Artery

White blood cells

Platelets

Red blood cells

• Deliver O2
• Remove metabolic wastes
• Maintain temperature, pH, and fluid volume
• Protection from blood loss- platelets
• Prevent infection- antibodies and WBC
• Transport hormones
 Plasma-55%

Buffy coat-<1%

Formed
elements-45%
90% Water
8% Solutes:
• Proteins
– Albumin (60 %)
– Alpha and Beta Globulins
– Gamma Globulins
– fibrinogens
• Gas
• Electrolytes
• Organic Nutrients
• Carbohydrates
• Amino Acids
• Lipids
• Vitamins
• Hormones
• Metabolic waste
• CO2
• Urea
• Platelets
• Leukocytes
• Erythrocytes (red blood cells)
• Leukocytes (white blood cells)
• Platelets (thrombocytes)
Erythrocytes
Erythrocyte7.5m in dia
   Anucleate
   Hematopoiesis- production of RBC
   Function- transport respiratory gases
   Hemoglobin- quaternary structure, 2  chains
and 2  chains
   Lack mitochondria. Why?
  1 RBC contains 280 million hemoglobin
molecules
   Men- 5 million cells/mm3
   Women- 4.5 million cells/mm3
   Life span 100-120 days and then destroyed in
spleen (RBC graveyard)
Hemoglobin
 Hematopoiesis
• Hematopoiesis (hemopoiesis):
blood cell formation
– Occurs in red bone marrow of
axial skeleton, girdles and
proximal epiphyses of humerus
and femur
 Hematopoiesis
• Hemocytoblasts (hematopoietic stem
cells)
– Give rise to all formed elements
– Hormones and growth factors push the cell
toward a specific pathway of blood cell
development
• New blood cells enter blood sinusoids
 Erythropoiesis
• Erythropoiesis: red blood cell
production
– A hemocytoblast is transformed into
a proerythroblast
– Proerythroblasts develop into early
erythroblasts
 Erythropoiesis

– Phases in development
1. Ribosome synthesis
2. Hemoglobin accumulation
3. Ejection of the nucleus and
formation of reticulocytes
– Reticulocytes then become
mature erythrocytes
 Stem cell Committed Developmental pathway
cell Phase 1 Phase 2 Phase 3
Ribosome Hemoglobin Ejection of
synthesis accumulation nucleus

Proerythro- Early Late Reticulo- Erythro-

Hemocytoblast blast erythroblast erythroblast Normoblast cyte cyte

Figure 17.5
Regulation of Erythropoiesis
• Too few RBCs leads to tissue hypoxia
• Too many RBCs increases blood
viscosity
• Balance between RBC production and
destruction depends on
– Hormonal controls
– Adequate supplies of iron, amino acids,
and B vitamins
 Hormonal Control of
Erythropoiesis

• Erythropoietin (EPO)
– Direct stimulus for erythropoiesis
– Released by the kidneys in
response to hypoxia
Hormonal Control of
Erythropoiesis
 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)
 Hormonal Control of
Erythropoiesis
• Effects of EPO
– More rapid maturation of committed bone
marrow cells
– Increased circulating reticulocyte count in
1–2 days
• Testosterone also enhances EPO
production, resulting in higher RBC
counts in males
Blood Cell Production
Formation & Destruction of RBCs
 RBC Diseases
Anemia- when blood has low O2 carrying
capacity; insufficient RBC or iron deficiency.
Factors that can cause anemia- exercise,
B12 deficiency
 RBC Diseases
Sickle-cell anemia-
•HbS results from a change in just one of the 287
amino acids in the  chain in the globin molecule.
•Found in 1 out of 400 African Americans.
•Homozygous for sickle-cell is deadly, but in malaria
infested countries, the heterozygous condition is
beneficial.
Transmission of Malaria
Sickle Cell Anemia
Sickle cell is prevalent in parts of all of
the following areas:
•Africa
•Mediterranean countries (such as Greece,
Turkey, and Italy)
•The Arabian peninsula
•India
•Spanish-speaking regions (South America,
Central America, and parts of the
Caribbean)
Distribution of the sickle cell gene
 Genetics of Sickle Cell Anemia

Genetics of Sickle Cell Anemia

 1 parent has sickle cell 1 doesn’t

HbA HbA

Hb S HbAHbS HbAHbS

Hb S HbAHbS HbAHbS

A = Normal
S = sickle cell
 both parents are carriers for sickle cell

HbA HbS

Hb A HbAHbA HbAHbS

HbS HbAHbS HbSHbS

A = Normal
S = sickle cell
 RBC Diseases
Polycythemia- excess of erythrocytes, 
viscosity of blood;
8-11 million cells/mm3
Usually caused by cancer; however, naturally
occurs at high elevations
Blood doping- in athletesremove blood 2
days before event and then replace it- banned
by Olympics.
 4,000-11,000 cells/mm 3

Never let monkeys eat bananas

Granulocytes
Neutrophils- 40-70%
Eosinophils- 1-4%
Basophils- <1%
Agranulocytes
Monocytes- 4-8%
Lymphocytes- 20-45%
 Eosinophil Lymphocyte
Basophil

platelet

Neutrophil
Monocyte
Leukocyte Squeezing Through Capillary Wall
Leukopenia
• Abnormally low WBC count—drug induced
Leukemias
• Cancerous conditions involving WBCs
• Named according to the abnormal WBC
clone involved

