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PACES > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Management of Asthma?

A

o Use a stepwise approach as per BTS
o Initial SABA
o If not controlling symptoms then ICS
o Can add in ICS with LABA (combined therapy)
o Can then add in montelukast
o If none of these are appropriate then can use PO steroids or refer to respiratory team

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2
Q

Diagnostic tests in Asthma?

A

o Spirometry and reversibility – obstructive picture with an improvement in FEV1 of 12% or atleast 200ml FEV1 following bronchodilator
o Fractional exhaled nitric oxide (biomarker of lung inflammation) of >40 parts per billion in steroid naïve adults is diagnostic
Eosinophilia and high IgE levels are supportive
Diurnal variation of PEFR diary supportive

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3
Q

Causes of airflow obstruction?

A

Asthma
COPD
Obliterative bronchiolitis
Bronchiectasis

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4
Q

Indications for a VATS procedure?

A
  • Lobectomy/wedge resection
  • Decortication
  • Bullectomy or pleurectomy for recurrent pneumothorax
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5
Q

When may surgery be indicated for a pneumothorax and what is option?

A

Recurrent pneumothorax or ongoing problems such as air leak
Pleurectomy
Pleurodesis
Bullectomy if bullae

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6
Q

Open surgery versus VATS for pneumothorax?

A

VATS less invasive and therefore lower risk with lower risk of pain, wound problems and associated in general with earlier hospital discharge and return to normal activity
o After VATS there is a risk of recurrent pneumothorax 5% and following open surgery there is a 1% risk

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7
Q

Indications for a lobectomy?

A
  • Main is malignancy
  • TB
  • Aspergilloma
  • Lung abscess
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8
Q

What steps are included in work up for pneumonectomy/lobectomy and what values are needed?

A
  • Full HX and Exam
  • Full lung function tests including transfer factor
  • Cardio-pulmonary exercise testing
  • Need to have an FEV1 >1.5L for a pneumonectomy
  • Need to have a FEV1 >2L for a lobectomy
  • In order to have a good prognosis post op for lobectomy need a VO2 max of 15mls/kg/min
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9
Q

What are the histological classifications of Lung Ca?

A
  • SCLC – about 20%
  • NSCLC – adenocarcinoma, squamous carcinoma, large cell carcinoma and neuro-endocrine tumours
    o Squamous cell carcinoma most strongly associated with smoking and central
  • Adenocarcinoma peripheral and may be seen in non smokers
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10
Q

What are the broad treatment options for SCLC and NSCLC?

A
  • SCLC
    o Rapidly progressive, presents late, rarely amenable to surgery, early disease/limited disease get chemo-rad, late disease get palliative chemo
    o Prophylactic cranial irradiation may be given to patients with limited disease to prevent brain mets and prolong survival
  • NSCLC:
    o Stage 1 or 2 treatment may be curative surgery or radical RT, may use adjuvant chemotherapy if high risk features such as mediastinal LN involvement on resected tissue
    o Some stage 3 may undergo curative surgery if mediastinal LNs not involved, otherwise radical chemoradiotherapy
    o Stage 4 – palliatively, presence of specific mutations such as EGFR, ALK and PDL1 mean specific therapies can be used
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11
Q

What are the 3 respiratory causes of clubbing?

A
  • Interstitial lung disease
  • Suppurative lung disease: CF, bronchiectasis, lung abscess
  • Lung Ca
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12
Q

How is COPD managed?

A

Short acting and long acting therapies
SA beta agonists and SA muscarinic antagonists and LA versions of both along with inhaled corticosteroids
Smoking cessation including specialist clinics which have been shown to help people stop smoking

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13
Q

Investigations in interstitial lung disease?

A
  • Bedside observations
  • Baseline bloods
  • Screening blood tests of connective tissue disorder
  • If relevant from the history allergy testing eg. Avian precipitans
  • ABG
  • Imaging – CXR, HRCT
  • Lung function tests and spirometry
  • More advanced investigations include: bronchoscopy with BAL or transbronchial or endobronchial biopsy for histological diagnosis
  • Echo – RH function and ?signs pulm HTN
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14
Q

How can HRCT be used in diagnosis of ILD?

