PowerPoint ® Lecture Slides prepared by Janice Meeking, Mount Royal College C H A P T E R Copyright © 2010 Pearson Education, Inc. 17 Blood

PowerPoint® Lecture Slides prepared by Janice Meeking, Mount Royal College

C H A P T E R

Copyright © 2010 Pearson Education, Inc.

17

Blood


Figure 17.1

1 Withdrawblood and placein tube.

2 Centrifuge theblood sample.

Plasma• 55% of whole blood• Least dense componentBuffy coat• Leukocytes and platelets• <1% of whole bloodErythrocytes• 45% of whole blood• Most dense component

Formedelements

• Hematocrit• Percent of blood volume that is RBCs • 47% ± 5% for males• 42% ± 5% for females


Physical Characteristics and Volume

•Sticky, opaque fluid

•Color scarlet to dark red

•pH 7.35–7.45

•38C

•~8% of body weight

•Average volume: 5–6 L for males, and 4–5 L for females


Functions of Blood

1. Distribution of

• O2 and nutrients to body cells

• Metabolic wastes to the lungs and kidneys for elimination

• Hormones from endocrine organs to target organs


Functions of Blood

2. Regulation of

• Body temperature by absorbing and distributing heat

• Normal pH using buffers

• Adequate fluid volume in the circulatory system


Functions of Blood

3. Protection against

• Blood loss

• Plasma proteins and platelets initiate clot formation

• Infection

• Antibodies

• Complement proteins (small proteins that amplify other immune cells ability to kill pathogens)

• WBCs defend against foreign invaders


Blood Composition

•Blood: a fluid connective tissue composed of

• Plasma

• Formed elements

•Erythrocytes (red blood cells, or RBCs)

•Leukocytes (white blood cells, or WBCs)

•Platelets


Blood Plasma

•90% water

•Proteins

•mostly produced by the liver

•60% albumin

•36% globulins

•4% fibrinogen


Blood Plasma

•Nitrogenous by-products of metabolism—lactic acid, urea, creatinine

•Nutrients—glucose, carbohydrates, amino acids

•Electrolytes—Na+, K+, Ca2+, Cl–, HCO3–

•Respiratory gases—O2 and CO2

•Hormones


Formed Elements (WBC, RBC, platelets)


Formed Elements

•Only WBCs are complete cells

•RBCs have no nuclei or organelles

•Platelets are cell fragments

•Most formed elements survive in the bloodstream for only a few days

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

Copyright © 2010 Pearson Education, Inc. Figure 17.2

Platelets

Neutrophils Lymphocyte

Erythrocytes Monocyte


RBCs or Erythrocytes


Erythrocytes

•Biconcave discs, anucleate, essentially no organelles

•Filled with hemoglobin (Hb) for gas transport


2.5 µm

7.5 µm

Side view (cut)

Top view


Erythrocytes

•Structural characteristics contribute to gas transport

• Biconcave shape—huge surface area relative to volume

• >97% hemoglobin (not counting water)

•No mitochondria; ATP production is anaerobic; no O2 is used in generation of ATP

•A great example of how structure and function work together!


Erythrocyte Function

•Hemoglobin structure

• Protein globin: two alpha and two beta chains

•Heme pigment bonded to each globin chain (4)

•Iron atom in each heme can bind to one O2 molecule; binds reversibly

•Each Hb molecule can transport four O2

•Normal Hb: 12-16 in women, 13-18 in men


Hemegroup

(a) Hemoglobin consists of globin (two alpha and two beta polypeptide chains) and four heme groups.

(b) Iron-containing heme pigment. Globin chains

Globin chains


Hemoglobin (Hb)

•O2 loading in the lungs

• Produces oxyhemoglobin (ruby red)

•O2 unloading in the tissues

• Produces deoxyhemoglobin or reduced hemoglobin (dark red)

•CO2 loading in the tissues

• Produces carbaminohemoglobin (carries 20% of CO2 in the blood)


Hematopoiesis

•Hematopoiesis (hemopoiesis): blood cell formation

• Formed in red marrow

•Red marrow is found mainly in the flat bones, such as pelvis, sternum, cranium, ribs, vertebrae, and scapula. Also in the spongy epiphyseal plates of long bones like the femur and humerus.


