Physiology Flashcards

(26 cards)

1
Q

Internal respiration vs external respiration

A
  • Internal respiration refers to the mitochondrial respiration (i.e., the oxidation of carbon-containing compounds to form CO2)
  • External respiration refers to the dual processes of (1) transporting O2 from the atmosphere to the mitochondria and (2) transporting CO2 from the mitochondria to the atmosphere
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2
Q

Oxygen percentage in atmosphere

A

About 21%

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3
Q

Nitrogen percentage in atmosphere

A

About 78%

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4
Q

CO2 percentage in atmosphere

A

0.04%

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5
Q

What is found in the pleural cavity?

A

About 10 mL of pleural fluid normally occupies the virtual space between the parietal and the visceral pleura

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6
Q

What produces pleural fluid?

A

Blood vessels in parietal pleura produce an ultrafiltrate of the plasma

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7
Q

Anatomical dead space volume

A

~150 mL in healthy young males and >100 mL in females

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8
Q

Total lung capacity volume

A

Averages 5 to 6 L in adults

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9
Q

Number of lobes in right and left lung

A
  • 3 lobes in right lung
  • 2 lobes in left lung
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10
Q

How can the several divisions of the bronchi be called?

A
  • We can refer to them by generation number
  • About 23 generation in the airway
  • Zeroth generation refers to the trachea, first generation are the main left and right bronchi, second generation
  • Up to 10th generation we call the airways bronchi
  • At about the 11th generation they are called bronchioles
  • , The most distal conducting airways are the terminal bronchioles (generation ~16)
  • At generation ~17. we have respiratory bronchiole
  • Respiratory bronchioles extend from generation ~17 to generation ~19
  • Alveolar ducts (generations 20 to 22) finally terminate blindly as alveolar sacs (generation 23)
  • The aggregation of all airways arising from a single terminal bronchiole (i.e., the respiratory bronchioles, alveolar ducts, and alveolar sacs), along with their associated blood and lymphatic vessels, is a terminal respiratory unit or primary lobule
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11
Q

Differences in histology of the airways as we go up generations

A
  • As generation number increases (i.e., as airways become smaller), the amount of cilia, the number of mucus-secreting cells, the presence of submucosal glands, and the amount of cartilage in the airway walls all gradually decrease
  • Airways maintain some cartilage to about the 10th generation
  • 11th generation onwards don’t have cartilage
  • Up to generation 16 no alveoli are present
  • Alveoli first appear budding off bronchioles at generation ~17
  • Respiratory bronchioles extend from generation
    ~17 to generation ~19, the density of alveoli gradually increasing with generation number
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12
Q

Purpose of cartilage in airway

A

Cartilage is important for preventing airway collapse, which is especially a problem during expiration

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13
Q

How do bronchioles which lack cartilage remain patent?

A
  • Bronchioles can maintain a patent lumen only because the pressure surrounding them may be more negative than the pressure inside and because of the outward pull (radial traction or tethering) of surrounding tissues
  • Thus, bronchioles are especially susceptible to collapse during expiration
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14
Q

Velocity of air throughout the respiratory system?

A
  • The linear velocity of air in the first four generations is higher than that in the trachea, which may be important during coughing
  • Same velocity for each generation of conducting airways
  • In succeeding generations, the aggregate cross-sectional area rises, at first slowly and then very steeply
  • As a result, the linear velocity falls to very low values (e.g. the terminal bronchioles (generation 16) have a velocity 1.4% of the value in the trachea)
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15
Q

Mechanism of movement of air through airways

A
  • Long-distance movement of gases from the nose and lips to the end of the generation-16 airways occurs by convection
    -However, the short-distance movement of gases from generation-17 airways to the farthest reaches of the alveolar ducts occurs by diffusion, as does the movement of gases across the gas exchange barrier
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16
Q

Gas exchange barrier width

A
  • ~0.6 µm
  • At the type I cells, the alveolar wall (i.e., pneumocyte plus endothelial cell) is typically 0.15 to 0.30 µm thick
17
Q

Diameter of alveoli

A

Range from 75 to 300 µm

18
Q

Pneumocyte 1 vs 2 coverage of alveoli

A

Type I cells cover 90% to 95% of the alveolar surface

19
Q

Differences between type of 1 and 2 pneumocytes

A
  • Cuboidal type II cells exist in clusters and are responsible for elaborating pulmonary surfactant
  • The type I cells are much thinner than the type II cells
20
Q

What contributes to surfactant production?

