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Respiratory Flashcards

1
Q

COPD definition

A

COPD is caused by chronic bronchitis and emphysema.

Progressive airflow obstruction, due to an abnormal inflammatory response within the lungs due to cigarette smoke / other inhaled particles.

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2
Q

MRC dyspnoea scale

A
  1. No breathlessness except on strenuous exercise
  2. SOB when hurrying or walking up a slight hill
  3. Walks slower than contemporaries on level ground due to SOB, or has to stop for breath
  4. Stops for breath after walking 100m or for a few minutes
  5. Too SOB to leave the house or breathless when dressing
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3
Q

GOLD COPD staging

A

I (mild) - FEV1 >80% predicted
II (moderate) - FEV1 50-80% predicted
III (severe) - FEV1 30-50% predicted
IV (very severe) - <30% predicted or >50% + chronic respiratory failure

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4
Q

Investigations for COPD

A

Bedside: lung function studies, sputum culture, observations, peak flow

Bloods: FBC (anaemia), CRP + WCC (infection), albumin (chronic disease), ABG (hypoxaemia +/- hypercapnia), A1AT levels

Imaging: CXR and HRCT

Other: BMI calculation, echo (to evaluate for pulmonary HTN)

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5
Q

What treatments are available to help patients stop smoking?

A

Behavioural: ‘5 A’s’ approach endorsed by BTS, group counselling

Nicotine replacement therapy (patches, gum, inhalers, nasal sprays)

Medications: bupriopion, varenicline

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6
Q

What are the treatment options available for COPD?

A

Non-pharmacological: pulmonary rehab, optimise nutrition, vaccination (influenza + pneumococcal)

Pharmacological:
1. Short-acting bronchodilators - short-acting b2 agonists and short-acting anticholinergics (combination treatment)
2. Long-acting bronchodilators - long-acting b2 agonists and long-acting anticholinergics
3. LABA + ICS if asthmatic features or steroid-responsive
3. LABA + LAMA if no asthmatic features or steroid responsiveness
4. LABA + LAMA + ICS
5. Theophylline - not recommended for initial treatment

Oxygen: LTOT - indicated in patients with Pa02 <7.3 or Pa02 <8 with secondary polycythaemia, nocturnal hypoxaemia, cor pulmonale, pulmonary HTN. 15h / day

NIV: considered in pts with chronic T2RF despite adequate treatment

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7
Q

Describe the role of surgery in patients with COPD

A

Lung volume reduction surgery

Bullectomy

Lung transplant

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8
Q

What causes an acute exacerbation of COPD?

A

60% infection:
- viruses (rhinovirus, influenza, parainfluenza, coronavirus, adenovirus), - bacteria (haemophilus influenza, moraxella catarrhalis, strep pneumoniae, pseudomonas)

10% environmental pollution

30% unknown aetiology

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9
Q

How are infective exacerbations of COPD treated?

A

Controlled o2 to achieve o2 sats of 88-92%

Salbutamol + ipratropium nebs

Oral corticosteroids: improve lung function and reduce length of hospital stay

Antibiotics: initially empirical tx with aminopenicillin, macrolides or tetracycline

Aminophylline: not recommended as first-line treatment due to side effects

Discharge planning should involve a community COPD treatment team

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10
Q

Describe the use of NIV in the treatment of IECOPD

A

BIPAP - provides pressure support via a facemask with higher IPAP than EPAP
- improves oxygenation, increases removal of co2, increases functional residual capacity, increases tidal volume, decreases respiratory effort
- has been shown to decrease the need for I + V, reduces mortality, results in fewer complications.

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11
Q

Indications for NIV

A

pH <7.35 despite maximal medical and controlled o2 therapy.

Able to consent to treatment and have potential for recovery for QOL acceptable for patient.

Exclusion criteria: life-threatening hypoxaemia, severe comorbidity, facial injuries, vomiting, upper airway obstruction, undrained pneumothorax, bowel obstruction, upper GI surgery, haemodynamic instability.

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12
Q

Pre-requisites for starting NIV

A

Ceiling of care and resus decision needs to be made prior to starting.

