1. Blood: a fluid connective tissue composed of
Blood Composition
Blood: a fluid connective tissue composed of
Plasma
Formed elements
Erythrocytes (red blood cells, or RBCs)
Leukocytes (white blood cells, or WBCs)
Platelets

2. Blood Composition Hematocrit Percent of blood volume that is RBCs
47% ± 5% for males
42% ± 5% for females

3. • Least dense component
Formed
elements
Plasma
• 55% of whole blood
• Least dense component
Buffy coat
• Leukocytes and platelets
• <1% of whole blood
Erythrocytes 1
Withdraw
blood and place
in tube.
Centrifuge the
blood sample. 2
• 45% of whole blood
• Most dense
component
Figure 17.1

4. Physical Characteristics and Volume
Sticky, opaque fluid
Color scarlet to dark red
pH 7.35–7.45
38C
~8% of body weight
Average volume: 5–6 L for males, and 4–5 L for females

5. Functions of Blood Distribution of ? Protection against Blood loss
Plasma proteins and clot formation
Infection
Antibodies
WBCs defend against foreign invaders

6. Proteins are mostly produced by the liver
Blood Plasma
90% water
Proteins are mostly produced by the liver
60% albumin
36% globulins
4% fibrinogen

7. Platelets
Erythrocytes
Monocyte
Neutrophils
Lymphocyte
Figure 17.2

8. 2.5 µm
Side view (cut)
7.5 µm
Top view
Figure 17.3

9. Structural characteristics contribute to gas transport
Erythrocytes
Structural characteristics contribute to gas transport
Shape—huge surface area
>97% hemoglobin
No mitochondria
No nucleus

10. (a) Hemoglobin consists of globin (two alpha and two beta polypeptide
b Globin chains
Heme
group
a Globin chains
(a) Hemoglobin consists of globin (two
alpha and two beta polypeptide
chains) and four heme groups.
(b) Iron-containing heme pigment.
Figure 17.4

11. O2 unloading in the tissues
Hemoglobin (Hb)
O2 loading in the lungs
Produces oxyhemoglobin (ruby red)
O2 unloading in the tissues
Produces deoxyhemoglobin or reduced hemoglobin (dark red)
CO2 loading in the tissues
Produces carbaminohemoglobin (carries 20% of CO2 in the blood)

12. Hematopoiesis; blood cell formation
Occurs in red bone marrow, girdle and proximal epiphyses of humerus and femur

13. Erythropoiesis:red blood cell production
Stem cell
Committed
cell
Developmental pathway
Phase 1
Ribosome
synthesis
Phase 2
Hemoglobin
accumulation
Phase 3
Ejection of
nucleus
Proerythro-
blast
Early
erythroblast
Late
erythroblast
Reticulo-
cyte
Erythro-
cyte
Hemocytoblast
Normoblast
Figure 17.5

14. Regulation of Erythropoiesis
Too few RBCs leads to tissue hypoxia
Too many RBCs increases blood viscosity
Balance depends on
Hormonal controls
Adequate supplies of iron, amino acids, and B vitamins

15. Hormonal Control of Erythropoiesis
Erythropoietin (EPO)
Direct stimulus for erythropoiesis
Released by kidneys in response to hypoxia
Testosterone also enhances EPO production, resulting in higher RBC counts in males

16. Hormonal Control of Erythropoiesis
Causes of hypoxia
Hemorrhage or increased RBC destruction reduces RBC numbers
Insufficient hemoglobin (e.g., iron deficiency)
Reduced availability of O2 (e.g., high altitudes)

17. 1 5 4 2 3 IMBALANCE Homeostasis: Normal blood oxygen levels Stimulus:
Hypoxia (low blood
O2- carrying ability)
due to
• Decreased RBC count
• Decreased amount of hemoglobin
• Decreased availability of O2 5
O2- carrying ability of blood increases.
IMBALANCE
Enhanced erythropoiesis increases RBC count. 4
Kidney (and liver to a smaller extent) releases erythropoietin. 2 3
Erythropoietin stimulates red bone marrow.
Figure 17.6

18. Fate and Destruction of Erythrocytes
Life span: 100–120 days
Macrophages engulf dying RBCs in spleen
Iron is salvaged for reuse
Heme is degraded to yellow bilirubin
Liver secretes bilirubin (in bile)) into the intestines
Degraded pigment leaves the body in feces as stercobilin

