Anemia is characterized by low levels of hemoglobin or red blood cells. It can be caused by inadequate red blood cell production, increased destruction, or blood loss. Anemia is classified based on red blood cell morphology, etiology, or pathophysiology. Common types include iron deficiency anemia, megaloblastic anemia caused by vitamin B12 or folate deficiencies, and hemolytic anemias where red blood cells are destroyed faster than they can be replaced. Symptoms vary depending on severity but can include fatigue, paleness, and shortness of breath.

1. SIMI JOJU .K
1ST
YEAR M-PHARM
PHARMACY PRACTICE

2. DEFINITION
Anemia's are a group of diseases characterized
by a decrease in either the hemoglobin (Hgb)
or the volume of red blood cells (RBC’s) in
blood.
Results in decreased oxygen-carrying
capacity of the blood.
WHO define Anemia in adult as hemoglobin
levels less than 13g/dl in males, less than
12g/dl in females and less than 13g/dl in
pediatrics.

3. Anemia can result from :
1) Inadequate RBC production.
2) Accelerated loss of RBC mass.
3) host of systemic disorders such as infection, chronic
renal diseases or malignancy.

4. ETIOLOGY
 Etiology basically consist of three mechanism:
1) Reduced Hemoglobin synthesis which may be due to lack
of nutrients or bone marrow failure. This leads to either reduced
proliferation of precursors or defective maturation of precursors or both.
2) Increased hemoglobin loss due to hemorrhage (red cell
loss) or heamolysis (red cell destruction)
3) Decreased red cell production i.e. disturbance in stem cell
proliferation or differentiation.

5. Classification :-
Anemias can be classified on the basis of
1. Morphology of the RBCs,
2. Etiology, or
3. Pathophysiology.

6. 1. Morphological Class
Anemias are classified by RBC size as
Macrocytic Anemias
Megaloblastic anemias
 Vitamin B12 deficiency anemia
 Folic acid deficiency anemia
Microcytic, hypochromic anemias
Iron deficiency anemia
Genetic anomaly
 Sickle cell anemia
 Thalassemia
 Other hemoglobinopathies (abnormal hemoglobins)

7. Normocytic anemias
Recent blood loss
Hemolysis
Bone marrow failure
Anemia of chronic disease
Renal failure
Endocrine disorders
Myeloplastic anemias

9. Deficiency
Iron
Vitamin B12
Folic acid
Pyridoxine
impaired bone marrow function
Anemia of chronic disease
Anemia of the elderly
Malignant bone marrow disorders
Peripheral
Bleeding (hemorrhage)
Hemolysis (hemolytic anemias)
Etiology Class

10. Pathophysiology Class
Excessive blood loss
Recent hemorrhage
Trauma
Peptic ulcer
Gastritis
Hemorrhoids

11. • Chronic hemorrhage
– Vaginal bleeding
– Peptic ulcer
– Intestinal parasites
– Aspirin and other NSAIDs
Excessive RBC destruction
Inadequate production of mature RBCs

13. Iron deficiency Anemia (IDA)
Decreased level of ferritin and serum iron,as well as
decreased transferrin saturation.Hb and Hematocrit
decrease later.
Daily requirement of Iron 0.9mg in males, 2mg
females, in pregnancy it is 3-5mg and in infant it is
0.5mg.
 Iron deficiency results from prolonged negative iron
balance.

14. Pathophysiology of IDA
Diminished total body iron content, developing in stages
over a period of negative iron balance
Iron depletion – Stage One
Iron deficient erthyropoiesis – Stage Two
Iron deficiency anemia – Stage Three
Stage One
Iron storage is exhausted - indicated by decrease in serum ferritin
levels No anemia – RBC morphology is normal.

15. Stage Two
Insufficient iron to insert into protoporphyrin ring to form heme
– Protoporphyrin accumulates in cell and complexes with zinc
to form ZPP No anemia, no hypochromia, but slight
microcytosis may be decreased
Stage Three
All laboratory tests for iron status become abnormal, Most
significant finding is microcytic, hypochromic anemia and there is
hyperplasia of erythroids.

16. Signs of IDA
1) Pale skin and mucous membrane
2) Painless glossitis (Inflammation of the tongue)
3) Angular stomatitis (Inflammation of the mucous membrane
of the mouth)
4) Koilonchia (Spoon shaped nails)
5) Dysphagia
6) Pica (Unusual cravings)
7) Atrophic Gastritis
8) Poikilocytes (misshapen red cells appear on the blood smear
as cigar-or pencil-shaped forms)
Chronic Iron
deficiency

17.  Symptoms
1) Faintness
2) Fatigue
3) Dizziness
4) Irritability
5) Malaise
6) Palpitation
7) Headache
8) Shortness of breath
9) Angina
10) Ankle edema

18. Megaloblastic Anemia
Macrocytic anemia is divided into two types:
1. Megaloblastic anemia
2. Non megaloblastic anemia
The two major causes are:
1. Folate deficiency
2. Vitamin B12 deficiency
Pernicious anemia is a specific disease caused by malabsoption of
Vit. B12.
Important to distinguish B12 from folate deficiency.

