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Blood > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Fetus hematopoietic organs

A

liver & spleen

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2
Q

adult hematopoietic organs

A

bone marrow- pelvis, ribs, vertebrae, skull, epiphyses of the femur & humerus

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3
Q

Blood cells are produced in the:

A

bone marrow

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4
Q

bone marrow contains:

A

stem cells

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5
Q

stem cells produce three types of blood cells:

A

WBCs, RBCs, & plts

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6
Q

blood islands

A

clusters of stem cells in the human embryo

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7
Q

chief site of blood cell formation until shortly before birth

A

liver and spleen

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8
Q

_____ of development, hematopoeisis commences in the bone marrow

A

fourth month

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9
Q

up until age 18, all of the marrow throughout the skeletonis hematopoietically active. after that:

A

only the vertebrae, ribs, sternum, skull, pelvis & proximal areas of humerus & femur are active

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10
Q

in adults, only about ___ of marrow space is active in hematopoiesis

A

half

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11
Q

hematon:

A

separate microenvironments of developing progenitor cells. isolated by reticular cells

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12
Q

important hematopoietic components that provide growth factors, collagen & cell adhesion proteins

A

endothelial cells, firboblasts, macrophages, & adipocytes

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13
Q

pluripotent

A

stem cells- unique potential to ultimately become any of the mature hematopoietic cells

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14
Q

stem cells are characterized by:

A

high proliferative capacity
potential to differentiate along all lineage pathways
property of self renewal

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15
Q

important property of stem cells

A

property of self renewal- ability to generate additional stem cells through mitosis w/out differentiation

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16
Q

hematopoietic cytokines

A

protein molecules actively secreted by cells of bone marrow & influence proliferation & differentiation of stem cells into mature blood cells

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17
Q

Platelets & RBCs do not have

A

a nucleus

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18
Q

WBCs include:

A

granulocytes (eos, baso, neutro)
monocytes/macrophages
lymphocytes (B&T cells)

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19
Q

most common PMN

A

neutrophils

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20
Q

neutrophils have

A

multi-lobe nucleus

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21
Q

primary neutrophils contain

A

proteins (defensisns), proteolytic enzymes, lysozymes

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22
Q

secondary neutrophils contain

A

NADH oxidase components

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23
Q

Basophils

A

basic
involved in allergic rxns
Heparin & histamine

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24
Q

Eosinophils

A

acid
defense against paracites
high numbers in GIT & lungs

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25
Q

Monocytes circulate in the ___ and

marcophages are found in ____

A

blood stream; tissues (liver & lymphh nodes)

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26
Q

most common type of blood cell

A

RBCs

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27
Q

diameter of a typical RBC

A

6-8 microns

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28
Q

RBCs produce energy via

A

glycolysis

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29
Q

production of RBCs can be stimulate dby

A

erythropoietin

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30
Q

main sites of destruction of RBCs

A

liver & spleen

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31
Q

hemoglobin is eventually excreted as

A

bilirubin

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32
Q

platelets aka

A

thrombocytes

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33
Q

platelets are

A

fragmented pieces of megakaryocyte cytoplasm released from bone marrow into the blood stream

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34
Q

what is required for the differientiation of stem cells into platelets

A

thrombopoietin

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35
Q

CBC contains

A

RBC & WBC count, Hgb, Hct, RDW, reticulocyte count, platelet count & mean platelet count, MCV< MCH< MCHC

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36
Q

Hct

A

% volume of blood composed of RBCs

usually 3X Hgb

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37
Q

Anemia

A

reduction in the oxygen carrying capacity of blood

decrease RBC volume measured by Hct or Hgb

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38
Q

anemia classification based on:

A

appearance (size) of RBCs
degree of Hgb- color
underlying mechanism

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39
Q

< folate or B12 causes defective

A

DNA synthesis and therefor can’t make RBCs

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40
Q

< iron cause deficient

A

heme synthesis

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41
Q

hemolytic anemia

A

> RBCs destruction
shortened lifespan of RBCs
accumulation of hgb catabolism products
erythropoiesis

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42
Q

spherocytosis:

A

abnormal shape, can’t fit through vessels

disorder of RBC membrane cytoskeleton

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43
Q

thalassaemia syndromes

A

deficient globin synthesis

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44
Q

sickle cell anemia

A

structural abnormal globin synthesis

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45
Q

extravascular hemolysis

A

phagocytic destruction of senescent RBCs takes place within the phagocytic cells of the spleen

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46
Q

intravascular hemolysis

A

lyses of RBCs occur within the vascular compartment. occurs when RBCs are damaged by mechanical injury, complement(transfusion), exogenous toxic factors (malaria)

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47
Q

characteristics of intravascular hemolysis

A

hemoglobinemia, hemoglobinuria, jaundice, methemoglobinuria(oxidized Hgb), hemosiderinuria

