1. 17
Blood

2. Blood Composition Blood Fluid connective tissue
Plasma – non-living fluid matrix
Formed elements – living blood "cells" suspended in plasma
Erythrocytes (red blood cells, or RBCs)
Leukocytes (white blood cells, or WBCs)
Platelets
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3. Figure 17.1 The major components of whole blood.
Slide 4
Formed
elements
Plasma
• 55% of whole blood
• Least dense component
Buffy coat
• Leukocytes and platelets
• <1% of whole blood
Erythrocytes
Withdraw blood
and place in tube. 1
Centrifuge the
blood sample. 2
• 45% of whole blood
(hematocrit)
• Most dense component
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4. Functions of Blood Functions include
Distributing food and oxygen, carries waste to lungs and kidneys, carries hormones
Regulating body temperature,normal pH and fluid levels
Protection from blood loss (clotting) and prevents infection (WBC)
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5. Over 100 dissolved solutes
Blood Plasma
90% water
Over 100 dissolved solutes
Nutrients, gases, hormones, wastes, proteins, inorganic ions
Plasma proteins most abundant solutes
Remain in blood; not taken up by cells
Proteins produced mostly by liver
60% albumin; 36% globulins; 4% fibrinogen
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6. Formed Elements RBC WBC and Platelets
Most blood cells originate in bone marrow and do not divide
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7. Platelets Erythrocytes Monocyte Neutrophils Lymphocyte
Figure Photomicrograph of a human blood smear stained with Wright's stain.
Platelets
Erythrocytes
Monocyte
Neutrophils
Lymphocyte
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8. Structural characteristics contribute to gas transport
Erythrocytes
Structural characteristics contribute to gas transport
Biconcave shape—huge surface area relative to volume
>97% hemoglobin (not counting water)
No mitochondria; ATP production anaerobic; do not consume O2 they transport
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9. Blood cell formation in red bone marrow
Hematopoiesis
Blood cell formation in red bone marrow
Composed of reticular connective tissue and blood sinusoids
In adult, found in axial skeleton, girdles, and proximal epiphyses of humerus and femur
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10. Figure 17.6 Erythropoietin mechanism for regulating erythropoiesis.
Slide 1
IMBALANCE
Homeostasis: Normal blood oxygen levels
Stimulus:
Hypoxia
(inadequate O2
delivery) due to 1
O2-carrying
ability of blood
rises. 5
IMBALANCE
• Decreased
RBC count
• Decreased amount
of hemoglobin
• Decreased
availability of O2
Enhanced
erythropoiesis
increases RBC count. 4
Kidney (and liver to
a smaller extent)
releases
erythropoietin. 2
Erythropoietin
stimulates red
bone marrow. 3
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11. Fate and Destruction of Erythrocytes
Life span: 100–120 days
No protein synthesis, growth, division
Old RBCs become fragile; Hb begins to degenerate
Get trapped in smaller circulatory channels especially in spleen
Macrophages engulf dying RBCs in spleen
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12. Fate and Destruction of Erythrocytes
Heme and globin are separated
Iron salvaged for reuse
Heme degraded to yellow pigment bilirubin
Liver secretes bilirubin (in bile) into intestines
Degraded to pigment urobilinogen
Pigment leaves body in feces as stercobilin
Globin metabolized into amino acids
Released into circulation
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13. Figure 17.7 Life cycle of red blood cells.
Slide 1
Low O2 levels in blood stimulate
kidneys to produce erythropoietin. 1 2
Erythropoietin levels rise in blood.
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 spleen,
liver, and bone marrow; the
hemoglobin is broken down. 5
Hemoglobin
Heme
Globin
Bilirubin is
picked up
by the liver.
Iron is stored
as ferritin or
hemosiderin.
Amino
acids
Iron is bound to transferrin
and released to blood
from liver as needed
for erythropoiesis.
Bilirubin is secreted into
intestine in bile where
it is metabolized to
stercobilin by bacteria.
Circulation
Raw materials are
made available in blood
for erythrocyte synthesis. 6
Food nutrients
(amino acids, Fe,
B12, and folic acid)
are absorbed from
intestine and enter
blood.