Initial pressures: IPAP 12-16 and EPAP 4-5 with oxygen adjusted to reach target sats of 88-92%.

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13
Q

How does CPAP differ from NIV?

A

CPAP maintains the same pressure support throughout the breathing cycle, splinting open the upper airways, recruiting collapsed alveoli and reducing ventilation / perfusion mismatch.

It is used in the treatment of acute pulmonary oedema, OSA and T1RF.

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14
Q

What is cor pulmonale? What is its significance?

A

Right-sided cardiac dysfunction secondary to pulmonary hypertension. The pulmonary HTN must be of a respiratory cause.

Untreated cor pulmonale causes right-sided heart failure and death.

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15
Q

What are the indications for LTOT?

A

LTOT targets = o2 for >16 hours/day, with aim of achieving Pa02 >8 kPa.

Pa02 <7.3 or Pa02 7.3 - 8 kPa in a patient with cor pulmonale.

All patients with FEV1 <30% predicted, signs of RHF and o2 sats <92% should be considered for LTOT.

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16
Q

How would you classify severity of COPD?

A

Based on the presence of symptoms and the percentage predicted of their FEV1.

GOLD staging:

Mild: FEV1 >80%
Moderate: FEV1 50-80%
Severe: FEV1 30-50%
Very severe: FEV1 <30%

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17
Q

Name the common causes of community-acquired pneumonia.

A

Common: strep pneumoniae, haemophilus influenzae, staph aureus

Atypical: mycoplasma pneumoniae, legionella pneumophila, coxiella burnetii

Viruses: influenza, CMV, VZV, Covid-19

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18
Q

List the possible complications of pneumonia.

A

Parapneumonic effusion
Empyema
Cavitation
Lung abscess
Septic shock
Respiratory failure / ARDS
Hepatitis
Haemolytic anaemia
Erythema multiforme

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19
Q

How can we assess the severity of community-acquired pneumonia?

A

CURB-65 score

0-1: low-risk, consider home treatment
2: increased risk
3-5: high risk, admit, consider ITU referral

Confusion (AMTS 8 or less)
Urea >7 mmol/l
Resp rate >30/min
BP <90 systolic and <60 diastolic
Age >65 years

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20
Q

Define hospital-acquired pneumonia.

A

HAP occurs >72 hours after admission to hospital.

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21
Q

What is the difference between an empyema and a complicated parapneumonic effusion?

A

Empyema is pus in the pleural cavity with pH <7.2

Complicated parapneumonic effusion has pH <7.2 but is clear

Parapneumonic effusion has pH >7.2 and is clear

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22
Q

How would consolidation be differentiated from effusion on clinical examination?

A

Tactile vocal fremitus: sound is increased through tissue (consolidation) and decreased through fluid (effusion)

Vocal resonance: is indicative of consolidation when whispered sounds are heard clearly through affected lung tissue

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23
Q

Other than guiding the clinical management of the patient, what other information does a CURB-65 score offer?

A

Indicates mortality associated with the severity of the pneumonia. Higher score = higher mortality rate.

0-1 <5% mortality rate
2- 9% mortality rate
3-5 15-40% mortality rate

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24
Q

Which patients are at high risk of pneumonia?

A

COPD, immunocompromised, the elderly, alcoholics

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25
Q

Respiratory causes of clubbing

A

ABCDEF

Abscess / asbestosis
Bronchiectasis
Cystic fibrosis
Dirty tumours (mesothelioma / bronchogenic carcinoma)
Empyema
Fibrosing alveolitis (IPF)

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26
Q

What is the pathogenesis of CF?

A

Autosomal recessive disease due to defect on CFTR gene on chromosome 7. F508 is the most common mutation.

Frequency in Caucasians is 1:2500 live births (1 in 25 chance of being a carrier).

CFTR gene located in all exocrine tissues. Defective CFTR prevents chloride moving out of cells, which results in osmosis of water into cells, resulting in thick viscous secretions, easily amenable to infection.

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27
Q

What other systems are affected in CF patients?

A

Multisystem disease, with lung disease being the major cause of morbidity and mortality.

