Respiratory Flashcards
what two types of disease are included within the definition of COPD?
emphysema and chronic bronchitis it’s chronic obstruction with *irreversible airflow obstruction –> air trapping and hyperinflation
define chronic bronchitis
narrowing of airways and mucosal oedema –> mucus hypersecretion –> cough + excessive mucus = persistent cough+mucus for 3/12 for 2 consecutive years
list some features that would suggest it is more likely the patient has COPD than asthma
onset >35yo, smoking/pollution related, chronic dyspnoea (instead of attacks), sputum production, lack of diurnal FEV1 variation
give 2 causes of COPD
**smoking, occupational exposure (particles and gases) alpha-1 antitrypsin deficiency
what generally causes early-onset COPD?
alpha-1 antitrypsin deficiency - produced in liver.
give 3 risk factors of COPD
smoking, pollutant exposure, frequent lower resp infections in childhood, age.
describe the pathology seen in chronic bronchitis
narrow airways. hypertrophy and hyperplasia of mucus secreting glands of the bronchial tree. bronchial wall inflammation. mucosal oedema. ulceration of epithelial layer - heals squamous instead of columnar (squamous metaplasia).
describe the pathology seen in emphysema
elastin breakdown –> dilation and destruction of alveoli - expiratory airflow limitation and air trapping
which disease is predominant in each of pink puffers and blue bloaters?
pink puffers = predominantly emphysema blue boaters = predominantly chronic bronchitis
what are the features of a pink puffer?
increased alveolar ventilation -= nearly normal PaO2 + normal/low PaCO2 - breathless but not cyanosed - may progress to type 1 resp failure they retain CO2 making it normal, will be old and thin, using accessory muscles
what are the features of a blue bloater?
decreased alveolar ventilation - low PaO2 and high PaCO2 - cyanosed but not breathless - poss. cor pulmonale - rely on hypoxic drive as respiratory centres are insensitive to CO2. peripheral oedema and overweight from RHF.
what is cor pulmonale?
enlargement and failure of right side of the heart due to disease of lungs/pulmonary blood vessels - leads to oedema and raised JVP Rx = LTOT + loop diuretic
explain how cigarette smoke causes COPD
causes mucous gland hypertrophy in larger airways - increase in neutrophils, macrophages and lymphocytes in airway walls - release of inflammatory mediators - inflammatory cells attracted - structural changes - break down of connective tissue
what is alpha1-antitrypsin?
a protease inhibitor - inactivated by cigarette smoke
give 3 symptoms of COPD
cough, sputum, dyspnoea, wheeze
give 3 signs of COPD
tachypnoea, use of accessory muscles of respiration, barrel chest, hyperinflation, decreased cricosternal distance, resonant/hyperresonant percussion, quiet breath sounds, wheeze, cyanosis, cor pulmonale
give 3 complications of COPD
acute exacerbations ± infection (pneumococcal vaccine + yearly flu jab) cor pulmonale (RHF secondary to long standing lung disease/COPD) resp. failure *depression polycythaemia, pneumothorax, lung carcinoma
give 3 differential diagnoses of COPD
asthma, bronchiectasis, pulmonary embolism, congestive heart failure, pneumothorax
what would be the results of a lung function test in a COPD patient? other Ix?
reduced FEV1/FVC ratio (obstruction = FEV1/FVC <0.7) - NON-reversible, reduced PEFR. raised TLC. obstructive pattern. CXR = see other card for findings FBC - ?polycythaemia sputum culture if ?IECOPD ABG - hypoxia ± hypercapnia
what might you see on CXR in a COPD patient?
flattened diaphragm increased intercostal spaces hyperlucent lungs increased AP diameter
how would you conduct a steroid trial in COPD? what information would it give you?
patient given oral prednisolone for 2 wks. if FEV1 rises by >15% the COPD is steroid responsive - will benefit from long-term inhaled corticosteroids
how would you treat COPD?
Lifestyle: smoking cessation, annual influenza vax & pneumococcal vaccine
Bronchodilator therapy: short-acting beta2 or short-acting muscarinic antagonist (ipratropium or tiotropium) is first-line treatment
If no asthmatic features/steroid responsiveness features then: add LABA or LAMA
If asthmatic features/features suggesting steroid responsiveness: LABA + inhaled ICS. If patient remains breathless offer triple therapy e.g. LAMA + LABA + ICS.
describe non-pharmacological treatment of COPD
pulmonary rehab programmes. smoking cessation. low BMI = diet advice ± supplements. long-term oxygen therapy (LTOT).
describe the features of the airway obstruction seen in asthma
reversible. bronchial muscle constriction. mucosal swelling/inflammation. increased mucous production.
give 2 diseases associated with asthma
eczema, hay fever, any allergy - atopy
what is atopy?
