Introduction

 Your blood has two

basic parts :
• blood cells, which
are also called
blood corpuscles
• plasma, the fluid in
which the blood
cells are
suspended
Plasma
 92 % terdiri dari air dan 7 - 8 % terdiri dari zat
padat
 zat-zat padat tsb. adalah
• albumin, globulin, dan fibrinogen
• unsur anorganik berupa natrium, kalsium, kalium,
fosfor, besi dan yodium
• unsur organik berupa zat-zat nitrogen non protein,
urea, asam urat, xantin, kreatinin, asam amino, lemak
netral, fosfolippid, kolesterol, glukosa dan berbagai
jenis enzim amilase, protease dan lipase
Basic parts of the blood
 Plasma
 White blood cells :
• Neutrophil
• Eosinophil
• Basophil
• Lymphocyte
• Monocyte
 Platelets
 Red blood cells
5
Istilah deskriptif & cara pengukuran
 Jumlah sel darah
 Hitung jenis sel darah
 Anisositosis : variasi abnormal dalam ukuran sel
 Poikilositosis : variasi abnormal dalam bentuk
 Sferosit : sel di mana rasio diameter/tebal
berkurang
 Polikromasia : sel berbeda dalam distribusi warna
• Normokrom : Hb normal dalam darah
• Hipokrom : sel pucat pd anemia defisiensi zat besi
 Siderosit : sel mengandung granula besi anorganik
Kelainan Sel Darah Merah / Eritrosit
 Anemia
• Anemia normositik normokrom / normokrom
normositer
• Anemia makrositik normokrom / normokrom
makrositer
• Anemia mikrositik hipokrom / hipokrom mikrositer
 Anemia Aplastik
 Anemia Defisiensi Besi
 Anemia megaloblastik
 Polisitemia
Hematologic
Disorders
 What Is a Complete Blood Count?
 White blood cells (WBCs). The normal range is 4,500 to 10,000 cells
per microliter (cells/mcL). (A microliter is a very tiny amount – one
millionth of a liter).
 RBC (red blood cell count). The normal range for men is 5 million to
6 million cells/mcL; for women it’s 4 million to 5 million cells/mcL.
 Hb or Hbg (hemoglobin). The normal range for men is 14 to 17
grams per deciliter (gm/dL); for women it’s 12 to 15 gm/dL.
 Hct (hematocrit). How much of your blood is red blood cells. A low
score on the range scale may be a sign that you have too little iron,
the mineral that helps produce red blood cells. A high score could
mean you’re dehydrated or have another condition. The normal
range for men is between 41% and 50%. For women the range is
between 36% and 44%.
 What Is a Complete Blood Count?
• MCV (mean corpuscular volume). This is the
average size of your red blood cells. If they’re
bigger than normal, your MCV score goes up.
That could indicate low vitamin B12 or folate
levels. If your red blood cells are smaller, you
could have a type of anemia. A normal-range
MCV score is 80 to 95.
• Platelets. These play a role in clotting. This
test measures the number of platelets in
your blood. The normal range is 140,000 to
450,000 cells/mcL
 MCH (mean corpuscular hemoglobin).How much
hemoglobin (a protein) is in your typical red blood
cell. It carries oxygen to your organs and tissues. It
also moves carbon dioxide from your organs and
tissues back to your lungs.
 MCHC (mean corpuscular hemoglobin
concentration). This measures how concentrated
the hemoglobin is in your typical red blood cell. It’s
how densely packed the hemoglobin molecules are
inside the cells.
 RDW (red cell distribution width). How your much
your red blood cells vary in size.
 Reticulocyte Count. Your results figure out
what could be causing your anemia.
 MPV (mean platelet volume). The size of the
platelets in your blood.
 PDW (platelet distribution width). How
much your platelets vary in size.
 White Blood Cell Differential. There are five
types of white blood cells. This test shows
how many of each type you have:
neutrophils, lymphocytes, monocytes,
eosinophils, and basophils.
Measures of Morphology
• Mean Corpuscular Volume (MCV)
• (Hct X 10)/RBC
• Mean Corpuscular Hemoglobin
(MCH)
• (Hgb X 10)/RBC
• Mean Corpuscular Hemoglobin
Concentration (MCHC)
• (Hgb/Hct) X 100
 Complete Blood Count Normal Adult Values

