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Haematology > Hematopoesis > Flashcards

Hematopoesis Flashcards

1
Q

TPO does what

A

stimulates BFU(EMeg)–> CFU-MEG for platelet production

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2
Q

EPO does what

A

Stimulates BFU-E->CFU-E for RBC production

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3
Q

G-CSF does what

A

stimulates CFU-GM–>CFU-G for neutrophil production

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4
Q

GM-CSF does what?

A

acts on all blast cell lines

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5
Q

Cells involved in myeloposiesis (aka granulopoiesis)

A

Monocytes, Neutrophils, Eosinophils, basophils

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6
Q

Cells involved in ertyhropoiesis

A

red blood cells

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7
Q

cells involved in thrombopoiesis

A

platelets

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8
Q

cells involved in lymphopoiesis

A

T cells, B cells, NK cells

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9
Q

Which cells are defined as blasts (<4%)

*not identifyable microscopically but by their responsiveness to growth factors

A

PSC–>CFEGEMM and common myeloid progenitor

then BFUE-CFUGM-CFUbaso
all of these are acted on by GMCSF

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10
Q

List normal maturation of granulocyte

A 
Blast-->
Promyelocyte-->
myelocyte-->
Metamyelocyte-->
bands-->
neutrophil
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11
Q

mature species outnumber younger species why?

A

because maturation is a process of DIFFERENTIATION alongside a process of DIVISION
(age=increase in rounds of division)

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12
Q

key regulator of granulopoiesis/ myelopoiesis

A

GM-CSF

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13
Q

eosinophils branch of when during myelopoiesis–>

A

between morphological bast stage and promyelocytes (in response to GM-CSF

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14
Q

G-CSF role in myelopoeisis

A

acts more specifically on neutrophil precursors

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15
Q

list the maturation of RBC’s

A 
blast-->
pronormoblast-->
basophillic erythroblast-->
polychromatophillic erythroblast-->
normochromic erythroblast
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16
Q

erythropiesis is under the control of which growth factor

A

Erythropoietin

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17
Q

EPO production is regulated by?

A

Hypoxia–> causes HIF-1 to be up-regulated which goes to nucleus and up-regulates EPO to be made and released by renal peritubular capillaries

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18
Q

renal failure can cause

A

ANEMIA: loss of EPO production and timely release

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19
Q

describe nascent RBC’s

A

–> anucleate, polychromatic reticulocytes

larger than usual, filled with RNA, so will stain with methylene blue

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20
Q

Do blasts have nuclei

A

YES

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21
Q

Pletelet maturation

A

blast–> immature megakaryocyte–> mature megakaryocyte–>platelets

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22
Q

platelet production is under control of –>

A

TPO

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23
Q

describe megakaryocytes

A

poly ploid (16-32 haploid nuclei)–> extend snake-like protoplatelets into bone marrow blood vessels

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24
Q

TPO is made in the

A

liver

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25
Q

How does TPO work

A

binds megakaryocytes–>stimulates production from immature precursors and platelet production from immature megakaryocytes

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26
Q

low platelet count…

A

–> allows more TPO to bind megakaryocytes, stimulating more thrombopoiesis.

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27
Q

hematopoetic GFR’s work via

A

JAK2 signal transduction

*acquired mutations here will give you cancer!

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28
Q

red cell production requirements

A

heme synthesis
globin synthesis
DNA synthesis
regulation

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29
Q

heme synthesis

A

iron
B6
succinyl Coa
glycine

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30
Q

hemoglobin=

A

heme + globin

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31
Q

heme=

A

iron + protoporphyrin

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32
Q

heme synthesis also requires…

A

B12 and folate

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33
Q

DNA synthesis requires

A
  1. dNTP’s–>thymidine (THYMINE)–>which requires B12 and folate
  2. deoxynucleotide reductase
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34
Q

proper regulation of EPO requires

A

healthy kidneys

normal bone marrow micro-environment

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35
Q

Iron deficieny results in–>

A

red cells without enough hemoglobin

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36
Q

most common cause of microcytic hypochromatic anemia

A

iron Deficiency anemia

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37
Q

RDW correlates with

A

anisocytosis

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38
Q

Characteristic but not diagnostic of Iron def. anemia

A

poikilocytosis and anisocytosis

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39
Q

why is free plasma iron bad

A

causes free radicals
>would augment bacterial growth
(ergo iron is low during inflammatory state and hepcidin is up)

40
Q

gastric environment that favors iron uptake

A

acidic (low pH)–>therefore co-admin of Vitamin C will increase the amount of iron one takes up

41
Q

iron is absorbed in the…

A

deodenum

42
Q

b12 is absorbed in the

A

illuem

43
Q

iron travels in the blood

A

with ternsferrin–> in the ferrous state Fe3++

44
Q

dietary iron–>

A

usually Fe+++

45
Q

iron is transported into the enterocyte via

A

DMT1–> in the fe++ state

46
Q

how does fe+++/transferrin get into the bone marrow to make heme

A

binds to transferrin receptor in erythroid precursors in the bone marrow

47
Q

storage form of iron

A

ferritin

48
Q

where is iron stored

A

macrophages in the liver, spleen bone marrow

49
Q

how does iron get from gastric lumen into enterocyte

A

dmt-1

50
Q

how is heme iron absorbed

A

heme carrier protein 1

51
Q

how does iron get from enterocyte to plasma

A

ferroportin

52
Q

inhibitor of feroportin

A

hepcidin

53
Q

how is DMT1 regulated

A

iron dependent regulation of its mRNA

54
Q

hepcidin transcription is increased by

A

IL-6 9we dont want the bacteria to have iron

55
Q

TIBC goes up or down in infection

A

down–>bind up iron making it unavailable to bacteria

56
Q

transporter responsible for moving iron from macrophages in storage pool–>making it available in plasma for erythroid precursors

