Anemias

Introduction
1-Anemia is a group of diseases
characterized by a decrease in either
hemoglobin (Hb) or the volume of red
blood cells (RBCs), resulting in decreased
oxygen-carrying capacity of blood.

2-The World Health Organization defines

anemia as Hb less than 13 g/dL in men or
less than 12 g/dL in women
 Pathophysiology
1-The functional classification of anemias is found
in Fig. -1.

2- Morphologic classifications are based

on cell size.
2- Morphologic classifications are based on
cell size.
A-Macrocytic cells are larger than normal
and are associated with deficiencies of
vitamin B12 or folic acid.

B-Microcytic cells are smaller than normal

and are associated with iron deficiency,
whereas normocytic anemia may be
associated with recent blood loss or chronic
disease.

3-Iron-deficiency anemia (IDA),

characterized by decreased levels of
ferritin (most sensitive marker) and
serum iron, and decreased transferrin
saturation, can be caused by inadequate
dietary intake, inadequate gastrointestinal
(GI) absorption, increased iron demand
(eg, pregnancy), blood loss, and chronic
diseases.
4-Vitamin B12 and folic acid deficiency
anemias, macrocytic in nature, can be caused
by inadequate dietary intake, malabsorption
syndromes, and inadequate utilization.
A-Deficiency of intrinsic factor causes
decreased absorption of vitamin B12 (ie,
pernicious anemia).

B-Folic acid deficiency anemia can be

caused by hyperutilization due to
pregnancy, hemolytic anemia,
malignancy, chronic inflammatory
disorders, long-term dialysis, or growth
spurt.

C-Drugs can cause anemia by reducing

absorption of folate (eg, phenytoin) or
through folate antagonism (eg,
methotrexate).
5-Anemia of inflammation (AI) is a newer
term used to describe both anemia of
chronic disease and anemia of critical
illness.

A-AI is an anemia that traditionally has

been associated with malignant,
infectious, or inflammatory processes,
tissue injury, and conditions associated
with release of proinflammatory
cytokines.

B-Serum iron is decreased but in

contrast to IDA, the serum ferritin
concentration is normal or increased.
Clinical presentation
1-Acute-onset anemia is characterized by
cardiorespiratory symptoms such as
palpitations, angina, orthostatic light-
headedness, and breathlessness.

2-Chronic anemia is characterized by

weakness, fatigue, headache, orthopnea,
dyspnea on exertion, vertigo, faintness,
cold sensitivity, pallor, and loss of skin
tone.

3-IDA is characterized by glossal pain,

smooth tongue, reduced salivary flow,
pica (compulsive eating of nonfood
items), and pagophagia (compulsive
eating of ice).
4-Neurologic effects (eg, numbness and
paraesthesisas) of vitamin B12 deficiency
may precede hematologic changes.
Psychiatric findings, including irritability,
depression, and memory impairment,
may also occur with vitamin B12
deficiency. Anemia with folate deficiency
is not associated with neurologic
symptoms.
Diagnosis
1-Rapid diagnosis is essential because
anemia is often a sign of underlying
pathology. Severity of symptoms does not
always correlate with the degree of
anemia.

2-Initial evaluation of anemia involves a

complete blood cell count (CBC),
reticulocyte index, and examination of
the stool for occult blood.
3-The earliest and most sensitive
laboratory change for IDA is decreased
serum ferritin (storage iron)

4-In macrocytic anemias, mean

corpuscular volume is usually elevated .
Vitamin B12 and folate concentrations
can be measured to differentiate
between the two deficiency anemias.

5-In AI , serum iron is usually decreased,

but, unlike IDA, serum ferritin is normal
or increased.
Treatment
Goals of Treatment: The goals are to
return hematologic parameters to normal,
restore normal function and quality of life,
and prevent long-term complications.

Iron-deficiency anemia
1-Oral iron therapy with soluble
ferrous iron salts, which are not
enteric coated and not slow or
sustained release (as the iron
is carried past the first part of
the duodenum into an area of
the gut where absorption may be
poor.) is recommended at a daily
dosage of 150 200 mg elemental
iron in two or three divided
doses.
2-Iron is best absorbed from meat, fish,
and poultry. Administer iron at least 1
hour before meals because food
interferes with absorption, but
administration with food may be needed
to improve tolerability.

3-Consider parenteral iron for patients

with iron malabsorption, intolerance of
oral iron therapy, or nonadherence.

4-Iron dextran, sodium

ferric gluconate, iron
sucrose, ferumoxytol, and
ferric carboxymaltose are
available parenteral iron
preparations with similar
efficacy but different
pharmacokinetics,
bioavailability, and adverse
effect profiles.
 Vitamin B12 deficiency anemia
1-Oral vitamin B12 supplementation is as
effective as parenteral, even in patients
with pernicious anemia, because the
alternate vitamin B12 absorption
pathway is independent of intrinsic factor.

2-Parenteral therapy acts more rapidly than oral

therapy and is recommended if neurologic
symptoms are present. Initiate daily oral
cobalamin administration after symptoms
resolve.

3-Continue vitamin B12 for life in patients with

pernicious anemia.
Folate-deficiency anemia
1-Oral folic acid, 1 mg daily for 4 months,
is usually sufficient for treatment of folic
acid deficiency anemia, unless the
etiology cannot be corrected.

2-If malabsorption is present, a dose of

1 5 mg daily may be necessary.
Parenteral folic acid is available but
rarely necessary.
 Anemia of inflammation
1-Treatment of AI is less specific than that
of other anemias and should focus on
correcting reversible causes. Reserve iron
therapy for an established IDA; iron is
not effective when inflammation is
present. RBC transfusions are effective
but should be limited to Hb of 7 8 g/dL.

2-Erythropoiesis-stimulating agents (ESAs)

can be considered, but response can be
impaired in patients with AI.

Iron, cobalamin, and folic acid

supplementation may improve response to
ESA treatment.
3-Potential toxicities of exogenous ESA
administration include increases in blood
pressure, nausea, headache, fever, bone
pain, and fatigue.

Hb must be monitored during ESA

therapy.

An increase in Hb greater than 12 g/dL

with treatment or a rise of greater than 1
g/dL every 2 weeks has been associated
with increased mortality and
cardiovascular events.

4-In patients with anemia of critical

illness, parenteral iron is often used but is
associated with a theoretical risk of
infection.
Anemia in pediatric populations
1-Infants aged 9 12 months: Administer
ferrous sulfate 3 6 mg/kg/day (elemental
iron) divided once or twice daily between
meals for 4 weeks. Continue for two
additional months in responders to replace
storage iron pools.

2-The dose and schedule of vitamin B12

should be titrated according to clinical and
laboratory response. The daily dose of folic
acid is 1 mg.
 Evaluation of therapeutic outcomes
1-IDA: Positive response to oral iron therapy
is characterized by an increase in Hb seen at
2 weeks. Hb should return to normal after 2
months; continue iron therapy until iron
stores are replenished and serum ferritin
normalized (up to 12 months).

2-Megaloblastic anemia: Signs and

symptoms usually improve within a few days
after starting vitamin B12 or folic acid
therapy.

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