Subnormal level of Hb causes lowered oxygen carrying
capacity of the blood. This in turn, initiates
compensatory physiologic adaptations such as:
Increased release of oxygen from Hb
Increased blood flow volume
Maintenance of the blood volume
Redistribution of blood flow to maintain the cerebral
The speed of onset of anemia: rapidly progressive anemia causes
more symptoms than anemia of slow-onset as there is less time for
The severity of anemia: mild anemia produces no symptoms or
signs but a rapidly developing severe anemia (Hb<6.0 g/dl) may
produce significant clinical features.
The age of the patient: the young patient due to good
cardiovascular compensation tolerate anemia quite well as
compared to the elderly.
The heamoglobin dissociation curve: in anemia, the affinity of
heamoglobin for oxygen is depressed as 2,3-BPG in the red cells
The presenting features are:
Generalized muscular weakness
In older patients, there may be symptoms of
cardiac failure, angina pectoris, intermittent
claudication, confusion and visual disturbances.
A). Haemoglobin Estimation:
Cynmethaemoglobin (HCN) method employing Drabkin’s solution and a
If pregnancy, there is haemodilution and, therefore, the lower limit in normal pregnant
women is less (10.5 g/dl) than in the non pregnant state.
B).Peripheral Blood Film Examination:
Stain with Romanowsky dyes (Leishman’s stain, May-Grunwal’s stain, Jenner-Giemsa
stain, Wright’s stain)
C). Red Cell Indices:
In Fe deficiency and thalassaemia, MCV, MCH and MCHC are reduced.
In anemia due to acute blood loss and haemolytic anemia, MCV, MCH and MCHC
are all within normal limits.
In megaloblastic anemia, MCV is raised above the normal range.
D). Leucocyte Count and Platelet Count
E). Reticulocyte Count
F). Erythrocyte Sedimentation Rate
G). Bone Marrow Examination
I. Anemias due to increased
a). Acute post-haemorrhagic blood
b). Chronic blood loss
II. Anemias due to impaired red
a).Cytoplasmic maturation defects
i. Fe deficiency anaemia
b).Nuclear Maturation Syndromes
i. Vitamin B12/ Folic acid
ii. Megaloblastic anemia
c).Defect In Stem cell proliferation
i. Aplastic Anemia
pure red cell aplasia
d).Anaemia of chronic disorders
e).Bone Marrow Infiltration
f). Congenital anaemias
III. Anaemias due to increased
red cell destruction(Haemolytic
a). Extrinsic red cell
b). Intrinsic red cell abnormalities
I. Microcytic, hypochromic:
MCV, MCH, MCHC are all reduced e.g. after Fe
deficiency anaemia and in certain non-iron deficient
II. Normocytic, normochromic:
MCV, MCH, MCHC are all normal e.g after acute blood
loss, haemolytic anaemias, bone marrow failure,
anaemia of chronic disorders
III. Macrocytic, normochromic:
MCV is raised e.g in megaloblastic anaemia due to
deficiency of vitamin B12 or folic acid.
ANAEMIA OF BLOOD
Depending upon the rate of blood loss due to
haemorrhage, the effects of post-
haemmorhagic anaemia appear.
When the loss of blood
i. Immediate threat to life due
to hypovolemia which may
result in shock and death.
ii. If patient survives, shifting
of interstitial fluid to
haemodilution with low
iii. Hypoxia stimulates
erythropoeitin resulting in
When the loss of blood is slow
and insidious, the effects of
anaemia will become apparent
only when the rate of loss is
more than the rate of
production and the iron stores
This results in Fe deficiency
anaemia as seen in other
Acute Blood Loss Chronic Blood Loss
Hypochromic anaemia due to Fe deficiency is the
commonest cause of anaemia the world over.
Fe deficiency is the most important cause of microcytic
hypochromic anemia which all the three red cell indices
(MCV, MCH, MCHC) are reduced and occurs due to
defective Hb synthesis.
It is of two types:
a).Hypochromic anaemia due to Fe deficiency
b).hypochromic anaemia other than Fe deficiency
The commonest nutritional deficiency disorder present
throughout the world is iron deficiency but its prevalence is
higher in developing countries.
The factors responsible for iron deficiency in different
populations are variable and are best understood in the
context of normal iron metabolism.
