Hematopoietic Agents Flashcards
1
Q
A connective tissue that consists of plasma (liquid) plus formed elements (red, white blood cells & platelets)
A
Blood
2
Q
functions of blood
A
1- transports oxygen, carbon dioxide, nutrients, hormones, heat & waste
2- regulates pH, body temperature, & water content of cells
3- protects against blood loss through clotting, & against disease through phagocytic white blood cells & proteins such as antibodies, interferons & complement
3
Q
fluid part of blood
A
plasma
4
Q
plasma without clotting factors
A
serum
5
Q
blood cells
A
erythrocytes- carry oxygen
leukocytes- role in immunity
thrombocytes- blood clotting
6
Q
leukocyte, neutrophil, monocyte
A
white blood cell
7
Q
erythrocyte
A
red blood cell
8
Q
-blood cell production
-occurs mainly in red bone marrow after birth
-hematopoiesis
A
hemopoiesis
9
Q
hematopoietic stem cells
A
*stem cells that give rise to the various types of blood cells in the body
*found primarily in the bone marrow
*can also be found in cord & peripheral blood
*can differentiate into red/white blood cells, & platelets
10
Q
pluripotent stem cell
A
*a type of stem cell that has the ability to differentiate into almost any cell type in the human body
*can be derived from different sources, such as:
*embryonic stem cell- early stage
embryos
*induced pluripotent stem cell-
reprogrammed from adult
cells
* can differentiate into 3 germ layers: ectoderm, mesoderm, & endoderm
11
Q
myeloid stem cell
lymphoid stem cell
A
come from pluripotent stem cell
12
Q
precursor cells
A
blasts
13
Q
myeloid stem cell
CFU-E
A
colony forming unit- erythrocyte
↓
proerythroblast
↓ (nucleus ejected)
reticulocyte
↓
red blood cell (erythrocyte)
14
Q
myeloid stem cell
CFU-Meg
A
colony forming unit- megakaryocyte
↓
Megakaryoblast
↓
megakaryocyte
↓
platelets
15
Q
myeloid stem cell
CFU-GM
A
colony forming unit- granulocyte macrophage
granular leukocytes:
eosinophil
basophil
neutrophil
16
Q
lymphoid stem cell
T, Y, NK lymphoblast
A
T lymphocyte (T cell)
B lymphocyte (B cell) - plasma cell
Natural Killer cell
17
Q
Agranular leukocytes
A
T cell
B cell
NK cell
Macrophage (from monocyte)
18
Q
mast cell
A
from myeloid stem cell
19
Q
requirements for formation and maintenance of healthy blood cells
A
1- IRON: formation of hemoglobin, the protein in red blood cells responsible for carrying oxygen
2- FOLIC ACID: (Vit B9) especially important during pregnancy and periods of rapid growth
3- COBALAMIN: (Vit B12) works closely with folate to make DNA and red blood cells
4- COPPER: involved in iron metabolism, the production of hemoglobin, and the formation of red blood cells
5- PYRIDOXINE: (Vitamin B6) formation of hemoglobin, regulate blood sugar levels
20
Q
HEMATOPOIETIC GROWTH FACTORS
A
Erythropoiesis: erythropoietin
Myelopoiesis: granulocyte macrophage colony stimulating factor (GM-CSF) & granulocyte colony stimulating factor (G-CSF)
Thrombopoiesis: IL-11, thrombopoietin
21
Q
HEMATOPOIETIC DISORDERS
A
↓RBC Anemia
↑RBC Polycythemia
↓WBC Leukopenia
↑WBC Leukocytosis
↓Platelets Thrombocytopenia
↑Platelets Thrombocytosis
22
Q
anemia
A
a group of diseases characterized by a decrease in hemoglobin( (Hb) or red blood cells (RBCs),
resulting in decreased oxygen-
carrying capacity of blood
World Health Organization definition:
Hb <13 g/dL (<130 g/L; <8.07 mmol/L) in men
Hb <12 g/dL (<120 g/L; <7.45 mmol/L) in women
23
Q
CLASSIFICATION OF ANEMIAS
A
Hypoproliferative
Maturation disorders
Hemorrhage/hemolysis
24
Q
Hypoproliferative anemia
A
*marrow damage
*iron deficiency
*↓ stimulation:
-renal disease
-inflammation
-metabolic disease
25
maturation disorder anemia
*cytoplasmic disease:
-thalassemia
-iron deficiency
-sideroblastic
