Ch 14: Red Blood Cells and Bleeding Disorders Flashcards
1
Q
what are the three main components of blood
A
formed elements, Buffy coat, and plasma
2
Q
formed elements make up what percentage of blood
A
45%
3
Q
buffy coat makes up what percentage of blood
A
<1%
4
Q
plasma makes up what percentage of blood
A
55%
5
Q
what are the three components of plasma and what are their percentages
A
water - 91%
proteins - 7%
other solutes - 2%
6
Q
what are the two components of the Buffy coat and what are their percentages
A
platelets - <1%
leukocytes - <1%
7
Q
what is the main component of formed elements in the blood and what is its percentage
A
erythrocytes (red blood cells) - >99%
8
Q
what are the four proteins found in plasma
A
albumin
globulin
fibrinogen
prothrombin
9
Q
what is the most important protein in plasma
A
albumin
10
Q
what are 4 other solutes in plasma
A
ions
nutrients
waste products
gases
11
Q
what are the 5 types of leukocytes in the Buffy coat
A
neutrophils
lymphocytes
monocytes
eosinophils
basophils
12
Q
what are the three types of granulocytes
A
neutrophils
eosinophils
basophils
13
Q
what are the two types of agranulocytes
A
lymphocytes
monocytes
14
Q
what is hematocrit
A
percentage of blood (by volume) composed of red blood cells
15
Q
what is the normal hematocrit in males
A
40-50%
16
Q
what is the normal hematocrit in females
A
36-44%
17
Q
what do all blood cells come from and where are they found
A
hemopoietic (pluripotent) stem cells (HSC) which are found in the bone marrow
18
Q
hemopoietic (pluripotent) stem cells differentiate into which two lineages
A
lymphoid and myeloid stem cells
19
Q
lymphoid stem cells differentiate into which 3 blood cells
A
natural killed cells
B cells
T cells
20
Q
myeloid stem cells differentiate into which 4 precursor blood cells
A
myeloblast
monoblast
megakaryoblast
erythroblast
21
Q
what 3 types of blood cells do myeloblasts differentiate into
A
neutrophils
eosinophils
basophils
22
Q
monoblasts differentiate into which type of blood cells
A
monocyte
23
Q
megakaryoblasts differentiate into which type of cell
A
platelets
24
Q
erythroblasts differentiate into which type of cell
A
erythrocytes (red blood cells)
25
what does the suffix "blast" refer to
an immature cell
26
what percentage of red bone marrow space in adults is involved in hematopoiesis
50%
27
normal bone marrow contains what 4 things and their percentages
granulocytes - 60%
erythroid (erythrocyte precursor) - 20%
lymphocytes and monocytes - 10%
unidentified cells - 10%
28
what is hematopoiesis
development of blood cells
29
what percentage of granulocytes are stored vs functional
50% stored
50% functional
30
what percentage of thrombocytes are stored vs functional
30% stored
70% functional
31
what percentage of erythrocytes (red blood cells) are stored vs functional
0% stored
100% functional
32
what are three main storage sites of granulocytes
liver
spleen
bone marrow
33
what is erythropoiesis
development of red blood cells
34
what is erythropoietin
hormone released by the kidneys that stimulates maturation of erythrocytes
35
what is the normal shape of an erythrocyte
biconcave disk
36
what is happening during the late stage of an erythroblast
nucleus shrinks and is ejected out of the cell along with other organelles
37
what is happening during the reticulocyte phase of an erythroblast
remaining organelles are rejected
cell enters blood stream in its biconcaved disk form
38
what are 4 things that trigger the kidneys release of erythropoietin
decrease in red blood cells
decrease in hemoglobin synthesis
decrease in blood flow
hemorrhage
39
how long does it take reticulocytes to mature in the blood to become red blood cells
1-2 days
40
what is the normal percentage range of reticulocytes in the blood
0.5-1.5%
41
what is hemoglobin
large oxygen binding protein
42
what is the structure of hemoblogin
4 polypeptide subunits; 2 alpha and 2 beta chains
each polypeptide is bound to a heme group
43
what is a heme group
iron containing compound found on a hemoglobin molecule
4 in each hemoglobin molecule
44
what is Fe2+
ferrous iron
form that can bind to oxygen
45
what is Fe3+
ferric iron
form that cannot bind to oxygen
46
what happens when oxygen binds to a heme group on a hemoglobin molecule
the iron attached to the heme becomes oxidized and forms a red molecule called oxyhemoglobin (HbO2)
47
what is oxyhemoglobin (HbO2)
hemoglobin that has oxygen bound to its heme groups
48
what is deoxyhemoglobin
hemoglobin that does not have oxygen bound to its heme groups
