Obstructive diseases Flashcards

1
Q

lung – systemic venous blood before it returns to the left ventricles

A

filtrates

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2
Q

difficulty breathing

A

dyspnea

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3
Q

treatment for obstructive diseases are –

A

similar regardless of underlying pathology

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4
Q

invasive procedures may be necessary for treatment of –

A

pleural diseases, interstitial lung diseases and malignancies

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5
Q

what does spirometry measure

A

vital capacity, timed volumes

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6
Q

– allows for air-flow studies

A

spirometry

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7
Q

blood gases are taken from – to measure pH, pCO2, pO2

A

artery

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8
Q

pH is determined by–

A

respiratory and metabolic acid production

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9
Q

pCO2 is determined by –

A

ventilation rate

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10
Q

pO2 is determined by –

A

ventilation rate, O2 content of inhaled air, diffusion from alveoli to pulmonary capillaries

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11
Q

normal range of pH

A

7.35 - 7.45

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12
Q

normal range of pCO2

A

35-45 mmHg

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13
Q

normal range of pO2

A

80-100 mmHg

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14
Q

pulse oximetry measures –

A

O2 saturation through skin

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15
Q

compare pulse oxymetry and blood gas measurement

A

pulse oximetry is less accurate but quicker

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16
Q

continuous flow-volume loops are useful in detecting –

A

laryngeal and tracheal lesions

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17
Q

how can ventilation/perfusion studies be assessed?

A

nuclear scans

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18
Q

pulse oximetry is a noninvasive test to monitor the percentage of –

A

hemoglobin saturated with oxygen

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19
Q

nuclear ventilation/perfusion scans can detect – and also evaluate lung function in advanced COPD

A

pulmonary embolism

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20
Q

COPD is united by presence of –

A

persistent airflow limitation (and dyspnea)

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21
Q

COPD is caused by –

A

chronic bronchitis or emphysema

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22
Q

what is more common chronic bronchitis or emphysema?

A

chronic bronchitis

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23
Q

Asthmatic patients with emphysema and/or bronchitis are considered to have –

A

“asthmatic bronchitis”

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24
Q

aging (after 20) –>

A

less alveoli and lung capillaries

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25
Q

lung functions that are affected by aging –

A

compliance, lung volume, airflow, diffusing capacity

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26
Q

can purely age-related change lead to clinically significant symptoms

A

no

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27
Q

in smokers, injury due to inflammation is – and accelerates the effects of aging

A

superimposed on

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28
Q

a key enzyme that inhibits human proteases, such as neutrophil elastase

A

alpha1-antitrypsin

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29
Q

alpha1-antitrypsin deficiency results in a susceptibility to –

A

alveolar injury

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30
Q

exposure to environmental toxins have effect similar to that of –

A

smoking

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31
Q

obesity affects –

A

lung mechanics

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32
Q

what is deconditioning?

A

respiratory muscle weakness

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33
Q

deconditioning progresses dyspnea to –

A

severe COPD

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34
Q

factors that lead to deconditioning

A

dyspnea –> lack of physical activity
severe anxiety –> increases respiratory rate
difficulty eating –> compromises muscle energy supply

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35
Q

where does damage occur for emphysema?

A

terminal part of respiratory tree

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36
Q

emphysema: alveoli become –

A

distended (can’t fully empty, some break)

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37
Q

emphysema: terminal bronchioles lose –

A

elastic recoil

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38
Q

emphysema: terminal bronchioles collapse during –

A

expiration

39
Q

emphysema: lungs become –

A

hyperinflated

40
Q

emphysema: patient usually has severe dyspnea noticeable during expiration / uncomfortable sensation when breathing during exercise

A

pink puffer

41
Q

emphysema: late hypoxemia and CO2 retention can lead to –

A

pneumothorax

42
Q

where is the damage for chronic bronchitis?