Stem cell

HemocytoblastProerythro-blast

Earlyerythroblast

Lateerythroblast Normoblast

Phase 1Ribosomesynthesis

Phase 2Hemoglobinaccumulation

Phase 3Ejection ofnucleus

Reticulo-cyte

Erythro-cyte

Committedcell

Developmental pathway


Regulation of Erythropoiesis

•Too few RBCs leads to tissue hypoxia

•Too many RBCs increases blood viscosity

•Balance between RBC production and destruction depends on

•Hormonal controls

• Adequate supplies of iron, amino acids, and B vitamins


Hormonal Control of Erythropoiesis

•Erythropoietin (EPO)

•Direct stimulus for erythropoiesis

•Released by the kidneys in response to hypoxia



•Causes of hypoxia

•Hemorrhage or increased RBC destruction reduces RBC numbers

• Insufficient hemoglobin (e.g., iron deficiency)

•Reduced availability of O2 (e.g., high altitudes)



•Effects of EPO

•More rapid maturation of committed bone marrow cells

• Increased circulating reticulocyte count in 1–2 days

•Testosterone also enhances EPO production, resulting in higher RBC counts in males

Copyright © 2010 Pearson Education, Inc. Figure 17.6, step 5

Kidney (and liver toa smaller extent)releaseserythropoietin. Erythropoietin

stimulates redbone marrow.

Enhancederythropoiesisincreases RBCcount.

O2- carryingability of bloodincreases.

Homeostasis: Normal blood oxygen levels

Stimulus:Hypoxia (low bloodO2- carrying ability)

due to• Decreased

RBC count• Decreased amount

of hemoglobin• Decreased

availability of O2

1

2

3

4

5

IMBALANCE

IMBALANCE


Dietary Requirements for Erythropoiesis

•Nutrients—amino acids, lipids, and carbohydrates

• Iron

• Stored in Hb (65%), the liver, spleen, and bone marrow

• Stored in cells as ferritin and hemosiderin

•Vitamin B12 and folic acid—necessary for DNA synthesis for cell division


Fate and Destruction of Erythrocytes

•Life span: 100–120 days

•Old RBCs become fragile, and Hb begins to degenerate

•Macrophages engulf dying RBCs in the spleen


Low O2 levels in blood stimulatekidneys to produce erythropoietin.1



Erythropoietin levels risein blood.2




Erythropoietin and necessaryraw materials in blood promoteerythropoiesis in red bone marrow.

3





3

New erythrocytesenter bloodstream;function about 120 days.

4


Fate and Destruction of Erythrocytes

•Heme and globin are separated

• Iron is salvaged for reuse

•Heme is degraded to yellow the pigment bilirubin

• Liver secretes bilirubin (in bile) into the intestines

•Degraded pigment leaves the body in feces as stercobilin

•Globin is metabolized into amino acids


Aged and damaged redblood cells are engulfed bymacrophages of liver,spleen, and bonemarrow; thehemoglobin isbroken down.

5 Hemoglobin

Aminoacids

GlobinHeme

Circulation

Iron storedas ferritin,hemosiderin

Bilirubin

Bilirubin is picked up from bloodby liver, secreted into intestine inbile, metabolized to stercobilin bybacteria, and excreted in feces.


Aged and damaged redblood cells are engulfed bymacrophages of liver,spleen, and bonemarrow; thehemoglobin isbroken down.

5

Raw materials aremade available in bloodfor erythrocyte synthesis.

6

Hemoglobin

Aminoacids

Globin

Iron is bound totransferrin and releasedto blood from liver asneeded for erythropoiesis.

Food nutrients,including amino acids,Fe, B12, and folic acid,are absorbed fromintestine and enterblood.

Heme

Circulation


Bilirubin



Low O2 levels in blood stimulate kidneys to produce erythropoietin.

