Respiratory - Asthma & COPD Flashcards

1
Q

What is asthma?

A

A chronic inflammatory condition of the airways that causes episodic exacerbations of reversible bronchoconstriction, from airway hypersensitivity.

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2
Q

What are some triggers of asthma?

A
  • infection
  • night time or early morning
  • exercise
  • animals
  • cold / damp
  • dust
  • strong emotions
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3
Q

Presentation of asthma.

A
  • dry cough
  • wheeze
  • shortness of breath
  • history of other atopic conditions (e.g. eczema, hayfever, food allergies)
  • worse at night
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4
Q

Give some differentiates for a wheeze.

A
  • acute asthma exacerbation
  • bronchitis
  • pulmonary oedema
  • foreign body entrapment
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5
Q

What is the pathophysiology of asthma?

A

Type 1 Hypersensitivity Reaction:

  1. Allergens are presented to Th2 cells by dendritic cells
  2. A disproportionate inflammatory response arises, with Th2 cells releasing cytokines
  3. Cytokines stimulate the production of IgE
  4. IgE causes mast cell degranulation, and the subsequent release of inflammatory mediators (histamine, leukotrienes and prostaglandins)
  5. Increased numbers of mucus secreting goblet cells and smooth muscle hyperplasia, with mucus plugging in fatal and severe asthma
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6
Q

What are the clinical features of mild asthma?

A
  • no features of severe asthma
  • PEFR >75%
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7
Q

What are the clinical features of moderate asthma?

A
  • no features of severe asthma
  • PEFR 50-75%
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8
Q

What are the clinical features of severe asthma?

A
  • PEFR 33-50%
  • cannot complete sentences in 1 breath
  • respiratory rate >25/min
  • heart rate >110bpm
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9
Q

What are the clinical features of life threatening asthma?

A
  • PEFR <33%
  • SpO2 <82% (oximetry)
  • PaO2 <8kPa (ABG)
  • normal PaCO2 (ABG)
  • cyanosis
  • poor respiratory effort
  • silent chest
  • exhaustion
  • confusion
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10
Q

What are the clinical features of near fatal asthma?

A
  • raised PaCO2 (ABG)
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11
Q

NICE recommend which first line investigations for asthma?

A
  • fractional exhaled nitric oxide (FeNO)
  • spirometry with bronchodilator reversibility
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12
Q

Outline the principles behind FeNO testing in asthma diagnosis.

A

Nitric oxide is a biomarker for asthma, which provides an indication of the level of inflammation in the lungs.

If FeNO is raised, this indicates airway inflammation and is supporting of a diagnosis of asthma.

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13
Q

Outline the principles behind spirometry testing in asthma diagnosis.

A

Spirometry will show an obstructive pattern of disease: FVC normal, but FEV1 reduced (thus FEV1/FVC < 0.7).

If given a bronchodilator (e.g. SABA; salbutamol), there will be reversibility of the obstruction, and FEV1/FVC will improve by +12%.

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14
Q

If there is diagnostic uncertainty of asthma following FeNO and spirometry investigation, which further testing can be used to follow up?

A
  • peak flow variability
  • direct bronchial challenge with histamine
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15
Q

BTS/SIGN (2019) guidelines for the treatment of asthma as follows.

A
  1. SABA inhaler as required for infrequent wheezy episodes (e.g. salbutamol)
  2. Add a regular low dose inhaled corticosteroid (e.g. beclametasone)
  3. Add a LABA inhaler (e.g. salmeterol)

If asthma contorl remains suboptimal following the addition of inhaled LABA, then:
- increase the dose of inhaled corticosteroids from low dose to medium dose
- consider adding a leukotriene receptor antagonist (e.g. montelukast)

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16
Q

What non-pharmacological management can be offered to a patient with asthma?

A
  • individual asthma self-management programme
  • yearly flu jabs
  • yearly asthma review
  • advise exercise
  • smoking cessation
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17
Q

What is an acute exacerbation of asthma?

A

A rapid deterioration in asthma symptoms, triggered by any of the typical asthma triggers such as infection, exercise or cold weather.

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18
Q

How does acute asthma present?

A
  • progressively worsening shortness of breath
  • use of accessory muscles
  • tachypnoea
  • symmetrical expiratory wheeze on auscultation
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19
Q

How should acute moderate asthma be generally managed?

A
  1. A-E approach - oxygen titrated to maintain SpO2 > 94%
  2. Nebulised SABA (e.g. 5mg salbutamol)
  3. 40mg oral prednisolone STAT*

*IV hydrocortisone can be administered if PO route not available.

20
Q

How should acute severe asthma be managed?

A
  1. A-E approach - oxygen titrated to maintain SpO2 > 94%
  2. Nebulised SABA (e.g. 5mg salbutamol)
  3. Nebulised ipratropium bromide 500mcg
  4. 40mg oral prednisolone STAT*

*IV hydrocortisone can be administered if PO route not available.

