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  1. Weight: 15-20 gm
  2. Divided into lobules composed of 20-40 evenly dispersed follicles
  3. Maintain BMR
  4. Hyperthyroidism:Q
Hypermetabolic state caused by elevated levels of free T3 & T4
  1. Diffuse toxic hyperplasia (Graves disease) (accounts for 85% of cases)
  2. Toxic multinodular goiter
  3. Toxic adenoma 
  1. ​Clinical features are due to
    1. Hypermeabilic state
    2. Sympathetic activity Cardiac manifestations are earliest & most consistent feature of hyperthyroidism. Uncommon cases:
      1. Acute or subacute thyroiditis
      2. Hyperfunctioning thyroid carcinoma
      3. Choriocarcinoma of H. mole
      4. TSH secreting Pituitary adenoma
      5. Neonatal thyrotoxicosis associated with maternal Graves disease.
      6. Struma ovarii
      7. Iodide induced hyperthyroidism
      8. Iatrogenic hyperthyroidism 
  2. Diagnosis: Q

Initial Screening: TSH & free T 4 levels

(TSH -low in prim, hyperthyroidism)

(Free T4 - )

Radioactive Iodine uptake: Rare Case T3 thyrotoxicosis in which TSH
T 4 normal, T3

  1. Hypothyroidism:
  2. Primary - defect in thyroid (parenchyma hormone synth.)
  3. Sec. - TSH deficiency
  4. Teritary - TRH deficiency
  5. Cretinism in children
  6. Myxedema in adults 

Thyroiditis: Q

Inflammation of thyroid gland.

  1. Acute illness with severe thyroid pain: Infectious thyroiditis, subacute granulomatous thyroiditis
  2. Little inflammation associated with hematogenous spread Pneumocystis infection are chronic; seen in immunocompromised patients prim. Thyroid dysfunction
    1. Subacute lymphocytic (painless) thyroiditis,
    2. Fibrous (Riedel) thyroiditis

'Hashimoto thyroiditis:

  • Most common cause of hypothyroidism in areas where Q iodine levels are sufficient
  • Autoimmune destruction Q of thyroid gland with lymphocytic infiltration - Struma lymphomatosa . 45-65 yrs.
  • Female: male:: 10:1 to 20:1
  • Familial clustering, HLA-DR5, HLA-DR3 associated Q
  • Usual course: gradual loss of thyroid fn. (Initially, thyroid follicular disruption ž transient hyperthyroidism)
  • freq. of other autoimmune diseases 


  1. Both cellular & humoral factors
  2.   * Primarily defect in T- cells (T cell activation, - suppressor T cells, cytotoxic T cells)
  3. Activated B cells produce Ab against Q
    1. Thyroglobulin & thyroid Peroxidase - Nearly all patients have it; not specific
    2. TSH receptor - Ab specific for Hashimoto & Graves disease
    3. Iodine transporter
  4. Apoptosis by Fas-Fas L system by IL-
  5. Painless enlargement of thyroid
  6. In Hashimotos Disease block action of TSH → Hypothyroidism
  7. In Grave Disease stimulates Thyroid Hormone → Hyperthyroidis
Morphology: Q
  1. Thyroid: Diffusely enlarged capsule intact
  2. CIS: Pale, gray-tan, firm, somewhat nodular
  3. Extensive infiltration of parenchyma by mononuclear inflammatory infiltrate: lymphocytes, plasma cells well developed germinal centers
  4. Hurthle cells+ (eosinophilia, granular); help Q in differentiating from lymphoma.
  5. Fibrosis doesn't extend beyond capsule)
Early: Thyrotoxicosis Q
  1. Later: Hypothyroidism
    ↑ risk of dev. B cell lymphoma
Subacute (Granulomatous) thyroiditis:
  1. Syn.: De Quervain thyroiditis
  2. 30-50 yrs.; Female: Male = 3 to 5:1
  3. Post-viral inflammation (URI
  4. Incidence in summer
Viruses: Coxsackie, mumps, measles, adenovirus, others Q
  1. Associated with HLA-B5.   
  2. Gland: U/L,  B/L enlarged, firm,
  3. Intact capsule, may be slightly adherent to surrounding structures
  4. Cut Surface- firm, yellow white
  5. Pathogenesis - Virus induced host tissue damage/viral direct damage
  6. Microscopy
  • Early: active: inflammatory phase: follicles disrupted by neutrophils forming micro abscess. Q
  • Followed by lymphocytes, histiocytes, plasma cells.
  • Multi nucleated: giant cells
  • Later stages: chronic inflammation & fibrosis
  1. Clinically: 
    Sudden or gradual
  • Pain in neck, sore throat
  • Fever, fatigue, anorexia, myalgia
  • Thyroid inflammation & hyperthyroidism are transient, diminish in 2-6 weeks
  • May be followed by period of transient, usually asymptomatic hypothyroidism, lasting 2-8 weeks
  • Recovery virtually always complete (Initially, T3 & T4 , TSH is low)
- Radioactive I2 uptake is low
- TFT normalizes in 6-8 wks. after recovery

