Emphysema

Question 1

Emphysema?

Answer 1

Characterized by the destruction of the alveoli, its walls and its elasticity.

Question 2

What does destruction of alveolar walls and capillary beds cause?

Answer 2

• Loss of compliance (decreased elastic tissue of the alveoli [reduced stretch & recoil when filling/emptying NOT decrease in compliance)
• Enlarged distal airspaces (by destroying the walls adjoining the millions of alveoli, fewer & larger alveoli are created -> decreased SA for exchange)

Question 3

Etiology of emphysema?

Answer 3

• Smoking

- Genetic deficiency of alpha-1 antitrypsin

Question 4

Trypsin?

Answer 4

breaks down proteins in gut, but also breaks down aging structures for regeneration of tissues

Question 5

Alpha-1 antitrypsin?

Answer 5

Opposes the breakdown of protein so that trypsin does not excessively breakdown useful tissue

Question 6

What happens if deficient in alpha-1 antitrypsin?

Answer 6

functional tissue of the respiratory tract is lost (trypsin breaks down walls of alveoli and capillaries)

Question 7

What does alpha-1 antitrypsin do in terms of the lungs?

Answer 7

Protects the lungs from breakdown

Question 8

What inhibits alpha-1 antitrypsin?

Answer 8

smoking

Question 9

Explain the pathology of chronic bronchitis.

Answer 9

Cigarette smoke inhibits alpha 1 antitrypsin (antitrypsin is an inhibitor, so by inhibiting an inhibitor, no inhibition of trypsin exits -> allows trypsin to freely break down structures in the respiratory tract causing damage. The activity of trypsin is no longer limited but the concentration of the protease remains the same. Smoke also attracts inflammatory cells to the area (lungs). Inflammation -> inflammatory damage (on top of the damage being caused by trypsin) Furthermore, inflammatory cells can result in a release of more trypsin (increase concentration of trypsin) -> trypsin is usually helpful in aiding healthy tissue regrowth by breaking down tissue to regenerate new functional tissue, but with an increase concentration and no limitation of trypsin activity, sever damage to the alveoli occurs. Trypsin destroys the alveolar walls.

Question 10

When alpha-1 antitrypsin is inhibited, what happens to the concentration and limit of trypsin?

Answer 10

Trypsin is no longer limited but the concentration of the protease remains the same.

Question 11

What is the result of trypsin destroying the alveolar walls?

Answer 11

instead of many many little air sacs with walls dividing them providing surface area for gaseous exchange, the destruction of wall surface results in larger air pockets and less surface area for gas exchange.

Question 12

Is the destruction reversible?

Answer 12

NO it is irreversible resulting in permanent distended air spaces where there is no gas exchange

Question 13

Bullae?

Answer 13

Large airspaces

Question 14

Blebs?

Answer 14

Small airspaces

Question 15

Where does air become trapped and what does this cause?

Answer 15

Between alveoli -> causes an increase in the work of breathing

Question 16

What will be the ventilation:perfusion ratio?

Answer 16

It will be normal. This does not reflect their level of health, as the only reason it is normal is that both ventilation and perfusion are impaired..

Question 17

Why is ventilation impaired?

Answer 17

D/t the increase of dead space (area where no gaseous exchange takes place)

Question 18

Why is perfusion impaired?

Answer 18

B/c the capillaries that adjoin alveoli are also damaged in the process

Question 19

Acinus?

Answer 19

refers to the functional unit of the respiratory system (includes terminal bronchioles, respiratory bronchioles, and alveoli)

Question 20

Acini?

Answer 20

lobed sacs containing groups of alveoli

Question 21

What are the 2 types of emphysema?

Answer 21

1. centrilobular

2. panacinar

Question 22

What is centrilobular also referred to as?

Answer 22

Centriacinar or proximal acinar

Question 23

Centrilobular?

Answer 23

When most of the damage occurs in the terminal and respiratory bronchioles, while the alveoli are mostly intact

Question 24

Panacinar?

Answer 24

when there is damage to the entire acinus (branches+alveoli)

Question 25

Do these individuals spend more time in exhalation or inhalation?

Answer 25

In exhalation

Question 26

Manifestations of emphysema

Answer 26

• insidious onset
• dyspnea
• increased ventilatory effort
• barrel chest
• hypoxemia & hypercapnia
• pursed lip breathing and nasal flaring

Question 27

Why does dyspnea occur?

Answer 27

• d/t decrease gas exchange and hypoxia

- d/t decrease lung volume by destruction and increased dead space

Question 28

Is dyspnea on rest or exertion or both?

Answer 28

Initially on exertion only, later on exertion and rest

Question 29

How do you know that a pt has increased ventilatory effort?

Answer 29

Evidence by use of accessory muscles

Question 30

Barrel chest?

Answer 30

The chest becomes fixed in an inspiratory position because air is trapped between alveoli

Question 31

What is the normal ratio of APD:TD?

Answer 31

1:2

Question 32

What is the ratio in pt with barrel chest and why?

Answer 32

In a pt with barrel chest the anteroposterior diameter is significantly higher resulting in a ratio of 1:1 or even 2:1
[these individuals use there accessory muscles all the time, even when resting]

Question 33

When do individuals with barrel chest use their accessory muscles?

Answer 33

All the time, even when resting