 Blood performs a number of functions

dealing with:
 Substance distribution
 Regulation of blood levels of particular
substances
 Body protection
 Blood transports:
 Oxygen from the lungs and nutrients from the
digestive tract
 Metabolic wastes from cells to the lungs and
kidneys for elimination
 Hormones from endocrine glands to target organs
 Blood maintains:
 Appropriate body temperature by absorbing and
distributing heat to other parts of the body
 Normal pH in body tissues using buffer systems
 Adequate fluid volume in the circulatory system
 Blood prevents blood loss by:
 Activating plasma proteins and platelets
 Initiating clot formation when a vessel is
broken
 Blood prevents infection by:
 Synthesizing and utilizing antibodies
 Activating complement proteins
 Activating WBCs to defend the body against
foreign invaders
 Average volume of blood:
 5–6 L for males; 4–5 L for females (Normovolemia)
 Hypovolemia - low blood volume
 Hypervolemia - high blood volume
 Viscosity (thickness) - 4 - 5 (where water = 1)
 The pH of blood is 7.4
 Osmolarity = 300 mOsm or 0.3 Osm
 This value reflects the concentration of solutes in the plasma
 Salinity = 0.85%
 Reflects the concentration of NaCl in the blood
 Temperature is 38C, slightly higher than “normal”
body temperature
 Blood accounts for approximately 8% of body weight
 Blood is the body’s only fluid tissue (a
connective tissue)
 2 major components
 Liquid
= plasma (55%)
 Formed elements (45%)
 Erythrocytes, or red blood cells (RBCs)
 Leukocytes, or white blood cells (WBCs)
 Platelets - fragments of megakaryocytes in marrow
 Plasma
(55% of whole blood)

Buffy coat:
leukocyctes and
platelets
(<1% of whole blood)
Formed
elements
Erythrocytes
1 Withdraw blood 2 Centrifuge (45% of whole blood)
and place in tube
 Blood plasma components:
 Water = 90-92%
 Proteins = 6-8%
 Albumins; maintain osmotic pressure of the blood
 Globulins
 Alpha
and beta globulins are used for transport purposes
 Gamma globulins are the immunoglobulins (IgG, IgA, etc)
 Fibrinogen; a clotting protein
 Organic nutrients – glucose, carbohydrates, amino
acids
 Electrolytes – sodium, potassium, calcium,
chloride, bicarbonate
 Nonprotein nitrogenous substances – lactic acid,
urea, creatinine
 Respiratory gases – oxygen and carbon dioxide
 Formed elements comprise 45% of blood
 Erythrocytes, leukocytes, and platelets make up
the formed elements
 Only WBCs are complete cells
 RBCs have no nuclei or organelles, and platelets are
just cell fragments
 Most formed elements survive in the
bloodstream for only a few days
 Most blood cells do not divide but are renewed
by cells in bone marrow
 Biconcave disc
 Folding increases surface area (30% more surface area)
 Plasma membrane contains spectrin
 Give erythrocytes their flexibility

