Respirology Flashcards
What happens to the total lung capacity and the residual volume in obstructive disease and restrictive disease?
The TLC and RV is increased in obstructive disease, and decreased in restrictive disease.
What happens to the FEV/FVC ratio in obstructive and restrictive lung disease?
In obstructive disease, the FEV/FVC ratio is decreased.
In restrictive disease the FEV/FVC ratio is increased or normal.
What happens to the residual volume/total lung capacity in obstructive disease? What happens in restrictive disease?
In obstructive disease the RV/TLC in increased or normal. In restrictive disease, it is normal.
What condition produces these PFT results?
Lung volumes normal
FEV/FVC normal
DLco decreased
Aneamia or pulmonary vascular disease
What condition produces these PLF results?
Reduced FEV/FVC <80% predicted. No change after giving a bronchodilator
High TLC and low DLco
Emphysema
What condition produces the following PFTs?
FEV/FVC <80% predicted, no change after bronchodilators
Normal TLC
Normal DLco
Chronic bronchitis
What condition do these Pulmonary lung function tests suggest?
FEV/FVC <80% predicted
Improvement with bronchodilators
Asthma
What condition do these PFT results suggest? Reduced FEV1 FEV/FVC >80% predicted Low TLC Low RV Low DLco
Interstitial lung disease
What condition do these PFT results suggest? Low FEV1 FEV/FVC >80% Low TLC Low RV DLco normal FRC low Normal RV
Chest wall disease
What do these PFT results suggest? Low FEV1 FEV1/FVC >80% Low TLC Low RV Low FRC Increased RV
Neuromuscular disease
Diffusion capacity for carbon monoxide DLco decreases with what four factors?
Decreased surface area (eg emphysema)
Decreased heamoglobin
Interstitial lung disease
Pulmonary vascular disease
List four factors that cause the DLco to increase?
Asthma
Pulmonary haemorrhage
Polycythemia
Increased pulmonary blood volume
What is consolidation? What signs suggest consolidation? What conditions cause consolidation?
Consolidation ‘airspace disease’ is an area of normally compressible lung tissue that has filled with liquid, a condition marked by induration or a normally aerated lung.
Signs include air bronchi grams, silhouette sign, and less visible blood vessels.
Common DDxs include:
Acute: water (pulmonary oedema), pus (pneumonia), blood (haemorrhage)
Chronic: neoplasm (lymphoma), inflammatory(eosinophilic pneumonia), chronic infection (TB, fungal)
What is a reticular pattern? What are the signs of a reticular pattern? What are the common DDx’s for a CXR with a reticular pattern?
A reticular pattern indicates interstitial disease. A reticular pattern is an opacity of crisscrossing thin well defined linear densities, ‘net like’ or ‘honeycomb’.
Signs include increased pulmonary markings or honey combing.
DDx’s are interstitial lung disease (IPF, CVD, asbestos, drugs)
What signs indicate a nodules pattern on X-ray? What are the common DDx’s for nodular X-rays?
Signs are cavitory vs non cavitory nodular x rays.
Cavitory DDx’s include neoplasm (primary vs metastatic lung cancer), infectious (TB, fungal), and inflammatory (Wegeners, RA)
Non cavitory DDx’s include all of those above, as well as sarcoid, kaposis sarcoma (in HIV), and silicosis.
How do you calculate the anion gap? What is a normal anion gap?
[Na+] - [Cl-] - [HCO3-] = 10-15 mmol/L.
If the anion gap is increased, is the change in the anion gap the same as the change in bicarbonate? If not, consider a mixed metabolic picture.
What is the DDx’s for respiratory acidosis do to decreased PaCO2 due to hypo ventilation respiratory centre depression?
Shows a decreased resp rate.
- drugs (anaesthesia, sedatives, narcotics)
- trauma
- increased ICP
- encephalitis
- stroke
- central apnoea
What is the differential diagnosis of respiratory acidosis due to increased PaCO2 due to hypoventilation from decreased vital capacity?
This is caused by neuromuscular diseases.
- myasthenia gravis
- guillame barre
- poliomyelitis
- muscular dystrophies
- ALS
- myopathies
- chest wall disease (obesity, kyphoscoliosis)
What are the DDx’s of respiratory acidosis from pulmonary disease?
