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17.3 Flashcards

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1
Q

diameter of RBCs

A

7.5 micro meters

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2
Q

what is the purpose behind RBCs having structural proteins

A

allowing the RBC to deform yet spring back into shape

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3
Q

spectrin

A

maintains the biconcave shape of an erythrocytes

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4
Q

how is the small size and shape of an RBC significant

A

huge surface are relative to volume

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5
Q

how is the disc shape of an RBC significant

A

ideally suited for gas exchange, no point withing the cytoplasm is far from the surface

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6
Q

erythrocytes are over ____ hemoglobin

A

97%

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7
Q

what is the significance of RBCs lacking mitochondria

A

Because erythrocytes lack mitochondria and generate ATP by anaerobic mechanisms, they do not consume any of the oxygen they carry, making them very efficient oxygen transporters

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8
Q

Hemoglobin, the protein that makes red blood cells red, binds easily and ______ with _____ , and most oxygen carried in blood is bound to hemoglobin.

A

reversibly

oxygen

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9
Q

Normal values for hemoglobin are

A

13-18 g/100 ml in adult males

12-16 g/100 ml in adult females.

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10
Q

Hemoglobin is made up of the _____ bound to the ______

A

red heme pigment

protein globin

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11
Q

Globin consists of

A

4 polypeptide chains
2 alpha
2 beta

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12
Q

each polypeptide chain of the globin is bound to

A

a red ringlike heme group

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13
Q

Each heme group bears an

A

iron ion (Fe2+) set like a jewel in its center

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14
Q

A hemoglobin molecule can transport ____ molecules of oxygen because each ____ atom can combine reversibly with ____ molecule of ____

A

four
iron
one
oxygen

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15
Q

A single red blood cell contains about

_______ so each of these tiny cells can scoop up about ______

A

250 million hemoglobin molecules

1 billion molecules of oxygen

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16
Q

why is hemoglobin contained in erythrocytes

A

prevents it from leaking out of the plasma and clogging up the kidneys

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17
Q

Oxygen loading occurs in the ____, and the direction of transport is from ________. As oxygen-deficient blood moves through the lungs, oxygen diffuses from the air sacs of the lungs into the blood and then into the erythrocytes, where it binds to the iron in hemoglobin. The iron is partially oxidized by the oxygen. As a result, the protein, now called _____, assumes a new three-dimensional shape and becomes ruby red.

A

lungs
lungs to tissue cells
oxyhemoglobin

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18
Q

In body tissues, the process is reversed. Oxygen detaches from iron, hemoglobin resumes its former shape, and the resulting ________, or _______ becomes dark red. The released oxygen diffuses from the blood into the tissue fluid and then into tissue cells.

A

deoxyhemoglobin

reduced hemoglobin

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19
Q

About 20% of the carbon dioxide transported in the blood combines with hemoglobin, but it binds to _________ rather than to the heme group. This formation of _________occurs more readily when hemoglobin is in the reduced state. Carbon dioxide loading occurs in the _____, and the
direction of transport is from ____to ____, where carbon dioxide is eliminated from the body

A

globin’s amino acids
carbaminohemoglobin
tissues
tissues to lungs

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20
Q

Blood cell formation is referred to a

A

hematopoiesis

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21
Q

Hematopoiesis occurs in the

A

red bone marrow

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22
Q

the bone marrow is composed largely of a ___ bordering on wide blood capillaries called _________

A

soft network of reticular connective tissue

blood sinusoids

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23
Q

what is found in the reticular connective tissue network

A

macrophages, reticular cells, fat cells

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24
Q

On average, the marrow turns out an

ounce of new blood containing

A

100 billion new cells everyday

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25
Q

all the formed elements arise from

A

the hematopoietic stem cell, sometimes called a hemocytoblast

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26
Q

once a cell is committed to a specific blood cell pathway, it ______. This commitment is signaled by the appearance of membrane surface ______ that respond to specific hormones or growth factors, which in turn ____ the cell toward further specialization

