Human Anatomy and Physiology

Eleventh Edition

Chapter 17
Blood
Diagrams have Alt-tags
17.1 Functions of Blood
• Functions include
– Transport
§ Delivering O2 and nutrients to body cells
§ Transporting metabolic wastes to lungs and kidneys for elimination
§ Transporting hormones from endocrine organs to target organs
– Regulation
§ Maintaining body temperature by absorbing and distributing heat
§ Maintaining normal pH using buffers; alkaline reserve of bicarbonate ions
§ Maintaining adequate fluid volume in circulatory system
– Protection
§ Preventing blood loss
– Plasma proteins and platelets in blood initiate clot formation
§ Preventing infection
– Agents of immunity are carried in blood
• Antibodies
• Complement proteins
• White blood cells
17.2 Composition of Blood
• Blood is the only fluid tissue in body

• Type of connective tissue

– Matrix is nonliving fluid called plasma
– Cells are living blood cells called formed elements
§ Cells are suspended in plasma
§ Formed elements
– Erythrocytes (red blood cells, or RBCs)
– Leukocytes (white blood cells, or WBCs)
– Platelets

• Spun tube of blood yields three layers:

– Erythrocytes on bottom (~45% of whole blood)
§ Hematocrit: percent of blood volume that is RBCs
– Normal values:
• Males: 47% ± 5%
• Females: 42% ± 5%
– WBCs and platelets in Buffy coat (< 1%)
§ Thin, whitish layer between RBCs and plasma layers
– Plasma on top (~55%)
The Major Components of Whole Blood

Figure 17.1 The major components of whole blood.

Physical Characteristics and Volume
• Blood is a sticky, opaque fluid with metallic taste

• Color varies with O2 content

– High O2 levels show a scarlet red
– Low O2 levels show a dark red

• pH 7.35–7.45

• Makes up ~8% of body weight

• Average volume:
– Males: 5–6 L
– Females: 4–5 L
Blood Plasma
• Blood plasma is straw-colored sticky fluid
– About 90% water

• Over 100 dissolved solutes

– Nutrients, gases, hormones, wastes, proteins, inorganic ions
– Plasma proteins are most abundant solutes
§ Remain in blood; not taken up by cells
§ Proteins produced mostly by liver
§ Albumin: makes up 60% of plasma proteins
– Functions as carrier of other molecules, as blood buffer, and contributes
to plasma osmotic pressure
Table 17.1-1 Composition of Plasma

Table 17.1 Composition of Plasma.

Formed Elements
• Formed elements are RBCs, WBCs, and platelets

• Only WBCs are complete cells

– RBCs have no nuclei or other organelles
– Platelets are cell fragments

• Most formed elements survive in bloodstream only few days

• Most blood cells originate in bone marrow and do not divide

Blood Cells

Figure 17.2 Blood cells.

Function of Erythrocytes
• RBCs are dedicated to respiratory gas transport

• Hemoglobin binds reversibly with oxygen

• Normal values: Males 13–18g/100ml; Females: 12–16 g/100ml

• Hemoglobin consists of red heme pigment bound to the protein globin

– Globin is composed of four polypeptide chains
§ Two alpha and two beta chains
– A heme pigment is bonded to each globin chain
§ Gives blood red color
§ Each heme’s central iron atom binds one O2
Function of Erythrocytes
• Each Hb molecule can transport four O2

• Each RBC contains 250 million Hb molecules

• O2 loading in lungs
– Produces oxyhemoglobin (ruby red)

• O2 unloading in tissues
– Produces deoxyhemoglobin, or reduced hemoglobin (dark red)

• CO2 loading in tissues

– 20% of CO2 in blood binds to Hb, producing carbaminohemoglobin
Production of Erythrocytes
• Hematopoiesis: formation of all blood cells
• Occurs in red bone marrow; composed of reticular connective tissue and blood
sinusoids
– In adult, found in axial skeleton, girdles, and proximal epiphyses of humerus and
femur
• Hematopoietic stem cells (hemocytoblasts)
– Stem cell that gives rise to all formed elements
– Hormones and growth factors push cell toward specific pathway of blood cell
development
– Committed cells cannot change
• New blood cells enter blood sinusoids
Erythropoiesis: Formation of Red Blood Cells

Figure 17.5 Erythropoiesis: formation of red blood cells.

