1. Chapter 19: Blood

2. Homeostasis
Transports O2, CO2, nutrients, & hormones to & from body cells
Helps to regulate pH & temperature
Provides protection against disease

3. Figure 19-1 The Composition of Whole Blood.

4. White Bood Cells (WBCs)
Hemopoiesis
Red bone marrow
Hemocytoblasts
(Hematopoietic
stem cells)
Myeloid Stem Cells
Lymphoid Stem Cells
Progenitor Cells
EPO
GM-CSF
G-CSF
M-CSF
Blast Cells
Proerythroblast
Erythroblast stages
Reticulocyte
Erythrocyte
Ejection of
nucleus
Red Blood Cells
(RBCs)
White Bood Cells (WBCs)
Myelocytes
Band Cells
Megakaryocyte
Myeloblast
Monoblast
Lymphoblast
Platelets
Promonocyte
Prolymphocyte
Basophil
Eosinophil
Neutrophil
Monocyte
Lymphocyte
Granulocytes
Agranulocytes

5. Erythrocytes RBCs Contain hemoglobin which carries O2
Production = destruction
Males have about 5.4million/ul
Females have about 4.8 million/ul

6. Figure 19-2 The Anatomy of Red Blood Cells.
LM × 477
Colorized SEM × 2100
Red blood cells
7.2–8.4 μm
Blood smear a
When viewed in a standard blood smear, RBCs appear as two-dimensional objects, because they are flattened against the surface of the slide. b
The three-dimensional shape of RBCs. c
A sectional view of a mature RBC, showing the normal ranges for its dimensions.
Red blood cell (RBC)
Rouleau (stacked RBCs)
Nucleus of endothelial cell
Blood vessels (viewed in longitudinal section)
LM × 1430
Sectioned capillaries d
When traveling through relatively narrow capillaries, RBCs may stack like dinner plates.

7. Clinical Note 19-1 Abnormal Hemoglobin.
Sickling in Red Blood Cells

8. Hemoglobin β chain 1 α chain 1 Heme β chain 2 Heme α chain 2
Hemoglobin molecule

9. Figure 19-4 Recycling of Red Blood Cell Components.
Events Occurring in Macrophages
Events Occurring in the Red Bone Marrow
Macrophages monitor the condition
of circulating RBCs, engulfing them
before they hemolyze (rupture), or
removing Hb molecules, iron, and
cell fragments from the RBCs that
hemolyze in the bloodstream.
Developing RBCs absorb amino acids
and Fe2+ from the bloodstream and
synthesize new Hb molecules.
Macrophages in spleen,
Liver, and red bone marrow
RBC
formation
Fe2+
Fe2+ transported in bloodstream
by transferrin
Heme
Amino acids
Average life span of
RBC is 120 days
90%
Biliverdin
New RBCs
released into
bloodstream
Old and
damaged
RBCs
Bilirubin
10%
In the bloodstream,
The rupture of RBCs
Is called hemolysis.
Bilirubin bound
to albumin in
bloodstream
Hemoglobin that is not
phagocytized breaks down,
and the alpha and beta
chains are eliminated in urine.
Liver
Kidney
Bilirubin Hb
Absorbed into the bloodstream
Urobilins
Excreted
in bile
Eliminated
In urine
Urobilins,
stercobilins
Bilirubin
Events Occurring in
the Kidney
Events Occurring in the Liver
Events Occurring in the Large Intestine
Eliminated
in feces
Bilirubin released from
macrophages binds to albumin
and is transported to the liver
for excretion in bile.
Bacteria convert bilirubin to urobilins
and stercobilins. Feces are yellow-brown
or brown due to the presence of urobilins
and stercobilins in varying proportions.
The kidneys excrete some
hemoglobin, as well as
urobilins, which gives
urine its yellow color.

10. Day 2: Basophilic erythroblast Day 3: Polychromatophilic erythroblast
RED BONE MARROW
Day 1: Proerythroblast
Day 2: Basophilic erythroblast
Erythroblasts
Day 3: Polychromatophilic erythroblast
Day 4: Normoblast
Ejection of nucleus
Days 5–7: Reticulocyte
Enters bloodstream
Erythropoiesis
Hypoxia (cellular O2 deficiency) main stimulus for production
Caused by
High altitude
Anemia
Circulatory problems
Mature red blood cell