GI: pancreatic enzyme insufficiency (malabsorption, diabetes, focal biliary cirrhosis, cholelithiasis)

Reproductive: male subfertility due to defective sperm transport

MSK: osteoporosis

ENT: sinus disease and nasal polyps

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28
Q

What organisms commonly colonise the respiratory tract in CF patients?

A

Haemophilus influenza
Staph aureus
Pseudomonas species
Burkholderia cepacia complex (CI to transplantation in some centres)

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29
Q

What is the prognosis for CF patients?

A

Median survival is 32 years and increasing, many patients live into their 40s and lead active lives.

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30
Q

What are the main complications of bronchiectasis?

A

Pulmonary: recurrent infection, haemoptysis, empyema, cor pulmonale

Extrapulmonary: anaemia, metastatic infections, secondary amyloidosis

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31
Q

What other conditions are known to be associated with bronchiectasis?

A

CTD (e.g., RA)
Chronic sinusitis
Inflammatory bowel disease
Marfan’s syndrome

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32
Q

What are the major pathogens associated with bronchiectasis?

A

Pseudomonas aeruginosa
Streptococcus
Haemophilus influenza

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33
Q

What is bronchiectasis?

A

Abnormal and permanently dilated airways with bronchial wall thickening.
This manifests as a cough with production of thick sputum.

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34
Q

What are the causes of bronchiectasis? (PMMII)

A

Post-infective bronchial damage: severe bacterial / viral pneumonias, measles and pertussis, TB and other mycobacterial infections.

Mucociliary clearance defects: CF, primary ciliary dyskinesia, Kartagener’s syndrome, Young’s syndrome

Mechanical: obstruction (tumour, foreign body)

Immunodeficiency: primary (immunoglobulin deficiency), secondary (HIV)

Immunological: allergic bronchopulmonary aspergillosis

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35
Q

What is the differential diagnosis of bilateral lower-zone crackles?

A

Bronchiectasis: coarse crackles heard in early-mid inspiration

Lung fibrosis: fine end-inspiratory crackles

Pulmonary oedema: fine/coarse bibasal crackles with signs of overload

Bilateral pneumonia: coarse crackles with fever / bronchial breathing

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36
Q

What organisms are commonly found in the sputum of patients with CF, and which are most important for prognosis?

A

Haemophilus influenzae, staph aureus, moraxella catarrhalis, strep pneumoniae, atypical mycobacteria.

Burkholderia cepacia, pseudomonas and mycobacterium abscessus infection are poor prognostic indicators.

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37
Q

What are the respiratory complications associated with CF?

A

Infective exacerbations
Pneumothorax
Haemoptysis
Aspergillus lung disease
Respiratory failure

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38
Q

Are you aware of any new treatments available for CF?

A

The CFTR modulators - Ivacaftor, Orkambi, Symkevi (make the chloride channel functional)

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39
Q

What are the risk factors for active pulmonary TB infection?

A

Place of birth - sub-Saharan Africa and Asia
Age
HIV / AIDS
Homelessness
Previous prison stays
Sex workers
Co-morbidities: diabetes, renal disease, malignancy
Immunosuppressed

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40
Q

How do you treat pulmonary TB?

A

Notifiable disease: contact tracing
Antibiotics (RIPE): rifampicin, isoniazid, pyrazinamide, ethambutol. RI continued for 4 months, P and E stopped after 2 months.

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41
Q

What are the side effects of TB medications?

A

Rifampicin: reduces efficacy of AEDs and COCP. Red discolouration of secretions and urine

Isoniazid: hepatitis, peripheral neuropathy

Pyrazinamide: hepatic toxicity, peripheral neuropathy, gout

Ethambutol: optic neuritis (e, for eye)

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42
Q

What are the complications of pulmonary TB?

A

Pneumothorax
Empyema
Abscess

43
Q

What are the extrapulmonary manifestations of TB?

A

CNS: TB meningitis, tuberculoma
Pericardial TB
Spinal TB
Prostatitis, epididymitis
Miliary TB (haematogenous spread)

44
Q

Discuss past surgical treatments of TB.

A

Induced pneumothoraces
Phrenic nerve crush
Plombage
Thoracoplasty

45
Q

What tests are used in the diagnosis of TB?

