1

Approach to Patients
with

Anemia
By Dr / Mohammed Basiony
2
 BLOOD COMPONENTS

CELLS 45%
PLASMA 55%

RBCs WBCs Platelets 3

?How Are Blood Cells Formed

4
 Red Blood Cells (RBCs)
 Largest cellular
component of blood,
about 40-45% of blood
volume
 Comprised mostly of
hemoglobin
 Transport oxygen

 Red blood cells

normally last about 120
days before they are
removed by the spleen
5
 Hemoglobin
 Red pigment molecule
which gives RBCs
(and blood) its color
 Contains 4 molecules
of heme and 4 of
globin (2 alpha chains
and 2 beta chains)
 Each molecule of heme
contains one iron ion

6
 Reticulocyte Count
 Reticulocytes are “young” red blood cells that
were recently released from the bone marrow.
 Normally, reticulocytes comprise 0.5 - 2% of
all red blood cells.
 Increased reticulocytes (reticulocytosis) is a
normal response to blood loss or anemia. Since
reticulocytes are larger, the MCV (and RDW)
may be elevated.
 The combination of anemia with a low or
normal reticulocyte count indicates that the
bone marrow is unable to respond normally,
either due to lack of essential ingredients (iron
deficiency, vitamin B12 or folate deficiency),
bone marrow disease, or chronic disease.
7
 White Blood Cells
Monkey
Banana
Never
Let
Eat
60
31360
 There are several types of White Blood Cells
 They are all involved in immunity but in somewhat
different ways
 neutrophils – involved in acute infections with bacteria.
Immature form is called a “band”
 Lymphocytes – involved in many types of infection,
especially viruses -Produce antibodies and “memory
cells” - Are further divided into T-cells and B-cells
 Eosinophils – involved in parasitic infections and
allergies
 Basophils – involved in parasitic infections and allergies

 Monocytes – involved in bacterial and parasitic

infections 8
Dr/ m.m.elfeky
 Platelets
 Really more of a fragment of
a cell
 They are broken off from a
very large cell in the bone
marrow called a
megakaryocyte
 Primary function is to aid
in blood clotting
 Lifetime in the blood is 7-
10 days after which they
are destroyed in the spleen
 Their clotting function is
permanently inhibited by
aspirin 9
 Plasma
 Plasma is the liquid component
of blood
 Comprised mostly of water, but
also includes:
 Protein (albumin, globulin,
fibrinogen)
 Lipids (cholesterol,
triglycerides)
 Dissolved salts and minerals
(sodium, calcium, potassium)
 Glucose

10
 The Three Basic Measures

Measurement Normal
Range
A. RBC count 5 million 4 to 6
B. Hemoglobin 15 g% 12 to 17
C. Hematocrit 45 38 to 50

Ax3=Bx3=C

11
 Special Considerations in
Determining Anemia
 Acute Bleeding
 Dropin Hgb or Hct may not be shown until 36 to
48 hours after acute bleed (even though patient
may be hypotensive)
 Pregnancy
 In third trimester, RBC and plasma volume are
expanded by 25 and 50%, respectively.
 Labs will show reductions in Hgb, Hct, and RBC
count, often to anemic levels, but according to
RBC mass, they are actually polycythemic
 This affect HB - RBC count - HT ------but no
effect on MCV
 Volume Depletion
 Patient’s
who are severely volume depleted may
not show anemia until after rehydrated 12
 Descriptive Terms Used on
Peripheral Smears
 Anisocytosis: marked variation in RBC sizes
(visual counterpart of increased RDW)
 Poikilocytosis: marked variation in the shape of
RBCs
 Hypochromia : RBCs are paler than normal
because they contain less hemoglobin (visual
counterpart of decreased MCH)
 Macrocytosis: increased number of large RBCs
(visual counterpart of increased MCV)
 Microcytosis: increased number of small RBCs
(visual counterpart of decreased MCV) 13
 How to read
 1st look for HB
 3 possibilities:

A - normal its ok.