Regulation and Requirements of
Erythropoiesis
• Too few RBCs lead to tissue hypoxia

• Too many RBCs increase blood viscosity

• > 2 million RBCs are made per second

• Balance between RBC production and destruction depends on:

– Hormonal controls
– Dietary requirements
Regulation and Requirements of
Erythropoiesis
• Hormonal control
– Erythropoietin (EPO): hormone that stimulates formation of RBCs
§ Always small amount of EPO in blood to maintain basal rate
§ Released by kidneys (some from liver) in response to hypoxia
– At low O2 levels, oxygen-sensitive enzymes in kidney cells cannot
degrade hypoxia-inducible factor (HIF)
– HIF can accumulate, which triggers synthesis of EPO
– Causes of hypoxia:
§ Decreased RBC numbers due to hemorrhage or increased destruction
§ Insufficient hemoglobin per RBC (example: iron deficiency)
§ Reduced availability of O2 (example: high altitudes or lung problems such as
pneumonia)
– Too many erythrocytes or high oxygen levels in blood inhibit EPO production
– EPO causes erythrocytes to mature faster
§ Testosterone enhances EPO production, resulting in higher RBC counts in
males
Erythropoietin (EPO) Mechanism for
Regulating Erythropoiesis

Figure 17.6 Erythropoietin (EPO) mechanism for regulating erythropoiesis.

Clinical – Homeostatic Imbalance 17.1
• Some athletes abuse artificial EPO
– Use of EPO increases hematocrit, which allows athlete to increase stamina and
performance

• Dangerous consequences:
– EPO can increase hematocrit from 45% up to even 65%, with dehydration
concentrating blood even more
– Blood becomes like sludge and can cause clotting, stroke, or heart failure
Regulation and Requirements of
Erythropoiesis
• Dietary requirements for erythropoiesis
– Amino acids, lipids, and carbohydrates
– Iron: available from diet
§ 65% of iron is found in hemoglobin, with the rest in liver, spleen, and bone
marrow
§ Free iron ions are toxic so iron is bound with proteins:
– Stored in cells as ferritin and hemosiderin
– Transported in blood bound to protein transferrin
– Vitamin B12 and folic acid are necessary for DNA synthesis for rapidly dividing cells
such as developing RBCs
Fate and Destruction of Erythrocytes
• Life span: 100–120 days

• RBCs are anucleate, so cannot synthesize new proteins, or grow or divide

• Old RBCs become fragile, and Hb begins to degenerate

• Can get trapped in smaller circulatory channels, especially in spleen

• Macrophages in spleen engulf and breakdown dying RBCs

• RBC breakdown: heme, iron, and globin are separated

– Iron binds to ferridin or hemosiderin and is stored for reuse
– Heme is degraded to yellow pigment bilirubin
§ Liver secretes bilirubin (in bile) into intestines, where it is degraded to pigment
urobilinogen
– Urobilinogen is transformed into brown pigment stercobilin that leaves
body in feces
– Globin is metabolized into amino acids
§ Released into circulation
Erythrocyte Disorders
• Most erythrocyte disorders are classified as either anemia or polycythemia

