Iron deficiency anemia

Iron deficiency anemia Muhammad Asif Zeb

Lecturer Hematology

Khyber Medical university

Peshawar

Anemia is a medical

condition in which the

hemoglobin concentration is

less than normal (for the age and sex of the individual)

Mild anemia

With hemoglobin level 9-12 g/dl

Moderate anemia

With hemoglobin level 6-9g/dl

Severe anemia

With hemoglobin level <6g/dl

Severity

Iron deficiency anemia is the most common form of anemia

caused from too little iron in the body

About 20% of women,

90% of pregnant women,

and 3% of men

do not have enough iron in their body.

Most body iron is present in haemoglobin in circulating red

cells

The macrophages of the reticuloendotelial system store iron

released from haemoglobin as ferritin and hemosiderin

Small loss of iron each day in urine, faeces, skin and nails

and in menstruating females as blood (1-2 mg daily)

Body Iron Distribution

Iron distribution

an adult male

ingest about 15 mg of iron of which only 10% will be

absorbed, giving him 1.5

mg/day of iron that can be used for red cell production or

stored in the reticuloendothelial system (RES)

Iron Metabolism

iron ingestion

duodenum

10% if ingested iron is absorbed

conversion of iron from the Fe3

(ferric) to the Fe2(ferrous)

transportation of iron from GI tract to bone marrow via transferrin(mono ferric\di ferric)

1 gram of transferrin binds 1.4 mg of iron

(total iron binding capacity)

iron

in bone marrow for the developing

normoblast for use of hemoglobin synthesis

erythrocytes

macrophages

reticuloendothelial system

Iron is stored mainly in the liver in reticuloendothelial

system as

Hemosiderin

Ferritin

Hemosiderin is the major long term storage form of iron ;

release slowly,

Ferritin is the primary storage form of soluble iron ;release

readily at time of need.

Iron Storage

Ferritin Iron storage protein

In humans, it acts as a buffer against iron deficiency and iron overload

Consists of: Apoferritin – protein component

Core- ferric, hydroxyl ions and oxygen

Largest amount of ferritin-bound iron is found in:

Liver hepatocytes (majority of the stores)

BM

Spleen

Excess dietary iron induces increased ferritin production

Partially digested ferritin= HAEMOSIDERIN- insoluble and can be detected in tissues (hepatocytes) using Perl’s Prussian blue stain

Water insoluble protien iron complex

Visible by light microscope

It has higher iron to protein ration up to 37% than ferritin up to 20%

Formed by partial digestion of ferritin aggregates by lysosomal enzymes.

Hemosidrin is present predominately in macrophages rather than hepatocytes.

Hemosidrin

Transferrin (Tf)

Transports iron from palsma to erythroblast

Mainly synthesized in the liver

Fe3+ (ferric) couples to Tf

Apotransferrin = Tf without iron

Contains sites for max 2 iron molecules

Synthesis is inversely proportional to iron store

Iron deficiency anaemia develops in three stages

iron depletion

Iron deficient erythropoiesis

iron deficiency anaemia

Pathophysiology of IDA

Iron stores are exhausted as indicated by decreased serum

ferritin, serum iron normal

No anaemia

Erythrocyte morphology is normal

Iron Depletion

There is insufficient iron to insert into the protoporphyrin

ring to form heme,

Serum iron is also depleted.

Anaemia and hypochromia are still not detectable

Erythrocytes may became slightly microcytic

Iron Deficient Erythropoiesis

Long standing negative flow leads to IDA

Blood loss significantly shorten this stage

Classic microcytosis and hypochromia

The situation represents advanced stage of severely

deficient body iron

Iron Deficiency Anemia

Blood Loss

Gastrointestinal Tract Menstrual Blood Loss Urinary Blood Loss (Rare) Blood in Sputum (Rarer)

Increased Iron Utilization Pregnancy Infancy Adolescence Polycythemia Vera

Causes of Iron Deficiency

Anemia

Malabsorption Tropical Sprue Gastrectomy Chronic atrophic gastritis

Dietary inadequacy Parasitic infection Hook worm

• Fatigability

• Dizziness

• Headache

• Irritability

• Dry, pale skin

• Spoon shaped nails, Koilonychias

• Pica (Appetite for non food substances such as clay)

• Splenomegaly (10%)

• Increased platelet count

Sign and Symptoms

Laboratory Diagnosis

Rbc count normal-decrease

Hemoglobin decreased

Wbc conut normal

Palatelets normal-increase(in chronic bleeding)

RDW increased

(is the first sign to appear even before microcytosis of the

cell occurs in the iron depletion stage of anemia )

Complete Blood Count

Red cell Indices

PCV decreased

MCV decreased

MCH decreased

MCHC decreased

DLC normal-increase(in chronic infections)

RBC morphology

Anisocytosis

microcytosis

Hypochormia

Poikilicytosis Tear drop cells

Elliptocytes

Target cells

Peripheral Film

Normal- rdeuced-slightly

Reticulocyte Count

Serum iron low

Serum ferritin low

TIBC(total iron binding capacity) inreased

Tansferrin saturation % low

Iron Profile

Bone marrow is hyper cellular with polychromatic

normoblast predominance

Erythroid series is small and have tiny projection from the

cytoplasm

Iron stain; Negative

Bone Marrow

Feaces examination for parasites

LFT in case if liver damage

Investigations Occasionally

Required

Iron is released from the hemosidrine molecules by treating

the slide with weak acid solution .the free iron combines

with potassium ferrocynide to produce ferric Ferro cyanide.

Free iron will appear greenish blue

Prussian-blue Stain

Procedure

Air dry film

Fix with methanol 10-20min

Place slide in solution of 10g /l potassium Ferro cyanide in 0.1 mol/l HCL for 30 min

Wash in running tap water for 1 min

Rinse in distilled water

Counter stain with neutral red for10-15 sec

Differential diagnosis

Thank You