Chapter 19

GRD121: Anatomy & Physiology B

General Requirements Department
Dr. Fahmi Tarmoom
Learning outcomes (General)
• Explain the functions of the blood.
• Describe the physical characteristics and
principal components of blood.
• Explain the origin of blood cells.
• Describe the structure, function, life cycle,
and production of red blood cells
(erythrocytes).
• Describe the structure, functions, and
production of white blood cells (leucocytes).
• Describe the structure, function, and origin
of platelets
 Learning outcomes (General)
Dr. Fahmi Tarmoom

• Describe the three mechanisms that

contribute to hemostasis
• Explain the various factors that promote and
inhibit blood clotting.
• Distinguish between the ABO and Rh blood
types
• Explain why it is so important to match
donor and recipient blood types before
administering a transfusion
 19.1 Functions and
(1) Transport Properties of Blood
Dr. Fahmi Tarmoom

• Oxygen, carbon dioxide, nutrients, hormones,

Functions of

heat and waste products.

the Blood

(2) Regulates

• pH, body temperature, and water contents of

cells
(3) Protection

• Against blood loss through clotting, and against

disease through phagocytic white blood cells and
proteins such as antibodies, interferons and
complement
 • Blood is a sticky, opaque (Unclear, vague) fluid
with a metallic taste
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Physical Characteristics

• Color varies from scarlet (oxygen-rich)

to dark red (oxygen-poor)

and Volume

• The pH of blood is 7.35–7.45

• Temperature is 38C, slightly higher than “normal”

body temperature

• Blood accounts for approximately 8% of body

weight – 20% of the extracellular fluid

• Average volume of blood is 5–6 L for males, and

4–5L for females
Non-formed Elements

Formed Elements
 Composition of Formed Elements
• Erythrocytes, leukocytes, and platelets
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make up the formed elements

1. Only WBCs are complete cells
2. RBCs have no nuclei or organelles
3. Platelets are just cell fragments (Remaining
of cells)
• Negative feedback systems regulate the total
number of RBCs and platelets in circulation.
• The abundance of the different types of WBCs,
varies in response to challenges by invading
pathogens and other foreign antigens
 Haematocrit

• Upon centrifugation - heavier cellular

elements settle to bottom, lighter plasma
rises to the top

• Large proportion of cells are erythrocytes,

the haematocrit or packed cell volume
(represents the percentage of total
blood volume that is occupied by
erythrocytes.)
 Haematocrit
Dr. Fahmi Tarmoom

• Normal haematocrit ~ 42% for

women and 45% for men.

• The white blood cells and

platelets form a thin, cream-
colored layer, the 'buffy' coat in • See anaemia &
polycythaemia
between the erythrocytes and section

plasma layers. 9

Physiological
• Represent < 1% of total
conditions influencing
blood volume. the haematocrit
Dr. Fahmi Tarmoom
19.2 Formation of Blood Cells
• Hematopoiesis: occurs in Red Bone Marrow.
• Stem cells in the red bone marrow sometimes
called pluripotent stem cells or hemocytoblasts.

• Stem cells reproduce themselves, proliferate and

differentiate into cells that give rise to blood cells.

• Myeloid stem cells form RBCs, platelets,

granulocytes and monocytes.

• Lymphoid stem cells give rise to lymphocytes

Stem cells: Specialized cells that can divide through mitosis

 Progenitor Cells

Haemopoiesis
 • Biconcave discs, anucleated, essentially no
Structural Characteristics
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organelles
19.3 Red Blood Cells

• Filled with hemoglobin (Hb), a protein that

functions in gas transport

• Contain the plasma membrane

• Proteins such as spectrin attached to plasma

membrane that:

1. Give erythrocytes their flexibility

2. Allow them to change shape as necessary

 Erythrocytes (RBCs) –
Functions
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• Globin – 4 polypeptide chains