11. Table 19-1 RBC Tests and Related Terminology.

12. Table 19-3 Formed Elements of the Blood (Part 1 of 4).

13. Leukocytes WBCs Granular Agranular Monocytes Neutrophils Eosinophils
Basophils
Agranular
Monocytes
Migrate into tissues where they differentiate into macrophages
Lymphocytes
LM × 1500 d
RBC
Eosinophil
Basophil
Monocyte
Lymphocyte
Neutrophil c b a e

14. Functions of WBCs Fight pathogens by phagocytosis or immune responses
Leave bloodstream & move into tissue
Emigration or diapedesis
Use adhesion molecules to accomplish this

15. Table 19-3 Formed Elements of the Blood (Part 2 of 4).

16. Table 19-3 Formed Elements of the Blood (Part 3 of 4).

17. Platelets
Large cell, megakaryocyte, fragments creating small pieces containing vesicles
Chemicals in vesicles promote blood clotting

18. Table 19-3 Formed Elements of the Blood (Part 4 of 4).

19. Hemostasis Responses that stop bleeding 1 2 3 4 Vascular Phase
Platelet Phase
Coagulation Phase
Clot Retraction 1 2 3 4
The vascular phase of hemostasis lasts for
about 30 minutes after the injury occurs.
The endothelial cells contract and release
endothelins, which stimulate smooth
muscle contraction and endothelial division.
The endothelial cells become “sticky” and
adhere to platelets and each other.
The platelet phase of hemostasis begins with the
Attachment of platelets to sticky endothelial
surfaces, to the basement membrane, to exposed
collagen fibers, and to each other. As they become
activated, platelets release a variety of chemicals
that promote aggregation, vascular spasm, clotting,
and vessel repair.
Coagulation, or blood clotting, involves a complex sequence of steps leading to the
conversion of circulating fibrinogen (a soluble protein) into fibrin (an insoluble protein).
As the fibrin network grows, blood cells and additional platelets are trapped in the fibrous tangle, forming a blood clot that seals off the damaged portion of the vessel.
Once the fibrin
meshwork has formed,
platelets and red blood
cells stick to the fibrin
strands. The platelets
then contract, and
the entire clot begins
to undergo clot
retraction, a process
that continues over
30–60 minutes.
Knife blade
Blood vessel injury
Vascular spasm
Release of chemicals
(ADP, PDGF, Ca2+,
platelet factors)
Plasma in
vessel lumen
Platelet
adhesion to
damaged
vessel
aggregation
Interstitial
fluid
Platelet plug
may form
Cut edge of
vessel wall
Endothelium
Basement
membrane
Vessel
wall
Contracted smooth
muscle cells
Extrinsic Pathway
Common Pathway
Intrinsic Pathway
Tissue factor
complex
Clotting factor
(VII)
(Factor III)
Tissue
damage
Activated
proenzymes
(usually Factor XII)
factor (PF-3)
Clotting factors
(VIII, IX)
Factor X
activator
Prothrombin
Thrombin
Fibrin
Fibrinogen
Ca2+
Blood clot containing
trapped RBCs
SEM × 1200

20. Vascular Spasm Contraction of smooth muscle in vessel wall
Knife blade
Blood vessel injury
Vascular spasm 1
The vascular phase of hemostasis lasts for about 30 minutes after the injury occurs. The endothelial cells contract and release endothelins, which stimulate smooth muscle contraction and endothelial division. The endothelial cells become “sticky” and adhere to platelets and each other.
Vascular Phase
Contraction of smooth muscle in vessel wall
Probably due to
Damage to muscle
Substances released from platelets
Reflexes from pain receptors

21. Platelet Plug Formation
Endothelium 2
The platelet phase of hemostasis begins with the attachment of platelets to sticky endothelial surfaces, to the basement membrane, to exposed collagen fibers, and to each other. As they become activated, platelets release a variety of chemicals that promote aggregation, vascular spasm, clotting, and vessel repair.
Platelet Phase
Vessel wall
Plasma in vessel lumen
Interstitial fluid
Platelet adhesion to damaged vessel
Platelet aggregation
Platelet plug may form
Cut edge of vessel wall
Contracted smooth muscle cells
Release of chemicals (ADP, PDGF, Ca2+, platelet factors)
Platelet adhesion
Stick to collagen
Platelet release reaction
Release of chemicals in vesicles
Platelet aggregation
Large numbers of platelets stick forming platelet plug
Basement membrane

22. Coagulation Blood clotting
Series of chemical reactions that end in formation of fibrin
If blood clots too easily, have thrombosis
If blood clotting takes too long, have hemorrhage

