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1) Cause of hypoproliferative anemia
Mild iron-deficiency anemia
[ In addition to mild to moderate iron-
deficiency anemia, the hypoproliferative anemias can be caused by four categories:
(1) chronic inflammation, (2) renal disease, (3) endocrine and nutritional deficiencies
(hypometabolic states), and (4) marrow damage.]
Chronic inflammation
[ With chronic inflammation, renal
disease, or hypometabolism, endogenous erythropoietin production is inadequate
for the degree of anemia observed. As a result of the lack of adequate erythropoietin
stimulation, an examination of the peripheral blood smear will disclose only an
occasional reticulocyte.]
Renal disease
Endocrine deficiencies
All of the above
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2) Hypoproliferative anemia – True statement
Normocytic and normochromic red cells
[ Hypoproliferative anemias are
characterized by normocytic and normochromic red cells and an inappropriately low
reticulocyte response (reticulocyte index <2.5).]
Low reticulocyte count
Caused by iron deficiency
[ Causes of hypoproliferative anemias
are early iron deficiency (before hypochromic microcytic red cells develop), acute
and chronic inflammation, malignancies, renal disease, protein malnutrition and
endocrine deficiencies and anemias from marrow damage. When moderate anemia
is present (hemoglobin 10–13 g/dL), the bone marrow remains hypoproliferative.
With severe prolonged iron-deficiency anemia, erythroid hyperplasia of the marrow
develops, rather than hypoproliferation.]
Most common type of anemia
[ Hypoproliferative anemias are the
most common type of anemia. The most common cause is acute and chronic
inflammation. The anemia of inflammation, like iron deficiency, is due in part to
abnormal iron metabolism.]
All of the above
T [ The anemias associated with renal
disease, inflammation, cancer, protein malnutrition and endocrine deficiencies and
anemias from marrow damage are due to an abnormal erythropoietin response to
the anemia.]
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3) What is the first stage in the development of iron deficiency?
Iron depletion
T [ There are four stages of iron lack.
These are iron depletion (or negative iron balance), iron-deficient erythropoiesis and
iron-deficiency anemia. In iron depletion stage, there is a decrease in storage iron
without a decrease in hemoglobin or other iron containing compounds. This stage is
also called negative iron balance.]
Iron-deficient erythropoiesis
[ After all iron stores are exhausted,
lack of iron affects the production of hemoglobin and other compounds that require
iron. Iron-deficient erythropoiesis develops.]
Iron-deficiency anemia
[ Further decrease in the body iron
produces iron-deficiency anemia. Iron deficiency is the most common cause of
anemia worldwide.]
[ Hypochromic red cells appear only
after weeks of iron-deficient erythropoiesis.]
4) What is the first stage in the development of iron deficiency?
a. Hypochromic microcytic red cells
[ Hypochromic microcytic red cells
develops only when frank iron deficiency anemia is present.]
b. Negative iron balance
T [ The first stage in the development
of iron deficiency is negative iron balance (or iron depletion). Negative iron balance
is present when the demands for iron or the losses of iron exceed capacity to
absorb iron from the diet. Then, the necessary iron is supplied by mobilization of
iron from reticuloendothelial storage sites. During this early period of negative iron
balance, only tests which measure body iron stores are abnormal.]
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c. Fall in the serum iron
d. Decrease in percent transferrin saturation
e. Rise in red cell protoporphyrin level
5) Negative iron balance
[ Blood loss in excess of 10–20 mL of
red cells per day is greater than the amount of iron that the gut can absorb from a
normal diet.]
[ The demands for red cell production
by the fetus outstrip the mother's ability to provide iron.]
Adolescent growth
Inadequate dietary iron intake
All of the above
T [ Common causes of negative iron
balance are blood loss (e.g., GI loss, menorrhagia), pregnancy, rapid growth spurts
in the adolescent, or inadequate dietary iron intake. In these conditions, the iron
deficit must be made up by mobilization of iron from RE storage sites. During this
period, iron stores decrease. Tests of iron storage are serum ferritin level or the
appearance of stainable iron on bone marrow aspirations. As long as iron stores are
present, the serum iron, total iron-binding capacity (TIBC), and red cell
protoporphyrin levels remain within normal limits. At this stage, red cell morphology
and indices are also normal.]
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6) Depletion of iron-store can be detected early by all except
Marrow iron stores
[ Depletion of iron-stores can be
detected early by measurements of marrow iron stores, serum ferritin, and total ironbinding capacity. These 3 tests are sensitive to early iron-store depletion. Bone
marrow aspiration and biopsy can provide information about macrophage storage
iron by grading of marrow hemosiderin stained with Prussian blue.]
