ANAEMIA

Dr. Jayesh Beladiya

Assistant Professor
1
 INTRODUCTION

 It is a hematological condition in which there is a

quantitative deficiency of circulating haemoglobin,
often accompanied by altered number of red blood
cell.

2
 CLASSIFICATION OF ANEMIA

Pathophysiological
 Anaemia due to increased blood loss :

 Acute post hemorrhagic anemia

 Chronic blood loss anemia

 Anaemia due to impaired red cell production

 Cytoplasmic maturation defects

 Iron deficiency anemia

 Thallassemic syndromes

 Nuclear maturation defects

 Vit .B12 /folic acid deficiency anemia: megaloblastic

3
anemia
CONT…
 Defects in stem cell proliferation and differentiation
 Aplastic anaemia

 Pure red cell aplasia

 Anaemia of chronic disorder

 Bone marrow infiltration

 Congenital anaemia

 Anaemia due to increased red cell destruction

 Extrinsic red cell abnormalities

 Intrinsic red cell abnormalities

4
CONT…
Morphological
1) Microcytic, Hypochromic
2) Normocytic, Normochromic
3) Macrocytic, Normochromic

5
6
 IRON DEFICIENCY ANAEMIA

 Body iron is insufficient for normal function of Hb, iron

containing enzyme myoglobin and cytochrome system
process.
 Iron essential element for many physiological process
like erythropoiesis, tissue respiration, several enzyme
catalysed reaction.
 Average body contain 3 to 5 gm of element iron
distributed in two major components function iron as Hb
and storage as ferritin and himosiderin.
 Transferin a specific iron binding protein in blood that
transport iron.
7
 Causes Association

Dietary Starvation, poverty, vegetarianism,

religious practice

Blood loss
Women and girls Menstruation, pregnancy,
postmenopausal bleeding

General Peptic ulcer, Ulcerative colitis

Malabsorption Chronic inflammation ,partial and

total gastroctomy ,celiac disease

8
Increased requirement Rapid growth ,pregnancy
PATHOPHYSIOLOGY
 The elimination of iron is not controlled physiologically
so homeostasis maintained by controlling iron
absorption.
 Absorption of iron is insufficient so mismatch between
body’s iron requirement and iron absorption.
 Diet deficient in animal protein or ascorbic acid may not
provide protein or ascorbic acid to meet iron demand.
 Tetracycline, Penicillamine, floroquinolones bind iron in
GIT and reduced absorption of iron.
 Gut increases demand of fetal red cell production during
pregnancy.
9
DIAGNOSIS
 Cases are identified on basis of
 Medical history
 Full blood count
 Peripheral smears
 Total binding capacity
 Serum ferritin help to establish the iron status of the
patient

10
TREATMENT
 Oral or Parenteral iron
 30-40 mg element iron is used to treat iron deficiency
anaemia
 Oral iron the ferrous form is cheap , safe and effective in
most patient
 Parenteral therapy used for those unable to tolerate oral
therapy
 ferrous sulphate and ferrous gluconate are used
 Iron dextran (i.m.),iron gluconate(i.v.) ,iron sorbitol
citrate(inj.)
11
 MEGALOBLASTIC ANAEMIA

 Vit.B12 deficiency anaemia

 Preceded by various stages of B12 depletion
 Daily requirement of B12 for human is 0.5-1.0 ug
 Vit.B12 is an essential cofactor for important enzymatic
reaction like
 Formation of succinyl co –A
 Formation of methionine
 Inter conversion of leucine

12
PATHOPHYSIOLOGY
 One molecules of vit.B12 combines with one molecule of
glycoprotein called intrinsic factor.
 Intrinsic factor protects the vit.B12 from breakdown by
microorganism.
 Vit.B12 enters the ileal cell and transport through blood
attached to transport protein.
 Intrinsic factor produced gastric parietal cell so
gastroctomy leads to vit.B12 deficiency

13
DIAGNOSIS
 Identifying risk factors by obtaining complete dietary,
medication history and laboratory tests
 Measurement of plasma B12 considered as test for
diagnosis
 Additional assessment of products like methymalonic
acid and homocysteine are advantageous
 A shilling test is a method for assessing B12
malabsorption

14
TREATMENT
 Dietary changes: fresh liver, eggs, meat, milk, dairy
products, fish and shell fish
 Vit.B12 supplement : oral-2mg
parenteral-100-1000mg
intranasal-400mg

15
 FOLATE DEFICIENCY ANEMIA

 Depletion of stores leading to deficiency that result in

megaloblastic anaemia
 Folate is essential in early pregnancy for fetal neural
development
 Reduced form of folate are cofactor for transmylation
reaction in the biosynthesis of purines and thymidylates
of nucleic acid leading to bone marrow suppression
 Minimum daily requirement of folate is 50 to 100 ug/day

16
PATHOPHYSIOLOGY
 During DNA synthesis folate oxidized to dihydrofolate
which is inactive and activated by the enzyme DHFR
 It is inhibited by methotrexate, co-trimoxazole
trimethoprim, pyrimethamine

