ANEMIA

Dr. Dileep Kumar

Lecturer of Physiology
SMC, JSMU
Definition
 Decrease in either the hemoglobin (Hb) or the
volume of RBCs → oxygen-carrying capacity.

 Anemia is defined as decrease in the circulating red

blood cell mass
<12 g/dL [hematocrit {Hct} <36%] in women
<14 g/dL [Hct<41%] in men
 Most common hematologic disorder

 Rather sign than a disease itself

Etiology

 RBC Loss (without RBC destruction)

 Deficient RBC production

 Increased RBC destruction

RBC Loss (without RBC Destruction)

Hemorrhage
◼ Trauma

◼ Disorders: e.g. cancer, ulcers, IBD

Menstrual flow
Gynecological disorders (e.g. endometriosis, fibroids)
Pregnancy (especially at gestation)
Parasitism
◼ Hookworms
Deficient RBC Production

➢ Neoplasia ➢ Iron Deficiency

➢ Leukemia ➢ Aplastic anemia

➢ Metastasis to bone ➢Chloramphenicol

marrow administration
➢ Renal disease (lack of
➢ Osteogenic sarcoma
erythropoietin production)
➢ Myelofibrosis
➢Increased RBC
➢ Pernicious anemia
destruction over
erythropoiesis
Increased RBC Destruction
Intrinsic Abnormalities
◼ Thalassemia
◼ G6PD
◼ Sickle Cell Anemia

Extrinsic Abnormalities
◼ Infections
◼ Malaria(Plasmodiumm species)
◼ Mycoplasma

◼ Lead poisoning
 Normal RBC's
Zone of central pallor about 1/3 the size of the
RBC
➢ Smaller RBCs
➢Increased zone of central pallor →hypochromic microcytic
anemia.
Right Arrow→ RBC with a malarial parasite in the
shape of a ring. Three other RBC's in this
smear are also infected with a ring trophozoite.
Arrow at left is a gametocyte of P vivax.
Classification
- Based on Morphology
 Macrocytic Anemia – vit B12, folate deficiency
 Microcytic Hypochromic – IDA, sickle cell anemia
 Normocytic – recent blood loss, hemolysis, renal
failure

- Based on Etiology
- Based on Pathophysiology
 Hematological Tests

 Complete blood count (CBC) or Complete Blood

Examination (CBE) is routinely ordered test

 Helps in diagnosis of multiple haematological

disorders
Routine Tests
 RBC count
 WBC count
 Hemoglobin (Hb)
 Hematocrit (Hct)
 RBC indices (specifically assess RBCs)
◼ Mean cell volume (MCV)
◼ Mean cell hemoglobin (MCH)
◼ Mean cell hemoglobin concentration (MCHC)
RBC count:
Male: 4.6 to 6.2 X106 cells /mm3
Female: 4.2 to 5.4 X106 cells /mm3

WBC count:
5000 to 10,000 cells /cu mm of blood

Hemoglobin (Hb):
Male: 14 to 18g/dl
Female: 12 to 16g/dl
Hematocrit (Hct) / Packed cell volume (PCV):

Volume of erythrocytes / L of whole blood indicating

the proportion of plasma and red cells.

Range:
Male: 42 to 52 %
Female: 37 to 47%
Mean cell volume (MCV):
Repesents average volume of RBCs
MCV = Hct / RBC count
Range:
Male: 80 to 96 fl (femtolitres – 10 -- 15)
Female: 82 to 98 fl
Mean cell hemoglobin (MCH):

It is the percent volume of Hb per RBC

Derived by dividing Hb by RBC count
Range: 27 to 33 pg /cell [picograms = 10 –12]
True increase in folate deficiency & decrease
in iron deficiency
A low MCH corresponds with hypochromic
RBCs - as seen in iron deficiency anaemia
Mean cell hemoglobin concentration (MCHC):

Is derived by dividing Hb by Hct

Range: 31 to 35 g/dl

Iron deficiency is the only anaemia in which

the MCHC is low
Reticulocytes:

Gives indirect measurement of RBC

production

Range: 0.5 to 2.5 % of RBCs

Peripheral Blood Smear
 Gives information on functional status of bone
marrow

 Information on anisocytosis, poikilocytosis

Serum Iron (50-100mcg/dL)

 Concentration of iron bound to transferrin

 Shows diurenal variation (20 – 30%)
 20 – 25 % day to day variation
 Decreases in infection and inflammation
 Best interpreted with TIBC
 in IDA, ACD
 in hemolytic anemias, iron overload
Ferrtin

 Cellular storage protein for iron

 Stores upto 4500 atoms of iron
 Accsessed for metabolic needs
 Plasma level reflects overall iron storage
 1 ng/mL → 10 mg of total iron stores
 50 – 100 ng/ mL
 <10 -15 ng/mL → specific for IDA
 Inc Ferritin → iron overload state
TIBC (250 – 400 mcg%)
 Indirect measurment of iron binding capacity of
serum transferrin

