Respiratory Medicine

Respiratory Medicine ASTHMA 1. Define the classical features of asthma including episodic wheeze, cough and reversible airways obstruction. • • • • • • Attacks of wheezing Episodic SOB Worst at night Associated with cough, esp. at night Specific triggers Reversible with bronchodilators 2. Classify asthma into early and late onset and discuss the characteristics of a typical patient who is likely to present with each. • Early onset Ø Atopic individuals Ø Intrinsic Ø +ve skin prick identifies specific allergen(s) Ø Can occasionally be from workplace exposure in adults • Middle age onset Ø Cryptogenic / extrinsic Ø No identifiable causative agent 3. Outline common precipitants of an asthma attack. • • • • • • • • Environmental – grass, pollen, pets Atmospheric – sulphur dioxide, ozone Irritants – perfume, cigarette smoke Drugs – NSAIDS, Beta-blockers Occupational – Isocyanates, colophony fumes Viral – rhinovirus, paraflu, RSV Cold air Emotion 4. Describe the clinical features of an acute asthma attack including marked breathlessness, tachycardia, pulsus paradoxus, widespread expiratory wheezing in both lung fields and a quiet chest if very severe. • hyperresponsive airway + trigger • bronchial inflammation – eosinophils, mast cells, T cells, plasma exudates, oedema, hypertrophic smooth muscle, mucus plugging and epithelial damage. • Airflow limitation Ø Starts within minutes of insult Ø Reversible with treatment Ø Widespread wheeze Ø Tachycardia Ø Pulsus paradoxus 5. Describe the blood gas abnormalities associated with severe asthma and highlight other clinical indices of severity. Severe Asthma • Unable to complete sentence in 1 breath • >25 breaths /minute • Tachycardia >110 • PEF <50% Life Threatening Asthma • Silent chest • Cyanosis • Poor respiratory effort • Exhaustion confusion coma • Bradycardia / hypotension • PEF <30% normal • PaCO2 >6kPa • PaO2 <8kPa on 100% oxygen • Low, falling PH, Bicarb normal 6. Outline the stepped approach to treatment of an acute asthma attack and describe the mechanisms of action of the main drugs used. This would include beta2-agonists, anticholinergics, and inhaled and oral steroids. • Community Rx Ø Sulbutamol / terbutaline inhaler (nebuliser if possible) Ø Hydrocortisone IV if possible Ø Oxygen 40-60% Ø Oral prednisolone • Hospital Rx Ø Ø Ø Ø Ø Ø Ø Ø Reassess Oxygen if not already given Salbutamol nebs 4hrly Ipratropium neb Hydrocotisone IV 4hrly / 24hrs Oral Prednisolone 2 / 52 Theophyline Intubation and ventilation as a last resort. 7. Describe how to use inhaler devices and be able to formulate management plans. • If standard inhaler Ø Get good seal with mouth Ø Depress cylinder and breathe in sharply • If Accuhaler Ø Breathe in sharply with good seal • If using spacer device Ø Get good seal with mouth Ø Depress cylinder Ø Breath through spacer 8. Describe the morphology and pathological consequences of asthma. • Necrosis of airway epithelium • Smooth muscle hypertrophy • Sub epithelial collagen deposition 9. Discuss the importance of identifying occupational asthma. LAWSUITS!!!! And avoidance of precipitants CHRONIC OBSTRUCTIVE PULMONARY DISEASE /EMPHYSEMA 1. Define the term chronic obstructive pulmonary disease (COPD). • Progressive airflow limitation, not fully reversible, and associated with abnormal inflammatory response 2. Describe the typical history of a patient with COPD. • Male • Smoker • Ex-miner, crop duster, builder etc. • Repeated RT infections • May be associated with high atmospheric pollution and or alpha1-antitrypsin deficiency 3. Describe the pathology underlying COPD and emphysema. • Thoracic muscle hypertrophy • Increase in mucus producing cells • Bronchial inflammation • Epithelial ulceration – leading to Ø Columnar à squamous Ø Scarring and thickening Ø Narrowing • loss of elastic recoil (emphysema) 4. List recognised risk factors for the condition including smoking, pollution and alpha-1 antitrypsin deficiency. • Duh 5. Elicit the physical signs of COPD including central cyanosis, chest hyperinflation, intercostal recession, and