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By Dr Bashir Ahmed Dar

Chinki pora sopore kashmir
Associate professor of Medicine
Classification of Anemia
I. Etiologic Classification
1. Impaired RBC production
2. Excessive destruction
3. Blood loss
II. Morphologic Classification
1. Macrocytic anemia
2. Microcytic hypochromic anemia
3. Normochromic normocytic anemia
Impaired RBC Production
1. Abnormal bone marrow
1.1 Aplastic anemia
1.2 Myelophthisis : Myelofibrosis, Leukemia,
Cancer metastasis
2. Essential factors deficiency
2.1 Deficiency anemia : Fe, Vit. B12, Folic acid, etc
2.2 Anemia in renal disease : Erythropoietin
3. Stimulation factor deficiency
3.1 Anemia in chronic disease
3.2 Anemia in hypopituitarism
3.3 Anemia in hypothyroidism
Excessive Destruction of RBC(cont.)
Hemolytic anemia
1. Intracorpuscular defect
1.1 Membrane : Hereditary spherocytosis
Hereditary ovalocytosis, etc.
1.2 Enzyme : G-6PD deficiency, PK def., etc.
1.3 Hemoglobin : Thalassemia, Hemoglobino-
Excessive Destruction of RBC
2. Extracorpuscular defect
2.1 Mechanical : March hemolytic anemia
MAHA (Microangiopathic HA)
2.2 Chemical/Physical
2.3 Infection : Clostridium tetani
2.4 Antibodies : HTR, SLE
2.5 Hypersplenism
Blood Loss

1. Acute blood loss : Accident, GI bleeding

2. Chronic blood loss : Hypermenorrhea
Parasitic infestation
Macrocytic Anemia
MCV > 94
MCHC > 31
1. Megaloblastic dyspoiesis
1.1 Vit. B12 deficiency : Pernicious anemia
1.2 Folic acid deficiency : Nutritional megaloblas-

tic anemia, Sprue, Other malabsorption

1.3 Inborn errors of metabolism : Orotic aciduria,
1.4 Abnormal DNA synthesis : Chemotherapy,
Anticonvulsant, Oral contraceptives
Microcytic Hypochromic Anemia
MCV < 80
MCHC < 31
1. Fe deficiency anemia : Chronic blood loss,
Inadequate diet, Malabsorption, Increased
demand, etc.
2. Abnormal globin synthesis : Thalassemia with or
without Hemoglobinopathies
3. Abnormal porphyrin and heme synthesis :
Pyridoxine responsive anemia, etc.
4. Other abnormal Fe metabolism :
Normocytic Normochromic Anemia
MCV 82 - 92
MCHC > 30
1. Blood loss
2. Increased plasma volume : Pregnancy, Overhydration
3. Hemolytic anemia : depend on each cause
4. Hypoplastic marrow : Aplastic anemia, RBC aplasia
5. Infiltrate BM : Leukemia, Multiple myeloma,
Myelofibrosis, etc.
6. Abnormal endocrine : Hypothyroidism, Adrenal
insufficiency, etc.
7. Kidney disease / Liver disease / Cirrhosis
Hemolytic Anemia
What is Hemolysis

- Premature destruction of dead cells.

- Causes hereditary and acquired disorders.

- Hemolysis occurs at two sites:


- Hemolysis occurs within systemic


- Hemoglobin is released into plasma.

- Hemoglobin is lost through kidneys or

catabolized in the liver.
- Trapping of red cells in spleen or liver

- Lyses of trapped red cells.

- Release of lysed hemoglobin and

catabolism within the sequestering organ.
Classification of Hereditary
Hemolytic Anemia
• Based on side effect:

- Metabolic defect

- Membrane defect

- Hemoglobin defect
A) Metabolic defect:
- Defect in hexose monophosphate shunt: G-
6-PD deficiency.

- Defects of glycolysis; pyrovate kinase def.,

glucose phosphate isomerase def.

- Defects in red cell nucleotide metabolism:

pyramidine-5-nucleotidase def.
B) Membrane defect:
- Heriditary spherocytosis

- Heriditary elliptocytosis

- Hereditary pyropoikilocytosis
C) Hemoglobin defect:

- Thalassemias

- Sickle cell anemia

- Hemoglobin C disease

- Hemoglobin E disease

- Unstable hemoglobin
Laboratory Findings
• Chemistry

 Hyperbilirubinemia, predominantly unconjugated bilirubin

due to breakdown of heme ring by reticuloendothelial cells
in the liver.

 elevated LDH: released from destroyed cells.

 Hemoglobinemia: free hemoglobin level increases in

hemolysis esp. intravascular hemolysis: levels of 10-20
mg/dl gives plasma amber color and 50-100 gm/dl reddish
 Hemoglobinuria: red-brown color of urine due to free
hemoglobin and methamoglobin.

 Decreased Heptaglobin level: it is a alpha-2-globin produced

in the liver. It binds free hemoglobin thus level is reduced in

 Hemosidrinuria: it reflects extensive hemolysis for a

prolonged period of time. When hemoglobin is filtered by
nephron, proximal tubular cells metabolize hemoglobin and
iron accumulate in the cells. Cells then exfoliate in the urine
and iron can be detected by Prussian blue reaction.
Drug-Induced Acute Hemolysis
• Drugs that have been linked to G6PD:
• Primaquine (an antimalarial)
• Sulphonamide antibiotics
• Sulphones (e.g. dapsone, used against leprosy)
• Other sulphur-containing drugs: glibenclamide (an anti-diabetic drug)
• Nitrofurantoin (an antibiotic often used for urinary tract infections)
• Vitamin K analogues
• Several others
• Henna can cause a hemolytic crisis in G6PD deficient infants
Acquired hemolytic anaemia
Immune haemolytic anaemias
Are caused by AB production by the body
against its own red cells.

Divided into  1) warm 37c

2) cold  4 c
• IgG alone ,Bind at 37c

• Usually IgM
• Bind to red cell at 4c
Coombs Test
Antiglobulin Test


Red cell with Anti-immunoglobulin
bound antibody to
membrane antigen
Coombs Test
Antiglobulin Test


Non-Immune Hemolytic Anemias
Hemolytic anaemias due to mechanisms or agents
other than antibodies +/or complement e.g.:
• Mechanical (traumatic)
• Toxins
• Infections
• Splenomegaly (hypersplenism)
• Burn (physical)
• Renal failure and liver failure
• Chemical
Mechanical (Traumatic)
This is due to(Fragmentation)
direct trauma (stress) to the RBCs
causing fragmentation of the RBCs & intra-
vascular hemolysis. The fragmented cells can be
seen on peripheral blood smears & are called

Due to:
1. Prosthetic valves
2. Patches
3. Valvular diseasse e.g., stenosis

Mechanical (Traumatic)
1. Microangiopathic: mechanical hemolysis due to
contact between the RBCs & the abnormal intema
of thrombosed, narrowed, necrotic small vessels or
fibrin strand formation.
Caused by many diseases e.g., DIC (disseminated
intravascular coagulation), malignant hypertension,
disseminated malignancies especially mucin
secreting adenocarcinomas, TTP (thrombocytopenic
purpura), hemolytic uremic syndrome (HUS).