Airway Diseases Flashcards

1
Q

what are the 3 main airway diseases?
what do they affect?

A

Asthma
COPD
Bronchiectasis (not covered in this lecture)

They affect the small airways of the lungs

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2
Q

what are the 2 basic lung function tests?
what are they used for?

A

Spirometry
Flow volume loop

both spirometry and flow volume loop can be used:
To help differentiate between obstructive and restrictive disease
To tell you the severity of condition
To tell you if the treatment is working (repeat tests)

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3
Q

using spirometry, what would be the indicators that we’re dealing with either obstructive airway disease or restrictive lung disease?

A

Spirometry is the main test for defining airway diseases
In obstructive airway diseases:
- You have narrowing of the airways
- FEV1/FVC ratio < 0.7
- This indicates airflow obstruction
In restrictive lung disease:
- Reduced VC
- Normal/Increased FEV1/FVC ratio (no problem with airway diameter)

Graphs: (Blow out as hard and as fast as you can)
1. Normal
2. Obstructive airway disease:
3. Restrictive lung disease picture
(NB: Same gradient so FEV1 remains the same)

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4
Q

using flow volume loop, what would be the indicators that we’re dealing with either obstructive airway disease or restrictive lung disease?

A

Y Axis is flow
X axis is volume
Positive y axis = expiration
Negative Y axis = Inspiration

Obstructive air way disease:
- Reduced peak flow
- Scooped out descending limb
- The more severe the airway obstruction, the lower the peak flow and the greater the scoop
NB: eventually same volume of lung is breathed (crosses x axis at same distance as normal loop)
- Asthma is reversible so you can get normal flow loop volume after treatment (bronchodilators)

Restrictive air way disease:
- Normal peak flow is reached
- No problem with how quickly you can blow out (same gradient as normal)
- Problem with how much you can blow out overall (reaches x axis earlier)

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5
Q

what is asthma?

A

a chronic inflammatory disorder of the airways leading to airflow obstruction

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6
Q

how is the airflow obstruction variable for asthma?

A

Airflow obstruction is variable:
You get diurnal variability of Peak expiratory flow rate of >20% (diagnostic of asthma)
If treated using bronchodilator –> Increase in FEV1 by at least 12% and increase of 200ml of volume
Asthma is due to Airway hyperresponsiveness
This is sometimes associated with atopy/allergies…

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7
Q

explain the pathogenesis of asthma

A

Asthma can be driven by exposure to Allergens.
There allergens are detected by dendritic cell which then induce a Th2 inflammatory response of airways
This can:
- Drive the release of IgE from β cells
- Drive the release of Inflammatory mediators e.g. leukotrienes from mast cells
- Drive the release of other inflammatory mediators from eosinophils

These released substances can then all cause asthma.
Asthma can also be driven by exposure to bacteria/viruses and prenatal programming in the same way.
Knowledge of the causes of asthma can help us design treatment
Asthma drugs are being developed to block different things in Th2 pathway
E.g. IgE & leukotrienes

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8
Q

what changes to the airways does asthma cause?

A

Asthma causes airway wall inflammation –> reduced diameter of airways –> increased airway resistance
Asthma also causes mucus secretion –> block small airways
Asthma causes hyperresponsive of air way wall –> contraction of smooth muscle –> reduce diameter of airways –> increased airway resistance
With treatment this should be reversible/episodic.
On-going airway inflammation will cause airway wall scaring (permanent)
Mucus secretion can be temporary or permanent.

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9
Q

what are the symptoms of asthma?

A

Diurnal variation (symptoms worse in the morning and late at night – can keep you awake)
- Coughing
- Chest tightness
- Wheezing (whistling noise made on expiration)
- Shortness of breath
NB: Symptoms are the tip of the iceberg. By the time you start to develop noticeable symptoms you will already have had the conditions below for quite some time.

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10
Q

what happens during an asthma attack?

A

During an asthma attack your airways narrow via:
- Contraction of smooth muscle surrounding airway
- Swelling of inner lining (epithelium) due to inflammation
- Increase in mucus production

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11
Q

what are signs that you have good control of your asthma?

A
  • No daytime symptoms
  • No night time awakenings due to asthma
  • No exacerbations (asthma attack)
  • No need for reliever medication
  • You should only be taking your twice daily steroid inhaler
  • No limitation of physical activity
  • Normal lung function: FEV1 and/or PEF >80% predicted
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12
Q

name 5 Asthma triggers including examples

A
  1. Allergens:
    Pollens, Dust mites, Foods, Moulds, Animal dander
  2. Irritants:
    Second-hand smoke, Aerosols, Volatile organic compounds, Ozone, Particulate matter
  3. Other:
    Viral respiratory infections
  4. Changes in weather:
    Going from hot house => cold air, wind, humid environment, Exercise
  5. Endocrine factor: Changes in hormonal levels during menstrual period/pregnancy
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13
Q

what is occupational asthma?
give examples

A

You job can result in:
- Worsening of pre-existing asthma
- Development of asthma
Examples:
Flour dust –> bakers
Exposure to Isocyanates –> used in paint, varnishes, plastics, insulation
Colophony –> soldering
Proteolytic enzymes –> cleaners
Therefore, it is important to get an occupational history
Symptoms go away when not at work

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14
Q

what are the different things you can do to manage asthma?

A

Patients with asthma should have a written asthma management plan including:
- Identification of asthma triggers and ways to reduce/avoid exposure to them
- Medication
- Peak flow monitoring e.g. peak flow diary
- Emergency plan (when to call Dr and when to take steroids orally)

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15
Q

what are the pros of using a peak flow diary?
what do the different colours on the chart mean?