Serum ferritin
[ Measurement of plasma ferritin is the
most useful indirect estimate of body iron stores. Normal serum ferritin is 50 to 200
µg/L. When the serum ferritin level is <15 µg/L, marrow iron stores are absent.]
Total iron-binding capacity
[ Normal TIBC = 300 to 360 µg/dL.]
RBC morphology
T [ RBC morphology remains normal in
negative iron balance and iron-deficient erythropoiesis. Abnormal RBC morphology
(i.e., hypochromic microcytic red cells) develops only when frank iron deficiency
anemia is present. When hemoglobin falls to 8 g/dL, hypochromia (MCH < 27 pg),
microcytosis (MCV < 80 fL), poikilocytes and target cells appear on the blood smear.
Poikilocytosis (variation in shape) and anisocytosis (variation in size) appear as
cigar- or pencil-shaped forms on the blood smear. The erythroid marrow becomes
increasingly ineffective. Target cells are not seen in iron-deficiency anemia]
RBCs are microcytic (smaller) and hypochromic (central areas of pallor)
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Indication of iron-deficient erythropoiesis
a. Fall in the serum iron
[ When iron stores become depleted,
the serum iron begins to fall. Gradually, the TIBC and red cell protoporphyrin levels
increases. As long as the serum iron remains within the normal range, hemoglobin
synthesis is unaffected despite the decreasing iron stores. Normal serum iron is 50
to 170 µg/dL.]
b. Fall in percent transferrin saturation
[ Once the transferrin saturation falls
to 15 to 20%, hemoglobin synthesis becomes impaired. This is a period of irondeficient erythropoiesis. Microcytic cells first appear in the peripheral blood smear.
Gradually, the hemoglobin and hematocrit begin to fall, reflecting iron-deficiency
anemia. The transferrin saturation at this point is 10 to 15%.]
c. Rise in red cell protoporphyrin level
[ Protoporphyrin is an intermediate
product in heme synthesis. When there is inadequate iron supply to erythroid
precursors heme synthesis is impaired and protoporphyrin accumulates within the
red cell. Normal values are <30 µg/dL of red cells. In iron deficiency, values are > 100
µg/dL. The most common causes of increased red cell protoporphyrin levels are iron
deficiency and lead poisoning.]
d. All of the above
T [ Iron-deficient erythropoiesis can be
detected by fall in the serum iron (normal serum iron = 50 to 170 µg/dL), percent
transferrin saturation (normal = 20 to 50%), and % of marrow sideroblasts (normal =
40 to 60%). Red cell protoporphyrin level rise (normal protoporphyrin level = 30 to 50
Page 7 of 30
Serum ferritin level is typically <20 ng/mL (Serum ferritin level is normal or elevated in
patients who also have anemia of chronic disease, active liver disease, renal insufficiency,
or malignancy)
Decreased serum iron level
Normal or elevated total iron-binding capacity
Normal or low erythrocyte count
Transferrin saturation is usually <15%
Serum transferrin receptor concentration is elevated in most cases
Anemia with or without microcytosis is a late development
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8) First test to become abnormal in iron deficiency anemia
a. Fall in serum ferritin level
T [ Tests of body iron stores are serum
ferritin level and the presence of stainable iron on bone marrow aspirations. Normal
serum ferritin level is 50 to 200 µg/L. Serum ferritin level less than 20 µg/L indicates
iron store depletion and iron deficiency. See table below.]
b. Fall in serum iron
[ The serum iron level represents the
amount of circulating iron bound to transferrin. As long as iron stores can be
mobilized, the serum iron, total iron-binding capacity, and red cell protoporphyrin
levels remain normal. The serum iron begins to fall only after iron stores have been
c. Rise in total iron-binding capacity
[ Then, the TIBC and red cell
protoporphyrin levels increase. The TIBC is an indirect measure of the circulating
transferrin. The normal range for TIBC is 300–360 µg/dL. Transferrin saturation is
normally 25–50%. It is obtained by the following formula: serum iron x 100 ÷ TIBC.
