1. The Cardiovascular System: The Blood Lecture Outline
Chapter 19
The Cardiovascular System: The Blood
Lecture Outline

2. INTRODUCTION
Blood inside blood vessels, interstitial fluid around body cells, and lymph inside lymph vessels constitute one’s internal environment.
To obtain nutrients and remove wastes, cells must be serviced by blood and interstitial fluid.
Blood, a connective tissue, is composed of plasma and formed elements.
Interstitial fluid bathes body cells (Figure 19.1).
The branch of science concerned with the study of blood, blood-forming tissues, and the disorders associated with them is called hematology.
Principles of Human Anatomy and Physiology, 11e

3. Chapter 19 The Cardiovascular System: The Blood
Principles of Human Anatomy and Physiology, 11e

4. Fluids of the Body Cells of the body are serviced by 2 fluids blood
composed of plasma and a variety of cells
transports nutrients and wastes
interstitial fluid
bathes the cells of the body
Nutrients and oxygen diffuse from the blood into the interstitial fluid & then into the cells
Wastes move in the reverse direction
Hematology is study of blood and blood disorders
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5. Functions of Blood Transportation
O2, CO2, metabolic wastes, nutrients, heat & hormones
Regulation
helps regulate pH through buffers
helps regulate body temperature
coolant properties of water
vasodilatation of surface vessels dump heat
helps regulate water content of cells by interactions with dissolved ions and proteins
Protection from disease & loss of blood
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6. Physical Characteristics of Blood
Thicker (more viscous) than water and flows more slowly than water
Temperature of degrees F
pH 7.4 ( )
8 % of total body weight
Blood volume
5 to 6 liters in average male
4 to 5 liters in average female
hormonal negative feedback systems maintain constant blood volume and osmotic pressure
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7. Techniques of Blood Sampling
Venipuncture
sample taken from vein with hypodermic needle & syringe
median cubital vein (see page 717)
why not stick an artery?
less pressure
closer to the surface
Finger or heel stick
common technique for diabetics to monitor daily blood sugar
method used for infants
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8. COMPONENTS OF BLOOD
Blood consists of 55% plasma and 45% formed elements (Figure 19.1).
Blood plasma consists of 91.5% water and 8.5% solutes.
Principal solutes include proteins (albumins, globulins, fibrinogen), nutrients, enzymes, hormones, respiratory gases, electrolytes, and waste products.
Table 19.1 summarizes the chemical composition of plasma.
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9. Components of Blood Hematocrit 55% plasma 45% cells 99% RBCs
< 1% WBCs and platelets
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10. Blood Plasma 0ver 90% water 7% plasma proteins created in liver
confined to bloodstream
albumin
maintain blood osmotic pressure
globulins (immunoglobulins)
antibodies bind to foreign substances called antigens
form antigen-antibody complexes
fibrinogen
for clotting
2% other substances
electrolytes, nutrients, hormones, gases, waste products
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11. Formed Elements of Blood
Red blood cells ( erythrocytes )
White blood cells ( leukocytes )
granular leukocytes
neutrophils, eosinophils, basophils
agranular leukocytes
lymphocytes = T cells, B cells, and natural killer cells
monocytes
Platelets (special cell fragments)
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12. FORMATION OF BLOOD CELLS
Blood cells are formed from pluripotent hematopoietic stem cells (Figure 19.3).
Bone marrow may be obtained through aspiration or biopsy. The sample is then sent to pathology for examination.
Originating from the pluripotent stem cells are the myeloid stem cells and lymphoid stem cells.
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13. Hematocrit Percentage of blood occupied by cells female normal range
% (average of 42%)
male normal range
% (average of 46%)
testosterone
Anemia
not enough RBCs or not enough hemoglobin
Polycythemia
too many RBCs (over 65%)
dehydration, tissue hypoxia, blood doping in athletes
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14. Blood Doping
Injecting previously stored RBC’s before an athletic event
more cells available to deliver oxygen to tissues
Dangerous
increases blood viscosity
forces heart to work harder
Banned by Olympic committee
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15. Formation of Blood Cells
