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Related Concept Videos

Chronic Obstructive Pulmonary Disease II: Emphysema01:23

Chronic Obstructive Pulmonary Disease II: Emphysema

Emphysema, a major phenotype of chronic obstructive pulmonary disease (COPD), is characterized by irreversible destruction of alveolar walls and permanent enlargement of distal airspaces. Unlike chronic bronchitis, which primarily affects the airways, emphysema predominantly involves the lung parenchyma, where structural damage leads to airflow limitation.PathophysiologyIt most commonly results from prolonged exposure to cigarette smoke and other toxic gases, particularly cigarette smoke.
Chronic Pancreatitis II: Pathophysiology01:21

Chronic Pancreatitis II: Pathophysiology

Chronic pancreatitis is a progressive and irreversible inflammation of the pancreas, most often caused by long-term alcohol abuse, but it can also be related to ductal obstruction, smoking, or genetic factors.Chronic pancreatitis occurs when the pancreas is repeatedly exposed to harmful agents like alcohol, smoking, ductal obstruction, or genetic predisposition. These factors lead to the release of toxic metabolites and inflammatory cytokines, sustaining chronic inflammation in the pancreatic...
Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation
Other Pulmonary Disorders01:17

Other Pulmonary Disorders

Respiratory disorders encompass a range of conditions with varying levels of severity. Asthma, marked by chronic airway inflammation and hypersensitivity, is one such condition. It can lead to airway obstruction due to factors like bronchial spasms, mucosal edema, increased mucus secretion, or epithelial damage. Asthma triggers are diverse, ranging from allergens to emotional upset, and treatment focuses on both immediate relief through bronchodilators and long-term inflammation suppression.
Atelectasis II: Pathophysiology01:10

Atelectasis II: Pathophysiology

Atelectasis develops when alveoli lose their air and collapse inward. Because lung tissue is naturally elastic, these air sacs shrink rather than remaining open. Collapsed alveoli are no longer ventilated, reducing their role in gas exchange. Blood flow may continue in these regions, creating a ventilation–perfusion mismatch. Clinical findings include decreased breath sounds, dullness to percussion, reduced chest expansion, and decreased tactile fremitus as sound transmission through collapsed...
Chronic Obstructive Pulmonary Disease-I: Introduction01:20

Chronic Obstructive Pulmonary Disease-I: Introduction

Chronic Obstructive Pulmonary Disease (COPD) is a long-lasting respiratory condition requiring continuous attention and care. It is a progressive lung disease that leads to breathing challenges due to airflow obstruction. It manifests as persistent respiratory symptoms and restricted airflow resulting from abnormalities in the airways and alveoli, usually due to long-term exposure to harmful particles or gases. COPD mainly consists of two primary conditions: emphysema and chronic bronchitis.

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Updated: May 12, 2026

Assessment of Glutamine as a Fuel Source for Alveolar Macrophages Exposed to Chronic Ethanol Using an Extracellular Flux Bioanalyzer
08:37

Assessment of Glutamine as a Fuel Source for Alveolar Macrophages Exposed to Chronic Ethanol Using an Extracellular Flux Bioanalyzer

Published on: November 15, 2024

Alcoholic lung disease.

Corey D Kershaw1, David M Guidot

  • 1Division of Pulmonary, Allergy, and Critical Care Medicine, Emory University School of Medicine, Atlanta, Georgia.

Alcohol Research & Health : the Journal of the National Institute on Alcohol Abuse and Alcoholism
|April 16, 2013
PubMed
Summary
This summary is machine-generated.

Alcohol abuse significantly increases the risk of acute respiratory distress syndrome (ARDS), a severe lung injury. Understanding the alcoholic lung is crucial for developing new treatments for this often-fatal condition.

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Chronic Intermittent Ethanol Vapor Exposure Paired with Two-Bottle Choice to Model Alcohol Use Disorder
05:12

Chronic Intermittent Ethanol Vapor Exposure Paired with Two-Bottle Choice to Model Alcohol Use Disorder

Published on: June 23, 2023

Area of Science:

  • Pulmonology
  • Toxicology
  • Genetics

Background:

  • Alcohol abuse is an independent risk factor for acute respiratory distress syndrome (ARDS), increasing incidence by 3-4 fold.
  • Alcohol-related lung injury causes tens of thousands of excess deaths annually in the US, comparable to alcohol-related cirrhosis.
  • The link between alcohol abuse and ARDS is recent and not widely recognized, even among lung researchers.

Purpose of the Study:

  • To highlight the significance of alcohol abuse as a cause of acute lung injury.
  • To explore the underlying mechanisms of alcohol-mediated lung damage.
  • To advocate for systems biology approaches in studying the alcoholic lung.

Main Methods:

  • Review of experimental and clinical studies on alcohol's effects on the lung.
  • Discussion of the potential for genomics and proteomics in understanding alcohol-induced lung diseases.
  • Emphasis on the need for systems biology approaches.

Main Results:

  • Alcohol abuse is a major, under-recognized contributor to ARDS and pneumonia.
  • Mechanisms linking alcohol abuse to lung injury are being elucidated.
  • Novel therapeutic targets for alcohol-mediated lung injury are being identified.

Conclusions:

  • The alcoholic lung presents a critical area for research due to high mortality and environmental-host interactions.
  • Systems biology approaches, including genomics and proteomics, are well-suited for studying alcohol-induced lung diseases.
  • Further research is needed to develop targeted therapies for vulnerable populations.