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Composition of Blood
• Consists of formed elements (cells) suspended & carried in plasma (fluid part)
• Total blood volume is about 5L
• Plasma is straw-colored liquid consisting of H20 & dissolved solutes– Includes ions, metabolites, hormones, antibodies
13-7
Physical Characteristics of Blood• Average volume of blood:
– 5–6 L for males; 4–5 L for females (Normovolemia)– Hypovolemia - low blood volume– Hypervolemia - high blood volume
• Viscosity (thickness) - 4 - 5 (where water = 1)• The pH of blood is 7.35–7.45; x = 7.4• Salinity = 0.85%
– Reflects the concentration of NaCl in the blood
• Temperature is 38C, slightly higher than “normal” body temperature
• Blood accounts for approximately 8% of body weight
Plasma Proteins
• Constitute 7-9% of plasma• Three types of plasma proteins: albumins, globulins, &
fibrinogen– Albumin accounts for 60-80%
• Creates colloid osmotic pressure that draws H20 from interstitial fluid into capillaries to maintain blood volume & pressure
• Globulins carry lipids– Gamma globulins are antibodies (immunoglobulins)
• Fibrinogen serves as clotting factor– Converted to fibrin – Serum is fluid left when blood clots
13-8
Formed Elements
• Are erythrocytes (RBCs) & leukocytes (WBCs)
• RBCs are flattened biconcave discs– Shape provides increased surface area
for diffusion– Lack nuclei & mitochondria– Each RBC contains 280 million
hemoglobins
13-9
Leukocytes
• Have nucleus, mitochondria, & amoeboid ability
• Can squeeze through capillary walls (diapedesis)– Granular leukocytes help detoxify foreign substances &
release heparin• Include eosinophils, basophils, & neutrophils
13-10
Leukocytes continued
• Agranular leukocytes are phagocytic & produce antibodies
• Include lymphocytes & monocytes
13-11
Platelets (thrombocytes)
• Are smallest of formed elements, lack nucleus
• Are fragments of megakaryocytes • Constitute most of mass of blood
clots• Release serotonin to vasoconstrict &
reduce blood flow to clot area• Secrete growth factors to maintain
integrity of blood vessel wall• Survive 5-9 days
13-12
Components of Whole Blood
Withdraw blood and place in tube
1 2 Centrifuge
Plasma(55% of whole blood)
Formed elements
Buffy coat:leukocyctes and platelets(<1% of whole blood)
Erythrocytes(45% of whole blood)
• Hematocrit • Males: 47% ± 5%
• Females: 42% ± 5%
Hematopoiesis
• Is formation of blood cells from stem cells in marrow (myeloid tissue) & lymphoid tissue
• Erythropoiesis is formation of RBCs– Stimulated by erythropoietin (EPO) from kidney
• Leukopoiesis is formation of WBCs– Stimulated by variety of cytokines
• = autocrine regulators secreted by immune system
13-13
Life Cycle of Red
Blood Cells
Erythropoiesis
• 2.5 million RBCs are produced/sec
• Lifespan of 120 days• Old RBCs removed
from blood by phagocytic cells in liver, spleen, & bone marrow– Iron recycled back
into hemoglobin production
13-14
Erythropoietin Mechanism
Figure 17.6
Imbalance
Reduces O2 levels in blood
Erythropoietin stimulates red bone marrow
Enhanced erythropoiesis increases RBC count
Normal blood oxygen levels Stimulus: Hypoxia due to decreased RBC count, decreased availability of O2 to blood, or increased tissue demands for O2
Imbalance
Start
Kidney (and liver to a smaller extent) releases erythropoietin
Increases O2-carrying ability of blood
• Erythropoiesis requires:– Proteins, lipids, and carbohydrates– Iron, vitamin B12, and folic acid
• The body stores iron in Hb (65%), the liver, spleen, and bone marrow
• Intracellular iron is stored in protein-iron complexes such as ferritin and hemosiderin
• Circulating iron is loosely bound to the transport protein transferrin
Dietary Requirements of Erythropoiesis
RBC Antigens & Blood Typing
• Antigens present on RBC surface specify blood type• Major antigen group is ABO system
– Type A blood has only A antigens– Type B has only B antigens– Type AB has both A & B antigens– Type O has neither A or B antigens
13-15
Transfusion Reactions
• People with Type A blood make antibodies to Type B RBCs, but not to Type A
• Type B blood has antibodies to Type A RBCs but not to Type B
• Type AB blood doesn’t have antibodies to A or B
• Type O has antibodies to both Type A & B
• If different blood types are mixed, antibodies will cause mixture to agglutinate
13-16
Transfusion Reactions continued
• If blood types don't match, recipient’s antibodies agglutinate donor’s RBCs
• Type O is “universal donor” because lacks A & B antigens– Recipient’s antibodies won’t
agglutinate donor’s Type O RBCs
• Type AB is “universal recipient” because doesn’t make anti-A or anti-B antibodies– Won’t agglutinate donor’s
RBCs
• Insert fig. 13.6
13-17
• May occur in an Rh- mom pregnanet with an Rh+ fetus• Hemolytic disease of the newborn – Rh+ antibodies of a
sensitized Rh– mother cross the placenta and attack and destroy the RBCs of an Rh+ baby
• Rh– mother becomes sensitized when Rh+ blood (from a previous pregnancy of an Rh+ baby or a Rh+ transfusion) causes her body to synthesis Rh+ antibodies
• The drug RhoGAM can prevent the Rh– mother from becoming sensitized
• Treatment of hemolytic disease of the newborn involves pre-birth transfusions and exchange transfusions after birth
Hemolytic Disease of the Newborn
Hemostasis
• Is cessation of bleeding
