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yr3 medicine- respiratory > Asthma & COPD > Flashcards

Asthma & COPD Flashcards

1
Q

What is asthma?

A

Chronic, inflammatory airway disease characterised by intermittment airway obstruction and hyper-reactivity to a variety of stimuli. Airway obstruction is reversible (but not always completely reversible in some pts)

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2
Q

Discuss the pathophysiology of asthma

A
  1. Genetic and environmental factors lead to atopy- patients have predisposition to allergic hypersensitivity in airway
  2. Macrophages engulf allergen and process and present antigens to TH2 cells
  3. TH2 cells release cytokines causing the activation of B cells, mast cells and eosinophils
  4. B cells produce IgE antibodies
  5. IgE binds to surface of mast cell and basophils
  6. Re-exposure:
  • Immediate response (type 1 hypersensitivity reaction): allergen binds to antigens on mast cells & eosinophils causing cross linnking of antigens which then causes degranulation of mast cells & basophils causing histamines, leucotrienes and other mediators to be relesed
  • Late/delayed response (type IV hypersensitivity reaction): activated inflammatory cells (including mast cells, eosinophils, neutrophils) release cytokines which release mediators and cytokines to cause airway inflammation. *NOTE: Eosinophils release leukotriene C4 and other mediators- some of which are toxic to epithelial cells and cause shredding of epithelia
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3
Q

What are the 3 main factors that contribute to airway narrowing in asthma?

A
  • Bronchial smooth muscle contraction
  • Mucosal swelling/inflammation
  • Increased mucus production
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4
Q

State some risk factors for asthma

A
  • Family history
  • Atopy
  • Allergens (e.g. animals, chemicals, pollen, allergens from work etc..)
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5
Q

What are the symptoms of asthma

A
  • Intermittent dyspnoea
  • Wheeze (polyphonic, high pitched, expiratory)
  • Cough (often dry, worse in evening/night and morning
  • Atopy
  • Nasal polyps
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6
Q

State some asthma triggers

A
  • Cold air
  • Exercise
  • Smoking
  • Emotion e.g. stress
  • Allergens
  • Infection
  • Pollution
  • NSAIDs
  • Beta blockers
  • Food & drink e.g. dairy products, orange juice
  • URTs
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7
Q

Explain why NSAIDs can make asthma worse

Explain why betablockers can make asthma worse

A
  • NSAIDS: block COX enzymes hence more arachidonic acid is fed into the lipoxygenase pathway; iincreases amoutn of asthmogenic leukotrienes produced
  • Beta blockers: bind to B2 receptors in bronhcial smooth muscle and cause bronchoconstriction
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8
Q

When taking a history from someone with suspected asthma, what are some key questions you need to ask to try and establish a.) if it is asthma b.) severity?

A
  • Triggers?
  • Dinural variation (do symptoms or peak flow vary over day)
  • Exercise tolerance
  • Does it disturb their sleep
  • Acid reflux
  • Other atopic diseases
  • Questions about home e.g. any pets, carpets, soft furnishings etc..
  • Are symptoms worse at work/better when not at work?
  • Days off work/school
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9
Q

State some signs you might find on clinical examination of someone with asthma

(NOTE: just asking for signs in someone with mild asthma. Not askng about acute severe, life threatening or fatal)

A
  • Tachypnoea
  • Audible wheeze
  • Decreased air entry
  • Widespread polyphonic wheeze
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10
Q

State what investigations you would order if you suspect someone may have asthma, include:

  • Bedside
  • Bloods
  • Imaging
  • Others
A

Bedside

  • PEFR (can look at dinural variation in peak flow: evening compared to morning- morning usually lower. Difference >20% suggests asthma. BUT NOT OFTEN USED DIAGNOSTICALLY NOW AS WE HAVE OTHER OBJECTIVE TESTS)

Bloods

  • FBC (look for raised eosinophils or neutrophils)
  • Aspergillus serology
  • IgE

Imaging

  • CXR (exlcude other pathologies e.g. aspergilloma. May also see hyperinflation.)

Others

  • Spirometry with bronchodilator reversibility
  • FeNO test (fractional exhaled nitric oxide): there are 3 types of nitric oxide synthases; one of these is inducible and levels rise in inflammatory cells- particularly eosinophils hence levels of NO correlate with levels of inflammation.