Iron Deficiency Anemia
Iron deficiency anemia develops when the supply of iron
is inadequate for the requirement of Hb synthesis.
Initially, negative iron balance is covered by mobilization
from the tissue stores so as to maintain Hb synthesis.
It is only after the tissue stores of iron are exhausted
that the supply of iron to the marrow becomes
insufficient for Hb formation and thus a state of iron
A).Females in reproductive period of life:
Highest incidence in women.
i. Blood Loss: Most important cause of anemia in women
during child bearing age group.
due to persistant and heavy menstrual blood loss.
young girls at the start of menstruation may develop mild
anemia due to blood loss.
ii. Inadequate Intake: prevalent in women of lower economic
besides diet deficient in iron, other factors such as
anorexia, impaired absorption and diminished bioavailability
may act as contributory factors.
iii. Increased Requirements: During adolescence and
pregnancy the body’s iron demands are increased.
during a normal pregnancy, 750 mg of iron may be
siphoned off from the mother - 400 mg to foetus + 150 mg to
placenta + 200 mg lost at parturition and lactation
B).Post Menopausal Females:
i. Post menopausal uterine bleeding: due to
carcinoma of uterus.
i. Bleeding from alimentary tract: due to
carcinoma of stomach and large bowel and
i. Gastrointestinal Tract: due to peptic ulcer,
haemarrhoids, hook worm infestation,
carcinoma of stomach and large bowel,
oesophageal varices, hiatus hernia, chronic
aspirin ingestion and ulcerative colitis.
ii. Urinary Tract: due to haematuria and
iii. Nose: repeated epistaxis
iv. Lungs: haemoptysis from various causes.
D).Infants and Children:
Peak incidence at 1-2 years of age.
Principal cause is increased demand of iron
which is not met by inadequate intake of iron in
Normal full term infants have sufficient iron
stores, while premature infants have
inadequate reserves because iron stores from
the mother are mainly laid down during the last
trimester of pregnancy.
Anemia: onset of iron deficiency anemia is
Usual symptoms are weakness, fatigue,
dyspnoea on exertion, palpitations and pallor of
the skin, mucous membranes and sclerae.
Older patients may develop angina and
congestive cardiac failure.
Patients may have dietary cravings such as
Menorrhagia is a common symptom in iron
Epithelial Tissue Changes:
Long standing iron deficiency anemia causes
epithelial tissue changes in some patients.
Koilonychia (spoon shaped nails)
Dysphagia (a feature of Plummer Vinson
Stage 1: Storage iron depletion
Stage 2: Iron deficient erythropoeisis
Stage 3: Frank iron deficiency anemia where
the RBCs become microcytic and
Blood Picture and Red Cell Indices
ii. Red Cells: Hypochromic and Microcytic and there is Anisocytosis and
Target cells, elliptical forms and polychromatic cells are often present.
Normoblasts are uncommon.
RBC count is below normal level but is proportionate to the fall in Hb
iii. Reticulocyte Count: Normal or reduced but may be slightly raised (2-
5%) in cases after haemorrhage.
iv. Absolute Values: MCV, MCH, MCHC are reduced.
v. Leucocytes: TLC, DLC are usually normal.
vi. Platelets: usually normal but may be slightly to moderately raised in
patients who have had recent bleeding.
Bone Marrow Findings
i. Marrow Cellularity: Increased due to erythroid hyperplasia
ii. Erythropoeisis: Normoblastic erythropoeisis with
predominance of small polychromatic normoblasts
(micronormoblasts). These normoblasts have a thin rim of
cytoplasm around the nucleus and ragged and irregular cell
iii. Other Cells: Myeloid, Lymphoid and Megakaryocytic cells
are normal in number and morphology.
iv. Marrow Iron: Iron staining (Prussian blue reaction) shows
deficient reticuloendothelial iron stores and absence of
siderotic iron granules from developing normoblasts.
1. Correction of the disorder: Appropriate surgical,
medical and preventive measures are instituted to
correct the cause of blood loss.
2. Correction of iron deficiency:
a. Oral therapy: Administration of iron salts such as
ferrous sulfate, ferrous fumerate, ferrous gluconate
and polysaccharide iron.