A

CXR: enlarged hilum, consolidation, cavitation, pleural effusion, granuloma
Sputum staining: Ziehl-Neelsen stain for acid-fast bacilli
Bronchoscopy and washings
Biopsies of extrapulmonary manifestations
Whole-blood interferon tests
Always consider an HIV test in patients with suspected TB

46
Q

Causes of upper zone fibrosis

A

BREASTS

B: berylliosis
R: radiation fibrosis
E: extrinsic allergic alveolitis, eosinophilic pneumonia
A: allergic bronchopulmonary aspergillosis, ankylosing spondylitis
S: sarcoidosis
T: tuberculosis
S: silicosis

47
Q

Causes of lower zone fibrosis

A

RATIO

Rheumatoid arthritis
Asbestosis
connective Tissue disease
Idiopathic pulmonary fibrosis
Other causes (bronchiectasis, chemical or drug exposure)

48
Q

CXR and CT appearances of pulmonary fibrosis?

A

CXR - reticulonodular shadowing in affected areas

HRCT - reticular pattern, ensuing fibrosis causes ‘honeycomb’ appearance

49
Q

What is Hamman-Rich syndrome?

A

An acute, rapidly progressive lung fibrosis known as acute interstitial pneumonia (IAP). It may respond to steroids but has a poor overall outcome (6-month survival is 22%).

50
Q

What different types of CT imaging do you know about and when should each be used?

A

High-resolution CT - most useful for assessment of interstitial processes (fibrosis / emphysema) and endobronchial changes with ‘tree in bud’ appearances.

Dynamic (standard CT) - most useful for assessment of pneumonia or malignancy and mediastinal pathology (staging LNs).

CTPA - main diagnostic investigation for PE.

51
Q

What are the main treatments available for pulmonary fibrosis?

A

Corticosteroids
Immunosuppressants: cyclophosphamide, azathioprine, MTX, ciclosporin
Anti-oxidant: NAC + corticosteroids + azathioprine
Supplemental oxygen
Lung transplant (60% 1-year survival)

52
Q

In addition to steroids and immunosuppressives, are you aware of any other treatments for pulmonary fibrosis?

A

Anti-fibrotic agents: evidence for their use in IPF is limited and they are rarely used in clinical practice (pirfenidone).

Can use bosentan or warfarin for their role in pulmonary hypertension.

53
Q

Comment on prognosis and list favourable prognostic factors in IPF.

A

Mean survival 2.8 years
5-year survival is 50%
Favourable prognostic factors include the NSIP subtype

54
Q

Which disorders typically have high lymphocyte count on BAL?

A

Hypersensitivity pneumonitis
Sarcoidosis
Organising pneumonia
Lymphocytic interstitial pneumonia

55
Q

Describe the ‘rheumatoid lung’ (LIPO)

A

Lung fibrosis
Intrapulmonary nodules
Pleural effusions
Obliterative bronchiolitis

Can get Caplan’s syndrome: rheumatoid pneumoconiosis in people with RA who have breathed in coal dust / silica

56
Q

Causes of transudates?

A

CCF
Hypoalbuminaemia (nephrotic syndrome)
All failures (cardiac, renal, hepatic)
Meig’s syndrome (ovarian fibromas and pleural effusions)

57
Q

Causes of exudates?

A

Parapneumonic effusion
Lung infarction
Lung malignancy
Connective tissue disorders

58
Q

Investigations for pleural effusion?

A

CXR, USS guided pleural tap - sent for LDH, pH, protein, amylase, glucose, cytology, microscopy and culture

59
Q

Light’s criteria for pleural effusion?

A

Exudates demonstrate:

  1. The ratio of pleural albumin to serum albumin is >0.5
  2. The ratio of pleural LDH to serum LDH >0.6
  3. Pleural LDH >2 thirds of the upper limit of normal serum LDH
60
Q

What causes a pleural effusion that is low in glucose?

A

MEAT:

Malignancy
Empyema
Arthritis (RA)
TB

61
Q

List some drugs that cause a pleural effusion

A

Amiodarone, phenytoin, methotrexate, nitrofurantoin, beta-blockers

62
Q

What is the main indication for a thoracoscopy?