ready development of IgE antibodies against common environmental antigens
explain the hygiene hypothesis
the idea that growing up in a clean environment may predispose towards IgE response, as there is no childhood exposure to allergens, bacteria etc - suppression of natural development of immune system
what is asthma? briefly explain the pathophysiology
- chronic inflammatory airway disease with intermittent obstruction and hyperreactivity - inflammation –> constriction, oedema, mucus hypersecretion - chronically this –> airway remodelling, airway hyperresponsiveness - acute = bronchoconstriction, chronic = airway hyperresponsiveness, airway remodelling = persistent obstruction - linked to IgE and mast cells - allergen triggers release of histamine, leukotrienes and TNFa - increased vascular permeability + hypersecretion of mucus = airway oedema - increased airway tone + smooth muscle responsiveness - later it’s eosinophil mediated - increased goblet sells etc.
give 3 precipitants of an asthma attack
cold air, exercise, emotion, allergens, infection, smoking, pollution, *NSAIDs, beta blockers
what investigations would you perform to diagnose asthma?
peak expiratory flow rate - diurnal variation, marked dip in PEFR in AM - variation of >15%. reversibility testing - increase in PEF or FEV1 >15% after salbutamol. spirometry = FEV1 <80% + FEV1/FVC = < 70% CXR = normal or hyperinflation skin prick test if want to test allergens
Asthma management in child less than 5?
- SABA
- (if not controlled on previous step OR newly-diagnosed with symptoms > 3/week or night-time waking) = SABA + 8-week trial of paediatric MODERATE dose ICS
- SABA + low dose ICS + leukotriene
- stop leukotriene and refer to paediatric asthma specialist
Stepwise management in 5 to 16 year old?
Newly diagnosed = SABA
Not controlled on previous step OR newly-diagnosed with symptoms > 3/week or night-time waking = SABA + low dose ICS
Then = SABA + low dose ICS + leukotriene
Then = SABA + low dose ICS + LABA
Then = SABA + moderate dose ICS
Then = SABA + high dose ICS
Note: this is pretty much the same as adult management
how would you manage an acute asthma attack?
OSHITME O2 (aim 94-98% sats) Salbutamol nebs Hydrocortisone IV (or oral pred if mild) Ipatropium bromide nebs with senior help: Theophylline Magnesium Escalate/ITU
how to beta 2 agonists work?
activate beta 2 receptors, inducing smooth muscle relaxtion in lungs.
describe what is happening in the lungs of a patient with extrinsic allergic alveolitis (hypersensitivity pneumonitis)
inhalation of allergens provokes a hypersensitivity reaction, with complement activation, granuloma formation and obliterative bronchiolitis.
give 2 causes of EAA (hypersensitivity pneumonitis)
Farmer’s lung. Bird-fancier’s lung - proteins in bird droppings. Malt-worker’s lung. Bagassosis/Sugar worker’s lung. humidifier fever. Mushroom workers. Cheese washer’s lung. Wine maker’s lung.
give 3 clinical features of EAA seen after exposure to the allergen
fevers, rigors, myalgia, dry cough, dyspnoea, crackles (no wheeze)
give 3 chronic features of EAA
increasing dyspnoea, weight loss, exertional dyspnoea, type I respiratory failure, cor pulmonale
what would been seen on CXR of a patient with EAA?
fibrosis/mottling of upper lobes and honeycomb lung
list some investigations that might be performed on a patient with EAA
bloods - neutrophilia, raised ESR CXR. lung function tests (reversible restrictive). broncheoalveolar lavage.
how would you treat EAA in an acute and a chronic situation?
acute - remove allergen, give O2 + oral prednisolone. chronic - avoid exposure (facemask), long-term steroids.
list 3 occupational lung diseases
EAA (e.g. Farmer’s lung). Coal worker’s pneumonconiosis. Silicosis. Asbestosis. Byssinosis. Berylliosis.
what causes the fibrosis seen in coal worker’s pneumoconiosis?
inhalation of coal dust particles - ingested by macrophages - these die and release their enzymes - fibrosis
what would a CXR show in coal worker’s pneumoconiosis?
round opacities in upper zone.
what causes progressive massive fibrosis? what are the features of this?
progression of coal worker’s pneumoconiosis. progressive dyspnoea, fibrosis + eventual cor pulmonale.
give some examples of jobs at risk of silicosis
metal mining, stone quarrying, sand blasting, pottery/ceramic manufacture
what do investigations show in silicosis?
CXR - diffuse miliary/nodular pattern in upper and mid-zones + egg shell calcification of hilar nodes. Spirometry - restrictive.
what disease are patients with silicosis at greater risk of?
