Chest Medicine (week 6) Flashcards
Name 3 chest pathologies that affect the airways?
COPD
Asthma
Bronchiectasis
Name 3 chest pathologies that affect the Interstitium/parenchyma?
Pulmonary fibrosis
Hypersensitive pneumonitis
(emphysema)
Name 3 chest pathologies that affect the pleura?
Pleural effusion
Pleural maliganancy
Pleural thickening
Name 3 chest pathologies that affect the vasculature?
PE
Pulmonary HTN
Name 4 chest pathologies that affect the lungs ventilation?
Sleep disordered breathing
Obesity hypoventilation
Neuromuscular disease
Thoracic cage abnormalities
What parameters are tested in spirometry?
FEV1 (forced expiratory volume in 1 SEC)
VC (vital capacity)
FVC (forced vital capacity - how much total air)
What is the significance of FEV1/VC ratio?
FEV1/VC ratio <70% = obstructive
FEV1/VC ratio normal = restrictive
What is the FEV1/VC ratio of obstructive disease? Give 3 examples of obstructive pathologies.
FEV1/VC ratio <70% = obstructive
COPD, Asthma, Bronchiectasis
What is the FEV1/VC ratio of restrictive disease? Give 4 examples of restrictive pathologies.
FEV1/VC ratio normal = restrictive Pulmonary Fibrosis Hypersensitivity pneumonitis Neuromuscular disorders Thoracic cage abnormalities
What are the 3 pulmonary function tests?
Spirometry, Lung Volumes (flow volume loop), Transfer Factor
What is the characteristic flow volume loop shape of large airway obstruction?
Hamburger shape
What is the characteristic flow volume loop shape of small airway obstruction?
(COPD) Church and steeple
What are the 2 main measurements of lung volumes?
TLC (total lung capacity)
RV (residual volume)
What patterns of lung volumes are seen in an obstructive pathology?
TLC increases with hyperventialtion
RV increases with gas trapping
What patterns of lung volumes are seen in an Restrictive pathology?
TLC falls (definition of restriction) RV falls but proportionally the same
What are the 2 parameters of transfer factor that we measure?
TLCO (transfer factor of CO)
KCO (coefficient of CO) - per unit volume
What is transfer factor a measurement of?
Functionality of the alveolar-capillary membrane
What factors affect the TLCO? Which conditions are these seen in?
- Ventilation Perfusion Mismatch - common in many lung diseases
- Reduction in the area of alveolar-capillary membrane - e.g. emphysema
- Increased thickness of alveolar-capillary membrane - e.g. pulmonary fibrosis
- Pulmonary Blood flow - e.g. pulmonary hypertension
- Haemoglobin concentration - e.g. anaemia leads to a decrease in TLCO
How do we use TLCO and KCO in unison?
KCO is a useful measurement to give information on functionality ‘per unit volume’ of lung
- I.e. 2 full functioning lungs TLCO = 100%, KCO = 100%.
But in someone with a pneumonectomy (1 lung)
- TLCO = 50% but KCO would be 100%.
What is the TLCO & KCO pattern for the obstructive pathologies (asthma and COPD)?
Asthma - TLCO = normal, KCO = normal
COPD - TLCO = decreased, KCO = decreased
What is the TLCO & KCO pattern for restrictive pathologies, both intrapulmonary (IPF) and extrapulmonary (obesity)?
Intrapulmonary (IPF) - TLCO = decreased, KCO = decreased
Extra-pulmonary (obesity) - TLCO = decreased, KCO = Increased (to keep up with demand)
What are the differentials of a diffusely abnormal CXR?
Cardiac failure/ pulmonary oedema Pneumonia/ ARDS Idiopathic pulmonary fibrosis (IIPs) Sarcoidosis Pneumoconiosis Hypersensitivity pneumonitis
What is the difference between HRCT and spiral/helical CT? When is it appropriate to use each?
HRCT
- Finely detailed pictures of parts of the lung e.g. 1mm slice every 10mm
- Good if suspect diffuse condition [fibrosis; HP; bronchiectasis]
Spiral or Helical
- Less detailed imaging but done in continuum therefore do not miss small nodules etc
What is pneumoconiosis?
Lung disease caused by mineral dust
What is the prevalence of occupational lung disease in terms of % of COPD, asthma, cancer and hypersensitivity pneumonitis?
Asthma - 15% of cases
COPD - 15% of cases
Cancer - 2% of cases
Hypersensitivity pneumonitis - 80% of cases
Name 3 types fibrogenic lung diseases?
Silicosis, Coal worker’s pneumoconiosis, Asbestosis
How does silicosis present? (CXR, biopsy and lung function)
Early CXR: Diffuse nodules (differentiate from TB, sarcoidosis & diffuse malignancy)
Late CXR: Solid mass in upper zone
Restrictive lung function
Biopsy: Dense fibrosis with birefringent particles
What is the characteristic biopsy findings of silicosis?
Biopsy: Dense fibrosis with birefringent particles
sparkly nodules - diagnostic
How does coal workers pneumoconiosis present? (CXR, biopsy and lung function)
Early CXR: Diffuse nodules (differentiate from TB, sarcoidosis & diffuse malignancy)
Late CXR: Solid mass in upper zone
Restrictive lung function
Biopsy: Dust accumulation around terminal bronchioles with fibrosis.
