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PATH1000 > COPD > Flashcards

COPD Flashcards

1
Q

dyspnoea

A

shortness of breath

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2
Q

COPD incldues

A

includes chronic bronchitis and emphysema and sometimes asthma

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3
Q

what is COPD

A
  • chronic obstructive lung disease
  • is preventable and treatable
  • irreversible
  • lung condition characterised by chronic respiratory symptoms due to abnormalities of the airways and/or alveoli that cause persistent airflow obstruction
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4
Q

tidal volume

A

amount of air inspired or expired with each breath

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5
Q

inspiratory reserve volume

A

amount that can be forcefully inspired after inspiration of tidal volume

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6
Q

expiratory reserve volume

A

amount that can be forcefully expired after expiration of tidal volume

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7
Q

residual volume

A

volume still remaining in respiratory passages and lungs after more forceful expiration

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8
Q

inspiratory capacity

A

tidal volume plus inspiratory reserve volume

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9
Q

functional residual capacity

A

expiratory reserve volume plus residual volume

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10
Q

vital capacity

A

sum of inspiratory reserve volume, tidal volume and expiratory reserve volume

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11
Q

total lunch capacity

A

sum of inspiratory and expiratory reserve volumes, tidal volume and residual volume

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12
Q

spirometry

A

process of measuring volumes of air that move into and out of the lungs

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13
Q

FVC

A

forced vital capacity
- the volume of air forcefully expired after a maximum inspiration and maximum rapid exhalation

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14
Q

FEV1

A

forced expiratory volume in 1 second

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15
Q

carbon monoxide diffusion capacity

A

measures the ability of the lungs to transfer gas from inhaled air to the red blood cells in the pulmonary capillaries

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16
Q

divisions of the respiratory system

A

upper
- nose
- pharynx
lower
- larynx
- trachea
- lungs

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17
Q

conducting zone

A

zone exclusively for air movement
from the nose to the bronchioles

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18
Q

respiratory zone

A

within the lungs and is where gas exchange between air and blood takes place

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19
Q

right vs left lung

A

right has 3 lobes
left has 2 lobes

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20
Q

obstructive

A
  • air flow limitation because of partial / complete blockage
  • decreased expiratory air flow
  • emphysema, chronic bronchitis, asthma, bronchiectasis
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21
Q

restrictive

A

reduced expansion of lung parenchyma (tissue)
- decrease lung capacity
- pulmonary fibrosis, rheumatoid arthritis

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22
Q

obstructive vs restrictive graph

A

obstructive
- reduced FEV1
- longer to reach outcome
- decreased FEv1/FVC ratio
restrictive
- FEV1/FVC ratio increased/normal
- decreased FEV1
- decreased FVC

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23
Q

asthma

A

chronic airway inflammation
hyper responsiveness of tracheobronchial tree to various stimuli leading to bronchoconstriction

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24
Q

asthma symptoms

A

wheezing, breathlessness. chest tightness, coughing
- vary in intensity
- worse at night or early in the morning

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25
Q

long term changes in asthma

A
  • increase in bronchial blood vessels
  • increased smooth muscle
  • thickening of collagen layers
  • loss of normal distensibility of the airway
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26
Q

atopic vs non atopic asthma

A

atopic - most common, specific allergens eg pollen dust
- family history
non-atopic
- intermittent
- persistant

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27
Q

3 main changes in asthma

A
  • smooth muscles constrict
  • inflammation redness and swelling
  • increased mucous production
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28
Q

emphysema

A

enlargement and destruction of alveolar walls
- loss of elasticity
- trapping of air

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29
Q

chronic bronchitis

A

inflammation and thickening of mucous membranes
- accumulation of musus and pus leading to obstruction
- bronchial oedema (swelling of bronchioles)
- increase in size and number of mucous glands and goblet cells
- narrowing of airways
- smooth muscle hypertrophy with fibrosis
- thick mucus which can’t be clearer because of impairs ciliary function
= lead to pulmonary infection and ineffective repair

30
Q

asthma

A
  • reversible airflow obstruction
  • thick mucus, smooth muscle spasm causing obstruction of small airways
31
Q

hemoptysis

A

coughing up blood

32
Q

hypoventilation

A

CO2 removal doesn’t match CO2 production, increase in CO2
- respiratory acidosis
hypercapnia = high CO2 in blood

33
Q

hyperventilation

A

lungs remove CO2 faster then it is produced
hypocapnia = decreased CO2 in blood
- repsiratory alkalosis

34
Q

cyanosis

A

bluish discolouration of skin and mucous membranes eg lips

35
Q

clubbing

A

enlargement of end of the fingers or toes
= chronic hypoxemia (trapped air)

36
Q

hypoxaemia

A

reduced oxygenation of arterial blood
lead to tissue hypoxia

37
Q

hypoxia

A

reduced oxygenation of cells in tissues

38
Q

atelectasis

A

collapse of lung tissue

39
Q

chronic bronchitis criteria

A

hyper secretion of mucus and cough for at least 3 months of the year for at least 2 years

40
Q

smoking and chronic bronchitis

A
  • interferes with ciliary action
  • causes direct damage to airway epithelium and inhibits the ability of bronchial and alveolar leukocytes
  • triggers inflammation
  • bronchial oedema, hypertrophy and hyperplasia of goblet cells
  • impaired mucus clearance
  • metaplasia of epithelial
  • smooth muscle constriction
  • floppy airways
    = increase risk of infection
41
Q

primary and secondary emphysema

A

primary - inherited disorder
secondary - smoking

42
Q

emphysema mechanism

A

smokers have increase in antiproteinases and anti oxidants

43
Q

what does destruction of alveoli produce

A

bullae - large air spaces within lung parenchyma
blebs - air spaces adjacent to pleurae
- results in ventilation perfusion