A

To investigate an exudative effusion of uncertain cause, as it yields a better diagnostic rate than pleural tap, and pleural biopsies can be taken at the same time.

It can also be used to drain the effusion and perform pleurodesis.

63
Q

Are there weaknesses of Light’s criteria in differentiating transudates from exudates?

A

25% of patients with transudates are mistakenly identified as having exudates by Light’s criteria.

If a transudative effusion is suspected clinically, calculate the serum/pleural albumin gradient. If this value is <1.2 g/dl then this is 100% specific and 95% sensitive for an exudate.

64
Q

What are parapneumonic effusions?

A

Exudative effusions that accompany approximately 40% of bacterial pneumonias. They can be:

Simple: sterile and resolves with treatment of pneumonia
Complicated: 1/2 of hemithorax or empyema (requires pleural drainage via chest drain)

65
Q

Outline the management of a pleural effusion. What additional management is needed in cases of recurrent effusions?

A

Supportive: o2, IV fluids, chest physio
Diagostic +/- therapeutic thoracocentesis or chest drain insertion
Effusions should be drained slowly
Treatment of underlying cause: diuretics, antibiotics

For recurrent effusions: continuous tube thoracostomy, pleurodesis (common in malignant effusions), pleuro-peritoneal shunt (rarely used)

66
Q

Differentiate between a thoracoscopy and mediastonoscopy.

A

Thoracoscopy (VATS): surgical procedure involving visualisation of the pleural cavity for diagnosis and therapeutics. A mediastinoscopy visualises the mediastinum.

A thoracoscopy scar is observed laterally, whereas a mediastinoscopy is located anteriorly over the mediastinum.

67
Q

What is ‘yellow nail syndrome’?

A

A rare cause of exudative pleural effusions. Patients with this condition also have yellow curved nails, lymphoedema, bronchitis / bronchiectasis, sinusitis, nephrotic syndrome and hypothyroidism.

68
Q

In obesity-related hypoventilation syndrome (OSA, hypercapnia, restrictive defect on PFTs), how many types of ‘abnormal’ respiratory events are described during sleep?

A

3 types of apnoea have been recognised:

Central: cessation of ventilatory drive from the respiratory centres in the brain.
Obstructive: collapse of the upper airway, more easily treatable with weight loss, removal of obstruction and weight loss.
Mixed: central and obstructive

69
Q

What causes the ‘obstruction’ in OSA?

A

At least 2 of:

Upper airway narrowing
Upper airway collapse
Abnormality in control of upper airway muscle tone

70
Q

Outline treatment for OSA and OHVS

A

Weight loss
Smoking and alcohol reduction
CPAP therapy delivered by nasal/face mask (1st line treatment)
NIV may be used instead of CPAP in OHVS (hypercapnia)
LTOT where indicated
Oral mandibular advance devices
Surgery: UPPP
Medications: orlistat, fluoxetine, modafanil

71
Q

What complications are associated with OSA?

A

Cardiac arrhythmias, systemic hypertension, MI stroke, OHVS, pulmonary HTN, increased mortality

72
Q

How can one estimate body fat at the bedside?

A

Measuring skinfold thickness at the biceps, triceps, subscapular and suprailiac regions

73
Q

Name some diseases where obesity is a manifestation

A

Endocrine: hypothyroidism, PCOS, hypothalamic disease, Cushing’s syndrome

Genetic: Prader-Willi syndrome, Laurence-Moon-Bardet-Biedl syndrome

74
Q

Describe the risk factors for developing lung cancer

A

Smoking (90% of cancers associated with smoking, adenocarcinoma is the only one that isn’t)

Radiation therapy, environmental exposure to smoke, asbestos, radon, metals.

Pulmonary fibrosis, COPD, A1AT deficiency, FH of lung cancer.

75
Q

Describe the histological classification of lung cancer.

A

Non-small cell lung cancer: 75-80% of lung cancers.
Adenocarcinoma > squamous cell > alveolar > large cell

Small-cell lung cancer: 15% of lung cancers.
Rapidly proliferating tumour with early metastasis.

76
Q

Name the common sites of lung cancer metastases.

A

Liver, adrenal glands, bone, brain.