 Anucleate, no centrioles, no organelles

 End result - no cell division
 No mitochondria means they generate ATP anaerobically
 Prevents consumption of O2 being transported
 Filled with hemoglobin (Hb) - 97% of cell contents
 Hb functions in gas transport
 Hb + O HbO2 (oxyhemoglobin)
2
 Most numerous of the formed elements
 Females: 4.3–5.2 million cells/cubic millimeter
 Males: 5.2–5.8 million cells/cubic millimeter
Figure 17.3
 Erythrocytes are dedicated to respiratory gas
transport
 Hemoglobin reversibly binds with oxygen and
most oxygen in the blood is bound to
hemoglobin
 Composition of hemoglobin
 A protein called globin
 made up of two alpha and two beta chains
A heme molecule
 Each heme group bears an atom of iron, which can bind to
one oxygen molecule
 Each hemoglobin molecule thus can transport four
molecules of oxygen
Figure 17.4
 Oxyhemoglobin – hemoglobin bound to
oxygen
 Oxygen loading takes place in the lungs
 Deoxyhemoglobin – hemoglobin after oxygen
diffuses into tissues (reduced Hb)
 Carbaminohemoglobin – hemoglobin bound to
carbon dioxide
 Carbon dioxide loading takes place in the tissues
 The life span of an erythrocyte is 120 days
 Old erythrocytes become rigid and fragile, and
their hemoglobin begins to degenerate
 Dying erythrocytes are engulfed by
macrophages
 Heme and globin are separated
 Iron
is removed from the heme and salvaged for
reuse
 Stored as hemosiderin or ferritin in tissues
 Transported in plasma by beta-globulins as transferrin
 Heme is degraded to a yellow pigment
called bilirubin
 Liver secretes bilirubin into the intestines as
bile
 Intestines metabolize bilirubin into
urobilinogen
 Urobilinogen leaves the body in feces, in a
pigment called stercobilin
 Globin is metabolized into amino acids
which are then released into the
circulation
 Hematopoiesis – blood cell formation
 Occurs in the red bone marrow (myeloid tissue)
 Axial skeleton and girdles
 Epiphyses of the humerus and femur
 Marrow contains immature erythrocytes
 Composed of reticular connective tissue
 Hemocytoblasts give rise to ALL formed
elements
 Lymphoid stem cells - give rise to lymphocytes
 Myeloid stem cells - give rise to all other blood cells
 Erythropoietin (EPO) release by the kidneys
is triggered by:
 Hypoxia due to decreased RBCs
 Decreased oxygen availability
 Increased tissue demand for oxygen
 Enhanced erythropoiesis increases the:
 RBC count in circulating blood
 Oxygen carrying ability of the blood
 Erythropoiesis requires:
 Proteins, lipids, and carbohydrates
 Iron, vitamin B12, and folic acid
 The body stores iron in Hb (65%), the
liver, spleen, and bone marrow
 Intracellular iron is stored in protein-iron
complexes such as ferritin and
hemosiderin
 Circulating iron is loosely bound to the
transport protein transferrin
 Polycythemia
 Abnormal excess of erythrocytes
 Increases viscosity, decreases flow rate of blood
 Anemia – blood has abnormally low oxygen-
carrying capacity
 Itis a symptom rather than a disease itself
 Blood oxygen levels cannot support normal
metabolism
 Signs/symptoms include fatigue, paleness, shortness
of breath, and chills
 Hemorrhagic anemia – result of acute or
chronic loss of blood
 Hemolytic anemia – prematurely ruptured
erythrocytes
 Aplastic anemia – destruction or inhibition of
red bone marrow
 Iron-deficiency anemia results from:
A secondary result of hemorrhagic anemia
 Inadequate intake of iron-containing foods
 Impaired iron absorption
 Pernicious anemia results from:
 Deficiency of vitamin B12
 Lack of intrinsic factor needed for absorption of B 12
 Treatment is intramuscular injection of B 12
 Thalassemias – absent or faulty globin
chain in hemoglobin
 Erythrocytes
are thin, delicate, and deficient
in hemoglobin
 Sickle-cell anemia – results from a
defective gene
 Codes for an abnormal hemoglobin called
hemoglobin S (HbS)
 This defect causes RBCs to become sickle-
shaped in low oxygen situations
 Polycythemia – excess RBCs that increase
blood viscosity
 Three main polycythemias are:
 Polycythemia vera
 Secondary polycythemia
 Leukocytes, the only blood components that are complete
cells:
 4,800 - 10,000/cubic millimeter
 Protect the body from infectious microorganisms
 Can leave capillaries via diapedesis
 Move through tissue spaces (amoeboid motion)
 Many are phagocytic (possess numerous lysosomes)
 Two major types of leukocytes
 Granulocytes: Neutrophils, Eosinophils, Basophils
 Agranulocytes: Monocytes, Lymphyocytes
 Leukocytosis – WBC count over 11,000/mm3
 Normal response to bacterial or viral invasion
 Leukopenia - a decrease in WBC count below 4,800/mm3
 Leukemia - a cancer of WBC
 Granulocytes – neutrophils, eosinophils, and
basophils
 Contain cytoplasmic granules that stain
specifically (acidic, basic, or both) with Wright’s
stain
 Are larger and usually shorter-lived than RBCs
 Have lobed nuclei
 Are all phagocytic cells
 Account for 65-75% of total WBC’s
 Neutrophils have two types of granules that:
 Take up both acidic and basic dyes
 Give the cytoplasm a lilac color
 Contain peroxidases, hydrolytic enzymes, and
defensins (antibiotic-like proteins)
 Neutrophils are our body’s bacteria slayers
 Eosinophils account for 1–4% of WBCs
 Have red-staining, bilobed nuclei
 Have red to crimson granules
 Function:
 Lead the body’s counterattack against parasitic
infections
 Lessen the severity of allergies by phagocytizing
immune complexes (ending allergic reactions)
 Account for 0.5-1% of all WBCs
 Have U- or S-shaped nuclei with two or three
conspicuous constrictions
 Are functionally similar to mast cells
 Have large, purplish-black (basophilic) granules
that contain histamine
 Histamine – inflammatory chemical that acts as a
vasodilator and attracts other WBCs (antihistamines
counter this effect)
 Account for 20-25% or more of WBCs and:
 Have large, dark-purple, circular nuclei with a thin
rim of blue cytoplasm
 Are found mostly enmeshed in lymphoid tissue
(some circulate in the blood)
 Most important cells of the immune system
 There are two types of lymphocytes: T cells
and B cells
T cells - attack foreign cells directly
 B cells give rise to plasma cells, which produce
antibodies
 Monocytes account for 3–7% of leukocytes
 They are the largest leukocytes
 They have purple-staining, U- or kidney-shaped
nuclei
 They leave the circulation, enter tissue, and
differentiate into macrophages
 Leukopoiesis is hormonally stimulated by two
families of cytokines (hematopoietic factors) –
interleukins and colony-stimulating factors
(CSFs)
 Interleukins
are numbered (e.g., IL-1, IL-2), whereas
CSFs are named for the WBCs they stimulate (e.g.,
granulocyte-CSF stimulates granulocytes)
 Macrophages and T cells are the most important
sources of cytokines
 Many hematopoietic hormones are used clinically
to stimulate bone marrow
 All leukocytes originate from hemocytoblasts
 The mother of all blood stem cells
 Hemocytoblasts differentiate into myeloid stem
cells and lymphoid stem cells
 Myeloid stem cells become myeloblasts or
monoblasts
 Granulocytes form from myeloblasts

