The document discusses different types of anemias classified based on morphology, etiology, and pathophysiology. It describes macrocytic anemias like megaloblastic anemia caused by vitamin B12 or folate deficiency. Microcytic anemias discussed include iron deficiency anemia and sickle cell anemia. Normocytic anemias can result from blood loss, hemolysis, or bone marrow failure. Etiologies include deficiencies, impaired bone marrow function, or peripheral causes like bleeding or hemolysis. Diagnosis and treatment of various anemias like iron deficiency, vitamin B12 deficiency, and folate deficiency anemia are also summarized.

1. -Manithottiyle Angelo Simon
2301310005
Pharm D 4th year
SRM College of Pharmacy
SRM University

2.  Anemias are a group of diseases characterized by a decrease in haemoglobin or
RBCs, resulting in decreased oxygen carrying capacity of blood.
 The decrease may result from blood loss, increased destruction of RBCs
(hemolysis), or decreased production of RBCs.
 Anemia, like a fever, is a sign that requires investigation to determine the
underlying etiology.
 The most serious complications of severe anemia arise from tissue hypoxia. Shock,
hypotension, or coronary and pulmonary insufficiency can occur. This is more
common in older individuals with underlying pulmonary and cardiovascular
disease.

3.  BASED ON MORPHOLOGY
 BASED ON ETIOLOGY
 BASED ON PATHOPHYSIOLOGY

4. A)BASED ON MORPHOLOGY
1) Macrocytic anemias
 Where cells are larger than normal.
 Mean corpuscular volume(MCV) >100 fL
Megaloblastic anemia
 Cells are larger than normal in size because of impaired DNA synthesis.
 Vitamin B12 deficiency
 Folate deficiency
 Can be caused by inadequate dietary intake, decreased absorption and inadequate
utilization.
 Deficiency of intrinsic factor can cause a decrease in absorption of vitamin B12 in the
GIT which is caused by alcohol dependence, pernicious anemia etc.
 Folate deficiency can be caused due to hyper utilization during pregnancy, hemolytic
anemia, myelofibrosis, malignancy, chronic inflammatory disorders, long-term dialysis or
growth spurt .
 Drugs can cause anemia by reducing absorption of folate (eg. phenytoin) or by interfering
with corresponding metabolic pathways(eg. methotrexate).

5. 2) Microcytic anemia
 RBCs are lesser in size than normal.
 MCV <80fL
 MCHC <32 g/dL
Iron deficiency anemia
 Iron deficiency anemia develops when body stores of iron drop too low to support
normal red blood cell (RBC) production.
 Inadequate dietary iron, impaired iron absorption, bleeding, or loss of body iron in
the urine may be the cause.
Sickle-cell anemia
 RBCs become sickle shaped.
 Presence of abnormal hemoglobin called hemoglobin S in RBC.
 Genetic causes; abnormal genes which are inherited from parents.
 Present from birth.
 Most infants do not present any symptoms until they are 5-6 months age.
 Causes painful swelling of the hands and feet called dactylitis, fatigue and jaundice
in children.
 Some complications are: Acute pain(sickle-cell or vaso-occlusive crisis), acute chest
syndrome, stroke, pulmonary hypertension, liver complications etc.

6. Sickle cell anemia

7. Thalassemia
 Inherited blood disorders that can result in abnormal formation of hemoglobin.
 2 types: Alpha-thalassemia and Beta-thalassemia.
 Hemoglobin consists of 4 globin chains bound to the heme molecule.
 There are 4 major types of globins: alpha (α), beta (β), gamma (γ), and delta (δ).
The dominant hemoglobin in adults (hemoglobin A) is composed of 2 alpha and 2
beta chains.
 Two minor forms of hemoglobin constitute a small percentage of normal blood:
hemoglobin F , composed of 2 alpha chains and 2 gamma chains, and hemoglobin
A2, composed of 2 alpha chains and 2 delta chains.
 A very tightly controlled globin chain production process keeps the ratio of alpha
chains to non-alpha chains at 1.00 (± 0.05).
 In thalassemia , this ratio is disrupted.
 Alpha thalassemias involve HBA1 and HBA2 genes.
 Beta thalassemias are due to mutations in HBB gene.
 Patients are always at risk of severe anemia and require lifelong transfusions.
 Iron overload: Patients have excessive iron levels in the body either from the
disease or continuous transfusions. Iron gets accumulated in tissues and causes
damage to heart, liver and endocrine system.
 Iron chelation therapy is required to manage iron overload.