Subacute Lymphocytic (painless) thyroiditis: (Syn.: Silent thyroiditis; lymphocytic thyroiditis) Q
  1. Middle aged adults, female, especially in Postpartum period (1-10% of all cases of hyperthyroidism)
  2. Mild hyperthyroidism & goitrous involvement of gland
  3. HLA DR-3 & HLA DR-5 assoc.
  4. Variant of Hashimoto's thyroiditis
    1. Ab to thyroglobulin & thyroid peroxidase
    2. Family h/o All disease
→ Patchy disruption & collapse of thyroid follicles with multifocal i.i of lymphocytes (Plasma cells, germinal centres → not conspicuous) 
  1. Clinical Manifestations: Hyperthyroidism (develop in 1-2 wks; last from 2-8 wks)
  2. Gland: minimally & diffusely involved, non tender
  3. No infiltrative ophthalmopathy
  4. T3 & T4, ↓ TSH, rI2 uptake
    ↑ Riedel’s Thyroiditis: 
(Syn.: Riedel's struma, fibrous thyroiditis, invasive thyroiditis)
  1. Rare
  2. Adults to elderly patients
  3. V. firm, binds soft tissue of neck in iron collar; trachea; slit like
Clin. DID:
Carcinoma: Stony hard, shows hyalinized fibrous tissue replacing the gland and extending into peripheral skeletal muscle
Path: D/D: Fibrosing variant of Hashimoto thyroiditis
→ Belongs to group of idiopathic disorders:
Inflammatory Fibro-sclerosis
  • Mediastinal or retroperitoneal fibrosis
  • Sclerosing cholangitis
  • Inflammatory pseduo-tumor of the orbit
  • Steroid therapy effective in some
Graves Disease: Q
  1. Most common cause of endogenous hyperthyroidism -  Triad of
    a. Hyperthyroidism due to hyperfunctional diffuse enlargement of gland
    b. Infiltrative ophthalmopathy
    c. Localized, infiltrative dermopathy
  2. 20-40 yrs.; Female: Male 7: 1
  3. Familial clustering, Genetic factors are imp.
  4. HLA B8, HLA DR3 Q        
Pathogenesis Q Autoimmune disease; Ab to TSH receptors Ab. (Antibodies)
  1. Ab to TSH receptors or thyroid stimulating immunoglobulin (TSH) / LA TS (long acting thyroid stimulator): IgG Ig which binds to adenylate cyclase which increases cAMP responsible for t thyroid hormone
  2. Thyroid growth stimulating immunoglobulin: Proliferation of thyroid follicular epithelium)
  3. TSH binding inhibitor immunoglobulin
  4. Prevents TSH from binding normal to its receptor
  5. When hyperthyroidism supervenes on pre-existing Hashimoto thyroiditis Hashitoxicosis
These antibodies are triggered by Q
a) molecular mimicry
b) 'primary T cell autoimmunity
Symmetrically enlarged
Hypertrophy & hyperplasia
  1. Soft, meaty app., smooth
  2. Capsule intact
  3. Crowding with papillae; scalloped margins, Colloid Pale (Papillae lack F/V core unlike papill. Ca.)
  4. ↑ in amount of lymphoid tissue
  5. ↑ T3. ↑ T4, ↓ TSH
  6. ↑ rI2, uptake
Diffuse & Multinodular Goiter:
  1. Reflect impaired synthesis of thyroid hormone
  2. M. often caused by dietary 12 deficiency
  3. ↑TSH → hypertrophy & hyperplasia of gland
    Degree of enlargement is proportional to level & duration of thyroid hormone deficiency  
Diffuse Non-toxic (Simple) Goitre: Q
  1. No nodules
  2. Colloid filled follicles (Colloid Goitre)
  3. Endemic-> 10% of population affected; lack of low dietary iodine
  4. Alps, Andes, Himalayas
  5. Female preponderance
  6. Peak: Puberty- young adult life
  7. -Because of ingestion of Goitrogens & hereditary enzyme deficiencies
Goitrogens: Substances which interfere with thyroid hormone synthesis. eg., excessive Ca, vegetables of Brassica & cruciforme families (e.g., Cabbage, cauliflower, Brussels sprouts, turnips, cassava)
Hereditary enzyme defects (AR): - Involves Q
  1. iodine transport       
  2. organification
  3. dehalogenase
  4. iodotyrosine
Two stages: 
1. Hyperplastic Stage - diffuse, symm. Enlarged, thyroid follicular hyperplasia
2. Colloid involution

