Blood 1

 Introduction
 Properties of blood
 Composition of blood
 Functions of blood
 Red blood cells
 Erythropoiesis
4/15/2014 3BLOOD AND ITS COMPONENTS

 Erythrocyte sedimentation rate
 White blood cells
 Platelets

 Coagulation of blood
 Test for clotting
 Bleeding time
 Clotting time
 Prothrombin time
 Partial Prothrombin time
 Thrombin time
 Bleeding disorders

 Connective tissue in fluid form
 Fluid of life
 Fluid of growth
 Fluid of health

 Color
 Volume
 Reaction and pH
 Specific gravity
 Viscosity

 Blood cells
 RBC
WBC
 Platelets
 Plasma
 Serum

 Plasma –
 Straw colored clear liquid part of the blood
 Contains 91-92% water and 8-9% solids
 Serum –
 Clear straw colored fluid that is left after blood
has been clotted.
 Serum is same as plasma but only difference
serum is devoid of fibrinogen ( its absent because
fibrinogen is converted into fibrin during blood
clotting).

 MOLECULAR WEIGHT:-
Albumin:69,000
Globulin:1,56,000
Fibrinogen:4,00,000
 ONCOTIC PRESSURE –
 The plasma proteins are responsible for the
oncotic or osmotic pressure. Normally it is about
25 mm Hg.
 SPECIFIC GRAVITY-
 The specific gravity plasma proteins is
1.026.
 BUFFER ACTION –
 Hydrogen ions is responsible for buffer
action. The plasma protein have 1/6th of
total buffering action of blood.

 Nutrient function
 Respiratory function
 Excretory function
 Transport of hormones and enzymes
 Regulation of water balance
 Regulation of acid – base balance
 Regulation of body temperature
 Storage function
 Defensive function

 Non – nucleated cells
 Normal value
 4 and 5.5 millions per cu mm of blood
 Males – 5 millions/ Cu mm
 Females – 4.5 millions/ Cu mm

 Morphology of RBC
 Disk shaped and biconcave
 Advantages of biconcave shape of RBC
 Normal size
 Diameter – 6.9 – 7.4µ
 Thickness – Periphery – 2.2µ
and centre - 1µ
 Surface area – 120 sq. µ
 Volume – 85 - 90 cu.µ

 Rouleaux formation
 Specific gravity
 1.092 to 1.101
 Packed cell volume
 Suspension stability
 Lifespan of RBC – 120 days. After the lifetime
the senile RBC are destroyed in
reticuloendothelial system.

 Transport of oxygen from lungs to the tissues
 Transport of CO2 from tissues to the lungs
 Buffering action in blood – Hb acts as buffer
 In blood group determination

 Physiological variations
 Increase in RBC count
 Age
 Gender
 High altitude
 Muscular exercise
 Emotional conditions
 Increased environmental temp.
 After meals
 Decrease in RBC count
 High barometric pressure
 During sleep – all the activities decreases
 Pregnancy – decrease in ECF vol. – increase in plasma
vol. resulting in hemodilution.

Birth – 8 to10
millions/cc
Count decreases
causing
physiological
jaundice
Infants and
growing children
have increased
count

Before
puberty and
menopause
count is same
as males
During
reproductive
age the
count is less
than that of
males

Temporary
increase in
RBC count
after exercise
mild hypoxia
and
contraction of
spleen.
Spleen stores
RBC.
Hypoxia
increases the
sympathetic
activity
resulting in
secretion of
adrenaline.
Adrenaline
contracts the
spleen and
hence RBC
are produced

High altitude
hypoxia
Stimulation of
kidney
Production of
erythrpotein
Stimulation of
bone marrow
Production of
RBC
Emotional
conditions
Increased
sympathetic activity
Increased secretion
of adrenaline
Contraction of
spleen
Release of RBC

 Pathological variations
 Pathological polycythemia
RBC count increases 7millions/cc of blood
Two types:
1.Primary
2.Secondary

