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BDS2 BAMS > Asthma and COPD > Flashcards

Asthma and COPD Flashcards

1
Q

2 types of cough

A

productive and non-productive

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2
Q

wheeze

A

expiratory noise
(breathe out, organ sounding nose - airways resonate at different frequency, can’t fake a wheeze – something bad happening in an airway)

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3
Q

stridor

A

inspiratory noise (breathe in, blockage in big airway, choking)

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4
Q

dyspnoea

A

distress on effort with breathing

  • know breathing not working well,
  • uncomfortable with breathing
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5
Q

2 types of pain in respiratory system

A

general

inspiratory

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6
Q

general pain in respiratory system

A

cough

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7
Q

inspiratory pain in respiratory system

A

sudden sharp in a particular part, inflammatory change in chest well – pleurisy (inflammation of chest wall) pain when past certain point e.g. after broken rib. Specific pain rather with generalised as with cough)

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8
Q

respiratory symptoms (5)

A

cough

wheeze

stridor

dyspnoea

pain (general/inspiratory)

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9
Q

respiratory signs (5)

A

chest movement with respiration

rate of respiration (12-15/min)

air entry (symmetrical? reduced)

vocal resonance

percussion note (resonant, dull)

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10
Q

what should chest movement with respiration be like

A

Expansion should be same on both side – hand on waist and thumbs on back and move at same rate and distance

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11
Q

what is normal rate of respiration

A

12-15/min

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12
Q

how can the rate of respiration be changed

A

Change with

  • exercise,
  • altitude (increase with as O2 lower, need faster ventilation),
  • asthma – cannot ventilate properly compensate by breathing more
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13
Q

why can it be useful to measure of rate of respiration over a course of time

A

guide to see how people change over course of treatment

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14
Q

how to assess air entry

A

with a stethoscope

symmetrical? reduced?

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15
Q

what happens to vocal resonance is there is exudate in lungs

A

sounds odd = Exudate in lungs can hear what they are saying

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16
Q

what happens to vocal resonance is there is air in lungs

A

noise out front

very little sound echos in lungs

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17
Q

respiratory investigations (5)

A

Sputum examination

CXR - chest radiograph

Pulmonary function

  • PEFR - maximum flow rate – gas breathe out total
  • FEV1 – forced expiratory volume - gas breathe out in 1 sec
  • FEV1/VC - measure of resp. function

Bronchoscopy – flexible tube in

VQ scan - ventilation/perfusion mismatch

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18
Q

PEFR

A

maximum flow rate – gas breathe out total

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19
Q

FEV1

A

forced expiratory volume - gas breathe out in 1 sec

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20
Q

FEV1/VC

A

measure of resp. function

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21
Q

ventilation/perfusion mismatch because

A

more alveoli not ventilated, less oxygenated blood. Embolism in legs can lodge in lungs blocks flow to certain part. See if blood and oxygen go to same place – need to match up

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22
Q

what should lungs appear like on X-ray

A

black as filled with air

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23
Q

4 types of respiratory disease

A

infections (pneumonia)

airflow obstruction

gas exchange failure

tumours

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24
Q

airflow obstructions respiratory diseases

A

asthma

Chronic Obstructive Pulmonary Disease

restrictive pulmonary change – lungs become stiff so elastic tissue replaced by fibrous tissue

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25
Q

gas exchange failure respiratory diseases

A

reduced surface area, fibrosis, fluid

  • poor surface area
  • lost alveoli due to damage
  • less space for gas exchange to occur
  • lungs have collapsed or fluid in lungs
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26
Q

respiratory failure =

A

combination of alveolar and ventilation problems

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27
Q

asthma reversibility

A

short term is reversible, long term causes permanent lung damage (good to bad)

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28
Q

COPS reversibility

A

COPD is always destructive, but will have reversible component on top (bad to more bad)

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29
Q

2 chronic airflow obstruction diseases

A

asthma and COPD

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30
Q

what 3 things can exacerbate and cause remission of chronic airflow obstruction

A

infection

exercise

cold air

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31
Q

%asthma in children and adults

A

5-10% children (common)

2-5% adults

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32
Q

bronchial hyper reactivity in asthma

A
  • Overreaction to minor stimulation
  • Immune response disproportionate
  • Too many chemical mediators
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33
Q

what causes asthma

A

bronchial hyper reactivity

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34
Q

3 responses in asthma which create the problem

A

Inflammation of airways that is not needed – narrows the tube (mucosal oedema)