Obstructive disease: asthma, COPD
Parenchymal disease: COPD, pulmonary oedema, pneumothorax, pneumonia, interstitial lung disease (late stage), acute respiratory distress syndrome.
What is the differential diagnoses for respiratory alkalosis due to a decreased PaCO2 secondary to hyperventilation as a result of hypoxemia.
Pulmonary disease (pneumonia, oedema, PE, interstitial fibrosis)
Severe aneamia
Heart failure
High altitude
Or mechanical hyperventilation
What are the differential diagnoses for respiratory alkalosis due to decreased PaCO2 from hyperventilation as a result of hyperventilation due to respiratory centre stimulation?
CNS disorders Hepatic failure Gram negative sepsis Pregnancy Anxiety Pain Drugs (ASA, progesterone, theophylline, catecholamines, psychotropics)
What is the effect of acidosis and alkalosis on potassium?
Acidosis leads to hyperkalemia, alkalosis leads to hypokaleamia.
How do you calculate the alveolar arteriole gradient? What should the Aa gradient be on room air?
Aa gradient = PaO2 alveolar - PaO2 arteriole = [150 - 1.25(PaCO2))] - PaO2
A normal Aa is <15mmHg and increases with age.
What causes hypoxemia with a normal Aa gradient and increased PaCO2?
HypoventilTion
What causes hypoxemia with a normal Aa gradient and normal PaCO2?
Low FiO2 (eg altitude)
What causes hypoxemia, with a high Aa that does not improve after giving 100% O2?
- shunt
- atelectasis
- intraalveolar filling (eg pulmonary oedema, pneumonia)
- intra cardiac shunt
- vascular shunt within lungs
What causes hypoxemia with an increased Aa gradient that improves with oxygen?
V/Q mismatch Airway disease (asthma, COPD) Interstitial lung disease Alveolar disease Pulmonary vascular disease
What is asthma?
Asthma is a chronic inflammatory disorder of the airways resulting in episodes of reversible bronchi spasm causing airflow obstruction. It is associated with reversible airflow limitation and airway hyperresponsiveness to endogenous or exogenous stimuli.
Px with dyspnoea, wheezing, chest tightness, cough, sputum, respiratory distress and symptoms worse at night.
There is an improvement of >12% of FEV after giving bronchodilators.
What are the causes of obstructive Airways disease?
Asthma, COPD, bronchiectasis, cystic fibrosis and inhalation of a foreign body
What is chronic obstructive pulmonary disease?
COPD is the progressive development of airway obstruction that is not completely reversible. Patients typically have periodic exacerbations characterised by weight loss, lung hyperinflation, and gas trapping. There are 2 subtypes characterised by chronic bronchitis and emphysema. These subtypes usually coexist to various degrees.
There is a gradual decrease in FEv1 over time with episodes of acute exacerbations.
Define chronic bronchitis
Chronic bronchitis is a productive cough on most days for at least 2 consecutive years. The obstruction is due to the narrowing of the airway lumen by mucosal thickening and excess mucous.w
What is emphysema?
Emphysema is the dilation and destruction of air spaces distal to the terminal bronchiole without obvious fibrosis. There is decreased elastic recoil of the lung parenchyma causing decreased expiratory driving pressure, airway collapse, and air trapping.
There are two types of emphysema.
Centracinar emphysema is when the respiratory bronchioles are predominantly affected. The typical form seen in smokers primarily affects upper lung zones.
Panacinar emphysema is where the respiratory bronchioles, alveolar ducts, and alveolar sacs are affected. This accounts for less than 1% of emphysema cases such as in a1 antitrypsin deficiency, and primarily affects the lower lobes.
What are the presenting symptoms of bronchitis? What are the signs?
Bronchitis presents with ‘blue bloater’ signs and symptoms
- chronic productive cough with purulent sputum and heamoptysis
- initially only mild dyspnoea
- cyanosis (hypoxemia and hypercapnia)
- peripheral oedema for RVF (Cor pulmonale)
- crackles, wheezes
- prolonged obstructive expiration
- frequently obese
What are the signs and symptoms of someone presenting with emphysema?
