FAQ'S
 
 
 
 
  • Thyroid gland develops from an invagination of tongue endoderm
  • Grows inferiorly around the hyoid to anterior trachea
  • Parafollicular cells originate from ultimobranchial apparatus near inferior portion of pharyngeal pouch
  • Ultimobranchial organ seen in lower vertebrates
  • Parafollicular Cells are of different origin than thyroid follicular cells
 
 
  • Persistence of a portion of thyroglossal duct
  • Commonest congenital error1
  • Asymptomatic , sub hyoid1
  • Evident in late teens1
  • Whole thyroglossal tract to be removed
 
 
 
 
  • Anywhere along the line of descent
  • May be the only thyroid tissue
  • Base of tongue occasional site
  • Foramen caecum only remnant
  • Distal portion of the duct – pyramidal lobe
 
 
 
 
  • Present in 50% of pts
  • Isolated rest of normal thyroid tissue
  • Lying below the infr pole of thytroid
  • Nodular changes in the rset may present as goitre
 
 
  • Embryological remanant of thyroglossal tract
  • Frequency 55-76%
  • Commonly in the left side of isthmus
  • Cause for recurrence
 
 
  • Posterolateral projection of thyroid tissue
  • Resulting at the point where medial lateral thyroid fuse
  • Grades 1-3
  • RLN medial to the ZT
 
 
  • Brownish-red, highly vascular gland
  • Location: ant neck at C5-T1, overlays 2nd – 4th tracheal rings
  • Consist of rt and lt lobe connected by an isthumus
  • Avg weight: 25-30 g in adults(slightly more in women,iodine content)
 
 
 
 
  • Conical in shape
  • Apex at the level of oblique line of thyroid cartilage
  • Base at the level of fourth or fifth tracheal ring
  • Dimensions:5cm x 3cm x 2cm
  • Postromedial aspect:lateral ligament
 
 
  • Lateral surface: sternothyroid
  • More anteriorly: sternohyoid, superior belly of omohyoid, SCM
  • Medial suface: larynx and trachea
  • Superior pole: inf pharyngealconstrictor: posterior part of cricothyroid: ELN(medial)
  • Inferior pole: trachea,RLN
 
 
  • Lateral - sternothyroid
  • Anterior
  • Omohyoid muscle
  • Sternohyoid
  • Inferior - SCM (lower portion)
  • Motor nerve supply from the ansa cervicalis enters these muscles inferiorly.
  • Posterolateral surface: carotid sheath,CCA
  • Anterior border: anterior br of sup thyroid artery
  • Posterior border: inferior thyroid artery
  • Sternohyoid
  • Lower part: parathyroid
  • Left: thoracic duct
 
 
 
 
  • It connects lower parts of two lobes
  • It measures 1.25cm in width and length
  • It overlies second and third tracheal rings
  • Size and site may vary
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
  • Congenital hypothyroidism
  • Acquired hypothyroidism
 
 
  • Autoimmune CLT (Chronic lymphocytic thyroiditis, Hashimoto thyroiditis)
  • Subacute thyroiditis
  • Goitrogen ingestion
  • Endemic goiter
  • Euthyroid sick syndrome (non-thyroidal illness)
  • Irradiation of the thyroid gland
  • Infiltrative and storage disorders of the thyroid gland (histiocytosis X and cystinosis)
  • Surgical excision
 
 
 
 
  • Acute – Suppurative
    1. Bacterial, fungal, parasitic
  • Sub acute
    1. Granulomatous
    2. Lymphocytic – sporadic & post partum
  • Chronic –
    1. Hashimoto’s thyroiditis
    2. Riedel’s thyroiditis
 
 
 
 
  • Goitrous(Hashimoto’s thyroiditis)
  • Atrophic(primary myxoedema)
  • Juvenile thyroiditis
  • Postpartum thyroiditis
  • Silent thyroiditis
  • Focal variant
 
