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Hematology week 1 > Hematopoiesis > Flashcards

Hematopoiesis Flashcards

1
Q

Hematopoiesis

A

the formation and development of blood cells.

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2
Q

Hematopoiesis includes:

A

Erythropoiesis, Leukopoiesis, Thrombopoiesis

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3
Q

Erythropoiesis

A

formation and development of red blood cells

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4
Q

Leukopoiesis

A

formation and development of white blood cells.

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5
Q

Thrombopoiesis

A

formation and development of platelets.

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6
Q

mesoblastic stage

A

The yolk sac 0-2 months

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7
Q

hepatic stage

A

The liver and spleen are the main organs involved in hemopoiesis from two months to seven months of fetal life, and they continue to produce blood cells until about two weeks after birth

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8
Q

myeloid stage

A

5-9 months BM

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9
Q

the most important hemopoietic site, and it is the only source of new blood cells during normal childhood and adulthood

A

BM

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10
Q

spongy tissue in the middle of the bones where new blood cells are formed.

A

BM

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11
Q

when is the marrow in all bones is active and contributes to blood cell formation; red marrow.

A

at birth

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12
Q

The red marrow is gradually replaced() and becomes inactive; ()

A

by fibrous and fatty tissues
yellow marrow

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13
Q

By the age of 20 years, the red marrow is limited to the

A

flat bones and the ends of long bones.

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14
Q

There are two types of stem cells in the BM:

A
  • Haematopoietic stem cells: form blood cells; WBC’s, RBC’s, platelets.
  • Stromal stem cells: generate other types of cells; fat, cartilage, bone
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15
Q

Hematopoiesis is regulated by glycoproteins ()

A

known as hemopoietic growth factors

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16
Q

hemopoietic growth factors,

A

which can regulate the proliferation and differentiation of hemopoietic progenitor cells as well as the function of mature blood cells.

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17
Q

The biological effects of growth factors are mediated through

A

specific receptors on target cells.

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18
Q

The main sources of growth factors are: 5

A
  • T-lymphocyte.
  • Monocyte.
  • Endothelial cells.
  • Fibroblast.
  • Kidney (erythropoietin and thrombopoietin)
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19
Q

Hemopoietic Growth Factors act on stromal cells

A

IL1 TNF

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20
Q

Hemopoietic Growth Factors pluripotent stem cells

A

stem cell factor VEGF

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21
Q

Hemopoietic Growth Factors multipotent progenitor cells

A

IL3 GM-CSF IL-6 G-CSF thrombopoietin

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22
Q

Hemopoietic Growth Factors on committed progenitor cells

A

IL-5 G-CSF M-CSF thrombopoietin erythropoietin

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23
Q

Hemopoiesis Requirements

A

1-Hemopoietic growth factors
2-Nutrients
3- Vitamins
4- Metals

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24
Q

Erythropoeisis stages

A
  • Proerythroblast: the first cell to be identified as belonging to the red blood cell line.
  • Basophil erythroblasts: first generation cells resulting from divisions of proerythroblasts; with little hemoglobin produced.
  • Polychromatophil and orthochromatic erythroblasts: hemoglobin concentration increases; nucleus condenses.
  • Reticulocyte: nucleus remnant extruded from cell and endoplasmic reticulum reabsorbed; cells pass from bone marrow to blood capillaries (diapedesis).
  • Mature erythrocyte: remaining basophilic material of reticulocyte disappears.
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25
Q

Erythropoietin

A

Is a glycoprotein hormone, mainly produced by the kidneys (90%) in response to hypoxia; 10% produced in the liver.

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26
Q

Renal tissues hypoxia leads to

A

increased level of hypoxia inducible factors HIF (1 and 2)à secretion of erythropoietin.

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27
Q

Erythropoietin stimulates erythropoiesis by

A

increasing the number of progenitor cells committed to erythropoiesis:
* Stimulates production of proerythroblasts.
* Promotes the rapid development of proerythroblasts.

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28
Q

Factors That Enhance RBCs Production

A

Vitamin B12 (Cobalamin)
Folic acid
Iron

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29
Q

Vitamin B12 is required for

A

DNA synthesis, maturation of RBCs, and myelin formation

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30
Q

Cobalamin Daily requirement is

A

about 1-3 microgram.

