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Respiratory Flashcards

1
Q

What conditions have a high FENO?

A

Asthma (Eosinophilic asthma specifically)

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2
Q

What conditions have a high DLCO?

A
  • Asthma
  • Polycythaemia
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3
Q

What conditions have a reduced DLCO?

A
  • COPD
  • ILD
  • PE
  • Neuromuscular Disease
  • Anaemia
  • Heart Failure
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4
Q

What conditions have a normal DLCO?

A

Obesity

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5
Q

Causes of Raised A-a Gradient

A

V/Q Mismatch
R/L Shunt
Diffusion defect

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6
Q

A-a Gradient formula

A

(150 - PaCO2/0.8) - PaO2
Normal = 5-10mmHg for young adult, add 1mmHg for each decade of life

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7
Q

Risk Factors for EGFR mutant Lung Cancer

A

Asian
Female
Non smoker

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8
Q

Most common mutation in non small cell lung cancer

A

KRAS

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9
Q

Most common histopathological subtype of lung cancer

A

Adenocarcinoma

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10
Q

Which type of lung cancer are EGFR and ALK mutations present in?

A

Adenocarcinoma

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11
Q

Which type of lung cancer are CTLA-4 and PD-1/PD-L1 mutations present in?

A

Squamous Cell Carcinoma

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12
Q

When considering Fleischner Guidelines, what patient factors would make a patient high risk?

A

Heavy smoking
Older age
Upper lobe
Irregular/spiculated margin

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13
Q

Follow up for single solid nodule <6mm

A

Low risk: no routine follow up
High risk: Consider CT at 12 months particularly if suspicious

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14
Q

In what conditions does Pulus Paradoxus occur?

A

Tamponade, Asthma, COPD

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15
Q

What is Allergic Bronchopulmonary Aspergillosis?

A

Type 4 hypersensitivity due to colonisation of airway with Aspergillus (i.e. not infection). Can result in eosinophilic pneumonia, and upper lobe predominant bronchiectasis.

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16
Q

What’s a key cause of a lack of improvement in Oxygen Saturations with supplemental oxygen?

A

Methaemoglobinaemia

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17
Q

What is the most common cause of death in COPD? (Mild, and severe?)

A

Mild: CVD
Severe: Respiratory Failure

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18
Q

In asbestosis, are straight blue or curly white fibres more carcinogenic and why?

A

Straight blue, as they can get further into the lungs

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19
Q

Of the causes of hypoxaemia, which has a normal A-a gradient?

A

Hypoventilation

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20
Q

As CO2 rises, what should happen to HCO3?

A

For every increase of 10 in CO2 above 40, bicarb should rise by:
Acute: 1
Chronic: 4

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21
Q

Which causes of ILD are predominantly in upper zones?

A

Farmer’s
Ankylosing Spondylitis
Sarcoid
Silicosis
Tuberculosis
Eosinophilic Granuloma
Neurofibromatosis

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22
Q

Which causes of ILD predominantly involve the lower zones?

A

Rheumatoid Arthritis
Scleroderma
Asbestosis

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23
Q

What is the mechanism of Omalizumab? What condition is it indicated in?

A

Blocks IgE interactions. Indicated in severe Allergic Asthma and chronic rhinosinusitis with nasal polyps

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24
Q

What is the mechanism of Benralizumab? What are the indications?

A

Anti- IL-5. Indicated in Eosinophilic Asthma (also EGPA)

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25
Q

What is the most common cause of spontaneous secondary pneumothorax?

A

1st: COPD (50-70%)
2nd: Lung Cancer

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26
Q

What medical therapy is indicated for CTEPH in patients who have inoperable disease or recurrence post surgery?

And what is its mechanism?

A

Riociguat

Soluble Guanylate Cyclase stimulator, targets NO - cGMP pathway to cause vasodilation

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27
Q

What is the key complication of Cystic Fibrosis in males, and what is the mechanism?

A

Infertility due to obstructive azoospermia secondary to congenital lack of vas deferens

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28
Q

What does the Delta F508del mutation do to CFTR function?

A

CFTR works, but isn’t transported to the cell membrane and thus is dysfunctional. (Class II)

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29
Q

What is the mechanism of Ivacaftor?

A

CFTR potentiator → improves function/opening of the channel

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30
Q

What is the mechanism of Bosentan and Macitentan?

A

Endothelin antagonism -> pulmonary vasodilation

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31
Q

What is the mechanism of Elexacaftor and Tezacaftor?

A

Both bring the CFTR protein to the surface

32
Q

What happens if DNAse is given in the same nebuliser as hypertonic saline?