 
  • Hashimoto’s thyroiditis – commonest (>90%)
  • Etiology uncertain
  • Most plausible hypothesis – Antigen induced
  • Characteristic feature – variable proportions of lymphocytes,fibrosis and follicle damage
  • Variable/ fluctuating course
  • Passes through all 3 phases
  • Pain exclusive in granulomatous variant
  • >90% recovery in granulomatous form
  • About 75% in painless lymphocytic variant
  • Persistent goiter with/without hypo – rule
  • 5% cases - ophthalmopathy
 
 
  • Type I autoimmune polyglandular syndrome
  • Type II autoimmune polyglandular syndrome
  • Rheumatologic conditions- RA,SLE, SS etc.,
  • Others- Chronic active hepatitis,PBC,MVP
  • Turner’s and Down syndrome
 
 
 
 
  • E/o malignancy – ptc
  • Goiter with pressure symptoms
  • Recurrent/ refractorily painful thyroiditis
  • Indeterminate biopsy- lymphoma Vs thyroiditis
  • Presence of dominant mass- T4 unresponsive
  • Progressive thyromegaly despite T4 therapy
  • Cosmetic reasons
  • Risk of DTC in HT- 8 to 37 %*
  • Commonest is papillary cancer with high propensity to lymphoma
  • Local pressure symptoms
  • Clark*– 21/ 75 cases successfully treated
  • Lindem**– 21/ 41 cases
  • Essential to differentiate from subacute form
  • Options are total thyroidectomy* or near total thyroidectomy with RAI remnant ablation
  • Presence of dominant mass- T4 unresponsive
  • Progressive thyromegaly despite T4 therapy
 
 
  • Begin with toxic symptoms
  • Low iodine uptake in scintigraphy
  • Leakage of preformed hormones
  • Development of goitre
  • Initial hyperthyroid stage followed by recovery with in between breif period of eu&hypothyroid stage
 
 
 
 
  • No primary role of surgery
  • Indicated only in persistent goiter with compressive symptoms&cosmetic reasons
  • For repeated painful relapses*
  • Painless variant needs to be differentiated from hashimoto’s thyroiditis
  • Postpartum variant needs to be differentiated from Graves disease
 
 
  • Surgery is
 
 
  • Surgery- to relieve compressive symptoms
  • Reports of total thyroidectomy* –
 
 
 
 
  • Thyroid gland-remarkably resistant to infection
  • Commonest predisposing factor – preexisting thyroid disease*
  • Most common route of spread-pyriform fistula**
  • Mostly preceded by upper respiratory infection**
 
 
 
 
 
 
  • From infected 3,4 branchial pouches*
  • From infected thyroglossal tract
  • Via blood stream from LRT, GIT, GTU**, skin***
  • Via lymphatics from head& neck sepsis
  • Along fascial planes- retro& post pharyngeal
  • Direct inoculation eg., at surgery****
 
 
  • >90% anterior neck pain, tenderness,fever,radiating pain,erythema,hyperemia,unilateral/bilateral lobar enlargement and fluctuance in 1 to 3 d.
  • Dysphagia,dysphonia.
  • RLN palsy, persistent goiter, hypothyroidism, tracheal perforation*
  • Via lymphatics from head& neck sepsis
 
 
  • Non- thyroidal causes – clinical
  • H/o irradiation, radio-iodineand drug intake
  • Subacute thyroiditis- clinical, investgations
  • TFT
  • Thyroglobulin
  • Leukocytosis, ESR
  • X ray neck
  • X ray neck
  • FNAC* – cytology, Gram stain, culture, special stains( Gomori silver methanamine)
  • MRI,CT, radionuclide imaging when in doubt
 
 
  • FNAC – iv antibiotics - drainage/ lobectomy
  • Treat the cause - mainly in children/adolescents
  • Subacute thyroiditis- clinical, investgations
 
 
 
 
  • Overactivity of thyroid gland (hyperthyroidism)