*More info in paeds asthma

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11
Q

Who should be offered:

  • Spirometry with bronchodilator reversibility
  • FeNO test
A
  • Spirometry with bronchodilator reversibility: all children ≥ 5yrs and all patients ≥ 17yrs
  • FeNO test: all ≥ 17yrs and request it in children aged 5-16yrs if normal spirometry or inconclusive
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12
Q

What spirometry results suggest asthma in adults and in children?

A

FEV1/FVC ratio

  • FEV1/FVC ratio < 70% (obstructive)

Bronchodilator reversibility

  • Adults: FEV1 improvement of ≥12% or of ≥200ml
  • Children: FEV1 improvement of ≥12%
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13
Q

What FeNO results suggest asthma in adults and in children?

A
  • Adults: ≥40ppb
  • Children: ≥35ppb
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14
Q

Patients may have occupational asthma (chemicals at work worsen asthma); state some examples chemicals that can be associated with occupational asthma

A
  • Isocyanates (most common) e.g. spray painting, foam moulding adhesives
  • Platinum salts
  • Flour
  • Epoxy resins

*Serial measurements of peak flow are recommended at and away from work

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15
Q

At what age does asthma often present?

A

Children (often present <6yrs)

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16
Q

Discuss the long term management of asthma, include:

  • Conservative management
  • Pharmacological management

*NOTE: not asking about exacerbations just long term

A

Conservative

  • Avoid triggers
  • Use self-managment plans
  • Educate/teach pts- including teaching them correct inhaler technique and assessing their technique

Pharmacological

  • Note that BTS and NICE guidelines differ. NICE says to add LTRA before LABA
  • BTS and NICE shown on next flashcards
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17
Q

Outline the NICE guidance for long term pharmacological management of asthma

A
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18
Q

Outline the BTS guidance for long term pharmacological management of asthma

A
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19
Q

Define what is mean by the following according to NICE:

  • Low dose ICS
  • Moderate dose ICS
  • High dose ICS
A
  • Low dose ICS: ≤ 400 micrograms
  • Moderate dose ICS: >400 micrograms to ≤ 800micrograms
  • High dose ICS: >800 micrograms
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20
Q

BTS recommend we should consider stepping down treatment every 3 months or so (note you may not go straight from e.g. step 3 to step 2 may do gradually). When reducing dose of ICS, by what % do BTS recommend we reduce it by?

A

Reduce by 25-30% at a time

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21
Q

State some asthma phenotypes

A
  • Allergic asthma: childhood, atopy, respond well to ICS
  • Non-allergic asthma: less responsive to ICS
  • Adult onset asthma
  • Asthma with persistent airflow limitation: due to airway remodeeling
  • Asthma with obesity
  • Nocturnal asthma
  • Samter’s triad (asthma, nasal polpys, sensitivity to NSAIDs)
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22
Q

We can use the ACT (asthma control test) to identify current level of asthma control; what are the questions in the ACT and what is the max score for each

A
  • 20/25= okay
  • <20= concern
  • <15= go to doctor
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23
Q

Asthma exacerbations can be mild, moderate, acute severe, life threatening or near fatal. Describe what a pt presents with to be classed as each category

A

Mild

  • PEFR >75% of best or predicted
  • No features of severe asthma

Moderate

  • PEFR 50-75% of best or predicted
  • No features of severe asthma

Acute Severe

  • PEFR 33-50% of best or predicted
  • Cannot complete sentences in 1 breath
  • Resp rate >25/min
  • HR >110/min

Life-threatening​

  • PEFR <33% of best or predicted
  • Near or fully silent chest
  • Sats <92%
  • ABG pO2 <8kPa
  • ABG normal pCO2
  • Cyanosis/hypoxia
  • Poor respiratory effort
  • Bradycardia
  • Hypotension
  • Exhaustion, confusion, arrhythmias

Near Fatal

  • Raised pCO2
  • Require mechanical ventilation with raised inflation pressures
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24
Q

What is the relevance/meaning of a normal pCO2 in acute asthma attacks?

A

Indicates exhaustion and should therefore be classes as life threatening.

