Anemia................................................................................................................................................................. 1
Mechanism of Anemia......................................................................................................................................2
Tests for Anemia...............................................................................................................................................3
Reticulocyte Count......................................................................................................................................3
Mean Cell Volume (MCV)........................................................................................................................... 3
Absolute Reticulocyte Count (ARC)...........................................................................................................3
Serum Ferritin......................................................................................................................................4
Free Erythrocyte Protoporphyrin (FEP)............................................................................................... 4
Serum Iron...........................................................................................................................................4
Total Iron-Binding Capacity (TIBC)...................................................................................................... 4
Transferrin Saturation.......................................................................................................................... 4
Soluble Transferrin Receptor...............................................................................................................4
Hemoglobin Concentration of R.......................................................................................................... 4
Prussian Blue (Fe7(CN)18)................................................................................................................. 4
Disorders of Iron Kinetics and Heme Metabolism........................................................................................... 5
Iron-Restricted Anemia..................................................................................................................................... 5
Iron-Deficiency Anemia...............................................................................................................................5
Pathogenesis........................................................................................................................................ 5
Anemia of Chronic Disease/Inflammation................................................................................................7
Sideroblastic Anemia........................................................................................................................................8
Acquired: Lead Poisoning.......................................................................................................................... 8
Hereditary: Porphyrias................................................................................................................................ 8
Hemochromatosis............................................................................................................................................ 9
Anemias Caused by Defects of DNA Metabolism......................................................................................... 10
Megaloblastic Anemia............................................................................................................................. 10
Pernicious Anemia.............................................................................................................................10
Nonmegaloblastic Anemia.......................................................................................................................10
Laboratory Tests................................................................................................................................ 11
Bone Marrow Failure..................................................................................................................................... 12
Aplastic Anemia.......................................................................................................................................12
Congenital Aplastic Anemia – Fanconi Anemia.................................................................................12
Inherited Aplastic Anemia – Dyskeratosis Congenita........................................................................12
Pure Red Cell Aplasia............................................................................................................................. 13
Acquired Pure Red Cell Aplasia........................................................................................................ 13
Congenital Pure Red Cell Aplasia – Diamond-Blackfan Anemia.......................................................13
Myelophthisic Anemia..............................................................................................................................13
Anemia of Chronic Disease..................................................................................................................... 13
Thalassemia.................................................................................................................................................. 14
, Anemia
- A decrease in the oxygen carrying capacity of the blood
- Due to a reduction in the hemoglobin concentration of the blood
- Caused by a decreased: RBC count, Hemoglobin content, Hematocrit
Clinical Findings Rationale
(Classical symptoms) A reduction in the oxygen-carrying capacity of the blood also causes a
fatigue and shortness of decrease in the oxygen-delivery in tissues. Thus, resulting in a decrease in
breath the available energy for use. The body prioritizes the more important
organs such as the brain and heart.
Jaundice Anemia may be due to an increase in RBC destruction – hemolytic
anemia. When RBCs are destroyed, hemoglobin is released. Hemoglobin
is broken down into heme, globin, and iron. Heme is further degraded
into biliverdin, then bilirubin (a yellowish pigment).
Tachycardia Patients usually exhibit tachycardia when experiencing a rapid fall in
hemoglobin. The decrease in oxygen is compensated through a fast rate
(to increase the circulation of blood)
Result Physiologic Adaptation
Anemia from ACUTE blood ↓ blood volume ↑ heart rate
loss ↓ blood pressure ↑ respiratory rate
↑ cardiac output
CHRONIC/SEVERE Anemia Tissue hypoxia Shift in the oxygen dissociation
curve to the right
- ↓ 2,3-DPG
- ↑ O2 affinity to tissues
NOTE: A decrease in oxygen delivery to tissues due to a decrease in hemoglobin concentration triggers an
increase in EPO secretion to stimulate the erythroid precursors in the bone marrow to release more RBCs.
However, this response also prompts the release of more immature RBCs in the circulation – reticulocytes.
These immature reticulocytes are called “shift reticulocytes” or stress reticulocytes.”