• Heme in each of 4 chains
• Iron ion can combine reversibly with one
oxygen molecule
• Also transports 20 % of total carbon dioxide
Combines with amino acids of globin

• Nitric oxide (NO) binds to hemoglobin

Releases NO causing vasodilation to improve
blood flow and oxygen delivery
Figure 17.4 Structure of hemoglobin
 • Oxyhemoglobin – hemoglobin bound to oxygen
• Oxygen loading takes place in the lungs
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• Deoxyhemoglobin – hemoglobin after oxygen

Erythrocytes
Function of

diffuses into tissues (reduced Hb)

• Carbaminohemoglobin – hemoglobin bound to

carbon dioxide
• Carbon dioxide loading takes place in the
tissues

• Normal Hb : 14-18 gm/dl male and 12-16 gm/dl

female
• Adult male has 5.5 million per microliter and, adult
female has 4.8 million per microliter.
 • Live only about 120 days
• Cannot synthesize new components – no
Fate and Destruction
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nucleus
of Erythrocytes
• Ruptured red blood cells removed from
circulation and destroyed by fixed phagocytic
macrophages in spleen and liver
• Breakdown products recycled
• Globin’s amino acids reused
• Iron reused
• Non-iron heme ends as yellow pigment urobilin
in urine or brown pigment stercobilin in feces
Dr. Fahmi Tarmoom

Figure 17.7 Life cycle of red blood cells

Dr. Fahmi Tarmoom

Erythropoiesis

Phase 1 – ribosome synthesis in early erythroblasts

Phase 2 – hemoglobin accumulation in late erythroblasts
and normoblasts
Phase 3 – ejection of the nucleus from normoblasts and
formation of reticulocytes (immature RBCs)
Reticulocytes then become mature erythrocytes
Ribosomes: molecules within the living cell responsible
for (protein synthesis)
 Regulation and Requirements
for Erythropoiesis
Dr. Fahmi Tarmoom

• Erythropoiesis is hormonally controlled and

depends on adequate supplies of iron, amino
acids, and B vitamins plus copper and cobalt.

• Not to forget the IF (intrinsic factor) provided by

the gastric mucosa

• (Generally, when there is no enough oxygen in

circulatory system, kidneys detect this and secret
hormone Erythropoietin (EPO))
 Hormonal Control
of Erythropoiesis
Dr. Fahmi Tarmoom

More reticulocytes enter

circulating blood
 • Anaemia is the inability of blood to carry enough
Erythrocyte Disorders oxygen to meet body needs.
Dr. Fahmi Tarmoom

• Anaemia is classified depending on the cause:

1. Production of insufficient or defective erythrocyte –
release of low number or defective red blood cells –
example: Iron deficiency, vit.B12/folic acid deficiency
and bone marrow failure (aplastic anemia)

2. Blood loss or excessive erythrocyte breakdown

(hemo-lysis).

• Anaemia can cause abnormal changes in red cell

size or colour
Dr. Fahmi Tarmoom Erythrocyte Disorders
 Erythrocyte Disorders
1. Iron deficiency anaemia

• Red cell count is normal but the cell is small,

Dr. Fahmi Tarmoom

variable in size and less Hb than normal. Can

result from:
• Deficient intake – poorly planned veg. diet, babies
weaned much past the first year, older adults,
alcohol dependent.

• High requirements – In pregnancy, chronic blood

loss (peptic ulcer), menorrhagia or Ca. of the GIT.

• Malabsorption – increased pH of the stomach, or

removal of part of the stomach or the small intestine
 2. Vitamin B12 /folic acid deficiency anemias

Erythrocyte Disorders • Causes reduction in the rate of DNA and RNA,

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so delaying cell divisions (the cells grow larger

between divisions)

• Circulating cells are immature, some nucleated

(> MCV)

• The life span is reduced (40-50 days) –

decreased production and early lysis causes
anemia. Types:
• Pernicious anaemia

• Dietary deficiency of Vit. B12

• Complication Irreversible neurological damage.