expiratory wheeze. • Productive cough • Widespread wheeze • Breathlessness • Worse in cold, fog and with pollution If severe; • Tachypnoea • Prolonged expiration • Use of accessory muscles • Intercostal recession on inspiration • Lip pursing on expiration • Poor chest expansion • Hyperinflated chest • Loss of normal cardiac and liver dullness • Cyanosis • Oedema • Rarely breathless If hypercapnic; • peripheral vasodilatation • bounding pulse • flapping tremor • ultimately drowsiness and confusion 6. Outline the investigation of a patient with suspected COPD • Bloods – FBC, PCV  , ABG – hypercapnia low P02 • CXR – hyperinflation, flattened hemidiaphragms, large pulmonary arteries, decreased peripheral vascular markings, • ECG – RA/RV hypertrophy (cor pulmonare) • Lung function – fev1- <80&, fev1:fvc <70% 7. Discuss the treatment with monitored oxygen therapy, physiotherapy, bronchodilators, antibiotics and steroids • stop smoking • encourage exercise • pulmonary rehab • ipratropium or salmeterol • +/- inhaled steroid. • Mucolytics • Oxygen therapy to maintain pa02 at >8 (rx @ 7.3) 8. Discuss methods of helping people to stop smoking. • New leaf • Councelling • Patches • Fake fags • Gum • Beatings • Electric shock therapy • More beatings • Ban smoking • Beat the living s**t out of them 9. Discuss the importance of monitored oxygen therapy in treatment. • Increases 3 year survival by 50% if 15 hrs a day are given 10. Discuss the indications for assisted ventilation and outline how this is undertaken. Assisted ventilation should only be given if the patient is suffering an acute on chronic episode eg infection NEVER give assisted ventilation to a worsening of chronic disease – they are going to die anyway it is unnecessarily invasive. BRONCHIECTASIS 1. Describe the typical history of a patient with bronchiectasis and describe how it differs from COPD. 2. Outline the morphology and pathological consequences of bronchiectasis • Widened bronchi and bronchioles 5-6x diameter • Most commonly at bases • Purulent secretions • Chronic bronchial wall inflammation • Epithelium replaced by granulation tissue • Bleeding and haemoptysis • Fibrous scarring with lung obliteration and respiratory failure Complications; • Chronic suppuration • Lung abscess • Haematogenous spread • Amyloidosis 3. List recognised risk factors for bronchiectasis including inherited causes (Kartagener's syndrome, cystic fibrosis-see separate section), post-infectious, and immunocompromised patients. • Congenital – bronchial wall deficiency, pulmonary sequestration • Mechanical – foreign body • Obstruction – post TB stenosis, tumour • Post-infective damage – pneumonia, all types • Granuloma and fibrosis – TB, sarcoidosis, fibrosing alveolitis • Immune over-response – aspergillosis, post-lung transplant • Genetic – CF, cilliary dyskinesia • Immune deficiency – Ig deficiency, HIV, malignancy, steroids • Acquired – Young’s Syndrome 4. Elicit the physical signs of bronchiectasis including persistent purulent sputum and, in some patients, finger clubbing, central cyanosis, and coarse crackles over affected lung. • Yellow/Green sputum post-infection • Position dependent • Persistent halitosis • Recurrent febrile episodes, malaise and pneumonia • Clubbing • Coarse crackle over infected areas, often bases • Continuous foul thick mucus • Haemoptysis • Breathlessness • Cyanosis 5. Outline the investigations of a patient with suspected bronchiectasis including CXR, sputum culture and chest CT scanning. • sputum culture • CXR – cystic shadows, thickened bronchial walls – tramline and ring • Spirometry shows obstructive pattern • Brochoscopy • Ct scanning can give better views of chest 6. Discuss the treatment with postural drainage and physiotherapy and antibiotics for infective exacerbation • BD postural drainage • Chest physio, to aid drainage • Abx for infection, promptly • Ciprofloxacin if pseudomonas • Bronchodilators if asthma copd etc. • Steroids if inflammatyory / allergic component • Syrgery may be used in severe disease CYSTIC FIBROSIS 1. Describe the clinical