A

Good way of monitoring how well asthma is being controlled and how effective treatment is.
Green: where you want to be
Yellow: acceptable
Red: Danger zone, risk of severe life-threatening asthma attack.

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16
Q

what are the 2 Inhaled asthma therapies (medication)?

A

Inhalation of β2 agonist (bronchodilators)
Inhaled steroids

17
Q

what does inhalation of β2 agonist (bronchodilators) do?

A

These agonists bind to β2 receptors on smooth muscle walls, causing them to relax
E.g. Salbutamol (SA), salmeterol (LA)
These agonists can be:
Short acting: work quickly for rescue therapy. (blue inhaler)
Long acting: maintain relaxation of smooth muscle throughout the day

18
Q

what do inhaled steroids do?
example?

A

E.g. fluticasone
These reduce inflammation
They also
Improve lung function
Reduce symptoms
Reduce exacerbations
Reduce oral steroid use
Reduce hospital admissions
Reduce mortality

19
Q

what is the step-wise approach to prescribing asthma medication?

A

Step 1: Patient given short acting beta agonist (blue inhaler) which they used as required.
Step 2: If this does not work patient takes regular inhaled steroid at a low to moderate dose in conjunction with blue inhaler
Step 3: if symptoms still persist, we add a Long-acting beta agonist with the inhaled steroid.
Step 4: If this does not work, we increase the dose of steroid and try using leukotriene antagonist or theophylline (tablets which cause bronchodilation)
Step 5: Oral steroid tablets (try to avoid due to side effects)
If patient becomes well controlled at one step, we can try to move them down.

20
Q

when are oral steroids used?

A

Rarely needed in maintenance therapy
Predominantly used in acute exacerbations
If required, keep dose as low as possible
Monitor for side effects
(Diabetes, osteoporosis, cataracts)

21
Q

name 3 newer interventions in asthma?

A

Monoclonal antibodies class of drugs –> targeting asthma pathogenesis
Omalizumab - anti IgE
Delivered via SC injection

22
Q

what is COPD?

A

Chronic obstructive pulmonary disease
Characterised by airflow obstruction that is NOT fully reversible - does not improve with bronchodilator drugs
There is fixed damage to the lungs

23
Q

what is the pathogenesis of COPD?

A

Regular smoking and being susceptible to its effects is the main cause
Cigarettes stimulate inflammatory cells in the lungs (macrophages + neutrophils)
These cells release proteases and oxidants
Both of these lead to parenchymal damage and mucus hypersecretion
This results in airflow limitation:
- Air way inflammation and damage to mucociliary function of airways.
- This leads to narrowing or airways (bronchospasm)
- This then causes structural damage to lungs
- Also cigarette smoke can also causes systemic changes in blood stream which exacerbates inflammation.

24
Q

why does lung function decline faster in COPD patients?

A

Everyone’s lung function decreases with age.
We can measure lung function as FEV1 (% of value at 25)
FEV1 decreases at a faster rate in COPD patients
COPD is obtained via smoking regularly and being susceptible to its effects.
Stopping smoking will not reverse any damage already done but the decline in future lung function is a lot slower.

25
Q

how do you assess for COPD?

A

Measure Sputum production
Breathlessness score (MRC dyspnoea score)
Exacerbation frequency
Smoking history
BMI (BODE index score) - a low BMI is a bad prognostic factor as it indicates muscle
Signs of right heart failure - caused by hypoxia
Spirometer Results - to grade severity of disease (image)
Pulse oximetry - drops in oxygen levels

26
Q

what is the MRC dyspnoea score?

A
27
Q

how do you classify patients when assessing their COPD?

A

COPD can exist on its own but can also exist with asthma.
In COPD…
Pathologically patient may have chronic bronchitis like symptoms, where they have obstruction due to mucus production and chronic cough.
Radiologically (CT scan) lots of emphysema and parenchyma damage of lungs and hole in lung.
There is a spectrum where there are reversible and irreversible elements.
When treating patients, we try to classify them in this Venn diagram so we can target treatment appropriately.

28
Q

how do you differentiate asthma and COPD?

A
29
Q

how do you manage COPD?

A

COPD is not reversible so the main aim of management is to maximise bronchodilation
This can be done via:
Short acting β2 agonist (SABA), e.g. salbutamol
Long acting muscarinic antagonist (LAMA), e.g. tiotropoim
Muscarinic receptors on smooth muscles will cause bronchoconstriction so targeting them with antagonists will cause bronchodilation.
Combination of long acting bronchodilators → LAMA/MABA
Add inhaled steroid in selected patients → LABA/ICS and LAMA
NB inflammation does not play a big role in COPD so we don’t initiate steroid inhaler until patient is severe:
FEV1 less than 50%
Frequent exacerbations
blood eosinophilia is present

30
Q

what are the 4 tests for COPD?

A
  1. Spirometry
  2. Lung volume Tests
    - In COPD there is loss of elastic recoil of lung parenchyma so you we can’t expel all air out.
    - This causes gas trapping which causes an increase in - - - TLC even though FEV1 is reduced.
  3. Gas transfer Tests
    - In COPD there is damage to lung parenchyma
    - This results in reduced gas transfer of O2 from alveoli to capillaries
  4. Quality of life and comorbidities
    - Breathlessness scores, cardiovascular disease (systemic component)