A

bronchial tubes

43
Q

chronic bronchitis: decreased – of bronchi and bronchioles

A

lumen

44
Q

chronic bronchitis due to –

A

inflammation, enlarged mucus gland, and fibrosis

45
Q

chronic bronchitis: elastic recoil is –

A

usually normal

46
Q

chronic bronchitis: patient feels obstruction during inspiration and expiration

A

blue bloater

47
Q

chronic bronchitis: patient has productive cough

A

lasts 3 months/year for at least 2 consecutive years

48
Q

chronic bronchitis: early hypoxemia and CO2 retention can lead to –

A

cor pulmonale (R sided failure)

49
Q

normal breathing for children

A

12-20 breaths/min

50
Q

normal breathing for resting adults

A

12-16 breaths/min

51
Q

normal breathing for older patients

A

12-18 breaths/min

52
Q

normal breathing for older patients in long-term care

A

16-25 breaths/min

53
Q

sputum production in emphysema

A

scant (little)

54
Q

sputum production in chronic bronchitis

A

copious and purulent

55
Q

bradypnea is a form of hypoventilation with a respiratory rate of –

A

less than 10 breaths/min

56
Q

COPD signs: weight loss occurs in many long time sufferers and –

A

can’t be nutritionally reversed

57
Q

COPD signs: – chest diameter

A

increased antero-posterior

58
Q

COPD signs: lung sounds

A

decreased and abnormal

59
Q

chest x ray of COPD

A

hyperinflated lungs (hyperblack)

60
Q

TLC in emphysema

A

increased

61
Q

TLC in chronic bronchitis

A

normal or slightly decreased

62
Q

RV in emphysema

A

increased

63
Q

RV in chronic bronchitis

A

increased

64
Q

diffusing capacity in emphysema

A

very decreased

65
Q

diffusing capacity in chronic bronchitis

A

decreased

66
Q

anteroposterior view of COPD lungs

A

darker and more vascularity

67
Q

lateral view of COPD lungs

A

increased AP diameter
flattened diaphragm
increased retrosternal air space

68
Q

why does oxygen therapy need to be done very carefully?

A

some patients rely on hypoxemia for their ventilator drive

69
Q

exacerbations of COPD are associated with –

A

transient decreases in lung function

70
Q

severe hypoxia may lead to –

A

angina, acute coronary syndrome, heart failure

71
Q

T/F: in elderly smokers COPD may coexist with heart failure

A

true (cor pulmonale)

72
Q

asthma is hyperreactivity of –

A

bronchial musculature

73
Q

asthma involves airway –

A

inflammation and reversible obstruction

74
Q

common aeroallergens

A

animal dander, dust mite, mold, cockroach, pollens

75
Q

asthma may also be precipitated by exercise, acid reflux (aspirin), – an dinfections

A

temp changes

76
Q

inflammatory cells, cytokines and other – are involved in asthma

A

mediators

77
Q

what are targeted in treatment of asthma

A

histamine and leukotrienes

78
Q

tachypnea

A

20-45 breaths/min

79
Q

in mild asthma cases, – may be the only symptoms

A

cough

80
Q

drop in systolic P during inspiration

A

pulsus paradoxus

81
Q

O2 saturation in hypoxemia

A

90%

82
Q

treatment of asthma

A

medications and avoid causal agents

83
Q

bronchiectasis

A

irreversible dilation of airways

84
Q

bronchiectasis: destruction of muscular and elastic components of –

A

bronchial walls

85
Q

disease of exocrine glands (may also involve salivary gland dysfunction)

A

cystic fibrosis

86
Q

the cause of bronchiectasis following pneumonia,

A

tuberculosis or fungal infections

87
Q

diagnosis of bronchiectasis

A

high resolution CT scan

88
Q

most bronchiectasis patients have –

A

chronic cough and sputum production

89
Q

complications of bronchiectasis –, recurrent pneumonia, low oxygen levels

A

cor pulmonale

90
Q

treatment of bronchiectasis: –, bronchodilators, physiotherapy

A

antibiotics

91
Q

occasional treatment of bronchiectasis

A

surgical resection

92
Q

rare treatment of bronchiectasis

A

lung transplant

93
Q

long standing hypoxemia is associated with –

A

poor tissue perfusion and CV complications