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31
Q

B12 is absorbed from the

A

terminal ileum.

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32
Q

Absorption requires binding of B12 to the intrinsic factor that is produced

A

gastric parietal cells in the stomach.

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33
Q

B12 deficiency can cause

A
  • Megaloblastic anemia.
  • Impairment in myelination of the nervous system; subacute combined degeneration of the cord.
34
Q

Vit b12 absorption mechanism 3 sites

A

◦ Stomach: Cobalamin is released from ingested proteins by pepsin and binds to the glycoprotein haptocorrin (R-protein){released by salivary glands}, which protects it from gastric acid.
◦ Duodenum: Cobalamin is released from haptocorrin by trypsin and binds to intrinsic factor (IF), a protein produced by the parietal cells of the stomach that facilitates cobalamin absorption in the ileum.
◦ Terminal ileum: cubilin receptor‐mediated endocytosis of the intrinsic factor-cobalamin complex → breakdown of IF in enterocytes, release of cobalamin, followed by binding to carrier protein transcobalamin II and then enters the plasma → cobalamin is either delivered to metabolically active tissues or stored in the liver

35
Q

B12 deficiency is usually due:

A
  • Inadequate intake:
    • Vegetarian diet. * Malabsorption:
    • Lack of intrinsic factor or parietal cells:
    • Pernicious anemia, damage of the parietal cells by
      autoantibodies.
    • Post-gastrectomy. * Atrophic gastritis.
  • Diseases of the terminal ileum: * Crohn’s disease.
    • Bacterial overgrowth.
  • Transcobalamin deficiency.
36
Q

Causes of folic acid deficiency:

A
  • Inadequate folate intake.
  • Malabsorption: barbiturates, phenytoin, and oral contraceptives. * Impaired metabolism: methotrexate or rare enzyme deficiencies
37
Q

The biochemical basis of megaloblastic anaemia caused by

A

vitamin B12 or folate deficiency

38
Q

Vitamin B12 is needed to convert

A

methyl THF, which enters the cells from plasma, to THF, from which polyglutamate forms of folate are synthesized.

39
Q

Dietary folates are all converted to

A

methyl THF (a monoglutamate) by the small intestine.

40
Q

Iron absorption occurs in the

A

upper small intestine; mainly duodenum and upper jejunum.
* Free iron must be in the reduced form [Fe++].

41
Q

Factors that help in iron absorption:

A
  • HCl of the stomach.
  • Vitamin C.
42
Q

Factors inhibiting iron absorption:

A
  • Phosphates and phytates (in plants): form insoluble complexes.
  • Some drugs: e.g. tetracyclin. * Alkalis.
43
Q

Iron Transport And Storage

A
  • Absorbed from the intestinal tract by the aid of apotransferrin.
  • Iron in the blood is transported mainly bound to transferrin.
  • Transferrin is normally about 30% saturated.
  • Excess iron is stored mainly in the liver as ferritin.
  • Ferritin is soluble and readily gives iron when it is needed.
  • Another storage form of iron is haemosidrin, it is insoluble,
    formed when the iron body contents are abnormally large.
  • Deposition of haemosidrin in soft tissues in large amounts (haemosidrosis) may cause damage (Bronze diabetes).
44
Q

Iron Requirements

A
  • Daily iron needs in males is 1 mg and in females is 2 mg.
  • Iron absorption efficiency in the intestine is only 10–15 %,
    therefore, dietary requirements for iron is 10-20 mg/day.
  • Daily loss in males is 0.6-1 mg and in females 1-2 mg.
  • Increased iron demand: * Pregnancy.
  • Lactation.
  • Growing children.
45
Q

Iron Deficiency

A
  • Iron deficiency causes anaemia characterized by small, pale red cells (microcytic hypochromic anaemia).
  • Causes of iron deficiency:
  • Poor intake.
  • Increased needs:
  • Early childhood and adolescence, pregnancy and lactation.
  • Decreased absorption:
  • Achlorhydria, inflammatory bowel diseases.
  • Increased loss:
  • Heavy menstrual cycles.
  • Bleeding (ulcers, intestinal worms).
46
Q

where do leukocytes originate from

A

pluripotent hematopoietic stem cells

47
Q

Pluripotential cells differentiate into

A

myeloid stem cells and lymphoid stem
cells.