 Monoblasts enlarge and form monocytes

 Lymphoid stem cells become lymphoblasts

 Lymphoblasts develop into lymphocytes
Figure 17.11
 Leukemia refers to cancerous conditions
involving white blood cells
 Leukemias are named according to the
abnormal white blood cells involved
 Myelocyticleukemia – involves myeloblasts
 Lymphocytic leukemia – involves lymphocytes
 Acute leukemia involves blast-type cells
and primarily affects children
 Chronic leukemia is more prevalent in
older people
 Immature white blood cells are found in the
bloodstream in all leukemias
 Bone marrow becomes totally occupied with
cancerous leukocytes
 Severe anemia ensues due to excess
production of WBC’s
 The white blood cells produced, though
numerous, are not functional
 Death is caused by internal hemorrhage and
overwhelming infections
 Treatments include irradiation, antileukemic
drugs, and bone marrow transplants
 Platelets are fragments of megakaryocytes
 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
 Platelets not involved in clotting are kept
inactive by Nitric Oxide (NO) and prostaglandins
 RBC membranes have glycoprotein antigens
on their external surfaces
 These antigens are:
 Unique to the individual
 Recognized as foreign if transfused into another
individual
 Promoters of agglutination and are referred to as
agglutinogens
 Presence or absence of these antigens is used
to classify blood groups
 Humans have 30 varieties of naturally
occurring RBC antigens
 The antigens of the ABO and Rh blood groups
cause vigorous transfusion reactions when
they are improperly transfused
 Other blood groups (M, N, Dufy, Kell, and
Lewis) are mainly used for legalities
 The ABO blood groups consists of:
 Two antigens (A and B) on the surface of the
RBCs
 Two antibodies 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
Table 17.4
 Presence of the Rh agglutinogens on RBCs is
indicated as Rh+; 85% of population is +
 Lack of antigen indicated as Rh -; 15% of
popn.
 Anti-Rh antibodies are not spontaneously
formed only 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
 May occur in an Rh- mom pregnanet with an Rh+
fetus
 Hemolytic disease of the newborn – Rh+ antibodies of
a sensitized Rh– mother cross the placenta and attack
and destroy the RBCs of an Rh+ baby
 Rh– mother becomes sensitized when Rh+ blood (from
a previous pregnancy of an Rh+ baby or a Rh+
transfusion) causes her body to synthesis Rh+
antibodies
 The drug RhoGAM can prevent the Rh– mother from
becoming sensitized
 Treatment of hemolytic disease of the newborn
involves pre-birth transfusions and exchange
transfusions after birth
 Transfusion reactions occur when
mismatched blood is infused
 Donor’s cells are attacked by the
recipient’s plasma agglutinins causing:
 Diminished oxygen-carrying capacity
 Clumped cells that impede blood flow
 Ruptured RBCs that release free hemoglobin
into the bloodstream
 Circulating hemoglobin precipitates in the
kidneys and causes renal failure
46
47
 Anemias (or anaemias) are diseases
characterized by low oxygen transport
capacity of the blood, because of low red
cell count or some abnormality of the red
blood cells or the hemoglobin
 Iron deficiency anemia is the most common
anemia

