RBC Flashcards

1
Q

Jobs of the RBC

A

prevent renal loss
carry carbonic anhydrase
buffer for the blood (like other proteins)

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2
Q

what is the role of carbonic anhydrase

A

allows us to sequester CO2 as bi carbonate

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3
Q

biconcave disc allows for

A

flexible membrane and they can bend on themselves to move through very tight spaces like where capillaries turn; better exchange for gases as well

as well as enhanced surface area

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4
Q

RBC amount in body and amt of Hgb carried

A

5.2 M/100 microliters of blood in men

always near carrying cappacity

14-16 gm of hemoglobin on average

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5
Q

production of RBC

A

begins in yok sac
moves with the incorporation of abdominal contents and then production is taken over by the liver spleen and nodes

finally this moves to the bone marrow in around the 8th or 9th month of life and this is the final placement of the RBC

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6
Q

role of glycoproteins

A

give RBC negative charge and repel from other cells or clumping

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7
Q

describe the production of RBC beginning with the stem cell

A

pluripotent stem cells becomes erythroid progenitor

stops having the potential to turn into other types of cells

the daughter of this progenitor are “committed stem cells”

CFU can be played out from these

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8
Q

most important mediator of RBC production

A

EPO

this is a renal hormone 90% of it comes from the kidney

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9
Q

what triggers EPO and what is necessary for this production

A

Sympathetic response -(bleeding)

need B12 and folic acid for the

DNA synthesis and replication
because these cells are very high turnover they require a lot of this for cell division

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10
Q

how does the absence of B12 or folate influence the production of RBC

A

in the absence of B12 or folate the nucleus foes not keep up with the cytoplasms and doe not do the replication that it needs to

resulting in a large cell

macrocytic anemia

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11
Q

pernicious anemia

A

failure to absorb B 12 leads to pernicious anemia

in order to absorb we need a intrinsic factor that will bind and carry for absorption in the intestine

atrophic stomach
bipass surgery
autoimmune deficiency can destroy intrinsic factor and limit absorption

can lead to pernicious anemia

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12
Q

how does EPO influence RBC growth

what happens if EPO does not exist

A

CFU and common erythropoytin cells that express the EPO receptor

the EPO is a growth factor that stimulates the final differentiation of the stem cells

in the absence of these cells die

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13
Q

EPO receptor

how it works when activated

what are JAK and STAT

A

homodrimeric
formed from two proteins

when bound there is a confirmation change that will stimulate tyrosine kinase molecule activity in cytoplasm

two transcription factors will induce transcription that will lead to the completion of the differentiation process

JAK and STAT are these two factors

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14
Q

two lineages that arise from pluripotent stem cell

A

lymphoid stem cell (only lymphocytes)

myeloid stem cells

can have cancers in both of these lineages

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15
Q

erythrocyte is part of what lineage

A

myeloid stem cell lineage

a lot of steps in between myeloid cell and erythrocyte

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16
Q

what is the preerythroblast

where is it located and what role does it play

A

first cell to make Hgb

confined to the bone marrow

WILL NOT FIND IN BLOOD

will move through stages of development

proerythroblast will force organelles like the nucleus out and the nucleus will become pyknotic

as the Hgb levels increase the cell will get smaller

17
Q

basophil erythroblast

A

will stain with basic dyes because it is acidic on the inside hence the name
(BLUE)

this is the intermediate in between the proerythrobalst and the reticulocyte

18
Q

reticulocyte

A

baby RBC

nucleus and protein apparatus/machinery is gone

DOES NOT HAVE A NUCLEUS

contains a few polyribosomes and continues to make protein after nucleus is gone based on mRNA left over

(Hgb levels will continue to rise)

will be able to move into the blood stream and will speak to how aggressively the body is trying to pump out RBC and how much EPO is being produced in response to stress

19
Q

Hgb

A

speherical tetramer of 4 subunits

pyrroles from succinyl coA and glycine

4 pyrroles form protoporphyrin IX

Addition of iron to protoporhyrin forms Heme

globin polypeptide completes a hemoglobin subunit

(heme plus globin)

which contains iron these are comitted stem cells

20
Q

HgBA

what is it an what is the prophyrin ring

A

two alpha and two beta subunits (usually a 1:1 combination)

porphyrin ring on which iron binds nitrogen molecules

2 dimers from the tetrame

majority found in most of us

21
Q

which type of iron binds ocygen

A

ferrous Fe2

Fe3 accumulates and causes oxidative stress

22
Q

methemoglobin

A

generated by the oxidation of heme to the ferric state causing bluish brown color

high ocygen affinity of methmoglobin means to oxygen is delivered

some globin mutations can stablize iron in this state

you can also get a methemoglobinemia form toxins that oxidize heme orin like nitrate

23
Q

what is the molecule responsible for stabilizing Hgb prior to oxygen binding

A

oxygen changes to state of the protein

and keeps 2,3, diphosphoglycerate from stabilizing in unbound state

when this occurs DPG can no longer keep oxygen from binding and the 02 affinity increase

24
Q

why are RBC not really cells

A

no nuclei and no mitochondria
this is why we call them erythrocytes

b/c they would steal the O2 from the tissues

very limited protein repair and membrane maintance is allowed but this is in part of the reason why we see such a short lifespan

25
Q

how does a RBC undergo metabolism

A

Embden-Myerhof pathway

allows for metabolism
through this glycolytic pathway within the cell

can’t do atp metabolism with oxygen

anaerobic and produces latic acid and 2,3, DPG as biproducts

need glucose form the blood stream and NADH as an essential cofactor

26
Q

what is required for the Embden-Myerhof pathway

A

need glucose form the blood stream and NADH as an essential cofactor

27
Q

pathophys of SCA

A

hydrophobic
distortion of the sickle due to a valine substitution for a glutamate hemoglobin leads to mishaping after deoxygenation

allow for aggregation of polymers and sickling

28
Q

how does acidosis and small flow vessels lead to increase intravascular hemolysis with sickle cell anemia

A

acidosis decreases affinity for oxygen

small low flow vessels

where Hgb has lots of time to dump oxygen

29
Q

low haptoglobin indicates what

A

intravascular hemolysis because it is gathering HgB

this recycling can lead to an increase in unconjugated bilirubin

jaundice

also see increase in reticulocytes

30
Q

complications of SCA

A

increased reticulocytes leads to an increase in bone formation

stuck in bones causing dactylitis

bone pain

spleenic infarct

31
Q

oxygen binding influences itself by

A

a. Loose association of oxygen with hemoglobin molecule

b. Binding of each molecule of oxygen makes hemoglobin more receptive to the next

32
Q

cellular storage form and what it is composed of

A

i. Ferritin is the storage form of iron in our body = important

33
Q

insoluble form of iron that occurs when ferritin is maxed out

A

hemosiderin

34
Q

Hypochromic anemia from failure of

A

transferrin to enter erythroblasts

can’t make chromogen
hypochromic

Can’t make hemoglobin without the iron

35
Q

Apotransferrin in blood binds Fe

A

form transferrin (very similar to absorption)

this is how iron is transported

36
Q

life span of the RBC and how we use this

A

i. When we do A1c, we are looking at glucose molecules stuck to the hemoglobin molecules

37
Q

how does the spleen help with the death of RBC

A

Cells rupture in transit through small spaces, often in the spleen

Spleen is there to recover the old RBCs

many macrophages ingest and return iron to the blood, porphyrin lost as bilirubin