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Hematology > RBC and cancer metabolism > Flashcards

RBC and cancer metabolism Flashcards

1
Q

After 120 days, RBCs aredegraded by the spleen. What causes this?

A

Inability to squeeze through splenic veins

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2
Q

What is intravascular hemolysis?

A

RBCs are damaged while circulating through the circulation

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3
Q

What is the key biological marker of intravascular hemolysis?

A

Hb

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4
Q

What is extravascular hemolysis?

A

RBCs lose their flexibility too early, and are degraded by the spleen

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5
Q

What is the key finding of extravascular hemolysis?

A

Splenomegaly

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6
Q

Why is the no serological marker of extravascular hemolysis?

A

Spleen cleans blood

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7
Q

What is the cause for sphereocytic anemia?

A

Problems with RBC membranes–cells lose their membranes, round off, and are filtered by the spleen

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8
Q

What is the cause of non-spherocytic anemia?

A

Metabolic RBC problems, leading to degradation of RBC membrane

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9
Q

What is the marker for nonsphereocytic anemia?

A

Deficiency of glycolytic or pentose phosphat pathway enzymes

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10
Q

Defect in RBC metabolism generally lead to what type of anemia (sphereocytic? intra/extravascular)?

A

nonsphereocytic hemolytic anemia, with both intra and extracellular hemolysis

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11
Q

What is the MOA of bili lights?

A

Unfolds bilirubin, increasing hydrophilicity

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12
Q

What is the cause of the limited life span of RBCs?

A

no protein synthesis

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13
Q

What is the cause of hereditary sphereocytosis?

A

Spectrin mutation leads to rounded, short liverd cells

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14
Q

What is the marker for extravascular hemolysis?

A

Bilirubin

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15
Q

What is the state that Fe needs to be kept in to be useful? What is the energy carrier molecule that is used to do this?

A

2+ (ferrous)

NADH

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16
Q

What are the two minerals that RBCs need to balance? What is the energy carrier molecule that is used to do this?

A

K and Ca

ATP

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17
Q

What protein side chain needs to be kept reduced in RBCs? What is the energy carrier molecule that is used to do this?

A

SH groups

NADPH

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18
Q

What are the four things that RBC metabolism does for the cell?

A
  1. Maintain heme
  2. Defend mineral balance
  3. Keep proteins reduced
  4. Maintain shape
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19
Q

What are the two rate limiting steps in glycolysis?

A

Hexokinase reaction

PFK1 reaction

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20
Q

How is glycolysis in RBCs regulated? What is the physiological consequence of this?

A

acidity (enzymes are pH dependent. Thus acidosis or alkalosis will result in hemolytic anemia)

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21
Q

What happens to RBC metabolism if there is a metabolic acidosis?

A

Switch to burning lactate, to bring the pH back toward optimal

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22
Q

What is the “energy clutch” part of glycolysis of RBCs? Why is this important?

A

ability to perform glycolysis without the gain of ATP

not enough ADP to produce pyruvate

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23
Q

What are the three signs that a RBC is failing?

A

Fills with Ca
Release K
Lose biconcave shape

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24
Q

RBCs do not have mitochondria. What energy source is thus unable to be utilized by RBCs?

A

Fat

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25
Q

What is the step that is bypassed in glycolysis for the energy clutch?

A

from 1,3 bisphosphoglycerate to 3 phosphoglycerate

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26
Q

Draw out glycolysis pathway, with energy clutch step.

A

Draw out glycolysis pathway, with energy clutch step.

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27
Q

What is the major purpose for the energy clutch step?

A

ATP/ADP gain is 0, get NADH

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28
Q

What are the two enzymes that are utilized in the energy clutch pathway?

A

Diphosphoglycerate mutase

DPG phosphatase

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29
Q

What is the intermediate that is formed between disphosphoglycerate mutase and DPG phosphatase?

A

2,3 BP glycerate

30
Q

What is the role of 2,3 BPG outside of glycolysis?

A

maintains the T state of Hb, allowing for more oxygen delivery to tissue at lower [oxygen]

31
Q

What is the signal for RBCs to start using the energy clutch pathway? What is the enzyme that controls this?

A

lower pH

PFK1

32
Q

In cells other than RBCs, what is the enzyme that is regulated by insulin/glucagon?

33
Q

If the energy clutch is utilized, what is the only output of glycolysis?