49
how is methemoglobin formed
when hemoglobin releases its oxygen into the tissues, it can become oxidized to form methemoglobin (Fe3+)
50
what is a normal percentage of methemoglobin in the blood
<1%
51
what is methemoglobin reductase
enzyme that reactivates hemoglobin by reducing Fe3+ back to Fe2+
52
what is methemoglobulinemia and what are its two causes
excess methemoglobin and a decreased ability to deliver oxygen to the tissues
two causes: deficiency in methemoglobin or toxic insult
53
what is toxic insult of methemoglobinemia
some kind of toxin leads to high levels of methemoglobin
leads to brown appearance of blood
54
what are the three treatments for methemoglobinemia
treated with: methylene blue, vitamin C, or giving blood
55
what are the three things those with methemoglobinemia present with
presents with: headache, lightheadedness, and dyspnea
56
what is carboxyhemoglobin and how is it formed
complex of hemoglobin and carbon monoxide (CO)
CO changes shape of hemoglobin making it unable to unload oxygen into tissue
57
where are the three main storage locations of iron
liver cells
spleen macrophages
bone marrow macrophages
58
where is iron first absorbed within the body
duodenum
59
what transports iron throughout the plasma and where is it made
the glycoprotein transferrin which is made in the liver
60
where is iron lost at a rate of 1-2mg/day
lost in the skin, gut, and endometrium
61
what three things destroy old RBC
macrophages of the bone marrow, spleen, and liver
62
how long do red blood cells live before they're destroyed
120 days
63
explain how red blood cells are destroyed
RBC become trapped in the sinusoids of the spleen and spleen macrophages digest them
64
what happens to hemoglobin after a red blood cell is destroyed
it is broken down into amino acids, iron, and bilirubin
65
what happens to bilirubin after a red blood cell is destroyed
it is excreted in feces and urine
66
what happens to iron and amino acids after a red blood cell is destroyed
they are recycled in the bone marrow to make new hemoglobin
67
what is anemia
reduction of the total circulating red cell mass below normal limits
leads to hypoxia because there are less RBC available to carry oxygen
68
what three things do those with anemia present with
progressive weakness (fatigue)
pallor
dyspnea (labored breathing)
69
what are the two things that are used to diagnosis anemia
hematocrit and hemoglobin concentration
70
what is macrocytic-normochromatic anemia
a type of anemia that is caused by impaired maturation of erythroid precursors in bone marrow
leads to a large but normal colored RBC
71
what is an example of macrocytic-normochromic anemia
pernicious anemia
72
what is microcytic-hypochromic anemia
a type of anemia that is cause by disorders of hemoglobin synthesis
leads to a small and very pale red blood cell
73
what are two examples of microcytic hypochromic anemia
iron deficiency; thalassemia
74
what is normocytic-normochromic anemia
a type of anemia caused by diverse etiologies (origins)
leads to a normal sized and color red blood cell
75
what is an example of normocytic-normochromic anemia
aplastic anemia
76
what are the three main mechanisms of classifying anemia
blood loss
increased red cell destruction (hemolysis)
decreased red cell production
77
what is acute blood loss
loss of intravascular blood volume and all its components due to trauma
causes an increase in reticulocyte counts and eventually cardiovascular collapse or death
78
what is chronic blood loss
loss of blood that induces anemia with it exceeds regenerative capacity of bone marrow or when iron reserves are depleted
caused by GI lesions or GYN disturbances
79
what is hemolytic anemia and what are the three things its characterized by
accelerated destruction of red blood cells
characterized by:
shortened RBC life span
accumulation of hemoglobin degradation products
elevated erythropoietin and erythropoiesis levels
80
what is extravascular hemolysis
destruction of RBCs outside of the blood vessels
alterations make RBC less deformable making them get stuck in the spleen
spleen macrophages destroy the cells, leading to anemia, splenomegaly, and jaundice
81
what are two examples of extravascular hemolysis
hereditary spherocytosis and sickle cell anemia
82
what is intravascular hemolysis
destruction of RBCs within the vessel
caused by mechanical injury, complement, parasites, or toxins
RBC is lysed, hemoglobin is released and binds to haptoglobin to form complex
