1. Blood = Transport Medium
Components of the Circulatory System
Heart = Pump
Blood = Transport Medium
Blood vessel = Passageways

2. Functions of Blood Transports: Defense: Maintains Homeostasis
Nutrients
Foreign organisms
Electrolytes
Injury/infection
O2 & CO2
Waste Products
Clotting process
Hormones
Body temperature
Maintains
Homeostasis

3. Components of Blood Blood is a mixture of cellular components
suspended in plasma:
1. Erythrocytes (RBCs)
2. Leukocytes (WBCs)
3. Thrombocytes (platelets)
Total Blood Volume: 8 % of body weight
Plasma (water + dissolved solutes)
2.75 / 5.5 liters of blood is plasma
(remaining is the cellular portion)

4. Blood vessel
White blood cell
Red blood cell
platelet
Plasma

5. Hematocrit “Packed Cells”
RBCs heaviest – packed at bottom after centrifugation
Average 45% for men / 42 % for women
Important clinical diagnostic marker
Anemia = Low percentage of erythrocytes
Hematocrit – mostly RBCs b/c they are the most abundant type of blood cell (99%)
Plasma = rest of blood not occupied by RBCs (55% of whole blood for males/ 58% for females)

6. Centrifuged Blood Sample

7. Separation of Components
Plasma = Less Dense
Platelets / WBC’s
Hematocrit
“Packed Cells”
More Dense

8. Components of Plasma Blood plasma Consists of: Other components:
Water 90%
Plasma Proteins 6-8 %
Electrolytes (Na+ & Cl-) 1%
Other components:
Nutrients (e.g. Glucose and amino acids)
Hormones (e.g. Cortisol, thyroxine)
Wastes (e.g. Urea)
Blood gases (e.g. CO2, O2)

9. Functions of Plasma 1. Water: 2. Electrolytes:
* Transport medium; carries heat
2. Electrolytes:
* Membrane excitability
* Osmotic distribution of fluid b/t ECF & ICF
* Buffering of pH changes
3. Nutrients, wastes, gases, hormones:
No function – just being transported
4. Plasma Proteins (See Next Slide)

10. Plasma Proteins Plasma Proteins: (albumins, globulins, fibrinogen)
1. Maintaining colloid osmotic balance (albumins)
2. Buffering pH changes
3. Transport of materials through blood (such as water insoluble hormones)
4. Antibodies (e.g. gamma globulins, immunoglobulins)
5. Clotting factors (e.g. fibrinogen)

11. 3 Cellular Elements of Blood
1. Red Blood Cells
2. White Blood Cells
3. Platelets

12. Production of Formed Elements
Hematopoiesis or hemopoiesis: Process of blood cell production
Stem cells: All formed elements derived from single population
Proerythroblasts: Develop into red blood cells
Myeloblasts: Develop into basophils, neutrophils, eosinophils
Lymphoblasts: Develop into lymphocytes
Monoblasts: Develop into monocytes
Megakaryoblasts: Develop into platelets

13. Hematopoiesis

14. 1. RBC’S (Erythrocytes)
Shape - a biconcave disc with large surface area
Can change shape
No Nucleus / organelles
Contains hemoglobin
Primary Function = Transport oxygen from the lungs to the cells of the body & assist with CO2 removal

15. Mechanism of Transport
HEMOGLOBIN
* 4 Heme Molecules =
* 4 Oxygen Molecules
*Oxygenated Hemoglobin
Bright Red (systemic)
*Deoxygenated Hemoglobin
Blue (venous circulation)
Minutia- Every erythrocyte has more than 250 million hemoglobin molecules- which means each RBC can carry more than a billion oxygen molecules!!!!

17. RBC’S (Erythrocytes) cont…
Lack intracellular organelles necessary for cellular repair, growth, division
Short Life Span (~120 days)
Aged RBC
Fragile - prone to rupture
Ruptured RBC’s are destroyed in spleen
Phagocytic WBC’s “clear the debris”

18. Formation of New RBC’s
Ruptured cells must be replaced by new cells by a process called……… ..Erythropoiesis
Secretion of the hormone erythropoietin
New RBC’s (and platelets & leukocytes) are produced
in the Bone Marrow
We each have trillion RBCs going through our vessels.
Every second, we replace 2-3 million RBCs!