B - high polycythemia.
C - low anemia

Dr/ m.m.elfeky
 HB
polycythemia
WBC WBC
plat plat

Primary Secondar
y
polycyth polycythe
emia mia

15
Dr/ m.m.elfeky
 HB
- Anemia :
is defined as the lowering of hemoglobin concentration
below the established normal levels……….…coming
- Anemia is a clinical sign not a diagnostic entity.
-Most common hematological disorder by far…
-Almost always a secondary disorder
- Hematocrit (Hct): pcv
is the proportion, by volume, of the blood occupied by
red blood cells. The hematocrit (Hct) is expressed as a
percentage, normal levels are :
45% in Adult male & 40% in Adult female
For example, a hematocrit of 25% means that there are 25
milliliters of red blood cells in 100 milliliters of blood.
16
 HB

HB •11
•12
Female
male

HB •13
•14
child
infant

17
Dr/ m.m.elfeky
 Red Cell Indices
Are measurements that indicate the size and
hemoglobin content of red cells:
M.C.V (Mean Corpuscular Volume)

M.C.H (Mean Corpuscular Hemoglobin)

M.C.H.C (Mean Corpuscular Hemoglobin

Concentration)

18
 M.C.V (Mean Corpuscular Volume):
Referred to the average volume of red cells , normally = 77 - 99 fl
It can be calculated from an independently-measured red blood
cell count and hematocrit:

MCV  (femtoliters) = 10 x HCT(percent) ÷ RBC (millions/µL)

MICROCYTOSIS & MACROCYTOSIS : 

By definition, microcytosis is taken to mean the presence of RBCs
with a MCV less than normal, while macrocytosis means the
presence of RBCs with an MCV greater than normal.

19
 M.C.H (Mean Corpuscular Hemoglobin):

or "mean cell hemoglobin" (MCH), is a measure of the

mass of hemoglobin contained by a red blood cell. It
is diminished in microcytic anemias, and increased in
macrocytic anemias. It is calculated by dividing the
total mass of hemoglobin by the RBC count :-
MCH=Hb/RBC
A normal value in humans is 27 to 32 picograms/cell

20
 M.C.H.C
(Mean Corpuscular Hemoglobin Concentration):

is a measure of the concentration of hemoglobin in a given

volume of packed red blood cell.
It is diminished ") hypochromic") in microcytic anemias,
and normal ("normochromic") in macrocytic anemias
(due to larger cell size, though the hemoglobin amount or
MCH is high, the concentration remains normal).
It is calculated by dividing the hemoglobin by the hematocrit:
M.C.H.C = Hb / Hct
A normal value is 30 to 36 g/dl.
21
 RDW
Red cell distribution width

 It is correlates with the degree of

anisocytosis

 Normal range from 10-15%

 <21 in thalathemia.
 >21 in IDA
 elevated RDW is the first hematological
manifestation of iron deficiency anemia, and
hence a very sensitive screening test for that
particular disorder
22
 Mentzer index
 Differentiate iron deficiency anemia from
thalassemia trait
 = MCV / RBC in millions
 An index > 13 indicates iron deficiency
 An index < 13 indicates thalassemia trait

23
 Signs &Symptoms of Anemia
- Cardiovascular :
Exertional Dyspnea Palpitations Orthopnea
Tachycardia Angina Claudications
Cardiomegally Bounding peripheral Pulses
Murmurs Vascular bruits Pedal edema

- Neurological :
Headache Tinnitus Dizziness
Faintness Fatigue Cold Sensitivity
Loss of Concentration

24
 Signs &Symptoms of Anemia
- Skin :
Pallor of skin , mucous membranes, nail beds and palms.
- Gastrointestinal :
Anorexia Nausea Constipation
Diarrhea
- Respiratory :
Increased Respiratory Rates
- Genitourinary :
Menstrual irregularity Amenorrhea Menorrhagia
Loss of libido or potency
- Fundus Examination :
Retinal Exudates Rarely Papilloedema 25
Is the patient Anemic or not ?
Anemic means single or total
decrease in :
- Hb
- Hct
- RBCs count in millions
But…?
What Type of Anemia..?
This depends on the RBCs indices
26
 Red Cell Indices
According to MCV & MCH
Normal Decreased
77-99 > 77
Normocytic Microcytic
Normochromic Hypochromic
Anemia Increased Anemia
<99
Macrocytic
Anemia

27
 Normocytic Normochromic Anemia
It may be due to :
- Acute Blood Loss
- Aplastic Anemia
- Hemolytic Anemia ( Except Thalasemia)
- A.O.C.D (Anemia Of Chronic Diseases)

Which of Which ….?