19. Stages of B12 deficiency
Stage B12conc. Mean corpuscular Hb Signs &
vol. Symptoms
Normal Normal Normal Normal None
-ve bal. ” ” ” ”
Depletion of
Stores Slight ↓ ” ” Possible
B12 def. Moderate ↓ ↑ ” ”
Erythropoiesis
B12 def.
Anemia Severe ↓ ↑ ↓ Probable

20. Etiology of Vitamin B12 Deficiency
The three major causes are:
1. Inadequate intake
2. Malabsorption syndrome
3. Inadequate utilization
Deficiency occurs from inadequate intake or malabsorption.
The only dietary source of Vit. B12 (cyanocobalamin) is from
food of animal origin. It is present in meat, fish, eggs, cheese
and milk. Daily requirements are between 0.5-1.0 μg.
Malabsorption occurs if the distil ileum is removed during
stagnant loop syndrome, tropical sprue and fish tapeworm
infestation.

21. Pathophysiology of Vitamin B12
Vitamin B12 works closely with folate in the synthesis of
building blocks for DNA and RNA.
 It is a water soluble vitamin obtained exogenously by
ingestion of meat, fish, poultry, diary products and fortified
cereals.

22. Most circulating
cobalamin complex
Free cobalaminFree cobalamin
Binding complexBinding complex
Cobalamin – R- Protein
complex
Cobalamin – R- Protein
complex
Release of cobalaminRelease of cobalamin
StomachStomach
Dietary cobalaminDietary cobalamin
Complex secreated
into circulation
Mucosal cell receptors
(cubilin) in distal ileum
Cobalamin -Intrinsic factor
complex
Cobalamin -Intrinsic factor
complex
Pepsin and HCL
R- Protein
Cobalamin -R- Protein complex
from Bile
Degradation by pancreatic
enzymes
Intrinsic factor

23. Symptoms
Apathy
Weakness
Fatigue
Palpitation
Breathlessness
Sore tongue
Glossitis
Burning of mouth
Nausea
Heart burn

24. FOLIC ACID Deficiency
Most common Vitamin deficiency
Critical in early pregnancy
The four major causes are:
1. Inadequate intake of folic acid
2. Decreased absorption
3. Hyper utilization
4. Inadequate utilization
5. Drugs (Azathioprine, methotrexate, phenytoin etc…)
Etiology of Folic acid Deficiency

25. Clinical manifestation
1. Megaloblastosis
2. Glossitis
3. Diarrhea
4. Weight loss
5. Fatigue
6. Pallor
7. palpitation
8. Chronic folate deficiency predisposes patients to thrombosis,
depression and neoplasia
9. Anisocytosis and poikilocytosis

26. Pathophysiology
GI cells and RBCGI cells and RBC
Methyltetrahydrofolate
monoglutamate
Methyltetrahydrofolate
monoglutamate
FolateFolate
MonoglutamateMonoglutamate
PolyglutamatePolyglutamate
Dietary FolateDietary Folate
Dihydrofolate
Enzymes in the gut
Absorption
Methylation/ Reduction
Specific carrier
Methyl
FolateFolate
Polyglutamate
DHF Reductase

27. Hemolytic Anemia
Hemolytic anemia decreases the life span of erythrocytes
If the rate of destruction of the erythrocytes exceeds the
rate of production, then anemia results
Wide range of hemolytic anemia with both genetic and
acquired disorders

28. Classification of Hemolytic Anemia
1. Abnormalities of red blood cell interior
a.) Enzyme deficts
b.) Hemoglobinopathies
2. RBC membrane abnormilities
a.) Heridity spherocytosis
b.) Paroxyysmal nocturnal hemoglobinuria
c.) Spur cell anemia
3. Extrensic factors
a.) Splenomegaly
b.) Antibody immune hemolysis
c.) Microangiopathic hemolysis
d.) Infections, toxins etc.
Intra-
corpuscular
Extra-
corpuscular
Hereditary
Acquired

29. Etiology
1. Sickle cell anemia:
 It is due to abnormal hemoglobin called hemoglobin S (HbS),
normal hemoglobin is usually HbA
 α chains are normal and β chains are abnormal. HbS has
valine substituted for glutamic acid as the 6th
amino acid in the
β polypeptide compared with HbA
 The molecules of HbS polymerize into long chain and
precipitate inside the cells because of this RBC’s attain sickle
shape and become more fragile leading to hemolysis
 Hemolysed sickle cell aggregate and block the blood vessels
leading to infarction.

