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Heme/Genetics > Hematopoiesis > Flashcards

Hematopoiesis Flashcards

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1
Q

What are the layers in an aliquot of blood?

A
  • top: plasma
  • middle: thin line of WBCs (buffy coat)
  • bottom: RBCs (heaviest)

unable to see platelet layer

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2
Q

Normal hematocrit in males and females

A
  • male: 40-50%

- female: 35-40%

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3
Q

Hematocrit trend from newborn to child

A

Higher HCT in new borns (45-60%) but then drops down to around 35% until the age of 10

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4
Q

Why does hematocrit decrease during pregnancy?

A

-normally decreased during 3rd trimester d/t volume expansion; have a lot more fluid and plasma

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5
Q

Make up of plasma

A
  • 90% water
  • 10% dissolved substances:
  • 7% protein
  • 2% aa, vitamins, hormones, lipids
  • 0.9% inorganic salts
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6
Q

What is the main protein in plasma? (4% of the 7% total)

A

albumin (plasma also includes immunoglobulins, fibrinogen, prothrombin)

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7
Q

What is “normal saline” that is given for IV fluids based off of?

A

Normal saline is classified as 0.9% saline d/t our physiologic saline being 0.9% of our plasma

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8
Q

Plasma vs. Serum

A
  • If not centrifuged, blood will clot spontaneously, which uses up the clotting factors leaving the serum with no clotting elements
  • Plasma contains all things discussed previously (PA: plasma, all)
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9
Q

Coulter Counter

A

device to measure blood counts; extremely accurate until you get above 100k WBCs/mL like in leukemia

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10
Q

A blue colored stain in a blood smear indicates why kind of cell?

A

basophilic

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11
Q

A yellowish-pink stain in a blood smear indicates what kind of cell?

A

eosinophilic (eosin is red but stains yellow/pink)

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12
Q

A salmon pink stain in a blood smear indicates what kind of cell?

A

Neutrophilic (Does not take up eosin or basophilic stain)

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13
Q

What is the process that drives erythropoiesis?

A

Erythrogenin stimulates the transformation of erythropoietinogen to erythropoietin

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14
Q

Erythrogenin

  • where produced
  • why
A
  • produced by kidney

- in response to hemorrhage, high altitude, anemia, etc.

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15
Q

Erythropoietinogen is produced by what?

A

liver

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16
Q

Native erythropoietin is produced by what?

A

kidney

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17
Q

Hemoglobin

A

-tetramer w/ 2 alpha globin chains and 2 beta globin chains

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18
Q

What produces alpha and beta polypeptides/chains?

A

mRNA

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19
Q

What is each globin chain bound to in Hgb?

A

w/ a porphyrin containing iron

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20
Q

Variations in Hgb are d/t what?

A

differences in aa sequence of globin chains

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21
Q

Most of our circulating hgb is what kind?

A

alpha 1 (HgbA1)

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22
Q

Steps in the formation of hgb

A
  1. 2 CoA + 2 glycine = 4 pyrrole
  2. 4 pyrrole -> protoporphyrin
  3. Fe attaches to protoporphyrin to get a heme
  4. heme insterts into the globin
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23
Q

Fe binding in hgb formation

A
  • 1 heme will insert itself in into every globin chain
  • The Fe in heme has 2 binding sites for oxygen
  • this means 1 Hgb molecule can carry 8 elemental oxygen atoms (4 O2 molecules)
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24
Q

HgbS

A
  • sickle cell disease

- substitution of aa at position 6 on beta globin chain

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25
Q

Effect of HgbS

A
  • can’t carry O2 as well

- causes conformational change – sickle shaped RBC

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26
Q

HgbF

A
  • primary Hb when born (80%)
  • 2 alpha and 2 gamma globin chains
  • higher affinity for oxygen
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27
Q

When does the primary Hgb shift from F to A1 ?

A
  • by 6 mos

- 97% now HgbA1

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28
Q

What is significant about HbgF in possible tx for sickle cell?

A
  • gamma globin not effected in sickle cell

- can take hydroxuria to de-repress HgbF gene

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29
Q

Since 97% of our circulating Hgb is alpha-1, what is the remaining 3%?

A
  • 2% HgbA2 (2 alpha, 2 delta)

- 1% remaining HgbF

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30
Q

Red marrow

A
  • hematogenous/active
  • all bones in new born
  • flat bones and vert. in adults
  • ongoing hematopoeisis
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31
Q

Yellow marrow

A
  • long bones of adults
  • energy storage
  • can convert to red marrow in times of stress
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32
Q

Where does marrow begin to form in an embryo?

A
  • yolk sac (3rd or 4th week)
  • then liver/spleen (until month 2)
  • then bones when they are formed
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33
Q

What is the first bone to form in the body?

