominant nodule
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Multinodular Goiter
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Multinodular Goiter
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Toxic Multinodular Goiter
Toxic multinodular goiters usually occur in
individuals older than 50 years of age
Symptoms and signs of hyperthyroidism aresimilar to Graves' disease
Extrathyroidal manifestations are absent
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Thyroid Neoplasms
I. Primary Tumours
Epithelial
Malignant Lymphomas Mesenchymal tumours
II. Metastatic Tumours
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Epithelial Thyroid Neoplasms
Tumours of follicular cells
Benign (adenomas)
Follicular adenoma
Malignant (carcinomas)
Follicular carcinoma (10-20%)
Papillary carcinoma (75-85%)
Undifferentiated (anaplastic) carcinoma (
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Follicular Adenoma
Benign, encapsulated tumor showing evidence
of follicular differentiation
Common
Predominantly young to middle women
Presents as solitary thyroid nodule Painless nodular mass, cold on isotopic scan
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Follicular Adenoma
Solitary, Variably sized,
encapsulated, well-
circumscribed with
homogenous gray-white to red-brown
cut-surface
+/- degenerativechanges
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Plummer's Disease (Toxic
Adenoma)
Hyperthyroidism from a single
hyperfunctioning nodule
Physical examination usually reveals a
solitary thyroid nodule without palpablethyroid tissue on the contralateral side
RAI scanning shows a "hot" nodule with
suppression of the rest of the thyroid
gland.
Rarely malignant
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Follicular Carcinoma
Second most common form, 10-20%
Females > Males, average age ~ 45 - 55 yr
Rare in children
Solitary nodule, painless, cold on isotopic scan
Widely invasive Vs minimaly invasive
50% 10 yr survival Vs 90%10 yr survival
Haematogenous route is preferred mode of spread
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Follicular Carcinoma
Solitary round or oval
nodule
Thick capsule
Composed of follicles
Capsular invasion or
vascular invasion
within our outsidecapsular wall
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Papillary Carcinoma
Commonest thyroid malignancy, 75-85%
Female:Male = 2.5:1
Mean age at onset = 20 - 40 yr
May affect children
Prior head & neck radiation exposure
Indolent, slow-growing painless mass cold onisotopic scan
Cervical lymphadenopathy may be presentingfeature
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Papillary Carcinoma
Variable size
(microscopic to
several cm)
Solid or cystic
Infiltrative or
encapsulated
Solitary ormulticentric (20%)
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Papillary Carcinoma
Papillae or follicles
Psammoma bodies
NUCLEAR
FEATURES***
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Papillary Carcinoma
Nuclear Features
Optically clear (ground
glass, Orphan Annie)
nuclei
Nuclear
pseudoinclusions or
nuclear grooves
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Papillary Carcinoma
Prognosis
Excellent but following factors play importantrole:
Age and sex
Size
Multicentricity
Extra-thyroid extension
Distant metastasis
Total encapsulation, pushing margin of growth &cystic change
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Anaplastic Carcinoma
Rare; < 5% of thyroid carcinomas
Highly malignant and generally fatal < 1yr.
Elderly 65 yrs; females slightly > males
Rapidly enlarging bulky neck mass
Dysphagia, dyspnoea, hoarseness
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Anaplastic Carcinoma
Large, firm, necrotic mass
Frequently replaces entire thyroid gland
Extends into adjacent soft tissue, trachea andoesophagus
Highly anaplastic cell on histology with:
Giant, spindle,small or mix cell population
Foci of papillary or follicular differentiation
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Anaplastic Carcinoma
Cellular pleomorphism
+/- multinucleated
giant cells
High mitotic activity
Necrosis
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Medullary Thyroid Carcinoma (MTC)
Malignant tumour of thyroid C cells producing
cacitonin
5 % of all thyroid malignancies
Sporadic (80%)
Rest in the setting of MEN IIA or B or asfamilial without associated MEN syndrome
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Medullary Thyroid Carcinoma (MTC)
Sporadic MTC
Middle-aged adults
Female:male = 1.3:1
Unilateral involvement of gland
+/- cervical lymph node metastases
Indolent course with 60-70% 5-yr survival after
thyroidectomy
l i l d i l i &
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Multiple Endocrine Neoplasia Types IIA &
IIB
Germ-line mutation in Retprotooncogene on
chromosome 10q11.2
MEN IIA: MTC, phaeochromocytoma, parathyroidadenoma or hyperplasia
MEN IIB: MTC, phaeochromocytoma, mucosalganglioneuromas, Marfanoid habitus, other skeletal
abnormalities
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Medullary Thyroid Carcinoma (MTC)
Associated with MEN IIA
Younger patients in twenties
Multicentric and bilateral
Slow growing
Associated with MEN IIB
Even younger patientsin teens
Aggressive with early metastasis
Poor prognosis
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Medullary Thyroid Carcinoma (MTC)
Histology same forsporadic & familial
Solid, lobular or
insular growthpatterns
Tumour cells round,polygonal or spindle-
shaped Amyloid deposits in
many cases
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Medullary Thyroid Carcinoma (MTC)
Amyloid deposits stain
orange-red with
Congo Red stain
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Prognosis of Thyroid Carcinomas
Papillary Best prognosis
Follicular
Medullary
Anaplastic Worst prognosis
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Secondary Tumours
Direct extensions from: larynx, pharynx,
oesophagus etc.
Metastasis from:
renal cell carcinoma, large intestinal
carcinoma, malignant melanoma, lung
carcinoma, breast carcinoma etc.
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Solitary thyroid nodule
Papillary carcinoma
Follicular carcinoma
Medullary carcinoma
Follicular adenoma
Hyperplastic (dominant) nodule
Metastatic neoplasms FINE NEEDLE ASPIRATION CYTOLOGY