6. Respiration I - Alveolar and Systemic Gas Exchange Flashcards

1
Q

what is the name for ALVEOLI CELLS

A

PNEUMOCYTES

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2
Q

what type of cells are TYPE 1 ALVEOLAR CELLS / PNEUMOCYTES

A

SQUAMOUS EPITHELIAL

  • THIN, FLATTENED
  • large, thin cytoplasm
  • central nucleus (fried egg appearance)
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3
Q

what type of cells are TYPE 2 ALVEOLAR CELLS / PNEUMOCYTES

A

CUBOIDAL EPITHELIAL CELLS

  • distinct apical MICROVILLI
  • LARGE nucleus
  • abundant cytoplasm with MITOCHONDRIA, extensive ER, GOLGI
  • SECRETORY CELLS
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4
Q

what do TYPE 2 PNEUMOCYTES do

A

SECRETE SURFACTANT

(Secretory Cells)

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5
Q

TYPE 2 PNEUMOCYTES are HIGHLY METABOLIC so have important roles in:

A
  • SURFACTANT PRODUCTION
  • SURFACTANT HOMEOSTASIS
  • REPAIRING ALVEOLI (upon injury)
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6
Q

TYPE 1 PNEUMOCYTES contribute to the..

A

AIR-BLOOD BARRER

Overlies capillaries on alveolar wall

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7
Q

which PNEUMOCYTE comprises 90% of the ALVEOLAR WALL

A

TYPE 1

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8
Q

TYPE 1 play a role in

A

GAS EXCHANGE

(PASSIVE role)

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9
Q

what is the DISTANCE of GAS EXCHANGE

A

0.1 - 1.5 μm
(MAX 1.5)

  • SHORT DISTANCE for maximum EFFICIENCY
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10
Q

what is the ROLE of SURFACTANT (from Type 2 pneumocyte)

A

REDUCE SURFACE TENSION

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11
Q

how does SURFACTANT REDUCE SURFACE TENSION (what happens without)

A

SURFACE TENSION created by FLUID LINING ALVEOLI
- H20 COHESION (attract to each other/stick)
tension pulls alveolar walls inwards causing COLLAPSE

SURFACTANT MOLECULES INTERPOSE between H20 MOLECULES
- have HYDROPHILIC and HYDROPHOBIC Regions
- interfere with H BONDING between H2O molecules

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12
Q

by REDUCING SURFACE TENSION what are the 3 MAIN FUNCTIONS of SURFACTANT

A
  • INCREASE LUNG COMPLIANCE
    facilitate changes in volume/expansion of lungs
  • STABILISING ALVEOLAR SIZE
    LAPLACE LAW
  • keeping LUNGS DRY / PREVENT FLUID ACCUMULATION
    surface tension would draw in fluid from interstitium
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13
Q

how does SURFACTANT STABILISE ALVEOLAR SIZE
- LAPLACE LAW
1. what would happen without
2. what does surfactant do

A
  1. without:
    SURFACE TENSION REDUCES ALVEOLI SIZE
    SMALLER alveoli have HIGH PRESSURE
    air moves from high to low pressure, from small alveoli into large alveoli
    therefore Small ALVEOLI COLLAPSE
  2. smaller size alveoli have MORE DENSE SURFACTANT
    - STABILISES SIZE
    - REDUCES PRESSURE
    - PREVENT COLLAPSE
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14
Q

what is INFANT RESPIRATORY DISTRESS SYNDROME

A
  • LACK OF SURFACTANT

fetus starts to produce surfactant 24-28 WEEKS GESTATION

if born premature/before 35 weeks, may have insufficent
- ALVEOLI COLLAPSE

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15
Q

what does DALTON’S LAW state

A

the TOTAL PRESSURE is EQUAL to the SUM of the PARTIAL PRESSURES

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16
Q

OXYGEN and CARBON DIOXIDE MOVE DOWN..

A

GRADIENTS of PARTIAL PRESSURE

between Alveoli and Pulmonary Capillary Blood
and between Systemic Capillary Blood and Interstitial Fluid

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17
Q

what does HENRY’S LAW state

A

the SOLUBILITY of a GAS IN A LIQUID is
PROPORTIONAL to its PARTIAL PRESSURE Above the Liquid and the SOLUBILITY COEFFICIENT of the GAS In the Liquid

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18
Q

what does FICK’S LAW state

A

the AMOUNT of GAS DIFFUSING IN unit time through the resistance of a barrier is
INVERSELY PROPORTIONAL to the THICKNESS of the BARRIER
and
DIERECTLY PROPORTIONAL to the SURFACE AREA of the BARRIER, DIFFUSION CONSTANT (D), and PARTIAL PRESSURE DFFERENCE (GRADIENT) on each side

(INCREASE THICKNESS BARRIER, DECREASE AMOUNT DIFFUSION)

(INCREASE SURFACE AREA, INCREASE DIFFUSION
INCREASE DIFFUSION CONSTANT, INCREASE DIFFUSION
INCREASE PRESSURE DIFFERENCE, INCREASE DIFFUSION)

19
Q

what does GRAHAM’S LAW state

A

the RATE of DIFFUSION is
DIRECTLY PROPORTIONAL to the SOLUBILITY COEFFICIENT
and
INVERSELY PROPORTIONAL to the SQUARE ROOT of its MOLECULAR WEIGHT

(INCREASE SOLUBILITY, INCREASE RATE)
(INCREASE SIZE, DECREASE RATE
smaller size faster diffusion)

