Goiter pathophysiology: Difference between revisions

Jump to navigation Jump to search
Line 70: Line 70:


==Microscopic Pathology==
==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].
*On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].



Revision as of 17:21, 11 September 2017

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: [1]
  • Thyroglobulin (Tg) gene
  • Thyroid-stimulating hormone receptor (TSHR) gene
  • Na+/I- symporter (NIS) gene
  • Multinodular goitre marker 1 (MNG1) on chromosome 14 [1]

Associated Conditions

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].

References

  1. 1.0 1.1 Brix TH, Hegedüs L (2000). "Genetic and environmental factors in the aetiology of simple goitre". Ann. Med. 32 (3): 153–6. PMID 10821321.

Template:WH Template:WS