*nuclear maturation defect:
-folate deficiency
-vit B12 deficiency
-refractory anemia
26
hemorrhage/hemolysis anemia
*blood loss
*intravascular hemolysis
*autoimmune disease
*hemoglobinopathy
*metabolic/membrane defect
27
CLASSIFICATIONS OF ANEMIA
Based on Size
* Macrocytic- increased MCV of over 100, megaloblastic and non-megaloblastic, due to impaired DNA synthesis
* Normocytic- normal MCV of between 80-100 fL, haemolysis or underproduction of normal-sized RBCs
* Microcytic- MCV of less than 80, results in smaller and paler (hypochromic) RBCs, iron deficiency anaemia
28
CLASSIFICATIONS OF ANEMIA
Based Hemoglobin
Content
* Normochromic- red blood cells have a normal amount of hemoglobin
* Hypochromic-- ed blood cells that have less hemoglobin than normal, resulting in a paler appearance
29
CLASSIFICATIONS OF ANEMIA
Based on Shape
* Normal
* Abnormal
30
amount of Hb per volume of whole blood
Hemoglobin (Hb)
31
the actual volume of RBCs in a unit volume of whole blood (in %)
Hematocrit (Hct)
32
– actual count of RBCs per unit of blood
RBC Count
33
Mean Corpuscular Volume (MCV = Hct/RBC)
– average volume of RBCs
34
Mean Corpuscular Hb (MCH = Hb/RBC)
– average amount of Hb in a RBC
35
Mean Corpuscular Hb Concentration (MCHC = Hb/Hct)
– concentration of Hb in a volume of RBCs
36
– an indirect assessment of new RBC production; can differentiate hypoproliferative marrow from a compensatory marrow response to
an anemia
Reticulocyte Production Index (RPI)
37
RBC Distribution Width (RDW)
– variability of RBC size
38
best indicator of iron deficiency or overload; in equilibrium
with storage ferritin in RES; can be used to estimate total body iron stores
Serum ferritin –
39
diagnose pernicious anemia
Schilling test –
40
– for hemolytic anemia
Coombs test
41
the iron portion of a heme group binds oxygen for transport by
hemoglobin
42
most common cause of chronic anemia
strictly conserved
IRON
43
*is toxic because of its ability to induce the formation of damaging reactive oxygen species:
*Fe2+ + H2O2 → Fe3+ + OH* + OH−
*needs to be bind to proteins to be transported to decrease its toxicity.
Free iron
44
*membrane transporter
*transports dietary Fe2+ heme through the apical surface into enterocytes
Heme Carrier Protein
45
*membrane transporter
*transports Fe2+ through membranes
Divalent Metal Ion Transporter-1
(DMT-1 or SLC11A2)
46
*membrane transporter
*exporter of iron from cells (e.g., enterocytes, RBCs)
Ferroportin or Iron-Regulated
Protein 1 (IREG1 or SLC40A1)
47
*enzyme
*reduces dietary free Fe3+
to Fe2+ prior to absorption via DMT-1
Duodenal Cytochrome b (Dcytb)
48
*storage protein
*binds Fe3+ for storage in liver, spleen and bone marrow; iron is readily mobilized; can bind up to 4500 Fe3+
/ferritin;
*most sensitive indicator of body iron stores
Ferritin
49
*storage protein
*stores excess iron; iron is not readily mobilized
Hemosiderin
50
*transport protein
*binds Fe3+ for transport in the plasma; binds 2 Fe3+/transferrin;
*usually 1/3 saturated with iron; *reflects total iron-binding
capacity
Transferrin (Tf)
51
TfR
*receptor
*facilitates receptor mediated endocytosis of transferrin
52
*enzyme
*a Cu-containing ferroxidase in the plasma:
*oxidizes Fe2+ to Fe3+
Ceruloplasmin
53
*enzyme
*a Cu-containing ferroxidase in the enterocyte membrane:
*oxidizes Fe2+ to Fe3+
Hephaestin
54
*regulatory protein
*regulates ferroportin;
*the central molecule in iron
homeostasis
Hepcidin
55
– less abundant but better absorbed
Fe2+ in heme from animal sources
56
– more abundant but less absorbed because of oxalates, phytates, tannins, and phenolic compounds that chelate or precipitate iron
Free Fe3+ in plant sources
57
10–15 mg of dietary elemental Fe/day.
