1. Chapter 17a Circulation Characteristics of Blood RBC and Erythropoiesis

2. Overview of Vessels
Arteries: blood vessels that move AWAY from the heart
Veins: vessels that move TOWARD the heart
Capillaries: Small vessels created by repeated branching of arteries and veins
1 epithelial cell layer thick
allows for gas, waste, and nutrient exchange at the tissue level

3. Blood Circulation
5. O2 and nutrients diffuse across capillary walls into tissues
6. CO2 and waste move from tissues into vessels
4. Blood leaves left ventricle of the heart via aorta and moves into arteries towards tissues
1. O2 deficient blood moves into veins that enter the right atrium of heart
2. Right ventricle pumps blood through the pulmonary artery, which carries blood to lungs, where it releases CO2 and picks up O2
3. O2 rich blood returns to the heart via pulmonary veins and enters left atrium of heart

4. Heart Anatomy (pump your blood song)
Aortic Valve
= L Semi-lunar Valve
Pulmonary Valve
= R Semi-lunar Valve
L Atrioventricular valve
= Mitral Valve
= Bicuspid Valve
R Atrioventricular valve
= Tricuspid valve

5. Heart Valves (Cross Section; Inferior View)

6. Physical Characteristics of Blood
Body’s only fluid tissue
Sticky plasma
Color: scarlet (O2 rich) to dark red (O2 poor)
pH: 7.35–7.45 (slightly basic)
Temperature: 38C (100.4F)
8% of total body weight
AVG volume:
males: L
females: L

7. Functions of Blood Distribution: Transportation of
Oxygen from lungs to cells
Nutrients from intestines to cells
Metabolic wastes from cells to lungs and kidneys for elimination
Hormones from endocrine glands to target organs

8. Functions of Blood 2. Regulation: Maintenance of Body temperature
pH with buffer proteins and solutes
pH imbalances interfere w/ cell activities, causing tissue damage
Fluid volume

9. Functions of Blood 3. Protection: Fights infections
Synthesizing and employing antibodies
Activating complement proteins
Activating WBCs to destroy foreign invaders

10. Functions of Blood 3. Protection: b. Prevention of blood loss by
Activating plasma proteins and platelets
Initiating clot formation when a vessel is broken

11. Composition of Blood Composed of liquid plasma (matrix) and
formed elements (cellular)

12. Composition of Blood Hematocrit = % of RBCs out of total blood volume
Males: 47% Females: 45%

13. Blood Plasma 90% water by volume > 100 solutes, including:
1. Proteins
Albumin (liver protein):
blood buffer; maintains osmotic pressure
Globulins:
α, β (liver proteins) : transport lipids, metal ions, fat-soluble vitamins
Gamma ɣ: antibodies during immune response
Fibrinogen: clotting protein

14. Blood Plasma 90% water by volume > 100 solutes, including:
2. Lactic acid, urea, creatine
3. Hormones: ex. insulin, erythropoietin, and others
4. Organic nutrients: carbohydrates, amino acids, lipids
5. Electrolytes: Na+, K+, CA2+, Cl-, bicarbonate (HCO3), etc.
6. Respiratory gases: O2 and CO2

15. Formed Elements
Erythrocytes (RBC), leukocytes (WBC), and platelets (for clotting)
Only WBCs are complete cells
RBCs have no nuclei or organelles
platelets are just cell fragments
Most survive in the bloodstream for only a few days (RBC: 100 – 120 days)
Most are amitotic (do not divide)
replaced by stem cells in bone marrow

16. Components of Formed Blood

17. Erythrocyte (RBC) Characteristics
Biconcave discs  High SA/V ratio (> 30% than spherical)
Contributes to blood’s viscosity
anucleate (no nucleus), and no organelles, no mitochondria
 anaerobic ATP generation; do not use any O2 that they transport
Contain spectrin membrane protein on cytoplasmic face
 Flexibility
Ability to change shape
Ease of movement through narrow capillaries

18. Gas Transport RBCs with > 97% hemoglobin (Hb)
 protein used for transport of O2 and CO2
Binding Hb to CO arrests cellular respiration

19. Hemoglobin (Hb) Structure
4 Globin proteins, each globin bound to a heme group
Heme = red pigment w/ an atom of iron (Fe)
 binds to O2 and changes to scarlet red
Fun Fact:
1 Hb can transport 4 O2 molecules
One RBC has 250 million Hb molecules
The cell transports 1 billion molecules of O2!

