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RESP > Lecture 9: Obstructive airway diseases > Flashcards

Lecture 9: Obstructive airway diseases Flashcards

1
Q

Give some examples of obstructive airway diseases:

A
  • asthma

- COPD: emphysema, chronic bronchitis

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2
Q

What is asthma?

A

Chronic inflammatory airway disease

  • affects small airways
  • intermittent obstruction and hyper-reactivity
  • usually reversible
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3
Q

What is the structure of the airways?

A

(from inside to outside)

  • mucosa & pseudostratified epithelium
  • submucosa
  • smooth muscle
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4
Q

What are the 2 types of asthma?

A

Atopic

Non-atopic

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5
Q

What is atopic asthma?

A

-asthma
-eczema
-hayfever
Develops due to a type 1 hyerpsensitivity reaction
-first exposure to an allergen
-macrophages present this
-stimulating T helper cells
-these THcells make IgE antibodies
-IgE attach themselves to mast cells
-IgE cross over, causing mast cell degranulation
-histamines, leukotrienes, and cytokines cause inflammation (oedema), increased mucus production and bronchoconstriction causing narrowing/blockage of the small airways

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6
Q

What are the symptoms of asthma?

A

-breathless (harder to exhale)
-chest tightness
-wheeze
-cough (dry, tends to be at night, parasympathetic system: don’t take in as much oxygen, and it causes bronchoconstriction)
-atopy
(intermittent symptoms)

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7
Q

What are signs of asthma?

A

Respiratory rate: increased
Pulse: increased
Oxygen sats: low
Listening to chest: wheeze

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8
Q

How do we diagnose asthma with investigations?

A

-peak flow
-spirometry (low FEV1:FVC-obstructive)
(reversibility with bronchodilator)

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9
Q

How do we manage asthma?

A

Divide into probabilities
Low- little/no typical features (other diagnosis more likely), rule out/treat other causes
Intermediate- some symptoms/treatment for other causes aren’t working
High- typical presentation of asthma, so start treatment straight away

  • patient education (remove triggers)
  • pharmacology
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10
Q

How do we treat asthma?

A

Step 1:

  • Promote sympathetics: bronchodilation, Beta 2 receptors in lungs, so give short acting B2 agonists
    e. g. salbutamol= BLUE INHALER (RELIEVER INHALER)
  • BROWN INHALER (PREVENTER INHALER): corticosteroid, to reduce inflammation

Step 2: (if symptoms are bad)

  • long acting beta agonist and corticosteroid: PURPLE INHALER
  • still have reliever

Step 3:

  • increase steroid dose
  • add leukotriene receptor antagonist (this is released from mast cells)

If still no improvement, check to see if you have the correct diagnosis/ if inhaler technique is correct

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11
Q

How can you aid childrens asthma medication?

A

Add a spacer for children if they find inhaler technique hard

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12
Q

When do we need to give emergency management?

A 
-(ABC)
Actuely severe
-can't complete full sentences
-oxygen sats low >/+ 92%
-resp rate increased >/=25
-wheeze 
-HR >/= 110 bpm
-if well enough PEFR is 33-50% of best predicted value

Life-threatening

  • cyanosis
  • drowsy
  • poor respiratory effort/silent chest-no airflow
  • oxygen sats <92%
  • if they can, PEFR <33%
  • arrythmia/hypotension
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13
Q

What are the ABG’s for acute severe asthma?

A 
Hyperventilation
-low CO2
-increased pH
-low pO2 as they are hypoxic
=respiratory alkalosis
(type 1 respiratory failure)
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14
Q

What are the ABG’s for life threatening asthma?

A

ABG’s look normal

  • deteriorating
  • rising pCO2, as resp rate is going down
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15
Q

How do we manage acute severe/life threatening asthma?

A
  • oxygen
  • salbutamol (nebuliser: mask)
  • steroids (orally/IV)
  • admit them
  • chest X-Ray (rule out pneumothorax)
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16
Q

What is the difference between type 1 and 2 respiratory failure?

A

1: low pO2, low pCO2
2: low pO2, high pCO2

17
Q

What is atopy?

A

Genetic tendency to develop allergic diseases

-associated with heightened immune response to common allergens

18
Q

What is emphysema?

