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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.
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The respiratory zone of the human body, which stands in contrast to the conducting zone, comprises the structures that actively participate in the exchange of gases. The initiation of this zone is marked by the terminal bronchioles converging into respiratory bronchioles, the tiniest bronchiole classification. The respiratory bronchioles give way to the alveolar ducts that opens into a congregation of alveoli. Actively involved in gas exchange, alveoli resemble tiny sacs similar to clusters of...
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Chronic bronchitis is a key phenotype of chronic obstructive pulmonary disease (COPD), characterized by airway-centered inflammation and mucus overproduction. It develops from long-term exposure to harmful particles or gases, most commonly cigarette smoke, which triggers a persistent inflammatory response.Cellular and Structural ChangesInflammation initially affects the large bronchi and later the smaller airways, with infiltration by immune cells, including neutrophils, macrophages, and...
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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...
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Related Experiment Video

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Refined Murine Model of Idiopathic Pulmonary Fibrosis
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Extensive pulmonary alveolar microlithiasis.

Nuttapol Rittayamai1, Nisa Muangman2, Ruchira Ruangchira-Urai3

  • 1Division of Respiratory Diseases and Tuberbulosis, Department of Medicine, Faculty of Medicine Siriraj Hospital, Mahidol University Bangkok, Thailand.

Respirology Case Reports
|December 5, 2014
PubMed
Summary
This summary is machine-generated.

Pulmonary alveolar microlithiasis, a rare lung disease, involves abnormal phosphate transport due to SLC34A2 gene mutations. This case highlights extensive microlithiasis in an elderly woman presenting with dyspnea and diffuse calcification.

Keywords:
Alveolar microlithiasisSLC34A2 genecomputed tomography of chesthypoxemiapulmonary calcification

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Area of Science:

  • Pulmonology
  • Genetics
  • Rare Diseases

Background:

  • Pulmonary alveolar microlithiasis (PAM) is a rare interstitial lung disease characterized by the accumulation of calcium phosphate microliths in the alveoli.
  • Mutations in the SLC34A2 gene, encoding a sodium-dependent phosphate co-transporter, are implicated in the pathogenesis of PAM.
  • The condition typically presents with progressive dyspnea and diffuse pulmonary calcification on imaging.

Purpose of the Study:

  • To report a case of extensive pulmonary alveolar microlithiasis in an elderly female patient.
  • To describe the clinical presentation, diagnostic findings, and histopathological confirmation of the disease.

Main Methods:

  • Case report of an elderly woman with progressive dyspnea.
  • Diagnostic imaging including chest radiography.
  • Histopathological examination of lung tissue obtained via open lung biopsy.

Main Results:

  • Chest radiograph showed diffuse pulmonary calcification.
  • Open lung biopsy revealed widespread intra-alveolar laminated calcium deposits.
  • Findings were consistent with extensive pulmonary alveolar microlithiasis.

Conclusions:

  • This case underscores the importance of considering pulmonary alveolar microlithiasis in elderly patients with unexplained dyspnea and diffuse pulmonary calcification.
  • Genetic factors, specifically SLC34A2 mutations, play a crucial role in the development of this rare disorder.
  • Histopathological confirmation remains essential for diagnosing pulmonary alveolar microlithiasis.