A

cannot change
receptors
push

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27
Q

erythrocyte production is called

A

erythropoiesis

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28
Q

stages of erythropoiesis

A 
Hematopoietic stem cell (hemocytoblast)
Proerythroblast
Basophilic erythroblast 
Polychromatic erythroblast
Orthochromatic erythroblasts
Reticulocyte
Erythrocyte
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29
Q

what is the committed cell called

A

Proerythroblast

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30
Q

what are the 3 phases of the developmental pathway

A

1- ribosome synthesis
2- hemoglobin accumulation
3- ejection of nucleus

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31
Q

The entire process from hematopoietic stem cell to reticulocyte takes about

A

15 days

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32
Q

usually the erythrocytes become fully mature within how many days of their release into the bloodstream

A

2 days

as their ribosomes are degraded by intracellular enzymes.

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33
Q

Reticulocytes account for ____ of all erythrocytes in the

blood of healthy people.

A

1-2%

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34
Q

provide a rough index of the rate of RBC formation-reticulocyte counts below or above this range indicate abnormal rates of erythrocyte formation.

A

Reticulocyte counts

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35
Q

hypoxia is

A

oxygen deprivation

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36
Q

To ensure that the number of erythrocytes in blood remains within the homeostatic range, new cells are produced at the incredibly rapid rate of more than

A

2 million per second in healthy people

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37
Q

what are the 3 things that regulate erythropoiesis

A

iron
amino acids
certain B vitamins

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38
Q

a glycoprotein hormone, stimulates

the formation of erythrocytes

A

erythropoietin

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39
Q

which organ plays a major role in EPO production

A

kidneys and the liver kinda :)

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40
Q

When certain kidney cells become hypoxic

(oxygen deficient), oxygen-sensitive enzymes are unable to carry out their normal functions of degrading an

A

HIF hypoxia inducible factor

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41
Q

As HlF accumulates, it

A

accelerates the synthesis and release of

erythropoietin

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42
Q

The drop in normal blood oxygen levels that triggers EPO formation can result from:

A

low count of RBCs due to hemorrhage
excessive RBCs destruction
Insufficient hemoglobin/RBC (iron deficiency)
Reduced availability of O2 (high altitudes, Pneumonia)

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43
Q

Conversely, too many erythrocytes or excessive oxygen in

the bloodstream depresses

A

EPO production

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44
Q

Note that it is not the number of erythrocytes in blood that controls the rate of erythropoiesis. lnstead, control is

A

based on their ability

to transport enough oxygen to meet tissue demands.

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45
Q

Notice that hypoxia does not activate the bone marrow ____. Instead it stimulates the ____ , which in turn provide the hormonal stimulus that activates
the _____.

A

directly
kidneys
bone marrow

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46
Q

which type of athletes abuse EPO

A

professional bike racers and marathon runners seeking increased stamina and performance.

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47
Q

By injecting EPO, healthy athletes increase their normal

hematocrit from ___ to ___

A

45% to as much as 65%

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48
Q

why is EPO injecting dangerous

A

because during the race or whatever the blood concentrates even further and this may lead to clotting, stroke, or even heart failure

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49
Q

which hormone enhances EPO production

A

testosterone

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50
Q

The raw materials required for erythropoiesis include:

A

nutrients
2 B vitamin complex
Iron

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51
Q

which two vitamin B complex are we talking about

A

B12

Folic Acid

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52
Q

Free iron ions (Fe2+, Fe3+) are ___, so iron is

stored inside cells as protein-iron complexes such as ____ and _____

A

toxic
ferritin
hemosiderin

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53
Q

In blood, iron is transported loosely bound to a transport protein called _______, and developing erythrocytes take up iron as needed to
form hemoglobin

A

transferrin

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54
Q

lifespan of RBCs

A

100 to 120 days

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55
Q

old RBCs become trapped in __

A

the spleen and this is the reason behind it being called the RBC graveyard

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56
Q

the iron core of the heme group is __

A

bound to protein (as ferritin or

hemosiderin), and stored for reuse

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57
Q

The balance of the heme group is degraded to

A

bilirubin

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58
Q

a yellow pigment

that is released to the blood and binds to albumin for transport.