21
Q

How should acute life-threatening asthma be managed?

A
  1. A-E approach - oxygen titrated to maintain SpO2 > 94%
  2. IV SABA (e.g. salbutamol)
  3. IV aminophylline
  4. Nebulised ipratropium bromide 500mcg
  5. 40mg oral prednisolone STAT*

*IV hydrocortisone can be administered if PO route not available.

Urgent ITU / anaesthetic assessment and CXR required.

22
Q

Explain the principles behind the following ABG result, in a patient presenting with an acute exacerbation of asthma.

PaO2: 11 kPa (11 – 13 kPa)

pH: 7.49 (7.35 – 7.45)

PaCO2: 3.2 kPa (4.7 – 6.0 kPa)

HCO3–: 22 (22 – 26 mEq/L)

BE: +2 (-2 to +2)

A

Uncompensated respiratory alkalosis.

Respiratory alkalosis occurs as tachypnoea causes a drop in PaCO2.

There is no metabolic compensation as this is an acute respiratory alkalosis.

23
Q

Explain the principles behind the following ABG result, in a patient presenting with an acute exacerbation of asthma.

PaO2: 7.0 kPa (11-13 kPa)

pH: 7.29 (7.35 – 7.45)

PaCO2: 9.1 kPa (4.7 – 6.0 kPa)

HCO3–: 26 (22 – 26 mEq/L)

Base excess: +1 (-2 to +2)

A

Uncompensated respiratory acidosis.

This is a sign of LIFE-THREATENING or NEAR FATAL asthma exacerbation - the patient is tiring, hypoventilating and thus PaCO2 is rising.

There is no metabolic compensation as this is an acute respiratory acidosis.

A-a = 9.62 - 7.00 = 2.62 kPa (ie. this is a respiratory cause)

PaO2 = 7.0kPa

PAO2 = 21 - (9.1 / 0.8) = 9.62kPa

24
Q

Following an acute exacerbation of asthma, what is the criteria to ensure safe discharge?

A
  • PEFR > 75%
  • stop regular nebulisers for 24hrs prior to discharge
  • inpatient asthma nurse review
  • prescribe 5 day course of prednisolone
  • GP follow up within 2 working days
  • respiratory clinic follow up within 4 weeks

It is important to optimise asthma control after an acute attack - patients should be discharged with an asthma action plan, and you should consider prescribing a ‘rescue pack’ or steroids for the person to initiate in future if they have another exacerbation of asthma.

25
Q

Give some differentials for eosinophilia.

A
  • airway inflammation (asthma or COPD)
  • hayfever
  • lymphoma
  • SLE
  • parasitic infection
26
Q

What is COPD?

A

Chronic obstructive pulmonary disease (COPD) is a non-reversible, long term airflow obstruction caused by damage to the lung tissue. The damage to the lung tissues makes it more difficult to ventilate the lungs, and thus prone to developing infections.

27
Q

What is the pathophysiology behind COPD?

A

COPD = chronic bronchitis + emphysema

Pathophysiology:
- mucous gland hyperplasia
- loss of cilial function
- emphysema: alveolar wall destruction causing irreversible enlargement of air spaces distal to the terminal bronchiole
- chronic inflammation and fibrosis of the small airways

28
Q

What are the causes of COPD?

A
  • smoking (most common)
  • inherited a-1 antitrypsin deficiency
  • industrial exposure (e.g. soot)
29
Q

Presentation of COPD.

A
  • chronic SOB
  • cough with sputum production
  • wheeze
  • recurrent respiratory infections

Differential diagnoses include lung cancer, fibrosis and heart failure.

30
Q

What is the MRC dyspnoea scale?

A

A 5 point scale recommended by NICE for assessing the impact of a patient’s breathlessness:

Grade 1 - breathless on strenuous exercise
Grade 2 - breathless on walking uphill
Grade 3 - breathless that slows walking flat
Grade 4 - stop to catch breath after 100m walking on flat
Grade 5 - unable to leave the house due to breathlessness

31
Q

How is COPD investigated?

A
  • spirometry
  • CXR (exclude lung cancer)
  • FBC (anaemia or polycythaemia)
  • sputum culture (chronic infections)
  • ECG and echocardiogram (heart function)
  • TLCO reduced
32
Q

Outline the principles of spirometry testing in COPD diagnosis.

A

Spirometry will show an obstructive pattern of disease: FVC normal, but FEV1 reduced (thus FEV1/FVC < 0.7%).

If given a bronchodilator (e.g. SABA; salbutamol), there will be no reversibility of the obstruction (ie. FEV1/FVC will not improve).

33
Q

How can severity of airflow obstruction be assessed?