Iron-deficiency states are associated with saturation levels below 18%.]
d. Fall in transferrin saturation
[Transferrin saturation is normally 25–
50%. It is obtained by the following formula: serum iron x 100 ÷ TIBC. Irondeficiency states are associated with saturation levels below 18%. A transferrin
saturation >50% indicates that a disproportionate amount of the iron bound to
transferrin is being delivered to nonerythroid tissues. If this persists for an
extended time, tissue iron overload may occur.]
e. Abnormal red cell indices
[ At this stage, red cell morphology
and indices are also normal. Hemoglobin synthesis is not affected as long as the
serum iron is normal. When the transferrin saturation falls to 20%, hemoglobin
synthesis is impaired. This is the stage of iron-deficient erythropoiesis. Peripheral
blood smear may show microcytic cells. Gradually, the hemoglobin and hematocrit
fall and iron deficiency anemia develops. The transferrin saturation at this point is
less than 10%. Only at this stage, red cell morphology and indices become
abnormal. When hemoglobin falls to 8 g/dL, hypochromia and microcytosis become
prominent. Poikilocytes appear. Poikilocytes are red cells with abnormal shapes
(cigar shaped, pencil-shaped, or target cells). With severe prolonged iron deficiency
anemia, erythroid hyperplasia of the marrow develops rather than
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Iron store
Serum ferritin level
1–300 mg
300–800 mg
800–1000 mg
1–2 g
Iron overload
9) Iron deficiency anemia – True statement
a. Serum ferritin levels falls
[The level of serum ferritin reflects the
amount of stored iron. The normal values for serum ferritin are 30-300 μg/L in males
and 15-200 μg/L in females. In simple iron deficiency, a low serum ferritin confirms
the diagnosis. However, ferritin is an acute-phase reactant, and levels increase in
the presence of inflammatory or malignant diseases. In the presence of
inflammation, up to 30% of patients with true iron deficiency have serum ferritin
levels greater than 100 μg/L. This can obscure the diagnosis of iron deficiency.
Assays for serum transferrin receptor are useful to diagnose iron deficiency in the
presence of the inflammation. See below.]
b. Decreases iron saturation of transferrin
c. Increased free protoporphyrin in erythrocytes
d. Decreased reticulocyte hemoglobin level
e. All
T [ Red-cell production is not affected
until iron stores are depleted. Serum ferritin levels, which indicate iron stores, falls.
When the stores have been used up, the iron saturation of transferrin decreases.
The first biochemical clues of iron deficiency are increased levels of free
protoporphyrin and zinc protoporphyrin in erythrocytes. The levels of soluble
transferrin receptor increase. This is because the lack of iron limits the production
of new red cells. Frank anemia with microcytosis is detected later. A decreased
reticulocyte hemoglobin level is a useful early indicator of iron-deficient
Page 10 of 30
Iron deficiency
Anemic of chronic disease (low-normal MCV)
Sideroblastic anemia
Lead poisoning
10) Best single test to confirm iron deficiency
Plasma iron
[ Plasma iron and total iron binding
capacity are measures of iron availability. They are affected by many factors besides
iron stores. Plasma iron has a marked diurnal and day-to-day variation. It becomes
very low during an acute phase response but is raised in liver disease and
Serum ferritin levels
T [ The most accurate initial diagnostic
test for iron deficiency anemia is the serum ferritin measurement. Plasma ferritin is
the best single test to confirm iron deficiency. It is a measure of iron stores. Patients
with a serum ferritin concentration less than 25 mcg per L have a very high
probability of being iron deficient. Serum ferritin values greater than 100 mcg per L
indicate adequate iron stores and a low likelihood of iron deficiency anemia. Total
iron-binding capacity, transferrin saturation, serum iron, and serum transferrin
receptor levels may be helpful if the ferritin level is between 46 and 99 ng per mL.]
Transferrin levels
[ Transferrin levels are lowered by
malnutrition, liver disease, an acute phase response and nephrotic syndrome. It is
raised by pregnancy or the oral contraceptive pill. A transferrin saturation of less
than 16% is consistent with iron deficiency but is less specific than a ferritin
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11) Falls in iron deficiency
Total iron-binding capacity
[ The serum iron falls and the total
iron-binding capacity (TIBC) rises in iron deficiency.]
Transferrin receptors
[ All proliferating cells express
membrane transferrin receptors to acquire iron. A small amount of this receptor is
shed into blood and found in a free soluble form there. When iron stores are poor,
cells up-regulate transferrin receptor expression. The number of transferrin
receptors increases in iron deficiency. Hence the levels of soluble plasma
transferrin receptor increase. This test can now be used to distinguish depletion of
storage iron. This test can help to distinguish between iron deficiency and anaemia
of chronic disease. It may avoid the need for bone marrow examination. In difficult
cases it may still be necessary to examine a bone marrow aspirate for iron stores.]