presentation of a patient with cystic fibrosis with respect to disease of the lung and pancreas. • 40% respiratory disease • 30% failure to thrive • 20% diagnosis at birth due to meconium ileus • 10% liver disease, nasal polyps and sinusitis All due to abnormally viscous mucus 2. Describe the genetic defect and how it is inherited. • Autosomal recessive gene on chromosome 7 • Carriers 1in 22 • Sufferers 1 in 2500 of all live births 3. Describe the pathology of the lungs. • Obstruction – stagnation and infection • Bronchiectasis and haemoptysis • Lung hyperinflation ude to trapped air, increased risk of pneumothorax • Hypoxia, scarring and destruction of lung parenchyma • Pulmonary hypertension and cor pulmonale 4. Describe the usual organisms causing lung infection. • SA and pseudomonas 5. Describe the main principles of treatment including physiotherapy, antibiotics, pancreatic enzymes DNAse, and lung transplantation. • MDT team Chest • • • • • • • • postural drainage and physio Abx for infection and prophylaxis with flucloxacillin Mucolytics Bronchodilators Oxygen Diuretics Non-invasive ventilation Heart-lung transplant GI • • • • pancreatic enzyme replacement fat soluble vitamin supplements ursodeoxycholic acid for impaired liver function may need transplant if cirrhosed Other • diabetic rx • screen for osteoporosis • rx arthritis, sinusitis, vasculitis, fertility and genetic counselling 6. Describe the non-respiratory manifestations of cystic fibrosis GI • pancreatic insufficiency; steatorrhoea, diabetes • distal intestinal obstruction syndrome – similar to meconium ileus • • gallstone cirrhosis Other • male infertility • osteoporosis • arthritis • vasculitis • nasal polys • sinusitis • hypertrophic pulmonary osteoarthropathy PNEUMONIA 1. Describe the typical presentation of a patient with a community-acquired pneumonia and the features that identify severe pneumonia. Presents with; • Cough • SOB • Chest pain • Malaise / lethargy • Anorexia • • • • • • • • Signs RR, HR raised Low BP Respiratory distress Creps and bronchial breathing Increase vocal fremitus and resonance Pleural rub Sweating Cyanosis • • • • • • • Sever community acquired is CURB 65 C – confusion U – Urea >7 R – Resp. rate >30 B – BP <90 <60 65 + years old 1-2 = hospital referral 3+ = urgent referral, may kak it 2. List the common pathogens causing community acquired and hospital acquired pneumonia. Community: • Typical Ø Strep. Pneumoniae Ø Mycoplasma Ø Haem. Influenzae • Atypical Ø Chlamydia Ø S. Aureus Ø Legionella Hospital: • Gram –ve (pseudomonas, klebsiella) • S.Aureus inc MRSA Immunosupressed • Pneumocystis – AIDS defininig • Aspergillus • CMV 3. Outline factors that predispose to pneumonia including smoking, endobronchial lesions, influenza epidemics (staphylococcus aureus infections), pets (psittacosis), Spanish holidays (Legionnaire's disease) and AIDS (pneumocystis pneumonia). • • • • • • • • Lung disease Smoking Alcohol – aspiration Immunosupression Chronic disease Pets; birds cats and dogs – extrinsic fibrosing alveolitis and psittacosis Holidays – legionella – spain, TB – Africa, Yorkshire AIDS – pneumocystis 4. Describe the pathology of acute lobar pneumonia and bronchopneumonia. LOBAR • Organisms colonise and spread through distal air spaces • Acute inflammatory exudate enters air spaces • Lobe becomes consolidated • Seen esp in vagrants and alcoholics BRONCHOPNEUMONIA • Primary bronchial infection • Spreads outward • Patchy consolidation • Often lower lobes 5. Outline the investigation of a patient presenting with a community-acquired pneumonia. • Bloods – FBC, WCC, U&E (hydration), CRP (inflammation), LFTs (mycoplasma), cultures • ABG – if hypoxic / cyanosed • Sputum – if productive cough; gram stain and culture • Urine – legionella and pneumococcal AB • CXR – look for effusion, consolidation, air bronchogram 6. Discuss treatment including general supportive measures, appropriate antibiotic regimens analgesia and physiotherapy. • Supportive – iv fluid, oxygen • Antibiotics Ø CAP amoxicillin & erythromycin Ø Severe CAP cefotaxime & clarithromycin Ø HAP Augmentin +/- cephalosporin IV Ø Aspiration – anti anaerobes • Chest physiotherapy – can help clear secretions 7. Describe the complications of pneumonia including septicaemia, lung abscess and empyema. • • • Lung abscess Ø Ø Ø Ø commonest with aspiration, SA and klebsiella persistant worsening pneumonia swinging fever, malaise, weight loss anaemia, raised ESR Ø Ø Ø Ø Pus in pleural cavity Normally follows ruptured abscess High fever severe illness Neutrophil granulocytosis Empyema Septicaemia Ø Can lead to infective endocarditis Ø Meningitis and other systemic infection • others – respiratory failure, effusion, hypotension, pericarditis, AF and jaundice TUBERCULOSIS 1. Describe the process of infection by the tubercle bacillus together with the route of spread. • Infection is usually inhalation, can be ingestion • Bacilli enter lungs and lymph nodes • Transient response; T-cell sensitisation, cytokines and exudate • Exudate initially neutrophils , later macrophages • Chronic response; after 3-8 weeks, cytokines, increased macrophages and type IV immune response • 1o infection subpleural, mid / upper zones, usually asymptomatic • GHON focus forms as bacilli are surrounded, central caseation occurs – mmmmm cheese • Can reactivate 2. Discuss the presentation of post-primary tuberculosis from reactivation of infection. • Reactivation – pulmonary TB with cavitation , apex / upper zone • Apical, bilateral – fibrosis, decreased volume, bronchiectasis and pleural thickening • Gradual onset of Sx weeks to months Ø Tiredness Ø Malaise Ø Anorexia Ø Weight loss Ø Fever Ø Cough Ø Purulent mucoid of blood stained sputum Ø Recurrent colds and dull ache in chest Ø Little to find on examination Ø Night sweats uncommon 3. Outline common predisposing factors including ethnicity, debility, alcohol, malnutrition, diabetes and steroid therapy. • Ethnicity Ø Asian sub continent 40x Ø West indies 4x Ø Eastern Europe 4x • Genetic – HLA linked • Co-existing disease eg diabetes • Nutrition • Alcohol • Impaired immunity, HIV steroids etc 4. Outline the investigation of a patient with suspected TB. • • • • • sputum sample mc+s,for acid fast bacilli, if –ve BAL biopsy any non-pleural lesions PCR – use of BAL, sputum or aspirate from lesion CXR for consolidation, cavitation, fibrosis, and calcification Mantoux test 5. Outline the principles of treatment of confirmed cases and the principles of contact tracing. • NEED TO CHECK 6. List the common sites and outline the pathological features of non-pulmonary TB infection including involvement of the meninges, kidneys, spine, peripheral joints, gastrointestinal tract, pericardium and adrenal glands. • • • • • miliary TB haematological spread, classic cxr but also liver, lymph nodes and bone marrow meningeal – subacute meningial sx, GU – sterile pyuria, loin pain, frequency and dysuria Bone – vertebral collapse and paravertebral abscess Pericardium - primary exudative allergic reaction, can cause constrictive pericarditis 7. Describe in broad outline how the patient would have been treated between 1930 and 1970 and the implications of this for current treatment. • Lobar collapse, look for ping pong balls on x-ray and thoracotomy scars 8. Describe the global picture of TB, its relation to the AIDS epidemic and the causes and consequences of multidrug resistant tuberculosis. HIV alters presentation in the following ways – • Mantoux may be –ve • Atypical presntatons • Latent reactivation common • BCG has no effect • Few afb seen • Culture essential as often multi-resistant strains • CXR atypical • Extrpulmonary more common • HAART and TB antibiotics interact to increase toxicity • As retrovirals work, inflammatory response builds against TB and can kill PNEUMOTHORAX 1. Describe its typical clinical presentation and the recognised risk factors. • Pleuritic chest pain • SOB • Worsening of pre-existing lung disease • Asymptomatic – depends on size • Decreased breath sounds, decreased resonance and fremius • Hyperresonant • Deviated trachea, RD, BP fall and raised HR, distended veins if tension 2. Distinguish between an 'ordinary' and a tension pneumothorax and outline the clinical features that would point toward a diagnosis of a tension pneumothorax. • a monkey could do this 3. Outline the underlying pathology. • Rupture of pleural blebs in young males • Lung deflateion due to loss of negative pressure in pleural space 4. Elicit the classical physical signs including reduced chest expansion, resonant percussion note and reduced or absent breath sounds. 