 2. Vitamin B12 /folic acid deficiency anemias

Erythrocyte Disorders • Cause a form of megaloblastic anaemia, seen in

Dr. Fahmi Tarmoom

B12 deficiency but NO neurological damage.

Due to:

• Dietary deficiency – pregnancy, anorexia,

alcoholism, infants with delayed mixed diet.

• Malabsorption from the jejunum, caused by

coeliac disease, tropical sprue or the use of
anticonvulsant drugs,

• Interference with folate metabolism, cytotoxic

and anticonvulsants drugs
 3. Aplastic (hypoplastic) anaemia

Erythrocyte Disorders • Results from bone marrow failure.

Dr. Fahmi Tarmoom

• All three types of formed elements are low, the

condition is called pancytopenia.

• Occasionally inherited – but known causes

include:
• Drugs – cytotoxic therapy

• Ionizing radiation

• Some chemicals, e.g. benzene and its derivatives

(toluene, dimethylbenzene, and trimethylbenzene)

• Viral disease, including hepatitis

• Symptoms: infection, anemia and bleeding.

 4. Hemolytic anemias (Sickle-cell anemia)

(Congenital Hemolytic • Abnormal hemoglobin become misshapen when

Erythrocyte Disorders
Dr. Fahmi Tarmoom

deoxygenated (sickled)
• Large numbers of red blood cells being destroyed.
Anemias)
• They obstruct blood flow, intravascular clotting,
tissue ischemia and infarction.
• Acute episodes (sickle crises) – acute pain in
affected area (hands and feet)
• Long term problems – cardiac and kidney disease,
retinopathy and poor tissue healing;
• Slow growth in children, and delay in sexual
maturity.
 4. Hemolytic anaemia (Thalassemias)
(Congenital Hemolytic
Erythrocyte Disorders
Dr. Fahmi Tarmoom

• Inherited condition – abnormal hemoglobin

production this will;

• Reduce erythropoiesis and stimulate hemolysis

Anemias)

• May present from mild and asymptomatic to

profound and life threatening.

• Symptoms include bone marrow expansion and

splenomegaly.

• Treatment, regular transfusion (may lead to Iron

overload)
 Hemolytic Disease of the Newborn
(Congenital Hemolytic
Erythrocyte Disorders
• Hemolytic disease of the newborn – Rh+ antibodies of a
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sensitized Rh– mother cross the placenta and attack and

destroy the RBCs of an Rh+ baby.
Anemias)

• Rh– mother becomes sensitized (Making antibodies)

when Rh+ blood (from a previous pregnancy of an Rh+
baby or a Rh+ transfusion) causes her body to synthesis
Rh+ antibodies.

• The Antibody of the mother passes to fetus via Placenta

and attack the blood cells of the fetus and destroy it and
lead to ?anaemia and ? death.
 Hemolytic Disease of the Newborn
(Congenital Hemolytic
Erythrocyte Disorders
• The drug RhoGAM can prevent the Rh– mother from
Dr. Fahmi Tarmoom

becoming sensitized (Prevent Rh –ve mother from

making antibody during pregnancy). Should be given
Anemias)

within 72 hours of the delivery.

• Treatment of hemolytic disease of the newborn

involves pre-birth transfusions and exchange
transfusions after birth.
Erythrocyte Disorders Blood Transfusion Reactions
(Acquired Hemolytic • Donor’s cells are attacked by the recipient’s
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plasma agglutinins causing:

Anemias)
1. Diminished oxygen-carrying capacity

2. Clumped cells that impede blood flow(affect

blood flow)

3. Ruptured RBCs (dead RBCs) that release free

hemoglobin into the bloodstream
• Circulating hemoglobin precipitates in the kidneys and
causes renal failure.
 Polycythemia are of two types:
1. Polycythemia vera (Primary Polycythemia) –
Dr. Fahmi Tarmoom

bone marrow cancer; and ↑ RBCs and ↑ Hct (80%)

