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x M2 Respiration > 7. COPD > Flashcards

7. COPD Flashcards

1
Q

what is COPD?

A

disease with progressive airflow limitation that is not fully reversible. associated with abnormal inflammatory response of lungs to toxins (can be smoking)

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2
Q

two types of COPD?

A

chronic bronchitis, emphysema

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3
Q

defn of chronic bronchitis?

A

productive cough on most days for a minimum of 3 mo/year for at least 2 yrs. clinical dx

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4
Q

def of emphysema?

A

enlargement of airspaces distal to the terminal bronchiole, destruction of the alveolar walls. no fibrosis. pathological dx.

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5
Q

risk factors for COPD?

A

cig smoke
occupational dust and particles
environmental tobacco smoke
air pollution

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6
Q

how does exposure to inhaled toxins yield the COPD disease state?

A

inflammatory process in response to the inhaled toxins, neutrophils release proteases, leads to inflammation and loss of elastic recoil

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7
Q

the two main problems in COPD?

A
  1. small airway disease (airway inflammation/remodeling)

2. parenchymal destruction (loss of elastic recoil)

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8
Q

what does the ‘obstructive’ element of COPD refer to?

A

airway narrowing and airflow obstruction

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9
Q

if smoke primarily affects small airways, then the phenotype will be?

A

chronic bronchitis – mucosal inflammation, fibrosis

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10
Q

if smoke primarily affects parenchyma and alveoli, then the phenotype will be?

A

emphysema – disrupted alveolar attachments, loss of elastic recoil

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11
Q

phenotype of chronic bronchitis?

A

productive cough, hypoxia/cyanosis, pulmonary HTN

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12
Q

phenotype of emphysema?

A

breathlessness, cachexia (wasting)

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13
Q

what is alpha-1-anti-trypsin?

A

protein made in liver, inhibitor of circulating proteases in the lungs. (ie, inhibits proteases from damaging lung)

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14
Q

what will happen if someone has an alpha-1-anti-trypsin deficiency? (recessive trait)

A

w this deficiency + cig smoking, will dev COPD earlier on than would with just cigs.

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15
Q

if someone has an alpha-1-anti-trypsin deficiency but does not smoke cigs, will they dev COPD?

A

improbable

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16
Q

using spirometry, how would you dx obstructive disease?

A

based on FEV1/FVC radio. usually lower than 70% of normal.

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17
Q

if FEV1/FVC ratio is low, what are the 3 possible diagnoses?

A
  • chronic bronchitis
  • emphysema
  • CF
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18
Q

what happens with FRC in emphysema?

A

incr due to reduced elastic recoil of the lung. hypervolume

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19
Q

what happens with FRC in chronic bronchitis?

A

FRC is normal, elastic recoil is not affected.

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20
Q

what happens with RV in emphysema?

A

RV is increased due to air trapping. pt is unable to exhale all the air completely.

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21
Q

what happens with RV in chronic bronchitis?

A

RV is increased due to air trapping. pt is unable to exhale all the air completely.

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22
Q

what happens with FVC in emphysema?

A

may be normal or decr, due to air trapping.

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23
Q

what is FVC/VC?

A

total amt of air that can be exhaled after a deep inhalation. dependent on RV.

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24
Q

what happens with FVC in chronic bronchitis?

A

may be normal or decr, due to air trapping.

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25
Q

what is FRC?

A

balance between the outward expansion of the chest wall and the inward/elastic recoil of the lung

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26
Q

what is RV?

A

amt of air in the lungs at the end of forced vital capacity

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27
Q

what is TLC?

A

amt of air in the lungs after a deep inhalation. detd by the elastic recoil of the lungs and insp muscle strength.

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28
Q

what happens with TLC in emphysema?

A

inc due to reduced elastic recoil of the lung

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29
Q

what happens with TLC in chronic bronchitis?

A

normal because elastic recoil is not affected.

30
Q

what happens with DLCO in emphysema?

A

decr due to destruction of the alveolar-cap membranes as a result of proteases

31
Q

what happens with DLCO in chron bron?

A

DLCO is normal (disease is in airways, not gas exchange units)

32
Q

the list of possible treatments for COPD?

A
  • smoking cessation
  • pharm treatments (bronchodilators, glucocorticosteroids, A1AT therapy)
  • 02
  • pulmonary rehab
  • surgery
33
Q

have any drugs been shown to modify the long term decline in lung function?

A

no

34
Q

what do bronchodilators do?

A

inc cAMP which relaxes bronchial smooth muscle.

35
Q

what is the deal with glucocorticosteroids?

A

anti-inflammatory. ok using inhaled. not good for long term oral therapy because side effects outweigh benefits.

36
Q

what does pulmonary rehab consist of?

A

exercise training - most pts with COPD have reduced the physical activities to reduce dyspnea. lungs have become deconditioned.

37
Q

what might exacerbate COPD?

A
  • environmental toxins
  • bacterial infection
  • viral infection
38
Q

how is obstructive airway disease defined?

A

anything that causes an obstruction of flow of air

39
Q

what is the first airway structure without cartilage and sub-mucosal glands? what about muscle in this area?