10-15% (1-2 mg/day) of is absorbed.
occurs the duodenum and proximal jejunum
58
On the apical surface:
Fe2+-heme –
via heme
carrier protein (HCP)
59
On the apical surface:
Free Fe3+ –
via DMT-1
enhanced by vitamin C (a coenzyme
for duodenal cytochrome b (Dcytb)
that reduces Fe3+ to Fe2+)
60
release of Fe2+ from heme via
heme oxygenase
oxidization of Fe2+ to Fe3+ to be
stored as intracellular ferritin
In the enterocyte:
61
exit of Fe2+ via ferroportin and
oxidation by hephaestin (Cu-
containing) to Fe3+
On the basolateral surface:
62
combination of Fe3+ combines with apotransferrin, to form
and circulate as
transport of transferring to cells that store or use it iron
transferrin (Tf)
63
CELLULAR UPTAKE OF IRON
*binding of transferrin-bound Fe3+ to transferrin receptors (TfR) on erythroblasts and other iron-requiring cells
*receptor mediated endocytosis of transferrin-bound Fe3+ forming an endosome w/ slightly acidic pH
*release of Fe3+ from transferrin
*reduction of Fe3+ to Fe2+ by membrane-bound oxidoreductase
*transport of Fe2+ from the endosome to the cytosol via DMT-1
*storage or use of Fe2+
64
STORAGE OF IRON
*in most cells especially in intestinal mucosal cells, the liver, spleen
and bone marrow
*oxidation of Fe2+ to Fe3+
*binding of Fe3+ to apoferritin forming ferritin.
*In iron overload, it is stored as hemosiderin, a form of degraded
ferritin complexed with additional iron that cannot be readily mobilized.
65
USE OF IRON IN HEME SYNTHESIS
*mobilization of iron from storage (ferritin)
*transport as transferrin to cells that require iron for heme synthesis
(e.g. erythroblasts)
66
RECYCLING OF IRON
*exit of Fe2+ from heme degradation in macrophages via ferroportin
*oxidized of Fe2+ to Fe3+ by ceruloplasmin (Cu-containing)
*release of Fe3+ and transport as transferrin
*Recycled iron meets approximately 90% of daily need.
67
EXCRETION OF IRON
*through defecation or bleeding
*trace amounts in bile, urine, and sweat
*no more than 1 mg daily
68
REGULATION OF
IRON METABOLISM
BY HEPCIDIN
*When plasma iron levels are high,
hepatic synthesis of hepcidin
increases.
*Hepcidin binds to ferroportin,
triggering its internalization and
degradation.
*In enterocytes, iron absorption is
blocked.
*In RBCs, iron liberation is blocked.
*Plasma iron levels are reduced
(hypoferremia).
69
IDA
*the most common nutritional deficiency in developing and developed countries
Etiology:
most common in adults: blood loss, usually in the GIT
increased iron requirements e.g., growing children, pregnant women
increased losses of iron e.g., menstruating women ≈30 mg of iron with each menstrual period
*microcytic hypochromic anemia
70
increased demand for iron
-rapid growth in infancy or adolescence
-pregnancy
-erythropoietin therapy
71
increased iron loss
-chronic blood loss
-menses
-cute blood loss
-blood donation
-phlebotomy as treatment for polycythemia vera
72
decreased iron intake or absorption
-inadequate diet
-malabsorption from disease (sprue, chron's disease)
-malabsorption from surgery (gastrectomy & some forms of bariatric surgery)
-acute or chronic inflammation
73
the demands for/losses of iron
exceed the body’s ability to
absorb iron; red cell
morphology and indices are
normal
Negative iron balance:
74
impaired hemoglobin
synthesis
Iron-deficient erythropoiesis:
75
microcytic hypochromic cells
Iron deficiency anemia:
76
ORAL IRON THERAPY
*corrects IDA as rapidly and completely as parenteral Fe if absorption is
normal, except in advanced CKD undergoing hemodialysis and treatment with erythropoietin
*contain Fe2+ ion – most efficiently absorbed
*200–400 mg of elemental Fe/day to correct iron deficiency most rapidly
*continued for 3-6 months after correction of iron deficiency
*take before meals; may be taken with meals to reduce GI irritation
*A/E: nausea, epigastric discomfort, abdominal cramps, constipation, diarrhea, black stools
77
PARENTERAL IRON THERAPY
*reserved for patients who are unable to tolerate or absorb oral Fe with
extensive chronic anemia who cannot be maintained with oral Fe alone:
advanced CKD requiring hemodialysis and treatment with erythropoietin
postgastrectomy conditions and previous small bowel resection
inflammatory bowel disease involving the proximal small bowel
malabsorption syndromes
*contain Fe3+ ion as colloid containing particles with a core of iron
*oxyhydroxide surrounded by a core of carbohydrate
*
Bioactive iron is released slowly from the stable colloid particles.