Do Reticulocytic Count
Normal Low or Absent High
A.O.C.D e.g.: B.M.F - Acute Blood Loss
TB, SLE, Malignancy, “Aplastic Anemia” ( search for evidence
Rh. Arthritis
of the cause)

Note: BM biopsy or BM
- Evidence of the cause
aspiration show : - Hemolytic
- Anemia May be Micro- Acellular or Hypo- Anemia
cytic Hypochromic cellular BM
28
Hemolytic Anemia
- low Hb &/or Hct & /or RBCs count
- Normal RBCs indices
- Reticulocytosis

Do Indirect Serum Billirubin

Unconjugated Hyper-billirubinemia
“ jaundice”

Other Evidences of Hemolysis e.g.:-

- Hemoglobinuria - Hemoglobinemia (increased free Hb)

- Decreased Haptoglobin.

?..……… What is the Further Step

Coombs Test
29
 Coombs Test
Positive Negative
Immune Non-immune
Hemolytic Anemia: Hemolytic Anemia:
May be due to :
- Membrane Defect e.g. Spherocytosis
(lab show increased O.F.) & P.N.H
- Iso immune - Enzyme Defect
- Auto immune e.g. G6PD (lab : Enz. assay)
- Hb Defect (Hemoglobinopathy)
e.g. Sickle Cell Anemia (lab: Hb
Electrophoresis).
- Others : Malaria (lab: Bl. Film)
30
N
a
fr
s
o
t
r
ia NN anemia
c
n
rW
eB
ea
tC
m
n
i&
iec
m
ap
i
cl
a
oa
I
t
u
f
n
p
t
a
in
c
n
cy
rt
eo 31
Dr/ m.m.elfeky
 Hemolytic Anemia (CRC>2% + no blood loss)

Sickled Bite Target Schisto- parasite Acantho-

Sphero-cytes
cells cells cells cytes inclusions cytes

DAT DAT Hgb electro- G6PD PT/PTT

(+) (-) phoresis level Crea
platelets

Thalas- TTP-HUS
Auto- Malaria
Heredi- semias DIC
Immune Sickle Babe- Liver
tary G6PD Hemo- Prosthe-
Hemo- Cell siosis Ds
Sphero- Deficiency globino- tic Valve
lytic Ds Barto-
cytosis pathy Malignant
Anemia nella
Liver Ds HTN
32
 Hereditary Spherocytosis
 Inherited nonimmune hemolytic anemia
 anemia, splenomegaly, jaundice
 Gallstones common
 Aplastic crisis – from viral infections
 Dx: (+) spherocytes in PBS AND
Direct Coombs Test negative + osmotic
fragility test
 Tx:

Conservative mgt: folic acid, immunize

(pneumovax, meningovax, H flu vaccine)
33
34
Sickle Cell Anaemia

35
 ( G6PD ) Deficiency
 Pivotal
enzyme in HMP Shunt & produces
NADPH to protect RBC against oxidative stress
 Most common enzymopathy -10% world’s
population
 Protection against ????
 X-linked
 Its level sample taken 3weeks after the
attack???
36
 Drugs to be avoided in G6PD
 Antimalarial drugs
deficiency
 primaquine
 Sulphonamide and sulphons
 sulphapuridine, salazopyrine

 Antibacterial
 nalidixic acid, Nitrofurantion

 Analgesics
 asprin

 Antihelminthics
 B-Naphthol, Niridazole

 Miscellaneous Naphthaline, Vit K analogues 37

Autoimmune Hemolytic Anemia
 Warm-antibody mediated
 IgG antibody.
 most common.
 Diagnosed by POSITIVE Coomb’s Test..
 Can be caused by drugs .
 Treated with corticosteroids or splenectomy if
refractory
 Cold agglutinin Disease
 IgM antibodies.
 Does not respond to corticosteroids, but
usually mild.

