Respiratory Flashcards
Pathophysiology of asbestos and interstitial lung disease
Pleural plaques - fibrous thickening in pleura or diaphragm
Asbestos effusion - inflammation in pleura leading to leaky blood vessels and excess fluid in pericardial space
Asbestosis - fibrosis of lungs caused by asbestos dust
mesothelioma
Bronchial carcinoma
Aetiology of asbestos and interstitial lung disease
person inhales fibres - accumulate in lung tissue - immune (macrophage and neutrophil response) - fibrosis and scarring - thickening - pain and restricted breathing
Epidemiology of asbestos and interstitial lung disease
More common in cities and in those working in industry
Clinical presentation of asbestos and interstitial lung diseases
Pleural plaques: asymptomtic, mild effort and dysponea
Pleural effusion: Pleuratic pain, dysponea, dry cough, fever, malaise, hiccups, tachypnoea
Mesothelioma: pleuritic pain and dysponea
Asbestosis: progressive dysponea and finger clubbing
Bronchus carcinoma: progressive dysponea
Diagnostic tests and results: Asbestos and interstitial lung disease- CXR
Pleural plaques: thickening of the parietal pleura
thickening of the diaphragmatic pleura, calcification
pleural effusion: Opaque shadowing, gravity dependent
Mesothelioma: pleural effusion, usually unilateral
Asbestosis: diffuse bilateral streaky shadows, honey comb lung
Diagnostic tests and results: Asbestos and interstitial lung disease- CT scan
Asbestosis: can identify minor degrees of fibrosis not visible on Xray
Diagnostic tests and results: Asbestos and interstitial lung disease- Auscultation
Asbestosis: bilateral basal end-inspiratory crackles
Diagnostic tests and results: Asbestos and interstitial lung disease- Pulmonary function tests
restrictive pattern
reduced gas transfer in asbestosis
Asbestos and interstitial lung disease - Treatment
Life style modification:
- smoking cessation
- Vaccination
- oxygen therapy
Most people with asbestosis will not need medication:
- low dose morphine
- side effect constipation
No treatment for pleural plaques
- small/simple pleural effusions will resolve alone
- large/complicated (infected) ones can be drained
- Malignant recurrent pleural effusions can be solved by instilling a sclerosing agent such as tetracycline or talc - pleurodesis
Pathophysiology: Asthma
Chronic inflammation of the conducting zones of the airways = increased contractility of the smooth muscle. Leads to bronchoconstriction and wheezing breathing.
- bronchoconstriction
- airway remodelling
- mucus hypersecretion
Pathophysiology: asthma
What are the 3 classical characteristics of asthma
- Airflow limitation/bronchoconstriction
- Airway hyperresponsiveness/excess mucus production
- bronchial inflammation
Pathophysiology: asthma
What does the severity of asthma depend on?
Inflammation and remodelling
Pathophysiology of Asthma
What are the principles behind inflammation in asthma
Inflammation:
-increased mast cells in epithelium, smooth muscle and mucous glands
these release histamine, tryptase, prostaglandin D2 and leukotrienes, which cause immediate asthmatic reaction .
release cytokines, chemokines and growth factors which contribute to chronic aspects
- increased eosinophils in bronchial walls and secretions
Number and activation of eosinophils decreased by corticosteroids
-increased dendritic cells and lymphocytes in mucous membranes of airways and alveoli
affected by corticosteroids
Pathophysiology of Asthma
What are the principles behind remodelling in asthma
- Submucosa is stressed and damaged - increased susceptibility to respiratory viral infections and pollutants
- increase in number and activity of goblet cells
- repair collagens, proteoglycans and matrix proteins deposited under basement membrane - increases inflammation through these molecules via cell signalling
- hyperplasia of smooth muscle: contracts more easily and stays contracted for longer
- smooth muscle secretes cytokines, chemokines and growth factors which sustain chronic inflammation
- central and peripheral neural reflexes contribute to irritability
Aetiology of asthma
allergic (extrinsic) or Nonallergic (intrinsic)
- Environmental exposure to allergen (pollen, domestic pets)
- Occupational sensitisers (industrial, drugs, bleaches, dyes, metal salts, antibiotics, latex, increased risk in smokers)
- Atmospheric pollution (sulphur dioxide, ozone)
- Drugs (NSAIDs, beta blockers- parasympathetic innervation causes bronchoconstriction, adrenaline antagonises this in normal state via beta 2 receptors on smooth muscle- in asthmatic subjects inhibition of this effect by beta blockers may induce asthma attacks)
- Viral infections (rhinovirus, parainfluenza)
- Cold air (typically symptoms after exposure)
- Emotion
- Irritant dusts, vapour and fumes (perfume, cigarette smoke, solvents, dust, car exhaust fumes)
- Genetic factors (several genes have been found to be associated, including those coding for interleukins)
