OUTLINE
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II.
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VI.
VII.
VIII.
IX.
X.
HEMATOPOIESIS
Definition of Terms
Blood Cells
Hematopoiesis
Hematopoietic Growth Factors
a. Erythropoietin
b. G-CSF and GS-CSF
Iron
Cobalamin
Folic Acid
Anemia
a. Iron-deficiency anemia
b. Megaloblastic Anemia
c. Anemia of Chronic Disease
Hemostasis
a. Vitamin K
b. Fibrinolytic inhibitors
c. Serine Protease Inhibitors: Aprotinin
Self-test
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production from undifferentiated stem cells of circulating
erythrocytes, and platelets
produces over 200 billion new blood cells/d in the normal
person and more in conditions that cause loss or
destruction of blood cells
requires iron, folic acid, cobalamin and growth factors for
proliferation and differentiation of blood cells
DEFINITION OF TERMS
Hematinics
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agents that tend to stimulate blood cell formation or to
increase the hemoglobin in the blood
Hemostasis
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finely regulated dynamic process of maintaining fluidity of
the blood, repairing vascular injury and limiting blood loss
while avoiding vessel occlusion (thrombosis) and
inadequate perfusion of vital organs
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dysregulated hemostasis include hereditary or acquired
defects in the clotting mechanism and secondary effects of
Infection or cancer
Hemostatics
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agents that maintain hemostasis
Coagulants
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exogenous substances used to promote coagulation. The
exogenous blood coagulation factors are considered to be
coagulants only when administered as drugs.
BLOOD CELLS
Blood
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blood volume: 4-4.5L in females ; 4.5-5L in males
functions include:
transport of various molecules (O2, CO2, nutrients,
metabolites, vitamins, electrolytes, etc.),
heat (regulation of body temperature)
transmission of signals (hormones)
buffering
immune defense
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The young red cell is called a retlculocyte and normally
takes about 4 days to mature into an erythrocyte.
In health, erythropoiesis is regulated and maintained within
a narrow range.
<l% of the body's total red blood cells are produced/day
It is stimulated by hypoxia. However, oxygen lack does not
act directly on the haemopoietic tissues but instead
stimulates the production of a hormone, erythropoietin
and other hematopoietic factors.
HEMATOPOIETIC GROWTH FACTORS
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Red blood cells (RBCs) - transport O2 and pH regulation
White blood cells (WBCs) - divided into neutrophilic,
eosinophilic and basophilic, granulocytes, monocytes, and
lymphocytes. (Neutrophils play a role in nonspecific
immune defense; monocytes and lymphocytes participate
in specific immune responses)
Platelets (thrombocytes) - hemostasis
glycoprotein hormones that regulate the proliferation and
differentiation of hematopoietic progenitor cells in the bone
marrow
includes erythropoietin (epoetin alfa), granulocyte colonystimulating factor (G-CSF), granulocyte-macrophage
colony-stimulating factor (GM-CSF), and interleukin-11 (IL11)
Erythropoietin
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This hormone stimulates hemopoietic tissues to produce
red cells.
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It is inactivated by the liver and excreted in the urine. It is
now established that erythropoietin is formed within the
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kidney by the action of a renal erythropoietic factor
erythrogenin on plasma protein, erythropoietinogen.
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other tissues.
In the absence of adequate iron, small erythrocytes with
insufficient hemoglobin are formed.
Absorption: 1mg/day; 2 mg in menstruation, birth and
Hypoxia serves as stimulus for the increase in the production of EPO
by the kidneys. EPO, in turn stimulates hematopoeitic organs to
increase production of RBCs.
G-CSF and GM-CSF (Myeloid Growth Factors)
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produced by endothelium, macrophages, and a number of
other immune cells. The natural human glycoprotein exists
in two forms.
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is present on precursor cells in the bone marrow, and, in
response to stimulation by this factor, initiates proliferation
and differentiation into mature granulocytes.