Most blood cells types need to be continually replaced
die within hours, days or weeks
process of blood cells formation is hematopoiesis or hemopoiesis
In the embryo
occurs in yolk sac, liver, spleen, thymus, lymph nodes & red bone marrow
In adult
occurs only in red marrow of flat bones like sternum, ribs, skull & pelvis and ends of long bones
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16. Hematopoiesis
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17. Stages of Blood Cell Formation
Pluripotent stem cells
.1% of red marrow cells
replenish themselves as they differentiate into either myeloid or lymphoid stem cells
Myeloid stem cell line of development continues:
progenitor cells(colony-forming units) no longer can divide and are specialized to form specific cell types
example: CFU-E develops eventually into only red blood cells
next generation is blast cells
have recognizable histological characteristics
develop within several divisions into mature cell types
Lymphoid stem cell line of development
pre-B cells & prothymocytes finish their develop into B & T lymphocytes in the lymphatic tissue after leaving the red marrow
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18. Hemopoietic Growth Factors
Regulate differentiation & proliferation
Erythropoietin (EPO)
produced by the kidneys increase RBC precursors
Thrombopoietin (TPO)
hormone from liver stimulates platelet formation
Cytokines are local hormones of bone marrow
produced by some marrow cells to stimulate proliferation in other marrow cells
colony-stimulating factor (CSF) & interleukin stimulate WBC production
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19. Medical Uses of Growth Factors
Available through recombinant DNA technology
recombinant erythropoietin (EPO) very effective in treating decreased RBC production of end-stage kidney disease
other products given to stimulate WBC formation in cancer patients receiving chemotherapy which kills bone marrow
granulocyte-macrophage colony-stimulating factor
granulocyte colony stimulating factor
thrombopoietin helps prevent platelet depletion during chemotherapy
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20. Blood Cells
Myeloid stem cells give rise to RBCs, platelets, and all WBCs except for lymphocytes.
Lymphoid stem cells give rise to lymphocytes.
Myeloid stem cells differentiate into progenitor cells or precursor cells (blast cells) which will develop into the actual formed elements of blood.
Lymphoid stem cells differentiate into pre-B and prothymocytes which develop into B-lymphocytes and T-lymphocytes, respectively.
This process of hemopoiesis (or hematopoiesis) is stimulated by several hematopoietic growth factors. These hematopoietic growth factors stimulate differentiation and proliferation of the various blood cells.
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21. Red Blood Cells or Erythrocytes (Figure 19.4a)
Contain oxygen-carrying protein hemoglobin that gives blood its red color
1/3 of cell’s weight is hemoglobin
Biconcave disk 8 microns in diameter
increased surface area/volume ratio
flexible shape for narrow passages
no nucleus or other organelles
no cell division or mitochondrial ATP formation
Normal RBC count
male 5.4 million/drop ---- female 4.8 million/drop
new RBCs enter circulation at 2 million/second
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22. Hormones Erythropoietin increases the number of RBC precursors.
Thrombopoietin increases the number of platelet precursors.
Cytokins (colony-stimulating factors and interleukins) increase the number of WBC precursors.
Growth factors, available through recombinant DNA technology, hold great potential for use in patients who cannot normally form the blood cells.
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23. Hemoglobin Globin protein consisting of 4 polypeptide chains
One heme pigment attached to each polypeptide chain
each heme contains an iron ion (Fe+2) that can combine reversibly with one oxygen molecule
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24. Transport of O2, CO2 and Nitric Oxide
Each hemoglobin molecule can carry 4 oxygen molecules from lungs to tissue cells
Hemoglobin transports 23% of total CO2 waste from tissue cells to lungs for release
combines with amino acids in globin portion of Hb
Hemoglobin transports nitric oxide & super nitric oxide helping to regulate BP
iron ions pick up nitric oxide (NO) & super nitric oxide (SNO)& transport it to & from the lungs
NO causing vasoconstriction is released in the lungs
SNO causing vasodilation is picked up in the lungs