9. 3)Normocytic anemia
 Common form of anemia that occurs with older age.
 Manifests with a decrease in haemoglobin and hematocrit but not MCV or MCH or
MCHC.
 Causes include:
Recent blood loss
Hemolysis
Bone marrow failure
Anemias of chronic disease
Renal failure
Endocrine disorders
Myelodysplastic anemias(Blood cancer)
 Anemias of chronic disease is a hypoproliferative anemia associated with chronic
infectious or inflammatory processes, tissue injury, or conditions that release
proinflammatory cytokines.
 The pathogenesis is based on shortened RBC survival, impaired bone marrow
response, and disturbance of iron metabolism.

10. 1)Deficiency
 Iron
 Vitamin B12
 Folic acid
 Pyridoxine
2)Central-caused by impaired bone marrow function
 Anemia of chronic disease
 Anemia of the elderly(normocytic anemia)
 Malignant bone marrow disorders
Myelodysplastic syndrome, leukaemia, aplastic anemia, multiple myeloma,
PNH(Paroxysmal nocturnal hemoglobinuria).
3)Peripheral
 Bleeding (hemorrhage)
 Hemolysis(Hemolytic anemia)

11. Hemolytic anemia
 A condition in which there is premature destruction of RBCs before their life span
of 120 days is completed and the bone marrow is not able to compensate for the
RBC loss.
 Mild anemia is asymptomatic but severe anemia can be life threatening and can
cause angina and cardiopulmonary decompensation.
 Hereditary disorders may cause hemolysis as a result of erythrocyte membrane
abnormalities, enzymatic defects, and hemoglobin abnormalities. Hereditary
disorders include the following:
 Glucose-6-phospate dehydrogenase deficiency
 Sickle cell disease
 Hereditary spherocytosis
 Acquired causes of hemolysis include the following:
 Immune disorders
 Toxic chemicals and drugs
 Antiviral agents (eg, ribavirin )
 Physical damage
 Infections [18]

12. 1)Excessive blood loss
 Recent hemorrhage
 Trauma
 Peptic ulcer
 Gastritis
 Haemorrhoids
2)Chronic hemorrhage
 Vaginal bleeding
 Peptic ulcer
 Intestinal parasites
 Aspirin and other NSAIDs
3)Excessive RBC destruction
 RBC antibodies
 Drugs
 Physical trauma to RBCs

13.  Excessive sequestration in the spleen
 Heredity
 Disorders of hemoglobin synthesis
4)Inadequate production of mature RBCs
 Deficiency of nutrients(B12, folic acid, iron, protein)
 Deficiency of erythroblasts
Aplastic anemia
Isolated(often transient) erythroblastopenia
Folic acid antagonists
Antibodies
5)Conditions with infiltration of bone marrow
 Lymphoma
 Leukaemia
 Myelofibrosis
 Carcinoma

14. 7)Endocrine abnormalities
 Hypothyroidism
 Adrenal insufficiency
 Pituitary insufficiency
8)Chronic renal disease
9)Chronic inflammatory disease
 Granulomatous diseases
 Collagen vascular diseases
10)Hepatic diseases
Paleness of skin due to iron deficient anemia

15.  Aplastic anemia is a syndrome of bone marrow failure characterized by peripheral
pancytopenia and marrow hypoplasia.
 Although often normocytic, mild macrocytosis can also be observed in association
with stress erythropoiesis and elevated fetal hemoglobin levels.
 Occurs primarily due to bone marrow failure.
 On morphologic evaluation, the hematopoietic elements in the bone marrow are
less than 25%, and they are largely replaced with fat cells.
 Symptoms:
Fatigue
Dyspnea
Paleness
Tachycardia
Frequent infections
 Mostly genetic cause

16.  Signs and symptoms depend upon the onset and cause of the anemia, and on the
individual.
Acute-onset anemia:
 Tachycardia
 Light headedness
 Breathlessness
Chronic anemia:
 Weakness
 Fatigue
 Vertigo
 Faintness
 Cold sensitivity
 Pallor
 Loss of skin tone

17. Iron-deficiency anemia:
 Glossal pain
 Smooth tongue
 Reduced salivary flow
 Pica(compulsive eating of non-food items)
 Pagophagia (compulsive eating of ice)
Vitamin B12 and folate deficiency anemia:
 Pallor
 Icterus
 Gastric mucosal atrophy
Pica

