Right ventricular outflow tract obstruction pathophysiology

Right ventricular outflow tract obstruction Microchapters
Home
Patient Information
Overview
Anatomy of Pulmonary Valve
Classification
Pulmonary valve stenosis
Pulmonary subvalvular stenosis
Pulmonary supravalvular stenosis
Pulmonary atresia
Pathophysiology
Causes
Differentiating Right ventricular outflow tract obstruction from other Diseases
Epidemiology and Demographics
Risk Factors
Natural History, Complications and Prognosis
Diagnosis
History and Symptoms
Physical Examination
Electrocardiogram
Chest X Ray
Echocardiography
Cardiac Catheterization
Pulmonary Angiography
Treatment
Indications For Surgery
Surgery
Pre-Operative A/P
Post-Operative A/P
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Special Scenarios
Pulmonary artery conduits/Prosthetic Valves
Double-Chambered Right Ventricle
Case Studies
Case #1
Right ventricular outflow tract obstruction pathophysiology On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Right ventricular outflow tract obstruction pathophysiology
CDC on Right ventricular outflow tract obstruction pathophysiology
Right ventricular outflow tract obstruction pathophysiology in the news
Blogs on Right ventricular outflow tract obstruction pathophysiology
Directions to Hospitals Treating Right ventricular outflow tract obstruction pathophysiology
Risk calculators and risk factors for Right ventricular outflow tract obstruction pathophysiology

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

Overview

pulmonic stenosis is most commonly secondary to acute rheumatic fever. Generally, the initial valvulitis is associated with valvular regurgitation but over a period of 2 or more years, the commissures fuse and the valves thicken and calcify. The chordal supporting structure also calcifies and retracts. The result is the typical “fish mouth deformity”. 70% of the time; the mitral valve is involved in isolation, and 25% of the time; the aortic valve is involved as well.

Pathophysiology

Physiology

The normal physiology of [name of process] can be understood as follows:

Pathogenesis

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

OR

• It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
• [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
• Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
• [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
• The progression to [disease name] usually involves the [molecular pathway].
• The pathophysiology of [disease/malignancy] depends on the histological subtype.

Genetics

[Disease name] is transmitted in [mode of genetic transmission] pattern.

OR

Genes involved in the pathogenesis of [disease name] include:

• [Gene1]
• [Gene2]
• [Gene3]

OR

The development of [disease name] is the result of multiple genetic mutations such as:

• [Mutation 1]
• [Mutation 2]
• [Mutation 3]

Associated Conditions

Conditions associated with [disease name] include:

• [Condition 1]
• [Condition 2]
• [Condition 3]

Gross Pathology

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

Microscopic Pathology

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