78
PARENTERAL IRON THERAPY
Ferric Carboxymaltose
Iron Isomaltoside/
Ferric Derisomaltose
79
IRON TOXICITY
Acute Toxicity
* necrotizing gastroenteritis, with vomiting, abdominal pain, and bloody
diarrhea followed by shock, lethargy, and dyspnea
* improvement often noted, but may be followed by severe metabolic acidosis,
coma, and death
* Treatment: whole bowel irrigation, deferoxamine (IV), activated charcoal is
not effective
80
IRON TOXICITY
Chronic Toxicity (Hemochromatosis)
* excess iron is deposited in the heart, liver, pancreas, and other organs
* can lead to organ failure and death
* Treatment: phlebotomy weekly; deforoxamine (IV), deferasirox (PO), &
deferiprone (PO) less effective
81
RBC TRANSFUSION
*reserved for individuals who have symptoms of anemia,
*cardiovascular instability, and continued and excessive blood loss from whatever source and who require
immediate intervention
Hb <7 g/dL (<70 g/L)
82
MEGALOBLASTIC ANEMIA
*caused by abnormal DNA metabolism resulting from vitamin B12 or
folate deficiency
*The rate of RNA and cytoplasm production exceeds the rate of
DNA production.
*The maturation process is retarded, resulting in immature large
RBCs (macrocytosis).
macrocytic, normochromic anemia
83
VITAMIN B12
(COBALAMIN)
3 major structural components:
planar group or corrin
nucleus with a central cobalt
atom
5,6-dimethylbenzimidazolyl
nucleotide
variable R group
84
VITAMIN B12
ultimate source:
microbial synthesis
not synthesized by animals or plants
85
VITAMIN B12
chief dietary source:
meat (especially liver), eggs, and dairy products
5–30 mcg of vitamin B12/day
1–5 mcg absorbed/day
86
ACTIVE FORMS OF VITAMIN B12 IN THE BODY
5’-deoxyadenosylcobalamin
* bonded to 5’-carbon of 5’-deoxyadenosine
Methylcobalamin
* bonded to carbon of a methyl group
87
VITAMIN B12 ABSORPTION
Passive Absorption
* occurs equally through buccal, duodenal, and ileal mucosa
* rapid but extremely inefficient
* <1% of an oral dose being absorbed
88
VITAMIN B12 ABSORPTION
Active Absorption
* occurs through the distal ileum
* efficient for small oral doses of cobalamin
* pepsin and hydrochloric acid release the cobalamin from animal
proteins
* mediated by gastric intrinsic factor (IF) produced by parietal cells
89
VITAMIN B12 STORAGE AND EXCRETION
*avidly stored, primarily in the liver
*total vitamin B12 storage pool: 3000–5000 mcg
*only trace amounts normally lost in urine and stool
90
*megaloblastic, macrocytic anemia
*associated w/ mild or moderate leukopenia or thrombocytopenia
*hypercellular bone marrow with an accumulation of megaloblastic
erythroid and other precursor cells
VITAMIN B12 DEFICIENCY ANEMIA
91
would take ≈5 years for all stored vitamin B12 to be exhausted
and for __________ to develop if B12 absorption were stopped
megaloblastic anemia
92
VITAMIN B12 DEFICIENCY ANEMIA
Etiology:
Malabsorption Syndromes – pernicious anemia (lack of intrinsic
factor), inadequate gastric acid
Inadequate Intake – rare; in strict vegans, chronic alcoholics,
elderly who have tea and toast diet
Inadequate Utilization
93
TREATMENT OF VITAMIN B12 DEFICIENCY ANEMIA
Cyanocobalamin (PO, IV)
* bonded to cyanide group
Hydroxocobalamin (PO, IV)
* bonded to hydroxyl group
* more protein-bound, longer t1/2
94
TREATMENT OF VITAMIN B12 DEFICIENCY ANEMIA
PO
initial dose: 1-2 mg qd for 2 weeks
maintenance dose: 1 mg qd
IV (if there are neurologic abnormalities)
initial dose: 1 mg qd for 1 week
maintenance dose: 1 mg monthly
95
FOLIC ACID
(PTEROYLGLUTAMIC ACID)
*required for biochemical
reactions that provide
precursors for synthesis of
amino acids, purines, & DNA
*3 major structural components:
bicyclic pteridine ring
PABA
polyglutamate tail
96
FOLIC ACID
Absorption
* Dietary Source:
yeast, liver, kidney, and green
vegetables
* complete in the
proximal jejunum
* 500–700 mcg of
dietary folate/day
* 50–200 mcg
absorbed/day
97
FOLIC ACID
Storage
* in the liver and other tissues
* relatively low stores
98
99
FOLIC ACID
Elimination
* in the urine and stool
* destroyed by catabolism
100
FOLIC ACID
In the body:
1. partly or completely reduced to di- or tetrahydrofolate (THF) derivatives,
2. usually contain a single carbon unit, and
3. 70–90% of natural folates are folate-polyglutamates
101
FOLIC ACID DEFICIENCY ANEMIA
*can develop within 1–6 months due to low body stores and high daily requirements
Etiology:
Inadequate Intake – “junk food,” alcoholics, food faddists, the
impoverished, chronically ill or demented
Decreased Absorption – malabsorption syndromes
Increased Folate Requirements – increased rate of cell division i.e.,.
