Resp Pathology Flashcards
What happens to lung volumes/physiology during obstructive diseases?
Airway disease with increased resistance to airflow due to partial or complete obstruction meaning air is released slower so gas is trapped
-increased size
-increased RV
increased lung capacity
-decreased FEV1 and FVC and FEV1/FVC
What happens to lung volumes/physiology during restrictive diseases?
parenchymal (tissue) disease resulting in reduced expansion of lung parenchyma, loss of gas exchange surface area, increased thickness of membrane and decreased lung capacity
Lug is stiffer and less compliant
- decreades size, RV, TLC, FVC
-increased FEV1 and FEV1/FVC
Define wheeze, stridor and stertor and when they occur?
Wheeze - polyphonic high pitch sound on expiration (asthma)
Stridor - single high pitch sound on inspiration
Stertor - single low pitch sound usually at back of throat (snoring)
Outline the 5 obstructive lung diseases, where, what, causes and clinical features of each?
- Bronchitis - bronchus, mucosal gland hypertrophy, smoking/air pollution, cough/sputum
- Asthma - bronchus, sm. hypertrophy/mucus, immunologic/triggers, cough/wheeze/SOB
- Emphysema - acinus/alveoli, air space enlargement/wall destruction, smoking, dyspnoea,
- Bronchiectasis - bronchus, airway dilatation/scarring, infection, cough/sputum/fever
- Small airway disease - bronchiole, inflammation/scarring/obliteration, smoke/pollution, cough/dyspnoea
What are the 4 types of asthma?
- Atopic - IgE mediated hypersensitivity reaction in children associated with allergic rhinitis and eczema triggered by allergens
- Drug induced - asprin or others
- Occupational - fumes, organic chemicals or dust, gases
- Non-atopic asthma - only intrinsic type that is triggered by resp infections, pollutnts, exercise, cold with no family history
Pathogenesis of asthma?
- Early phase - bronchoconstriction triggered by histamine, prostaglandins, leukotrienes, mucus
- Late phase - inflammaotry mediators stimulate epithelial cells to produce chemokines, recruit Th2 and eosinophils
- Th2 produce IL5 (eosinophils), IL13 (mucus production), IL4 (IgE causing mast cells to degranulate
- Airway remodelling - due to repeated bouts of asthma causing sm. hypertrophy, mucus gland hypertrophy and increased collagen.
Histological aspects of asthma?
mucus plugging bronchi, focal necrosis of epithelium with eosinophilic infiltration and oedema of walls, thickening of basal membrane, hypertrophy of sm and mucus glands
What is emphysema and outline pathogenesis and 2 main causes?
abnormal and permanent enlargement of airspaces distal to terminal bronchus. air trapped and loss of recoil due to damage of lung parenchyma and damage to walls without interstitial fibrosis.
Pathogenesis - development of alveolar wall destruction due to repeated damage to acini, chronic inflammation, imbalance of protease/antiprotease activity (a1 antitrypsin found in bronchial mucus to protect against proteases which destroy lung wall
1. Smoking/air pollution - induces accumulation of neutrophils and macrophages and inhibits a1 antitrypsin resulting in inflammation and damaging protease activity
2. a1 antitrypsin deficiency - genetically predisposed. Cirrhosis is liver as a1 antitrypsin is produced in liver but cannot be transported out
Clinical features of emphysema and complications?
Clinical - progressive dyspnea with symptoms developing after 1/3 lung tissue affected. Barrel chest with decreased exercise tolerance. Chest is hyper resonant and wheezing/coughing is bronchitis associated
Complications - resp failure with acidosis as cannot compensate by blowing off CO2, Right sided heart damage as damage to lungs, pneumothorax
Macro and micro of emphysema?
Macro - pale spongy hyperinflated lungs, may have emphysematous bullae (blisters) which can rupture causing pneumothorax, anthracosis
Micro - damage to alveolar walls, large alveolar spaces, only see end damage
What are the 4 types of pathological emphysema
- Centracinar - centrilobar, proximal acinar sparing distal acinar. Loss of resp bronchioles (smokers)
- Panacinar - all lung fields, especially bases with loss of acinus from resp bronchioles to alveolar (a1 antitrypsin deficiency)
- Distal acinar - least common affecting distal acinus, often forming bullae
- Irregular - associated with scarring, clinically significant
What are the three features of a clinical diagnosis of chronic bronchitis?
- productive cough with sputum on most days for 3 months of the year for 2 years
- presence of airflow obstruction (wheeze, SOB)
- approx 75 mL sputum per day
How is cough, SOB and infection rate different in emphysema and bronchitis?
Emphysema - SOB develops early, cough develops late in disease and less infectious
Bronchitis - productive cough early, SOB develops late in disease with frequent infections
Cause of bronchitis?
chronic irritation leading to hypersecretion of mucus (without eosinophils) in large airways and inflammation (lymphocytes, plasma cells, neutrophils) of bronchus with infectious episodes of pneumonia. Squamous metaplasia, secondary fibrosis, systemic manifestations
What is bronchiectasis and major causes of it?
Permanent and abnormal dilatation of bronchus/bronchioles due to obstruction or infection. Leads to increased infection as mucociliary elevator cannot clear mucus, so bacterial proliferation. Persistent cough with foul smelling sputum usually on waking. Caused by tumour, foreign body, infection or congenital (CF, Kartagenes syndrome)
Obstruction - dustal collapse - inflammation and increased secretion - bronchodilated leading to necrosis of lung - scar tissue - contraction of airway - dilated
What is ALI? and outline the pathology?
reduced lung expansion with abrupt onset of significant hypoxemia and diffuse pulmonary infiltrates in absence of cardiac failure
Pathology - diffuse alveolar damage with hyaline membranes, haemorrhagic and heavy lungs, reactive proliferation of type 2 pneumocytes
What is chronic interstitial lung disease, common features and 4 main catagories?
Group of disorders with inflammation and fibrosis of the pulmonary connective tissue, mainly the interstitium between alveolar walls. Common features include reduced compliance, reduced diffusion capacity due to expansion, reduced lung volumes
Main categories
1. Fibrosing - usual interstitial pneumonia, pneumoconiosis, autoimmune
2. Granulomatous - sarcoid, hypersensitivity pneumonitis
3. Smoking related
3. Eosinophilic
What type of ILD is usual interstitial pneumonia?
Fibrosing ILD with unknown cause. Areas of recent and old scarring with subplueral, fibroblastic foci with patchy interstitial fibrosis and inflammation leading to honeycomb lung.
What type of IDL is hypersensitivity pneumonitis and what is it?
Granulomatous IDL.
developed through inhalation ofantigen with malfunction of Treg cells forming immune complexes early and type IV hypersensitivity leading to inflammation and fibrosis
aka - farmers lung, bird fanciers lung, hot tub lung, aircon lung, byssinosis (textile workers)
Influenza-like syndrome a few hours after exposure with repeated episodes leading to centriacinar emphysema. Can progress to respiratory failure with gas transfer impeded. Chronic leads to honeycomb lung due to peribronchiolar and subpleural inflammatory infiltrates with giant cells and fibrosis