• White Blood Cells 5,000 – 10,000/mm3

• Red Blood Cells 4.5 – 5.5 million/mm3 (4 – 5
females)
• Hemoglobin 14 – 17 g/dl (12 – 16 females)
• Hematocrit 42 – 52% (36 – 48 females)
• Mean Corpuscular Volume 84 – 96 fL
• Mean Corpuscular Hemoglobin 28 – 34 pg/cell
• Mean Corpuscular Hemoglobin Concentration 32
– 36 g/dl
• Platelets 140,000 – 400,000/mm3
• Red cell Distribution Width 11.5 – 14.5%
• Mean Platelet Volume 7.4 – 10.4 fL
White Blood Cells Differential
Granulocytes (Polymorphonuclears)
• Neutrophils Segmens 50 – 62%
• Neutrophils Band/Stabs 3 – 6%
• Eosinophils 0 – 3%
• Basophils 0 – 1%

Agranulocytes (Mononuclears)
• Monocytes 3 – 7%
• Lymphocytes 25 – 40%
BLOOD DISORDERS
Alterations in Erythrocyte Function
• Anemias
• reduction in the total number of circulating
erythrocytes or a decrease in the quality or
quantity of hemoglobin
• Etiology
• Impaired Erythrocyte Production
• Blood Loss
• Increased Erythrocyte Destruction
• Combination of the Above Causes
Anemias
• Classification based on Morphology
• Size: normocytic, macrocytic, microcytic
• Color: normochromic, hypochromic,
hyperchromic
• Other
• Anisocytic – varied size
• Poiilocytosis – varied shape
ANEMIA
• Iron-Deficiency Anemia (most
common)
• Aplastic Anemia – bone marrow
does not produce enough Red
Blood Cells
• Hemorrhagic anemia – due to
extreme blood loss
• Pernicious anemia – B12
deficiency
• Sickle Cell Anemia (genetic)
Blood loss leads to a particular
type of anemia
 Iron Deficiency anemia
 anemia of chronic
disease
 B12 deficiency anemia
and folic acid
deficiency
 Sickle cell anemia
 Thalassemia
 Hemolytic anemia
What are the symptoms of
anemia
 Weak
 pale
 tired
 faint
 and/or breathless
 palpitations
 increases awareness
of your heartbeat
Clinical Manifestations of Anemia
• Gradual vs. Sudden
• gradual = usually less symptomatic because of
compensation
• sudden = usually more symptomatic
• Magnitude
• Hgb of 8 g would be more likely to be symptomatic
• Hgb of 12 g would be less likely to be symptomatic
• Classic Signs of Anemia
• Pallor
• Fatigue
• Dyspnea on Exertion (DOE)
• Dizziness
Clinical manifestations
• Compensatory Manifestations
• Cardiovascular (stress response) to pump the decreased
amount of oxygen to the vital organs most efficiently
• Tachycardia
• Palpitations
• Vasoconstriction
• Respiratory – to increase the effectiveness of
breathing in order to optimize the uptake of oxygen
• tachypnea
• increased breathing depth
• Other
• increased plasma volume – interstitial fluid moves into the
vascular space
• salt and water retention ( because of activation of the Renin-
Angiotensin-Aldosterone (RAA) system)
Macrocytic-Normochromic Anemia
(Megaloblastic)
• Characterized by defective DNA synthesis that
produces a pattern of ineffective erythropoiesis,
resulting in unusually large stem cells in the bone
marrow called megaloblasts that mature into
unusually large and fragile erythrocytes that may
die prematurely resulting in increased bilirubin
levels.
• Complete Blood Count characteristics
• Anemia
• Macrocytic
• Normochromic or Hyperchromic
Megaloblast Anemias
• Pernicious Anemia – Vit B12 Deficiency
• Pernicious means highly injurious or destructive,
indicating its fatal potential if untreated
• Etiology
• Chronic condition caused by malabsorption of vitamin
B12
• Decreased intake of Vitamin B12 (strict vegetarians)
• Animal products
• Meat, shellfish
• Milk, eggs
• Stored in liver for 3-5 years
Pernicious Anemia cont
• Etiology