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25. RBCs
Production of abnormal hemoglobin can result in serious blood disorders such as thalassemia and sickle cell anemia. (Figure 19.15)
The blood test, hemoglobin A1c, can be used to monitor blood glucose levels in diabetics
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26. RBC Life Cycle RBCs live only 120 days
wear out from bending to fit through capillaries
no repair possible due to lack of organelles
Worn out cells removed by fixed macrophages in spleen & liver
Breakdown products are recycled
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27. Recycling of Hemoglobin Components
In macrophages of liver or spleen
globin portion broken down into amino acids & recycled
heme portion split into iron (Fe+3) and biliverdin (green pigment)
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28. Fate of Components of Heme
Iron(Fe+3)
transported in blood attached to transferrin protein
stored in liver, muscle or spleen
attached to ferritin or hemosiderin protein
in bone marrow being used for hemoglobin synthesis
Biliverdin (green) converted to bilirubin (yellow)
bilirubin secreted by liver into bile
converted to urobilinogen then stercobilin (brown pigment in feces) by bacteria of large intestine
if reabsorbed from intestines into blood is converted to a yellow pigment, urobilin and excreted in urine
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29. Erythropoiesis: Production of RBCs
Erythrocyte formation, called erythropoiesis, occurs in adult red bone marrow of certain bones (Figure 19.3).
The main stimulus for erythropoiesis is hypoxia (Figure 19.6).
Proerythroblast starts to produce hemoglobin
Many steps later, nucleus is ejected & a reticulocyte is formed
orange in color with traces of visible rough ER
Reticulocytes escape from bone marrow into the blood
In 1-2 days, they eject the remaining organelles to become a mature RBC
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30. Feedback Control of RBC Production
Tissue hypoxia (cells not getting enough O2)
high altitude since air has less O2
anemia
RBC production falls below RBC destruction
circulatory problems
Kidney response to hypoxia
release erythropoietin
speeds up development of proerythroblasts into reticulocytes
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31. Normal Reticulocyte Count
Should be .5 to 1.5% of the circulating RBC’s
Low count in an anemic person might indicate bone marrow problem
leukemia, nutritional deficiency or failure of red bone marrow to respond to erythropoietin stimulation
High count might indicate recent blood loss or successful iron therapy
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32. WHITE BLOOD CELLS
Leukocytes (white blood cells or WBCs) are nucleated cells and do not contain hemoglobin. Two principal types are granular (neutrophils, eosinophils, basophils) and agranular (lymphocytes and monocytes) (Figure 19.7).
Granular leukocytes include eosinophils, basophils, and neutrophils based on the straining of the granules.
Agranular leukocytes do not have cytoplasmic granules and include the lymphocytes and monocytes, which differentiate into macrophages (fixed and wandering).
Leukocytes have surface proteins, as do erythrocytes. They are called major histocompatibility antigens (MHC), are unique for each person (except for identical siblings), and can be used to identify a tissue.
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33. WBC Physiology Less numerous than RBCs
5000 to 10,000 cells per drop of blood
1 WBC for every 700 RBC
Leukocytosis is a high white blood cell count
microbes, strenuous exercise, anesthesia or surgery
Leukopenia is low white blood cell count
radiation, shock or chemotherapy
Only 2% of total WBC population is in circulating blood at any given time
rest is in lymphatic fluid, skin, lungs, lymph nodes & spleen
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34. Function of WBCs
Different WBCs combat inflammation and infection in different ways.
Neutrophils and wandering or fixed macrophages (which develop from monocytes) do so through phagocytosis.
Eosinophils combat the effects of histamine in allergic reactions, phagocytize antigen-antibody complexes, and combat parasitic worms.
Basophils develop into mast cells that liberate heparin, histamine, and serotonin in allergic reactions that intensify the inflammatory response.
B lymphocytes, in response to the presence of foreign substances called antigens, differentiate into tissue plasma cells that produce antibodies.
T lymphocytes destroy foreign invaders directly.
