COPD Flashcards
3 characteristics of COPD
- chronic airflow obstruction
- symptoms progressive
- not completely reversible (most of the time irreversible)
stats about COPD
- 2% of UK pops affected
- 1/8 emergency admissions
- 11.7% global prevalence
- <50% of smokers develop COPD in their lifetime, but nearly all COPD patients are smokers
- second most common resp disease after asthma
- 3M COPD deaths annually
why are women more likely to be affected by COPD
they have smaller lungs, but since men smoke, more men are actually affected than women.
Initial presentations of COPD
- breathlessness
- ongoing cough +/- sputum
- recurrent chest infections
- wheeze
End stage presentation of COPD
- weight loss
- fatigue, drowsiness
- flapping tremor
- cyanosis
- severe breathlessness
- cor pulmonale
- ankle swelling
- raised JVP
- hyperinflated chest, tight lips, resp effort
- cachexia: loss of muscle mass (from high metabolism)
- pyrexial: increased tempt
causes of COPD
- smoking
- genetic predisposition (AAT (alpha antitrypsin) deficiency will result in the person diagnosed with COPD before 45)
describe pathology of AAT(alpha1 antitrypsin) deficiency
AAT are protease inhibitors made in the liver that reduces elastase released by activated neutrophils. Without AAT, elastase will damage lung tissue whenever inflammatory response is activated, which is what happens.
This is also why smoking makes it worse (particles result in inflammatory response)
this enzyme is produced in the liver and therefore liver damage can also result in this condition.
mMRC dysponoea scale (0-4 grades)
Grade 0. breathless only with strenuous exercise
- DOB when hurrying on flat ground or up the hill
- walks slower than ppl their age on lower ground + need to stop for breath
- stopping for breath every 100 yards on flat ground
- too tired to come outside
4 determinants of whether or not this is COPD
- COPD symptoms present
- history correlates with COPD (risk, >35 yrs, not asthma)
- spirometry test indicates COPD (confirmed airflow obstruction if FEV1/FVC<70%) - only do this test when you think it is COPD to confirm (note that in COPD, you can still get FVC up to normal if you try very hard during exhalation, but FEV1 will definitely fall)
- reduced peak expiratory flow
5 spirometry stages
- FEV1 = 80% of normal value
- 50-79%
- 30-49%
- <30%
- End stage (mostly dead)
things in CXR that indicates COPD
- bulla
- hyperinflated lungs (more than 6 anterior and 10 posterior ribs)
- small, deflated heart
- flat diaphragm due to hyperinflation
3 tests to differentiate btw asthma and COPD
- lung function tests
- radiology
- response to asthma treatment
what is the most common cause of COPD exacerbations
infection - mostly viral infection, bacteria less common
primary care for acute exacerbations
inhalers (bronchodilators + steroids - short + long term)
oral steroids
antibiotics
self management in community if possible
secondary care for acute exacerbations
- O2
- nebs bronchodilators
- beta2 and antimuscarinic
- oral/IV corticosteroids
- possibly antibiotics
triggers for severe exacerbations
- viral or bacterial infections
- sedative drugs
- pneumothorax
- trauma (that would lead to pneumothorax)
investigations done for COPD
- CXR
- blood gases
- full blood count (look for infection, anaemia, clotting)
- Urea and Electrolytes (check renal function)
- sputum culture
- ventilation test
- electrocardiograph
- blood cultures
- biochemistry and blood glucose
- theophylline concentration in those using a theophylline preparation.
type I vs II resp failure
type I: decrease in PO2 only - pure hypoxia, there is not enough O2 in the arteries
- problem with diffusion
type II: decrease in PO2 and increase in PCO2 - because you cannot get enough air in
- problem with ventilation or perfusion
- chronic type II failure –> hypoxic drive, flapping tremors
diseases related to COPD
type I/II resp failure cor pulmonale secondary polycythaemia chronic bronchitis emphysema
describe secondary polycythaemia
body produces extra erythrocytes (RBC) because there is low PO2, resulting in increased viscosity and hypertension.
describe chronic bronchitis
BLUE BLOATERS (airways-based COPD) daily productive cough of >3 months at a time for more than 2 years, fat and hypoxic because they are not breathing in enough, have raised CO2 levels and pitting edema, hypoxic (low O2 saturation)
describe emphysema
PINK PUFFERS (emphysema-based COPD) permanent enlargement and destruction of lung tissue , old and thin, very breathless, quiet chest, very sensitive to CO2 drive to breathe (there will be increased CO2 retention), have normal O2 saturation
nonpharma management
smoking cessation (only helps in the long run, the immediate effect would be less heart attacks)
treating other pre-existing conditions that contributes to breathlessness
vaccinations (best to use combination treatment pneumococcus+influenza) - only relieves symptoms, prevent exacerbations, and improve QoL, mortality remains unchanged.