 TIBC (Total Iron Binding Capacity) when

body iron stores are low

 Low serum iron and TIBC → IDA

 Actual measurement of protien, serum

transferrin
IRON DEFICIENCY ANEMIA
 Iron deficiency is the most common nutritional
deficiency in developing and developed
countries.
 More than 500 million people worldwide are
estimated to have IDA
 IDA is a leading cause of infant morbidity and
mortality
 children younger than 2 years, adolescent
girls, pregnant females, and elderly older than
65 years are at risk
BODY IRON DISTRIBUTION

Metabolically Active Iron

 Haemoglobin
 “Serum” iron bound to a protein transferrin
in blood
 Tissue Iron: in cytochromes and enzymes
 Myoglobin: oxygen reserve in muscles
Storage Iron

 Ferritin: found in blood, tissue fluids, and

cells

 Haemosiderin: found in macrophages

and assessed by staining bone marrow
with Prussian Blue stain
Food content of Iron &
absorption

12 – 15
6 1 mg of
2000 - mg of
mg/1000 10% elemental
2500 Kcal elemental iron
Kcal iron
Etiology
 Results from imbalance between physiologic
iron need and supply
 Situations that increase the demand for iron
are frequent blood donations, participation in
endurance sports, menstruation, pregnancy
and lactation, infancy, and adolescence
 Occult blood loss from a single gastrointestinal
lesion has been shown to be a frequent cause
of “idiopathic” IDA
 Increased demand for iron and/or
hematopoiesis
 Rapid growth in infancy or adolescence
 Pregnancy
 Erythropoietin therapy
 Increased iron loss
 Chronic blood loss
 Menses
 Acute blood loss
 Blood donation
 Phlebotomy as treatment for polycythemia
vera
 Decreased iron intake or absorption
 Inadequate diet
 Malabsorption from disease (sprue, Crohn’s
disease)
 Malabsorption from surgery (post-gastrectomy)
 Acute or chronic inflammation
Pathophysiology
 Risk of iron deficiency is related to levels of iron
loss, iron intake, iron absorption, and physiologic
demands
 The margin between the amount of iron available
for absorption and the body’s iron requirement is
narrow for growing infants and female adults
 Manifestations of iron deficiency occur in three
stages:
Prelatent
Latent
IDA
Laboratory Findings
 Low serum iron and ferritin levels and high
TIBC
 In early stages, RBC size is not changed. Low
ferritin concentration is the earliest and most
sensitive indicator
Renal or hepatic disease, malignancies, infection,
or inflammatory processes may increase ferritin
values
 In the later stages of IDA, Hb and Hct →
microcytic hypochromic anemia develops
preceded with Microcytosis
 Low Transferrin saturation values likely
indicate IDA
low serum transferrin saturation values also may
be present in inflammatory disorders
 TIBC usually helps to differentiate the
diagnosis TIBC >400 mcg/dL → IDA, values
<200 mcg/dL → inflammatory diseases
 With continued progression of IDA,
anisocytosis occurs and poikilocytosis
develops
Treatment
 The severity and cause of IDA determines the
approach to treatment
 Dietary supplementation and administration of
therapeutic iron preparations
 Iron is poorly absorbed from vegetables, grain
products, dairy products, and eggs
 Best absorbed from meat, fish, and poultry
 Different formulations

General recommendation is administration of approx 200 mg

of elemental iron daily, in 2 or 3 divided doses to maximize
Parentral preparations
 Poor enteral absorption, continued blood loss,
intolerance to oral iron – prompts for parentral
therapy
 Dose (mL) = 0.0442 (Desired Hb - Observed
Hb) x LBW + (0.26 x LBW)
 For males: LBW = 50 kg + 2.3 kg for each inch
of patient’s height over 5 feet
For females: LBW = 45.5 kg + 2.3 kg for each
inch of patient’s height over 5 feet
Preparations
 Iron dextran
Anaphylaxis noted in 1 out of 300 patients
25mg of test dose in 50 mL normal saline
Proceed if no reaction in 1 hour
Pain and brown staining at injection site, flushing,
hypotension, fever, chills, myalgia, Anaphylaxis
 Ferric Gluconate
Administered as 10 mL (125 mg of elemental iron)
in 100 mL normal saline intravenously over 1 hour
cramps, nausea, vomiting, flushing, hypotension,
intense upper gastric pain, rash, and pruritus.
Monitoring Patient’s Response

 in reticulocyte begin in 3rd or 4th day of therapy

 in reticulocyte peak in 7th or 10th day of therapy
 By second week of therapy reticulocyte will back
to normal
 Hemoglobin increased by 2 gm/dL, Hematocrit
increased by 6% Within 3 weeks
 Anemia is resolved within 2 months
 Another 3-6 months of Iron therapy