03b: RBC Flashcards

1
Q

List some things transported by blood.

A
  1. Water
  2. Heat
  3. Gasses
  4. Defense components
  5. Proteins
  6. Nutrients/salt/waste
  7. Messengers (hormones)
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2
Q

Amount of blood per kg BW in male and female.

A

Male: 75 mL/kg
Female: 65 mL/kg

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3
Q

How many liters blood in average person?

A

5-6 L

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4
Q

Clinically, one “unit” of blood is what volume?

A

450 mL

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5
Q

Concentration of Hb in a RBC:

A

30g/dL RBC

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6
Q

Why is Hb packaged in RBC?

A

Has short half-life in circulation

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7
Q

RBC is about (X) thick and has a diameter of (Y).

A
X = 1-2 micrometers
Y = 8 micrometers
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8
Q

What can occur to RBCs in slow-flowing blood?

A

Form rouleaux (stack together like roll of coins)

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9
Q

RBC rouleaux more seen in which cases?

A
  1. Diseases that increase RBC stickiness (change surface proteins)
  2. Pregnancy
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10
Q

T/F: RBC transports lots of oxygen, but does not use it.

A

True

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11
Q

RBC mitochondria produce ATP at (slower/faster) rate than other cells.

A

No mitochondria! Only ATP production by anaerobic glycolysis

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12
Q

If an RBC is depleted of ATP:

A

Shape changes (crenated)

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13
Q

Glucose enters RBC via which transporter(s)?

A

None; just by simple diffusion

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14
Q

Why/how does crenation of RBC happen?

A
  1. ATP depletion
  2. Dysfunction of Na/K and Ca pump
  3. Ca accumulates in cell (spiky appearance)
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15
Q

Sickle cell disease arises from:

A

One AA change in Hb

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16
Q

Which conditions begin the sickle cell crisis? Why?

A

Low oxygen or low pH; causes HbS to crystallize into long, rigid rods (gives cell sickle shape)

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17
Q

Why is a sickle shape problematic?

A

Cells not flexible, block vasculature, decrease oxygen and increase LA buildup (cycle)

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18
Q

Methemoglobin is (X) and functions to (Y).

A

X = oxidized form of Hb (has ferric ion)

Non-functional!

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19
Q

Oxidized Hb transforms into:

A

Dysfunctional Hb (methemoglobin)

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20
Q

T/F: oxidation of Hb is reversible.

A

True

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21
Q

(X) restores the iron to (Y), making Hb functional again.

A
X = methemoglobin reductase
Y = ferrous state (Fe2+)
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22
Q

RBC requires NADH because it acts as a(n) (X) for (Y).

A
X = cofactor
Y = methemoglobin reductase
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23
Q

NADH levels in RBC maintained by:

A

Glycolysis

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24
Q

Why is it important to maintain adequate H2O2 levels in RBC?

A

It’s not… H2O2 is potent oxidizing species for Hb

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25
Q

What’s the effect of H2O2 on RBC?

A

Cross-links Hb cysteines (inactivated protein)

26
Q

H2O2 levels in RBC are kept in check by:

A

Reaction with reduced GSH (glutathione)

27
Q

H2O2 + GSH equals…

A

Glutathione-peroxidase,

which then becomes oxidized glutathione and water

28
Q

Reduced GSH levels are kept in check by:

A

Glutathione reductase

29
Q

RBC requires NADPH because it acts as a(n) (X) for (Y).

A
X = cofactor
Y = glutathione reductase
30
Q

NADPH levels in RBC are kept in check by:

A

G6PD (in phosphogluconate pathway)

31
Q

Deficiency in (NADH/NADPH) can cause (X) anemia.

A

NADPH;

X = hemolytic

32
Q

The Luebering-Rapoport pathway is an off-shoot of (X). It’s important in producing (Y) for RBC.

A
X = glycolysis
Y = 2,3-DPG
33
Q

What’s the effect of 2,3-DPG in RBC?

A

Changes Hb affinity for oxygen (binds it less tightly if 2,3-DPG present)

34
Q

Formation of RBCs in fetus is dependent on:

A

Yolk sac (liver and spleen) and bone marrow

35
Q

Describe role of kidney in RBC formation.

