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Physiology

of
Blood
Functions of Blood
Blood performs a number of functions to the body:
Blood transports:
O2, CO2, nutrients, metabolic wastes, and hormones.
Blood maintains
body temperature, normal blood pH, and adequate fluid
volume in circulatory system.
Blood prevents blood loss by
activating plasma proteins & platelets, and initiating clot
formation to prevent bleeding.
Blood prevents infection by
synthesizing & utilizing antibodies and activating WBCs
2 to defend the body.
Physical Characteristics of Blood
Is a sticky, opaque fluid with a metallic taste.
Is a viscous fluid, heavier & thicker than water.
It is circulates within a closed series of vessels: systemic &
pulmonary circuits that are in series with each other.
Its color varies from scarlet (O2-rich) to dark red (O2-poor)
pH of the blood = 7.357.45
Salt content of the blood = 0.9%
To of blood = 38C - slightly higher than normal body To
It accounts for 20% of ECF volume & 8% of the normal
adult body weight.
Average blood volume:
Male = 56 Liter
Female = 45 Liter
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Composition of Blood
Blood is the bodys only the fluid connective tissue.
Blood constitutes - liquid plasma (55%) &
- formed elements (45%)

Formed elements in the blood are:


Erythrocytes or red blood cells (RBCs)
Leukocytes or white blood cells (WBCs)
Thrombocytes or platelets

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Components of Whole Blood

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Plasma
Plasma is the liquid portion of the blood.
It makes up 55% of the blood volume.
Plasma has the osmolality of 300 mosm/L.

Composition of plasma:
1. Water (91.5%)
2. Plasma proteins (7%): albumin, globulins, clotting
proteins (fibrinogen), & all others.
3. Other solutes (1.5%):
Electrolytes
Nutrients: CHO, amino acids, fats, & vitamins
Metabolic waste products: urea & creatinine
Respiratory gases: O2 & CO2
Hormones & enzymes
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Hematopoiesis
Hematopoiesis is the process of blood cell formation.

(Hemocytoblast cell)

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Erythrocytes (Red blood cells)
Function: major function of RBCs is
transport of Hgb, which in turn:
Transport O2 & CO2
Shape: - biconcave disk
- has no nucleus & no organelles
Normal RBCs count:
Male = 5.2 millions/mm3
Female = 4.6 millions/mm3
Hematocrit (Hct): proportion of the
blood volume that is the blood cells.
Normal range = 40 to 45%.
Hemoglobin (Hgb) = 1/3 of Hct
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Erythropoiesis: Production of Erythrocytes
Areas of the Body That Produce RBCs:
During IUL RBCs are produced in the yolk sac, liver, and red
bone marrow.
In children & adults:
The bone marrow of essentially all bones produces RBCs until
person is 5 years old.
After age of 20, most RBCs are produced from the marrow of the
membranous bones, such as vertebrae, sternum, ribs, and ilia.
Bone marrow makes different types of blood cells, including
Red blood cells to carry oxygen around our bodies.
White blood cells to fight infection.
Platelets to help the blood clot.
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Regulation of RBC Production
The total mass of RBCs in the circulatory system is
regulated within narrow limits, so that
Adequate number of RBC is always available to provide
sufficient transport of O2 from the lungs to the tissues,
If too few RBCs leads to tissue hypoxia
If too many RBCs blood viscosity
Erythropoiesis requires diets rich in:
Proteins, lipids & carbohydrates
Iron, Vit-B12, Vit-C & folic acid
Vit-B12 & folic acid are essential for maturation of RBCs
(for synthesis of DNA).

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Regulation of RBC Production, contd
Tissue oxygenation is most essential regulator of RBC
production
Any condition that decreases O2 transportation to the tissue,
increases rate of RBC production.

Erythropoietin stimulates RBC production, and its


formation increases in response to hypoxia.
The principal stimulus for RBC production in low O2 states is a
circulating hormone called erythropoietin (EPO), produced
from JG-cells of kidneys (90%) & hepatocytes.

