2. Definition
• Defined as a decrease in circulating red blood cell mass- Hb less than 12g/dl
or Hct <36% for non pregnant women and Hb< 13g/dl or Hct <39% in men
• Anemia is basically an objective sign of disease and needs further evaluation
to determine the underlying cause and appropriate treatment.
4. ERYTHROPOIETIN
• Glycoprotein hormone
• Produced by peri tubular capillary lining of cells in kidney
• Small amount by liver
• EPO gene regulation is done by HIF 1alpha
5. RETICULOCYTES
• They are prematurely released RBCs from the bone marrow
• Appear in circulation due to EPO stimulation or bone marrow damage(fibrosis,
infiltration by malignant cells)
• Appear greyish blue due to residual ribosomal RNA
• Reticulocyte count - 1-2 %
6. CORRECTION
• RC% = (No. of reticulocytes/RBC) X 100
• First correction - CRC
• CRC = (Hb/15) x RC OR (Hct/45)x RC
• This is done to correct reticulocyte count based on the reduced number of
RBCs
7. Second correction
• This is done if there are polychromatophilic macrocytes
• They are known as shift cells - prematurely released reticulocytes
• CRC/2 (correction factor can be 1-3)
• This is known as reticulocyte production index (RPI)
8. CLASSIFICATION
• ETIOLOGICAL-
• Blood loss - acute and chronic
• Decreased RBC production
• Increased RBC destruction (Hemolysis)
• MORPHOLOGICAL
• Microcytic when MCV is less than 80fl
• Normocytic-MCV IS 80-96 fl
• Macrocytic - MCV more than 96fl
8
10. HISTORY
• Acute -Patient with abrupt onset of anemia tolerate diminished RBC mass
poorly.Experience symptoms of fatigue, malaise, dyspnea, syncope angina
• Chronic anemia are usually less symptomatic.Experience symptoms with
increased activity or exertion.
• CVS AND PULMONARY FEATURES-
• Exertional fatigue,
• dizziness, palpitations
• Angina
• Symptoms of cardiac failure
11. • GI FEATURES
• occult bleeding (Malena)
• PICA (consumption of substances of no nutritional value like ice, clay)
• Dysphagia in pernicious anemia
12. • CNS FEATURES
• Peripheral neuropathy,paresthesia,seizures (Vit B12 def )
• confusion
• dementia
• Restless leg syndrome (IDA)
13. • OBSTETRIC AND MENSTRUAL HISTORY- symptoms of menorrhagia
• PAST HISTORY- GI surgery ,gastric atrophy, renal disease,rheumatologic
disease, history of blood transfusion
• Hookworm infection
• FAMILY HISTORY - hemoglobinopathies
• DRUG INTAKE -
• DIETARY INTAKE- vegetarian/non vegetarian,PICA
• Symptoms suggestive of other cytopenias like bruising,recurrent infections
14. PHYSICAL EXAMINATION
• Vitals - PR and BP
• HEAD TO FOOT EXAMINATION
• Pallor- Is examined at lower palpebral conjunctiva, palms, tongue, mucous
membrane of mouth, Nail bed skin
• scleral icterus- haemolytic anemia
• Glossitis - pernicious anemia
• lymphadenopathy
• Sternal tenderness
15. • Koilonychia - iron defieciency anemia
• Petechia in skin- suggests of bone marrow failure or anemia due to bleeding disorde
• Chronic leg ulcers- sickle cell anaemia, hereditary spherocytosis
• THALASSEMIA FEATURES
16.
17. • knuckle hyperpigmentation-
• CVS
• signs of congestive cardiac failure
• flow murmur
• RESPIRATORY SYSTEM
• Wheeze in acute chest syndrome
• PAH due to vascular occlusion in sickle cell anaemia
18. • CNS
• Ataxia
• decreased vibratory and position sense
• GIT
• Splenomegaly- extra medullary hematopoiesis
22. IRON DEFICIENCY ANEMIA
• Mcc of anemia
• usually chronic with a low reticulocyte count
• causes-1.Increased iron loss -GI loss, menses, hookworm infection,
• 2. decreased iron intake or absorption - bariatric surgery, gastrectomy,
crohn’s disease, celiac disease
• 3. increased iron requirement - pregnancy, rapid growth in infancy or
adolescence
• 4.Drugs - glucocorticoids,NSAIDs,proton pump inhibitors
24. LAB
• S Fe and TIBC
• S Ferritin low
• Bone marrow iron stores
• Red cell protoporphyrin levels
• S levels of transferrin receptor protein
25.