A

bilirubin

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59
Q

Liver cells pick up ____ and in turn secrete it in ____
into the intestine, where it is metabolized to ______. Most of this degraded pigment leaves the body in feces, as a brown pigment called _____.

A

bilirubin
bile
urobilinogen
stercobilin

60
Q 
The protein (globin) part of hemoglobin is metabolized or broken down to \_\_\_\_\_\_\_ which are
released to the circulation.
A

amino acids

61
Q

Most erythrocyte disorders can be classified as

A

anemia and polycythemia

62
Q

anemia can be due to

A

blood loss
not enough RBC production
too many RBC destruction

63
Q

is a condition in which
the blood’s oxygen-carrying capacity is too low to support
normal metabolism.

A

anemia

64
Q

anemia is usually a ___ of some disorder

A

sign

65
Q

what is the hallmark of anemia

A

blood oxygen levels that are

inadequate to support normal metabolism

66
Q

describe anemia individuals

A

fatigued
pale
short of breath
chilled

67
Q

blood loss anemia example

A

hemorrhagic anemia

68
Q

what are the two types of hemorrhagic anemia

A

acute or chronic

69
Q

describe blood loss of acute hemorrhagic anemia give example

A

rapid as in following being stabbed by a knife

70
Q

treatment of acute hemorrhagic anemia

A

replace lost blood

71
Q

what would be the reason behind chronic hemorrhagic anemia

A

due to hemorrhoids or an undiagnosed bleeding ulcer

72
Q

describe blood loss of chronic hemorrhagic anemia

A

Slight but persistent blood loss

73
Q

for chronic hemorrhagic anemia once the _____ is resolved normal erythropoietic mechanisms replace the lost blood cells.

A

primary problems

74
Q

A number of problems can decrease erythrocyte production. These problems
range from

A

lack of essential raw materials (such as iron) to

complete failure of the red bone marrow

75
Q

what is generally a secondary result of hemorrhagic anemia

A

iron deficiency anemia

76
Q

iron deficiency anemia can also be a result of

A

inadequate intake of iron-containing foods

or unpaired iron absorption.

77
Q

in iron deficiency anemia The erythrocytes produced under these conditions, called ______
are small and pale because they cannot synthesize their normal complement of hemoglobin.

A

microcytes

78
Q

treatment for iron deficiency anemia

A

increase iron intake in diet or through iron supplements.

79
Q

is an autoimmune disease that most often

affects the elderly.

A

Pernicious anemia

80
Q

in Pernicious anemia The immune systern of these individuals destroys cells of

A

their own stomach mucosa

81
Q

normally cells of the stomach muscosa proudce

A

intrinsic factors

82
Q

intrinsic factors must be present for

A

vitamin B 12 to be absorbed by intestinal cells

83
Q

Without vitamin B 12, the developing erythrocytes

A

grow but cannot divide

84
Q

what does Pernicious anemia do to the cells

A

large, pale cells called macrocytes result

85
Q

treatment for Pernicious anemia

A

regular intramuscular injections of vitamin B 12 or application of a B 12 containing gel to the nasal
lining once a week.

86
Q

what can lack of vitamin B12 in a diet lead to

A

anemia

87
Q

anemia due to lack of vitamin B12 is a problem for which group of people

A

strict vegetarians because meats, poultry, and fish provide ample vitamin B 12.

88
Q

which anemia is caused by a lack of EPO

A

renal anemia

89
Q

renal anemia frequently accompanies

A

renal diseases

90
Q

treatment for renal anemia

A

administer EPO

91
Q

anemia due to destruction of red bone marrow due to drugs, chemicals, radiation, virus is

A

aplastic anemia

92
Q

for aplastic anemia that cause is usually

A

unknown

93
Q

in aplastic anemia anemia is just a

A

sign because destruction of Red bone marrow will impair formation of all the formed elements presenting defects in blood clotting immunity

94
Q

aplastic anemia treatment options

A

Blood transfusions provide a stopgap treatment until

stem cells harvested from a donor’s blood, bone marrow, or umbilical cord blood can be transplanted.