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35. Function of WBCs
WBCs leave the blood stream by emigration (Figure 19.8).
Some WBCs, particularly neutrophils and macrophages, are active in phagocytosis.
The chemical attraction of WBCs to a disease or injury site is termed chemotaxis.
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36. WBC examination
A differential white blood cell count is a diagnostic test in which specific white blood cells are enumerated. Because each type of WBC plays a different role, determining the percentage of each type in the blood assists in diagnosing the condition.
Table 19.2 shows the significance of elevated or depressed counts of the various WBCs.
Bone marrow transplants may be used to treat several types of anemia, leukemia, and numerous other blood disorders. (Clinical Application)
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37. WBC Anatomy and Types
All WBCs (leukocytes) have a nucleus and no hemoglobin
Granular or agranular classification based on presence of cytoplasmic granules made visible by staining
granulocytes are neutrophils, eosinophils or basophils
agranulocytes are monocyes or lymphocytes
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38. Neutrophils (Granulocyte)
Polymorphonuclear Leukocytes or Polys
Nuclei = 2 to 5 lobes connected by thin strands
older cells have more lobes
young cells called band cells because of horseshoe shaped nucleus (band)
Fine, pale lilac practically invisible granules
Diameter is microns
60 to 70% of circulating WBCs
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39. Eosinophils (Granulocyte)
Nucleus with 2 or 3 lobes connected by a thin strand
Large, uniform-sized granules stain orange-red with acidic dyes
do not obscure the nucleus
Diameter is 10 to 12 microns
2 to 4% of circulating WBCs
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40. Basophils (Granulocyte)
Large, dark purple, variable-sized granules stain with basic dyes
obscure the nucleus
Irregular, s-shaped, bilobed nuclei
Diameter is 8 to 10 microns
Less than 1% of circulating WBCs
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41. Lymphocyte (Agranulocyte)
Dark, oval to round nucleus
Cytoplasm sky blue in color
amount varies from rim of blue to normal amount
Small cells microns in diameter
Large cells microns in diameter
increase in number during viral infections
20 to 25% of circulating WBCs
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42. Monocyte (Agranulocyte)
Nucleus is kidney or horse-shoe shaped
Largest WBC in circulating blood
does not remain in blood long before migrating to the tissues
differentiate into macrophages
fixed group found in specific tissues
alveolar macrophages in lungs
kupffer cells in liver
wandering group gathers at sites of infection
Diameter is microns
Cytoplasm is a foamy blue-gray
3 to 8% o circulating WBCs
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43. Emigration & Phagocytosis in WBCs
WBCs roll along endothelium, stick to it & squeeze between cells.
adhesion molecules (selectins) help WBCs stick to endothelium
displayed near site of injury
molecules (integrins) found on neutrophils assist in movement through wall
Neutrophils & macrophages phagocytize bacteria & debris
chemotaxis of both
kinins from injury site & toxins
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44. Neutrophil Function Fastest response of all WBC to bacteria
Direct actions against bacteria
release lysozymes which destroy/digest bacteria
release defensin proteins that act like antibiotics & poke holes in bacterial cell walls destroying them
release strong oxidants (bleach-like, strong chemicals ) that destroy bacteria
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45. Monocyte Function
Take longer to get to site of infection, but arrive in larger numbers
Become wandering macrophages, once they leave the capillaries
Destroy microbes and clean up dead tissue following an infection
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46. Basophil Function Involved in inflammatory and allergy reactions
Leave capillaries & enter connective tissue as mast cells
Release heparin, histamine & serotonin
heighten the inflammatory response and account for hypersensitivity (allergic) reaction
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47. Eosinophil Function Leave capillaries to enter tissue fluid
Release histaminase
slows down inflammation caused by basophils
Attack parasitic worms
Phagocytize antibody-antigen complexes
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48. Lymphocyte Functions B cells destroy bacteria and their toxins