• Anemia
– Blood has abnormally low O2-carrying capacity that is too low to support normal
metabolism
– Sign of problem rather than disease itself
– Symptoms: fatigue, pallor, dyspnea, and chills
– Three groups based on cause
§ Blood loss
§ Not enough RBCs produced
§ Too many RBCs being destroyed
Erythrocyte Disorders
• Anemia (cont.)
– Blood loss
§ Hemorrhagic anemia
– Rapid blood loss (example: severe wound)
– Treated by blood replacement
§ Chronic hemorrhagic anemia
– Slight but persistent blood loss
• Example: hemorrhoids, bleeding ulcer
– Primary problem must be treated to stop blood loss
– Not enough RBCs being produced
§ Iron-deficiency anemia
– Can be caused by hemorrhagic anemia, but also by low iron intake or
impaired absorption
– RBCs produced are called microcytes
• Small, pale in color
• Cannot synthesize hemoglobin because there is a lack of iron
– Treatment: iron supplements
Erythrocyte Disorders
• Anemia (cont.)
– Not enough RBCs being produced (cont.)
§ Pernicious anemia
– Autoimmune disease that destroys stomach mucosa that produces
intrinsic factor
– Intrinsic factor needed to absorb B12
– B12 is needed to help RBCs divide
– Without B12 RBCs enlarge but cannot divide, resulting in large
macrocytes
– Treatment: B12 injections or nasal gel
– Can also be caused by low dietary intake of B12
• Can be a problem for vegetarians
§ Renal anemia
– Caused by lack of EPO
– Often accompanies renal disease
• Kidneys cannot produce enough EPO
– Treatment: synthetic EPO
Erythrocyte Disorders
• Anemia (cont.)
– Not enough RBCs being produced (cont.)
§ Aplastic anemia
– Destruction or inhibition of red bone marrow
– Can be caused by drugs, chemicals, radiation, or viruses
• Usually cause is unknown
– All formed element cell lines are affected
• Results in anemia as well as clotting and immunity defects
– Treatment: short-term with transfusions, long-term with transplanted stem
cells
– Too many RBCs destroyed:
§ Premature lysis of RBCs
– Referred to as hemolytic anemias
§ Can be caused by:
– Incompatible transfusions or infections
– Hemoglobin abnormalities: usually genetic disorder resulting in abnormal
globin
• Thalassemias
• Sickle-cell anemia
Erythrocyte Disorders
• Anemia (cont.)
– Too many RBCs destroyed:
§ Thalassemias
– Typically found in people of Mediterranean ancestry
– One globin chain is absent or faulty
– RBCs are thin, delicate, and deficient in hemoglobin
– Many subtypes that range in severity from mild to extremely severe
• Very severe cases may require monthly blood transfusions
§ Sickle-cell anemia
– Hemoglobin S: mutated hemoglobin
• Only 1 amino acid is wrong in a globin beta chain of 146 amino
acids
– RBCs become crescent shaped when O2 levels are low
• Example: during exercise
– Misshaped RBCs rupture easily and block small vessels
• Results in poor O2 delivery and pain
Erythrocyte Disorders
• Anemia (cont.)
– Too many RBCs destroyed:
• Sickle-cell anemia (cont.)
– Prevalent in black people of the African malarial belt and their
descendants
– Possible benefit: people with sickle cell do not contract malaria
• Kills 1 million each year
• Individuals with two copies of Hb-S can develop sickle-cell anemia
• Individuals with only one copy have milder disease and better
chance of surviving malaria
– Treatment: acute crisis treated with transfusions; inhaled nitric oxide
– Prevention of sickling:
• Hydroxyurea induces formation of fetal hemoglobin (which does not
sickle)
• Stem cell transplants
• Gene therapy
• Nitric oxide for vasodilation
Sickle-Cell Anemia

Figure 17.8 Sickle-cell anemia.

Erythrocyte Disorders
• Polycythemia
– Abnormal excess of RBCs; increases blood viscosity, causing sluggish blood flow
– Polycythemia vera: Bone marrow cancer leading to excess RBCs
§ Hematocrit may go as high as 80%
§ Treatment: therapeutic phlebotomy
– Secondary polycythemia: caused by low O2 levels (example: high altitude) or
increased EPO production
– Blood doping: athletes remove, store, and reinfuse RBCs before an event to
increase O2 levels for stamina
General Structure and Functional
Characteristics
• Leukocytes, or WBCs, are only formed element that is complete cell with nuclei and
organelles

