• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/16

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

16 Cards in this Set

  • Front
  • Back

Definition

Diffuse interstitial fibrosis of the lung as a consequence of exposure to asbestos fibres



Abnormalities include: plaques, pleural thickening, pleural effusions or rounded atelectasis

Epidemiology

Exposure common among workers in the shipyard, construction, and building maintenance industries



Typically seen in individuals who began working with asbestos prior to the 1980s and are now usually >50 years of age

Aetiology

Inhalation of asbestos fibres. Asbestos is a fibrous silicate, which exists as a naturally occurring mineral. Chrysotile is the primary asbestos mined



Airborne asbestos particles <10 microns can be inhaled

Pathophysiology

Fibres deposit at alveolar duct bifurcations and cause an alveolar macrophage alveolitis.



Release cytokines, such as tumour necrosis factor and interleukin-1beta and oxidant species, which initiate a process of fibrosis



Starts in lower lobes and may progress to extensive fibrosis and honeycombing



Clearance of asbestos fibres is through lymphatic drainage and the pleural cavities

Signs, symptoms and risk factors

Symptoms: dyspnoea, cough



Signs: crackles and maybe clubbing



Risk factors: occupational exposure and duration of occupational exposure



Investigations

CXR: lower zone fibrosis and pleural thickening


Spirometry: restrictive


HRCT: same as CXR but clearer



Lung biopsy: asbestos mineral fibres

DDx

Idiopathic pulmonary fibrosis, Connective tissue disease, auto-immune (sarcoidosis) and silicosis

Criteria

1. Structural changes on CXR



2. Occupational exposure



3. Exclusion of alternatives

Treatment

Smoking cessation


Supportive care (antibiotics and steroids on standby + bronchodilator if it helps


Pulmonary rehab and oxygen


Lung transplant (end stage respiratory failure


Managment

Monitoring with CXR and PFTs. Risk of lung cancer and mesothelioma


Smoking cessation

Prognosis

Varies depending on level of exposure and progression of fibrosis

IPRATROPIUM BROMIDE

Antimuscarinic bronchodilator - Cholinergic receptor angonist - Decreases cGMP > decreases calcium > smooth muscle relaxation

TIOTROPIUM BROMIDE

Antimuscarinic bronchodilator. Decreases cGMP > decreases calcium > smooth muscle relaxation but longer acting. Acts on M3 receptors

METACLOPROMIDE

Anti-emetic. Dopamine agonist. Inhibits gastric smooth muscle

OMEPRAZOLE

PPI acts on H+ K+ ATPASE. Blocks final step of acid production

RAMIPRIL

ACE inhibitor. Stops conversion of ATI to ATII. ATII increaes blood pressure via RAAS system by stimulating ADH, increases aldosterone and binds to smooth muscle by binding to smooth muscle