44
Q

air trapping

A

causes hyper expansion of the chest
- increases the workload of breathing
= hypoventilation and hypercapnia

45
Q

what does destruction of alveolar wall and pulmonary capillaries cause

A
  • pulmonary artery hypertension
  • cor pulmonale
46
Q

cor pulmonale

A
  • right sided heart failure
  • enlargement of right ventricle due to high blood pressure in the lungs
47
Q

pathophysiology of emphysema

A
  • smoking = loss of elasticity by protease - destruction of alveoli - elimination of portion of the capillaries and increase are in acinus
    = decrease surface for gas exchange
  • cause blebs and bullae
  • air trapping = barrel chest
  • increase work for breathing
  • floppy airways = hypercapnia and hypoventilation
    = weight loss, muscle weakness, respiratory acidosis = increase risk of infection
    = pneumothorax
48
Q

when is asthma considered reversible

A
  • FEV1 increases by more then 200ml post bronchodilator
49
Q

asthma vs COPD symptoms

A

asthma
- vary over time often triggered by exposure
COPD
- continuous especially during exercise

50
Q

asthma vs COPD lung function between symptoms

A

asthma
- normal between symptoms
COPD
- persistent airflow limitation

51
Q

asthma vs COPD onset

A

asthma
- usually childhood
COPD
- usually 40+

52
Q

asthma vs COPD response to brochodilator and steroids

A

asthma = good
COPD = bad

53
Q

type 1 respiration failure

A

low oxygen

54
Q

type 2 respiratory failure

A

low oxygen and high carbon dioxide

55
Q

bronchiectasis

A

permanent dilation of bronchi and bronchioles caused by destruction of the muscles and elastic tissue resulting from chronic necrotising infections

56
Q

bronchiectasis pathophysiology

A
  • airways are scarred and inflamed with thick mucous
  • airways become widened and cannot clear themselves properly = infected by bacteria
  • pockets in airways = trapped mucus = infection
57
Q

pneumonitis

A

inflammation of lung parenchyma due to chemical or physical agents
- secondary infection may result in pneumonia

58
Q

pneumonia

A

infection of lower respiratory tract
- result when pulmonary defence mechanisms are impaired

59
Q

tuberculosis

A
  • transmitted from person to person
  • highly contagious
60
Q

latent vs active TB

A

latent
- lives but doesn’t grow in the body
- doesn’t make person feel sick
- can’t spread
active
- grows in the body
- makes a person feel sick
- can spread from person to person

61
Q

pleural effusion

A

presence of fluid in pleural spaces
- due to abscess draining into pleural space comes from blood or lymphatic vessels lying beneath pleural space

62
Q

empyema

A
  • pus in pleural space and develops when the pulmonary lymphatics become blocked
  • contaminated lymphatic fluid into pleural space
63
Q

pneumothorax

A

gas or air in pleural space
- caused by rupture of visceral pleura which surrounds the lungs
- causes lung to collapse

64
Q

thrombosis

A
  • blood clot if blood vessel
  • caused by many things
    eg injury, alterations in blood flow, changes in blood composition
  • life threatening
65
Q

haematoma

A
  • life saving
  • extravascular clot eg when injury
66
Q

embolism

A
  • thrombus that travels
  • carried in the blood stream from its origin
  • why people use compression stockings to stock the pooling of blood
67
Q

pulmonary oedema

A
  • excess water in the lungs
  • caused by left sided heart disease
  • left ventricle fails - increase in pulmonary hydrostatic pressure - fluid moves from capillary into the interstitial space
68
Q

right sided heart failure

A
  • chronic hyperaemia due to lung disease = pulmonary vasoconstriction
  • narrowed pulmonary capillaries = pulmonary hypertension
  • right side of heart has to work harder
    = enlargement of heart muscles = reduced BV in right ventricle
69
Q

determining if obstructive or restrictive with data

A
  1. FEV1 = if low it can be obstructive or restrictive
  2. Ratio (FEV1%): low = obstructive, high/normal = restrictive
    Confirmation
  3. TLC/RV: reduced = restrictive, increased = emphysema (build up of air in alveoli)
  4. Asthma = FEV1 improved by more then 200ml (0.2L), reversibility
70
Q
  1. Explain the pathophysiology behind the scarring and thickening of the airways noted in people with smoking associated chronic bronchitis.
A

Thickening – caused by swelling of epithelial cells as well as hypertrophy and hyperplasia of goblet cells, smooth muscles thicken all contributed to the thickening of the airways
Scarring – metaplasia and lose of cilia as well as scarring of the smooth muscles
o Healing by scarring – replacement of healthy tissue with non functioning tissue

71
Q
  1. Explain to your patient the pathophysiology behind ‘floppy airways’, early airway closure and why they ‘pursed lips breathe’.
A

o after smoking we lose elasticity the walls of the alveoli and this reduces the surface area for gas exchange and lose in capillaries as well as thickened and inflamed bronchioles
o cant rely on elastic recoil as much and we have to force the air out, there is a chance that the airway may close early = floppy airways trapping more air in the alveoli. Leading to hyperinflated lungs = barrelled chest
o Pursed lip breathing increases the pressure in the airways and allows them to get more air out
o Eg paper straw becomes floppy and cant get anything through the straw

72
Q
A

PATH1000 (8 decks)

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