TB
what are the clinical features of asbestosis?
dry cough, progressive dyspnoea. O/E - clubbing, diffuse, fine end-inspiratory crackles, pleural plaques. CT = ground glass opcaities.
what two diseases are asbestosis patients at greater risk of?
bronchial adenocarcinoma and mesothelioma
in what industries might workers get byssinosis? and for berylliosis?
byssinosis - cotton mill workers. berylliosis - beryllium-copper alloy used in aerospace industry, electronics, atomic reactors.
describe the pathogenesis of bronchiectasis
chronic infection of bronchi/bronchioles leads to inflamed, thickened and irreversibly damaged walls with permanent dilation. mucociliary transport mechanism is impaired.
give 2 of the main organisms involved in bronchiectasis
H influenza, Strep pneumonia, Staph aureus, Pseudomonas aeruginosa
give 3 possible causes of bronchiectasis
congenital - CF. post-infection - measles, pertussis, pneumonia, TB, HIV. Other - bronchial obstruction (tumour, foreign body), allergic bronchopulmonary aspergillosis (ABPA), hypogammaglobulinaemia, rheumatoid arthritis, UC.
give 3 clinical features of bronchiectasis
persistent cough, copious purulent sputum, intermittent haemoptysis, finger clubbing, coarse inspiratory crepitations, wheeze
give 2 possible complications of bronchiectasis
pneumonia, pleural effusion, pneumothorax, haemoptysis, cerebral abscess, amyloidosis
name 3 investigations you would carry out in bronchiectasis and their results
*sputum culture. *CT scan - shows the dilated airways. CXR - cystic shadows, thickened bronchial walls. spirometry - obstructive pattern. broncoscopy - locate site of haemoptysis, exclude obstruction, obtain samples.
how would you manage a patient with bronchiectasis?
physiotherapy - postural drainage. Abx - flucloxacillin for staph, amoxicillin for strep, tazocin for pseudomonas. bronchodilators - salbutamol nebulisers. Oral/inhaled corticosteroids.
what causes cystic fibrosis?
autosomal recessive mutation in the CF transmembrane conductase regulator gene on chromsome 7. defective chloride secretion and increased sodium absorption over airway epithelium - produces very viscous and sticky mucous.
give 3 respiratory symptoms of CF
cough, wheeze, recurrent infections, bronchiectasis, pneumothorax, haemoptysis, respiratory failure, cor pulmonale
give 3 extrapulmonary features of CF
pancreatic insufficiency - DM, steatorrhoea. intestinal obstruction, gallstones, cirrhosis, male infertility, osteoporosis, arthritis, vasculitis, sinusitis.
name 3 investigations you would carry out in CF and their results
sweat test - increased sodium and chloride secretion in sweat. faecal elastase - screens for pancreatic dysfunction. genetic screening for CF mutations. CXR - hyperinflation, bronchiectasis.
how would CF be managed?
physiotherapy. Abx for exacerbations. mucolytics - DNase (dornase alfa). bronchodilators. fat soluble vit supplements. pancreatic enzyme replacement.
what is sarcoidosis? what genes is it associated with?
multisystem granulomatous disorder of unknown cause. associated with HLA-DRB1 and DQB1 alleles.
what is seen on transbronchial biopsy in sarcoidosis?
infiltration of alveolar walls and interstitial spaces with mononuclear cells - later, granulomas
how does acute sarcoidosis present?
erythema nodosum ± polyarthralgia
give 3 pulmonary features of sarcoidosis?
dry cough, progressive dyspnoea, decreased exercise tolerance, chest pain.
give 3 extra-pulmonary features of sarcoidosis
lymphadenopathy, hepatomegaly, splenomegaly, uveitis, conjunctivitis, glaucoma, Bell’s palsy, neuropathy, meningitis, brainstem and spinal syndromes, space occupying lesions, erythema nodosum, cardiomyopathy, arrhythmias, hypercalcaemia, renal stones, pituitary dysfunction
what are the features of sarcoidosis on CXR?
bilateral hilar lymphadenopathy ± pulmonary infiltrates/fibrosis
list some differential diagnoses for bilateral hilar lymphadenopathy
sarcoidosis, infection (TB, mycoplasma), malignancies, silicosis, EAA
what investigations would you carry out, apart from CXR, in sarcoidosis, and what might they show?
SERUM ACE is raised. lung function - restrictive pattern, reduced TLC, reduced FEV1/FVC ratio. tissue biopsy - non-caseating granuloma.
how would you treat sarcoidosis?
if symptomatic - corticosteroids (prednisolone). if severe - IV methylprednisolone or methotrexate.
what is the underlying pathology of idiopathic pulmonary fibrosis?
disruption of alveolar epithelium and basement membrane activates inflammation. fibroblasts convert to myofibroblasts - synthesise collagen and aggregate to form fibrotic foci.
give 3 symptoms and 3 signs of idiopathic pulmonary fibrosis
symptoms - dry cough, exertional dyspnoea, malaise, weight loss, arthralgia. signs - cyanosis, finger clubbing, fine end-inspiratory crepitations.
what investigations would you carry out in idiopathic pulmonary fibrosis? what do they show? which one is needed for diagnosis?
