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BDS2 - respiratory system > obstructive airways disease > Flashcards

obstructive airways disease Flashcards

1
Q

what are some respiratory symptoms

A
  • cough
  • wheeze
  • stridor
  • pain
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2
Q

what is a cough

A
  • can be productive = produces stuff, such as sputum (green, white, red), or blood
  • or can be non-productive = dry cough
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3
Q

what is a wheeze

A
  • expiratory noise
  • each airway makes a different noise = will have a different noise depending on which airway is blocked
  • means something bad is happening
  • can’t fake a wheeze
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4
Q

what is a stridor

A
  • inspiratory noise

- blockage in big airway = choking

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5
Q

what is dyspnoea

A
  • distress on effort

- patient knows breathing is not right and is uncomfortable when they breathe

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6
Q

what pain is experienced

A
  • can be general or inspiratory
  • if a patient has been coughing for a few days they will have rib pain
  • if patient has chest wall problems they will have pain
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7
Q

what are respiratory signs

A
  • chest movement with respiration
  • rate of respiration
  • air entry
  • vocal resonance
  • percussion note
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8
Q

what does chest movement show

A
  • want to check expansion is the same on both sides

- place thumb at ribs and hands round patients back to check and thumbs should move at same time

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9
Q

what does rate of respiration show

A
  • should be 12-15/min
  • good to know
  • in asthma, patient will have a higher rate as they can’t ventilate properly so compensate by increasing rate
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10
Q

what does air entry show

A
  • is it symmetrical?

- is it reduced?

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11
Q

what does vocal resonance show

A
  • someone with healthy lungs should have lots of air in them and when you press your ear to their chest you wont be able to hear what they say
  • if someone has liquid in their liquids in their lungs you ca hear what they say with ear to chest
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12
Q

what does percussion note show

A
  • resonance, dull

- tap to see if it makes hollow or solid noise

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13
Q

what are some respiratory examinations

A
  • sputum examination
  • CXR chest radiograph
  • pulmonary function
  • bronchoscopy
  • VQ scan
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14
Q

what is tested for in pulmonary function

A
  • PEFR = maximum flow rate
  • FEV1 = forced expiratory volume in 1 second
  • FEV1/VQ = measure of respiratory function
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15
Q

how is a bronchoscopy done

A
  • flexible tube placed down throat
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16
Q

what is a VQ scan

A
  • ventilation/perfusion mismatch
  • shows difference between oxygenation and ventilation
  • looks t blood flow and gas flow to lungs and see if they match
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17
Q

what are some respiratory disease

A
  • infections = pneumonia
  • airflow obstruction = problem getting gas in and out of lungs, changes ability of lungs to stretch
  • gas exchange failure = reduces surface area, fibrosis, fluid, don’t have ability to get gas from alveoli to blood
  • tumours
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18
Q

what are examples of airflow obstruction

A
  • asthma
  • COPD
  • restrictive pulmonary change
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19
Q

what is chronic airflow obstruction

A
  • reversible airway obstruction
  • asthma is reversible if it lasts 10 mins to a week but over 40 years it will cause damage to lungs
  • COPD is always obstructive, there is always an element from which you can’t recover
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20
Q

what can make chronic airflow obstructions worse

A
  • infections
  • exercise
  • cold air
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21
Q

how common is asthma

A
  • 5-10% children = is thought to be an overreaction to mild stimulants, children should go outside and okay to keep immune system active
  • 2-5% adults
  • bronchial hyper-reactivity
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22
Q

what happens in asthma

A
  • get an inflammation of airways
  • inflammation of lining which narrows the tube
  • mucus glands go into hyper secretion secreting slimy ‘goo’ which makes airways even narrower
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23
Q

what will patients notice in asthma

A
  • a wheeze and a cough
  • wheeze from narrow airway
  • cough due to mucus
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24
Q

what is the mechanisms of asthma

A
  • triad of = airway smooth muscle constriction, inflammation of mucosa (swelling), increased mucus secretion
  • cough, wheeze, shortness of breath
  • diurnal variation = worst in the morning and at night
25
Q

what is the peak expiratory flow rate

A
  • changes as airways narrowed
  • morning are all the same and nights are all the same
  • varies at different times of the day
26
Q

