Chapter 10 Blood
Blood is the "river of life" that surges within us. It transports
everything that must be carried from one place to another within the
body-nutrients, wastes (headed for elimination from the body), and
body heat-through blood vessels. For centuries, long before modern
medicine, people recognized that blood was vital (some believed
"magical"), and its loss was always considered to be a possible cause
of death. In this chapter, we consider the composition and function of
this life-sustaining fluid. The means by which it is propelled
throughout the body is discussed in Chapter 11.
Composition and Functions of Blood
 Indicate the composition and volume of whole blood.
o Being the only fluid tissue, blood contains both a complex connective tissue in which living
blood cells, the formed elements, are suspended in a nonliving fluid matrix called plasma
 Contains – water, salts, plasma proteins, nutrients, waste products, respiratory
gases, hormones, red blood cells, white blood cells, platelets
 Blood accounts for ~8% of body weight - ~6 quarts in a healthy male
 Describe the composition of plasma and discuss its importance in the body.
o Plasma – 90% water – dissolved substances include nutrients, metal ions (salts),
respiratory gases, hormones, plasma proteins, and various wastes and products of cell
metabolism
 Plasma proteins – most abundant solutes in plasma – except for antibodies and
protein-based hormones, most plasma proteins are made by the liver
 Albumin – contributes to the osmotic pressure of blood, acting to keep water
in the bloodstream
 Clotting proteins – help stem blood loss when blood vessels are injured
 Antibodies – help protect the body from pathogens
 Plasma proteins are not taken up by cells to be used as food fuels or metabolic
nutrients unlike other solutes such as glucose, fatty acids, and oxygen
 List the cell types making up the formed elements and describe the major functions of each type.
o Erythrocytes – small, biconcave disks with depresses centers – red blood cells – ferry
oxygen in blood cells to all cells in the body – anucleate (no nucleus when mature) with
very few organelles
 Hemoglobin – iron-containing protein that transports the bulk of oxygen carried in
the blood and to a lesser degree, carbon dioxide
 Each RBC contains ~250 million hemoglobin molecules, each capable of
binding 4 molecules of oxygen
 No mitochondria so make ATP vie anaerobic mechanisms so they don’t use the
oxygen they carry
o Leukocytes – white blood cells – crucial to body defense against disease (bacteria,
viruses, parasites, tumor cells, dead cells) – less than 1% of total blood volume – the only
complete cells in blood with a nucleus and the usual organelles
 Not confined to the blood vessels like RBC are – are able to slip out of blood vessels
via diapedesis to get to areas of tissue damage and infection – respond to
chemicals that diffuse from the damaged cells in a process called positive
chemotaxis – move to the area by ameboid motion following the diffusion gradient
Granulocytes – granule-containing WBCs – lobed nuclei, which consist of
several rounded nuclear areas connected by thin strands of nuclear material –
granules stain with Wright’s stain
 Neutrophils – have a multilobed nucleus and very fine granules that
respond to both acid and basic stains and the cytoplasm stains pink –
phagocytes at sites of acute infection
 Eosinophils – blue-red nucleus and brick-red cytoplasmic granules –
numbers increase during allergies and infections by parasitic worms
 Basophils – contain large histamine-containing granules that stain
dark blue – histamine is an inflammatory chemical that makes blood
vessels leaky and attracts other WBCs to the site
 Agranulocytes – lake visible cytoplasmic granules with normal looking nuclei
 Lymphocytes – large dark purple nucleus that occupies most of the
cell volume – live in lymphatic tissue where they help in immune
responses
 Monocytes – abundant cytoplasm and indented nucleus – change into
macrophages to fight chronic infections such as tuberculosis
o Platelets – not cells but fragments of multinucleate cells called megakaryocytes, which
rupture, releasing thousands of anucleate pieces that quickly seal themselves off from
surrounding fluids – appear as darkly staining, irregularly shaped bodies scattered among
the other blood cells – normal platelet count is 300,000/mm3 – needed for the clotting
process that occurs when blood vessels are broken
 Define anemia, polycythemia, leucopenia, and leukocytosis, and list possible causes for each
condition.