Mononucleosis
• highly contagious viral disease caused by
Epstein-Barr virus; excessive # of
agranulocytes; fatigue, sore throat, recover
in a few weeks
 Platelets
• Small fragments of megakaryocytes
• Formation is regulated by
thrombopoietin
• Blue-staining outer region, purple
granules
• Granules contain serotonin, Ca2+,
enzymes, ADP, and platelet-derived
growth factor (PDGF)
Stem cell Developmental pathway

Hemocyto- Promegakaryocyte
blast Megakaryoblast Megakaryocyte Platelets

Figure 17.12
Hemostasis- stoppage of bleeding
Platelets: 250,000-500,000 cells/mm3

Tissue Damage

Platelet Plug

Clotting Factors
Hemostasis:
1. Vessel injury

2. Vascular spasm

3. Platelet plug formation

4. Coagulation
 Hemostasis
(+ feedback)

Clotting Factors
thromboplastin

Prothrombin Thrombin

Fibrinogen Fibrin
Traps RBC & platelets

Platelets release thromboplastin

Blood Clot
Platelet Fibrin thread

RBC
 Disorders of Hemostasis
• Thromboembolytic disorders:
undesirable clot formation
• Bleeding disorders:
abnormalities that prevent
normal clot formation
Thromboembolytic Conditions
• Thrombus: clot that develops and
persists in an unbroken blood vessel
– May block circulation, leading to tissue death
• Embolus: a thrombus freely floating in
the blood stream
– Pulmonary emboli impair the ability of the
body to obtain oxygen
– Cerebral emboli can cause strokes
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
Thrombocytosis- too many platelets due to
inflammation, infection or cancer

Thrombocytopenia- too few platelets

• causes spontaneous bleeding
• due to suppression or destruction of bone
marrow (e.g., malignancy, radiation)
– Platelet count <50,000/mm3 is diagnostic
– Treated with transfusion of concentrated
platelets
 
• Impaired liver function
– Inability to synthesize procoagulants
– Causes include vitamin K deficiency,
hepatitis, and cirrhosis
– Liver disease can also prevent the
liver from producing bile, impairing fat
and vitamin K absorption
• Hemophilias include several similar
hereditary bleeding disorders
• Symptoms include prolonged
bleeding, especially into joint
cavities
• Treated with plasma transfusions
and injection of missing factors
Hemophiliac- a sex-linked recessive trait, primarily
carried by males (x chromosome)
Type A
Type B
Type AB
Type O
Blood type is based on the presence of 2 major antigens in
RBC membranes-- A and B
Blood type Antigen Antibody
A A anti-B
B B anti-A
A&B AB no anti body
Neither A or B O anti-A and anti-B

Antigen- protein on the surface of a RBC membrane

Antibody- proteins made by lymphocytes in plasma which are

made in response to the presence of antigens.
They attack foreign antigens, which result in clumping
(agglutination)
 Type A

b
b
b

b
b

b
 Type B

a a
a

a
a

a
 Type O

a b
a

a
a
b
b
a
a b
Type AB
Rh Factor and Pregnancy

                                                                                                              

RH+ indicates protein

RH- indicates no protein
 Rh Factor
and
Pregnancy

Rh+ mother w/Rh- baby– no problem

Rh- mother w/Rh+ baby– problem
Rh- mother w/Rh- father– no problem
Rh- mother w/Rh- baby-- no problem

RhoGAM used @ 28 weeks

Type AB- universal recipients
Type O- universal donor
 
Rh factor:
Rh+ 85% dominant in pop
Rh- 15% recessive

Blood Type Clumping Antibody

A antigen A anti-A serum antibody anti-b
B antigen B anti-B serum antibody anti-a
AB antigen A & B anti A & B serum -
O neither A or B no clumping w/ either anti A or B anti-a,
anti-b
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
Blood Type & Rh How Many Have It Frequency

O Rh Positive 1 person in 3 37.4%

O Rh Negative 1 person in 15 6.6%
A Rh Positive 1 person in 3 35.7%
A Rh Negative 1 person in 16 6.3%
B Rh Positive 1 person in 12 8.5%
B Rh Negative 1 person in 67 1.5%
AB Rh Positive 1 person in 29 3.4%
AB Rh Negative 1 person in 167 .6%
ABO Blood Types
Phenotype Genotype
O i i
A I A I A or I A
i
B I I or I
B B B

i
AB IAIB
 Punnett square
Type A and Type B cross
IB i

IA IAIB I Ai

IA I AI B IAi
 INQUIRY
1. What is an erythrocyte, leukocyte, and thrombocyte?
2. What 2 things do red cells lack compared to white
cells?
3. What dietary component is needed for the production
of red blood cells?
4. The largest cells in the blood that leave the
bloodstream to become macrophages are ____.
5. In an acute infection, the white cell count would show
as ______.
6. Erythroblastosis fetalis , also known as hemolytic
newborn disease, occurs in ____ mothers carrying
____ fetuses.
7. What antigens and antibodies found on AB red cells?
8. In a transfusion, what type blood can you give a type
O person?