pregnancy; hemolytic anemia, myelofibrosis, malignancy, chronic
inflammatory disorders e.g., Crohn disease, RA, or psoriasis; long-term
dialysis; burn patients; growth spurts
102
FOLIC ACID DEFICIENCY ANEMIA
Etiology: Drugs
DNA Synthesis Inhibitors:
azathioprine, 6-mercaptopurine, 5-
fluorouracil, hydroxyurea, and zidovudine
Folate Antagonists:
methotrexate, pentamidine, trimethoprim, triamterene
Alcohol – interferes with folic acid absorption & utilization, and
decreases hepatic stores of folic acid
103
TREATMENT OF FOLIC ACID DEFICIENCY ANEMIA
Folate PO: 1 mg daily for 4 months
If malabsorption is present: 1 to 5 mg daily
104
ANEMIA OF INFLAMMATION (AI)
*anemia of chronic disease and anemia of critical illness
*a diagnosis of exclusion
*traditionally associated w/ malignant, infectious, or inflammatory
*processes, tissue injury, and conditions associated with release of
proinflammatory cytokines
*Serum Fe is decreased but unlike IDA, serum ferritin concentration is
normal or increased.
105
TREATMENT OF AI
correct the reversible causes
Iron
for iron deficiency
not effective when there is inflammation
Parenteral Iron - often used in anemia of critical illness but is
associated with a theoretical risk of infection
RBC Transfusion
Erythropoietin
106
ERYTHROPOIETIN
*34- to 39-kDa glycoprotein
*primarily produced by peritubular interstitial cells of the kidneys
Pharmacodynamics:
binds to erythropoietin receptor (a JAK/STAT receptor) on RBC progenitors
induces release of reticulocytes from
the bone marrow
usually given w/ Fe
107
RECOMBINANT ERYTHROPOIETIN (IV, SC)
Epoetin alfa
(rHuEPO)
Epoetin alfa
(rHuEPO)
* produced in a mammalian cell
expression system
* t1⁄2: 4–13 hours in CKD
* given 3x/week
108
RECOMBINANT ERYTHROPOIETIN (IV, SC)
Darbepoetin Alfa
* more heavily glycosylated
* longer t1⁄2 (2-3x)
* given weekly
109
RECOMBINANT ERYTHROPOIETIN (IV, SC)
Methoxy
Polyethylene
Glycol–Epoetin Beta
* isoform of erythropoietin
covalently attached to a long
polyethylene glycol polymer
* long t1⁄2
* given every 2 weeks or monthly
110
ERYTHROPOIETIN: USES
*anemia in CKD
*HIV-infected patients treated with zidovudine
*cancer patients treated with myelosuppressive cancer
chemotherapy (not methoxy polyethylene glycol–epoetin beta due
to increased mortality)
*patients scheduled to undergo elective, noncardiac, nonvascular
surgery
*best response in endogenous erythropoietin <100 IU/L
111
ERYTHROPOIETIN: A/E
hypertension and thrombotic complications
an increase in Hb >12 g/dL or a rise of >1 g/dL every 2 weeks has been associated with increased cardiovascular events,
thromboembolic events, stroke, and mortality
recommended that Hb not exceed 11 g/dL
112
ERYTHROPOIETIN: ILLICIT USE
performance-enhancing drug
“blood doping”
113
SIDEROBLASTIC ANEMIA
*impaired Hb synthesis and accumulate iron in the perinuclear
mitochondria of erythroid precursors (ringed sideroblasts)
*Treatment: 50 mg pyridoxine PO qd
114
COPPER DEFICIENCY ANEMIA
Treatment:
0.1 mg/kg of cupric sulfate PO qd
1–2 mg/day cupric sulfate added to the solution of nutrients for
parenteral administration
115
RIBOFLAVIN DEFICIENCY
hypoproliferative anemia
treated w/ riboflavin
116
G-CSF
* stimulates proliferation and differentiation of progenitors committed to the neutrophil
lineage