 Persistent increase in RBC count above 14
millions/cc of blood.
 Always associated with increased white blood
cell count above 24ooo/cc of blood.
 Occurs in myeloproliferative disorders like
malignancy of red bone marrow

 Secondary to some of the pathological
conditions:
 Respiratory disorders like emphysema
 Congenital heart disease
 Ayerza’s disease – hypertrophy of right ventricle
and obstruction of blood flow to lungs.
 Chronic carbon monoxide poisoning
 Poisoning by chemicals like phosphorus, and
arsenic
 Repeated mild hemorrahages

 Process of origin, development and
maturation of erythrocytes.

 Changes during Erythropoiesis
 Reduction in size of RBC
 Disappearance of nucleoli and nucleus
 Appearance of hemoglobin
 Change in the cytoplasm properties of the
cytoplasm

 STAGES OF ERYTHROPOIESIS
The various stages between stem cells and
matured red blood cell are;
 Proerythroblasts
 Early normoblasts
 Intermediate normoblasts
 Late normoblasts
 Reticulocytes
 Matured erythrocytes

RBCs after 120 days
Fragile
Membranes of RBC rupture
Phagocytized by Reticulo endothelial system
Tissue macrophages
 Kupffer cells
 Spleen
FATE OF RBC

Heme Globin Amino acid
pool- reuse
Free Iron Straight chain of
4 pyrole nuclei
Transported in
blood by transferrin
Reused

Straight chain of 4 pyrole nuclei
Biliverdin
Free Bilirubin (released by Macrophages)
Combination with plasma Albumin
Blood Interstitial fluids
Liver kidney-- Nil
Free Bilirubin
HEME OXYGENASE
BILIVERDIN REDUCTASE

 The rate at which the erythrocytes
settle down.
 Methods:
 Westergren’s method
 Wintrobe’s method

 Normal values:
 Westergren's method
 Males – 3 to 7 mm
 Females – 5 to 9 mm
 Infants – 0 to 2 mm
 Wintrobe’s method
 Males – 0 to 9 mm
 Females – 0 to 15 mm
 Infants – 0 to 5 mm

 Physiological variation
 Age – less in children and infants
 Gender – more in females than in males
 Menstruation – increases because of loss of blood
 Pregnancy – from 3rd to paturition ESR increases
because of hemodilution

 Pathological variation
 Increased in
 Tuberculosis
 All types of anemia except sickle cell anemia
 Malignant tumors
 Rheumatoid arthritis
 Rheumatic fever
 Liver diseases
 Decreased in
 Allergic conditions
 Sickle cell anemia
 Polycythemia
 Severe leukocytosis

 ESR is an easy, inexpensive and non specific
test , which helps in diagnosis as well as in
prognosis.
 Certain disorders like:
 Pulmonary TB
 Rheumatoid arthritis
 Polymyalgia rheumatica
 Temporal arteritis

 Specific gravity of RBC – Increases so ESR also
increases
 Rouleaux formation – increases the ESR
 Increase in size of RBC – increases so ESR also
increases
 Viscosity of blood – increases so ESR
decreases
 RBC count – increases so viscosity increases
so ESR decreases.

4/15/2014BLOOD AND ITS COMPONENTS 41
GOOD
MORNING

 Hb is the iron containing coloring matter of
RBC
 The main function of red cells is to carry O2
to the tissues and to return carbon dioxide
(CO2) from tissues to the lungs.
 In order to achieve this gaseous exchange the
red cells contain the specialized protein
haemoglobin.
 Each red cell contains approximately 640
million Hb molecules.