Transferrin saturation
T [ Transferrin saturation is serum iron
divided by TIBC. Iron deficiency is regularly present when the transferrin saturation
falls below 19%.]
All of the above
None of the above
12) Negative iron balance occur in
a. Blood loss
[ Negative iron balance is present
when the demands for iron or the losses of iron exceed capacity to absorb iron from
the diet. Blood loss in excess of 10 to 20 mL of red cells per day is greater than the
amount of iron that the gut can absorb from a normal diet.]
b. Pregnancy
[ In pregnancy, the demands for red
cell production by the fetus are more than the mother's ability to supply iron.]
c. Growth spurts in the adolescent
[ Pregnancy and rapidly growing child
are the most common causes of negative iron balance.]
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d. Inadequate dietary iron intake
e. All of the above
T [ See table below.]
Increased demand for iron and/or hematopoiesis
Rapid growth in infancy or adolescence
Increased iron loss
Blood loss
Decreased iron intake or absorption
Inadequate diet
Malabsorption (sprue, Crohn's disease, surgery)
Acute or chronic inflammation
The most common pathologic cause of iron deficiency is blood loss.
In men and post-menopausal women, iron deficiency almost always due to gastrointestinal
blood loss (gastric or colorectal malignancy, gastritis, peptic ulceration, inflammatory
bowel disease, diverticulitis, polyps and angiodysplastic lesions). In men over the age of 40
years and in post-menopausal women with a normal diet, the gastrointestinal tract should
be investigated by endoscopy or barium studies.
Worldwide, the most frequent cause of gastrointestinal blood loss is hookworm infection.
In women of child-bearing age, menstrual blood loss, pregnancy and breastfeeding are the
common causes of iron deficiency.
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13) Marrow iron stores are absent when the serum ferritin level is
a. Undetectable
b. Less than15 ug/L
T [ Marrow iron stores are absent
when the serum ferritin level is less than15 ug/L.]
c. Less than 25 ug/L
d. Between 50 ug/L
14) A 50-year-old male is admitted for evaluation of general weakness. Physical examination
shows systolic murmur. There is no cheilosis or koilonychia. Hb=7gms%. What is the next
best investigation?
a. Echocardiogram
b. Coronary angiogram
c. Endoscopy
T [ A cardinal rule is that iron
deficiency in an adult male means gastrointestinal blood loss until proven
otherwise. Cheilosis is fissures at the corners of the mouth. Koilonychia is
spooning of the fingernails. Both are present only in advanced tissue iron
d. Glycosylated hemoglobin
[ This is used in diabetic patients for
assessing control of blood sugar in the previous 3 months.]
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15) What does serum iron level indicate?
a. Free ferrous iron in the blood
b. Free ferric iron in the blood
c. Both free ferrous and ferric iron in the blood
d. Iron bound to transferrin
T [ The normal serum iron level of 50 to
150 ug/dL represents the amount of circulating iron bound to transferrin. There is a
diurnal variation in the serum iron value. The TIBC (total iron binding capacity) is an
indirect measure of the circulating transferrin. The normal TIBC is 300 to 360 ug/dL.
Free iron is toxic to cells and does not normally circulate in the blood. Transferrin is
normally only 25 to 50% saturated. Transferrin saturation = serum iron X 100 ÷ TIBC.
Transferrin saturation below 18% indicates iron deficiency. Transferrin saturation
rate of more than 50% indicates that tissue iron overload may occur.]
e. C and D
16) What is the most common cause of increased red cell protoporphyrin levels?
a. Hepatic porphyrias
b. Erythropoietic porphyrias
c. Iron deficiency
T [ The most common causes of
increased red cell protoporphyrin levels are iron deficiency and lead poisoning.
Protoporphyrin is an intermediate in the pathway to heme synthesis. When heme
synthesis is impaired, protoporphyrin accumulates within the red cell. Normal
protoporphyrin levels are less than 30 ug/dL of red cells. In iron deficiency,
protoporphyrin levels more than 100 ug/dL are seen.]