95
Q

erythrocytes rupture, or lyse, prematurely.

A

hemolytic anemia

96
Q

hemolytic anemia can be due to

A

Hemoglobin abnormalities, transfusion of mismatched blood,
and certain bacterial and parasitic infections are possible
causes

97
Q

thalassemias are common in

A

people of Mediterranean ancestry

98
Q

example of too many RBCs being destroyed

A

thalassemias and sickle cell anemia

99
Q

in both thalassemias and sickle cell anemia the _____ part of hemoglobin is abnormal and the erythrocytes produced are ____ and ____

A

globin
fragile
rupture prematurely

100
Q

what is the main problem in thalassemias

A

One of the globin chains is absent or faulty, and the erythrocytes are thin, delicate, and deficient in hemoglobin.

101
Q

severe thalassemias require

A

monthly blood transfusions

102
Q

Thalassemia protects these people from _____ due to the blood cells’ easy degradation.

A

malaria

103
Q

In α thalassemia, production of the ______ is affected. The α globin chains are encoded by ___
closely linked genes _________. __ loci encode the α chain.

A

alpha globin chain
2
chromosome 16
4

104
Q

In β thalassemia production of the _______ is affected. The β globin chains are encoded by a ____ gene on
_____. ___loci encode the β chain.

A

beta globin chain
single
chromosome 11
2

105
Q

Deletion of one of the α loci has a high prevalence in people of _________ making them more likely to develop α thalassemia.

A

African or Asian descent,

106
Q

Thalassemia is a group of

A

inherited (autosomal recessive) diseases

107
Q

In autosomal recessive disease, ____ parents must be ____ for a child to be affected

A

both

carriers

108
Q

in thalassemia there is ____ risk with each pregnancy for an affected child.

A

25%

109
Q

60-80 million people in the world are carrying the beta thalassemia _____alone

A

trait

110
Q

India and Pakistan are seeing a large increase of thalassemia patients due to

A

lack of genetic counseling and screening

111
Q

which type of thalassemia does not require medical care or follow up

A

Mild thalassemia

112
Q

Patients with β thalassemia trait should be warned about what

A

that their blood picture resembles iron deficiency and can be misdiagnosed.

113
Q

what should patients with mild thalassemia avoid

A

empirical use of iron therapy

114
Q

why is counselling important for people with thalassemia

A

Counseling is indicated in all persons with genetic disorders, especially when the family is at risk of a
severe form of disease that may be prevented

115
Q

require medical treatment, and a blood transfusion regimen is effective in prolonging
life.

A

severe thalassemia

116
Q

Medical therapy for β-thalassemia primarily involves

A

iron chelation

117
Q

Medical therapy for β-thalassemia primarily involves iron chelation. The antioxidant can be incorporated into the redox machinery of β-thalassemic RBC and defend the cell from ____, possibly interfering with ______, a reactive intermediate in the hydroperoxide-dependent Hb degradation.

A

oxidation

perferryl-Hb

118
Q

complications in thalassemia patients

A 
iron overload
infection
bone deformities
enlarged spleen
slowed growth rates
heart problems
119
Q

People with thalassemia can get an overload of ___ in their bodies, either from the disease itself
or from frequent _______. Too much iron deposition can result in damage to the ___, ___and
_____, which includes glands that produce hormones that regulate processes throughout the body. Without iron chelation therapy, patients with beta-thalassemia will accumulate potentially ______.

A

iron
blood transfusions
heart, liver, and endocrine system
fatal iron levels

120
Q

people with thalassemia have an increased risk of infection if the ____ has been removed as a
treatment.

A

spleen

121
Q

Thalassemia can ___the bone marrow, causes bones to ____. This can result in abnormal
____, especially in the face and skull. Makes bones _____ increasing the risk of broken bones.

A

expand
widen
bone structure
thin and brittle

122
Q

the spleen aids in fighting infection and filters unwanted material, such as old or damaged blood
cells. Thalassemia is often accompanied by the destruction of a large number of red blood cells, and the task of removing these cells causes the spleen to ____. _____can make anemia worse, and it can ____the life of transfused red blood cells. Severe enlargement of the spleen may necessitate its ____.