19. Figure 11-4

20. Too few, Too many
Anemia – low hematocrit (below-normal oxygen-carrying capacity of the blood)
Nutritional, pernicious, aplastic, renal, hemorrhagic, hemolytic
Polycythemia- abnormally high hematocrit (too many RBCs in circulation)
Primary, secondary
Nutritional- dietary deficiency of factors needed for erythropoiesis
Pernicious- inability to absorb enough ingested vitamin B12 from the digestive tract (deficiency of intrinsic factor)
Aplastic- failure of the bone marrow to produce enough RBCs
Renal- kidney disease (inadequate erythropoietin secretion)
Hemorrhagic- loss of a lot of blood
Hemolytic- rupture of too many RBCs (e.g. sickle cell disease)
POLYCYTHEMIA- primary- erythropoiesis proceeds at an excessive, uncontrolled rate.- not subject to normal erythropoietin regulatory mechanism -makes blood super viscous
Secondary- an appropriate erythropoietin-induced adaptive mechanism to improve blood’s oxygen carrying capacity in response to a prolonged reduction in oxygen delivery to the tissues. (normally in people at high elevations- where less oxygen is available in the atmosphere)

21. WBC’ s
RBC’s

22. 2. White Blood Cells (Leukocytes)
Mobile units of body’s defense system:
“Seek and Destroy” Functions:
Destroy invading microorganisms
Destroy abnormal cells (ie: cancer )
Clean up cellular debris (phagocytosis)
3. Assist in injury repair

23. 5 - Types of WBC’s Each WBC has a specific function Granulocytes
Agranulocytes
Each WBC has a specific function

24. Blood Cell Origin and Production
Bone Marrow
All leukocytes ultimately originate from the same undifferentiated multipotent stem cells in the red bone marrow that also give rise to erythrocytes and platelets
All new WBCs except for lymphocytes are produced in the bone marrow. Most new lymphocytes are produced by colonies of cells in lymphoid tissues, such as lymph nodes and tonsils.
Circulation
Figure 11-8

25. Neutrophils Eosinophils Basophils Types of WBC’s
Polymorphonuclear Granulocytes
Neutrophils
Eosinophils
Basophils

26. 1. NEUTROPHILS * 50-70% of all leukocytes (most abundant of WBC’s)
* Important in inflammatory
responses
* Phagocytes that engulf
bacteria and Debris

27. 2. EOSINOPHILS * 1-4% of the WBC's * Attack parasitic worms
* Important in allergic reactions

28. 3. BASOPHILS * 0.5% of the WBC's * Release histamine and heparin
* Important in Allergic
Reactions
* Heparin helps clear fat from blood

29. Mononuclear Agranulocytes
Types of WBC’s
Mononuclear Agranulocytes
4. Monocytes
5. Lymphocytes
(B and T cells)

30. 4. MONOCYTES * 2-6 % of the WBC's * Exit blood (diapedesis)
to become macrophages
* Phagocytic = defend against
viruses and bacteria

31. 5. LYMPHOCYTES * 25-33 % of the WBC's * B-lymphocytes:
Produce Antibodies
* T-lymphocytes:
Directly destroy virus-
invaded cells and cancer
cells
B cells responsible for antibody-mediated (or humoral) immunity. – An Ab binds with and marks for destruction (by phagocytosis) the specific foreign matter that induced production of the Ab.
T cells directly destroy their specific target cells by releasing chemicals that punch holes in the cell (process is called cell-mediated immunity)

32. Blood vessel
White blood cell
Red blood cell
Platelets
Plasma

33. 3. Platelets (Thrombocytes)
Platelets are produced by the bone marrow. They are not whole cells, but are fragments of extraordinarily large bone marrow-bound megakaryocytes.
The hormone THROMBOPOIETIN (produced by liver) increases the # of megakaryocytes in the bone marrow, stimulating them to produce more platelets
* Cell fragments bound to megakaryocytes
* “Bud Off” and are released into the blood

34. Function of Platelets Stop bleeding from a damaged vessel * Hemostasis
Three Steps involved in Hemostasis
1. Vascular Spasm
2. Formation of a platelet plug
3. Blood coagulation (clotting)

35. Steps in Hemostasis *DAMAGE TO BLOOD VESSEL LEADS TO: Vascular Spasm:
Immediate constriction of blood vessel
Vessel walls pressed together – become “sticky”/adherent to each other
Minimize blood loss

36. Steps in Hemostasis 2. Platelet Plug formation: (figure 11-10)
a. PLATELETS attach to exposed collagen
b. Aggregation of platelets causes release of chemical mediators (ADP, Thromboxane A2)
c. ADP attracts more platelets
d. Thromboxane A2 (powerful vasoconstrictor)
* promotes aggregation & more ADP
Platelets will not adhere to normal vascular surfaces, but they do adhere to injured vessel surfaces when underlying collagen is exposed, forming a plug at the defect.
The aggregated platelets release chemicals that induce other platelets passing by to become sticky and pile on top of the growing plug.
Leads to formation of platelet plug !

