1. Cardiovascular System: Blood
Clinical Anatomy
Tony Serino, Ph.D.

2. Blood: Topic Objectives
Be able to describe the physical properties of the blood including its components.
Be able to explain how blood cells develop and what key ingredients are necessary in RBC development.
Understand hemoglobin structure and the effect of a point mutation.
Understand the molecular basis of blood typing and be able to interpret blood typing tests results.
Be able to apply blood types in transfusions and list their abundance.
Be able to describe the characteristics of WBC types and their abundance, be able to use differential WBC count data to interpret selected clinical diagnosis.
Be able to describe platelet formation and their characteristics and functions.
Be able to describe hemostatic reflexes and the clotting process
Be able to explain the results of bleeding and clotting tests and the types of bleeding disorders.

3. Blood Liquid connective tissue
Arises from hemopoietic tissue: 1. myeloid tissues (Red bone marrow) 2.lymphoid tissues (thymus, spleen, lymph nodes, tonsils, etc.
In fetus, liver and yolk sac are hemopoietic

4. Properties of the Blood
Volume 4-6L (5-6L men, 4-5L women) based on body size (8% of total body weight) pH
5X the viscosity of water
Hematocrit = 45

5. Blood Composition

6. Plasma Composition 90% water 10% suspended or dissolved constituents
Plasma Constituents (10%)
0.9% NaCl + other electrolytes
Nutrients
Plasma proteins: albumin, globulins, fibrinogen
Dissolved gases: O2, CO2, N2

7. Functions of the Blood Transportation media Osmoregulation
Acid-Base balance
Protection

8. Hemopoiesis (RBC development)
Rate controlled by erythropoietin secretion
Availability of Fe++, folic acid, vitamin B12 and amino acid precursors for hemoglobin production

9. RBC Production Control

10. Formed Elements

11. RBC (erythrocyte) Lives 120 days Non-nucleated biconcave disc
million/mm3
1/3 of cytoplasm is hemoglobin

12. Rouleau

13. Hemoglobin

14. Hemoglobin Metabolism

15. Point Mutation in Sickle Cell

16. Sickle Cell Anemia

17. Blood Types

18. Anti-D
Blood Typing

19. ABO Blood Group Summary

20. WBC Development

21. WBC Development

22. Distribution of WBC

23. Neutrophil
Most abundant circulating WBC (55-65% of WBCs), highly phagocytic, 1st to arrive at site of infection

24. Eosinophil
2-4% of WBC, combat irritants that trigger inflammation, phagocytic for Ag-Ab complexes, destroy worm infections, limit inflammation

25. Basophil
Least abundant WBC (0.5% of WBC), trigger inflammation, contain vesicles with vasoactive compounds

26. Monocyte
3-8% of WBC, highly phagocytic and chemotaxic, arrive second to neutrophils at site of infection but in more massive numbers, can undergo diapedesis; some take up permanent residence in some tissues (often has a C-shaped nucleus)

27. Lymphocyte
Second most abundant WBC (20-30% of WBC), function in specific immunity, two types: T and B cells

28. Platelet Development

29. Platelets 150-400 thousand/mm3 2-4 mcm in diameter
Function in clotting and vessel repair

30. Hemostasis (stoppage of bleeding)
Extravascular Mechanisms
Tightening of skin and muscles around injury
Behavior response (elevate, applied pressure)
Vascular Mechanisms
Vasoconstriction (vascular spasms)
Intravascular Mechanisms
Platelets –plug formation and factor secretion (PF3)
Clotting factors (extrinsic and intrinsic system)

31. Platelet Plug and Clotting
Platelet aggregation is increased by the stuck platelets releasing Thromboxane which stimulates vasoconstriction and attracts more platelets to area. Prostacyclin inhibits this and is released by non-damaged endothelial cells
The common clotting pathway

32. Platelet stimulated
(TF)
(PF3) or
(TF)
(PF3)
(Stabilizing Factor)

33. Coagulation Summary
Coagulation may be triggered by intrinsic or extrinsic pathway, but in the body the extrinsic path is the one most commonly used.
Activated Factors X, V, Ca2+, and PF3 or TF combine to change Xa into prothrombin activator which catalyzes prothrombin to thrombin
Thrombin then catalyzes Fibrinogen to Fibrin turning the blood into a gel-like state
Activate Factor XIII stabilizes and strengthens the fibrin.
Finally the platelets in the clot contract, squeezing the plasma from the clot. (Clot retraction)
After 2 days, enzymes in clot activate plasminogen into plasmin with begins dissolving clot

34. Fibrin Clot

35. Bleeding and Coagulation Tests
Bleeding time –the time it takes a small wound to stop bleeding
Coagulation (clotting) time –the time it takes to form a blood to clot in a test tube (test intrinsic system) but not that sensitive
Thrombin time –measures the time for blood to clot in a tube when thrombin is added
Prothrombin time (pro-time, PT) –evaluates the extrinsic mechanism
Partial Thromboplastin time (PTT) –tests the intrinsic system, more sensitive than clotting time

36. Bleeding Disorders Thrombocytopenia Impaired Liver Function
–decrease number of platelets
Impaired Liver Function
responsible for many of the clotting factors in the blood
Vit. K used as co-factor in many clotting factor syntheses; liver bile salts help in absorbing this vitamin
Hemophilia –hereditary bleeding disorders
Class A (classical) –deficiency of factor VIII; most common hemophilia (83%)
Class B deficiency of factor IX
A & B is sex (X) linked trait; mainly seen in males
Class C deficiency of factor XI –less severe; seen in both sexes