A

clavicle

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34
Q

Order of cell maturation in erythropoiesis

A
  1. pro erythroblast
  2. basophilic erythroblast
  3. polychromatic erythroblast
  4. Normoblast
  5. Erythrocyte
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35
Q

Proerythroblast stage of erythropoiesis

A
  • arises from stem cell
  • lg cell
  • multiple nucleoli
  • basophilic d/t ribosomes
  • can divide
  • Hgb synthesis begins
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36
Q

basophilic erythroblast stage of erythropoiesis

A
  • shrinks
  • blueish granules (basophilic)
  • can divide once
  • clock face
  • Hgb increasing
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37
Q

polychromatophilic erythroblast stage of erythropoiesis

A
  • shrinks further
  • nucleus is 50% of cell
  • enough Hgb formed to take on pink color over blue
  • multiple divisions
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38
Q

Normoblast stage of erythropoiesis

A
  • smaller still
  • small/dense nucleus
  • pyknotic nucleus stops division
  • Hgb major protein in cytoplasm
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39
Q

Erythrocyte stage of erythropoiesis

A
  • nucleus has extruded
  • mature RBC
  • 80% hgb
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40
Q

Mature RBC (erythrocyte) characteristics

A
  • lives about 120 days
  • 7.2 microns in diameter
  • biconcave and flexible
41
Q

Size variations of RBCs

A
  • microcytes: <6 micron diameter
  • macrocytes: >9 micron diameter
  • hypochromic: not making enough Hgb, cells are small
42
Q

Main causes of hypochromic microcytic anemia?

A
  1. Fe deficiency anemia
  2. lead poisoning
  3. anemia of chronic disease
  4. thalassemia
43
Q

Howell-Jolly bodies

A
  • retained DNA fragments found in disease states

- RBC w/ blue dot in it – indication of chronic disease

44
Q

If the howell-jolly bodies are in a circular in formation, what is the condition?

A
  • Cabot rings

- indication that a problem is present just not specific as to what

45
Q

Erythrocyte maturation summary

A
  • decreased cell volume
  • decreased nuclear diameter leading to extrusion
  • increase in cytoplasmic Hgb
  • decrease in non-nuclear organelles
46
Q

Platelets

A
  • aka thrombocytes

- enucleated disklike cell fragments 2-3 micron in diameter

47
Q

Platelets bud from what?

A

megakaryocytes in marrow

48
Q

platelet membranes

A
  • rich in GAGs and glycoprotein

- gives a sticky quality to adhere to exposed collagen

49
Q

d/t the “stickiness” of platelet membranes, what do they bind to?

A

-vWF (von Willebrand Factor) outside of vessels

50
Q

Contents of platelets as they bud off of megakaryocytes

A
  • thromboplastin
  • serotonin
  • thrombostenin (contracts clots)
51
Q

fxn of thromboplastin

A
  • converts prothrombin to thrombin

- thrombin coverts fibrinogin to fibrin

52
Q

platelet life span

A
  • 7-10 days

- 10% are replaced daily -this is fairly high turnover so taken out of circulation in spleen

53
Q

Effects of aspirin on platelets

A
  • interferes w/ thromboplastin – this prevents fibrin formation and coagulation
  • prolongs bleeding time
54
Q

Return to normal after aspirin use

A
  • have to replace 30% new platelets
  • this is 3 days
  • so technically you only need to take aspirin every 3 days, but adherence would be poor then
55
Q

Granulocyte type luekocytes

A
  • neutrophilic
  • eosinophilic
  • basophilic
56
Q

Agranulocyte leucocytes

A
  • lymphocytes

- monocytes

57
Q

Other names for neutrophils

A
  • Polymorphonuclear leukocytes
  • Polymorphonuclear neutrophils
  • Polys
  • PMNs
  • Segmented neutrophils
  • Segs
58
Q

WBC maturation in granulocyte series

A
  1. stem cell
  2. myeloblast
  3. promyeloblast - can develop into any of the 3 granulocytes
  4. myelocyte (eosinophilic, neutrophilic, basophilic)
  5. metamyelocyte
  6. stab cell
  7. completely differentiated cell
59
Q

What point in granulocyte maturation divides the cells that are in marrow vs. circulation

A
  • up to metamyelocyte = marrow

- stab cells on = circulation

60
Q

significant of neutrophilic band cell count

A
  • normal conditions: 4% band cells in circulation
  • then nucleus condenses to form mature neutrophil
  • infection: band count increases to 9% or higher
  • only good indicator in pts who are not immunocompromised
61
Q

What would a bone marrow biopsy look like in leukemia

A
  • early stage cells are present in peripheral circulation
  • no young RBCs
  • classified by youngest cell present (i.e myeloblastic leukemia)
62
Q

Neutrophilic lineage

A
  • neutrophilic myelocyte: nucleus becomes eccentric and indented
  • metamyelocyte: deeper indented nucleus; decrease in protein synth.; high glycogen storage
  • band stage
63
Q

If nuetrophilic bands are present at higher than 3-5%, what is it called?

