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CHEST X-RAY SEMINAR
By
Sailee Kamat Bambolkar
Karrishma Karampure
Mansi Karnik
Pneumoconiosis
It can be deïŹned as a permanent alteration of lung
structure due to the inhalation of mineral dust and
the tissue reactions of the lung to its presence.
Strictly speaking the term ‘pneumoconiosis
includes those occupational lung diseases which
are due to exposure to inorganic or mineral dust
that is retained in the lung parenchyma and
incites ïŹbrosis.’
Diseases due to
inorganic dust
Coal worker’s
pneumoconiosis
Silicosis
Asbestosis
Siderosis
Berylliosis
Diseases due to organic
dust
Bysinosis
Farmer’s lung
Malt worker’s lung
Mushroom worker’s
lung
Bagassosis
Aetiology
1.
2.
3.
The type of lung disease varies according to the nature of the
inhaled dust. Some dusts are inert and cause no reaction at all
while the others cause immunologic damage and predispose to
tuberculosis or neoplasia.
The tissue response to the inhaled dust may be one of the following
3 types;
Fibrous nodules e.g. in coal worker’s pneumoconiosis and silicosis
Interstitial ïŹbrosis e.g. Asbestosis
Hypersensitivity reaction e.g. Berylliosis.
Signs and symptoms
1.
2.
1.
2.
1.
2.
1.
2.
Simple Coal Worker’s Pneumoconiosis
Develops after prolonged exposure (15-20 years) to coal dust
Patients present with cough and dyspnoea.
Progressive Massive Fibrosis
This condition progresses even after the miner leaves the industry.
Clinically presence of cough with blackish expectoration and progressive
breathlessness.
Silicosis-Chronic or Simple Silicosis
Develops after many decades of exposure to relatively low levels of silica.
Upper lobes mostly involved, presence of gradually progressive dyspnoea dry
cough.
Acute Silicosis
Occurs after exposure to very high levels of dust over few months and fatal
within years.
Characterised by pulmonary oedema interstitial inïŹ‚ammation and
accumulation of proteinaceous surfactant like ïŹ‚uid within alveoli.
1.
2.
1.
Asbestosis
Moderate to severe exposure for at least 10 years.
Clinically presence of progressive exertion dyspnoea, ïŹnger
clubbing and end inspiratory crepitations over the lung bases
Berylliosis
Presence of cough, progressive breathlessness, night sweats and
anthralgia.
Diagnosis
X-ray
CT scan
HRCT
Pulmonary Function Tests
Lung Biopsy
Specialised testing of lymphocyte function
(a) INORGANIC
SILICOSIS
ASBESTOSIS
COAL WORKERS PNEUMOCONIOSIS
Simple coal workers pneumoconios
BERYLLIOSS
(b) ORGANIC
BAGASOSIS
THANKYOU

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CHEST X-RAY SEMINAR FINAL.pdf

  • 1. CHEST X-RAY SEMINAR By Sailee Kamat Bambolkar Karrishma Karampure Mansi Karnik
  • 2. Pneumoconiosis It can be deïŹned as a permanent alteration of lung structure due to the inhalation of mineral dust and the tissue reactions of the lung to its presence. Strictly speaking the term ‘pneumoconiosis includes those occupational lung diseases which are due to exposure to inorganic or mineral dust that is retained in the lung parenchyma and incites ïŹbrosis.’
  • 3. Diseases due to inorganic dust Coal worker’s pneumoconiosis Silicosis Asbestosis Siderosis Berylliosis Diseases due to organic dust Bysinosis Farmer’s lung Malt worker’s lung Mushroom worker’s lung Bagassosis Aetiology
  • 4.
  • 5. 1. 2. 3. The type of lung disease varies according to the nature of the inhaled dust. Some dusts are inert and cause no reaction at all while the others cause immunologic damage and predispose to tuberculosis or neoplasia. The tissue response to the inhaled dust may be one of the following 3 types; Fibrous nodules e.g. in coal worker’s pneumoconiosis and silicosis Interstitial ïŹbrosis e.g. Asbestosis Hypersensitivity reaction e.g. Berylliosis.
  • 6. Signs and symptoms 1. 2. 1. 2. 1. 2. 1. 2. Simple Coal Worker’s Pneumoconiosis Develops after prolonged exposure (15-20 years) to coal dust Patients present with cough and dyspnoea. Progressive Massive Fibrosis This condition progresses even after the miner leaves the industry. Clinically presence of cough with blackish expectoration and progressive breathlessness. Silicosis-Chronic or Simple Silicosis Develops after many decades of exposure to relatively low levels of silica. Upper lobes mostly involved, presence of gradually progressive dyspnoea dry cough. Acute Silicosis Occurs after exposure to very high levels of dust over few months and fatal within years. Characterised by pulmonary oedema interstitial inïŹ‚ammation and accumulation of proteinaceous surfactant like ïŹ‚uid within alveoli.
  • 7. 1. 2. 1. Asbestosis Moderate to severe exposure for at least 10 years. Clinically presence of progressive exertion dyspnoea, ïŹnger clubbing and end inspiratory crepitations over the lung bases Berylliosis Presence of cough, progressive breathlessness, night sweats and anthralgia.
  • 8. Diagnosis X-ray CT scan HRCT Pulmonary Function Tests Lung Biopsy Specialised testing of lymphocyte function
  • 10.
  • 13. Simple coal workers pneumoconios