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RESPIRATORY > COPD AND ALPHA-1-ANTITRYPSIN > Flashcards

COPD AND ALPHA-1-ANTITRYPSIN Flashcards

1
Q

What is COPD?

A

Common, treatable but incurable, largely preventable lung condition characterised by persistent respiratory symptoms and airflow obstruction. This obstruction results from chronic inflammation caused by exposure to noxious particles or gases (usually tobacco smoke but also from environmental and occupational exposures)

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2
Q

What exists within the umbrella term of COPD?

A

Chronic bronchitis
Emphysema
Chronic obstructive airways disease

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3
Q

What is an exacerbation of COPD?

A

acute episodes of worsening COPD symptoms (such as increased breathlessness, cough and sputum) which are beyond normal day-to-day variations.

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4
Q

Outline the epidemiology of COPD?

A

Historically its been much higher in men than women but in more recent years its prevalence is almost equal in men and women
It’s the second largest cause of emergency admissions in the UK and affects around 3 million people with 2 million being undiagnosed

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5
Q

What are risk factors for COPD?

A

Tobacco smoking
Occupation exposure to dusts, fumes, chemicals
Exposure to high levels of indoor air pollutants from burning wood and other biomass materials
Genetic abnormalities e.g. alpha 1 antitrypsin deficiency
Factors affecting lung growth and development in-utero (e.g. maternal smoking and pre-term birth) and childhood e.g. severe resp tract infection
Asthma

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6
Q

What are the complications of COPD?

A

Reduced QOL and increased morbidity and mortality
Depression and anxiety
Cor pulmonale
Frequent chest infections
Secondary polycythemia as a result of hypoxia
Resp failure due to increased airway resistance
Pneumothorax
Lung cancer
Muscle wasting and cachexia

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7
Q

How much of a risk factor is smoking for COPD?

A

90% of cases of COPD are associated with smoking but only 10% of smokers will develop it which indicates the presence of a co-factor such as a genetic predisposition

In the absence of other co-factors, COPD is unlikely to develop in patients with a smoking history <10-15 pack years.

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8
Q

How do you calculate pack years?

A

Number of cigarettes smoked per day, divided by 20, multiplied by the number of years smoked

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9
Q

What is alpha-1-antitrypsin deficiency?

A

an autosomal recessive disorder with co-dominant expression characterised by a deficiency in alpha-1 antitrypsin.
Alpha-1 antitrypsin is a protease inhibitor that is synthesised by the liver. It acts in the lung parenchyma to oppose the action of elastase. Elastase is a protease that causes the breakdown of elastin, a protein important to the structural integrity of the alveoli. This causes emphysema.

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10
Q

Whats the difference between emphysema from smoking and from alpha-1-antitrypsin deficiency?

A

Alpha 1 antitrypsin deficienc typically causes emphysema which is panlobular with a lower zone predominance
Emphysema from smoking is typically centriacinar

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11
Q

What does it mean by ‘COPD is a disease of both the airways and the alveoli’?

A

Disease of airways - chronic bronchitis
Disease of alveoli - emphysema

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12
Q

What is chronic bronchitis?

A

inflammation of the bronchi, defined as a chronic productive cough for three or more months a year in two consecutive years where other causes are excluded

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13
Q

What are the key inflammatory cells in the pathogenesis of COPD?

A

neutrophils
CD8+ T lymphocytes
macrophages

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14
Q

Whats the pathophysiology of chronic bronchitis?

A

Chronic inflammation of bronchial tubes due to exposure to irritants
Hypertrophy of mucus-secreting glands of bronchial tree, an increase in the number of goblet cells = increased mucus secretion
Smooth muscle in the airways becomes thicker and narrows the bronchioles. This narrowing is further aggravated by Bronchospasm.
Mucus blocks airway as cilia are unable to cope
Walls of bronchioles become inflamed and continual inflammation causes eventual fibrosis

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15
Q

What is emphysema?