20. Forms of Hb Oxyhemoglobin – Hb bound to oxygen O2
O2 loading happens in the lungs
Deoxyhemoglobin – Hb after O2 diffuses into tissues
Carbaminohemoglobin – Hb bound to CO2
CO2 loading happens in the tissues
How does loading and unloading of respiratory gasses happen? Watch this video and take notes to find out…

21. Hematopoiesis Blood Cell Formation Occurs in red bone marrow of:
Axial skeleton and girdles
Epiphyses of the humerus and femur
Hemocytoblasts (adult stem cells of blood):
- give rise to all formed elements
Erythropoeisis: specific formation of RBC

22. Erythropoiesis Developmental Pathway
Phase 1: Ribosome synthesis for globulin protein formation
Phase 2: Hemoglobin accumulates
Phase 3: Nucleus and Organelles eject
 Reticulocytes: still w/ remnants of RER and ribosomes
 Erythrocytes: complete RBC, all ribosomes degraded by enzymes
Fun Fact: process takes 15 days; 2 million RBCs made/minute

23. Dietary Needs 1. Iron (Fe) 2. vitamin B12 and folic acid
65% of Fe in body is in Hb
Remainder stored in liver, spleen, marrow as protein-iron complexes: ferritin and hemosiderin
free iron ions Fe2+ and Fe3+ are toxic, increasing free radicals, causing cell death
2. vitamin B12 and folic acid
For normal DNA synthesis
3. Lipids, CHO, Amino Acids
Iron lost daily via waste
0.9 mg/day lost by men
1.7 mg by women (menstrual bleeding)

24. Control of Erythropoiesis
Delicate balance btw RBC formation and destruction
Too few RBC hypoxia (lack of O2 in tissues)
Too many RBC  blood is too viscous
Hormonal Controls
Erythropoietin (EPO):
hormone made by kidneys
directly stimulates RBC formation
EPO released in response to:
Tissue hypoxia
Increased tissue demand for O2

25. EPO Mechanism Imbalance Start Stimulus: Hypoxia due to
decreased RBC count,
decreased amount of
hemoglobin, or decreased
availability of O2
Homeostasis: Normal blood oxygen levels
Increases
O2-carrying
ability of blood
Imbalance
Reduces O2 levels
in blood
Kidney (and liver to a smaller
extent) releases erythropoietin
Enhanced
erythropoiesis
increases
RBC count
Erythropoietin
stimulates red
bone marrow

26. Fate of Erythrocytes RBC w/ no nuclei, no DNA, no new proteins
Fragile, lose shape, becomes rigid
Hb degenerate
RBCs often trapped and fragmented in spleen
Dying RBC engulfed and destroyed by macrophages
Components of Hb are broken down and some parts recycled for reuse.

27. Life Cycle of Erythrocytes
Low O2 levels in blood stimulate
kidneys to produce erythropoietin.
Erythropoietin levels
rise in blood.
Erythropoietin and necessary
raw materials in blood promote
erythropoiesis in red bone marrow.
New erythrocytes
enter bloodstream;
function about
120 days.
Aged and damaged red
blood cells are engulfed by
macrophages of liver, spleen,
and bone marrow; the hemoglobin
is broken down.
Hemoglobin

28. Destruction of Hb
1. Heme and Globin separated
Hemoglobin
Heme
Globin

29. Destruction of Hb 1. Heme and Globin separated
Hemoglobin
Heme
Globin
2. Globin metabolized into AA and released into blood
Amino
acids

30. Destruction of Hb 1. Heme and Globin separated
Hemoglobin
Heme
Globin
2. Globin metabolized into AA and released into blood
3. Heme degraded into yellow pigment Bilirubin
Bilirubin
Iron stored
as ferritin,
hemosiderin
Amino
acids

