1. Chapter 10 Blood

2. Physical Characteristics of Blood
Color range
- O2-rich blood is scarlet red
- O2-poor blood is dull red
pH betw 7.35–7.45
slightly higher than body temp

3. Blood Only fluid classified as connective tissue
- Living cells = formed elements
- Non-living matrix = plasma

4. Hematocrit
Depends on age and, after adolescence, the sex of the individual.
Newborns: 55-68%
One (1) week of age: 47-65%
One (1) month of age: 37-49%
Three (3) months of age: 30-36%
One (1) year of age: 29-41%
Ten (10) years of age: 36-40%
Adult males: 42-54%
Adult women: 38-46%
Low hematocrit = anemic
High hematocrit = high altitudes, smokers,
dehydration, lung disease, tumors

5. Blood Plasma 55% of blood sample ~ 90 % water
Many dissolved substances
- Salts/electrolytes (metal ions)
- Proteins
- Respiratory gases
- Hormones
- Nutrients
- Waste products

6. Plasma Proteins Albumin – regulates osmotic pressure
Clotting proteins – help to stem blood loss when a blood vessel is injured
Antibodies – help protect the body from antigens

7. Formed Elements 1. Erythrocytes = red blood cells
2. Leukocytes = white blood cells
3. Platelets = cell fragments

8. 1. Erythrocytes (Red Blood Cells)
Carry O2 & little CO2
Anatomy-
- Biconcave disks
- Essentially bags of hemoglobin
- Anucleate (no nucleus)
- Contain very few organelles
Outnumber WBCs 1000:1

9. Hemoglobin Iron-containing protein
Binds strongly, but reversibly, to oxygen
has four oxygen binding sites
Each RBC has 250 million hemoglobin molecules
Normal blood contains g of hemoglobin per 100 ml.

10. 2. Leukocytes (White Blood Cells)
Defense against disease
Have nucleus & organelles
move into and out of vessels (diapedesis)
ameboid motion
Respond to chemicals released by damaged tissues

11. Leukocyte Levels in the Blood
Normal 4, ,000 cells per ml
Abnormal leukocyte levels
- Leukocytosis
+ 11,000 WBC/ml
Indicates an infection
- Leukopenia
- 4,000 WBC/ml
Commonly caused by drugs

12. Types of Leukocytes Granulocytes Agranulocytes Have granules
neutrophils, eosinophils, & basophils
Agranulocytes
No visible granules
lymphocytes & monocytes
Figure 10.4

13. Granulocytes Neutrophils Eosinophils Basophils
- Multilobed nucleus w/granules
- phagocytes at infection
Eosinophils
- Large brick-red granules
- Respond to allergies & parasitic worms
Basophils
- histamine-containing granules
- Initiate inflammation

14. Agranulocytes Lymphocytes Monocytes Nucleus fills most of the cell
important role in immune response
Monocytes
Largest of the WBC
macrophages
Fight chronic infection L

15. 3. Platelets
Derived from ruptured multinucleate cells (megakaryocytes)
Needed for the clotting process
Normal platelet count = 300,000/ml

16. Hematopoiesis - Blood cell formation
Red bone marrow
Adults – flat bones & epiphyseal plates, not shaft
Hemocytoblast – common stem cell
Differentiation
Lymphoid stem cell make lymphocytes
Myeloid stem cell produces other formed elements

17. Starts in the Red Bond Marrow

18. Leukemia
Chronic Leukemia —Early in disease, abnormal blood cells can still work; people may not have any symptoms. Symptoms increase as leukemia cells increase.
Acute Leukemia —blood cells abnormal; cannot work. Abnormal cells increases rapidly. Worsens quickly.
Leukemia can arise in lymphoid cells or myeloid cells.

