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Riki Tenggara

Program Sp2 Gastro_Entero_Hepato


RSCM-FKUI

A N EM IA D EFIS IEN S I FE
D A N PA LLO R

Pallor or pale
Is a change of skin color to become pale
is a reduced amount of oxyhaemoglobin

in skin or mucous membrane, a pale


color which can be caused by
illness, emotional shock or stress, stimulant use,

lack of exposure to sunlight, anaemia or


genetics.

It is more evident on the face and palms.

It can develop suddenly or gradually,


depending on the cause
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Pallor is not usually clinically

significant unless it is accompanied


by a general pallor (pale lips,
tongue, palms, mouth and other
regions with mucous membranes).
It is distinguished from similar
symptoms such as
hypopigmentation (loss of skin
pigment).
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Possible causes
Anemia
Shock, cardiogenic shock or

hemorrhagic shock
Migraine attack or headache
Hypoglycemia
Frostbite
Hypothyroidism
Emotional responses

Exam ination

Exam ination

Pallor caused by PosturalC olor C hanges


of Chronic A rterialInsuf c
i
fiency

If pain or diminished pulses suggest

arterial insufficiency, look for


postural color changes.
Raise both legs, as shown at the right, to
about 60 until maximal pallor of the
feet developsusually within a minute.
In light-skinned persons, either
maintenance of normal color, as seen in
this right foot, or slight pallor is normal.

Anem ia
Anemia is most often recognized by abnormal

screening laboratory tests.


Patients less commonly present with
advanced anemia and its attendant signs and
symptoms.
Acute anemia is nearly always due to blood
loss or hemolysis.
If blood loss is mild, enhanced O 2 delivery is
achieved through changes in the O 2hemoglobin dissociation curve mediated by a
decreased pH or increased CO2 (Bohr effect).

Approach to the patient w ith anem ia


The evaluation of the patient with anemia

a careful history and physical


examination.
Nutritional history related to drugs or alcohol
intake and family history of anemia should
always be assessed.
Certain geographic backgrounds and ethnic
origins are associated with an increased
likelihood of an inherited disorder of the
hemoglobin molecule or intermediary
metabolism. (Sickle cells disease & Hb-pathy)

Approach to the patient w ith anem ia


symptoms and signs such as bleeding,

fatigue, malaise, fever, weight loss, night


sweats, and other systemic symptoms.
Clues to the mechanisms of anemia may
be provided on physical examination by
findings of
Infection
blood in the stool
lymphadenopathy, splenomegaly, or

petechiae.
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Splenomegaly and lymphadenopathy

suggest an underlying
lymphoproliferative disease
while petechiae suggest platelet
dysfunction

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physical examination may demonstrate a forceful

heartbeat, strong peripheral pulses, and a systolic


"flow" murmur.
The skin and mucous membranes may be pale if
the hemoglobin is <80100 g/L (810 g/dL). This
part of the physical examination should focus on
areas where vessels are close to the surface such
as the mucous membranes, nail beds, and palmar
creases.
If the palmar creases are lighter in color than the
surrounding skin when the hand is hyperextended,
the hemoglobin level is usually <80 g/L (8 g/dL).

Initialblood test to check the pallor


I. Complete blood count (CBC)
A. Red blood cell count
1. Hemoglobin
2. Hematocrit
3. Reticulocyte count
B. Red blood cell indices
1. Mean cell volume (MCV)
2. Mean cell hemoglobin (MCH)
3. Mean cell hemoglobin concentration (MCHC)
4. Red cell distribution width (RDW)
C. White blood cell count
1. Cell differential
2. Nuclear segmentation of neutrophils
D. Platelet count
E. Cell morphology
1. Cell size
2. Hemoglobin content
3. Anisocytosis
4. Poikilocytosis
5. Polychromasia

Specifi
c blood test for anem ia
II. Iron supply studies
A. Serum iron
B. Total iron-binding capacity
C. Serum ferritin

III. Marrow examination


A. Aspirate
1. M/E ratioa
2. Cell morphology
3. Iron stain
B. Biopsy

1. Cellularity
2. Morphology

The laboratory measurements that reflect the

availability of iron for hemoglobin synthesis


include the serum iron, the TIBC, and the
percent transferrin saturation. The percent
transferrin saturation is derived by dividing the
serum iron level (x 100) by the TIBC.
The normal serum iron ranges from 927 mol/L (50

150 g/dL), while


the normal TIBC is 5464 mol/L (300360 g/dL)
the normal transferrin saturation ranges from 25
50%.
A diurnal variation in the serum iron leads to a
variation in the percent transferrin saturation.

The serum ferritin is used to evaluate total-body

iron stores. Adult males have serum ferritin levels


that average ~100 g/L, corresponding to iron
stores of ~1 g. Adult females have lower serum
ferritin levels averaging 30 g/L, reflecting lower
iron stores (300 mg). A serum ferritin level of 10
15 g/L represents depletion of body iron stores.
However, ferritin is also an acute-phase reactant
and, in the presence of acute or chronic
inflammation, may rise several-fold above baseline
levels. As a rule, a serum ferritin > 200 g/L means
there is at least some iron in tissue stores.

