Prepared by: Maha Nahal

Introduction .1
Anemia .2
Iron deficiency anemia .3
G6PD deficiency .4
.A plastic Anemia .5
ITP.5
Blood
Blood is the fluid of life
:Blood is composed of
Plasma ◦
RBC ◦
WBC ◦
Platelets ◦
:Plasma consists of
.water 90% ◦

.solutes: albumin, electrolytes and proteins % 10 ◦

Proteins consist of clotting factors, globulins, ◦

. circulating antibodies and fibrinogen
 RBC’s travel through the body delivering
.oxygen and removing waste
RBC’s are red because they contain a protein 
chemical called hemoglobin which is bright
.red in color
Hemoglobin contains iron, making it an 
excellent vehicle for transporting oxygen and
. carbon dioxide
 Average life cycle is 120
. days

The bones are continually

. producing new cells
.The battling(fighting) blood cells
The white blood cells are continually on the 
.look out for signs of disease

:When a germ appears the WBC will

.Produce protective antibodies ◦
Surround it and devour the bacteria ◦
 WBC life span is from a few days to a few
.weeks
.WBC’s will increase when fighting infection
Platelets are irregularly-shaped, colorless
.bodies that are present in blood
Their sticky surface lets
them form clots
.to stop bleeding
:Hgb
Normal levels are 11 to 16 g / dl
:Panic levels are
Less than 5 g / dl
More than 20 g / dl
Describes a condition in which the number of 
RBCs or Hgb concentration is reduced below
.normal
Normally the RBCs carry the oxygen to body
.tissues
In anemia, there is a decrease in the oxygen – 
carrying capacity of the blood that leads to
.decrease oxygen available to tissue
This reduced oxygen carrying capacity will be 
associated with an increased heart rate and
.cardiac out put

The effect of anemia on circulatory system 

can be profound. As viscosity of blood
depends on concentration of RBC, the
resulting hemo-dilution of severe anemia
decreases peripheral resistance, causing
.greater quantity of blood to return to heart
The increased circulation with in the heart 
produces murmur. Since the workload
increased, cardiac failure may occur
Inadequate production of HB or RBC’s which)1
: may be due to

lack of some substances necessary in the )a

formation of cells ( Iron, folic acid ….etc)

Decreased number of red cell precursors )b

.which may be congenital or acquired
)eg. Toxic or Chemical agents(

Excessive loss of RBC’s( hemolysis or)2

hemorrhage)
:Etiology /pathophysiology

Excessive blood loss from acute or chronic ◦
hemorrhage
Destruction (hemolysis) of erythrocytes: result of ◦
intra-corpuscular defect with in RBC as in Sickle
cell anemia,or extra-corpuscular factor as
. infection, chemical or immune factor
Decreased production of erythrocytes: bone ◦
marrow failure as disease or neoplasm or
.deficiency of iron
  Muscle weakness, fatigue, frequent resting,
shortness of breath, poor sucking in
infant, pale skin, Pica: eating clay, ice,
paste
CNS Manifestation: Headache, dizziness, 
slowed thought process, decreased attention
. span, apathy, depression
Shock: poor peripheral perfusion, skin moist 
and cool, low blood pressure, increased heart
. rate
 Includes
;History -
Physical assessment-
.laboratory findings-
 HB level and RBC’s count)1

Hematocrite or packed RBC’s )2

( the ratio of the volume
volume of RBC’s to the volume
of whole blood)
 :Red blood cells indices )3
Mean corpuscular volume(MCV)=
(Hte/ RBC’s count= normal 75-100
fimtoliter)
macrocytic anemiaIf >100
If < 75 microcytic anemia
If 75-100normocytic anemia
(Mean Corpuscular Hemoglobin
= )MCH

Average quantity of HB per

individual red cell (HB/RBC’s
= count
-Normal 27
31picogramme
Mean Corpuscular Hemoglobin Concentration
Average concentration of HB in a =)MCHC(
= volume of packet RBC’s
% HB/Hematocrite = Normal 32-35
Both MCH and MCHC are used
to
determined the content of HB in RBC’s
If normal MCH and MCHC =
Normocytic anemia
If low MCH and MCHC =Hypochromic
anemia
 Peripheral blood smear (film ))4
Reticulocytes count = reflect the state of )5
activity of the BM (Normal value is 0.5-1.5%
of the red blood cells )
Level < 0.5 represent inactive BM , High level
represent BM regeneration
Other specific tests include = BM )6
examination, HB electrophoresis, Osmotic
fragility,Serum iron,B12,Folic acid…etc
 Treat cause
Identify age if child, for example; iron deficiency anemia 
occurs more frequently in infants between 6-24 months of
. age and during the growth spurt of adolescence
Racial or ethnic background is significant as black and Asian
has an abnormal Hgb ( thalassemia and sickle cell anemia)
Infants drink lots of artificial milk lead to iron deficiency 
anemia
.Frequent blood tests
During the last trimester of pregnancy, iron 
transferred from mother to the fetus, which is
adequate for first 5-6 months of full term
infants, but 2-3 months for premature
.infants
Clinical manifestations
Pallor, irritability, anorexia, PICA( Ice , paper) -
.Over weight as high ingestion of milk
Pale
Poor muscle development and prone to infection
Low HB, RBC’s count, & Low hematocrite -
Microcytic, hypochromic RBC’s ( reduction in the -
diameter of cell ,small size and pal color)
Low serum iron, low saturation -
Etiology
.Inadequate supply of iron
.Inadequate iron stores
.Impaired iron absorption
.Blood loss
Inability to form hemoglobin as lack of
.vitamin B 12
.Parasite infection
Etiology: Lack of iron in the diet or
the child’s inability to use the iron he
ingest 1- Low birth weight, Prematurity,
twins decreased storage of iron >=
Continued or excessive milk administration -2
without iron enriched food
Blood loss = Occult bleeding may be due to -3
. a lesion of the GI tract
Malabsorption = ex: celiac disease -4
 

