Respiratory Flashcards
Why do we measure lung function?
Evaluation of the breathless patient.
-screening for COPD or occupational lung disease
-lung cancer-fitness for treatment
-pre-operative assessment
-disease progression and treatment response
monitoring of drug treatment
pulmonary complications of systemic disease
Potential pitfalls of spirometry?
- Appropriately trained technician
- Effort and technique dependent
- Patient frality
- Pain, patient too unwell
What is tidal volume?
During normal quiet breathing the amount of air that moves in and out of the lungs with each breath. Normally 500ml.
What is inspiratory reserve volume?
The volume of air that can be inspired beyond the tidal volume.
What is the expiratory reserve volume?
The volume of air that can be expired after a tidal expiration.
What is the residual volume?
Volume of air (approx. 1200ml) that remains in the lungs after the most strenuous expiration. The residual volume prevents atelectasis.
What is the vital capacity?
The total amount of exchangeable air. VC=TV+IRV+ERV.
What is total lung capacity?
The sum of all lung volumes and is normally around 6L in males.
What is FEV1?
Forced expiratory volume in one second. The maximal volume of gas, which can be expired from the lungs in the first second of a forced expiration from full inspiration.
What is FVC?
Forced vital capacity. Maximal volume of gas, which can be expired from the lungs during a forced expiration from full inspiration.
What is the FEV1/FVC(%)?
Proportion of the FVC, which can be expelled during the first second of expiation-expressed as a percentage. Derived by calculating FEV1/FVC x 100. If less than 70=obstructive airflow.
What is the peak expiratory flow?
The maximum expiratory flow that can be sustained for a minimum of 10msecs.
What is ventilation?
Refers to the movement of gas into and out of the alveoli. Expressed as V.
What is perfusion?
Refers to the blood flow through the pulmonary capillaries. Expressed as Q.
What is COPD?
Chronic obstructive pulmonary disease. Largely irreversible airflow obstruction, includes emphysema and chronic bronchitis. Smokers disease. Alveolar destruction.
What is asthma?
Recurrent reversible airflow obstruction due to inflammatory changes in the airways. Bronchial hyper-reactivity. Causes wheezing, coughing, hyperinflation.
What are xanthines?
Bronchodilators. Narrow therapeutic window, many drug interactions. Cause cause cardiac dysrhythmias and seizures. Use of xanthines has declined, but still used in lower doses for anti-inflammatory effects.
What is mild COPD?
> 80% FEV1
What is moderate COPD?
50-80% FEV1
What is severe COPD?
30-50% FEV1
What is very severe COPD?
<30% FEV1
In reversibility testing, what is suggestive of asthma?
After having given salbutamol, 15% AND 400ml reversibility of FEV1.
Obstructive lung disease
FEV1/FVC ratio less than 70%. Asthma and COPD.
Restrictive lung disease
FEV1 and FVC reduced but FEV1/FVC ratio over 70 (normal). Causes interstitial lung disease, obesity, chest wall abnormality.
What are causes of obstructive lung disease?
Asthma and COPD
What are causes of restrictive spirometry disease?
Interstitial lung disease, chest wall abnormality, previous pneumonectomy, neuromuscular disease, obesity, poor effort/technique.
What is sarcoidosis?
A multi or single organ disease of unknown aetiology which is characterised by ‘non-necrotising Granulomatous inflammation’. Diagnosis of exclusion.
What are the lung signs of sarcoidosis?
Stage 1-bilateral hilar lymphadenopathy without infiltration
Stage 2- bilateral hilar lymphadenopathy with infiltration
Stage 3- infiltration alone.
Stage 4-fibrotic bands, bullae, hilar retraction, bronchiesctasis and diaphragmatic tenting.
What causes pulmonary fibrosis?
Smoking, radiation, post infection, drugs, other chronic conditions eg. RA.
Idiopathic pulmonary fibrosis
Age>50, M:F 2:1, progressive breathlessness, bibasilar crackles, clubbing, peripheral interstitial pattern. Subpleural honeycombing. Hacking dry cough, fatigue and weakness, appetite and weight loss.
What is a ‘fibroblastic focus’?
Histological feature of UIP (usual interstitial pneumonia). Temporal heterogeneity is also a feature.
Smoking predisposes you to what types of lung cancer?
Squamous and small cell lung cancer.
Signs and symptoms of lung cancer
Cough, haemoptysis, SOB, chest pain, weight loss, general malaise.
