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Table of Contents
Definition / general | Essential features | Terminology | Epidemiology | Pathophysiology | Etiology | Diagrams / tables | Clinical features | Diagnosis | Laboratory | Case reports | Treatment | Clinical images | Peripheral smear description | Microscopic (histologic) images | Negative stains | Additional referencesCite this page: Amita R Iron deficiency anemia. PathologyOutlines.com website. http://www.pathologyoutlines.com/topic/hematologyirondefanemia.html. Accessed May 25th, 2019.
Definition / general
- Develops when iron stores are too low to support normal red blood cell (RBC) production
Essential features
- Occurs when iron deficiency is severe enough to diminish erythropoiesis and cause development of anemia
Terminology
- Also called nutritional anemia
Epidemiology
- Single most prevalent deficiency state on worldwide basis
Pathophysiology
- Infants:
- Total body iron decreases from 250 mg (80 parts per million/ppm) to 60 ppm in first 6 months of life, due to consumption of iron deficient milk diet
- Cow milk consumption results in greater incidence of iron deficiency, due to higher concentration of calcium, which competes with iron for absorption
- Growing children must obtain approximately 0.5 mg more iron daily than is lost to maintain a normal body concentration of 60 ppm
- Adult males:
- Absorb and lose about 1 mg of iron from a diet containing 10 - 20 mg daily
- Lose body iron in sloughed epithelium, in secretions from the skin and gut lining, and from small daily losses of blood from the GI tract (0.7 mL daily)
- Those with severe siderosis from blood transfusions can lose a maximum of 4 mg daily via these routes without additional blood loss
- Adult females:
- Lose an average of 2 mg of iron daily during childbearing years; must absorb a similar quantity to maintain equilibrium
- Lose about 500 mg of iron with each pregnancy
- Menstrual losses are highly variable; range from 10 - 250 mL (4 - 100 mg) per period
- Iron absorption:
- 3 pathways, but most absorbed iron is derived from heme
- Digested enzymatically free of globin; enters enterocytes as a metalloporphyrin; released from heme within the cell by heme oxygenase to pass into the body as inorganic iron
- Most dietary inorganic iron is ferric; enters absorptive cell via integrin-mobilferrin pathway (IMP)
- Some dietary iron is reduced in gut lumen and enters absorptive cell via the divalent metal transporter-1 (DMT 1 / DCT 1 / Nramp 2)
- Proteins of both pathways interact within enterocyte with paraferritin (large protein complex capable of ferric reduction)
- Excess iron is stored as ferritin to protect cell from oxidative damage
- Iron leaves cell to enter plasma, facilitated by ferroportin and hephaestin (associates with an apotransferrin receptor)
- Enterocyte is informed of body requirements by transporting iron from plasma into cell using holotransferrin receptor
- 3 pathways, but most absorbed iron is derived from heme
Etiology
- Dietary deficiency: substances that diminish absorption of ferrous and ferric iron include phytates, oxalates, phosphates, carbonates and tannates
- Malabsorption of iron:
- Prolonged achlorhydria may produce iron deficiency because acidic conditions are required to release ferric iron from food
- Starch and clay eating produce malabsorption of iron and iron deficiency anemia
- Extensive surgical removal of proximal small bowel or chronic diseases (e.g., untreated sprue or celiac syndrome) can diminish iron absorption
- Bleeding for any reason produces iron depletion
- Hemosiderinuria, hemoglobinuria (paroxysmal nocturnal hemoglobinuria, brisk intravascular hemolytic anemia associated with implantation of artificial valves)
- Pulmonary hemosiderosis
Diagrams / tables
Images hosted on other servers:
Iron equilibrium in the body
Clinical features
- Fatigue and diminished capability to perform hard labor
- Leg cramps on climbing stairs
- Craving ice (in some cases, cold celery or other cold vegetables) to suck or chew
- Poor scholastic performance
- Cold intolerance
- Reduced resistance to infection
- Altered behavior (e.g., attention deficit disorder)
- Dysphagia with solid foods (from esophageal webbing)
- Worsened symptoms of comorbid cardiac or pulmonary disease
Diagnosis
- Low serum iron and ferritin levels with an elevated total iron binding capacity / TIBC are diagnostic of iron deficiency
- A normal serum ferritin can be seen in patients with iron deficiency plus either hepatitis or anemia of chronic disorders
Laboratory
- Complete blood count shows low mean corpuscular volume (MCV) and low mean corpuscular hemoglobin concentration (MCHC)
- Reticulocyte hemoglobin content (CHr) value is a strong predictor of iron deficiency and iron deficiency anemia
- Peripheral blood smear:
- Microcytic and hypochromic RBCs with marked anisopoikilocytosis in chronic cases
- Platelets usually are increased
- In contrast to thalassemia, target cells are usually not present
- Testing includes:
- Serum iron, total iron binding capacity (TIBC) and serum ferritin
- Evaluation for hemosiderinuria, hemoglobinuria and pulmonary hemosiderosis
- Hemoglobin electrophoresis and measurement of hemoglobin A2 and fetal hemoglobin
- Reticulocyte hemoglobin content
Images hosted on other servers:
RBC indices and biochemical markers
of microcytic anemia (Medscape)
Case reports
- Iron deficiency anemia of unknown cause (Clinics (Sao Paulo) 2010;65:531)
- Pica and refractory iron deficiency anaemia (J Med Case Rep 2008;2:324)
Treatment
- Correct the etiology and replenish iron stores
- Iron therapy:
- Oral ferrous (sulphate) iron salts
- Reserve parenteral iron for those unable to absorb oral iron or with increasing anemia despite adequate doses of oral iron
- Reserve transfusion of packed RBCs for those experiencing significant acute bleeding or in danger of hypoxia or coronary insufficiency
Clinical images
Images hosted on other servers:
Koilonychia: abnormal
fingernail shape
Atrophic glossitis
Peripheral smear description
- For anemia due to hemorrhage, maximal changes in RBC cellular indices occur by 120 days, when all normal erythrocytes produced prior to hemorrhage are replaced by microcytes
- Before this, the peripheral smear shows a dimorphic population of erythrocytes: normocytic cells produced before bleeding and microcytic cells produced after bleeding - this is reflected in the red blood cell distribution width (RDW)
- Earliest evidence of iron deficient erythropoiesis is reflected by increased RDW
Microscopic (histologic) images
Images hosted on other servers:
Prussian blue stain: normal (left), anemia (right)
Negative stains
Images hosted on other servers:
Slide 38: Prussian blue staining of bone
marrow aspirate shows absence of iron
Additional references
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