26. • DIAGNOSTIC TESTS
• Bone marrow biopsy shows absent staining to iron is the definitive test to
diagnose
• ID IS NOT THE FINAL DIAGNOSIS, IT IS INDICATIVE OF AN UNDERLYING
ETIOLOGY
27. TREATMENT
• Oral iron therapy -
• ferrous sulphate is the most common prescribed formulation
• Dosage - 100-200mg of elemental iron per day (50mg/day)
• with normal bone marrow and normal EPO stimulus this results in RBC production of
• 2-3 times of normal
• Goal of treatment is to correct anemia +0.5-1g for stores
• Duration is 6-12 months
28. • Reticulocyte response begins in 4-7 days
• Reticulocyte response peeks in 1-1.5 weeks
• Increase in Hb 14-21 days
• Normal iron stores 4-5 months
• Absence of response – rule out compliance , absorption issues
29. • Parenteral iron therapy -
• Indications-
• Inadequate response to oral iron
• poor absorption
• intolerance to oral preparation
• Need for rapid response
• Persistant bleeding
• GI causes- bariatric surgery,celiac sprue
• Organ dysfunction - CKD,
30. • Total iron requirement-
• MODIFIED GANZONI FORMULA- weight x (15-hb) x 2.4+ 500
• IV PREPARATIONS
• First generation- iron dextran
• Second generation - iron sucrose, ferric gluconate
• Third - ferumoxytol,ferric carboy maltose, iron isomaltoside
31. • RED CELL TRANSFUSION
• Indications
• severe anemia with hemodynamic instability
• excessive blood loss which needs an immediate intervention
• ADVANTAGES
• can correct anemia acutely
• transfused RBC provide a source of iron for reutilisation
33. THALASSEMIA
• Inherited disorders characterised by reduced Hgb synthesis associated with
mutations in either alpha or beta gene of molecule
• BETA THALASSEMIA - decreased production of beta globin chain that results
in excess alpha globin chain synthesis forming insoluble alpha tetramers
which leads to ineffective erythropoiesis
• ALPHA THALASSEMIA - Due to deletion of one or more alpha globin chains
leading to beta globin excess
34. • DIAGNOSIS
• Peripheral smear - microcytic hypochromic RBCs with target cells, tear
drop cells (s/o extra medullary heamtopoiesis)
• DIAGNOSTIC -Hgb electrophoresis ( increased percentage of Hgb A2
and HgbF )
• For alpha thalassemia - alpha globin gene analysis
35. • TREATMENT
• In severe forms of the disease- RBC transfusions done to maintain an Hb level o
• coupled with oral iron chelation to prevent accumulation of iron
• Repeated transfusions can lead to iron overload
• Iron chelation therapy is indicated when ferritin is consistently >1000 ng/ml
oral - deferasirox,deferiprone
IV- deferoxamine
• Hydroxyurea - to increase HgbF
36. • To improve ineffective erythropoiesis - Luspatercept (enhances late stage
erythropoiesis) given s/c 1mg/kg every 3 weeks
38. SIDEROBLASTIC ANEMIA
• Characterised by abnormal iron metabolism associated with the presence of ring
sideroblasts in the developing RBCs
• ETIOLOGY
• ACQUIRED
• Primary sideroblastic anemia (MDS)
• Secondary sideroblastic anemia is caused by
• drugs like chloramphenicol,cycloserine,ethanol,isoniazid,
• lead and zinc toxicity
• HEREDITARY
• X linked-ALA synthetase deficiency
39. • Fe profile - all increases except TIBC
• Peripheral smear - Papenheimer bodies- siderocyte stained with ramonowsky
stain due to non heme iron deposition
• Marrow iron stores increase
Investigations
44. MACROCYTIC ANEMIA
• Group of disorders characterised by presence of distinctive morphological
appearances of developing red cells in bone marrow.
• Can be
1. Megaloblastic - nuclear maturation defect
2. Non megaloblastic - nuclear maturation normal
45. • MEGALOBLASTIC NON MEGALOBLASTIC
• Nuclear maturation defect Normal
• CAUSES
• VIT B12 deficiency- chronic liver disease
• Pernicious anemia, thyroid diseases
• nutritional deficiency drugs
• Folate deficiency - dietary,antifolates
• Folate deficiency- mcc is dietary deficiency,
48. DIAGNOSIS
• MCV high
• Earliest PS finding is macro ovalocyte
• PS- anisocytosis,poikilocytosis
• hypersegmented neutrophil (>5 lobes)
• leucopenia due to decrease in granulocyte and lymphocyte
• BONE MARROW - hypercellular with accumulation of primitive cells
• megaloblasts
• giant band forms
• enlarged hyperploid megakaryocyte are characteristic
51. COBALAMIN DEFICIENCY
1. S.cobalamin - normal range -148-738pmol/l
2. S MMA - used for early diagnosis of cobalamin deficiency
3. S Homocysteine -high in both early cobalamin and folate deficiency
53. TREATMENT OF B12 AND FOLATE DEFICIENCY
• B12 for replenishing stores - 1000mcg IM inj at 3-7 day interval for 8 weeks.
• Maintenance dose - 1000mcg IM monthly
• oral doses 50mcg daily
• Folate - 5 to 15 mg FA daily at least 4 months till all folate deficient cells are
replaced
• Folinic acid - mtx/DHF reductase inhibitors
54. In megaloblastic anemia ,when only FA is corrected,
• Anemia is corrected due to tetrahydrofolate formation from FA .
• Neurological manifestations worsen as methionine
is not formed ( methyl B12 absent)
55. HEMOLYTIC ANEMIA
• There is premature destruction of RBC so to compensate there is increase in
production capacity of RBCs by bone marrow
• When the rate of production exceeds the bone marrow capacity of producing
more will manifest as haemolytic anemia