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Regulation of RBC Production, contd
Erythropoietin (EPO) release by the kidneys is
triggered when there is:
Hypoxia due to RBCs count
Decreased oxygen availability, or
Increased tissue demand for O2
Enhanced erythropoiesis increases:
RBCs count in circulating blood, and
Oxygen carrying ability of the blood.

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Erythropoietin Mechanism to control RBC Production
Start
Stimulus: Hypoxia
Normal blood oxygen levels due to RBCs count,
availability of O2 in
Increases the blood, or tissue
O2-carrying demands for O2
ability of blood Reduces O2
levels in blood

Erythropoietin
Enhanced stimulates red Kidney 90% & liver
erythropoiesis bone marrow 10% releases EPO
increases RBCs count
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Hemoglobin
Hgb in the RBCs is intended for transport of
respiratory gases (O2 & CO2).
Normal concentration of Hgb:
Male = 16 g/dl (14-18 g/dl)
Female = 14 g/dl (12-16 g/dl)
Hemoglobin molecule:
Has a protein globin & heme part
4 heme molecules are conjugated with 4 globin molecules
to form a hemoglobin.

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Structure of Hemoglobin

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Types of Hemoglobin
Several slight variations are found in different subunit of
the Hb chains, depending on amino acid composition of the
polypeptide portion.
The different types of Hb include:
1. Adult Hb (HbA-2 2)
2. Fetal Hb (HbF -2 2)
3. Sickled Hb (HbS-2 2)
Most common form of Hb in adult human is HbA
In adult Hb, the globin part has 4 polypeptide chains:
2 -chains & 2 -chains
In case of Sickled Hb, in two of the -chains at position-6
valine is wrongly substituted for glutamate.
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Hemoglobin, contd
Hb is reversibly binds with O2 & most of the O2 in the blood is
transported in combination with Hb.
Each heme group bears an atom of iron, which can bind to one O2
molecule.
So, each Hb molecule can transport four molecules of O2
Oxyhemoglobin: when Hb is bound to O2 .
O2 loading is takes place in the lungs.
Deoxyhemoglobin/reduced Hb/deoxygenated Hb: Hb after O2
diffuses into tissues.
Carbaminohemoglobin: when Hb is bound to CO2.
CO2 loading is takes place in tissues & is returned to lungs to be
eliminated in expired air.
Carboxyhemoglobin or carbon monoxy hemoglobin: when Hb
is combined with CO.
Note: Because the affinity of Hb for CO is much more (200-250 times)
than its affinity for O2. So that, CO displaces O2 from Hb, thereby
17 reducing the O2 carrying capacity of the blood.
Destruction of Erythrocytes
The life span of an erythrocyte is 120 days.
Old erythrocytes become rigid and fragile & their Hb begins
to degenerate.
Older erythrocytes are engulfed by the tissue macrophages
(reticuloenothelial system) in the spleen.
Heme & globin are separated & iron released from Hb pass
back into the blood for production of new RBCs or to the
liver for storage.
Heme part is converted into bilirubin, which is released into
the blood & later removed from body by the liver.

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Important notes
The normal Hgb becomes 100% saturated when blood is
equilibrated with 100% O2 (PO2, 760 mm Hg)
1gm of Hgb when fully saturated combines with 1.34 ml
of O2. Thus Hgb concentration is an index of O2 carrying
capacity of the blood.
Thus, normal values of O2 carrying capacity in males is
1.34 x 16 = about 21 ml%, and in females is 1.34 x 14 =
about 18.5 ml%.

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Destruction of RBCs, contd
Jaundice
Is a yellowish discoloration of the skin & the sclera due to
excessive bilirubin in the plasma.
Normal level of plasma bilirubin is = 0.5 mg/dl.
The skin & sclera look yellow, when the bilirubin level rises
greater than1.5 mg/dl.