38
 Treatment of Autoimmune
Hemolytic Anemia
 Treat underlying disease if indicated
 Prednisone (1 mg/kg/day for 2 weeks, then taper)
 Splenectomy
 Other
 Immunosuppressive agents (Rituximab)

 IVIG

 Similar approach to ITP

39
 Thrombotic Thrombocytopenic Purpura
(TTP)
 Thrombocytopenia and microangiopathic
hemolytic anemia, fever, renal insufficiency,
neurologic symptoms
 Schistocytes in smear.
 Hemolytic Uremic Syndrome
 Thrombocytopenia, Microangiopathic
hemolytic anemia, renal insufficiency

40
 Red Cell Indices
According to MCV & MCH
Decreased

Microcytic
Hypochromic
Increased Anemia

Macrocytic
Anemia

41
Microcytic Hypochromic Anemia
- The Commonest Cause is:
Iron Deficiency Anemia
-Other Causes: - Thalasemias
- Sedroplastic Anemia
- Lead Poisoning
- A.O.C.D

Which of Which ….?

Do Iron Studies:
- Serum Iron
- Serum Ferritin
- T.I.B.C (Total Iron Binding Capacity)
- Transferrin Saturation

42
 According to Iron Studies
A.C.O.D Sideroplastic Thalassemia Iron
Anemia Deficiency
Anemia
Serum Fe

N or Normal Serum
Ferritin

Normal T.I.B.C

Transferrin
Saturation
43
 Thalassemia
Notes: Iron
- Hb Electrophoresis will Studies
show: Serum Fe
Persistence of
hb f major type Serum
Ferritin
hb a2 minor type
-Rdw <21 T.I.B.C
-Mntzer index>13
-HPLC =
Transferrin
high performance
chromatography Saturation
A more accurate substitute for
HB electropheresis

44
 Thalassemia
clinical picture
 general manifestation of anaemia→see before
 general maifrstations of ↑ haemolysis→jaundice,dark
stool.dark urine.
 maifrstations of ↑ medullary erythropoiesis→enlarged head,
frontal&parietal bossing , protruded maxilla, depressed
nasal bridge, slantig of eye&epicathic folds.
 maifrstations of ↑ extramedullary
erythropoiesis→hepatomegaly &spleenomegaly,
lymphadenopathy
 -growth retardation
 mainfestations of complications→Haemosidrosis,2ry
hypersplenism,complications of tranfusion 45
Hair on end - Thalassemia
Major

46
Thalassemia minor
is an inherited form of hemolytic anemia that is less severe
than thalassemia major. This blood smear from an individual
with thalassemia shows small (microcytic), pale
(hypochromic), variously-shaped (poikilocytosis) red blood
cells. These small red blood cells (RBCs) are able to carry less
oxygen than normal RBCs

47
Thalassemia, being a genetic disease, runs in a family. Most
are silent carriers or suffer mild anemia. Severe cases such as
the Hemoglobin H disease with enlarged spleen, small body
and malnourished look shows more prominent symptoms.
[Pic below: Enlargement of spleen, small body]

48
Target Cells

1-thalathemia.
2-post splenectomy.
3-liver disease.

