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pathophysiology > COPD > Flashcards

COPD Flashcards

1
Q

1 cause of COPD

A

cigarette smoking

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2
Q

A heredity deficiency of _____ may result in early onset and severe COPD.

A

alpha-1 antitrypsin

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3
Q

polymorphisms

A

genes that code for TNF, surfactant, proteases and antiproteases

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4
Q
  • airway inflammation and obstruction of the major and small airways
  • chronic productive cough for at least 3 consecutive months over 2 consecutive years
A

chronic bronchitis

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5
Q

Loss of lung elasticity & abnormal enlargement of the airspaces distal to the terminal bronchioles with destruction of the alveolar walls & capillary beds

A

emphysema

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6
Q
  • permanent dilation of the bronchi and bronchioles
  • caused by destruction of the muscle and elastic supporting tissue due to vicious cycles of infection & inflammation
A

bronchiectasis

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7
Q

onset of COPD

A

occurs midlife

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8
Q

clinical features of COPD

A

persistent or worsening dyspnea, chronic cough

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9
Q

pathologic changes in COPD

A

squamous metaplasia of epithelium, parenchymal destruction, mucus gland metaplasia & enlargement

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10
Q

a respiratory disorder largely caused by smoking, characterized by progressive, partially reversible airway obstruction and lung hyperinflation, systemic manifestations, and increasing frequency and severity of exacerbations.

A

COPD

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11
Q

occurs with emphysema due to protease mediated degradation of connective tissue elements in the lungs.

A

loss of lung elastic recoil

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12
Q

occurs due to an imbalance between the lung’s repair and defense mechanisms.

A

Peribronchiolar fibrosis

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13
Q

contributes to airway remodeling

A

fibrosis of the small airways

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14
Q

the persistent changes that occur within the structural components of the airways in response to inflammation.

A

airway remodeling

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15
Q

mucus hyperplasia and increased expression of mucin genes results in…

A

increased airway secretions

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16
Q

due to hyperactivity of the bronchi with bronchoconstriction due to persistent inflammation

A

increased tone in airway smooth muscle

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17
Q

first feature of chronic bronchitis

A

hypersecretion in the large airways

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18
Q

airway obstruction causes….

A

ventilation-perfusion mismatch, hypercapnia, and hypoxemia.

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19
Q

cor pulmonale

A

enlargement of the right ventricle

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20
Q

enzymes that digest proteins

A

proteases

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21
Q

Characterised by a breakdown of elastin in the alveolar septa and bronchial walls as well as breakdown of alveolar and bronchial wall components by proteases

A

emphysema

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22
Q

where are proteases released from?

A

neutrophils, alveolar macrophages and other inflammatory cells

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23
Q

____ contributes to air trapping.

A

decreased elastic recoil in bronchial walls

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24
Q

septal destruction in the alveoli destroys portions of the pulmonary capillary bed causing ______.

A

ventilation-perfusion mismatch and hypoxemia.

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25
Q

the action of elastin is normally inhibited by ____

A

alpha-1-antitrypsin

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26
Q

the most serious a1-antitrypsin deficiency is caused by ___

A

PIZ variant which is found in 5% of the population

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27
Q

what is the most common form of emphysema?

A

Centriacinar emphysema

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28
Q
  • the destruction is confined to the terminal and respiratory bronchioles.
  • upper parts of the lung
A

centriacinar emphysema

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29
Q
  • there is involvement of the peripheral alveoli and later the more central bronchioles.
  • lower parts of the lung
A

panacinar emphysema

30
Q

this form of emphysema is more common in individuals with inherited a1-antitrypsin deficiency

A

panacinar emphysema

31
Q

appearance of barrel chest is due to

A

air trapping

32
Q

expanded thorax results in

A

decreased tidal volume, hypoventilation and hypercapnia

33
Q

____ is a central feature of COPD

A

inflammation

34
Q

leads to damage & remodeling of the lung parenchyma -> airflow limtiation

A

inflammation

35
Q

___ immunity activated at all stages of COPD

A

innate

36
Q

____ immunity activated in more severe disease

A

adaptive

37
Q

____ mediate both types of immunity

A

cytolines

38
Q

___ likely link innate and adaptive immunity in COPD

A

dendritic cells

39
Q

what are the most important inflammatory cells in COPD?

A

neutrophils, macrophages and CD8+ T lymphocytes

40
Q

what are the most important proteases involved in emphysema?

A

Elastases, cathepsins and matrix metalloproteinases

41
Q

secrete inflammatory mediators that active neutrophils and CD8+ T lymphocytes.

A

macrophages

42
Q

secrete inflammatory mediators that active neutrophils and CD8+ T lymphocytes.

A

TNF-a

43
Q

activates macrophages to secrete inflammatory cytokines, chemokines and matrix metalloproteinase.

A

IL-B

44
Q

s a link between innate and acquired immunity and stimulates C-reactive protein release from the liver.

A

IL-6

45
Q

is newly described pro-inflammatory cytokine and is correlated with disease severity.

A

IL-32

46
Q
  • belongs to the IL-7 family
  • plays a role in dendritic cell programming by stimulating specific chemokines which then attract T helper lymphocytes and cytotoxic T lymphocytes
A

Thymic stromal lymphopoeitin (TSLP)

47
Q

induce leukocyte chemotaxis specifically promoting neutrophil activation and migration.

A

Chemockines, growth factors, anti-inflammatory cytokines

48
Q

It plays an important role in regulating energy and is decreased in persons with COPD.

A

leptin

49
Q

An elevated ____ during exacerbations is correlated with the severity of exacerbations

A

serum amyloid A

50
Q

increased ____ has been linked to health and exercise capacity and appears to be a significant predictor of BMI.

A

CRP

51
Q

may be caused by disturbances in ventilation, gas exchange or ventilation-perfusion relationships as well as increase work of breathing or diseases that damage the lung parenchyma.

A

dyspnea

52
Q

occurs as breathing with effort depletes energy stores.

A

fatigue and exercise intolerance

53
Q

is a reflex that is stimulated in COPD by excessive secretions and/or inhaled irritants

A

cough

54
Q

is caused by inflammation in the airways

A

sputum production

55
Q

occurs as air passes through narrowed airways

A

wheezing

56
Q

often seen due to prolonged expiratory phase.

A

hypoventilation

57
Q

may be present related to inadequate gas exchange in COPD.

A

hypoxemia

58
Q

helps to prevent expiratory airway collapse.

A

pursed lip breathing

59
Q

is caused by hypoxemia.

A

cyanosis

60
Q

are caused by abnormal secretions, mucus or fluid in the airways.

A

crackles

61
Q

usually associated with upper airway obstruction

A

inspiratory wheezing

62
Q

usually associated with lower airway obstruction

A

expiratory wheezing

63
Q

indicates more advanced disease

A

FEV1 <80%

64
Q

not always reduced in early stages of COPD

A

FVC

65
Q

confirms airflow limitation

A

FEV1/FVC post-bronchodilatory <0.70

66
Q

main pharmacological therapy for COPD

A

bronchodilators

67
Q

decrease bronchoconstriction by reducing muscle tone and glandular mucus.

A

inhaled anticholingeric

68
Q

It is important to identify the _____ names and what they are prior to administering

A

generic

69
Q

can also be used especially in patients with significant mucus hypersecretion.

A

mucolytics

70
Q

third line treatment

A

methylxanthines

71
Q

the only intervention shown to slow the rate of lung function decline.

A

smoking cessation

pathophysiology (5 decks)

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