Respiratory 2.45-2.52 Flashcards
KCO significance?
Means drops if lung itself is affected e.g. COPD; but if extrapulmonary then TLCO decreases but KCO normal or even SUPERNORMAL to compensate
TLCO and KCO in obesity ie extrapulmonary restriction?
TLCO decreased, KCO increased/normal
Burden of occupational lung disease?
Causes 15% COPD/asthma, 2% lung cancer, 80% EAA; plus mesothelioma, infection, pneumoconiosis
Fibrogenic and non-fibrogenic occupational lung disease?
Silicosis, CWP and asbestosis all fibrogenic; non-fibrogenic includes siderosis (Fe) and baritosis (barium)
Silicosis?
Silica dust. Need unnatural forces to get small enough particules ie sandblasting, masonry, mining/quarrying. Much smaller lethal exposure than CWP. Restrictive pattern; dense fibrosis. Nodules are bifringent and sparkling. Get classic silicosis, acute silicosis, COPD, cancer, (TB) i.e. increases everything.
Early and late appearance of silicosis?
- Early = diffuse, well-defined nodules on CXR. Predominately upper lobe. May see calcification. On CT, may see hilar and mediastinal l’dopathy, lymph node calcifciation. (DD sarcoid, Tb, diffuse malignancy);
- Late.See multiple solid masses in upper zone; usually symmetrical/bilateral, graduallly migrating towards the hilum.
CWP?
Fibrogenic pneumoconiosis; coal deposition. Same appearance as silicosis i.e. simple gives nodular upper zone shadowing, progressive massive fibrosis gives multiple large opacities (predominately upper/middle zones). See dust accumulation around terminal bronchioles on histology.
Causes of high TLCO?
Polycythaemia, asthma (may be normal), exercise (increased pulmonary blood volume), pulmonary haemorrhage
Pleural thickening?
aka benign diffuse pleural thickening. Can occur in silicosis/Tb/radiation/chronic
pneumonia/empyema but will be unilateral; bilateral in asbestos. SOB, restriction. Fibres cause inflammation, leading to chronic pleural effusions and fibrosis (thickening). 15-20 years latency . Irreversible but usually not progressive. DD inc. mesothelioma. Need regular screening
Asbestosis?
Diffuse interstitial fibrosis; parenchymal (separate to pleural disease). Basal! Rare for fibrosis. Get severe SOB, increased risk of lung cancer. Hear fine end inspiratory crackles. Get restrictive deficit, TLC and VC down. Ratio preserved. Diffusion impaired (TLCO/KCO) so get hypoxaemia. Can get cor pulmonale eventually.
Diagnosing asbestosis?
Imaging or histology consistent with it, evidence of causation (occupational history, markers of exposure (pleural plaques, recovery of asbestos bodies), exclusion of alternative possibilities HRCT better than CXR.. Most will have concurrent pleural plaques.
Key differential for asbestosis?
IPF. Occupational history, pleural plaques; clubbing less common in asbestosis. Important for treatment. Remember not all asbestos lung disease is asbestosis!
Malignant mesothelioma?
Long latency (40 years), breathlessness, pain, sweats, weight loss and anorexia. Death in 18 months. Pleura “enroaches” onto lung; may see reduction in lung volume so mediastinum shifts towards lesion. Predilection for direct invasion and metastasis.
Diagnosing mesothelioma?
CXR and CT for suspicion; confirm with aspiration[thoracentesis] for malignant cells/tissue biopsy [thoracoscopy]. DD HF, Tb.
How many years is generally needed for CWP?
~20. Silicosis is fewer (remember graph)
Findings that point towards EAA?
BAL with lymphocytosis, compatible CXR and HRCT, IgG to farmer’s lung-type microbes etc., histology, compatible history or evidence of exposure from Ab, decreased TLCO, positive challenge test
BAL in EAA?
Negative findings are useful to rule out EAA; positive (i.e. alveolar lymphocytosis) is useful but may also be found in asymptomatic people (false positives)
Treating EAA?