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pregnancy (3-15% in a normal person and ~25% in iron
deficient states)
iron needed in body: 10-20 mg /day
(women>children>men)
Only 3 – 15% of Fe intake is absorbed in the duodenum
and proximal jejunum. Normal Fe intake for males is 5 –
10 mg/day; for females, 10 – 20 mg/day.
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G-CSF stimulates proliferation and differentiation of
progenitors already committed to the neutrophil lineage
GM-CSF’s biologic actions:
stimulates proliferation and differentiation of early and
late granulocytic progenitor cells as well as erythroid
and megakaryocyte progenitors
stimulates the function of mature neutrophils together
with interleukin-2 stimulates T-cell proliferation
IRON
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It forms the nucleus of the iron-porphyrin heme ring, which
together with globin chains forms hemoglobin.
Hemoglobin reversibly binds oxygen and provides the
critical mechanism for oxygen delivery from the lungs to
4
(1) Intestinal epithelial cells actively absorb inorganic iron and
heme iron.
(2) Non-heme iron in foods and iron in inorganic iron salts and
complexes must be reduced to ferrous iron (Fe2+) before it
can be absorbed by intestinal mucosal cells.
(3) Iron crosses the luminal membrane by 2 mechanisms:
active transport (via DMT1) of ferrous iron and absorption
of iron complexed with heme.
(4) When total body iron stores are high and iron requirements
by the body are low, the excess iron is diverted into ferritin
in the mucosal cells.
(5) When total body iron stores are low or iron requirements
are high, newly absorbed iron is immediately transported
by transferrin from the mucosal cells to the bone marrow
to support hemoglobin production.
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5
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Distribution
(1) actively transported into the blood or complexed with
apoferritin and stored as ferritin,
(2) transported by transferrin to erythroid precursors in
the bone marrow for synthesis of hemoglobin (as
previously described)
(3) transported to hepatocytes for storage as ferritin.
NOTES:
Apoferritin synthesis is regulated by the levels of free iron. When
these levels are low, apoferritin synthesis is inhibited and the balance
of iron binding shifts toward transferrin. When free iron levels are
high, more apoferritin is produced to sequester more iron and protect
organs from the toxic effects of excess free iron.
Ferritin is detectable in serum. Since the ferritin present in serum is in
equilibrium with storage ferritin in reticuloendothelial tissues, the
serum ferritin level can be used to estimate total body iron stores.
FOLIC ACID
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provide precursors for the synthesis of amino acids,
purines, and DNA
deficiency is common and consequences include
congenital malformations and vascular diseases
average diet contains 500-700 µg of folates daily,
50-200 µg of which is usually absorbed in proximal jejunum
(5-20 mg of folates are stored in the liver and other tissues)
pregnant women may absorb as much as 300-400 µg of
folic acid daily
sources are yeast, liver, kidney, and green vegetables.
folates are excreted in the urine and stool
folic acid deficiency and megaloblastic anemia can develop
within 1-6 months after the intake of folic acid stops
Metabolism
COBALAMIN
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serves as a cofactor for several essential biochemical
reactions in humans
deficiency is secondary to inadequate absorption
consists of a porphyrin-like ring with a central cobalt atom
attached to a nucleotide
deoxyadenosylcobalamin and methylcobalamin are the
active forms
Cyanocobalamin and hydroxocobalamin and other
cobalamins found in food sources are converted to the
active forms
ultimate source of vitamin B12 is from microbial synthesis
average diet contains 5-30 µg of vit B12 daily
1-5 µg of which is usually absorbed
requires intrinsic factor; complex is absorb in the ileum
average adult storage pool of 3000-5000 µg
daily requirement: 2 µg (it would take about 5 years for all
of the stored vitamin B12 to be exhausted and for
megaloblastic anemia to develop if B12 absorption
stopped)
bound to a plasma glycoprotein, transcobalamin II
excess vitamin B12 is transported to the liver for storage.
