Iron Deficiency Anemia:

Iron deficiency anemia (IDA) is a common type of

anemia caused by insu8icient iron in the body,
Causes of Iron Deficiency Anemia
1. Inadequate Dietary Intake: Insu8icient
consumption of iron-rich foods (e.g., red meat,
leafy greens, fortified cereals) can lead to
deficiency, especially in vegetarians or those
with poor diets.
2. Increased Iron Demand: Periods of rapid
growth (infancy, adolescence, pregnancy) or
increased physiological needs (e.g.,
menstruation) increase iron requirements.
3. Blood Loss: Chronic blood loss is a major
cause, including:
o Heavy menstrual bleeding (menorrhagia).
o Gastrointestinal bleeding (e.g., ulcers,
hemorrhoids, colorectal cancer).
o Parasitic infections (e.g., hookworm).
4. Malabsorption: Conditions like celiac disease,
inflammatory bowel disease, or gastric bypass
surgery impair iron absorption.
 5. Other Factors: Chronic diseases (e.g., cancer,
kidney disease) or genetic conditions a8ecting
iron metabolism can contribute.
Symptoms
Symptoms of IDA vary based on severity but
commonly include:
• Fatigue and weakness.
• Pale skin and mucous membranes.
• Shortness of breath.
• Dizziness or lightheadedness.
• Cold hands and feet.
• Brittle nails and hair loss.
• Pica (craving non-food substances like dirt or
ice).
• Restless legs syndrome (in some cases).
Diagnosis
IDA is diagnosed through clinical evaluation and
laboratory tests, including:
• Complete Blood Count (CBC): Shows low
hemoglobin, low hematocrit, and low mean
 corpuscular volume (MCV, indicating microcytic
anemia).
• Serum Ferritin: Low levels (<15–30 ng/mL)
indicate depleted iron stores.
• Serum Iron and Total Iron-Binding Capacity
(TIBC): Low serum iron with high TIBC suggests
IDA.
• Transferrin Saturation: Reduced in IDA.
• Peripheral Smear: Discussed in detail below.
Treatment
1. Iron Supplementation: Oral iron (e.g., ferrous
sulfate) is the first-line treatment. Intravenous
iron may be used in severe cases or if oral iron is
poorly tolerated.
2. Dietary Changes: Increasing intake of iron-rich
foods and enhancing absorption with vitamin C.
3. Addressing Underlying Causes: Treating
conditions causing blood loss or malabsorption.
4. Monitoring: Follow-up blood tests to assess
response to treatment.
Complications
Untreated IDA can lead to:
• Heart problems (e.g., tachycardia, heart failure
due to increased cardiac workload).
• Developmental delays in children.
• Pregnancy complications (e.g., preterm delivery,
low birth weight).
• Reduced immune function.

