Goiter pathophysiology

Goiter Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Goiter from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
Chest X Ray
CT
MRI
Echocardiography or Ultrasound
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
Goiter pathophysiology On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Goiter pathophysiology All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Goiter pathophysiology
CDC on Goiter pathophysiology
Goiter pathophysiology in the news
Blogs on Goiter pathophysiology
Directions to Hospitals Treating Cushing’s disease
Risk calculators and risk factors for Goiter pathophysiology

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 too 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.

• 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].