A

NICE - loss of parenchymal lung texture.
Enlargement of alveoli in the lungs due to damage of the walls

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16
Q

Outline the pathophysiology of emphysema?

A

Inhalation of toxins -> initiation of immune/inflammatory response -> alveolar macrophages secrete inflamatory mediators (IL-6, IL-8, IL1, TNF alpha) ->IL-1 and TNF alpha recruit neutrophils (chemotaxis) -> neutrophils secrete proteases, mainly elastase, and macrophages secrete proteases (=imbalance between proteases and antiproteases) -> destruction of elastic fibres and surrounding tissues -> reduced area for gas exchange and chronic hypoxia.

Loss of elastin has two effects:
Collapse: the alveoli are prone to collapse.
Dilation and bullae formation: alveoli dilate and may eventually join with neighbouring alveoli forming bullae.

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17
Q

How does COPD lead to cor pulmonale?

A

Chronic hypoxia causes vasocontriction of pulmonary arteries, which leads to elevated pulmonary arterial pressure. The chronic elevation of pulmonary arterial pressure subsequently leads to right heart failure. This presents with classical features including raised jugular venous pressure, cyanosis, ankle oedema, parasternal heave and hepatomegaly.

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18
Q

How does COPD present?

A

Breathlessness - persistent, progressive over time, worse on exertion
Chronic/recurrent cough
Regular sputum production
Frequent LRTI
Wheeze
Reduced exercise tolerance

In severe COPD - weight loss, anorexia, fatigue, ankle swelling in cor pulmonale

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19
Q

What are signs of COPD?

A

Dyspnoea
Cyanosis
Pursed lip breathing
Use of accessory muscles
Barrel chest
Wheeze
Coarse crackles
Loss of cardiac dullness
Cachexia
Downward displacement of liver
Signs of CO2 retention - drowsy, asterixis, confusion
Signs of cor pulmonale - peripheral oedema, left parasternal heave, raised JVP, hepatomegaly

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20
Q

Why do COPD patients typically have pursed lip breathing?

A

prevents alveolar collapse by increasing the positive end expiratory pressure
It also slows the respiratory rate which can improve gas exchange in the lungs

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21
Q

How should you investigate COPD?

A

Physical examination
BMI
Obs
Sputum culture
ABG
FBC
Spirometry
Alpha-1-antitrypsin level
CXR or CT scan
ECG and echocardiogram if cor pulmonale is suspected

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22
Q

What will spirometry show in COPD?

A

post-bronchodilator FEV1/FVC ratio < 0.7 is needed for diagnosis

FVC may be normal but is often reduced due to air trapping
FEV1 is reduced
FEV1/FVC <70%

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23
Q

What is reversibility testing? What are typical results for COPD?

A

Spirometry before and after inhalation of a bronchodilator

COPD is characterised by limited reversibility post-bronchodilator, which helps differentiate it from asthma.

Note reversibility testing is not necessary for the diagnosis as its usually distinguishable from asthma based on history and examination

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24
Q

How is severity of COPD assessed?

A

Using the predicted FEV1%

Stage 1 (mild) - FEV1 >80% of predicted
Stage 2 (moderate) - 50-79%
Stage 3 (severe) - 30-49%
Stage 4 (very severe) - <30%

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25
Q

What is the predicted FEV1%?

A

refers to how the patients’ FEV1 compares to the average FEV1 in a population of similar age, sex and body composition

There are standard formulas available to determine the predicted FEV1 for men and women at different ages. This is then used alongside the patients’ FEV1 to work out the predicted FEV1 %.

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26
Q

What is used to grade the severity of breathlessness?