Enzymatic reactions that use folates. (1) shows the vit B12-dependent
reaction that allows most dietary folates to enter the THF cofactor pool and
becomes the “folate trap” in vit B12 deficiency. (2) shows the dTMP cycle. (3)
shows the pathway by which folic acid enters the THF cofactor pool.
ANEMIA
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Two essential enzymatic reactions in humans that require vit B12. In (A),
methylcobalamin serves as an intermediate in the transfer of a methyl group
from N5-methylTHF to homocysteine, forming methionine. In (B), vit B12 is
required in the isomerization of methylmalonyl-CoA to succinyl-CoA by the
enzyme methylmalonyl-CoA mutase.
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There is a reduction in blood hemoglobin concentration due
to a decrease in the number of circulating erythrocytes
and/or in the amount of hemoglobin they contain.
It occurs when the erythropoietic tissues cannot supply
enough normal erythrocytes to the circulation.
In anemias due to abnormal red cell production, increased
destruction and when demand exceeds capacity, plasma
erythropoietin levels are increased.
However, anemia can also be caused by defective
production of erythropoietin as, for example, in renal
disease.
It is a deficiency in oxygen-carrying erythrocytes, is the
most common and can easily be treated
includes iron deficiency anemia, megaloblastic anemia,
hemolytic anemia, hemoglobinopathies etc
treatment: supplementation of iron, folic acid, cobalamin,
growth factors and transfusion
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A. Iron deficiency anemia
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most common cause of chronic anemia and one of the
most prevalent forms of malnutrition
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Stages:
 negative iron balance - in which the demands for (or
losses of) iron exceed the body's ability to absorb iron
from the diet. This stage can result from a number of
physiologic mechanisms including blood loss,
pregnancy (in which the demands for red cell
production by the fetus outstrip the mother's ability to
provide iron), rapid growth spurts in the adolescent, or
inadequate dietary iron intake
 iron-deficient erythropoiesis – once transferrin
saturation falls to 15 – 20% and so hemoglobin
synthesis becomes impaired
 iron-deficiency anemia – once hemoglobin and
hematocrit begin to fall
Clinical Manifestations: pallor, fatigue, dizziness,
exertional dyspnea, other generalized sx of tissue hypoxia,
tachycardia, increased cardiac output, vasodilation
• Treatment:
oral Fe++ salts
o A/E: nausea, epigastric discomfort, abdominal
cramps, constipation, diarrhea, black stools
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anaphylaxis and death (48-72H)
Iron-sucrose complex and iron sodium gluconate
complex
o Less likely to cause anaphylactic reactions
• Toxicity
acute iron toxicity
o seen in children
o include necrotizing gastroenteritis, with vomiting,
abdominal pain, and bloody diarrhea followed by
shock, lethargy, and dyspnea; complications
include severe metabolic acidosis, coma, and
death
o treated with Deferoxamine, a potent ironchelating compound, can be given systemically
to bind iron that has already been absorbed and
to promote its excretion in urine and feces
chronic iron toxicity
o secondary to iron overload (hemochromatosis)
o results when excess iron is deposited in the
heart, liver, pancreas, and other organs
o leads to organ failure and death
o can be treated by intermittent phlebotomy and
Deferasirox by reducing liver iron concentrations
B. Megaloblastic anemia
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group of disorders characterized by the presence of
distinctive morphologic appearances of the developing red
cells in the bone marrow
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cause is deficiency of either cobalamin (vitamin B12) or
folate or genetic or acquired abnormalities affecting the
metabolism of these vitamins or defects in DNA synthesis
not related to cobalamin or folate
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causes
cobalamin deficiency or abnormalities of cobalamin
metabolism*
folate deficiency or abnormalities of folate
metabolism**
therapy with anti-folate drugs (e.g. Methotrexate)
independent of either cobalamin or folate deficiency
and refractory to cobalamin and folate therapy:
o some cases of AML, myelodysplasia
o therapy with drugs interfering synthesis of DNA
[e.g. Cytosine arabinoside, hydroxyurea, 6mercaptopurine, azidothymidine (AZT)]
o orotic aciduria (responds to uridine)
o thiamine-responsive
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parenteral iron
o reserved for patients with documented iron
deficiency who are unable to tolerate or absorb
oral iron and for patients with extensive chronic
blood loss who cannot be maintained with oral
iron alone
Iron dextran
