Occupational lung disease, restrictive lung disease & ventilatory failure Flashcards
Describe the main conditions associated with asbestos inhalation
Mesothelioma:
- Caused by light exposure, with an interval of 20-40 years between exposure to disease onset
- There will be pleuritic pain, increasing dyspnoea and a unilateral pleural effusion on CXR
- Survival is poor, with median survival of 2 years from diagnosis
Asbestosis:
- Caused by heavy exposure, with an interval of 5-10 years from exposure to disease
- There will be progressive dyspnoea, with diffuse bilateral streaky strikes on CXR with honeycombing
- The outcome is poor and can progress after exposure ceases
There can also be asbestos-related carcinoma of the bronchus, with features above plus those of bronchial carcinoma
What is pneumoconiosis?
Pneumoconiosis is disease of the lungs caused by inhalation of dusts, generally used to refer to pathology caused by coal dust
Describe the pathology of simple and complicated pneumoconiosis
- The coal dust is toxic to macrophages (normal defence for inhaled dusts), thus there will be a local inflammatory response similar to that seen in COPD
- If this becomes chronic, there will be fibrosis leading to restructive lung disease
- Silicates are the main dusts causing industrial pulmonary fibrosis, often mixed with coal
Simple coalworker’s pneumoconiosis:
- Presence of small nodules (2-5mm) on CXR, not associated with any clinically significant impairment of respiratory function
- May develop progressive massive fibrosis
Progressive massive fibrosis:
- Presence of large nodules (>10mm) on CXR, and the disease progresses relentlessly leading to a mixed obstructive and restrictive pattern
- It may present long after active exposure to coal dust, and culminates in COPD (dyspnoea and cough productive sputum, sometimes black)
- This can progress to respiratory failure
Define restrictive lung disease
Causes?
Restrictive lung disease involves processes that reduce the patient’s total lung capacity, without loss of ability to inspire and expire adequately.
Causes:
- Recurrent exogenous injury and responsive endogenous stimuli lead to transformation, disruption and apoptosis of epithelial cells in the lung.
- Cytokines are released, stimulating angiogenesis and myofibroblast proliferation: leading to collagen construction and development of “fibrotic foci”.
Define obstructive lung disease
Obstructive deficits involve maintenance of normal total lung capacity, but a decline in ability to inspire and expire as easily
What are the main groups of disease leading to pulmonary fibrosis?
- Localised fibrosis may be caused by: (STABS)
- systemic sclerosis
- tuberculosis
- asbestosis
- berylliosis
- sarcoidosis
- Diffuse fibrosis may be caused by:
- Idiopathy pulmonary fibrosis
- Rheumatoid lung
- Tuberous sclerosis
- Neurofibromatosis
- Langerhans’ cell histiocytosis
How does is fibrosis classified?
How do they differ in presentation and on X-ray?
Localised or generalised fibrosis
- Localised fibrosis physical signs at the chest wall include:
- reduced chest wall movement on affected side
- mediastinal displacement towards the lesion
- dull to percussion
- bronchial breath sounds
- increased vocal resonance
- coarse crackles
- Generalised fibrosis will lead to:
- reduced global expansion
- increased vocal resonance
- fine crackles.
Localised fibrosis gives streaky shadowing on CXR, whereas generalised fibrosis gives a honeycomb lung picture.
How can you distinguish between type 1 and type 2 respiratory failure?
Type I Respiratory failure:
- PaO2 low (<8kPa)
- PaCO2 normal or low
It is typically caused by a ventilation/perfusion (V/Q) mismatch; the volume of air flowing in and out of the lungs is not matched with the flow of blood to the lungs
caused by diseases of the lung parenchyma
Type II Respiratory failure:
- PaO2 low (<8kPa)
- PaCO2 high (>6kPa)
Type 2 respiratory failure is caused by inadequate alveolar ventilation; both oxygen and carbon dioxide are affected
What are the implications of having a high arterial pCO2?
Clinical features?
Hypercapnia results in a respiratory acidosis. This may eventually lead to unconsciousness and death
Clinical features of hypercapnia are:
- Headache, tachycardia, bounding pulse, CO2 retention flap and papilloedema as well as feature of acidosis:
- Kussmal respiration: air hunger, giving deep and laboured breathing
- Cardiovascular dysfunction
- Potassium abnormalities: acidosis leads to potassium loss from cells, leading to hypokalaemia if renal function is good, or hyperkalaemia if impaired
- Cerebral dysfunction: confusion or coma
- Peripheral vasodilation & increased permeability: leadiing to oedema
Distinguish between acute and chronic type II respiratory failure and respiratory and metabolic causes of acidosis
Chronic type II respiratory failure is caused most commonly by COPD.
Acute causes include morphine overdose, airway collapse, foreign body, etc.
Chronic respiratory acidosis will exist alongside metabolic compensation, whereas acute respiratory acidosis will not – the metabolic compensation is not a fast process.
Respiratory acidosis is caused by a high pCO2, whereas metabolic acidosis is caused by a negative base excess
What are the causes of ventilatory failure?
(type 2 respiratory failure)
Occurs when alveolar ventilation is insufficient to excrete the volume of CO2 being produced by tissue metabolism
- Severe pulmonary disease:
- asthma
- COPD
- pulmonary fibrosis
- obstructive sleep apnea
- Reduced respiratory drive
- CNS pathology
- sedative drugs
- Thoracic wall disease
- rib fracture (pain)
- kyphoscoliosis
- flail chest
- Neuromuscular disease
- diaphragmatic paraylsis
- Myasthenia gravis
- Guillian-Barre
- cord lesions
- Poliomyelitis
What is the effect of chest wall and spinal deformity on respiratory function?
Deviation in the shape of the chest wall away from normal is going to have logical effects on respiratory function, through change/limitation in the ability of the chest to expand