.Decrease Hgb level

.Decrease HCT
Decrease MCV<70mm3 in infants is
.diagnostic
.RBC smaller volume
Decreased serum iron and total iron binding 
.capacity
 Iron supplement (ferrous iron with vitamin C) for 3 months .Should 
be given in 3 divided doses between meals. Ferropel dose is (2-6)
mg/kg/day
Decrease milk intake for children to less than 500ml/day to
.encourage intake of solid food that contains iron
Liquid preparation of iron may temporarily stain the teeth, so clean 
.teeth after administration
.Dietary iron rich .Note that stool will change to green black color
seldom administered if level of Intramuscular or intravenous iron is
Hgb fails to rise after one month therapy. Injection must be injected
deeply into large muscles no more than 1cc at site, without
.massaging
if there is if Hb is less than 4 orTransfusions for severe anemia
infection
 PREVENTION *

Adequate diet include vegetables, -

meat and vitamins for full term
infants
Administration of iron (2 mg/kg) -
from the age of 2 months for low
birth weigh and premature infants
IMBALANCE NUTRITION less than .1
body requirement r/t
. inadequate iron

KNOWLEDGE DEFICIENT r/t cause .2

and treatment of iron deficiency
. anemia
A condition in which all formed elements of the 
blood is depressed
Inherited as an autosomal recessive trait (child 
with congenital abnormalities )
Acquired a plastic anemia (radiations ,drug
) chemical ,chemotherapy,
Assessment ( fatigue,anorexia,petechia ,GI 
bleeding)
HYPOPLASTIC ANEMIA
also genetic or acquired ) RBC only affect (
 :Etiology
Congenital: Fanconi syndrome, a rare hereditary 
disorder characterized by pancytopenia, hypoplasia
of the bone marrow, and patchy brown
discoloration of the skin due to the disposition of
melanine
Infection–Radiation-Drugs: chemotherapy and 
antibiotics as chloramphenicol–Industrial and
.house hold chemicals
Autoimmune and allergic state. Suppression or 
.erythropoiesis from multiple transfusion therapy
Anemia, leuckopenia, and decreased platelet 
.count
Bone marrow aspiration: conversion of red
bone marrow to yellow, fatty bone marrow
 Immunosuppressive therapy
Replacement of bone marrow through 
.transplantation
Anti lymphocyte globulin suppresses
T-cells
.dependent autoimmune responses
Methyl prednisone
Androgens to stimulate erythropoietin
Glucose-6-phosphate Dehydrogenose
)Enzyme to maintenance of RBC life(

Transmitted as a sex-linked -
recessive
Mediterranean and middle eastern -
groups have high frequencies of
G6OD deficiency
Clinically
Usually no evidence of hemolysis is apparent
until 48-96 hours after the patient has
ingested a substance which has oxidant
properties
Antipyretic,Sulfonamide, Anti malarial, or fava(
producing an acute and severe ) beans
hemolytic syndrome called FAVISM, Hb level
become very low, presence of
hemoglobinemia/-uria, mild jaundice,
splenomegally and increased reticulocyte count
G6PD deficiency is an
important cause of
neonatal hemolysis and
neonatal jaundice
 Fatigue
Pallor
Low back pain
Shortness of breath
Tachycardia
Jaundice
Dark urine (Cola color)
Spleenomegaly
 Diagnosis
Low G6PD activity in red blood
cells
Treatment
When hemolysis has occurred =>
Red blood cell transfusion
Prevention
Avoiding ingestion of fava
beans
or oxidant substances
Isan acquired hemorrhagic disorder that is
characterized by excessive destruction of
platelets (thrombocytopenia) and purpura
(discoloration caused by petetchia beneath
the skin)
Causes: Unknown, Autoimmune and after
.upper respiratory tract infection
:Diagnosis
Clinical symptoms
Platelet count < 20.000 mm3, so
tests that


relate to bleeding time are abnormal
 :Treatment
Supportive, Activity is restricted
Corticosteroids and Gamma globulin
.increase platelet count
.Packed RBC
Spleenectomy