5. Outline the investigation of a patient with a suspected pneumothorax. • If tension suspected Ix = Rx 16G cannula 2ndICS MCL then chest drain • If simple then x-ray, ABG and standard bloods esp clotting 6. Outline the treatment options including chest aspiration or an intercostal underwater chest drain. • small pneumothorax, no treatment, monitor with CXR • Med / large / tension – aspirate air via 3 way tap • If large or recurrent, use intercostal chest drain with underwater seal, can do pleurodesis and pleurectomy 7. Outline the emergency treatment of a tension pneumothorax. • Wide bore canula, 2nd intercostal space midclavicular line • Then chest drain 8. Outline the indications for surgical pleurectomy and pleurodesis. • Recurrent large pneumothoraces, especially those which are clinically / physiologically significant. • Risk benefit of surgery vs risk of future pneumothorqaces LUNG CANCER 1. Outline the major pathological classification of lung cancers and their prognosis. • Squamous Ø 50-60% Ø Men>women Ø 50+ Ø Smokers Ø Tumour in hilum, projects to bronchi, obstruction can look like pneumonia • • • Adenocarcinoma Ø Ø Ø Ø Ø 10% Peripheral Pleural and lymphatic spread F>m Few signs at early stage Ø Ø Ø Ø Ø Ø Endocrine origin Early spread Lymph nodes Inoperable at diagnosis Can have some response to chemo If extensive (bilateral) 6wks – 9 months (with chemo) Ø Ø Ø Ø Asbestos related, long development time Pleaural CA, encases lung Thoacoscopy and biopsy Poor prognosis Small (Oat) cell Mesothelioma 2. Describe risk factors that increase the risk of lung cancer. • Air puultion • Smoking • Toxic substances • Asbestos • Radiation • Radon gas • Genetic predisposition • Owning a donkey 3. Outline the epidemiology of lung cancer in developed countries. • 90% are smokers • 20% of all smokers develop lung cancer • Biggest Ca killer in UK 4. Describe the common clinical presentation of lung cancer including persistent cough, haemoptysis, dyspnoea, and weight loss. • cough 41% • chest pain 22% • pain and cough 15% • haemoptysis 7% • chest infection • malaise • weight loss • SOB • • • • • • • • • Hoarseness Asyptomatic Finger clubbing SVC obstruction Persistant lymphadenopathy Abnormal CXR Stridor Metastesis All above 5% 5. Outline local metastatic manifestations of lung cancer including recurrent laryngeal nerve palsy, Horner's syndrome, and SVC obstruction. 6. Outline non-metastatic manifestations of lung cancer, including hypertrophic osteoarthropathy and dermatomyositis. 7. Discuss relevant investigations including CXR, sputum cytology, bronchoscopy or transthoracic lung biopsy depending on the site of the lesion. • CXR • Spirometry • Sputum cytology • Bronchoscopy • MRI • CT • Pet Scan • Bone scan • Liver US • Blood tests 8. Outline the treatment options for a patient with confirmed lung cancer including surgery, chemotherapy and radiotherapy. • • • • • Excision – peripheral tumours, no spread Curative radiotherapy – if inadequate respiratory reserve Chemotherapy – if disseminated tumour Palliative radiotherapy – obstruction of bronchi, or blood vessels Drainage / pleurodesis for effusions PLEURAL EFFUSION 1. Classify causes of a pleural effusion including infective (pneumonia), inflammatory (SLE, rheumatoid disease), neoplastic, metabolic (uraemia, hypoproteinaemia) and cardiac causes. • Raised hydrostatic pressure • Decreased oncotic pressure • Decreased pressure in pleural space • Increased capillary permeability • Impaired lymphatic drainage • Fluid from peritoneum or pericardium Transudate • Low protein <30g/l • LD <200 IU/l • HF • Pericarditis • Low serum protein • HYPOTHYROID • OVARIAN TUMOURS Exudate • Pleural inflammation / impaired lymph drainage • Infection • Autoimmune • Lymph abnormality • Yellow nail syndrome • Pulmonary infarct • Bronchial Ca 2. Obtain a relevant history from a patient with a pleural effusion including features such as weight loss, smoking, previous cancer (lung ca), recent pneumonia, TB exposure, asbestos exposure, heart disease (LVF), connective tissue disease and trauma. 