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Respiratory > 3. Asthma + Acute Asthma > Flashcards

3. Asthma + Acute Asthma Flashcards

1
Q

Define asthma.

A

A chronic, inflammatory condition of the airways that causes episodic exacerbations of bronchoconstriction.

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2
Q

Describe the pathophysiology seen in the airways of someone with asthma.

A

A type of obstructive lung disease - characterised by paroxysmal + reversible airway bronchoconstriction, as a result of inflammation of the respiratory airways + bronchial hyperrresponsiveness.

Main issue: narrowing of the airway
1. Smooth muscle contraction
2. Thickening of the airway wall by cellular infiltration and inflammation
3. Presence of secretions within the airway lumen

Asthma = type 1 hypersensitivity reaction

  1. Allergen present
  2. Allergen stimulates Type 2 Helper T cells (TH2) to produce cytokines such as:
    - IL-4 -> Facilitates class switching to IgE
    - IL-5 -> Facilitates release of eosiniphils
    - IL-13 -> Stimulates mucus production
  3. 1st exposure to allergen:
    - Induces sensitisation of mast cells, in which IgE binds to IgE receptors on the mast cells
  4. 2nd exposure to allergens:
    - Induces degranulation of mast cells
    - Mast cells release their granule contents; produce cytokines & other inflammaotry mediators e.g. histamine, prostaglandin D2, and leukotrienes, C4, D4, E4.
  5. Resulting airway inflammation –> leads to airway remodelling
  6. Characterised by:
    - bronchial smooth muscle hypertrophy
    - bronchoconstriction
    - mucous gland hypertrophy
    - vasodilation
    - increased vascular permeability
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3
Q

Describe the 4 main features of the airway obstruction seen in asthma.

A

Reversible.
Bronchial muscle constriction.
Mucosal swelling/inflammation.
Increased mucous production.

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4
Q

Explain the hygiene hypothesis.

A

The idea that growing up in a clean environment may predispose towards IgE response, as there is no childhood exposure to allergens, bacteria etc.

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5
Q

What are the 2 main types of asthma?

A
  1. Allergic/eosinophilic asthma (70%):
    - Allergens (e.g. fungal allergens and pets etc.) & atopy
  2. Non-allergic/non-eosinophilic (30%):
    - Exercise, cold air & stress
    - Smoking & non smoking associated
    - Obesity associated
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6
Q

What are the 2 types of allergic asthma?

A
  1. Extrinsic (atopic):
    - Type 1 hypersensitivity reaction triggered by extrinsic allergens e.g. dust, mold
    - Occurs most frequently in atopic individuals or those with atopic Fx
    - Childhood asthma often accompanied by eczema
  2. Intrinsic:
    - Non-immune
    - Often starts in middle-aged and attacks are usually triggered by
    respiratory infections.
    - Viral infections, stress, exercise, smoking
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7
Q

What is atopy?

A

Individuals who readily develop IgE antibodies (produced by B cells) against common environmental antigens.

E.G. house-dust mites, grass pollen and fungal spores.

Leading to elevated IgE serum levels -> which is linked to airway hyper-responsiveness and the prevalence of asthma.

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8
Q

Give 3 precipitants/triggers of an asthma attack.

A
  1. Occupational sensitisers
    e.g. wood dust, bleaches & dyes, isocyanates (industrial coating & spray painting) & latex can cause occupational asthma
  2. Cold air & exercise
  3. Atmospheric pollution and irritant dusts
  4. Diet - more fruit and veg is protective
  5. Emotion - high risk asthma attacks with those that are anxious
  6. Drugs e.g. NSAIDs (particularly aspirin), Beta-blockers
  7. Allergen induced asthma
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9
Q

Give 3 risk factors for asthma.

A
  1. Family history of asthma
  2. Exposure to allergens - dust mites, pets, tobacco smoke (living in city environments)
  3. History of atopic diseases - eczema, allergic rhinitis
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10
Q

give 2 diseases associated with asthma

A

eczema, hay fever, any allergy - atopy

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11
Q

Describe the clinical presentation of asthma - symptoms.

A
  1. Wheeze
  2. Intermittent dysponea (difficulty breathing)
  3. Cough (maybe nocturnal)
  4. Chest tightness
  5. Diurnal variation
  6. Episodic SOB
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12
Q

Describe the clinical presentation of asthma - signs.

