chapter 17: blood 1 17 blood (rbc). chapter 17: blood 2 overview of blood circulation blood leaves...
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Chapter 17: Blood 1
17Blood
(RBC)
Chapter 17: Blood 2
Overview of Blood Circulation
Blood leaves the heart via arteries that branch repeatedly until they become capillaries
Oxygen (O2) and nutrients diffuse across capillary walls and enter tissues
Carbon dioxide (CO2) and wastes move from tissues into the blood
Chapter 17: Blood 3
Overview of Blood Circulation
Oxygen-deficient blood leaves the capillaries and flows in veins to the heart
This blood flows to the lungs where it releases CO2 and picks up O2
The oxygen-rich blood returns to the heart
Chapter 17: Blood 4
Composition of Blood
Blood is the body’s only fluid tissue
It is composed of liquid plasma and formed elements
Formed elements include:
Erythrocytes, or red blood cells (RBCs)
Leukocytes, or white blood cells (WBCs)
Platelets
Hematocrit – the percentage of RBCs out of the total blood volume
Chapter 17: Blood 5
Components of Whole Blood
Figure 17.1
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)
Chapter 17: Blood 6
Physical Characteristics and Volume
Blood is a sticky, opaque fluid with a metallic taste
Color varies from scarlet (oxygen-rich) to dark red (oxygen-poor)
The pH of blood is 7.35–7.45
Temperature is 38C, slightly higher than “normal” body temperature
Blood accounts for approximately 8% of body weight
Average volume of blood is 5–6 L for males, and 4–5 L for females
Chapter 17: Blood 7
Functions of Blood
Blood performs a number of functions dealing with:
Substance distribution
Regulation of blood levels of particular substances
Body protection
Chapter 17: Blood 8
Distribution
Blood transports:
Oxygen from the lungs and nutrients from the digestive tract
Metabolic wastes from cells to the lungs and kidneys for elimination
Hormones from endocrine glands to target organs
Chapter 17: Blood 9
Regulation
Blood maintains:
Appropriate body temperature by absorbing and distributing heat
Normal pH in body tissues using buffer systems
Adequate fluid volume in the circulatory system
Chapter 17: Blood 10
Protection
Blood prevents blood loss by:
Activating plasma proteins and platelets
Initiating clot formation when a vessel is broken
Blood prevents infection by:
Synthesizing and utilizing antibodies
Activating complement proteins
Activating WBCs to defend the body against foreign invaders
Chapter 17: Blood 11
Blood Plasma
Blood plasma contains over 100 solutes, including:
Proteins – albumin, globulins, clotting proteins, and others
Nonprotein nitrogenous substances – lactic acid, urea, creatinine
Organic nutrients – glucose, carbohydrates, amino acids
Electrolytes – sodium, potassium, calcium, chloride, bicarbonate
Respiratory gases – oxygen and carbon dioxide
Chapter 17: Blood 12
Formed Elements
Erythrocytes, leukocytes, and platelets make up the formed elements
Only WBCs are complete cells
RBCs have no nuclei or organelles
platelets are just cell fragments
Most formed elements survive in the bloodstream for only a few days
Most blood cells do not divide but are renewed by cells in bone marrow
Chapter 17: Blood 13
Erythrocytes (RBCs)
Biconcave discs, anucleate, essentially no organelles
Filled with hemoglobin (Hb), a protein that functions in gas transport
Contain the plasma membrane protein spectrin and other proteins that:
Give erythrocytes their flexibility
Allow them to change shape as necessary
Chapter 17: Blood 14
Erythrocytes (RBCs)
Figure 17.3
Chapter 17: Blood 15
Erythrocytes (RBCs)
Erythrocytes are an example of the complementarity of structure and function
Structural characteristics contribute to its gas transport function
Biconcave shape that has a huge surface area relative to volume
Discounting water content, erythrocytes are more than 97% hemoglobin
ATP is generated anaerobically, so the erythrocytes do not consume the oxygen they transport
Chapter 17: Blood 16
Erythrocyte Function
Erythrocytes are dedicated to respiratory gas transport
Hemoglobin reversibly binds with oxygen and most oxygen in the blood is bound to hemoglobin