o IV infusion or IM injection
o give total dose of iron required to correct the
hemoglobin deficit and provide the patient with
500 mg of iron stores; second is to give repeated
small doses of parenteral iron over a protracted
period
o formula: kg x 2.3x 15 – hgb in g/dl + 500mg
o dilute in D5 0.9 NaCl; given 60-90mins
o include headache, light-headedness, fever,
arthralgias, nausea and vomiting, back pain,
flushing, urticaria, bronchospasm, and, rarely,
*Causes of Cobalamin Deficiency Sufficiently Severe to cause
Megaloblastic Anemia
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nutritional (vegans)
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malabsorption (pernicious anemia)
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gastric causes (congenital absence of instrinsic factor or
functional abnormality, total or partial gastrectomy)
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intestinal causes
 intestinal stagnant loop syndrome: jejunal
diverticulosis, ileocolic fistula, anatomic blind loop,
intestinal stricture, etc
 ileal resection and Crohn's disease
 selective malabsorption with proteinuria
 tropical sprue
 transcobalamin II deficiency
 fish tapeworm
Malabsorption of Cobalamin May Occur in the Following Conditins
but is not usually sufficiently severe and prolonged to cause
megaloblastic anemia
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Gastric causes
 simple atrophic gastritis (food cobalamin
malabsorption)
 Zollinger-Ellison syndrome
 Gastric bypass surgery
 Use of proton pump inhibitors
Intestinal causes
 Gluten-induced enteropathy
 Severe pancreatitis
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HIV infection
Radiotherapy
GVH disease
Deficiencies of cobalamin, folate, protein, ? Riboflavin, ?
Nicotinic acid
Therapy with colchicine, para-aminosalicylate, neomycin,
slow-release Kcl, anticonvulsant drugs, metformin,
phenformin, cytotoxic drugs
Alcohol
Treatment:
1. Erythropoietin
 originally purified from the urine of patients with severe anemia
 recombinant human erythropoietin (rHuEPO, epoetin alfa) is
produced in a mammalian cell expression system
 CHF: usual dose is 50–150 U/kg 3x/week IV
 hemoglobin levels of 10–12 g/dL are usually reached within
4–6 weeks if iron levels are adequate; 90% of these
patients respond
 4-13H half life; Darbepoetin alfa with a longer half life
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Treatment: Cobalamin
a) Oral preparations: 500-1000 µg
b) parenteral injection is available as cyanocobalamin or
hydroxocobalamin
100-1000 µg of vitamin B12 IM daily or every other day for
1-2 weeks then maintenance therapy consists of 100-1000
µg IM once a month for life
Toxicity: rapid increase in hematocrit and hemoglobin and include
hypertension and thrombotic complications
2. Myeloid Growth Factors
 originally purified from cultured human cell lines
 recombinant human G-CSF (rHuG-CSF; filgrastim) is
produced through bacterial expression and recombinant human
GM-CSF (rHuGM-CSF; sargramostim) is produced in a yeast
expression
 serum half-lives of 2-7 hours after IV or SQ; longer for
pegfilgrastim
NOTE:
- if neurologic abnormalities are present, maintenance should be
given every 1-2 weeks for 6 months before switching to monthly
injections
- oral cobalamins are not used to treat Vit B12 deficiency with
neurologic manifestations but can be used for pernicious anemia
(500µg BID)
Uses:
 myelosuppressive chemotherapy producing neutropenia
 in autologous stem cell transplantation
**Folate Deficiency
Causes : (please refer to Table on the last page)
Treatment : Folic Acid oral preparations:
- 400 µg folic acid daily for adults are satisfactory
- 600 µg for pregnant women
- 500 µg for nursing mothers
A/E:
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C. Anemia of Chronic Disease
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encompasses inflammation, infection, tissue injury, and
conditions (such as cancer) associated with the release of
proinflammatory cytokines—is one of the most common
forms of anemia seen clinically and probably the most
important in the differential diagnosis of iron deficiency
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low serum iron, increased red cell protoporphyrin, a
hypoproliferative marrow, transferrin saturation in the range
of 15–20%, and a normal or increased serum ferritin
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Decrease EPO response – interleukin, TNF
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Hepcidin – found in liver in chronic inflammation decreases
iron uptake and metabolism
G-CSF causes bone pain
GM-CSF can cause fever, malaise, arthralgias, myalgias, and a
capillary leak syndrome characterized by peripheral edema and
pleural or pericardial effusions; allergic reactions
HEMOSTASIS
Intrinsic and extrinsic pathways of blood coagulation. Both results to
the activation of factor X.