A

HRCT can be diagnostic – ground glass changes suggest inflammation which may be responsive to steroids, established fibrosis may represent end stage fibrosis not response to steroids
- HRCT is a high resolution CT scan without contrast which can be used to image the lung parenchyma particularly in ILD and bronchiectasis

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15
Q

Management of ILD broadly?

A
  • MDT approach inc. physio, OT, resp nurses with SOB and improving QoL
  • If underlying connective disorder treat this with disease modifying agents
  • non-specific interstitial pneumonia may use immunosuppressive agents and steroids
  • If pt had idiopathic fibrosis can consider anti fibrotic agents such as pirfenidone
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16
Q

What would be the typical findings of spirometry and lung function tests in ILD?

A
  • Spirometry to show a restrictive pattern, reduction in both FEV1 and FVC with a preserved ratio
  • Reduction in TLC as well as transfer factor
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17
Q

How is a diagnosis of ILD made?

A
  • Diagnosis may be made without histology if on MDT review the team are reasonably confident of the diagnosis from the history, examination, lung function and radiology
  • For some cases, bronchoscopy with BAL or endobronchial or transbronchial biopsy for diagnosis such as sarcoidosis or extrinsic allergic alveolitis
  • Decision to pursue a biopsy is made on a case by case basis and decided by MDT
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18
Q

What is the prognosis of IPF?

A
  • IPF has the worst prognosis and median survival is 2-3y with a 30% 5y survival
  • Poor prognostic factors include: increasing age, dyspnoea, low or declining PFTs, PAH< co-existing emphysema, extensive radiogreaphic involvement, low exercise tolerance, exertional desaturation, universal interstital pneumonia on histopathology
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19
Q

What is the treatment for IPF?

A
  • Pulmonary rehab
  • Supportive treatments: LTOT
  • Nintedanib or pirfenidone can be considered in patients with FVC 50-80% of predicted to slow progression
  • Pts with no absolute contraindications should be referred for consideration of lung transplant
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20
Q

What is the treatment for non specific interstitial pneumonia?

A
  • Can use immunosuppressive treatment if moderate to severe disease
  • Oral or IV glucocorticoids
  • Steroid sparing agents such as azathioprine or mycophenolate mofetil
  • Prognosis is significantly better than IPF and about half to 2/3 of patients are stable or have improved at longer term follow up but 5y mortality still high at 15-25%
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21
Q

What is your waffle for the causes of interstitial lung disease?

A
  • Broadly: idiopathic, related to connective tissue disease, related to an occupational exposure or related to a drug exposure
  • Exposure to asbestosis, dust such as silica or berrilium
  • Exposure to allergens for example birds in extrinsic allergic alveolitis
  • Radiation
  • Drugs such as chemotherapeutic agents, amiodarone, methotrexate, nitrofurantoin
  • Connective tissues disorders: SLE, scleroderma, RA, polymyositis and mixed connective tissue disease
  • Idiopathic causes such as sarcoidosis, cryptogenic organising pneumonia and idiopathic interstitial lung disease which included idiopathic pulmonary fibrosis
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22
Q

Causes of predominantly upper zone fibrosis?

A

CHARTS
Coal workers pneumoconiosis
Histiocytosis X
Ankylosing spondylitis
Radiation
TB
Sarcoidosis and silicosis

23
Q

Causes of predominantly lower zone fibrosis?

A

Rheumatoid arthritis
Asbestosis
SLE, scleroderma, sjogrens
Idiopathic pulmonary fibrosis
Drugs

24
Q

Features of cystic fibrosis you may see?