  • Graves' disease
  • Neonatal Graves' disease
  • Autoimmune functional nodule
  • TSH-induced hyperthyroidism
  • Tumor-produced thyroid stimulators
  • Iodine-induced thyrotoxicosis (Jod-Basedow)
  • Toxic nodular goiter

  • Receiving exogenous thyroid hormone

 
 
  • Multisystem autoimmune disorders
  • Classic triad
  • Incidence: 10 – 15% in childhood thyroid disorders
  • Increases with age (peak in adolescence) and family history
  • Male:female = 1:4-5
 
 
 
 
  • Thyroid function test
  • Positive autoantibodies
  • Radioiodine uptake : elevated
 
 
 
 
  • Medical treatment
  • Radiation Therapy
  • Surgical treatment
 
 
  • Male sex
  • Large goiters
  • High titers of TSH receptor Ab & TPO at 6 months after initiation of ATD
  • High baseline T4 & T3 values
  • H/O > 1 prior relapse
 
 
  • Most common cause hyperthyroidism in elderly
  • Accounts for 10-15% of HT
  • It take many years to evolve
  • High baseline T4 & T3 values
 
 
 
 
 
 
 
 

Clinically recognizable enlargements of the thyroid gland characterized by excessive growth and structural and/or functional transformation of one or several areas within the normal thyroid tissue.

  • Adenomatous goiter
  • Non toxic diffuse goiter
  • Non toxic nodular goiter
  • Colloid nodular goiter
 
 
  • Multifactorial
    1. Iodine deficiency
    2. Dyshormonogenesis
    3. Goitrogens
    4. Heredity
    5. Growth factors
 
 
  • 15.5% population (UK- Wickham survey)
  • 14.9% I2 Deficient & 9.8% I2 sufficient (Denmark- Knudsen et al)
  • Females : Males :: 5:1 to 10:1 (Non-endemic areas)
 
 

Hegedus L, et al. Endocrine review. 2003. 24(1): 102-132

 
 
  • Genetic factors
    1. Point mutation- Tg gene at Chr. 8 (Corel et al)
    2. MNG-1 gene at Chr. 14 (Bignell et al)
    3. TSH receptor gene mutation (Hegedus et al)
    4. Sodium Iodide symporter (Hegedus et al)
    5. GD-1 on Chr.14 (Tomer et al)
 
 
  • Primary
    1. Normal follicular cells have functional heterogeneity? genetic
    2. Replicating follicular cells acquire inheritable qualities
    3. Subsequent functional and structural abnormalities in growing goiters
  • Secondary
    1. TSH Stimulation (iodine deficiency, goitrogens, inborn errors of thyroid hormone synthesis)
 
 
  • Genetic heterogeneity:
    1. Developing follicular epithelial cells are functionally polyclonal.*
    2. Widely differing qualities in growth & thyroid hormone synthesis, viz. iodine uptake, thyroglobulin production, iodo-thyrosine coupling, endocytosis.
 
 
 
 
  • 17% sub-clinical hyperthyroidism*
  • 9-10% incidence of overt hyperthyroidism (12 yr follow up)**
  • Hyperthyroidism
    1. Differentiated from graves disease by H.S. Plummer in 1928
    2. Thyrotoxicosis Πduration
    3. 5-7th decade
    4. CHF, arrhythmias more common
    5. Emotional liability, Proximal muscle weakness
    6. Absence of exophthalmos
  • Carcinomatous change
    1. Reported literature 4-17%*
    2. Papillary thyroid cancer
 
 
 
 
 
 
  • Ultrasound
  • Scintigraphy
  • CT scan
  • MRI scan
  • PET scan
 
 
  • Indications
    1. Toxicity in a MNG
    2. Aim- visualize hot nodule suitable for I131 therapy
  • Malignancy in hot nodules 1%
  • Malignancy in cold nodules 8-25%
 
 
  • No advantage over USG for intra-thyroidal lesions.
  • Indications
    1. Substernal goiters
    2. Malignancy
    3. Recurrent goiters
  • PET differentiate Benign v/s malignant*
 