complex is cleared by phagocytes which leads to anemia, jaundice, and hemoglobinemia
83
what is the consequence of intravascular hemolytic anemia
haptoglobin that was bound to hemoglobin is removed by mononuclear phagocytes
lack of haptoglobin allows hemoglobin to oxidize to methemoglobin
too much methemoglobin reduces oxygen levels in the blood
84
what is an acquired genetic defect that leads to increased red cell destruction (hemolysis)
antibody mediated destruction
85
what is warm autoimmune hemolytic anemia
-causes
-intravascular vs extravascular
most common type of immunohemolytic anemia
IgG binds to Rh antigens on RBC at 37 degrees Celsius (normal body temperature)
50% primary (idiopathic)
50% secondary to things like lymphomas, SLE, and chronic lymphocytic leukemia (CLL)
destruction is mostly extravascular
86
what is cold agglutinin autoimmune hemolytic anemia
-which conditions is it most seen
-intravascular vs extravascular
type of immunohemolytic anemia
IgM binds to RBC at cold temps (0-4 degrees celsius)
binding causes agglutination of seen mostly in fingers, toes, and ears and can lead to gangrene
can appear following infections like mycoplasma, EBV, CMV
IgM releases RBC once temperature increases
destruction is mostly extravascular
87
what is cold hemolysin autoimmune hemolytic anemia
-in what conditions is it most seen
-intravascular or extravascular
type of immunohemolytic anemia
IgG autoantibodies bind to P blood group antigen in peripheral regions of the body when cold
RBC is destroyed once body warms up
often seen in children following viral infections
destruction is mostly intravascular
88
what are the two main types of acquired, extrinsic, genetic defects that cause antibody mediated destruction of RBC and therefore anemia
immunohemolytic
drug induced hemolytic
89
what is the hapten model of drug-induced hemolytic anemia
drug like penicillin binds to red blood cells
body now views RBC as foreign and creates antibodies against the drug
leads to hemolysis by complement or phagocytosis
90
what is the immune complex formation of drug-induced hemolytic anemia
drug like quinidine binds to a carrier protein
antibodies against drug bind to this quinidine/carrier protein complex
complex binds to C3b receptors on RBC
RBC is now seen as foreign and is destroyed by complement
91
what is the autoimmune model of drug-induced hemolytic anemia
body makes antibodies against drugs such as alpha-methydopa
antibodies mistakenly bind to RBC and cause it to be destroyed by phagocytosis
92
how is drug-induced hemolytic anemia treated
remove offending drug
splenectomy
93
what are the two types of intrinsic, inherited genetic defects that cause hemolytic anemia
RBC membrane disorders
enzyme deficiencies
94
what is hereditary spherocystosis (HS)
type of RBC membrane disorder
75% of cases are autosomal dominant
mutations affect RBC membrane skeleton
hereditary spherocyte cells lose membranes as they age which lead to a spherocyte shape
can't deform as they go through vessels as well which causes them to be removed through an extravascular process (spleen macrophages)
only live 10-20 days
presents with: anemia and splenomegaly
95
what four things in the RBC membrane are most commonly mutated in hereditary spherocytes
ankyrin
band 3
spectrin
band 4.2
all lead to pieces of RBC being cleaved until it is sphere shaped and destroyed by splenic macrophage
96
what is a glucose-6-phosphate-dehydrogenase deficiency (G6PD)
inherited, intrinsic enzyme deficiency
X-linked recessive disorder where there are mutations that destabilize G6PD enzyme
enzyme can no longer neutralize compounds like hydrogen peroxide, making RBC more susceptible to oxidative injuries
damaged cells will be lysed, leading to anemia
97
what is the glucose-6-phosphate-dehydrogenase (G6PD) variant seen in american blacks
G6PD-
98
what is the glucose-6-phosphate-dehydrogenase (G6PD) variant seen in mediterraneans
G6PD
99
what are the 3 triggers of glucose-6-phosphate-dehydrogenase deficiency (G6PD)
infections (viral and pneumonia)
drugs (sulfonamide and nitrofurantoin)
foods (fava beans)
100
explain how deficiency of glucose-6-phosphate-dehydrogenase (G6PD) enzyme damages RBCs are how they are removed after 2-3 days
deficiency of enzyme leads to high oxidant build up which damages RBCs by cross-linking globin chains (intravascular)
cross-linking leads to denaturing of red cell and formation of heinz bodies
heinz bodies get trapped in spleen, form bite cells and spheryocytes, and are removed by macrophages (extravascular)