d. Gout
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17) Highest numbers of transferrin receptors
a. Enterocytes
b. Erythroid cells
T [ Erythroid cells have the highest
numbers of transferrin receptors on their surface. Transferrin receptor protein (TRP)
is released by cells into the circulation. Serum levels of TRP reflect the total
erythroid marrow mass. TRP levels are elevated is absolute iron deficiency. Normal
values are 4 to 9 ug/L determined by immunoassay. TRP may be used to measure
expansion of the erythroid marrow in response to recombinant erythropoietin
c. Hepatocytes
d. Reticuloendothelial cells
18) Highly characteristic symptom of severe iron deficiency
a. Pica
T [ Signs related to iron deficiency
depend on the severity and chronicity of the anemia. The symptoms and signs of
iron deficiency include pallor, fatigue, poor exercise tolerance, and decreased work
performance. In both children and adults, pica can develop. Pica is characterized by
the inappropriate consumption of nonnutritive substances. It disappears with iron
treatment. Physical findings that may be associated with the iron-deficient state
include glossitis (atrophy of the papillae of the tongue) and angular stomatitis See
figure below). Severe, long-standing iron deficiency may also be associated with
koilonychia (spooning of the fingernails) and the Plummer–Vinson syndrome
(dysphagia due to an esophageal web). The diagnosis of iron deficiency is typically
based on laboratory results.]
b. Convulsions
c. Bleeding
[ Bleeding is not characteristic of
severe iron deficiency. Bleeding may cause iron deficiency.]
d. Microcytic hypochromic anemia
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Atrophic glossitis and angular stomatitis
19) Highly specific for iron deficiency
[ Pagophagia is a variant of pica in
which ice is obsessively consumed. It is a highly specific symptom of iron
deficiency. It resolves within a few days to 2 weeks after beginning iron therapy.]
[ In koilonychia, the fingernails are
thin, friable, and brittle. The distal half of the nail has a concave or “spoon” shape.
This results from impaired nail bed epithelial growth. This is pathognomonic of iron
deficiency but occurs in a small minority of patients. See figure below.]
Blue sclera
[ The sclerae have a bluish hue. This
sign is also a highly specific and sensitive indicator of iron deficiency. The bluish
tinge results from thinning of the sclera, which makes the choroid visible. This
thinning result from impairment of collagen synthesis by iron deficiency.]
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All of the above
T [ Signs and symptoms common to all
anemias are pallor, palpitations, tinnitus, headache, irritability, weakness, dizziness,
easy fatigability, and other vague nonspecific complaints. Because iron deficiency
often is of insidious onset and prolonged duration, circulatory and respiratory
adaptive responses minimize these manifestations. Therefore, low hemoglobin
concentrations may be very well tolerated with minimal symptoms.]
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Blue sclera
20) Plummer-Vinson syndrome does not have
[ The combination of glossitis, a sore
or burning mouth, dysphagia, and iron deficiency is called the Plummer-Vinson or
Paterson-Kelly syndrome.]
Iron deficiency
Pernicious anemia
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21) A 30-year-old female is being investigated for microcytic hypochromic anemia. Serum iron
is 160 ug/dL. TIBC is 360 ug/dL. Serum ferritin is 160 ug/L. What is the diagnosis?
a. Iron deficiency
[ Only 4 conditions cause hypochromic
microcytic anemia. Most common cause is iron deficiency. Others are thalassemias,
chronic inflammatory diseases, and myelodysplastic syndromes. In iron deficiency
anemia, serum iron is less than 30 ug/dL, TIBC is more than 360 ug/dL, and serum
ferritin is less than 15 ug/L. See table below.]
b. Inflammation
[ The anemia of chronic disease is
usually normocytic and normochromic. The ferritin level is normal or increased. The
TIBC is typically below normal. Serum iron may be low.]
c. Thalassemia
T [ In the thalassemias, serum iron
and ferritin are normal or increased, TIBC is normal, and hemoglobin pattern is
abnormal. In myelodysplasia, serum ferritin is normal or increased.]
d. Any of the above
Micro/hypo with
Serum iron
Normal to high
Normal to high
Ferritin (µg/L)
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Serum iron
ACI/AI + Iron
Serum total iron-binding
Low normal–↓
Transferrin saturation
Low normal–↓
Serum ferritin
Serum soluble transferrin
Bone marrow iron stores
Iron-containing normoblasts
in bone marrow
22) Which of the following has the highest elemental iron?
a. Ferrous sulphate
[ Ferrous sulphate 325 mg tablet
contains 65 mgs of elemental iron (20%).]
b. Ferrous gluconate
contains 39 mgs of elemental iron (12%).]