How do you measure transfer factor in the lungs?
Single breath of a very small concentration of carbon monoxide (CO has a very high affinity to Hb). Measure concentration in expired gas to derive uptake in the lungs.
What affects ‘transfer factor’?
Alveolar surface area, pulmonary capillary blood volume, haemoglobin concentration, ventilation perfusion mismatch.
When is ‘transfer factor’ reduced?
In emphysema, interstitial lung disease, pulmonary vascular disease and anaemia (increased in polychthaemia.
What are the 2 ways to measure residual volume?
Cannot be measured by spirometry.
1) Helium dilution (inspire known quantity of inert gas).
2) Body plethysmography (respiratory manoevures in a sealed box lead to changes in air pressure-can derice lung volumes).
What is oximetry?
Non-invasive measurement of saturation of haemoglobin by oxygen.
What are the main causes of hypoxaemia?
- Hypoventilation eg. drugs, neuromuscular disease.
- Ventilation/perfusion mismatch eg. COPD, pneumonia
- Shunt eg. congenital heart disease
- Low inspired oxygen
What is a ‘shunt’?
An extreme form of V/Q mismatch where blood bypasses the lungs entirely. Does not correct with oxygen administration.
What is the treatment for exacerbation of COPD?
O-Oxygen-24% aiming for SpO2 of 88-92%
N-Nebulised salbutamol and ipratropium bromide
A-Amoxicillin (oral)
P-Predinosolone
Definition of respiratory failure
PO2 less than 8kPa at sea level.
What is Cor Pulmonale?
Clinical syndrome of right sided heart failure secondary to lung disease and salt and water retention leading to peripheral oedema. Treatment is diuretics to control peripheral oedema.
What are the signs of Cor Pulmonale?
Peripheral oedema, raised jugular venous pressure, a systolic parasternal heave, loud pulmonary second heart sound.
What are the effects of cigarettes smoking on the respiratory system?
- Cilial motility is reduced
- Airway inflammation
- Hypertrophy of Goblet cells
- Increased protease activity, decreased anti-proteases
- Oxidative stress
- Squamous metaplasia=higher risk of lung cancer.
What is chronic bronchitis?
Clinical syndrome of COPD. The production of sputum on most days for at least 3 months in at least 2 years.
What is emphysema?
Abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles.
Centri-acinar emphysema
Damage around respiratory bronchioles. More in the upper lobes.
Pan-acinar emphysema
Uniformly enlarged from the level of terminal bronchiole distally. Can get large bullae. Associated with alpha1 anti-trypsin deficiency.
What are the 3 types of emphysema?
1) Centriacinar (causes airflow obstruction)
2) Panacinar (causes airflow obstruction)
3) Paraseptal (doesn’t cause airflow obstruction)-can lead to pneumothorax.
What is the mechanism of airflow obstruction in COPD?
Loss of elasticity and alveolar attachments due to emphysema-airways collapse on expiration. Causes air trapping and hyperinflation- increased work of breathing- breathlessness.
Type 2 respiratory failure
Blue bloater-low respiratory drive. Low oxygen, high Co2. Cyanosis, warm peripheries, flapping tremor, right heart failure.
Type 1 respiratory failure
Pink puffer-high respiratory drive. Low O2 and low CO2. Pursed lip breathing, uses accessory muscles, wheeze, tachypnoea, desaturates on exercise.
What are dermatophytes?
Fungi that cause common infections of skin, nails and hair. Only colonise keratinised areas.
Name some systemic fungal infections
1) Fungal meningitis (Crytococcus neoformans)
2) Aspergillosis of the lungs (Aspergillus fumigatus)
3) Pneumocystis pneumonia (pneumocystis jiroveci)
What causes fungal meningitis?
Crytococcus neoformans
What can Aspergillus fumigatus cause?
1) Allergic bronchopulmonary aspergillosis (ABPA)
2) Invasive pulmonary aspergillosis (IPA)
3) Aspergilloma
What is the treatment for pneumonia caused by Pneumocystis jiroveci?
Trimethoprim-sulfamethoxazole.
What is the largest class of antifungal agents?
‘Azoles’ eg. Miconazole and Clotrimazole. Many applications.
MOA of ‘Azoles’
Azoles are inhibitors of 14-methlysterol alpha-demethylase. This is important enzyme in the ergosterol pathway. Ergosterol is a key component of fungal plasma membrane.
