2. Objective
By the end of this course, the student should
be know the:
1. Definition of anaemia
2.Symptoms and signs of anaemia
3.Physiologic compensation for anaemia
4.Classification of anaemia
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3. Definition of anaemia
Anaemia is a medical condition defined as
a reduction in red blood cells ,hemoglobin
and or hematocrit according to gender
and age of individual.
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4. General symptoms and signs
• Easy fatigue and loss of energy
• Tachycardia rapid heart beat.
• Shortness of breath.
• Difficulty concentrating
• Dizziness
• Pale skin
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5. Physiologic compensation
for anaemia
1- Decreased hemoglobin oxygen affinity:
Increase the production of 2,3-DPG which
2- Redistribution of blood flow to vital organ:
eg: brain and liver.
3- Increased cardiac output:
The heart can respond to tissue hypoxia by
increased cardiac output.
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8. Morphological classification
• Which based on red cell
appearance of STD blood film
& red cell indices calculated
from Hb , PCV & RBCS count
values:
I. Normocytic normochromic
anaemias
II. Macrocytic anaemias
III. Microcytic hypochromic
anaemias.
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9. Normocytic normochromic
anaemias
MCV : normal (80-95fL)
MCH : normal (≥27pg)
These include:
1. ACD.
2. Acute hemorrhage.
3. Hemolytic Anaemia.
4. A plastic anaemia.
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12. Etiological classification
I.I. Impaired red cell production (bone marrow defect).Impaired red cell production (bone marrow defect).
II.II. Excessive red cell destruction (hemolytic anaemia)Excessive red cell destruction (hemolytic anaemia)
III.III. Blood loss anaemiaBlood loss anaemia
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13. Etiological classification
I.I. IMPAIRED RED CELL PRODUCTIONIMPAIRED RED CELL PRODUCTION
1. Inadequate supply of nutrients essential for
erythropoiesis:
– Iron deficiency
– Vitamin b-12 deficiency
– Folic acid deficiency
– Protein malnutrition
5. Reduction in erythropoietin production:
– Chronic renal disease
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14. Etiological classification
I.I. IMPAIRED RED CELL PRODUCTIONIMPAIRED RED CELL PRODUCTION
4. Infiltration of bone marrow by neoplastic cell:
– Leukemia
– Lymphoma
– Myeloproliferative Disorder
• Polycythemia
• Essential Thrombocythemia
• Chronic Myeloid Leukemia
• Myelofibrosis
– Myeloma
– Myelodysplastic Disorders
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15. Etiological classification
I.I. IMPAIRED RED CELL PRODUCTIONIMPAIRED RED CELL PRODUCTION
5. Chronic disorders:
– Infection
– Connective tissue disorders
– Inflammatory disorders
– Disseminated malignancy
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16. Etiological classification
II. Exessive red cell destruction (haemolytic anaemia)
i. Due to intrinsic defects in RBCs
a.Congenital
1.Membrane defects:
i. Hereditary spherocytosis
ii. Hereditary elliptocytosis
2.Enzyme defects :
i. G6PD deficiency
ii.Pyruvate kinase deficiency
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17. Etiological classification
II. Exessive red cell destruction (haemolytic anaemia)
i. Due to intrinsic defects in RBCs
a. Congenital
3. Haemoglobin defects:
i. Haemoglobinopathies: Sickle cell anaemia
ii.Thalasaemia: α thalasaemia and β
thalasaemia
b. Acquired
Paroxysmal Nocturnal Haemoglobinuria (PNH)
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18. Etiological classification
II. Exessive red cell destruction (haemolytic anaemia)
i. Due to extrinsic defects in RBCs
a. Immune mechanisms
1. Autoimmune acquried haemolytic anaemia ◊
◊warm antibody ◊ cold antibody
2. Haemolytic Disease of New Born (HDN)
3. Drug induced haemolytic anaemia
b. Non immune mechanisms
1. Cardiac haemolytic anaemia
2. Microangiopathic haemolytic anaemia
3. March haemolytic anaemia
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19. Etiological classification
II. Exessive red cell destruction (haemolytic anaemia)
i. Due to extrinsic defects in RBCs
c. Miscellaneous
1. Due to action of certain drugs, chemical
or physical agents
2. Due to parasitic infection e.G. Malaria
,hookworm….Etc
3. Due to burns.
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20. Etiological classification
III. BLOOD LOSS ANAEMIA
a. Overt blood loss
• Surgery
• Accident
• Menorrhagia
• Recurrent bleeding from any other site
a. Occult blood loss
• Gi bleeding
• Genti-urinary bleeding
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Increase the production of 2,3-DPG which shifts the hemoglobin-oxygen dissociation curve to the right, thus allowing the hemoglobin to release the oxygen easily
anaemia selective vasoconstriction of blood vessels subserving certain nonvital areas allows more blood to flow into critical areas. The main donor sites who sacrifice their aerobic lifestyle are the skin and kidneys. Shunting of blood away from cutaneous sites is the mechanism behind the clinical finding of pallor, a cardinal sign of anaemia. Although the kidney can hardly be thought of as a nonvital area, it receives (in the normal state) much more blood flow than is needed to meet its metabolic requirements. Although (by definition) total body red cell mass is decreased in anaemia, in the chronically anemic patient the total blood volume paradoxically is increased, due to increased plasma volume. It is as if the body were trying to make up in blood quantity what it lacks in quality.