 Average Hb in blood is 14 to 16g/dL
 Age
 At birth – 25g/dL
 After 3rd month – 20g/dL
 After 1 year – 17g/dL
 From puberty onwards – 14 – 16g/dL
 Gender
 In adult males – 15g/dL
 In adult females – 14.5g/dL

 Transport of gases
 Oxygen
 Oxygen + Hb known as oxygenation occurs resulting in
the formation of oxyHb
 Iron in this state remains as ferrous
 Its an unstable compound and the combination is
reversible
 Carbon dioxide
 Carboxyhaemoglobin is formed
 Unstable and reversible
 Hb has 250 times affinity for Co2 as compared to
oxygen

 IRON
 In ferrous form, unstable and loose form
 In some abnormal conditions gets converted into
ferric form – stable form
 Porphyrin
 Pigment part
 Formed by 4 pyrrole rings
 Attached by methane bridges
 Globin
 4 polypeptide chains
 2 alpha and 2 beta

B
B
A
A
heme

Hb A Hb A2 Hb F
structure a2b2 a2d2 a2g2
Normal % 96-98 % 1.5-3.2 % 0.5-0.8 %

 Haem synthesis starts with
the condensation of
glycine and succinyl
coenzyme A under the
action of a rate limiting
enzyme -aminolaevulinic
acid synthase.
 -ALA will be formed.
 Pyridoxal phosphate (vit.
B6) is a coenzyme for this
reaction.

 A series of biochemical
reactions will follow.
 Two molecules of -ALA
condense to form a pyrrole
called porphobilinogen
(PBG)
 Four PBG condense to form
a tetrapyrrole
uroporphyrinogen III.
 UPG III is then converted
to coproporphyrinogen.

 CPG then changes to
protoporphyrin which
ultimately combines with
iron in the ferrous state
(Fe2+) to form haem.
 Iron is brought to the
developing red cells by a
carrier protein (
transferrin) which attaches
to special binding sites on
the surface of these cells.
 Transferrin releases iron
and returns back to
circulation.

 Each molecule of haem
combines with a globin
chain.
 A tetramer of four
globin chains each with
its own haem group in
a pocket is formed to
make up a
haemoglobin molecule.

Heme Globin Amino acid
pool- reuse
Free Iron Straight chain of
4 pyrole nuclei
Transported in
blood by transferrin
Reused

Straight chain of 4 pyrole nuclei
Biliverdin
Free Bilirubin (released by Macrophages)
Combination with plasma Albumin
Blood Interstitial fluids
Liver kidney-- Nil
Free Bilirubin
HEME OXYGENASE
BILIVERDIN REDUCTASE

584/15/2014BLOOD AND ITS COMPONENTS

 Hemoglobinopathies
 Hemoglobin in thalassemia and related
disorders

 Hemoglobin S –
 Found in SC anemia
 Alpha chains are normal and beta chains are
abnormal
 Hemoglobin C –
 Beta chains are abnormal
 In people with HB C diseases characterized by mild
hemolytic anemia and splenomegaly
 Hemoglobin E
 Beta chains are abnormal
 Hemoglobin M
 Abnormal Hb present in the form of methHB
 Occurs due to mutation
 Blue baby syndrome

 HB in thalessemia and related disorders
 Abnormal Hb are present
 Polypeptide chains are decreased

 Thalassemia is an inherited blood disorder
that causes mild or severe anemia.
 The anemia is due to reduced hemoglobin
and fewer red blood cells than normal.
Hemoglobin is the protein in red blood cells
that carries oxygen to all parts of the body.

 In people with thalassemia, the genes that
code for hemoglobin are missing or variant
(different than the normal genes). Severe
forms of thalassemia are usually diagnosed in
early childhood and are lifelong conditions.

 Alpha and beta, are named for the two
protein chains that make up normal
hemoglobin.
 The genes for each type of thalassemia are
passed from parents to their children. Alpha
and beta thalassemias have both mild and
severe forms.

 Four genes are involved in making the alpha
globin part of hemoglobin—two from each
parent.
 Alpha thalassemia occurs when one or more
of these genes is variant or missing.

 People with only one gene affected are
called silent carriers and have no sign of
illness.
 People with two genes affected (called
alpha thalassemia trait, or alpha
thalassemia minor) have mild anemia and
are considered carriers.
 People with three genes affected have
moderate to severe anemia, or
hemoglobin H disease.
 Babies with all four genes affected (a
condition called alpha thalassemia major,
or hydrops fetalis) usually die before or
shortly after birth.