• Make up <1% of total blood volume

– 4800 to 10,800 WBCs per µl blood

• Function in defense against disease

– Can leave capillaries via diapedesis
– Move through tissue spaces by amoeboid motion and positive chemotaxis
• Leukocytosis: WBC count over 11,000 per μl
• Increase is a normal response to infection
• Leukocytes grouped into two major categories:
– Granulocytes: contain visible cytoplasmic granules (neutrophils, eosinophils,
basophils)
– Agranulocytes: do not contain visible cytoplasmic granules (lymphocytes,
monocytes)
• Mnemonic to remember decreasing abundance in blood: Never let monkeys eat
bananas (neutrophils, lymphocytes, monocytes, eosinophils, basophils)
Types and Relative Percentages of
Leukocytes in Normal Blood

Figure 17.9 Types and relative percentages of leukocytes in normal blood.

Leukocytes

Figure 17.10 Leukocytes.

Granulocytes
• Granulocytes: three types
– Neutrophils, eosinophils, basophils

• Larger and shorter-lived than RBCs

• Contain lobed, rather than circular, nuclei

• Cytoplasmic granules stain specifically with Wright’s stain

• All are phagocytic to some degree

 Granulocytes
• Neutrophils
– Most numerous WBCs
§ Account for 50–70% of WBCs
– About twice the size of RBCs
– Granules stain with both acid and basic dyes
– Granules contain either hydrolytic enzymes or
antimicrobial proteins, defensins
– Also called polymorphonuclear leukocytes (PMNs or
polys) because nucleus is lobular
§ Cell has anywhere from three to six lobes
– Very phagocytic
§ Referred to as “bacteria slayers”
§ Kill microbes by process called respiratory
burst
– Cell synthesizes potent oxidizing
substances (bleach or hydrogen peroxide)
– Defensin granules merge with phagosome
§ Form “spears” that pierce holes in membrane of
ingested microbe
Granulocytes
• Eosinophils
– Account for 2–4% of all leukocytes
– Nucleus has two lobes connected by a broad
band; resembles ear muffs
– Red-staining granules contain digestive
enzymes
§ Release enzymes on large parasitic
worms, digesting their surface
– Also play role in allergies and asthma, as well
as immune response modulators
Granulocytes
• Basophils
– Rarest WBCs, accounting for only 0.5–1% of
leukocytes
– Nucleus deep purple with one to two
constrictions
– Large, purplish black (basophilic) granules
contain histamine
§ Histamine: inflammatory chemical that acts
as vasodilator and attracts WBCs to
inflamed sites
– Are functionally similar to mast cells
Agranulocytes
• Agranulocytes lack visible cytoplasmic granules

• Two types: lymphocytes and monocytes

• Both have spherical or kidney-shaped nuclei

Agranulocytes
• Lymphocytes
– Second most numerous WBC, accounts for 25%
– Large, dark purple, circular nuclei with thin rim of
blue cytoplasm
– Mostly found in lymphoid tissue (example: lymph
nodes, spleen), but a few circulate in blood
– Crucial to immunity
– Two types of lymphocytes
§ T lymphocytes (T cells) act against virus-
infected cells and tumor cells
§ B lymphocytes (B cells) give rise to
plasma cells, which produce antibodies
Agranulocytes
• Monocytes
– Largest of all leukocytes; 3–8% of all WBCs
– Abundant pale blue cytoplasm
– Dark purple-staining, U- or kidney-shaped nuclei
– Leave circulation, enter tissues, and differentiate
into macrophages
§ Actively phagocytic cells; crucial against
viruses, intracellular bacterial parasites, and
chronic infections
– Activate lymphocytes to mount an immune
response
Production and Life Span of Leukocytes

