Iron Deficiency Anemia

Cause:
1. Inadequate intake
2. Increased need
3. Impaired absorption
4. Chronic blood loss
Laboratory Diagnosis

• Screening
• Diagnostic
• Specialized
Response to Treatment
Reticulocyte hemoglobin - corrected within 2 days
Reticulocyte count- begin to increase 5 to 10 days
Anemia of Chronic Inflammation
• the term used to describe the hypoproliferative anaemia
seen in response to systemic illness or inflammation
• is the second most prevalent form of anaemia
• the most common amongst patients with chronic
illnesses
• central feature - sideropenia with abundant iron store
Hepcidin
• hormone produced by hepatocytes to regulate body iron
levels, particularly absorption of iron in the intestine and
release of iron from macrophages
• Hepcidin interacts with the transmembrane protein
ferroportin, which exports iron from enterocytes into the
plasma, reducing the amount of iron absorbed into the blood
from the intestine.
• Macrophages and hepatocytes also use ferroportin to export
iron into plasma and are affected by hepcidin.
Hepcidin
• an acute phase reactant, so levels increase during
inflammation, regardless of iron levels in the body

Acute phase reactants

- inflammation markers that exhibit significant
changes in serum concentration during inflammation
- either increase or decrease in response to
inflammation
Mechanism of Hepcidin during Inflammation

Increased levels of Hepcidin during inflammation

can cause decrease level of iron in the circulation

Decreased levels of iron in the circulation means

no available iron for bacteria to use for growth

Which will eventually cause rapid/increase

death to invading bacteria
Lactoferrin
• an iron-binding protein in the granules of neutrophils.
• Its avidity for iron is greater than that of transferrin.
• important intracellularly for phagocytes to prevent
phagocytized bacteria from using intracellular iron for
their metabolic processes
Ferritin
• Increased levels of ferritin in the plasma also bind
some iron. Because developing RBCs do not have a
ferritin receptor, this iron is unavailable for
incorporation into hemoglobin
Sideroblastic Anemia
Lead Poisoning
• The conversion of aminolevulinic acid to
porphobilinogen; the result is the accumulation of
aminolevulinic acid.
• The incorporation of iron into protoporphyrin IX by
ferrochelatase (also called heme synthetase); the
result is accumulation of iron and protoporphyrin
Porphyrias
Iron Overload
• Excess accumulation of iron results from acquired or
hereditary conditions in which the body’s rate of iron
acquisition exceedsthe rate of loss, which is usually about 1
mg/day.
• Regardless of the source of the iron, the body’s first reaction
is to store excess iron in the form of ferritin and, ultimately,
hemosiderin within cells