Pulmonary: Restrictive Lung Diseases

Front 1

What feature do all restrictive lung diseases have in common?

Back 1

The are associated with decreased lung or chest wall distensibility (compliance)

Front 2

Restrictive Lung Disease
1) Does TLC increase or decrease?
2) Why?

Back 2

1) Decrease
2) Because the CW cannot expand the lungs to such a degree anymore because they are less compliant. The same amount of CW pressure will be move the lungs less.

Front 3

Restrictive Lung Disease
1) Does FRC increase or decrease?
2) Why?

Back 3

1) Decrease
2)Because although the CW recoil will remain the same, the force exerted by the lungs (inward recoil) will be greater. This will shrink the lungs.

Front 4

Restrictive Lung Disease
1) Does Residual Volume increase or decrease?
2) Why?

Back 4

1) Decrease
2) Small airways are tethered open by recoil pressure. They do not shut until lower lung volume.

Front 5

Restrictive Lung Disease
1) Does Tidal Volume increase or decrease?
2) Why?

Back 5

1) decrease
2) TLC decreases proportionally more than residual volume

Front 6

Restrictive Lung Disease
1) Does FEV1 increase or decrease?
2)Does FEV1/FVC increase or decrease?
3) reconcile these two facts.

Back 6

1) decrease
2) Same
3) They decrease proportionally. The amount of expelled air is decreased, but the rate is unchanged.

Front 7

Name three types of molecules that can be found in the interstitial matrix

Back 7

collagen
elastins
Proteoglycans

Front 8

1) What does diffusion capacity measure
2) What two factors go into diffusion capacity its basic form
3) Which on is increased in restrictive lung disease? Does this increase or decrease diffusion capacity?
4) What is the significance of it being called "D1CO" in the PFT

Back 8

1) The ability of the lung to transfer gasses
2) Partial Pressure gradient, gas, surface area (not actually in the constant obviously) thickness of barrier
3) Increased thickness of barrier- interstitial fibrosis decreases diffusion capacity
4) We use Carbon monoxide to test diffusion capacity because it binds so tightly to hemoglobin once taken up. This means that no back-pressure is generated and flow of the gas will be one way

Front 9

1) Does the decreased diffusion capacity due to interstitial thickening in restrictive lung disease decrease Arterial P02 at rest
2) Why?
3) When does it decrease arterial PO2
4) Why does this occur
5) What other characteristics of restrictive lung disease predispose to decreased arterial CO2

Back 9

1) No
2) Although the mural thickness is increased, the RBC is in the capillary long enough that it can afford to equilibrate more slowly. It is generally in there for .75 seconds. Healthy lungs equilibrate with blood in .25 seconds, while restricted lungs may take up to .5 seconds. This is still enough time.
3) During ecercise
4) Arterial transit time is decreased down below the ~.5 seconds it is taking the blood to equilibrate with the air across the thickened alveolar wall. Thus, it is leaving with some CO2 and not enough O2
5) In normal people, we would simply ecruit more capilaries such that the lungs could accomodate a larger CO without decreasing RBC transit time. Obliteration of capillaries in RLD makes this impossible and transit time must be reduces.

Front 10

What two factors cause hypoxemia at rest in RLD?

Back 10

1) Airway distortion causes can cause low V to airways wht have high Q
2) Heterogeneous dispersion of compliance across the lung parenchyma. This can also cause V/Q mismatch by preferentially ventilating areas of greater compliance.

Front 11

Does CO2 equilibrate faster or slower across the alveolar/capillary barrier than O2. Why?
2) Why do some people screw this up?
3) Does Arterial PCO2 go up, down, or nowhere in RLD?

Back 11

1) about same, because although it has a higher ability to diffuse, it takes a long time to bind to hemoglobin. This creates some active equilbration in both directions rather than "one-way flow"
2) Because Co2 actually diffuses faster, it is made slower by its binding properties.
3 Same, because we can blow it off by increasing minute ventilation

Front 12

Name two reasons that RLD pathophysiology causes exercise to cause more decrease in arterial O2 than one would expect if the only finding in RLD was interstitial thickening.

Back 12

1) In normal people, we would simply recruit more capillaries such that the lungs could accommodate a larger CO without decreasing RBC transit time. Obliteration of capillaries in RLD makes this impossible and transit time must be reduced,

2)Pulmonary HTN due to the disease may cause decreased CO by the left heart causing tissue hypoperfusion. This will cause a decrease in mixed venous PO2 which cannot be made up for because the lung is already shot on time to accomplish gas equilibration.

Front 13

There are a ton of diseases/causes for RLD. What one group did we learn about extensively in Path?

Back 13

Interstitial Pneumonia

Front 14

What are some fact about the patient that modify their likelihood of having a specific cause of RLD.

Back 14

AGE
SEX
Cigarettes
Meds (Past and present)
Exposures

Front 15

What are some physical exam signs that can have implication suggesting a cause of RLD?

Back 15

dysphagia
sinusitis
arthritis/arthralgia
skin changes
telangiectasias
calcinosis (Ca++ deposit in soft tissue)
Sclerodactyly (skin tightness in fingers and toes)

Front 16

What radiological study is used in trying to dertimine a ause of RLD?

Back 16

High resolution CT scan.

Front 17

Why does each of these things decrease the ability of the lung to exchange gas?
1) emphysema
2) surgical resection
3)Interstitial fluid or inflammation
4)interstitial scarring
5) anemia
6) pulmonary emboli

Back 17

1)Loss of surface area and VC
2) Loss of SA
3) Thicker wall
4) Thicker wall and smaller V
5) Slower uptake means higher back pressure
6) Decreased VC