? Diffuse and Multinodular Goiters
? Neoplasms of the Thyroid
? Congenital cyst
? TFT
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? Hyperthyroidism-Thyrotoxicosis is a hypermetabolic state caused by
elevated circulating levels of free T3 and T4
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? Primary
? Secondary
? most common causes of thyrotoxicosis
?Diffuse hyperplasia of the thyroid associated with Graves disease
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(approximately 85% of cases)
? Hyperfunctional multinodular goiter
? Hyperfunctional thyroid adenoma
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Clinical manifestation-
? weight loss despite increased appetite
? left ventricular dysfunction
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? hypermotility, diarrhea, and malabsorption? Proximal muscle weakness and decreased muscle mass are common
(thyroid myopathy)
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? osteoporosisThyroid storm-
? underlying Graves disease
? during infection, surgery, cessation of antithyroid medication, or any
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form of stress.? febrile and present with tachycardia
apathetic hyperthyroidism-
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vHypothyroidism-structural or functional derangement that interfereswith the production of thyroid hormone
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? Primary? Secondary
Primary hypothyroidism-
?Congenital- endemic iodine deficiency
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?Autoimmune-? most common cause of hypothyroidism in iodine-sufficient areas of
the world
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? Hashimoto thyroiditis? Circulating autoantibodies, including antimicrosomal, antithyroid
peroxidase, and antithyroglobulin antibodies
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?Iatrogenic-? Surgical resection
? Radiation
? drugs
Clinical manifestations of hypothyroidism
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? Cretinism? Myxedema
1.Cretinism- congenital hypothyroidism
ETIOPATHOGENESIS-
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1.Developmental anomalies2. Genetic defect in thyroid hormone synthesis
3. Foetal exposure to iodides and antithyroid drugs
4. Endemic cretinism
? CLINICAL FEATURES-slow to thrive, poor feeding, constipation, dry
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scaly skin, hoarse cry and bradycardia
? rise in TSH level and fall in T3 and T4 levels
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? Myxoedema-non-pitting oedema due to accumulation of hydrophilicmucopolysaccharides in the ground substance of dermis and other
tissues
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ETIOPATHOGENESIS.1.Ablation of the thyroid by surgery or radiation
2. Autoimmune (lymphocytic) thyroiditis (termed primary idiopathic
myxoedema)
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3. Endemic or sporadic goitre4. Hypothalamic-pituitary lesions
? CLINICAL FEATURES-cold intolerance, mental and physical lethargy,
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constipation? Thyroiditis
1. Hashimoto thyroiditis
2. granulomatous (de Quervain) thyroiditis
3. subacute lymphocytic thyroiditis
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? Hashimoto Thyroiditis-destruction of the thyroid gland and gradual
and progressive thyroid failure.
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Pathogenesis-
? Anti -thyroglobulin and anti-thyroid peroxidase Ab
? Cytotoxic T lymphocyte-associated antigen-4 (CTLA4) and protein
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tyrosine phosphatase-22 (PTPN22)MORPHOLOGY-
? gross-diffusely enlarged
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? Cut surface- firm, pale, yellow-tanClinical Course.
? Hypothyroidism
? preceded by transient thyrotoxicosis
? Increased risk for developing other autoimmune diseases
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? Subacute Lymphocytic (Painless) Thyroiditis- subset of HT
similar to Hashimoto thyroiditis, however, fibrosis and H?rthle cell
metaplasia are not prominent.
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Granulomatous Thyroiditis-De Quervain thyroiditis
? 40 and 50
? F:M(4:1)
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Pathogenesis-? viral infection
MORPHOLOGIC FEATURES.
? Grossly, asymmetric moderate enlargement
? Cut surface-firm and yellowish-white
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Microscopically-vary to the stage
? acute inflammation
? granulomatous appearance
? advanced cases may show fibroblastic proliferation
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? RIEDEL'S THYROIDITIS-
MORPHOLOGIC FEATURES.
? Grossly-contracted, stony-hard, asymmetric
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? Cut section- hard and devoid of lobulations? Microscopically, there is extensive fibrocollagenous replacement,
marked atrophy of the thyroid parenchyma
GRAVES' DISEASE (DIFFUSE TOXIC GOITRE)-
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? most common cause of endogenous hyperthyroidismClinical findings
? Hyperthyroidism (thyrotoxicosis)
? Diffuse thyroid enlargement
? Ophthalmopathy
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ETIOPATHOGENESIS-
? Genetic factor association-HLA-DR3, CTLA-4 and PTPN22
? Autoimmune disease association
? Autoantibodies- against TSH-receptor autoantigen
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?Thyroid-stimulating immunoglobulin (TSI)?Thyroid growth-stimulating immunoglobulins
?TSH-binding inhibitor immunoglobulins
? Other factors-female,stress, and smoking
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MORPHOLOGIC FEATURES-? Grossly-moderately, diffusely and symmetrically enlarged
? Cut surface-homogeneous, red-brown and meaty and lacks the
normal translucency
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Histology-
? epithelial hyperplasia
? colloid is markedly diminished
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? increased vascularity and accumulation of lymphoid cellsGOITRE-Thyroid enlargement caused by compensatory hyperplasia and
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hypertrophy of the follicular epithelium in response to thyroidhormone deficiency
?Diffuse goitre (simple nontoxic goitre or colloid goitre).