Types of Jaundice
1. Hemolytic jaundice: due to destruction of RBCs.
2. Hepatic or hepatocellular jaundice: due to damaging of the
liver cells (infective or toxic).
3. Obstructive jaundice: due to obstruction of biliary pathways.
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Anemia
It is a deficiency of Hgb in the blood, which can be caused
by either too few RBCs or too little Hgb in the cells.
Classification of Anemia
1. Deficiency anemia: caused by deficiency of iron, vit-B12,
folic acid & proteins.
2. Aplastic anemia: due to depression of bone marrow as
result of excessive X-ray Rx, certain industrial chemicals,
drugs, and leukemia.
3. Hemolytic anemia: a result of prematurely ruptured
erythrocytes or formation of fragile RBCs.
4. Hemorrhagic anemia (Blood loss anemia): a result of
acute or chronic loss of blood.
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Deficiency Anemia
Iron deficiency anemia
Number one deficiency anemia worldwide
Common in infants & females
Occurs due to
Inadequate intake of iron-containing foods
Impaired iron absorption
Can be treated with a replacement therapy

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Pernicious anemia
Causes
Deficiency of Vitamin B12
o Failure to absorb vit B12 from GI tract is a common cause of
RBCs maturation failure, due to gastric atrophy that fails to
produce normal gastric secretions.
Deficiency of Intrinsic Factor (IF)
o Occurs in gastroectomy, gastric atrophy, and in defective IF
secretion.
o Parietal cells of gastric glands secrete a glycoprotein called IF,
which combines with vit B12 in the food & makes it available
for absorption by the gut.
Treatment
IV injection of vit-B12 through the whole life.
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Polycythemia
A condition of production of RBCs, > 6 million/mm3
Causes
1. Chronic hypoxia: occurs as a result of high altitude,
heart failure, & respiratory failure.
2. Primary over activity of bone marrow
Effect: blood viscosity, venous return, BV, & BP.
Types of Polycythemia:
Physiologic polycythemia: a common type of secondary
polycythemia, occurs in natives who live at high altitudes.
Polycythemia vera/primary polycythemia: it is a
pathological condition in which RBCs count may reach to
78 million/mm3 & a Hct level of 6070%.
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Leukocytes (WBCs)
Also called the white blood cells (WBCs).
Are formed partially in bone marrow (granulocytes and
monocytes & a few lymphocytes) & partially in the lymph
tissue (lymphocytes).
After formation, they are transported in the blood to different
parts of the body.
WBCs are transported to areas of serious infection and
inflammation, where providing a defense against infections.
The granulocytes & monocytes have a special ability to
seek out & destroy a foreign invader.

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Leukocytes, contd
Granulocytes & monocytes protect the body against invading
organisms mainly by ingesting them - that is, by phagocytosis.
Leukocytes, the only blood components that are complete
cells: contain nucleus, and other organelles.
Make up 1% of the total blood volume. Less numerous than
RBCs.
Normal WBCs count: 400010000/mm3. Average: 7000/mm3
Function:
General inammatory & immune functions of WBCs include:
Destruction of invading microorganisms (bacteria & viruses).
Identication and destruction of cancer cells.
Phagocytosis of tissue debris including dead & injured cells.
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Types of WBCs
Granular leukocytes Agranular leukocytes
PMN - cells: - Neutrophils - Monocytes
- Eosinophils - Lymphocytes
- Basophils
WBC differential count:
Neutrophils: 60-70%, 3000-7000/mm3
Eosinophils: 2-4%, 100-440/mm3
Basophils: 0.5-1%, 20-50/mm3
Monocytes: 3-8%, 100-700/mm3
Lymphocytes: 25-30%, 1500-3500/mm3
Granulocytes & monocytes are formed only in bone marrow.
Lymphocytes & plasma cells are produced mainly in the
lymphogenous tissues (lymph glands, spleen, thymus, & tonsils).
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Formation of Leukocytes

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Primary Functions of WBCs
Neutrophils
The most abundant WBCs
Have multilobed nuclei (PMN-cells)
The first line of defense
Phagocytic cells (ingest bacteria)

Basophils
Account for 0.5% of WBCs
Basophils liberate heparin into the blood, a
substance that can prevent blood coagulation.