• Defective gastric secretion of Intrinsic factor
(IF) from parietal cells of gastric mucosa
• Congenital
• Following partial or complete gastrectomy
• Autoimmune gastric atrophy
• Chronic atrophic gastritis
• Heavy alcohol, hot tea, smoking
• More common in elderly
Pernicious Anemia
• Clinical Manifestations
• Classic signs of anemia
• Neurologic manifestations with severe anemia (<7 g/dl)
• Vitamin B12 is necessary for the synthesis of myelin
• Parasthesias of feet and fingers
• Ataxia
• Loss of position and vibration sense
• Spasticity
• Sore tongue, beefy red (unknown cause)
• Hyperbilirubinemia
• Jaundice/icterus
• “Lemon yellow” skin – combination of pallor and jaundice
• Hepatosplenomegaly – enlarged liver and spleen
Pernicious Anemia
• Evaluation
• Complete Blood Count analysis
• Clinical manifestation analysis
• B12 levels
• Schilling test – Vit B12 absorption is
measured by administering radioactive
Vitamin B12 and measuring its excretion in
the urine
• Intrinsic factor evaluation
• Bone marrow aspiration and analysis
Pernicicous Anemia
• Treatment
• Vitamin B12 administration
• Injection if IF deficiency is the problem
• Orally, IF deficiency is not the problem
• Dietary adjustments
• Blood transfusion
• Monitor reticulocyte count for evidence of
response to therapy
Vitamin B12
• Cyanocobalamin
• Routes: PO, Intranasally, IM, SC
• Oral Preferred
• Adverse effects: hypokalemia
• PO: 1000-10,000 micrograms/day tx
6 micrograms/day dietary supplement
• IM, SC: typically 30 micg/day x 5-10days
then 100 to 200 micg/month
• Intranasal 500 micg/spray once a week
B12 Treatment Considerations
• Monitor B12 levels
• Monitor Hemogram and
reticulocytes
• Give Folic acid with B12 for severe
anemia
• Folic acid caution
Folate Deficiency
• Megaloblastic anemia
• Etiology low folic acid levels
• Sources: liver, yeast, fruits, leafy vegetables, eggs, milk
• Absorbed in upper small intestine and is not IF
dependent
• Circulates through the liver with very little storage
• Deficiency is most common with select groups
• Pregnancy and lactation (increased need)
• Fad diets with decreased intake of folate
• Alcoholic persons (ETOH interferes with folate
metabolism)
• Chronically malnourished
• Sprue
Folate deficiency anemia
• Clinical Manifestations
• Classic signs of anemia
• No neurologic manifestations
• Manifestations related to malnourishment
• painful ulcerations of cheeks and tongue
• fissuring of lips and mouth
• Gastrointestinal symptoms
• Dysphagia
• Flatulence
• Watery diarrhea
Folate Deficiency Anemia
•Evaluation
•Complete Blood Count
•Clinical Manifestations
•Folic acid levels
•Bone marrow aspiration and
analysis
Folate deficiency anemia
• Treatment
• Folic acid requires B12 to be converted to
active form
• In large amounts, Folic acid is converted via
an alternate pathway
• Two forms of treatment are available
• Active form: leucovorin, folinic acid,
citrovorum factor
• Inactive form: folacin, folate,
pterolyglutamic acid, folic acid
• Inactive form is more common
Folic Acid
• Indications
• Treatment of Folic acid deficiency anemia
• Prophylaxis for deficiency during pregnancy
• Initial tx of severe B12 deficiency
• Adverse effects: no known
• Routes: PO, IM, SC, IV
• Dosage: 1000 – 2000 micrograms/day
400 micrograms/day
Folic Acid
•Treatment Guidelines
•Monitor Complete Blood
Count and reticulocytes
•If malabsorption is cause, diet
alone will not be sufficient
•Oral is preferred
Microcytic-Hypochromic Anemia
