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JC WCS > Respiratory JC015: Shortness Of Breath In A Construction Site Worker: Occupational Lung Diseases, Pulmonary Fibrosis, Workman's Compensation > Flashcards

Respiratory JC015: Shortness Of Breath In A Construction Site Worker: Occupational Lung Diseases, Pulmonary Fibrosis, Workman's Compensation Flashcards

1
Q

Interstitial lung diseases

A
  • Aka Pulmonary fibrosis
  • Heterogeneous —> Different pathological processes —> Different treatment

Types:
1. Inhaled substances
- Inorganic: **Silicosis, **Asbestosis
- Organic: ***Hypersensitivity pneumonitis

  1. ***Drug-induced
    - Antibiotics
    - Chemotherapy
    - Immune-checkpoint inhibitor
    - Antiarrhythmic
    - Statins
  2. Connect tissue disease
    - ***Systemic sclerosis
    - RA
  3. Infection
    - Atypical pneumonia
    - Pneumocystis pneumonia
    - TB
    - Chlamydia
    - RSV
  4. Idiopathic
    - ***Idiopathic pulmonary fibrosis
    - Sarcoidosis
  5. Malignancy
    - Lymphangitis carcinomatosis
  6. Radiation
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2
Q

Pulmonary Interstitium

A

Microscopic space between Alveolar epithelium (gas exchange unit) and Capillary endothelium (vascular compartment)
—> Crucial for gas exchange

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3
Q

***Pathophysiology of ILD / Pulmonary fibrosis

A

Key site of injury and pathogenesis:
- ***Alveolar-capillary interface

Pathophysiology:
Formation of lung fibrosis (Scarring of lung tissue)
—> **Thickening of interstitium
—> Loss of thin elastin-rich connective component containing capillary blood vessels
—> **Blockade of effective gas exchange across alveolus
—> Worsening dyspnea

  • Acute and Chronic diseases processes
  • Many differently causes / patterns

Early stage:
- ***Alveolitis (injury with inflammatory cell infiltration)

Late stage:
- ***Fibrosis (uncontrolled persistent inflammation)

Effect:
1. ↑ in Interstitial tissue (in response to external stimulus) —> **↓ Lung compliance (less distensible) —> Restrictive deficit
2. **Hypoxia
3. **Pulmonary hypertension
4. **Cor pulmonale
5. HF

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4
Q

Chronic Interstitial Lung Diseases

A
  1. IPF / UIP
  2. Sarcoidosis
  3. Hypersensitivity pneumonitis
  4. Pneumoconiosis
  5. CT diseases
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5
Q

Idiopathic Pulmonary Fibrosis (IPF) / Usual Interstitial Pneumonia (UIP)

A

Definition:
- Progressive interstitial fibrosis of ***unknown cause

  • Variable association with inflammation
  • Clubbing
  • Chronic
  • ***Progressive decline in lung function (e.g. FVC)
  • Ultimately fatal

Usual Interstitial Pneumonia pattern (UIP)
- a form of IPF
- NOT equate to diagnosis of IPF

Diagnosis:
IPF is diagnosed only if known causes of ILD are ***excluded
—> Environmental exposure: Asbestosis
—> CT disease
—> Drug toxicity
—> Chronic hypersensitivity pneumonitis

Pathology:
- Local **persistent inflammation —> Fibrosis at **Subpleural + **Basal segments (Location of terminal bronchiole, alveoli)
- Terminal lung structures replaced by dilated spaces surrounded by fibrous walls —> **↓ Compliance + ***↓ DLCO

Epidemiology:
- Presentation at ***advanced age
- No gender difference

Risk factors:
- **Smoking
- **Environmental pollutants (e.g. exposure to metal / wood dusts, hairdressing, raising birds
- Undiagnosed GERD (repeated micro-injury)
- Familial pulmonary fibrosis (<5%)

Prognosis:
- Poor

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6
Q

Diffuse Parenchymal Lung Diseases (DPLD)

A

Same as Interstitial Lung Disease
***DPLD = ILD

Broad term, classified according to etiology:

  1. DPLD of known etiology (HP, drugs, collagen-vascular)
  2. **Idiopathic Interstitial Pneumonia (IIP)
    - Chronic fibrosing —> **    IPF, ***NSIP
    - Smoking related —> RBILD, DIP
    - Acute / Subacute —> AIP, COP
    (Very rare IIPs: LIP, PPFE)
  3. Granulomatous DPLDs (Sarcoidosis)
  4. Other forms of DPLD (Eosinophilic pneumonia, LAM, HX etc.)
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7
Q