Smooth muscles on outside constrict

Mucous glands go into hypersecretion

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35
Q

what 3 things always line inside of airways

A

mucus
muscles
glands

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36
Q

mechanisms in asthma

A

Triad of airway

  • smooth muscle constriction
  • inflammation of the mucosa (swelling)
  • increased mucus secretion

P/c - COUGH!, wheeze, Shortness of Breath

  • Wheeze – narrowing of airway
  • Cough – excess mucous, body trying to mouth out of irritated airways into trachea

diurnal variation - worse early morning
- follows pattern depending on time of day, -dependent on circadian rhythm

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37
Q

triad of airway changes in asthma

A
  • smooth muscle constriction
  • inflammation of the mucosa (swelling)
  • increased mucus secretion
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38
Q

patient complaints in asthma

A

COUGH!, wheeze, Shortness of Breath

  • Wheeze – narrowing of airway
  • Cough – excess mucous, body trying to mouth out of irritated airways into trachea
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39
Q

how does peak expiratory flow rate change with airway

A

gas out of lungs

Slower with narrowing

Vary at different times of day

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40
Q

4 asthma triggers

A

Infections

Environmental stimuli

  • dust
  • smoke
  • chemicals at work

Cold air
- Children – change in temperature of gas going in

‘Atopy’

  • Hyper response of Immune system
  • Asthmas often with eczema, allergies
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41
Q

why would you perform a skin prick test in asthma investigations

A

Testing reactivity of skins (Not of lungs)

Can narrow down range of things that are problem

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42
Q

immune response to asthma is

A

biphasic

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43
Q

biphasic immune response to asthma

A
  • early asthma response – breathless
  • survive this (can die in 20 mins sometimes)
  • seem to get better
  • 6 hours later – worse again

Some mediators work quicker and some slower

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44
Q

asthma trigger/stimuli

A

is innocuous

immune response not needed

45
Q

6 respiratory drugs

A

Beta-adrenergic Agonists
Anticholinergic
Corticosteroids

Leukotriene inhibitors
Chromones

Theophyllines

46
Q

nebulised beta-adrenergic agonists

A

as effective as IV
o Bubble gas through liquid and inject
o Can direct into lungs
o Very effective rapidly

47
Q

action of beta-adrenergic agonists

A 
Relax bronchial smooth muscle 
- Reduce bronchoconstriction 
- Reduce resting bronchial tone 
- Make hole slightly wider 
Nothing for oedema, or secretion

PROTECTIVE against stimuli
- Take puffer before exercise if exercise induced
Short & Long acting

48
Q

when should you take beta-adrenergic agonists

A

PROTECTIVE against stimuli

- Take puffer before exercise if exercise induced

49
Q

2 types of inhaled bronchodilators

A

salbutamol (blue)

salmeterol (green)

50
Q

role of anticholinergics

A

Act on muscarinic receptors

Reduce BASAL tone only
- Good in COPD

‘neurogenic’ triggers

51
Q

when are theophyllines used

A

SEVERE asthma due to potential adverse effects
- Adenosine inhibition
CNS Stimulation, Diuresis, arrhythmia

52
Q

best drug for asthma treatment

A

corticosteroids

treat all 3 symptoms of asthma

53
Q

corticosteroid action

A

No mucosal oedema, bronchoconstriction or muscosal secretion
- immune cell and epithelial cell actions

Take brown puffer everyday – stop asthma symptoms

54
Q

problem with corticosteroid

A

Take 3 or 4 days to work – no use in emergency

Tablets will help quicker but still likely next day

Steroid by injection best chance of stopping biphasic

55
Q

when to use a corticosteroid

A

if β2 agonist >3 times each week

56
Q

are there any side effects of corticosteroid

A

Inhaled corticosteroid for asthma has no evidence if daily dose <1500ug
Children <800ug

SPACER recommended if daily dose exceeds 800ug in adult
- Or breath activated devices

57
Q

mild asthma treatment

A

bottom, blue puffer and/or brown puffer

  • Low dose inhaled steroid or sodium cromoglycate/nedocromil
  • Occasional beta-agonist only

blue puffer better and go home inemergency

58
Q

tiers of asthma

A

mild
moderate
severe

ID as treat differently in emergency

59
Q

moderate asthma treatment

A

Green/purple/pink

  • Long-acting beta agonist, theophylline, anti-muscarinic drugs
  • High-dose inhaled steroid

treat and then decide (wont get bad as fast)

60
Q

severe asthma treatment

A

Ever hospital admitted or steroid tablets more than once a year
- Oral steroid

will not make better, improve but biphasic need to go to causality soon can die in 20 mins of attack. Organise ambulance and then treat