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Primary Functions of WBCs, contd
Eosinophils
Eosinophils account for 24% of WBCs
Absorb histamine during allergic conditions, thus severity
of allergies.
Produced in large numbers in people with parasitic
infections, and migrate into tissues diseased by parasites.
They kill big parasites by producing hydrolytic enzymes.
Monocytes
Account for 38% of the WBCs
Are highly phagocytic cells
Are the largest WBCs
They leave the circulation, enter tissue, and differentiate into
30 macrophages.
Lymphocytes
Lymphocytes constitute about 30% of the total number of WBCs.
The two types of lymphocytes are:
B lymphocytes
T lymphocytes
The primary function of the B lymphocytes is to produce antibodies,
which are molecules that identify & lead to destruction of foreign
substances such as bacteria.
The B lymphocytes & the antibodies they produce are responsible
for humoral immunity.
T lymphocytes provide immunity against viruses & cancer cells. These
lymphocytes directly attack & destroy their targets by forming holes
in the target cell membrane, causing cell lysis.
The T lymphocytes are responsible for cell-mediated immunity.
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Leukocytes Disorders: Leukemia
Leukemia refers to the cancerous conditions
involving the WBCs.
Leukemia can be classified into
Acute leukemia
Rapid onset (children & adults)
Chronic leukemia
Symptoms develop slowly (mostly adults)

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Leukemia
Immature WBCs are found in the bloodstream in all
leukemia.
Bone marrow becomes totally occupied with cancerous
WBCs.
The WBCs produced, though numerous, are not functional.
Death is can caused by internal hemorrhage & massive
infections.
Treatments include irradiation, anti-leukemic drugs, and
bone marrow transplants.

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Immunity
Immunity is the body's ability to resist or eliminate
potentially harmful foreign materials or abnormal cells.
Consists of the following activities:
Defence against invading pathogens (viruses & bacteria).
Removal of 'worn-out' cells (e.g. old RBCs) & tissue debris (e.g.
from injury or disease).
Identification & destruction of the abnormal or mutant cells
(primary defence against cancer).
Rejection of 'foreign' cells (e.g., organ transplant).
Inappropriate responses:
o Allergies - response to normally harmless substances
o Autoimmune diseases
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Types of Immunity
A. Natural/innate/immunity or Non-specific immunity
Examples:- Phagocytosis
- HCl in the stomach
- Skin barrier
- Lysozymes in saliva
B. Acquired/adaptive immunity or Specific immunity
Features:- Specific
- Memory
- Recognition of self & non-self

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Types of acquired immunity
1. Humoral immunity/Antibody mediated immunity
B-Lymphocytes: are specialized for such type of immunity.
2. Cellular immunity/Cell mediated immunity
T-Lymphocytes: are specialized for such type of immunity.
Lymphocytes & their origin
Bone Marrow
Lymphoblasts (lymphocyte stem cells)

Lymphocytes
Thymus gland Bone marrow in man

T-Lymphocytes B-Lymphocytes

Enter the circulation


Filtered into lymphoid tissues
36 Lymph node, Spleen & Bone marrow
Active immunity Vs Passive immunity
Active ('natural'):- production of antibodies as a result of
exposure to an antigen (immunization).
Passive:- direct transfer of antibodies formed by another
person (or animal),
E.g., transfer of IgG antibodies from mother to the fetus across
placenta or in colostrum ('first milk') OR treatment for rabies or
poisonous snake venom.

