Asthma and COPD Flashcards
2 types of cough
productive and non-productive
wheeze
expiratory noise
(breathe out, organ sounding nose - airways resonate at different frequency, can’t fake a wheeze – something bad happening in an airway)
stridor
inspiratory noise (breathe in, blockage in big airway, choking)
dyspnoea
distress on effort with breathing
- know breathing not working well,
- uncomfortable with breathing
2 types of pain in respiratory system
general
inspiratory
general pain in respiratory system
cough
inspiratory pain in respiratory system
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)
respiratory symptoms (5)
cough
wheeze
stridor
dyspnoea
pain (general/inspiratory)
respiratory signs (5)
chest movement with respiration
rate of respiration (12-15/min)
air entry (symmetrical? reduced)
vocal resonance
percussion note (resonant, dull)
what should chest movement with respiration be like
Expansion should be same on both side – hand on waist and thumbs on back and move at same rate and distance
what is normal rate of respiration
12-15/min
how can the rate of respiration be changed
Change with
- exercise,
- altitude (increase with as O2 lower, need faster ventilation),
- asthma – cannot ventilate properly compensate by breathing more
why can it be useful to measure of rate of respiration over a course of time
guide to see how people change over course of treatment
how to assess air entry
with a stethoscope
symmetrical? reduced?
what happens to vocal resonance is there is exudate in lungs
sounds odd = Exudate in lungs can hear what they are saying
what happens to vocal resonance is there is air in lungs
noise out front
very little sound echos in lungs
respiratory investigations (5)
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
PEFR
maximum flow rate – gas breathe out total
FEV1
forced expiratory volume - gas breathe out in 1 sec
FEV1/VC
measure of resp. function
ventilation/perfusion mismatch because
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
what should lungs appear like on X-ray
black as filled with air
4 types of respiratory disease
infections (pneumonia)
airflow obstruction
gas exchange failure
tumours
airflow obstructions respiratory diseases
asthma
Chronic Obstructive Pulmonary Disease
restrictive pulmonary change – lungs become stiff so elastic tissue replaced by fibrous tissue
gas exchange failure respiratory diseases
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
respiratory failure =
combination of alveolar and ventilation problems
asthma reversibility
short term is reversible, long term causes permanent lung damage (good to bad)
COPS reversibility
COPD is always destructive, but will have reversible component on top (bad to more bad)
2 chronic airflow obstruction diseases
asthma and COPD
what 3 things can exacerbate and cause remission of chronic airflow obstruction
infection
exercise
cold air
%asthma in children and adults
5-10% children (common)
2-5% adults
bronchial hyper reactivity in asthma
- Overreaction to minor stimulation
- Immune response disproportionate
- Too many chemical mediators
what causes asthma
bronchial hyper reactivity
3 responses in asthma which create the problem
Inflammation of airways that is not needed – narrows the tube (mucosal oedema)
Smooth muscles on outside constrict
Mucous glands go into hypersecretion
what 3 things always line inside of airways
mucus
muscles
glands
mechanisms in asthma
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
triad of airway changes in asthma
- smooth muscle constriction
- inflammation of the mucosa (swelling)
- increased mucus secretion
patient complaints in asthma
COUGH!, wheeze, Shortness of Breath
- Wheeze – narrowing of airway
- Cough – excess mucous, body trying to mouth out of irritated airways into trachea
how does peak expiratory flow rate change with airway
gas out of lungs
Slower with narrowing
Vary at different times of day
4 asthma triggers
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
why would you perform a skin prick test in asthma investigations
Testing reactivity of skins (Not of lungs)
Can narrow down range of things that are problem
immune response to asthma is
biphasic
biphasic immune response to asthma
- 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
asthma trigger/stimuli
is innocuous
immune response not needed
6 respiratory drugs
Beta-adrenergic Agonists
Anticholinergic
Corticosteroids
Leukotriene inhibitors
Chromones
Theophyllines
nebulised beta-adrenergic agonists
as effective as IV
o Bubble gas through liquid and inject
o Can direct into lungs
o Very effective rapidly
action of beta-adrenergic agonists
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
when should you take beta-adrenergic agonists
PROTECTIVE against stimuli
- Take puffer before exercise if exercise induced
2 types of inhaled bronchodilators
salbutamol (blue)
salmeterol (green)
role of anticholinergics
Act on muscarinic receptors
Reduce BASAL tone only
- Good in COPD
‘neurogenic’ triggers
when are theophyllines used
SEVERE asthma due to potential adverse effects
- Adenosine inhibition
CNS Stimulation, Diuresis, arrhythmia
best drug for asthma treatment
corticosteroids
treat all 3 symptoms of asthma
corticosteroid action
No mucosal oedema, bronchoconstriction or muscosal secretion
- immune cell and epithelial cell actions
Take brown puffer everyday – stop asthma symptoms
problem with corticosteroid
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