These preparations having varying amounts of
elemental iron ranging from 39 to 105 mg.
Optimal absorption is obtained by giving iron fasting,
but if side effects occur (nausea, abdominal
discomfort, diarrhoea) iron can be given along with
food or with a lower iron preparation.
3. Parenteral Therapy:
Indicated in cases who are:-
i. Intolerant to oral iron therapy
ii. In GIT disorders (Malabsorption)
iii. Women with severe anemia a few weeks before expected
date of delivery
A common preparation is Iron Dextran which may be given
as a single IM or as IV infusion after dilution with dextrose or
Adverse effects of dextran are anaphylactoid reaction,
haemolysis, hypotension, circulatory collapse, vomiting and
Newer iron complexes such as sodium ferric gluconate and
iron sucrose can be administered as repeated IV injections
with much lower side effects.
Was first described by Addison in 1885 as a
chronic disorder of middle-aged and elderly
indivisual of either sex in which IF secretion
ceases owing to atrophy of gastric mucosa.
The average age at presentation is 60 years but
rarely can be seen in children under 10 years
(Juvenile Pernicious Anemia)
Vitamin B12 is an ‘Erythrocyte Maturing Factor’ or
‘Haemopoeitic Factor’ and present in foods(liver,
beef, milk and dairy products).
Probably an autoimmune disorder with a genetic predisposition and
the disease is associated with HLA types A2, A3 and B7 and blood
Similarly binding and blocking antibodies (Anti Parietal Ab) to IF are
found in most patients.
Also associated with other autoimmune disorders like thyroid
disorders, type I diabetes mellitus, ulcerative colitis, Addisons
disease and acquired agammaglobulinemia.
Relatives of patients have increased incidence.
Corticosteroids have been reported to be beneficial in curing this
Most characteristic pathologic finding is gastric
atrophy affecting the acid-pepsin secreting
portion of stomach, sparing the antrum.
Gastric epithelium may show cellular atypia.
Complications include: peripheral neuropathy,
spinal cord damage.
Onset is insidous and progresses slowly.
Characterized by a triad of symptoms: generalized
weakness, a sore, painful tongue.
Anemia, glossitis, neurological(subacute degeneration
of spinal cord, retrobulbar neuritis), gastrointestinal
manifestations(diarrhoea, anorexia, weight loss,
dyspepsia), hepatosplenomegaly, CHF and
Pain and burning sensation in lingual areas
‘Beefy red’ tongue (entirely or in patches)
Shallow ulcers resembling apthous ulcers.
Gradual atrophy of pappilae of tongue referred
to as ‘Bald Tongue’; ‘Hunter’s glossitis’;
Patients become intolerant to dentures.
A). Blood: RBC count is decreased to 1,000,000 or less per cubic
Many cells exhibit Macrocytosis.
Poikilocytosis is also present.
Hb is increased in proportion to the size of the RBCs.
Polychromatophillic cells, stippled cells, nucleated cells, Howell-Jolly
bodies and Cabot’s ring puctuate basophilia.
Mild to moderate thrombocytopenia is noticed.
Coexistent iron deficiency is common because achlorhydria prevents
solubilisation of dietery ferric iron from foodstuffs.
B). Serum: Indirect bilirubin maybe elevated.
Serum lactate dehydrogenase is markedly increased.
Serum pottasium, cholesterol and skeletal alkaline
phosphatase are decreased.
C). Gastric secretions: Total gastric secretions are reduced
to about 10%.
Most patients are achlorhydric.
IF is absent or markedly decreased.
D). Bone Marrow: biopsy and aspirate are hypercellular and
show trilineage differentiation.
Major Criteria Minor Lab
1. Low serum B12
level in presence of
anemia in bone
3. Positive test for IF
4. Positive gastric
parietal cell Ab
Family history of
Parenteral vitamin B12 replacement therapy.
Symptomatic and supportive therapy such as
physiotherapy for neurologic deficits and occasionally
Follow up for early detection of cancer of stomach.
Corticosteroid can improve gastric lesion with a return
of acid secretion.
Mental and neurologic damage can become
irreversible without therapy.
1. Shafer’s textbook of oral pathology
2. Navel’s textbook of oral pathology
3. Textbook of pathology-Harsh Mohan
4. Burket’s oral medicine