Obstructive diseases (Chapter 4) Flashcards

1
Q

Areas that can cause increased resistance to airflow

A

1) Inside the lumen
2) in the wall of the airway
3) in the peribronchial region

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2
Q

Causes of resistance to airflow in lumen

A

Due to partial obstruction of the airway lumen

  • excessive secretions (chronic bronchitis)
  • pulmonary edema (acutely)
  • aspiration of foreign material
  • postoperatively with retained secretions
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3
Q

Causes of resistance to airflow in the wall of the airway

A
  • contraction of bronchial smooth muscle (asthma)
  • hypertrophy of mucous glands (chronic bronchitis)
  • inflammation and edema (bronchitis and asthma)
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4
Q

Causes of resistance to airflow in the peribronchial region

A
  • destruction of lung parenchyma may cause loss of radial traction and consequent narrowing (i.e. emphysema)
  • bronchus compressed locally by an enlarged lymph node or neoplasm
  • peribronchial edema can cause narrowing
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5
Q

Chronic obstructive pulmonary disease

A
  • term applied to patients who have emphysema, chronic bronchitis or a mixture of the two
  • it is often hard to distinguish between chronic bronchitis and emphysema –> therefore COPD is convenient, nondescript label that avoids making false diagnosis
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6
Q

Emphysema -what characterizes it

A

-enlargement of the air spaces distal to the terminal bronchiole with destruction of their walls (anatomic definition - diagnosis is presumtive in living patient - can’t dissect when living!!)

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7
Q

Typical histologic appearance of emphysematous lung

A
  • loss of alveolar walls and consequent enlargement of airspaces
  • destruction of part of the capillary bed
  • strands of parenchyma containing blood vessels coursing across large dilated airspaces
  • small airways are narrowed, tortuous and reduced in number
  • thin, atrophied walls of small airways
  • some loss of larger airways
  • structural changes well seen with naked eye
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8
Q

What structures are affected in emphysema (location)

A

The parenchyma distal to the terminal bronchioles (the acinus)

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9
Q

Types of emphysema

A
  • acinus may not be damaged uniformly - how it is damaged categorizes the type of emphysema
    1) Centriacinar emphysema - destruction limited to the central part of the lobule (peripheral alveolar ducts and alveoli unscathed)
    2) Panacinar emphysema -distension and destruction of the whole lobule
    3) Paraseptal emphysema - disease most marked in the lung adjacent to the interlobular septa
    4) Bullous emphysema-large cystic areas or bullae develop
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10
Q

Topographic distribution of centriacinar emphysema

A
  • more marked in the apex of the upper lobe

- spreads down the lung as the disease progresses

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11
Q

Why centriacinar emphysema starts in the apex - hypothesis

A

-higher mechanical stresses in this area which predispose to structural failure of the alveolar walls

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12
Q

Panacinar emphysema topographic distribution

A

-no regional preference or possibly is more common in the lower lobes

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13
Q

When is it difficult to distinguish between the two types of emphysema

A

When emphysema is severe + these may coexist in one lung

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14
Q

Emphysema associated with alpha1-antitrypsin deficiency

A
  • in patients who are homozygous for the Z gene
  • frequently develop severe panacinar emphysema which usually begins in the lower lobes
  • disease usually becomes evident by age 40 and often occurs without a cough or smoking history
  • heterozygotes do not seem to be at risk
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15
Q

Pathogenesis of emphysema

A

hypothesis..
-excessive amounts of the enzyme lysosomal elastase are released from the neutrophils in the lung
-results in destruction of elastin = important structural protein
+
-neutophil elastase cleaves type IV collagen (important in determine the strength of the thin side of the pulmonary capillary and therefore the integrity of the alveolar wall)

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16
Q

Cigarette MOA development emphysema

A

1) stimulates macrophages to release neutrophil chemoattractants (such as C5a)
2) reduces the activity of elastase inhibitors
3) Exagerration