1



3

Aged and damagedred blood cells areengulfed by macrophagesof liver, spleen, and bonemarrow; the hemoglobinis broken down.

5

New erythrocytesenter bloodstream;function about 120 days.

4

Raw materials aremade available in bloodfor erythrocyte synthesis.

6

Hemoglobin

Aminoacids

Globin

Iron is bound totransferrin and releasedto blood from liver asneeded for erythropoiesis.

Food nutrients,including amino acids,Fe, B12, and folic acid,are absorbed fromintestine and enterblood.

Heme

Circulation


Bilirubin



Erythrocyte Disorders

•Anemia: blood has abnormally low O2-carrying capacity

• A sign rather than a disease itself

• Accompanied by fatigue, paleness, shortness of breath, and chills


Causes of Anemia

1. Insufficient erythrocytes

• Hemorrhagic anemia: acute or chronic loss of blood

• Hemolytic anemia: RBCs rupture prematurely

• Aplastic anemia: destruction or inhibition of red bone marrow


Causes of Anemia

2. Low hemoglobin content

• Iron-deficiency anemia

• Secondary result of hemorrhagic anemia or

• Inadequate intake of iron-containing foods or

• Impaired iron absorption

• Heavy menstruation


Causes of Anemia

• Pernicious anemia

•Deficiency of vitamin B12

•Lack of intrinsic factor needed for absorption of B12

•Treated by intramuscular injection of B12 or application of Nascobal

•Common in elderly and those with GI disorders that cause malabsorption, like Crohn’s, IBD, etc.


Causes of Anemia

3. Abnormal hemoglobin

• Thalassemias

• Absent or faulty globin chain

• RBCs are thin, delicate, and deficient in hemoglobin


Causes of Anemia

• Sickle-cell anemia

•Defective gene codes for abnormal hemoglobin (HbS)

•Causes RBCs to become sickle shaped in low-oxygen situations


1 2 3 4 5 6 7 146

1 2 3 4 5 6 7 146

(a) Normal erythrocyte has normal hemoglobin amino acid sequence in the beta chain.

(b) Sickled erythrocyte results from a single amino acid change in the beta chain of hemoglobin.


Erythrocyte Disorders

•Polycythemia: excess of RBCs that increase blood viscosity

•Results from:

• Polycythemia vera—bone marrow cancer

• Secondary polycythemia—when less O2 is available (high altitude) or when EPO production increases


Leukocytes or WBCs


Leukocytes

•Make up <1% of total blood volume

•Can leave capillaries via diapedesis

•Move through tissue spaces by ameboid motion and positive chemotaxis (toward a chemical stimulus)

•Normal range: 4-11,000/mm3

•Leukocytosis: WBC count over 11,000/mm3

•Normal response to bacterial or viral invasion


Formedelements

Platelets

Leukocytes

Erythrocytes

DifferentialWBC count(All total 4800 –10,800/l)

Neutrophils (50 – 70%)

Lymphocytes (25 – 45%)

Eosinophils (2 – 4%)

Basophils (0.5 – 1%)

Monocytes (3 – 8%)

Agranulocytes

Granulocytes


Granulocytes

•Granulocytes: neutrophils, eosinophils, and basophils

•Cytoplasmic granules stain specifically with Wright’s stain

• Larger and shorter-lived than RBCs

• Lobed nuclei

• Phagocytic


Neutrophils

•Most numerous WBCs

•Aka polymorphonuclear leukocytes (PMNs)

•Granules contain hydrolytic enzymes or defensins

•Very phagocytic—“bacteria slayers”

•THE MARINES “FIRST ONES IN”


Eosinophils

•Red to crimson (acidophilic) coarse, lysosome-like granules

•Allergies and digest parasitic worms that are too large to be phagocytized


Basophils

•Rarest WBCs

•Large, purplish-black (basophilic) granules contain histamine

•Histamine: an inflammatory chemical that acts as a vasodilator and attracts other WBCs to inflamed sites

•Are functionally similar to mast cells

Copyright © 2010 Pearson Education, Inc. Figure 17.10 (a-c)