* activates the phagocytic activity of mature neutrophils and prolongs their survival
* mobilizes hematopoietic stem cells
117
GM-CSF
* broader biologic actions
* stimulates proliferation and differentiation of early and late granulocytic progenitor cells,
erythroid and megakaryocyte progenitors
* stimulates the function of mature neutrophils
* stimulate T-cell proliferation
* mobilizes peripheral blood stem cells, but significantly less efficacious & more toxic than G-
CSF
118
G-CSF (IV, SC)
* Filgrastim (rHuG-CSF) – produced in a bacterial expression system
* Tbo-Filgrastim – similar to filgrastim, with minor structural differences
and equivalent activity
* Pegfilgrastim – filgrastim covalent conjugated to polyethylene glycol;
longer t1⁄2
* Lenograstim – glycosylated recombinant G-CSF
119
GM-CSF (IV, SC)
* Sargramostim (rHuGM-CSF) – produced in a yeast expression system
120
MYELOID GROWTH FACTORS: USES
Neutropenia
* Cancer patients treated with myelosuppressive cancer chemotherapy
* Severe chronic neutropenia
* Patients recovering from bone marrow transplantation
Stem cell or bone marrow transplantation
* Patients with nonmyeloid malignancies or other conditions being treated with stem cell or bone marrow transplantation
Mobilization of peripheral blood progenitor cells (PBPCs)
* Donors of stem cells for allogeneic or autologous transplantation
121
MYELOID GROWTH FACTORS: A/E
G-CSF
* better tolerated
* bone pain
* splenic rupture – rare but serious complication for PBSC mobilization
GM-CSF
* less tolerated
* fever, malaise, arthralgias, myalgias
* capillary leak syndrome characterized by peripheral edema and pleural
or pericardial effusions
122
MEGAKARYOCYTE GROWTH FACTORS
Thrombopoietin
* Romiplostim
* high affinity binding to the human Mpl receptor
* Eltrombopag
* binds to the transmembrane domain of the Mpl receptor
IL-11
* Oprelvekin
* binds to cytokine receptors to stimulate the growth of multiple lymphoid and myeloid cells
* increases the number of peripheral platelets and neutrophils
123
RECOMBINANT MEGAKARYOCYTE GROWTH
FACTORS
Thrombopoietin
* Romiplostim (SC)
* thrombopoietin agonist peptide covalently linked to antibody fragments to extend t1⁄2
* t1⁄2: 3–4 days
* Eltrombopag (PO)
* small nonpeptide thrombopoietin agonist molecule
* t1⁄2: 26–35 hours
IL-11 – produced by fibroblasts and stromal cells in the bone marrow
* Oprelvekin (Recombinant IL-11, SC)
* produced by expression in Escherichia coli
* t1⁄2: 7-8 hours
124
MEGAKARYOCYTE GROWTH FACTORS: USES
Thrombopoietin
* Romiplostim
* idiopathic thrombocytopenic purpura
* Eltrombopag
* idiopathic thrombocytopenic purpura
* thrombocytopenia in patients with hepatitis C to allow initiation of interferon therapy
IL-11
* Oprelvekin
* nonmyeloid malignancies who receive myelosuppressive cancer chemotherapy
125
MEGAKARYOCYTE GROWTH FACTORS: A/E
Thrombopoietin
* portal vein thrombosis in chronic liver disease
* marrow fibrosis
* rebound thrombocytopenia
* Romiplostim
* increased blast count and risk of progression to acute myeloid leukemia
* Eltrombopag
* potentially hepatotoxic
IL-11
* Oprelvekin
* fatigue, headache, dizziness
* cardiovascular effects: anemia (due to hemodilution), dyspnea (due to fluid accumulation asd854` qqin the lungs), and transient atrial arrhythmias
* hypokalemia
