1. INTRODUCTION TO THE CARDIOVASCULAR SYSTEM: BLOOD

2. Functions and Components of the Circulatory System
Transport -- of O2 from lungs to tissues; transport of CO2 from tissues to lungs. -- Nutrients, hormones, wastes, blood cells with various functions Components -- Heart -- Arteries – blood moves away from heart -- Veins – blood moves toward the heart -- Capillaries – thin-walled; where exchange occurs

3. Composition of Blood
Figure 13.1
55%
45%
Hematocrit is a blood test that measures the percentage of the volume of whole blood that is made up of red blood cells.

4. Plasma
-- contains water, electrolytes, hormones, proteins
Proteins: albumins – (most) – maintain osmotic pressure (keep H2O in blood) fibrinogen – soluble clotting factor globulins – α- , β- carry lipids γ – globulins are part of the immune system
All proteins are made by the liver except the γ-globulins, which are made by B-lymphocytes.

5. Formed Elements – Red Blood Cells (RBCs)
-- Made from stem cells in bone marrow
6 μm in diameter; capillaries are 7-8μm RBCs must squeeze through
No organelles
Live for only about 120 days
Liver and spleen detect damaged RBCs and remove them.
RBCs are constantly replenished
Approx. 5 million RBCs per cm3 (1 cm3 = 1 ml)
Erythrocytes
Flattened biconcave discs

6. This is the protein that carries oxygen in your RBCs
Fe is the symbol for IRON. Iron binds to oxygen. This is why Iron is important in your diet. Without iron, you can’t bring oxygen to your body cells to make ATP.
Heme is recycled from old red blood cells by the liver and spleen. Iron travels to the bone marrow attached to a protein carrier called transferrin. Though we recycle iron in heme, we still need some in our diet.

7. A deficiency of RBCs or a reduction in the amount of hemoglobin
Types of Anemia
A deficiency of RBCs or a reduction in the amount of hemoglobin
they contain
There are a variety of types of anemia:
1) iron deficiency anemia
hemoglobin deficient
lack of iron
3) pernicious anemia
excess of immature RBCs
inability to absorb B12
2) aplastic anemia
bone marrow damaged
toxic chemicals
radiation
Thalassemias are genetic defects that occur in one of the genes that controls the regulation of hemoglobin and then leads to a defective hemoglobin or lowered amount of hemoglobin
4) sickle cell anemia
abnormal shape of RBCs
defective gene

8. Sickle Cell Anemia
Hemoglobin protein has one defective amino acid
RBC does not transport O2 as well
Respiratory problems, etc.
Malarial resistance

9. Formed Elements – Leukocytes: GRANULOCYTES
ALSO SEE
TABLE 13.2
DIAPEDESIS
CHARACTERISTICS OF GRANULOCYTES:
--have cytoplasmic protein granules that take up stain
-- they all have polymorphic nuclei
-- eosinophils – take up acid stain; they increase in number when a patient has a parasitic infection
-- neutrophils – most common WBC, %; phagocytes; take up neutral stain
-- basophils – take up a blue dye, inflammatory reactions
AGRANULOCYTES:

10. Formed Elements – Leukocytes: AGRANULOCYTES
ALSO SEE
TABLE 13.2
CHARACTERISTICS –they do not stain, no granules, large nuclei
-- Lymphocytes – 2nd most common; T- and B-cells T cells (thymus); B cells make antibodies
-- Monocytes – phagocytic; when they leave the bloodstream they are called macrophages
-- Platelets (thrombocytes) – membrane-bound pieces of cytoplasm from a megakaryocyte.
AGRANULOCYTES:

11. HEMATOPOIESIS/ ERYTHROPOIESIS
Hematopoiesis – formation of all blood cells from bone marrow stem cells Erythropoiesis – RBC formation stimulated by erythropoietin; organelles are ejected. Erythropoietin – formed in kidney - stimulated by low oxygen levels - travels to bone marrow  RBC’s

13. Ab = abbreviation for antibody

14. Clumping
-- the antigen is grabbed by the tips of the Y-shaped Ab. This causes clumping (agglutination). -- clumping blocks the flow of blood through the capillaries. -- do NOT confuse clumping with clotting.

15. Visualize How Agglutination is used for blood typing.
No clumping when anti B is added to type A
Clumping: anti-A is added to type A
Clumping: anti-B is added to type B
No clumping when anti A is added to type B
Clumping: anti-B is added to type AB
Clumping: anti-A is added to type AB

16. Rh ANTIGEN: Rh positive (Rh+) indicates presence of Rh antigen; Rh negative (Rh-) indicates its absence.
FIRST PREGNANCY
SECOND PREGNANCY
Rh factor
Treatment: Mom is given RhoGAM, which prevents her from making anti-Rh Ab

17. Blood clotting Normal blood vessel: Platelets repel each other
Endothelium -- prevents platelets from contacting collagen -- Secrete PGI2 and NO, which act as vasodilators, and inhibit platelet aggregation
-- Secrete an enzyme which breaks down ADP
Broken endothelium
Endothelial cells don’t secrete PGI2 and NO
Platelet release reaction: they release ADP, serotonin and a prostaglandin: Thromboxane A2, which makes platelets sticky (positive feedback) + more A2 is made, etc. [PLATELET PLUG]
3) Fibrinogen is converted to fibrin, which forms a mesh. [FIBRIN WEB]

18. Platelet Aggregation (Blood Clotting)
A) Intact endothelium – platelet aggregation is prevented. B) Broken endothelium – platelets adhere to collagen by von Willebrand’s factor, which anchors the platelets to collagen This process is helped by ADP and thromboxane A2, a prostaglandin. C) A platelet plug is formed.
Fig. 13.7

19. ASPIRIN
Aspirin inhibits the enzyme that forms Thromboxane A2, and so it is used to prevent clots.

20. Creating the Fibrin Network
Intrinsic pathway – blood will clot on its own without the addition of any external chemicals; -- initiated by exposure to hydrophilic surfaces (e.g. glass) or to negatively charged structures (collagen) -- a sequence of reactions leads fibrinogen (soluble) to be converted to fibrin Extrinsic pathway – the pathway for blood to clot using a chemical released by damaged tissues; ultimately fibrinogen is converted to fibrin.

21. Inborn Errors of Metabolism
Hemophilia A Hemophilia B X-linked diseases deficiency in different blood clotting factors
Von Willebrand’s Disease autosomal Different types: dominant and recessive inheritance patterns Deficiency in Von Willebrand’s factor

22. Healing
-- getting rid of the fibrin mesh after the endothelium heals -- Plasminogen (inactive) is converted to plasmin by Tissue Plasminogen Activator (TPA) -- Plasmin degrades fibrin!
TPA has been used to treat clots. It’s called Alteplase.

23. ANTICOAGULANTS – clot prevention
Lowering Ca2+ with EDTA or sodium citrate
Heparin – inactivates thrombin, which converts fibrinogen to fibrin
Warfarin (coumadin) – blocks the activation of vitamin K, which is required to make blood clotting factors