this presentation includes a clinical approach to anemia .

1. ANEMIA

11. DEFINITION
↓ RBCs Count Or
Hb Content Or
Packed red cell volume (HV)

12. ETIOLOGY

13. ↓ RBCs PRODUCTION
 Iron
 Folic acid
 Vit. B12
 EPO
 Thyroxin
 Androgen

14. Aplastic anemiaSTEM CELLS
 Megaloblastic anemia
 Sideroblastic anemia
ERYTHROBLASTS
Myelodyplasia - Myelofibrosis - Tumor infiltration.INFILTRATION
 Drugs(chloramphenicol, sulphonamides, Carbimazole)
 Irradiation  Chemotherapy
SUPPRESSION

15. ETIOLOGY
↓ PRODUCTION
BLOODLOSS
DESTRUCTION

16. BLOODLOSS
trauma, melena, hematemesis,
menometrorrhagia
OBVIOUS
BLEEDING
Slowly bleeding ulcer or carcinomaOCCULT
BLEEDING
repeated diagnostic testing , hemodialysis
losses, excessive blood donation
during surgical procedures
IATROGENIC

17. ETIOLOGY
↓ PRODUCTION
BLOODLOSS
DESTRUCTION

18. DESTRUCTION

19. EXTRAVASCULAR DESTRUCTION OF RBCs
INTRINSIC RED BLOOD CELL DEFECTS
Enzyme deficiencies (eg, G6PD)
Hemoglobinopathies (eg, sickle cell disease, thalassemias)
Membrane defects (eg, hereditary spherocytosis)
EXTRINSIC RED BLOOD CELL DEFECTS
Liver disease
Hypersplenism
Infections (eg, malaria)
Oxidant agents (eg, dapsone, nitrites, aniline dyes)
Other agents (eg, lead, copper, snake and spider bites)
Autoimmune hemolytic anemia (warm- or cold-reacting, drugs)
IVIG infusion

20. INTRAVASCULARDESTRUCTION OF RBCs
Microangiopathy (eg, aortic stenosis, prosthetic valve)
Transfusion reactions (eg, ABO incompatibility)
Infection (eg, severe malaria)
Paroxysmal cold hemoglobinuria.
Paroxysmal nocturnal hemoglobinuria
IV infusion with hypotonic solutions

21. MORPHOLOGIC APPROACH

22. MICROCYTIC ANEMIA: MCV <80 FL
Iron deficiency anemia
Thalassemic disorders (# Globin)
Anemia of inflammation/anemia of chronic
disease (late)
Sideroblastic anemia (eg, congenital, lead,
alcohol, drugs; uncommon) (# Heme)

25. NORMOCYTIC ANEMIA (MCV 80 : 100 FL)
Acute blood loss
Iron deficiency anemia (early)
Anemia of inflammation/anemia of chronic disease
Bone marrow suppression (may also be macrocytic)
Bone marrow invasion  Aplastic anemia
Chronic renal insufficiency
Endocrine dysfunction (Hypothyroidism – Hypopituitarism)

26. MACROCYTIC ANEMIA: MCV >100 FL
Alcohol abuse
Folate deficiency
Vitamin B12 deficiency
Myelodysplastic syndromes
Acute myeloid leukemias.
Reticulocytosis (Hemolytic anemia - Response to blood loss -
Response to appropriate hematinic (eg, iron, B12, folic acid)
Drug-induced anemia (eg, Hydroxyurea, AZT, chemotherapeutics)
Liver disease

30. APPROACH
(A) (B)
(C)

31. MAJOR QUESTIONS?
•Is the patient bleeding (now or in the past)?
•Is there evidence for increased RBC destruction (hemolysis)?
•Is the bone marrow suppressed?
•Is the patient iron deficient? If so, why?
•Is the patient deficient in folic acid or vitamin B12? If so, why?

