The document discusses various types of anemia including their causes, symptoms, diagnostic tests, and treatment. It covers iron deficiency anemia, thalassemia, sickle cell anemia, hereditary spherocytosis, megaloblastic anemia, and aplastic anemia. The key signs and findings for each type are outlined along with recommended treatment approaches.

1. Anaswara P R
Roll no: 18

2.  Anemia is present when the hemoglobin level is more two standard deviations below
the mean for child age and sex.
 According to third NATIONAL FAMILY HEALTH SURVEY (NHFS3), 79% of Indian
children have anemia, including 71% of urban children and 84% of rural areas.
 Anemia refers to reduction in oxygen carrying capacity of blood leading to tissue
hypoxia.
 Decreased production and increased breakdown of RBC can lead to anemia

4. • The 2 major categories are decreased production and increased destruction or
loss.
• Decreased RBC production may be a consequence of ineffective erythropoiesis or a
complete or relative failure of erythropoiesis
• Increased destruction or loss may be secondary to hemolysis, sequestration, or
bleeding.
• The peripheral blood reticulocyte percentage or absolute number will help to
make a distinction between the 2 physiologic categories.

5. • The normal reticulocyte percentage of total RBCs during most of childhood is
approximately 1%, with an absolute reticulocyte count of 25,000-75,000/mm3.

6.  1. SIZE
 NORMOCYTE – NORMAL SIZE ( MCV = 75FL )
 MICROCYTE. – SMALL SIZE ( MCV <75 FL )
 MACROCYTE – LARGE CELLS ( MCV > 105 FL )
 2. SHAPES
 ANISOCYTOSIS – variation in size
 POIKILOCYTOSIS – variation in shape
 SPHEROCYTE – small round cells.

7.  NORMOCYTIC ANEMIA
 ACUTE BLOOD LOSS
 CHRONIC DISEASES
 HYPOPLASTIC ANEMIA – DEC. RBC PRODUCTION
 HEMOLTYTIC ANEMIA ( G6PD, AHA )
 MICROCYTIC ANEMIA
 IRON DEFICIENCY ANEMIA
 HEMOLYTIC ANEMIA ( thalassemia , hereditary spherocytosis )
 CHRONIC DISEASES
 MACROCYTIC ANEMIA
 HEMOLYTIC ANEMIA ( CHRONIC HEMOLYSIS )
 FOLIC ACID DEFICIENCY
 VITAMIN B12 DEFICIENCY

8.  Pallor – in nail beds, oral mucous membrane and conjunctiva.
 Fatigue & generalized muscular weakness
 Anorexia, irritability & inadequate school performance
 Dysnoea on excertion, palpitation , tachycardia
 Nervous system symptoms include dizziness , headache,humming in
ears,tinnitus,lack of concentration.

9.  . 1. AGE
 . Neonate – neonatal blood loss, fetomaternal hemorrhage, haemolytic disorders.
 CHILDHOOD 6m-2yr = nutritional anemia
 After 4-6m beta thalassemia
 Adolescent growth spurt,menstruating & pregnant teens
 . 2. SEX
 ⚫ X linked diseases will be seen in male
 ⚫ include G6PD deficiency and PK deficiency
 . 3. FAMILY HISTORY
 ⚫ all hemoglobinopathies and thalassemia syndromes are inherited in AUTOSOMAL
DOMINANT condition.
 • Spherocytosis is inherited as autosomal dominant

10.  4. DIET HISTORY
 ⚫Iron deficiency develops when there is poor breast fooding and improper time
and quality of weaning food, both of which are exaggerated by bottle feeding
⚫Pica is both an effect and a cause of iron deficiency besides seen in lead pisoning
 ⚫ Megaloblastic anemia is due to folate deficiency is common in those villagers
who consume a lot of goat milk
 5.DRUG HISTORY
.

11.  -7. INFECTION AND INFESTATION HISTORY
 ⚫ G6PD deficiency induced hemolysis can be precipitated by many inf. And drugs to
treat such inf.
 ⚫ Hemolysis could also be induced by malaria.
 ⚫Bone marrow suppression can occur following many viral infections, kala Azar,
fulminant sepsis or drugs
 ⚫ Nutritional anemia can be precipitated by worms due to worms due to
malabsorption, nutrients deficiency and micro bleeding especially in hook worm
infestations.