101
what does glucose-6-phosphate-dehydrogenase (G6PD) deficiency protect you from
RBC's without enough glucose-6-phosphate-dehydrogenase impair the growth of plasmodium falciparum malaria
102
what is the most common type (98%) of hemoglobin in normal adults
HbA (alpha 2, beta 2)
103
what is the second most common type (2%) of hemoglobin in normal adults
HbA2 (alpha 2, delta 2)
104
what is the fetal hemoglobin
HbF (alpha 2, gamma 2)
105
what is the sickle hemoglobin
HbS (alpha 2, beta 2 s)
106
which type of hemoglobin is elevated 4-8% in those with beta-thalassemia
HbA2 (alpha 2, delta 2)
107
what is significant about hemoglobin production at the chromosomal level
alpha globin comes from alpha gene on chromosome 16 which is turned on during embryonic development - you get 2 from mom and two from dad
beta globin comes from beta gene on chromosome 11 - you get two from mom and two from dad
108
which type of hemoglobin is elevated in those with beta-thalassemia trait
HbA2 (2 alpha, 2 delta)
109
what is the mechanism of thalassemia syndromes
mutation in globin genes leads to decrease synthesis of alpha or beta chains
chains are damaged by precipitants
110
what are three consequences of thalassemia syndromes
anemia, hypoxia, and red cell hemolysis
111
why do thalassemia syndromes cause anemia
decreased production of hemoglobin leads to decreased life span of RBCs and therefore anemia
112
what causes A-Thalassemia
inherited deletions reduced or stop synthesis of alpha-globin chains
113
what causes B-thalassemia
mutations lead to diminished synthesis of B-globin chains
Bdegree: no beta chain synthesis at all
B+: decreased beta chain synthesis
114
what do the RBCs of thalassemia syndromes looks like
microcytic-hypochromic due to decreased hemoglobin synthesis
115
what is B-thalassemia major (Cooley's anemia) and what treatment does it require
severe case of reduced beta globin
require blood transfusions
116
what's another name for B-thalassemia major
Cooley's anemia
117
what is B-thalassemia major caused by
point mutations that lead to defects in transcription, splicing, or translation of B-globin mRNA
118
what is B-Thalassemia intermedia and what treatment does it require
severe cases of reduced beta globin
do not require regular blood transfusions
119
what do those with B-thalassemia minor or trait present with
asymptomatic with mild or absent anemia
red cell abnormalities seen
120
what type of thalassemia is silent carrier and what does it present with
type of a-thalassemia
asymptomatic with no red cell abnormalities
121
what is silent carrier a-thalassemia caused by
mainly gene deletions
122
what do those with a-thalassemia trait present with
asymptomatic with mild or absent anemia
red cell abnormalities seen
123
what type of thalassemia is HbH disease, how bad is it, and how is it treated
type of A-thalassemia
severe
does not require blood transfusions
124
what happens to those with a-thalassemia major
aka hydrops fetalis
lethal in utero without transfusions
125
what is another name for a-thalassemia major
hydrops fetalis
126
how does B-thalassemia affect your heart and liver
erythroblasts of those with B-thalassemia are abnormal and therefore can't be made into red blood cells so they die in the bone marrow
less RBCs means there are less places for the absorbed iron to go
unabsorbed iron causes overload in the heart and liver leading to secondary hemochromatosis
127
what is another term for the systemic iron overload of the heart and liver
secondary hemochromatosis
128
how does B-thalassemia affect your skeleton
erythroblasts of those with B-thalassemia are abnormal and therefore can't be made into red blood cells so they die in the bone marrow
reduced number of RBCs leads to anemia, tissue hypoxia, and erythropoietin increase
increased erythropoietin leads to bone marrow expansion and therefore skeletal deformities
129
what happens to the abnormal erythroblasts that are not destroyed in the bone marrow in those with B-thalassemia
the hypochromic cell with a-globin aggregate gets lysed in the spleen
reduced RBCs leads to anemia, tissue hypoxia, and erythropoietin increase
increased erythropoietin leads to bone marrow expansion and therefore skeletal deformities
130
what is sickle cell anemia
autosomal recessive disorder where there is a point mutation in B-globin chain
glutamic acid is replaced with valine
sickled hemoglobin can carry oxygen but once they drop oxygen off, they become deoxygenated and sickled