• Promoted by reactions initiated by vessel injury:– Vasoconstriction restricts blood flow to area– Platelet plug forms
• Plug & surroundings are infiltrated by web of fibrin, forming clot
13-19
Role of Platelets
• Platelets don't stick to intact endothelium because of presence of prostacyclin (PGI2--a prostaglandin) & NO– Keep clots from
forming & are vasodilators
13-20
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Role of Platelets
• Damage to endothelium allows platelets to bind to exposed collagen– von Willebrand factor
increases bond by binding to both collagen & platelets
– Platelets stick to collagen & release ADP, serotonin, & thromboxane A2 • = platelet release reaction
13-21
Role of Platelets continued
• Serotonin & thromboxane A2 stimulate vasoconstriction, reducing blood flow to wound
• ADP & thromboxane A2 cause other platelets to become sticky & attach & undergo platelet release reaction– This continues until
platelet plug is formed 13-22
• Platelet plug becomes infiltrated by meshwork of fibrin• Clot now contains platelets, fibrin & trapped RBCs
– Platelet plug undergoes plug contraction to form more compact plug
Role of Fibrin
13-23
• Can occur via 2 pathways:– Intrinsic pathway clots damaged vessels & blood left in test tube
• Initiated by exposure of blood to negatively charged surface of glass or blood vessel collagen– This activates factor XII (a protease) which initiates a series of clotting factors– Ca2+ & phospholipids convert prothrombin to thrombin
» Thrombin converts fibrinogen to fibrin which polymerizes to form a mesh
– Damage outside blood vessels releases tissue thromboplastin that triggers a clotting shortcut (= extrinsic pathway)
Conversion of Fibrinogen to Fibrin
13-24
Fig 13.913-25
Dissolution of Clots
• When damage is repaired, activated factor XII causes activation of kallikrein – Kallikrein converts plasminogen to plasmin
• Plasmin digests fibrin, dissolving clot
13-26
Anticoagulants
• Clotting can be prevented by Ca+2 chelators (e.g. sodium citrate or EDTA)– or heparin which activates antithrombin III (blocks
thrombin)
• Coumarin blocks clotting by inhibiting activation of Vit K– Vit K works indirectly by reducing Ca+2 availability
13-27
Prostaglandins (PGs)
• Are produced in almost every organ
• Belong to eicosanoid family -- all derived from arachidonic acid of plasma membrane
11-72
• Have wide variety of functions– Different PGs may exert antagonistic effects in tissues
• Some promote smooth muscle contraction & some relaxation
• Some promote clotting; some inhibit
– Promotes inflammatory process of immune system– Plays role in ovulation– Inhibits gastric secretion in digestive system
Prostaglandins (PGs) continued
11-73
• Cyclooxygenase (COX) 1 & 2 are involved in PG synthesis – Are targets of a number of inhibitory non-steroidal anti-
inflammatory drugs (NSAIDs)• Aspirin, indomethacin, ibuprofen inhibit both COX 1 & 2 thereby
producing side effects• Celebrex & Vioxx only inhibit COX 2 & thus have few side effects
Prostaglandins (PGs) continued
11-74
• Polycythemia– Abnormal excess of erythrocytes
• Increases viscosity, decreases flow rate of blood
• Anemia – blood has abnormally low oxygen-carrying capacity– It is a symptom rather than a disease itself– Blood oxygen levels cannot support normal
metabolism– Signs/symptoms include fatigue, paleness,
shortness of breath, and chills
Erythrocyte Disorders
Anemia: Insufficient Erythrocytes
• Hemorrhagic anemia – result of acute or chronic loss of blood
• Hemolytic anemia – prematurely ruptured erythrocytes
• Aplastic anemia – destruction or inhibition of red bone marrow
• Iron-deficiency anemia results from:– A secondary result of hemorrhagic anemia– Inadequate intake of iron-containing foods– Impaired iron absorption
• Pernicious anemia results from:– Deficiency of vitamin B12
– Lack of intrinsic factor needed for absorption of B12
– Treatment is intramuscular injection of B12
Anemia: Decreased Hemoglobin Content
Anemia: Abnormal Hemoglobin
• Thalassemias – absent or faulty globin chain in hemoglobin – Erythrocytes are thin, delicate, and deficient in
hemoglobin
• Sickle-cell anemia – results from a defective gene– Codes for an abnormal hemoglobin called hemoglobin
S (HbS)
– This defect causes RBCs to become sickle-shaped in low oxygen situations
Polycythemia
• Polycythemia – excess RBCs that increase blood viscosity
• Three main polycythemias are:– Polycythemia vera– Secondary polycythemia– Blood doping
• Leukemia refers to cancerous conditions involving white blood cells
• Leukemias are named according to the abnormal white blood cells involved– Myelocytic leukemia – involves myeloblasts– Lymphocytic leukemia – involves lymphocytes
• Acute leukemia involves blast-type cells and primarily affects children
• Chronic leukemia is more prevalent in older people
Leukocytes Disorders: Leukemias
• Immature white blood cells are found in the bloodstream in all leukemias
• Bone marrow becomes totally occupied with cancerous leukocytes
• Severe anemia ensues due to excess production of WBC’s
• The white blood cells produced, though numerous, are not functional
• Death is caused by internal hemorrhage and overwhelming infections
• Treatments include irradiation, antileukemic drugs, and bone marrow transplants
Leukemia