Occupational diseases 1

Define pneumoconiosis Any [blank_start]chronic[blank_end] pulmonary diseases with [blank_start]non-organic depositions[blank_end]

The 2 types of pneumoconiosis include: [blank_start]Collagenous pneumoconiosis[blank_end] [blank_start]Non-collagenous pneumoconiosis[blank_end]

Examples of collagenous pneumoconioisis are: [blank_start]Silicosis[blank_end] [blank_start]Asbestosis[blank_end] [blank_start]Anthracosis[blank_end]

Examples of non-collagenous pneumoconiosis are: [blank_start]Siderosis[blank_end] [blank_start]Baritosis[blank_end] [blank_start]Stenosis[blank_end]

Stages of pathogenesis of pneumoconiosis: Dust particles are [blank_start]trapped in alveolar ducts[blank_end] [blank_start]Macrophages[blank_end] engulf them [blank_start]Inflammation[blank_end] and [blank_start]IL-1 production[blank_end] occurs [blank_start]Pneumoconiosis[blank_end] occurs More [blank_start]reactive[blank_end] particles cause [blank_start]fibroblast[blank_end] stimulation

Define silicosis A type of [blank_start]pneumoconiosis[blank_end] that occurs with people handling [blank_start]silica[blank_end]

State the symptoms for each form of silicosis: Mild: [blank_start]asymptomatic[blank_end] Moderate: [blank_start]wheezing[blank_end], [blank_start]SOB[blank_end], [blank_start]chronic coughing[blank_end] Severe: [blank_start]peripheral cyanosis[blank_end], [blank_start]swollen legs[blank_end]

What are the forms of diagnosis for silicosis? [blank_start]X-ray[blank_end] [blank_start]CT scan[blank_end] [blank_start]Lung tissue sample[blank_end]

Examples of differential diagnosis for silicosis: Diffuse [blank_start]pulmonary fibrosis[blank_end] Disseminated [blank_start]pulmonary infections[blank_end] Disseminated [blank_start]pulmonary neoplasm[blank_end] Systemic [blank_start]autoimmune diseases[blank_end]

State the treatment for silicosis: Avoid [blank_start]exposure[blank_end] Sprays = [blank_start]corticosteroids[blank_end], [blank_start]bronchodilators[blank_end] Extreme cases = [blank_start]lung transplant[blank_end]

Silicosis can be prevented by: Wearing a [blank_start]mask[blank_end]

Asbestosis is a [blank_start]progressive[blank_end], [blank_start]irreversible[blank_end] silicosis caused by inhaling [blank_start]asbestos fibres[blank_end] (hydrogenated [blank_start]magnesium silicate[blank_end]).

Sources of asbestosis are: [blank_start]Pipes[blank_end], [blank_start]boilers[blank_end], [blank_start]furnaces[blank_end] [blank_start]Textiles[blank_end] and [blank_start]paper[blank_end] products [blank_start]Battery[blank_end] boxes

Pathogenesis of asbestosis: Asbestos fibres are [blank_start]inhaled[blank_end] They are deposited at the [blank_start]duct bifurcation[blank_end] This causes [blank_start]alveolar macrophage alveolitis[blank_end] These activated macrophages release [blank_start]cytokines[blank_end] This initiates [blank_start]fibrosis[blank_end] (usually in the [blank_start]lower lobes[blank_end]) Pre-bronchial fibrosis with [blank_start]cellular infiltrate[blank_end] may [blank_start]narrow[blank_end] the airway and cause [blank_start]reduced[blank_end] air flow

Clinical manifestation of asbestosis: Initial symptoms: [blank_start]fatigue[blank_end], [blank_start]chest pain[blank_end], [blank_start]exertional dyspnoea[blank_end] Later symptoms: [blank_start]cough[blank_end], [blank_start]sputum[blank_end] with different quantity and quality, [blank_start]haemoptysis[blank_end], [blank_start]permanent dyspnoea[blank_end] On auscultation: [blank_start]inspiratory crackles[blank_end] Radiography: - [blank_start]S2[blank_end] or [blank_start]T2[blank_end] irregular opacities in the [blank_start]middle[blank_end] and [blank_start]low[blank_end] lung zones [blank_start]bilaterally[blank_end] [blank_start]- Honeycomb[blank_end] structures = signs of [blank_start]bronchiectasis[blank_end] in [blank_start]basal[blank_end] lung area X-ray = [blank_start]pleural thickening[blank_end] (fibrosis, hyalinosis, calcinosis)