20
Q

properties that MAXIMISE GAS EXCHANGE

A
  • LARGE SURFACE AREA (70m^2) (300-600 million alveoli)
  • DENSE NETWORK CAPILLARIES
  • THIN Alveolar-Capillary MEMBRANE
  • SURFACTANT production to REDUCE SURFACE AREA and facilitates EXPANSION of LUNGS (further increases Surface Area)
21
Q

SURFACE AREA of GAS EXCHANGE surface

22
Q

does CO2 or O2 DIFFUSE FASTER and why

A

CO2 20X FASTER than o2

  • MORE SOLUBLE
23
Q

CO2 MORE SOLUBLE so what does this mean

A

20X FASTER DIFFUSION RATE

does NOT NEED as big PARTIAL PRESSURE GRADIENT/DIFFERENCE to DIFFUSE
from blood (45 mmHg) to Alveoli (40mmHg)

OXYGEN NEEDS BIG GRADIENT
Alveoli (104 mm Hg) to Blood (40 mm Hg)

24
Q

when does DIFFUSION CAPACITY INCREASE

A

during EXERCISE

  • LARGER TIDAL VOLUMES - inflate alveoli, INCREASES SURFACE AREA
    more pulmonary capillaries perfused
    increased PAO2 due to increased ventilation
    INCREASED PARTIAL PRESSURE GRADIENT
25
when can you have REDUCTION in DIFFUSION CAPACITY
- THICKENING of AIR-BLOOD BARRIER Pulmonary Oedema - REDUCTION in ALVEOLI SURFACE AREA Emphysema
26
how much of OXYGEN in the blood is carried by HAEMOGLOIN
97% - 1 Hb : 4 X O2 (1 O2 to each HAEM group - Fe2+)
27
remaining 3% of OXYGEN in blood is where
DISSOLVED in PLASMA and other BLOOD CELLS
28
HAEMOGLOBIN is a ... PROTEIN
TETRAMERIC PROTEIN - 2 ALPHA chains - 2 BETA chains 4 non-protein Haem groups with Fe2+ (O2 binding site)
29
at top end of OXYHAEMOGLOBIN DISSOCIATION CURVE above 90% saturated Hb, how would change in PO2 affect %O2 in Hb
would have to be a substantial drop in available O2 before Hb Saturation would be significantly affected
30
at STEEP area of OXYHAEMOGLOBIN DISSOCIATION CURVE around P02 of 5 kPa and 50% saturated Hb, how would change in PO2 affect %O2 in Hb
small drop in O2 partial pressure will cause BIG DROP in Hb Saturation BENEFICIAL - MORE O2 will be RELEASED from Hb and become AVAILABLE
31
when does OXYHAEMOLOBIN DISSOCIATION CURVE move to the RIGHT and what does this mean
when NEEDS MORE AVAILABLE O2 eg EXERCISE - DECREASED AFFINITY - Increased P50
32
when does OXYHAEMOLOBIN DISSOCIATION CURVE move to the LEFT and what does this mean
when LOW CO2 eg at LUNGS - INCREASED AFFINITY - DECREASED P50
33
where is CO2 in the BLOOD
- 7% DISSOLVED in PLASAM and INTRACELLULAR FLUID of blood cells - 23% BOUND to HAEMOGLOBIN - 70% present as BICARBONATE HCO3- IONS
34
where does CO2 bind in Hb
to the GLOBIN (O2 binds to HAEM Group)
35
how does CO2 become HCO3-
CO2 + H20 -> H2CO3 carbonic acid -> HCO3- + H+
36
how does Hb act as a BUFFER
BINDS/RELEASES CO2 (gives HCO3- buffer)
37
BICARBONATE BUFFER SYSTEM
- CO2 from cell metabolism diffuses into RBC and Dissociates into HCO3- (exhanged for Cl-) and H+ H+ BINDS Hb (decreases Hb affinity for O2) - in LUNGS H+ DISPLACED from Hb O2 from air BINDS Hb (INCREASED AFFINITY for O2) HCO3- exchanged back into RBC (chloride shift) BINDS to H+ to BUFFER (so not lower pH) HCO3- + H+ -> H2CO3 -> CO2 + H2O - REVERSE REACTION. MORE CO2 production.
38
what is the CHLORIDE SHIFT / HAMBURGER SHIFT
In BICARBONATE BUFFER SYSTEM HCO3- EXCHANGED for CL- - Maintains ELECTRICAL BALANCE in RBC and PLASMA during CO2 DISSOCIATION (eg. CO2 into RBC, forms HCO3-, moves out into plasma exchanged for Cl-. at lungs HCO3- exchanged back into RBC to BIND H+)
39
what is the BOHR EFFECT
when INCREASE H+ causes Hb to LOSE AFFINITY for / UNBIND O2 - H+ BINDS deoxyhaemoglobin - increase O2, INCREASES AFFINITY for O2, DISPLACES H+
40
what is HALDANE EFFECT
when INCREASED OXYGEN in blood causes DISPLACEMENT OF CO2 FROM Hb - FREES CO2 so can be expelled
41
what is called when H+ IONS cause HbO2 to GIVE UP O2
BOHR EFFECT
42
what is it called when INCREASED OXYGENATION of blood DISPLACES CO2 from Hb
HALDANE EFFECT
43
PULMONARY ARTERY function
DEOXYGENATED BLOOD from Heart TO LUNGS - only artery with Deoxygenated
44
PULMONARY VEIN function
OXYGENATED BLOOD from LUNGS TO HEART - only Vein with Oxygenated