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FRACP Shuyu > Respiratory > Flashcards

Respiratory Flashcards

1
Q

FEV1/FVC cut off for COPD

A

<0.7

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2
Q

Chronic bronchitis definition

A

daily sputum production for at least 3 months of 2 or more consecutive years

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3
Q

What FEV1 chances to consider asthma or coexisting asthma and COPD

A

FEV1 increases >400mL following bronchodilator

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4
Q

What imaging modality if better to detect PEs in COPD

A

CTPAs. VQ scans may be difficult to interpret in COPD patients because regional lung ventilation may be compromised leading to matched defects

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5
Q

SABA/SAMA combinations in COPD

A

Provides additional benefits compared to using SAMA alone and decreased need for corticosteroids

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6
Q

GOLD ABCD

A

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

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7
Q

GOLD A management

A

A bronchodilator of any type

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8
Q

GOLD B management

A

LABA or LAMA If persistent symptoms then combination LAMA/LABA

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9
Q

GOLD C management

A

LAMA If further exacerbations, LAMA+LABA combination or LABA + ICS combination

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10
Q

GOLD D management

A

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

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11
Q

Pneumococcal vaccination for <65 COPD

A

PPSV23

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12
Q

How many generations of airways between the trachea and alveoli

A

23

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13
Q

how to distinguish between inflammation vs persistent airway remodeling components of airway hyperresponsiveness

A

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

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14
Q

Asthma step up therapy for controllers

A

Low dose ICS -> low dose ICS/LABA -> med/high dose ICS/LABA -> add on treatment (e.g. anti IgE, tiotropium)

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15
Q

Most effective strategy of reducing progression in COPD

A

Smoking cessation

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16
Q

Light’s criteria

A

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

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17
Q

Most likely cause of transudative pleural effusion

A

cardiac failure

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18
Q

How to confirm diagnosis of heart failure as the cause of pleural effusion?

A

NT-proBNP >1500 pg/mL (+ve LR 15.2; neg LR 0.06)

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19
Q

Best pleural fluid test for diagnosis of pleural mycobacterium tuberculosis

A

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

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20
Q

Biomarkers in malignant pleural effusion (tumour biomarkers and mesothelioma)

A

Tumours: CEA, CYFRA 21-1, CA 15-3 Mesothelioma: Mesothelin, fibulin 3

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21
Q

What are the predictors of mortality in a pleural infection

A

Urea, age, prulence of fluid, infection source (CAP vs HAP), albumin

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22
Q

Indication of ICC insertion in pleural infection without preceding trial of antibiotics

A

pH < 7.2 Macroscopically purulent or gram stain/culture positive

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23
Q

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

A

Intrapleural tissue plasminogen activator (tPA) and deoxyribonuclease (DNAse)

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24
Q

how does pleural fluid pH need to be fun?

A

<1hr on a pH analyser for accuracy

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25
Q
A

Central sleep apnoea

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26
Q

What AHI (apnoea-hypopnea index) is normal?

A

<5

(per hour)

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27
Q

What AHI (apnoea and hypopnoea index) constitutes severe OSA

A

>30

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28
Q

based on AHI

Clinical diagnosis of OSA

A
  • AHI>5/hr plus one symptom attributable to OSA (eg. daytime sleepiness, snoring, choking, mood disorder, HT, etc
  • AHI >15/hr
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29
Q

what does use of CPAP in sleep apnoea reduce?

A

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.

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30
Q
A
  1. Variable intra-thoracic upper airway obstruction
  2. Variable extra-thoracic upper airway obstruction

Flattened inspiratory loop suggests extra thoracic obstruction

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31
Q

When is measuring total lung volumes clinically useful and which volumes are not measured during spirometry

A

Restrictive lung diseases

TLC, FRC, RV

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32
Q

What lung volumes increases with age

A

Residual volume and funtional residual capacity

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33
Q

Anatomical airway vs physiological dead space

A

anatomical dead space is until the terminal bronchioles

physiological dead space includes alveolar dead space from disease e.g. PE

34
Q

indications for lytic therapy in PE

A

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

35
Q

When is O2 therapy indicated in COPD.

A

PaO2 <55mmHg

If PulHTN and polycythemia, then PaO2 <60 mmHg

Of note, the only thing that improves mortality benefit in COPD is oxygen therapy

36
Q

Pulmonary function tests in pumonary vascular disease

A

low TLCO but everything else low

37
Q

evidence for pulmonary rehabilitation exercise program

A

improve quality of life scores

38
Q

evidence for nocturnal BPAP for chronic hypercapnia in COPD

A

evidence of mortality benefit

https://jamanetwork.com/journals/jama/fullarticle/2627985

39
Q

Factors that reduce TLCO

A

Abnormalities in the:

  • Gas exchange barrier
    • Emphysema
    • Thickening of membranes - ILD
  • Blood
    • PHT
    • Anaemia
  • Decrease in lung volume
40
Q

How to distinguish between gas trapping and real restriction on lung volumes?