77
Q

Which paraneoplastic syndromes are associated with lung cancer?

A

SCLC: most commonly assoc with paraneplastic syndromes.
- ECTH and ADH causing Cushing’s syndrome and SIADH. Lambert-Eaton myaesthenic syndrome.

Squamous cell: PTHrP resulting in hypercalcaemia.

Adenocarcinoma: hypertrophic pulmonary osteoarthropathy (HPOA) - results in gross finger clubbing and arthritis with radiological evidence of subperiostial new bone formation.

78
Q

Describe the staging classification of SCLC.

A

Limited disease: confined to ipsilateral hemithorax. Median range of survival 15-20 months.

Extensive disease: metastatic disease outside ipsilateral hemithorax. Median range of survival 8-13 months.

79
Q

What other prognostic factors help guide treatment in lung cancer?

A

WHO performance score
Weight loss

80
Q

Describe the management of patients with NSCLC

A

Discuss at lung cancer MDT
Lung cancer CNS
Surgery: lobectomy / pneumonectomy (depends on lung function and comorbidities)
Radical radiotherapy
Chemotherapy offered to patients with stage III or IV cancer with good performance status.
Palliative: for stage IV disease. Radiotherapy to control local symptoms, involvement of palliative care team and EoL care and support.

81
Q

Describe the management of SCLC.

A

Combination treatment with radiotherapy and platinum-based chemotherapy.

Prophylactic cranial irradiation considered in patients who respond to treatment - reduces incidence of brain metastasis.

82
Q

What are the signs of Pancoast’s syndrome?

A

Pancoast’s syndrome is caused by an apical lung tumour with involvement of the brachial plexus and cervical sympathetic nerves which results in:

Anhydrosis
Ptosis
Miosis
Enophthalmos

83
Q

What are the common causes of SVC obstruction?

A

Lung cancer
Lymphoma (NHL)
Others: thymoma, solid tumours w/ LN mets, post-radiation fibrosis, thoracic aortic aneurysm, thrombosis

84
Q

Describe the management of SVCO.

A

Unless evidence of respiratory compromise or cerebral oedema, the cause should be investigated before treatment is started.

Steroids
Endovascular stent
Chemo / radiotherapy

85
Q

What are the clinical signs and symptoms of SVCO?

A

Oedema of the face, neck and upper body
Prominent neck and chest wall vessels
Facial plethora
Stridor
Headache worse on bending forward
Dizziness

86
Q

Main causes of a posterolateral thoracotomy scar, and clinical presentation on examination?

A

Pneumonectomy: empty unilateral cavity, fills with fluid giving dull percussion note and decreased breath sounds.

Lobectomy: hyperinflation of ipsilateral lobes occurs, which may partially mask clinical signs making them difficult to appreciate.

Open lung biopsy: if clinical findings don’t fit with pneumo/lobectomy, the scar may be explained by an open lung biopsy which is shorter (3-4cm).

87
Q

How would you differentiate between a lobectomy and pneumonectomy?

A

Pneumonectomy: traches deviates towards side of surgery, decreased breath sounds over entire lung field, reduced chest expansion.

Lobectomy: trachea may be shifted away from the side of surgery, audible breath sounds in lobes that remain, chest expansion may be reduced.

88
Q

What are the criteria for lung surgery in lung cancer?

A

Patients must have an FEV1 >1.51, and transfer factor of >50%.

They cannot have any evidence of pulmonary hypertension and no evidence of metastatic disease.

Surgery is only beneficial in peripheral, non-small cell disease.

89
Q

What are the indications for a lung transplant?

A

People with emphysema (usually A1AT deficiency).
Idiopathic pulmonary fibrosis
Idiopathic pulmonary hypertension
Bronchiectasis and CF

90
Q

What are the absolute contraindications for lung transplantation?

A

Malignancy in last 2 years
Substance abuse
Chest wall deformity
Poor social support
Psychiatric illness
Advanced extrapulmonary organ dysfunction
Noncurative infections such as HIV

91
Q

What are some reasons for performing a pneumonectomy / lobectomy?

