Obstructive Lung Disease-Parks, Baker

Question 1

Give the def for...
total lung capacity
vital capacity
tidal volume
functional residual capacity
inspiratory capacity
inspiratory reserve volume
expiratory reserve volume
residual volume.

Answer 1

total lung capacity–Everything! VC + RV
vital capacity: How much you can breathe in & out if you try really hard
tidal volume: how much you breathe in & out normally
functional residual capacity: the extra air you can expire if you try really hard + RV
inspiratory capacity: the amount of air you normally breathe in + the amount you can breathe in if you try really hard
inspiratory reserve volume: the extra air you can only breathe in if you try hard
expiratory reserve volume: the amount of air you can expire if you try hard
residual volume: the amount of air that remains in your lungs & you can’t expire

Question 2

OF the following which can't be measured?
total lung capacity
vital capacity
tidal volume
functional residual capacity
inspiratory capacity
inspiratory reserve volume
expiratory reserve volume
residual volume.

Answer 2

Can’t measure RV or TLC. Need body plethysmography for that.

Question 3

What can be normally measured in an in-office spirometry test? What do they mean?

FVC (L)
FEV1 (L)
FEV1/FVC
PEF (L/min)
FEF 25-75 (L/s)
FET (s)

Answer 3

FVC (L): vital capacity
FEV1 (L): amount of air expired in first second
FEV1/FVC: ratio
PEF (L/min): peak expiratory flow–>how fast the air is coming out
FEF 25-75 (L/s): looks @ flow when 25%-75% of air is out
FET (s): dunno!

Question 4

What can be measured in a full PFT w/ spirometry & body plethysmography? Explain.

Answer 4

Body plethysmography is like a person breathing in a closed box. Obeys Boyle’s Law: P1V1=P2V2. Measure the pressure change in the box when they breathe in & out to calculate residual volume & total lung capacity.
Also measures DLCO: looks @ gas exchange across alveoli from air–>blood by measuring transfer of CO. If you have compromised alveoli from emphysema–>will have decreased DLCO.

Question 5

What will happen to the following in a person with Obstructive pulmonary disease? 
FEV1
FVC
FEV1/FVC
FEF25-75
TLC
RV

Answer 5

FEV1: down
FVC: down
FEV1/FVC: down
FEF25-75: down
TLC: up
RV: up

Question 6

Why does RV & TLC increase in obstructive lung disease?

Answer 6

b/c air builds up & can’t be expired.

eventually can pop your lung-pneumothorax.

Question 7

What are the subtypes of obstructive pulmonary disease?

Answer 7

COPD: chronic bronchitis, emphysema
asthma
bronchiectasis

Question 8

What is the funny name for chronic bronchitis & emphysema?

Answer 8

chronic bronchitis: blue bloaters

emphysema: pink puffers

Question 9

What is the prevalence of COPD? Men & women? Biggest risk factor?

Answer 9

6.2%
men a little less than women
smoking is the biggest risk factor, but only 10-15% of smokers develop COPD.

Question 10

What are some trends that we have seen since the 1960s w/ respect to COPD & smoking?

Answer 10

COPD & asthma deaths have increased since the the 1960s, while other causes of death have decreased.
Tobacco use peaked in the 1960s.

Question 11

How many cigarettes in a pack?

Answer 11

20

Question 12

How does Nevada stack up w/ COPD & deaths etc?

Answer 12

COPD deaths & prevalence high in NV

Question 13

WHat happened in 2000 w/ respect to men & women & COPD?

Answer 13

the number of deaths by COPD in women exceeded those in men.

Question 14

What are the 4 leading causes of death as of 2010?

Answer 14

1. Heart disease
2. Cancer
3. COPD, asthma
4. cerebrovascular
   * *note: smoking is very responsible for #3, and can contribute to numbers 1-4.

Question 15

How is emphysema defined?

Answer 15

anatomically

Irreversible enlargement of the airspaces distal to the terminal bronchioles
Airspace wall destruction without fibrosis

Question 16

What are the 4 types of emphysema? Which 2 are the most important?

Answer 16

1. centriacinar-important & most common!
2. panacinar–important & less common
3. paraseptal
4. irregular

Question 17

Describe the characteristics of centriacinar emphysema.

Answer 17

Most common (>95%)
Initial sparing of the distal acinus.  Involved later. Targets resp bronchioles first.
Upper lobes/apical segments
Associated with heavy smoking
Walls with black pigment
Associated with chronic bronchitis

Question 18

Describe the characteristics of panacinar emphysema.

Answer 18

Less common
Airspace enlargement from respiratory bronchiole to alveoli (no sparing). Begins by targets alveolar ducts & alveoli.
Lower lobes/anterior margins
Most severe at the lung bases
Associated with α1-antitrypsin deficiency

Question 19

What is the pathogenesis of emphysema?

Answer 19

You smoke & put nicotine & ROS in your body.
Nicotine promotes inflammation.
ROS causes release of IL8, LTB4, TNF, promoting inflammation.
ROS also inactivates alpha 1 AT.
Have lots of neutrophils b/c of inflammation, not enough alpha 1 AT & you get a large release of elastase!
Elastase destroys the elastic tissue of alveoli.
They dilate & lose their elastic recoil.
OBSTRUCTIVE PULM DISEASE!
If you have alpha 1 AT deficiency congenitally, at much greater risk for this pathology.

Question 20

Describe the genetics of alpha 1 antitrypsin deficiency.

Answer 20

Pi (Proteinase inhibitor) locus of chromosome 14
“M” allele & “Z” allele
PiM x 2 copies = PiMM
Normal
PiZ x 2 copies = PiZZ
Panacinar Emphysema-prob get emphysema no matter what.
PiM + PiZ = PiMZ
Typically has reduced levels of α1AT, but asymptomatic
However, add smoking and risk increases significantly. Maybe ok if they don’t smoke.

Question 21

What is a bleb?

Answer 21

a piece of thinned lung tissue on a lung w/ emphysema that is like a balloon & easy to pop.
If it pops–>pneumothorax.

Question 22

What are ways by which you can get obstructive physiology?

Answer 22

1. Loss of elastic recoil (increased elastase)
2. Small airway inflammation
   - mucus plugging (via goblet cell metaplasia)
   - just a bunch of inflammatory cells up in there!
   - smooth muscle hypertrophy & peribronchial fibrosis