1. Composition of Blood
• Consists of formed elements (cells) suspended &
carried in plasma (fluid part)
• Total blood volume is about 5L
• Plasma is straw-colored liquid consisting of H20 &
dissolved solutes
– Includes ions, metabolites, hormones, antibodies
13-7
2. Physical Characteristics of Blood
• 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 7.35–7.45; x = 7.4
• 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
3. Plasma Proteins
• Constitute 7-9% of plasma
• Three types of plasma proteins: albumins, globulins, &
fibrinogen
– Albumin accounts for 60-80%
• Creates colloid osmotic pressure that draws H 20 from interstitial fluid into
capillaries to maintain blood volume & pressure
• Globulins carry lipids
– Gamma globulins are antibodies (immunoglobulins)
• Fibrinogen serves as clotting factor
– Converted to fibrin
– Serum is fluid left when blood clots
13-8
4. Formed Elements
• Are erythrocytes (RBCs) &
leukocytes (WBCs)
• RBCs are flattened biconcave discs
– Shape provides increased surface area
for diffusion
– Lack nuclei & mitochondria
– Each RBC contains 280 million
hemoglobins
13-9
5. Leukocytes
• Have nucleus, mitochondria, & amoeboid ability
• Can squeeze through capillary walls (diapedesis)
– Granular leukocytes help detoxify foreign substances &
release heparin
• Include eosinophils, basophils, & neutrophils
13-10
7. Platelets (thrombocytes)
• Are smallest of formed elements,
lack nucleus
• Are fragments of megakaryocytes
• Constitute most of mass of blood
clots
• Release serotonin to vasoconstrict &
reduce blood flow to clot area
• Secrete growth factors to maintain
integrity of blood vessel wall
• Survive 5-9 days
13-12
8. Components of Whole Blood
Plasma
(55% of whole blood)
Buffy coat:
leukocyctes and
platelets
(<1% of whole blood)
1 Withdraw blood
2 Centrifuge
and place in tube
• Hematocrit
• Males: 47% ± 5%
• Females: 42% ± 5%
Erythrocytes
(45% of whole blood)
Formed
elements
9. Hematopoiesis
• Is formation of blood cells from stem cells in
marrow (myeloid tissue) & lymphoid tissue
• Erythropoiesis is formation of RBCs
– Stimulated by erythropoietin (EPO) from kidney
• Leukopoiesis is formation of WBCs
– Stimulated by variety of cytokines
• = autocrine regulators secreted by immune system
13-13
11. Erythropoiesis
• 2.5 million RBCs are
produced/sec
• Lifespan of 120 days
• Old RBCs removed
from blood by
phagocytic cells in
liver, spleen, & bone
marrow
– Iron recycled back
into hemoglobin
production
13-14
12. Erythropoietin Mechanism
Imb
ala
nce
Start
Normal blood oxygen levels
Imb
ala
nce
Increases
O2-carrying
ability of blood
Stimulus: Hypoxia due to
decreased RBC count,
decreased availability of O2
to blood, or increased
tissue demands for O2
Reduces O2
levels in blood
Enhanced
erythropoiesis
increases RBC
count
Erythropoietin
stimulates red
bone marrow
Kidney (and liver to a
smaller extent) releases
erythropoietin
Figure 17.6
13. Dietary Requirements of
Erythropoiesis
• 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
14. RBC Antigens & Blood Typing
• Antigens present on RBC surface specify blood type
• Major antigen group is ABO system
–
–
–
–
Type A blood has only A antigens
Type B has only B antigens
Type AB has both A & B antigens
Type O has neither A or B antigens
13-15
15. Transfusion Reactions
• People with Type A blood make
antibodies to Type B RBCs, but
not to Type A
• Type B blood has antibodies to
Type A RBCs but not to Type B
• Type AB blood doesn’t have
antibodies to A or B
• Type O has antibodies to both
Type A & B
• If different blood types are
mixed, antibodies will cause
mixture to agglutinate
13-16
16. Transfusion Reactions continued
• If blood types don't match,
recipient’s antibodies
agglutinate donor’s RBCs
• Type O is “universal donor”
because lacks A & B antigens
• Insert fig. 13.6
– Recipient’s antibodies won’t
agglutinate donor’s Type O
RBCs
• Type AB is “universal
recipient” because doesn’t
make anti-A or anti-B
antibodies
– Won’t agglutinate donor’s
RBCs
13-17
17. Hemolytic Disease of the Newborn
• 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
18. Hemostasis
• Is cessation of bleeding
• Promoted by reactions initiated by vessel injury:
– Vasoconstriction restricts blood flow to area
– Platelet plug forms
• Plug & surroundings are infiltrated by web of fibrin, forming
clot
13-19
19. Role of Platelets
• Platelets don't
stick to intact
endothelium
because of
presence of
prostacyclin
(PGI2--a
prostaglandin) &
NO
QuickTime™ and a
TIFF (LZW) decompressor
are needed to see this picture.
