Chapter 16 Blood
Objectives:
1.
Describe the composition and physical characteristics of whole blood. Explain why is it
classified as a connective tissue.
2. List the functions of blood.
3. Discuss the composition and functions of Plasma.
4. Describe the structural characteristics, functions, and production of erythrocytes.
5. Describe the chemical makeup of hemoglobin.
6. List the classes, structural characteristics, and functions of leukocytes.
7. Describe the structure and functions of platelets.
8. Give examples of disorders caused by abnormalities of each of the formed elements. Explain
the mechanism of each disorder.
9. Describe the process of hemostasis. List the factors that limit clot formation and prevent
undesirable clotting.
10. Give examples of hemostatic disorders. Indicate the cause of each condition.
11. Describe the ABO and Rh blood groups. Explain the basis of transfusion reactions.
12. Explain the importance of blood testing as a diagnostic tool.
Whole blood: composed of formed elements (the cellular components) and plasma. Colored scarlet to
dark red. pH of 7.35-7.45. 5-6L in males, 4-5L in females. Plasma = 55%, Buffy coat < 1%, RBC’s =
45%. Hematocrit (percentage of RBC’s) in males = 47 + 5%, females 42 + 5%. See figure 16.1
Functions of Blood:
1. Distribution: O2, nutrients, metabolic wastes, hormones
2. Regulation: body temperature, pH (w/ buffers), fluid volume
3. Protection: prevent blood loss (platelets and clotting proteins), prevent and combat infection
Plasma: See Table 16.1


90% water, 100 dissolved solutes (table 16.1) such as nutrients, gases, hormones, wastes,
products, ions, proteins
Plasma proteins: albumin (made by the liver) is the most abundant to maintain osmotic pressure of
the blood, others act as shuttles, buffers, clotting proteins, and for immunity (to name a few).
Formed Elements
1. Erythrocytes: (see hematocrit). Approx 5 million/ml See figure 16.3
 Red blood cells (RBC’s), biconcave discs, anucleate, flexible for travel through capillaries
 Huge surface area to volume ratio, suited for gas exchange
a. hemoglobin: binds easily and reversibly to oxygen (4 globin and 4 heme). See figure 16.4
 4 molecules of oxygen per 1 molecule of hemoglobin (Hb)
b. hematopoiesis: formation of blood. Erythropoiesis: formation of RBC’s See figure 16.5
 occurs in bone marrow, cells arise from pluripotent stem cells
 Iron (Fe), Vit B12, and Folic Acid necessary


Life span 100-120 days; damaged cells (ragged cell membranes) become trapped in
spleen, iron is salvaged & stored, rest of heme is degraded to bilirubin (in liver), then
secreted in bile to intestines. See figure 16.7
erythropoietin from kidneys stimulates RBC’s due to hypoxia caused by See figure 16.6
i. reduced #’s of RBC’s (hemorrhage or excess RBC destruction)
ii. reduced availability of O2 (high altitude or pneumonia)
iii. increased tissue demands (aerobic exercise or homeostatic imbalance)
c. erythrocyte disorders
i.
anemia: low oxygen carrying capacity
 hemorrhagic anemia: blood loss
 hemolytic anemia: RBC’s lyse (Hb abnormal, transfusion mismatch,

ii.
parasitic/bacterial infections)
aplasic anemia: destruction or inhibition of bone marrow (toxins, drugs, ionizing
radiation)
decreased hemoglobin content
 iron deficiency anemia
 pernicious anemia: lack of Vit B12
 abnormal hemoglobin: sickle cell anemia See figure 16.8
iii. polycythemia: too many RBC’s makes blood viscous, sludgy (blood doping)
2. Leukocytes:4000-11,000/ml. See figure 16.9 and Table 16.2