48
 Iron deficiency anemia occurs when the
dietary intake or absorption of iron is
insufficient, and hemoglobin, which contains
iron, cannot be formed

49
 Sickle-cell disease is a genetic disease that
results in abnormal hemoglobin molecules
 When these release their oxygen load in the
tissues, they become insoluble, leading to mis-
shaped red blood cells

50
51
 These sickle shaped red cells are rigid and
cause blood vessel blockage, pain, strokes,
and other tissue damage
 Thalassemia is a genetic disease that results
in the production of an abnormal ratio of
hemoglobin subunits

52
 Spherocytosis is a genetic disease that causes
a defect in the red blood cell's cytoskeleton,
causing the red blood cells to be small,
sphere-shaped, and fragile instead of donut-
shaped and flexible
 Pernicious anemia is an autoimmune disease
wherein the body lacks intrinsic factor,
required to absorb vitamin B12 from food

53
 Vitamin B12 is needed for the production of
hemoglobin
 Aplastic anemia is caused by the inability of
the bone marrow to produce blood cells
 Pure red cell aplasia is caused by the
inability of the bone marrow to produce only
red blood cells

54
 Hemolysis is the general term for excessive
breakdown of red blood cells. It can have
several causes
 The malaria parasite spends part of its life-
cycle in red blood cells, feeds on their
hemoglobin and then breaks them apart,
causing fever

55
 Both sickle-cell disease and thalassemia are
more common in malaria areas, because
these mutations convey some protection
against the parasite
 Polycythemias (or erythrocytoses) are
diseases characterized by a surplus of red
blood cells. The increased viscosity of the
blood can cause a number of symptoms

56
 In polycythemia vera the increased number
of red blood cells results from an
abnormality in the bone marrow
 Several microangiopathic diseases, including
disseminated intravascular coagulation and
thrombotic microangiopathies, present with
pathognomonic (diagnostic) RBC fragments
called schistocytes

57
 These pathologies generate fibrin strands
that sever RBCs as they try to move past a
thrombus
 Several blood tests involve red blood cells,
including the RBC count (the number of red
blood cells per volume of blood) and the
hematocrit (percentage of blood volume
occupied by red blood cells)

58
 The blood type needs to be determined to
prepare for a blood transfusion or an organ
transplantation

59
60
 Anemia (AmE) or anaemia (BrE), from the
Greek (Ἀναιμία) (an-aîmia) meaning "without
blood," is defined as a qualitative or
quantitative deficiency of hemoglobin, a
molecule found inside RBCs
 Since hemoglobin normally carries oxygen
from the lungs to the tissues, anemia leads
to hypoxia (lack of oxygen) in organs

61
 Since all human cells depend on oxygen for
survival, varying degrees of anemia can have
a wide range of clinical consequences

62
 Anemia is the most common disorder of the
blood
 There are several kinds of anemia, produced
by a variety of underlying causes

63
 The three main classes of anemia:
 Excessive blood loss (acutely such as a
hemorrhage or chronically through low-volume
loss)
 Excessive blood cell destruction (hemolysis)
 Eeficient RBC production (ineffective
hematopoiesis)