– Keep clots from
forming & are
vasodilators
13-20
20. Role of Platelets
• Damage to endothelium
allows platelets to bind
to exposed collagen
– von Willebrand factor
increases bond by binding
to both collagen &
platelets
– Platelets stick to collagen
& release ADP, serotonin,
& thromboxane A2
• = platelet release reaction
13-21
21. Role of Platelets continued
• Serotonin & thromboxane
A2 stimulate
vasoconstriction,
reducing blood flow to
wound
• ADP & thromboxane A2
cause other platelets to
become sticky & attach &
undergo platelet release
reaction
– This continues until
platelet plug is formed
13-22
22. Role of Fibrin
• Platelet plug becomes infiltrated by meshwork of fibrin
• Clot now contains platelets, fibrin & trapped RBCs
– Platelet plug undergoes plug contraction to form more compact plug
13-23
23. Conversion of Fibrinogen to Fibrin
• Can occur via 2 pathways:
– Intrinsic pathway clots damaged vessels & blood left in test tube
• Initiated by exposure of blood to negatively charged surface of glass or
blood vessel collagen
–
–
This activates factor XII (a protease) which initiates a series of clotting factors
Ca2+ & phospholipids convert prothrombin to thrombin
» Thrombin converts fibrinogen to fibrin which polymerizes to form a mesh
– Damage outside blood vessels releases tissue thromboplastin that
triggers a clotting shortcut (= extrinsic pathway)
13-24
25. Dissolution of Clots
• When damage is repaired, activated factor
XII causes activation of kallikrein
– Kallikrein converts plasminogen to plasmin
• Plasmin digests fibrin, dissolving clot
13-26
26. Anticoagulants
• Clotting can be prevented by Ca+2 chelators (e.g.
sodium citrate or EDTA)
– or heparin which activates antithrombin III (blocks
thrombin)
• Coumarin blocks clotting by inhibiting activation of
Vit K
– Vit K works indirectly by reducing Ca+2 availability
13-27
27. Prostaglandins (PGs)
• Are produced in almost every organ
• Belong to eicosanoid family -- all derived from arachidonic acid of
plasma membrane
11-72
28. Prostaglandins (PGs) continued
• Have wide variety of functions
– Different PGs may exert antagonistic effects in tissues
• Some promote smooth muscle contraction & some relaxation
• Some promote clotting; some inhibit
– Promotes inflammatory process of immune system
– Plays role in ovulation
– Inhibits gastric secretion in digestive system
11-73
29. Prostaglandins (PGs) continued
• Cyclooxygenase (COX) 1 & 2 are involved in PG synthesis
– Are targets of a number of inhibitory non-steroidal antiinflammatory drugs (NSAIDs)
• Aspirin, indomethacin, ibuprofen inhibit both COX 1 & 2 thereby
producing side effects
• Celebrex & Vioxx only inhibit COX 2 & thus have few side effects
11-74
30. Erythrocyte Disorders
• Polycythemia
– Abnormal excess of erythrocytes
• Increases viscosity, decreases flow rate of blood
• Anemia – blood has abnormally low
oxygen-carrying capacity
– It is a symptom rather than a disease itself
– Blood oxygen levels cannot support normal
metabolism
– Signs/symptoms include fatigue, paleness,
shortness of breath, and chills
31. Anemia: Insufficient
Erythrocytes
• Hemorrhagic anemia – result of acute or
chronic loss of blood
• Hemolytic anemia – prematurely ruptured
erythrocytes
• Aplastic anemia – destruction or inhibition
of red bone marrow
32. Anemia: Decreased Hemoglobin
Content
• 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 B12
– Treatment is intramuscular injection of B12
33. Anemia: Abnormal Hemoglobin
• 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
34. Polycythemia
• Polycythemia – excess RBCs that increase
blood viscosity
• Three main polycythemias are:
– Polycythemia vera
– Secondary polycythemia
– Blood doping
35. Leukocytes Disorders:
Leukemias
• Leukemia refers to cancerous conditions involving
white blood cells
• Leukemias are named according to the abnormal
white blood cells involved
– Myelocytic leukemia – involves myeloblasts
– Lymphocytic leukemia – involves lymphocytes
• Acute leukemia involves blast-type cells and
primarily affects children
• Chronic leukemia is more prevalent in older
people
36. Leukemia
• 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
