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White blood cells
Platelets
Red blood cells
Artery
• 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%
Formed
elements-45%
Buffy coat-<1%
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→7.5µm in dia
•   Anucleate
•   Hematopoiesis- production of RBC
•   Function- transport respiratory gases
•   Hemoglobin- quaternary structure, 2 α chains
and 2 β 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
Figure 17.5
Stem cell
Hemocytoblast
Proerythro-
blast
Early
erythroblast
Late
erythroblast Normoblast
Phase 1
Ribosome
synthesis
Phase 2
Hemoglobin
accumulation
Phase 3
Ejection of
nucleus
Reticulo-
cyte
Erythro-
cyte
Committed
cell
Developmental pathway
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
Anemia- when blood has low O2 carrying
capacity; insufficient RBC or iron deficiency.
Factors that can cause anemia- exercise,
B12 deficiency
RBC DiseasesRBC Diseases
Sickle-cell anemia-
•HbS results from a change in just one of the 287
amino acids in the β 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.
RBC DiseasesRBC Diseases
Transmission of Malaria
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)
Sickle Cell Anemia
Distribution of the sickle cell gene
Genetics of Sickle Cell Anemia
Genetics of Sickle Cell Anemia
HbA
HbS
HbA
HbS HbA
HbS
HbA
HbS
HbA
HbS
HbA
HbS
1 parent has sickle cell 1 doesn’t
A = Normal
S = sickle cell
HbS
HbS
HbA
HbA HbA
HbA
HbA
HbS
HbA
HbS
HbS
HbS
both parents are carriers for sickle cell
A = Normal
S = sickle cell
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.
RBC DiseasesRBC Diseases
Granulocytes
Neutrophils- 40-70%
Eosinophils- 1-4%
Basophils- <1%
Agranulocytes
Monocytes- 4-8%
Lymphocytes- 20-45%
Never let monkeys eat bananas
4,000-11,000 cells/mm 3
Basophil Eosinophil
Neutrophil
Lymphocyte
Monocyte
platelet
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)
Figure 17.12
Stem cell Developmental pathway
Hemocyto-
blast Megakaryoblast
Promegakaryocyte
Megakaryocyte Platelets
Hemostasis- stoppage of bleeding
Tissue Damage
Platelet Plug
Clotting Factors
Platelets: 250,000-500,000 cells/mm3
Hemostasis:
4. Coagulation
1. Vessel injury
2. Vascular spasm
3. Platelet plug formation
Hemostasis
(+ feedback)
Prothrombin Thrombin
Fibrinogen Fibrin
Clotting Factors
thromboplastin
Traps RBC & platelets
Platelets release thromboplastin
Blood Clot
Fibrin threadPlatelet
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 AType A
Type BType B
Type ABType AB
Type OType 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 AType A
b
b
b
b
b
b
b
Type BType B
a
a
a
aa
a
a
Type OType O
a
a
a
ba
a
a
b
b
b
Type ABType AB
Rh Factor and Pregnancy
RH- indicates no protein
RH+ indicates proteinRH+ indicates 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
Figure 17.16
Serum
Anti-A
RBCs
Anti-B
Type AB (contains
agglutinogens A and B;
agglutinates with both
sera)
Blood being tested
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)
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
PhenotypePhenotype GenotypeGenotype
OO i ii i
AA II AA
II AA
or Ior I AA
ii
BB II BB
II BB
or Ior I BB
ii
ABAB II AA
II BB
Type A and Type B cross
IA
IA
IB i
IA
iIA
IB
IA
IB IA
i
Punnett square
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?

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Blood Erythrocytes (red blood cells) Leukocytes (white blood cells) Platelets (thrombocytes)

  • 1.