19. Fate of Erythrocytes Can’t divide, grow, or make proteins
Wear out in 100 to 120 days
Eliminated by phagocytes in spleen or liver
Replaced by division of hemocytoblasts

20. Control of Erythrocyte Production
Rate is controlled by a hormone (erythropoietin)
Kidneys produce most erythropoietin
Negative feedback from blood O2 levels

21. Control of Leukocytes
colony stimulating factors (CSFs) and interleukins stimulate production of leukocytes.

22. Hemostasis Stoppage of blood flow Result of a break in a blood vessel
Hemostasis involves three phases
1. Platelet plug formation
2. Vascular spasms
3. Coagulation

23. 1. Platelet Plug Formation
Collagen fibers are exposed by a break in a blood vessel
Platelets become “sticky” and cling to fibers
Anchored platelets release chemicals to attract more platelets
Platelets pile up to form a platelet plug

24. 2. Vascular Spasms Anchored platelets release serotonin
Serotonin causes blood vessel muscles to spasm
Spasms narrow the blood vessel, decreasing blood loss

25. 3. Coagulation Injured tissues release thromboplastin
PF3 (a phospholipid) interacts with thromboplastin, blood protein clotting factors, and calcium ions to trigger a clotting cascade
Prothrombin activator converts prothrombin to thrombin (an enzyme)
Thrombin joins fibrinogen proteins into hair-like fibrin
Fibrin forms a meshwork (the basis for a clot)

26. Blood Clotting Blood usually clots within 3 to 6 minutes
The clot remains as endothelium regenerates
The clot is broken down after tissue repair
Vitamin "K" is derived from the German "koagulation" -essential for the functioning of several proteins involved in blood clotting

27. Undesirable Clotting Thrombus Embolus Clot in unbroken vessel
Deadly in heart
Embolus
Thrombus that breaks away and floats in bloodstream
Can later clog vessels in critical areas such as the brain

28. Bleeding Disorders 1.Thrombocytopenia 2. Hemophilia
Platelet (thrombocyte) deficiency
normal movements can cause bleeding
Petechiae – purple blotches
2. Hemophilia
Hereditary bleeding disorder
Normal clotting factors are missing
Sex-linked genetic disorder

29. Bleeding Disorders 3. Anemia a. Hemorrhagic – massive bleeding
b. Hemolytic – bacterial infection
c. Pernicious – lack of B12 absorption
d. Aplastic – damage of bone marrow
e. Iron-deficiency – diet, menstral
flow, bleeding ulcer
f. Sickle-cell – recessive genetic disorder; sickling due to increase O2 levels

30. Bleeding Disorders
4. Polycythemia – abnormal increase of RBCs; from bone cancer or response to high altitude; causes high viscosity.
5. pH disorders – regulated by kidneys & resp. sys.
a. alkalosis – too basic
b. acidosis – too acidic

31. Blood Groups and Transfusions
Large losses of blood have serious consequences
15 to 30 % = weakness
+ 30 % = shock; can be fatal
Transfusions = only way to replace blood quickly
Transfused blood must be of the same blood group

32. Human Blood Groups over 30 common RBC antigens (proteins)
Worst transfusion reactions caused by ABO and Rh antigens
Unmatched blood types:
Lysed RBCs release hemoglobin which blocks kidneys, causes fevers, vomit, etc.

33. Human Blood Groups Blood contains genetically determined proteins
A foreign protein (antigen) may be attacked by the immune system
Blood is “typed” by using antibodies that will cause blood with certain proteins to clump (agglutination)

34. ABO Blood Groups
Based on the presence or absence of two antigens (A & B)
Blood Types
Type A – has A antigen, anti-B antibody
Type B – has B antigen, anti-A antibody
Type AB – has both A & B antigens, Universal Recipient
Type O – lacks A & B antigens, has both anti-A anti-B antibodies; Universal Donor

35. Rh Blood Groups
Named because one of eight Rh antigens (agglutinogen D) found first in Rhesus monkey
Most Americans are Rh+
Anti-Rh antibodies not automatically formed; formed after exposed to Rh+
Problems can occur in mixing Rh+ blood into a body with Rh– blood

36. Rh Dangers During Pregnancy
Rh– mom with Rh+ baby- problems for the unborn child
1st pregnancy usually no problems
2nd pregnancy, the mom’s antibodies attack the Rh+ blood
hemolytic disease of the newborn
Destruction of RBCs, anemia, brain damage, death
Fetal transfusions
Give RhoGAM serum to prevent sensitivity to Rh antigen

37. Blood Typing Blood mixed with anti-A and anti-B serum
Coagulation or no coagulation leads to determining blood type
Cross matching – testing for agglutination of donor RBCs by the recipient’s serum, and vice versa

38. Developmental Aspects of Blood
Sites of blood cell formation
fetal liver and spleen
bone marrow takes over by 7th month
Fetal hemoglobin can pick up more O2
Physiological Jaundice – liver can’t keep up with rapid fetal RBC destruction