Reduce exposure, give steroids; stopping immediately usually not the best thing to do!
What are Light’s criteria?
- Pleural fluid protein divided by serum protein >0.5
- Pleural LDH / serum LDH >0.6
- Pleural LDH >2/3 ULN for serum LDH.
Pleural fluid is an exudate if one or more are met.
How does mineral dust cause lung disease?
Particles become lodged, are taken up by macrophages, which are activated and released cytokines etc. As silica etc. is indigestible, macrophage dies, particle is taken up by another and process is perperuated.
Two types of occupational asthma?
- Sensitiser-induced OA (90%). Latency period between first exposure and immunological response (allergy); IgE mediated (so must be reaction to protein?)
- Irritant-induced OA = RADS (reactive airway dysfunction syndrome). Occurs a few hours after exposed to high concentration of irritant; acutely dangerous but may have chronic sequelae (i.e. lifelong asthma)
IgE in occupational asthma?
Total IgE raised indicates atopy and therefore predilection; can look for specific IgE to allergen but may get false negatives.
Use of methylcholine challenge?
Take baseline FEV1; inhale increasing doses of potent bronchoconstrictor; get PD20 (dose needed to reduce FEV1 by 20%. If very low, indicates airway hyper-responsiveness (hallmark of asthma).
Why are OA symptoms often worse after work?
Get late response after ~12 hours; must observe for this when testing for OA. Same as with allergy (early is mast cell degranulation following specific IgE cross-linking; late is mast cell mediated and recruits lymphocytes/eosinophils to site; takes 8-12 hours).
Causative agents for OA?
- HMW allergens (flour, dander, enzymes). Proteins, make specific IgE and get type 1 HS response. Natural counterparts.
- LMW agents (CHEMICALS) e.g. isocyanates, epoxy resins. Small and very reactive; react with proteins to give novel allergens but are not themselves allergens; may be no specific IgE (hence FNs). No natural counterparts.
Features of OA?
Onset often in one year of new work, have latent phase of asymptomatic exposure, get evening/night-time symptoms (delayed response), worse when working and BETTER AT WEEKENDS/HOLIDAYS, worse with heavier exposure/no protection, associated nasal/eye symptoms, other workers likely to be affected?
Sputum eosinophils in OA?
Induce fresh sputum with hypertonic saline; associated with inhalation challenge testing (PD20). Levels of eosinophilic airway inflammation. Suppressed by cigarette smoking. More associated with HMW than LMW.
Risk factors for OA?
Atopy increases risk of OA in HMW agents; smoking increases risk of sensitisation to flour, seafood, isocyanatesm platinum salts, coffee and castor bean. Atopy also means develop sensitisation to HMW (IgE forming) FASTER
Most common causes of OA in UK?
Isocyanates (e.g. paint-spraying), flour/grain, latex, cleaning products.
Preventing OA?
- Limiting exposure (ventilation, RPE, reallocation)
- Pre-employment screening not effective unless history of sensitisation to certain Ag
- Health surveillance could be key in identifying early
Prognosis OA?
Loss of income, 1/3 achieve symptomatic recovery; likely to worsen if remain exposed. 1/3 unemployed <6 years after diagnosis
Post-OA?
Once becomes established, can get symptoms triggered by “normal” asthma factors like cold/exercise etc. Means can miss “better on weekends”!
Serial PEFs/spirometry in OA?
Done when at work and when away; may show variable AW obstruction (hallmark of asthma) and possible relationship between symptoms/PFTs/work. Assessment may be difficult as can exaggerate or underplay.
Serial methycholine measurements?
Should show sequential improvement away from work and rapid deterioration when return
Chronic bronchitis pathophysiology?
Chronic/recurrent excessive mucus secretion in the bronchial tree; caused by smoke irritation so should improve when stops smoking. Caused by mucous gland hypertrophy and increased number of goblet cells.