turn into plasma cells that produces antibodies
T cells
attack viruses, fungi, transplanted organs, cancer cells & some bacteria
Natural killer cells
attack many different microbes & some tumor cells
destroy foreign invaders by direct attack
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49. Complete Blood Count Screens for anemia and infection
Total RBC, WBC & platelet counts; differential WBC; hematocrit and hemoglobin measurements
Normal hemoglobin range
infants have 14 to 20 g/100mL of blood
adult females have 12 to 16 g/100mL of blood
adult males have 13.5 to 18g/100mL of blood
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50. Differential WBC Count
Detection of changes in numbers of circulating WBCs (percentages of each type)
indicates infection, poisoning, leukemia, chemotherapy, parasites or allergy reaction
Normal WBC counts
neutrophils 60-70% (up if bacterial infection)
lymphocyte 20-25% (up if viral infection)
monocytes % (up if fungal/viral infection)
eosinophil % (up if parasite or allergy reaction)
basophil <1% (up if allergy reaction or hypothyroid)
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51. Bone Marrow Transplant
Intravenous transfer of healthy bone marrow
Procedure
destroy sick bone marrow with radiation & chemotherapy
donor matches surface antigens on WBC
put sample of donor marrow into patient's vein for reseeding of bone marrow
success depends on histocompatibility of donor & recipient
Treatment for leukemia, sickle-cell, breast, ovarian or testicular cancer, lymphoma or aplastic anemia
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52. PLATELETS
Thrombopoietin stimulates myeloid stem cells to produce platelets.
Myeloid stem cells develop into megakaryocyte-colony-forming cells that develop into megakaryoblasts (Figure 19.2).
Megakaryoblasts transform into megakaryocytes which fragment.
Each fragment, enclosed by a piece of cell membrane, is a platelet (thrombocyte).
Normal blood contains 250,000 to 400,000 platelets/mm3. Platelets have a life span of only 5 to 9 days; aged and dead platelets are removed by fixed macrophages in the spleen and liver.
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53. PLATELETS
Platelets help stop blood loss from damaged vessels by forming a platelet plug. Their granules also contain chemicals that promote blood clotting.
A complete blood count (CBC) is a test that screens for anemia and various infections. It usually includes counts of RBCs, WBCs, and platelets per μL of whole blood; hematocrit and differential white blood cell count. The amount of hemoglobin in grams per ml is also determined.
Table 19.3 summarizes the formed elements in blood.
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54. Platelet (Thrombocyte) Anatomy
Disc-shaped, micron cell fragment with no nucleus
Normal platelet count is 150, ,000/drop of blood
Other blood cell counts
5 million red & 5-10,000 white blood cells
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55. Platelets--Life History
Platelets form in bone marrow by following steps:
myeloid stem cells to megakaryocyte-colony forming cells to megakaryoblast to megakaryocytes whose cell fragments form platelets
Short life span (5 to 9 days in bloodstream)
formed in bone marrow
few days in circulating blood
aged ones removed by fixed macrophages in liver and spleen
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56. STEM CELL TRANSPLANT FROM BONE MARROW AND CORD-BLOOD
Bone marrow transplant replaces diseased marrow with healthy marrow.
Patient’s diseased marrow is destroyed.
Healthy marrow is supplied by a donor or the patient.
There are several problems with this method.
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57. Cord-blood transplant
Stem cells are taken from the umbilical cord and frozen
This method offers several advantages over marrow transplant.
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58. HEMOSTASIS
A clot is a gel consisting of a network of insoluble protein fibers (fibrin) in which formed elements of blood are trapped (Figure 19.10).
The chemicals involved in clotting are known as coagulation (clotting) factors; most are in blood plasma, some are released by platelets, and one is released from damaged tissue cells (Table 19.4).
Blood clotting involves a cascade of reactions that may be divided into three stages: formation of prothrombinase (prothrombin activator), conversion of prothrombin into thrombin, and conversion of soluble fibrinogen into insoluble fibrin (Figure 19.11).
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59. HEMOSTASIS