what are some triggers of asthma

A
  • infections
  • environmental stimuli = dust, smoke, chemicals at work
  • cold air = more of an issue for children
  • atopy = when the general response of the immune system is a problem
27
Q

what is a skin prick test for asthma

A
  • good but it only tests the skin, doesn’t test lungs as could be different
  • narrows down possibilities however
28
Q

what type of immune response is asthma

A
  • biphasic immune response
  • early response is a wheeze etc
  • if you survive this then 6 hours later you will get the late response with increased bronchial hyper-responsiveness
29
Q

how long can it take for someone to die from asthma

A
  • 20 minutes
30
Q

how is asthma treated

A
  • need to give patient initial treatment after early response to get them better but also need to give more to prevent late response
  • need to give beta agonist and steroids to prevent late phase
31
Q

what is the treatment for asthma based on severity

A
  • very strategic
  • 1-5 (1 OK, 5 bad)
  • 1 = occasional beta agonist
  • 2 = low dose inhaled steroid or sodium cromoglycate
  • 3 = high dose inhaled steroid
  • 4 = long acting beta agonist, theophylline, antimuscuranic drugs
  • 5 = oral steroid
32
Q

what do the different colours of puffer mean

A
  • brown/blue = mild asthma
  • purple/pink = moderate asthma
  • take steroid tablets = severe
33
Q

how do you treat mild asthma

A
  • treat with blue puffer and send home
34
Q

how do you treat severe asthma

A
  • you’re not going to fix them, only make it slightly better
  • need to go to hospital soon
35
Q

what are some respiratory drugs

A
  • beta-adrenergic agonists
  • anticholinergic
  • corticosteroids
  • leukotriene inhibitors = good for delayed phase
  • chromones
  • theophyllines
36
Q

what are beta adrenergic agonists

A
  • given by puffer or nebuliser
  • relax bronchial smooth muscle = reduce bronchoconstriction, reduce resting bronchial tone
  • protective against stimuli
  • short and long acting
  • but = do nothing for mucosal oedema, only quick fixes, don’t address fundamental issues of asthma
37
Q

what are anticholinergic

A
  • act on muscarinic receptors = good for muscles
  • reduce basal tone only = good in COPD, not so much asthma
  • neurogenic triggers
38
Q

what are theophylline

A
  • used in severe asthma due to potential adverse effects
  • adenosine inhibition = CNS stimulation, diuresis, arrhythmias
  • immunomodulatory
39
Q

what are corticosteroids

A
  • most effective treatment for asthma = ‘fix’ asthma
  • why you are to take brown puffer everyday, takes a few days to kick in so wont work in emergencies however
  • don’t get mucosal oedema, secretion or bronchoconstriction
  • immune cell and epithelial cell actions
  • use if beta2 agonist > 3 times a week
  • to prevent late phase need to give by injection
40
Q

what are the problems with corticosteroids

A
  • can cause adrenal suppression and osteoporosis
  • no evidence of this if daily dose <1500 micrograms however or <800micrograms in children
  • spacer is recommended if daily dose exceeds 800 micrograms in the adult
41
Q

what are other names for COPD

A
  • chronic obstructive pulmonary disorder
  • chronic obstructive airways disease
  • chronic bronchitis and emphysema = most descriptive
42
Q

what is COPD

A
  • destruction of alveoli and cartilaginous airways
  • airways are inflamed and narrowed
  • restricted airways caused by chronic bronchitis, with inflames walls and lined with mucus
  • get abnormal alveoli with enlarged sacs, compared with normal alveoli = gas exchange compromised by fewer alveoli and ventilation compromised by obstructed airways
  • get big holes where alveoli used to be= still lined by gas exchange tissue
43
Q

what is emphysema

A
  • destruction of alveoli

- dilation of others to ‘fill space’