49
 Thalassemia
TTT
 Packed RBC transfusion:
defeciet × body weight ×3
Every 3 cm packed RBC ↑ HB 1gm/kg
 Iron chelating agents:
a-parentral→desferoxamine
b-Oral→deferasirox. (Exjade)
 folic acid………1-5mg/day.
 vaccination…….pueumococci,meningococci,haem
ophilus influenza
50
 Thalassemia
TTT
 lasix 1mg/kg/dose following blood
transfusion(to avoid volume over load)
 antibiotic………erythromycin or long acting
pencillin /3 weeks
 CST
 bone marrow transplantation….is the only
radical treatment

51
 Sideroplastic Anemia
Notes: Iron
Sedroplastic Anemia is due Studies
to: Serum Fe
- B6 Deficiency
- Drugs e.g.: INH Normal Serum
Ferritin
- Inherited
Blood film show: Normal T.I.B.C
RBCs contain Iron
Granules Transferrin
Saturation
Treated by:
B6 supply

52
Many rounded sideroblasts are present in this field.
This is the hallmark feature of sideroblastic anemia

53
 Lead Poisoning
Notes:
-History is Suggestive.
-Reduced IQ.
-Hearing problems--Failure at school

- Elevated Serum Lead level.

- Purely Motor Neuropathy (foot and wrist drop)
- Lead colic
- Blood Film show:
Basophilic Stippling of RBCs

54
Basophilic Stippling of RBCs
Basophilic stippling appears as round, dark-blue granules in
red blood cells on smears stained with supra vital stains such
as brilliant cresyl blue.
They may be observed in lead poisoning, exposure to some
drugs, severe burns, or septicemia. The granules are
precipitated ribosomes and mitochondria

55
Iron Deficiency Anemia

56
Iron  is the most common cause of anemia &
it’s the most important cause of microcytic
hypochromic anemia.
Iron Protoparphyin

Haem + Globin

Hemoglobin

57
.Duodenal epithelial cell uptake of heme and nonheme iron
59
Body iron distribution & transport:
Transport & storage of iron is largely mediated by 3
proteins transferrin, transferrin receptor 1 & ferretin

Transferrin (TF):
It delivers iron to tissues that have transferrin
receptors… then its reutilized.
At the end of their life, RBCs are broken down
in the macrophages of RES & the iron is
released from Hb, enters the plasma &
provides most of the iron on TF. Only a small
proportion of plasma transferrin iron comes
from dietary iron absorbed.
Ferritin
Storage form of iron. 58
 No excretion
 The general need to conserve the metal is
reflected in the absence of any physiological
mechanism for excretion of iron, control of
iron balance being at the level of iron
absorption.

61
Table (1): Distribution of body iron:

Hb 65%

Ferretin & hemosiderin 30%

Myoglobin 3.5%

Haemenzymes 0.5%

Transferrin bound iron 0.1%

60
 Table (2): Daily iron requirements:

Urine, Sweat,
Menses Pregnancy Growth Total
Faces

0.5 – 1
Adult ♂ 0.5 – 1
mg/day
Postmenopausal ♀ 0.5 – 1 0.5 – 1

Menstruating ♀ 0.5 – 1 0.5 – 1 1–2

Pregnant ♀ 0.5 – 1 1–2 1.5 – 3

Children 0.5 – 1 0.6 1.1

♀ (12 – 15 years) 0.5 – 1 0.5 – 1 0.6 1.6 – 2.6

Iron absorption through the duodenum

61
Dietary iron:
There are 2 types of iron in the diet; haem
iron and non-haem iron
Haem iron is present in Hb containing
animal food like meat, liver & spleen
Non-haem iron is obtained from cereals,
vegetables & beans
Milk is a poor source of iron, hence
breast-fed babies need iron supplements
62
Table (3): Iron absorption:
Through duodenum

Factors  absorption Factors  absorption

Haem iron Inorganic iron
Ferrous Ferric
Acids (Hcl, vit C) Alkalis e.g. antacids
Preciptating agents:
Solubizing agents (sugars)
phytates
Iron  Iron 
Pregnancy Infection
Hereditary hemosiderosis Tea

63
 IRON ABSORPTION
 Haem iron is not affected by ingestion of
other food items.
 It has constant absorption rate of 20-30%

which is little affected by the iron balance

of the subject.
 Heam iron is present in food of animal origin
1,5-6mg/100gm of diet.
 Absorption of Haem Iron > Fe ++ > Fe+++
64
 IRON ABSORPTION
 The absorption of non-haem iron varies
greatly from 2% to 100% because it is
strongly influenced by:
 The iron status of the body.
 The solubility of iron salts.

