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Block 2 > Clinical Aspects Of Airway Disease > Flashcards

Clinical Aspects Of Airway Disease Flashcards

1
Q

At what age does asthma occur?

A

Any

Most common in childhood (3-5yrs)

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2
Q

Is asthma common?

A

10-15% of UK population

Incidence increasing worldwide

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3
Q

Does asthma have a high mortality?

A

1000-2000 people/yr die from acute asthma

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4
Q

What 3 factors can bring on asthma?

A
  1. Genetic
  2. Environmental
  3. Acute
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5
Q

What are the causes and triggers of asthma?

A
  • Environmental allergen e.g. moulds, dust, grass pollen, pet hair
  • Viral infections e.g. rhinovirus, parainfluenza virus, RSV
  • Cold air
  • Emotion
  • Irritant vapours & fumes
  • Genetic factors
  • Drugs e.g. NSAIDs, beta-blockers
  • Atmospheric pollution e.g. sulphur dioxide, ozone, particulates
  • Exercise
  • Occupational sensitizers
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6
Q

What are the 2 types of asthma?

A
  1. Extrinsic/atopic: result of inappropriate adaptive immune response to an inhaled Ag so associated with atopy esp. eczema & hayfever (eosinophilic inflammation)
  2. Intrinsic/non-atopic: triggered by factors not related to allergies so no personal/family history of asthma/atopy (neutrophilic inflammation)

OFTEN OVERLAP

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7
Q

What is the difference between the onsets of the 2 types of asthma?

A
  1. Extrinsic/atopic: typical onset in childhood

2. Intrinsic/non-atopic: typical onset in middle age often following an upper airway infection

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8
Q

What are the 2 phases of extrinsic asthma?

A

Sensitisation

Effector

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9
Q

What is the pathophysiological features of asthma?

A

Airway obstruction (reversible)

Airway hyperresponsiveness

Airway inflammation

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10
Q

What happens inside the airways in asthma?

A
  • Mucus accumulation due to increased goblet cells in mucosa & hypertrophy of submucosal glands
  • Mucus plug with eosinophils & desquamated epithelial cells
  • Hypertrophy & hyperplasia of SMCs so muscle layer thickened
  • Thickened basement membrane
  • Oedema due to dilated blood vessels
  • Chronic inflammation due to recruitment of IS cells e.g. eosinophils, macrophages, neutrophils, lymphocytes & mast cells
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11
Q

What nerve reflex is involved in asthma?

A

Cholinergic reflex

Activated via sensory nerve irritation & causing SM to constrict

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12
Q

What are the 3 phases of asthma pathogenesis?

A
  1. Immediate/early: Allergen stimulates IgE production from B cells & IgE-sensitized MCs produce histamine, tryptase, PDG2, LTC4/D4 & PAF which constricts SM
  2. Late: Th2 cells produce IL-3, IL-5, GM-CSF & TNF whilst eosinophils release ECP + MCP & neutrophils release proteases + PAF -> vascular leak, cell infiltration & mucus secretion
  3. Re-modelling (chronic): SM hypertrophy, SM/epithelial cell hyperplasia, epithelial damage & BM thickening
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13
Q

What are the main problems of the early/acute and the late/chronic asthma response?

A

Acute: transient bronchial constriction due to factors released by IgE-sensitized histamine

Chronic: infiltration of inflammatory immune cells like T cells, eosinophils & neutrophils

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14
Q

What is asthma?

A

Chronic inflammatory condition with often acute exacerbations called “asthma attacks”

Closely associated with ‘atopy’/allergy

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15
Q

What are the symptoms of asthma?

A 
Cough
Wheeze
Chest tightness
SOB
Worst at night often
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16
Q

What are signs of asthma during exacerbation?

A 
Difficulty completing sentences
Wheeze (audible)
Tachypnoea 
Tachycardia
Use of accessory muscles
Reduced breath sounds (if severe)
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17
Q

Why do patients with asthma get woken in the morning by wheezing?

A

Cyclical secretion of steroids i.e. cortisol exacerbate airway narrowing

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18
Q

How is asthma diagnosed?

A
  • Trial of treatment & assess response (can also give irritant e.g. Ag or histamine)
  • Reversibility on spirometry before/after salbutamol
  • Diurnal variation on peak flow monitoring
  • Fractional exhaled NO (FeNO)

BUT NO GOLD STANDARD TEST

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19
Q

Why can a fractional exhaled NO (FeNO) test help to diagnose asthma?

A

Measures eosinophilic inflammation in airways -> secrete more NO in breath if their is inflammation present at the time

20
Q

If you are assessing someone for asthma, but symptoms are always present i.e. does not get better/worst, what should you do?

A

Consider other diagnoses e.g. COPD or lung cancer

21
Q

What changes can be seen in CO2 in an Arterial Blood Gas (ABG) in asthma?

A

Normal in mild cases

CO2 drops due to hyperventilation when bronchospasm is not too bad but when airway spasms get bad there is trapping so CO2 starts to rise again becoming normal at some stage (worrying) & eventually high in very severe cases

22
Q

What are the 3 first line treatments in the management of acute asthma?

A
  1. O2 (to maintain sats 94-98%)
  2. B2-agonist bronchodilators e.g. salbutamol or terbutaline nebulised or MDI via spacer (repeat at 15-30 min intervals) - IV salbutamol may have role in severe cases
  3. Corticosteroids e.g. prednisolone or hydrocortisone (continue for min 5 days)
23
Q

What other treatments may you give for acute asthma management?

