2. ANEMIA
Quantitative and qualitative reduction of RBCs leading
to low oxygen carrying capacity of the blood
irrespective of age & sex.
Normal Hb:
Males: 14-18 gm/dl
Females:12-15.5 gm/dl
3. CLASSIFICATION OF ANEMIA
Blood loss
Due to increased red cell destruction-HEMOLYSIS
Due to increased red cell production
4. HEMOLYTIC ANEMIA
Defined as anemia's resulting from an increase in the
rate of red cell destruction.
INTRAVASCULAR HEMOLYSIS-Red cells undergo
lysis in the circulation and release their contents into
plasma.
EXTRAVASCULAR HEMOLYSIS-Red cells are taken
up by the cells of the RE system where they are
destroyed and digested.
6. LIST OF HEMOLYTIC ANEMIAS
Hereditary spherocytosis
Hereditary elliptocytosis
Sickle cell disease
Thalassemia
Hemolytic anemia due to G6PD deficiency
Immunohemolytic anemia
Paroxysmal nocturnal hemoglobinuria
7. RBC INDICES
Mean Corpuscular Volume
MCV=PCV per 100 ml blood/RBC count in
million per µL.
Normal=78-94 fL.
8. Mean Corpuscular Hemoglobin
MCH=Hemoglobin in gm per dL/RBC count in
million per µL.
Normal=28-32 pg.
9. Mean Corpuscular Hemoglobin Concentration
MCHC=Hb in gm per dL/PCV per 100 ml blood
Normal=30-37%
10. LABORATORY EVALUATION OF
HAEMOLYSIS
A. Test of increased red cell breakdown
1.Serum bilirubin-unconjugated bilirubin is
increased (van den Bergh reaction-indirect
positive)
2.Urine urobilinogen is raised.
3.Faecal stercobilinogen is raised.
4.Serum haptoglobin(α-globulin binding protein)
is reduced or absent.
5.Plasma lactate dehydrogenase is raised.
11. B.Test for increased red cell
production
1.Reticulocyte count reveals reticulocytosis which is
generally early and is hence most useful initial test of
marrow erythroid hyperplasia.
2.Routine blood film(PS) shows macrocytosis,
polychromasia and presence of normoblasts.
3.Bone marrow shows erythroid hyperplasia with usually
raised iron stores.
4.X-ray of bones shows evidence of expansion of marrow
space, especially in tubular bones and skull.
22. C.Test of Damage to Red Cell
1.Routine blood film.
2.Osmotic fragility test.
3.Coomb’s antiglobulin test.
4.Eletrophoresis for abnormal hemoglobin
5.Estimation of HbA2.
6.Estimation of HbF.
7.Tests for sickling.
8.Screening test for G6PD deficiency.
23. D.Tests for Shortened Red Cell Life
Span
A shortened red cell survival is best tested by 51Cr
labeling method. Normal RBC life span of 120 is
shortened to 20-40 days in moderate haemolysis and
to 5-20 days in severe haemolysis.
26. IMMUNOHEMOLYTIC ANEMIA-
COOMB’S TEST
Immunohemolytic anemia's are a group of
anemia's occurring due to antibody production by the
body against its own red cells. It is induced by one of
the following three types of antibodies:
1.Autoimmune hemolytic anemia
a. Warm antibody AIHA
b. Cold antibody AIHA
2.Drug induced immunohemolytic anemia
3.Isoimmune hemolytic anemia
27. IMMUNOHEMOLYTIC ANEMIA-
COOMB’S TEST (Contd.)
An important diagnostic tool in all cases of
immunohemolytic anemia's is Coomb’s antiglobulin
test.
It is the test for detection of Rh-antibodies in
saline(direct Coomb’s) or after addition of
albumin(indirect Coomb’s).
32. SICKLING TEST
It is done under condition of reduced oxygen tension
by an oxygen consuming reagent, sodium
metabisulfate.
It is a confirmatory test for sickle cell disease.
Editor's Notes
Marrow smear from a patient with hemolytic anemia. The marrow reveals greatly increased numbers of maturing erythroid progenitors (normoblasts).
Hereditary spherocytosis (peripheral smear). Note the anisocytosis and several dark-appearing spherocytes with no central pallor. Howell-Jolly bodies (small dark nuclear remnants) are also present in red cells of this asplenic patient
G6PD deficiency: effects of oxidant drug exposure (peripheral blood smear). Inset, Red cells with precipitates of denatured globin (Heinz bodies) revealed by supravital staining. As the splenic macrophages pluck out these inclusions, “bite cells” like the one in this smear are produced
Sickle cell disease (peripheral blood smear). A, Low magnification shows sickle cells, anisocytosis, and poikilocytosis. B, Higher magnification shows an irreversibly sickled cell in the center.
A, Spleen in sickle cell disease (low power). Red pulp cords and sinusoids are markedly congested; between the congested areas, pale areas of fibrosis resulting from ischemic damage are evident. B, Under high power, splenic sinusoids are dilated and filled with sickled red cells
Thalassemia: x-ray film of the skull showing new bone formation on the outer table, producing perpendicular radiations resembling a crewcut
Microangiopathic hemolytic anemia. A peripheral blood smear from a person with hemolytic-uremic syndrome shows several fragmented red cells