A

Medical research council (MRC) dyspnoea scale

  1. Breathlessness on strenuous exercise.
  2. Breathlessness on hurrying or slight hill.
  3. Walks slower than contemporaries on ground level due to breathlessness OR have to stop to catch breath when walking at own pace.
  4. Stops to catch breath after 100 metres OR a few minutes of walking
  5. Breathlessness on minimal activity (dressing) or unable to leave the house due to breathlessness
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27
Q

What features of supportive of COPD versus asthma?

A

Smoker or ex-smoker
Symptoms in older adults (> 35 years old)
Chronic productive cough
Persistent/progressive breathlessness
Night time waking with symptoms uncommon
Variability uncommon (diurnal or day-to-day)

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28
Q

What are chest X-ray features of COPD?

A

Hyperexpanded/inflation
Hyperlucent lung fields
Flattened hemidiaphragms
Hypodense
Saber-sheath trachea

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29
Q

When should you perform a CT scan for COPD?

A

Symptoms disproportionate to spirometric assessment
Alternative diagnosis suspected (e.g. bronchiectasis, fibrosis)
Lung cancer suspected or to investigate abnormalities on chest x-ray

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30
Q

When should I refer a person with COPD to a respiratory specialist?

A

If lung cancer is suspected
Diagnostic uncertainty
If COPD is very severe (<30% predicted) or rapidly declining
If cor pulmonale is suspected
If they’re <40 or there is FHx of alpha-1-antitrypsin deficiency
If they have frequent infections

Others - assessing need for oxygen therapy, long term ventilation, steroids, nebuliser therapy or lung surgery

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31
Q

Who should you suspect cor pulmonale in?

A

People with…
Peripheral oedema.
Raised JVP
Systolic parasternal heave.
A loud pulmonary second heart sound (over the second left intercostal space).
Hepatomegaly.

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32
Q

When shopudl you suspect alpha-1-antitrypsin deficiency?

A

in people with early onset of symptoms, minimal smoking history or a positive family history

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33
Q

Outline how post-bronchodilator spirometry is done?

A

Spirometry should be carried out 15–20 minutes after the person has inhaled a short-acting bronchodilator (for example 400 micrograms salbutamol delivered via a spacer device — local protocols may vary).
Airflow obstruction is defined as a post bronchodilator ratio of forced expiratory volume in 1 second (FEV1) to forced vital capacity (FVC) of less than 0.7.

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34
Q

What are DDx of COPD?

A

Asthma
Bronchiectasis
HF
Interstitial lung disease
Anaemia
TB
CF
Upper airway obstruction

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35
Q

What can trigger an acute exacerbation of COPD?

A

RTI - commonly rhinovirus
Smoking
Environmental pollutants

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36
Q

What are typical symptoms of an acute exacerbation of COPD?

A

Increased breathlessness, cough, sputum production or change in sputum colour
Increased wheeze, chest tightness, URTI symptoms, reduced exercise tolerance, ankle swelling, increased fatigue, acute confusion

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37
Q

What is pulmonary rehabilitation?

A

This refers to a multidisciplinary programme that aims to optimise the physical and social performance of patients suffering from long-term chronic lung conditions like COPD. It involves exercise training, health education, and breathing techniques over a series of sessions. Nutritional education and behavioural techniques are also utilised.
Pulmonary rehabilitation is offered to any patient with COPD who feels disabled by their condition.

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38
Q

When should I refer a person with COPD for pulmonary rehabilitation?

A

If they are functionally disabled by COPD i.e. MRC grade 3 or above
If they have had a recent hospitalisation for an acute exacerbation

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39
Q

Why should you not start oxygen therapy without a specialist assessment?

A

Oxygen is a treatment for hypoxaemia (not breathlessness).
Long-term oxygen therapy (LTOT) can improve survival in people with stable COPD and chronic hypoxia.
Inappropriate oxygen therapy in people with COPD may cause respiratory depression.

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40
Q

When should I refer a person with COPD for assessment for oxygen therapy?

