COPD Flashcards

1
Q

what is copd

A

lung disease that cases obstructed air flow from the lungs

  • affects approx 5% of world pop
  • chronic bronchitis and emphysema
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2
Q

Chronic bronchitis

A

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

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3
Q

Emphysema

A

alveoli are destroyed as a result of damaging exposure to cig smoe and other particulate matter

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4
Q

Flow of COPD

A

COPD–> expiratory flow limitation/air trapping–> dyspenea–> inactivity–> deconditioning–> reduced exercise tollerance (ultimatly exacerbates symptoms)

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5
Q

exacerbation symptoms of copd

A

exacerbation–> worsoning expiratory flow/ dynamic hyperinflation( less room to inspire new air) –> increased ventilatory drive, tachypnoea, dyspnoea, decreased RV preload, increased LC afterload

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6
Q

causes of systematic inflamation

A
Noxious gases partiicles
AATD deficiancy( cellular damage, oxidative stress)
Endothelial dysfunction, apoptosis
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7
Q

Affects of systematic inflammation on brain, cardiac tissue, muscle tissue

A

Brain- cellular damage, neuroinflammation, hemodynamic impairment

Cardiac tissue- pre thrombotic status (before clotting), reduced fibrinolysis

Muscle tissue- muscle wasting, sarcopenia

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8
Q

What is Alpha 1 anti trypsin deficiency (AATD)

A

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
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9
Q

Cardiovascular dysfunction w/ copd

A

lung inflamation–> increase Tnfa–> increase c reactive pro.–> atherosclerosis

lung inflamation–> increase iL6–> coagulation

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10
Q

Skeletal muscle dysfunction w COPD

A

circulating TNFa–> TnF-R binding–> increase ROS in mito–> pro loss

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11
Q

etiology of muscle function in COPD (lower limb) and how exercise can help it

A

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
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12
Q

Eitology of muscle function in COPD (repiratory muscles)

A

BAD’

  • oxidative stress (decrease pro synthesis)
  • Apoptosis

Good

  • increase type 1
  • increase mito density
  • increase myoglobin
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13
Q

How COPD affects VO2 max

A

decrease capillaeries and mitochondria
decrease muscle blood flow
increase afterload and decrease preload
decrease end expiratory lung volume

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14
Q

exercise training recomendation for someone w copd

A

endurance- 20-30 min @60% 3-5xw
Resistance- 2-3 x week
Respiratory- resisted breathing 2x day 30 breathes

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