48
Q

Myeloid stem cells become

A

myeloblasts or monoblasts.

49
Q

Myeloblasts develop into

A

eosinophils, neutrophils, and basophils.

50
Q

Monoblasts develop into

A

monocytes.

51
Q

Lymphoid stem cells become and develop into

A

lymphoblasts.
* Lymphoblasts develop into lymphocytes

52
Q

what are small, granulated bodies that lack nuclei and are 2–4 μm in diameter; normally have a half-life of about 4 days.

A

platelets

53
Q

The sequential developmental pathway of platelet is

A

hemocytoblast, megakaryoblast, promegakaryocyte, megakaryocyte, and platelets.

54
Q

what is the major regulator of platelet formation

A

Thrombopoietin (TPO)

55
Q

where is Thrombopoietin (TPO) formed

A

95% is produced by the liver.

56
Q

Between 60 and 75% of the platelets that have been extruded from the bone
marrow are in

A

in the circulating blood, and the remainder are mostly in the spleen.

57
Q

what causes an increase in platelet count

A

Splenectomy

58
Q

As ATP becomes depleted how will the RBC look

A

cell will become a sphere and loose the ability to deform (becomes rigid)

59
Q

The main metabolic pathways in RBCs, which in turn affect their life span, are:

A

Glycolysis
Hexose MonoPO4 shunt
Luebering-Rapoport shunt

60
Q

provides necessary ATPS for existence; maintenance of red cell volume, shape and flexibility.

A

Glycolysis:

61
Q

provides NADPH for keeping glutathione in reduced form, which is necessary to prevent hemolysis.

A

Hexose MonoPO4 shunt:

62
Q

produces 2,3-DPG, which decreases Hb affinity for oxygen.

A

Luebering-Rapoport shunt

63
Q

Hemoglobin and red blood cell membrane are usually protected from oxidant stress by

A

GSH

64
Q

converts Glu-6-P to 6-Phosphogluconate by G-6-PD thereby producing NADPH.

A

HMP shunt

65
Q

G6PD def

A

impaired synthesis of NADPH & GSH
&
RC r susceptible to oxidant stress

66
Q

Provides 90% of ATP

A

Embden-Meyerhof Glycolytic Pathway

67
Q

Provides adequate amounts of ATP necessary to
o Maintain erythrocyte shape, flexibility, and membrane
integrity
o Regulate intracellular cation concentrations o Sodium, potassium, calcium pumps

A

Embden-Meyerhof Glycolytic Pathway

68
Q

Embden-Meyerhof Glycolytic Pathway Utilizes the enzyme

A

Utilizes the enzyme pyruvate kinase

69
Q

Also referred to as Phosphogluconate pathway

A

Hexose Monophosphate Shunt

70
Q

G6PD is the enzyme utilized

A

Hexose Monophosphate Shunt

71
Q

NADPH together with glutathione protects against oxidative injury from toxic reducing oxidants

A

Hexose Monophosphate Shunt

72
Q

Ifpathwayisdefective,globinchainsinhemoglobin denature and precipitate as aggregates called

A

Heinz bodies

73
Q

Heinz bodies damage

A

the red cell membrane and causes the cell to be destroyed

74
Q

Folic acid is normally found in

A

in green vegetables, some fruits and liver; easily destroyed by cooking.

75
Q

folic acid daily requirement

A

Daily requirement is 100-200 microgm and storage in the body is relatively small

76
Q

folic acid Deficiency develops

A

rapidly in case of inadequate intake or increase needs.

77
Q

Folic acid is needed for

A

DNA synthesis and is essential for cell replication and the normal neural tube development.

78
Q

Causes of folic acid deficiency:

A
  • Inadequate folate intake.
  • Malabsorption:
  • Impaired metabolism
79
Q

Deficiency of folic acid leads to

A

Deficiency leads to maturation failure and production of fewer red cells with large size; macrocytic anaemia.

80
Q

Malabsorption of folic acid caused by which drugs

A

barbiturates, phenytoin, and oral contraceptives.

81
Q

which enzyme causes folic acid deficiency

A

methotrexate

Hematology week 1 (5 decks)

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