A

Oxygen saturations of 92% or less breathing air.
Very severe (FEV1< 30% predicted) or severe (FEV1 30–49% predicted) airflow obstruction.
Cyanosis.
Polycythaemia.
Peripheral oedema.
Raised jugular venous pressure.

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41
Q

What vaccinations should COPD patients be offered?

A

Pneumococcal vaccine
Seasonal influenza vaccine

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42
Q

What non-pharmacological management is given to all COPD patients?

A

Explain diagnosis, risk factors etc
Give patient information from the British lung foundation and NHS websites
Offer support to stop smoking at every opportunity
Offer pneumococcal and influenza vaccines
Offer pulmonary rehabilitation if indicated
Develop a personalised self-management plan
Optimise treatment for comorbidities

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43
Q

How should you manage breathlessness in COPD?

A

Step 1 - SABA or SAMA to use as needed

Step 2 -
no asthmatic or steroid responsive features - combined LABA plus a LAMA.
Asthmatic or steroid responsive features - LABA plus an ICS

Step 3 -
No asthmatic or steroid responsive features - 3 month trial of LABA, LAMA + ICS and if no improvement at 3 months then go back to LABA and LAMA
Asthmatic or steroid responsive features - if person continues to have day-to-day symptoms adversely affecting quality of life or has 1 severe or 2 moderate exacerbations of COPD within a year, offer LABA plus LAMA plus ICS.

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44
Q

Whats the risk of taking inhaled corticosteroids for COPD?

A

Increased risk of pneumonia

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45
Q

Whats the moa of beta-receptor agonists for COPD?

A

Bind to β2 adrenergic receptors on bronchial smooth muscle cells which activates the enzyme adenylyl cyclase which leads to increased cAMP production that ultimately cause relaxation of the smooth muscle.

β2-agonists also stimulate the β2 receptors on immune cells like mast cells and decrease the release of inflammatory mediators like leukotrienes and prostaglandins. This, in turn, decreases the inflammation, swelling, and irritation in the respiratory tract.
Ultimately, all these events help dilate the narrowed airways and improve air flow.

46
Q

What are examples of SABAs?

A

albuterol (aka salbutamol), metaproterenol, and terbutaline.

47
Q

What are side efefcts of beta-2 agonists?

A

Arrhythmias; headache; palpitations; muscle cramp; tremor: hyperglycaemia (uncommonly). Bronchospasm paradoxical (very rare)

48
Q

What are examples of LABAS?

A

Salmeterol
Formoterol
Olodaterol

49
Q

Whats the MOA of muscarinic antagonists for COPD?

A

They enter the lungs and bind to M3 muscarinic receptors on the tracheal and bronchial smooth muscles. This blocks acetylcholine from binding to the receptors, leading to less smooth muscle constriction.

50
Q

What are examples of SAMAs?

A

ipratropium bromide and oxitropium bromide

51
Q

What are examples of LAMAs?

A

tiotropium, aclidinium, umeclidinium, and glycopyrrolate (also called glycopyrronium)

52
Q

What are the main side effects of Anticholinergics e.g. muscarinic anatgonsist?

A

a dry mouth
constipation
a cough
headaches
feeling sick (nausea)

53
Q

What are examples of inhaled corticosteroids for COPD?

A

Beclometasone
Fluticasone

54
Q

How do inhaled corticosteroids work for COPD?

A

work by reducing inflammation within the lungs. They are thought to reduce the number of exacerbations, improve the efficacy of bronchodilators and decrease dyspnoea in stable COPD.

55
Q

What is seretide?

A

Salmeterol and fluticasone
I.e. a LABA and ICS combined

56
Q

What is ultibro?

A

Indacaterol and glycopyrronium
I..e LABA and LAMA combined

57
Q

What is Trimbow?

A

formoterol/glycopyrronium/beclometasone
I.e. LABA, LAMA and ICS combined

58
Q

What are the delivery systems for COPD treatment?

A

Inhalers
Spacers
Nebulisers

59
Q

What is a spacer?