34
Q

Low pH causes increased or decreased production of 2,3 BPG? What is the effect this has on acidosis?

A

Reduces

causes increase oxygen in the blood, increasing pH

35
Q

What is the Bohr effect?

A

Lower pH will decrease Hb affinity for oxygen

36
Q

Explain how the Bohr effect and the loss of 2,3 BPG at low pH are not at odds.

A

Low 2,3 BPG allows more oxygen pick up by RBCs, then as RBCs enter hypoxic tissues, will release oxygen

37
Q

Draw out the PPP.

38
Q

What is the output of the PPP?

39
Q

low intracellular NADPH levels activates what enzyme to start the PPP?

A

glucose-6-phosphate dehydrogenase

40
Q

What happens to the pentose products after they exit the PPP?

A

Reenter into glycolysis

41
Q

Does the PPP occur in RBCs?

42
Q

How is the PPP regulated?

A

Low NADPH will activate glucose-6-phosphate dehydrogenase

43
Q

What is the protein in RBCs that prevent the oxidation of proteins?

A

Glutathione

44
Q

What are Heinz bodies?

A

Damaged Hb

45
Q

What is the enzyme that converts superoxide to hydrogen peroxide?

A

superoxide dismutase

46
Q

Hydrogen peroxide is reduced to water by what enzyme?

A

glutathione peroxidase

47
Q

The elections donated by GSH come from where?

48
Q

What is the enzyme that keeps glutathione in the reduced state?

A

Glutathione reductase (duh)

49
Q

True or false: Genetic deficiencies usually result in intravascular hemolysis

A

False–usually extravascular, although less often it can be intravascular

50
Q

G6PD deficiency is transmitted how?

A

X-linked recessive

51
Q

Why is it that most pts with G6PD deficiencies do well?

A

Hematpoietic system is able to compensate

52
Q

What are the symptoms of G6PD deficiency?

A

Jaundice with infection d/t increased bilirubin production

53
Q

What is the food that pts with G6PD deficiency should avoid?

A

fava beans

54
Q

What are the drugs that pts with G6PD deficiencies should avoid?

A

Those that produce ROS

55
Q

What is the problem with pyruvate kinase deficiency?

A

RBCs run out of ATP, causing premature degeneration

56
Q

What are the symptoms of pyruvate kinase deficiency?

A

splenomegaly
Jaundice
Gallstones

57
Q

A peripheral blood stain of a pts with G6PD deficiency will show what?

A

Bites out of RBCs (Heinz bodies)

58
Q

What is the major difference between pyruvate kinase deficiency and G6PD deficiency?

A

ROS is an issue with G6PD, while it is not for pyruvate kinase deficiency

59
Q

A peripheral blood stain of a pts with pyruvate kinase deficiency will show what?

A

Blebbing of RBCs d/t loww of energy

60
Q

What is in grey top tubes that allows for analysis of RBC metabolism? Why are these used?

A

sodium fluoride / potassium oxalate

Fluoride inhibits enolase
Oxalate is an anticoag

61
Q

Tumor cells get most of their energy from what process? What is the substrate that they produce?

A

Glycolysis

Lactate

62
Q

Why do CA cells undergo anaerobic glycolysis often?

A

Not enough blood supply to the tumor

63
Q

What is the role of HIF1-alpha in tumor cells?

A

Increased expression increases expression of glucose transporters

64
Q

What is the cycle whereby the liver takes up lactate and converts ito pyruvate?

A

Cori cycle

65
Q

What is the name of the filament that serves as an anchor for plasma proteins in RBCs?

A

beta-spectrin

66
Q

What is the name of the protein that attaches to beta spectrin, and allows for the attachment of surface proteins?

A

Ankyrin

band 3

67
Q

RBC cytoskeletal defects usually present how?

A

As heriditary sphereocytosis

68
Q

What is the most common cytoskeletal defect?

A

akyrin defect

69
Q

Blood smears of pts with RBC cytoskeletal defects will show what?

A

SPhereocytes

70
Q

What do sphereocytes look like histologically?

A

Round without pale center as is usualy for RBCs

71
Q

What is the gene that causes paroxysmal noctural hemoglobinuria? What chromosome is this located on?

A

PIGA gene

X-chromosome

72
Q

RBCs with the PIGA gene defect are susceptible to what? Why?

A

complement attack d/t loss of protein attachment

Hematology (32 decks)

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