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Hematology > Hematopoiesis & Its Impairments > Flashcards

Hematopoiesis & Its Impairments Flashcards

1
Q

What percentage of BM cells are pluripotent stem cells?

A

1 in 20 million

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2
Q

What receptors do pluripotent stem cells have on their surface?

A

The have growth factor receptors, i.e. GM-CSF.

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3
Q

What are Burst Forming Units (BFU) and Colony Forming Units (CFU)?

A

They are the precursors to Red Blood Cells, from Common myeloid progenitor cells.

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4
Q

What can we normally see microscopically in the bone marrow? Percentages?

A

Erythropoiesis (20-30%)
Myelopoiesis (60-70%)
Thrombopoiesis

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5
Q

What is the order of differentiation of granulocyte precursors?

A

Blasts - Promyelocytes - Myelocytes - Metamyelocytes - Bands and Neutrophils

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6
Q

What mnemonic can be used to remember the differentiation order of granulocyte precursors?

A

Blast and Play My Metal Bands and Nothing (Else)

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7
Q

What is a characteristic of blast cells visibly?

A

They have smudgy chromatin

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8
Q

What is a charac of promyelocytes?

A

Larger than blasts with immature nucleus. Has primary blue granules.

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9
Q

What is a charac of myelocytes?

A

Small, prominent golgi with red granules.

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10
Q

What is a characteristic of metamyelocyte?

A

Nucleus beings to indent

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11
Q

At what two stages of granulocyte development can we regulate maturation with G-CSF?

A

Between Blasts and Promyelocytes

Between Promyelocytes and Myelocytes

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12
Q

What are the three end products that can form from blast cells?

A

Bands and Neutrophils
Megakaryocytes
Normochromic Erythroblasts

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13
Q

What do megakaryocytes make?

A

Platelets

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14
Q

What is the prominent characteristic of megakaryocytes?

A

They are more segmented than neutrophils. Also, they are polyploidy.

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15
Q

Explain the regulation of thrombopoeisis.

A

The liver produces a constant amount of TPO. In normal people, this binds to platelets and megakaryocytes (producing more platelets). In thrombocytopenia, more able to bind to megakaryocytes , leading to increased thrombopoeisis.

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16
Q

What are the stages of development to erythroblasts from blasts?

A

Blast to pronormoblast to basophilic erythroblast to polychromatophilic erythroblast to normochromic erythroblast.

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17
Q

What is the mnemonic to remember the development of erythroblasts?

A

Bored Princes Bump Plenty of Nights

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18
Q

What are characteristics of pronormoblasts?

A

Large with dark blue cytoplasm

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19
Q

What are characteristics of basophilic erythroblasts?

A

Smaller Nucleus with blue nucleus

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20
Q

What are characteristics of polychromatophilic erythroblasts?

A

Grey cytoplasm

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21
Q

What must normochromic erythroblasts do before they become mature?

A

They must extrude their nucleii.

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22
Q

Visually compare the BM of someone age 5 and age 35

A

Age 5 has 80-90% cellularity
Age 35 has 40% cellularity

Has increasing amounts of fatty deposits.

23
Q

What does heme synthesis require?

A

Iron, B6, Succinyl CoA, Glycine (B12 and Folate)

24
Q

What does globin synthesis require?

A

Normal Globin Genes, Amino Acids

25
Q

What does DNA synthesis require?

A 
Deoxynucleoside Triphosphates
Ribonucelotide Reductase (which required Thymidine which requires B12 and Folate)
26
Q

What are the three ways to become anemic?

A

Losing red cells
Not making enough red cells
Both

27
Q

What ways do we describe cells that are iron deficient?

A

Microcytosis, Hypochromia, Anisocytosis, Poikilocytosis

28
Q

When giving someone an iron supplement, what is a good co-administration to recommend that they take as well?

A

Vitamin C, which reduces Dietary Ferric Iron to Ferrous Iron (absorbable).

29
Q

Explain the overall iron uptake process?

A

Dietary Ferric Iron in the GI tract is reduced to Ferrous Iron by Vitamin C or low pH. Then, it’s transported into the plasma. Once here, it’s oxidized to Ferric Iron again, where it becomes bound to transferrin. Organs possess transferrin receptors, allowing the iron to brought into cells.

30
Q

Why is the transferrin important in the plasma?

A

Prevents free iron from making superoxides

31
Q

What is serum ferritin?

A

Safely stored iron

32
Q

What is serum iron?

A

The amount of iron that is bound to transferrin in the plasma

33
Q

What levels change during iron deficiency?

A

Reduced serum iron
Reduced iron saturation
Increased soluble transferrin receptor (allowing as much iron uptake as possible)
Transferrin will be upregulated

34
Q

What is the TIBC?

A

Total Iron Binding Capacity. The blood’s ability to bind iron to transferrin. Functions as an indirect measure of transferrin levels (which is more expensive to directly measure)

35
Q

In iron deficiency how do macrophages in the spleen and liver assist?

A

They contain ferritin, which they release into the plasma. At this point, the iron is available to be brought into the bone marrow macrophages to be used as red cell precursors.

36
Q

What are characteristics of beta thalassemia?

A

Microcytic, Hypochromic, frequent target cells, normal or increased numbers of red blood cells.

37
Q

What CBC values change in Beta Thalassemia?

A

RBC goes up

Hg, Hct, and MCV go down

38
Q

What is the beta gene located?

A

On chromosome 11, with 6 total copies

39
Q

What is hemoglobin a?

A

alpha2 beta2

40
Q

What is hemoglobin a2?

A

alpha2 delta 2

41
Q

What is fetal hemoglobin?

A

alpha2 gamma2

42
Q

Where the gene locus for alpha globin?

A

On chrom 16, with 4 fxnal copies (harder to knock out)

43
Q

What area has a high rate of alpha thalassemia with one defective allele

A

SE asians

44
Q

1 Defective allele in alpha thalassemia leads to what?

A

Almost nothing

45
Q

2 defective alpha allels leads to what?

A

mild microcytic anemia, xs hg gamma4 at birth. 3% of african americans

46
Q

3 defective alpha alleles?

A

hb H disease, variable degree of microcytic anemia

47
Q

Four defective alpha allels?

A

you’re dead, common in SE asia

48
Q

What is the significance of comparing nuclear and cytoplasmic development in impaired dna synthesis of rbcs?

A

normal/enhanecd maturation of cytoplasm with reduced nuclear maturation

49
Q

What causes megalobastic anemia?

A

Impaired b12 uptake
impaire folate uptake
drug effect
intrinsic bm dysfunction

50
Q

Is delayed nuclear development common in megaloblastic anemias?

A

Yes, it’s the central feature

51
Q

What comes from the spleen that is essential in causing increased erythropoeisis?

A

EPO

52
Q

What does hepcidin do?

A

Impairs the release of Fe2+ to transferrin from storage .

53
Q

How does IL6 regulated hepcidin?

A

It upregulates it’s release because iron is great food for bacteria. So IL6 works to diminish serum iron

Hematology (7 decks)

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