A

RBC formation increased if low oxygen levels detected by JG Apparatus; kidney will secrete more EPO

36
Q

Iron used to synthesize Hb comes from:

A
  1. Old RBC (mainly)
  2. Body stores
  3. GI tract
37
Q

Old RBCs are taken up by (X). This occurs mostly in which organ? Why?

A

X = macrophages

Spleen - finest sieve in entire body and old RBC lose flexibility/can’t pass

38
Q

Most RBC meet their end by:

A

Extra-vascular hemolysis

39
Q

Macrophage breaks down Hb into which main components?

A
  1. Globin
  2. Fe
  3. Porphyrin ring
40
Q

In extravascular hemolysis, what’s the fate of globin?

A

Recycled into AA pool

41
Q

In extravascular hemolysis, what’s the fate of Fe?

A

Recycled by immediately binding Transferrin (which will take it to developing RBC)

42
Q

In extravascular hemolysis, what’s the fate of porphyrin ring?

A

Can’t be recycled, so converted to bilirubin

43
Q

In extravascular hemolysis, what’s the fate of bilirubin?

A
  1. Binds plasma albumin
  2. taken to hepatocyte
  3. secreted in feces as urobilinogen
44
Q

What’s the first step in intravascular hemolysis?

A
  1. Immediate oxidation of Hb to methemoglobin

2. Breakdown of tetramer to Hb dimer

45
Q

In intravascular hemolysis, what’s the fate of methemoglobin?

A

Breaks down into globin and heme

46
Q

In intravascular hemolysis, what’s the fate of heme?

A

Binds hemopexin and carried to liver

47
Q

In intravascular hemolysis, what’s the fate of Hb dimer?

A
  1. Binds haptoglobin and carried to liver

2. If haptoglobin all full, goes straight to kidney and secreted in urine

48
Q

In intravascular hemolysis, what’s the function of liver?

A

Takes either Hb dimer or heme and breaks them down into Fe and bilirubin (eventually secreted in feces)

49
Q

Why/when does our body produce CO?

A

Extravascular hemolysis; conversion of porphyrin ring to bilirubin in macrophage releases CO

50
Q

What are the clinical methods to test for (extra/intra)-vascular hemolysis? About how long is each test valid following event?

A

Intravascular;

  1. Test for low haptoglobin levels (up to 5 days)
  2. Hemoglobinuria; Test for presence of Hb in urine (up to 2 days)
51
Q

Why would inflammation cause hypoproliferative anemia?

A

Fe released by RBC death are taken up by bacteria, so low Fe content

52
Q

Too few (X) can cause anemia.

A

X = RBC or Hb

53
Q

Most common reason behind anemia is:

A

Hypoproliferation (production is too slow)

54
Q

Hemolysis refers to:

A

Abnormally rapid destruction of RBC

55
Q

In blood typing, the concern is agglutination of (donor/recipient/both) blood.

A

Donor (Ab in donor blood very dilute so they have no effect on recipient)

56
Q

Cell with D antigen are termed:

A

Rh-positive

57
Q

Describe the relationship between (deficiency/excess) of Vitamin (X) and (Y) anemia.

A

Deficiency;
X = B12
Y = hypoproliferative/pernicious

Condition leads to large-scale destruction of erythrocyte precursors

58
Q

In (X) anemia, intestinal absorption is compromised due to failure of (Y) cells to (Z).

A
X = pernicious
Y = parietal cells (in stomach)
Z = produce intrinsic factor
59
Q

Vitamin (X) is critical in which stage of RBC development?

A

X = B12 (and folic acid)

Proliferation of erythrocyte precursors in bone marrow

60
Q

Renal disease can cause (X) anemia because of (Y) (destruction/production).

A

X = hypoproliferative

X = inadequate erythropoietin production

61
Q

Thalassemia can be a cause for (X) anemia due to (Y) (destruction/production)

A

X = hypoproliferative

Y = abnormal Hb synthesis (and thus destruction of RBC precursors in marrow)