CXR - reticular shadowing, decreased lung volume, bilateral lower zone HRCT = ground glass opacification, honeycombing if severe, reticular pattern. lung function tests - restrictive pattern, increased FEV1/FVC ratio. need a lung biopsy to diagnose **ask them about occupation!*
management of idiopathic pulmonary fibrosis
MDT! 6/12 assessment for pulmonary rehab. supportive = O2 therapy, physio, exercise/wt loss, vaccinations, smoking cessation. pirfenidone = antifibrotic drug, inhibits TGFB (transforming growth factor beta) collagen synthesis. acute exacerbation = admit, high dose pred ± cytotoxic, check for infective cause. lung transplant if extreme median survival only 2-5yrs!
name 3 causes of pulmonary hypertension
hereditary, SLE, systemic sclerosis, rheumatoid arthritis, drugs, HIV, portal hypertension, schistosomiasis, chronic haemolytic anaemia, COPD, pulmonary fibrosis, mitral valve disease, sarcoidosis
define pulmonary hypertension
disease of small pulmonary arteries characterised by vascular proliferation and remodelling - progressive increase in pulmonary vascular resistance. elevated pulmonary artery pressure (mean pulmonary artery pressure >25mmHg at rest, pulmonary capillary wedge pressure <15mmHg) poor prognosis as most get secondary right ventricular failure (cor pulmonale) types = idiopathic, hertable, secondary.
give 3 clinical features of pulmonary hypertension
exertional dyspnoea, lethary, peripheral oedema, loud pulmonary second sound, right parasternal heave. Graham Steel murmur = pulmonary regurg murmur (high pitched early diastolic) RHF signs (oedema, RV heave, ascites, pulsatile hepatomegaly, raised JVP)
give 3 signs that pulmonary hypertension has progressed to right heart failure (cor pulmonale)
elevated JVP, hepatomegaly, pulsatile liver, peripheral oedema, ascites, pleural effusion
what is the eventual end treatment of primary pulmonary hypertension?
heart and lung transplant
what 3 investigations would you carry out in pulmonary hypertension and what would they show?
CXR - enlarged proximal pulmonary arteries which taper distally (pruning) ECG - RVH, P pulmonale (peaked P waves) transthoracic echo - RV dilation/hypertrophy r heart catheterisation (Swan-Ganz) - measures pressures.
how would you treat pulmonary hypertension?
CCB (nifedipine or amlodipine) or sildenafil (PDE5 inhibitor, augments pulmonary vascular response to nitric oxide) warfarin (target INR 21.5-2.5) - reduce thrombosis risk. furosemide/salt reduction - oedema. lifestyle - low level, graded exercise. supp. O2 if needed.
what is a haemothorax?
blood in the pleural space
what is a chylothorax?
chyle (lymph + fat) in the pleural space
what is an empyema?
pus in the plerual space
what is a pleural effusion? define transudates and exudates
excessive fluid in the pleural space (potential space between visceral and parietal pleura) transudates = low protein content (< 30g/L) exudates = high protein content (>30)
give 3 causes of a transudate pleural effusion
cardiac failure, constrictive pericarditis, fluid overload, cirrhosis, nephrotic syndrome, Meig’s synd (R pleural effusion + ovarian fibroma + ascites) increased venous pressure and fluid overload = disruption of hydrostatic and oncotic forces across pleural membranes (hypoproteinaemia can cause it too)
give 3 causes of an exudate pleural effusion
pneumonia, TB, rheumatoid arthritis, SLE, bronchogenic carcinoma, malignant metastases, lymphoma, mesothelioma, lymphangitis carcinomatosis. Dressler’s synd (comp. of MI) increased permeability of pleural capillaries secondary to infection, inflammation or malignancy.
what would you hear on auscultation of a patient with a pleural effusion?
on side of the effusion: unilateral reduced chest expansion, stony dull percussion note, diminished breath sounds. if really large effusion - trachea deviates away.
what investigations would you perform to diagnose a pleural effusion? what would they show?
CXR - small effusions= blunted costophrenic angles. larger = water-dense shadows with concave upper borders. 200ml effusion visible on PA, 50ml on lateral view. diagnostic pleural aspiration/thoracocentesis (US guided) - send for clinical chemistry, bacteriology and cytology. (if unilateral and clinical picture suggests transudate just Rx cause instead of bothering with aspirating)
how would you treat a symptomatic pleural effusion?
pleural tap, repeat if necessary - up to 1.5l (otherwise fluid shift + pulmonary oedema). can use chest drain for controlled removal. don’t tap if transudates!!
learn spirometry graphs!!