o Anemia – a decrease in the oxygen-carrying ability of the blood for any reason – a lowerthan-normal number of RBC or abnormal or deficient hemoglobin content in the RBCs such
as sickle-cell anemia
o Polycythemia – an excessive or abnormal increase in the number of erythrocytes – may
result from bone marrow cancer or a normal physiological response to living at high
altitudes where air is thinner and therefore less oxygen is available – excessive RBCs
increases blood viscosity causing it to flow sluggishly in the body and impairs circulation
o Leukocytosis – a total WBC count above 11,000 cells/mm3 – generally indicated that a
bacterial or viral infection is stewing in the body
 Explain the role of the hemocytoblast.
o All the formed elements arise from this common type of stem cell in a process called
hematopoiesis that occurs in red bone marrow, or myeloid tissue
 Development differs for each type but once the cell is committed to a specific blood
pathway, it cannot change
 Hemocytoblasts form two types of descendants that form all the other cells –
lymphoid stem cells that result in lymphocytes and myeloid stem cells that result
in all other types
 Rate of erythrocyte production is controlled by the hormone erythropoietin
produced primarily by the kidneys and less by the liver
 Rate of leukocytes is stimulated by the hormones colony stimulating factor
and interleukins, which are stimulated by chemical signals sent out by cells
in danger
 Rate of platelets is accelerated by the hormone thrombopoietin

Hemostasis
 Describe the blood-clotting process.
o See figure 10.6 on page 316
o Platelet plug forms – platelets become sticky and cling to the damaged site and anchored
platelets release chemicals that attract more platelets to the site so that a small mass called
a platelet plug or white thrombus is formed
o Vascular spasms occur – the anchored platelets also release serotonin which causes that
blood vessel to go into spasms that narrow the blood vessel at that point, decreasing blood
loss until clotting can occur
o Coagulation events occur
 The injured tissues are releasing thromboplastin, a factor that plays a role in
clotting
 PF3, a phospholipid that coats the surfaces of the platelets, interacts with
thromboplastin, other blood protein clotting factors, and calcium ions (Ca 2+) to
form an activator that triggers the clotting cascade
 This prothrombin activator converts prothrombin that is present in the plasma to
thrombin, an enzyme
 Thrombin then joins soluble fibrinogen proteins into long hair-like molecules of
insoluble fibrin, which forms a meshwork that traps the RBCs and forms the basis of
the clot
 Within the hour, the clot begins to retract, squeezing serum (plasma minus the
clotting proteins) from the mass and pulling the ruptured edges of the blood vessel
closer together
 Name some factors that may inhibit or enhance the blood-clotting process.
o Undesirable clotting – sometimes form in intact blood vessels, especially those in the legs
– a clot that develops and persists in unbroken vessels is called a thrombus and if it is
large enough, it may prevent blood flow to the cells beyond the blockage – may be caused
by anything that roughens the endothelium of a blood vessel and encourages clinging of
platelets such as burns, physical blows, or an accumulation of fatty material – treated with
anticoagulants such as aspirin, heparin, and dicumarol
 If the clot is in the heart, a heart attack may occur killing heart tissue and/or the
person
 If a thrombus breaks away from the vessel wall and floats freely in the blood stream,
it becomes an embolus, which if it lodges in a small vessel in the brain could result
in a cerebral embolus and cause a stroke
 Slowly flowing blood or blood pooling is another problem especially in immobilized
patients because clotting factors are not washed away as usual and so they
accumulate
o Bleeding disorders – usually caused by platelet deficiency and deficits of clotting factors
 Thrombocytopenia – results from an insufficient number of platelets resulting in
normal movements causing spontaneous bleeding from small blood vessels showing
up as small purplish blotches called petechiae on the skin – can arise from any
condition that suppresses myeloid tissue such as bone marrow cancer, radiation, or
certain drugs
 Vitamin K deficiency – when the liver is unable to make its usual supply of clotting
factors, abnormal bleeding may result as vitamin K is needed to make clotting
factors – treated with vitamin K or with whole blood transfusions when the liver
function is severely impaired
 Hemophilia – hereditary bleeding disorder – results from a lack of any of the factors
needed for clotting – even minor tissue trauma results in prolonged bleeding and can
be life-threatening – repeated bleeding into joints causes them to become disabled
and painful – treated with transfusion of fresh plasma or injections of purified clotting
factors they lack
Blood Groups and Transfusions
 Describe the ABO and Rh blood groups.
