IRON DEFICIENCY

ANEMIA

DR. FERNANDO MEDINA RUIZ

 ABNORMAL HEMOGLOBIN
PRODUCTION
 Heme-disorders

 Disorders of globin synthesis

Hipoproliferativa

Microcytic
Defects in the
hypochromic
maturation
anemia
 ABNORMAL HEME SYNTHESIS
 Disorders of Iron Metabolism

 IRON DEFICIENCY ANEMIA:

Lack of iron for heme synthesis by reduced intake, impaired
absorption, increased requirements or chronic blood loss.

 SIDEROACRESTIC ANEMIA:
• Adequate or excessive deposits of iron but there is lack of
insertion for the ring of protoporphyrin to form heme.
 SYNTHESIS OF DEFECTIVE
GLOBIN
Deletion or defect of globin genes
(thalassemias)
 All body cells require iron for:

• Vital functions in oxidative metabolism

• Growth and cell proliferation
• Transport and storage of oxygen.

• Iron should be linked to protein compounds

• The free iron is toxic and harmful to the cells

 DISTRIBUTION OF IRON
 Iron is found in the body:

 InTOTAL
the formCONCENTRATION
of compounds which serve OF to
IRON
metabolic or IS FROM
enzymatic 2 TO 5myoglobin,
functions: G.
hemoglobin, cytochromes and other proteins
for transport and utilization of oxygen.

 InHEMOGLOBIN
storage form of ISiron,
THEferritin
MAINand
FRACTION OF BODY IRON.
haemosiderin.
 FERRITIN

 A very important iron storage in bone marrow,

spleen and liver.

 It is a form of water-soluble iron that fails to be

visualized by microscopy.

 Its synthesis is proportional to the total amount

of iron deposits.
 FERRITIN

 Works to recycle iron intended for

hematopoiesis.

 It is a way to have readily available iron

 Hemosiderin
 Iron protein aggregate which is insoluble in
water.

 Readily visible in unstained tissue specimens.

 Form-iron storage in the long term.

 Not easily mobilized.

 Hemosiderin

 Low concentrations of iron as ferritin

predominates.

 High concentrations of iron, most of the iron

stores is as hemosiderin.
 DETERMINATION
 Serum iron of 70-201 mg / dL, 95% bound to
transferrin (third saturated with iron)

 Laboratory tests to determine iron status:

 Quantification of serum iron

 Quantification of the percentage of transferrin
saturation
 Ferritin
 As a general rule

 The changes in iron stores are associated with

fluctuations in serum iron and transferrin,
therefore:
o Transferrin saturation below 15%: iron
deficiency
o Saturation above 55%:
 Iron overload: Hemochromatosis (defecto en

eliminar hierro),
 Hemosiderosis (sobrecarga de hierro[excesiva/prolongada] + muchas
transfusiones).
 As a general rule
 The interstitial space allows exchange iron with
transferrin body cells.

 Most of the combined iron transferrin in

normoblasts are sent to the developing bone
marrow.

 The combined transferrin iron comes from that

absorbed in the mucosa, but most derived from
monocyte-macrophage system.
 As a general rule

Ferritin values ​ • Iron deposits

There are inespecific increases in
less than 12Mg /iron stores:
L decrease
Neoplasms
Chronic infections
Values ​greater
•
Liver Iron overload.
Disorders
Chronic
than 1000 mg / L inflammatory diseases
 CUTS BONE MARROW
 Sideroblasts are normoblasts-containing granules of
iron and can be dyed.

 Normoblasts and developing reticulocytes contain

scattered ferritin molecules necessary for heme
synthesis.

 Macrophages from the bone marrow also contain

ferritin and hemosiderin if body iron stores are normal.
IRON DAILY REQUIREMENTS
1 mg.

 Maintaining humans lifetime constant iron

concentration.

 Iron body remains for reuse. The absorption

and daily loss is small (1 mg/ day).
Pregnancy

 3-4 mg daily over the whole pregnancy

 During pregnancy 1000 mg are needed

 The daily diet provides about 10 to 20 mgs of
iron.

 It absorbs 10 to 15% of ingested iron.

 Women during menstruation, require 2 mgs of

iron daily.
 The fetus accumulates 250 mg of this maternal
stores of iron through the placenta.

