1. Blood

2. Blood Functions Transport Regulate Defense O2 and CO2 Gases Nutrients
Carbs, proteins, fats
urea and uric acid
Estrogen, testosterone, ADH, insulin
Between 7.45 to 7.48
Acts as a heat resevoir to distribute it
tissues get fluid from blood
Has ability to stop blood loss
Defend against foreign invaders
Transport
Gases
Nutrients
metabolic wastes
hormones
Regulate pH
temperature
fluid
Defense
blood loss
infectious agents

3. Blood Composition Erythrocytes Leukocytes Platelets
Cells = Formed Elements
(not all are technically cells)
Erythrocytes
aka RED blood cells
count ~ 5.0 million/drop
Leukocytes
aka White blood cells
count ~ 4,000 – 11,000/drop
Platelets
aka Thrombocytes
count 250,000 – 500,000/drp

4. Blood Composition Matrix = Plasma 90% Water 8% Proteins albumin
globulins
fibrinogen
2% Other
gases
nitrogenous wastes
nutrients
electrolytes

5. ERYTHROCYTES Biconcave discs Lack nucleus Lack mitochondria
Contain hemoglobin
Carry oxygen and some carbon dioxide

6. HEMOGLOBIN HEME PORTION Has central Fe atom that
carries one oxygen molecule
Each Hemoglobin is like a
4 passenger TAXI

7. HEMOGLOBIN GLOBIN PORTION *each chain has one heme
4 protein chains
*each chain has one heme
*each RBC carries 250 million hemoglobin molecule
*Therefore each RBC carries ONE BILLION O2

8. HEMOGLOBIN
When oxygen is bound to hemoglobin it is called oxyhemoglobin.
When oxygen is NOT bound to hemoglobin it is called deoxyhemoglobin
20% of CO2 is transported
in hemoglobin, but does not
compete with oxygen site of heme

9. CO

10. So how can we get rid of CO?

11. Skiing the Rockies

13. Erythropoiesis: formation of erythrocytes
Hematopoiesis
Formation of blood
Erythropoiesis: formation of erythrocytes
Starts with hemocytoblasts
Occurs in red bone marrow

14. Hemocytoblast Proerythroblast Early erythroblast Late erythroblast
Stem cell
Hemocytoblast
Committed cell
Proerythroblast
Ribosome production
Early erythroblast
Late erythroblast
Hemoglobin production
When hemoglobin content reaches ~35%, organelles get ejected. Eventually nucleus gets ejected.
Normoblast
Reticulocyte
Gets released into blood stream
Erythrocyte
Mature cell

15. 3 to 5 days Hemocytoblasts
Time it takes for erythropoiesis
Hemocytoblasts
Total time to replace RBCs is about ONE week
3 to 5 days
Reticulocytes
2 days more
Erythrocytes

16. Erythropoietin (EPO) Regulates RBC production
Normal rates 2 million/sec
Kidneys control production of EPO

17. mechanism for regulating erythropoiesis
IMBALANCE
Homeostasis: Normal blood oxygen levels
Stimulus:
Hypoxia (low blood
O2- carrying ability)
due to
• Decreased RBC count
• Decreased amount of hemoglobin
• Decreased availability of O2 1
IMBALANCE

18. Kidney (and liver to a smaller extent) releases erythropoietin.
IMBALANCE
Homeostasis: Normal blood oxygen levels 1
Stimulus:
Hypoxia (low blood
O2- carrying ability)
due to
• Decreased RBC count
• Decreased amount of hemoglobin
• Decreased availability of O2
IMBALANCE
Kidney (and liver to a smaller extent) releases erythropoietin. 2

19. 1 2 3 IMBALANCE Homeostasis: Normal blood oxygen levels Stimulus:
Hypoxia (low blood
O2- carrying ability)
due to
• Decreased RBC count
• Decreased amount of hemoglobin
• Decreased availability of O2 1
IMBALANCE
Kidney (and liver to a smaller extent) releases erythropoietin. 2
Erythropoietin stimulates red bone marrow. 3

20. 1 4 2 3 IMBALANCE Homeostasis: Normal blood oxygen levels Stimulus:
Hypoxia (low blood
O2- carrying ability)
due to
• Decreased RBC count
• Decreased amount of hemoglobin
• Decreased availability of O2 1
IMBALANCE
Enhanced erythropoiesis increases RBC count. 4 2
Kidney (and liver to a smaller extent) releases erythropoietin. 3
Erythropoietin stimulates red bone marrow.

