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
what is the peak expiratory flow rate
- changes as airways narrowed - morning are all the same and nights are all the same - varies at different times of the day
26
what are some triggers of asthma
- 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
what is a skin prick test for asthma
- good but it only tests the skin, doesn't test lungs as could be different - narrows down possibilities however
28
what type of immune response is asthma
- 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
how long can it take for someone to die from asthma
- 20 minutes
30
how is asthma treated
- 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
what is the treatment for asthma based on severity
- 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
what do the different colours of puffer mean
- brown/blue = mild asthma - purple/pink = moderate asthma - take steroid tablets = severe
33
how do you treat mild asthma
- treat with blue puffer and send home
34
how do you treat severe asthma
- you're not going to fix them, only make it slightly better - need to go to hospital soon
35
what are some respiratory drugs
- beta-adrenergic agonists - anticholinergic - corticosteroids - leukotriene inhibitors = good for delayed phase - chromones - theophyllines
36
what are beta adrenergic agonists
- 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
what are anticholinergic
- act on muscarinic receptors = good for muscles - reduce basal tone only = good in COPD, not so much asthma - neurogenic triggers
38
what are theophylline
- used in severe asthma due to potential adverse effects - adenosine inhibition = CNS stimulation, diuresis, arrhythmias - immunomodulatory
39
what are corticosteroids
- 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
what are the problems with corticosteroids
- 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
what are other names for COPD
- chronic obstructive pulmonary disorder - chronic obstructive airways disease - chronic bronchitis and emphysema = most descriptive
42
what is COPD
- 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
what is emphysema
- destruction of alveoli | - dilation of others to 'fill space'
44
what are the GOLD classifications of COPD
``` - 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
how can COPD progress to respiratory failure
- reduced surface area for gas exchange - thickening of alveolar mucosal barrier - can't oxygenate enough to get sufficient amount to tissues
46
what are the causes of COPD
- smoking = mainly - environmental lung damage = coal, silica, beryllium, asbestos, occupational lung diseases - hereditary = emphysema
47
what is occupational lung disease
- 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
how is COPD managed
- 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
what is the problem with management of COPD
- 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
what is type 1 respiratory failure COPD
- hypoxaemia = low oxygen - caused by hypoxia - thickening of alveolar barrier = more difficult for alveolar infusion of oxygen
51
what is type 2 respiratory failure COPD
- 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
what is failure of oxygenation in respiratory failure
- 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
what is failure of ventilation in respiratory failure
- 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
what is normal breathing control
- 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
what is COPD type 2 breathing control
- 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
what is the oxygen use in COPD
- 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
what is home O2 therapy
- 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
what home O2 therapy is used
- in cylinder with a mask | - an O2 concentrator = saves patient having a cylinder, takes in room air and removes nitrogen
59
how does airflow obstruction impact dentistry
- 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