Gas Exchange/ Transport Flashcards

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1
Q

Trachea

A

Tube that allows air to travel into and out of the lungs to and from the atmosphere

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2
Q

The Lungs

A

Take in fresh air (oxygen) from atmosphere and get rid of carbon dioxide from blood

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3
Q

Bronchi

A

Tubes (right and left) that carry air into lungs (from trachea) and out of lungs

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4
Q

Bronchioles

A

Smaller tubes that carry air to and from the alveoli (from the bronchi) - ↑SA

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5
Q

Alveoli

A

-Clusters of air sacs (↑SA) at ends of bronchioles
-Carry out gas exchange with the blood (O2 and CO2)

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6
Q

How is alveoli structure adapted to its function? (TRIM)

A

-Thin walls – surrounded by a single layer of epithelial cells (minimizes diffusion distance): capillary walls only one cell thick too (endothelial cells)
-Rich capillary network surrounding each alveolus – maintains high concentration gradient (O2/ CO2) between lungs and blood for diffusion
-Increased SA:V ratio – small, spherical shape increases surface area while decreasing volume
-Moist – cells lining each alveolus secrete fluids to allow gases to dissolve (dissolved oxygen diffuses easier into blood) and prevent alveoli from collapsing on themselves/ sticking together

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7
Q

Type I Pneumocytes

A

Squamous (flattened) and extremely thin to minimize diffusion distance and increase surface area for gas exchange

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8
Q

Type II Pneumocytes

A

cuboidal with granules (store components to make surfactant); function is to secrete pulmonary surfactant - a liquid substance that reduces/ decreases surface tension (ensuring all alveoli expand at the same rate and none of them collapse in on themselves due to unequal pressure)

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9
Q

Red Blood Cells in an Electron Micrograph

A

Red blood cells are not right up against the alveolar space

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10
Q

Type II Pneumocytes on an Electron Micrograph

A

less flattened (sort of cuboidal but mostly just less flattened) cells up against the alveolar space

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11
Q

Type I Pneumocytes on an Electron Micrograph

A

flattened cells right up against the alveolar space

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12
Q

Describe Ventilation

A

Ventilation (exchange of air between lungs and atmosphere through breathing) involves the internal and external intercostal muscles (between ribs), the diaphragm (below lungs) and abdominal wall muscles, and it is driven by a negative pressure mechanism

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13
Q

Inspiration (breathing in)

A

a. Diaphragm muscles contract (flatten downwards) and external (on outside) intercostal muscles contract (pull ribs up and out)
b. Thoracic cavity volume and lung volume increase (pressure of air in lungs drops below atmospheric pressure – air rushes in through mouth or nasal passage to equalize)

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14
Q

Expiration (breathing out)

A

a. Diaphragm muscles relax (curves upward), abdominal wall muscles contract (pushing diaphragm up), external intercostal muscles relax (ribs fall), and internal (on inside) intercostal muscles contract (pulling ribs back down)
b. Thoracic cavity volume and lung volume decrease (pressure of air in lungs rises above atmospheric pressure – air rushes out to equalize)

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15
Q

Describe the function of the ventilation system.

A

-Because gas exchange is a passive process (diffusion),
the lungs function to continually cycle fresh air into the alveoli (high O2 in alveoli allows diffusion of O2 into the blood and low CO2 in alveoli allows diffusion of CO2 out of blood and into alveoli)
-Maintains a high concentration of O2 AND a low concentration of CO2 in the alveoli in the lungs
-Ensures that O2 diffuses from the lungs through the alveoli walls INTO the blood (capillaries) and CO2 diffuses OUT of the blood (capillaries) through the alveoli walls and into the lungs (most cell respiration is aerobic – requires O2 and produces CO2)
-Allows continual cycling of the air in the lungs with the air in the atmosphere to maintain concentration gradients between the alveoli and the capillaries for gas exchange

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16
Q

What is emphysema?

