COPD - Chronic Obstructive Pulmonary Disease
Chronic bronchitis
blue bloaters
inflammatory change
muscularity dysfunction
increase # + secretion of goblet cells
excessive mucus production
decrees O2 + increase CO2 + V/Q mismatch
hypocampia
resp. acidosis
increase CO2 + decrease O2
polycithemia
make more RBC to compensate = increase heamiglobin
cynosis risk
pulmanory hypertension
pulmanory vessles constrict
shunt blood flow to healthier alveoli
alveller hypoxia
decrease O2 + increase CO2
Emphysema
pink puffers
inflammatory response
elastic break down + destruction of alveoli walls
loss of alveoli intergrity + recoil
air trapping
macrephagia stimulated
proteases
cytokines
attract neutrofills
produce elastase
specifically targets = loss of elastic recoil
decrease perfusion = air trapping = increase end exptaritory volume = effort in breathing accessory muscles
Burden
15% over 45
4th leading cause of death
permanent + disabling + frequently progressive
85% caused by smoking
Hosp. discharge = Maori + Pacific 3-4x greater chance being admitted to hospital for COPD
Promote awareness
contact general practice earlier
barriers
slow progress nature
financial barriers
support for stop smoaking
symptoms of COPD
high impact on Maori + Pacific communities
Support not blame
engage with person
judgement + blame prevents theroputic relationship + engaging with health
be seen as welcoming and supporting
Testing
Spirometry
recommended method for diagnosing device that allows electronic analysis of results
offered to any person over 40
chronic cough sporadic / unproductive
chronic sputum production
Dyspepsia - persistent/progressive/ worse w excersize
Hx exsposer to tobacco + occupational smoke + dust + chemicals
family Hx of COPD
performed when clinically stable + without infection
don't use bronchodilator 6hrs b/f testing / long acting 12hrs before
measure values
before + 10-15 min after administrating short acting beta-2 agonist
b/f and 30 -45 min after admin of short acting anticholinergic
diagnosis
post - bronchodilator forced expiatory volume in one second to forced vital capacity ration
peak expiratory flow rate = not be used in diagnosis + management
assessing severity
severity assessment
level of breathlessness
spirometry results
exacerbation risk
presence of co morbidities
Management
cessation of smoke
motivating smoking cessation
ABC
brief advice + cessation support
primary management focus
pharmacological treatment
pulmonary rehabilatation
exacerbation management
pulmonary rehabilitation
programs to break cycle of COPD
decreased physical activity b/c dyspnoea = further loss of fitness
rehab = reduce hospitalisation
reduce muscle wasting + weight loss
psycho social support = reduce anxiety + depression
6 week time frame
longer program = greater effectiveness
family involvement
weight loss