A
  • Ipratropium bromide as nebuliser when poor initial response to bronchodilators
  • Mg sulphate (safe bronchodilator) or IV in acute asthma with poor response OR life-threatening/near-fatal
  • Antibiotics in presence of infection
24
Q

What are the 4 categorized types of acute asthma in terms of severity?

A
  1. Moderate acute
  2. Acute severe
  3. Life-threatening
  4. Near-fatal
25
Q

What drugs can be used for bronchodilation in asthma?

A

B2 agonists
Anticholinergics
Leukotriene antagonists

26
Q

What drugs can be used to reduce airway inflammation in asthma?

A

Glucocorticoids

27
Q

What are the 4 different types of inhaler treatment for asthma?

A
  1. Relivers
  2. Controllers
  3. Preventers
  4. Combinations
28
Q

What is COPD?

A

Umbrella term for chronic, mostly irreversible, obstructive airway changes

29
Q

What are the different types of COPD?

A

Chronic bronchitis (secretions)
Emphysema (tissue destruction)
Chronic asthma
Other inflamamtory conditions

30
Q

Is COPD common?

A

COPD changes present in 50% of older smokers (COPD present in 10-20% of heavy smokers so genetic factors must affect susceptibility)

Predicted to become 3rd commonest cause of death worldwide by 2020

31
Q

Does COPD have a big impact on the population?

A

Accounts for 7% of all sick days from work

32
Q

What are the causes of COPD?

A

Mainly smoking
Other pollutants
α1-antitrypsin deficiency

33
Q

What is the pathophysiological features of chronic bronchitis?

A

Larger airways e.g. bronchus & larger bronchioles

Mucus gland hypertrophy & hyperplasia

Hypersecretion of mucus due to increased goblet cells in mucosa

Infiltration with neutrophils & CD8 lymphocytes

34
Q

What is the pathophysiological features of emphysema?

A

Lobules/acini affected e.g. peripheral bronchioles & alveoli

Air space enlargement

Alveolar wall destruction

35
Q

What are the 2 types of emphysema?

A

Centriacinar: respiratory bronchioles affected

Panacinar: alveolus & alveolar ducts affected

36
Q

What is the immune response demonstrated in emphysema?

A

Smoking/air pollutant & genetic predisposition causes:

  • Inflammatory cells & mediator release e.g. neutrophils, macrophages & CD8 T cells releasing LT, ILs, TNF etc. amplifying inflammation & inducing structural changes
  • Protease-anti-protease imbalance as proteases released from inflammatory & epithelial cells that break down connective tissue + congenital anti-protease (α1-antitrypsin) deficiency
  • Oxidative stress due to ROS stimulated by smoke & released by inflammatory cells causing tissue damage/inflammation

= alveolar wall destruction

37
Q

What are the enlarged areas of lung called in emphysema? What problem can this cause?

A

Bullous/bulla

> 1cm in diameter -> can burst causing a pneumothorax

38
Q

What are the reversible causes of airflow obstruction in COPD?

A
  • Accumulation of inflammatory cells, mucus & plasma exudate in bronchi
  • SM contraction in peripheral & central airways
  • Dynamic hyperinflation during exercise
39
Q

What are the irreversible causes of airflow obstruction in COPD?

A
  • Fibrosis & narrowing of airways
  • Loss of elastic recoil due to alveolar destruction
  • Destruction of alveolar support that maintains patency of small airways
40
Q

What are the symptoms of COPD?

A

Productive cough (sputum)
Wheeze
Breathlessness (dyspnoea)
Frequent infective exacerbations with purulent sputum
Signs of respiratory failure & cor pulmonale

41
Q

How do you diagnose COPD? What would you expect to see in these tests?

A
  • Spirometry mainly (reduced FEV1:FVC ratio)
  • CXR (hyperinflation or normal)
  • Hb (raised in chronic hypoxia)
42
Q

How can you manage COPD?

A
  • Smoking cessation advice
  • Bronchodilator therapy (short-acting B2 agonist e.g. salbutamol or short-acting anticholinergic e.g. ipratropium)
  • Combination therapy (long acting B2 agonist e.g. salmeterol, formoterol + inhaled steroid e.g. beclomethasone, fluticasone)
  • Home O2
  • Pulmonary rehab & MDT management
  • Vaccines e.g. pneumococcal (single dose) & annual influenza
43
Q

What can pulmonary rehabilitation and multidisciplinary management involve?

A 
Education
Exercise
Self-management strategies
Nutrition
Dyspnoea management
Anxiety & depression management
Social assessment
Smoking cessation support
Occupational therapy
Palliative care
44
Q

What is the only way to potentially prolong life expectancy in COPD? How does this work?

A

Smoking cessation

FEV1 in a non-smoker or non-susceptible smoker will decrease with age with rate increasing slightly with age but do not develop clinically significant airflow obstruction

FEV1 causes airflow obstruction in susceptible smokers & you will never restore FEV1 lost but you may revert rate of loss back to normal (screening smoker’s lung function in early-middle age may be useful to prevent severe COPD)

45
Q

How would you manage acute exacerbations of COPD?

A

Inhalers
Nebulisers
Corticosteroids (oral predinosolone for 7 days)
Antibiotics (e.g. amoxicillin, doxycycline)
Non-invasive ventilation

46
Q

What are the main immune cells involved in COPD and what effect do they have?

A

Macrophages, CD8 T cells & neutrophils

-> small airway narrowing & alveolar destruction

47
Q

What is the main difference between asthma and COPD?

A

Asthma’s airways effects are reversible whilst COPD is irreversible

Block 2 (45 decks)

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