A
  • Bronchiectasis – coarse crackles, classically in upper lobes, might also have expiratory wheeze
  • Clubbing
  • Low BMI (combo of pancreatic insufficiency and a catabolic state)
  • Signs of supplemental feeding (as above)
    o Standard gastrostomy tube
    o Gastrostomy button – more discreet
  • Portacath or other long term venous access – need for IV abx
    o Circular port which lies under the skin and tunnelled line tip of which lies in SVC
    o Usually upper chest wall, lateral chest wall, abdominal wall
  • LTOT/AOT
  • CF related diabetes
    o Look for evidence of CBG monitoring on fingers
    o Insulin pump
    o Libre device
  • Cystic fibrosis liver disease
    o Can lead to portal hypertension with splenomegaly and hyposplenism
  • Osteopenia/osteoporosis
    o Low impact fractures such as rib fractures from coughing
  • Male infertility due to absence of vas deferens
  • Female subfertility
  • Sinus disease
    o Nasal polyps
  • Increased risk allergic bronchopulmonary aspergillosis and pneumothoraces
  • Haemoptysis
    o May require bronchial artery embolization
  • Constipation
    o Distal intestinal obstruction syndrome (DIOS) in adults
    o Meconium ileus in infants
  • Gall stones
  • Renal stones
25
Q

What are the genetics of CF?

A
  • Autosomal recessive
  • Mutation in the long arm of Chr 7 resulting in a defective CFTR protein, over 2000 types of mutation have been described, the comments in UK is delta F508
  • 90% of CF patients in UK have atleast one copy of the delta F508 mutation, 50% are homozygous
26
Q

How is CF diagnosed?

A
  • Previously diagnosed in infancy following meconium ileus or failure to thrive
  • Now all infants screened as part of Guthrie test
  • Measurement of immunoreactive trypsin levels via heel prick test
  • If levels sufficiently raised then CF suspected
  • Diagnosis then made via screening for commonest mutations on a blood sample and via sweat test
27
Q

Waffle about the microbiology of CF related lung disease?

A
  • By adulthood most people will have chronic colonisation with a bacteria
  • In childhood infection with staphylococcus aureus predominates
  • With age increased chance of becoming colonised with pseudomonas
  • Some are colonised with very resistant bacteria such as burkholderia cepacia or non tuberculous mycobacteria
  • Infection with burkholderia cenocepacia or mycobacterium abscessus holds poor prognosis and is a contraindication to lung transplantation
28
Q

Treatment of CF?

A
  • Postural draining, active cycle of breathing techniques and exercise
  • Nebulised mucolytics such as recombinant DNA-ase and hypertonic saline
  • Oral azithromycin and nebulised antibiotics
  • Regular courses of IV abx – can be given IP or OP
  • Creon for enzyme replacement
  • Fat soluble vitamins
  • High calorie requirement may require additional feeding through NG or gastrostomy tube
  • Insulin therapy for CF related diabetes
  • Newer CFTR modulating drugs such as Ivacaftor
29
Q

What is the rough prognosis of CF?

A
  • Varies depending on mutations, complications and adherence to treatment
  • Survival is improving
  • Majority of individuals with CF are adults
  • Median life expectancy is 47y old
30
Q

Contraindications to lung transplant?

A
  • Malignancy within the last 5y (or within 2y if malignancy of low risk eg. BCC)
  • Significant heart, liver, brain or renal dysfunction
  • Infection with highly virulent/resistant organisms
  • Significant chest wall or spinal deformities
  • High or low BMI
  • Smoking or using elicit drugs
  • Compliance issues
  • Poor functional status with poor rehab potential
31
Q

Complications post lung transplant?

A
  • Hyperacute rejection (primary graft dysfunction):
    o Common and most people experience at least one episode in the first 6/12 post transplant
  • Chronic rejection is usually due to bronchiolitis obliterans syndrome
    o Leading cause of death after 1st year, incidence of 50% by 5Y
  • Infective:
    o Bacterial, mycobacterial, fungal and viral
  • Increased risk of malignancy:
    o Post transplant lymphoproliferative disease is the most common one in the first year post transplant
    o Skin malignancy also common and needs screening for
  • Side effects of immunosuppression medications:
    o Steroid side effects
    o Tacrolimus – tremor and can also develop diabetes
32
Q

Indications for lung transplant (and single vs double)?