18. Glossitis

19.  Rapid diagnosis is essential because it anemia is often a sign of underlying
pathology.
 Signs and symptoms
 Complete Blood count
 Reticulocyte index
 Peripheral blood smear report
 Stool examination
 Serum iron for Iron-deficiency anemia
 TIBC(Total Iron Binding Capacity)
 Macrocytic anemias-Raised MCV(80-110 FL)
 Hypersegmented polymorphonuclear leukocytes for macrocytic anemia

20. Iron deficiency anemia:
 Oral iron therapy containing soluble ferrous iron salts which are not enteric coated and not
slow or sustained release is recommended at a daily dosage of 200 mg in two or 3 divided
doses.
 In case of dietary absorption iron is best absorbed from meat, fish and poultry and poorly
from vegetables, grain products, diary products and eggs.
 Parenteral iron is required in cases where there is malabsorption of iron from diet ,
intolerance of oral iron or non compliance. Parenteral administration however does not
hasten the hematologic process.
SALT ELEMENTAL IRON(%) ELEMENTAL IRON
PROVIDED
Ferrous sulphate 20 60-65mg/324-325 mg tab
18 mg iron/5 ml syrup
44mg iron/5 ml elixir
15 mg iron/0.6 ml drop
Ferrous sulphate(exsiccated) 30 65 mg/200 mg tablet
60 mg/187 mg tab
50 mg/160 mg tab

21. SALT ELEMANTAL IRON(%) ELEMENTAL IRON
PROVIDED
Ferrous gluconate 12 36 mg/325 mg tablet
27 mg/240 mg tab
Ferrous fumarate 33 33 mg/ 100 mg tab
63-66mg/200 mg tab
106 mg/324-325 mg tab
33 mg/5 ml suspension
Polysaccharide iron
complex
100 150 mg cap
50 mg tab
100 mg /5 ml elixir
Carbonyl iron 100 50 mg caplet

23. Vitamin B12 Deficiency anemia:
 Oral vitamin B12 supplementation is as effective as parenteral therapy.
 Oral cobalamin is initiated at 1-2 mg daily for 1-2 weeks followed by 1 mg daily.
 Parenteral therapy is more rapid acting than oral therapy and should be given if
neurologic symptoms are present.
 An intranasal gel formulation can be advantageous for patients who are homebound, have
cognitive impairment, or experience dysphagia.
 A widely used regimen is cyanocobalamin 1000 µg daily for a week, then weekly for a
month, and then monthly. When symptoms resolve, daily oral administration can be
initiated.
Folate-deficiency anemia:
 Oral folate 1 mg daily for 4 months is usually sufficient, unless the underlying etiology
cannot be corrected..
 If malabsorption is present, the daily dose should be increased to 5 mg.
Anemia of chronic disease:
 Treatment must focus on correcting reversible causes.
 Iron therapy is not effective when inflammation is present.
 Epoetin alfa is a human erythropoietin produced in cell culture using recombinant DNA
technology which stimulates erythropoiesis and facilitates formation of new RBCs.

24.  It is used in cases of anemia associated with chronic renal failure and chemotherapy.
 In case of renal failure associated anemia it is to be used only if hemoglobin levels go
<10 g/dl.
 Initial dosage is 50-100 units/kg thrice weekly.
 If no increase in hemoglobin after 6-8 weeks of administration then increase to 150
units/kg thrice weekly or in patients with AIDS to 300 units/kg weekly.
Hemolytic Anemia:
 Management consists of administration of folic acid supplements.
 Corticosteroids such as prednisone prevents phagocytosis of antibody covered RBCs and
thus is useful in autoimmune hemolytic anemia.
 Iron supplements are contraindicated in hemolytic anemia.
Thalassemia:
 Management includes administration of folic acid supplements and iron chelation
therapy.
 Iron chelating agents- Deferoxamine mesylate & Deferasirox.
 Approximately 8mg of iron is bound by 100 mg of deferoxamine from ferritin and
hemosiderin but not from transferrin and it gets excreted in urine and bile.
 Given via IM inj, SC bolus, slow infusion or continuous infusion.
 Deferasirox is available as tablet for oral suspension and it binds to iron with affinity ratio
of 2:1