A

ferroportin

57
Q

Most useful measure of iron metabolism in anemias of unknown etiology

A

serum ferritin

measures storage iron

58
Q

simplest measure of transferrin-bound iron

A

serum iron

*but does not directly address iron stores

59
Q

Serum ferritin is propoertional to

A

amount of storage pool iron in the body

60
Q

TIBC=

A

total amount of transferrin in ciruclation

61
Q

transferrin saturation

A 
serum iron (transferrin bound fe)// total transferrin
*tells us how active transport system is
62
Q

UIBC=

A

TIBC-serum ferritin

63
Q

WHen would you see an increase in Soluble Transferrin receptor?

A

when iron storage pool is depleted following loss of serum iron
*macrophages increase the amount of transferrin receptors–> manifests as increase in sTFR–>

64
Q

reliable indicator between anemia or chronic disease and iron deficiency anemia

A

sTFR will be increased in iron deficiency anemia and NOT in anemia of chronic disease

65
Q

ferritin is an

A

accute phase protein and will be elevated in inflamatory states

66
Q

markers of Iron defieincy anemia

A
  1. increased soluble transferrin receptor
  2. decreased serum ferritin
  3. decreased serum iron
  4. increased TIBC
  5. increased ferroportin
67
Q

normal iron/transferrin levels increase or decrease hepdicin production

A

increase–>which decreases ferroportin and iron uptake

68
Q

below average iron/transferrin levels increases or decreases hepcidin production

A

decreases –.ferroportin is increased and more iron is absorbed

69
Q

reduced globin production=

A

thalassemia

70
Q

characters of beta thalassema

A

microcytic, hypochromic, with target cells (nonspecific)

71
Q

differentiates beta thal from IDA

A

MCV < 70 and a NORMAL or increased NUMBER OF BLOOD CELLS

72
Q

IDA HAS NORMAL OR REDUCED # OF RBC’S

A

reduced

73
Q

confirmation of beta thal–>

A

hg electrophoresis

74
Q

normal heomoglobin : HgbA

A

alpha2beta2

75
Q

HgA2

A

alpha2delta2

76
Q

fetal Hgb

A

Alpha2gamma2

77
Q

beta thalassemia will result in which types of Hgb in the adult

A

over production of Hgb delta–> so increased Hgb A2

78
Q

beta thalassemias are more susceptible to…

A

point mutations

79
Q

alpha thals are more susceptible to

A

deletions

80
Q

Hgb H

A

three deletions of alpha globin gene–> result is beta tetramers–>increased afinity for O2–>poor deivery

81
Q

Hgb Bart;s–>

A

deletion of four ALPHA alleles–>result is gamma tetramer, and fetus dies

82
Q

which alpha thal can be confused for IDA

A

alpha thalassemia type 3

83
Q

Type 2 alpha thal in adulthood

A

> normal hgb electrophoresis as adults

>mild microcytic anemia

84
Q

Type 2 alpha thal prenatal

A

excess Hgb Barts at birth

85
Q

Dx of Thalassemia 2 trait

A

Pcr based (electrophresis and/or sequencing)

86
Q

overall cause of megaloblastic anemia

A

inhibition of DNA synthesis

87
Q

causes leading to megaloblastic anemia

A
  1. pernicious anemia–>b12 def.
  2. impaired folate uptake
  3. drug effect (HAART and hydroxyurea)
  4. Myelodysplastic syndrome
88
Q

Most megaloblastic anemias can be dx with…

A

bone marrow biopsy

89
Q

the urge to breath is regulated by Co2

A

co2 concentration–> not o2

90
Q

2 overall causes of reduced circulating red cell mass

A
  1. decreased produciton of RBC’s

2. increased loss of RBCs

91
Q

discuss anemia of chronic inflammation

A

IL6 induces liver to produce–> increased hepcidin (acute phase reactant)–> decreased uptake and release from macorphages storage pool (via destrcution of ferroportin) –> erythroppiesis comes to a screeching HALT

92
Q

normocytic anemias

A
  1. anemia of chronic disease
  2. thalassemias (sickle cell)
  3. pregnancy
  4. hemolysis
  5. b2 or b6 defiency
93
Q

Anemia of chronic disease will present as what?

everybody is ordered off the street

A
  1. increased hepcidin–>ferroportin inhibited
  2. therefore decreased serum iron
  3. decreased transferrin
  4. decreased TIBC
  5. increased ferritin
    * iron shunted from plasma–>into storage macrophages!***
94
Q

confirmation of anemia of CD

A

bone marrow biopsy

95
Q

chronic disease that can cause anemia

A

cancer of any type RA
TB
AIDS

96
Q

reticulocyte count with ACD and IDA

A

will be low–> unable to compensate

also could be an EPO problem

Haematology (7 decks)

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