A

Real restriction: TLC < LLN

Gas trapping: RV/TLC > ULN

41
Q

KCO

A

TLCO/VA transfer coefficient

Gas exchange per unit lung volume

42
Q

Variable intrathoracic obstruction flow volume loop

A
43
Q

reduction in both inspiratory and expiratory loops (flow volume loop)

A

Fixed upper airway obstruction — Firm tracheal lesions (eg, tracheal stenosis)

44
Q
A

ILD

quick desaturation

45
Q
A

COPD

46
Q
A

Cardiac dysfunction

47
Q

What is the relationship of airway resistance to airway generation?

A
48
Q

What is indirect and direct challenges of airway hyperresponsiveness

A

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
49
Q

Does indirect or direct cause detect inflammation more?

Does indirect or direct cause detect airway remodelling more?

A

Inflammation - mannitol, hypertonic saline

Persistent airway remodelling - direct challenge

50
Q

Which out of the direct and indirect challenges for airway hyperresponsiveness is more sensitivite/specific?

A

Direct challenges are more sensitive

Indirect challenges are more specific

51
Q

Step up stages in asthma controller management

A

low dose ICS -> low dose ICS/LABA -> med/high ICS/LABA -> add on tx (e.g. tiotropium, anti-IgE, anti-IL-5)

52
Q

2x2 grid for GOLD ABCD classification

A

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

53
Q

Initial pharmacological management of stable COPD based on ABCD GOLD classification

A
54
Q

Period of monitoring for solid vs sub-soild nodules as per Fleischner Society Guidelines

A

Solid >6mm if stable after 2 years. STOP

Subsolid >6mm scan after 3-6 months for resolution. If stable after 5 years. STOP

55
Q

Granulomatous interstitial lung disease

A

Sarcoid

Hypersensitivity pneumonitis

56
Q

Causes of UIP

A

– Idiopathic pulmonary fibrosis
– Asbestosis
– Connective tissue related ILD e.g. RA

57
Q

Radiological features of UIP pattern (usual interstitial pneumonia)

A
  • 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
58
Q

What is the best pulmonary function test predictor of mortality for idiopathic pulmonary fibrosis

A

serial FVC trends

59
Q

What is the most sensitive pulmonary function testing for change in interstitial lung disease when there is a mix of emphysema and fibrosis

A

Serial DLCO

60
Q

most important function of BAL in the diagnostic evaluation of interstitial lung disease

A

to exclude chronic hypersensitivity pneumonitis (lymphocytic cellular pattern)

should only be performed in selected patients

61
Q

When should a lung biopsy be performed in the evaluation of interstitial lung disease?

A

Unclear for UIP pattern on chest HRCT to look for alternative diagnosis

62
Q

What are the adverse effects of Pirfenidone?

A

photosensitivity, nausea, rash, diarrhoea

63
Q

nintedanib MOA

A

An intracellular inhibitor that targets multiple tyrosine kinases

64
Q

Nintedanib SE

A

GI upset, diarrhoea, nausea

65
Q

NSIP radiology features

A

ground-glass opacities w basal predominance or diffuse

subspleural sparing is a specific feature

honeycombing is not a major feature

there is traction bronchiectasis

66
Q

What conditions are associated with NSIP

A

Connective tissue disease

67
Q

When to use radial EBUS vs linear EBUS

A

radial EBUS for peripheral lesions

Linear EBUS for peribronchial/peritracheal/mediastinal lesions

68
Q

risk of death as a result of bronchoscopy

A

1/2500

69
Q

What is the most common type of mutation in NSCLC

A

KRAS

70
Q

difference between OSA and obesity hypoventilation syndrome on sleep study oximetry

A

OHS has prolonged hypoxia that doesn’t resolve

71
Q

maintenance of wakefulness test

A

measures ability to stay awake - e.g. measure of response to treatment

72
Q

silicosis imaging findings

A
  • nodules in upper zones
  • eggshell calcification
73
Q

what infectious disease is associated with silicosis

A

2-30x risk of tuberculosis

74
Q

PFT changes that indicate progressive disease in ILD

A

>10% FVC

>15% DLCO

75
Q

hypersensitivity pneumonitis CT findings

A

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

76
Q

what population of people get lymphangioleiomyomatosis (LAM)

A

women of child-bearing age or people with tuberous sclerosis

77
Q

When to do spirometry for COPD (inpatient vs outpatient)

A

Timing generally does not influence diagnosis

78
Q

What is the strongest predictor of future COPD exacerabtion?

A

Exacerbation in the previous year

79
Q

Evidence for pulmonary rehabilitation in COPD

A

Improvement in QOL

Decrease in hospitalisations

No change in mortality

80
Q

Role of prophylactic antibiotics in COPD

A

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

81
Q
A

FRACP Shuyu (65 decks)

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