Hemoglobin is composed of the protein globin, made up of two alpha and two beta chains, each bound to a heme group
Each heme group bears an atom of iron, which can bind to one oxygen molecule
Each hemoglobin molecule can transport four molecules of oxygen
Chapter 17: Blood 17
Structure of Hemoglobin
Figure 17.4
Chapter 17: Blood 18
Hemoglobin
Oxyhemoglobin – hemoglobin bound to oxygen
Oxygen loading takes place in the lungs
Deoxyhemoglobin – hemoglobin after oxygen diffuses into tissues (reduced Hb)
Carbaminohemoglobin – hemoglobin bound to carbon dioxide
Carbon dioxide loading takes place in the tissues
InterActive Physiology®: Respiratory System: Gas TransportPLAYPLAY
Chapter 17: Blood 19
Production of Erythrocytes
Hematopoiesis – blood cell formation
Hematopoiesis occurs in the red bone marrow of the:
Axial skeleton and girdles
Epiphyses of the humerus and femur
Hemocytoblasts give rise to all formed elements
Chapter 17: Blood 20
Production of Erythrocytes: Erythropoiesis
A hemocytoblast is transformed into a committed cell called the proerythroblast
Proerythroblasts develop into early erythroblasts
The developmental pathway consists of three phases
Phase 1 – ribosome synthesis in early erythroblasts
Phase 2 – hemoglobin accumulation in late erythroblasts and normoblasts
Phase 3 – ejection of the nucleus from normoblasts and formation of reticulocytes
Reticulocytes then become mature erythrocytes
Chapter 17: Blood 21
Production of Erythrocytes: Erythropoiesis
Figure 17.5
Chapter 17: Blood 22
Circulating erythrocytes – the number remains constant and reflects a balance between RBC production and destruction
Too few red blood cells leads to tissue hypoxia
Too many red blood cells causes undesirable blood viscosity
Erythropoiesis is hormonally controlled and depends on adequate supplies of iron, amino acids, and B vitamins
Regulation and Requirements for Erythropoiesis
Chapter 17: Blood 23
Hormonal Control of Erythropoiesis
Erythropoietin (EPO) release by the kidneys is triggered by:
Hypoxia due to decreased RBCs
Decreased oxygen availability
Increased tissue demand for oxygen
Enhanced erythropoiesis increases the:
RBC count in circulating blood
Oxygen carrying ability of the blood
Chapter 17: Blood 24
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
Chapter 17: Blood 25
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
Chapter 17: Blood 26
Fate and Destruction of Erythrocytes
The life span of an erythrocyte is 100–120 days
Old erythrocytes become rigid and fragile, and their hemoglobin begins to degenerate
Dying erythrocytes are engulfed by macrophages
Heme and globin are separated and the iron is salvaged for reuse
Chapter 17: Blood 27
Fate and Destruction of Erythrocytes
Heme is degraded to a yellow pigment called bilirubin
The liver secretes bilirubin into the intestines as bile
The intestines metabolize it into urobilinogen
This degraded pigment leaves the body in feces, in a pigment called stercobilin
Globin is metabolized into amino acids and is released into the circulation
Hb released into the blood is captured by haptoglobin and phgocytized
Chapter 17: Blood 28
Recycling of Hemoglobin
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)
Chapter 17: Blood 29
Life Cycle of Red Blood Cells
Figure 17.7
Chapter 17: Blood 30Figure 17.7
Chapter 17: Blood 31
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
Chapter 17: Blood 32
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
Chapter 17: Blood 33
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; application of Nascobal
Anemia: Decreased Hemoglobin Content
Chapter 17: Blood 34
Anemia: Abnormal Hemoglobin
Thalassemias – absent or faulty globin chain in hemoglobin
Erythrocytes are thin, delicate, and deficient in hemoglobin
Chapter 17: Blood 35
Severe, chronic anemias (such as thalassemias and sickle cell anemia) can increase the bone marrow response to form RBC's. This drive for erythropoiesis may increase the mass of marrow and lead to increase in marrow in places, such as the skull seen here, that is not normally found. Such an increase in marrow in skull may lead to "frontal bossing" or forehead prominence because of the skull shape change.