• Characterized by erythrocytes that
are abnormally small and contain
abnormally reduced amounts of
hemoglobin
• Complete Blood Count characteristics
• Anemia
• Microcytic
• Hypochromic
Fe Deficiency Anemia
• Pathophysiology
• The body maintains a balance between iron
that is in use as Hgb and iron that is in
storage for future Hgb synthesis
• As old RBCs are broken down, iron is recycled
• Inadequate intake of iron-rich foods
• Children with increased need related to
growth
• Pregnancy
• Iron poor diet
Fe Deficiency Anemia
• Pathophysiology (cont.)
• Increased iron loss through bleeding,
• Menorrhagia – excessive menstrual bleeding
• Medications that cause GI bleeding (ASA, NSAIDS)
• Hemorrhoids
• Ulcerative Colitis (bloody diarrhea)
• Chronic blood loss with gastric or duodenal ulcers
• Neoplasms which erode into blood vessels
• Decreased iron related to parasitic infection (i.e.
hookworms metabolize iron)
Fe Deficiency Anemia
• Clinical Manifestations
• Classic signs of anemia
• Structural and functional changes in epithelial tissue
as a result of impaired capillary circulation (usually
not present unless the anemia is severe, < 7 g/dl)
• nails – brittle, thin, coarsely ridged, spoon-shaped
(koilonychia)
• Tongue – sore, red, burning caused by atrophy of the
papillae (glossitis)
• Sore, dry skin at the corners of the mouth called “angular
stomatitis”
• Difficulty swallowing related to a mucous web at the level
of the hypopharynx and epiglottis (consisting of mucous
& inflammatory cells)
Fe Deficiency Anemia
• Clinical manifestations
• Deficient iron containing enzymes
• gastritis
• headache
• Neuromuscular changes probably related to hypoxia
(gait problems are rare)
• numbness
• tingling
• Confusion, disorientation, memory loss (elderly)
• Pica (eating disorders)
Fe Deficiency Anemia
• Evaluation
• Complete Blood Count analysis
• Clinical manifestation analysis
• Serum Iron profile
• Plasma Iron (Fe)
• Total Iron Binding Capacity (TIBC)
• Transferrin – carrier protein for iron
• Ferritin – storage form of iron
• Free Erythrocyte Protoporphyrin (FEP) – indicator of
heme synthesis within erythrocytes
• Bone Marrow aspiration and analysis
Fe Deficiency Anemia
• Treatments
• eliminate causes of blood loss
• administer iron
• offer dietary counseling
• blood transfusion
• monitor reticulocyte count for
evidence of response to therapy
Iron Therapy
• Oral Iron Preparations
• Iron Salts
• Ferrous Sulfate (DOC)
• Ferrous Fumarate
• Ferrous Gluconate
• Carbonyl Iron
• Parenteral Iron
• Iron Dextran
• Sodium-ferric Gluconate Complex ad Iron
Sucrose
Ferrous Sulfate
• Least expensive
• Standard by which other therapies
are judged
• Indications
• Tx of Iron Deficiency Anemia
• Prophylaxis
• Adverse Effects
• Gastro Intestinal side effects
• Staining of teeth (liquid forms
Ferrous Sulfate
• Toxicity
• Rare from therapeutic dosing
• Mostly accidental or intentional overdosing
• Adult fatality rare
• Child mortality common
• Normal Vaginal Delivery, shock, then
acidosis, gastric necrosis, hepatic failure,
pulmonary edema, vasomotor collapse
• Early dx saves lives :Fe levels and gastric x-
ray
Ferrous Sulfate
• Drug Interactions
• Antacids decrease iron absorption
• Tetracyclines decrease absorption of both
• Ascorbic acid increases absorption and side
effects
• Formulations Immediate Release (IR) and
Sustained Release (SR)
• Dosage and administration
• Elemental Iron is key
• Relationship to meals
Microcytic Hypochromic Anemia