A

Spacers are plastic devices with a mouthpiece at one end and a hole for a metered-dose inhaler (MDI) to be inserted at the other:
They require less coordination than use of a MDI alone and allow carers to help people with cognitive impairment or functional problems.
They slow down the particles of the drug and allow more time for evaporation of the propellant, so that more of the drug can be inhaled.
They increase the proportion of the drug delivered to the airways and reduce the amount of drug deposited in the oropharynx (thereby reducing local adverse effects and systemic absorption).
They are useful in people with poor inhalation technique.

60
Q

Who should you consider nebuliser therapy for?

A

people with distressing or disabling breathlessness despite maximal therapy using inhalers.
Nebulised therapy should not be prescribed without an assessment of the person’s and/ or carer’s ability to use it.

61
Q

What add on treatments can be considered in COPD?

A

Oral corticosteroids
Oral theophylline (slow release)
Oral mucolytic therapy
Oral prophylactic antibiotic therapy
Oral phsophodiesterase-4 inhibitors

62
Q

Whats the moa of theophylline?

A

relaxes the smooth muscles located in the bronchial airways and pulmonary blood vessels by phosphodiesterase 3 inhibition

63
Q

When should oral mucolytic therapy be considered?

A

if a person with stable COPD develops a chronic cough productive of sputum.

64
Q

What are oral mucolytic licensed for COPD use?

A

Carbocisteine and acetylcysteine

65
Q

Who should be considered for prophylactic oral macrolide therapy?

A

people with COPD who have had more than three exacerbations requiring steroid therapy and at least one exacerbation requiring hospital admission in the previous year

66
Q

What prophylactic antibiotic therapy is given in some COPD cases?

A

Treatment with azithromycin 500 mg three times per week, should be considered for a minimum of 6–12 months to assess evidence of efficacy in reducing exacerbations.

67
Q

Before commencing prophylactic oral macrolides, what should you do?

A

Optimise non-pharmacological and pharmacological therapies, including smoking cessation, optimised inhaler technique, optimised self-management care plan, airway clearance techniques, and attendance at pulmonary rehabilitation course.
Perform ECG (electrocardiogram) to assess QTc interval.
Perform baseline liver function tests.
Counsel people with COPD about potential adverse effects, including gastrointestinal upset, hearing and balance disturbance, cardiac effects, and microbiological resistance.
Arrange microbiological assessment of sputum before therapy, including investigation for non-tuberculous mycobacteria (NTM).
Consider accurate assessment of baseline exacerbation rate and a CT scan to exclude a possible diagnosis of bronchiectasis.

68
Q

What monitoring should be done after starting oral macrolides?

A

If adverse gastrointestinal effects occur at this higher dose of azithromycin clinicians can consider a dose reduction to 250 mg three times per week.
Liver function tests should be checked 1 month after starting treatment and then every 6 months. An ECG should be performed 1 month after starting treatment to check for new QTc prolongation. If present, treatment should be stopped.
Subsequent follow up at 6 and 12 months should determine whether benefit is being derived from therapy by using objective measures such as the exacerbation rate, CAT score or quality of life as measured by a validated assessment tool. If there is no benefit treatment should be stopped.
It is not necessary to stop prophylactic azithromycin during an acute exacerbation of COPD unless another antibiotic with potential to affect the QT interval has also been prescribed.

69
Q

What information should self-management plans offer for people with COPD?

A

Advice and info on…
COPD and its symptoms
Non-pharmacological measures
Importance of vaccines
Apporpate use of inhaled therapies
Early recognition and management of exacerbations
Details of local and national organisations and online resources that can provide more information and support such as the British Lung Foundation

70
Q

What is the walk test?

A

Involves asking the person to walk for a standardised length of time (usually 6 or 12 minutes).
Failure to complete the test and/or moderate to severe respiratory distress measured on a visual analogue scale indicates a possible need for in-flight oxygen.