 In infancy, the rapid growth of the body and

the total hemoglobin content requires more
iron in food consumption ratio (tissue growth).
 Preterm infants

 More risk of a rapid decline in iron because

much of the placental transfer of iron occurs in
the last trimester of pregnancy

 They have a higher rate of postnatal growth

than term infants.
 PHASES OF IRON DEFICIENCY

1 -. Reduced Iron Storage (Ferritin and

hemosiderin)

2 -. Decreased serum iron and ferritin.

3 - Iron Deficiency Anemia.

FIRST PHASE:

 Iron absorption in the gut is generally high at

this stage in an attempt to compensate for the
negative iron balance. Iron deposits in bone
marrow and liver begin to decrease.
SECOND PHASE:

 Iron deposits are exhausted.

Erythropoiesis is limited to the
 amount
The serum ofironironandwhich
serum can be are
ferritin
recycled
diminished.

 There are no changes in the red blood cell.

THIRD AND LAST STAGE OF IRON
DEFICIENCY

 Iron deficiency anemia (iron deficiency).

 All laboratory tests are abnormal.

 Blood count shows red blood cells with

hypochromia and microcytosis.
 At this stage, the patient has taken several
months to iron deficiency.

 Proper correction of iron deficiency anemia

requires 3 to 6 months of replacement therapy.
 SYMPTOMS
 No early-phase clinical manifestation.
• weakness
• Lethargy hypoxia
• Koilonychia (concavity on nails)
Pica: compulsive ingestion of strange
• glossitis
 When the decrease
substances: of iron stores
ice (pagophagia), earthis(geophagy)
complete
anemia, • gastritissuch as:
causing symptoms
starch (amilofagia).
• dizziness
• headache
 SYMPTOMS IN CHILDREN
• Irritability
• Memory loss
• Difficulty in learning
• Deficiency in the immune system.

 With the lack of iron in the intestine, some metals

are absorbed in larger amounts, may have
absorption even toxic metals such as lead,
cadmium and plutonium.
 LABORATORY:
Hypochromic microcytic anemia:

Microcytosis: M.C.V. 55 to 74 FL.

Hypochromia: M.C.H. 22-26 pgs.

Anemia can be mild, moderate or severe.

Hemoglobin figures may vary from 6-12 grams.

The red blood cell count and hematocrit are not
good indicators of the degree of anemia, no
proportion to the marked decline in
hemoglobin.

The leukocyte count is usually normal.

Platelets normal or increased numbers

frequently.
 Hypochromic microcytic anemia:

 Serum iron decreases, usually less than 30 mg /

dl.

 Transferrin saturation, is decreased to less than

15%.

 Serum Ferritin is low: less than 12 mg/ L

 The diagnostic sensitivity of the TIBC is below
ferritin test for diagnosis of iron deficiency.

 Ferritin allows differentiation between iron

deficiency anemia and other hypochromic
microcytic anemias (thalassemia, anemia of
chronic conditions).
 LABORATORY & DX.
 Stains for iron show absence of hemosiderin in
macrophages, invariable characteristic of iron
deficiency.

 Sideroblasts are reduced or absent.

 Assessment of iron stores using serum iron and

ferritin, eliminate the need for bone marrow
study.
 TREATMENT
 Oral-administration of ferrous sulfate.
The hemoglobin should rise until it
 reaches normal limits,
Iron supplements usually
with food between lower
or administer 6
todoses
10 weeks. There
especially whenisthere
a rapid increasetoinoral
is intolerance
the
ironnumber of reticulocytes.
preparations.


ItTheis usually
parenteral required
treatmentprolonged
(intramuscular,
(6
intravenous)treatment,
months) iron is more dangerous
even afterand expensive
the
than the oralhas
hemoglobin route, must betoindicated
returned normal. in special
situations.
 A 19 year old female, refers unhealthy eating habits and
irregular and abundant menstrual bleeding. For 2 months has
had fatigue, weakness, headache, easy hair loss, and inability
to concentrate in school. The P.E. patient with marked pallor
of integuments, hair and nails very fragile. No visceromegaly.
Hb. 7g., M.C.V. 65 microns, M.C.H. 22 pgs., leukocytes
6,200 x mm3, platelets 450,000 x mm3. Reticulocytes 0.2%

 What is your haematological diagnosis?

