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Hema 1 > Erythrokinetics > Flashcards

Erythrokinetics Flashcards

1
Q

Dynamics of RBC production and destruction

A

Erythrokinetics

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2
Q

Collection of all stages of RBC throughout the body in the BM, PB, vascular spaces within organs

A

Erythron

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3
Q

The entirety of all erythroid cells (rbcs), whether it is
mature or immature

A

Erythron

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4
Q

refers only to the cells in circulation

A

RBC mass

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5
Q

a stimulus to RBC production

A

Hypoxia

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6
Q

main role of RBC

A

carry oxygen

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7
Q

It has the ability to sense adequacy of oxygen supply to tissues

A

Primary oxygen-sensing system

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8
Q

Location of primary oxygen-sensing system (be very specific)

A

Peritubular fibroblast of the kidney

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9
Q

Mechanism of POSS

A

Once inadequacy of O2 supply is detected, it triggers EPO production

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10
Q

Diminished or decrease of tissue oxygenation in our body

A

Hypoxia

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11
Q

Organ responsible in detecting oxygen adequacy in tissues

A

Kidney

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12
Q

Give 2 very important features of oxygen sensing system

A
  1. It has mechanism to detect inadequacy or adequacy if O2
  2. It has a mechanism that can influence or trigger the increase of RBC production by triggering EPO
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13
Q

Major stimulatory cytokine or stimulatory hematopoietic growth factor for RBCs

A

erythropoietin

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14
Q

most sensitive cell to EPO

A

Colony Forming Unit - E / CFU-E

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15
Q

erythroid progenitor cells that has the most EPOR

A

CFU-E

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16
Q

First human hematopoietic growth factor to be identified

A

Erythropoietin

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17
Q

Location of gene for EPO

A

Chromosome 7

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18
Q

it regulates the increase of EPO production as a response / physiologic adaptation to hypoxia

A

Hypoxia-Inducible Factors (HIFs)

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19
Q

EPO is found in the ff cells:

A

Erythroid Progenitor Cells (BFU-E and CFU-E)

Early erythroid precursor cells (Pronormoblast and Basophilic Normoblast)

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20
Q

Transcription factor that mediates EPO

A

GATA1

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21
Q

It serves as the primary source of EPO from newborn to adulthood / throughout life

A

Kidney

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22
Q

Specific part of the kidney where EPO in produced

A

peritubular insterstitial cells of kidney

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23
Q

It is primary source of EPO in the newborn

A

Liver

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24
Q

Complete the statement: EPO is a thermostable, nondialyzable, glycoprotein hormone that has ________ unit & _______ unit

A

carbohydrate ; terminal sialic acid

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25
Q

Nice to know: molecular weight of EPO

A

34 kD

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26
Q

3 major actions of EPO in increasing RBC Production

A
  1. It promotes early release of reticulocytes from the BM
  2. MAJOR ACTION: Prevents apoptotic cell death
  3. Reduces the time needed for cells to mature in the BM
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27
Q

Refers to reticulocytes released to the peripheral blood earlier than intended

A

Shift / stress reticulocye

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28
Q

In normal process, reticulocytes will stay in the BM for:

A

1-2 days or 2-3 days before released in circulation

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29
Q

In normal process, retics are in the circulation for a period of ___ before becoming RBCs

A

24 hrs / day

30
Q

Location of developing cells in the BM

A

hematopoietic / extra vascular cords

31
Q

developing blood cells are separated from the vascular sinuses by 2 layers of cells, namelyL

A

Adventitial Cells
Endothelial Cells

32
Q

What does the EPO does in the cells surrounding the developing RBCS in order to release shift reticulocytes

A

Conformational change that causes widening of spaces between the reticular adventitial cells

33
Q

It secretes extracellular fluids that anchor developing cells

A

stromal cells

34
Q

developing cells are arranged in their proper location by:

A

semi extracellular matrix

35
Q

Adhesive molecule in charge of anchoring developing cells in their proper location

A

fibronectin

36
Q

EPO’s action to be able to release shift/stress retics despite of being anchored in the hematopoietic cord

A

down regulate or reduce the expression of receptors for adhesive molecules

37
Q

Where are receptors for adhesive molecules found

A

membrane of reticulocytes

38
Q

In cases where the body has increase RBC demand, the reticulocytes will be released in the circulation in _____, depending on the severity of the condition