61
Q

names for COPD

A

Chronic Obstructive Pulmonary Disease
Chronic Obstructive Airways Disease COAD
Chronic Bronchitis & Emphysema
- Most descriptive – destructive (emphysema) and chronic inflammation (bronchitis)

62
Q

severe asthma when

A

Ever hospital admitted or steroid tablets more than once a year

63
Q

COPD is

A

• MIXED airway reversible obstruction and destructive lung disease (alveoli and cartilaginous airways – never able to fully return to normal)
- asthma & emphysema

airways are inflamed
reduced SA for gas exchange and lung function
- gas exchange compromised by fewer alveoli
- ventilation compromised by restricted airway

64
Q

emphysema

A

destruction of alveoli
- big spaces where alveoli used to be still lined by gas exchange tissue but far less alveoli

dilation of other to ‘fill space’
- markings going further into lungs where black air space should be

65
Q

GOLD 1 or 2 classification of COPD

A

disease state
- mild or moderate

lung function
- FEV1 50-80%

clinical state
- cough or little to no breathlessness

66
Q

GOLD 3 classification of COPD

A

disease state
- severe

lung function
- FEV1 30-50%

clinical state

  • cough and sputum
  • breathlessness on exertion
67
Q

GOLD 4 classification of COPD

A

disease state
- very severe

lung function
- FEV1 30%

clinical state 
- wheeze and cough 
- breathlessness on mild exertion 
over inflated lungs 
- cyanosis and peripheral oedema in some
68
Q

how can COPD progress to respiratory failure

A

o reduced surface area for gas exchange
o thickening of alveolar mucosal barrier

boiler not working, not enough air oxygenated
- not enough area for gas exchange
- not enough ventilation of air in and out
combination of reduced SA and poor exchange most common

69
Q

disease state in GOLD 1 or 2

A

mild or moderate

70
Q

diseases state in GOLD 3

A

severe

71
Q

Disease state in GOLD 4

A

very severe

72
Q

lung function in GOLD 1 or 2

A

FEV1 50-80%

73
Q

lung function in GOLD 3

A

FEV1 30-50%

74
Q

lung function in GOLD 4

A

FEV 30%

75
Q

clinical state in GOLD 1 or 2

A

cough or little to no breathlessness

76
Q

clinical state in GOLD 3

A
  • cough and sputum

- breathlessness on exertion

77
Q

clinical state in GOLD 4

A
  • wheeze and cough
  • breathlessness on mild exertion
    over inflated lungs
  • cyanosis and peripheral oedema in some
78
Q

how can poor ventilation in COPD occur

A

o airway narrowing (reversible?)

o restrictive lung defects

79
Q

respiratory failure occurs when

A

cannot oxygenate enough air for tissue needs

80
Q

Causes of COPD (3)

A

smoking

environmental lung damage
- occupational lung diseases coal, silica, beryllium, asbestos

hereditary – emphysema
- lack enzymes in alveoli

lungs fibrous and stuff not open enough to allow ventilation

81
Q

how can occupational lung disease lead to respiratory failure? (2)

A

fibrosis (dust related)

tumours

82
Q

what causes fibrosis in occupational lung disease

A

dust related

o Coal
o Silicon
o Beryllium
o Asbestos – dust created when try and remove

83
Q

tumours in occupational lung disease

A

caused by Asbestos - mesothelioma

  • Tumour of pleural lining
  • Liquid Between chest and lung walls
  • Chronic inflammation can lead to tumour formation
84
Q

smoking progressive effect on lung function

A

more smoking that you do the worse lung function

- Forced expiratory volume gets progressively less

85
Q

6 ways to manage COPD

A

Smoking cessation – stop getting worse
- Will help even late on in disease

Long acting bronchodilator
- Improve ventilation as there is not way to
improve gas exchange (cannot change alveoli)

Inhaled steroids (<50% FEV)

(systemic steroids)

Oxygen support
- Increase concentration of inspired oxygen due to respiratory failure as cannot increase volume inspired so increase quality

Pulmonary rehabilitation therapy

86
Q

difference between asthma and COPD management effects

A

Everyone different in how they respond – need to try and see what works for them

Doesn’t reflects severity of disease - Reflects reversibility of disease (unlike asthma)

87
Q

what does COPD treatment reflext

A

reversibility of disease not severity (unlike asthma)

88
Q

2 outcomes of COPD

A

type 1 respiratory failure

type 2 respiratory failure

89
Q

type 1 respiratory failure

A

no longer properly oxygenate the blood)