  • 2. White blood cells Platelets Red blood cells Artery
  • 3. • Deliver O2 • Remove metabolic wastes • Maintain temperature, pH, and fluid volume • Protection from blood loss- platelets • Prevent infection- antibodies and WBC • Transport hormones
  • 5. 90% Water 8% Solutes: • Proteins – Albumin (60 %) – Alpha and Beta Globulins – Gamma Globulins – fibrinogens • Gas • Electrolytes
  • 6. • Organic Nutrients • Carbohydrates • Amino Acids • Lipids • Vitamins • Hormones • Metabolic waste • CO2 • Urea
  • 8. • Erythrocytes (red blood cells) • Leukocytes (white blood cells) • Platelets (thrombocytes)
  • 10. Erythrocyte→7.5µm in dia •   Anucleate •   Hematopoiesis- production of RBC •   Function- transport respiratory gases •   Hemoglobin- quaternary structure, 2 α chains and 2 β 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)
  • 12. Hematopoiesis • Hematopoiesis (hemopoiesis): blood cell formation –Occurs in red bone marrow of axial skeleton, girdles and proximal epiphyses of humerus and femur
  • 13. 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
  • 14. Erythropoiesis • Erythropoiesis: red blood cell production – A hemocytoblast is transformed into a proerythroblast – Proerythroblasts develop into early erythroblasts
  • 15. Erythropoiesis – Phases in development 1. Ribosome synthesis 2. Hemoglobin accumulation 3. Ejection of the nucleus and formation of reticulocytes – Reticulocytes then become mature erythrocytes
  • 16. Figure 17.5 Stem cell Hemocytoblast Proerythro- blast Early erythroblast Late erythroblast Normoblast Phase 1 Ribosome synthesis Phase 2 Hemoglobin accumulation Phase 3 Ejection of nucleus Reticulo- cyte Erythro- cyte Committed cell Developmental pathway
  • 17. 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
  • 18. Hormonal Control of Erythropoiesis • Erythropoietin (EPO) –Direct stimulus for erythropoiesis –Released by the kidneys in response to hypoxia
  • 20. 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)
  • 21. 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
  • 24. Anemia- when blood has low O2 carrying capacity; insufficient RBC or iron deficiency. Factors that can cause anemia- exercise, B12 deficiency RBC DiseasesRBC Diseases
  • 25. Sickle-cell anemia- •HbS results from a change in just one of the 287 amino acids in the β 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. RBC DiseasesRBC Diseases
  • 27. 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) Sickle Cell Anemia
  • 28. Distribution of the sickle cell gene
  • 29.
  • 30. Genetics of Sickle Cell Anemia Genetics of Sickle Cell Anemia
  • 31. HbA HbS HbA HbS HbA HbS HbA HbS HbA HbS HbA HbS 1 parent has sickle cell 1 doesn’t A = Normal S = sickle cell
  • 32. HbS HbS HbA HbA HbA HbA HbA HbS HbA HbS HbS HbS both parents are carriers for sickle cell A = Normal S = sickle cell
  • 33. 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. RBC DiseasesRBC Diseases
  • 34. Granulocytes Neutrophils- 40-70% Eosinophils- 1-4% Basophils- <1% Agranulocytes Monocytes- 4-8% Lymphocytes- 20-45% Never let monkeys eat bananas 4,000-11,000 cells/mm 3
  • 36. Leukocyte Squeezing Through Capillary Wall
  • 37. 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
  • 38. 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)
  • 39. Figure 17.12 Stem cell Developmental pathway Hemocyto- blast Megakaryoblast Promegakaryocyte Megakaryocyte Platelets
  • 40. Hemostasis- stoppage of bleeding Tissue Damage Platelet Plug Clotting Factors Platelets: 250,000-500,000 cells/mm3
  • 41. Hemostasis: 4. Coagulation 1. Vessel injury 2. Vascular spasm 3. Platelet plug formation
  • 42. Hemostasis (+ feedback) Prothrombin Thrombin Fibrinogen Fibrin Clotting Factors thromboplastin Traps RBC & platelets Platelets release thromboplastin
  • 44. Disorders of Hemostasis • Thromboembolytic disorders: undesirable clot formation • Bleeding disorders: abnormalities that prevent normal clot formation
  • 45. 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
  • 46. 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
  • 47. 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
  • 48. • 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
  • 49. • Hemophilias include several similar hereditary bleeding disorders • Symptoms include prolonged bleeding, especially into joint cavities • Treated with plasma transfusions and injection of missing factors
  • 50. Hemophiliac- a sex-linked recessive trait, primarily carried by males (x chromosome)
  • 51. Type AType A Type BType B Type ABType AB Type OType O
  • 52. 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)
  • 57. Rh Factor and Pregnancy RH- indicates no protein RH+ indicates proteinRH+ indicates protein
  • 58. 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
  • 59. 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
  • 60. Figure 17.16 Serum Anti-A RBCs Anti-B Type AB (contains agglutinogens A and B; agglutinates with both sera) Blood being tested 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)
  • 61. 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%
  • 62. ABO Blood Types PhenotypePhenotype GenotypeGenotype OO i ii i AA II AA II AA or Ior I AA ii BB II BB II BB or Ior I BB ii ABAB II AA II BB
  • 63. Type A and Type B cross IA IA IB i IA iIA IB IA IB IA i Punnett square
  • 64. 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?