A

Pneumocyte type 2 in the alveoli and Clara cells in the respiratory brochioles

21
Q

Composition of pulmonary surfactant

A
  • Complex mixture of lipids and proteins
  • Lipids make 90% of surfactant with about of the lipid made up of dipalmitoylphosphatidylcholine (DPPC)
  • Second most common lipids in pulmonary surfactant are phophatidylchole molecules with unsaturated fatty acid-chains
22
Q

Function of surfactant

A

-To increase pulmonary compliance.
- To prevent atelectasis at the end of expiration.
- To facilitate recruitment of collapsed airways.
- Substantially eases the expansion of the lungs
- Lipids are responsible for the surface-active properties (reduces surface tension)

23
Q

Blood supply to the lungs

A
  • Receives two blood supplies: the pulmonary arteries and the bronchial arteries
  • The pulmonary arteries, by far the major blood supply to the lung, carry the relatively deoxygenated mixed-venous blood.
  • After gas exchange in the alveoli, the blood eventually collects in the pulmonary veins.
  • The bronchial arteries supply the conducting airways
  • At the level of the respiratory bronchioles, capillaries derived from bronchial arteries anastomose with those derived from pulmonary arteries
  • Small amount of the bronchial blood drains into the azygos and accessory hemiazygos veins
24
Q

Particle trapping in respiratory system

A
  • Nasal hairs tend to filter out large particles (greater than ~15 µm in diameter)
  • The turbulence set up by these hairs—as well as the highly irregular surface topography of the nasal passages—increases the likelihood that particles larger than ~10 µm in diameter will impact and embed themselves in the mucus that coats the nasal mucosa
  • Moreover, air inspired through the nose makes a right-angle turn as it heads toward the trachea. The inertia of larger particles causes them to strike the posterior wall of the nasopharynx, which coincidentally is endowed with large amounts of lymphatic tissue that can mount an immunological attack on inspired microbes
  • Of the larger particles that manage to escape filtration in the upper airways, almost all will impact the mucus of the trachea and the bronchi
  • Smaller particles (2 to 10 µm in diameter) also may impact a mucus layer. In addition, gravity may cause them to sediment from the slowly moving air in small airways and to become embedded in mucus. Particles with diameters below ~0.5 µm tend to reach the alveoli suspended in the air as aerosols. The airways do not trap most (~80%) of these aerosols but expel them in the exhaled air
25
WHat happens to particles that were not captured in the airways and are now in the alveoli
- The lung has a variety of strategies for dealing with particles that remain on the surface of the alveoli or penetrate into the interstitial space - Alveolar macrophages (on the surface) or interstitial macrophages may phagocytose these particles, enzymes may degrade them, or lymphatics may carry them away - In addition, particles suspended in the fluid covering the alveolar surface may flow with this fluid up to terminal bronchioles, where they meet a layer of mucus that the cilia propel up to progressively larger airways - There, they join larger particles—which entered the mucus by impaction or sedimentation—on their journey to the oropharynx - Coughing and sneezing reflexes triggered by airway irritation, accelerate the movement of particulates up the conducting airways
26
Molecules processed and not processed in the lung
- UNAFFECTED: PGA1, PGA2, PGI2, histamine, epinephrine, dopamine, Angiotensin II, arginine vasopressin, gastrin, oxytocin - LARGELY REMOVED: PGE1, PGE2, PGF2α, leukotrienes, serotonin, bradykinin, Angiotensin I (converted to angiotensin II)