Goiter pathophysiology

Goiter Microchapters
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Overview

The exact pathogenesis of [disease name] is not fully understood.

OR

It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].

OR

[Pathogen name] is usually transmitted via the [transmission route] route to the human host.

OR

Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.

OR

[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].

OR

The progression to [disease name] usually involves the [molecular pathway].

OR

The pathophysiology of [disease/malignancy] depends on the histological subtype.

Pathophysiology

Pathogenesis

• Goiters may can occur as a result of either hypothyroidism, hyperthyroidism, or when the levels of thyroid hormone are normal.
• Thyroid enlargement (goiter) and hypothyroidism may occur due to compensatory responses as a result of a severe underlying disorder.
• When the thyroid gland can't secrete enough thyroid hormone to cater to the metabolic requirements, it may lead to simple goiter.
• In order to compensate for inadequate hormone synthesis the thyroid gland enlarges, this type of compensation overcomes mild to moderate hormonal impairment.
• When the TRH-TSH thyroid hormone axis is interfered, it results in the structural and functional changes of the thyroid gland.
• Increased TSH production is trigerred by a deficiency in thyroid hormone synthesis or intake.
• In order to normalize thyroid hormone levels, the increase in TSH leads to increased cellularity and hyperplasia of the thyroid gland and whne this process is continuous, it leads to goiter.
• Thyroid hormone deficiency may be related to iodine deficiency, inborn errors of thyroid hormone synthesis and goitrogens.
• Goiters may from as a result of a many TSH receptor agonists. The TSH receptor get stimulated under the following condition:
  • Adenoma of the pituitary
  • Adenoma of the hypothalamus
  • Pituitary resistance to thyroid hormone
  • TSH receptor antibodies
  • Tumors producing hCG (human chorionic gonadotropin)

• The pathophysiological consequences of goitres results from one of the following:
  • The effect of thyroid hormone dysfunction
  • The effect of enlarged thyroid gland
  • The effect of primary disease causing goitre

• The effect of thyroid hormone dysfunction:
  • Thyroid hyperfunction (hyperthyroidism) → Features of hyperthyroidism
  • Thyroid hypofunction (hypothyroidism) → Features of hypothyroidism

• The effect of enlarged thyroid gland:
  • Effect on the trachea → dyspnea
  • Effect on the esophagus → dysphagia
  • Effect on the superior venacava → distended neck veins
  • Effect on the recurrent laryngeal nerve → horsiness of voice

• The effect of primary disease causing goitre:
  • The effect depends on the underlying disease

Genetics

• Goiter may be caused by a mutation in the following genes which vary from one family to the other:

• Thyroglobulin (Tg) gene
• Thyroid-stimulating hormone receptor (TSHR) gene
• Na+/I- symporter (NIS) gene

• Multinodular goitre marker 1 (MNG1) on chromosome 14

Gross Pathology

• On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].

Microscopic Pathology

Microscopic studies that aid in the histopathological analysis:

• Fine needle aspiration cytology (FNAC)
• Open biopsy

• On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].