Resp final

Question 1

“perfect” serum marker

Answer 1

• tissue specificity
• quickly released with injury and detectable
• can tell from normal levels
• biological sensitivity and specificity
• marker levels tell effectiveness of therapy
• remain in blood for hrs to days (delayed detection)

Question 2

COPD

Answer 2

PROGRESSIVE AIRWAY DISEASE (NOT REVERSIBLE)

Question 3

pathogenesis of COPD

Answer 3

noxious agent –> inflammation –> COPD

Question 4

chronic bronchitis

Answer 4

excessive mucous production

Question 5

emphysema

Answer 5

enlargment of air spaces distal to terminal bronchioles with destruction of alveolar walls

Question 6

3 mechanisms of airway obstruction

Answer 6

1) partially blocked lumen (CB) due to excessive mucous secretion (decreases radius and increases resistance)

2) thickening airway wall (CB) mucous gland hypertrophy and hyperplasia
- REID INDEX= y/x healthy<0.4 and COPD > 0.4

3) loss of radial traction (E) due to loss of elastin from damage therefore, permanently collapsed and can’t get air out (low alveolar pressure) AND degrade tissue therefore decrease SA for gas exchange
* 3rd reason for PAH (digest lung therefore cause increase R)

Question 7

diagnosing COPD

Answer 7

VC decreased because can’t get air out

FEV1/FVC= 60% COPD

Question 8

assessing COPD

Answer 8

best with FEV1 with bronchodilator, chest X-ray (flatter diaphragm curve), arterial blood gas measurement (hypoxia), alpha 1 anti trypsin deficiency screening

Question 9

dyspnea

Answer 9

distressing experience of respiratory discomfort

disease aspect: with exercise COPD feel they can’t get enough air

Question 10

severity of COPD

Answer 10

0: at risk – normal spirometry but have chronic symptom of coughing
1: mild – FEV1>80%
II: moderate – IIA: FEV1 btw 50 and 80%
IIB: FEV1 btw 30 and 50%
III: severe – FEV1 less than 30 or 50% with respiratory failure or clinical signs of RH failure

accelerated loss of FEV1 with COPD up to 70 ml/yr (normal only 30)

Question 11

defence of lung

Answer 11

fight and remove foreign particles by lymphocytes and macrophages use proteases
protease inhibitors used to limit damage and prevent healthy lung being damaged
with an imbalance between proteases and protease inhibitor you get degraded elastin and alpha 1 trypsin

Question 12

dynamic hyperinflation

Answer 12

restricted ventilatory response to exercise

• continue doing same TV but at increasing lung volumes (unproductive work)
• with COPD get increased FRC and compliance curve is more flat

Question 13

Exercise intolerance

Answer 13

1) dynamic hyperinflation increases load on res muscles
- high pressure change needed for change in volume of lung
- inspiration starts while intrathoracic pressure still positive
- diaphragm operates at less advantageous position on F-l curve
2) peripheral skeletal muscles dysfunction (increased fast fibres)
3) diaphragmatic endurance and strength reduced (increase proportion of slow oxidative fibres)

therefore, atrophy and fibre type shifting (steroid use, hypoxia and malnutrition)

Question 14

diaphragmatic muscle injury

Answer 14

inflamed and dead fibres

- severity of airway obstruction is related to increased area of abnormal muscle

Question 15

diaphragm fibre type shifting with disease

Answer 15

increase SO fibres with FEV1<60%

F production decreased (secondary)

Question 16

what happens to heart in COPD

Answer 16

1) blood O2 decreases progressively via local control, pulmonary blood vessels constrict
2) loss of lung parenchyma decreased # pulmonary capillaries (increase R cause pulmonary hypertension)
3) FRC increases to higher and higher LV’s

all contribute to RVH

Question 17

Cor pulmonale

Answer 17

RVH

• abnormal heart beat
• pushes septum left therefore decrease L ventricle volume and compliance and decrease CO cause inadequate perfusion to organs

Question 18

what do COPD patients usually die from

Answer 18

RVF as result of pulmonary hypertension