Chapter 17: Blood 36
Anemia: Abnormal Hemoglobin Sickle-cell anemia – results from a defective gene coding
for an abnormal hemoglobin called hemoglobin S (HbS)
HbS has a single amino acid substitution in the beta chain
This defect causes RBCs to become sickle-shaped in low oxygen situations
Chapter 17: Blood 37
Anemia: Abnormal Hemoglobin
Chapter 17: Blood 38
Polycythemia
Polycythemia – excess RBCs that increase blood viscosity
Three main polycythemias are:
Polycythemia vera
Secondary polycythemia
Blood doping
Chapter 17: Blood 39
17Blood
(WBC and Homeostasis)
Chapter 17: Blood 40
Leukocytes (WBCs)
Leukocytes, the only blood components that are complete cells:
Are less numerous than RBCs
Make up 1% of the total blood volume
Can leave capillaries via diapedesis
Move through tissue spaces
Leukocytosis – WBC count over 11,000 per cubic millimeter
Normal response to bacterial or viral invasion
Chapter 17: Blood 41
Granulocytes
Granulocytes – neutrophils, eosinophils, and basophils
Contain cytoplasmic granules that stain specifically (acidic, basic, or both) with Wright’s stain
Are larger and usually shorter-lived than RBCs
Have lobed nuclei
Are all phagocytic cells
Chapter 17: Blood 42
Account for 0.5% of WBCs and:
Have U- or S-shaped nuclei with two or three conspicuous constrictions
Are functionally similar to mast cells
Have large, purplish-black (basophilic) granules that contain histamine
Histamine – inflammatory chemical that acts as a vasodilator and attracts other WBCs (antihistamines counter this effect)
Basophils
Chapter 17: Blood 43
Eosinophils account for 1–4% of WBCs
Have red-staining, bilobed nuclei connected via a broad band of nuclear material
Have red to crimson (acidophilic) large, coarse, lysosome-like granules
Lead the body’s counterattack against parasitic worms
Lessen the severity of allergies by phagocytizing immune complexes
Eosinophils
Chapter 17: Blood 44
Neutrophils have two types of granules that:
Take up both acidic and basic dyes
Give the cytoplasm a lilac color
Contain peroxidases, hydrolytic enzymes, and defensins (antibiotic-like proteins)
Neutrophils are our body’s bacteria slayers
Neutrophils
Chapter 17: Blood 45
Agranulocytes – lymphocytes and monocytes:
Lack visible cytoplasmic granules
Are similar structurally, but are functionally distinct and unrelated cell types
Have spherical (lymphocytes) or kidney-shaped (monocytes) nuclei
Agranulocytes
Chapter 17: Blood 46
Account for 25% or more of WBCs and:
Have large, dark-purple, circular nuclei with a thin rim of blue cytoplasm
Are found mostly enmeshed in lymphoid tissue (some circulate in the blood)
There are two types of lymphocytes: T cells and B cells
T cells function in the immune response
B cells give rise to plasma cells, which produce antibodies
Lymphocytes
Chapter 17: Blood 47
Monocytes account for 4–8% of leukocytes
They are the largest leukocytes
They have abundant pale-blue cytoplasms
They have purple-staining, U- or kidney-shaped nuclei
They leave the circulation, enter tissue, and differentiate into macrophages
Monocytes
Chapter 17: Blood 48
Macrophages:
Are highly mobile and actively phagocytic
Activate lymphocytes to mount an immune response
Monocytes
Chapter 17: Blood 49
Summary of Formed Elements
Table 17.2
Chapter 17: Blood 50
Summary of Formed Elements
Table 17.2
Chapter 17: Blood 51
Leukopoiesis is hormonally stimulated by two families of cytokines (hematopoietic factors) – interleukins and colony-stimulating factors (CSFs)
Interleukins are numbered (e.g., IL-1, IL-2)
CSFs are named for the WBCs they stimulate (e.g., granulocyte-CSF stimulates granulocytes)
Macrophages and T cells are the most important sources of cytokines
Many hematopoietic hormones are used clinically to stimulate bone marrow
Production of Leukocytes
Chapter 17: Blood 52
All leukocytes originate from hemocytoblasts
Hemocytoblasts differentiate into
myeloid stem cells