 If two people with alpha thalassemia trait
(carriers) have a child, the baby could have a
mild or severe form of alpha thalassemia or
could be healthy.

 Two genes are involved in making the beta
globin part of hemoglobin—one from each
parent. Beta thalassemia occurs when one or
both of the two genes are variant.

 If one gene is affected, a person is a carrier
and has mild anemia. This condition is called
beta thalassemia trait, or beta thalassemia
minor.
 If both genes are variant, a person may have
moderate anemia (beta thalassemia
intermedia, or mild Cooley’s anemia) or severe
anemia (beta thalassemia major, or Cooley’s
anemia).
 Cooley’s anemia, or beta thalassemia major, is
a rare condition. A survey in 1993 found 518
Cooley’s anemia patients in the United States.
Most of these persons had the severe form of
the illness, but there may be more who are
not diagnosed.

1. Thalassemia is passed from parents to
children through their genes.
2. Thalassemia affects both males and
females.
3. Beta thalassemias affect people of
Mediterranean origin or ancestry
(Greek, Italian, Middle Eastern) and
people of Asian and African descent.
4. Alpha thalassemias mostly affect people
of Southeast Asian, Indian, Chinese, or
Filipino origin or ancestry.

 The symptoms of thalassemia depend on the
type and severity of the disease.
 Symptoms occur when not enough oxygen
gets to various parts of the body due to low
hemoglobin and a shortage of red blood cells
in the blood (anemia).

1. Fatigue (feeling tired) and weakness
2. Pale skin or jaundice (yellowing of the skin)
3. Protruding abdomen, with enlarged spleen and
liver
4. Dark urine
5. Abnormal facial bones and poor growth
Babies with all four genes affected (a condition called
alpha thalassemia major, or hydrops fetalis) usually
die before or shortly after birth

1. Thalassemia is diagnosed using blood
tests, including a complete blood count (CBC)
and special hemoglobin studies.
2. A CBC provides information about the amount
of hemoglobin and the different kinds of
blood cells, such as red blood cells, in a
sample of blood. People with thalassemia
have fewer red blood cells than normal and
less hemoglobin than normal in their blood.
Carriers of the trait may have slightly small
red blood cells as their only sign.
3. Hemoglobin studies measure the types of
hemoglobin in a blood sample.

 is usually diagnosed in early childhood because
of signs and symptoms, including severe anemia.
Some people with milder forms of thalassemia
may be diagnosed after a routine blood test
shows that they have anemia.
 Doctors suspect thalassemia if a child has
anemia and is a member of an ethnic group that
is at risk for thalassemia.

 To distinguish anemia caused by iron deficiency
from anemia caused by thalassemia, tests of the
amount of iron in the blood may be done.
 Iron-deficiency anemia occurs because the body
doesn’t have enough iron for making
hemoglobin.
 The anemia in thalassemia occurs not because
of a lack of iron, but because of a problem with
either the alpha globin chain or the beta globin
chain of hemoglobin. Iron supplements do
nothing to improve the anemia of thalassemia,
because missing iron is not the problem.

 Family genetic studies are also helpful in
diagnosing thalassemia. This involves taking a
family history and doing blood tests on family
members.
 Prenatal testing can determine if an unborn
baby has thalassemia and how severe it is likely
to be.

Treatment for thalassemia depends on the type
and severity of the disease.
 People who are carriers (they have
thalassemia trait) usually have no symptoms
and need no treatment.

 Those with moderate forms of thalassemia (for
example, thalassemia intermedia) may need
blood transfusions occasionally, such as when
they are experiencing stress due to an infection.
 If a person with thalassemia intermedia worsens
and needs regular transfusions, he or she is no
longer considered to have thalassemia
intermedia; instead, the person is said to have
thalassemia major, or Cooley’s anemia.