Blood coagulation. With tissue factor (TF), factor VII forms an activated
complex (VIIa-TF) that catalyzes the activation of factor IX to factor IXa. The
cascade proceeds as shown, resulting ultimately in the conversion of
fibrinogen to fibrin.
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Clotting Factors:
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inhibits fibrinolysis by free plasmin
inhibits the plasmin-streptokinase complex in patients who have
received that thrombolytic agent
reduce bleeding by as much as 50% from many types of surgery
increased risk of myocardial infarction, stroke, and renal
damage in aprotinin-treated patients
association with anaphylaxis has been reported in <0.5% of
cases
SELF-TEST
1. Vitamin K
 found primarily in leafy green vegetables
 dietary requirement is low, synthesized by bacteria that colonize
the human intestine
 2 natural forms exist: vitamins K1 and K2. Vitamin K1
(phytonadione) is found in food and Vitamin K2 (menaquinone)
is found in human tissues and is synthesized by intestinal
bacteria
 vitamins K1 and K2 require bile salts for absorption from the
intestinal tract
 vitamin K1 is available in oral and parenteral forms
 effect delayed for 6 hours but the effect is complete by 24 hours
when treating depression of prothrombin activity by excess
warfarin or vitamin K deficiency
 IV administration should be slow( rapid infusion can produce
dyspnea, chest and back pain, and even death.)
 vitamin K repletion is best achieved with intravenous or oral
administration,
 administered to all newborns to prevent the hemorrhagic
disease of vitamin K deficiency, which is especially common in
premature infants.
2. Fibrinolytic Inhibitors
 adjunctive therapy in hemophilia
 therapy for bleeding from fibrinolytic therapy
 prophylaxis for rebleeding from intracranial aneurysms
 postsurgical bleeding and bladder hemorrhage secondary to
radiation- and drug-induced cystitis.
a) Aminocaproic acid
 similar to lysine; synthetic inhibitor of fibrinolysis
 competitively inhibits plasminogen activation
 rapidly absorbed orally and cleared by the kidney
 oral dosage is 6 g QID; IV at a 5 g loading dose should be
infused over 30 minutes to avoid hypotension
 AE: intravascular thrombosis from inhibition of plasminogen
activator, hypotension, myopathy, abdominal discomfort,
diarrhea, and nasal stuffiness.