become myeloblasts or monoblasts
Myeloblasts develop into eosinophils, neutrophils, and basophils
Monoblasts develop into monocytes
lymphoid stem cells
Lymphoid stem cells become lymphoblasts
Lymphoblasts develop into lymphocytes
Formation of Leukocytes
Chapter 17: Blood 53
Formation of Leukocytes
Figure 17.11
Chapter 17: Blood 54
Leukemia refers to cancerous conditions involving white blood cells
Leukemias are named according to the abnormal white blood cells involved
Myelocytic leukemia – involves myelocytes
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
Chapter 17: Blood 55
Immature white blood cells are found in the bloodstream in all leukemias
Bone marrow becomes totally occupied with cancerous leukocytes
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
Chapter 17: Blood 56
Platelets are fragments of megakaryocytes with a blue-staining outer region and a purple granular center
Their granules contain serotonin, Ca2+, enzymes, ADP, and platelet-derived growth factor (PDGF)
Platelets function in the clotting mechanism by forming a temporary plug that helps seal breaks in blood vessels
Platelets (not involved in clotting) are kept inactive by NO and prostaglandin I2
Platelets
Chapter 17: Blood 57
Genesis of Platelets
The stem cell for platelets is the hemocytoblast
The sequential developmental pathway is hemocytoblast, megakaryoblast, promegakaryocyte, megakaryocyte, and platelets
Figure 17.12
Chapter 17: Blood 58
Hematopoiesis
Chapter 17: Blood 59
A series of reactions designed for stoppage of bleeding
During hemostasis, three phases occur in rapid sequence
Vascular spasms
Platelet plug formation
Coagulation (blood clotting)
Hemostasis
Chapter 17: Blood 60
Vascular Spasm
Immediate vasoconstriction in response to injury
Chapter 17: Blood 61
Platelets do not stick to each other or to the endothelial lining of blood vessels
Upon damage to blood vessel endothelium (which exposes collagen) platelets:
1. With the help of von Willebrand factor (VWF) adhere to collagen
Are stimulated by thromboxane A2
2. Stick to exposed collagen fibers and form a platelet plug
3. Release serotonin and ADP, which attract still more platelets
The platelet plug is limited to the immediate area of injury by PGI2
Platelet Plug Formation
Chapter 17: Blood 62
Platelet Adhesion
Platelets stick to exposed collagen underlying damaged endothelial cells in vessel wall
Chapter 17: Blood 63
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.
Chapter 17: Blood 64
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.
Chapter 17: Blood 65
A set of reactions in which blood is transformed from a liquid to a gel
Coagulation follows intrinsic and extrinsic pathways
The final three steps of this series of reactions are:
1. Prothrombin activator is formed
2. Prothrombin is converted into thrombin
3. Thrombin catalyzes the joining of fibrinogen into a fibrin mesh
Coagulation
Chapter 17: Blood 66
May be initiated by either the intrinsic or extrinsic pathway
Triggered by tissue-damaging events
Involves a series of procoagulants
Each pathway cascades toward factor X
Once factor X has been activated, it complexes with calcium ions, PF3, and factor V to form prothrombin activator
Coagulation Phase 1: Two Pathways to Prothrombin Activator
Chapter 17: Blood 67
Prothrombin activator catalyzes the transformation of prothrombin to the active enzyme thrombin
Coagulation Phase 2: Pathway to Thrombin
Chapter 17: Blood 68
Thrombin catalyzes the polymerization of fibrinogen into fibrin
Insoluble fibrin strands form the structural basis of a clot
Fibrin causes plasma to become a gel-like trap
Fibrin in the presence of calcium ions activates factor XIII that:
Cross-links fibrin
Strengthens and stabilizes the clot
Coagulation Phase 3: Common Pathways to the Fibrin Mesh
Chapter 17: Blood 69
Overview of the Clotting Cascade
Prothrombinase is formed by either:
1. intrinsic pathway
2. extrinsic pathway.