1. Those with severe thalassemia have a
serious and life-threatening illness.
2. They are treated with regular blood
transfusions, iron chelation therapy, and
bone marrow transplants.
3. Without treatment, children with severe
thalassemia do not live beyond early
childhood.

 Severe forms of thalassemia are treated by
regular blood transfusions.
 A blood transfusion, given through a needle in a
vein, provides blood containing normal red
blood cells from healthy donors. In thalassemia
treatment, blood transfusions are done on a
schedule (often every 2–4 weeks) to keep
hemoglobin levels and red blood cell numbers at
normal levels. Transfusion therapy can allow a
person with severe thalassemia to feel better,
enjoy normal activities, and live longer.

 Transfusion therapy, while lifesaving, is
expensive and carries a risk of transmitting viral
and bacterial diseases (for example, hepatitis).
Transfusion also leads to excess iron in the blood
(iron overload), which can damage the liver,
heart, and other parts of the body. To prevent
damage, iron chelation therapy is needed to
remove excess iron from the body.

 Iron chelation therapy uses medicine to
remove the excess iron that builds up in the
body when a person has frequent blood
transfusions. If the iron is not removed, it
damages body organs, such as the heart and
liver.

 The medicine, deferoxamine, works best when
given slowly under the skin, usually with a small
portable pump overnight.
 This therapy is demanding and sometimes is
mildly painful, so some people stop chelation
therapy. A pill form of iron chelation
therapy, deferasirox, was approved in November
2005 for use in the United States.
 People who have iron overload should not take
vitamins or other supplements that contain
iron.

 Surgery may be needed if body organs, such
as the spleen or gall bladder, are affected.
 For example, if the spleen becomes inflamed
and enlarged, it may be removed.
 If gallstones develop, the gall bladder may
be removed.

 Bone marrow or stem cell transplants have
been used successfully in some children with
severe thalassemia. This is a risky
procedure, but it offers a cure for those
children who qualify.

 People with severe thalassemia are more likely
to get infections that can worsen their anemia.
They should get an annual flu shot and the
pneumonia vaccine to help prevent infections.
 Folic acid is a B vitamin that helps build red
blood cells. People with thalassemia should
take folic acid supplements.
 Researchers are also studying other
treatments, such as gene therapy and fetal
hemoglobin.

 They are the measurements that describe the size
and oxygen carrying protein (hemoglobin) content
of red blood cells. The indices are used to help in
the differential diagnosis of anemia.
 The relationships between the hematocrit, the
hemoglobin level, and the RBC are converted to
red blood cell indices through mathematical
formulas.
 The indices include these measurements: mean
corpuscular volume (MCV); mean corpuscular
hemoglobin (MCH); and mean corpuscular
hemoglobin concentration (MCHC).

 The MCV is the average volume of the RBC in cubic
microns
 MCV = Hct (%) X 10 / RBC count (10-12/L)
 Example: Hct = 45%, RBC count = 5.0x1012/L;
therefore,
 MCV = 45.0x10 / 5.0 = 90fL
 Cells of normal size (MCV is 80-100cu. microns) are
called normocytic, smaller cells are microcytic, and larger
cells are macrocytic.

 Microcytic cells are found in:
 Patients with iron deficiency anemia.
 Thalassemia.
 Macrocytic cells are found in:
 Patients with liver disease or hypothyroidism
 When there is asynchrony in RBC maturation (termed
megaloblastic anemia's).
 Folate and vitamin B12 deficiencies.