The clotting cascade can be initiated by either the extrinsic pathway or the intrinsic pathway.
Normal coagulation requires vitamin K and also involves clot retraction (tightening of the clot) and fibrinolysis (dissolution of the clot).
The fibrinolytic system dissolves small, inappropriate clots and clots at a site of damage once the damage is repaired.
Plasmin (fibrinolysin) can dissolve a clot by digesting fibrin threads and inactivating substances such as fibrinogen, prothrombin, and factors V, VIII, and XII.
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60. Hemostasis
Stoppage of bleeding in a quick & localized fashion when blood vessels are damaged
Prevents hemorrhage (loss of a large amount of blood)
Methods utilized
vascular spasm
platelet plug formation
blood clotting (coagulation = formation of fibrin threads)
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61. Vascular Spasm
Damage to blood vessel produces stimulates pain receptors
Reflex contraction of smooth muscle of small blood vessels
Can reduce blood loss for several hours until other mechanisms can take over
Only for small blood vessel or arteriole
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62. Platelet Plug Formation
Platelets store a lot of chemicals in granules needed for platelet plug formation
alpha granules
clotting factors
platelet-derived growth factor
cause proliferation of vascular endothelial cells, smooth muscle & fibroblasts to repair damaged vessels
dense granules
ADP, ATP, Ca+2, serotonin, fibrin-stabilizing factor, & enzymes that produce thromboxane A2
Steps in the process
(1) platelet adhesion (2) platelet release reaction (3) platelet aggregation
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63. Platelet Adhesion
Platelets stick to exposed collagen underlying damaged endothelial cells in vessel wall
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64. Platelet Release Reaction
Platelets activated by adhesion
Extend projections to make contact with each other
Release thromboxane A2 & ADP activating other platelets
Serotonin & thromboxane A2 are vasoconstrictors decreasing blood flow through the injured vessel
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65. Platelet Aggregation
Activated platelets stick together and activate new platelets to form a mass called a platelet plug
Plug reinforced by fibrin threads formed during clotting process
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66. Blood Clotting Blood drawn from the body thickens into a gel
gel separates into liquid (serum) and a clot of insoluble fibers (fibrin) in which the cells are trapped
If clotting occurs in an unbroken vessel is called a thrombosis
Substances required for clotting are Ca+2, enzymes synthesized by liver cells and substances released by platelets or damaged tissues
Clotting is a cascade of reactions in which each clotting factor activates the next in a fixed sequence resulting in the formation of fibrin threads
prothrombinase & Ca+2 convert prothrombin into thrombin
thrombin converts fibrinogen into fibrin threads
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67. Overview of the Clotting Cascade
Prothrombinase is formed by either the intrinsic or extrinsic pathway
Final common pathway produces fibrin threads
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68. Extrinsic Pathway
Damaged tissues leak tissue factor (thromboplastin) into bloodstream
Prothrombinase forms in seconds
In the presence of Ca+2, clotting factor X combines with V to form prothrombinase
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69. Intrinsic Pathway Activation occurs
endothelium is damaged & platelets come in contact with collagen of blood vessel wall
platelets damaged & release phospholipids
Requires several minutes for reaction to occur
Substances involved: Ca+2 and clotting factors XII, X and V
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70. Final Common Pathway Prothrombinase and Ca+2
catalyze the conversion of prothrombin to thrombin
Thrombin
in the presence of Ca+2 converts soluble fibrinogen to insoluble fibrin threads
activates fibrin stabilizing factor XIII
positive feedback effects of thrombin
accelerates formation of prothrombinase
activates platelets to release phospholipids
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71. Clot Retraction & Blood Vessel Repair
Clot plugs ruptured area of blood vessel
Platelets pull on fibrin threads causing clot retraction
trapped platelets release factor XIII stabilizing the fibrin threads
Edges of damaged vessel are pulled together
Fibroblasts & endothelial cells repair the blood vessel
