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Delta Med - Respiratory > Respiratory 1 - Hot topics in respiratory medicine (1) > Flashcards

Respiratory 1 - Hot topics in respiratory medicine (1) Flashcards

1
Q

What is the overall survival for Lung Ca in Victoria?

A

14% five year survival
NSCLC survival improved from 11% to 18% over 20y
Most patients die from lung Ca
Even those presenting with early stage disease - long term survival is only 18-22% overall for NSCLC

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2
Q

What were the outcomes of the ELCAP study for lung cancer screening?

A

Used low dose CT initially - if nodule found, proceeded to HRCT. Calcified nodules with a smooth edge 20mm = benign.

11mm - Bx, bronch, VATS

Screening detected 599 nodules, 27 cancers, of which 26 were resectable. 233 were non calcified and 28 required Bx.

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3
Q

What were features of the Mayo clinic lung cancer screening trial?

A

Low dose CT scan and annual induced sputum. Smokers, otherwise fit for surgery.

Detected 25 lung cancers, and 66% of participants had nodules detected. Unexpected pathology in 14%

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4
Q

What were findings of the national lung screening trial?

A

3 x yearly LDCT and 3x annaul CXR, shown to provide a 20% reduction in mortality.
Associated reduction in smoking in both arms.
High rate of false positives.
? cost effectiveness, f/u of benign lesions, ? correct population

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5
Q

What are overall outcomes of lung cancer screening?

A

LDCT screening reduces mortality, comparable to CRC and Breast cancer screening.
Management of nodules based on volume is safe.
Does carry risk of radiation/dx of other conditions etc.

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6
Q

What are features of PET imaging in the Ix of pulmonary nodules?

A

False positives are common due to infection and inflammation.
PET misses

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7
Q

What is the role of Chemotherapy in NSCLC?

A

75-80% of lung cancer cases - 30% are candidates for resection, 30% have locally advanced inoperable disease and 40% have metastatic disease.

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8
Q

What is the ideal chemotherapy regime for NSCLCC?

A

cisplatin/paclitaxel
cisplatin/gemcytabine
cisplatin/docetaxel
carboplat/paclitaxel

all are equivalent and improve response rates, one year survival (modest) - also improved QoL.

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9
Q

What are the three main histological subtypes of Lung cancer?

A
  1. adenocarcinoma (most common)
  2. squamous cell carcinoma
  3. large cell carcinoma

Now to a degree being supplanted by molecular analysis - EGFR, KRAS, ALK etc.

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10
Q

What are first line TKIs in EGFR +ve lung cancer?

A

gefininib was tested in the IPASS study - which found that there was a significant improvement in progression free survival in patiehts who were EGFR mutation positive NSCLC, but poorer survival in EGFR -ve lung cancer (treated with carboplatin and paclitaxel).

Non significant survival benefit

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11
Q

What are AEs associated with gefitinib therapy?

A 
Rash (71%)
Raised ALT (55.3%)
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12
Q

What AEs are associated with combined carboplatin/paclitaxel in lung cancer Rx?

A

Neutropenia 77%
Anaemia 64%
Loss of appetite 57%
Peripheral neuropathy 55%

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13
Q

What is the benefit of continuous vs as needed ICS in mild intermittent asthma?

A

Daily ICS was not superior to intermittent ICS when considering exacerbation rate, QoL, rate of FEV1 decline over a year

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14
Q

What was the outcome of the START study in mild persistent asthma?

A

Daily ICS found to provide a 44% reduction in hospital or AE treatment for asthma
Reduced rates of severe, life-threatening attacks
More sx free days and lower po steroid requirement
Significantly improved FEV1

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15
Q

What is the relationship between exacerbations and lung function?

A

Frequent exacerbations may contribute to accelerated decline in lung function over time in both adults and children.

Once daily ICS within 2 years of Dx reduces risk of exacerbations and is associated with an attenuation in the decline of lung function.

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16
Q

What is the rationale of treatment of moderate-persistent asthma?

A

Addition of LABA to low dose ICS better than high dose ICS:
- improves control with respect to PEFR, symptoms, spirometry and exacerbations

Current thought that asthma is a combination of airway inflammation and abnormal airway smooth muscle.

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17
Q

What is the optimised dose of ICS in asthma?

A

The dose of peak effect appears to be 600ug of fluticasone daily - has best improvement in FEV1, PEF nocte/mane and B-agonist use.

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18
Q

What effect dose increasing ICS dose have upon side effects in Asthma?

A

risk of AEs increases 25% for each 1000ug/day increase in dose above 1000ug/day

AEs include brusing, cataracts, OP, dysphonia and thrush

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19
Q

What is the predominant cell type involved in classic asthma?

A

Th2 respinse - steroid responsive

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20
Q

What are features of eosinophilic bronchitis?