A

bronchioles. first airway with circumferential smooth muscle (spiral)

40
Q

what are some features of bronchitis that we might see on slides?

A
  • hypersecretion of mucus in airways, goblet cell hyperplasia.
  • clustered inflammatory cells, alveolar macrophages
41
Q

what is a bronchospasm in the setting of COPD

A

spasm of the smooth muscle-surrounded airways. referred to as an asthmatic component to COPD.

42
Q

what can repair of damaged lung look like?

A

either re-epithelialization and restoration, or fibrous remodeling and scarring. re-epithelialization can either be native epithelium or metaplastic.

43
Q

what does resp mucosa generally look like

A

ciliated, pseudostratified with scattered goblet cells

44
Q

what will happen with continuous irritation and inflammation?

A

epithelium undergoes metaplasia. final mucosa may become squamous type. precursor to certain lung cancers

45
Q

what are the three patterns of emphysema (at the alveolar level)?

A
  • centriacinar
  • panacinar
  • distal acinar (aka paraceptal)
46
Q

describe centriacinar emphysema?

A

destruction limited to resp bronchioles and central portions of acinus. most severe in upper lobes, assocd with cig smoking. smoking will damage most proximal tissue first.

47
Q

describe panacinar emphysema?

A

involves entire alveolus distal to the term bronchiole. most severe in lower long, generally develops in pts with A1AT deficiency

48
Q

describe distal acinar emphysema?

A

least common, localizes to fibrous septa or pleurae, leads to bullae formation.

49
Q

in emphysema, what is it that actually destroys the tissue?

A

neutrophil elastase.
macrophage elastase
oxidants/reactive 02 species

50
Q

neutrophil elastase does what?

A

destroys elastin and thus decr elastic recoil. also attacks connective tissue matrix thus degrading the supporting structures of the lung

51
Q

what do oxidants/ROS do?

A

deplete anti-oxidants, incite tissue damage

52
Q

definition of asthma?

A

hyper-responsiveness of tracheobronchial tree, leads to repeated episodes of bronchoconstriction and inflammation.

53
Q

what is atopy?

A

genetic predisposition to type 1 hypersensitivity reaction

54
Q

in asthma, what do the T2 helper cells do?

A

induce bronchial allergic inf response: interleukin secretion and stimulation of B lymphocytes to produce IgE (mast cell, vasodilation, edema)

55
Q

what is the problem with the T2 helper response in asthma?

A

normally T1 and T2 cells maintain balance in our airways. in asthma, there is an imbalance with greater T2 response.

56
Q

what happens when IgE (from T2 activity) triggers mast cell activation?

A

vasodilation, edema. Eosinophils may be recruited which secrete major basic protein which is damaging to epithelium, and causes further constriction.

57
Q

what changes to the airway occur w asthma?

A

fibrosis of submucosa, thickened bronchial smooth muscle which may lead to spasms, thickened mucus secretions

58
Q

bronchiectasis: definition

A

abnormal permanent dilatation of airways that affects airflow. usually secondary to chronic infection.

59
Q

is bronchiectasis reversible

A

nope.

60
Q

The types of cells in alveoli: what do they do?

A

Epithelial cell. comma shaped, flat.
P1 = type I pneumocyte. fragile, is site of gas exchange. cytoplasm is like arms extending out. can be confused with E.
P2 = Type II pneumocyte. has regenerative properties. makes surfactant.
M = macrophage. cleanup.

61
Q

with irritated epithelium, what happens to the relative amts of goblet cells and cilia?

A

in bronchi: make more goblet cells, more mucus. fewer ciliated cells. basically trade pseudostratified tissue for mucus tissue.

62
Q

what is the Reid index?

A

measure of the relative thickness of submucosal tissue to full epithelial surround. if less than 0.4, ok. if greater, consistent with chronic bronchitis

63
Q

what is the difference between normal mucosa and squamous metaplasia?

A

normal: pseudostratified ciliated. every cell hits basement membrane.
squamous met: truly stratified. less ciliated.

64
Q

which type of emphysema pattern is associated with spontaneous pneumothorax?

A

paraseptal (distal acinar)/bullus.

65
Q

in A1AT deficiency, what emphysema pattern will you see?

A

panacinar, because deficiency is everywhere. may also see further damage in bases of lungs because neutrophils tend to congregate there (slightly more bloodflow/perfusion there)

66
Q

what are the 2 types of asthma?

A

intrinsic, extrinsic

67
Q

intrinsic asthma means what?

A

non-allergic. due to cold, exercise, resp tract infections

68
Q

extrinsic asthma means what?

A

allergic. initiated by a type 1 hypersensitivity reaction.

69
Q

asthma: histology?

A
  • incr submucosal mucus glands
  • hypertrophied smooth muscle
  • inflammatory infiltrate with eosinophils
  • thick mucus plug
70
Q

what will you find in the mucus of an asthmatic?

A
  • Charcot Leyden crystals (degranulated eosinophil membranes

- Curschmann spirals – whorls of shed epithelium

71
Q

what characterizes bronchiactesis?

A

permanent airway dilatation. like an old rubber band that will not spring back. brittle.

x M2 Respiration (36 decks)

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