30. 2. Thalassaemias
It is also known as Cooley’s anemia or Mediterranean anemia
Due to inherited abnormalities of hemoglobin
It is of two types
1. α Thalassaemias
2. β Thalassaemias (more common)
Defective synthesis of globin genes
Production of α and β chains become imbalanced
Precipitation of polypeptide Precipitation of polypeptide
chain in the immature RBC chain in the mature RBC
Disturbance in the process Hemolysis
of Erythropoiesis

31. α Thalassaemia (fetal life) β Thalassaemia
α chains are less, absent or β chains are less, absent or
abnormal with excess of abnormal with excess of
γ chains. α chains.
Defective Erythropoiesis and Hemolysis
G6PD deficiency:
G6PD is an erythrocyte enzyme that is indirectly involved in the
production of reduced Glutathione.
Glutathione is produced in response to and protects the red cells
from oxidizing reagents.

32. Pathophysiology
Normal 120 days life span of RBC.
Hemolysis RBC lifespan less than 120 days due to
1. Membrane defects
2. Alteration in hemoglobin solubility or stability
3. Changes in intracellular metabolic process
These changes can be intrinsic or extrinsic in origin
Intracorpuscular changes Extracorpuscular changes are
are genetically determined cause of hemolytic anemia
(direct effect on membrane)

33. Hereditary spherocytosis: RBC’s lose their flexible biconcave
characteristics and become tight spheres destroyed by
reticuloendothilial cells, causing pigment bile stones, mild
jaundice and splenomegaly.
Sickle cell and Thalassaemia: Alteration in hemoglobin
solubility and stability cell deformation hemolysis
G6PD Deficiency
G6PD deficiency i.e. decrease in G6PD
Decrease production of NADPH in erythrocytes
NADPH is needed to keep glutathione in reduced form
Hemoglobin in reduced from and helps erythrocytes deal with
oxidative stress

34. Clinical Manifestation
Acute haemolytic anemia:
1. Malaise
2. Fever
3. Abdominal pain
4. Dark urine and jaundice
5. Haemoglobulinaemia
6. Hyperbilinaemia
7. Reticulocytosis
8. Increased urobilinogen levels in urine
Chronic haemolytic anemia:
1. Splenomegaly
2. Normochromic and normocytic anemia

35. Anemia of CHRONIC DISEASE
It is an hypoproliferative anemia that has traditionally been
associated with infections, inflammatory, hepatic disease or
neoplastic disease lasting for more than 1 to 2 months.
ACD is a response to stimulation of the cellular immune
system by various underlying disease processes. ACD
commonly develops in AIDS patients, especially those with
opportunistic infections or malnutrition, HIV infects
hematopoietic cells, which can lead to abnormal hematopoiesis
and bone marrow suppression. In addition, the drugs used to
treat AIDS and associated illness can cause bone marrow
suppression.
Etiology

37. Pathophysiology
In this anemia RBC’s have shortened life span.
This anemia may be due to a block in release of iron from the
endothelial cells of the marrow.
Cytokinins such as IL1, γ interferon and TNF released during
these illness may inhibit the production of RBCs
Signs and Symptoms
1. Fatigue
2. Breathlessness
3. Swollen feet
4. Chest pain

38. Aplastic Anemia
It is group of disorders characterized by pancytopenia in
peripheral blood, variable hypocellularity in bone marrow,
absence of underlying malignant or myeloproliferative disease.
ETIOLOGY
1. Congenital – rare
2. Acquired- virus or chemical
Other etiologies
Hepatitis, infectious mononucleosis, dengue and influenza
Regular exposure to irradiation
Major component of inherited conditions

39. Causes
Damage to the bone marrow's stem cells causes
aplastic anemia. When stem cells are damaged, they
don't grow into healthy blood cells.
The cause of the damage can be acquired or
inherited. Acquired aplastic anemia is more
common, and sometimes it's only temporary.
Aplastic anemia that's inherited is rare.
In more than half of the people who have aplastic
anemia, the cause of the disorder is unknown. Some
research suggests that stem cell damage may occur
because the body's immune system attacks its own
cells by mistake.

40. ANTIANEMIC DRUGS
 Erythropoietin
Ferrous sulfate
Deferoxamine
Folic acid
Vitamin B : Cyanocobalamin, hydroxocobalamin⑫
Iron dextran

41. ALGORITHM