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BDS2 BAMS - Respiratory medicine > 2 Obstructive airways disease > Flashcards

2 Obstructive airways disease Flashcards

1
Q

What respiratory symptoms are there

A
  • Cough (dry, sputum, blood)
  • Wheeze (expiratory)
  • Stridor (inspiratory)
  • Dyspnoea (distress on effort)
  • Pain (general/inspiratory)
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2
Q

What respiratory signs are there

A
  • chest movement with respiration
  • rate of respiration (12-15/min)
  • air entry - symmetrical? reduced?
  • vocal resonance (if air in lungs you can’t hear them speak when your ear is against their chest)
  • percussion note
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3
Q

What respiratory investigations can you have done?

A
  • sputum examination
  • chest radiograph
  • pulmonary function (PEFR, FEV1, FEV1/VC)
  • bronchoscopy
  • VQ scan
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4
Q

What different respiratory diseases are there

A
  • infections
  • airflow obstruction (asthma, COPD, restrictive pulmonary change)
  • gas exchange failure
  • tumours
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5
Q

What chronic obstructive respiratory diseases are there

A

asthma and COPD

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6
Q

What is the main difference between asthma and COPD

A

asthma: ‘reversible’ airway obstruction
COPD: irreversible, gets worse with time

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7
Q

What things can exacerbate asthma

A
  • infections
  • exercise
  • cold air
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8
Q

What happens in an asthma attack

A
  1. airway smooth muscle constriction
  2. inflammation of the mucosa (swelling)
  3. increased mucus secretion
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9
Q

What does a patient complain of in asthma

A

cough, wheeze, SoB

worse early morning (diurnal variation)

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10
Q

How does asthma affect someones peak expiratory flow rate?

A

the narrower their airways, the longer it will take for air to get out of the lungs

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11
Q

What can trigger asthma

A
  • infections
  • environmental stimuli (dust/smoke/chemicals)
  • cold air
  • ‘atopy’ (people who get asthma also have other problems like allergies)
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12
Q

What happens to an asthmatic patient’s FEV1 after the inhalation of an allergen (KNOW)

A

The early asthmatic response is IgE dependent, related to mast cell degranulation, and is blocked by B2 agonists

The late response is due to cellular inflammation, associated with increased bronchial responsiveness, and is blocked by corticosteroids. Has an increased hyper-responsiveness e.g. increased diurnal rhythm (blocked by steroids)

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13
Q

What does the high phasic immune response of asthma attacks mean for treatment of them

A

For first attack: beta 2 agonists

For second attack: steroids

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14
Q

What is the natures of the immunology of asthma

A

sudden and delayed onset

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15
Q

What inhalers would someone with mild asthma have

A
  • blue (beta agonist)

- brown (steroid)

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16
Q

If someone has anything other than a blue or brown inhaler what does this mean

A

they at least have moderate asthma

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17
Q

If someone has ever been hospitalised for asthma what does this mean

A

they have severe asthma

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18
Q

If someone with moderate or severe asthma had an attack in your surgery what should you do

A

call an ambulance

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19
Q

What are the respiratory drugs

A
  • beta-adrenergic agonists
  • anticholinergic
  • corticosteroids
  • leukotriene inhibitors
  • chromones
  • theophyllines
20
Q

What do beta-adrenergic agonists do

A
  • relax bronchial smooth muscle (reduce bronchoconstriction, reduce resting bronchial tone)
  • protective against stimuli
  • short and long acting
  • nebulised as effective as IV
21
Q

what do antichonlinergics do

A
  • act on muscarininc receptors

- reduce basal tone only (good in COPD)