Diagnosis of asbestosis: [blank_start]Work environmental[blank_end] history (dust exposure) [blank_start]Chest x-ray[blank_end] (irregular and subpleural opacities) [blank_start]Transbronchial lung[blank_end] autopsy [blank_start]Bronchoalveolar[blank_end] lavage fluid investigation [blank_start]Spirometry[blank_end] [blank_start]ABG analysis[blank_end]

Differential diagnosis of asbestosis, talcosis and kaolinosis: Disseminated [blank_start]pulmonary infections[blank_end] Disseminated [blank_start]pulmonary neoplasm[blank_end] Systemic [blank_start]autoimmune diseases[blank_end]

Treatment for asbestosis, talcosis, kaolinosis includes: [blank_start]Antioxidants[blank_end] [blank_start]Anti-inflammatory[blank_end] drugs [blank_start]Gene therapy[blank_end]

Prevention of asbestosis, talcosis and kaolinosis includes: [blank_start]Decrease[blank_end] dust concentration in [blank_start]work environment[blank_end] [blank_start]Masks[blank_end] [blank_start]Early detection[blank_end] and [blank_start]preventative treatment[blank_end]

Talcosis is the inhalation of [blank_start]talc[blank_end] (hydrogenated [blank_start]magensium silicate[blank_end]) and [blank_start]silicates[blank_end]. This includes [blank_start]iron[blank_end], [blank_start]calcium[blank_end] and [blank_start]quartz[blank_end]. Its sources are: [blank_start]paints[blank_end], [blank_start]cosmetics[blank_end] and [blank_start]pharmaceuticals[blank_end]

Pathogenesis of talcosis is the same as asbestosis but leads to [blank_start]mild diffuse pulmonary fibrosis[blank_end] and [blank_start]granulomatosis[blank_end].

Clinical manifestations of talcosis are: [blank_start]Slow[blank_end] progressing [blank_start]dyspnoea[blank_end] [blank_start]Cough[blank_end] and [blank_start]sputum[blank_end] similar to asbestos On auscultation: [blank_start]crackles[blank_end] in [blank_start]lower[blank_end] lung areas On chest x-ray: [blank_start]mild diffuse pulmonary fibrosis[blank_end] with [blank_start]irregular[blank_end] opacities [blank_start]Lung functional impairments[blank_end] appear later

Kaolinosis is a [blank_start]silicosis[blank_end] caused by inhalation of [blank_start]kaolin[blank_end]. Kaolin is a [blank_start]hydrogenated aluminium silicate[blank_end] e.g. quartz. Its sources include: [blank_start]firebrick[blank_end] production, [blank_start]paper[blank_end] and [blank_start]plastic[blank_end] production

Clinical manifestations of kaolinosis: Early stage: no [blank_start]significant[blank_end] pulmonary symptoms (develop slowly and later) On chest x-ray: [blank_start]small round opacities[blank_end]

Coal worker's pneumoconiosis is caused by [blank_start]long-term exposure[blank_end] to [blank_start]coal[blank_end] dust and [blank_start]long-term smokers[blank_end].

Pathogenesis of coal worker's pneumoconiosis includes: [blank_start]Coal dust[blank_end] enters the lungs and reaches the [blank_start]terminal bronchioles[blank_end] The dust is engulfed by [blank_start]macrophages[blank_end] and accumulates in the [blank_start]alveoli[blank_end] An [blank_start]immune response[blank_end] is activated [blank_start]Fibroblast[blank_end] growth factors and [blank_start]cytokines[blank_end] are released This causes [blank_start]interstitial fibrosis[blank_end] - leading to [blank_start]emphysema[blank_end] and [blank_start]ischaemic necrosis[blank_end]

Clinical manifestations are: [blank_start]cough[blank_end], [blank_start]sputum[blank_end] and [blank_start]dyspnoea[blank_end] Severe lung impairment leads to [blank_start]cor pulmonale[blank_end], [blank_start]hepatomegaly[blank_end] X-ray: [blank_start]small round nodules[blank_end] in early infection, nodules form [blank_start]large opacities[blank_end] in later infection Differential diagnosis: [blank_start]asbestosis[blank_end], [blank_start]silicosis[blank_end]