A

not synonymous with asthma
diagnosed with >2.5% eosinophils on sputum
a cause of steroid responsive chronic cough
no evidence of airway hyperrresponsiveness
responds to ICS and oral steroids
atopy at the same rate as the general population

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21
Q

What are features of neutrophilic, non-eosinophilic asthma?

A

Identified by sputum analysis
Stable asthma phenotype with time
Associated with activation of the innate immune response in airways (TLRs, IL8, IL1B, endotoxin)
Less steroid responsive than eosinophilic asthma

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22
Q

What are features of GORD and influenza vaccination in asthma?

A

75% of difficult to control asthma have GERD evidence on pH monitoring, however treating these does not improve asthma.

Influenza vaccination does not cause exacerbations, however has not been shown to be protective against exacerbations.

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23
Q

What is lebrikizumab and it’s role in asthma treatment?

A

anti-IL-13 mAb - important in driving the Th2 asthma response.
FEV1 shown to be higher in group when lebrikizumab added to mod/high dose ICS +/- LABA.

High FENO (Th2 biomarker) - predictive of response

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24
Q

What is omalizumab and it’s role in asthma treatment?

A

Anti IgE molecule that prevents IgE binding to mast cells.

Improves asthma symtom control and allows lower doses of ICS and reduces frequency of exacerbations.

RR of hospitalisation/ED visits for asthma 0.4

25
Q

What is the role of ICS in COPD?

A

Early studies suggested they did not prevent decline in FEV1, however subsequent evidence shows improvement in FEV1 following optimisation of lung function with prednisone.
Also reduce frequency and severity of exacerbations.

26
Q

What is the role of LABA and ICS in COPD?

A

Shown to improve stabilising PFTs and delaying exacerbations when LABS is added to ICS.

Reduces rates of exacerbations with RR of 0.7, QoL, daily symptoms. One exacerbation was averted with every 2-4 y of treatment.

27
Q

What are some risks of adding ICS to LABA in COPD?

A

increased oral candidiasis RR2.1 and skin bruising 2.1 and pnuemonia (fluticasone 1.78 and budesoine 1.62.)

28
Q

What is the role of antibiotics in the treatment of COPD exacerbations?

A

60% of AEs of COPD due to bacterial infection.
Lower mortality has been demonstrated in patients admitted with ECOPD and treated w antibiotics (1 vs 1.8%). 13% reduction in 30 day readmission rate.
No difference in risk of readmission for c. diff colitis.

29
Q

What is the role of tiotropium in the treatment of COPD?

A

UPLIFT study showed improved exacerbations, FEV1, symptoms scores and QoL however did not slow the rate of lung function with tiotropium - now 1st line therapy in COPD vs ICS.

30
Q

What are two other anticholinergic agents used in COPD (other than tiotropium)?

A

Aclinadium - shown to improve trough FEV1 and respiratory symptoms.
Umeclidinium - improved lung function, health status and dyspnoea scores.

31
Q

What is the role of seretide in additio to ICS and LABA?

A

addition of seretide to tiotropium significantly improves QoL, frequency of all cause hospitalisations and lung function

32
Q

What are systemic effects of COPD?

A

Sekeltal muscle changes in COPD:

  • muscle atrophy
  • quads > arms
  • decreased oxidative capacity
  • reduced capillary to fibre ratio
  • contributes to exercise limitation
  • causes include chronic disuse, systemic inflammation, nutritional effects, steroid therapy, hypoxia
33
Q

What are benefits of pulmonary rehabilitation in COPD?

A

Benefits across all COPD severity
Maximum benefit following acute exacerbation
Benefits extend to patients recovering from other illness
variable long-term effects

34
Q

What is occuring with COPD death?

A

only major cause of death currently increasing in prevalence

35
Q

What are causes of mortality in COPD?

A 
Respiratory 35%
CArdiac 27%
Cancer 21%
Other 10%
Unknown 7%
36
Q

What is the role of LVRS in patients with COPD?

A

shown to reduce mortality 0.86 RR in patients, esp those with 6MWT low and upper zone emphysema only.

37
Q

What are features of the BODE index in COPD?

A 
Consists of:
BMI
Obstruction (FEV1 % predicted)
Dyspnoea (MRC) 
Exercise capacity (6MWT)

Predicts outcome of medical management and a increase of 1 BODE point is associated with a significant increase in mortality

38
Q

What is the natural history of ILD?

A

traditionally quoted 50% 5 year survival rates.
Note that UIP has highest mortality rate (50% at 2 years), and that prolonged survival likely suggests another pathology.

39
Q

What are the 4 main categories of diffuse lung disease?

A

1) Drug induced lung disease
2) Idiopathic interstitial pneumonias
3) Granulomatous lung diseases
4) Other (pLAM, histiocytosis x)

40
Q

What are features of sarcoidosis?