(a) Neutrophil; multilobed nucleus

(b) Eosinophil; bilobed nucleus, red cytoplasmic granules

(c) Basophil; bilobed nucleus, purplish-black cytoplasmic granules


Agranulocytes

•Agranulocytes: lymphocytes and monocytes

• Lack visible cytoplasmic granules

•Have spherical or kidney-shaped nuclei


Lymphocytes

•Large, dark-purple, circular nuclei with a thin rim of blue cytoplasm

•Mostly in lymphoid tissue; few circulate in the blood

•Crucial to immunity


Lymphocytes

•Two types

• T cells act against virus-infected cells and tumor cells (cell mediated immune response)

• B cells give rise to plasma cells, which produce antibodies (humoral immune response)


Monocytes

•The largest leukocytes

•Abundant pale-blue cytoplasm

•Dark purple-staining, U- or kidney-shaped nuclei


Monocytes

•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

Copyright © 2010 Pearson Education, Inc. Figure 17.10d, e

(d) Small lymphocyte; large spherical nucleus

(e) Monocyte; kidney-shaped nucleus

Copyright © 2010 Pearson Education, Inc. Table 17.2 (1 of 2)


Leukopoiesis

•Production of WBCs

•Stimulated by chemical messengers from bone marrow and mature WBCs

• Interleukins (e.g., IL-1, IL-2)

•All leukocytes originate from hemocytoblasts


Hemocytoblast

Myeloid stem cell Lymphoid stem cell

Myeloblast Myeloblast MonoblastMyeloblast Lymphoblast

Stem cells

Committedcells

Promyelocyte PromyelocytePromyelocyte Promonocyte Prolymphocyte

Eosinophilicmyelocyte

Neutrophilicmyelocyte

Basophilicmyelocyte

Eosinophilicband cells

Neutrophilicband cells

Basophilicband cells

Developmentalpathway

Eosinophils NeutrophilsBasophils

Granular leukocytes

(a) (b) (c) (d) (e)Monocytes Lymphocytes

Agranular leukocytes

Some becomeSomebecome


Leukocyte Disorders

•Leukopenia

• Abnormally low WBC count—drug/toxin induced

•Leukemias

• Cancerous conditions involving WBCs

• Named according to the abnormal WBC clone 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


Leukemia

•Bone marrow totally occupied with cancerous leukocytes

•Immature nonfunctional WBCs in the bloodstream

•Death caused by internal hemorrhage and overwhelming infections

•Treatments include irradiation, antileukemic drugs, and stem cell transplants


Platelets


Platelets

•Form a temporary platelet plug that helps seal breaks in blood vessels

•Circulating platelets are kept inactive and mobile by NO (nitric oxide) and prostacyclin from endothelial cells of blood vessels


Stem cell Developmental pathway

Hemocyto-blast Megakaryoblast

PromegakaryocyteMegakaryocyte Platelets


Hemostasis


Hemostasis

• Fast series of reactions for stoppage of bleeding

1. Vascular spasm

2. Platelet plug formation

3. Coagulation (blood clotting)


Vascular Spasm

•Vasoconstriction of damaged blood vessel

•Triggers

•Direct injury

•Chemicals released by endothelial cells and platelets

• Pain reflexes


Collagenfibers

Platelets

Fibrin

Step Vascular spasm• Smooth muscle contracts, causing vasoconstriction.

Step Platelet plugformation

• Injury to lining of vessel exposes collagen fibers; platelets adhere.

• Platelets release chemicals that make nearby platelets sticky; platelet plug forms.

Step Coagulation• Fibrin forms a mesh that traps red blood cells and platelets, forming the clot.

