ANAEMIA

Prof. Dr. Mousa Qasim Hussein

17th Sep. 2023
 anaemia refer to a state in which the level
of haemoglobin in the blood below the
reference range appropriate for age and
sex.
The clinical features of anaemia reflect
diminished oxygen supply to the tissues .
Symptoms and signs help to indicate the
clinical severity of anaemia. A full history
and examination is needed to identify the
underlying cause
 A rapid onset of anaemia (e.g. due to
blood loss) causes more profound
symptoms than a gradually developing
anaemia.
Individuals with cardiorespiratory disease
are more susceptible to symptoms of
anaemia.
ANAEMIA
Non-specific symptoms
• Tiredness
• Lightheadedness
• Breathlessness
• Development/worsening of ischaemic
symptoms, e.g. angina or claudication
Non-specific signs
• Mucous membrane pallor
• Tachypnoea
• Raised jugular venous pressure
• Tachycardia
• Flow murmurs
• Ankle oedema
• Postural hypotension
Causes of anaemia
Decreased or ineffective marrow production
• Lack of iron, vitamin B12 or
folate
• Hypoplasia/myelodysplasia
• Invasion by malignant cells
• Renal failure
• Anaemia of chronic disease
Normal marrow production but increased
removal of cells
• Blood loss
• Haemolysis
• Hypersplenism
The clinical assessment and investigation of
anaemia should gauge its severity and
define the underlying cause

Clinical assessment
• Iron deficiency anaemia is the most common type of anaemia
worldwide. A thorough gastrointestinal history is important,
looking in particular for symptoms of blood loss.
Menorrhagia is a common cause of anaemia in pre-menopausal
females, so women should always beasked about their periods.
A dietary history should assess the intake of iron
and folate, which may become deficient in
comparison to needs (e.g. in pregnancy or during
periods of rapid growth.
• Past medical history may reveal a disease that is
known to be associated with anaemia, such as
rheumatoid arthritis (anaemia of chronic disease), or
previous surgery (e.g. resection of the stomach or
small bowel, which may lead to malabsorption of
iron and/or vitamin B12).
Family history and ethnic background may raise suspicion of
haemolytic anaemias, such as the haemoglobinopathies
and hereditary spherocytosis. Pernicious anaemia may
also run in families but is not associated with a clear
Mendelian pattern of inheritance.

• A drug history may reveal the ingestion of drugs that

cause blood loss (e.g. aspirin and anti-inflammatory
drugs), haemolysis (e.g. sulphonamides) or aplasia (e.g.
chloramphenicol).
On examination
there may be specific findings related to the aetiology of the
anaemia; for example, a patient may be found to have a right
iliac fossa mass due to an underlying caecal carcinoma.
Haemolytic anaemias can cause jaundice.
Vitamin B12 deficiency may be associated with neurological
signs, including peripheral neuropathy, dementia and signs of
subacute combined degeneration of the cord .
Sickle-cell anaemia may result in leg ulcers, stroke or
features of pulmonary hypertension. Anaemia may be
multifactorial and the lack of specific symptoms and signs
does not rule out silent pathology
Investigations
Schemes for the investigation of anaemias are often based on the
size of the red cells, which is most accurately indicated by the
MCV in the FBC.
Commonly, in the presence of anaemia:
-A normal MCV (normocytic anaemia) suggests either acute
blood loss or the anaemia of chronic disease, also known as the
anaemiaof infammation (ACD/AI) .
- A low MCV (microcytic anaemia) suggests iron defciency or
thalassaemia or sometimes ACD/AI .
-A high MCV (macrocytic anaemia) suggests vitamin B12 or folate
defciency or myelodysplasia
ANAEMIAS
Around 30% of the total world
population is anaemic and half
of these, some 600 million
people, have iron deficiency.