o ABO blood groups are based on which of two antigens, type A or type B a person
inherits – absence of both antigens results in type O blood while presence of both antigens
results in type AB blood, only A or B antigens leads to either type A or type B blood
 Antibodies are formed during infancy against the ABO antigens not present in your
own RBCs
o Rh blood groups – so named because one of the eight Rh antigens (agglutinogen D)
was originally identified in Rhesus monkeys
 Rh+ people have RBCs that carry the Rh antigen while RH- people do not carry the Rh
antigen
 Anti-Rh antibodies are not automatically formed and present in the blood of Rh people but once an Rh- individual receives Rh+ blood, their immune system begins
producing antibodies so the second time they receive the wrong blood type,
hemolysis (rupturing of the RBCs) will occur
 When an Rh- woman is carrying an Rh+ fetus the first time there is usually no
problems and a healthy baby is delivered but the mother becomes sensitized to the
Rh+ antigens that have passed through the placenta into her bloodstream and she
will produce anti-Rh+ antibodies unless treated with RhoGAM shortly after giving
birth
 RhoGAM is an immune serum that prevents the sensitization and her
immune response
 If no treatment is given, and she becomes pregnant again with another Rh +
baby, her antibodies will cross the placenta and destroy the baby’s RBCs,
which produces a condition known as hemolytic disease of the newborn
where the baby is anemic and hypoxic resulting in brain damage or the
death of the baby
 Explain the basis for a transfusion reaction.
o It is important to determine the blood group of both the donor and the recipient before
blood is transfused because agglutination could occur killing the recipient
o The plasma membranes of RBCs bear genetically determined proteins (antigens, which is a
substance that the body recognizes as foreign and stimulates the immune system to release
antibodies against it), which identify each person as unique therefore another person’s RBCs
with foreign antigens on them will be attacked by the recipient’s immune system
 Agglutination occurs when the binding of the antibodies causes the RBCs to clump,
which leads to the clogging of small blood vessels throughout the body
 The donor RBCs are lysed and their hemoglobin is released into the bloodstream
where the released molecules could block the kidney tubules and cause kidney
failure – treatment is aimed at preventing kidney damage by infusing alkaline
fluids to dilute and dissolve the hemoglobin and diuretics to flush it out of the body
in urine
o The Rh factor must also match between the donor and recipient to further reduce the
danger to the recipient
Developmental Aspects of Blood
 Explain the basis of physiologic jaundice seen in some newborn babies.
o Fetal hemoglobin (HbF) differs from the hemoglobin formed after birth in that fetal
hemoglobin has a greater ability to pick up oxygen – after birth fetal blood cells are
gradually replaced by RBCs that contain the typical hemoglobin A (HbA)
o Physiologic jaundice occurs when the fetal RBCs are destroyed at such a rapid rate that
the immature infant liver cannot rid the body of hemoglobin breakdown products in the bile
fast enough
 Indicate blood disorders that increase in frequency in the aged.
o Iron-deficiency anemia is common in women because of their monthly blood loss during
menses
o The young and old are particularly at risk for leukemia
o With increasing age, chronic types of leukemia, anemia, and diseases involving undesirable
clot formation are more prevalent, however, these are usually secondary to disorders of the
heart, blood vessels, or immune system
o The elderly are particularly at risk for pernicious anemia because the stomach mucosa
(which produces intrinsic factor) atrophies with age