(We would expect their pCO2 to be low due to hyperventilation due to hypoxia)

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25
Q

Discuss how you would manage mild to moderate asthma exacerbations

A

Short course of oral steroids e.g. prednisolone 30-60mg daily

Increase salbutamol use (pmdi)

*NOTE: don’t have to taper/ween off steroids so long as duration of course was <3 weeks

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26
Q

State some differential diagnoses for someone who you suspect is having an acute severe asthma attack

A
  • Acute infectious exacerbation COPD
  • PE
  • Anaphylaxis
  • Pulmonary oedema
  • URT obstruction
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27
Q

State briefly (i.e. just name drugs don’t state doses) how you manage an acute severe or life threatening asthma attack

THINK OSHITME

A
  • ABCDE management
  • Oxygen
  • Salbutamol (pmdi or via nebuliser. Nebulised SABA is recommended in life-threatening)
  • Steroids e.g. prednisolone or IV hydrocortisone
  • Ipatropium bromide nebuliser
  • Other drugs e.g. Magnesium sulfate, theophylline, aminophylline IV
  • Escalate (ma need intubation & ventilation)
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28
Q

Describe in detail, including drug doses, how you manage acute severe asthma attacks

A
  1. ABCDE
  2. Oxygen: aim sats 94-98%. Do ABG is sats <92%
  3. Salbutamol: 5mg nebulised (can repeat after 15 mins)
  4. Steroids: either 40mg oral prednisolone STAT or 100mg IV hydrocortisone if PO not possible
  5. Ipatropium bromide: 500ug nebulised
  6. Other drugs e.g. Magnesium sulfate 1.2-2g IV over 20 mins; IV aminophylline 5mg/kg loading dose over 20 mins followed by continous infusion at 1mg/kg/hr, IV salbuatmol; IV salbutamol
  7. ITU intervention for e.g. Intubation & ventilation, ECMO

NOTE: beyond magnesium sulfate you need a senior. So if magnesium shows no improvement you need senior to come and manage. Consider an urgent portable CXR if becomes life-threatening asthma attack

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29
Q

If after administering oxgyen, nebulised salbutamol, steroids, nebulised ipatropium and magnesium sulfate your pt- who is havine an acute severe asthma attack- starts to improve, what would you do?

A
  • Continue nebulised salbutamol every 4-6hr
  • Continue nebulised ipatropium every 6hr
  • Prednisolone 40mg PO OD for 5-7 days
  • Monitor PEFR
  • Aim sats 94-98%
30
Q

Following an acute severe-near fatal asthma attack, what are the criteria for safe asthma discharge?

A
  • PEFR >75%
  • Stable on discharge medication (so no oxygen or nebulisers) for 24hrs
  • Inpatient asthma nurse review to assess inhaler technique
  • Provide PEFR and written asthma action plan
  • Pt needs to have at least 5 days of prednisolone (hence if discharged before 5 days will need to be sent home with some)
  • GP follow up in 2 working days
  • Resp clinic follow up in 4 weeks
  • Consider psychological factors
31
Q

BTS guidelines recommend ABG for patients with O2 sats less than….?

A

< 92%

32
Q

State some side effects of salbutamol that you must be aware of

A
  • Tachycardia
  • Arrhythmias
  • Tremor
  • Decrease K+
33
Q

State some side effects of ipatropium bromide that you must be aware of

A
  • Arrhythmias
  • Headache
  • Dry mouth
  • Cough
  • Constipation
  • Dizziness
  • Nausea & vomitting
  • Diarrhoea
34
Q

State some side effects of aminophylline

A
  • Tachycardia
  • Arrhythmias
  • Nausea
  • Seizures
  • Decrease K+
35
Q

If a pt has eosinophilic asthma, what will they respond well to?

A

Steroids

36
Q

Asthma pts with eosinophilia often respond well to steroids; however, there are numerous causes of eosinophilia. State some differentials for eosinophilia

A
  • Airway inflammation (asthma or COP)
  • Hayfever/allergies
  • Drugs
  • Allergic bronchopulmonary aspergillosis
  • Drugs
  • Churg-Strauss/vasculitis
  • Eosinophilic pneumonia
  • Parasties
  • Lymphoma
  • SLE
  • Hypereosinophilic syndrome
37
Q

What is Churg-Strauss syndrome?

A

Eosinophilic Granulomatosis with Polyangiitis (EGPA), previously known as Churg-Strauss Syndrome, is an inflammatory disease of small and medium sized blood vessels. The lungs and skin are commonly affected but it can affect other organs including the heart, kidneys, nerves and bowels. Eosinophils are found in very high levels in EGPA, both in blood tests and in affected parts of the body. People with EGPA often have severe asthma that presents as an adult.