What are the different diseases you can get with asbestos exposure?
Heavy exposure: Lung Ca & asbestosis
Light exposure: pleural plaques, pleural fibrosis & mesothelioma.
(Heavy = lungs, Light = pleura)
What is the prognosis of pleural plaques, characteristic CXR appearance, and the associated clinical pattern?
Not associated with other asbestos conditions (good prognosis)
>10 yr latency, usually asymptomatic
CXR: holly leaf appearance
What is the prognosis of benign diffuse pleural thickening, characteristic CXR appearance, and associated clinical pattern??
Forms a small pleural effusion and leaves patient slightly breathless due to restriction.
Rarely progresses.
CXR: blunt costophrenic angles from effusion
What is asbestosis?
Basal diffuse interstitial fibrosis caused primarily by heavy asbestos exposure
How does asbestosis present clinically and on investigation?
Slow onset SOB with exercise Fine end-inspiratory crackles Restrictive abnormality on PFTs Patients may have clubbed fingers (like IPF) CXR = Basal reticular shadowing
What is the treatment and progression of asbestosis?
No treatment (symptom relief) Progresses slower than IPF
What is the latency and progression of malignant mesothelioma?
~ 25 year latency
Progression to death ~18 months
How will a patient with malignant mesothelioma present?
Breathless, chest pain, sweats, anorexia and w. loss.
CXRL bulky pleural masses, thickening, unilateral pleural effusion
CT: thick grey pleura (reduces size of chest wall (pain) & lung fields (breathless))
What is asthma?
Whats the clinical picture?
Chronic airway inflammation
(Reversible) airflow obstruction caused by airway hyper-responsiveness
Wheeze, cough, shortness of breath, tightness
Nocturnal, early mornings (diurnal variation)
Whats the difference between occupational asthma and work-aggravated asthma?
Occupational Asthma
- Asthma which is caused directly by exposures to some agents at work (or is substantially worsened) – always get worse with increased exposure
“Work-Aggrevated” Asthma
- Previous asthma and symptoms are increased because of exposures at work (eg exercise, dust, cold)
What are the 2 types of Occupational Asthma (OA)?
What is the difference between them?
- Sensitiser-induced OA
- ~90% of cases of OA (like an allergy - IgE)
- Latency period between 1st exposure to a “sensitiser” and immunologically-driven symptoms - Irritant-induced OA
- ~ Reactive airways dysfunction syndrome (RADS)
- Few hours after high concentration exposure to irritant gas, fume, vapours at work. Sometimes 1 exposure is enough.
What is the allergen work exposure limit?
4mg/m3
What are the key investigations in Occupational Asthma?
Total IgE level Skin prick tests Peak flow readings at work and home Airway responsiveness measurements Inhalational challenge test
What is the key feature in history pointing towards occupational asthma?
Symptoms better at weekend or on holiday
Others include:
Onset often within one year of new work
Latent interval of asymptomatic exposure
Worsening during the week
Worse with heavier exposures
Associated nasal/ eye symptoms (IgA sensitisation)
Other workers often affected
Associated with rhinoconjunctivitis and dermatitis
What is the most effective treatment for occupational asthma?
Redeployment to avoid asthmagen exposure
What is the most common agent causing occupational asthma in the UK?
Isocyanates from paint spraying or Wheat Flour (bakers asthma)
What are the key investigations in Occ Asthma?
- Serial PEF measurements (home and work)
- Allergy tests : skin prick/ serum IgE levels
- Challenge tests
• Methacholine challenge (strong bronchoconstrictor)
• Workplace visit/challenge test (take PEFR every hr for 3 days)
• Direct inhalational challenge test
%FeNO is sometimes used in the diagnosis of OA
• Fractional exhaled nitric oxide (NO)
• NO released by inflamed bronchial epithelial cells in asthma and is a surrogate marker for eosinophilic inflammation in the airways. - Sputum eosinophils in OA
• Eosinophilic airway inflammation is a hallmark of asthma.
• Suppressed in cigarette smokers (won’t work as a marker)
What is the Scoring system for occupational asthma? What score indicates Oc Asthma?
OASYS score (range 0-4) ≥2.4 - highly suggestive of Occ Asthma
What is the methacholine challenge test? What score are you looking for in Oc Asthma?
Methacholine (very strong bronchoconstrictor, non-selective muscarinic antagonist)
Take basic FEV1, then breath in increasing doses of methacholine (1.5µg – 3.2mg), repeating the lung function.
You look for a PD20 (the amount of methacholine that causes a 20% drop in FEV1)
Compare this score at work and on holiday
What are the 2 broad categories of Oc asthma causative agents?
High molecular weight allergens
• Flour – bakers, Animals – labs, shops, Enzymes - detergents
Low molecular weight agents
• Isocyanates (most common) – paints, Acrylates - superglue & 100s of others
How do high molecular weight allergens drive Oc Asthma?
Usually proteins with Specific IgE antibodies
- Similar to asthma driven by Cf mites, animals, pollen
How do low molecular weight allergens drive Oc Asthma?
Reactive chemicals with often no specific IgE
- Very small so body barely recognises them, however they are very reactive and react with proteins within your lungs alveoli to make NEOANTIGENS (new proteins). Because there is a change in the protein structure, the body thinks they are foreign and will develop an immune response to them.