?Nodular goitre (multinodular goitre or adenomatous goitre).
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? ETIOLOGY. Epidemiologically, goitre occurs in 2 forms: endemic, andnon-endemic or sporadic.
qEndemic goitre.
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? Endemic zone- more than 10% of the population is termed endemicgoitre
? Goitrogens
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qSporadic (non-endemic) goitre-
? Increased demand as in puberty and pregnancy
? Genetic factors.
? germline mutations in DICER1 gene
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?PTEN hamartoma tumor syndrome? Dietary goitrogenes
? Drug induced goiter
? Hereditary defect in thyroid hormone synthesis and transport
? Inborn errors of iodine metabolism
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MORPHOLOGIC FEATURES-
? Gross-moderate enlargement,symmetric and diffuse
? Cut surface-gelatinous and translucent brown
Histologically -stage
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? Hyperplastic stage-papillae,new follicles? Involution stage-large follicles distended by colloid and lined by
flattened follicular epithelium
Nodular Goitre (Multinodular Goitre, Adenomatous Goitre)-
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? nodular goitre is regarded as the end-stage of long-standing simplegoitre.
? tumour-like enlargement of the thyroid gland and characteristic
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nodularity
MORPHOLOGIC FEATURES.
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? Grossly, asymmetric and extreme enlargement, weighing 100-500 gmor even more
? Five cardinal macroscopic features are as under
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1. Nodularity with poor encapsulation
2. Fibrous scarring
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3. Haemorrhages4. Focal calcification
5. Cystic degeneration
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? Cut surface- poorly-circumscribed multinodular
Histologically,
? Partial or incomplete encapsulation of nodules
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? follicles varying from small to large? Areas of haemorrhages
? Fibrous scarring with foci of calcification
? Micro-macrocystic change
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THYROID TUMOURS
FOLLICULAR ADENOMA-most common
Pathogenesis-Somatic mutations of the TSH receptor signal ing
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pathway are found in toxic adenomas, as well as in toxic multinodular
goiter.
? TSHR and GNAS mutations,50%
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? RAS or PIK3CA (<20%)? <10% of follicular adenomas harbor PAX8- PPARG fusion genes
MORPHOLOGIC FEATURES.
? Grossly, the follicular adenoma is characterised by four features
1.solitary nodule
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2. complete encapsulation3. clearly distinct architecture inside and outside the capsule
4. compression of the thyroid parenchyma outside the capsule
? small ,up to 3 cm in diameter
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? cut section-grey-white to red-brownHistologically,
? complete fibrous encapsulation
? epithelial cells forming follicles of various size
? surrounding thyroid tissue shows signs of compression
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Thyroid CarcinomaMajor subtypes of thyroid carcinoma-
? Papillary carcinoma (>85% of cases)
? Follicular carcinoma (5% to 15% of cases)
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? Anaplastic (undifferentiated) carcinoma (<5% of cases)? Medullary carcinoma (5% of cases)
Papillary Carcinomas-
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? Fusion gene RET/PTC(RET/papillary thyroid carcinoma) and are present in approximately
20% to 40%
? NTRK1, 5-10%
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? BRAF gene, advance stageFollicular Carcinomas-
? RAS or the PI-3K/AKT
? PIK3CA amplifications
? PTEN, a tumor suppressor gene
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Anaplastic (Undifferentiated) Carcinomas-RAS or PIK3CA mutations)
Second hit ,inactivation of TP53 or activating mutations of -catenin
Medullary Thyroid Carcinomas-
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? MEN-2 syndrome? RET mutations
Papil ary Carcinoma-
most common form of thyroid cancer
MORPHOLOGY-
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Gross-solitary or multifocal
Cut surface-greyish-white, hard, Fibrosis,calcification and papillary foci
microscopic hallmarks-
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? branching papillae? Ground glass or Orphan Annie eye nuclei,intranuclear cytoplasmic
inclusion
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Variants-
? follicular variant
? tall-cell variant
? diffuse sclerosing variant
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? papillary microcarcinomaFol icular Thyroid Carcinoma-
? 5% to 15% of primary thyroid cancers, but are more frequent in areas
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with dietary iodine deficiencyMORPHOLOGY-
? Solitary nodule
? Cut surface-grey-white with areas of haemorrhages, necrosis and cyst
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formation
Microscopically,-
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? follicles of various sizes,solid trabecular pattern? Vascular invasion and direct extension
? lymphatic invasion is rare
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Anaplastic (Undifferentiated) Carcinoma-? <5%
? 100% moratality
Microscopy-
? pleomorphic giant cells
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? spindle cells? mixed spindle and giant cells
Medul ary Carcinoma
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Congenital Anomalies-
Thyroglossal duct cyst
? most common congenital neck mass
? Midline neck
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