71
Q

What is the hypoxic challenge test>

A

Is performed in a specialist lung function unit and is used to assess whether a person needs in-flight oxygen.
Measures the person’s response to a simulated aircraft cabin environment.
In this investigation, 15% oxygen is administered and the person is monitored continuously by pulse oximetry.
A partial pressure of arterial oxygen (PaO2) of 6.6 kPa or an oxygen saturation of 85% is used as the cut-off value below which supplemental oxygen is recommended for air travel.

72
Q

How should I manage a person with end-stage COPD?

A

Ensure they have an advanced care plan and discuss end-of-life issues including advanced decisions
Coordinate care with a respiratory nurse specialist, district nurse, palliative care team, and social services as appropriate.
Optimise treatment
Discuss hospice admission
Consider what practical and emotional support can be provided for family and carers

73
Q

How should I treat a person with an acute exacerbation of COPD who does not require admission?

A

Advise the pt to increase doses or frequency of short acting bronchodilators (not exceeding maximum dose)
Consider oral corticosteroids for those with significant increases in breathlessness that interfered with daily activities - 30mg oral prednisolone
Consider need for Antibiotics - amoxicillin, doxycycline or clarithromycin are fist line (if not improvement after 3 days then send a sputum sample for culture and suspectibility testing)

74
Q

What is long term oxygen therapy?

A

When pt breathe supplementary oxygen for at least 15 hours a day

75
Q

Who should be assessed for long term oxygen therapy?

A

Measure arterial blood gases on 2 occasions at least 3 weeks apart in pt with stable COPD on optimal management
If pO2 is <7.3kPa or 7.308 with secondary polycythemia/peripheral oedema/pulmonary hypertension, then offer LTOT

76
Q

Whats the advice for long term oxygen therapy and smoking?

A

NICE advise the following:
do not offer LTOT to people who continue to smoke despite being offered smoking cessation advice and treatment, and referral to specialist stop smoking services.

77
Q

What is the structured risk assessment that NICE suggest should be carried out before offering long term oxygen therapy?

A

NICE suggest that a structured risk assessment is carried out before offering LTOT, including:
the risks of falls from tripping over the equipment
the risks of burns and fires, and the increased risk of these for people who live in homes where someone smokes (including e‑cigarettes)

78
Q

What are the criteria NICE suggest to determine whether a pt has asthmatic/steroid responsive features?

A

any previous, secure diagnosis of asthma or of atopy
a higher blood eosinophil count - note that NICE recommend a full blood count for all patients as part of the work-up
substantial variation in FEV1 over time (at least 400 ml)
substantial diurnal variation in peak expiratory flow (at least 20%)

79
Q

When should oral theophylline be considered?

A

After trials of short and long-acting bronchodilators or to people who cannot used inhaled therapy

80
Q

What should you do with the dose of oral theophylline if macrolide or fluoroquinolone are Co prescribed and why?

A

Reduce the dose
As these antibiotics can inhibit it the breakdown of theophylline in the liver leading to an accumulation of the drug in the body. If taking both then monitor theophylline levels and reduce dose accordingly to prevent toxicity. This is particularly important if pt have pre-existing conditions that increase the risk of theophylline toxicity e.g. liver disease, kidney disease, COPD, congestive HF

81
Q

How should you manage cor pulmonale in COPD?

A

Loop diuretic and consider long term oxygen therapy

82
Q

What factors may improve survival in patients with stable COPD?

A

Smoking cessation
Long term oxygen therapy in pt who fit the criteria
Long volume reduction surgery in selected patients

83
Q

What are the most common infective causes of COPD exacerbations?

A

bacteria 70%
Haemophilus influenzae (most common cause)
Streptococcus pneumoniae (most common cause of pneumonia)
Moraxella

respiratory viruses 30%
human rhinovirus is the most important pathogen

84
Q

How should you manage severe exacerbations of COPD that require secondary care?