[ Ferrous gluconate 325 mg tablet
Page 21 of 30
c. Ferrous fumarate
T [ Ferrous fumarate 325 mg tablet
contains 107 mgs of elemental iron (33%). Oral iron is best taken on an empty
stomach. Foods may inhibit iron absorption. Iron should be given for 6 to 12 months
after the anemia has been corrected. This is to provide iron stores of at least 1 g of
iron. Gastrointestinal irritation is the most prominent complication of oral iron
therapy. Ferrous succinate has 35% elemental iron. Colloidal ferrichydroxide has
50% iron. It is the elemental iron content in one dose that is important and not the
total iron compound. Sustained release preparations are not very useful since iron
is absorbed in the duodenum.]
d. All have equal amounts
Iron compound
% elemental iron
Ferrous succinate
Ferrous fumarate
Ferrous sulfate
Ferrous gluconate
23) Oral therapy of choice for most persons
Ferrous gluconate
[ Iron salts are suitable for many
children and adults. The most commonly used preparation is ferrous sulfate.
Ferrous gluconate, ferrous fumarate, polysaccharide-iron complex, and entericcoated iron preparations can be used similarly. However, most are more expensive.]
Ferrous sulphate
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Carbonyl iron
T [ Carbonyl iron consists of
microspheres of pure iron. It causes less gastrointestinal toxicity than iron salts and
is equally effective in correcting iron deficiency. In patients with anemia, the
hemoglobin concentration usually increases about 1.0 g/dL weekly. Continue
treatment until anemia is corrected and serum ferritin concentration is > 50 µg/mL.
Microcytosis typically resolves several months after iron stores are replete. Oral
iron should be given for long enough to correct the Hb level and to replenish the
iron stores. This can take 6 months.]
Dietary iron
Enteric-coated iron preparations
[ Iron is absorbed mainly from the
duodenum. Slow-release preparations release iron beyond its main sites of
absorption. Therefore, enteric-coated iron preparations may not offer any
24) A 30-year-old female has presented with menorrhagia. Blood smear shows hypochromic
microcytic anemia. Serum iron is 20 ug/dL, TIBC is 390 ug/dL, and serum ferritin is 10 ug/L.
2 days after oral iron therapy, reticulocyte count is not increasing. What should you do?
a. Investigate for thalassemia
b. Investigate for myelodysplastic syndromes
[ The diagnosis of myelodysplasia
requires microscopic examination of bone marrow cell morphology.]
c. Investigate for malabsorption
d. Continue oral iron therapy
T [ The diagnosis is iron deficiency
anemia. The reticulocyte count usually begins to increase within 4 to 7 days after
iron therapy. The reticulocyte count peaks at about 10 days. The absence of a
reticulocyte response is most commonly due to noncompliance. It may also be due
to poor adsorption or a wrong diagnosis.]
Page 23 of 30
e. Give parenteral iron
[ IV iron is given for patients unable to
tolerate oral iron. IV iron is also used in those unable to absorb oral iron and in
those getting recombinant erythropoietin therapy. Erythropoietin induces a large
demand for iron. Oral iron may not be absorbed in adequate amounts to meet this
large demand. Rate of response with IV iron is not faster than oral iron given in
correct doses. IV iron may cause anaphylaxis. IV iron gluconate may be safer than
IV iron dextran. Arthralgias, skin rash, and low-grade fever may develop several
days after the infusion of a large dose of iron.]
25) Not an indication for IV iron therapy
a. Noncompliant patients
[ Noncompliance is the most common
cause of treatment failure. Oral therapy often fails in patients who take antacids, H2
blockers, proton pump antagonists, or calcium supplements.]
b. Unable to take oral iron
[ Reserve intravenous iron therapy for
noncompliant patients, those unable to take oral iron, patients who absorb iron
poorly, patients who have not had a satisfactory therapeutic response to oral iron
replacement, and patients in whom recurrent bleeding causes iron loss in excess of
what can be replaced at an acceptable rate with oral therapy.]
c. Chronic hemodialysis patients
[ For chronic hemodialysis patients,
intravenous iron administration is the only suitable route of replacement. Many
patients with nondialysis chronic renal disease, chronic inflammation, or
malignancy and all hemodialysis patients require erythropoietin therapy to maximize
response to iron replacement.]
d. To induce a more rapid erythropoietic response
T [ Intravenous therapy does not
induce a more rapid erythropoietic response than is possible with oral replacement.]
e. No satisfactory therapeutic response to oral iron replacement
Page 24 of 30
26) What is the most common cause of unsuccessful therapy with oral iron supplements?
a. Poor compliance
T [ The most common cause of
unsuccessful therapy with oral iron supplements is poor compliance due to adverse
gastrointestinal effects. Another common cause is chronic or recurrent blood loss
associated with angiodysplasia of the gastrointestinal tract or chronic anticoagulant
b. H2 receptor blockers
[ Some commonly prescribed drugs
markedly decrease iron absorption, including antacids, H2 blockers, proton pump
antagonists, calcium supplements, and tetracycline.]
c. Malabsorption
[ Gastrectomy, achlorhydria, celiac
disease, and gastric or intestinal bypass are often associated with iron
malabsorption. Many patients who have inadequate responses to oral iron therapy
require intravenous iron replacement.]
d. Chronic renal insufficiency
[ In persons with chronic disease or
renal insufficiency and in those receiving anticancer chemotherapy, erythropoietin
therapy is often necessary to induce a satisfactory erythropoietic response.]