22
Q

what do theophyllines do

A
  • used in severe asthma

- adenosine inhibition

23
Q

what do corticosteroids do

A
  • immune cell and epithelial cell actions

- use if beta2 agonist > 3 times each week

24
Q

what is the most effective asthma treatment

A

corticosteroids

25
Q

potential side effects of corticosteroids

A

adrenal suppression
osteoporosis
(no evidence if daily dose <1500µg/ children <800µg)

spacer recommended if daily dose exceeds 800µg in the adult

26
Q

what is the order of asthma risk assessment

A 
SA B2 agoinst
LD inhaled steroid
LA B2 agonist
Others
Oral steroid hospitalised
27
Q

What are the different elements of COPD

A

bronchitis and emphysema

mixed airway reversible obstruction and destructive lung disease

28
Q

How do alveoli appear in a patient with COPD

A

abnormal, enlarged sacs

29
Q

How do the airways in a patient with COPD appear

A

restricted, caused by chronic bronchitis with inflammed walls and lined with mucus

30
Q

What is emphysema

A

destruction of alveoli

dilation of others to ‘fill space’

31
Q

Describe the gold classification of COPD

A

Gold 1 or 2

  • mild/moderate
  • FEV1 50%-80%
  • cough, little or no breathlessness

Gold 3

  • severe
  • FEV 30-50%

Gold 4

  • very severe
  • FEV1 30%
  • wheeze and cough, breathless on mild exertion over inflated lungs, cyanosis and peripheral oedema in some
32
Q

How can COPD progress to respiratory failure

A
  • reduced surface area for gas exchange
  • thickening of alveolar mucosal barrier (reduces ventilation)

normally bit of both

33
Q

Why does COPD result in poor ventilation

A
  • airway narrowing (reversible?)

- restrictive lung defects

34
Q

Causes of COPD?

A
  • SMOKING
  • environmental lung damage (occupational lung diseases e.g. coal, silica, beryllium, asbestos)
  • hereditary - emphysema (lack enzymes which maintain form of alveoli)
35
Q

How can occupational lung disease lead to respiratory failure

A

Fibrosis (dust related- coal, silicon etc)

Tumours (e.g. asbestos –> mesothelioma. tumour of the plural lining)

36
Q

What is included in the management of COPD

A
  • smoking cessation (will help ventilation)
  • long acting bronchodilator
  • inhaled steroids? (<50% FEV)
  • (systemic steroids)
  • oxygen support
  • pulmonary rehabilitation therapy
37
Q

Can you tell what stage someone with COPD is at based on their medicines

A

nope (people react differently including amount and type of drug)

38
Q

What is type 1 respiratory failure

A

hypoxaemia and thickening of alveolar barrier

(Low oxygen
Co2 normally normal
Problem is not enough functioning alveoli
Alveolar diffusion fails)

39
Q

What is type 2 respiratory failure

A

Hypercapnia and ventilation failure

40
Q

How might someone get type 2 respiratory failure

A
  • airway blockage/ narrowing
  • ventilation problems - muscles
  • acute/chronic infections
41
Q

Why can oxygenation fail

A
  • poor alveolar ventilation
  • diffusion abnormality
  • ventilation perfusion mismatch
42
Q

Why can ventilation fail

A

Acute
- 20% reduction in ventilation needed for PaCo2 >6.6kPa

Chronic
- renal compensation for acidosis
(contributions from reduced compliance, airway obstruction, muscle dysfunction)

43
Q

What drives breathing in healthy individuals

A

CO2 drive controls ventilation

oxygen saturation usually ok

44
Q

What drives breathing in individuals with COPD

A

Hypoxia drives ventilation

CO2 tolerance

45
Q

Describe how oxygen should be used as treatment in COPD

A

Acute

  • use until medical help arrises
  • watch respiratory rate and SaO2

Chronic
- fixed % delivery

46
Q

How does obstructive respiratory disease apply specifically to dentists

A
  • ability to attend for treatment (home oxygen is inflammable)
  • use of inhaled steroids = candida risk (rinse mouth, use spacer device)
  • smokers = oral cancer risk

BDS2 BAMS - Respiratory medicine (4 decks)

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