A

a chronic/progressive disease where the walls of the alveoli are damaged and lose their elasticity (feeling of shortness of breath) - a form of COPD (chronic obstructive pulmonary disease)

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17
Q

Causes of emphysema

A

SMOKING/ tobacco/marijuana/fumes/coal dust/air pollution (irritants cause damage, then phagocytes (WBC’s) come to “help” damaged tissue/ secrete elastase, which breaks down elastic fibers in alveolar walls) - Note that in rare cases, hereditary gene mutation causes deficiency in elastase enzyme inhibitor (which causes hereditary emphysema)

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18
Q

Consequences of Emphysema

A

Healthy alveoli break down/ rupture, turn into large, irregularly shaped structures with gaping holes, ↓ elasticity (so ↑total lung volume at rest), ↓ SA, ↓O2 can reach the bloodstream

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19
Q

Treatments of Emphysema

A

No cure, but certain treatments can help alleviate symptoms/ delay disease = bronchodilators (improve airflow by relaxing bronchial muscles), inhaled steroids (reduce inflammatory response/ phagocytes), oxygen supplementation, elastase enzyme inhibitors, surgery (remove damaged tissue/ lung transplant)

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20
Q

What is lung cancer?

A

a cancerous growth (uncontrolled cell division) within the lungs.

21
Q

Causes of lung cancer

A

carcinogens (smoking, asbestos)/air pollution/ certain infections/genetic predispositions

22
Q

Consequences of lung cancer

A

*Malignant cancer cells can take over healthy tissues of the bronchioles & alveoli – then eventually spread (metastasize) to the brain/bones/liver/adrenal gland
* Lung tissues become dysfunctional, can lead to internal bleeding, coughing up blood, wheezing, respiratory distress and weight loss

23
Q

Give a basic definition of ventilation

A

The exchange of air between lungs and atmosphere (through breathing)

24
Q

Ventilation Rate

A

Number of inhalations/exhalations/ breaths per minute

25
Q

Tidal volume

A

Volume of air taken in with each inhalation/out with each exhalation

26
Q

Pneumocytes

A

Cells that make up the lining of each alveolus in the lungs

27
Q

Gas Exchange

A

The exchange of oxygen and carbon dioxide in the alveoli (lungs) and in the bloodstream (by diffusion)

28
Q

Respiration

A

The transport of oxygen to cells producing energy; it involves ventilation, gas exchange, and cell respiration

29
Q

Cellular Respiration

A

The release of ATP from organic molecules (enhanced by oxygen – aerobic respiration)

30
Q

Coronary Occlusion

A

Narrowing of arteries that supply oxygen and nurtrients to the heart

31
Q

Effect of Exercise on Ventilation

A

The rate of ventilation is controlled by the respiratory control center in the medulla oblongata and during exercise the rate of ventilation changes in response to the amount of CO2 in the blood

Exercise increases metabolism (cell respiration rate)
This increases CO2 in the blood, which
DECREASES the pH of the blood (becomes more
acidic) - normal range = 7.35-7.45 (~7.4 average)
Chemoreceptors in the carotid artery (neck) and the aorta (heart) detect CO2/ O2 levels and blood pH; Chemoreceptors in the medulla detect CO2 changes (as pH changes in cerebrospinal fluid)
Chemoreceptors send impulses to the respiratory/ breathing center (in medulla oblongata)
Medulla sends impulses to the diaphragm and intercostal muscles to increase rate of contraction (increasing ventilation rate/ hyperventilation)
As ventilation rate increases, CO2 levels in blood decrease, pH rises and is restored
As CO2 levels drop and pH is restored, breathing rate decreases
As breathing rate decreases, CO2 levels rise again, pH drops again and the cycle continues

32
Q

How does a spirometer measure ventilation rate?

A

Spirometer measures volume of gas inhaled/ expelled per breath - Note: changes in volume are shown as increasing (breathing in) or decreasing (breathing out) over time on a graph and each breath is one “wave” (shows tidal volume - amount of O2 in or out in in one breath)

33
Q

Hemoglobin

A

(oxygen binding protein in RBC’s)
-4 polypeptide chains, each with heme group; heme binds REVERSIBLY/ COOPERATIVELY with oxygen = O2 binding changes shape so hemoglobin has HIGHER affinity for O2 and binds more of it more readily/ easily (and vice versa too) - promotes oxygen loading in lungs and oxygen release at/ to respiring tissues