deoxygenated hemoglobin forms long polymers that distort the RBC
lifespan of RBC is reduced significantly
131
what percentage of African Americans are heterozygous for sickle cell anemia
8-10%
132
what does it mean when you're heterozygous for HbS
you have sickle cell trait and are most of the time asymptomatic
133
what does it mean when you're homozygous for HbS
you will be symptomatic
134
in someone with heterozygous sickle cell trait, what percentage of their hemoglobin is HbS vs HbA
HbS: 40%
HbA: 60%
135
in someone with homozygous sickle cell, what percentage of their hemoglobin is HbS vs HbA
all is HbS
136
explain the mechanism which causes a cell to become sickled
point mutation in B-globin gene switches out a glutamic acid for valine
when RBCs drop off their oxygen, the deoxygenated cell forms long polymers, sickling the cell
137
what are the four factors that affect the rate and degree of sickling
interaction of HbS with other types of hemoglobin in cell
mean cell hemoglobin concentrations
intracellular pH
transit time of red cells through microvascular beds
138
what happens to the mean hemoglobin concentration if the cells are dehydrated
increase in concentration of hemoglobin which increases amount of sickling
139
how does the intracellular pH affect the rate and degree of sickling
decreased intracellular pH reduces affinity of O2
O2 won't stick well which leads to deoxygenation
140
how does the transit time of RBCs through microvascular beds affect rate and degree of sickling
longer the transit time, the more sickling that happens in spleen, bone marrow, and inflamed vessels
141
what are three complications of sickle cell anemia
episodic vessel blockage (tissue infarction of bone marrow and spleen)
repeated bouts of sickling lead to permanent RBC membrane damage, eventually leading to anemia
autosplenectomy
142
what is autosplenectomy
seen in sickle cell anemia
erythrostasis in spleen (red blood cells get stuck in spleen)
leads to infarction and fibrosis of spleen with eventual shrinkage
143
what does sickle cell anemia protect you from
plasmodium falciparum malaria
144
how is sickle cell anemia treated
hydration
blood transfusions
hydroxyurea
145
what is hydroxyurea used for and what does it do
used to treat sickle cell anemia
inhibits DNA synthesis
increases HbF levels
anti-inflammatory
146
what is aplastic anemia
chronic primary hematopoietic (bone marrow) failure which leads to pancytopenia
can present with anemia, leukopenia (neutropenia), and thrombocytopenia
onset is gradual
cells are normochromic, normocytic
147
what is pancytopenia
low levels of RBCs, WBCs, and platelets typically caused by an issue with the bone marrow
148
what is the major acquired cause of aplastic anemia (with percentage)
idiopathic (cause unknown) - 60% of all cases
149
what is the most common chemical agent cause of aplastic anemia
idiosyncratic (distinct) chemicals
150
what is a major physical agent that causes aplastic anemia
viral infections
151
what are two major inherited conditions that cause aplastic anemia
fanconi anemia
telomerase defects
152
what is the extrinsic pathogenesis of aplastic anemia
immune-mediated suppression of bone marrow progenitors (antibodies destroy cells)
cells aren't being made
153
what is the intrinsic pathogenesis of aplastic anemia
mutation within stem cells stops them from acting correctly
can be caused by things like being exposed to a virus
154
give an example of intrinsic pathogenesis of aplastic anemia
pluripotent stem cell is affected by environmental insult such as virus or drug that alters stem cells
altered stem cells express new antigens which activates T cells to destroy them
or
reduces proliferative and differentiate capacity
both lead to marrow aplasia
155
how is aplastic anemia diagnosed and what does it show
through bone marrow biopsy
shows lots of adipocytes with little cellular components
156
how is aplastic anemia treated
avoidance of toxin
blood transfusion
stimulation of hematopoiesis
stem cell transplantation
157
what is fanconi anemia
type of aplastic anemia caused by inherited genetic defect
autosomal recessive
destroyed multiprotein complex that is required for DNA repair
affects bone marrow in early life
leads to underdeveloped kidneys and spleen
leads to bone abnormalities in thumbs or radii
158
what are telomerase defects
inherited cause of aplastic anemia
mutation of telomerase enzyme which results in premature hematopoietic stem cell exhaustion and marrow aplasia
stem cells die without the telomerase enzyme