1. How Does Iron Absorption Take Place?

Iron absorption is a tightly regulated process
primarily occurring in the duodenum and proximal
jejunum of the small intestine, where the acidic
environment and specific transporters facilitate
uptake. The process involves dietary iron in two
forms: heme iron (from hemoglobin and myoglobin
in animal products) and non-heme iron (from plant-
based foods and supplements).
Steps of Iron Absorption
1. Dietary Sources and Forms:
o Heme Iron: Found in meat, poultry, and
fish, it is highly bioavailable (15–35%
 absorption rate) and absorbed directly as a
heme molecule.
o Non-Heme Iron: Found in grains,
vegetables, and supplements, it exists as
ferric (Fe³⁺) or ferrous (Fe²⁺) iron, with lower
bioavailability (2–20%).
2. Luminal Processing:
o In the stomach, gastric acid and peptic
enzymes break down food, releasing iron.
Gastric acid converts ferric iron (Fe³⁺) to the
more soluble ferrous iron (Fe²⁺), which is
better absorbed.
o Heme iron is released from
hemoglobin/myoglobin and remains intact
as a porphyrin complex.
3. Absorption at the Enterocyte:
o Non-Heme Iron:
§ Ferrous iron (Fe²⁺) is transported into
the enterocyte (intestinal cell) via the
divalent metal transporter 1 (DMT1)
on the apical membrane.
 § Ferric iron (Fe³⁺) must first be reduced
to Fe²⁺ by duodenal cytochrome b
(Dcytb), a reductase enzyme on the
enterocyte surface.
o Heme Iron:
§ Heme is absorbed intact via a heme
carrier protein 1 (HCP1) or other
transporters.
§ Once inside the enterocyte, heme is
broken down by heme oxygenase,
releasing Fe²⁺, which joins the same
intracellular iron pool as non-heme
iron.
4. Intracellular Handling:
o Absorbed iron is either:
§ Stored as ferritin in the enterocyte (for
later use or lost when enterocytes are
sloughed o8).
§ Exported into the bloodstream via
ferroportin, the only known iron
exporter, located on the basolateral
membrane.
5. Systemic Transport:
o Exported Fe²⁺ is oxidized to Fe³⁺ by
hephaestin (a ferroxidase) or
ceruloplasmin in the blood.
o Fe³⁺ binds to transferrin, a plasma protein
that transports iron to tissues like the bone
marrow for erythropoiesis or to the liver for
storage.
6. Regulation of Absorption:
o Iron absorption is tightly regulated by
hepcidin, a liver-derived hormone.
Hepcidin inhibits ferroportin, reducing iron
export from enterocytes and macrophages
when iron stores are high.
o Low iron levels, hypoxia, or increased
erythropoiesis suppress hepcidin,
enhancing absorption.
o Dietary factors also influence absorption:
§ Enhancers: Vitamin C (ascorbic acid)
reduces Fe³⁺ to Fe²⁺ and prevents
precipitation.
 § Inhibitors: Phytates (in grains),
polyphenols (in tea/co8ee), and
calcium compete with iron for
absorption.
Factors AUecting Iron Absorption
• Iron Status: Absorption increases when body
iron stores are low and decreases when stores
are adequate.
• Dietary Composition: Heme iron is absorbed
more e8iciently than non-heme iron.
• Gastrointestinal Health: Conditions like celiac
disease or H. pylori infection impair absorption.
• Inflammation: Chronic inflammation increases
hepcidin, reducing absorption.

2. Peripheral Smear Findings in Iron Deficiency

Anemia
A peripheral blood smear is a microscopic
examination of a stained blood film that provides
valuable insights into RBC morphology, aiding in the
diagnosis of IDA. In iron deficiency anemia, the
peripheral smear typically reveals characteristic
findings due to impaired hemoglobin synthesis and
reduced RBC production.
Key Peripheral Smear Findings
1. Microcytic, Hypochromic RBCs:
o Microcytosis: RBCs are smaller than
normal (mean corpuscular volume [MCV]
<80 fL). This is due to reduced hemoglobin
synthesis, leading to smaller cell size.
o Hypochromia: RBCs appear pale with a
larger central pallor (area of central
clearing) due to decreased hemoglobin
content. The mean corpuscular hemoglobin
(MCH) and mean corpuscular hemoglobin
concentration (MCHC) are low.
2. Anisocytosis:
o Variation in RBC size, indicated by an
increased red cell distribution width (RDW).
This reflects the presence of RBCs of
di8erent sizes as iron deficiency progresses.
3. Poikilocytosis:
o Variation in RBC shape. Common abnormal
shapes include:
 § Pencil Cells: Elongated, cigar-shaped
RBCs, a hallmark of IDA.
§ Target Cells (Codocytes): Occasionally
seen, with a bullseye appearance due
to excess membrane relative to
hemoglobin.
§ Elliptocytes: Oval-shaped RBCs, less
common but may appear in severe
cases.
4. Reduced Reticulocytes:
o Reticulocyte count is typically low,
reflecting decreased RBC production due to
insu8icient iron for erythropoiesis.
5. Other Findings:
o Platelet Count: May be normal or elevated
(reactive thrombocytosis) in response to
chronic blood loss or inflammation.
o White Blood Cells (WBCs): Usually normal
unless an underlying condition (e.g.,
infection) is present.
Comparison with Other Anemias
• Thalassemia: Also microcytic and hypochromic
but typically shows more target cells, basophilic
stippling, and less anisocytosis. RDW is often
normal in thalassemia, unlike IDA.
• Anemia of Chronic Disease: May be
normocytic or mildly microcytic, with normal or
low RDW and less pronounced hypochromia.
• Sideroblastic Anemia: May show dimorphic
RBCs (normal and microcytic) with ringed
sideroblasts in bone marrow (not seen in
peripheral smear).