MOA of Amphotericin B
Forms a channel in the fungal membrane leading to leakage of intracellular cations. Does this by binding to ergosterol and intercalating into cell membrane. Hydrophobi side of amphotericin B interacts with ergosterol.
Amphotericin B
Anit-fungal agents. Has to be given IV, at high levels interact with cholesterol. Best given as ambisome- part of a liposome. Allows better movement through body and reduced toxicity.
MOA of amoxicillin
Inhibits bacterial cell wall synthesis.
MOA of clarithryomycin
Bacteriostatic drug inhibiting protein synthesis.
MOA of doxycyline
Bacteriostatic drug-inhibits action of amino acids to growing peptide.
MOA of corticosteroids in an asthma attacke
Bind to activated glucocorticoid receptors to suppress multiple pro-inflammatory genes that are activated in asthmatic airways reversing histone acetylation.
MOA of B2 agonist
Bronchodilator. Acts on B2 receptors to stimulate adenyl cyclase to increase intracellular cAMP-relaxation of bronchial smooth muscle.
MOA of anti-muscarinics eg. Ipatropium bromide
Bronchodilator. Inhibition of cholinergic M1 and M3 receptors in the lung-reduction in cGMP and inhibition of parasympathetic-mediated bronchoconstriction.
MOA of methylxanthines eg. Theophylline
Non-selective inhibition of phosphodiesterase-increased intracellular cAMP-bronchial smooth muscle relaxation. Immunomodulatory action-improved mucociliary clearance and anti-inflammatory effect.
MOA of leukotriene receptor antagonists eg. Motelukast
Bind with high affinity to cysteinyl leukotriene receptor (CysLT1) inhibiting action of LTD4 in smooth muscle cells of the airway and airway macrophages-reduced airway oedema and smooth muscle contraction.
Obstructive sleep apnoea defintion
Recurrent episodes of partial or complete upper (pharyngeal) airway obstruction during sleep, intermittent hypoxia and sleep fragmentation.
Obstructive sleep apnoea syndrome
Manifests as excessive daytime sleepiness.
What is retrognathia?
A type of malocclusion which refers to an abnormal posterior positioning of the maxilla or mandible, particularly the mandible, relative to the facial skeleton and soft tissues.
Symptoms of OSA
Snorer, witnessed apnoeas, disruptive sleep, unrefreshed sleep, daytime tiredness, fatigue, low mood, poor concentration.
Assessment of OSA
Weight, BMI, BP, neck circumference (>40cm), craniofacial appearance (posterior mandible, small jaw?), tonsils, nasal patency.
What is the mallampati score?
Used to assess ease of intubation in a patient or to assess for OSA.
Class I-Complete visualisation of soft palate.
Class II-Complete visualisation of uvula.
Class III- Visualisation of bottom of uvula.
Class IV-Soft palate not visible at all.
Define apnoea
Cessation, or near cessation of airflow leading to a 4% oxygen desaturation lasting more than or equal to ten seconds.
Define hypopnoea
Reduction of airflow to a degree insufficient to meet the criteria for an apnoea.
Define respiratory effort related arousals
Arousals associated with a change in airflow that does not meet the criteria for apnoea or hypopnea.
Apnoea-hypopnoea index (AHI)
Calculated by adding the number of apnoeas and hypopnoeas and dividing the total sleep time (in hours). AHI> or equal to 15 suggests OSA. Or 5-15 with compatible symptoms.
Oxygen-desaturation index
Number of times per hour of sleep that the SpO2 falls more than or equal to 4% from baseline.
CPAP
Continuous Positive Airways Pressure. Treatment for OSA. Splints airway open, stops snoring and sleep fragmentation. A mask over the nose gently directs air into the throat to keep the airway open.
What causes bilateral hilar adenopathy?
1) Sarcoidosis
2) Lymphoma
3) TB
4) Malignancy
What are the 3 causes of a ‘white out’ on CXR?
1) Pleural effusion
2) Pneumonectomy
3) Lung collapse
What is a pneumothorax?
Air within the plural cavity. Can be traumatic, iatrogenic or spontaneous.
Causes of traumatic pneumothorax
- Stabbing
- Fractured rib
Causes of iatrogenic pneumothorax
Normally heals in 72 hours
- CT guided lung biopsy
- Pleural aspiration
Spontaneous pneumothorax
Primary-young patient, no underlying lung disease
Secondary- underlying lung disease (COPD, cystic fibrosis).
How do you manage a tension pneumothorax?