Terminology

A

IPF: Idiopathic pulmonary fibrosis
NSIP: Nonspecific interstitial pneumonia

RBILD: Respiratory bronchiolitis–associated interstitial lung disease
DIP: Desquamative interstitial pneumonia

AIP: Acute interstitial pneumonia
COP: Cryptogenic organizing pneumonia (previous known as Bronchiolitis obliterans with organizing pneumonia (BOOP) (SpC Medicine))

LIP: Idiopathic lymphocytic interstitial pneumonia
PPFE: Idiopathic pleuroparenchymal fibroelastosis

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8
Q

Examples of drugs that can cause ILD / Pulmonary fibrosis

A

Anti-cancer drugs
- ***Bleomycin
- Immune-checkpoint inhibitors (i.e. Immunotherapy)

Cardiac drugs
- ***Amiodarone

Antibiotics
- Cephalosporin
- **Sulfasalazine
- **Nitrofurantoin

***Illicit drugs (esp. inhalational drugs)
- Cocaine
- Heroin

Miscellaneous:
- **High flow oxygen
- **Inhalation / Aspiration of fat-containing substances (e.g. drugs containing mineral oils, certain laxatives, petroleum jelly)
- ***Radiotherapy

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9
Q

***Clinical features of ILD

A
  1. ***Dyspnea exacerbated by exertion
  2. ***Cough: dry, non-productive + persistent
  3. Fatigue (∵ poor gas exchange)
  4. ***Tachypnea (often laboured)
  5. Loss of appetite + Weight loss
  6. Chest pain
  7. Fever
  8. ***Central cyanosis
  9. ***Cor pulmonale
  10. Respiratory insufficiency + failure

S/S:
- >50 yo
- Dry, non-productive cough on exertion
- Progressive exertional dyspnea (SOB with exercise)
- Dry, inspiratory bibasilar “Velcro-like” crackles (i.e. **Fine crackles) —> **not change with coughing (vs Bronchiectasis / Pneumonia)
- **Clubbing
- Abnormal lung function test —> **Restriction pattern (FEV1/FVC >80%) + ***Impaired gas exchange (↓ DLCO)

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10
Q

***Initial assessment of patients with Suspected ILD

A
  1. History:
    - Medical / Drug
    - **CT disease symptoms
    - **    Environmental / Occupational exposure
    - Smoking
    - Family
    - Gastric reflux
  2. Examination:
    - ***Clubbing
    - Fever
    - Eye signs
    - Rashes
    - Arthritis
    - Hepatosplenomegaly
    - Crackles
  3. Investigations (Tailored towards S/S):
    - **CXR
    - Oximetry
    - **    Spirometry
    - **Blood tests: **Arterial blood gas, **AutoAb (to rule out CT disease)
    - Urinalysis
    - **    ECG
  4. Refer to chest physician
  5. Further assessment:
    - **High resolution CT chest (HRCT: best mode of investigation to diagnose ILD)
    - Bronchoscopy +/- Lavage
    - **    Transbronchial biopsy (only if history / imaging not conclusive of diagnosis / malignancy cannot be ruled out)
    - Surgical lung biopsy
    - Detailed pulmonary function test
    - ECG
  6. Discussion at multidisciplinary meeting, review management plan
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11
Q

Diagnosis of UIP and IPF

A
  1. ***Exclusion of known / environmental / occupational causes (can be difficult)
  2. ***Exclusion of collagen vascular diseases (can be difficult)
  3. HRCT scan techniques
  4. Local expertise in ILD
  5. Multidisciplinary discussion
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12
Q

UIP pattern vs NSIP pattern

A

Based on HRCT

UIP:
1. Subpleural, Basal predominance
2. **Reticular abnormality (Network)
3. **Honeycombing +/- Traction bronchiectasis
4. Absence of features consider to be inconsistent with UIP pattern

NSIP:
1. More **ground glass opacity (Hazy patches)
2. Reticulation usually comes with a **Peribronchovascular distribution
3. Less Honeycomb changes and Traction bronchiectasis