 What factors are contributing to this condition?

 Is there a differential diagnosis?

 What therapeutic measures are needed?

 Caso Clínico

 Femenino de 34 años de edad, en ninguno de sus 4 embarazos ha

recibido tratamiento médico. Desde hace 6 meses refiere astenia,
adinamia, con sangrado menstrual abundante y deseo de comer cosas
extrañas (hielo, tierra). A la E.F. paciente con palidez marcada, pelo
frágil, uñas cortas y quebradizas. No visceromegalia. Laboratorio con
Hemoglobina 7 grs., V.G.M. 65 micras, H.C.M. 22 picogramos,
leucocitos 7,200 xmm3, plaquetas 200,000 xmm3, reticulocitos 0.5%.
Ferritina sérica disminuída ++. Se reporta hipocromía ++ y
microcitosis ++.
 ¿Cuál es el diagnóstico más probable en esta paciente?
 ¿Cuáles han sido los factores predisponentes de este padecimiento?
• Mencione algunos diagnósticos diferenciales.
• ¿Cuáles serían las medidas terapéuticas más apropiadas?
 Caso Clínico
 Femenino de 34 años de edad, nulípara, con adecuada ingesta, que
desde hace 6 años tiene el diagnóstico de Artritis reumatoide, motivo
por el cual ha recibido diversos medicamentos. La paciente refiere
astenia, adinamia y dolor en las articulaciones de sus manos. E.F. se
observa paciente con palidez de tegumentos, no visceromegalia y se
confirma la presencia de deformidad articular de los dedos de las
manos. Laboratorio con Hemoglobina 9 grs. V.G.M. 80 micras, H.C.M.
26 pgs., leucocitos 6,800 xmm3, plaquetas 180,000 xmm3. Ferritina
sérica normal, se reporta hipocromía +.
 ¿Qué tipo de anemia presenta esta paciente?
 ¿Existe algún diagnóstico diferencial?
 ¿Es útil la administración de hierro en este caso?
 Padecimiento Examen físico
DEFICIENCIA actual
DE HIERRO
Palidez de tegumentos
Al llegar a consulta la
generalizada
paciente refiere astenia,
Desnutrición
debilidad muscular, cefalea,
EDAD: 19 AÑOS Decadencia en el estado
vértigos, falta de
SEXO: FEMENINO general
concentración, trastornos
Soplo sistólico en ápex
del sueño, déficit de ingesta
Taquicardia
de alimentos y ciclos
menstruales irregulares con
Antecedentes
mucho sangrado. Además
personales no
nos comenta haber iniciado
patológicos
con una alimentación
vegana Casa urbana
Cuenta con todos los
Antecedentes
servicios
familiares
2 perros
Madre con hipertensión Mala alimentación
Padre con obesidad Sedentarismo
2 hermanos sanos
 Estudios de Exámenes
laboratorio auxiliares
● Hemograma
● Hemoglobina: 10 grs completo
● V.G.M: 70 micras ● ferritina sérica
● H.C.M: 23 picogramos ● hierro sérico
● leucocitos 7,200
● plaquetas 200,000 xmm3
● reticulocitos 0.5%
● ferritina sérica disminuida +
+: 10mg/ml Diagnóstico
● Hierro sérico: 50 mcg/dl diferencial
● hipocromía ++
● microcitosis + ● Talasemia
● Anemia
mieloblástica
● Anemia
sideroblástica
● Saturnismo
● Hipercarotene
mias
 Diagnóstico Evolución

Anemia ferropénica Al iniciar el tratamiento la

Desnutrición en 2do grado hemoglobina deberá de
empezar a elevarse hasta llegar
a sus límites normales dentro
Tratamiento de 6-10 semanas, además de
un incremento de reticulocitos.
Se debe corregir la causa primaria
tomando en cuenta el cambio a
una dieta adecuada y la
administración de hierro por vía
oral o parenteral.
Vía oral: 3-6 mg/kg/día,
fraccionada en 1-3 tomas diarias
media hora antes de comer.
Vía parenteral: en caso de
intolerancia o patología digestiva
en dosis que no excedan de 1,5
mg/kg/día, a administrarse cada 2-
3 días.