44
Q

what are the GOLD classifications of COPD

A 
- GOLD 1 or 2 
= mild to moderate disease state
= lung function - FEV1 50-80%
= clinical state - cough, little or no breathlessness 
- GOLD 3
= severe disease state 
= lung function - FEV1 30-50%
= clinical state - cough and sputum, breathlessness on exertion 
- GOLD 4 
= very severe disease state 
= lung function - FEV1 30%
= clinical state - wheeze and cough, breathlessness on mild exertion, over inflated lungs, cyanosis and peripheral oedema in some
45
Q

how can COPD progress to respiratory failure

A
  • reduced surface area for gas exchange
  • thickening of alveolar mucosal barrier
  • can’t oxygenate enough to get sufficient amount to tissues
46
Q

what are the causes of COPD

A
  • smoking = mainly
  • environmental lung damage = coal, silica, beryllium, asbestos, occupational lung diseases
  • hereditary = emphysema
47
Q

what is occupational lung disease

A
  • can lead to respiratory failure
  • fibrosis = dust related (coal, silica, beryllium, asbestos)
  • tumours = from asbestos (mesothelioma), tumour of pleural lining, lungs lining most affected
  • asbestos is only a problem when you try and remove it
  • more smoking you do, worse lung volume you have
48
Q

how is COPD managed

A
  • smoking cessation = 1st thing
  • long acting bronchodilator = improve ventilation (as can’t improve gas exchange as can’t replace alveoli) so need to keep remaining healthy
  • inhaled steroids = if <50% FEV
  • oxygen support
  • pulmonary rehabilitation therapy
49
Q

what is the problem with management of COPD

A
  • there is no rule of thumb
  • patient tries both bronchodilators and steroids to see which works
  • treatment doesn’t reflect the extent of the disease
  • cannot asses severity of disease by medication alone
50
Q

what is type 1 respiratory failure COPD

A
  • hypoxaemia = low oxygen
  • caused by hypoxia
  • thickening of alveolar barrier = more difficult for alveolar infusion of oxygen
51
Q

what is type 2 respiratory failure COPD

A
  • hypercapnia = problem with CO2
  • ventilation failure = CO2 moves easily in and out of alveoli but problem is ventilating O2 going in to alveoli
  • airway blockage or narrowing = oedema of mucosal lining or tumour
  • ventilation problems = muscles, if you have a neuromuscular disease it will gradually get worse as you can’t breath properly
  • acute or chronic infections = most common reason, most patients have chronic COPD then get infections, cause fluid and swelling of airways causing sudden deterioration
52
Q

what is failure of oxygenation in respiratory failure

A
  • when PaO2<8.0kPa on air in arteries when breathing
  • surrogate - SaO2<90% on air
  • key thing is patient is hypoxic due to = poor alveolar ventilation, diffusion abnormality, ventilation perfusion mismatch
  • blood is going to one part of the lungs but ventilation is occurring elsewhere
53
Q

what is failure of ventilation in respiratory failure

A
  • PaCO2>6.7kPa
  • can get in acute or chronic respiratory failure
  • 20% reduction in ventilation needed
  • CHRONIC ventilation failure = renal compensation for acidosis
  • contributions from = reduced compliance, airway obstruction, muscle dysfunction
54
Q

what is normal breathing control

A
  • brain only works with sugar and O2
  • CO2 drives controls for ventilation
  • driver for taking a breath is hypercapnia = when you hold your breath CO2 amount increases
  • O2 saturation usually OK
  • CO2 slowly increases therefore sensitivity of cO2 receptors becomes less and less
55
Q

what is COPD type 2 breathing control

A
  • CO2 tolerance = don’t have same need to breathe as CO2 threshold higher
  • hypoxia drives ventilation
  • when you give them O2 they can stop breathing = it will stop the hypoxia but then also stop their desire to breathe
  • need to give small amounts of O2 and count respiratory rate as you do
56
Q

what is the oxygen use in COPD

A
  • in the acute stage use O2 until medical help arrives
  • give patient O2 and watch respiratory rate and oxygen saturation = if these get lower then need to take off O2
  • in chronic stage, sue O2 with care = fixed % delivery
57
Q

what is home O2 therapy

A
  • if you get to the point whee you can’t maintain O2 at room air you need O2 daily
  • is good but only if patient uses it properly
  • chronic hypoxia increases risk of cardiac events
58
Q

what home O2 therapy is used

A
  • in cylinder with a mask

- an O2 concentrator = saves patient having a cylinder, takes in room air and removes nitrogen

59
Q

how does airflow obstruction impact dentistry

A
  • can patient attend appointment
  • use of inhaled steroids = candida risk, can land inside mouth and cause local immune suppression and fungal infection so need to rinse mouth and use spacer device
  • smokers = 2 times more likely of getting oral cancer

BDS2 - respiratory system (4 decks)

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