A

While the FEV1/FVC ratio can give an impression as to whether the pathology is of obstructive or restrictive nature, FEV1 alone can be used to assess the severity of obstruction.

Stage 1: FEV1 >80% of predicted
Stage 2: FEV1 50-79% of predicted
Stage 3: FEV1 30-49% of predicted
Stage 4: FEV1 <30% of predicted

34
Q

What is the long term management of COPD, if the patient does not have asthma?

A
  1. SABA inhaler (e.g. salbutamol) or SAMA (e.g. ipratropium bromide)
  2. LABA (e.g. salmeterol) + LAMA (e.g. tiotropium bromide)

In more severe cases, additional options are:
- oral mucolytic therapy to break down sputum (e.g. carbocysteine)
- long term prophylactic antibiotics
- long term oxygen therapy at home

35
Q

What is the long term management of COPD, if the patient has asthma?

A
  1. SABA inhaler (e.g. salbutamol)
  2. LABA (e.g. salmeterol) + ICS (e.g. beclomethasone)

In more severe cases, additional options are:
- oral mucolytic therapy to break down sputum (e.g. carbocysteine)
- long term prophylactic antibiotics
- long term oxygen therapy at home

36
Q

Outline the principles behind long term oxygen therapy (LTOT) for severe COPD.

A

In severe COPD, complications of chronic hypoxia can cause renal and cardiac damage. LTOT is used >16hrs/day for a survival benefit, if PaO2 < 7.3kPa.

37
Q

What are the contraindications to long-term oxygen therapy in severe COPD?

A
  • smokers (fire hazard)
  • CO2 retainer
38
Q

What non-pharmacological treatment can be offered to patients with COPD?

A
  • smoking cessation
  • pneumococcal and annual flu vaccine
  • pulmonary rehabilitation
39
Q

What are the principles behind pulmonary rehabilitation?

A

Many COPD patients avoid exercise and physical activity as it causes breathlessness, however this may lead to a cycle of increasing social isolation and inactivity, worsening symptoms.

Pulmonary rehabilitation is a 12 week programme giving an individualised exercise regime, nutritional advise and disease education.

40
Q

Which professionals may be involved in the management of a COPD patient?

A
  • hospital doctors
  • general practitioners
  • specialist nurses
  • physiotherapists
  • pharmacists
  • occupational therapists
  • dieticians
41
Q

What is an exacerbation of COPD?

A

The acute worsening of COPD symptoms such as cough, shortness of breath, sputum production and wheeze.

It is usually triggered by vital or bacterial infection.

42
Q

How should an acute exacerbation of COPD be managed?

A
  1. A-E approach including ABG - titrate oxygen depending on PaCO2
  2. Nebulised salbutamol or ipatropium bromide
  3. Prednisolone 30mg stat PO or IV hydrocortisone
  4. Antibiotics if raised CRP / WCC or purulent sputum
43
Q

Distinguish the types of respiratory failure that may be seen on ABG:

a) Type 1 respiratory failure

b) Type 2 respiratory failure

A

a) low PaO2, with normal PaCO2

b) low PaO2, with high PaCO2

44
Q

Explain the principles behind the following ABG result, in a patient presenting with an acute exacerbation of COPD.

PaO2: 8.9 kPa (11-13 kPa)

pH: 7.31 (7.35 – 7.45)

PaCO2: 9.1 kPa (4.7 – 6.0 kPa)

HCO3–: 30 (22 – 26 mEq/L)

Base excess: +5 (-2 to +2)

A

This patient is in type 2 respiratory failure (hypoxic and hypercapnic).

The ECG shows a partially compensated respiratory acidosis, as the bicarbonate is raised.

As it takes weeks for bicarbonate to raise in response to respiratory acidosis, we can deduce this patient is a CHRONIC RETAINER OF CO2.

45
Q

Give the target SpO2 of a chronic retainer. Explain why the target is different.

A

88-92%

As the patient’s are chronic CO2 retainers, over-oxygenation places the patient at risk of worsening hypercapnia.

This is due to the Haldane effect: Hb has a higher affinity for O2 than CO2, therefore will preferentially displace CO2. This causes the CO2 to diffuse into the blood, rising PaCO2. Thus hypercapnia is worsened, and respiratory acidosis worsens.

Note if respiratory acidosis worsens - and therefore as blood pH falls - Hb’s affinity for O2 also falls, making hypoxia more likely.

46
Q

What is the COPD care bundle?

A

A bundle of 5 high impact actions to ensure the best clinical outcomes for a patient admitted with an acute exacerbation of COPD.

  1. Review patient’s medications and use of inhaler
  2. Provide written self management plan and emergency drug pack
  3. Assess and offer referral for smoking cessation
  4. Assess for suitability of pulmonary rehabilitation
  5. Arrange follow up call within 72 hours of discharge