Stercobilin
is excreted
in feces.
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14. Erythrocyte Disorders
Anemia
Blood has abnormally low O2-carrying capacity
Sign rather than disease itself
Blood O2 levels cannot support normal metabolism
Accompanied by fatigue, pallor, shortness of breath, and chills
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15. Causes of Anemia: Blood Loss
Hemorrhagic anemia
Blood loss rapid (e.g., stab wound)
Treated by blood replacement
Chronic hemorrhagic anemia
Slight but persistent blood loss
Hemorrhoids, bleeding ulcer
Primary problem treated
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16. Causes of Anemia: Low RBC Production
Iron-deficiency anemia
Caused by hemorrhagic anemia, low iron intake, or impaired absorption
Microcytic, hypochromic RBCs
Iron supplements to treat
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17. Causes of Anemia: Low RBC Production
Pernicious anemia
Autoimmune disease - destroys stomach mucosa
Lack of intrinsic factor needed to absorb B12
Deficiency of vitamin B12
RBCs cannot divide  macrocytes
Treated with B12 injections or nasal gel
Also caused by low dietary B12 (vegetarians)
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18. Figure 17.8 Sickle-cell anemia.
Val
His
Leu
Thr
Pro
Glu
Glu … 1 2 3 4 5 6 7
146
Normal erythrocyte has normal
hemoglobin amino acid sequence
in the beta chain.
Val
His
Leu
Thr
Pro
Val
Glu … 1 2 3 4 5 6 7
146
Sickled erythrocyte results from a
single amino acid change in the
beta chain of hemoglobin.
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19. Function in defense against disease
Leukocytes
Function in defense against disease
Can leave capillaries via diapedesis
Move through tissue spaces by ameboid motion and positive chemotaxis
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20. Lymphocytes
Two types
T lymphocytes (T cells) act against virus-infected cells and tumor cells
B lymphocytes (B cells) give rise to plasma cells, which produce antibodies
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21. Cancerous leukocytes fill red bone marrow
Leukemia
Cancerous leukocytes fill red bone marrow
Other lines crowded out  anemia; bleeding
Immature nonfunctional WBCs in bloodstream
Death from internal hemorrhage; overwhelming infections
Treatments
Irradiation, antileukemic drugs; stem cell transplants
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22. Fast series of reactions for stoppage of bleeding
Hemostasis
Fast series of reactions for stoppage of bleeding
Requires clotting factors, and substances released by platelets and injured tissues
Three steps
vasoconstriction
Platelet plug formation
Coagulation (blood clotting)
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23. Hemostasis: Vascular Spasm
Vasoconstriction of damaged blood vessel
Triggers
Direct injury to vascular smooth muscle
Pain reflexes
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24. Hemostasis: Platelet Plug Formation
Positive feedback cycle
Damaged endothelium exposes collagen fibers
Platelets stick to collagen fibers via plasma protein
Swell, become spiked and sticky, and release chemical messengers
ADP causes more platelets to stick and release their contents
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25. Hemostasis: Coagulation
Reinforces platelet plug with fibrin threads
Blood transformed from liquid to gel
Series of reactions using clotting factors (procoagulants)
Vitamin K needed to synthesize 4 of them
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26. Figure 17.13 Events of hemostasis.
Slide 1
Step Vascular spasm
• Smooth muscle contracts,
causing vasoconstriction.
Step 2 Platelet plug
formation
• 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 3 Coagulation
• Fibrin forms a mesh that traps
red blood cells and platelets,
forming the clot.
Fibrin
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27. Figure 17.15 Scanning electron micrograph of erythrocytes trapped in a fibrin mesh.
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28. Actin and myosin in platelets contract within 30–60 minutes
Clot Retraction
Stabilizes clot
Actin and myosin in platelets contract within 30–60 minutes
Contraction pulls on fibrin strands, squeezing serum from clot
Draws ruptured blood vessel edges together
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29. https://www. youtube. com/watch. v=P7KjyxN-_m4 https://www. youtube
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