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48
Q

haptoglobin levels go ____ in intravascular anemia

A

down

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49
Q

characteristics of extravascular hemolysis

A

do NOT have Hgb-emia or Hgb-uria
jaundice
mayhave decreased haptoglobin
may have hypertrophy of mononuclear phagocytes-> splenomegaly

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50
Q

hereditary spherocytosis

A

anemia due to RBC membrane protein disorder
autosomal dominant
RBC are spherical due to deficiency in RBC protein spectrin
can have chronic hemolytic anemia
splenomegaly
jaundice

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51
Q

spectrin

A

major component of RBC cytoskeleton

along with Band 3, are responsible fore maintenance of normal shape, strength & flexibility

52
Q

G6PDH deficiency

A

leads to hemolytic anemia due to inability to neutralize oxidative stress
H2O2 accumulates in RBCS

53
Q

how does accumulation of H2O2 cause RBC lysis?

A

cause oxidation of sulfhydryl groups like globin chains in RBCs-> denaturation of Hgb & formation of Heinz bodies

54
Q

Heinz bodies damage

A

RBC membrane and cause extravascular hemolysis

55
Q

causes of oxidative stress

A

Drugs, infections, fava beans

56
Q

Coombs’ test

A

distinguish between anemia caused by immune mediated response & other forms of anemia
Coombs- antihuman antibodies

57
Q

Direct Coomb’s test

A

detect antibodies bound to RBCs

58
Q

Indirect Coombs’ test

A

detects antibodies in the serum

59
Q

3 key defects in erythropoiesis:

A
  1. defective DNA synthesis due to lack of B12 or folate- Macrocytic
  2. impaired heme synthesis due to lack of iron- Microcytic
  3. impaired erythropoiesis due to marrow stem cells failure- normocytic
60
Q

major form of B12 deficiency anemia

A

pernicious macrocytic anemia- results from lack of intrinsic factor resulting in malabsorption of B12

61
Q

B12 & folate are ______ in the DNA synthetic pathway

A

coenzymes

synthesis of RNA & protein are unaffected

62
Q

to absorb B12 you need

A

intrinsic factor secreted by gastric parietal cells

63
Q

vitamin B12 aka

A

Cobalamin- complex organometallic compound

64
Q

_______ are the ultimate origin of cobalamin in the food chain

A

microorganisms

65
Q

B12 is released from protein bound form by

A

pepsin in the stomach

66
Q

free B12 binds to proteinsc called

A

cobalophilins or R-binders

67
Q

________ delivers B12 to the liver & other cells in the body

A

transcobalamin II

68
Q

Atrophic gastritis

A

loss of gastric mucosal folds & thinning of gastric mucosa with parietal cells-> no IF

69
Q

antibodies detected in pernicious anemia

A

Type 1: blocks binding of B12 to IF
Type 2: block binding of IF or IF-B12 to its receptor on ileal cells
type 3: bind to the gastric proton pump on parietal cells

70
Q

folate deficiency anemia is similar to B12 EXCEPT

A

NO neurological changes

71
Q

important metabolic rxns that depend on THF

A

synthesis of purine, methionine, & deoxythymidylate monophosphate

72
Q

form of folate in green veggies

A

folypolyglutamates

73
Q

most common anemia world wide

A

iron deficiency

74
Q

iron content in the body is distributed into:

A

functional(globin) & storage comparentments

75
Q

ferritin is stored within

A

parenchymal cells in the liver
mononuclear phagocytic cells in spleen & bone marrow
can be found within all tissues

76
Q

hemosiderosis

A

excess iron causes hemosiderin to accumulate within cells & tissues

77
Q

in iron deficiency, plasma ferritin is always

A

below 12mg/L

78
Q

in iron overload, plasma ferritin is at

A

high values approach 5000mg/L

79
Q

iron is stored in

A

ferritin

80
Q

iron is transported in plasma by

A

transferrin

81
Q

iron absorption takes place mainly in

A

the duogenum

82
Q

major function of plasma transferrin is to

A

deliver iron to cells

83
Q

_____ cells have high affinity receptors for transferrin

A

immature RBCs

84
Q

aplastic anemia common cause

A

exposure to chemicals/drugs-> suppression of multipotent myloid cells-> inadequate production of differentiated cell line

85
Q

anemia of chronic disease

A

associated with < erythroid porliferation & impaired iron utilization & may mimic iron deficiency

86
Q

common method to narrow possible cause of anemia

A

erythrocyte morphology- different anemias lead to different erythrocyte morphology

87
Q

RBC indices asses:

A

size & Hgb content of RBCs

88
Q

MCH (mean cell Hgb)

A

average amount of Hgb inside a RBCs

89
Q

goals of treatment

A

alleviate signs & symptoms
correct underlying etiology
prevent complications & recurrence