27) What is the daily requirement of iron during the last trimester of pregnancy?
a. 0.5 to 1 mg
[ RDI (recommended daily intake) in an
adult male is 13 microgram/Kg.]
b. 1 to 2 mg
[ RDI in an adult menstruating female
is 21 crogram/Kg.]
c. 3 to 5 mg
T [ Very high requirement of 80
microgram/Kg. RDI during infancy is 60 microgram/Kg.]
d. 5 to 10 mg
Page 25 of 30
28) Cause of anemia of chronic disease
Decreased release of iron from the bone marrow
T [ One of the most common types of
anaemia, particularly in hospital patients, is the anaemia of chronic disease,
occurring in patients with malignant disease, chronic infections such as
tuberculosis or chronic inflammatory disease such as Crohn's disease, rheumatoid
arthritis, systemic lupus erythematosus (SLE), and polymyalgia rheumatica. There is
decreased release of iron from the bone marrow to developing erythroblasts, an
inadequate erythropoietin response to the anaemia, and decreased red cell survival.
The exact mechanisms responsible for these effects are not clear.]
Inadequate erythropoietin response
Decreased red cell survival
High levels of hepcidin
[ High levels of hepcidin may play a
key role. Hepcidin, the key iron regulatory hormone, is made by the liver. It is
increased in inflammation and acts to suppress iron absorption and iron release
from storage sites.]
Any of the above
29) Anemia of chronic disease – True statement
Low serum iron
[ The anemia of chronic disease
(inflammation, infection, tissue injury, and cancer) is common and the most
important in the differential diagnosis of iron deficiency. The serum iron and the
TIBC are low. There is increased red cell protoporphyrin, a hypoproliferative
marrow, transferrin saturation in the range of 15–20%, and a normal or increased
serum ferritin.]
Caused by proinflammatory cytokines
[ It is associated with the release of
proinflammatory cytokines that suppress erythropoiesis. The proinflammatory
cytokines are tumor necrosis factor, interleukin 1 and gamma interferon. They
suppress erythropoietin production and the proliferation of erythroid progenitors.]
Page 26 of 30
Normal iron stores
[ There is inadequate iron delivery to
the marrow despite the presence of normal or increased iron stores. Serum ferritin
is normal or increased.]
Serum ferritin is normal
[ Serum ferritin is normal or increased
because of the inflammatory process. The serum ferritin values are often the most
distinguishing feature between true iron-deficiency anemia and the iron-deficient
erythropoiesis associated with inflammation. Typically, serum ferritin values
increase threefold over basal levels in the face of inflammation.]
All of the above
T [ The serum soluble transferrin
receptor level is normal. Stainable iron is present in the bone marrow, but iron is not
seen in the developing erythroblasts. Patients do not respond to iron therapy.]
30) Anemia of chronic disease – True statement
a. Serum iron is low
[ Serum iron is low. Transferrin is only
15 to 20% saturated. Red cell protoporphyrin is increased. Anemia is due to
inadequate iron delivery to the marrow.]
b. Serum ferritin is increased
[ Iron stores are normal or increased.
Serum ferritin is normal or increased (in contrast to true iron deficiency anemia).
The serum ferritin value is the most important feature which distinguishes true iron
deficiency anemia from the anemia associated with inflammation. Inflammation
increase serum ferritin levels. The anemia is due to the effects of inflammatory
c. Hypoproliferative
[ Bone marrow is hypoproliferative.
The red cell indices vary from normocytic, normochromic to microcytic,
d. All of the above
T [ The main causes are chronic
infections (tuberculosis, lung abscess, subacute endocarditis), non infectious
inflammatory diseases (rheumatoid arthritis, systemic lupus erythematous),
neoplastic disorders (Hodgkin`s disease, lung and breast carcinoma).]
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31) Which test is most useful to distinguish true iron deficiency anemia from the anemia
associated with inflammation?
Low serum iron
[ Typical laboratory findings include
low serum iron levels, low serum iron-binding capacity, increased serum ferritin, and
normocytic or slightly microcytic erythrocytes.]
