Respiratory Flashcards
FEV1/FVC cut off for COPD
<0.7
Chronic bronchitis definition
daily sputum production for at least 3 months of 2 or more consecutive years
What FEV1 chances to consider asthma or coexisting asthma and COPD
FEV1 increases >400mL following bronchodilator
What imaging modality if better to detect PEs in COPD
CTPAs. VQ scans may be difficult to interpret in COPD patients because regional lung ventilation may be compromised leading to matched defects
SABA/SAMA combinations in COPD
Provides additional benefits compared to using SAMA alone and decreased need for corticosteroids
GOLD ABCD
A - mMRC 0-1 and 0-1 moderate/severe exacerbation (not leading to hospital admission) B - mMRC 2 or more, 0-1 mod/severe exacerbation C - mMRC 0-1 and 1 or more mod/severe leading to hospital admission or 2 or more mod/severe exacerbation D - more than above
GOLD A management
A bronchodilator of any type
GOLD B management
LABA or LAMA If persistent symptoms then combination LAMA/LABA
GOLD C management
LAMA If further exacerbations, LAMA+LABA combination or LABA + ICS combination
GOLD D management
LAMA ->LAMA+LABA -> LABA + ICS -> LAMA + LABA + ICS Finally if further exacerbations: consider roflumilast if FEV1 <50% predicted and patient has chronic bronchitis Consider macrolide
Pneumococcal vaccination for <65 COPD
PPSV23
How many generations of airways between the trachea and alveoli
23
how to distinguish between inflammation vs persistent airway remodeling components of airway hyperresponsiveness
Indirect and direct challenges. Indirect challenges are mannitol, hypertonic saline, eucapnic voluntary hyperventilation, exercise challenge, adenosine monophosphate- to active mast cells to release histamine and other bronchoconstrictor mediators Direct challenges is with methacholine - to directly constrict airway smooth muscle via receptors on smooth muscle Inflammatory component of AHR has greater responsiveness to indirect stimuli and persistent airway remodeling is more responsive to direct stimuli
Asthma step up therapy for controllers
Low dose ICS -> low dose ICS/LABA -> med/high dose ICS/LABA -> add on treatment (e.g. anti IgE, tiotropium)
Most effective strategy of reducing progression in COPD
Smoking cessation
Light’s criteria
Exudate - at least one of: - ratio of pleural fluid protein to serum protein of >0.5 - ratio of pleural fluid LDH to serum LDH of >0.6 - Pleural fluid LDH >2/3 upper limit of normal serum LDH Increased false positive with people on diuretics
Most likely cause of transudative pleural effusion
cardiac failure
How to confirm diagnosis of heart failure as the cause of pleural effusion?
NT-proBNP >1500 pg/mL (+ve LR 15.2; neg LR 0.06)
Best pleural fluid test for diagnosis of pleural mycobacterium tuberculosis
Adenosine deaminase >50 U/L (sensitivity 95%, specificity 89%) Also as lymphocytes >50% normally Gold standard for TB diagnosis is thoracoscopy histology and AFB stain
Biomarkers in malignant pleural effusion (tumour biomarkers and mesothelioma)
Tumours: CEA, CYFRA 21-1, CA 15-3 Mesothelioma: Mesothelin, fibulin 3
What are the predictors of mortality in a pleural infection
Urea, age, prulence of fluid, infection source (CAP vs HAP), albumin
Indication of ICC insertion in pleural infection without preceding trial of antibiotics
pH < 7.2 Macroscopically purulent or gram stain/culture positive
What is a treatment option in patients with a pleural infection who has failed initial ICC/antibiotic treatment and is not suitable for VATS/surgery
Intrapleural tissue plasminogen activator (tPA) and deoxyribonuclease (DNAse)
how does pleural fluid pH need to be fun?
<1hr on a pH analyser for accuracy
Central sleep apnoea
What AHI (apnoea-hypopnea index) is normal?
<5
(per hour)
What AHI (apnoea and hypopnoea index) constitutes severe OSA
>30
based on AHI
Clinical diagnosis of OSA
- AHI>5/hr plus one symptom attributable to OSA (eg. daytime sleepiness, snoring, choking, mood disorder, HT, etc
- AHI >15/hr
what does use of CPAP in sleep apnoea reduce?
Blood pressure +/- stroke
Background:
There is RCT level studies demonstrating reduction in BP with CPAP. In 2016 (after this question was written) SAVE study demonstrated no reduction in AMI but ?reduction in stroke. CPAP use actually increases weight (because of reduced WOB), not sure about HF.
- Variable intra-thoracic upper airway obstruction
- Variable extra-thoracic upper airway obstruction
Flattened inspiratory loop suggests extra thoracic obstruction
When is measuring total lung volumes clinically useful and which volumes are not measured during spirometry
Restrictive lung diseases
TLC, FRC, RV
What lung volumes increases with age
Residual volume and funtional residual capacity
Anatomical airway vs physiological dead space
anatomical dead space is until the terminal bronchioles
physiological dead space includes alveolar dead space from disease e.g. PE
indications for lytic therapy in PE
selected patients with acute PE not associated with hypotension and with a low risk of beeding
but generally for hypotension who do not have a high risk of bleeding
When is O2 therapy indicated in COPD.