The classification of anaemia

by the size of the red cells (MCV) indicates the likely
cause
Iron deficiency anaemia
This occurs when iron losses or
physiological requirements exceed
absorption.
 causes
1-Blood loss
The most common explanation in men and post-
menopausal women is gastrointestinal blood loss .
This may result from :
1-occult gastric or colorectal malignancy, gastritis,
peptic ulceration, inflammatory bowel disease,
diverticulitis, polyps
and angiodysplastic lesions.
2-Worldwide, hookworm and schistosomiasis are
the most common causes of gut blood loss
 Gastrointestinal blood loss may be
exacerbated by the chronic use of aspirin or
non-steroidal anti-inflammatory drugs
(NSAIDs), which cause intestinal erosions
and impair platelet function.
In women of child-bearing age, menstrual
blood loss, pregnancy and breast feeding
contribute to iron deficiency by depleting
iron stores.
Very rarely, chronic haemoptysis or
haematuria may cause iron deficiency.
2-Malabsorption
Gastric acid is required to release iron from food and
helps to keep iron in the soluble ferrous state
Achlorhydria in the elderly or that due to drugs
such as proton pump inhibitors may contribute to the
lack of iron availability from the diet, as may previous
gastric surgery.
Iron is absorbed actively in the upper small intestine
and hence can be affected by coeliac disease
3-Physiological demands
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
Daily requirement:
-infants, children = 1-2mg/day
-adult male = 1mg/day
-premenopausal female = 2mg/day
-pregnant woman = 3mg/day, increased in
the last two trimesters to 5-6mg/day.
Iron absorption : by the proximal small
intestine, foods contain certain compounds
as phosphates and phagtates inhibit
absorption while ascorbic acid can promote
iron absorption.
Clinical features:
[Link] features of anemia([Link] and
reduce exercise capacity).
[Link] features of iron deficiency:
*spoon shaped nails (koilonychias)
*angular chilitis (painful hacks at the corner
of the mouth)
*atrophic glossitis (pale, smooth tongue)
spoon shaped nails (koilonychias)
spoon shaped nails (koilonychias)
angular chilitis (painful hacks at the corner of
the mouth)
I -Investigation :
Laboratory Tests in Anemia Diagnosis
I. Complete blood count (CBC)
A. Red blood cell count
1. Hemoglobin 2. Hematocrit 3. Reticulocyte count
B. Red blood cell indices
1. Mean cell volume (MCV) 2. Mean cell hemoglobin (MCH)
3. Mean cell hemoglobin concentration 4. Red cell distribution width
(RDW)
C. White blood cell count
1. Cell differential 2. Nuclear segmentation of neutrophils
D. Platelet count
E. Cell morphology
1. Cell size 2. Hemoglobin content 3. Anisocytosis
4. Poikilocytosis 5. Polychromasia
Investigations
Confirmation of iron deficiency
1-Serum ferritin is a measure of iron stores in
tissues and is the best single test to confirm iron
deficiency A subnormal level is most often due to
iron deficiency or, very rarely, hypothyroidism or
vitamin C deficiency. Ferritin levels can be raised in
liver disease and in the acute phase response; in
these conditions, a ferritin level of up to 100 μg/L
may still be compatible with low bone marrow iron
stores.
Adult males have serum ferritin values averaging 100 micro.g./L , while
adult females have levels averaging 30 [Link]/L.
2-Plasma iron and total iron binding capacity (TIBC) are
measures of iron availability;. Plasma iron has a
marked diurnal and day-to-day variation and becomes
very low during an acute phase response but is raised
in liver disease and haemolysis
normal range for serum irons (50-150micro.g/dl)
Normal TIBC (300-360micro.g/dl).
2-Levels of transferrin:
The binding protein for iron, are lowered by malnutrition,
liver disease, the acute phase response and nephrotic
syndrome, but raised by pregnancy and the oral
contraceptive pill.
A transferrin saturation (i.e. iron/TIBC × 100)
of less than 16% is consistent with iron deficiency but is
less specific than a ferritin measurement
4- membrane transferrin receptors
All proliferating cells express membrane transferrin
receptors to acquire iron; a small amount of this
receptor is shed into blood, where it can be detected in
a free soluble form.
At times of poor iron stores, cells up-regulate
transferrin receptor expression and the level of soluble
transferin receptors increase.