A

enlarge
splenomegaly
reduce
removal

123
Q

anemia can cause a child’s growth to ___. ___also may be delayed in children with thalassemia.

A

slow

puberty

124
Q

such as congestive heart failure and abnormal heart rhythms

(Arrhythmias) may be associated with

A

severe thalassemia.

125
Q

In sickle-cell anemia, the havoc caused by the abnormal hemoglobin, ______ results from a change in just ______ in a ______chain of the ____ molecule

A

HbS
1 of the 146 amino acids
beta
globin

126
Q

in sickle cell anemia This alteration causes the beta chains to link together under ______ forming _____
so that hemoglobin S becomes ______

A

low O2 conditoins
stiff rods
spiky and sharp

127
Q

in sickle cell anemia it causes the red blood cells to become __________ when they
unload oxygen molecules or when the oxygen content of the blood is lower than normal, as during vigorous exercise and other activities that increase metabolic rate

A

crescent shaped

128
Q

in sickle cell anemia
The stiff, deformed erythrocytes rupture easily and tend to jam up in small blood vessels. These events interfere with oxygen delivery, leaving the victims ________

A

gasping for air and in extreme pain

129
Q

what follows up sickle cell anemia

A

Bone and chest pain are particularly severe, and infection and stroke often follow

130
Q

______ is still the standard
treatment for an acute sickle-cell crisis, but preliminary results using _________ to dilate blood vessels are promising.

A

blood transfusions

inhaling nitric oxide

131
Q

While individuals
with two copies of the sickle-cell gene have sickle-cell anemia, individuals \Vi th only one copy of the gene (sickle-cell
trait) have a

A

better chance of surviving malaria

132
Q

____reduces the malaria
parasites’ ability to survive and enhances _____’ ability
to destroy infected RBCs and the parasites they contain.

A

sickling

macrophages

133
Q

treatment for sickle cell is focused on

A

preventing cells from sickling

134
Q

does fetal hemoglobin sickle

A

no even in those destined to have sickle cell anemia

135
Q

___, a drug used to treat chronic leukemia, switches

the fetal hemoglobin gene back on

A

hydroxyurea

136
Q

In children who are severely affected with sickle cell anemia , _______ offer a
complete cure, but carry high risks

A

bone marrow stem cell transplants

137
Q

is an
abnormal excess of erythrocytes that increases blood viscosity,
causing it to flow sluggishly.

A

polycythemia

138
Q

a bone marrow cancer, is characterized by dizziness and an exceptionally
high RBC count (8-l l million cells/µ!).

A

polycythemia vera

139
Q

people with polycythemia vera The hematocrit may
be as high as ___ and blood volume may ____, causing the vascular system to become engorged with blood and severely
______

A

80%
double
impairing circulation

140
Q

Severe polycythemia is treated by

A

removing some blood (a procedure called a therapeutic phlebotomy).

141
Q

result when less oxygen is available or EPO production increases.

A

Secondary polycythernias

142
Q

The secondary polycythemia

that appears in individuals living at high altitudes is a

A

normal physiological response to the reduced atmospheric pressure and
lower oxygen content of the air in such areas.

143
Q

what is the count of RBC in people with secondary polycythemia

A

6-8 million/µL are common in such people.

144
Q

practiced by some athletes competing in

aerobic events, is artificially induced polycythemia.

A

blood doping

145
Q

Some of the athlete’s red blood cells are drawn off and stored. The body quickly replaces these erythrocytes because removing blood triggers the erythropoietin mechanism. Then, when the stored blood is reinfused a few days before the athletic event, _______

A

a temporary polycythemia results

146
Q

Since red blood cells carry oxygen, the additional infusion should translate into increased oxygen-carrying capacity due to a higher hematocrit, and ______ should result. Other than the risk of ___and ____ due to high hematocrit and high blood viscosity, blood doping seems to work.

A

greater endurance and speed
stroke
heart failure

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