Gas Transport Flashcards

(64 cards)

1
Q

Hematocrit in adults, newborns, 2mo

A

40%-45%
55%
35%

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2
Q

plasma

A

water, proteins, electrolytes and nutrients, waste

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3
Q

buffy coat

A

WBCs, platelets

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4
Q

days RBCs live

A

120 days

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5
Q

RBCs are made where

A

red BM

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6
Q

RBC are broken down where

A

macrophages in red BM, liver, spleen

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7
Q

liver function in breakdown of RBCs

A

stores Fe+3 as Ferritin

and excretes bilirubin

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8
Q

what causes RBCs to be made

A
  1. low O2 in tissues, or low Hb
  2. kidneys release EPO (ERYTHROPOIETIN)
  3. red BM makes RBCs
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9
Q

how does the kidney make EPO

A

Hypoxia inducible factor is a TF that gets activated in the cytosol and binds to the DNA to transcribe the EPO

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10
Q

O2 consumption per min for our bodies

A

250 mL O2/min

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11
Q

amount of dissolved O2 in the blood

and how much is delivered per min

A

0.3 mL O2 in 100mL of blood

15ml O2/min

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12
Q

HbA
HbF
HbS
HbA1c

A

2 a chains, a B chains
2 a chains, 2 y chains
sickle cell
Diabetic glycosylated marker

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13
Q

poryhyrin complex

A

heme bounds to Fe+2

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14
Q

methemoglobulin

A

Fe+3

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15
Q

percent in arterial blood of
Dissolved CO2
HCO-3
Carbamino compounds

A

5%
90%
5%

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16
Q

percent in venous blood of
Dissolved CO2
HCO-3
Carbamino compounds

A

30%
60%
10%

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17
Q

PCO2 is what in venous circulation

solubility of CO2

A

45mmHg

higher then O2

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18
Q

how much CO2 do we make

A

200mL CO2/ min

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19
Q

how is HCO-3 made

3 ways

A
  1. CARBONIC ANHYDRASE : CO2 + OH- —-> HCO-3
  2. H2CO3 dissociatino —-> HCO-3 + H+
  3. CO-3 + H+ —-> HCO-3
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20
Q

what regulated HCO-3 production

2 things

A

carbonic anhydrase

HCO-3/Cl- exchanger

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21
Q

how does CO-2 enter RBCs from tissues

A

AQP1 channel

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22
Q

Hamburger shift

A

also called chloride shift

higher amount of Cl- causes more HCO- to leave the RBCs into circulation (due to HCO-3/Cl0 exchanger)

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23
Q

Co-2 goes where

A

to alveoli

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24
Q

oxygen - Hb dissociation curve

x and y axis

A

Right Y : O2 content
Left Y : Hb saturation (*with normal Hb amount in blood = 15g / 100mL)
X : PO2