1

2

3


Coagulation

• A set of reactions in which blood is transformed from a liquid to a gel

• Reinforces the platelet plug with fibrin threads


Coagulation


Coagulation

• Three phases of coagulation

1. Prothrombin activator is formed (intrinsic and extrinsic pathways)

2. Prothrombin is converted into thrombin

3. Thrombin catalyzes the joining of fibrinogen to form a fibrin mesh

Copyright © 2010 Pearson Education, Inc. Figure 17.14 (1 of 2)

Vessel endothelium ruptures,exposing underlying tissues(e.g., collagen)

PF3

released byaggregated

platelets

XII

XI

IX

XIIa

Ca2+

Ca2+

XIa

IXa

Intrinsic pathwayPhase 1Tissue cell traumaexposes blood to

Platelets cling and theirsurfaces provide sites formobilization of factors

Extrinsic pathway

Tissue factor (TF)

VII

VIIa

VIII

VIIIa

Ca2+

X

Xa

Prothrombinactivator

PF3

TF/VIIa complexIXa/VIIIa complex

V

Va

Copyright © 2010 Pearson Education, Inc. Figure 17.14 (2 of 2)

Ca2+

Phase 2

Phase 3

Prothrombinactivator

Prothrombin (II)

Thrombin (IIa)

Fibrinogen (I)(soluble)

Fibrin(insolublepolymer) XIII

XIIIa

Cross-linkedfibrin mesh


CLOTTING PATHWAYS

Measured by: PTT

Drugs: Heparin

Measured by PT/INRDrugs: Warfarin, ASA, Vitamin-E, EFA’sFactor

s 2-7-9-10

PROTHROMBIN ACTIVATOR made up of V&X: Started by X alone and V becomes active with + feedback

Extrinsic Pathway: Damage outside of blood vessels.

Intrinsic Pathway:Blood trauma (turbulence and viscosity) or collagen and blood contact.



Clot Retraction

•Actin and myosin in platelets contract within 30–60 minutes

•Platelets pull on the fibrin strands, squeezing serum from the clot


Clot Repair

•Platelet-derived growth factor (PDGF) stimulates division of smooth muscle cells and fibroblasts to rebuild blood vessel wall

•Vascular endothelial growth factor (VEGF) stimulates endothelial cells to multiply and restore the endothelial lining


Fibrinolysis

•Begins within two days

•Plasminogen in clot is converted to plasmin by tissue plasminogen activator (tPA), factor XII and thrombin

•Plasmin is a fibrin-digesting enzyme


Factors Preventing Undesirable Clotting

•Platelet adhesion is prevented by

• Smooth endothelial lining of blood vessels

• Antithrombic substances nitric oxide and prostacyclin secreted by endothelial cells

• Vitamin E quinine, which acts as a potent anticoagulant


Disorders of Hemostasis

•Thromboembolytic disorders: undesirable clot formation

•Bleeding disorders: abnormalities that prevent normal clot formation


Thromboembolytic Conditions

•Thrombus: clot that develops and persists in an unbroken blood vessel

•May block circulation, leading to tissue death

•Embolus: a thrombus freely floating in the blood stream

• Pulmonary emboli impair the ability of the body to obtain oxygen

•Cerebral emboli can cause strokes


Thromboembolytic Conditions

• Prevented by

• Aspirin

•Antiprostaglandin that inhibits thromboxane A2

• Heparin

•Anticoagulant used clinically for pre- and postoperative cardiac care

• Warfarin

•Used for those prone to atrial fibrillation


Disseminated Intravascular Coagulation (DIC)

•Widespread clotting blocks intact blood vessels

•Severe bleeding occurs because residual blood unable to clot

•Most common in pregnancy, septicemia, or incompatible blood transfusions


Bleeding Disorders

•Thrombocytopenia: deficient number of circulating platelets

• Petechiae appear due to spontaneous, widespread hemorrhage

•Due to suppression or destruction of bone marrow (e.g., malignancy, radiation)

• Platelet count <50,000/mm3 is diagnostic

• Treated with transfusion of concentrated platelets


Bleeding Disorders

•Impaired liver function

• Inability to synthesize procoagulants

•Causes include vitamin K deficiency, hepatitis, and cirrhosis

• Liver disease can also prevent the liver from producing bile, impairing fat and vitamin K absorption


Bleeding Disorders

•Hemophilias include several similar hereditary bleeding disorders

• Hemophilia A: most common type (77% of all cases); due to a deficiency of factor VIII

