Endocarditis pathophysiology

Revision as of 14:28, 11 July 2017 by Ahmed Younes (talk | contribs)
Jump to navigation Jump to search
https://https://www.youtube.com/watch?v=kW-85yk0ErQ%7C350}}

Endocarditis Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Infective Endocarditis from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications & Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-ray

Echocardiography and Ultrasound

CT scan

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease

Diagnosis and Follow-up

Medical Therapy

Intervention

Case Studies

Case #1

Endocarditis 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 Endocarditis pathophysiology

CDC onEndocarditis pathophysiology

Endocarditis pathophysiology in the news

Blogs on Endocarditis pathophysiology

to Hospitals Treating Endocarditis pathophysiology

Risk calculators and risk factors for Endocarditis pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Maliha Shakil, M.D. [2]

Overview

The pathogenesis of infective endocarditis includes valvular damage, altered and turbulent flow, bacteremia, and lack of blood supply to the valves.[1] Damaged endothelium becomes a site for attachment of infectious agents in infectious endocarditis. Nonbacterial thrombotic endocarditis is related to hypercoaguable states such as pregnancy or systemic bacterial infection.[2] The characteristic lesion of endocarditis is a vegetation. Vegetations are composed of fibrin, inflammatory cells, platelets, and microorganisms.[3]

Pathophysiology

Pathogenesis

Infective Endocarditis

The pathogenesis of infective endocarditis includes:[1][2]

Pathogenic Factors Mechanism
Valvular Damage
  • Altered and turbulent flow
  • Catheters, electrodes, and other intracardiac devices
  • Solid particles from repeated intravenous injections
  • Chronic inflammation
Bacteremia
Lack of blood supply to valves
  • Blunted immune response
  • Therapeutic drugs have difficulty reaching infected valves

Nonbacterial thrombotic endocarditis

  • Nonbacterial thrombotic endocarditis (NBTE), also called marantic endocarditis is most commonly found on previously undamaged valves.
  • The vegetations in NBTE are small, sterile, and tend to aggregate along the edges of the valve or the cusps.
  • Unlike infective endocarditis, NBTE does not cause an inflammation response from the body.
  • NBTE usually occurs due to hypercoaguable states such as systemic bacterial infection or pregnancy. NBTE may also occur in patients with cancer, particularly mucinous adenocarcinoma.
  • Libman-Sacks endocarditis is another form of sterile endocarditis; this form occurs more often in patients with lupus erythematosus and is thought to be due to the deposition of immune complexes.
  • Libman-Sacks endocarditis involves small vegetations, while infective endocarditis is composed of large vegetations. These immune complexes precipitate an inflammatory reaction, which helps to differentiate it from NBTE.
  • Unlike NBTE, Libman-Sacks endocarditis does not seem to have a preferred location of deposition and may form on the undersurfaces of the valves or even on the endocardium.[2]

Gross and Microscopic Pathology

The characteristic lesion of endocarditis is a vegetation. Vegetations are composed of fibrin, inflammatory cells, platelets, and microorganisms.[3] Characteristic features of endocarditis on gross pathology and histopathological analysis include:[4]

Endocarditis Subtype Features on Gross Pathology Features on Histopathological Microscopic Analysis
Infective Endocarditis
  • Left-sided valve involvement (mitral, aortic) more common generally
  • Right-sided valve involvement (pulmonic, tricuspid valve) more common in intravenous drug abusers
  • Valvular vegetations
  • Valvular destruction
  • Inflammatory infiltrate
  • Abundant neutrophils
  • Plasma cells may be present in subacute endocarditis
  • Microorganisms present
Nonbacterial Thrombotic Endocarditis
  • Round non-destructive vegetations, usually at the line of closure
  • Vegetations without inflammation and microorganisms

Pathology

Image courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

Videos

{{#ev:youtube|gk7cpP2ymOs}} {{#ev:youtube|BiNulEFh6rU}}

References

  1. 1.0 1.1 Infective endocarditis. Wikipedia (2015). https://en.wikipedia.org/wiki/Infective_endocarditis#Pathogenesis Accessed on September 21, 2015
  2. 2.0 2.1 2.2 Endocarditis. Wikipedia (2015). https://en.wikipedia.org/wiki/Endocarditis Accessed on September 21, 2015
  3. 3.0 3.1 Mylonakis E, Calderwood SB (2001). "Infective endocarditis in adults". N Engl J Med. 345 (18): 1318–30. doi:10.1056/NEJMra010082. PMID 11794152.
  4. Infective Endocarditis. Libre Pathology (2015). URL=http://librepathology.org/wiki/index.php/Infective_endocarditis Accessed on September 21, 2015

Template:WH Template:WS