 Integrity of gut mucosa.

 Presence of absorption inhibitors or

facilitators

65
 Iron absorption
 A single cup of tea taken with meal reduces iron
absorption by up to 11%.
 Some fruits inhibit the absorption of iron although
they are rich in ascorbic acid because of their high
phenol content e.g strawberry banana and melon.
 Calcium supplementation decreases bioavailability
of iron when metals are ingested simultaneously

66
 ?INHIBITION-HOW
 The dietary phenols & phytic acids
compounds bind with iron decreasing
free iron in the gut & forming
complexes that are not absorbed.
 Cereal milling to remove bran reduces
its phytic acid content by 50%.

67
Promoters of Iron Absorption
 Foods containing ascorbic acid like citrus fruits,
broccoli & other dark green vegetables because
ascorbic acid reduces iron from ferric to ferrous
forms, which increases its absorption.
 Foods containing muscle protein enhance iron
absorption due to the effect of cysteine containing
peptides released from partially digested meat, which
reduces ferric to ferrous salts and form soluble iron
complexes.

68
Clinical features:
General signs of anemia.
Painless glossitis, angular stomatitis.
Brittle or spoon nailes (kolinychia).
Dysphagia as a result of pharyngeal webs
(paterson-kelly or Plummer-vinson
syndrome).
Pica: persistent ingestion of nonnutritive
substances common in infants & young children

69
 Severe iron-deficiency anemia can lead to:
 problems with growth and development

in children
 angina (chest pain)

 leg pains (intermittent claudication)

72
Spoon Nails:
If nails look scooped out, like a spoon, it
.could be a sign of iron-deficiency anemia

70
 Left : Spoon shaped finger nails
Right : Showing angular cheilitis, and dry skin

71
Plummer Vinson Syndrome

72
Causes of iron deficiency:
I. Chronic blood loss:
Uterine.
Gastrointestinal: e.g. DU, OV, partial
gastrectomy, carcinoma of stomach,
caecum, colon rectum, colitis, piles.
Rarely hematuria, haemoglobinuria.
II. Increased demands- prematurity, growth
pregnancy.
III. Malabsorption.
IV. Poor diet.
73
 Stages of iron deficiency
Depletion of storage iron in liver,
bone marrow, muscle
serum ferritin
prelatent iron deficiency partially depl. : <30ug/l
fully depleted: <
12 ug/l
depletion of the transport iron pool
in blood plasma
serum iron
latent iron deficiency
TIBC = transferrin

loss of haemoglobin iron

hemoglobin
manifest iron deficiency Soluble Transferrin-
Receptor

74
 Important notes 2
Iron deficiency anemia in men or postmenopausal
women is primarily a result of gastrointestinal blood
losses; therefore, finding iron deficiency anemia in this
patient population warrants a through GI workup.

Iron deficiency anemia in women of reproductive age is

most often caused by menstrual blood loss.

75
 Iron Deficiency Anemia
Notes: Iron
- Search For The Cause: Studies
e.g.: Serum Fe
Chronic Blood Loss
Ankylostoma Serum
Cancer Colon Ferritin
Nutritional causes T.I.B.C
- Severe Aniso-cytosis and
Poikilo-cytosis: Transferrin
Increased R.D.W(N ≤ 13%) Saturation

76
Serum transferrin receptor 
Red cell protporphyrin  & red cell
ferretin 
BM:  iron from macrophages & from
erythroblasts
Investigation of the cause:
E.g. occult blood test upper & lower GIT
endoscopy.
Esinophilia think about?

77
 FOBT
 The fecal occult blood testing (FOBT) is negative
in about 50% of patients with GI cancer.
Therefore, a negative FOBT in the presence of
iron deficiency anemia should not discourage you
from pursuing a through GI workup.
 Preparation:
48-72h before testing avoid Red meat Vitamin
C supplements Pain relievers, such as aspirin,
ibuprofen and nitroglycerine

78
 The serum iron is not a helpful test in the
diagnosis of iron deficiency anemia because it is
subject to wide variability based on several
factors including age, gender, time of day, and
recent iron ingestion.