64
 Anemia can be classified in a variety of ways,
based on the morphology of RBCs, underlying
etiologic mechanisms, and discernible
clinical spectra, to mention a few

65
 There are two major approaches of
classifying anemias
 The "kinetic" approach which involves evaluating
production, destruction and loss
 The "morphologic" approach which groups anemia
by red blood cell size
 The morphologic approach uses a quickly
available and cheap lab test as its starting
point (the MCV)

66
 On the other hand, focusing early on the
question of production may allow the
clinician more rapidly to expose cases where
multiple causes of anemia coexist

67
68
 Anemia goes undetected in many people, and
symptoms can be small and vague
 Most commonly, people with anemia report a
feeling of weakness or fatigue in general or
during exercise, general malaise and
sometimes poor concentration

69
 People with more severe anemia often report
dyspnea (shortness of breath) on exertion
 Very severe anemia prompts the body to
compensate by increasing cardiac output,
leading to palpitations and sweatiness, and
to heart failure

70
 Pallor (pale skin, mucosal linings and nail
beds) is often a useful diagnostic sign in
moderate or severe anemia, but it is not
always apparent
 Other useful signs are cheilosis and
koilonychia

71
72
73
74
75
 Pica, the consumption of non-food such as
dirt, paper, wax, grass, ice and hair, may be
a symptom of iron deficiency, although it
occurs often in those who have normal levels
of hemoglobin

76
 Chronic anemia may result in behavioral
disturbances in children as a direct result of
impaired neurological development in
infants, and reduced performance in
children of school age

77
 Generally, clinicians request complete blood
counts in the first batch of blood tests in the
diagnosis of an anemia
 Apart from reporting the number of RBCs and
the hemoglobin level, the automatic
counters also measure the size of the RBCs
by flow cytometry, which is an important
tool in distinguishing between the causes of
anemia

78
 Examination of a stained blood smear using a
microscope can also be helpful, and is
sometimes a necessity in regions of the world
where automated analysis is less accessible

79
 In modern counters, four parameters (RBC
count, hemoglobin concentration, MCV and
are measured, allowing others (hematocrit,
MCH and MCHC) to be calculated, and
compared to values adjusted for age and sex
 Some counters estimate hematocrit from
direct measurements

80
 For adult men, a hemoglobin level less than
13.0 g/dl is diagnostic of anemia, and for
adult women, the diagnostic threshold is
below 12.0 g/dl

81
 Reticulocyte counts, and the "kinetic"
approach to anemia, have become more
common than in the past in part because
some automatic counters now have the
capacity to include reticulocyte counts

82
 A reticulocyte count is a quantitative
measure of the bone marrow's production of
new red blood cells
 The reticulocyte production index is a
calculation of the ratio between the level of
anemia and the extent to which the
reticulocyte count has risen in response

83
 If the degree of anemia is significant, even a
"normal" reticulocyte count actually may
reflect an inadequate response
 If an automated count is not available, a
reticulocyte count can be done manually
following special staining of the blood film

84
 In manual examination, activity of the bone
marrow can also be gauged qualitatively by
subtle changes in the numbers and the
morphology of young RBCs by examination
under a microscope
 Newly formed RBCs are usually slightly larger
than older RBCs and show polychromasia

85
 Even where the source of blood loss is
obvious, evaluation of erythropoiesis can
help assess whether the bone marrow will be
able to compensate for the loss, and at what
rate

86
 When the cause is not obvious, clinicians use
other tests: ESR, ferritin, serum iron,
transferrin, RBC folate level, serum vitamin
B12, hemoglobin electrophoresis, renal
function tests (e.g. serum creatinine)

87
 When the diagnosis remains difficult, a bone
marrow examination allows direct
examination of the precursors to red cells

88
89
 Sickle-cell disease or sickle-cell anemia is a
blood disorder characterized by red blood
cells that assume an abnormal, rigid, sickle
shape
 Sickling decreases the cells' flexibility and
results in their restricted movement through
blood vessels, depriving downstream tissues
of oxygen

90
 The disease is chronic and lifelong:
 Individuals are most often well, but their lives
are punctuated by periodic painful attacks and a
risk of various other complications
 Life expectancy is shortened, with older
studies reporting an average life expectancy
of 42 and 48 years for males and females,
respectively