A

-left shift

64
Q

mature neutrophil

A
  • 60-70% circulating WBCs
  • 2-5 lobes linked w/ chromatin thread
  • no nucleoli
  • live 12-14 hrs in circ.
  • live 1-4 days in con. tissue
65
Q

“drumstick” on mature neutrophil

A

-inactivated X chromosome

66
Q

Effect of epinephrine on seg count

A
  • elevated ct but not d/t infection

- caused by demarginalization

67
Q

main function of neutrophils

A
  • phagocytosis
  • of debri, bacteria, dead cells
  • if migrate to tissues all at once and die = pus
68
Q

Eosinophils

A
  • myelocyte and metamyelocyte stages
  • 2-4% of circulating WBCs
  • bilobed nucleus
69
Q

important enzyme in eosinophils

A
  • peroxidase
  • useful in killing protazoa
  • also have factors that inhibit mast cell degranulation
70
Q

increased eosinophils could indicate what things?

A
  • allergies
  • round worm infection
  • bacterial myocarditis
71
Q

basophils

A
  • same myelocyte to metamyelocyte stages
  • <1% of circulating WBCs
  • irregular nucleus
  • granuoles contain heparine and histamine
72
Q

agranulocytes

A
  • lymphocytes: B, T, and null

- monocytes

73
Q

Percentages of lymphocytes

A
  • T: 80%
  • B: 15%
  • null: 5%
74
Q

CD8+

A

killer/cytotoxic T cells

75
Q

CD4+

A

Helper T cells

76
Q

how do immune cells recognize other somatic cells?

A

-through cell surface markers

77
Q

primary markers are proteins of what?

A

-major histocompatibilty complex (MHC) = HLA (human leukocyte antigen)

78
Q

HLA markers in relation to disease

A
  • certain HLA markers tend towards certain disease states
  • for ex: ankylosing spondylitis (HLA B27), DM type 1, hemochromotosis, Sjogren’s
  • not the cause of disease but suggestive
79
Q

Class I MHCs

A

found on all body cells except for B cells

80
Q

Class II MHCs

A

found on B cells

81
Q

Explain the process of how a cell becomes recognizable as self

A
  1. in embryo, circulating antigens are endocytoced
  2. then they are processed into fragments and reintroduced as MHCs
  3. the new MHCs are packaged into granules and returned to cell surface as self
82
Q

Components of a T cell binding an antigen presenting cell

A
  • T cell receptor binds the MHC containing Ag fragment
  • the binding is stabilized by either CD4 or CD8
  • if T cell binds to non self = rejection
83
Q

clonal deletion

A

the removal of T and B cells that have receptors that recognize self before they are able to mature into immunocompetent lymphoctes

84
Q

What are the steps in the process of clonal deletion?

A
  • embryonic T cells have both CD4 and CD8 receptors
  • in the thymus they are presented to thymic cells
  • if embryonic T cell recognized self, have to delete it
  • if it doesn’t recognize self, allow to enter circulation where it will lose of the the receptors and become specified as CD4 or CD8
85
Q

What happens when the embyonic T cells that recognize self in the thymus are allowed to enter into circulation?

A

autoimmune disease

86
Q

CD4 T cells bind to what?

A

class II MHC on B cells

87
Q

B cell antibodies

A
  • IgM
  • IgA

-when Ag binds, they are indocytosed and returned as class II MHC

88
Q

What is the relationship between CD4 T cells and B cells?

A
  • T cell binds B cell and releases interleukins to cause proliferation of B cells
  • B cells begin producing antibodies against the Ag attached to its MHC
  • humoral immunity
89
Q

Without CD4 T cells what is the out come?

A
  • little or no B cell response

- loss of humoral immunity

90
Q

When does HIV transition to AIDS?

A
  • when CD4 count drops below 200

- can’t mount an immune rxn

91
Q

CD8 T cells bind to what?

A

Class I MHC on all cells except for B cells

92
Q

Action of CD8 T cells

A
  • binds non self and injects perforin into cells causing contents to leak out and lysis
  • cell mediated immunity
93
Q

What all can activate ia CD8 (killer T cell)?

A
  • non self Ag from infection
  • another MHC from different “self” cell
  • altered MHC from tumor
94
Q

Monocyte

A
  • not fully mature cell in circulation
  • exists 8-12 hrs in circulation
  • irregular horseshoe-shaped nucleus
95
Q

when monocytes migrate into tissues, what do they become?

A

macrophages

96
Q

Plasma cells

A
  • originate as B cells
  • not in circulation
  • few in number except where bacteria and foreign proteins are
  • clock faced nucleus
97
Q

When activated by Ag, what do plasma cells secrete?

A

IgE

98
Q

Function of IgE when produced by plasma cells

A

bind to mast cells which contain histamine, heparin, ECF-A (eosiniphil chemotactic factor of anaphylaxis) and SRS-A (slow-reacting substance of anaphylaxis)

99
Q

What cells are abundant in openings to the environment? (mouth, nose, anus, etc.)

A
  • monocytes

- plasma cells

Heme/Genetics (15 decks)

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