First year physio questions

Question: What textbook are you using? We can probably get the answers

1. Compliance would be lower. Surfactants, however, such as lipoprotein surfactants, reduce the surface tension of the fluid layer lining the lungs by disrupting the hydrogen bonds, increasing lung compliance and permitting lung inflation.

The ability of the lungs to reversibly change shape can be quantified using two parameters. One of these parameters is compliance, which is a measure of how easy it is to stretch the lung (during inhalation). The other measure is elastance, which is a measure of how readily the lung returns to its original shape (during exhalation). A highly compliant lung stretches more in response to a pressure change than does a less compliant lung. Compliance is a function of the change in lung volume divided by the change in transpulmonary pressure (delta_V / delta_P). Therefore, for a highly compliant lung, generating the same transpulmonary pressure upon inhalation will result in greater filling of the lung, which is desirable. A force that resists lung inflation (and thus reduces compliance) is surface tension of the thin layer of liquid that exists in the small airways and alveoli. Surface tension is generated mostly through hydrogen bonding, and causes two wet surfaces to stick together. This is detrimental to lung filling. For example, in premature human babies, surfactants are not present in the lungs in sufficient amounts to contribute to lung compliance, which makes breathing difficult. Surfactants, however, such as lipoprotein surfactants, reduce the surface tension of the fluid layer lining the lungs by disrupting the hydrogen bonds, increasing lung compliance and permitting lung inflation.

2. Read the description above for a complete explanation.

3. Fibrosis involves gradual exchange of normal lung parenchyma with fibrotic tissue. The replacement of normal lung with scar tissue causes irreversible decrease in oxygen diffusion capacity. In addition, decreased compliance makes pulmonary fibrosis a restrictive lung disease.

4. Upper airways.

5. Moderate to high-altitude living increases red-blood-cell concentrations because the body needs to compensate for the lack of oxygen at high altitudes. In order to increase oxygen count in the blood, more red blood cells are used so that more hemoglobin is available to carry more blood with every breath. This may give athletes a boost by giving them more endurance and stamina when they go back to normal conditions.

6. Blood returning to the heart from the tissues has a low PO2 (40 mmHg) and travels to the lungs via the pulmonary arteries.

7.

8. In emphysema there is actual breakdown of the alveoli; the tiny air sacs where oxygen and carbon dioxide are exchanged in the lungs. When they are broken down they are replaced with scar tissues and and a loss of surface area. Also the capillaries and tissues supporting these alveoli become damaged as well, losing elasticity. Gaseous exchange begins to drop more and more gradually. When emphysema is really bad the lungs begin to collapse and the person ends up needing a oxygen tank at all times to help breath or a respirator.

The text book is called Human Physiology: an integrated approach

Ya it's called Human Physiology: an integrated approach. Any ideas on 7? Thank you so much for the help Bio_man!

For #8:

In one type of inherited emphysema, the amino acid lysine replaces serine at the number 53 position of the enzyme anti-elastase. The change in amino acid sequence alters the protein’s three-dimensional structure, and enzyme activity drops to 15% of normal. In this form, anti-elastase is unable to inhibit another enzyme, elastase. Elastase then chews up the elastin fibers of the lung, resulting in the lung disease emphysema.

Patients with restrictive lung disease such as fibrosis have a decreased inspiratory capacity. Emphysema patients who have lost elastic recoil cannot expel as much air during passive expiration and have an increased functional residual capacity.

With the changes of emphysema, the lung becomes even more compliant but less elastic, resulting in a hyperinflated lung and the barrel chest associated with chronic emphysema.

5th edition?

1. Surfactant, made by the type II alveolar cells, reduces the surface tension in the fluid in the alveoli, thereby facilitating inflation and inhibiting collapse of the alveoli.

4. I know that asthma causes increased airway resistance.

5. Low atmospheric PO2 at high altitude low arterial sensed by kidney erythropoietin synthesized and released acts on bone marrow to increase production of red blood cells.

Spending several days at higher than normal altitude will stimulate erythropoiesis, due to the lower oxygen concentration in the air, which when breathed would result in hypoxemia. Athletes would be less competitive if they competed at a higher altitude than that in which they lived or trained, and more competitive if they lived and trained at a higher altitude than that in which they competed, at least in theory. While students may not know this, experimental results support the best regimen for maximizing performance at a low-altitude competition to be living at high altitude but training at low altitude. Neither living and training high nor living and training low achieved the same results. High-altitude training is necessary, however, for high-altitude competition.

7. I just finished doing something similar to this, I found that:

When PO2 increases: Arterioles: systemic constrict, pulmonary dilate.
When PCO2 increases: Bronchioles and systemic arterioles dilate.
When PO2 decreases: Arterioles: systemic dilate, pulmonary constrict.
When PCO2 decreases: Bronchioles and systemic arterioles constrict.

5th edition is fine!

Thanks for your help star. Yep, we have the question bank for that textbook.

Thanks so much for the help. Could you please remove this post bio_man. I think I might get in trouble from my school if this is found!