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Respiratory > Pathology of Obstructive Diseases > Flashcards

Pathology of Obstructive Diseases Flashcards

1
Q

What is atelectasis?

A

Incomplete expansion of the lung of collapse of previously inflated lung

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2
Q

What is the major issue with atelectasis?

A

Predisposes to infx

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3
Q

What is the resorptive type of atelectasis? What happens to the mediastinum with this?

A

Atelectasis that follows complete airway obstruction

Mediastinum will shift toward the affected side

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4
Q

What is compressive atelectasis? What happens to the mediastinum with this?

A

Excessive air, fluid, blood etc in pleural space causing compression

Mediastinum will shift away from the affected lung

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5
Q

What is patchy atelectasis? What usually causes this?

A

Loss of surfactant, usually post surgical complication

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6
Q

What is contraction atelectasis?

A

FIbrosis around the lung causing collapse

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7
Q

Which way does the trachea/mediastinum shift with a tension pneumothorax?

A

Away from the affected lung

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8
Q

What are the two primary causes of pulmonary congestion and edema?

A
  • Hemodynamic disturbances

- Microvascular injury

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9
Q

What happens in ARDS?

A

Breakdown of capillary cell walls and lung interstitium usually due to sepsis

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10
Q

What are the hemodynamic disturbances that can cause pulmonary edema?

A

Increased hydrostatic pressure from heart failure

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11
Q

What are the gross characteristics of pulmonary edema?

A

Heavy, wet lungs

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12
Q

What are the histological characteristics of hemodynamic pulmonary edema? (3)

A
  • Engorgement of alveolar capillaries
  • Intraalveolar HF cells
  • Fibrosis
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13
Q

What is transudate?

A

extravascular fluid with low protein content and a low specific gravity (

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14
Q

What is exudate?

A

any fluid that filters from the circulatory system into lesions or areas of inflammation.

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15
Q

What is the microvascular injury type of pulmonary edema?

A

Capillaries of alveolar septa. Either the endothelial cells, or the alveolar epithelial cells

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16
Q

What are the localized forms of microvascular injury type forms of pulmonary edema?

A

Pneumonia and ALI

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17
Q

What is the systemic form of microvascular injury type forms of pulmonary edema?

A

ARDS

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18
Q

What are the four major obstructive diseases?

A
  • Emphysema
  • chronic bronchitis
  • asthma
  • bronchiectasis
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19
Q

What is COPD?

A

Emphysema + chronic bronchitis

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20
Q

What is the main feature of obstructive pulmonary disease?

A

Air cannot get out of the lung efficiently

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21
Q

What is the main feature of restrictive pulmonary disease?

A

Air cannot get in the lung efficiently

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22
Q

Which of the obstructive diseases is/are reversible?

A

Asthma

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23
Q

What is the pathophysiology behind emphysema?

A

Breakdown of the elastin in alveoli, causing overexpansion

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24
Q

Which airways are primarily affected with emphysema?

A

Small airways–acinus and respiratory bronchioles

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25
Q

Which airways are primarily affected with chronic bronchitis?

A

Large airways–trachea and bronchi

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26
Q

What is the pathophysiology with chronic bronchitis?

A

Airway inflammation, causing mucus plugging

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27
Q

What is the pathophysiology behind asthma?

A

Bronchial hyperresponsiveness

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28
Q

What part of the airways are primarily affected with bronchiolitis? What happens here?

A

Bronchioles–fibrosis causes airway obstruction

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29
Q

What is the anatomic site affected with asthma?

A

Bronchi

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30
Q

What is the anatomic site affected with bronchiectasis? What happens here? Cause?

A

bronchus–breakdown of the airways due to an excessive inflammatory response. Involved bronchi become enlarged and thus less able to clear secretions

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31
Q

What are the ssx of bronchiectasis?

A

Productive, purulent cough, fever

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32
Q

In which obstructive lung diseases does tobacco play a major role?

A

Emphysema
Chronic bronchitis
Bronchiolitis

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33
Q

Which of the obstructive disorders primarily present(s) with wheezing?