A

Multisystem granulomatous disease
Nodular infiltrates in mid and upper zones
Mediastinal and hilar lymphadenopathy
Extrapulmonary manifestations include - ocular, hepatic, hypercalcaemia, rarely cardiac and CNS

41
Q

What are features of pulmonary lymphangioleiomyomatosis?

A

Females, predominantly premenopausal
cystic lung disease associated with pneumothorax
hyperinflation
associated with angiomyolipoma and chylous effusions.

42
Q

What are features of cryptogenic organising pneumonia?

A

Consolidation, sub-pleural and lower zones
Ground glass changes, pulmonary nodules and pleural tags and thickening.

Histology shows buds of granulation tissue in terminal broncioles/alevoli - fibrin exudates and collagen.

Causes include connective tissue disease, drugs, post infective

43
Q

What are features of desquamative interstitial pneumonia?

A

Smoking related - macrophages predominant with proliferating tissue

Ground glass attenuation

Basal and peripheral, diffusely spread

Half show features of fibrosis, anatomical distortion and traction bronchiectasis.

44
Q

What are features of RBILD?

A

No single predominant abnormality.
Ground glass attenuation
Centrilobular nodules and mild fibrosis

Strongly associated with smoking, generally resolves with cessation.

45
Q

What are features of acute interstitial pneumonia?

A 
Rapidly progressive
ARDS equivalent disease
50% mortality
Diffuse bilateral airspace opacification, in addition to evidence of alveolar damage on histology.
- interstitial thickening
- inflammatory infiltrate
- hyaline membranes (specific for AIP)
- organising pneumonia

Treat with high dose glucocorticoids.

46
Q

What are CT features of NSIP?

A

bilateral patchy and subpleural areas of ground glass changes, lower zone distribution.
often areas of irregular linear opacity
features suggestive of fibrosis but absence of gross honeycombing.
70% CT diagnosis concordance with expert radiologists
ground-glass attenuation
50% have features of fibrosis - anatomical distortion, traction bronchietasis.

STRONGLY ASSOCIATED WITH SCLERODERMA

47
Q

What are histological features of NSIP?

A

varying inflammation and fibrosis within alveolar walls.
no specific changes, c/w alternative diagnoses
temporally uniform - single hit disease
no fibroblastic foci

48
Q

What are clinical feature of UIP?

A

Usually male, progressive SOB, ex smokers

49
Q

What are radiological features of UIP?

A

lower zone and subpleural predominance
maximal posteriorally in bases, increasing anteiorally in upper zones.
reticular patter with honeycombing in 95% of cases
traction bronchiectasis and architectural distortion

50
Q

What are pathological features of UIP?

A

patchy, non uniform variably distributed interstitial changes.
temporal heterogeneity - fibroblastic foci in old collagen
predominantly collagen with minimal associated inflammatory cells
honeycombing (non-sp change)

51
Q

When should patients with ILD be referred for transplantation?

A

When DLCO falls to

52
Q

What drugs have not shown any definitive benefit in ILD?

A

Corticosteroids
Cytotoxics (AZA, Cyclophosphamide)
Cyclosporin A, D-penicillamine, Chlorambucil, MTX, Vincristine

53
Q

What are current recommendations for treatment?

A

Despite lack of evidence, attempt trial of treatment following expert opinion - AZA/Pred/NAC

54
Q

What were findings in the PANTHER-IPF trial?

A

Found reduced rate of progression on NAC/PNL/AZA vs NAC and placebo vs Placebo only.

Ceased early in 3 drug rebgimen due to excess deaths, hospitalisations and serious adverse events.

No evidence for FVC in study pop, however some trends to significance were noted.

55
Q

What were outcomes of the INSPIRE study?

A

Examine the use of IFN-gamma1B in IPF - found no improvement in survival.

Theory that elevated Th2 cytokines were noted in IPF, with anti-TGF-beta

56
Q

What is the MoA of pirfenidone?

A

Inhibits heart, liver and kidney fibrosis
inhibits production of TNFa, TGFb, IFNg, and IL-6 and O2 radicals.
Also increases IL-10

57
Q

What were findings in the PIRFENINDONE-ASCEND study?

A

Shown to improve proportion of patients with >10% FVC decline or death.

Also shown to improve proportion of patients with decline of >=50m on 6MWT or death.

Also shown to improve progression free survival

58
Q

What is the MoA of nintedanib?

A

Tyrosine kinase inhibitor, blocking VEGF, FGF and PDGFR

59
Q

What were outcomes in the IMPULSIS trial for nintedanib?

A

Shown to reduce rate of primary endpoint - annual rate of decline in FEV1
Also reduces time to 1st exacerbation

Delta Med - Respiratory (3 decks)

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