38
Q

Describe how you use a pressurised metered dose inhaler

A

Pressurised metered dose inhaler

  • Hold inhaler upright
  • Shake inhaler
  • Take cap off
  • Slightly tilt your chin up
  • Breathe out gently until you feel you can’t breathe out anymore
  • Put your mouth around inhaler to form tight seal
  • Simulatenously press the cannister and inhale slowly until your lungs feel full
  • Take inhaler out of your mouth, keep your lips sealed, and hold breath for 10 seconds (or as long as you can)
  • If you need to take two puffs, wait 30secs-1min then start process again
39
Q

Discuss the guidelines for stepping down asthma medications/inhalers

A

Should be joint decision between clinician and pt. Consider reductions every 3 months (only if asthma controlled):

  1. ) Reduce dose ICS by 25-50% whilst continuing LABA at same dose
  2. ) Half daily dose of combination treatment
  3. ) Dose of ICS should be reduced to lowest dose possible for asthma control
40
Q

Describe how you use a dry powder inhaler

A
  • Hold the inhaler horizontally
  • Slightly tilt your chin up
  • Breathe out gently and slowly away from inhaler until you feel like your lungs are empty
  • Put your lips around mouthpiece to make a tight seal
  • Breathe in quickly and deeply until your lungs feel full
  • Take inhaler out of your mouth, keep lips sealed and hold breath for 10 seconds (or as long as you can)
41
Q

What is COPD?

A
  • Chronic obstructive pulmonary disease (encompasses emphysema & chronic bronchitis)
  • Airflow obstruction that is not fully reversible. It is usually progressive and associated with inflammatory response of lungs to harmful particles or gas e.g. smoking. Features of disease include hyperinflation & mucus hypersecretion
42
Q

What is chronic bronchitis?

What is emphysema?

A
  • Chronic bronchitis is defined clinically as cough, sputum production on most days for 3 months of 2 sucessive years
  • Emphysema is defined histologically as enalrged air spaces distal to terminal bronchioles with destruction of alveolar walls
43
Q

Discuss the difference between blue bloaters and pink puffers

A

Blue Bloaters

  • Decreased alveolar ventilation
  • Low PaO2 and high PaCO2
  • Cyanosed but not breathless
  • Respiratory centres are relatively insensitive to CO2 hence rely on hypoxic drive to maintain respiratory effort
  • May go on to develop cor pulmonale

Pink Puffers

  • Increased alveolar ventilation
  • Near normal PaO2 and normal or low PaCO2
  • Breathless but not cyanosed
  • May progress to type 1 resp failure
44
Q

State some lung changes which occur in COPD

A
  • Mucus gland hyperplasia
  • Loss of cilial function
  • Emphysema
  • Chronic inflammation (macrophage & neutrophil infiltration)
  • Fibrosis of small airways
45
Q

State some potential causes of COPD

A
  • Smoking
  • Inherited alpha-1 antitrypsin deficiency
  • Industrial exposure e.g. soot, coal
46
Q

State the symptoms of someone with COPD

A
  • Cough- often productive (at start of disease worse in morning, as disease progresses becomes constant)
  • Dyspnoea
  • Wheeze
  • Cor pulmonale leading to peripheral oedema
47
Q

State what you might find on clinical examination of someone with COPD

A
  • Tachypnoea
  • Use of acessory muscles
  • Barrel chest
  • Decreased cricosternal distance (<3cm)
  • Decreased chest expansion
  • Resonant or hyperesonant percussion note
  • Quiet breath sounds (e.g. over bullae)
  • Wheeze
  • Cyanosis
  • Features of cor pulmonale e.g. peripheral oedema, raised JVP, hepatomegaly etc…
48
Q

What investigations would you want for someone with suspected COPD, include:

  • Bedside
  • Bloods
  • Imaging
  • Other

*For each, try to justify why you would do it

A

Bedside

  • ABG (see accurate PaO2 and PaCO2)
  • ECG (risk factors for COPD are similar to those for CVD. ECG might show RVH)
  • BMI

Bloods

  • FBC (haematocrit may be raised indicating polycythaemia, raised WCC if infection, anaemia)

Imaging

  • CXR: look for features of COPD
  • CT: features of COPD

Other

  • Post bronchodilator spirometry: obstructive patten FEV1:FVC ratio <70%
49
Q

What might you find on CXR of pt with COPD?