Serum ferritin
[ The serum ferritin value is an
important feature which distinguishes true iron deficiency anemia (decreased
ferritin) from the anemia associated with inflammation (increased serum ferritin
levels). In contrast to patients with iron-deficiency anemia, those with anemia of
chronic inflammation do not have elevated levels of serum transferrin receptor.]
Transferrin receptor concentration
T [ Detection of iron deficiency in the
presence of chronic infectious, inflammatory, or malignant disorders is problematic.
In such cases, even if iron lack contributes to the anemia of chronic disease, the
transferrin concentration (or total iron-binding capacity) will be decreased and the
plasma ferritin concentration will be increased. The serum transferrin receptor
concentration is not affected by inflammation. Therefore, its measurement usually
can determine whether iron stores are absent. If uncertainty remains, bone marrow
examination is definitive. If iron deficiency is present, iron stores are absent. If the
anemia of chronic disease alone is responsible, iron stores are present and typically
32) Plasma transferrin receptor – True statement
Majority of plasma transferrin receptors are derived from the erythroid marrow
[ Majority of plasma transferrin
receptors are derived from the erythroid marrow. Erythroid cells have the highest
numbers of transferrin receptors on their surface. Therefore, their concentration is
determined primarily by erythroid marrow activity.]
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Levels of circulating transferrin receptor decrease in erythroid hypoplasia
T [ Decreased levels of circulating
transferrin receptor are found in patients with erythroid hypoplasia (aplastic anemia,
chronic renal failure). Increased levels are present in patients with erythroid
hyperplasia (thalassemia major, sickle cell anemia, anemia with ineffective
erythropoiesis, chronic hemolytic anemia).]
Iron deficiency increases transferrin receptor concentrations
[ Iron deficiency also increases
transferrin receptor concentrations. Measurement of plasma transferrin receptor
concentration is a new test for detecting tissue iron deficiency. Increased plasma
transferrin receptor concentration is a reliable indicator of iron deficiency.
Measurement of plasma transferrin receptor concentration may help differentiate
between the anemia of iron deficiency and the anemia associated with chronic
inflammatory disorders.]
All of the above
33) Anemia of chronic disease – False statement
a. Decreased half-life of red cells
[ Anemia of chronic disease is
characterized by a small decrease in the half-life of red cells and iron-deficient
erythropoiesis. Iron-deficient erythropoiesis results from a defect in iron recycling.
Iron stores are normal, but this iron is not available to erythroid precursors. The only
effective treatment for anemia of chronic inflammation is correction of the
underlying disorder.]
Disturbance of the iron metabolism
[ The phagocyte system does not
release iron to the circulating transferrin. This prevents iron reutilization. Anemia is
usually normochromic-normocytic. Anemia may be hypochromic-microcytic
indicating progressive disease associated with iron deficiency. Low iron serum level
is necessary for the diagnosis. The serum level of ferritin is increased.]
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c. Very low erythropoietin levels
T [ False statement. In anemia of
chronic disease, erythropoietin levels increase due to tissue hypoxia. But, the
marrow response to this increase is not proportional. This suggests resistance to
erythropoietin action. The two forms of treatment are transfusions and
erythropoietin. Darbepoetin alfa is a modified erythropoietin. It has a half-life in the
circulation that is 4 times longer than epoetin alfa.]
d. All
e. None
34) Amount of iron in each unit of blood
a. 25 mg
b. 50 mg
c. 100 mg
d. 200 mg
T [ Each unit of blood contains 200 to
250 mg of iron. Repeated transfusion leads to rapid iron loading and cause
transfusional siderosis. Long-term transfusion therapy is a life-saving treatment for
patients with intractable anemia resulting from thalassemia, bone marrow failure, or
aggressive treatment of cancer.]
35) First to become iron-loaded in transfusional siderosis
a. Reticuloendothelial macrophages
T [ Reticuloendothelial macrophages
become iron-loaded before parenchymal tissue cells. Iron is ultimately deposited in
hepatocytes, the myocardium, and endocrine tissues.]
b. Hepatocytes
[ The body iron burden is best
determined by quantitative liver biopsy or magnetic-susceptibility measurement.
Measurement of serum ferritin and magnetic resonance imaging are less accurate
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c. Myocardium
[ Cardiomyopathy is more prominent in
patients with transfusional iron overload than in those with hemochromatosis. Iron
overload must be treated by Deferoxamine is given by continuous infusion.
Phlebotomy is usually not a treatment option for patients with transfusional
siderosis, because of their underlying diseases.]
d. Endocrine tissues