A

Becomes inactivated

33
Q

Ivacaftor monotherapy can work for which mutation?

A

G551d, as the protein is at the surface but doesn’t work properly. Increases weight, increased exercise tolerance, marked drop in pancreatitis.

34
Q

What is the key predictor of efficacy for Benralizumab and Mepolizumab?

A

Raised Eosinophils

35
Q

What are the key side effects/risks of Omalizumab?

A

Thrombocytopaenia
Can unmask/cause EGPA

36
Q

What is the mechanism of Mepolizumab, and what are the indications?

A

Binds to IL-5, reducing production and survival of eosinophils. Indicated in Eosinophilic asthma and EGPA

37
Q

What is the mechanism and indication/s for Dupilumab?

A

Inhibits IL-4 and IL-13, reducing atopy and immune response
Indicated in Eosinophilic asthma, atopic dermatitis, severe chronic rhinosinusitis with nasal poylps

38
Q

What is a key cause of irreversible loss of lung function post lung transplant?

A

Bronchiolitis Obliterans Syndrome. 50% of patients at 5 years post transplant. Risk increases with age

39
Q

What is a key risk factor for Post transplant lymphoproliferative disorder?

A

EBV positivity

40
Q

What is the key indication for a combined heart/lung transplant?

A

Almost exclusively congenital heart disease, e.g. Eisenmenger Syndrome

41
Q

What are the indications for Lung Transplant?

A

IPF
ILD other than IPF
CF
COPD
Alpha-1 antitrypsin Deficiency
Pulmonary Hypertension

42
Q

What are the features of low risk Pulmonary Hypertension?

A

No features of right heart failure
No progression of symptoms
No syncope
WHO Functional Capacity I or II
6MWD >440m
NT-proBNP <300
RA area <18cm^2
RAP <8mmHg

43
Q

What are the features of High Risk Pulmonary Hypertension?

A

Features of RHF present
Rapid progression of symptoms
Repeated syncope
WHO Functional Classification IV
6MWD <165m
NT-proBNP >1100
Ra area >26cm^2
RAP >14mmHg

44
Q

What is the key indication for the Endothelin Receptor Antagonists?

A

Indicated for low risk group 1 PAH either as monotherapy or with PDE5i.
Examples: Ambrisartan, Bosentan, Macitentan

45
Q

mPAP cut off for PAH diagnosis

A

Now >20, but PBS still uses 25

46
Q

What does a raised PAWP indicate in PAH diagnosis?

A

Suggestive of left ventricular dysfunction and thus suggestive of group II Pulmonary Hypertension

47
Q

Contraindications to Bronchoscopy

A

Respiratory insufficiency
Thrombocytopaenia (Plt <50 is cutoff)
Coagulopathy (INR >1.5)

Uncorrected bleeding diathesis is key issue, as can’t seen anything if there is bleeding, and very difficult to control it.

48
Q

How long does home oxygen therapy need to be used to see a mortality benefit in COPD?

A

At least 15 hours a day

49
Q

When is home oxygen indicated in COPD?

A

PaO2 <60mmHg
Doesn’t need to be as low if there are other complications such as PAH or polycythaemia

50
Q

Which immune cells are implicated in the pathogenesis of Asthma?

A

Mast Cells
Eosinophils
Th2

51
Q

Spirometry in Asthma

A

FEV1/FVC ratio >0.7
10% improvement post bronchodilator (or 8% if lung volumes normal)
This increase is compared to mean predicted value: ((post bronchodilator value - prebronchodilator value) x 100)/Predicted value

52
Q

What is the benefit of ICS in Asthma?

A

Reduces risk of exacerbation

53
Q

What is first line therapy for Asthma?

A

ICS-LABA used as a reliever

54
Q

When could a SABA be considered as first line therapy for asthma?

A

Daytime asthma symptoms <2 times a month
No waking due to asthma when using SABA alone
No history of severe flares in last 12 months
No risk factors for severe flares

55
Q

What is the stepwise approach to Asthma management?

A
  1. PRN ICS-LABA
  2. Regular ICS
  3. Low dose regular ICS-LABA
  4. Medium dose ICS-LABA
  5. High dose ICS-LABA, plus additional therapies
56
Q

What are the benefits of ICS/LABA vs ICS monotherapy in Asthma?

A

Improved FEV1
Reduced exacerbations
Improved quality of life

57
Q

When are biologics indicated in Asthma, and what is their benefit?

A

Indications: Frequent exacerbations despite maximal therapy, generally with high IgE titre or eosinophil count.
Benefits: reduce exacerbations, reduce oral steroid use, modest improvement in lung function

58
Q

When are Leukotrien Modifiers (Montelukast) indicated in Asthma, and what benefits do they provide?