Iron defi
ciency anem ia
Iron is a critical element in the function of all

cells, although the amount of iron required by


individual tissues varies during development. At
the same time, the body must protect itself
from free iron, which is highly toxic in that it
participates in chemical reactions that generate
free radicals such as singlet O2 or OH.
Consequently, elaborate mechanisms have
evolved that allow iron to be made available for
physiologic functions while at the same time
conserving this element and handling it in such
a way that toxicity is avoided

The iron-transferrin complex circulates in the

plasma until it interacts with specific transferrin


receptors on the surface of marrow erythroid cells.
Diferric transferrin has the highest affinity for
transferrin receptors; apotransferrin (transferrin
not carrying iron) has very little affinity.
While transferrin receptors are found on cells in
many tissues within the bodyand all cells at
some time during development will display
transferrin receptorsthe cell having the greatest
number of receptors (300,000 to 400,000/cell) is
the developing erythroblast

The iron cycle in hum an


In a normal individual, the average red cell life span is

120 days. Thus, 0.81.0% of red cells turn over each day.
At the end of its life span, the red cell is recognized as
senescent by the cells of the reticuloendothelial (RE)
system, and the cell undergoes phagocytosis.
Once within the RE cell, the hemoglobin from the
ingested red cell is broken down, the globin and other
proteins are returned to the amino acid pool, and the iron
is shuttled back to the surface of the RE cell, where it is
presented to circulating transferrin.
It is the efficient and highly conserved recycling of iron
from senescent red cells that supports steady state (and
even mildly accelerated) erythropoiesis

Evaluation of patient with


anemia

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Since each milliliter of red cells contains 1 mg

of elemental iron, the amount of iron needed to


replace those red cells lost through senescence
amounts to 1620 mg/d (assuming an adult
with a red cell mass of 2 L).
Any additional iron required for daily red cell
production comes from the diet.
Normally, an adult male will need to absorb at
least 1 mg of elemental iron daily to meet
needs, while females in the childbearing years
will need to absorb an average of 1.4 mg/d.
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Iron-deficiency anemia is the condition in which

there is anemia and clear evidence of iron lack.


The progression to iron deficiency can be divided
into three stages (Fig. 98-2). The first stage is
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 results 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.

Blood loss in excess of 1020 mL of red cells

per day is greater than the amount of iron that


the gut can absorb from a normal diet.
Under these circumstances the iron deficit
must be made up by mobilization of iron from
RE storage sites. During this period, iron
storesreflected by the serum ferritin level or
the appearance of stainable iron on bone
marrow aspirationsdecrease.
As long as iron stores are present and can be
mobilized, the serum iron, total iron-binding
capacity (TIBC), and red cell protoporphyrin
levels remain within normal limits. At this

Anemia hipokrom mikrositik

Normal smear

Komparasi anemia defisiensi Fe dan normal

D iff
erentialdiagnosis ofanem ia m ikrositik

D iff
erentialdiagnosis anem ia hipoproliferatif

Iron-D efi
ciency Anem ia:Treatm ent
The severity and cause of iron-deficiency anemia

will determine the appropriate approach to


treatment.
As an example, symptomatic elderly patients
with severe iron-deficiency anemia and
cardiovascular instability may require red cell
transfusions.
Younger individuals who have compensated for
their anemia can be treated more conservatively
with iron replacement. The foremost issue for
the latter patient is the precise identification of
the cause of the iron deficiency.

For the majority of cases of iron deficiency

(pregnant women, growing children and


adolescents, patients with infrequent episodes
of bleeding, and those with inadequate dietary
intake of iron), oral iron therapy will suffice.
For patients with unusual blood loss or
malabsorption, specific diagnostic tests and
appropriate therapy take priority.
Once the diagnosis of iron-deficiency anemia
and its cause is made, there are three major
therapeutic approaches.

Red CellTransfusion
Transfusion therapy is reserved for

individuals who have symptoms of


anemia, cardiovascular instability,
continued and excessive blood loss
from whatever source, and require
immediate intervention.
The management of these patients is
less related to the iron deficiency than
it is to the consequences of the severe
anemia.

Not only do transfusions correct the

anemia acutely, but the transfused


red cells provide a source of iron for
reutilization, assuming they are not
lost through continued bleeding.
Transfusion therapy will stabilize the
patient while other options are
reviewed

O ralIron Therapy
iron replacement therapy, up to 300 mg of

elemental iron per day is given, usually as three or


four iron tablets (each containing 5065 mg
elemental iron) given over the course of the day.
Oral iron preparations should be taken on an empty
stomach, since foods may inhibit iron absorption.
Some patients with gastric disease or prior gastric
surgery require special treatment with iron
solutions, since the retention capacity of the
stomach may be reduced.
The retention capacity is necessary for dissolving
the shell of the iron tablet before the release of iron

A dose of 200300 mg of elemental iron

per day should result in the absorption of


iron up to 50 mg/d.
This supports a red cell production level of
two to three times normal in an individual
with a normally functioning marrow and
appropriate erythropoietin stimulus.
However, as the hemoglobin level rises,
erythropoietin stimulation decreases, and
the amount of iron absorbed is reduced

The goal of therapy in individuals

with iron-deficiency anemia is not


only to repair the anemia, but also to
provide stores of at least 0.51.0 g of
iron.
Sustained treatment for a period of
612 months after correction of the
anemia will be necessary to achieve
this

Thank you

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