A

signs to suggest underlying reason but these are possibilities…..
Indications:
- COPD
- ILD
- CF
- Bronchiectasis
- Pulmonary vascular disease
Single versus double transplant:
- Single usually performed in COPD/ILD with double reserved for suppurative lung disease but given the increased survival with double then double may be used in other patients with COPD/ILD such as younger patients or those with co-existent pulmonary HTN

33
Q

What is the criteria to be met in adult patients to be eligible for lung transplant?

A

Criteria to be met in adults patients:
- Greater than 50% risk of death within 2y if transplant is not undertaken
- >80% likelihood of surviving 90 days post transplant
- >80% 5y survival from a general medical perspective provided there is adequate graft function

34
Q

What is the prognosis of lung transplant?

A

Prognosis:
- Overall median survival 6y
- Bilateral lung transplants do have better overall survival than single (7.5y versus 4.5y respectively)
- COPD and IPF have poorer 10y survival

35
Q

Causes of bronchiectasis?

A
  • Idiopathic
  • Cystic fibrosis
  • Primary ciliary dyskinesia (autosomal recessive)
  • Infections:
    o TB
    o Lobar pneumonia
  • Immunodeficiency
  • Exposure to moulds triggering allergic bronchopulmonary aspergillosis
  • Yellow nail syndrome (see below)
  • Rheumatoid arthritis
  • Inflammatory bowel disease
36
Q

Investigations in bronchiectasis?

A
  • Sputum cultures
    o General, fungal and mycobacterial culture
  • Spirometry – and helpful in disease monitoring
  • CXR (but may be normal in early disease)
  • HRCT Thorax
  • Bloods:
    o Routine bloods
    o Immunodeficiency
     HIV
     Immunoglobulin levels
     Pneumococcal serology
    o Aspergillus serology to screen for ABPA
    o Autoimmune screen if suggestion of CTD
    o All patients under 40 screening for common CFTR mutations
  • If Hx suggestive of PCD then referral to a specialist centre for nasal biopsy
37
Q

Management of bronchiectasis?

A
  • Daily Chest physio with postural drainage and active cycle of breathing techniques (may be enough alone)
    o Positive expiratory pressure devices can be used as an adjunct
  • Nebulised hypertonic saline as a mucolytic
  • Pneumococcal vaccination if serology non protective, annual influenza vaccine
  • Oral mucolytic with carbocisteine if often tried but ineffective
  • Prophylactic antibiotics such as azithromycin (macrolide with anti inflammatory properties)
  • Treatment of exacerbations with antibiotic therapy for a 2 week course guided by sputum culture, may need nebulised abx such as in pseudomonas infection
    o But rotating abx courses not recommended
  • Surgery is usually only in localised bronchiectasis with high exacerbations frequency despite maximal medical therapy
38
Q

What are the possible features of yellow nail syndrome?

A
  • Slow growing, discoloured, thickened, onycholysis can occur
  • Bronchiectasis
  • Pleural effusions (not always)
  • Lymphoedema (not always)
39
Q

What paraneoplastic conditions can occur win Lung Ca and which histological types are they associated with?

A

SCLC: SIADH, Cushing’s syndrome from ectopic ACTH and Lambert Eaton Myasthenic syndrome
SCC: Hypercalcaemia from ectopic ACTH

40
Q

Investigations in suspected lung malignancy?

A
  • CXR
  • Staging CT-TAP
  • Bloods – anaemia, co-existent infection, hypercalcaemia (bone mets or paraneoplastic), hyponatraemia (SIADH), deranged LFTs (liver mets), Clotting (most people need to undergo biopsy)
  • Tissues diagnosis – bronchoscopy for direct sampling, bronchoscopy and EBUS or CT guided biopsy
  • Enlarged LNs can have biopsy or FNA
  • Pleural effusion – diagnostic tap for cytology
  • If there was a potentially curative option do functional imaging with PET CT before work up (NSCLC)
  • Lung function – fitness for treatments esp. surgical resection
41
Q

Causes of pleural effusion?