– there is often spleen and liver enlargement

• It is more common in the over 60s

• Severe form needs therapeutic phlebotomy

2. Secondary polycythemia – due to less oxygen

availability and increased EPO production (e.g.
living in high altitudes, heart failure or heavy
smoking)
 • Leukocytes, the only blood components
that are complete cells:
Dr. Fahmi Tarmoom
Formed Elements –
Leukocytes (WBCs)
• Are less numerous than RBCs

• Make up 1% of the total blood volume:

(4800-10800 WBC/μl)

• Have nuclei

• Do not contain hemoglobin

• Granular or agranular based on staining

highlighting large conspicuous granules

Dr. Fahmi Tarmoom
 • 60-70% produced in bone marrow
• All leukocytes originate from hemocytoblasts
Production of Leukocytes:
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• Hemocytoblasts differentiate into (1)myeloid stem

cells and (2) lymphoid stem cells
Leukopoiesis

1. Myeloid stem cells become myeloblasts or

Monoblasts
• Myeloblasts develop into eosinophils, neutrophils,
and basophils
• Monoblasts develop into monocytes
2. Lymphoid stem cells become Lymphoblasts
• B and T Lymphocyte precursors develop into B and
T lymphocytes
 Progenitor Cells

Leukopoiesis
 Emigration of WBCs
• Many WBCs leave the
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bloodstream
• Emigration (formerly
Diapedesis)
• Roll along endothelium
• Stick to and then squeeze
between endothelial cells
• Precise signals vary for
different types of WBCs
 Dr. Fahmi Tarmoom
Formed Elements –
Leukocytes (WBCs)
Granulocytes:

• Contain granules of enzymes which help to

digest the invading microbes.

• Are larger and usually shorter-lived (2 days)

than RBCs (120 days)

• Only Neutrophils are phagocytes (specialized

cell that engulfs and ingests other cells or
particles(Microbes))
 Formed Elements –
Leukocytes (WBCs)
Dr. Fahmi Tarmoom

Eosinophils:

• Eosinophils account for 2–5% of WBCs

• Numerous in mucous membranes lining the

respiratory and digestive tracts

• Function of Eosinophils:

1. Lead the body’s counterattack against

parasitic worms (infections)

2. Regulating allergic reactions (histaminase)

such as asthma
 Formed Elements –
Leukocytes (WBCs)
Dr. Fahmi Tarmoom

Basophils:
• Account for 0.5 – 1 % of WBCs and
• Intensify inflammatory reaction and involved in
allergic reactions
• Similar in function to mast cells ( widespread in
the body, connective tissue of skin and mucous
membrane of respiratory and digestive systems)
• Release histamine, (an inflammatory
chemical) and heparin (an anticoagulant)
 Formed Elements –
Leukocytes (WBCs)
Dr. Fahmi Tarmoom

Neutrophils (PMNs) 50 – 70% of the WBCs:

• Neutrophils have two types of granules

• Contain enzyme lysozyme which destroy

certain bacteria, and strong oxidants, such
as superoxide anion, hydrogen peroxide,
and the hypochlorite anion. Also, defensins

• Neutrophils are our body’s bacteria slayers

(Bacteria killer)
Dr. Fahmi Tarmoom Leukocytes (WBCs)

Agranulocytes:

Monocytes and Lymphocytes:

• Monocytes account for 3–8% of white blood

cells – (the largest white blood cells)

• They leave the circulation, enter tissue,

and differentiate into macrophages

Macrophages (in the tissues)

• Are highly mobile and actively phagocytic

• Activate lymphocytes to mount (Increase) an

immune response
 Formed Elements –
Leukocytes (WBCs)
Dr. Fahmi Tarmoom

• Agranulocytes:

• Lymphocytes

• Account for 25% or more of WBCs and:

• There are two types of lymphocytes: T cells
and B cells

• T cells function in the immune response

• B cells give rise to plasma cells, which

produce antibodies
 • Leukocytosis: WBC count above
Dr. Fahmi Tarmoom

11,000cells / μl is a normal protective

Formed Elements –
Leukocytes (WBCs)
response to stresses such as invading
microbes, strenuous exercise, anesthesia
and surgery

• Leukopenia (below 4000/μl), caused by

radiation, shock and certain
chemotherapeutic agents like cyclosporine,
penicillin and interferons.
 Leukocytes Disorders:
Leukemias
• Leukemia: Cancerous conditions involving white
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blood cells, overproduction of abnormal white

blood cells in bone marrow.

• Also infectious mononucleosis – increase in the

number of WBCs
 Significance of High and Low
WBCs Count.
WBC Type High Count May Indicate Low Count May Indicate

Neutrophils Bacterial infection, burns, Radiation exposure, drug

stress, inflammation toxicity, Vit. B12 deficiency
and SLE
Lymphocytes Viral infections, some Prolonged illness, HIV,
Leukemias, infectious immunosuppression and
mononucleosis treatment with cortisol
Monocytes Viral of fungal infections, Bone marrow suppression,
tuberculosis, some treatment with cortisol
Leukemias, other chronic
disease
Eosinophils Allergic reactions, parasitic Drug toxicity, stress, acute
infections, autoimmune allergic reactions
disease
Basophils Allergic reaction, Leukemias, Pregnancy, ovulation, stress,
cancers and hypothyroidism hypothyroidism
 • Myeloid stem cells develop eventually into a
Megakaryocyte
Formed Elements –
Dr. Fahmi Tarmoom

• Splinters into 2000-3000 fragments

• Each fragment enclosed in a piece of plasma
Platelets

membrane
• Disc-shaped (2-4 μm in diameter) with many
vesicles but NO nucleus
• Help stop blood loss by forming platelet plug
• Granules contain blood clot promoting
chemicals (see next slide)
• Short life span – 5-9 days
Formed Elements –
Dr. Fahmi Tarmoom

Platelets

• Their granules contain serotonin, Ca2+, enzymes,

ADP, and platelet-derived growth factor (PDGF)

• Platelets function in the clotting mechanism by

forming a temporary plug that helps seal breaks

in blood vessels, and help stop bleeding

 Figure 17.12 Formation of platelets

Dr. Fahmi Tarmoom

Platelets counts in adults – 250,000/cubic

mm (150,000 – 400,000/cubic mm) – no sex
differences – infants reaches adult number
by the age of 3 months.
Thrombocytopenia – low platelet number
 Bone Marrow Transplant
• Recipient's red bone marrow replaced entirely by
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healthy, noncancerous cells to establish normal blood

cell counts
Transplants

• Takes 2-3 weeks to begin producing enough WBCs to

Stem Cell

fight off infections

• Graft-versus-host-disease – transplanted red bone
marrow may produce T cells that attack host tissues

Cord-blood transplant
• Stem cells obtained from umbilical cord shortly before
birth
• Easily collected and can be stored indefinitely
• Less likely to cause graft-versus-host-disease
Collagen fibers
and damaged
endothelium
Events of Hemostasis
(process causes bleed to stop, prevents blood loss)
Dr. Fahmi Tarmoom

Vascular spasm
Step 1 Smooth muscle contracts,
causing vasoconstriction.
Platelets

Platelet plug formation

Injury to lining of vessel
Step 2
exposes collagen fibers;
platelets adhere.

Liberated ADP, Platelets release

serotonin and chemicals that make
Thromboxane A2 nearby platelets sticky;
platelet plug forms.