19. Figure 17.7 Low O2 levels in blood stimulate
kidneys to produce erythropoietin. 1
Erythropoietin levels rise
in blood. 2
Erythropoietin and necessary
raw materials in blood promote
erythropoiesis in red bone marrow. 3
New erythrocytes
enter bloodstream;
function about 120 days. 4
Aged and damaged
red blood cells are
engulfed by macrophages
of liver, spleen, and bone
marrow; the hemoglobin
is broken down. 5
Hemoglobin
Heme
Globin
Bilirubin
Iron stored
as ferritin,
hemosiderin
Amino
acids
Iron is bound to
transferrin and released
to blood from liver as
needed for erythropoiesis.
Bilirubin is picked up from blood
by liver, secreted into intestine in
bile, metabolized to stercobilin by
bacteria, and excreted in feces.
Circulation
Food nutrients,
including amino acids,
Fe, B12, and folic acid,
are absorbed from
intestine and enter
blood.
Raw materials are
made available in blood
for erythrocyte synthesis. 6
Figure 17.7

20. Erythrocyte Disorders
Anemia: abnormally low O2-carrying capacity
A sign rather than a disease itself
Blood O2 cannot support normal metabolism
Accompanied by fatigue, paleness, shortness of breath, and chills

21. Insufficient erythrocytes
Causes of Anemia
Insufficient erythrocytes
Hemorrhagic anemia: acute or chronic loss of blood
Hemolytic anemia: RBCs rupture prematurely
Aplastic anemia: destruction or inhibition of red bone marrow

22. Low hemoglobin content
Causes of Anemia
Low hemoglobin content
Iron-deficiency anemia
Secondary result of hemorrhagic anemia or
Inadequate intake of iron-containing foods or
Impaired iron absorption

23. Causes of Anemia Pernicious anemia Deficiency of vitamin B12
Lack of intrinsic factor needed for absorption of B12
Treated by intramuscular injection of B12

24. Causes of Anemia Sickle-cell anemia
Defective gene codes for abnormal hemoglobin (HbS)
Causes RBCs to become sickle shaped in low-oxygen situations

25. (a) Normal erythrocyte has normal hemoglobin amino acid sequence
in the beta chain. 1 2 3 4 5 6 7
146
(b) Sickled erythrocyte results from
a single amino acid change in the
beta chain of hemoglobin. 1 2 3 4 5 6 7
146
Figure 17.8

26. Erythrocyte Disorders
Polycythemia: excess of RBCs that increase blood viscosity
Results from:
Polycythemia—bone marrow cancer
Secondary polycythemia—when less O2 is available (high altitude) or when EPO production increases
Blood doping

27. Differential WBC count (All total 4800 – 10,800/l) Formed elements
Platelets
Granulocytes
Neutrophils (50 – 70%)
Leukocytes
Eosinophils (2 – 4%)
Basophils (0.5 – 1%)
Erythrocytes
Agranulocytes
Lymphocytes (25 – 45%)
Monocytes (3 – 8%)
Figure 17.9

28. Table 17.2 (1 of 2)

29. Table 17.2 (2 of 2)

30. Leukopoiesis
Production of WBCs
Stimulated by chemical messengers from bone marrow and mature WBCs

31. Figure 17.11 Stem cells Hemocytoblast Myeloid stem cell
Lymphoid stem cell
Committed
cells
Myeloblast
Myeloblast
Myeloblast
Monoblast
Lymphoblast
Developmental
pathway
Promyelocyte
Promyelocyte
Promyelocyte
Promonocyte
Prolymphocyte
Eosinophilic
myelocyte
Basophilic
myelocyte
Neutrophilic
myelocyte
Eosinophilic
band cells
Basophilic
band cells
Neutrophilic
band cells
Eosinophils
Basophils
Neutrophils
Monocytes
Lymphocytes
(a)
(b)
(c)
(d)
(e)
Agranular leukocytes
Some
become
Granular leukocytes
Some become
Figure 17.11

32. Leukocyte Disorders Leukopenia Leukemias
Abnormally low WBC count—drug induced
Leukemias
Cancerous conditions involving WBCs
Named according to the abnormal WBC clone 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