 The MCH is the average weight of Hb in an RBC,
expressed in the units of picograms (pg), or 10-12g:
 MCH = Hb (g/dL) X 10 / RBC count (1012/L).
 The reference range for adults is 28-32pg.
 The MCH is not generally considered in the
classification of anemia's.
 Example:
 Hb=16.0 g/fl.
 RBC count=5.0x1012/l.
 MCH=16.0x10 / 5.0 = 32.0pg

 The MCHC is the average concentration of Hb
in each individual erythrocyte. The
 units used are gram per deciliter (formerly
referred to as a percentage).
 MCHC = Hb (g/dL) X 100 / Hct (%).
 Example: Hb =16 g /dl, Hct = 48%;
 MCHC=16 X 100 / 48 = 33.3g/dL

 Values of normochromic cells range from 32 to
37g/dL.
 Hypochromic cells are less than 32g/dL, and
those of hyperchromic cells are greater than
37g/dL.
 Hypochromic erythrocytes occur in thalassemia
and iron deficiency.
 Because there is a physical limit to the amount of
hemoglobin that can fit in a cell, there is no
hyperchromic category, a cell does not really
contain more than 37g/dL of Hb, but its shape
may have become spherocytic, making the cell
appear full.

 Hematocrit is defined as the volume occupied by
erythrocytes in a given volume of blood and is
usually expressed as a percentage of the volume of
the whole blood sample.
 The hematocrit may also be referred to as Packed
Cell Volume (PCV).

 Principle:
• The hematocrit is usually determined by spinning a blood-
filled capillary tube in a centrifuge.
 Specimen:
• Venous blood anticoagulated with EDTA or capillary blood
collected directly into heparinized capillary tubes can be
used. Specimens should be centrifuged within 6 hours of
collection.
• Hemolyzed samples cannot be used for testing.

 Reagents and equipment:
• Capillary tubes, heparinized for finger sticks (red tip) or
plain for anticoagulated blood (blue tip)
• Clay-type tube sealant
• Microhematocrit centrifuge
• Microhematocrit reader
• Kimwipes or gauze

 Procedure:
1. Fill two capillary tubes approximately three quarters
full with blood anti-coagulated with EDTA or heparin.
Alternatively, blood for heparinized capillary tubes
may be collected by capillary puncture. Wipe any
excess blood from the outside of the tube.
2. Seal the end of the tube with the colored ring with
nonabsorbent clay

3. Balance the tubes in the centrifuge with the clay ends
facing the outside away from the center, touching the
rubber gasket.
4. Tighten the head cover on the centrifuge and close
the top. Activate the centrifuge for 5 minutes
between 10,000 and 15,000 rpm
5. Determine the HCT by using a microhematocrit
reading device Read the level of RBC packing.
6. The values of the two Hcts should agree within 2%
(0.02).

Reference ranges:
•Newborn 53-65%
•Infant/child 30-43%
•Adult male 42-52%
•Adult female 37-47%

Normocytic normochromic anemia
Eg. Hemolytic anemia, anemia of
chronic disease, aplastic anemia
Macrocytic normochromic anemia
Eg. Vitt B12
Macrocytic hypochromic anemia
Eg. Protein deficiency
Microcytic and hypochromic anemia
Eg iron deficiency anemia

Hemorrhagic anemia
Hemolytic anemia
Nutrition deficiency anemia
Aplastic anemia
Anemia of chronic disease

 Excessive loss of blood
 Acute and chronic
 Acute
 Accident
 Decreased RBC count causes hypoxia which stimulates
the bone marrow to produce more no. of RBC.
 Chronic
 Internal or external bleeding over a long period of
time
 Like peptic ulcer, purpura, hemophilia and
menorrhagia

 Excessive destruction of RBC
 Two types:
 Extrinsic
 Liver failure
 Renal disorder
 Hypersplenism
 Burns
 Infections
 Intrinsic
 Generally inherited like sickle cell anemia and
thalassemia

 Sickle cell anemia/ SS disease/ Sickle cell
disease
 inherited blood disorder
 Alpha chains normal
 beta chains abnormal
 Mainly seen in black race
and in central Africa where
falciparum malaria is endemic

 Anemia – severe hemolytic anemia.
 Vaso – occlusive phenomenon – recurrent
vaso – occlusive due to obstruction to
capillary blood flow by sickled cells upon
deoxygenation or dehydration
 Micro infarcts – abdomen, chest , and joints
 Macro infarcts – bones, liver, kidney, spleen
 Other symptoms like impaired growth and
development and increased susceptibility to
infection due to markedly impaired splenic
function.