3. Describe the typical examination features of a pleural effusion. • small – asymptomatic • large – little discomfort if slow build up • pleurisy • SOB • Dull ache on affected side • Recurrent dry cough • Reuced chest wall movement • Mediastinal shift away • Stony dull to percussion • Reduced breath ssounds • Reduced resonance and fremitus 4. Describe the aetiology and clinical features of an empyema. • ruptured lung abscess, severe TB or infection of a transudate • pyrexia • rigors, chills, sweating malaise, weight loss • raised neutrophils • pleural pain • SOB • Cough and sputum • Signs of effusion • Must eradicate infection and re-expand lung 5. Discuss the investigation of a unilateral pleural effusion including indications for performing a pleural tap and biopsy. • CXR – look for loss of costophrenic angles, concave upper borders, flattened if pneumohaemothorax • All large effusions should be aspirated as a diagnostic / treatment method, can use ultrasound guidance. Send aspirate for microscopy, culture and biochemistry • Biopsy only if aspirate fails or is inconclusive 6. Discuss the management of pleural effusion including empyema. • Drain effusion – repeatedly if necessary <2l/24hrs, can use 3 way tap or chest drain • Pleurodesis – if recurrent effusions, malignant effusions. • Chest drain best for empyemas • Persistent collections and increasing pleural thickness requires surgery FIBROSING ALVEOLITIS 1. Describe the clinical features of fibrosing alveolitis. • dry cough • exertional dyspnoea • malaise • weight loss • arthralgia • • • cyanosis finger clubbing, fine end inspiratory creps 2. Outline the common causes including cryptogenic and connective tissue disease and list the differential diagnosis in patients who present with established pulmonary interstitial fibrosis. • RA • Cryptogenic • Sjogrens syndrome • Dermatomyositis • Sle • Connective tissue disease • Systemic sclerosis 3. Describe the pathological features. • Thickened alveolar walls due to scarring 4. Outline the blood tests, pulmonary function tests and radiological investigations of a patient with suspected fibrosing alveolitis and how they contribute to diagnosis. • Type II respiratory failure • CRP • IG • ANA +ve 30% • Decreased lung volume 5. Outline the treatment options including corticosteroids. • steroids • cyclophosphamide and steroids • lung transplant EXTRINSIC ALLERGIC ALVEOLITIS 1. Outline the nature of the allergic reaction underlying EAA and how this is used to establish the diagnosis. • Type III immune complex mediated response • Look for raised neutrophils and +ve serum precipitins 2. List common causes such as Farmer' lung, bird fancier's lung etc. • Bird or pigeon fanciers lung • Farmers / mushroom workers • Malt worker • Bagassosis 3. Describe the typical clinical presentation with episodic breathlessness several hours after exposure to the antigen. • fever • rigors • myalgia • dry cough • dyspnoea • crackles, no wheeze • 4. Outline the pathological consequences of repeated allergen exposure. • Weight loss • Type I respiratory failure • Restrictive lung defecit • Honeycomb lung – fibrosis 5. Outline the treatment options including removal of the allergen plus steroids and how response to treatment should be monitored. • Acute – remove allergen, give oxygen • 200mg Hydrocortisone IV • 40mg/24hr PO Pred reducing dose • • • Chronic – Avoid exposure Face mask, long term steroids ?Compensation if industrial OCCUPATIONAL LUNG DISEASE 1. Describe the clinical features of the main conditions associated with asbestos inhalation (pleural plaques, pleural effusion, mesothelioma, asbestosis