A
  1. Tachypnoea
  2. Hyperinflated chest
  3. Hyper-resonance on chest percussion
  4. Decreased air entry (sign of severe illness: silent chest)
  5. Wheeze on ausculation
    -> Bilateral widespread “polyphonic” wheeze heard by a healthcare professional
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13
Q

What is seen in sputum samples for an asthma attack (histology)?

A

Curshmann spirals:
- Where shed epithelium becomes whorled mucous plugs
- Blocks air exchange

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14
Q

What investigations would you perform to diagnose asthma?

A
  1. Fractional exhaled nitric oxide (FeNO) testing
    - Low: <25 parts per billion (ppb)
    - Intermediate: 25-50 ppb
    - High: >50 ppb
  2. Spirometry with bronchodilator reversibility (>5 years)
    -> Obstructive pattern:
    - FEV1 <80% of predicted normal
    - FEV1/FVC ratio <0.7
  3. Peak flow variability - Peak expiratory flow rate (PEFR)
    - Measured by keeping a diary of peak flow measurements several times per day for 2 to 4 weeks
  4. Direct bronchial challenge test with histamine or methacholine
    - A PC20 value (provocative concentration causing a 20% drop in FEV1) of 8 mg/ml or less is regarded as a positive result.
  5. Bloods - FBC - Normal or raised eosinophils
  6. CXR - normal or hyper-inflated
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15
Q

Which 3 investigations would be done for chronic asthma?

A
  1. Peak flow - PEFR
    - Variability >20%
  2. Fractional exhaled nitric oxide (FeNO)
    - Adults: >40 ppb
    - Children: >35 ppb
  3. Spirometry
    - FEV1/FVC <0.7 = obstructive spirometry
    - FEV1 low
    - FVC preserved
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16
Q

Give the stepwise management of mild to severe asthma (BTS guidelines).

A

SILCO:

  1. Short-acting B2-agonist (SABA)
    e.g. Salbutamol
  2. Add low-dose inhaled corticosteroid - ICS
    e.g. Beclamethasone
  3. Add long-acting B2-agonist (LABA)
    e.g. Salmeterol
    - Continue the LABA only if the patient has a good response.
    - If no benefit, stop LABA + Increase ICS dose.
    - If benefit but inadequate control, continue LABA + Increase ICS dose
  4. Consider 4th option:
    - Trial oral leukotriene receptor antagonist e.g. Montelukast
    - OR Trial oral Theophylline
    - OR Inhaled LAMA (I.E. Tiotropium)
    - OR Oral B2-agonist (Salbutamol)
  5. Add Oral prednisolone, refer to asthma clinic
  6. Titrate inhaled corticosteroid up to “high dose”. Combine additional treatments from step 4. Refer to specialist.
  7. Add oral steroids at the lowest dose possible to achieve good control.
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17
Q

What indicates the need to add step 2 (ICS) of asthma management?

A

If the patient reports symptoms 3 or more times per week or night-time waking.

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18
Q

Give the stepwise management of mild to severe asthma according to NICE guidelines.

A
  1. Short-acting B2-agonist inhaler (SABA)
    e.g. Salbutamol
    - As required for infrequent wheezy episodes
  2. ADD Low-dose Inhaled Corticosteroid (ICS)
  3. ADD Oral leukotriene receptor antagonist
    I.E. Montelukast
  4. ADD Long-acting B2-agonist inhaler (LABA)
    e.g. Salmeterol
    - Continue the LABA only if the patient has a good response.
  5. Consider changing to a maintenance and reliever therapy (MART) regime.
  6. Increase the inhaled corticosteroid to a “moderate dose”.
  7. Consider increasing the inhaled corticosteroid dose to “high dose”
    OR ADD Oral Theophylline
    OR ADD an inhaled LAMA (e.g. tiotropium)
  8. Refer to a specialist.

Summary:
1. SABA (e.g. salbutamol)
2. Inhaled corticosteroid (ICS, e.g. budesonide)
3. Leukotriene receptor antagonist (LRTA, e.g. montelukast)
4. LABA (e.g. salmeterol)
5. Increase ICS dose

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19
Q

For Beta agonist therapy, why do we use beta-2 receptor agonists?

A

Are Beta-2 selective I.E. work only in lungs (B1 is heart & B3 is
adipose tissue).

However, in high doses, the B2-agonists are not selective and will act on other receptors.