 Iron deficiency anemia
 Pernicious anemia/ Addison’s anemia
 Megaloblastic anemia

Country Men (%) Women
(%)
Pregnant
Women (%)
S. India 6 35 56
N. India 64 80
Latin America 4 17 38
Israel 14 29 47
Poland 22
Sweden 7
USA 1 13

Functions as electron transporter; vital
for life
Must be in ferrous (Fe+2) state for activity
In anaerobic conditions, easy to maintain
ferrous state
Iron readily donates electrons to oxygen
Ferric (Fe+3) ions cannot transport
electrons or O2
Organisms able to limit exposure to iron
had major survival advantage

 Blood Loss
 Gastrointestinal Tract
 Menstrual Blood Loss
 Urinary Blood Loss (Rare)
 Blood in Sputum (Rarer)
 Increased Iron Utilization
 Pregnancy
 Infancy
 Adolescence
 Polycythemia Vera
 Malabsorption
 Tropical Sprue
 Gastrectomy
 Chronic atrophic gastritis
 Dietary inadequacy (almost never sole cause)
 Combinations of above

Stainable Iron, Bone Marrow Aspirate
Serum Ferritin - Low in Iron Deficiency
Desaturation of transferrin
Serum Iron drops
Transferrin (Iron Binding Capacity)
Increases
Blood Smear - Microcytic, Hypochromic;
Aniso- & Poikilocytosis
Anemia

 Fatigue - Sometimes out of proportion to
anemia
 Atrophic glossitis
 Pica
 Koilonychia (Nail spooning)
 Esophageal Web

Correction of the disorder
Correction of iron deficiency
 Oral therapy
 Ferrous sulphate – 6omg TID
 Ferrous gluconate – 37mg
 Parenteral therapy
 Dose is calculated by multiplying the
grams of Hb below normal with 250.
 Given as single IM iron
dextran(interferon)
 Repeated inj. Of iron sorbitol citrate
(jectofer)

Dietary modification
Food fortification
Iron supplementation

Diet & nutrition education
eat more fruits and vegetable
no coffee or tea with meals
programmes should be targeted
to at risk groups
reduce phytic content of cereals
and legumes by fermentation

 Short term approach:
 supplementation with iron tablets.
 Long-term approach:
 food fortification with iron either for the whole
population (blanket fortification) or for specific
target groups like infants. It requires no
cooperation from users unlike taking iron
supplements.

 Iron compounds used in food fortification can
be divided into 4 groups
Freely water soluble (ferrous sulphate,
gluconate, lactate & ferric ammonium
citrate).
Poorly water soluble (ferrous fumarate,
succinate & saccharate).
Water insoluble (ferric pyrophosphate, ferric
orthophosphate & elemental iron).

 The major factors governing the choice of
iron compound include:
Bioavailability
Organoleptic problems
Cost
Safety
 Ideally we should go for a safe, cheap, highly
bioavailable iron, which causes no
organoleptic side-effects

 Freely water soluble iron are the most
bio-available, but causes unacceptable
colour & flavour change in many foods.
 Insoluble iron compounds are inert with
no organoleptic effects but it is poorly
absorbed
 Cost-wise elemental iron is the cheapest,
ferrous sulphate costs 10 times more, but
most expensive is EDTA
 Safety is of concern with EDTA & Bovine
Hb only because of potential problems

137
1. Vit. B12 deficiency
2. Folic acid deficiency
3. Other causes like drugs which interfere with DNA
synthesis, acquired defects of hemopoietic stem
cells and congenital enzyme deficiency.

138
Vitamin B12 Folic acid
Sources meat, fish green
vegetables, yeast
Daily requirement 2-5 ug 50-100 ug
Body stores 3-5 mg (liver) 10-12mg (liver)
Places of absorption ileum duodenum and proxymal
segment of
small intestine

 First described by Addison in 1855 as a
chronic disorder of middle aged and elderly
individual of either sex in which intrinsic
factor secretion ceases owing to atrophy of
the gastric mucosa.
 Average age is 60yrs.
 Bur rarely can be seen in children ( juvenile
pernicious anemia)
 Mostly seen in northern European descent
and American blacks and is uncommon in
South European.