Immediately insert venflon 2nd intercostal space midclavicular line to relieve pressure.
Tension pneumothorax
A medical emergency. Leads to increased intrapleural pressure-venous return is impaired, cardiac output and blood pressure falls. Can lead to cardiac arrest without intervention.
Pathophysiology of primary pneumothorax
Development of subpleural blebs/bullae at apex of lung. Spontaneous rupture leads to tear in visceral pleura. Air flows from airways to pleural space down a pressure gradient. Elastic lung then collapses.
When would you consider surgical pleurodesis to treat a pneumothorax?
If it is the 2nd pneumothorax on the same side or first contralateral event.
Risks factors for lung cancer
Smoking, environmental tobacco smoke, ionising radiation (radon, uranium), air pollution, asbestos, fibrosing conditions of the lungs, human papilloma virus.
Signs and Symptoms of lung cancer
Cough, haemoptysis, SOB, chest pain, weight loss/anorexia, malaise.
Central lung cancer signs
Haemoptysis, bronchial obstruction -SOB, retention pneumonia, and cough.
Peripheral lung cancer signs
May have few symptoms, pain if pleura or chest wall involved.
Where can lung cancer spread to locally?
Pleura, hilar lymph nodes, adjacent lung tissue, pericardium, mediastinum.
If you get lung cancer spread to the mediastinum, what can happen?
Superior vena cava obstruction, recurrent laryngeal nerve, phrenic nerve.
Small cell carcinoma of the lung
Most aggressive form of lung cancer, metastasises early and wide. Often initially response so chemo but often relapse. Oval to spindle shaped cells, scant cytoplasm, nuclear moulding.
What are the types of non-small cell carcinoma?
- Squamous cell carcinoma
- Adenocarcinoma
- Large cell carcinoma
- Other
Squamous cell carcinoma of the lung
Arises centrally from major bronchi. Slow growing and metastasises late. May undergo cavitation and block bronchi leading to retention pneumonia or collapse. A malignant epithelial tumour showing keratinization and/or intercellular bridges.
Define ‘lepidic’
Lepidic growth adenocarcinoma is defined as tumor cells proliferating along the surface of intact alveolar walls without stromal or vascular invasion pathologically.
Adenocarcinoma of the lung
Common tumour in females. Also seen in non-smokers. 2/3 arise peripherally, sometimes in relation to scarring.. Can be glandular, solid, papillary or lepidic, mucin production.
Large cell caricnoma
Diagnosis of exclusion. An undifferentiated malignant epithelial tumour that lacks the cytological features of SCLC and glandular or squamous differentiation.
Carcinoid tumour
Tumour of neuroendocrine cells. Central or peripheral. Typical or atypical. Can metastasise but much better prognosis than other conventional lung cancers.
Name some molecular targets identified for lung cancer treatment.
EGFR, 4-Anaplastic lymphoma kinase fusion gene, PDL1
Deletions in what exon are commonly associated with good response to EGFR inhibitors in lung cancer treatment?
Exon 19
How do you test for ALK fusion?
FISH or IHC for protein product.
What is mesothelioma?
Primary pleural tumour (also occurs in peritoneum, pericardium, tunica vaginalis of testes). Almost always due to asbestos exposure.
What is a ‘Pack year’ in relation to cigarettes?
1 pack year= 20 cigarettes/day for 1 year.
You would consider the diagnosis of COPD in people over 35 years old, smoker and ex-smokers with:
- Exertional breathlessness
- Regular sputum production
- Wheeze
- Chronic cough
- Frequent winter ‘bronchitis’
What signs on COPD might you see on a CXR?
Hyperinflation of lungs (more anterior ribs on show), flattened hemidiaphragms, bullae, pruned blood vessels-large proximal vessels. Heart can look longer and thinner due to increased intrathoracic pressure.
What is polycythaemia?
An abnormally increased concentration of haemoglobin in the blood, either through reduction of plasma volume or increase in red cell numbers. It may be a primary disease of unknown cause, or a secondary condition linked to respiratory or circulatory disorder or cancer. Can been seen in COPD if chronic hypoxaemia.
What is a Ghon complex?
Calcified areas of the lungs seen on chest x-ray, typical of TB.
Which of the antibiotic used in TB can cause visual disturbance?
Ethambutol can cause visual disturbance and deterioration.
What are the clinical components of COPD?
Chronic bronchitis and emphysema.
What is chronic bronchitis?