Coagulation: forming clot

Fibrin (protein) forms a
Step 3 mesh(network) that traps
red blood cells and
Platelet Plug
platelets, forming the clot.
Figure 17.13
 (2) Formation of platelet plug
Platelet factors released
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1) ADP: adenosine diphosphate

2) TXA2: Thromboxane A2
3) 5-HT: Serotonin
+ NO
• All 3 induce more platelet
aggregation
• TXA2 and 5-HT are
vasoconstrictors
ADP
TXA2
5-HT Vasoconstriction
 • Serum is blood plasma
minus clotting proteins
Dr. Fahmi Tarmoom

• Clotting – series of chemical

Blood Clotting

reactions culminating in
formation of fibrin threads
• Clotting (coagulation)
• factors – Ca2+, several
inactive enzymes, various
molecules associated with
platelets or released by
damaged tissues
Refer to
Page 598
Dr. Fahmi Tarmoom
Blood Clotting

Three
Stages

Also known as
Prothrombinase

Note: Once factor X is activated it combines with factor V in the presence of Ca

to form the active enzyme prothrombinase
 1. Production of fibrin from fibrinogen

2. Activates platelets
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Positive 3. Activates various clotting factors e.g. factors

feedback VIII, XI and factor XIII

4. Thrombin formation makes more thrombin

• (Thrombin also activates anti-clotting systems

which take effect after the clot has formed or
away from site of injury)

The Role of Thrombin

Dr. Fahmi Tarmoom
Clot Retraction and Fibrinolysis
• Clot retraction: (a process to stabilize the clot)

• Occur within 30 to 60 minutes;

• Because platelets have actin and myosin,

platelet contract – pull the fibrin strands –
compacting the clot – drawing the ruptured
edges closely together.

• PLUS, platelets produce Platelet-derived growth

factor (PDGF), stimulate the smooth muscle cells
and fibroblasts to divide and rebuild the blood
vessels.
Dr. Fahmi Tarmoom
Clot Retraction and Fibrinolysis
• Fibrinolysis: a process removing unneeded
clots when healing has occurred

• Clots presence, causes the endothelial cells to

secrete tissue plasminogen activator (tPA)

• tPA activate and convert plasminogen to plasmin

• Plasmin is confined to the site of the clot

• Note: also activating plasminogen - factor XIIa

and thrombin

• Fibrinolysis, begins within 2 days and continue

slowly for 7 days
Dr. Fahmi Tarmoom
Role of Vitamin K in Clotting
• Normal clotting depends on adequate levels of
vitamin K in the body.

• Required for the synthesis of 4 clotting factors.

• It is fat soluble produced by bacteria that inhabit

the colon

• People suffering from disorders that slow

absorption of lipid will lead to;

• Patient experiencing uncontrolled bleeding

Dr. Fahmi Tarmoom

1. Antithrombin III: produced by the liver, block the

action of several factors, factor XII, X, and II

2. Activated protein C: Blocks factors V and VIII

and stimulates fibrinolysis

3. Heparin: Inhibits thrombin-induced activation of

platelets and of factors IX, X, XI and XII (working

together with antithrombin III)

Dr. Fahmi Tarmoom

Intravascular
Clotting
• Thromboembolic Disorders: results from
conditions that causes undesirable clot formation.

• Bleeding Disorders: arise from abnormalities that

prevent normal clot formation.

• Disseminated intravascular coagulation: (DIC)

is when the coagulation system is inappropriately
activated. Formation of intravascular clots followed
by tendency to hemorrhage.
 Intravascular Clotting
• Thrombus – a clot that develops and
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persists in an unbroken blood vessel.

• Thrombi can block circulation, resulting in
tissue death.