31. Destruction of Hb 1. Heme and Globin separated
Hemoglobin
Heme
Globin
2. Globin metabolized into AA and released into blood
3. Heme degaded into yellow pigment Bilirubin
Bilirubin
Iron stored
as ferritin,
hemosiderin
Amino
acids
4. Iron stored safely as ferritin and hemosiderin in liver

32. Destruction of Hb 1. Heme and Globin separated
Hemoglobin
Heme
Globin
2. Globin metabolized into AA and released into blood
3. Heme degaded into yellow pigment Bilirubin
Bilirubin
Iron stored
as ferritin,
hemosiderin
Amino
acids
4. Iron stored safely as ferritin and hemosiderin in liver
5. Iron is bound to
transferrin protein and released into circulation
for erythropoiesis

33. Destruction of Hb 1. Heme and Globin separated
Hemoglobin
Heme
Globin
2. Globin metabolized into AA and released into blood
3. Heme degaded into yellow pigment Bilirubin
Bilirubin
Iron stored
as ferritin,
hemosiderin
Amino
acids
4. Iron stored safely as ferritin and hemosiderin in liver
5. Iron is bound to
transferrin protein and released into circulation
for erythropoiesis
6. The liver secretes bilirubin into intestine with bile from the gall bladder
7. The intestines metabolize it, and it leaves the body in feces as a pigment called stercobilin (brown poop)
Bilirubin is metabolized by intestines and excreted in feces

34. Destruction of Hb 1. Heme and Globin separated
Hemoglobin
Heme
Globin
2. Globin metabolized into AA and released into blood
3. Heme degaded into yellow pigment Bilirubin
Bilirubin
Iron stored
as ferritin,
hemosiderin
Amino
acids
4. Iron stored safely as ferritin and hemosiderin in liver
5. Iron is bound to
transferrin protein and released into circulation
for erythropoiesis
6. The liver secretes bilirubin into intestine with bile from the gall bladder
7. The intestines metabolize it, and it leaves the body in feces as a pigment called stercobilin (brown poop)
Bilirubin is metabolized by intestines and excreted in feces
Circulation
Food nutrients,
including amino
acids, Fe, B12,
and folic acid
are absorbed
from intestine
and enter blood
8. Raw materials are made available in
blood for erythrocyte synthesis.

35. Erythrocyte Disorders
Polycythemia – excess RBCs that increase blood viscosity
Causes clotting in small capillaries, leading to
Stroke
Heart Attack
3 types:
Polycythemia vera: bone marrow disease
20 polycythemia: people living at high altitudes.
Blood doping : enhancing RBC numbers to increase athletic performance
removing blood for a few days, then re-infusing it.

36. Erythrocyte Disorders
2. Anemia – blood has abnormally low oxygen-carrying capacity
Symptom; not a disease
Blood oxygen levels cannot support normal metabolism
Causes fatigue, paleness, shortness of breath, chills

37. Anemia: Insufficient Erythrocytes
Hemorrhagic anemia: due to acute or chronic loss of blood (ex. stab wounds)
Hemolytic anemia: RBCs prematurely destroyed (ex. abnormal proteins of RBCs, abnormal immune system, parasitic)
Aplastic anemia: bone marrow failure: does not produce enough RBCs

38. Anemia: Decreased Hb Content
Iron-deficiency anemia results from:
hemorrhagic anemia
Poor diet: lack of iron-containing foods
Impaired iron absorption
Pernicious anemia results from:
Inability to absorb vitamin B12
Not enough intrinsic factor (protein that aids in B12 absorption)

39. Anemia: Abnormal Hemoglobin
Thalassemias – absent or faulty globin chain in Hb
RBCs are thin, delicate, and deficient in Hb
Can lead to hemolytic anemia
Sickle-cell anemia – from abnormal Hb-S
Hb-S due to genetic mutation of a single amino acid (substitution), causing sickle-shape of RBC
Both conditions offered some protection from malaria