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Platelets
Platelets have a short life span,
normally just 5-9 days.
Aged & dead platelets are
removed by fixed macrophages
in spleen & liver.
Platelets function in the clotting Inactive platelets
mechanism by forming a
temporary plug that helps seal
breaks in the blood vessels.
Normal platelet count is
150,000 400,000/mm3

38 Active platelets
Hemostasis/Haemostasis
Hemostasis is a sequence of responses that stops
bleeding.
When successful, hemostasis prevents hemorrhage, i.e., the
loss of a large amount of blood from vessels.
When blood vessels are damaged or ruptured, the hemostatic
response must be quick, localized to region of damage, and
carefully controlled in order to be effective.
Hemostatic mechanisms can prevent hemorrhage from
smaller blood vessels, but extensive hemorrhage from
larger vessels usually requires medical intervention.

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Hemostasis, contd
There are three mechanisms that reduce blood loss:
1. Vascular spasm
2. Platelet plug formation
3. Blood coagulation (clotting)
Vascular spasm
It is immediate vasoconstriction in response to injury of the
arteries or arterioles that reduces blood loss.
The spasm is probably caused by damage to smooth muscle, by
substances released from activated platelets, and by reflexes
initiated by pain receptors.
In effect the reaction minimize the rate of bleeding by narrowing
diameter of the hole (rupture) on the wall of the blood vessels.

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Platelet Plug Formation
Platelets help stop blood loss from damaged small blood vessels by
forming a platelet plug.
Platelet plug is limited to the immediate area of the injury.
Normally, platelets do not stick to each other or to the
endothelial lining of the blood vessels.
Upon damage to the blood vessel endothelium (which exposes
collagen) the platelets:
adhere to collagen, and
stick to exposed collagen fibers & form a platelet plug.

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42
Blood coagulation (clotting)
A set of reactions in which blood is transformed from a
liquid to a gel (clot).
It is slow but has long lasting effect to stop bleeding.
Coagulation follows intrinsic & extrinsic pathways.

Stages of Blood Coagulation: has 3 steps of reactions:


1. Formation of prothrombin activators.
2. Conversion of prothrombin into thrombin by action of
prothrombin activators (prothrombinase).
3. Conversion of fibrinogen into fibrin thread by action of
thrombin.
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Fig. Blood clot formation

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Blood coagulation, contd
Coagulation is formed
primarily of fibrin threads (or
polymers), but also including
blood cells & platelets.

Blood clots in the right place


prevent the loss of blood from
ruptured vessels, but in the
wrong place can cause
problems such as a stroke due
to inappropriate clotting.

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Summary of Clotting
The 3rd major step in
hemostasis is coagulation, or
the formation of a blood clot.
3 essential steps lead to
clotting:
1. Activation of factor X
2. Conversion of prothrombin into
thrombin
3. Conversion of brinogen into
brin
All together, 12 clotting factors
are in the plasma.
These factors, which are
proteins synthesized in the
liver, are normally found
circulating in the plasma.
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Hemostasis Disorders: Thrombo-embolism
Thrombus: formation of a clot in the blood vessels.
o Thrombi can block circulation, resulting in tissue death & organ
failure.
o Coronary thrombosis - thrombus in blood vessel of the heart;
frequent cause of:
Myocardial infarction (heart attack)
Embolus: a thrombus (blood clot) freely floating in the
blood.
Pulmonary emboli - impair O2 delivery to the body.
Cerebral emboli - can cause cerebral stroke.

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Prevention of Undesirable Clots
Substances used to prevent undesirable clots are:
o Aspirin an anti-prostaglandin, inhibits initiation of
clotting mechanism so the platelets are less likely to stick
together.
o Heparin an anticoagulant used clinically for pre- &
postoperative cardiac care.
o Warfarin used for those prone to atrial fibrillation.

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Bleeding Disorders
Conditions That Cause Excessive Bleeding in the Human Beings
Excessive bleeding can result from deciency of any one of the
many blood-clotting factors. Three particular types of bleeding
tendencies are
1) Vitamin K deciency,
2) Hemophilia, and
3) Thrombocytopenia (platelet deciency)
Decreased Prothrombin, Factor VII, Factor IX, and Factor X
due to vitamin K deciency leads to severe bleeding.
With few exceptions, almost all the blood-clotting factors are
formed by the liver.