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72. Role of Vitamin K in Clotting
Normal clotting requires adequate vitamin K
fat soluble vitamin absorbed if lipids are present
absorption slowed if bile release is insufficient
Required for synthesis of 4 clotting factors by hepatocytes
factors II (prothrombin), VII, IX and X
Produced by bacteria in large intestine
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73. Hemostatic Control Mechanisms
Fibrinolytic system dissolves small, inappropriate clots & clots at a site of a completed repair
fibrinolysis is dissolution of a clot
Inactive plasminogen is incorporated into the clot
activation occurs because of factor XII and thrombin
plasminogen becomes plasmin (fibrinolysin) which digests fibrin threads
Clot formation remains localized
fibrin absorbs thrombin
blood disperses clotting factors
endothelial cells & WBC produce prostacyclin that opposes thromboxane A2 (platelet adhesion & release)
Anticoagulants present in blood & produced by mast cells
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74. Intravascular Clotting
Thrombosis
clot (thrombus) forming in an unbroken blood vessel
forms on rough inner lining of BV
if blood flows too slowly (stasis) allowing clotting factors to build up locally & cause coagulation
may dissolve spontaneously or dislodge & travel
Embolus
clot, air bubble or fat from broken bone in the blood
pulmonary embolus is found in lungs
Low dose aspirin blocks synthesis of thromboxane A2 & reduces inappropriate clot formation
strokes, TIAs and myocardial infarctions
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75. Anticoagulants and Thrombolytic Agents
Anticoagulants suppress or prevent blood clotting
heparin
administered during hemodialysis and surgery
warfarin (Coumadin)
antagonist to vitamin K so blocks synthesis of clotting factors
slower than heparin
stored blood in blood banks treated with citrate phosphate dextrose (CPD) that removes Ca+2
Thrombolytic agents are injected to dissolve clots
directly or indirectly activate plasminogen
streptokinase or tissue plasminogen activator (t-PA)
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76. Hemostatic Control Mechanisms
Clots are generally localized due to fibrin absorbing thrombin into the clot, clotting factors diffusing through blood, and the production of prostacyclin, a powerful inhibitor of platelet adhesion and release.
Substances that inhibit coagulation, called anticoagulants, are also present in blood. An example is heparin.
Patients who are at increased risk of forming blood clots may receive an anticoagulant drug such as heparin or warfarin. To prevent clots in donated blood, a substance that removes Ca+2 such as EDTA or CPD may be added to the blood.
Despite the anticoagulating and fibrinolytic mechanisms, blood clots sometimes form within the cardiovascular system.
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77. HEMOSTASIS Clotting in an unbroken blood vessel is called thrombosis.
A thrombus (clot), bubble of air, fat from broken bones, or piece of debris transported by the bloodstream that moves from its site of origin is called an embolus.
At low doses aspirin inhibits vasoconstriction and platelet aggregation thereby reducing the chance of thrombus formation. Thrombolytic agents are injected into the body to dissolve clots that have already formed. Streptokinase or tissue plasminogen activator (TPS) are thrombolytic agents.
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78. ABO Group
In the ABO system, agglutinogens (antigens) A and B determine blood types (Figure 19.12).
Plasma contains agglutinins (antibodies), designated as a and b, that react with agglutinogens that are foreign to the individual.
Table 19.5 indicates the incidence of ABO and Rh blood types.
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79. Blood Groups and Blood Types
RBC surfaces are marked by genetically determined glycoproteins & glycolipids
agglutinogens or isoantigens
distinguishes at least 24 different blood groups
ABO, Rh, Lewis, Kell, Kidd and Duffy systems
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80. ABO Blood Groups
Based on 2 glycolipid isoantigens called A and B found on the surface of RBCs
display only antigen A -- blood type A
display only antigen B -- blood type B
display both antigens A & B -- blood type AB
display neither antigen -- blood type O
Plasma contains isoantibodies or agglutinins to the A or B antigens not found in your blood
anti-A antibody reacts with antigen A
anti-B antibody reacts with antigen B
Principles of Human Anatomy and Physiology, 11e

