COPD Flashcards
what is copd
lung disease that cases obstructed air flow from the lungs
- affects approx 5% of world pop
- chronic bronchitis and emphysema
Chronic bronchitis
inflamation of the linning of the bronchial tubes which carry air to and from air sacs of lungs
-mucus blocks airway and inflammation further narrows it
Emphysema
alveoli are destroyed as a result of damaging exposure to cig smoe and other particulate matter
Flow of COPD
COPD–> expiratory flow limitation/air trapping–> dyspenea–> inactivity–> deconditioning–> reduced exercise tollerance (ultimatly exacerbates symptoms)
exacerbation symptoms of copd
exacerbation–> worsoning expiratory flow/ dynamic hyperinflation( less room to inspire new air) –> increased ventilatory drive, tachypnoea, dyspnoea, decreased RV preload, increased LC afterload
causes of systematic inflamation
Noxious gases partiicles AATD deficiancy( cellular damage, oxidative stress) Endothelial dysfunction, apoptosis
Affects of systematic inflammation on brain, cardiac tissue, muscle tissue
Brain- cellular damage, neuroinflammation, hemodynamic impairment
Cardiac tissue- pre thrombotic status (before clotting), reduced fibrinolysis
Muscle tissue- muscle wasting, sarcopenia
What is Alpha 1 anti trypsin deficiency (AATD)
genetic disorder that may result in lung disease
- 1/2500 ppl of european decent
- produced in liver, one of its functions is to protect lungs from neutrofil elasase ( enzyme that disrupts connective tissue) w/o leads to emphysema
Cardiovascular dysfunction w/ copd
lung inflamation–> increase Tnfa–> increase c reactive pro.–> atherosclerosis
lung inflamation–> increase iL6–> coagulation
Skeletal muscle dysfunction w COPD
circulating TNFa–> TnF-R binding–> increase ROS in mito–> pro loss
etiology of muscle function in COPD (lower limb) and how exercise can help it
BAD
- oxidative stress (decreases pro synthesis)
- Apoptosis
- Decrease % of type 1 fibres
- Decrease mitochondrial density
- Atrophy
Exercise
- IL6 leads to decrease in pro breakdown becuase it decreases TNFa
- liver releases IGF1 which releases mTOR which increases synthesis
Eitology of muscle function in COPD (repiratory muscles)
BAD’
- oxidative stress (decrease pro synthesis)
- Apoptosis
Good
- increase type 1
- increase mito density
- increase myoglobin
How COPD affects VO2 max
decrease capillaeries and mitochondria
decrease muscle blood flow
increase afterload and decrease preload
decrease end expiratory lung volume
exercise training recomendation for someone w copd
endurance- 20-30 min @60% 3-5xw
Resistance- 2-3 x week
Respiratory- resisted breathing 2x day 30 breathes