• Agranulocyte production:
– Monocytes: derived from myeloid line
§ Monoblast → promonocyte → monocyte
§ Share common precursor with neutrophils
§ Can live for several months
– Lymphocytes: derived from lymphoid line
§ T lymphocyte precursors give rise to immature T lymphocytes that mature in
thymus
§ B lymphocyte precursors give rise to immature B lymphocytes that mature
within bone marrow
§ Lymphocytes live from a few hours to decades
Leukocyte Disorders
• Leukemias
– Cancerous condition involving overproduction of abnormal WBCs
§ Usually involve clones of single abnormal cell
– Named according to abnormal WBC clone involved
§ Myeloid leukemia involves myeloblast descendants
§ Lymphocytic leukemia involves lymphocytes
– Acute (quickly advancing) leukemia derives from stem cells
§ Primarily affects children
– Chronic (slowly advancing) leukemia involves proliferation of later cell stages
§ More prevalent in older people
– Without treatment, all leukemias are fatal
– Immature, nonfunctional WBCs flood bloodstream
– Cancerous cells fill red bone marrow, crowding out other cell lines
§ Leads to anemia and bleeding
– Death is usually from internal hemorrhage or overwhelming infections
– Treatments: irradiation, antileukemic drugs; stem cell transplants
Formation of Platelets

Figure 17.12 Formation of platelets.

Table 17.2 Summary of Formed Elements
of the Blood

Table 17.2 Summary of Formed Elements of the Blood.

17.6 Hemostasis
• Hemostasis: fast series of reactions for stoppage of bleeding

• Requires clotting factors and substances released by platelets and injured tissues

• Three steps involved

– Step 1: Vascular spasm
– Step 2: Platelet plug formation
– Step 3: Coagulation (blood clotting)
Step 1: Vascular Spasm
• Vessel responds to injury with vasoconstriction

• Vascular spams are triggered by:

– Direct injury to vascular smooth muscle
– Chemicals released by endothelial cells and platelets
– Pain reflexes

• Most effective in smaller blood vessels

• Can significantly reduce blood flow until other mechanisms can kick in
Step 2: Platelet Plug Formation
• Platelets stick to collagen fibers that are exposed when vessel is damaged
– Platelets do not stick to intact vessel walls because collagen is not exposed
– Also prostacyclins and nitric oxide secreted by endothelial cells act to prevent
platelet sticking

• von Willebrand factor helps to stabilize platelet-collagen adhesion

• When activated, platelets swell, become spiked and sticky, and release chemical
messengers:
– ADP causes more platelets to stick and release their contents
– Serotonin and thromboxane A2 enhance vascular spasm and platelet
aggregation

• Positive feedback cycle: as more platelets stick, they release more chemicals, which
cause more platelets to stick and release more chemicals

• Platelet plugs are fine for small vessel tears, but larger breaks in vessels need additional
step
Events of Hemostasis

Figure 17.13 Events of hemostasis.

Step 3: Coagulation
• Coagulation (blood clotting) reinforces platelet plug with fibrin threads
– Blood clots are effective in sealing larger vessel breaks

• Blood is transformed from liquid to gel

• Series of reactions use clotting factors (procoagulants), mostly plasma proteins

– Numbered I to XIII in order of discovery
– Vitamin K needed to synthesize four factors

• Coagulation occurs in three phases

• Phase 1: Two pathways to prothrombin activator

– Initiated by either intrinsic or extrinsic pathway (usually both)
§ Triggered by tissue-damaging events
§ Involves a series of procoagulants
§ Each pathway cascades toward and ends with the activation of factor X
– Factor X then complexes with Ca2+, PF3 (platelet factor 3), and factor V to form
prothrombin activator
Step 3: Coagulation
– Intrinsic pathway
§ Called “intrinsic” because clotting factors are present within the blood
§ Triggered by negatively charged surfaces such as activated platelets, collagen,
or even glass of a test tube
– Extrinsic pathway
§ Called “extrinsic” because factors needed for clotting are located outside blood
§ Triggered by exposure to tissue factor (TF); also called factor III
§ Bypasses several steps of intrinsic pathway, so faster pathway
The Intrinsic and Extrinsic Pathways of
Blood Clotting (Coagulation)