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Bleeding Disorders, contd
Therefore, inability to synthesize factors regulating clotting
mechanism by the liver results severe bleeding disorders.
Causes: Vit. K deficiency, hepatitis & cirrhosis.

Inability to absorb fat can leads to vit. K deficiency as it is a


fat-soluble substance, absorbed along with fat.
Liver diseases prevent the liver from producing bile, which
is required for fat & vit. K absorption.

50
Bleeding Disorders, contd
Haemophilia
Hereditary sex-linked recessive bleeding disorder in males
XXh x XY
XX, XY, hXX, hXY
Bleeding time is prolonged.
There are three types of hemophilia:
1. Hemophilia-A: most common type (83% of all cases) due to
lack of F-VIII
2. Hemophilia-B: due to lack of F-IX
3. Hemophilia-C: due to lack of F-XI
Treatment: Replacement therapy
51
Blood Grouping
The surfaces of erythrocytes contain a genetically determined
assortment of antigens, composed of glycoproteins &
glycolipids.
These antigens are called agglutinogens.
Grouping depends on the presence or the absence of antigens
on the surface of RBCs membrane.
These antigens are:
Unique to the individual, and
Recognized as foreign if transfused into another individual who
does not have those same antigens on RBCs membrane.
Based on presence or absence of various antigens, the blood
is categorized into different blood groups.
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Major blood groups
There are at least 24 blood groups & more than 100
antigens that can be detected on the surface of RBCs.

Two major blood groups are:


ABO blood groups
Rh system
Other blood groups (medically less important)
include the Lewis, Kell, Kidd, & Duffy
53 systems.
ABO Blood Groups
Based on the of two glycolipid antigens (agglutinogens), A & B,
the ABO blood groups can be classified into 4 types of blood:
1. People whose RBCs display only antigen A have type A blood.
2. Those who have only antigen B are type B blood.
3. Individuals who have both A & B antigens are type AB blood.
4. Those who have neither antigen A nor B are type O blood.

Blood type Antigen present


A A
B B
AB A&B
54
O Neither A nor B
Agglutinins (Antibodies)
In the ABO blood grouping, plasma (serum) contains two
genetically determined agglutinins:
Anti-A antibodies (agglutinin-)
Anti-B antibodies (agglutinin-)
Based on the of two glycolipid antigens (agglutinogens) (A
& B), the ABO blood group can be classified into 4 types of
blood:
1. When agglutinogen A is present on RBCs membrane, anti-B
antibody is present in the serum.
2. When agglutinogen B is present on RBCs, anti-A antibody is
present in the serum.
3. When agglutinogen A & B exist together, neither anti-A nor
anti-B antibodies present in the serum.
4. When no agglutinogen on RBCs membrane, both anti-A &
55 anti-B antibodies are present in the serum.
ABO Blood Groups contd

Genetic combinations that determine blood type


are:
1. OO produces type O blood
2. AO & AA produce type A blood
3. BO & BB produce type B blood
4. AB produces type AB blood

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Ag-Ab Co-existence in the ABO Blood Groups

Blood type Antigen Antibody


A A anti-B
B B anti-A
AB A&B Neither
O Neither Both anti-A & anti-B

*Because the antibodies are large IgM-type antibodies


that do not cross the placenta, ABO incompatibility between
a mother and her fetus rarely causes problems.
57
Ag-Ab Co-existence, contd

58
ABO Blood Typing
To determine a blood type, a drop of blood sample is mixed
with a known prepared antibodies.
Known agglutinins
Blood
Anti-A Anti-B Blood type
samples
antibody antibody
1 + A
2 + B
3 + + AB
4 O
(+) = Agglutination reaction
59 () = No agglutination reaction
ABO Blood Group Cross Matching
Cross matching is a means to determine the compatibility of the
blood of donors with that of recipients for blood transfusion.

