Respiratory Flashcards

1
Q

What is the main risk factor for COPD?

A

Smoking

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2
Q

What condition does alpha1-antitrypsin deficiency make you more susceptible for? And what is the usual age of onset?

A

COPD (lung disease) and Liver disease. Lung disease usually comes on at the age of 20-50.

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3
Q

What are the signs of emphysema? (PP or BB)

A

Pink Puffer = Barrel chest, pursed lips, muscle wasting

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4
Q

What is the pathology of emphysema?

A

Reduced elasting which causes reduced surface area –> collapsed alveoli. Due to reduced recoil this causes air trapping.

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5
Q

What would the blood gases look like for a patient with suspected emphysema?

A

Normal. Due to the effort they put in (pursed lips).

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6
Q

What are the signs of Chronic Bronchitis? (PP or BB)

A

BB = Productive cough, oedema and raised JVP. VQ mismatch and right heart failure. Fibrosis may be present and they may be hypoxic.

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7
Q

What is the pathology of Chronic bronchitis?

A

Hypersecretion and reduced cilia = airway obstruction

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8
Q

What are the 2 main investigations for COPD diagnosis - and what would they show?

A

Chest X-ray –> flat diaphragm and hyperinflated

Spirometry - reduced exhalation. FEV1:FVC = less than 70%

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9
Q

What is the 1st line treatment for COPD (in most patients - non-pharmalogical)?

A

SMOKING CESSATION

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10
Q

What are the pharmacological options for patients with COPD? (1st option –> if there are exacerbations –> oral –> aids –> surgery)

A

Inhaler = B2 agonist (salbutamol) or M3 antagonist
+ corticosteroid inhaler if there are exacerbations
Oral = Theophylline (dilation) or Macrolides - reduce exacerbations for ex-smokers
Aids = Oxygen - long term or ambulatory
Surgery = Lung transplant or resection (remove damaged area so the rest is more efficient)

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11
Q

What is the definition of asthma?

A

Reversible widespread bronchoconstriction which varies over time.

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12
Q

What are the symptoms of asthma? (is there a time pattern)

A
Breathlessness 
Chest tightness 
Cough 
Wheeze 
- diurnal variation
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13
Q

Non-specific triggers of asthma?

A

Exercise, cold air, fumes and smoke

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14
Q

Specific triggers of asthma?

A

Allergens

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15
Q

What are the 2 forms of asthma?

A

Atopic (allergic) or Intrinsic

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16
Q
Atopic asthma - 
When is the onset?
What are other common co-morbidities?
What antibody is produced and where?
How do they respond to treatment?
A

Childhood onset
Eczema and rhinitis
IgE - systemically (skin prick test)
Good response to treatment

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17
Q
Intrinsic asthma - 
When is the onset?
What are other common co-morbidities?
What antibody is produced and where?
How do they respond to treatment?
A

Late onset (adulthood)
Sinusitis and polyps
IgE - locally
Reduced response to treatment - increased response when steroids are used.

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18
Q

Which cells in the lamina propria are increased in asthma- and what are their roles (3)

A
Mast cells - histamine release 
Neutrophils - pro-inflammatory 
T2 helper cells - become unregulated 
- IL 13/4 = activate mast cells 
- IL 9 = Activate MC complex 
- IL 5 = increased eosinophils
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19
Q

What are the 2 stages of a asthma attack?

A

Early - rapid FEV1 drop - mast degranulation

Late (4-12 hours) - eosinophil recruitment - gradual FEV1 drop

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20
Q

What are the investigations for asthma (2)?

A

FeNO - 40ppb +

Spirometry - FEV1:FVC = less than 70%

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21
Q
  1. What is the reliever treatment for asthma? (when do you move to next treatment) ?
A

SHort acting B2 agonist (salbutamol)

Move up pathway if using 3+ times a week

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22
Q
  1. Initial preventer treatment for asthma?
A

Low dose inhaled corticosteroid - beclomethasone

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23
Q
  1. Add on preventer treatment for asthma?
A

Long acting B2 agonist (salmeterol)

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24
Q
  1. 2nd add on for asthma?
A

Anti-leukotrienes (Montelukast) - reduce constriction and anti-inflammatory.
Theophylline - Increase cAMP (bronchodilator)
Long acting muscarinic antagonist (ipratropium) - reduce constriction and mucus

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25
Q
  1. Last resort treatment for asthma (medication)?
A

Oral steroids (prednisolone)

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26
Q

What are the 3 things to give in a status asthmaticus?