 Insidious onset and progress slowly
 Mainly due to Vit. B12 deficiency
 Anemia, Glossitis, Neurological abnormalities
( neuropathy, subacute combined
degeneration of the spinal cord, retrobulbar
neuritis) GIT manifestation ( diarrhoea,
anorexia, weight loss, dyspepsia),
hepatospleenomegaly, congestive heart
failure and hemorrhagic manifestation

 Hypergastrinaemia
 Pentagastrinaemia
 Haematologic findings -
 Rise in serum
bilirubin, LDH, haptoglobin, ferrritin and
iron.
 Chromosomal abnormalities are frequently
present in bone marrow cells which
disappear after therapy.

 Replacement therapy with vitamin B12
 Vitamin B12 administration intramuscular in dose 1000 (100) μg
per day for a week , then 100 μg 2x per week for 2 weeks, 1 x
per week 100μg for month
 Reticulocytosis begins 2 or 3 days after therapy started and
maximal number reached on day 5 to 8.
 Serum iron monitoring, after 7-10 days of vit.B12 treatment,
 If Fe deficiency is diagnosed we should start iron substitution
 100 ug vit.B12 i.m. every month, regimen that must be
maintained for the rest on the patients life.
 Physiotherapy for neurologic deficits and occasionally blood transfusion
 Follow up early detection of cancer of the stomach

145
1. Inadequate intake
- diet lacking fresh, slightly cook food; chronic alcoholism, total
parenteral nutrition,
2. Malabsorption
- small bowel disease (sprue, celiac disease,)
- alcoholism
3. Increased requirements:
- pregnancy and lactation
- infancy
- chronic hemolysis
- malignancy
- hemodialysis
4. Defective utilisation
Drugs:folate antagonists(methotrexate, trimethoprim, triamteren), purine
analogs (azathioprine), primidine analogs (zidovudine), RNA reductase
inhibitor (hydroxyurea), miscellaneous (phenytoin, N2)

146
1. Symptoms of anemia
2. Symptoms associated with vit. B12 or Folic acid
deficiency
neurologic manifestations (exclusivly in wit. B12 deficiency)
- megaloblastic madness or psychosis,
- subacute, combined degeneration of the
spinal cord (proprioceptive and vibratory
sensation, spinal ataxia)
gastrointestinal compraints (vit.B12 and folic acid
deficiency)
- loss of appetite
- glosstis (red, sore, smooth tongue)
- diarrhea or constipation

147
1. Blood cell count:
macrocytic anemia
thrombocytopenia
leucopenia (granulocytopenia)
low reticulocyte count
2. Blood smear:
hypersegmentation of granulocytes
macroovalocytes , anisocytosis, poikilocytosis

148
3. Laboratory features
indirect hyperbilirubinemia
elevation of lactate dehrogenase (LDH)
serum iron concentration- normal or increased
4. Bone marrow smear
hypercellular
increased erythroid /myeloid ratio
erythroid cell changes (megaloblasts, RBC precursor a abnormally
large with nuclear- cytoplasmic asynchrony)
myeloid cell changes (giant bands and metamyelocytes
, hypertsegmentation)
megakariocytes are decreased and show abnormal morphology

149
1. Establishing megaloblastic anemia
2. History: causes of folate deficiency
3. Absence neurologic symptoms
4. Low serum and red blood cell folic acid

150
FOLIC ACID DEFICIENCY ANEMIA
1. Oral administration of Ac. folicum 1 (5) mg
per day, for 3 months, and maintenance
therapy if it’s necessary.
2. Reticulocytosis after 5-7 days
3. Correction of anemia is over after 1-2
months therapy
4. Maintenance therapy if necessary

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