•Sideroblastic Anemia –
• group of hereditary and acquired
microcytic hypochromic anemias
characterized by inefficient iron
uptake resulting in dysfunctional
hemoglobin synthesis
Normocytic-Normochromic Anemia

• Characterized by erythrocytes that

are relatively normal in size and
hemoglobin content, but insufficient
in number
• Complete Blood Count characteristics
• Anemia
• Normocytic
• Normochromic
Aplastic Anemia
• Pathophysiology
• Caused by bone marrow failure
(hypoplasia or aplasia)
• Pancytopenia is common (RBC, WBC, &
platelet counts are all low)
• Pure red cell aplasia (PRCA) is an
associated condition - only red cells are
affected
Aplastic Anemia
• Etiology
• Acquired
• Primary - Idiopathic
• 50% of all confirmed cases
• 80% of Aplastic anemia occuring over age 50
• Secondary
• Chemicals
• Benzene
• Chloramphenicol
• Chemotherapy for cancer treatment
• Ionizing radiation
• Hereditary – Fanconi anemia – rare genetic anemia
• Has been observed to be a precursor to leukemia for some
persons (preleukemic condition)
Aplastic Anemia
• Clinical manifestations
• Classic signs of anemia
• If WBCs are low – expect infection
• If platetets are low – expect bleeding
• Evaluation
• Complete Blood Count
• Bone Marrow Biopsy analysis
Aplastic Anemia
•Treatment
• Treat underlying disorder
• Prevent further exposure to
causal agent
• Blood transfusions
• Bone Marrow Transplant
Post-Hemorrhagic Anemia
• Pathophysiology
• Caused by acute blood loss
• Immediate effects are those of volume
depletion
• Fluid Volume Deficit
• Hypovolemic Shock
• The stress response attempts to
compensate for the volume loss
Post Hemmorhagic Anemia
• Clinical Manifestations
• Sympathetic Nervous system (SNS) stimulation
• If greater than 50% blood loss
• Shock
• Lactic Acidosis
• Death
• Classic Signs of anemia
• If the blood loss becomes chronic – loss of iron
recycling results in the development of iron
deficiency anemia – with clinical manifestations as
described above
Post Hemmorhagic Anemia
•Evaluation
• Complete Blood Count analysis
• Vital signs assessment &Physical
examination
• History driven
• Look for bleeding if not
obvious
Post Hemmorhagic Anemia

•Treatment
•Stop the bleeding
•Administer fluids
•Blood transfusion
Hemolytic Anemia
• Pathophysiology
• Premature, accelerated destruction of RBCs
• Erythropoiesis is normal and often
accelerates in an attempt to compensate for
the increased destruction
• Elevated Bilirubin levels often occur as a
consequence of the increased destruction
• Jaundice
• Icterus (scleral icterus)
Hemolytic Anemia
• Etiology
• Acquired
• Immune Mediated
• Traumatic
• Infectious
• Toxic
• Physical
• Hypophosphatemic
Hemolytic Anemia
• Etiology cont.
• Hereditary
• Structural Defects
• Enzyme Deficiencies
• Defects of Globin synthesis or
structure
• Sickle cell anemia
• Thalassemia
Hemolytic Anemia
• Clinical Manifestations
• Classic Signs of Anemia
• Jaundice
• Splenomegaly
• Evaluation
• Complete Blood Count analysis
• Bone Marrow studies
• Clinical Manifestation analysis
• Other tests for immune status or Hgb examination
etc. depending on the cause of the hemolysis
Hemolytic Anemia
• Treatment
• Remove the cause
• Treat the underlying disorder
• Blood transfusions
• Splenectomy if that is a site where hemolysis
is occurring
• Corticosteroids to treat immune mediated
hemolysis
• Administration of folate, iron, erythropoietin
Anemia of Chronic Disease (ACD)