Production of sputum on most days for at least 3 months in at least 2 years (when other causes of chronic cough have been excluded).
What is emphysema?
Abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles.
Pink puffer
High respiratory drive, low PaO2 and low PaCO2, type 1 respiratory failure. Pursed lip breathing, uses acessory muscles.
Blue bloater
Low respiratory drive, Low PaO2 and high PaCO2, type 2 respiratory failure. Confusion, drowsiness, cyanosis. Loss of central sensitivity to CO2 and reliance on hypoxic drive to stimulate breathing.
What is the definition of an exacerbation of COPD?
Sustained worsening of the patients symptoms from their usual state which is beyond day-to-day variations, and is acute in onset. Commonly reported symptoms are worsening breathlessness, cough, increased sputum production and change in sputum colour. The change in these symptoms often necessitates a change in mediation.
What are the clinical signs of pleural effusion?
- Decreased breath sounds
- Stony dull to percussion
- Decreased tactile or vocal fremitus
CXR appearance of pleural effusions
Need >300ml of fluid to be present to see on CXR. Uniformly white appearance. Blunting of costophrenic and cardiophrenic angles. A meniscus at upper edge.
When is long-term oxygen therapy appropriate for a COPD patient?
Based on ABGs. PaO2 of less than 7.3 if they are well- indication for LTOT. Have to be a non-smoker for at least 3 months. or PaO2 of 7.3-8.0kPa AND any of secondary polycythaemia, nocturnal hypoxaemia, peripheral oedema, pulmonary hypertension.
What are features of a life threatening asthma attack?
PEF <33% best or predicted SpO2 <92% PaO2 <8kPa Normal PaCO2 (4.6-6kPa) Silent chest Cyanosis Poor respiratory effort Arrhythmia Exhaustion, altered conscious level
What is asthma?
A chronic inflammatory condition of the airways that causes recurrent episodes of wheezing, breathlessness, chest tightness and cough, particularly at night and/or early morning. These symptoms are usually associated with widespread but variable bronchoconstriction and airflow limitation that is at least partly reversible, either spontaneously or with treatment.
What are the key features of asthma?
- Increased airways hyper-responsiveness to a variety of stimuli resulting in episodic bronchoconstriction
- Inflammation of the bronchial walls
- Increased mucus secretion
Atopic asthma
Extrinsic asthma. Usually starts in childhood. Atopic individuals have a raised total serum IgE and the presence of specific IgE against common aeroallergens.
Non-atopic asthma
Intrinsic asthma. Often starts in middle age- possible triggers include respiratory viruses and air pollutants.
Causes and triggers of asthma
Environmental exposure to allergen, occupational sensitisers, viral infections, atmospheric pollution, drugs, irritant vapours and fumes, exercise, cold air.
Pathological features in asthmatic airways
Increased airway inflammatory cells Plasma exudation Oedema Smooth muscle hypertrophy Mucus plugging Shedding of epithelium
What is ‘stridor’?
A high-pitched, wheezing sound caused by disrupted airflow.
Serum osmolal gap=
measured osmolality- calculated osmolality
Calculated osmolality=
2 x (Na+ + K+) + urea + glucose (all in mmol/L)
Respiratory acidosis
pH less than 7.35 with a PaCO2 greater than 45mmHg.
Respiratory alkalosis
pH greater than 7.45 with a PaCO2 less than 35mmHg,
Metabolic acidosis
pH of less than 7.35 and a bicarbonate level of less than 22mEq/L.
Metabolic alklaosis
pH greater than 7.45 and bicarbonate greater than 26mEq/L.
PaO2
Partial pressure of oxygen that is dissolved in arterial blood. Normal range is 80 to 100mmHg.
SaO2
Arterial oxygen saturation. Normal range is 95-100%.
PaCO2
Amount of carbon dioxide dissolved in arterial blood. Normal range is 35 to 45mmHg.
HCO3
Calculated value of the amount of bicarbonate in the bloodstream. Normal range is 22-26mEq/litre.
What is bilateral hilar adenopathy and what causes it?
Bilateral enlargement of the lymph nodes of pulmonary hila. Caused by sarcoidosis, lymphoma, TB, malignancy.
What is Golden S Sign?
Golden S-sign is seen on both PA chest radiographs and on CT scans. It is named because this sign resembles a reverse S shape, and is therefore sometimes referred to as the reverse S-sign of Golden. Typical of right upper lobe collapse.
