ANEMIA

Joshi Nihar G.
Anaemia refers to a state in which the
level of haemoglobin in the blood is
below the reference range appropriate
for age and sex.
Other factors including pregnancy and
altitude also affect haemoglobin level.

Joshi Nihar G.
 CAUSES OF ANEMIA
Lack of iron, vitamin B12 , or folate
Hypoplasia/ myelodysplasia
Invasion by malignant cell
Renal failure
Anemia of chronic disease
Blood loss
Haemolysis
hypersplenism
Joshi Nihar G.
 CLINICAL ASSESSMENT
Iron deficiency anemia is the most common type of anemia
worldwide
A dietary history should assess the intake of iron and folate
Past medical history may reveal a disease that is know to
be associate with anemia
Family history and ethnic background may raise suspicion
of haemolytic anemia
A drug history may revel the ingestion of drug that causes
blood loss( eg., aspirin, sulphonamides,chloramphenicol)

Joshi Nihar G.
 EXAMINATION
Conjunctiva- pallor, jaundice
Mouth- lips : angular stomatitis, telangiectasia
gum hypertrophy, Tounge : colour, smoothness,
Buccal mucosae : petechia, tonsils
Hands- perfusion, telangectasia, skin crease
pallor, koilonchia
Fundi- hyperviscosity, engorged veins,
papilloedema, haemorrage

Joshi Nihar G.
 Skin- purpura, brusing
 Abdomen- masses, ascites, hepatomegaly,
splenomegaly, inguinal and femoral lymph nodes
 Joints- deformity, swelling, restricted movement
 Feet- peripheral circulation, toes : gangrene
 General observation- colour : pallor, plethora,
breathlessness
 Tachycardia
 Raised jugular venous pressure
 Ankle oedem, flow murmurs
 Postural hypotension
 Tiredness, lightheadedness
Joshi Nihar G.
Joshi Nihar G.
 INVESTIGATION
Schemes for investigation of anemia are most
often based on size of red blood cells, which is
most accurately indicated by MCV in the FBC.

Joshi Nihar G.
Commonly in presence of anemia :
 A normal MCV (normocytic anaemia)
suggests either acute blood loss or the
anaemia of chronic disease, also known as the
anaemia of inflammation
 A low MCV (microcytic anaemia) suggests
iron deficiency or thalassaemia
 A high MCV (macrocytic anaemia) suggests
vitamin B12 or folate deficiency or
myelodysplasia
Joshi Nihar G.
How to interpret white blood cells result??
Neutrophils
Neutrophilia : infection( bacterial, fungal),
trauma, infarction, inflammation, malignancy,
exercise, pregnancy
Neutropenia : infection (viral, bacterial), drugs,
autoimmune, alcohol,, bonemarrow infiltration,
Congenital

Joshi Nihar G.
Eosinophils
Eosinophilia : allergy, infection (parasitic), drug
hypersesitivity, vasculitis, malignancy, primary
bone marrow disorder
Basophils
Basophilia : myeloproliferative
disease,inflammation
Monocytes
Monocytosis : infection (bacterial),
inflammation, malignancy
Joshi Nihar G.
Lymphocytes
Lymphocytosis : infection (viral,
bacterial),lymphoproliferative disease, post
splenectomy
Lymphopenia : inflammation, lymphoma, renal
failure, sarcoidosis, drugs, congenital, HIV
infection

Joshi Nihar G.
 INCIDENCE
Around 30% of the total world population is
anemic and half of these, some 600 million
people, have iron deficiency.
Red cells in the bone marrow must aquire a
minimum level of haemoglobin before being
released into the blood stream.