• Pathophysiology
• Most common anemia in the
hospitalized patient
• Three pathogenic mechanisms cause
Anemia pf Chronic Disease
• Decreased erythrocyte lifespan
• Failure of mechanisms of
compensatory erythropoiesis
• Disturbances of the iron cycle
Anemia of Chronic Disease (ACD)
• Etiology
• Chronic Infections
• HIV
• Hepatitis C
• Chronic inflammatory diseases
• Rheumatoid Arthritis
• Systemic Lupus Erythematosus
• Inflammatory Bowel Disease
• Malignancies
Anemia of Chronic Disease (ACD)

• Clinical Manifestations
• Classic signs of anemia
• Usually normocytic-normochromic
but may be microcytic-hypochromic
if iron cycle is severely affected
• Manifestations of Iron deficiency
anemia if microcytic-hypochromic
Anemia of Chronic Disease (ACD)

• Evaluation
• Complete Blood Count analysis
• Screening for malignancies if chronic
infection or inflammation is not present
• Treatment
• Treat the underlying disorder
• Administer Erythropoietin
• Blood transfusion
Hemoglobin Blood Products
• Packed Red Blood Cells (PRBCs)
• No plasma; easier to store
• Less likelihood of fluid overload
• Whole Blood
• Contains clotting factors and proteins
• Both
• Used to replace blood losses
• Contains hemoglobin
• Can transmit viruses
• Carry oxygen to cells
• Contain citrates – may affect calcium levels
PRBCs and Whole Blood
• Poor shelf life, expensive (testing), availability varies
• Must be typed and cross-matched (time consuming)
• Many patients have developed antibodies against all
blood groups (patients with prior blood transfusions),
and PRBCs and whole blood must be "washed" to
remove antigens
• Can transmit viruses and other pathogens
• Adverse (allergic) reactions common
• Regiatered Nurse must follow strict protocols when
transfusing
• Nursing students are not allowed to transfuse PRBCs and
whole blood !!!
Other Blood Products
• Frosh Frozen Plasma (FFP)
• Albumin
• Platelets
• Clotting Factors
Kelainan Sel Darah Putih / Leukosit
 Leukositosis : Monositosis, Limfositosis,
granulositosis (neutrofilia, eosinofilia, basofilia)
 Leukopenia : Neutropenia
 Agranulositosis
 Leukemia
• Leukemia akut :
– Leukemia Myelogenik/Granulositik Akut.(AML/AGL)
– Leukemia Limfosistik Akut (LLA)
• Lekemia Kronis :
– Lekemia Granulositik Kronik (CGL)
– Leukemia Limfositik Kronik (CLL)
LEUKEMIA
 Is cancer of White Blood
Cells
 Abnormal blood cells
often multiply at an
increased rate
 There are two main types
of leukemia
• lymphocytic leukemia
• myelogenous leukemia
Limfoma : gangguan limfoproliferatif

 Limfoma Burkitt
 Limfoma Hodgkin dan non Hodgkin

 Multiple Myeloma :
• keganasan gangguan limfoproliferatif
yang berhubungan dengan sel plasma
Leukemia
• Type of cancer
• Overproduction of immature white blood
cells
• They take the place of RBCs

• Treatable with bone marrow transplants,

chemothemotherapy, radiation
Blood
Smear of a
patient with
Leukemia
Blood Smear; Leukemia
 St. Jude Hospital

Leukemia is one of the most common childhood cancers. It occurs

when large numbers of abnormal white blood cells fill the bone marrow
and sometimes enter the bloodstream.