Final common pathway produces fibrin threads.
Chapter 17: Blood 70
Extrinsic Pathway
Damaged tissues leak tissue factor (thromboplastin) into bloodstream.
In the presence of Ca+2, clotting factor X combines with factor V to form prothrombinase.
Prothrombinase forms in seconds.
Chapter 17: Blood 71
Intrinsic Pathway
Activation occurs.
endothelium is damaged & platelets come in contact with collagen of blood vessel wall
platelets damaged & release phospholipids
Substances involved: Ca+2 and clotting factors XII, X and V.
Requires several minutes for reaction to occur.
Chapter 17: Blood 72
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
Chapter 17: Blood 73
Clot retraction
stabilization of the clot by squeezing serum from the fibrin strands
Repair
Platelet-derived growth factor (PDGF) stimulates rebuilding of blood vessel wall
Fibroblasts form a connective tissue patch
Stimulated by vascular endothelial growth factor (VEGF), endothelial cells multiply and restore the endothelial lining
Clot Retraction and Repair
Chapter 17: Blood 74
Two homeostatic mechanisms prevent clots from becoming large
Swift removal of clotting factors
Inhibition of activated clotting factors
Factors Limiting Clot Growth or Formation
Chapter 17: Blood 75
Fibrin acts as an anticoagulant by:
binding thrombin
preventing its:
Positive feedback effects of coagulation
Ability to speed up the production of prothrombin activator via factor V
Acceleration of the intrinsic pathway by activating platelets
Thrombin not absorbed to fibrin is inactivated by antithrombin III
Heparin, another anticoagulant, also inhibits thrombin activity
Inhibition of Clotting Factors
Chapter 17: Blood 76
Unnecessary clotting is prevented by the structural and molecular characteristics of endothelial cells lining the blood vessels
Platelet adhesion is prevented by:
The smooth endothelial lining of blood vessels
Heparin and PGI2 secreted by endothelial cells
Vitamin E quinone, a potent anticoagulant
Factors Preventing Undesirable Clotting
Chapter 17: Blood 77
Thrombus – a clot that develops and persists in an unbroken blood vessel
Thrombi can block circulation, resulting in tissue death
Coronary thrombosis – thrombus in blood vessel of the heart
Hemostasis Disorders:Thromboembolytic Conditions
Chapter 17: Blood 78
Embolus – a thrombus freely floating in the blood stream
Pulmonary emboli can impair the ability of the body to obtain oxygen
Cerebral emboli can cause strokes
Hemostasis Disorders:Thromboembolytic Conditions
Chapter 17: Blood 79
Substances used to prevent undesirable clots include:
Aspirin – an antiprostaglandin that inhibits thromboxane A2
Heparin – an anticoagulant used clinically for pre- and postoperative cardiac care
Warfarin – used for those prone to atrial fibrillation
Prevention of Undesirable Clots
Chapter 17: Blood 80
Disseminated Intravascular Coagulation (DIC): widespread clotting in intact blood vessels
Residual blood cannot clot
Blockage of blood flow and severe bleeding follows
Most common as:
A complication of pregnancy
A result of septicemia or incompatible blood transfusions
Hemostasis Disorders
Chapter 17: Blood 81
Thrombocytopenia – condition where the number of circulating platelets is deficient
Patients show petechiae (small purple blotches on the skin) due to spontaneous, widespread hemorrhage
Caused by suppression or destruction of bone marrow (e.g., malignancy, radiation)
Platelet counts less than 50,000/mm3 is diagnostic for this condition
Treated with whole blood transfusions
Hemostasis Disorders: Bleeding Disorders
Chapter 17: Blood 82
Inability to synthesize procoagulants by the liver results in severe bleeding disorders
Causes can range from vitamin K deficiency to hepatitis and cirrhosis
Inability to absorb fat can lead to vitamin K deficiencies as it is a fat-soluble substance and is absorbed along with fat
Liver disease can also prevent the liver from producing bile, which is required for fat and vitamin K absorption