A

Oxygen therapy
Nebulised bronchodilator (IV theophylline if not responsive)
Steroid therapy
Non invasive ventilation may be used

85
Q

What is non-invasive ventilation?

A

a method of delivering mechanical ventilation to patients with respiratory failure without the need for invasive procedures such as tracheostomy or endotracheal intubation. NIV is often used as a treatment option for patients who experience acute exacerbations or chronic respiratory failure.
NIV involves the use of a machine that delivers a mixture of air and oxygen through a mask that covers the nose or mouth (or both) of the patient. The machine can provide different levels of positive airway pressure to support the patient’s breathing and reduce the work of breathing. This helps to improve gas exchange, increase oxygen levels in the blood, and reduce carbon dioxide levels.

86
Q

What are the benefits of non-invasive ventilation?

A

avoiding the need for intubation
reducing the risk of ventilator-associated pneumonia
improving patient comfort and quality of life
It can reduce the length of hospital stay and the need for mechanical ventilation
It may reduce mortality in some cases.

87
Q

When is non-invasive ventilation used?

A

when COPD is with a respiratory acidosis pH 7.25-7.35 (can be used for those who are more acidosis but a greater degree of monitoring is required)

88
Q

What are the 2 main types of non-invasive ventilation?

A

Continuous Positive Airway Pressure: CPAP provides a constant level of positive pressure throughout the respiratory cycle to keep the airways open and improve oxygenation. It is commonly used to treat obstructive sleep apnea and respiratory distress syndrome in premature infants. CPAP is not typically used to treat COPD, but it may be used in some cases to support breathing during acute exacerbations.

Bilevel Positive Airway Pressure (BiPAP): BiPAP provides two levels of positive pressure, one during inhalation and a lower level during exhalation, to support breathing and improve oxygenation. BiPAP is commonly used to treat acute exacerbations of COPD, chronic respiratory failure, and other respiratory conditions. BiPAP can be adjusted to provide different levels of pressure support, depending on the patient’s needs.

89
Q

What surgical interventions can be offered for COPD/A1ATD?

A

Lung reduction surgery
Bullectomy
Lung transplantation

90
Q

What is a bullectomy?

A

a surgical procedure in which a bullectomy is a surgical procedure in which a bulla, which is an abnormally large air-filled space in the lung, is removed.

91
Q

What is type 2 respiratory failure?

A

Hypercapnic failure
Lungs are unable to adequately remove CO2 from the blood leading to hypercapnia
Those with COPD are at risk of it

PaO2 <8kPa and raised PaCO2

92
Q

What are the target saturations for those with COPD?

A

88-92%

93
Q

How should you manage type 2 respiratory failure in pt with COPD?

A

oxygen therapy should be trialed using a venturi mask for 1 hour with repeat ABG. If there is persistent evidence of T2RF, or they decline during the trial period, then non-invasive ventilation should be considered

94
Q

What are the 2 settings on a BiPAP machine?

A

IPAP: inspiratory positive airway pressure (usually 10-15 cmH20)
EPAP: expiratory positive airway pressure (usually 4-5 cmH20)

95
Q

What can cause chronic bronchitis?

A

Cigarette smoke
Inhales irritants - smog, industrial pollutants, toxic chemicals, dust
Repeated exposure to infections - influenza, staphylococcus, streptococcus, mycoplasma pneumonia
Those with other respirairt disease have a higher predisposition
Chronic GERD

96
Q

How does cigarette smoke cause chronic bronchitis?

A

Smoke leads to chronic irritation
Its toxicity also destroys the ciliates epithelium and replaces it with squamous cells which ultimately reduces mucus clearance

97
Q

How does CF cause chronic bronchitis?

A

The loss of CFTR function leads to increased viscosity of mucus, increased mucus production and decreased mucus clearance. The recurrent respiratory infections and structural changes in the airways due to chronic inflammation can also lead to chronic bronchitis.