82
Normal Blood Film

79
MICROCYTES

80
HYPOCHROMIA

81
Severe Hypochromia

82
Anisocytosis with hypochromia and
microcytes (IDA)

84
Treatment:
I. Treatment of the cause.
II. Iron therapy:
1) Oral iron:
A- The best is ferrous sulphate ..
– Given on an empty stomach.
– S/E: abdominal pain, constipation.

B- Ferrous gluconate: contain less

elemental iron.

85
Treatment
 Ferrous sulphate 200mg 3times=195 E Fe./d
 If intollerant 200mg 2times or
 Ferrous gluconate 300mg/12 h = 70 E Fe/d
 Delayed iron releases not useful ????

 Ferro sanol duodenale tab 567.7 mg

sulphate

86
N.B:
Oral iron given for long enough both to
correct anemia & to replenish body iron
stores i.e. 3-4 months.

Causes of failure of response to oral iron:

Continuing haemorrage.
Failure to take tablets.
Wrong diagnosis.
Mixed  .
Malabsorption.

87
Parentral iron:
Ferric hydroxide – sucrose by slow i.v.
Iron dextran slowly i.v.
Ferric hydroxide polymaltose deep im.
N.B: used after failure of oral iron
malabsorption, intolerance to oral , essential to
replete body stores rapidly.
S/E anapylaxis.
1/1000 with sucrose -- 1/300 with dextran

88
 Iron preparations
 tab→ ferose F (100mg/tab)
ferro sannol (195mg E fe)
 Pediatric dose 6mg/kg/day
 Syrup
K-G-ron 15mg Ferromix 15mg
Sytron 28mg Vitaferrol 38mg
Feose 50mg
 Drops
hydroferrin 50mg/ml fer in sol 15/,6ml
89
 Iron preparations
 Parentral:
cosmofer amp (100mg/amp) dextran….
ferosac amp (100mg/amp) saccharate.
haemojet amp (100mg/amp) polymaltose.
(painful+ skin discolouration—z tract)
 Dose in milligrams :::
(target Hb – Actual Hb) X body weight X 0.24 + 500 mg
500 for (35kg or above)

90
 Monitoring Fe THERAPY
 Response to iron therapy can be documented
by an increase in reticulocytes 5-10 days after
the initiation of iron therapy.
 The hemoglobin concentration increases by
about 1 g/dL weekly until normal values are
restored.

91
 Prevention
American Academy of Pediatric recommendations..

a . Infants should be breastfed until at least age 5-6 months

if possible
b . Iron supplementation after age 5-6 months for breastfed
infants
c . Nonbreastfed infants should be given iron-fortified
formula
d. 1st foods introduced in infancy should be iron-fortified
cereals
e. No whole milk until after 1st birthday
95
 Red Cell Indices
According to MCV & MCH

Increased

Macrocytic
Anemia

92
 Macrocytic Anemia
 - In Which :
- low Hb &/or Hct & /or RBCs count
- Increased RBCs indices
 -TYPES :
A. Megaloblastic Macrocytic – B12 and Folate↓
B. Non Megaloblastic Macrocytic Anaemias
1. Liver disease/alcohol
2. Hypothyroidism
3. Myelodystrophy, BM infiltration
4. Accelerated Erythropoesis –as in ↑destruction
5. Drugs (cytotoxics, immunosuppressants, AZT,
anticonvulsants)
93
 MCV >100
Consider Lab
Rule out Drugs
Error

Retic ct LFT’s
High B12 &
Thyroid
Folate LOW
Blood Loss

Eval for Normal

Hemolysis

MMA & HC
LDH
Bilirubin normal
Haptoglobin Most commonly
Consider Bmbx Myelodysplasia
94
 Megaloblastic anemia
Vit B12:
Main food: animal produce only.
Minimal adult daily requirement: 1-2 g.
Absorption : terminal ileum

Folic acid:
Liver, greens & yeast.
Minimal requirement: 100 – 150 mg.
Absorption: jejunum. 95
Vit B12  :
Causes:
Nutritional: vegeterians.
Malabsorption: (much more common)
Gastric: pernicious anemia,  IF, cancer stomach, ch gastritis ,
gastrectomy.
Intestinal diverticulosis stricture etc.
Ileal resection – 2 causes??
Chronic tropical sprue.
Fish tapeworm.