81. RH blood groups Antigen was discovered in blood of Rhesus monkey
People with Rh agglutinogens on RBC surface are Rh+. Normal plasma contains no anti-Rh antibodies
Antibodies develop only in Rh- blood type & only with exposure to the antigen
transfusion of positive blood
during a pregnancy with a positive blood type fetus
Transfusion reaction upon 2nd exposure to the antigen results in hemolysis of the RBCs in the donated blood
Principles of Human Anatomy and Physiology, 11e

82. Hemolytic Disease of Newborn
Rh negative mom and Rh+ fetus will have mixing of blood at birth
Mom's body creates Rh antibodies unless she receives a RhoGam shot soon after first delivery, miscarriage or abortion
RhoGam binds to loose fetal blood and removes it from body before she reacts
In 2nd child, hemolytic disease of the newborn may develop causing hemolysis of the fetal RBCs
Principles of Human Anatomy and Physiology, 11e

83. Transfusions
Knowledge of blood types is essential to safe transfusion of blood and may also be used in proving or disproving paternity, linking suspects to crimes, or as a part of anthropology studies to establish a relationship among races.
The interactions of the blood types of the ABO system are summarized in Table 19.6.
Principles of Human Anatomy and Physiology, 11e

84. Transfusion and Transfusion Reactions
Transfer of whole blood, cells or plasma into the bloodstream of recipient
used to treat anemia or severe blood loss
Incompatible blood transfusions
antigen-antibody complexes form between plasma antibodies & “foreign proteins” on donated RBC's (agglutination)
donated RBCs become leaky (complement proteins) & burst
loose hemoglobin causes kidney damage
Problems caused by incompatibility between donor’s cells and recipient’s plasma
Donor plasma is too diluted to cause problems
Principles of Human Anatomy and Physiology, 11e

85. Universal Donors and Recipients
People with type AB blood called “universal recipients” since have no antibodies in plasma
only true if cross match the blood for other antigens
People with type O blood cell called “universal donors” since have no antigens on their cells
theoretically can be given to anyone
Principles of Human Anatomy and Physiology, 11e

86. Typing and Cross-Matching Blood for Transfusion
The Rh and ABO blood groups may be detected by a simple medical test, blood typing, in which a sample of blood is mixed with serum containing agglutinins to each of the major agglutinogens (AB, B, and Rh) (Figure 19.14).
Typing is the determination of blood types, whereas cross-matching is the mixing of donor and recipient blood for compatibility.
Principles of Human Anatomy and Physiology, 11e

87. DISORDERS: HOMEOSTATIC IMBALANCES
Anemia
Sickle-cell
Hemophilia
Disseminated intravascular clotting
Acute leukemia
chronic leukemia
Principles of Human Anatomy and Physiology, 11e

88. Anemia = Not Enough RBCs
Symptoms
oxygen-carrying capacity of blood is reduced
fatigue, cold intolerance & paleness
lack of O2 for ATP & heat production
Types of anemia
iron-deficiency =lack of absorption or loss of iron
pernicious = lack of intrinsic factor for B12 absorption
hemorrhagic = loss of RBCs due to bleeding (ulcer)
hemolytic = defects in cell membranes cause rupture
thalassemia = hereditary deficiency of hemoglobin
aplastic = destruction of bone marrow (radiation/toxins)
Principles of Human Anatomy and Physiology, 11e

89. Sickle-cell Anemia (SCA)
Genetic defect in hemoglobin molecule (Hb-S) that changes 2 amino acids
at low very O2 levels, RBC is deformed by changes in hemoglobin molecule within the RBC
sickle-shaped cells rupture easily = causing anemia & clots
Found among populations in malaria belt
Mediterranean Europe, sub-Saharan Africa & Asia
Person with only one sickle cell gene
increased resistance to malaria because RBC membranes leak K+ & lowered levels of K+ kill the parasite infecting the red blood cells
Principles of Human Anatomy and Physiology, 11e

90. Hemophilia Inherited deficiency of clotting factors
bleeding spontaneously or after minor trauma
subcutaneous & intramuscular hemorrhaging
nosebleeds, blood in urine, articular bleeding & pain
Hemophilia A lacks factor VIII (males only)
most common
Hemophilia B lacks factor IX (males only)
Hemophilia C (males & females)
less severe because alternate clotting activator exists
Treatment is transfusions of fresh plasma or concentrates of the missing clotting factor
Principles of Human Anatomy and Physiology, 11e

91. Disseminated Intravascular Clotting
Life threatening paradoxical presence of blood clotting and bleeding at the same time throughout the whole body
so many clotting factors are removed by widespread clotting that too few remain to permit normal clotting
Associated with infections, hypoxia, low blood flow rates, trauma, hypotension & hemolysis
Clots cause ischemia and necrosis leading to multisystem organ failure
Principles of Human Anatomy and Physiology, 11e

92. Leukemia Acute leukemia uncontrolled production of immature leukocytes
crowding out of normal red bone marrow cells by production of immature WBC
prevents production of RBC & platelets
Chronic leukemia
accumulation of mature WBC in bloodstream because they do not die
classified by type of WBC that is predominant---monocytic, lymphocytic.
Principles of Human Anatomy and Physiology, 11e

93. end
Principles of Human Anatomy and Physiology, 11e