A

asthma

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34
Q

Which of the lung volumes increase in obstructive diseases? What causes this?

A

Residual volume due to obstruction or loss of recoil (as in COPD)

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35
Q

What happens to the FVC1 with obstructive airway disease?

A

Decreases

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36
Q

What happens to FVC1/FVC with obstructive lung diseases?

A

Decreases

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37
Q

What happens to TLC and FVC with obstructive diseases?

A

Normal to increased

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38
Q

What happens to TLC with restrictive diseases?

A

Decreases

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39
Q

What happens to FVC with restrictive diseases?

A

Decreases

40
Q

What happens to FEV1/FVC in restrictive lung diseases? Why?

A

Normal–both FEV1 and FVC decrease since there is not a problem with getting air out, just how much that can be held

41
Q

Ssx of emphysema are not apparent until what fraction of the pulmonary parenchyma are incapacitated?

A

1/3

42
Q

What is the definition of emphysema?

A

Irreversible enlargement of airspaces distal to the terminal bronchioles without fibrosis

43
Q

What are the two major causes of emphysema?

A

Smoking and environmental pollutants

44
Q

What is the pathogenesis of COPD?

A

Smoking causes PMNs to increase in the lungs, which release elastase.

45
Q

What is notable about macrophages specifically in the role of COPD?

A

Macrophage elastase is not inhibited by alpha-1-antitrypsin.

Also release metalloproteases

46
Q

What is the oxidant model of COPD?

A

Oxidants in cigarette smoke and free radical formation inhibit antiprotease and cause damage

47
Q

What is the role of alpha-1-antitrypsin?

A

Inhibits elastase

48
Q

What are the cytokines that increase PMNs in the alveoli? (3)

A

IL-8
LTB4
TNF

49
Q

What causes the cirrhosis with alpha-1-antitrypsin deficiency?

A

Buildup of protein in the liver

50
Q

What is the gene that is mutated in alpha-1-antitrypsin?

A

PiMM goes to PiZZ

51
Q

What is the major functional difference between smoking induced COPD and alpha-1-antitrypsin induced?

A

Smoking merely inhibits antitrypsin, while alpha-1-antitrypsin causes a decrease in antitrypsin

52
Q

What is the stain that highlights antitrypsin in the liver?

A

PAS

53
Q

What is the anatomic site of smoking induced emphysema? How about for alpha-1-antitrypsin?

A 
smoking = centriacinar
alpha-1-antitrypsin = panacinar
54
Q

What are the four anatomic locations of emphysema? Which is clinically insignificant?

A

Centriacinar
Panacinar
Paraseptal
Irregular*-insignificant

55
Q

What is paraseptal emphysema?

A

lesion in the distal acinar, adjacent to areas of fibrosis, scarring, or atelectasis

56
Q

What is irregular emphysema?

A

Airspace enlargement with fibrosis

57
Q

What is centriacinar emphysema?

A

Respiratory bronchioles are fragmented with loss of septal tissue, creating enlarged areas

58
Q

Where in the lungs is the greatest damage with centriacinar emphysema?

A

Apical lungs

59
Q

What is panacinar emphysema?

A

Acini are uniformly enlarged from respiratory bronchioles to terminal blind alveoli

60
Q

Where is the lungs is panacinar emphysema most common?

A

Basilar portions

61
Q

Which two types of emphysema commonly occur together?

A

Panacinar and centriacinar

62
Q

What is distal acinar (paraseptal) emphysema? Where in the lung is this usually found?

A

Enlargement with destruction of the distal portion of the acinus, worst in the upper lung zones, adjacent to the pleura

63
Q

What is distal acinar (paraseptal) emphysema usually associated with? Why?

A

Spontaneous pneumothorax

d/t cyst like structure that form rupturing

64
Q

What are the histological characteristics of distal acinar (paraseptal) emphysema?

A

Scarring, fibrosis, or atelectasis

Cyst like structures

65
Q

What is irregular emphysema?