This can now be measured by immunoassay when a

raised level indicates iron deficiency.
In difficult cases, it may still be necessary to examine
a bone marrow aspirate for iron stores.
 Morphology of normal RBC

32
 Hypochromic Microytic Red Blood Cells
33
The cell size can easily be calibrated using
the nucleus of a small lymphocyte. A normal
red blood cell is usually the same size as the
nucleus of a small lymphocyte.
Sever iron deficiency anaemia
B/Investigation of the cause:
Depend on (age, sex, history and clinical
findings).
e.g.: men over 40, post-menopausal women
with normal diet upper &lower GI tract should
be investigated by endoscopy and barium
studies.
If celiac disease is suspected serum anti-
gliadin & anti-endomycin Ab and duodenal
biopsy are indicated.
In tropics stool, urine ex: for parasites.
 Management:
-depend on:
1. Aetiology of IDA.
2. Severity.
3. The ability of the patient to tolerate oral
preparations.
4. if the patient has angina, heart failure or evidence of
cerebral hypoxia.
Treatment:
1. Treat the underlying cause (bleeding,
malabsorption).
2. Blood transfusion: only for sever anemia, heart
failure, angina or evidence of cerebral hypoxia.
3. Iron replacemen
*oral iron preparations:
Ferrous sulphate 200mg 8 hourly (195mgof
elemental iron per day) for 3-6 months to
replete iron stores.
If the patient intolerant of ferrous sulphate
with dyspepsia and altered bowel habit so
either decrease the dose to 200mg 12 hourly
or change to ferrous gluconate 300mg 12
hourly (70mg of elemental iron per day).

Hb should be increased Ig/dl every 7-10 days

and reticulocyte response will be evident by
one week
failure to respond to treatment
adequately:
*non-adherence.
*continued blood loss.
*malabsorption
*incorrect diagnosis.
S.E: GI distress is form of abdominal pain,
nausea, vomiting, constipation or diarrhea.
parental iron therapy:
-indications:
1. Oral preparation intolerance.
2. Non-compliance.
3. Malabsorption and chronic gut disease.
4. Patient receiving recombinant
erythropoietin to guarantee adequate iron
delivery to support erythroid precursor
proliferation
 Previously, iron dextran or iron sucrose
was used, but new preparations of iron
isomaltose and iron 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.
ANAEMIA OF CHRONIC
DISEASE
This is a common type of anaemia, particularly in hospital
populations.

Characteristic features:
1. It occurs in the setting of chronic infections, chronic
inflammation or neoplasia.
2. The anaemia is not related to bleeding, haemolysis or
marrow infiltration,
3. mild, in the range of 85-115 g/l, and is usually associated
with a normal MCV (normocytic, normochromic), but up
to 25% may have reduced MCV
4. The serum iron is low but iron stores are normal or
increased, as indicated by the ferritin or stainable
marrow iron.
Clinical features
The clinical manifestations usually obscured by the
clinical Features of the underlying disease.
Moderate anaemia(Hb lessThan 10 g/dl) can exacerbate
the symptom of ischemic heart disease or respiratory
disease or contribute to fatigue or exertional
intolerance.
The diagnosis is based clinical features in conjugation
with laboratory Results.
Diagnosis and management
It is often diffcult to distinguish ACD associated with a
low MCV from iron deficiency.
Examination of the marrow may ultimately be required
to assess iron stores directly. A trial of oral iron can be
given in diffcult situations. A positive response occurs
in true iron defciency, but not in ACD. Measures that
reduce the severity of the underlying disorder
generally help to improve the ACD.
Trials of higher-dose intravenous iron are under way to
try to bypass the hepcidin-induced blockade.
THANK YOU