Defense against disease
Characteristics include margination (sticking to capillary walls), diapedesis (movement
through capillary walls), and chemotaxis (movement toward a chemical). Move by ameboid
motion
>11,000 WBC’s indicates leukocytosis and a normal homeostatic response to invasion
A. granulocytes: contain membrane bound cytoplasmic granules, lobed nuclei, and are
primarily phagocytic
i. neutrophils:




most numerous WBC (Never let monkeys eat bananas),
granules contain perioxidases and hydrolytic enzymes
attracted to sites of inflammation
phagocytic and partial to bacteria
ii. eosinophils:

attack parasitic worms, lessen severity of alleries
iii. basophils
 contain histamine
B. agranulocytes: no granules
i. lymphocytes: 2nd most numerous, T and B cells
ii. monocytes: largest cells, become macrophages
C. leukopoiesis: WBC production from bone marrow See figure 16.11
D. leukocyte disorders
i. leukopenia: abnormally low WBC count (drugs and anticancer therapies)
ii. leukemia: cancerous condition involving WBC’s; from a single clone
iii. infectious mononucleosis: caused by Epstein-Barr virus, excess
agranulocytes result
Platelets: fragments of megakaryocytes, called thrombocytes, regulated by thrombopoietin See figure
16.12
Hemostasis See figure 16.13
1. Vascular spasm:

constriction of damaged blood vessels to reduce blood flow due to direct
injury to smooth muscle, chemicals released from endothelial cells and reflexes from
pain receptors.
2. Platelet plug formation:

when endothelium is damaged, platelets swell and become spiky, get
sticky, and attach to collagen.
3. Coagulation: the ultimate reactions are:
a. Phase I: prothrombin activator (PA) is formed
b. Phase II: PA converts prothrombin to thrombin
c. Phase III: Thrombin catalyzes the joining of fibrinogen molecules to a fibrin mesh which traps
blood cells and seals holes.
Phase I:
Intrinsic Pathway
Extrinsic Pathway
-----
-- “short cut” since tissue factor
(TF) is released by damaged
cells
-- calcium is required
-- cascade leads to production of
prothrombin activator
blood remains in BV
collagen exposed
platelets cling and release PF 3
cascade of activated clotting factors
causes production of prothrombin
activator
Phase II: PA catalyzes transformation of prothrombin to thrombin
Phase III: Thrombin catalyzes fibrinogen to fibrin. Fibrin glues platelets together and makes a
web that forms a clot. Plasma becomes gel-like and traps formed elements. Thrombin and calcium
activate factor XIII that binds fibrin tightly together. See figure 16.14
Clotting Factors: enhance clot formation. Vitamin K is necessary for synthesis of other clotting factors.
Clot Retraction and Repair: platelets pull the clot together (w/ actin and myosin), squeezing out
serum. Platelet derived growth factor stimulates rebuilding.
Fibrinolysis: the breakdown of the clot that begins within 2 days of clotting. Removes unneeded clots
when healing occurs.
Factors limiting clot growth or formation

swift removal of clotting factors

inhibition of activated clotting factors by antithrombin III, protein C and heparin
Factors preventing undesirable clotting

smooth endothelium

antithrombic substances

Vitamin E quinine (vit E + oxygen is a potent anticoagulant)
Thromboembolytic conditions

Thrombus: a clot that develops and persists in an unbroken blood vessel

Embolus: a thrombus that breaks away

Arterio/Atherosclerosis, severe burns, inflammation

Slowflowing blood (bed ridden, long rides)

Prevention through aspirin, dicumerol, warfarin (Coumadin)
Bleeding disorders



Thrombocytopenia: lack of platelets, spontaneous bleeding can occur
Impaired liver function: procoagulants not made, lack of Vitamin K can cause
Inherited genetic disorders of clotting: hemophiliac
Blood Types See figure 16.15 and table 16.4




Due to presence or absence of antigens or agglutinogens, either type A or type B
Possible blood types include: Type A, Type B, Type AB, Type O
Blood Type
Antigen
Antibodies
A
A
B
B
B
A
AB
A,B
NONE
O
NONE
A,B
Rh factor: an additional antigen found on cells. Rh + : antigen present; Rh - : antigen absent.
Hemolytic disease of the newborn can result if an Rh – mother has an Rh + baby, RhoGAM is given
to prevent.