Joshi Nihar G.
Joshi Nihar G.
 IRON DEFICIENCY ANEMIA
These occurs when iron losses or physiological
requirements exceed absorption.
Blood loss
• most common in men and post menopausal women
is gastrointestinal blood loss (colorectal malignancy,
gastritis, peptic ulceration, inflammatiory bowel
disease, diverticulitis, polyps and angiodysplastic
lesions.
• Worldwide, hookworm and schistosomiasis are the
most common cause of gut blood loss.
Joshi Nihar G.
• Gastrointestinal blood loss – chronic use of
aspirin or NSAIDs.
• In women of child-bearing age, menstrual
blood loss, pregnancy and breastfeeding
contribute to iron deciency by depleting iron
stores.
Malabsorption
Achlorhydria in older people or that due to drugs
such as proton pump inhibitors may contribute to
the lack of iron availability from the diet.

Joshi Nihar G.
Physiological demand
At times of rapid growth, such as infancy
and puberty, iron requirements increase and
may outstrip absorption. In pregnancy, iron
is diverted to the fetus, the placenta and the
increased maternal red cell mass, and is lost
with bleeding at parturition.

Joshi Nihar G.
 Haematological physiology during
pregnancy
 Full blood count- increase plasma volume, low
normal haemoglobin, MCV may increase by 5fl,
progressive neutrophilia
 Depletion of iron stores- common and is treated with
oral iron supplements
 Vitamin b12- low serum level
 Folate- depleted and supplements recommended
 Coagulation factors- from second trimester increases
three fold

Joshi Nihar G.
 Investigations
Serum ferritin- low
Iron- low
TIBC (total iron binding capacity)- low
Endoscopy or radiological study
Stool and urine examination for parasites
Antibody testing

Joshi Nihar G.
 Management
• Transfusion not indicated in angina, heart
failure or evidence of cerebral hypoxia and
oral supplement is appropriate.
• Ferrous sulphate 200 mg 3 times daily (195
mg of elemental iron per day) is adequate and
should be continued for 3–6 months to replete
iron stores.

Joshi Nihar G.
Previously, iron dextran or iron sucrose was
used, but new preparations of ferric isomaltose
and ferric carboxymaltose have fewer allergic
effects and are preferred. Doses required can be
calculated based on the patient’s starting
haemoglobin and body weight. Observation for
anaphylaxis following an initial test dose is
recommended.

Joshi Nihar G.
 Anemia of chronic disease
ACD also known as anemia of inflammation
(AI) is common type of anemia in hospital
population. The anaemia is not related to
bleeding, haemolysis or marrow infiltration, is
mild
Haemoglobin range- 85–115 g/L
MCV- normal
Serum iron-low

Joshi Nihar G.
Pathogenesis
It has become clear that the key regulatory
protein that accounts for the findings
characteristic of ACD/AI is hepcidin, which is
produced by the liver . Hepcidin production is
induced by pro-inflammatory cytokines.
Inhibition or blockade of hepcidin is a potential
target for treatment of this form of anaemia.

Joshi Nihar G.
Diagnosis and management
• Ferritin- increased/normal
• Iron- low
• TIBC- low
A trial of oral iron can be given in difficult
situations.

Joshi Nihar G.
 Megaloblastic anemia
This results from a deficiency of vitamin B12 or folic
acid, or from disturbances in folic acid metabolism.
Folate is an important substrate of, and vitamin B12 a
co-factor for, the generation of the essential amino acid
methionine from homocysteine.

Joshi Nihar G.
Joshi Nihar G.
Joshi Nihar G.
 Management
Treatment should always include both folic acid and
vitamin b12 otherwise would worsen the
neurological condition.
Vit. B12 – hydroxycobalamine ; malabsorption –
1000ug IM for 6 doses 2 or 3 days apart,
neurological development- 1000ug on alternative
day.
Folic acid- oral folic acid for acute- 5mg daily for 3
week, 5mg once a week for adequate maintenance.

Joshi Nihar G.
 Pernicious anaemia
This is an organ-specific autoimmune disorder in
which the gastric mucosa is atrophic, with loss
of parietal cells causing intrinsic factor
deficiency. In the absence of intrinsic factor, less
than 1% of dietary vitamin B12 is absorbed.
Common in hashimotos thyroiditis, graves
disease, vitiligo or addisons disease.
Investigation- antiparietal cell antibodies are
present in 90% cases.
Joshi Nihar G.
 Haemolytic anemia
Haemolysis iindicates that there is shortening of
the normal red cell lifespan of 120 days.