91
 Sickle-cell disease occurs more commonly in
people (or their descendants) from parts of
the world such as sub-Saharan Africa, where
malaria is or was common, but it also occurs
in people of other ethnicities

92
 This is because those with one or two alleles
of the sickle-cell disease are resistant to
malaria since the sickle red blood cells are
not conducive to the parasites - in areas
where malaria is common there is a survival
value in carrying the sickle-cell genes

93
 Sickle-cell disease may lead to various acute
and chronic complications, several of which
are potentially lethal
 The vaso-occlusive crisis is caused by sickle-
shaped red blood cells that obstruct
capillaries and restrict blood flow to an
organ, resulting in ischemia, pain, and organ
damage

94
 Abnormal hemoglobin forms can be detected
on hemoglobin electrophoresis,

95
 The diagnosis can be confirmed with high
performance liquid chromatography (HPLC)
 Genetic testing is rarely performed, as other
investigations are highly specific for HbS and
HbC

96
 Sickle-cell anemia is caused by a point
mutation in the β-globin chain of
hemoglobin, causing the glutamate to be
replaced with the valine at the sixth position
 The β-globin gene is found on the short arm
of chromosome 11

97
 The association of two wild-type α-globin
subunits with two mutant β-globin subunits
forms haemoglobin S (HbS)
 Under low oxygen conditions, the absence of
a polar amino acid at position six of the β-
globin chain promotes the polymerization of
hemoglobin, which distorts RBCs into a sickle
shape and decreases their elasticity

98
99
 The cells include:
 Lymphocytes
 Monocytes
 Macrophages
 There are three types of granulocytes:
 Neutrophils
 Basophils
 Eosinophils

100
101
 Platelets, or thrombocytes, are the cells
circulating in the blood that are involved in
the cellular mechanisms of primary
hemostasis (bleeding stop) leading to the
formation of blood clots
 The term platelet should be reserved for
anucleated thrombocytes of mammals

102
103
 An abnormality or disease of the platelets is
called a thrombocytopathy which could be
either a decrease in number ie
thrombocytopenia, decrease in function ie
thrombasthenia or an increase in number ie
thrombocytosis

104
 Functions of platelets can be generalized
into a number of categories:
 Adhesion
 Aggregation
 Clot retraction
 Pro-coagulation
 Cytokine signaling
 Phagocytosis

105
106
107
 MW 66 000
 Single chain, 580 amino acids, sequence is
known
 Dimensions - Heart shaped molecule

108
109
 Albumin is the major transport protein in
blood plasma and can reversibly bind a wide
range of molecules

110
 “Colloid” osmotic pressure of blood is 80%
due to albumin
 relativelylow molecular weight
 regulates water distribution
 Transport of fatty acids
 Liver to tissues, binding

111
 Source of amino acids for tissue cells
(pinocytosis)
 60% albumin in tissue (interstitial) fluid

112
113
 20% of plasma proteins
 “” refers to electrophoretic mobility
 Represents a group of proteins of variable
structure
 immunoglobulins

 Main functional task is immunochemical

 Antibodies - combine with specific antigens

114
115
 Basic 4 chain structural unit
 MW = 160000
 Constant - same amino acid sequence for all
of the molecules
 Variable - varies between molecules- results
in specificity of molecules

116
 Two heavy and two light chains joined by
disulfide bonds
 Variable region - red - binds the antigen
Constant region (black) can activate
complement pathway or attach the Ab to
cells such as macrophages

117
1. IgG – Identifies microorganisms for
engulfment or lysis
2. IgE – Inhibits parasite invasion; involved in
allergic reactions
3. IgD – Unknown

118
4. IgA – Basis for passive immunity provided
by breast milk, agglutinates infectious
agents in secretions outside the body,
present in tears, mucous
5. IgM – Identifies microorganisms for
engulfment or lysis

119
 Primary function is antigen binding (immune
response)
 Secondary function is complement binding
(after antigen)

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 In lymphocytes (T and B)
 Made in response to presence of antigen
(“foreign” macromolecule, virus particle etc)

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 Coagulation
 Structure
 MW 340 000
 Sequence of amino acids is known (3000)

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 Coagulation - very important consideration
when processing blood outside of the body
 Structure must incorporate the ability to be
easily broken down after clotting

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