A

Causes:
- Exudative:
- Malignancy – current or previous scars
- Parapneumonic effusion
- TB
- Rheumatoid arthritis
- Pulmonary infarction
- Yellow nail syndrome - yellow nails, bronchiectasis, lymphoedema
- Others: pus in pleural space (empyema), haemothorax
- Transudative:
- Congestive cardiac failure
- Chronic liver disease – bilateral but can be unilateral R sided
- Renal failure
- Nephrotic syndrome

42
Q

Investigations in new pleural effusion?

A
  • Bloods: FBC, CRP, U&E, LFTs, Clotting, LDH for lights (+/- things like RF, blood cultures depending on suspected cause)
  • CXR, USS chest ?simple/septations and safety of aspiration, CT chest especially if cause unclear
  • Pleural aspiration – LDH, protein, MC&S, gram stain, AFBs, cytology, pH
  • Can consider pleural biopsy, thoracoscopy or bronchoscopy depending on suspected cause
43
Q

Management of pleural effusion?

A

Management:
- Chest drain if resp compromise, empyema (pH <7.2) or haemothorax
- PleurX drain in malignancy
- Pleurodesis – medical or surgical may be done in malignancy
- VATS procedure in complex pleural effusion
- Medical management of underling causeH

44
Q

How can you distinguish an exudative from transudative pleural effusion?

A

Exudate versus transudate:
- Protein >30 exudate, <30 transudate
- Light’s criteria for 25-30: Pleural fluid protein: serum protein >0.5, pleural fluid LDH:serum LHD >0.6 or pleural fluid LDH >2/3 upper limit LDH

45
Q

How much should you drain off a pleural effusion at once and why?

A
  • 1-1.5L depending on patients weight and frailty then clamp for 4h – prevent re-expansion pulmonary oedema
46
Q

Causes of predominantly neutrophilia in pleural fluid?

A

Bacterial infection

47
Q

Causes of a predominantly lymphocytosis in pleural fluid?

A

TB and malignancy

48
Q

If glucose in pleural fluid is particularly low (<1.6) what might this indicate?

A

Rheumatoid arthritis

49
Q

Grade severity of COPD?

A
  • FEV1 >80% = mild
  • FEV1 50-80% = mod
  • FEV1 30-50% = severe
  • FEV1 <30% = very severe
50
Q

Cor pulmonale - definition, mechanism and management?

A
  • Right sided heart failure secondary to chronic lung disease
  • Chronic hypoxia leads to constriction of pulmonary vasculature and pulmonary HTN leading to RHF
  • Management is LTOT to reduce the vasoconstriction and diuretics to relieve congestion which occurs as a result of the failure
51
Q

Types of pulmonary disease which can occur with RA?

A
  • Interstitial lung disease
  • Bronchiectasis (associated with condition or post infections as immunosuppressed)
  • Pleural effusions
  • Pleuritis
  • Raised hemi diaphragm from nerve involvement of vasculitic process
  • Obliterative bronchiolitis (obstructive disease)
  • Pulmonary nodules (more common in seropositive pts)
52
Q

Types of ILD seen in RA?

A
  • Can be usual interstitial pneumonia (UIP) histological pattern or a non specific idiopathic pneumonia (NISP) picture
  • Most connective tissue associated ILD is associated to NSIP but in RA UIP is more common
  • UIP more associated with end stage fibrosis and harder to treat than NISP which has more ground glass changes on HRCT and felt to be more associated with inflammation and potentially reversible with steroids or immunosuppression
  • Prognosis UIP worse than NISP and similar to that of IPF
  • No current licensed treatment for RA UIP type but current trials using the established anti fibrotics using id IPF
53
Q

In which patients may you use a VQ scan instead of CTPA in ?PE?

A
  • Poor renal function
  • Contrast allergy
  • High radiation risk eg. pregnant

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