• Coronary thrombosis – thrombus in blood

vessel of the heart.
Dr. Fahmi Tarmoom
Intravascular Clotting
• Embolus – a thrombus (clot) freely
floating in the blood stream
1. Pulmonary emboli can impair the ability of
the body to obtain oxygen

2. Cerebral emboli can cause strokes

• Example: stroke (embolus in brain),

lungs(pulmonary embolism), heart(cause heart
attack).
Dr. Fahmi Tarmoom
Haemorrhagic Disorders
Thrombocytopenia – is defined as a blood
platelet count below 150,000/mm3 -

This could be due to:

1. Reduced platelet production – as in Leukemias,

ionizing radiation and drugs (e.g. cytotoxic drugs)

2. Increased platelet destruction- occur in DIC and

autoimmune thrombocytopenic purpura
 Dr. Fahmi Tarmoom
Hemophilias
Inherited clotting disorder. It is sex-linked.

1. Hemophilia A – deficiency of factor VIII (anti

Congenital
Disorders

hemophilic factor) – account for 77% of cases

2. Hemophilia B (Christmas disease) – deficiency of

factor IX resulting in deficiency of thromboplastin

1. Both types above occur primarily in males (X-

linked condition)

3. Hemophilia C – deficiency of factor XI, less

severe and occur in both sexes
 • RBC membranes have glycoprotein antigens on
their external surfaces
Dr. Fahmi Tarmoom

• These antigens are:

Human Blood Groups
1. Unique to the individual
2. Recognized as foreign if transfused into another
individual
3. Promoters of agglutination (mix of antigen and
antibody) and are referred to as agglutinogens
(antigens)
• Presence or absence of these antigens is used to
classify blood groups.
• The antigens of the ABO and Rh blood groups cause
vigorous transfusion reactions when they are
improperly transfused.
 Antigen and antibody, and Rh
• Antigen: any foreign molecule that interact with
the cell of immune system and affect immune
response
Dr. Fahmi Tarmoom

• In blood: Antigen is protein on the surface of

RBC, A and B Antigen

• In Blood: Antibody A, Antibody B - each antibody

bind to specific antigen

• Rh: Rhesus (Rh) factor is an inherited protein

found on the surface of red blood cells.

• If your blood has the protein, you're Rh positive. If

your blood lacks the protein, you're Rh negative
 ABO Blood Groups
• The ABO blood groups consists of:
Dr. Fahmi Tarmoom

• Two agglutinogens, antigens (A and B) on the

surface of the RBCs
• Two antibodies (agglutinins) in the plasma
(anti-A and anti-B)
• An individual with ABO blood may have various
types of antigens and spontaneously preformed
antibodies
• Agglutinogens and their corresponding antibodies
cannot be mixed without serious hemolytic
reactions
 Rh Blood Groups
• There are eight different Rh agglutinogens, three of
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which (C, D, and E) are common

• Presence of the Rh agglutinogens on RBCs

is indicated as Rh+

• Anti-Rh antibodies are not spontaneously

formed in Rh– individuals.

• However, if an Rh– individual receives Rh+

blood, anti-Rh antibodies form.

• A second exposure to Rh+ blood will result in a

typical transfusion reaction.
 Summary of ABO Blood
Group Interactions
Characteristics Blood Type
A B AB O
Agglutinogens A B Both A and B Neither
(antigen) on RBCs A nor B

Agglutinin Anti-B Anti-A Neither anti-A Both anti-A

(antibody) in nor anti-B and anti-B
plasma
Compatible donor A, O B, O A, B, AB, O O
blood types (no
hemolysis)
Incompatible donor B, AB A, AB - A, B, AB
blood types
(hemolysis)

Table 19.6 page 602

Blood typing of ABO blood types

ABO Blood Typing

• Single drops of blood are mixed
with different antisera
• Agglutination with an antisera
indicates the presence of that
antigen on the RBC
Required Reading
Tortora. G.J., & Derrickson. B. (2017). Principles
of Anatomy & Physiology (15thed.). Wiley –
Chapter 19, pages 584-604.

Waugh A., Grant A. (2018). Ross & Wilson.

ANATOMY AND PHYSIOLOGY (13th ed.)
Elsevier – Chapter 4, pages 73-80.