34
Q

Myoglobin

A

(oxygen-binding protein in skeletal muscles)
* Composed of only ONE polypeptide chain with an iron-containing heme group (able to bind reversibly with oxygen – NO cooperative binding though b/c only one heme group, so binds only one oxygen molecule at a time)
* Binds to O2 and stores it IN muscle cells (acts as an “oxygen reserve”)
* Able to provide O2 to muscle cells when O2 in blood is very low; delays anaerobic respiration

35
Q

Oxygen Dissociation Curves in relation to each other

A

Myoglobin is furthest to the left, then fetal hemoglobin, then adult hemoglobin

The further left, the higher the oxygen affinity

36
Q

Adult Hemoglobin

A
  • Shows a sigmoidal (S-shaped) curve (due to its cooperative binding of oxygen molecules)
  • High saturation at high pressures (pO2)/ lungs = oxyhemoglobin forms when high pO2; Low saturation at low pressures/ concentrations (pO2)/ respiring tissues = oxyhemoglobin dissociates (unbinds/ breaks apart) at low pO2
37
Q

Fetal Hemoglobin

A

(Understand that fetal hemoglobin is different from adult hemoglobin, allowing the transfer of oxygen in the placenta onto the fetal hemoglobin)
* Fetal hemoglobin molecules have slightly different shape (molecular structure) than adult hemoglobin, making them have a HIGHER AFFINITY for oxygen (they bind it more readily/ easily - binds O2 more readily at lower pO2)
* Sigmoid shape dissociation curve but shifted LEFT (b/c it has a higher oxygen affinity)
* Higher affinity for oxygen ensures that oxygen moves from adult (mom’s) hemoglobin to fetal hemoglobin in the capillaries of the placenta

38
Q

Myoglobin

A
  • Higher affinity for oxygen than hemoglobin (saturated at extremely low O2 concentrations, so able to store oxygen in muscle cells no matter what concentrations are in body) – NOT an S-shaped curve b/c NO cooperative binding, like in hemoglobin. Only binds ONE O2 molecule at a time (only one heme group per myoglobin)
  • Releases oxygen to muscle cells when levels of O2 in
    blood are extremely low (from intense exercise),
    allowing aerobic respiration to continue/ delaying
    anaerobic respiration/ lactic acid formation!
39
Q

The Bohr shift explains….

A

the increased release of oxygen by hemoglobin in respiring tissues.

40
Q

Explain the Bohr Shift

A

Respiring tissues release MORE CO2 into the blood, which LOWERS the pH of the blood (it becomes more acidic)
↓in pH shifts the oxygen dissociation
curve to the RIGHT (Bohr shift/ effect),
causing ↓affinity of hemoglobin for
oxygen = MORE O2 is released to respiring
cells/ tissues! How?
* Excess CO2 diffuses into RBC’s and is
converted into carbonic acid
* Carbonic acid dissociates into H+ ions and
HCO3- ions
* H+ ions in the RBC bind to hemoglobin (causing it to change shape and have a LOWER affinity for oxygen, so O2 is released)
* MORE O2 is released at the same partial pressure due to Bohr effect

The Bohr shift ENSURES that respiring tissues have enough O2 when they need it the most (during ↑ physical activity/ exercise)!

41
Q

What happens at higher altitudes?

A

As altitude ↑ atmospheric pressure ↓ (less O2 because less air overall = lower partial pressure of O2)
Lower pO2 makes it more difficult for hemoglobin to take up and transport oxygen (lower pO2 = lower % Hb saturation in the lungs/ alveoli) – tissues and cells receive LESS oxygen (Symptoms of low oxygen intake/ hypoxia = breathlessness, headache, fatigue, rapid pulse, nausea - note that increased ventilation rate causes ↑ loss of H2O too)

42
Q

How does the body accumulate to high altitude over time?

A
  1. RBC production increases (more RBC’s = more hemoglobin = more O2 transport) - this causes kidneys to excrete excess fluid though = more urination = dehydration (so need more H2O)
  2. RBCs are produced with more hemoglobin molecules in them (these also have a slightly different structure which gives them a higher affinity for oxygen - shifts oxygen dissociation curve to the left - ↑ % saturation of Hb at lower pO2)
  3. Vital capacity increases (more air in/out per breath = increased rate of gas exchange)
  4. Muscles produce more myoglobin (capillaries become more dense too – more O2 diffusion into cells and binding by myoglobin)
  5. Kidneys secrete alkaline urine (remove excess HCO3- to improve buffering of blood pH)
  6. Greater lung surface area/ larger chest size – if living permanently at high altitude
43
Q

What are the benefits of high altitude training and why?