 CI: in patients with DIC or GU bleeding of the upper tract,
eg, kidney and ureters because of the potential for
excessive clotting
b) Tranexamic acid
 analog of aminocaproic acid
 orally with a 15 mg/kg loading dose followed by 30
mg/kg/day QID
3. Serine Protease Inhibitor : Aprotinin
Case for questions 1-4
A 23y/o pregnant woman is referred by her obstetrician for evaluation
of anemia. She is in her fourth month of pregnancy and has no
history of anemia; her grandfather had pernicious anemia. Her
hemoglobin is 10g/dL (normal, 12-16 g/dL)
1. If this woman has macrocytic anemia, an increased serum
concentration of transferring, and a normal serum
concentration of vitamin B12, the mostly likely cause of her
anemia is deficiency of
a. Cobalamin
b. Erythropoietin
c. Folic acid
d. Intrinsic factor
e. Iron
2. If the patient had deficiency on folic acid, her infant would
have a higher than normal risk of
a. Cardiac abnormality
b. Congenital neutropenia
c. Kidney damage
d. Limb deformity
e. Neural tube defect
3. The laboratory data for your pregnant patient indicate that
she does not have macrocytic anemia but instead has
microcytic anemia. Optimal treatment of normocytic or mild
microcytic anemia associated with pregnancy uses
a. A high-fiber diet
b. Erythropoietin injections
c. Ferrous sulfate tablets
d. Folic acid supplementation
e. Hydroxocobalamin injections
4. If this patient has a young child at home and is taking ironcontaining prenatal supplements, she should be warned
that they are a common source of accidental poisoning in
young children and advised to make a special effort to
keep these pills out of her child’s reach. Toxicity associated
with acute iron poisoning usually includes
a. Dizziness, hypertension and cerebral
hemorrhage
b. Hyperthermia, delirium and coma
c. Hypotension, cardiac arrhythmia and seizures
d. Necrotizing gastroenteritis, shock and metabolic
acidosis
e. Severe hepatic injury, encephalitis and coma
5. The iron stored in intestinal mucosal cells in complexed to
a. Apoferritin
b. Intrinsic factor
c. Oprelvekin
d. Transcobalamin II
e. Transferrin
6. Which of the following is the MOST likely to ne requires by
a 5 y/o boy with chronic renal insufficiency?
a. Cyanocobalamin
b. Deferoxamine
c. Erythropoietin
d. Filgrastim (G-CSF)
e. Oprelvekin (IL-11)
7. In a patient who require filgrastim(G-CSF) after being
treated with anticancer drugs, the therapeutic objective is
to prevent
a. Allergic reactions
b. Cancer recurrence
c. Excessive bleeding
d. Hypoxia
e. Systemic infections
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8.
The megaloblastic anemia that results from vitamin B12
deficiency is due to inadequate supplies of
a. Cobalamin
b. dTMP
c. folic acid
d. homocysteine
e. N5-methlytetrahydrofolate
Case for question 9-10
After undergoing surgery for breast cancer, a 53 y/o woman is
scheduled to receive 4 cycles if cancer chemotherapy. The cycles
are to be administered every 3-5 weeks. Her first cycle was
complicated by severe chemotherapy-induced thrombocytopenia.
9. During the second cycle of chemotherapy, it would be
appropriate to consider treating this patient with
a. Darpoetin alpha
b. Filgrastim
c. Iron dextran
d. Oprelvekin
e. Vitamin B12
10. 20 months after finishing her chemotherapy, the woman
had relapse of breast cancer. Te cancer was now
unresponsive to standard doses of chemotherapy. The
decision was made to treat the patient with higher-dose
chemotherapy followed by autologous stem cell
transplantation. Which of the following drugs is most likely
to be used to mobilize the peripheral blood stem cells
needed for the patient’s autologous stem cell
transplantation?
a. Erythropoietin
b. Filgrastim
c. Folic acid
d. Intrinsic factor
e. Oprelvekin
Greetings! :D
Merry Christmas and Happy New Year Everyone!
(sabi ng friend ko, bkit dw super sikat si Everyone? At in fairness,
halos lhat nga ng greetings sa fb ay naka-address kay Everyone.
Hehehe)
Again, congratulations to SINAG-TALA and SARANGGOLA NI BRO!