159
what are Vitamin B12 and Vitamin B9 deficiencies associated with
anemia of diminished erythropoiesis
both are coenzymes are required for synthesis of thymidine
presents with macrocytic-normochromic cells
160
what is vitamin B12
cobalamin
161
what is vitamin B9
folic acid
162
what is the mechanism of vitamin deficiency causing anemia
vitamin deficiencies lead to inadequate synthesis of thymidine and defective DNA replication
leads to enlarged abnormal hematopoietic precursors
megaloblasts in bone marrow have lots of hemoglobin and RBCs are large
163
what is the outcome of someone with anemia caused by nutritional deficiencies
marrow hyperplasia leads to most cells undergoing apoptosis
overall leads to pancytopenia
164
vitamin B12 deficiency can be caused by impaired absorption which will lead to what
pernicious anemia
165
what three major things lead to a vitamin B9 deficiency
decreased intake (alcoholics, poor, elderly)
increased requirement (pregnancy, cancer)
impaired utilization (antagonist drugs)
166
what is pernicious anemia caused by
type of megaloblastic anemia
autoimmune gastritis causes impaired production of intrinsic factor which leads to impaired absorption of vitamin B12
167
what is intrinsic factor
secreted by parietal cells of fundic mucosa
required for proper absorption of vitamin B12
168
what is autoimmune (chronic atrophic) gastritis
cause of pernicious anemia
inflammation of the stomach due to auto reactive T cells attacking gastric mucosa
or
H. pylori infection
both lead to formation of autoantibodies that attack parietal cells and therefore no intrinsic factor can be produced
169
how is the CNS involved in pernicious anemia
demyelination of dorsal and lateral tracts lead to loss of axon
causes sensory neuropathy and visual impairment
170
how is pernicious anemia diagnosed
through symptoms and low vitamin counts in the blood
171
how is pernicious anemia treated
with vitamin B12 injections
172
what is folic acid (vitamin B9) deficiency anemia
some factor leads to folic acid deficiency
it's required for DNA synthesis - makes thymidine
does not cause neurologic impairment
treated with oral folic acid
173
what is iron deficiency anemia (hypoferremia) including cell type
most common type of anemia in the world
microcytic-hypochromic cells due to insufficient hemoglobin synthesis
caused by dietary deficiency, chronic blood loss, impaired absorption, and increased requirement
don't present until levels are super low because you use all your store
174
how much iron is functional and where is it found
80%
found in hemoglobin, myoglobin, and iron containing enzymes
175
what are two types of iron containing enzymes
cytochrome and catalase
176
how much iron is stored and where is it stored
20%
stored as hemosiderin or bound to ferritin in the liver, mononuclear phagocytes in bone marrow, and spleen
177
how does hepcidin normally work
works to block ferroportin 1 from allowing iron absorption into bloodstream
178
what is the effect of low iron stores on hepcidin
low iron store leads to less plasma hepcidin which increases activity of ferroportin 1, allowing iron to be absorbed
179
what is myelophthisic anemia
type of space-occupying marrow lesion
bone marrow is being replaced and pushed out of the way due to lesions
immature, tear drop shaped cells released
usually caused by metastatic cancer
180
what are the three most common types of metastatic cancer which causes myelophthisic anemia
breast
lung
prostate
181
what is polycythemia
abnormally high levels of RBC with lots of hemoglobin
182
what's a relative cause of polycythemia
dehydration leads to decreased plasma volume and increased hemoconcentration
183
what's absolute polycythemia
increase of total red cell mass
two types: primary and secondary
184
what is primary absolute polycythemia
excess red blood cells due to an abnormality of stem cells in bone marrow
happens even with low erythropoietin levels
185
what are two types of primary absolute polycythemia
polycythemia vera (red cells grow in the bone marrow, no erythropoietin needed)
familiar EPO receptor gain of function mutation (continuous activation)
186
what is secondary absolute polycythemia
increased EPO secretion either from tumors
or
inherited defects in renal oxygen-sensing pathways which stimulates transcription of EPO gene
187
which carcinomas produce erythropoietin
renal cell carcinomas
188
what is Chuvash polycythemia
rare inherited defects in renal oxygen sensing pathways
stimulates transcription of EPO gene