A
  • alveolar wall damage (due to smoking)
  • larger alveoli form which can’t support the smaller airways (bronchioles)
  • bronchioles collapse and trap air inside the lung

Not reversible

19
Q

How does alpha-1 antitrypsin deficiency effect the lungs?

genetic

A

Balance action of protease enzymes/elastase which are produced in presence of infection/inflammation/smoking
-if you have this disease then elastase can break down elastin in the lungs leading to destruction of alveoli and therefore emphysematous change

20
Q

What is chronic bronchitis?

A

Chronic inflammation of the bronchioles

  • not allergic
  • chronic inflammation after exposure to tobacco/smoking

Irreversible

  • increased mucus production
  • inflammation of the airways
  • less associated with bronchoconstriction (as no degranulation of mast cells) so don’t respond that well to bronchodilators
21
Q

What are the clinical presentations of chronic bronchitis?

A

-chronic productive cough for at least 3 months consequetively

22
Q

What are the risk factors for COPD?

A
  • smoking
  • more common in men
  • increased age
  • childhood respiratory diseases
  • genetics (A1AT def)
  • exposure
23
Q

What are the symptoms of COPD?

A

Both emphysema and chronic bronchitis: breathlessness and wheeze

24
Q

How doyou diagnose patients with COPD?

A

-Spirometry: obstructive airway pattern (reduced FEV1:FVC)
-Poor bronchodilator reversibility
-chest XRay: air trapping: dense on X-ray, and hyperinflated chest
(hyperinflated if you can see >6 anterior or >10 posterior ribs)

25
Q

How do you detect the severity of COPD?

A
  • depends on how reduced the FEV1 is (NICE)

- Medical research council dyspnoea scale

26
Q

How do you manage COPD?

A

Prevention: stop smoking
Pharmacology:
-inhalers (SABA/LABA/anti-muscarinics/steroids)
(anti-muscarinics: ipratropium bromide/tiotropium-long acting)
Non pharmacological: flu vaccines, chest physiotherapy

27
Q

What is hypoxic drive?

A
  • increased pCO2 (causes a strong pulse) in chronic lung conditions which is consistently high
  • kidneys retain HCO3-, so no need for hyperventilation as pH is balanced (but pCO2 levels are still high)
  • chemoreceptors reset
  • peripheral chemoreceptors detect low pO2, this causes hyperventilation, so we don’t give patients too much oxygen because otherwise their respiratory rate will drop
28
Q

What saturation of oxygen do we want in COPD?

A

88-92%

29
Q

What is an acute exacerbation in COPD?

A

In response to infections/pollutants
-acute deterioration in symptoms (increased dyspnoea, cough, increased sputum volume, change in sputum colour from clear to green, wheeze, chest tightness)

  • accessory muscles used: ‘tripodding’
  • pursed lip breathing (increase pressure inside thoracic cavity to keep airways open)
  • may see cyanosis
30
Q

What are the differentials in acute exacerbation in COPD?

A

(could be pneumonia/heart failure)

  • CXR (rule out infection)
  • ABG (detect high pCO2)
  • FBC/CRP/U and E
  • sputum cultures
  • blood cultures
31
Q

How do you manage acute exacerbation in COPD?

A
  • SABA and ipratropium via nebuliser
  • steroids (orally/IV)
  • antibiotics
32
Q

What are some long term complications in COPD?

A

Chronic hypoxia: pulmonary hypertension due to vasoconstriction as underperfused (usually diverts blood to better alveoli), so you get pulmonary constriction which is widespread (harder to pump blood into pulmonary circulation: causes right sided heart failure)

Chronic respiratory failure

Chronic hypoxia: improve oxygen levels= polycythaemia (high conc of RBC in your blood)

33
Q

Compare and contrast asthma and COPD:

A

Asthma

  • younger people affected
  • allergens
  • dyspnoea, wheeze
  • dry, nocturnal cough
  • low pCO2 as hyperventilating
  • reduced FEV1:FVC ratio with revesibilty
  • respond better the B2 agonists

COPD

  • older people, caused by smoking
  • emphysema/chronic bronchitis
  • dyspnoea, wheeze
  • productive coough over a long time
  • hyperinflation is more common
  • chronic retention of pCO2
  • reduced FEV1:FVC ratio with poor revesibilty
  • respond better to muscarinic antagonists

RESP (18 decks)

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