90
Q

oral iron best absorbed in the:

A

Fe2+ (ferrous) form

91
Q

sickle cell syndrome:

A

a hereditary autosomal recessive genetic blood disorder affecting the hemoglobin beta chain

92
Q

Sickle cell syndrome is characterized by

A

red blood cells that ssume an abnormal, rigid, sickle shape

93
Q

Sickle cell syndrome results in

A

deformation, increased rigidity and destruction of RBCs

94
Q

Sickle cell trait (SCT)

A

only one abnormal allele; usually symptomatic

95
Q

sickle cell disease (SCD)

A

both alleles are mutated; develop SCA; multisystem disease associated with episodes of acute illness and progressive organ damage

96
Q

SCD results in

A

impaired circulation, vasocclusive disorders, vessel damage and RB destruction; severe morbidity and early mortality

97
Q

global distribution is indicative of two factors:

A
  1. survival advantage in malaria-endemic regions

2. subsequent migrations.

98
Q

patients with SCD experience

A

delayed growth (height & weight)

99
Q

Life expectancy in SCD

A

males-42

females-48

100
Q

life expectancy in SCT

A

males-60

females-68

101
Q

it is the mutation of __ chain that accounts for the disease

A

beta

102
Q

HgbS

A

Glutamic acid->valine(hydrophobic) at 6th AA

alters conformational structure of hgb

103
Q

HgbC

A

substitution of glutamic acid with lysine

104
Q

val6 of beta 2 chain in one HGS forms hydrophobic bonds with

A

Phe85 and Leu88 of second HbS beta-1 chain

105
Q

solubility od deoxygenated HgS is ____ than HbA

A

Substantially lower

106
Q

life span of sickled RBC

A

10-20 days

107
Q

3 main problems are primarily responsible for the clinical manifestation of the disease:

A
  1. impaired circulation
  2. destruction of RBCs
  3. stasis of blood flow
108
Q

factors promoting HbS polymerization

A 
low pO2/hypoxia (high altitudes)
increased CO2, low pH (physical inactivity)
increased 2-3BPG in RBC
high [HgS]
low [HgF]
109
Q

HgF

A

has gamma chains instead of beta, so no sickling

gamma globin chains bind HgS & inhibit HgS polymerization

110
Q

hallmarks of SCD

A

microvascular vasoocclusion, inflammation, system disease

111
Q

acute complications (sickle cell crisis)

A

vasoocclusive, splenic sequestration, aplastic, hemolytic

112
Q

vasoocclusive pain crisis

A

hand & food syndrome (dactylitis- sausage digit)- infancy
joint and extremities
abdomen
hepatic- older pts

113
Q

splenic sequestration crisis

A

splenic sinusoidal vaso-occlusion-> splenic sequestration -> acute splenomegaly & decreased circulating blood volume-> hypotension & shock/death

114
Q

aplastic crisis

A

destruction of erythroid precursors in marrow-> anemia
low reticulocyte count
associated with paravirus B19, strep pneumo, salmonella, & H. influenzae

115
Q

hemolytic crisis

A

particulary common in pts w/ G6PDH deficiency too
acute accelerated decrease in hemoglobin level & RBCs
transfusions are necessary

116
Q

second most common complication of SCD & most common cause of death in adult patients

A

acute chest syndrome

117
Q

SCD treatment

A 
lifelong multidisciplinary 
pain control
infection prophylaxis
chronic transfusion therapy
preventative therapies (HgF inducers)
curative treatment (allogeneic stem cell transplantation)
investigative therapies (gene therapy)
118
Q

hydroyurea

A

HgF inducer
inhibits production of deoxynucleotides via the inhibition of ribonucleotide reductase
can prevent painful crisis
induces proliferation of early erythroid progenitors & increase NO levels
antioxidant properties

119
Q

hydroxyurea decreases

A

frequency of acute chest syndrome, hospitalization, need for transfusion, morbidity & mortality

120
Q

hydroxyurea is a possible alternative to:

A

chronic transfusion to decrease recurrent stroke

121
Q

hydroxyurea side effects

A

significant bone marrow toxicity- leukopenia & thrombocytopenia
drowsiness, N/V/D, constipation, alopecia, abnormal liver enzymes, creatinine & BUN

122
Q

sodium butyrate

A

naturally occurring short-chain fatty acids
inhibits histone deacetylation
shown to heal leg ulcers

123
Q

decitabine

A

inhibits DNA methylation (prevents gamma->beta chain)

124
Q

only therapy offering curative potential for SCD

A

allogenic hematopoietic stem cell transplanation

125
Q

gene therapy in SCD

A

transfer of anti-sickling beta-globin genes

HIV lentiviral- mediated gene transfer can potentially correct hematological defects & organ damage

Blood (10 decks)

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