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25
oxygen - Hb dissociation curve venous PO2 Hb saturation O2 amount in blood
40mmHg PO2 75% 15mL O2
26
oxygen - Hb dissociation curve arterial PO2 Hb saturation O2 amount in blood
100mmHG PO2 97% 20mL O2
27
1g of HB carries how much O2
Hb carries = 1.34mL O2/g Hb
28
in 15g Hb/ 100mL blood what is the maximum amount of O2 that can be carried
maximum amount = 1.34 x 15 = 20.1mL O2/ dL blood 75% of this = 15mL O2/ dL blood (venous) 97% of this = 19.5mL O2 / dL blood (arterial)
29
ml of dissolved O2 in arterial circulation
0.3mL O2/ 100mL blood
30
P50 is what
50% O2 saturation of the Hb = 27mmHg PO2* = 10mL O2/ dL blood
31
what happens is you breath 100% O2
arterial O2 will be 20.1 mL O2/ dL blood and Hb saturation is 100% DISSOLVED O2 increases to 1.8mL O2/ Dl blood
32
RIGHT SHIFT
O2 if given off to tissues more easily, lower Hb-O2 affinity can happen due to anemia to tissues get O2 *effects the venous side more of dissociation curve
33
LEFT SHIFT
O2 has higher affinity for Hb and is not given off easily
34
what causes left shift
1. Methemoglobinemia (high Fe+3) 2. HbF 3. Polycythemia (high RBCs) 4. high pH (alkaline = low CO2) 5. low TEMP and low Co2
35
what causes right shift
1. HIGH TEMP 2. low pH (acidic = high PCO2) 3. HIGH 2,3-diphosphoglycerate (2,3-bisphosphoglycerate)
36
2,3-bisphosphoglycerate
product of RBCs when they : have low O2 = glycolysis stimulated chronic hypoxia or chronic anemia high altitudes
37
CO poisoning what happens Sx
CO competitively binds to Hb instead of O2 mimiks a LARGE LEFT SHIFT (stays of CO for a long time) Sx: headache, N,V
38
CO poisoning Tx:
breathe hyperbaric 100% O2 to displace CO and speed up the washout process 95% O2 and 5% CO2 = decrease pH for a right shift
39
normal O2 consumption
arterial O2- venous O2 = 20ml - 15ml = 5ml O2/ 100ml blood
40
O2 consumption during exercise for skeletal muscles
arterial O2- venous O2 = 20ml - 5ml = 15ml O2/ 100ml blood
41
Respiratory Quotient (RQ)
RQ = V of CO2 made/ V of O2 consumed = 200ml/250ml = 0.8* per minute
42
RQ of CARBS FATS PROTEIN
1: 1 = 1.0 7: 10 = 0.7 9: 10 = 0.9
43
mixed food RQ =
0.8
44
as HR increases and % O2 consumption increases what happens to RQ
INCREASES because CARBS breakdown increases a lot and fat breakdown increases a little and then decreases
45
Haldane effect
when Hb-O2 decreases, CO2 levels increase | HIGH HbO2 = larger amounts of CO2 release
46
3 things RBCs need to be healthy in their life cycle
1. calories are adequate 2. VIT B12 (cobalamin) + FOLATE (VIT B9) = DNA synthesis 3. FE+2 absorption, transportation, storage (liver)
47
Megaloblastic macrocytic anemia
X Folate VIT B9 | X VIT B12
48
Pernicious anemia
X absorption of VIT B12
49
microcytic anemia
low Fe+3 levels
50
hypochromic anemia
low transportation by transferrin of Fe+3 to developing erythroblasts
51
how much Fe is needed per day
absorption of 1.4mg for women | 1mg for men
52
HIGH levels of Fe
1. Fe3+ is absorbed by DMT1 --> Fe+2 from lumen to intestinal cells (can be stored in intestinal cells as Ferritin) 2. Fe+2 released to BVs (on transferrin) by Ferroportin as Fe+3
53
LOW levels of Fe
Hepcidin blocks Ferroportin from releasing Fe from the intestinal cells to the BVs (bound to transferrin) stored in intestinal cells as Ferritin
54
reason the most important thing for RBCs is ATP
1. maintain Fe+2 (not Fe+3) 2. ATPase fro ion transport 3. prevent oxidative damage 4. RBCs have no mitochondria to make energy or ATP
55
what happens when the 15g of Hb ----> 7.5f Hb (half of normal)
1. *Arterial Hb-O2 saturation % stays the same at 97%)* 2. Arterial O2 amount decreases to half = 9.8ml O2/ dL blood 3. Venous Hb-O2 saturation % decreases to 45% (from 75%) 4. Venous O2 amount decreases to 21ml O2/dL blood (from 40mL O2/dL blood)
56
side effect of O2-Hb saturation staying the same in arterial BF when the amount of Hb changes
cyanosis is not present *
57
Primary polycythemia
(genetic) LOW EPO (RBCs don't get enough O2 and over-production occurs) causes extra RBCs = increases Blood volume x2 increases viscosity x10 *still normal CO
58
secondary polycythemia
Hypoxia (HIGH EPO) extra RBCs * ABNORMAL CO
59
Physiologic Polycythemia
High altitude adaptation = causing body to get accustomed to low O2 = more RBCs are made * normal CO
60
Methemoglobinemia
high Fe+3 bound to Hb decreases O2 available to tissues, shift left in curve skin appears blue Fe+2 is oxidized from somthing or methemoglobulin reductase does not work
61
Hemachromatosis
OVERLOAD FE can lead to liver cirrhosis + skin pigmentation +DM = from X erythropoiesis, many blood transfusions, high Fe intake
62
V of CO2 in blood
50mL CO2/ 100mL blood
63
CO2 is mostly found how
as HCO-3
64
dissolved amount of CO2 | dissolved amount of O2
3mL CO2/ 100mL blood | 0.3mL O2/ 100mL blood