**4. Pathophysiology of goiter**

Thyroid stimulating hormone is the major trophic factor for thyroid gland. TSH acts on TSH receptors present on thyroid cells which are G protein coupled receptors. Downstream signaling leads to gene transcription leading to cell proliferation and differentiation (**Figure 2**).

The most common condition causing TSH dependent Goiter is iodine deficiency.

Goiter in chronic Hashimoto's thyroiditis is also secondary to elevated TSH levels.

In conditions like Graves' disease TSH receptors are stimulated by TSH stimulating antibodies Infection and neoplasia are examples for non-humoral causes of thyroid enlargement. Neoplastic enlargement occurs secondary to clonal expansion are usually are associated with underlying genetic alterations.

**7**

**Table 2.**

*Goiter: Overview of Aetiopathogenesis and Therapy DOI: http://dx.doi.org/10.5772/intechopen.90028*

**5. Differential diagnosis of swelling in anterior aspect of neck**

Extensive history should be taken in all patients with goiter (**Table 2**). Following points should be highlighted while taking history like place of residence (patients from high altitude areas iodine deficient), dietary iodine intake, family history of thyroid disorders, radiation exposure and any history of goitro-

**5.1 Approach to patient with goiter**

*5.1.1 History and examination*

genic drugs intake.

2.Neurogenic tumors

4.Bronchogenic cysts 5.Pericardial cysts 6.Lymphoma 7. Teratoma 8.Thyroglossal cyst

*Differential diagnosis of swelling in anterior aspect of neck.*

1.Goiter

3.Thymoma

**Figure 2.**

*TSH signaling pathway.*

*Goiter: Overview of Aetiopathogenesis and Therapy DOI: http://dx.doi.org/10.5772/intechopen.90028*

*Goiter - Causes and Treatment*

**3.5 Multinodular goiter**

**3.6 Infiltrative thyroid disorder**

sarcoidosis may affect thyroid gland.

orbitopathy, dermopathy and goiter.

condition.

**3.7 Graves' disease**

**3.8 Thyroid adenoma**

**3.9 Thyroid malignancies**

**4. Pathophysiology of goiter**

and differentiation (**Figure 2**).

invasion.

deficiency.

levels.

David Marine and Selwyn Taylor proposed that chronic intermittent stimulus leads to variable thyroid hyperplasia resulting in multinodular goiter [10]. Various factors including genetic heterogeneity of follicular cells, secondary elevation of TSH due to iodine deficiency, goitrogens, and inborn error of thyroid hormone synthesis are considered to be factors involved in pathogenesis of

Various infiltrative disorders like amyloidosis, histiocytosis, cystinosis and

This autoimmune condition is characterized by presence of TRAB (TSH receptor autoantibodies) in the serum. The clinical feature ranges from hyperthyroidism,

These are benign tumors, classified as either follicular (most common form) or papillary (rare) type. Adenomas may be hyper functioning when they are termed toxic adenoma. Follicular adenoma are histopathologically divided into Fetal (micro follicular), Colloid (macro follicular), Embryonal (atypical), Hurthle cell adenoma (oxyphil or oncocytic tumor) types. Among these with the exception of colloid type all other histopathological types have potential for micro

Thyroid malignancies are classified as papillary carcinoma (most common type), follicular carcinoma, medullary thyroid carcinoma, anaplastic carcinoma,

Thyroid stimulating hormone is the major trophic factor for thyroid gland. TSH acts on TSH receptors present on thyroid cells which are G protein coupled receptors. Downstream signaling leads to gene transcription leading to cell proliferation

The most common condition causing TSH dependent Goiter is iodine

Goiter in chronic Hashimoto's thyroiditis is also secondary to elevated TSH

ing antibodies Infection and neoplasia are examples for non-humoral causes of thyroid enlargement. Neoplastic enlargement occurs secondary to clonal expansion

In conditions like Graves' disease TSH receptors are stimulated by TSH stimulat-

thyroid lymphoma (rare) clinical features are explained below.

are usually are associated with underlying genetic alterations.

**6**

**Figure 2.** *TSH signaling pathway.*