17
DIAGNOSIS
 Full RBC cell count
 RBC folate concentration
 Serum folate concentration

18
TREATMENT
 Dietary manipulation : folate rich food include raw
spinach , broccoli ,cauliflower ,peanuts and nuts
 Oral supplementation : 400 ug daily

19
 THALASSEMIAS

 Diverse group of hereditary disorders in which there is

reduced rate of synthesis of one or more of the globin
polypeptide chains
 Genetically transmitted disorder
 Depending upon whether the genetic defect or deletion
lies in transmission of globulin chain genes

20
PATHOPHYSIOLOGY
 α-Thalassaemias :
 Defective synthesis of α- globulin chain resulting in
depressed production of hemoglobin that contains α-
chains
 Deletion of one or more α-chain genes located on short
arm of chromosome 16.
 Four types α-thalassaemias
 4 α-gene deletion
 3 α-gene deletion
 2- α gene deletion
 1- α gene deletion 21
 β-Thalassaemias :
 Decreased rate of synthesis resulting in reduced
formation of HbA in the red cells
 Most of β-thalassaemias arise from different types of
mutation of β-globin gene resulting from single base
changes
 β-thalassaemias classify into 2 types

1. Homozygous form: β-thalassaemia major

2. Heterozygous form : β-thalassaemia minor(trait)

22
DIAGNOSIS
 Reticulocyte count is high
 Serum bilirubin level is elevated
 Haemoglobin level mildly reduced
 Platelet count is reduced
 WBC count is raised

23
TREATMENT
 Regular blood transfusion
 Folic acid supplement
 Splenectomy
 Chelation therapy
 Bone marrow transplantation

24
 SICKLE CELL ANEMIA

 Severally malignant disorder associated with protean

clinical manifestations and decreased life expectancy

25
PATHOGENESIS
 Basic molecular lesions
 Mechanism of sickling
 Reversible-irreversible sickling
 Factors determining rate of sickling

26
DIAGNOSIS
 Moderate to severe anaemia
 Blood film shows sickle cells and target cells
 A positive sickling test
 Haemoglobin electrophoresis show no normal HbA but
show predominance of HbS

27
TREATMENT
 Bone marrow transplantation
 Pain releasing medication
 Stem cell transplant
 Blood transfusion
 Oxygen supplement

28
 APLASTIC ANAEMIA

 Define as pantocytopenia resulting from aplasia of bone

marrow
 The underlying defect in all cases appears to be
sufficient reduction in the number of hematopoietic
pluripotent stem cells which makes them unable too
divide and differentiate.

29
ETIOLOGY
 Primary aplastic anaemia :
Fanconi’s anaemia
Immune causes
 Secondary aplastic anaemia :
Drugs
Dose related aplasia
Idiosyncratic aplasia
Toxic chemicals
Infections
Miscellaneous 30
PATHOPHYSIOLOGY
 Deficient or defective stem cells.
 Suppression of stem cell function
 Disturbances in the bone marrow microenvironment
 T-cell–mediated destruction of marrow cells

31
DIAGNOSIS
 Anemia: Hemoglobin levels are moderately reduced.
 Leucopenia: Absolute granulocyte count particularly low
with relative lymphocytosis
 Thrombocytopenia: Platelet count is always reduced.
 Bone marrow aspiration: Severe depression of myeloid
cell so that chiefly consists of lymphocytes and plasma
cell.

32
TREATMENT
 General management :
Identification and elimination
Supportive care
 Specific treatment :
Marrow stimulating agents
Immunosuppressive therapy
Bone marrow transplantation

33
 G6PD DEFICIENCY ANAEMIA

 Defects in hexose monophophate shunt

 It affects millions of people thought world
 The G6PD gene therefore a sex linked trait affecting
males while female are carriers and are asymptomatic

34
PATHOGENESIS
 Individual with inherited deficiency of G6PD an enzyme
required for hexose monophosphate shunt for glucose
metabolism fail to develop adequate levels of reduced
glutathione in their red cells

35
DIAGNOSIS
 Screening test:

1. Methaemoglobin reduction test

2. Fluorescent screening test
3. Ascorbate cyanide screening test

 Direct enzyme assay on red cell:

36
TREATMENT
 Avoidance of oxidative stressors
 Blood transfusion
 Splenectomy
 Folic acid and iron potentially are useful in haemolysis
 Research is being done to identify medications that may
inhibit oxidative-induced hemolysis of G6PD-deficient
red blood cells

37
 FAQS
1. Discuss etiology, symptoms and pathogenesis of iron
deficiency anemia.
2. Write detail note on megaloblastic anemia.
3. Write short note on aplastic anemia.

38
 REFERENCES

 Harsh Mohan. Text book of pathology. The

hematopoietic system, Jaypee Brothers, Fifth Edition,
2008, 364-404.
 Roger Walker, Clive Edwards, Clinical Pharmacy and
therapeutics, Anemia, Churchill Livingstone, 3rd Edition,
2003, 725-743.
 H.P. Rang, M.M. Dale, J.M. Ritter, R.J. Flower Rang and
Dale’s Pharmacology. The hematopoietic system.
Churchill Livingstone, 6th Edition 2007, 347-354.

39
THANK YOU!!!!

40