resp Flashcards
Patients with ARDS require transfer to intensive care for cardio-respiratory support, where supportive treatment includes:
Ventilatory support - a low tidal volume is associated with better outcomes.
Haemodynamic support to maintain mean arterial pressure >60 mmHg.
DVT prophylaxis.
Nutritional support with enteral/parenteral means if necessary.
Regular repositioning of patient for pressure ulcer prophylaxis.
Note that antibiotics need only be administered if an infectious cause for the ARDS is identified (such as pneumonia or sepsis).
Investigation of ARDS
Chest x-ray reveals bilateral alveolar infiltrates, without other features of heart failure (such as cardiomegaly and Kerley B lines).
CT Scan may help further characterise changes found on XRay.
Asbestosis
Symptoms: dyspnoea, cough
Signs: crepitations on auscultation, finger clubbing, cyanosis, reduced chest expansion
Chest x-ray: linear interstitial fibrosis, pleural plaques, pleural thickening, atelectasis
Treatment for an aspiration pneumonia
IV cephalosporin and IV metronidazole.
Causes of bilateral hilar lymphadenopathy can be classified as follows:
Inflammatory: sarcoidosis
Infective: tuberculosis and mycoplasma
Neoplastic: bronchial carcinoma and lymphoma.
Interstitial lung disease can also cause bilateral hilar lymphadenopathy and may be inorganic (such as silicosis) or organic (such as extrinsic allergic alveolitis).
Guidelines from the British Thoracic Society (BTS) suggest that if a patient is experiencing 3 or more exacerbations per year
Bronchiectasis
if they are already on optimal medical management (including mucolytic treatment, in the form of saline nebulisers here) then they are a candidate for long term prophylactic antibiotics.
In pseudomonas infections they recommend oral macrolides or inhaled aminoglycosides, however individual agent choice should be made according to local guidelines which factor in information about regional resistant strains.
Cystic fibrosis can be diagnosed by:
Neonatal heel prick day between day 5 and day 9
Sweat test: sweat sodium and chloride >60mmol/L
Faecal elastase: this can provide evidence for abnormal pancreatic exocrine function.
Genetic screening: This can identify CF mutations
Cystic fibrosis
infective exacerbations are treated with:
nfective exacerbations are treated with:
antibiotics, although for patients with recurrent chest infections prophylactic long-term antibiotics may be prescribed.
Nebulised mucolytics (Dornase Alfa)
Bronchodilators (Inhaled corticosteroids or B2-agonists)
Important Features of Squamous cell carcinoma
of the lung
Most common type of lung cancer in the UK
Usually present as obstructive lesions of the bronchus leading to infection.
Occasionally cavitates (10% at presentation) Lung Ca that most commonly cavitates
On X-ray it is not possible to tell whether it is an abscess or a cancer (the border’s definition cannot be easily seen) but on the CT there is obviously a jagged border – indicating cancer.
Local spread is common, but metastasis are normally late (but frequent)
Often causes hypercalcaemia – by bone destruction or production of PTH analogues (PTHrp).
Also associated with clubbing and HPOA (Hypertrophic pulmonary osteoarthropathy)
Important Features of Adenocarcinoma of lung
Arises from mucous cells in the bronchial epithelium
Commonly invades the mediastinal lymph nodes and the pleura, and spreads to the brain and bones
Does not usually cavitate
Proportionally more common in non-smokers, women and in the Far Eastleast likely to be related to smoking
Most likely to cause pleural effusion (as are mesotheliomas
Exudative pleural effusions are caused by diseases which increase capillary permeability, including:
Infections such as pneumonia or TB.
Malignancy such as bronchial carcinoma, mesothelioma, or lung metastases.
Inflammatory conditions such as rheumatoid arthritis, lupus, or acute pancreatitis.
Pulmonary infarct (for example secondary to a pulmonary embolism) and trauma.
Transudative pleural effusions are caused by imbalances in the Starling forces that govern the formation of interstitial fluid.
Conditions that increase the capillary hydrostatic pressure (forcing fluid out of the pulmonary capillaries into the pleural space) include congestive cardiac failure.
Conditions that reduce the capillary oncotic pressure (impairing the reabsorption of fluid from the pleural space into the pulmonary capillaries) include cirrhosis, nephrotic syndrome/chronic kidney disease, and gastrointestinal malabsorption/malnutrition (eg. Coeliac disease).
Management of PCP
Treatment is based on clinical or radiological evidence of infection or clinical indicators of general immune deficiency.
The first choice agent in the treatment of PCP, regardless of severity, is Co-trimoxazole
Alternative therapy can be used if Co-trimoxazole does not eliminate infection. This includes Clindamycin-primaquine, dapsone, IV pentamidine.
If the patient has p02 <9.3kPa and an arterial alveolar 02 gradient >4.7kPa, is it important to consider adjuvant corticosteroids. This has a proven reduction of mortality.
drug induced fibrosis
Medications: Amiodarone, Nitrofurantoin and Bleomycin.
Pulmonary hypertension
Signs include a raised JVP, parasternal heave, loud P2, presence of an S3 sound, pansystolic murmur (tricuspid regurgitation) and an end-diastolic murmur (pulmonary regurgitation).