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13
Q

***Management of ILD

A

Medical treatment:
1. Occupational exposure
- avoid that environment

  1. Drug cause
    - discontinue drug
  2. Some idiopathic / CT-based causes (associated with **systemic sclerosis)
    - may be treated with **    Nintedanib (newer targeted kinase)
  3. **Systemic glucocorticoid
    - no longer recommended as 1st line (esp. in IPF with UIP patttern)
    - used in **    acute exacerbation
  4. ***Immunosuppressant
    - some patients may respond
  5. ***Supplemental O2
    - patients with hypoxaemia (in form of ambulatory O2 / LTOT therapy)
  6. **Sildenafil
    - in advanced IPF
    - vasodilator to relieve effects of **    pulmonary hypertension
    - 10mg QDS

Surgical treatment:
1. ***Lung transplantation
- most effective
- but severe risks of its own

Supportive care:
1. Supplemental O2
2. Patient education
3. Pulmonary rehabilitation
4. Vaccination (Influenza + ***Pneumococcal polysaccharide vaccine)
5. Palliative

Monitoring:
1. Regular follow-up ***lung function tests (FVC, TLC, DLCO, Kco)
—> information on disease progression

  1. ***Flexible bronchoscopy +/- BAL +/- Transbronchial biopsy (TBBx) (not necessarily needed)
    —> exclude infection / malignancy
  2. Thoracoscopic VATS biopsy (Video-assisted thoracoscopic surgery)
    - more invasive but more reliable
    - generates far more tissue
  3. ***6-minute Walk Test (6MWT)
    - functional assessment of exercise tolerance
    - assess how long patient can walk
  4. Breathlessness score
    - grade + assess symptoms
  5. Multi-disciplinary approach
    - physiotherapist
    - pulmonary rehab
    - occupational therapist
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14
Q

Spirometry

A

Suggestive but NOT diagnostic of restrictive lung physiology

Restrictive pattern:
- ***Narrowing of Flow-volume loop

Obstructive pattern:
- Shortening of Flow-volume loop

Diagnosis also depends on Measurement of lung volume
—> ***↓ in ALL volumes
—> ↓ VC, RV, FRC, TV, TLC (in different extent)

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15
Q

Nintedanib

A
  • Inhibitor of VEGF and Multiple angiokinase
  • Small molecule like Pirfenidone
  • VEGFR, FGFR, PDGFR inhibitor
  • Developed as anti-vascular anti-cancer therapy
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16
Q

Hypersensitivity Pneumonitis (Extrinsic Allergic Alveolitis)

A

?A form of IPF (Mentioned in lecture but not sure)

Chronic inflammatory disease
- Small airways
- Interstitial involvement
- Occasional granuloma

**Allergic origins
- Reaction to Organic dust / Inorganic dust
- **Type 3 / Type 4 hypersensitivity

Example:
- **Farmer’s lung: Thermophilic bacteria
- **Bird / Pigeon Fancier’s lung: Avian proteins
- ***Malt Worker’s lung: Fungi (Beer brewery)

Investigations:
- Precipitins (Ab that can precipitate when bind to Ag) / ***Ab often detectable in serum samples
- Unusual cases come to biopsy
- CT: Small airway sepsis-like changes

17
Q

Pneumoconiosis

A

Lung disease caused by **mineral dust exposure
1. **Asbestosis
2. ***Silicosis
3. Coal worker’s lung

Disease severity depends on:
1. Particle size
2. Reactivity of particles
3. Clearance of particles
4. Host response
5. Duration of exposure

Asbestos:
- a Silicate
- Serpentine (curved) fibres: relatively safe
- ***Amphibole (straight) fibres: highly dangerous to man (more immunogenic)

18
Q

Detrimental effects of inhaling dusts

A
  1. COPD
  2. Asthma
  3. ***Extrinsic Allergic Alveolitis (EAA) / Hypersensitivity Pneumonitis
  4. Fibrosing Alveolitis
  5. ***Pneumoconiosis
  6. ***Cancer
  7. Heart disease: Cardiorespiratory failure
  8. Other problems
19
Q

***Silicosis (矽肺病)

A

Occupational lung disease

Etiology:
- Inhalation of ***crystalline silica dust

Pathology:
- Inflammation + Scarring in form of **Nodular lesions in **upper lobes of lungs —> Pulling of structures upwards
- ***Hilar lymphadenopathy (“eggshell” calcification) —> widening of mediastinum