Hemostasis Disorders: Bleeding Disorders
Chapter 17: Blood 83
Hemophilias – hereditary bleeding disorders caused by lack of clotting factors
Hemophilia A – most common type (83% of all cases) due to a deficiency of factor VIII
Hemophilia B – results from a deficiency of factor IX
Hemophilia C – mild type, caused by a deficiency of factor XI
Hemostasis Disorders: Bleeding Disorders
Chapter 17: Blood 84
Symptoms include prolonged bleeding and painful and disabled joints
Treatment is with blood transfusions and the injection of missing factors
Hemostasis Disorders: Bleeding Disorders
Chapter 17: Blood 85
Whole blood transfusions are used:
When blood loss is substantial
In treating thrombocytopenia
Packed red cells (cells with plasma removed) are used to treat anemia
Blood Transfusions
Chapter 17: Blood 86
RBC membranes have glycoprotein antigens on their external surfaces
These antigens are:
Unique to the individual
Recognized as foreign if transfused into another individual
Promoters of agglutination and are referred to as agglutinogens
Presence or absence of these antigens is used to classify blood groups
Human Blood Groups
Chapter 17: Blood 87
Humans have 30 varieties of naturally occurring RBC antigens
The antigens of the ABO and Rh blood groups cause vigorous transfusion reactions when they are improperly transfused
Other blood groups (M, N, Dufy, Kell, and Lewis) are mainly used for legalities
Blood Groups
Chapter 17: Blood 88
The ABO blood groups consists of:
Two antigens (A and B) on the surface of the RBCs
Two antibodies in the plasma (anti-A and anti-B)
An individual with ABO blood may have various types of antigens and spontaneously preformed antibodies
Agglutinogens and their corresponding antibodies cannot be mixed without serious hemolytic reactions
ABO Blood Groups
Chapter 17: Blood 89
ABO Blood Groups
Table 17.4
Chapter 17: Blood 90
There are eight different Rh agglutinogens, three of which (C, D, and E) are common
Presence of the Rh agglutinogens on RBCs is indicated as Rh+
Anti-Rh antibodies are not spontaneously formed in Rh– individuals
However, if an Rh– individual receives Rh+ blood, anti-Rh antibodies form
A second exposure to Rh+ blood will result in a typical transfusion reaction
Rh Blood Groups
Chapter 17: Blood 91
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
Chapter 17: Blood 92
Transfusion reactions occur when mismatched blood is infused
Donor’s cells are attacked by the recipient’s plasma agglutinins causing:
Diminished oxygen-carrying capacity
Clumped cells that impede blood flow
Ruptured RBCs that release free hemoglobin into the bloodstream
Circulating hemoglobin precipitates in the kidneys and causes renal failure
Transfusion Reactions
Chapter 17: Blood 93
Blood Typing
When serum containing anti-A or anti-B agglutinins is added to blood, agglutination will occur between the agglutinin and the corresponding agglutinogens
Positive reactions indicate agglutination
Chapter 17: Blood 94
Blood Typing
Blood type being tested RBC agglutinogens Serum Reaction
Anti-A Anti-B
AB A and B + +
B B – +
A A + –
O None – –
Chapter 17: Blood 95
When shock is imminent from low blood volume, volume must be replaced
Plasma or plasma expanders can be administered
Plasma Volume Expanders
Chapter 17: Blood 96
Plasma expanders
Have osmotic properties that directly increase fluid volume
Are used when plasma is not available
Examples: purified human serum, albumin, plasminate, and dextran
Isotonic saline solution can also be used to replace lost blood volume
Plasma Volume Expanders
Chapter 17: Blood 97
Laboratory examination of blood can assess an individual’s state of health
Microscopic examination:
Variations in size and shape of RBCs – predictions of anemias
Type and number of WBCs – diagnostic of various diseases
Chemical analysis can provide a comprehensive picture of one’s general health status in relation to normal values
Diagnostic Blood Tests