A

Acini are irregularly involved, but are scarred and inflamed

66
Q

What is bullous emphysema? What is the major complication associated with this?

A

Subpleural emphysematous spaces that are greater than 1-2 cm in diameter

Can give rise to a pneumothorax

67
Q

What are the three major causes of death from emphysema?

A
  • respiratory acidosis/coma
  • Right heart failure
  • Massive pneumothorax
68
Q

What is the treatment for emphysema?

A

Bronchodilators

Steroids

69
Q

What is pink puffer?

A

Pt with severe emphysema, who overventilation but achieves adequate respiration

70
Q

What are blue bloaters?

A

Chronic bronchitis leads to hypercapnia and abundant sputum production

71
Q

What is the clinical definition of chronic bronchitis?

A

Persistent cough with production of sputum for at least 3 months of year, for 2 consecutive years

72
Q

What is the most common cause of chronic bronchitis?

A

cigarette smoking

73
Q

What is chronic bronchitis? What is it characterized by?

A

Chronic inflammation of the airways, characterized by hypertrophy of submucosal glands, and goblet cell metaplasia

74
Q

What is bronchiolitis obliterans?

A

obliteration of the lumen of bronchioles secondary to fibrosis from chronic bronchitis

75
Q

What is the Reid index?

A

Fraction of the submucosa (from BM to the cartilage) that is taken up by glands.

76
Q

What are the ssx of chronic bronchitis?

A

Persistent cough and sputum production, leading to outflow obstruction

77
Q

What are the non-neoplastic complications of chronic bronchitis?

A

Pulmonary HTN and HF

78
Q

What are the neoplastic complications of chronic bronchitis?

A

Squamous metaplasia and dysplasia of bronchial epithelium

79
Q

What are the two common infectious bacteria that cause chronic bronchitis?

A

H. Influenza

Strep Pneumonia

80
Q

What are the two common infectious viruses that cause chronic bronchitis?

A

Adenovirus

RSV

81
Q

How does cigarette smoking predispose patients to chronic bronchitis? (2)

A

Interfere with mucociliary escalator, and directly damaging the epithelium

82
Q

What is the elastic recoil like in emphysema? Chronic bronchitis?

A 
Emphysema = low
Bronchitis = normal
83
Q

When does a cough usually present with chronic bronchitis? Emphysema? How does this compare to the SOB with each?

A

Early with bronchitis
Late with emphysema

Flipped for dyspnea

84
Q

Which can lead to pulmonary HTN: chronic bronchitis or emphysema?

A

Bronchitis

85
Q

What are the CXR findings for chronic bronchitis? Emphysema?

A

Bronchitis = prominents vessels

COPD= hyperinflation

86
Q

What are the histological changes with chronic bronchiolitis? (3)

A

Goblet cell metaplasia with fibrous thickening of the wall and increased smooth muscle

87
Q

What are the long term complications of asthma?

A

chronic bronchitis or cor pulmonale

88
Q

What is status asthmaticus?

A

Unremitting asthma attack

89
Q

What are the two important questions to ask patients with asthma Why?

A

Have you been hospitalized or intubated for it

Increased probability of mortality

90
Q

What is atopic asthma? Non-atopic?

A

Atopic = Type I hypersensitivity

Non-atopic = idiopathic

91
Q

What are the cytokines released by Th2 cells in allergic asthma? (2)

A

IL-4

IL-5

92
Q

What is the major immune cell response to asthma?

A

Th2

93
Q

What is the early phase of allergic asthma?

A

antigen exposure causes asthmatic attack within 30 minutes

94
Q

What is the late phase of allergic asthma?

A

4-8 hours after initial attack, with new cells binding to left-over IgE triggering another attack

95
Q

Why is the vagal nerve stimulated to cause contraction in asthma?

A

Destruction of epithelial cells

96
Q

What are the two findings of asthma with alveolar lavage? What are each of these?

A

Curschmann spirals = whorls of shed epithelium

Charcot-Leyden crystals = crystalloids of eosinophilic proteins

Respiratory (34 decks)

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