At salamat sa lahat ng tumulong mula sa costumes ng chorvA
(FARIE!!!, Pia, Tin, Elaine, Ethel, Cocai, Unica, Fao, Yvette, Grethel)
to the stars (Gretch, Nice, Fiona, and those she asked to help :P),
tansan (Go Fao, Armin—the official spray painter hehe), cd flower
(Go Lexie, Nadinne), paper crane (Bau, Ria, Unica) , clouds, phoenix
(Go Ivan, Kuya Manny, Pia, Joy), paper mache (Go Bjorn, Robin,
Ewi, Jei, Yoj, Tin, Giselle), paper twine, hair blower (Go Cocai!), xray
(Paul, Judith), drawings (Berry), frame (Go Mike and Rocky!!!), stand
(Go Carlo!), etc ng lantern natin. Salamat din sa tulong at suporta ni
Pau2x (perfection!), Gelo, Andrew, Chad, Jen, Anna, Lance,
Madaam, Rika, Andrea, Mau, Faye (oops, may nakalimutan ba ko?
Sana wala. Pero kung meron man, maraming salamat pa rin sayo. :D
and of course, sa lahat ng hindi nahiya at nag-share ng kanilang
KALANDIAN at KAARTEHAN para gumanda ang ating parol (Casey,
Ate Rena, Vincent). GUJAB!!!!
Start na naman ng ating buhay-estudyante. Wala namang nagsabing
magiging madali ang lahat. Ang importante, alam natin kung sino ang
ating kakapitan (think Saranggola ni Bro) :D
Tandaan, anuman ang mangyari, anuman ang sabihin nila, si Bro,
ndi bumitiw sa krus...kaya, KAPIT LANG. :)
/dwtl-ssc 59
Lea E.
Answers
1. Deficiencies of folic acid or vitamin B12 are the most
common causes of megaloblastic anemia. If a patient with
this type of anemia has a normal serum vitamin B12
concentration, folate deficiency is the most likely cause of
the anemia. Answer is C.
2. Deficiency of folic acid during early pregnancy is
associated with increased risk of a neural tube defect in the
newborn. Answer is E.
3. The anemia most commonly associated with pregnancy is
iron deficiency microcytic anemia. In this condition, oral
iron supplementation is indicated. Answer is C.
4. Acute iron poisoning often causes severe gastrointestinal
damage resulting from direct corrosive effects, shock from
fluid loss in the gastrointestinal tract, and metabolic
acidosis from cellular dysfunction. Answer is D.
5. The iron stored in intestinal mucosal cells, macrophages
and hepatocytes is in ferritin, a complex of iron and the
protein apoferritn. Answer is A.
6. The kidney produces erythropoietin; patients with chronic
renal insufficiency often require exogenous erythropoietin
to avoid chronic anemia. Answer is C.
7. Filgrastim stimulates the production and function of
neutrophils, which are important cellular mediators of the
innate immune system, the first line of defense against
infections. Answer is E.
8. Deficiency of vitamin B12 leads to a deficiency in
tetrahydrofolate and subsequently a deficiency of the
dTMP required for DNA synthesis. Homocysteine and N5methyltetrahydrofolate accumulate. Answer is B.
9. Oprelvekin stimulates platelet production and decreases
the number of platelet transfusions required by patient
undergoing bone marrow suppression therapy for cancer.
Answer is D.
10. The success of transplantation with peripheral blood stem
cells depends on infusion of adequate numbers of
hematopoietic stem cells. Administration of G-CSF to the
donor (in the case of autologous transplantation, the
patient who also will be the recipient of the transplantation)
greatly increases the number of hematopoietic stem cells
harvested from the donor’s blood. Answer is B.
Faye Bautista | Ralph Bautista | Paul Bejosa | Berry Beriña | Alex Bondoc | Mafe Bonifacio | Mau Borja
Jei Chan | Ivan de Guzman | Lance Domingo | Ram Enerio | Joy Esguerra | Lea Esquivel | Nice Gelvosa
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