Asbestosis
Table of content
Overview
Pathophysiology
Causes
Risk factors
Incidence
Complications
Assessment
Diagnostic test results
Imaging
Treatment
Medication
Procedures
Surgery
Nursing considerations
Monitoring
Associated Nursing procedures
Patient teaching
Discharge planning
,Asbestosis
2
, Overview
Lung disease characterised by diffuse interstitial pulmonary
fibrosis resulting from working or living in areas with prolonged
exposure to airborne asbestos particles
Possibly developing 15 to 20 years after regular exposure to
asbestos ceases
Severity dependent on length of exposure and amount of asbestos
inhaled
Development of pleural plaques and mesotheliomas of the pleura
and the peritoneum
Also known as asbestos pneumoconiosis
Pathophysiology
Asbestos is a mineral fibre that when inhaled travels down the
airway and penetrates respiratory bronchioles and alveolar walls.
Mucus production and goblet cell formation are stimulated to
protect the airway and aid in expectoration.
Fibres are engulfed by macrophages, which release inflammatory
mediators, leading to fibroblast proliferation.
Fibres become encased in a brown, iron-rich, protein-like sheath
called asbestosis bodies.
3
Table of content
Overview
Pathophysiology
Causes
Risk factors
Incidence
Complications
Assessment
Diagnostic test results
Imaging
Treatment
Medication
Procedures
Surgery
Nursing considerations
Monitoring
Associated Nursing procedures
Patient teaching
Discharge planning
,Asbestosis
2
, Overview
Lung disease characterised by diffuse interstitial pulmonary
fibrosis resulting from working or living in areas with prolonged
exposure to airborne asbestos particles
Possibly developing 15 to 20 years after regular exposure to
asbestos ceases
Severity dependent on length of exposure and amount of asbestos
inhaled
Development of pleural plaques and mesotheliomas of the pleura
and the peritoneum
Also known as asbestos pneumoconiosis
Pathophysiology
Asbestos is a mineral fibre that when inhaled travels down the
airway and penetrates respiratory bronchioles and alveolar walls.
Mucus production and goblet cell formation are stimulated to
protect the airway and aid in expectoration.
Fibres are engulfed by macrophages, which release inflammatory
mediators, leading to fibroblast proliferation.
Fibres become encased in a brown, iron-rich, protein-like sheath
called asbestosis bodies.
3