Because these abnormal blood cells are defective, they don't help
protect the body against infection the way normal white blood cells do.
And because they grow uncontrollably, they take over the bone
marrow and interfere with the body's production of other important
types of cells in the bloodstream, like red blood cells (which carry
oxygen) and platelets (which help blood to clot).
Infectious mononucleosis
sometimes called "mono"
or "the kissing disease," is
an infection usually
caused by the Epstein-
Barr virus (EBV).

EBV is very common, and

many people have been
exposed to the virus at
some time in childhood.
Blood poisoning - Septicemia
• An infection enters the blood stream
• Can be deadly
• Treated with antibiotics
Pembekuan (Hemostasis)
 Trombosit : trombositopenia,
trombositosis
Gangguan plasma herediter :
Hemofilia
Defisiensi faktor plasma : vitamin
K. fibrinolisis, DIC (Disseminated
Intravascular Coagulopathy)
BLEEDING AND BRUISHING
 Bleeding occurs when
a blood vessel is
damaged
 Bleeding from a cut,
which should stop
within 5 or 10 minutes
 Two common bleeding
disorders :
• hemophilia
• Thrombocytopenia
Thrombocytopenia
• Low production of Platelets
• Causing bleeding or bruising
Thrombocytopenia
 The blood cells known
as platelets play a vital
part in the
mechanisms that stop
bleeding
 Your blood contain
considerably fewer
that the normal
number of platelets is
called
trombocytopenia
Jaundice
• In newborns, caused by the liver not
functioning fully
• Secretes bilirubin into the blood causing
the yellow color
• Exposure to flourescent lights (bili lights)
will break down the substance
SICKLE CELL ANEMIA
• Genetic
Disorder
• Abnormally
shaped blood
cells
• Parents can be
carriers
(asymptomatic)
Quick Genetics Review
A gene consists of 2 alleles
(represented by letters)

One allele is usually dominant over the

other
Example:
Genotype Phenotype
PP widow’s peak
Pp widow’s peak
pp straight hairline
Sickle Cell Anemia is actually codominant

AA = normal
Aa = sickle cell trait (few symptoms)
aa = sickle cell anemia
If both parents are carriers,
child has a ¼ chance of
having the disease
Complications

1.Pain
• Lethargy
• Lifelong anemia
(low red blood count)
• Organ failure
• Stroke
HEMOPHILIA
This disorder causes a failure of the blood
to clot

Patients can be treated with blood

transfusions that include clotting agents.
Hemophilia
 Is the best knows of
the bleeding
diseases
 Risk of being
disabled or dying
from hemophilia are
greatly reduced
because of effective
treatment
Queen Victoria

Carrier for Hemophilia

Hemophilia is carried on the X chromosome

Females X H X H normal
X H X h carrier
X h X h hemophiliac

Males X H Y normal
X h Y hemophiliac
Pedigree of Hemophilia
BLOOD TRANSFUSION
 If your blood level
is deficient - as a
result of disease or
hemorrhage - you
may given a blood
transfusion to
restore the blood
to the correct level
Blood Donor
 To give blood, a
donor visits a blood
bank, where a blood
test determines
whether the donor
has anemia
 Your bone marrow
will replace the
missing blood
BLOOD GROUPS & BLOOD MATCHING
 There are four main
Blood groups, and a
transfusion is safe and
effective if the donor
and the recipient are
compatible
 Bloods group A, B, AB, O
 Other bloods group :
Rhesus (Rh)
BLOOD GROUPS & BLOOD MATCHING
 There are four main
Blood groups, and a
transfusion is safe and
effective if the donor
and the recipient are
compatible
 Bloods group A, B, AB, O
 Other bloods group :
Rhesus (Rh)