Mechanism of Anemia
The normal lifespan of an RBC in circulation is approximately 120 days. In healthy or non-anemic individuals, the
rate of destruction is equal to the rate of production, meaning the bone marrow continuously produces RBCs to replace
those that are destroyed due to senescence. Adequate RBC production requires: Iron, Vitamin B12, Folate, and a normally
functioning globin. Folate and Vitamin B12 are necessary for purine and pyrimidine synthesis in the DNA.
INEFFECTIVE Erythropoiesis INSUFFICIENT Erythropoiesis
Production of Defective (the defective cells decreased
erythroid undergo apoptosis in the bone
precursors marrow)
EPO Increased due to a low decreased
hemoglobin content
Diseases - Megaloblastic anemia - Renal diseases
associated - Thalassemia - Infection with parvovirus B19
- Sideroblastic anemia
Loss of erythroid precursors due to an
, Tests for Anemia
Reticulocyte Count
- To determine whether an anemia is due to an RBC production defect or premature hemolysis and
shortened RBC survival defect
↑ RETICULOCYTE COUNT Hemolytic anemia, acute blood loss, increased RBC destruction
↓ RETICULOCYTE COUNT ↓ normal RBC production, chronic blood loss, decreased RBC
destruction
Note: Increased RBC destruction triggers the release of immature RBCs in the circulation to compensate
for the loss of red cells.
Mean Cell Volume (MCV)
- Key to classify anemia according to morphological size
- Microcytic -less than 80fL
- Caused by conditions that result in reduced hemoglobin synthesis
- Normocytic - 80-100 fL
- Caused by premature destruction and shortened RBC survival
- Characterized by an elevated reticulocyte count
- Caused by a decreased production of RBCs
- characterized by a decreased in reticulocyte
- Macrocytic - more than 100fL
- Caused by conditions that impair synthesis of DNA
- Vitamin B12 and Folate Deficiency
Absolute Reticulocyte Count (ARC)
- Useful for classifying anemias into decreased or ineffective RBC production and excessive RBC loss
Mechanism of Anemia......................................................................................................................................2
Tests for Anemia...............................................................................................................................................3
Reticulocyte Count......................................................................................................................................3
Mean Cell Volume (MCV)........................................................................................................................... 3
Absolute Reticulocyte Count (ARC)...........................................................................................................3
Serum Ferritin......................................................................................................................................4
Free Erythrocyte Protoporphyrin (FEP)............................................................................................... 4
Serum Iron...........................................................................................................................................4
Total Iron-Binding Capacity (TIBC)...................................................................................................... 4
Transferrin Saturation.......................................................................................................................... 4
Soluble Transferrin Receptor...............................................................................................................4
Hemoglobin Concentration of R.......................................................................................................... 4
Prussian Blue (Fe7(CN)18)................................................................................................................. 4
Disorders of Iron Kinetics and Heme Metabolism........................................................................................... 5
Iron-Restricted Anemia..................................................................................................................................... 5
Iron-Deficiency Anemia...............................................................................................................................5
Pathogenesis........................................................................................................................................ 5
Anemia of Chronic Disease/Inflammation................................................................................................7
Sideroblastic Anemia........................................................................................................................................8
Acquired: Lead Poisoning.......................................................................................................................... 8
Hereditary: Porphyrias................................................................................................................................ 8
Hemochromatosis............................................................................................................................................ 9
Anemias Caused by Defects of DNA Metabolism......................................................................................... 10
Megaloblastic Anemia............................................................................................................................. 10
Pernicious Anemia.............................................................................................................................10
Nonmegaloblastic Anemia.......................................................................................................................10
Laboratory Tests................................................................................................................................ 11
Bone Marrow Failure..................................................................................................................................... 12
Aplastic Anemia.......................................................................................................................................12
Congenital Aplastic Anemia – Fanconi Anemia.................................................................................12
Inherited Aplastic Anemia – Dyskeratosis Congenita........................................................................12
Pure Red Cell Aplasia............................................................................................................................. 13
Acquired Pure Red Cell Aplasia........................................................................................................ 13
Congenital Pure Red Cell Aplasia – Diamond-Blackfan Anemia.......................................................13
Myelophthisic Anemia..............................................................................................................................13
Anemia of Chronic Disease..................................................................................................................... 13
Thalassemia.................................................................................................................................................. 14
, Anemia
- A decrease in the oxygen carrying capacity of the blood
- Due to a reduction in the hemoglobin concentration of the blood
- Caused by a decreased: RBC count, Hemoglobin content, Hematocrit
Clinical Findings Rationale
(Classical symptoms) A reduction in the oxygen-carrying capacity of the blood also causes a
fatigue and shortness of decrease in the oxygen-delivery in tissues. Thus, resulting in a decrease in
breath the available energy for use. The body prioritizes the more important
organs such as the brain and heart.