12.  Dysmorphic features – congenital hypoplastic anemia and chronic haemolytic
anemia
 Jaundice. - hemolysis
 Tongue( atrophy of papillae)
 Purpura or bleeding – thrombocytopenia
 Kilonychia – severe iron defeciency
 Lymhadenopathy – leukaemia and lymphoma
 Splenomegaly – hemolysis, leukaemia and lymphoma

13.  CBC ( hb, hematocrit, MCV, MCH,MCHC,TLC, DLC,platelets )
 Peripheral blood film (microcytic, normocytic, macrocytic)
 Reticulocyte count – high (hemolysis), low (hypoplastic)
 ESR ,CRP( CHRONIC DISEASE AND INFLAMMATION)
 Serum ferritin, serum iron
 Hemoglobin electrophoresis ( hemoglobinopathies )
 Bone marrow examination ( leukemia )

15.  Decrease in total iron body content severe enough to diminish erythropoiesis.
 Laboratory diagnosis:
 Periheral smear: microcytic,hypochromic red cells with
anisocytosis,poikilocytosis ,increased RDW
 MCV,MCHC reduced
 Serum iron ,serum ferritin reduced,TIBC increased

16.  TREATMENT
 Oral iron 3-6 mg/kg/day,should be taken on empty stomach or in between meals.
 Parenteral iron : indications-
1. Intolerance to oral iron
2. Malabsortive states
3. Ongoing blood loss
 Total dose (mg)=(target Hb-actual Hb)x weight in kgx2.4+[15xweight(kg)]

17.  Laboratory findings
 Hb level ranges from 2-8g/dl
 MCV & MCH significantly low
 Reticulocyte count elevated to 5-8%
 PS shows hypochromasia,microcytosis
Polychromatophilia, nucleated RBCs,basophilic stippling
 HPLC shows absence of HbA & high levels of HbF,elevated HbA2

18.  MANAGEMENT
 Genetic counselling
 Hematopoietic stem cell transplantation
 Blood transfusion at an early age
 Chelation therapy for accumulated iron overload.
 Normal diet with following suplements- folic acid small doses of ascorbic acid (vit
C) & alpha –tocopherol(vit E).

19.  Laboratory findings
 Anemia & thrombocytosis are common
 Leukocytosis
 On PS sickle shaped cells,target cells found
 Presence of Howell-Jolly bodies indicates functional asplenia.
 Indirect bilirubin elevated due to hemolysis.
 Hemoglobin electrophoresis.

20.  Management
 Hospital management:
 Hydration & analgesia
 Blood transfusion in aplastic &
sequestration crisis.
 Oxygen supplementation in hypoxia
 Intubation & mechanical ventilation
if CVA has occurred.
 Preventive care:
 Penicillin or Amoxicillin prophylaxis
until 5 yrs.
 Pneumococcal,meningococcal &
hemophilus vaccines
 Lifelong folate supplements
 Hydroxyurea,10-15mg/kg /day
 Genetic counseling

22.  Laboratory findings:
 Anemia is normocytic normochromic
 Increased reticulocyte count
 Spherocytes & nucleated red cells in PS
 Positive direct coombs test
 Increased lactic dehydrogenase,indirect & total biliruin,aspartate
aminotranserase & urinary uroilinogen

23.  MANAGEMENT
 Supportive care
 Prednisolone 1mg/kg for 4 weeks,tapered over 4-6 months.
 In severe cases immunosuppressive agents like corticosteroids, aathioprine
,cyclosporines are used.
 Intravenous immunoglobulins ,splenectomy or hematopoetic stem cell
transplantation can be done in refractory cases.

25.  Laboratory findings
 CBC shows macrocytosis and cytopenias,hypersegmented neutrophils.
 Reticulocyte count
 Serum b12 and folate level
 Bone marrow cellular & show RBC precursor nuclear-cytoplasmic asynchrony.
 Serum chemistry :elevated LDH & bilirubin.

26.  TREATMENT
 Folate supplementation,1-5mg/day for 3-4 weeks.
 Parenteral vit B12 1mg IM
 In patients with pernicious anemia & malabsorptive states vit B12 1mg IM daily
for 2 weeks then weekly until the hemocrit value & monthly for life.
 Dietary counselling

27.  Hematopoietic stem cells are damaged by various mechanisms:
1. Acquired stem cell injury from viruses ,toxins or chemicals
2. Abnormal cellular control of hematopoiesis
3. Abnormal marrow environment
4. Immunologic suppression of hematopoiesis
5. Mutation in genes resulting in inherited bone marrow failure

28. Laboratory findings
 Pancytopenia
 PS shows macrocytic anemia
,thrombocytopenia & agranulocytosis
 Corrected reticulocyte count <1%
indicates reduced RBC production.
 Bone marrow aspirate & biopsy
shows reduced cellularity.
Management
 Supportive care: packed red cells for
anemia,platelets for
thrombocytopenia & antibiotics for
infection
 HSCT is the only curative therapy.