and lung cancer). Light Exposure Pleural plaques • Fibrotic plaques on parietal pleura • Usually asymptomatic or mild dyspnoea Mesothelioma • Highly malignant tumour • starts in pleura spreads to pericardium • 90% associayed with asbestos 20% also absbestosis • 2 yr survival max without rx • Pleuritic pain dyspnoea amd effusion Heavy exposure Asbestosis • usually with plaques ans mesothelioma • similar to fibrotic lung disease • progressive dyspnoea and clubbing with bibasal end inspiratory creps • Pulmonary hypertension +/- cor pulmonale • Restricitve deficit • Streaky shadow and honeycomb on cxr Lung Cancer • asbestosis, bilateral pleural thickening • bronchial cancer 2. Describe the natural history of pleural plaques, mesothelioma and asbestosis and outline the relation between these conditions and the duration of exposure to asbestos. • plaque à mesothelioma à asbestosis • increased time and level of exposure à 3. Discuss the effect of inhalation of coal dust on lung function and its relation to pneumoconiosis. • coal workers pnemoconiosis commonest uk dust disease • coal dust eaten by macrophages, die release enzymes cause fibrosis 4. Be aware that patients exposed to coal and asbestos can obtain industrial compensation. • compensation under social security act 1975 • coal miners account for 90% • asbestos if bilateral pleural thickening, asbestosis and mesothelioma • 5. Be aware that asthma can be due to occupational factors (see asthma). • determined y days off • common in • –vetinery medicine • animal handling • bakery • laundry work • 10 years to apply for compensation OBSTRUCTIVE SLEEP APNOEA 1. Outline the clinical presentation of a patient with obstructive sleep apnoea. • Fat Middle aged male • Snoring • Daytime somnolence • Snorts loudly when asleep • Poor quality sleep • Morning headache • Decreased cognitive function • Decreased libido 2. Describe the use of sleep studies in the investigation of the condition. • 15+ episodes of apnoea during 1 hour sleep is significant • Polysomnography – 02 sats, airflow of nose and mouth, ecg, eeg and emg chest and abdominal movement 3. Outline the principles of treatment of the condition. • weight reduction • avoid tobacco and alcohol • CPAP via nasal mask during sleep • Surgery is bollocks VENTILATORY FAILURE 1. Distinguish type-2 (ventilatory) from type-1 respiratory failure and understand the implications of having a high arterial pCO2. • Type I • Pa02 <8 • Pulmonary oedema, pneumonia, fibrosisng alveolitis • • • • Type II Low or normal oxygen PaCO2 >7 COPD respiratory depression Acute raised C02 – uncompensated repiratory acidosis Chronic raised C02 – compensated with renal HC03 retention 2. Describe the causes of ventilatory failure including central depression of the respiratory centre, neuromuscular and chest wall problems and chronic bronchitis (see section on COPD). • respiratory depression – opiates, CNS tumour, trauma • neuromuscular – MG, cord lesion, paralysed diaphragm, guillan barre, other drugs • chest wall – flail, kyphoscoliosis • airway / lung – asthma, chronic bronchitis, COPD, fibrosis, epiglotitis, OSA 3. Outline the effect of chest wall and spinal deformity on respiratory function. Chest wall • decreased expansion and inspiration • hypoventilation • type ii failure 4. Outline the conditions that may cause respiratory failure due to neuromuscular disease including Guillain-Barre syndrome and myasthenia gravis. • MG, GB, poliomyelitis, paralysed diaphragm, cervical cord lesion 5. Outline the treatment for acute ventilatory failure including the use of low concentrations of oxygen, physiotherapy and bronchodilators and be aware that IPPV in the intensive care setting or nasal IPPV on the ward may be needed for some patients. • Type I – give high flow oxygen, treat cause • Type II – give high flow oxygen until P02 recovers, monitor blood gasses and RR beware hypoxic driven patients • ALWAYS treat cause as well as symptoms if possible • If reversible cause, send to ITU as necessary • If irreversible cause then make comfortable – they will die