A

Lung malignancy / pulmonary mets
Localised bronchiectasis with uncontrolled haemoptysis
Old TB
Fungal infections (aspergilloma)
Traumatic lung injury
Large emphysematous bullae
CF

92
Q

What are the chest radiographic features in a pneumonectomy / lobectomy?

A

‘White out’ on one side (pneumonectomy)

Deviated trachea towards pneumonectomy / lobectomy

Compensatory hyperinflation of opposite lung/lobes

93
Q

What is the importance of pre-operative evaluation in pneumonectomy?

A

Pre-op evaluation is important due to the significant loss of lung function that follows.

Preop FEV1 >2L, low risk, no further PFTs in absence of pulmonary HTN.
Preop FEV1 <2L, high risk, need to have V/Q scanning.

Preop cardiopulmonary testing can also be performed.

94
Q

Are you aware of any subtypes of pneumonectomy?

A

Simple: removal of affected lung.

Extrapleural: removal of lung plus part of diaphragm, parietal pleura and pericardium on ipsilateral side. These linings are then replaced by surgical Gore-Tex. Primary use of EPP is in treatment of malignant mesothelioma.

95
Q

If a patient had a lobectomy secondary to lung malignancy, can you suggest a likely subtype of lung cancer?

A

Surgery has a greater role in the management of NSCLC rather than SCLC which has a poorer prognosis, and is almost always unsuitable for surgery by the time of presentation.

96
Q

What proportion of NSCLC’s are suitable for surgery?

A

Approx 25% of NSCLC will be suitable for surgical resection.

97
Q

Comment on operative mortality of a) lobectomy and b) pneumonectomy. Are there any differences between right and left sides?

A

Operative mortality for lobectomy: 2-4%
Mortality for pneumonectomy: 6%

Right sided pneumonectomy is associated with higher mortality. Reasons are unclear, but most likely due to life-threatening complications such as space empyema, pulmonary oedema and bronchopleural fistula.

98
Q

What is the ‘post-pneumonectomy syndrome’?

A

Results from the extrinsic compression of the distal trachea and mainstem bronchus due to mediastinal shifting and compensatory hyperinflation in the remaining lung.

Occurs almost exclusively in patients with right-sided pneumonectomy.

Consists of: progressive dyspnoea, cough, stridor and pneumonia.

99
Q

What is the definition of pulmonary hypertension?

A

Mean pulmonary artery pressure >25 mmHg with a pulmonary capillary or left atrial pressure <15 mmHg.

Caused by an increase in pulmonary blood flow, increase in pulmonary vascular resistance or elevated pulmonary venous pressure.

100
Q

Common causes of cor pulmonale?

A

COPD (10-40% of patient, poor prognostic indicator)
Interstitial lung disease
OSA
Hypoventilation disorders including obesity-related hypoventilation, neuromuscular disorders, kyphoscoliosis

101
Q

What are the indications for surgical management of pneumothoraces?

A

Surgery is not first-line management for pneumothorax.

However, with ongoing problems including air leak, or recurrent pneumothoraces – surgery is an option

Pleurodesis or pleurectomy may be offered

Bullectomy may be offered

Open thoracotomy and VATS – VATS is much less invasive and carries a lower risk of wound infection, ongoing pain and associated with earlier discharge. However, after VATS there is risk of recurrent pneumothorax, greater than open thoracotomy.

102
Q

What investigations would you request for a patient with suspected pulmonary fibrosis?

A

Bedside: lung function tests (FEV1/FVC >0.8 - restrictive), observations

Bloods: ABG (T1RF), ESR, rheumatoid factor, ANA

Imaging: CXR and HR-CT (honeycombing and ground-glass changes)

Special: lung biopsy (morbidity 7%), bronchoalveolar lavage (to exclude infection prior to immunosuppression, and if lymphocytes > neutrophils this indicates a better response to steroids and better prognosis)

103
Q

What treatments are available for a patient with pulmonary fibrosis?

A

Immunosuppression if likely to be inflammatory (NSIP) - steroids
Pirfenidone (anti-fibrotic)
N-acetylcysteine - free radical scavenger
Single lung transplant - in exams will be unilateral fine crackles with normal breath sounds on the other side

104
Q
A

PACES retrieval practice (10 decks)

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