A

Oxygen + B2 agonist nebuliser + Steroid (IV hydrocortisone/prednisolone)

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27
Q

If the first treatment for status asthmaticus doesn’t work (15-20 mins) what should be given next?

A

Ipratropium and Magnesium (reduces calcium levels)§

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28
Q

Multisystem disorder characterised by noncaseating granulomatous inflammation - What condition is this?

A

Sarcoidosis

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29
Q

A patient presents with sudden onset dyspnoea accompanied with some chest pain and a cough. They have a fever and have felt general malaise recently. They also state that they feel their clothes have been getting loser and they haven’t wanted food as much recently. O/E they have red bumps on their legs which are warm to the touch, hard and painful. They also have some anterior uveitis and mention some of their joints have been painful recently. What is the most likely diagnosis and how would you further investigate?

A
Acute sarcoidosis.
Want to do bloods: 
- increase in inflammatory markers 
- Normal ACE, IgG, Calcium and ALP 
Pulmonary function tests 
Chest x-ray = hilar lymphadenopathy.
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30
Q

What is the treatment/management for acute sarcoidosis?

A

Majority will resolve spontaneously if more severe than can give bed rest and NSAIDs. Steroids and immunosuppressants if continuously severe.

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31
Q

What are the symptoms of chronic sarcoidosis? (A GRUELLING Disease)

A
ACE increase 
Granulomas 
Arthritis 
Uveitis  
Erythema nodosum 
Lymphadenopathy 
Lupus pernio 
Idiopathic 
Non-caseating 
Gammaglobulinemia 
Vitamin D increase (calcium increase)
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32
Q

A patient comes in with left hyper resonance, Right tracheal deviation and a raised JVP. What is the most likely diagnosis and which side?

A

Left sided tension pneumothorax

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33
Q

What is a pneumothorax?

A

Air in the pleural space causing partial or total lung collapse

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34
Q

When and in who are pneumothorax most likely to occur?

A

More likely in men

Peak at 20-30 years and at 60-70 years

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35
Q

What is the presentation of a pneumothorax and how may they differ between the old and young?

A

Young = chest pain (anterior radiating to the back)
Old = Dyspnoea
Non-productive cough
Tympanic resonance and decreased respiratory murmur over the affected side.
12% can be asymptomatic

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36
Q

What is the difference between type 1 closed pneumothorax and type 2 open pneumothorax?

A

Type 1/Closed = spontaneous. Usually due to a small visceral pleura laceration which can spontaneously close and the air is reabsorbed. No invasive treatment is required.

Type 2/Open = Most likely due to lung disease (emphysema). Due to a large laceration in the visceral or parietal pleura which is unable to close. There are repeated shifts of the mediastinum and needs to be treated immediately!

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37
Q

How would you deal with a small asymptomatic pneumothorax?

A

Bed rest - lie of affected side, anticoagulate and give oxygen. Can be discharged.

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38
Q

In what pneumothorax case would you aspirate with a 16-18g cannula? And what would you do after aspirating?

A

Aspirate in 2nd intercostal space mid clavicular
Large primary or small secondary pneumothorax. Symptomatic patient.
Put on high flow oxygen and observe.

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39
Q

If a patient with a pneumothorax has been aspirated and has not improved or they have a large secondary pneumothorax what would you do?

A

Put in a chest drain - until there is no leak of air and the lung has expanded and fluid is being removed.
Chest drain into 5th-6th intercostal space mix axillary.

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40
Q

What is a tension pneumothorax?

A

Ruptured tissue causes a valve to be made so on inspiration air enters the cavity and on expiration it doesn’t leave causing there to be a total lung collapse.
Causing there to be a big mediastinal shift.

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41
Q

What is and when does vena cava kinking occur?

A

Vena cava gets compressed in a tension pneumothorax causing there to be decreased venous return = reduced cardiac output. This can lead to a arrhythmia.

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42
Q

What is the treatment for a tension pneumothorax?

A

MEDICAL EMERGENCY!
Immediate aspiration - cannula 2nd intercostal space midclavicular. Then a chest drain to be placed in once the initial relief has occurred.

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43
Q

When would surgery be thought about in the case of pneumothoraces?