Jaundice Anemia may be due to an increase in RBC destruction – hemolytic
anemia. When RBCs are destroyed, hemoglobin is released. Hemoglobin
is broken down into heme, globin, and iron. Heme is further degraded
into biliverdin, then bilirubin (a yellowish pigment).
Tachycardia Patients usually exhibit tachycardia when experiencing a rapid fall in
hemoglobin. The decrease in oxygen is compensated through a fast rate
(to increase the circulation of blood)
Result Physiologic Adaptation
Anemia from ACUTE blood ↓ blood volume ↑ heart rate
loss ↓ blood pressure ↑ respiratory rate
↑ cardiac output
CHRONIC/SEVERE Anemia Tissue hypoxia Shift in the oxygen dissociation
curve to the right
- ↓ 2,3-DPG
- ↑ O2 affinity to tissues
NOTE: A decrease in oxygen delivery to tissues due to a decrease in hemoglobin concentration triggers an
increase in EPO secretion to stimulate the erythroid precursors in the bone marrow to release more RBCs.
However, this response also prompts the release of more immature RBCs in the circulation – reticulocytes.
These immature reticulocytes are called “shift reticulocytes” or stress reticulocytes.”
Mechanism of Anemia
The normal lifespan of an RBC in circulation is approximately 120 days. In healthy or non-anemic individuals, the
rate of destruction is equal to the rate of production, meaning the bone marrow continuously produces RBCs to replace
those that are destroyed due to senescence. Adequate RBC production requires: Iron, Vitamin B12, Folate, and a normally
functioning globin. Folate and Vitamin B12 are necessary for purine and pyrimidine synthesis in the DNA.
INEFFECTIVE Erythropoiesis INSUFFICIENT Erythropoiesis
Production of Defective (the defective cells decreased
erythroid undergo apoptosis in the bone
precursors marrow)
EPO Increased due to a low decreased
hemoglobin content
Diseases - Megaloblastic anemia - Renal diseases
associated - Thalassemia - Infection with parvovirus B19
- Sideroblastic anemia
Loss of erythroid precursors due to an
, Tests for Anemia
Reticulocyte Count
- To determine whether an anemia is due to an RBC production defect or premature hemolysis and
shortened RBC survival defect
↑ RETICULOCYTE COUNT Hemolytic anemia, acute blood loss, increased RBC destruction
↓ RETICULOCYTE COUNT ↓ normal RBC production, chronic blood loss, decreased RBC
destruction
Note: Increased RBC destruction triggers the release of immature RBCs in the circulation to compensate
for the loss of red cells.
Mean Cell Volume (MCV)
- Key to classify anemia according to morphological size
- Microcytic -less than 80fL
- Caused by conditions that result in reduced hemoglobin synthesis
- Normocytic - 80-100 fL
- Caused by premature destruction and shortened RBC survival
- Characterized by an elevated reticulocyte count
- Caused by a decreased production of RBCs
- characterized by a decreased in reticulocyte
- Macrocytic - more than 100fL
- Caused by conditions that impair synthesis of DNA
- Vitamin B12 and Folate Deficiency
Absolute Reticulocyte Count (ARC)
- Useful for classifying anemias into decreased or ineffective RBC production and excessive RBC loss