Multinodular Goiter:
  1. Recurrent episodes of hyperplasia & involution → more irreg. Enlargement: MNG
  2. May be nonotoxic
Toxic MNG
  • MNGs produce most extreme thyroid enlargements
  • Normal thyroid cells: heterogenous with respect to response to TSH
  • Nodules reflect clonal prolif. of cells having differing Proliferative potentials
  • Both clonal & polyclonal nodule co-exist
Gross: Enlarged multinodular Q
  1. Varying morphology
  2. Hemorrhage, fibrosis, calcification, cystic change
Clinically: Mass effect
  1. Cosmetic effect
  2. Hyperfunctioning nodule developing in MNG: Plummer Syndrome
Solitary Thyroid Nodule (STN):
 2 to 4% of adult population (in USA)
 Female> Male
  1. Solitary nod. are more likely to be neoplastic than multiple nodules Q
  2. STN in younger pt. → more likely neoplastic
  3. STN in Male pt. → more likely neoplastic
  4. H/O radiation to head & neck → ↑ incid. of malignancies
  5. Hot nodules → most likely benign.
Adenomas Q
  1. Most common follicular adenoma
  2. Pathiogenesis: Chronic stimulation of cAMP pathway is a TSH receptors (due to somatic mutation common to GS α
  3. Solitary, spherical, encapsulated (thin, uniform capsule)
  4. Compresses adjacent thyroid
Subtypes includes:
  • Macrofollicular (Simple colloid)
  • Microfollicular (fetal)
  • Embryonal (trabecular)
  • Hurthle cell (oxyphil, oncocytic)
  • Atypical adenoma
  • Adenoma with papillae
Mostly: Cold nodules, relative to adjacent thyroid
(10% of cold nodules: Malignant)
(Malign. is rare in hot nodules)
Thyroid Carcinomas
  1. Early & middle adult life
  2. Female> Male
  3. Papillary Ca (75-80%0)
  4. Follicular Ca (10-20%)
  5. Medullary Ca (5%)
  6. Anaplastic Ca (<5%) 
  1. Ionizing radiation
  2. Hashimoto thyroiditis
  3. Nodular goiter
  4. RET p-onc: with medullary & papillary thyroid Ca: is a tyrosine kinase receptor
Papillary carcinoma Q
  1. 20-40 yrs
  2. associated with previous exposure to ionizing radiation
  3. ↑ incidence with Gardner Syndrome (FAP) & Cowden disease (familia/goiter & skin hamartomas) 
  4. Papillae with F IW stalk
Microscopy: Papillae with Fibrovascular  stalk
Orphan Annie eyed nuclei, intranuclear inclusion, longitudinal grooves
Psammoma bodies
  • Encapsulated variant well encapsulated; rare lymphatic /vascular spread: good prognosis
  • Follicular variant follicular architecture, poor prognosis
  • Tall cell variant → Poorest Prognosis
  • Tumor: Solitary / Multifocal
  • Lymphatic invasion
Follicular Ca: Q
  1. 2nd most common form of thyroid cancer of women of older age (40-50 yrs.)
  2. Single nodule, well circumsc. or infiltr.
  3. Capsule: thick, non-uniform
  4. Capsular infiltration & BV dissemination (to bone, lung, liver etc.) 
Medullary Ca : Neuro-endocrine neoplasm origin Q -parafollicular cells/ C cells (Secrete calcitonin)
(Other markers: CEA, somatostatin, serotonin, VIP)
  1. Sporadic in 80% cf cases
  2. Others with MEN syndromes., RET mutation
Solitary /Multiples lesion
B/L & multicentricity: most common in familial cases
Polygonal, spindle cells in nests / trabeculae with interspersed amyloid Seen

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