Joshi Nihar G.
Investigation indicating active haemolysis

Haemoglobin- low
Unconjug ated bilirubin- high
Lactate dehydrogenase- high
Reticulocytes- high
Haemoglobinuria
Urinary urobilinogen- high

Joshi Nihar G.
Autoimmune haemolytic anemia
This results from increased red cell destruction
due to red cell autoantibodies. The antibodies may
be IgG or IgM or mare rarely IgE or IgA.
Alloimmune haemolytic anemia
Alloimmune haemolytic anemia is caused by
antibodies against non-self red cells. It has two
main causes, occurring after:
• Unmatched blood transfusion
• Maternal sensitization to paternal antigens on
fetal cells
Joshi Nihar G.
Non- immune haemolytic anaemia
Occurs due to-
Endothelial damage : mechanical heart valve,
march haemoglobinuria, thermal injury
Infection : plasmodium falciparum malaria,
clostridium perfringens sepsis
Chemical or drugs : dapsone and sulfasalazine,
arsenic gas, copper, chlorates, nitrates and
nitrobenzene

Joshi Nihar G.
 Haemoglobinopathies
These disorders are caused by mutations affecting the
genes encoding the globin chains of haemoglobin.
Normal haemoglobin is composed of two alpha and two
non-alpha globin chains. Alpha globin chains are
produced throughout life, including in the fetus, so
severe mutations in these may cause intrauterine death.
Production of non-alpha chains varies with age; fetal
haemoglobin (HbF-αα/γγ) has two gamma chains, while
the predominant adult haemoglobin (HbA-αα/ββ) has
two beta chains. Thus, disorders affecting the beta
chains do not present until after 6 months of age
Joshi Nihar G.
The haemoglobinopathies can be classified into :
Qualitative abnormalities
Alteration in amino acid structure of polypeptide
chain of globin chain; Haemoglobin S- sickle cell
anaemia

Quantitative abnormalities
Mutation causing reduce rate of production of
globin chain- thalassaemia

Joshi Nihar G.
 Sickel cell anemia
Sickle-cell disease results from a single glutamic
acid to valine substitution at position 6 of the
beta globin polypeptide chain. It is inherited as
an autosomal recessive trait.

Joshi Nihar G.
Clinical and laboratory features of SCD

Joshi Nihar G.
 Management
Daily prophylaxis with folic acid
Seasonal vaccination
Aggressive rehydration, oxygen therapy,
adequate analgesic and antibiotic
Blood transfusion
allogeneic stem cell transplants from HLA-
matched siblings

Joshi Nihar G.
 Thalessaemia
Thalassaemia is an inherited impairment of
haemoglobin production, in which there is
partial or complete failure to synthesise a
specific type of globin chain. In alpha-
thalassaemia, disruption of one or both alleles on
chromosome 16 may occur, with production of
some or no alpha globin chains. In beta-
thalassaemia, defective production usually
results from disabling point mutations causing
no (β0) or reduced (β ) beta chain production.
Joshi Nihar G.
BETA THALESSAEMIA
Failure to synthesize beta chain
Beta thalessaemia major
profound hypochromic anaemia
Reduction or absence of haemoglobin A
Raised haemoglobin F
Erythroblastosis
Evidence that both parents have thalassaemia
minor

Joshi Nihar G.
Beta- thalassaemia minor (heterozygotes)
Mild anaemia
Punctate basophilia
Microcytic hypochromic erythrocytes
Treatment of beta- thalassemia major
Erythropoietic failure- allogenic transfusion,
folic acid 5mg daily
Iron load- iron chelaton therapy
Splenomegaly- splenectomy

Joshi Nihar G.
ALPHA THALESSAEMIA
Reduced or absent alpha chain synthesis
There are 2 alpha gene loci on chromosome 16
and therefore each individual carries four alpha
gene alleles
Treatment similar to that of beta thalassaemia.

Joshi Nihar G.