Emphysema

Question 1

emphysema

Answer 1

permanent tissue damage to airway, alveoli, and capillaries (all of parenchyma and vasculature)

Question 2

what does emphysema cause?

Answer 2

• enlarged distal airspaces (by destroying the walls adjoining the millions of little alveoli, fewer and larger alveoli are created -> decreased SA for gas exchange)
• l/o compliance (decreased elastic tissue of alveoli -> decreased stretch and recoil when filling & emptying)

Question 3

etiology

Answer 3

• smoking

- genetic deficiency of alpha-1 antitrypsin (~1% of all COPD)

Question 4

explain genetic deficiency of alpha-1 antitrypsin

Answer 4

• trypsin breaks down proteins in gut, but also breaks down aging structures for regeneration of tissues
• alpha-1 being the subclass and trypsin referring to the enzyme responsible for breaking down proteins
• alpha-1 antitrypsin opposes breakdown of protein so that trypsin doesn’t excessively break down useful tissues (manages proteases)
• if deficient in a1 antitrypsin, then functional tissue of the RT is lost (antitrypsin breaks down walls of alveoli and capillaries)
• a1 antitrypsin (antiprotease) protects the lungs from breakdown

Question 5

patho

Answer 5

• cigarette smoke inhibits a1 antitrypsin
• smoke attracts inflammatory cells to the lungs
• trypsin destroys alveolar walls -> larger air pockets and less SA for gas exchange
• both ventilation and perfusion are impaired

Question 6

explain how cigarette smoke inhibits a1 antitrypsin

Answer 6

• it opposes the effects of the antiprotease that suppresses trypsin’s actions, and allows trypsin to freely break down structures in the RT causing damage
• activity of trypsin is no longer limited but [protease] is the same

Question 7

explain what happens when smoke attracts inflammatory cells to the lungs

Answer 7

• inflmtn -> inflammatory damage
• inflammatory cells result in a release of more trypsin (increased [protease]) -> increase [ ] and no limitation of trypsin’s activity -> severe damage to alveoli occur

Question 8

explain destruction of alveolar walls

Answer 8

• its irreversible, resulting in permanent distended air spaces where there’s no gas exchange
• air becomes trapped between alveoli = increased work of breathing
• bullae and blebs: air spaces pushing against pleura

Question 9

why are ventilation and perfusion impaired?

Answer 9

• ventilation is impaired d/t increased dead space b/c of air spaces between alveoli
• perfusion is impaired b/c capillaries that adjoin alveoli are also damaged

Question 10

types of emphysema

Answer 10

1) centrilobular (aka centriacinar or proximal acinar)

2) panacinar

Question 11

centrilobular emphysema

Answer 11

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

Question 12

panacinar emphysema

Answer 12

damage to entire acinus (branches + alveoli)

Question 13

acinus

Answer 13

• functional unit of respiratory system

- includes terminal bronchioles, respiratory bronchioles, and alveoli

Question 14

acini

Answer 14

lobed sacs containing groups of alveoli