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20
Q

How do beta 2 agonists work?

A
  1. B2 agonist binds to B2 receptor coupled with Gs protein
  2. Results in adenyl cyclase converting ATP to cyclic AMP
  3. Increases in cyclic AMP leads to bronchodilation
  4. Inducing smooth muscle relaxation in the lungs
  5. Beta-agonists also inhibit mast cell activity
  6. Thereby reducing inflammatory response
21
Q

Give 2 examples of short-acting B2-agonists (SABA).

A
  1. Salbutamol
  2. Terbutaline
22
Q

Give 2 examples of long-acting B2-agonists (LABA).

A
  1. Salmeterol (partial agonist)
  2. Formoterol (full agonist)
23
Q

Give some possible side effects of B2-agonists.

A
  1. Tachycardia
  2. Palpitations
  3. Tremor/ trembling
  4. Headaches
  5. Muscle spasms
  6. Nausea
  7. Activation of ‘fight or flight’ receptors
24
Q

Why are beta-blockers contraindicated in asthmatics?

A

Beta-blockers can act on the beta2 receptors within the bronchi.

Blocking them induces bronchospasm, causing an asthma attack/worsening.

25
Q

Give some examples of inhaled corticosteroids (ICS).

A
  • Prednisolone
  • Beclomatasone
  • Budesonide
  • Fluticasone
26
Q

How do steroids work to help in an asthma attack?

A

Corticosteroids inhibit phospholipase A2.
Thus inhibiting the inflammatory cascade.
So dampening down the inflammatory reaction that occurs in an asthma attack.

27
Q

Give some possible side effects of inhaled corticosteroids (ICS).

A
  1. Oral thrush - oral candidiasis
  2. Sore throat
  3. Nosebleeds
  4. Coughing
28
Q

How do long-acting muscarinic antagonists (LAMA) work?

A
  • Act on airway M3 receptors.
  • Normally, ACh (parasympathetic) binds to M3 receptor bound to
    Gq protein, resulting in phospholipase C converting phosphate to
    DAG, resulting in protein kinase C production that results in smooth muscle contraction.
  • Muscarinic antagonists: block the muscarinic ACh receptors.
  • Causes smooth muscle relaxation.
29
Q

Give 1 example of a short-acting antimuscarinic and 1 example of a long-acting antimuscarinic.

A

Short-acting: ipratropium
Long-acting: tiotropium

30
Q

How do leukotriene receptor antagonists (LTRA) work to improve asthma symptoms?

A
  1. Leukotrienes are produced by the immune system and cause inflammation, bronchoconstriction and mucus secretion in the airways.
  2. LTRA block the action of leukotrienes on the CsyLT1 receptor on bronchial smooth muscle cells and mast cells.
  3. Blocks the effects of leukotrienes e.g. inflammation, mucous secretion, bronchoconstriction.
31
Q

Give an example of a leukotriene receptor antagonist (LTRA).

A

Montelukast

Zafirlukast

32
Q

What class of drug is theophylline?

A

Methylxanthines = non-selective phosphodiesterase (PDE) inhibitors

33
Q

How does theophylline work?

A

A competitive non-selective phosphodiesterase inhibitor:
- Prevent the conversion of cyclic-AMP to 5’-AMP.
- Resulting in a build up of cyclic-AMP.
- Inhibits leukotriene synthesis (major cause of bronchiole inflammation).
- Reduces inflammation and immunity.
- Causes smooth muscle relaxation.

34
Q

What is the problem with using theophylline?

A

Narrow therapeutic window
- Can be toxic in in excess so monitoring plasma theophylline levels in the blood is required.

35
Q

What are the blue and brown inhalers?

A

Blue:
- Active ingredient: Beta-2 agonists/long-acting anticholinergics
- Effect: Long-acting bronchodilator
- When to use: During asthma attacks
- Reason for use: For relief

Brown:
- Active ingredient: Corticosteroids
- Effect: Anti-inflammatory
- When to use: Every day to prevent attacks
- Reason for use: Prevention

36
Q

What is MART?

A

Maintenance and Reliever Therapy (MART):

-> A form of combined ICS + LABA treatment in which a single inhaler, containing both ICS and a fast-acting LABA, is used for both daily maintenance therapy and the relief of symptoms as required.

  • MART is only available for ICS and LABA combinations in which the LABA has a fast-acting component (e.g. formoterol).
37
Q

Compare COPD with asthma.