37. (+) Feedback promotes formation of platelet Plug !
Figure 11-10
Adenosine diphosphate (ADP) release causes the surface of nearby circulating platelets to become sticky so that they adhere to the first layer of aggregated platelets. These newly aggregated platelets release more ADP, causing more platelets to stick etc etc- in a positive-feedback fashion.
Platelet plug eventually broken because ADP release stimulates concurrent release of prostacyclin and NO from adjacent normal endothelium, which profoundly inhibit platelet aggregation- so platelet plug is limited to the defect
(+) Feedback promotes formation of platelet Plug !

38. Final Step in Hemostasis
Blood Coagulation (clot formation):
“Clotting Cascade”
Transformation of blood from liquid to solid
Clot reinforces the plug
Multiple cascade steps in clot formation
Fibrinogen (plasma protein) Fibrin
Thrombin

39. Thrombin in Hemostasis
Factor X
Figure 11-11

40. Clotting Cascade
Participation of 12 different clotting factors (plasma glycoproteins)
Factors are designated by a roman numeral
Cascade of proteolytic reactions
Intrinsic pathway / Extrinsic pathway
Common Pathway leading to the formation of a fibrin clot !

41. Hageman factor (XII) X
inactive
active
CLOT !

42. Clotting Cascade Intrinsic Pathway:
Stops bleeding within (internal) a cut vessel
Foreign Substance (ie: in contact with test tube)
Factor XII (Hageman Factor)
Extrinsic pathway:
Clots blood that has escaped into tissues
Requires tissue factors external to blood
Factor III (Tissue Thromboplastin)
Intrinsic pathway stops bleeding within cut vessel or clots blood outside the body
EXTRINSIC pathway clots blood that has escaped into tissues

43. Clotting Cascade Fibrin :
Threadlike molecule-forms the meshwork of the clot
Entraps cellular elements of the blood forms CLOT
Contraction of platelets pulls the damaged vessel close together:
Fluid squeezes out as the clot contracts (Serum)

44. Clot dissolution
Clot is slowly dissolved by the “fibrin splitting” enzyme called Plasmin
Plasminogen is the inactive pre-cursor that is activated by Factor XII (Hageman Factor) (simultaneous to clot formation)
Plasmin gets trapped in clot and slowly dissolves it by breaking down the fibrin meshwork
Figure 11-15

45. Clot formation: Too much or too little of a good thing…
Inappropriate clot formation is a thrombus (free-floating clots are emboli)
An enlarging thrombus narrows and can occlude vessels
Too little:
Hemophilia- too little clotting- can lead to life-threatening hemorrhage (caused from lack of one of the clotting factors)
Thrombocyte deficiency (low platelets) can also lead to diffuse hemorrhages

46. Blood Grouping
Determined by antigens (agglutinogens) on surface of RBCs
Antibodies (agglutinins) can bind to RBC antigens, resulting in agglutination (clumping) or hemolysis (rupture) of RBCs
Groups
ABO and Rh

47. ABO Blood Groups

48. Agglutination Reaction

49. Rh Blood Group First studied in rhesus monkeys Types
Rh positive: Have these antigens present on surface of RBCs
Rh negative: Do not have these antigens present
Hemolytic disease of the newborn (HDN)
Mother produces anti-Rh antibodies that cross placenta and cause agglutination and hemolysis of fetal RBCs

50. Diagnostic Blood Tests
Type and crossmatch
Complete blood count
Red blood count
Hemoglobin measurement
Hematocrit measurement
White blood count
Differential white blood count
Clotting

51. Blood Disorders Erythrocytosis: RBC overabundance
Anemia: Deficiency of hemoglobin
Iron-deficiency
Pernicious
Hemorrhagic
Hemolytic
Sickle-cell
Hemophilia
Thrombocytopenia
Leukemia
Septicemia
Malaria
Infectious mononucleosis
Hepatitis