33. Leukemia
Bone marrow totally occupied with cancerous leukocytes
Immature nonfunctional WBCs in the bloodstream
Death caused by internal hemorrhage and overwhelming infections
Treatments include irradiation, antileukemic drugs, and stem cell transplants

34. Platelets
Form a temporary platelet plug that helps seal breaks in blood vessels
Circulating platelets are kept inactive and mobile by NO and prostacyclin from endothelial cells of blood vessels

35. Developmental pathway
Stem cell
Developmental pathway
Hemocyto-
blast
Promegakaryocyte
Megakaryoblast
Megakaryocyte
Platelets
Figure 17.12

36. Fast series of reactions for stoppage of bleeding
Hemostasis
Fast series of reactions for stoppage of bleeding
Vascular spasm
Platelet plug formation
Coagulation (blood clotting)

37. Vasoconstriction of damaged blood vessel Triggers
Vascular Spasm
Vasoconstriction of damaged blood vessel
Triggers
Direct injury
Chemicals released by endothelial cells and platelets
Pain reflexes

38. • Smooth muscle contracts, causing vasoconstriction.
Step Vascular spasm 1
• Smooth muscle contracts,
causing vasoconstriction.
Step Platelet plug
formation 2
• Injury to lining of vessel
exposes collagen fibers;
platelets adhere.
Collagen
fibers
• Platelets release chemicals
that make nearby platelets
sticky; platelet plug forms.
Platelets
Step Coagulation 3
• Fibrin forms a mesh that traps
red blood cells and platelets,
forming the clot.
Fibrin
Figure 17.13

39. PF3 released by aggregated platelets Prothrombin activator
Phase 1
Intrinsic pathway
Extrinsic pathway
Vessel endothelium ruptures,
exposing underlying tissues
(e.g., collagen)
Tissue cell trauma
exposes blood to
Platelets cling and their
surfaces provide sites for
mobilization of factors
Tissue factor (TF)
XII
Ca2+
XIIa XI
VII
XIa
VIIa IX
Ca2+
IXa
PF3
released by
aggregated
platelets
VIII
VIIIa
IXa/VIIIa complex
TF/VIIa complex X Xa
Ca2+ V
PF3 Va
Prothrombin
activator
Figure (1 of 2)

40. Phase 2 Phase 3 Prothrombin activator Prothrombin (II) Thrombin (IIa)
Fibrinogen (I)
(soluble)
Fibrin
(insoluble
polymer)
Ca2+
XIII
XIIIa
Cross-linked
fibrin mesh
Figure (2 of 2)

41. Figure 17.15

42. Thromboembolytic Conditions
Prevented by
Aspirin
Antiprostaglandin that inhibits thromboxane A2
Heparin
Anticoagulant used clinically for pre- and postoperative cardiac care
Warfarin
Used for those prone to atrial fibrillation

43. Bleeding Disorders
Hemophilias include several similar hereditary bleeding disorders
Hemophilia A: most common type (77% of all cases); due to a deficiency of factor VIII
Hemophilia B: deficiency of factor IX
Hemophilia C: mild type; deficiency of factor XI
Symptoms include prolonged bleeding, especially into joint cavities
Treated with plasma transfusions and injection of missing factors

44. ABO Blood Groups
Types A, B, AB, and O
Based on the presence or absence of two agglutinogens (A and B) on surface of RBCs
Blood may contain anti-A or anti-B antibodies (agglutinins) that act against transfused RBCs with ABO antigens not normally present

45. Table 17.4

46. Rh Blood Groups
Anti-Rh antibodies are not spontaneously formed in Rh– individuals
Anti-Rh antibodies form if an Rh– individual receives Rh+ blood
A second exposure to Rh+ blood will result in a typical transfusion reaction
RhoGAM containing anti-Rh can prevent the Rh– mother from becoming sensitized

47. ABO Blood Typing

48. agglutinates with both sera)
Blood being tested
Serum
Anti-A
Anti-B
Type AB (contains
agglutinogens A and B;
agglutinates with both
sera)
RBCs
Type A (contains
agglutinogen A;
agglutinates with anti-A)
Type B (contains
agglutinogen B;
agglutinates with anti-B)
Type O (contains no
agglutinogens; does not
agglutinate with either
serum)
Figure 17.16