23. Coagulation 3 stages Extrinsic pathway Intrinsic pathway
Extrinsic & intrinsic pathways lead to formation of prothrombinase (prothrombin activator)
Prothrombinase converts prothrombin to thrombin
Thrombin converts fibrinogen to fibrin
Extrinsic pathway
Occurs rapidly
Tissue factor leaks into blood from outside vessel
Intrinsic pathway
Occurs more slowly
Its activators are either in direct contact with blood (endothelial cells) or contained within blood (platelets)

24. 3 Coagulation Phase Extrinsic Pathway Common Pathway Intrinsic Pathway
Figure The Vascular, Platelet, and Coagulation Phases of Hemostasis and Clot Retraction (Part 3 of 4). 3
Coagulation Phase
Coagulation, or blood clotting, involves a complex sequence of steps leading to the conversion of circulating fibrinogen (a soluble protein) into fibrin (an insoluble protein). As the fibrin network grows, blood cells and additional platelets are trapped in the fibrous tangle, forming a blood clot that seals off the damaged portion of the vessel.
Extrinsic Pathway
Common Pathway
Intrinsic Pathway
Factor X
Prothrombin activator
Tissue factor complex
Factor X activator complex
Prothrombin
Thrombin
Clotting factor (VII)
Clotting factors (VIII, IX)
Fibrin
Fibrinogen
Ca2+
Ca2+
Platelet factor (PF-3)
Tissue factor (Factor III)
Activated proenzymes (usually Factor XII)
Tissue damage
Blood clot containing trapped RBCs
SEM × 1200
Contracted smooth muscle cells

25. Table 19-4 Clotting Factors.

26. Clot Retraction 4 Tightening of the fibrin clot
Once the fibrin meshwork has formed, platelets and red blood cells stick to the fibrin strands. The platelets then contract, and the entire clot begins to undergo clot retraction, a process that continues over 30–60 minutes.
Clot Retraction
Tightening of the fibrin clot
Fibrin threads contract as platelets pull on them
Permanent repair can now take place

27. Vitamin K Required for the synthesis of 4 clotting factors
Normally produced by bacteria in large intestine

28. Fibrinolysis Dissolution of a clot
Plasminogen is incorporated into clot
Tissues & blood have substances that activate plasminogen to plasmin
Plasmin digests fibrin threads & inactivates some clotting factors

29. Other Mechanisms of Control
Prostacyclin
Produced by endothelial cells & WBCs
Opposes action of thromboxane A2
Inhibits platelet adhesion & release
Anticoagulants
Antithrombin
Blocks action of several factors
Heparin
Combines with antithrombin & increases its effectiveness
Activated protein C
Inactivates 2 major clotting factors

30. Intravascular Clotting
Thrombosis
Clotting in an unbroken vessel
Due to
Slow flow
Roughened endothelial surfaces from atherosclerosis, trauma
Called thrombus
If dislodges & begins to flow in blood, it is an embolus
This can lodge causing blockage

31. Blood Groups & Blood Types
Genetically determined antigens on surface of RBCs
Glycoproteins & glycolipids
Called agglutinogens
Organizes blood into different groups based on antigen on surface

32. ABO Blood Group
Type A
Type B
Type AB
Type O
Type A blood has RBCs with surface antigen A only.
Type B blood has RBCs with surface antigen B only.
Type AB blood has RBCs with both A and B surface antigens.
Type O blood has RBCs lacking both A and B surface antigens.
Surface antigen A
Surface antigen B
If you have type A blood, your plasma contains anti-B antibodies, which will attack type B surface antigens.
If you have type B blood, your plasma contains anti-A antibodies, which will attack type A surface antigens.
If you have type AB blood, your plasma has neither anti-A nor anti-B antibodies.
If you have type O blood, your plasma contains both anti-A and anti-B antibodies. a
Blood type depends on the presence of surface antigens (agglutinogens) on RBC surfaces. The plasma contains antibodies (agglutinins) that will react with foreign surface antigens.

33. Rh Blood Group
Presence or absence of Rh factor or D antigen on surface of RBCs
If present = +
If absent = -

34. Figure 19-7 Blood Type Testing.
Anti-A
Anti-B
Anti-D A+ B+
AB+ O−

35. Table 19-2 Differences in Blood Group Distribution.

36. Figure 19-6b Blood Types and Cross-Reactions.
RBC
Surface antigens
Opposing antibodies
Agglutination (clumping)
Hemolysis b
In a cross-reaction, antibodies react with their target antigens causing agglutination and hemolysis of the affected RBCs.

37. Hemolytic Disease of the Newborn