A

less than 24 hours

39
Q

these are cells with EPOR

A

Erythroid progenitor cells
erythroid precursor cells

40
Q

cells that respond to EPO in healthy circumstances

A

cells that are less sensitive to EPO

41
Q

In case of hypoxia, what type of cells respond to EPO

A

cell that are highly sensitive to EPO

42
Q

portion of EPOR where EPO binds

A

extracellular domain

43
Q

binding of EPO to EPOR activates the signal transducer _____, which is associated with the cytoplasmic domain of EPOR

A

Janus Kinase 2 / JAK 2

44
Q

After activation of JAK2, it will further cause the activation of diff. signal transduction pathways (STPs) going to the nucleus of the cell. One of which is the:

A

STAT5 Pathway / Signal transducer and activator of transcription 5

45
Q

It bears the receptor

A

target cell

46
Q

amount of RBC lost everyday

A

approximately 1%

47
Q

Under normal conditions: Loss of 1% RBC Daily will result to EPO increase but only to _____

A

compensate

48
Q

In severe anemia, the EPO production can increase ____ regardless of pathologic mechanism causing it

A

1,000-fold (1,000x)

49
Q

EPO production fluctuates significantly or significantly increase particularly during:

A

hypoxic conditions or
anemic stress

50
Q

What happens to hypoxia-inducible factors in non hypoxic conditions / normal state

A

HIFs are being subsequently degraded because we do not need them

51
Q

In hypoxic conditions, the one that senses / responds to it first is the:

A

Primary Oxygen Sensing System (POSS)

52
Q

What happens to HIFs in hypoxic conditions?

A

HIFs will accumulate then will activate certain transcription genes that will promote response to adopt to hypoxic conditions

53
Q

Binding of HIFs to EPO gene leads to

A

increased transcription of the EPO gene, leading to increase EPO protein production

54
Q

Once the normal tissue oxygenation is restored back to normal, what will then happen?

A

The peritubular interstitial cells detects this which leads to degradation of HIFs = No HIFs to binds to EPO genes, EPO production decreases, RBC production decreases

55
Q

other function of HIFs

A

enhance cellular iron
intestinal absorption
stimulate maturation and proliferation of erythroid progenitor cells

56
Q

How to differentiate shift/stress reticulocyte from normal/typical reticulocytes?

A

Apply Wright stain.

Normal polychromatic erythrocyte have pink as predominant and minimal blue.

Shift retics are more baophilic

57
Q

How long does it take for shift reticulocytes to mature in the circulation

A

24hrs (normal) + 48hrs = 72 hours / 3 days

58
Q

What causes the basophilia of shift reticulocytes

A

Ribosomes and rRNA

59
Q

Why can’t our body store RBCs?

A

All of RBCs must be in circulation because their primary function is to provide oxygen to tissues. We cannot store them because of their limited life spam of 120 days. In short, all of them will age and die.

60
Q

Body’s compensatory mechanism in case of emergency since we cannot store RBCs

A

Produces excess colony forming unit E

61
Q

Why our body produces excess CFU-E, and why not just BFU-E when it will also eventually mature into RBC?

A

CFU is more lineage restricted on what type of cell it will differentiate into

62
Q

Fas is expresses on these cells

A

Erythroid progenitor cells such as the BFU and CFU and early erythroid precursor cells such as pronormoblast and basophilic normoblast

63
Q

FAS L is expressed on these cells

A

More mature erythroid precursor cell such as the polychromatophilic normoblast, orthochromatophilic normoblast, and polychromatophilic erytheocytes

64
Q

In normal state, how does apoptosis occur when extra RBCs are not needed?

A

Fas-L bearing erythroid precursor cells collide with those Fas-bearing erythroid precursor cells. Fas-L bearing (ligand) cells bind with the Fas bearing (receptor), signal will be created and received by the cells bearing the receptors, leading to its death

65
Q

Give an example of anti-apoptotic molecule

A

BCL-XL

66
Q

Where is BCL-XL produced and expressed

A

Mitochondrial membrane of the developing cell

67
Q

Why is BCL-XL, an apoptotic molecule, expressed on the “mitochondrial membrane” of the developing cell

A

The mitochondria is capable of producing apoptotic substance, named “CYTOCHROME C”. We have to prevent release of this substance in exchange of apoptosis

68
Q

G0 is also known as

A

Resting phase

69
Q

G1 is also known as

A

Cell growth phase

70
Q

How does EPO reduces the time needed for cells to mature in the BM?

A

cytokine (EPO) decreases the transmit time from G0 (resting phase) to G1 (cell growth phase), for faster cell division or mitosis, thus increasing the rate of normoblastic proliferation.

71
Q

Erythrocyte destruction is termed as

A

Eryptosis

72
Q

Process of cellular aging is termed as

A

Senescence

Hema 1 (2 decks)

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