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Pleural Effusion I: Introduction

Pleural Effusion I: Introduction

Pleural effusion is an abnormal fluid accumulation in the pleural cavity, a narrow space between the lungs and the chest wall. It is not a disease per se but rather a symptom or indication of an underlying disease. In normal circumstances, this space contains a small amount of fluid (5 to 15 mL), a lubricant facilitating the non-frictional movement of the pleural surfaces.
There are two main types of pleural effusion: transudative and exudative. They are differentiated using Light's criteria,...

Pleural Effusion II: Symptoms and Management

Pleural Effusion II: Symptoms and Management

Pleural Effusion Overview
A pleural effusion is the abnormal collection of fluid between the parietal and visceral pleura layers of tissue that form the lining of the lungs and chest cavity. It can occur independently or due to surrounding parenchymal diseases, such as infection, malignancy, or inflammatory conditions.
Clinical Manifestations:

Pulmonary Tuberculosis III

Pulmonary Tuberculosis III

Tuberculosis (TB) is a contagious infection primarily affecting the lung parenchyma but which can also affect other body parts. TB can be classified based on disease development, presentation, and the affected anatomical site.
The first classification is based on the development of the disease, and it includes the following categories:

Amyloid Fibrils

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins. Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils.
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining, normally used to...

Amyloid Fibrils

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins. Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils.
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining, normally used to...

Pulmonary Tuberculosis II

Pulmonary Tuberculosis II

Tuberculosis, or TB, is a bacterial infectious disease caused by Mycobacterium tuberculosis. While its primary impact is on the lungs, leading to pulmonary tuberculosis, it can also affect various other organs, a condition referred to as extrapulmonary tuberculosis.
Here is a detailed explanation of its pathophysiology:
Transmission: The process begins when a person inhales droplet nuclei containing M. tuberculosis. These are typically released into the air when an individual with pulmonary or...

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Related Experiment Video

Updated: Jun 18, 2026

Imaging Features of Systemic Sclerosis-Associated Interstitial Lung Disease

Imaging Features of Systemic Sclerosis-Associated Interstitial Lung Disease

Published on: June 16, 2020

Primary systemic amyloidosis and persistent pleural effusions.

Dan Schwarz¹, Christopher Jue, William Sikov

¹Alpert School of Medicine, Brown University, Providence, Rhode Island, USA. dan_schwarz@brown.edu

Amyloid : the International Journal of Experimental and Clinical Investigation : the Official Journal of the International Society of Amyloidosis

|November 20, 2009

Summary

Persistent pleural effusions are rare in systemic amyloidosis (AL). This case suggests pleural amyloid deposition may cause these effusions, even without direct biopsy proof, impacting lymphatic drainage.

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Area of Science:

Medicine
Pulmonology
Cardiology

Background:

Primary systemic amyloidosis (AL) is a rare plasma cell disorder.
Persistent pleural effusions are an uncommon manifestation of AL.
Amyloid deposition in the pleura is hypothesized to cause effusions by impairing lymphatic drainage.

Observation:

A 73-year-old woman with AL presented with persistent bilateral pleural effusions.
The effusions were refractory to standard treatments like diuresis and thoracentesis.
The patient's cardiac and renal function did not adequately explain the persistent effusions.

Findings:

This case highlights a potential, albeit unproven, cause of refractory pleural effusions in AL.
The findings support the hypothesis that pleural amyloid deposition can lead to lymphatic dysfunction.
Suggests pleural amyloidosis as a potential etiology for persistent effusions in AL patients.

Implications:

This case broadens the understanding of AL's extrapulmonary manifestations.
Highlights the need to consider pleural amyloid deposition in AL patients with unexplained effusions.
May guide diagnostic and therapeutic strategies for managing pleural effusions in AL.