A
  • Hyperinflation
  • Bullae
  • Flat hemidiaphragm
50
Q

Discuss how we classify the severity of COPD

A
51
Q

State some potential complications of COPD

A
  • Acute exacerbations +/- infections
  • Polycythaemia
  • Respiratory failure
  • Cor pulmonale
  • Pneumothorax (ruptured bullae)
  • Lung carcinoma
52
Q

Discuss the long term management of stable COPD

A

Conservative

  • Smoking cessation
  • Pulmonary rehabilitation (if MRC grade 3 or above)
  • Vaccination
    • Annual influenza
    • One off pneumococcal
  • Treat co-morbidities

Pharmacological

  1. SABA or SAMA to use PRN
  2. Next step depends on if have asthmatic features:
  • No asthmatic features:
    • LABA + LAMA
      • If using SAMA switch to a SABA (as you don’t give dual anitmuscuranic therapy)
  • Asthmatic features:
    • LABA + ICS ​
    • LABA + LAMA + ICS
      • If using SAMA switch to SABA (as you don’t give dual antimuscarinic therapy)
  1. Other treatments eg:
  • Oral theophylline
  • Prophylactic antibiotics e.g. azithromycin
  • Mucolytics
  • LTOT
  • If have cor pulmonale, consider loop diuretics for oedema
  1. Lung volume reduction if required
53
Q

State 4 features that suggest COPD has asthmatic features

A
  • Any previous diagnosis of asthma or atopy
  • Higher blood eosinophil count
  • Substantial variation in FEV1 over time (at least 400ml)
  • Substantial diurnal variation in peak expiratory flow test (at least 20%)
54
Q

Which COPD pts do you offer smoking cessation and flu vaccination to?

A

All pts with COPD should be offered smoking cessation and flu vaccination

55
Q

Discuss pulmonary rehabilitation, include:

  • What it is
  • What the aims are
  • Why it is beneficial
  • Who it is offered to
A
  • Multidisciplinary treatment programme that incorpates physical training, disease education and nutrional counselling to reduce symptoms, improve health and boost confidence. Course is about 6-12 weeks with 2 x 2 hour sessions per week
  • To help people with chronic lung conditions stay active
  • Improve muscle strength, reduce breathlessness, improve fitness, help pt feel better, help manage condition better
  • Individuals with long term lung conditions e.g. bronchiectasis, CF, COPD, asthma, lung fibrosis
56
Q

Remind yourself of the MRC dyspnoea scale

A
57
Q

Discuss long term oxygen therapy, include:

  • Why it is beneficial
  • How many hours per day are required for survival benefit
  • Who should be assess for LTOT
  • Pt criteria for LTOT
A
  • Extended periods of hypoxia cause renal and cardiac damage- this can be prevented by LTOT
  • Continuous oxygen for at least 16 hours per day
  • Assess patients if any of the following:
    • very severe airflow obstruction (FEV1 < 30% predicted). *Can consider if FEV 30-49%
    • cyanosis
    • polycythaemia
    • peripheral oedema
    • raised jugular venous pressure
    • oxygen saturations less than or equal to 92% on room air
  • LTOT offered to pts who:
    • pO2
      • Either pO2 consistently <7.3kPa
      • Or pO2 7.3kPa to 8kPa with secondary polycythaemia, peripheral oedema or pulmonary hypertension
    • Non-smokers
    • Do not retain high levels of CO2
58
Q

Patients with COPD on LTOT should have supplementary oxygen for at least ____ hours per day

How do we assess whether pts would benefit from LTOT? (Asking how many ABGs we do how far apart)

A

15-16hrs per day

Assessment is done by measuring arterial blood gases on 2 occasions at least 3 weeks apart in patients with stable COPD on optimal management.

59
Q

COPD requires multidisciplinary management to improve quality of life; state some healthcare professionals involved in the management of COPD

A
  • Doctors
  • GPs
  • Specialist nurses
  • Physiotherapists
  • Pharmacists
  • OTs
  • Dieticians
60
Q

What is meant by an acute exacerbation of COPD?