Emphysema typically presents with symptoms of a ‘pink puffer’
- dyspnoea (+/- exertion)
- tachypnoea and decreased excercise intolerance
- minimal cough
- pink skin
- pursed lip breathing and acessory muscle use
- cachetic appearance due to anorexia and increased work of breathing
- hyperinflation/barrel chest, hyperresonant percussion
- decreased breath sounds
- decreased diaphragmatic excursion
How do you treat stable COPD?
COPDERS
C- Inhaled corticosteroids (poor response in COPD)
O- Oxygen. Home oxygen prevents Cor pulmonale and can decrease mortality
P- Prevention (vaccines for pneumococcus and influenza, smoking cessation)
D- Dilators. No mortality benefit. LAch (triotropium bromide) & SACh (ipratropium bromide) >SABA, LABA,
E- Experimental: lung volume reduction, lung transplant
R- Rehabilitation: patient education, eliminate irritant/allergens, excercise rehabilitation to improve physical endurance
What are the complications of COPD?
Chronic hypoxemia, pulmonary hypertension from vasoconstriction, and or pulmonale
What is an acute exacerbation of COPd and what are its causes?
An acute exacerbation of COPD is a sustained worsening of dyspnoea, cough, or sputum production leading to an increased use of medications. Acute exacerbations of COPD may be triggered by a viral URTI, bacterial infection, air pollution, CHF, PE, or an MI.
How do you manage a acute exacerbation of COPD?
Give oxygen. For CO2 retainers target 88-92%
Bronchodilators SABA + ACh
Systemic corticosteroids eg prednisone
Give antibiotics if sputum is purelent.
Rehabilitation for post exacerbation.
Consider ICU admission for life threatening exacerbations and ventilatory support (NIPPV, BiPAP, mechanical ventilation)
What is the MMRC scale?
Modified medical research scale for dyspnoea
What is bronchiectasis?
Bronchiectasis is irreversible dilatation of the airways due to destruction of the airways wall resulting from persistently infected mucous. The most common pathogen to cause this is pseudomonas aueroginosa. Bronchiectasis usually affects the medium sized airways.
What are the different causes of bronchiectasis?
- Obstruction: tumour, foreign body, thick mucous
- Post Infection: pneumonia, TB, measles, pertussis, allergic bronchopulmonary aspergillosis, mycobacterium avian complex (MAC)
- Impaired Defences: Cystic Fibrosis, Ciliary Dysfunction (Kartagener’s syndrome:situs inversus, bronchiectasis, sinusitis), hypogammaglobiaemia, defective leukocyte function
What are the signs and symptoms of Bronchiectasis?
Bronchiectasis may be difficult to differentiate from chronic bronchitis.
Signs and symptoms include:
-clubbing
- chronic cough purelent sputum, heamoptysis (can be massive)
- recurrent pneumonia
-local crackles (inspiratory and expiratory)
- wheezes
How is emphysema seen on CXR?
Diffuse hyoerinflation with flattening of the diaphragms, increased retro sternal space, bullae (Lucent, air containing spaces that have no vessels and are not perfused), and enlargement of the PA/RV (Cor pulmonale).
Findings do not correlate well with pathology and PFTs or high resolution CT are more informative (CT can differentiate between different types eg pan lobular, intra lobular, paraseptal)
What investigations do you order and what do you expect to see in bronchiectasis?
Obstructive pattern on PFTs
CXR: non specific findings. Increased marking, linear atelectasis, loss of volume in affected areas, cysts or tram tracking
High resolution CT: “signet ring” dilated bronchi with thickened walls where diameter bronchus >diameter of the accompanying artery.
Also take sputum cultures, serum Ig levels,
How do you treat bronchiectasis?
Vaccination for pneumococcal and influenza,
Antibiotics for exacerbations
Inhaled corticosteroids
Oral corticosteroids for acute major exacerbations
Chest physiotherapy
Excercise
Pulmonary resection for focal bronchiectasis.
What is interstitial lung disease?