A

Improved performance/ endurance (at lower oxygen levels, and when returning to lower altitude maintain benefits temporarily)
Due to:
* Higher concentration of hemoglobin/ RBC’s/ increased affinity of Hb for O2 = more O2 transported
* Improved gas exchange/ vital capacity (↑ lung surface area)
Increased capillaries/ myoglobin in skeletal muscles

44
Q

What are the risks of high altitude?

A

Altitude sickness/ lowered immunity/ stroke/ increased breakdown of muscle tissue
Effects only temporary/ require lengthy training time to achieve and may be unfair advantage to other competitors

45
Q

How is carbon dioxide carried in the blood?

A

Carbon dioxide is carried in the blood (from the tissues to the lungs) in one of three ways:
1. Bound to hemoglobin (HbCO2 - binds to globin, not heme, so does not compete with oxygen)
2. Dissolved in the blood plasma (in water portion - forms carbonic acid/ bicarbonate ions)
3. In erythrocytes (RBC’s) as carbonic acid (~75% of CO2 carried this way!):
a. CO2 diffuses into erythrocyte
b. CO2 combines with water to form carbonic acid, which is more soluble (H2CO3) – this reaction is catalyzed by carbonic anhydrase
c. Carbonic acid dissociates into H+ ions and bicarbonate ions (HCO3-)
d. Chloride shift: Bicarbonate ions are pumped OUT of erythrocytes and Cl- ions are pumped in (ensures overall charge remains the same)
e. Bicarbonate ions in blood plasma combine with sodium ions in the blood plasma(NaHCO3) – these are carried to the lungs
f. H+ ions in the erythrocyte lower the pH, causing hemoglobin to release oxygen (to respiring cells/ tissues)
g. Hemoglobin absorbs/ binds excess H+ ions to buffer/ maintain pH in the erythrocyte
h. In lungs, HCO3- pumped back into RBC’s and entire process reversed

46
Q

How is normal blood pH maintained?

A

Chemoreceptors are sensitive to changes in blood pH, and pH of blood is regulated to stay within the (VERY) narrow range of 7.35 to 7.45 (to avoid the onset of disease)

Chemoreceptors (such as those in the aorta/ carotid artery and medulla) detect changes in blood pH and can trigger body responses to maintain balanced pH in the blood:
* Changes in ventilation rate in lungs helps regulate CO2 in blood
* Kidneys control reabsorption of HCO3- (from filtered blood contents - called filtrate) back into blood; excess HCO3- excreted/ not reabsorbed

pH in blood is also maintained by plasma proteins:
* Plasma proteins act as pH buffers by removing excess H+ ions (that would ↑ acidity) or by removing excess OH- ions (that would ↑ alkalinity)
* Amino acids (building blocks of proteins) are zwitterions (both positive and negative charges) - Amine groups take on H+ ions (removing them from blood), carboxyl groups release H+ (adding them to blood
where they combine with OH-
ions to form water, removing
excess OH- ions from blood)

47
Q

Capillary

A

red blood cells carry O2/ CO2; endothelium one cell thick = minimize diffusion distance

48
Q

Hemoglobin Oxygen Dissociation Curve Overview

A

In general:
-At LOW pO2 (partial pressure of oxygen), affinity/ saturation of
hemoglobin is also LOW; happens when hemoglobin is RELEASING O2 to
respiring/ exercising cells/ tissues (oxyhemoglobin dissociates)
-At HIGH pO2, affinity/ saturation of hemoglobin is also HIGH; happens in
alveoli in lungs (forming more oxyhemoglobin in RBC’s)

For HEMOGLOBIN, shows an S-shaped (sigmoid) curve due to cooperative
binding of oxygen molecules with hemoglobin

49
Q

ventilation rate=

A

tidal volume x breathing rate