 
  • FNAC is procedure of choice for evaluation of all thyroid nodules
  • Cystic nodules that repeatedly reveal non diagnostic results need close follow up or surgical excision. Surgery should be strongly considered if the nodule is solid.
  • If indeterminate- thyroid scan should be done. If concordant autonomous nodule is not seen hemi / total thyroidectomy should be undertaken.
  • If benign on cytology, further immediate diagnostic procedure or treatment is usually not required.
  • In presence of 2 or more nodules larger than 1-1.5 cm, those with a suspicious sonographic appearance should be preferentially aspirated.
  • In presence of multiple nodules with none having a suspicious sonographic appearance, likelihood of malignancy is low and it is reasonable to aspirate the largest nodule only.
  • In case of low TSH, radio iodine scan should be done and compared to the USG to determine the functionality of the nodule larger than 1-1.5 cm. FNAC should be considered only for iso / non functioning nodules, among which, those with suspicious sonographic features should be aspirated preferentially.
 
 
  • Moderate goiters with no symptoms
  • Indications for therapy
    1. Strong
      1. Pressure symptoms
      2. Hyperthyroidism
      3. Rapid growth in one nodule / Suspected malignancy
      4. Retrosternal Extension
    2. Relative
      1. Cosmetic
      2. Patient concern
 
 
  • Regular follow up
  • Iodine supplementation
  • Levothyroxine supplementation
  • I131 therapy
  • Surgery
  • Percutaneous ethanol injection
 
 

 

What is the role of medical therapy for benign thyroid nodules?

 

  • Do not recommend routine suppression therapy of benign thyroid nodules.
  • Growing nodules that are benign after repeat biopsy should be considered for continued monitoring or intervention with surgery based on symptoms and clinical concern. There are no data on the use of levo-thyroxin in this subpopulation of patients.
  • TSH suppression
    1. I2 deficient areas leads to regression in nodule size.
    2. I2 sufficient areas-Data inconclusive.
 
 
 
 
  • Radioactive iodine therapy
    1. Need more dose
    2. Relatively resistant
    3. Thyroid volume may reduce by 43%
  • Surgery –total thyroidectomy
 
 
 
 
 
 
  • Basic investigation: TSH, fT4, USG, Scintigraphy, FNAC
  • Majority of asymptomatic patients- followed up
  • No role of LT4, Iodine therapy
  • Surgery and I131
  • Total thyroidectomy
 

Approach to a patient who walks into the clinic with a Thyroid Nodule

 

Definition…..

 

A discrete lesion within the Thyroid gland that is radiologically distinct from the surrounding thyroid parenchyma. ( Some palpable lesions may not correspond to distinct radiologic abnormalities)

  • Prevalence
    1. Palpation – 3%-7%
    2. High Resolutuin USG – 19%- 67%
    3. Increases with Age, Iodine deficiency
    4. Higher frequency in women
  • 10% life time probability of developing a thyroid nodule
  • Thyroid cancers occurs in 5% -15% of thyroid nodules
 
 
 
 
  • Benign
    1. Colloid Nodule
    2. Hashimotos Thyroiditis
    3. Simple or hemorrhagic cyst
    4. Follicular adenoma
    5. Sub acute Thyroiditis
  • Malignant
    1. PTC,FTC,Anaplastic Carcinoma
    2. MTC
    3. Thyroid Lymphoma
    4. Metastatic carcinoma
 
 
  • Hypothyroidism
    1. Congenital
      1. Dyshamonogenic
      2. Agenesis
    2. Acquired
    3. Thyroiditis
      1. Acute
      2. Subacute
      3. chronic
  • Hyperthyroidism
    1. Graves disease
    2. AFTN
    3. Toxic MNG
    4. Euthyroid
 
 
  • Medical history
  • Clinical examination
  • Analysis of thyroid hormones
  • Ultrasound
  • Thyroid c
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