Interstitial lung disease is an inflammatory or fibrosing process that occurs in the alveolar walls causing thickening and possible destruction of pulmonary vessels and fibrosis of interstitium leading to:
- decreased lung compliance (increased or normal FEV1/FVC)
- decreased lung volumes (decreased TLC, decreased VC, decreased RV)
- impaired diffusion(decreased DLCO)
- hypoxia usually without hypercapnia due to V/Q mismatch
- pulmonary HTN and Cor pulmonale occur with advance disease secondary to hypoxia and blood vessel destruction
What are the causes of ILD that affects the upper lobes?
FASSTEN
Farmer’s lung (hypersensitivity pneumonitis)
Anklylosing spondylitis
Sarcoidosis
Silicosis
TB
Eosinophilic granuloma (langerhans histiocytosis)
Neurofibromas oasis
What are the causes of Interstitial Lung Disease that affects the lower lobes?
BAD RASH
Bronchiolitis obliterates with organising pneumonia (BOOP)
Asbestosis / silicosis / pneumoconiosis / berylliosis
Drugs (amiodarone, methotrexate, nitrofurantoin, chemo)
Rheumatological disease (RA, SLE, polymyositis, dermatomyositis)
Aspiration
Scleroderma
Idiopathic pulmonary fibrosis
What are the signs and symptoms of interstitial lung disease?
- SOB especially on exertion
- dry crackles
- non productive cough
- cyanosis
- clubbing (especially in IPF and asbestosis)
- features of Cor pulmonale
- signs and symptoms vary with each type of ILD
What investigations do you order for ILD?
CXR/ HRCT: may be normal or show decreased lung volumes, reticular, nodular, or reticule doulas patterns, Kerley B lines, hilar/mediastinal adenopathy
Lines and ground glass appearance in early IPF, this progresses to honey combing in later disease
PFTs: decreased lung volume and compliance, normal or increased FEV/FVC. DLco decreased due to V/Q mismatch (less surface area for gas exchange) and pulmonary vascular disease.
ABGs: hypoxia and decreased CO2
May also do a bronchoscope, bronchi alveolar lavage, lung biopsy, cANCa(Wegeners) antiGbM (Goodpastures), ESr, ANA (lupus) RF, serum precipitating antibodies to inhaled organic antigens (hypersensitivity pneumonitis)
What is idiopathic pulmonary fibrosis? What symptoms would they present with? What investigations would you order?
IPF is a diagnosis of exclusion. IPF is also known as cryptogenic fibrosing alveolitis, or usual interstitial pneumonitis.mit commonly presents over the age of 50, with the incidence rising with age, and is more common in males than females. Pts present with dyspnoea on exertion, non productive cough, constitutional symptoms, late inspiratory fine crackles at the lung bases, and clubbing.
Investigations you would order include ESR, ANAs, RF
CXR, high resolution CT, and biopsy to exclude granulomas.
How do you treat idiopathic pulmonary fibrosis?
Oxygen and steroids. Lung transplantation, mean survival is 3-5 years after diagnosis.
What is sarcoidosis?
Sarcoidosis is an idiopathic non infectious granulomatous multi system disease other lung involvement in 90% of cases. It is characterised by non caseating granulomas. Proposed triggers include infectious, allergic, and environmental exposures, sarcoidosis typically affects young and middle aged patients. There is a higher incidence among black North Americans.
What are the presenting signs and symptoms of sarcoidosis?
Asymptomatic, or cough, dyspnoea, fever, arthralgia, malaise, erythema nodosum, chest pain
Chest exam usually normal
Common extra pulmonary manifestations include:
- cardiac (arrhythmias, sudden death)
- eye involvement (anterior uveitis)
- skin involvement (skin papular, erythema nodosum, lupus)
- peripheral lymphadenopathy
- arthralgia
- hepatomegaly
Hat is hypersensitivity pneumonitis?
Hypersensitivity pneumonitis is also known as extrinsic allergic alveolitis. It is caused by intense/repeated inhalation and sensitisation to certain organic agents. There is non IgE mediated inflammation of the lung parenchyma, lymphocytic inflammation and granulomas present.
Exposure is usually related to occupation or hobby.
Farmers lung = thermophillic actinomyces
Bird breeders/bird fanciers lung= chlamydia psittaci
Humidifier’s lung: aureobasidium pullulans
Sauna takers lung: aureobasidium spp.