98
Q

How do chronic bronchitis and emphysema present differently?

A

Chronic bronchitis typically presents with a productive cough
Emphysema almost exclusively presents with SOB

99
Q

What should COPD patients be given a home supply of?

A

Prednisolone and an antibiotic - so they can start these meds whilst contacting the GP (if by the time they have seen GP e.g. 24 hours later and still bad they should probably be sent into hopsital as often deteriorate very fast)

100
Q

What Is alpha-1-antitrypsin? What is its role?

A

A protease inhibitor normally produced by the liver
It’s role is to protect cells from enzymes such as neutrophil elastase. This is important as left unchecked neutrophil elastase leads to lung damage

101
Q

How is alpha-1-antitrypsin deficiency inherited?

A

Autosomal recessive disorder with co-dominant expression (both alleles are expressed but the clinical phenotype is only seen with inheritance of 2 abnormal genes)

102
Q

Outline the genetics behind alpha-1-antitrypsin deficiency?

A

Caused by a mutation in the SERPINA1 gene on chromosome 14
There are >100 genetic mutations that can lead to reduces or absent AAT. The major 3 types are the following:
M allele - normal
S allele - in 2-3% population
Z allele - most severe and found in 1% population

103
Q

Outline the genotypes seen in alpha-1-antitrypsin deficiency?

A

PiMM - homozygous for normal alleles
PiZZ - homozygous for abnormal Z allele - 80-100% chance of developing A1AD
PiSZ - compound homozygous - variable phenotype - 20-50% chance of A1AD
PiMZ - heterozygous - 1 abnormal gene so unlikely to have the clinical phenotype

(Pi - Protease Inhibitor)

104
Q

Whats the pathophysiology of alpha-1-antitrypsin deficiency?

A

Z allele - Abnormal AAT protein polymerises and accumulates within hepatocytes leading to cellular destruction, chronic scarring and fibrosis
Mutations that lead to a complete deficiency of AAT will not cause liver disease as no protein is created

If AAT is absent or significantly reduces, elastase isnt broken down so it breaks own elastin which is important for the integrity of alveoli = emphysema = oxygen transfer is reduced = chronic hypoxia and breathlessness

105
Q

What are clinical features of alpha-1-antitrypsin deficiency?

A

COPD features - Dyspnoea, wheeze, cough, ankle swelling (from cor pulmonale)
CLD features - jaundice, bruising, spider navel, palmar erythema,a hepatomegaly, ascites, leuconychia, confusion, asterixis

106
Q

How do we investigate alpha-1-antitrypsin deficiency?

A

Measure serum alpha-1-antitrypsin levels
Genotyping to look for the most common mutations

Others may include - Pulmonary function tests, pulmonary imaging, liver imaging

107
Q

How is alpha-1-antitrypsin deficiency managed?

A

Stop smoking
Pulmonary rehabilitation
Prompt treatment of respiratory infections
Manage according to COPD guidelines e.g. inhaled therapy, antibiotics and short courses of corticosteroids for infections
If established cirrhosis, 6 monthly liver USS and AFP monitoring
Consideration for a lung or liver transplant

108
Q

How do A1AT and COPD differ in terms of location of emphysema?

A

Emphysema is most prominent in the lower lobes in A1AT deficiency and the upper lobes in COPD

109
Q

How should you manage an acute exacerbation of COPD?

A

increase the frequency of bronchodilator use and consider giving via a nebuliser
give prednisolone 30 mg daily for 5 days
Consider antibiotics

110
Q

What are indications for giving antibiotics in an acute exacerbation of COPD?

A

Purulent sputum
Clinical signs of pneumonia

111
Q

Which antibiotics are given first line for an acute infective exacerbation of COPD?

A

amoxicillin or clarithromycin or doxycycline.

RESPIRATORY (22 decks)

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