A

Recurrent episodes
First episode but a high risk patient
Prolonged air leak

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44
Q

What are the surgical options for pneumothoraces?

A

Resection of a bullous dystrophic lung. Video assisted thoracic surgery. Can be a apex, bleb(mm), Bullae (cm) or giant bullae (over 1/3rd)

Pleurodesis - abrasion of parietal pleura (stick lung to chest so that nothing can get in the pleural space).
Pleurectomy = removal of parietal pleura. Create strong pleuroparenchymal adhesions.

45
Q

What drug can people not have post-pleurectomy?

A

NSAIDs§

46
Q

What is the primary mutation found in cystic fibrosis?

A

DeltaF508

47
Q

What is a normal CTFR and how does it work/what does it do?

A

Epithelial chloride channel - bronchial
Inactive form is inserted and then activated by ATP
It moves 90% of the chloride and negatively regulates the Na channel

48
Q

What is the consistency of normal mucous in the respiratory tract?

A

Thin layer with high elasticity and low viscosity
- traps particulates and pathogen and moves them along the mucociliary escalator
H2O, Na, and Cl move to maintain this

49
Q

What are the consequences of having the delta F508 mutation?

A

CTFR is never expressed = CF

50
Q

What is the pathophysiology of cystic fibrosis?

A

Large mucous production (thick) causing the failure of the mucociliary escalator.
More sodium into the cell due to the lack of negative regulation from the CTFR - increased activity of Na/K ATPase also causes a huge energy loss
Due to the increased sodium in the cell the water also moves into the cell causing the mucous to be thick
Cilia are unable to beat due to large amount of mucous causing bacterial colonisation

51
Q

What is the role of neutrophils in cystic fibrosis?

A

Move in to the mucous to try and clear the bacteria however become frustrated and phagocytose releasing O₂⁻ and proteases which leads to lung tissue destruction

52
Q

A 2 yr old child presents to the GP with their 4th chest infection in the year in which they are coughing up a lot of mucous. The child is generally failing to thrive and is on the 95th centile for weight and height. The child has also noticed that their sweat is very salty. What is the most likely diagnosis and what signs would you expect to see O/E?

A

Cystic fibrosis

  • finger clubbing
  • cyanosis
  • coarse crackles over areas of bronchiectstasis
53
Q

What are important differentials to think about in a cystic fibrosis presentation?

A

Pneumonia, malignancy, PE
coeliac if there is abdominal involvement
Primary ciliary dyskinesia

54
Q

What investigations would be done for a query cystic fibrosis?

A

Bedside
- urine dip = in case of diabetes
- Lung FTs - obstructive picture is most common
Bloods = FBC, U+Es, LFTs, CRP, glucose, vitamins (A, E,C)
Sputum culture - haemophilus influenza, staph aureus, pseudomonas aeruginosa
Sweat testing = high chloride (98%)
Genetic testing - CTFR
Stool test - faecal elastase (pancreatic insufficiency)
Imaging - CXR = bronchiectasis and hyperinflation
HRCT - bronchial thickening and bronchiectasis. Mucous plugging
CT angio - if there is haemoptysis

55
Q

What is the management of cystic fibrosis?

A
Physiotherapy and mucolytic agents to help clear the mucous. 
Prophylactic antibiotics (azithromycin) and early antibiotics in the case of acute exacerbations
56
Q

What is the main bacteria for TB?

A

Mycobacterium Tuberculosis

57
Q

How is TB spread?

A

Via droplet spread - sustained close contact

58
Q

What is the pathogenesis of TB?

A

MBTB goes into pulmonary alveoli –> alveolar macrophages and it replicates in them –> lymphocytes and fibroblasts come to the infected macrophage and cause granulation formation (protects the TB from spreading) –> centre of the granulation can die-caseous necrosis and lead to latent TB

59
Q

What is the main presentation of TB?

A
Pulmonary only (90%) 
cough +/- haemoptysis and shortness of breath for more than 2-3 weeks. 
Also have fever, night sweats and weight loss
60
Q

What are possible extrapulmonary symptoms of TB?

A

Only 10% of cases
Meningitis, choroiditis (red and inflamed eye), lupus vulgaris, constrictive pericarditis, dysuria, haematuria, RIF mass/pain, ascites, arthritis, osteomyelitis

61
Q

How is active TB diagnosed?