Occupational risk factors
- Stone mining + cutting
- Pneumatic drill worker
- Caisson worker
- Jade polisher, Gemstone cutter
- Ceramic workers
- Manual labourer in construction sites

Clinical features:
1. Dyspnea exacerbated by exertion
2. Cough: dry + persistent
3. Fatigue (∵ poor gas exchange)
4. Tachypnea (often laboured)
5. Loss of appetite + Weight loss
6. Chest pain

S/S:
- >50 yo
- Dry, non-productive cough on exertion
- Progressive exertional dyspnea (SOB with exercise)
- Dry, inspiratory bibasilar “Velcro-like” crackles (i.e. ***Fine crackles) —> not change with coughing
- Clubbing
- Abnormal lung function test —> Restrictive pattern + Impaired gas exchange

20
Q

Occupational risk factors: Asbestosis and Malignant pleural mesothelioma

A

Handling of ***asbestos products (石綿) (incorporated into construction work, commercial / household products)

Construction works:
- Demolition of fireproof coatings / bricks / pipes
—> shipyard workers, seamens

Commercial / Household:
- Demolition work
- Insulation wall layers with broken asbestos brick in floorings / roofings

21
Q

***Asbestosis (石綿肺)

A
  • ***Diffuse interstitial fibrosis
  • Develops after prolonged / heavy exposure

Pathogenesis:
Chronic inflammation
—> Fibroblasts proliferate in interstitium
—> Fibrosis
—> **Bronchiolar epithelium extend to line airspaces + Collapsed / **Amputated distal airway
—> Obstruction of usual gas exchange

End stage:
- Acini “simplified” —> Cystic space
- Bronchiolar epithelium grow into cystic space
- Honeycomb lung

Pathological features:
1. Interstitial fibrosis
2. **Obliteration of some air spaces
3. **Cystic dilatation of others (non-functional)
4. Chronic inflammatory cells (not always present)
5. **Asbestosis bodies
6. Abnormal pleural shadows on CXR
- **not conforming to any pulmonary Parenchymal anatomy
- **Pleural thickening (calcified)
- **Asbesto / Pleural plaque

22
Q

Management of Silicosis and Asbestosis

A
  • ***Irreversible with no cure
  • Treatment on alleviating symptoms + preventing complications
  • Silica and Asbestos: WHO Type 1 carcinogens
  1. Stop further exposure
    - Silica
    - Lung irritants (including tobacco smoking)
  2. Cough suppressant
  3. Antibiotics (if lung infection)
  4. TB prophylaxis (if positive tuberculin skin test / IGRA)
  5. Prolonged anti-TB drugs (Multi-drug regimen) (for active TB)
  6. **Monitor for malignancy
    - **    Mesothelioma: primary malignant neoplasm of mesothelial tissue (cancer derived from lining (mesothelium) of pleura, pericardium, peritonium) due to dust of Asbestos
23
Q

Occupation safety clinic

A

Evaluation of compensation

Must be HK resident

Once diagnosed with **Pneumoconiosis, **Mesothelioma
Referred to Pneumoconiosis Medical Board (Shau Kei Wan Chest Clinic)
—> Evaluate degree of lung function impairment
—> Stratified by ***FVC measurement

24
Q

From CPRS L67

A

Pathological features of IPF:
1. Interstitial fibrosis (stained pink)
- ↓ compliance —> stiff, rigid lung
- reduced capillaries —> ↓ gas exchange —> impaired perfusion
- alveolar fibrosis —> ↓SA + ↓ diffusion capacity —> VQ mismatch

  1. Obliteration and cystic dilation of air space

Gross appearance (restrictive pattern):
1. Rigid shrunken lung (sense/fibrosis)
2. Thickened alveolar wall (***pinhole alveolar space)
3. Honeycomb lung (End stage changes)

S/S:
1. Dry cough
2. SOB but no wheeze
3. Chronic hypoxia —> cyanosis
4. Coarse lines and nodules on CXR
5. Risk of lung cancer

Effects of chronic hypoxia
1. Pulmonary vasoconstriction
- Early: reversible
- Late: irreversible structural change: increased fibroblast and smooth muscle cell —> thickening of tunica media and intima
2. Polycythaemia: increased blood viscosity
3. Pulmonary hypertension (type 3)
4. Right ventricular hypertrophy / dilatation (systemic venous congestion)
5. Cor pulmonale

JC WCS (134 decks)

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