96
folic acid :
Causes:
Nutritional
Malabsorption e.g. jejunal resection,
crohn’s disease.
excess utilization (e.g. pregnancy,
hemolytic anemias).
excess loss (e.g. liver diseases)
drugs (e.g. sulfa salazine).
97
Pernicious anemia:
Autoimmune attack on the gastric mucosa  atrophy
of the stomach.
There is a chlorhydria & IF secretion  or absent.
H. pylori infection may initiate autoimmune gastritis.
More in female, peak at 60 years, blue eyes early
greying , Blood group A, familial.
May be associated autoimmune disease e.g. vitiligo,
Myxoedema, Hashimoto’s thyroditis hypogamma
globinemia, PAN, addison’s disease.
2-3%  cancer stomach.
90% show parital cell antibodies, antibodies blocking
IF binding to B12 or antibodies inhibit IF binding to
distal ileum.
98
Clinical features:
Features of anemia.
Mild jaundice (ineffective erythropoiesis).
Glossitis & angular stomatitis.
B12 neuropathy (subacute combined
degeneration): progressive neuropathy affecting
the peripheral sensory nerves & posterior &
lateral columns, the neuropathy is symmetrical
and affects the lower limbs (d.t.  methylation of
myelin).
Neural tube defect: anencephaly, spina bifida or
encephalocele infetus d.t. B12 or folate  in
mothers.
99
 Diagnosing Vitamin Deficiencies
Serum B12, serum & red cell folate:
In B12 :
Serum B12  (160 – 925 ng/L).
Serum folate N or  (3 – 15 g/L).
RBCs folate N or  (160 – 640 g/L).
In folic acid :
S. B12 N
S. folate  -- RBCs folate 
100
Effect of diet: A single meal may
falsely elevate serum folate levels
to normal. Hence, blood should
be drawn prior to transfusions,
meals, and therapy to achieve
.accurate results
105
 methylation of DNA,
myelin, proteins etc

1) S-adenyl homocysteine S-adenyl methionine

Methyl
Homocysteine Methionine
B12

Methyl THF THF

Deoxyd-
enosyl
2) Propinoyl COA  Methyl malonyl CoA Succinyl CoA
B12
102
Diagnosing Vitamin Deficiencies
 Methylmalonic acid and Homocysteine
 Good if Cobalamin and Folate are equivocal
 Both elevated = Cobalamin Deficiency
 95% Sensitivity
 99% Specificity

 If Homocysteine only elevated = Folate

Deficiency
 85% Sensitivity
 Anti-Intrinsic factor Antibodies Confirms
Pernicious Anemia
101
 Anemia - Macrocytic (MCV > 100)

 Macrocytic anemias may be asymptomatic until

the Hb is as low as 6 grams
 MCV 100-110 fl

must look for other causes of macrocytosis

 MCV > 110 fl
almost always folate or B12 deficiency

103
Schilling Test
The Schilling test is
performed to evaluate vitamin
B12 absorption.

Normally, ingested vitamin

B12 combines with intrinsic
factor, which is produced by
cells in the
stomach.
Certain diseases, such as
pernicious anemia, can result
when absorption of vitamin
B12 inadequate

109
Treatment:
I. Treatment of the cause.
II. B12:
Hydroxy cobalamin IM 1000 mg.
Initial dose 1000 mg daily for 2 weeks.
Weekly till HB normalization.
Maintenance 1000 mg every 3 weeks.
NB---given oral to hemophilia patients.
III. Folic acid
5 mg/day for 4 months.
105
 Treatment
If we start ttt with folic acid alone and there was vit
b12 deficiency neurological manifestations will
…worsen
If initial response is not maintained and blood film
was dimorphic mic&mac give iron therapy
……also

106
112