A

Asthma:
1. Intermittent airway obstruction
2. Improved with bronchodilators + steroids
3. Cellular inflammation - eosinophils, mast cells, T cells
4. Airway remodelling

COPD:
1. Progressively worsening airway obstruction
2. More permanent, less reversibility
3. Cellular inflammation - neutrophils, macrophages
4. Emphysema frequent
5. More common in > 50 YO

38
Q

Define acute asthma.

A

An acute exacerbation of asthma is characterised by a rapid deterioration in symptoms.
This could be triggered by any of the typical asthma triggers such as infection, exercise or cold weather.

39
Q

In terms of severity, what are the 3 levels of grading acute asthma?

A
  1. Moderate
  2. Severe
  3. Life-threatening
40
Q

Features of moderate acute asthma.

A
  1. Increasing symptoms
  2. Peak flow  50-75% best or predicted
  3. No features of acute severe asthma
  4. SATS >92% in air
41
Q

Features of severe asthma.

A

At least 1 of these:

  1. PEFR 33 - 50% best or predicted
  2. RR>= 25
  3. HR >=110
  4. Inability to complete sentences in 1 breath
42
Q

Features of life-threatening asthma.

A
  1. Silent chest on auscultation
    - No wheeze
    - Occurs when the airways are so tight that there is no air entry at all!
  2. Confusion + Exhaustion (poor respiratory effort)
  3. Bradycardia
  4. Cyanosis (PaO2 <8kPa)
  5. PEFR (Peak flow) < 33% predicted
  6. SATS <92%
  7. Normal CO2 (4.6-6kPa)
  8. Hypotension
  9. Haemodynamic instability (I.E. shock)
43
Q

Which 3 investigations would be done for acute asthma?

A

Should be ordered more urgently in the context of an acute asthma attack:

  1. ABG
    - Shows type 2 respiratory failure = low PaO2 + high PaCO2
    1) 1st: Initially - patients will have a respiratory alkalosis as tachypnoea causes a drop in CO2.
    2) A normal pCO2 or hypoxia is a concerning sign as it means they are tiring and indicates life threatening asthma.
    3) A respiratory acidosis due to high CO2 is a very bad sign in asthma.
  2. Bloods - to look for precipitating causes of an asthma attack e.g. infection
    - FBC
    - CRP
  3. CXR
    - To exclude differentials + possibly identify a precipitating infection
44
Q

What is the criteria for a patient to be discharged from hospital following an asthma attack?

A

Must be stable on their REGULAR asthma regime for 24 hours

45
Q

Management of a moderate acute attack.

A
  1. Nebulised beta-2 agonists
    (I.E. Salbutamol 5mg repeated as often as required)
  2. Nebulised ipratropium bromide
  3. Steroids. Oral prednisolone or IV hydrocortisone. These are continued for 5 days
  4. Antibiotics if there is convincing evidence of bacterial infection.
46
Q

Management of a severe acute attack.

A

Severe:

  1. Oxygen if required to maintain SATS 94-98%
  2. Aminophylline infusion
  3. Consider IV salbutamol
47
Q

Management of life-threatening acute attack.

A

Life threatening:

  1. IV magnesium sulphate infusion
  2. Admission to HDU / ICU
  3. Intubation in worst cases – however this decision should be made early because it is very difficult to intubate with severe bronchoconstriction.
48
Q

Management of an acute asthma attack.

A
  1. Ensure patient’s airway
  2. Ensure O2 saturations of 94-98%
    = 100% O2 with facemask.
  3. Give nebulisers of salbutamol and ipatropium bromide
  4. If severe:
    - Give IV hydrocortisone or Oral prednisolone
    (Give 40-50 mg Prednisolone for >5 days following an acute asthma attack).
  5. If severe:
    - Give IV Magnesium Sulphate
  6. If inadequate bronchodilatory response from nebulisers + severe:
    - Give IV Aminophylline
  7. Still no improvement:
    -> Intensive care
49
Q

What doe ABGs show for an acute asthma attack?

A

Initially:
- Patients will have a respiratory alkalosis as tachypnoea causes a drop in CO2.

Then:
- A normal pCO2 or hypoxia is a concerning sign as it means they are tiring and indicates life threatening asthma.

Then:
- A respiratory acidosis due to high CO2 is a very bad sign in asthma.

Respiratory (9 decks)

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