21. O2- carrying ability of blood increases.
IMBALANCE
Homeostasis: Normal blood oxygen levels
Stimulus:
Hypoxia (low blood
O2- carrying ability)
due to
• Decreased RBC count
• Decreased amount of hemoglobin
• Decreased availability of O2 1
O2- carrying ability of blood increases. 5
IMBALANCE
Enhanced erythropoiesis increases RBC count. 4 2
Kidney (and liver to a smaller extent) releases erythropoietin. 3
Erythropoietin stimulates red bone marrow.

23. Induced Polycythemia
Increasing the number of red blood cells in circulation
Training at higher altitudes
Blood doping

24. Who is he?

25. WHY DO BRUISES TURN YELLOW

26. Fate and destruction of RBCs
Hemoglobin
Aged and damaged red
blood cells are engulfed by
macrophages of liver,
spleen, and bone
marrow; the
hemoglobin is
broken down.
Heme
Globin
Bilirubin
Amino
acids
Iron stored
In liver
Iron is released to blood from liver as needed for erythropoiesis.
Bilirubin is picked up from blood
by liver, secreted into intestine in
bile, metabolized by bacteria,
and excreted in feces.
Urine gets its color from urochrome (comes from bilirubin)
Circulation
Food nutrients are
absorbed from
intestine and enter
blood.
Raw materials are
made available in blood
for erythrocyte synthesis.

27. Fate and destruction of RBCs
Circulation

28. Erythrocyte disorders
Anemias = abnormally LOW oxygen carrying capacity
low RBCs – blood loss, RBC destruction, defective bone marrow
low Hemoglobin content – low iron, B12 deficiency
abnormal hemoglobin – sickle cell
Polycythemia = abnormal excess of RBCs
increases blood viscosity
increases blood pressure
Can be due to disease, high altitude or blood doping

29. Leukocytes Granulocytes = have cytoplasmic granules
Basophils – release histamine (inflammation); contain heparin (anticoagulant)
Neutrophils – phagocytize bacteria
Eosinophils –role in allergies and asthma
Agranulocytes = lack cytoplasmic granules
Monocytes – phagocytize foreign invaders
Lymphocytes – involved in immune response

30. Leukopoiesis – formation of WBCs
Leukemia – abnormally high WBC count of abnormal WBCs
Leukopenia – low WBC count

31. Thrombocytes aka Platelets
Responsible for Blood Clotting

32. Hemostasis
Stoppage of blood flow

33. • Smooth muscle contracts, causing vasoconstriction.
Step Vascular spasm
• Smooth muscle contracts, causing vasoconstriction. 1

34. Step Platelet plug formation
Step Vascular spasm
• Smooth muscle contracts, causing vasoconstriction. 1
Step Platelet plug
formation
• Injury to lining of vessel exposes collagen fibers; platelets adhere. 2
Collagen fibers

35. Step Platelet plug formation
Step Vascular spasm
• Smooth muscle contracts, causing vasoconstriction. 1
Step Platelet plug
formation
• Injury to lining of vessel exposes collagen fibers; platelets adhere.
• Platelets release chemicals that make nearby platelets sticky; platelet plug forms. 2
Collagen fibers
Platelets

36. Chemicals that aid platelet plug formation
Serotonin
Enhances vasoconstriction
Thromboxane
Attracts platelets to the wound
What is aspirin, and how does it work?
Inhibits thromboxane
increases bleeding time

37. red blood cells and platelets, forming the clot.
Step 1: 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.
Step 3: Coagulation
Platelets
• Fibrin forms a mesh that traps
red blood cells and platelets,
forming the clot.
Fibrin

38. Inactive Clotting Factors Collagen exposure Ca+2 Prothrombin Activator
Becomes
The
catalyst
Collagen
exposure
Ca+2
Prothrombin
Activator
Active Clotting
Factors
Becomes
The
catalyst
Prothrombin
Thrombin
Fibrinogen
Fibrin

39. Fibrin
Platelets
RBC
Figure 17.15

40. Clot Retraction Platelets contract within 30–60 minutes
Platelets pull on the fibrin strands pulling ends of wound together

42. Fibrinolysis
Clot dissolving
Takes several days to occur