A

Chest x-ray - patchy nodal shadows (upper lobe)
3 sputum samples (seperate times and 1 in morning)
Ziehm-neelson - acid fast bacilli (50%)

62
Q

How is latent TB diagnosed?

A

TST test to screen high risk patients

Interferon gamma release assay

63
Q

What is the biggest risk for TB?

A

HIV

64
Q

where in the lung does TB primarily stay?

A

Ghon focus (upper lobe)

65
Q

What is the treatment for active TB?

A

Multi drug regime = isoniazid, pyrazinamide, ethambutol, rifamycins

66
Q

What is a possible side effect of ethambutol?

A

Optic neuritis - red/green colourblindness

67
Q

What is the treatment for latent TB?

A

single antibiotic for 3-6 months

68
Q

What is bronchiectasis?

A

Permanent dilation of bronchi - irreversible bronchial wall damage

69
Q

What are the causes of bronchiectasis?

A

Post infection - TB, childhood LRTI, ABPA
COPD/Asthma
primary ciliary dyskinesia, CF, alpha 1 anti-trypsin deficiency
RA
SLE
Sarcoidosis
Idiopathic (40%)

70
Q

What is the pathophysiology of bronchiectasis?

A

trauma –> immune recruitment –> inflammation –> loss of elastin and muscle = dilatation.
This increases the colonisation of bacteria which further causes inflammation and damage –> dilation

71
Q

How may bronchiectasis present? (signs and symptoms)

A
Cough - daily, mucopurulent, haemoptysis (50%) 
Dyspnoea 
rhinosinusitis - facial ache
Fatigue
Clubbing 
Coarse crepitus 
rhonchi (snoring) 
high pitched inspiratory squeaks and pops
72
Q

What bedside investigations could be done to confirm bronchiectasis?

A
Sats 
Sputum sample - pseudomonas aurgelia /haemophilus influenza 
lung function tests - obstructive 
ECG - can cause pulmonary hypertension (tall R waves and RAD) 
FBC, CRP 
autoimmune screen 
IgE (ABPA) 
CF genetic test (F508)
73
Q

What imaging can be done to confirm bronchiectasis?

A

CXR = severe - tram lines and ring shadows
HRCT - gold standard = bronchial dilation and thickening
Bronchoscopy - if it is localised

74
Q

Differential diagnosis for bronchiectasis - productive cough, dyspnoea, fatigue and rhinosinusitis?

A

COPD
Asthma
Pneumonia
chronic sinusitis

75
Q

What is the conservative management for bronchiectasis?

A

pulmonary rehab - physio
smoking cessation
vaccination - flu and pneumonia

76
Q

What is the medical management for bronchiectasis?

A

Mucoactive agent
long term antibiotics
bronchodilator - formoterol
Long term oxygen

77
Q

Surgery options for bronchiectasis and when to do them?

A

Lung resection

Lung replacement - if under 65, quickly worsening and no treatments have been effective

78
Q

What is pneumonia?

A

Infection of the lung tissue causing inflammation of the lung parenchyma and sputum fills the airways and alveoli

79
Q

What classifies as hospital acquired pneumonia?

A

48hrs after hospital admission

80
Q

What are the symptoms of pneumonia?

A
Shortness of breath 
Productive cough 
haemoptysis 
pleuritic chest pain 
fever 
delirium
81
Q

What are the signs of pneumonia?

A
Tachypnoea 
tachycardia 
hypoxic 
hypotension 
bronchial breathing 
focal coarse crackles 
dullness on percussion
82
Q

What does the CURB-65 score determine and what are the points for it?

A
Confusion 
Urea >7 
Respiratory rate >30 
BP <90 systolic 
if they are 65 and older 
0-1 = home treatment 
2 = hospital admission 
3+ = ICU
83
Q

What are the 2 main causes of pneumonia?

A

Streptococcus pneumoniae

Haemophilus influenza

84
Q

What are atypical causes of pneumonia (2) and how may people contract them/what are specific signs?

A

Legionnaires - hot tubs/AC. Causes SIADH = hyponatremia

Mycoplasma pneumoniae = erythema multiforme

85
Q

What investigations would be carried out if a patient was in hospital for pneumonia and what might be added on if they have severe pneumonia?