A

Sudden/acute worsening of COPD which often presents with increased level of dyspnoea, worsening of chronic cough, and/or an increase in the volume and/or purulence of the sputum produced, hypoxia, confusion

61
Q

COPD exacerbations can be infective or non-infective; what would make you think the exacerbation is infective?

A
  • Change in sputum colour or volume
  • Fever
  • Raised WCC +/- raised CRP
  • Pyrexia
62
Q

State some potential causes of an exacerbation of COPD

A
  • Bacterial infection
  • Viral infection
  • GORD & swallowing disorders leading to aspiration
63
Q

What are the most common bacterial causes of COPD exacerbations?

A
  • Haemophilus influenza (MOST COMMON)
  • Streptococcus pneumonia
  • Moraxella catarrhalis
64
Q

What investigations would you do for someone with suspected exacerbation of COPD, include:

  • Bedside
  • Bloods
  • Imaging
A

Bedside

  • Sputum sample (check infec)
  • ABG (check PaO2 and PaCO2- help guide O2 and other decisions)
  • ECG

Bloods

  • FBC (haematocrit, WCC, anaemia)
  • CRP (infection)
  • U&E (renal func)
  • Theophylline level if pt on therapy at home (narrow therapeutic index)
  • Blood cultures (?sepsis)

Imaging

  • CXR (exclude pneumothorax & infection)
65
Q

Discuss the management of an acute exacerbation of COPD

A
  • ABCDE
  • Controlled oxygen (via a venturi face mask)
  • Bronchodilators (e.g. salbutamol) *Can increase use of pmdi or have via nebuliser
  • Nebulised ipratropium
  • Steroids
    • 30mg prednisolone STAT OD for 7 days
    • 100mg IV hydrocortisone every 6hr
  • Antibiotics (if bacterial infection suspected. BNF recommend amoxicillin, clarithromycin or doxycycline first line)

If still unresponsive, consider:

  • Aminophylline IV
  • NIV if type 2 resp failure and pH 7.25-7.35
  • If pH <7.25 consider ITU referal
66
Q

You must give controlled oxygen therapy to pts with COPD exacerbation as you could remove hypoxic drive; discuss how you should control your oxygen therapy

A
  • Asses pt: do pulse oximetry to determine SATS and ABG to determine PaO2 and PaCO2
  • Always use venturi face mask. The % will vary dependent on if in CO2 retention
  • If pt is not in CO2 retention put on 28-40% oxygen and aim sats as you would for normal individual
  • If pt is in CO2 retention, put on 24-28% oxygen and aim sats for 88-92%
  • REPEAT ABG IN 30 MINS TO REASSESS AND POTENTIALLY ALTER OXGYEN
67
Q

Non-invasive ventilation may be required for an acute exacerbation of COPD; describe the two forms of NIV and state when we woudl use each

A

CPAP

  • “Continous positive airway pressure”
  • Blows constant pressure which is same when you breath both in and out. Breathing against increased resistance helps to keep airways open. Pressure can also help force ‘stuff’ out of alveoli
  • Useful for: type 1 respiratory failure e.g. acute pulmonary oedema, sleep apnoea, pneumonia, chest wall trauma

BIPAP

  • “Bi-level positive airway pressure”
  • Blow higher pressure when you breathe in and lower pressure when you breath out.
  • Useful for: hypercapnic respiratory failure, COPD with respiratory acidosis
68
Q

What is meant by the ceiling of care?

A

Discussion with pt, family and other healthcare professionals to decide at what point we decide to stop intensifying treatment

69
Q

Describe the different stages of the modified MRC dyspnoea scale

A
70
Q

Describe how the flow volume loop changes for someone with restrictive disease e.g. lung fibrosis

A
  • Loop shifts to right (decreased TLC)
  • Loop is narrower (decreased vital capacity)
  • Loop height reduced (PEFR reduced slightly)
71
Q

Discuss how the flow volume loop changes with obstructive diseases e.g. asthma & COPD

A
  • Shifts to the left (residual volume increases)
  • Decreaed height (decreased PEFR)
  • Scalloping
72
Q

State examples of restrictive and examples of obstructive diseases

A

Restrictive

  • Interstitial lung disease
  • Sarcoidosis
  • Obesity
  • Pregnancy
  • Scoliosis
  • Neuromuscular disorders

Obstructive

  • COPD
  • Asthma
  • CF
  • Bronchiectasis

yr3 medicine- respiratory (11 decks)

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