Figure 17.14 The intrinsic and extrinsic pathways of blood clotting (coagulation).
Step 3: Coagulation
• Phase 2: Pathway to thrombin
– Prothrombin activator catalyzes transformation of prothrombin to active enzyme
thrombin
Step 3: Coagulation
• Phase 3: Common pathway to the fibrin mesh
– Thrombin converts soluble fibrinogen to fibrin
– Fibrin strands form structural basis of clot
– Fibrin causes plasma to become a gel-like trap catching formed elements
– Thrombin (along with Ca2+) activates factor XIII (fibrin stabilizing factor), which:
§ Cross-links fibrin
§ Strengthens and stabilizes clot
– Anticoagulants: factors that normally dominate in blood to inhibit coagulation
Disorders of Hemostasis
• Thromboembolic conditions
– Thrombi and emboli
§ Thrombus: clot that develops and persists in unbroken blood vessel
– May block circulation, leading to tissue death
§ Embolus: thrombus freely floating in bloodstream
§ Embolism: embolus obstructing a vessel Example: pulmonary or cerebral
emboli
§ Risk factors: atherosclerosis, inflammation, slowly flowing blood or blood stasis
from immobility
– Anticoagulant drugs: used to prevent undesirable clotting
§ Aspirin: antiprostaglandin that inhibits
thromboxane A2; lowers heart attack incidence by 50%
§ Heparin: used clinically for pre- and postoperative cardiac care as well as to
prevent venous thrombosis
§ Warfarin and direct oral anticoagulants: reduce risk of stroke in patients prone
to atrial fibrillation in which blood pools in heart
– Interferes with action of vitamin K
Disorders of Hemostasis
• Bleeding disorders
– Thrombocytopenia: deficient number of circulating platelets
§ Petechiae appear as a result of spontaneous, widespread hemorrhage
§ Due to suppression or destruction of red bone marrow (examples: malignancy,
radiation, or drugs)
§ Platelet count <50,000/μl is diagnostic
§ Treatment: transfusion of concentrated platelets

• Figure 17.16 Petechiae.

Disorders of Hemostasis
• Bleeding disorders (cont.)
– Impaired liver function
§ Inability to synthesize procoagulants (clotting factors)
§ Causes include vitamin K deficiency, hepatitis, or cirrhosis
§ Liver disease can also prevent liver from producing bile, which is needed to
absorb fat and vitamin K
– Hemophilia
§ Includes several similar hereditary bleeding disorders
– Hemophilia A: most common type (77% of all cases) due to factor VIII
deficiency
– Hemophilia B: factor IX deficiency
– Hemophilia C: factor XI deficiency, milder
§ Symptoms include prolonged bleeding, especially into joint cavities
§ Treatment: injections of genetically engineered factors; has eliminated need for
plasma transfusion and risk of contracting hepatitis or HIV
17.7 Blood Transfusions
• Cardiovascular system minimizes effects of blood loss by:
1. reducing volume of affected blood vessels
2. stepping up production of RBCs

• Body can compensate for only so much blood loss

• Loss of 15–30% causes pallor and weakness

• Loss of more than 30% results in potentially fatal severe shock

Transfusing Red Blood Cells
• Whole-blood transfusions are used only when blood loss is rapid and substantial

• Infusions of packed red blood cells, or PRBCs (plasma and WBCs removed), are
preferred to restore oxygen-carrying capacity

• Blood banks usually separate donated blood into components; shelf life of blood is about
35 days