Donors Recipients Blood Types


Blood
Types A B AB O
A + +
B + _ +
AB + + +
O
(+) = Agglutination reaction
60 () = No agglutination reaction
Rh Factor
The Rh blood group is so named because the antigen was
discovered in the blood of the Rhesus monkey.
Grouped as Rh+ & Rh- based on the presence or absence of
agglutinogen D on the surface of RBCs.
People whose RBCs have Rh antigens (agglutinogen D) are
designated Rh+ (Rh positive); those who lack Rh antigens
are designated Rh- (Rh negative).
Agglutinins (anti-D antibodies) are not normally present in
the blood plasma, produced secondary to exposure of an Rh-
blood to Rh+ blood (antigen-D).
61
Rh Factor, contd
Normally, blood plasma does not contain anti-Rh
antibodies.
If an Rh- person receives an Rh+ blood transfusion,
however, the immune system starts to make anti-Rh
antibodies that will remain in the blood.
If a second transfusion of Rh+ blood is given later, the
previously formed anti-Rh antibodies will cause
agglutination & hemolysis of the RBCs in the donated
blood, and a severe reaction may occur.

62
Erythroblastosis Fetalis
The most common problem with Rh incompatibility, hemolytic
disease of the newborn (HDN), may arise during pregnancy.
Occurs when an Rh- mother marries an Rh+ father & conceives an
Rh+ fetus.
During delivery, there could be a leakage of Rh+ blood from the
fetus to the circulation of the mother.
Rh+ blood induces production of anti-D antibodies in the
circulation of the mother.
During 2nd conception of Rh+ fetus, anti-D antibodies cross the
placenta & attack RBCs of the fetus.
Injection of anti-Rh antibodies called anti-Rh gamma globulin
(RhoGAM) can be prevent HDN.
All Rh- women should receive RhoGAM soon after every
delivery, miscarriage, or abortion.
63 Limits the risk for subsequent births
ABO Blood Groups, contd

64
Blood Transfusion
A transfusion is the transfer of whole blood or blood
components (RBCs only or blood plasma only) into the
bloodstream or directly into the red bone marrow.
A transfusion is most often given to alleviate anemia, to
increase BV (e.g., after a severe hemorrhage), or to improve
immunity.
Whole blood transfusions are used:
When blood loss is substantial
In treating thrombocytopenia
Packed red cells (cells with plasma removed) are used to
treat anemia.
65
Blood Transfusions, contd

Precaution during blood transfusion


1. Determine blood group of the patient
2. Determine Rh factor
3. Do cross matching to see compatibility
4. Screen the blood for pathogens
5. Start with slow rate
6. Closely follow the patient

66
Transfusion Reactions
Transfusion reactions occur when mismatched blood is
infused.
In an incompatible blood transfusion, antibodies in the
recipients plasma bind to antigens on the donated RBCs,
which causes agglutination, or clumping of the RBCs.
Agglutination is an antigenantibody response in which
RBCs become cross-linked to one another.
As a result of the reaction:
o Diminished oxygen-carrying capacity.
o Clumped cells impede blood flow.
o Ruptured RBCs release free Hgb into the bloodstream
Circulating Hgb precipitates in the kidneys & causes renal
failure.
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Prevalence of ABO and Rh blood groups among
different ethnic groups
Frequency of blood groups (%)
Races
O A B AB Rh+

Whites 45 41 10 4 85

Blacks 48 27 21 4 88

Chines 36 28 23 13 100

Ethiopians 47 28 20 5 97
Diagnostic Blood Tests
Laboratory examination of blood can assess an
individuals state of health.
Microscopic examination:
o Variations in size & shape of RBCs predictions of
anemias.
o Type & number of WBCs diagnostic of various
diseases
Chemical analysis can provide a comprehensive
picture of ones general health status in relation to
normal values.

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