A

Indicated as an add on therapy for difficult to control eosinophilic and aspirin sensitivity asthma.
Reduce symptoms, improve quality of life, decrease need for SABA, prevent exercise induced asthma

59
Q

Treatment of Severe Asthma

A

Salbutamol and Ipratropium via nebuliser
Adrenaline if: poor respiratory effort, unresponsive, peri-arrest
IV Mg Sulphate
Oral steroid within first hour
Consider whether anaphylaxis is contributing/present

60
Q

Pregnancy and Asthma

A

Pregnancy can induce or worsen asthma

Consequences of poorly controlled asthma during pregnancy:
- Low birth weight
- Pre-eclampsia
- Premature labour
- Increased infant mortality

61
Q

Diagnostic Features of Allergic Bronchopulmonary Aspergillosis

A

Asthma or CF
Elevated total IgE >1000, or Aspergillus IgE RAST or positive Aspergillus skin prick tests
Consistent CT findings or total eosinophil count >0.5 or positive aspergillus precipitant

CT findings:
- Tree in bud pattern
- proximal upper lobe bronchiectasis
- mucus plugging
- mosaicism

62
Q

Management of Allergic Bronchopulmonary Aspergillosis

A

High dose steroids with slow wean (exacerbations common during weaning)
Antifungals for frequent relapses (Intraconazole has best evidence)
- Reduces circulating IgE
- Improves radiological appearance
- Reduces exacerbation frequency
Omalizumab emerging as another option for resistant disease with high IgE titres

63
Q

GOLD Classification of airflow impairment

A
  1. Mild (FEV1 >80%)
  2. Moderate (FEV1 50-80%)
  3. Severe (FEV1 30-50%)
  4. Very Severe (FEV1 <30%)
64
Q

Usual Interstitial Pneumonia

A

Findings: Honeycombing, traction bronchiectasis, subpleural reticular opacities

Lower lobe predominant

Seen in: IPF, Rheumatoid Arthritis, CTD-ILD, Asbestosis

65
Q

Non Specific Interstitial Pneumonia

A

Findings: Ground glass changes, subpleural sparing

Lower lobe predominant

Seen in: Systemic sclerosis, CTD-ILD

66
Q

BAL Cell Patterns

A

High Neutrophils: IPF, Asbestosis
High Lymphocytes: Hypersensitivity pneumonitis, sarcoid, berrylium
High Eosinophils: Eosinophilic pneumonia

67
Q

Hypersensitivity Pneumonitis Radiology

A

Acute findings: ground glass nodularity
Chronic findings: fibrotic changes akin to UIP with ground glass and mosaicism (gas trapping)

Centrilobar predominance

Seen in Hypersensitivity pneumonitis shockingly!

68
Q

Testing for Cushing Syndrome

A

Midnight Salivary Cortisol
High dose Dexamethasone test to confirm
Short Synacthen to determine if ACTH dependent or independent
Image adrenals if independent
Petrodollar sinus ACTH levels if dependent, may also be paraneoplastic

69
Q

Indication for Bilateral lung transplant

A

CF, Bronchiectasis, PAH

Survival advantage in younger patients

Can be done for COPD

70
Q

When may single lung transplant be done?

A

COPD
ILD without PAH

71
Q

Risks of Sleep Disorders

A

Obesity hypoventilation syndrome
Nacrolepsy
REM behavioural disorder

72
Q

Impact of CPAP on cardiovascular risk in OSA

A

Does not reduce risk of cardiovascular events in moderate to severe OSA

73
Q

Benefits of CPAP in OSA

A
  • Reduced respiratory events
  • Decreased daytime sleepiness
  • Small BP improvements
  • Decreased erectile dysfunction
  • Reduced risk of MVA
  • Improved QOL
74
Q

What medications appear to have benefit for OSA?

A

Tirzepatide - reduced AHI in obese patients with OSA
Sulthiame (Carbonic anhydrase inhibitor): ~50% reduction in AHI

75
Q

Distinguish OSA from CSA

A

Respiratory effort key
- OSA: ongoing respiratory effort, trying to overcome obstruction
- CSA: intermittent drop in respiratory effort

76
Q

Diagnosis of Obesity Hypoventilation Syndrome

A

Elevated pCO2 during or immediately after sleep, BMI >35, no other reason for hypercarbia (e.g. COPD, neuromuscular)

Patients usually hypersomnolent

77
Q

What lung volume is reduced in Obesity Hypoventilation Syndrome?

A

Expiratory reserve volume

BPT (20 decks)

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