32.  Age,
 Gender,
 Race,
 Family history
 Menstrual history
 Dietary history
 Occupational history

34. Etiology (tarry stools - ulcer-type pain, R.A, R.F)?
Urine color ?
Stool (float – color ? – Bulk – offensive ? – easily
flushed ?) Malabsorption
Fever ?
Drug history

36. B12 DEFICIENCY ?
•Early greying of hair
•Loss of proprioception ?
•Sore tongue

38. APPROACH
(A) (B)
(C)

39. Pallor (conjunctivae, nail beds, face, Palms)
Jaundice
Weight loss
Lymphadenopathy
Lower Limb edema
Arthritis (Felty’s syndrome)
GENERAL

40. Hypothyroidism
Splenomegaly – hepatomegaly
Bone tenderness (sternum- low
back)
Koilonychias
Angular stomatitis - glossitis
GENERAL

41. Ecchymosis.
Piles.
Early greying of hair (B12 ↓)
Cardiac examination (enlarged – S3 –
Murmur ?)
GENERAL

43. APPROACH
(A) (B)
(C)

44. CBC

45. CBC
FemaleMale
< 36 %< 41 %

46. CBC
> 10080 - 100< 80
MacrocyticNormocyticMicrocytic
Values in excess of 115 fL are almost exclusively
seen in vitamin B12 or folic acid deficiency

47. CBC
HighLow
MacrocyticMicrocytic

48. CBC
HighLow
H.S. – SCA↓ MCV & MCH

50. CBC
0.5% to 2.5%

51. CBC
Good BM response to Hemolysis or blood
loss
 Anemia +  Retics
↓ BM response e.g. Iron ↓ - Renal failure Stable anemia + ↓ Retics
Aplastic crisis (Parvovirus B19) – BM failure Hemolytic anemia + ↓ Retics
Aplastic anemia ↓ Retics + Pancytopenia
Pure red cell aplasia
 ↓ Retics + Anemia + Normal
platelets & WBCs

52. CBC
  neutrophils: Bacterial infection
  monocytes: myelodysplasia
  eosinophils: parasitic infections
Anemia
+
Leucocytosis
 bone marrow suppression or
replacement, hypersplenism, or
 deficiencies of B12 or folate
Anemia
+
Leucopenia

53. CBC
Bone marrow suppression or
replacement,
Hypersplenism, or
 Deficiencies of B12 or folate
Anemia
+
Thrombocytopenia
Infection
Essential thrombocytosis
Iron deficiency anemia
Anemia
+
Thrombocytosis

54. CBC
HYPERSPLENISMAPLASTIC ANEMIA
Hyperplastic bone
marrow
Aplastic bone
marrow

55. CBC
 RDWNormal RDW
 Early iron, vitamin B12, or
folate deficiency
 Dimorphic anemia (Iron &
folate deficiency)
 Anemia of chronic disease
 Acute blood loss or hemolysis
 Anemia of renal disease
Normocytes
 Iron deficiency
 Sickle cell-β-thalassemia
 Anemia of chronic disease
 Heterozygous thalassemiaMicrocytes
 Folate or vitamin B12 ↓
 Aplastic anemia
 Chronic liver diseaseMacrocytes

56. BLOOD SMEAR

57. BONE MARROW EXAMINATION
 PANCYTOPENIA.
 PRESENCE OF ABNORMAL CELLS IN CIRCULATION, e.g. BLASTS.
 MEGALOBLASTIC ERYTHROPOIESIS (FOLATE OR B12 DEFICIENCY),
 ABSENCE OF RBC PRECURSORS (PURE RED CELL APLASIA)

58. ↓ HB
Iron studies

67. CONDITION SERUM IRON TIBC FERRITIN COMMENT
Iron deficiency ↓ ↑ ↓ Responsive to iron
Chronic inflammation ↓ ↓  Unresponsive to iron
Thalassemia major ↑ N N
Reticulocytosis and indirect
bilirubinemia
Thalassemia minor N N - ↓ N  fetal Hb & Hb A2, target cells
Lead poisoning N N N Basophilic stippling of RBCs
Sideroblastic anemia ↑ N  Ring sideroblasts in marrow
Hemoglobin N N N Hemoglobin electrophoresis

68. ↓ HB
RETICS

70. ↓ HB
BM