• Human blood groups of donated blood must be determined because transfusion

reactions can be fatal
– Blood typing determines groups

• Human blood groups

– RBC membranes bear different many antigens
§ Antigen: anything perceived as foreign that can generate an immune response
§ RBC antigens are referred to as agglutinogens because they promote
agglutination
– Mismatched transfused blood is perceived as foreign and may be agglutinated and
destroyed
§ Potentially fatal reaction
 Transfusing Red Blood Cells
• Human blood groups (cont.)
– Humans have at least 30 naturally occurring RBC antigens
– Presence or absence of each antigen is used to classify blood cells into different groups
– Some blood groups (MNS, Duffy, Kell, and Lewis) are only weak agglutinogens
§ Not usually typed unless patient will need several transfusions
– Antigens of ABO and Rh blood groups cause most vigorous transfusion reactions;
therefore, they are major groups typed
– ABO blood groups
§ Based on presence or absence of two agglutinogens (A and B) on surface of RBCs
– Type A has only A agglutinogen
– Type B has only B agglutinogen
– Type AB has both A and B agglutinogens
– Type O has neither A nor B agglutinogens
§ Blood may contain preformed anti-A or anti-B antibodies (agglutinins)
– Act against transfused RBCs with ABO antigens not present on recipient's
RBCs
§ Anti-A or anti-B form in blood at about 2 months of age, reaching adult levels by 8–
10 years of age
Table 17.4 ABO Blood Groups

Table 17.4 ABO Blood Groups.

Transfusing Red Blood Cells
– Rh blood groups
§ 52 named Rh agglutinogens (Rh factors)
§ C, D, and E are most common
§ Rh+ indicates presence of D antigen
– 85% Americans are Rh+
§ Anti-Rh antibodies are not spontaneously formed in Rh– individuals
– Anti−Rh antibodies form if Rh– individual receives Rh+ blood, or Rh– mom
is carrying Rh+ fetus
§ Second exposure to Rh+ blood will result in typical transfusion reaction
Clinical – Homeostatic Imbalance 17.3
• Hemolytic disease of newborn, also called erythroblastosis fetalis only occurs in Rh–
mom with Rh+ fetus
• First pregnancy: Rh– mom exposed to Rh+ blood of fetus during delivery; first baby born
healthy, but mother synthesizes anti-Rh antibodies
• Second pregnancy: Mom’s anti-Rh antibodies cross placenta and destroy RBCs of Rh+
baby
• Baby treated with prebirth transfusions and exchange transfusions after birth
• RhoGAM serum containing anti-Rh can prevent Rh– mother from becoming sensitized
Transfusing Red Blood Cells
• Transfusion reactions
– Occur if mismatched blood is infused
– Donor’s cells are attacked by recipient’s plasma agglutinins
§ Agglutinate and clog small vessels
§ Rupture and release hemoglobin into bloodstream
– Result in:
§ Diminished oxygen-carrying capacity
§ Decreased blood flow beyond blocked vessel
§ Hemoglobin in kidney tubules can lead to renal failure
– Symptoms: fever, chills, low blood pressure, rapid heartbeat, nausea, vomiting
– Treatment: preventing kidney damage with fluids and diuretics to wash out
hemoglobin
– Type O universal donor: no A or B antigens
– Type AB universal recipient: no anti-A or anti-B antibodies
§ Misleading as other agglutinogens that cause transfusion reactions must also
be considered
– Autologous transfusions: patient predonates own blood that is stored and
available if needed
Transfusing Red Blood Cells
• Blood typing
– Donor blood is mixed with antibodies against common agglutinogens
§ If agglutinogen is present, clumping of RBCs will occur
– Blood is typed for ABO and for Rh factor in same manner
– Cross matching: typing between specific donor and specific recipient
§ Mix recipient’s serum with donor RBCs
§ Mix recipient’s RBCs with donor serum
Blood Typing of ABO Blood Types

Figure 17.17 Blood typing of ABO blood types.

17.8 Diagnostic Blood Tests
• Examination of blood can yield information on persons health:
– Low hematocrit seen in cases of anemia
– Blood glucose tests check for diabetes
– Leukocytosis can signal infection

• Microscopic examination of blood can reveal any variations in size or shape of RBCs
– Abnormal size, shape, or color could indicate anemia

• Differential WBC count looks at relative proportions of each WBC

– Increases in specific WBC can help with diagnosis

• Prothrombin time and platelet counts assess hemostasis

• CMP (comprehensive medical panel): blood chemistry profile that checks various
blood chemical levels
– Abnormal results could indicate liver or kidney disorders

• Complete blood count (CBC) checks formed elements, hematocrit, hemoglobin