when to use a corticosteroid
if β2 agonist >3 times each week
are there any side effects of corticosteroid
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
mild asthma treatment
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
tiers of asthma
mild
moderate
severe
ID as treat differently in emergency
moderate asthma treatment
Green/purple/pink
- Long-acting beta agonist, theophylline, anti-muscarinic drugs
- High-dose inhaled steroid
treat and then decide (wont get bad as fast)
severe asthma treatment
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
names for COPD
Chronic Obstructive Pulmonary Disease
Chronic Obstructive Airways Disease COAD
Chronic Bronchitis & Emphysema
- Most descriptive – destructive (emphysema) and chronic inflammation (bronchitis)
severe asthma when
Ever hospital admitted or steroid tablets more than once a year
COPD is
• 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
emphysema
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
GOLD 1 or 2 classification of COPD
disease state
- mild or moderate
lung function
- FEV1 50-80%
clinical state
- cough or little to no breathlessness
GOLD 3 classification of COPD
disease state
- severe
lung function
- FEV1 30-50%
clinical state
- cough and sputum
- breathlessness on exertion
GOLD 4 classification of COPD
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
how can COPD progress to respiratory failure
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
disease state in GOLD 1 or 2
mild or moderate
diseases state in GOLD 3
severe
Disease state in GOLD 4
very severe
lung function in GOLD 1 or 2
FEV1 50-80%
lung function in GOLD 3
FEV1 30-50%
lung function in GOLD 4
FEV 30%
clinical state in GOLD 1 or 2
cough or little to no breathlessness
clinical state in GOLD 3
- cough and sputum
- breathlessness on exertion
clinical state in GOLD 4
- wheeze and cough
- breathlessness on mild exertion
over inflated lungs - cyanosis and peripheral oedema in some
how can poor ventilation in COPD occur
o airway narrowing (reversible?)
o restrictive lung defects
respiratory failure occurs when
cannot oxygenate enough air for tissue needs
Causes of COPD (3)
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
how can occupational lung disease lead to respiratory failure? (2)
fibrosis (dust related)
tumours
what causes fibrosis in occupational lung disease
dust related
o Coal
o Silicon
o Beryllium
o Asbestos – dust created when try and remove
tumours in occupational lung disease
caused by Asbestos - mesothelioma
- Tumour of pleural lining
- Liquid Between chest and lung walls
- Chronic inflammation can lead to tumour formation
smoking progressive effect on lung function
more smoking that you do the worse lung function
- Forced expiratory volume gets progressively less
6 ways to manage COPD
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
difference between asthma and COPD management effects
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)
what does COPD treatment reflext
reversibility of disease not severity (unlike asthma)
2 outcomes of COPD
type 1 respiratory failure
type 2 respiratory failure
type 1 respiratory failure
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
type 2 respiratory failure
Hypercapnia (high CO2)
ventilation failure
- CO2 easily diffuse
Ventilating the gas that gets to the alveoli
what can cause type 2 respiratory failure (3)
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)
what are the 2 principles of respiratory failure
- Failure of oxygenation
* Failure of ventilation
failure of oxygenation occurs when
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
failure of ventilation occurs when
PaCO2 > 6.7kPa in arterial blood
20% reduction in ventilation needed
acute or chronic
acute respiratory failure failure of ventilation
Drop from coping to too low happens fairly quickly
20% reduction in ventilation needed
chronic ventilation failure
Renal compensation for acidosis
- Due to cigarette accumulation
- Increase in CO2 build up due to poor ventilation to alveoli
3 things which contribute to ventilation failure
- Reduced compliance
- Airway obstruction
- Muscle dysfunction
normal breathing control
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
COPD desire to breathe
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
what drives desire to breath in COPD
HYPOXIA drives ventilation not hypocania
- Oxygen sensitivity starts to kick in
- Rely on oxygen level to keep them breathing
delivering oxygen to COPD patient impact on desire to breath
Fine till you give oxygen, increase oxygen – stop breathing = distressful
- Take away hypoxia with desire to breathe
best way to deliver oxygen to COPD patient
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
dental emergency COPD treatment
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
when would a patient have home oxygen therapy
Respiratory failure to the point they are not able to oxygenate blood properly
• Cannot maintain oxygen from room air
2 ways to have home oxygen therapy
cylinders
oxygen concentrators
oxygen cylinders disadvantage
sit with mask on 24/7
oxygen concentrator
room air and remove nitrogen so higher oxygen concentration in inspired air
- Saves cylinders constantly as higher oxygen concentration
should oxygen be given 24 hours?
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
airflow obstruction and dentistry
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