PaO2 <55mmHg
If PulHTN and polycythemia, then PaO2 <60 mmHg
Of note, the only thing that improves mortality benefit in COPD is oxygen therapy
Pulmonary function tests in pumonary vascular disease
low TLCO but everything else low
evidence for pulmonary rehabilitation exercise program
improve quality of life scores
evidence for nocturnal BPAP for chronic hypercapnia in COPD
evidence of mortality benefit
https://jamanetwork.com/journals/jama/fullarticle/2627985
Factors that reduce TLCO
Abnormalities in the:
- Gas exchange barrier
- Emphysema
- Thickening of membranes - ILD
- Blood
- PHT
- Anaemia
- Decrease in lung volume
How to distinguish between gas trapping and real restriction on lung volumes?
Real restriction: TLC < LLN
Gas trapping: RV/TLC > ULN
KCO
TLCO/VA transfer coefficient
Gas exchange per unit lung volume
Variable intrathoracic obstruction flow volume loop
reduction in both inspiratory and expiratory loops (flow volume loop)
Fixed upper airway obstruction — Firm tracheal lesions (eg, tracheal stenosis)
ILD
quick desaturation
COPD
Cardiac dysfunction
What is the relationship of airway resistance to airway generation?
What is indirect and direct challenges of airway hyperresponsiveness
Indirect challenge:
- Activates mast cells to release histamine and other bronchoconstrictors
- E.g. mannitol, hypertonic saline, exrcise
Direct challenge:
- Directly constricts airway smooth muscle via receptors on smooth muscles
- E.g. metacholine, histamine
Does indirect or direct cause detect inflammation more?
Does indirect or direct cause detect airway remodelling more?
Inflammation - mannitol, hypertonic saline
Persistent airway remodelling - direct challenge
Which out of the direct and indirect challenges for airway hyperresponsiveness is more sensitivite/specific?
Direct challenges are more sensitive
Indirect challenges are more specific
Step up stages in asthma controller management
low dose ICS -> low dose ICS/LABA -> med/high ICS/LABA -> add on tx (e.g. tiotropium, anti-IgE, anti-IL-5)
2x2 grid for GOLD ABCD classification
Y axis: exacerbation history (0/1 vs 2 or more or any leading to hospitalisation)
X axis: mMRC 0-1 or mMRC 2 or more
Initial pharmacological management of stable COPD based on ABCD GOLD classification
Period of monitoring for solid vs sub-soild nodules as per Fleischner Society Guidelines
Solid >6mm if stable after 2 years. STOP
Subsolid >6mm scan after 3-6 months for resolution. If stable after 5 years. STOP
Granulomatous interstitial lung disease
Sarcoid
Hypersensitivity pneumonitis
Causes of UIP
– Idiopathic pulmonary fibrosis
– Asbestosis
– Connective tissue related ILD e.g. RA
Radiological features of UIP pattern (usual interstitial pneumonia)
- Apical basal gradient with bases being more affected
- Reticulation
- Traction bronchiectasis
- Honeycombing
- Architectural distortion
Inconsistent features:
- too much nodules, too much groundglass, too much moisac attenuation
What is the best pulmonary function test predictor of mortality for idiopathic pulmonary fibrosis
serial FVC trends
What is the most sensitive pulmonary function testing for change in interstitial lung disease when there is a mix of emphysema and fibrosis
Serial DLCO
most important function of BAL in the diagnostic evaluation of interstitial lung disease
to exclude chronic hypersensitivity pneumonitis (lymphocytic cellular pattern)
should only be performed in selected patients
When should a lung biopsy be performed in the evaluation of interstitial lung disease?
Unclear for UIP pattern on chest HRCT to look for alternative diagnosis
What are the adverse effects of Pirfenidone?
photosensitivity, nausea, rash, diarrhoea
nintedanib MOA
An intracellular inhibitor that targets multiple tyrosine kinases
Nintedanib SE
GI upset, diarrhoea, nausea
NSIP radiology features
ground-glass opacities w basal predominance or diffuse
subspleural sparing is a specific feature
honeycombing is not a major feature
there is traction bronchiectasis
What conditions are associated with NSIP
Connective tissue disease
When to use radial EBUS vs linear EBUS
radial EBUS for peripheral lesions
Linear EBUS for peribronchial/peritracheal/mediastinal lesions
risk of death as a result of bronchoscopy
1/2500
What is the most common type of mutation in NSCLC
KRAS
difference between OSA and obesity hypoventilation syndrome on sleep study oximetry
OHS has prolonged hypoxia that doesn’t resolve
maintenance of wakefulness test
measures ability to stay awake - e.g. measure of response to treatment
silicosis imaging findings
- nodules in upper zones
- eggshell calcification
what infectious disease is associated with silicosis
2-30x risk of tuberculosis
PFT changes that indicate progressive disease in ILD
>10% FVC
>15% DLCO
hypersensitivity pneumonitis CT findings
mosaic attenuation:
hypoattenuation and hypovascularity of scattered secondary lobules: hypoattenuating regions that persist on expiratory CT scans are indicative of air trapping, which is caused by bronchiolar inflammation and obstruction
what population of people get lymphangioleiomyomatosis (LAM)
women of child-bearing age or people with tuberous sclerosis
When to do spirometry for COPD (inpatient vs outpatient)
Timing generally does not influence diagnosis
What is the strongest predictor of future COPD exacerabtion?
Exacerbation in the previous year
Evidence for pulmonary rehabilitation in COPD
Improvement in QOL
Decrease in hospitalisations
No change in mortality
Role of prophylactic antibiotics in COPD
Macrolides x 3 /week prevents hospitalisation
Moxifloxacin/doxycycline doesn’t work
Doesn’t work in smokers
Not available on PBS for long term use
Target patients: otherwise optimised, cough/sputum