  • hypoxaemia (low oxygen)
  • thickening of alveolar barrier – gas diffusion fails

alveolar diffusion of oxygen issue
thicker the tissue barrier, harder for oxygen to get through
CO2 normal, oxygen level falls

Not enough functioning alveoli to diffuse blood with oxygen sufficiently

90
Q

type 2 respiratory failure

A

Hypercapnia (high CO2)

ventilation failure
- CO2 easily diffuse
Ventilating the gas that gets to the alveoli

91
Q

what can cause type 2 respiratory failure (3)

A

airway blockage or narrowing

ventilation problems
– muscles (motor neuron disease, chest muscles get less nerve innervation, breathe less)

acute on chronic
– infections (most common, coping with chronic COPD and infection on top and narrows airways too greatly, gas cannot get out of alveoli)

92
Q

what are the 2 principles of respiratory failure

A
  • Failure of oxygenation

* Failure of ventilation

93
Q

failure of oxygenation occurs when

A

When PaO2 <8.0kPa on air, in arterial blood
- hypoxic
Surrogate – SaO2 <90% on air

Poor alveolar ventilation
Diffusion abnormality in alveoli

Ventilation perfusion mismatch
- Blood flow to one area of lungs, ventilation to another area of the lungs

94
Q

failure of ventilation occurs when

A

PaCO2 > 6.7kPa in arterial blood

20% reduction in ventilation needed

acute or chronic

95
Q

acute respiratory failure failure of ventilation

A

Drop from coping to too low happens fairly quickly

20% reduction in ventilation needed

96
Q

chronic ventilation failure

A

Renal compensation for acidosis

  • Due to cigarette accumulation
  • Increase in CO2 build up due to poor ventilation to alveoli
97
Q

3 things which contribute to ventilation failure

A
  • Reduced compliance
  • Airway obstruction
  • Muscle dysfunction
98
Q

normal breathing control

A

desire to take a breathe,
brain still work (needs sugar and oxygen)

CO2 drive controls ventilation
- want to breathe due to CO2 build up – hypocapnia not hypoxia

Oxygen saturation usually OK

99
Q

COPD desire to breathe

A

CO2 tolerance

  • Gradually increases over several months
  • Carbon dioxide receptors less sensitive
  • Less desire to breathe as threshold set higher

HYPOXIA drives ventilation

  • Oxygen sensitivity starts to kick in
  • Rely on oxygen level to keep them breathing

Fine till you give oxygen, increase oxygen – stop breathing = distressful
- Take away hypoxia with desire to breathe

Slight increase in oxygen from room air (21-24% instead of 100%)
- Need to count respiratory rate – sensitive marker
- Usually 12
COPD can be around 20, will drop with oxygen delivery

100
Q

what drives desire to breath in COPD

A

HYPOXIA drives ventilation not hypocania

  • Oxygen sensitivity starts to kick in
  • Rely on oxygen level to keep them breathing
101
Q

delivering oxygen to COPD patient impact on desire to breath

A

Fine till you give oxygen, increase oxygen – stop breathing = distressful
- Take away hypoxia with desire to breathe

102
Q

best way to deliver oxygen to COPD patient

A

Slight increase in oxygen from room air (21-24% instead of 100%)
- Need to count respiratory rate – sensitive marker
- Usually 12
COPD can be around 20, will drop with oxygen delivery

103
Q

dental emergency COPD treatment

A

in the acute stage use oxygen until medical help arises (cannot give specific level – only 100% in practice)
- watch (respiratory rate, SaO2)

In the chronic stage, use oxygen with care – fixed percentage delivered

104
Q

when would a patient have home oxygen therapy

A

Respiratory failure to the point they are not able to oxygenate blood properly
• Cannot maintain oxygen from room air

105
Q

2 ways to have home oxygen therapy

A

cylinders

oxygen concentrators

106
Q

oxygen cylinders disadvantage

A

sit with mask on 24/7

107
Q

oxygen concentrator

A

room air and remove nitrogen so higher oxygen concentration in inspired air
- Saves cylinders constantly as higher oxygen concentration

108
Q

should oxygen be given 24 hours?

A

yes - needed for improvement

Oxygen only part/most of the time – then waste no improvement in survival
• Chronic hypoxia increases chance of acute cardiac events

109
Q

airflow obstruction and dentistry

A

Ability to attend for treatment
- home Oxygen - inflammable!

Use of inhaled steroids – steroid inside mouth, local immune suppression and then candida risk e.g. COPD, asthma
- rinse mouth
- use spacer device or breath activated
lower risk

Smokers - oral cancer risk (COPD)
- 2 times increase risk

BDS2 BAMS (54 decks)

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