A

CXR = consolidation
FBC, CRP, U+Es
Severe = sputum and blood culture and urinary antigens

86
Q

What is the treatment for mild and severe CAP?

A

Dependent on each trusts policy
mild = 5 day oral antibiotics - amoxicillin or macrolide
severe = 7-10 days oral antibiotics - amoxicillin and a macrolide

87
Q

What are possible complications of pneumonia?

A
sepsis 
pleural effusion 
empyema 
Lung abscess 
death
88
Q

What is a pleural effusion?

A

Collection of fluid in the pleural cavity

89
Q

What is exudate and what type of pleural effusion is this related to +examples ?

A
>3g protein - related to inflammation 
lung cancer 
pneumonia 
RA 
TB
90
Q

What is transudate and what type of pleural effusion is this related to and examples?

A
<3g protein - fluid shift relation 
congestive cardiac failure 
hypoalbuminemia 
hypothyroidism 
Meigs syndrome - right pleural effusion secondary to ovarian malignancy
91
Q

A patient comes into the GP for shortness of breath that came on quite suddenly. On examination there is dullness of the right sided lung base and reduced breath sounds in this area. The trachea is deviated to the left.. What is the most likely diagnosis and management plan?

A

Pleural effusion
CXR = costophrenic blunting, fluid in the fissures
If its large - meniscus and tracheal and mediastinal deviation.
Fluid sample
Treatment
- small - resolve underlying cause
large = aspirate and chest drain

92
Q

What is empyema?

A

infected pleural effusion
- pus, acidic, decreased glucose and increased LDH on the aspiration
Drain and give antibiotics

93
Q

What is pulmonary hypertension and what can it lead to?

A

Increased resistance and pressure in the pulmonary arteries leading to right heart strain and increased systemic venous pressure

94
Q

What are the 5 groups of pulmonary hypertension causes?

A
1 = primary PH or CT disease (SLE) 
2 = Left heart failure 
3 = chronic lung disease (COPD) 
4 = pulmonary vascular disease (PEmbolism) 
5 = Misc - sarcoidosis, glycogen storage disease
95
Q

What is the presentation for pulmonary hypertension?

A
Shortness of breath
syncope 
tachycardia 
Increased JVP 
hepatomegaly 
peripheral oedema
96
Q

What could possibly be seen on a ECG of a patient with pulmonary hypertension and why?

A

Right ventricular hypertrophy - increased R waves in V1-3

  • right axis deviation
  • RBBB
97
Q

What investigations can be done in the case of suspected pulmonary hypertension?

A

BNP
CXR
ECG
ECHO

98
Q

What is the management for primary pulmonary hypertension?

A

IV prostanoids
Endothelin receptor antagonists
Phosphodiesterase-5 inhibitors

99
Q

What are interstitial lung disease?

A

Conditions that affect the parenchyma causing inflammation and fibrosis

100
Q

What are the general symptoms for interstitial lung disease?

A

Progressive exertional dyspnoea
dry cough
arthralgia
malaise

101
Q

What is most likely to be found on examination of a patient with interstitial lung disease?

A

bilateral fine end inspiratory crepitations (velcro)
clubbing
Possible pulmonary effusion

102
Q

How is interstitial lung disease diagnosed?

A

HRCT - ground glass, honeycombing, bronchiectasis and opacities
Biopsy if HRCT is not clear

103
Q

What are the more specific symptoms/history of idiopathic pulmonary fibrosis?

A

3+ history of symptoms
no clear cause
50+

104
Q

What 2 drugs can be used for idiopathic pulmonary fibrosis?

A

Pirfenidone = antifibrotic and anti inflammatory

Nintedanib - monoclonal antibody for tyrosine kinase

105
Q

What drugs can cause interstitial lung disease?

A

Amiodarone, cyclophosphamide, methotrexate, nitrofurantoin

106
Q

What are the causes of secondary pulmonary fibrosis ?

A
Alpha-1 anti-trypsin deficiency 
RA 
SLE 
Sclerosis 
Sarcoidosis
107
Q

What is cryptogenic organising pneumonia and what is the treatment for it?

A
Focal inflammation (consolidation) 
- oral corticosteroids
108
Q

What properties does asbestos have and what conditions/signs is it likely to cause?

A

Fibrogenic and oncogenic
- fibrosis, pleural thickening and plaques
adenocarcinoma/mesothelioma