pulmonary rehab
nutritional assessment - BMI, make sure to eat meals with high vits and high proteins
psychological support
inhaled therapy for COPD
- short acting bronchodilators (temporary but immediate relief, used when there is symptoms) - SABA (salbuatmol), SAMA(ipratropium)
- long acting bronchodilators (long term effect for curative purposes, use everyday regardless of symptoms) - LAMA (antimuscarinic agents like umeclidinium, tiotropium), LABA (B2 agonist like salmeterol)
- high dose ICS and LABA (fluticasone/vitanterol, fostair MDI)
order of pharma treatment
SABA –> add LABA –> add 2 LABA –> add steroid
those eligible to Longterm Inhaler Therapy (2 categgories)
- PaO2<7.3 kPA
2. PaO2 = 7.3-8 kPa + polycythaemia/nocturnal hypoxia/peripheral edema/pulmonary hypertension
Ward management for ACEOPD (COPD exacerbation assessment)
give O2 - target saturation is 88-92% (don’t give too much to those who rely on hypoxic drive or they will lose the will to breathe)
bronchodilators through nebs
corticosteroids (only if we need to, a very short course)
oral/IV antibiotics
assess for evidence of resp failure
Palliative care of COPD (2 main methods)
you know you need this when you are at the stage of invasive ventilation
- management of breathlessness(pathological) and dysfunctional breathing(psychological) - give 5-10mg morphine
- anticipatory care plan, what they plan to do in the next exacerbation.
list examples of primary obstructive airway diseases
- COPD (chronic bronchitis, chronic obstructive disease)
- asthma
- emphysema
describe chronic bronchial asthma
- chronic bronchitis + asthma happening at the same time
- regulated by mast cells
- type I hypersensitivity (immediate hypersensitivity at re-exposure to the same antigen, regulated by IgE antibodies)
- reversible condition with medication if treated early
describe the 2 roles of mast cells in chronic bronchial asthma
- induction of acute inflammatory response
2. constriction of bronchial muscle
presentation of chronic bronchitis
- prolonged cough + sputum
- narrowed airways
- both large and small airways affected:
LARGE AIRWAYS: - mucous gland + goblet cells hyperplasia (indicates inflammation)
- inflammation + fibrosis
SMALL AIRWAYS:
- appearance of goblet cells (not normally there)
- scar formation in long-standing disease
difference between chronic bronchitis and chronic bronchial asthma
these two are often confused, but chronic bronchitis is more long-lasting
5 causes of narrowed airways
- fibrosis
- inflammation
- excess mucous secretion + clogging
- smooth muscle tone
- partial collapse of airway on expiration
causes of chronic bronchitis
- smoking
- dust
- atmospheric obstruction (not enough O2 in the air?)
- extremes of age (M>F)
- alpha 1 antitrypsin/antiprotease deficiency (rare)
pathology of emphysema
- increase in the size of airspace at terminal bronchioles, either from dilation or destruction of alveoli
- ascinus affected (usually 0.5-2 cm in size)
- no fibrosis
3 types of emphysema
- centriacinar - the most common (loss of tissue in the middle of the ascinus, numerous small holes at the top of the lungs)
- panacinar (severe and tends to wipe out the whole lung tissue)
- periacinar, bulla/scar emphysema (bulla formation at the edge of the ascinus, usually at the edge of the pleura. Asymptomatic unless popped, then it will result in pneumothorax, has bigger holes than the other types)
why do people with emphysema breathe with hyperinflated lungs
adaptive mechanism - keep the air inside the lungs at all time to keep the alveolar open - no need to overcome the initial inertia and therefore makes breathing easier
pathology of normal lung vs emphysema
NORMAL:
neutrophils and macrophages produce elastase (a protease) to kill pathogens, but will also damage lung tissue. Therefore, there are 2 countermeasures: 1. lung repair mech + elastin synthesis, 2. production of antiprotease (AAT)
EMPHYSEMA:
- increase pathogens in the lung from smoking
- increased elastase production
- inhibited antiprotease production
- decrease repair mechanism
what brings about COPD symptoms?
collapse of SMALL airways (collapse of large airways don’t make much of a difference)
importance of alveoli in preventing bronchioles from collapsing
elastin in the alveolar walls holds the bronchioles patent during inspiration
7 causes of hypoxaemia
- V/Q imbalance (responds to increase in FIO2)
- shunt (does not respond to increase in FIO2)
- diffusion impairment
- alveolar hypoventilation (this increases PCO2 and decreases PO2 )
- reduction in alveolar surface area
- reduced resp drive
- airway obstruction
why do blue bloaters tend to die of heart failure?
not getting enough O2 in –> heart works harder to pump the small amount of O2 around the body –> body responds by increasing number of RBCs, but that makes the blood more viscous and the heart to pump even harder –> heart failure
how does COPD lead to cor pulmonale?
hypoxic –> all pulmonary vessels in the lungs constrict in an attempt to divert blood somewhere else –> pulmonary hypertension –> RV works hard to pump blood to the lungs –> cor pulmonale (enlarged RV)