• Hemophilia B: deficiency of factor IX

• Hemophilia C: mild type; deficiency of factor XI

•Symptoms include prolonged bleeding, especially into joint cavities

•Treated with plasma transfusions and injection of missing factors


Transfusions

•Whole-blood transfusions are used when blood loss is substantial

•Packed red cells (plasma removed) are used to restore oxygen-carrying capacity

•Transfusion of incompatible blood can be fatal


Blood Types


Blood Groups

•Humans have 30 varieties of naturally occurring RBC antigens

•Antigens of the ABO and Rh blood groups cause vigorous transfusion reactions

•Other blood groups (MNS, Duffy, Kell, and Lewis) are usually weak agglutinogens


ABO Blood Groups

•Types A, B, AB, and O

•Based on the presence or absence of two agglutinogens (A and B) on the surface of the RBCs

•Blood may contain anti-A or anti-B antibodies (agglutinins) that act against transfused RBCs with ABO antigens not normally present

•Anti-A or anti-B form in the blood at about 2 months of age

Copyright © 2010 Pearson Education, Inc. Table 17.4


Rh Blood Groups

•There are 45 different Rh agglutinogens (Rh factors)

•C, D, and E are most common

•Rh+ indicates presence of D

•Rh+ = 85% of the population

•Rh- = 15% of the population


Rh Blood Groups

•Anti-Rh antibodies are not spontaneously formed in Rh– individuals

•Anti-Rh antibodies form if an Rh– individual receives Rh+ blood

•A second exposure to Rh+ blood will result in a typical transfusion reaction


Homeostatic Imbalance: Hemolytic Disease of the Newborn

•Also called erythroblastosis fetalis

•Rh– mother becomes sensitized when exposure to Rh+ blood causes her body to synthesize anti-Rh antibodies

•Anti-Rh antibodies cross the placenta and destroy the RBCs of an Rh+ baby


Homeostatic Imbalance: Hemolytic Disease of the Newborn

•The baby can be treated with prebirth transfusions and exchange transfusions after birth

•RhoGAM serum containing anti-Rh can prevent the Rh– mother from becoming sensitized


ABO Blood Typing

Blood Type Being Tested

RBC Agglutinogens

Serum Reaction

Anti-A Anti-B

AB A and B + +

B B – +

A A + –

O None – –


SerumAnti-A

RBCs

Anti-B

Type AB (containsagglutinogens A and B;agglutinates with bothsera)

Blood being tested

Type A (containsagglutinogen A;agglutinates with anti-A)

Type B (containsagglutinogen B;agglutinates with anti-B)

Type O (contains noagglutinogens; does notagglutinate with eitherserum)


Restoring Blood Volume

•Death from shock may result from low blood volume

•Volume must be replaced immediately with

• Normal saline or multiple-electrolyte solution that mimics plasma electrolyte composition

• Plasma expanders (e.g., purified human serum albumin, hetastarch, and dextran)

•Mimic osmotic properties of albumin

•More expensive and may cause significant complications


Diagnostic Blood Tests

•Hematocrit

•Blood glucose tests

•Microscopic examination reveals variations in size and shape of RBCs, indications of anemias

•RBCs too big = macrocytic anemia (B12/folic acid deficiency, etc.)

•RBCs too small = microcytic anemia (iron deficiency, thalassemia, etc.)


Diagnostic Blood Tests

•Differential WBC count

•Prothrombin time (PTT) and platelet counts assess hemostasis

•SMAC (or CMP), a blood chemistry profile

•Complete blood count (CBC)


Developmental Aspects

•Fetal blood cells form in the fetal yolk sac, liver, and spleen

•Red bone marrow is the primary hematopoietic area by the seventh month

•Blood cells develop from mesenchymal cells called blood islands

•The fetus forms HbF, which has a higher affinity for O2 than hemoglobin A formed after birth


Developmental Aspects

•Blood diseases of aging

•Chronic leukemias, anemias, clotting disorders

•Usually precipitated by disorders of the heart, blood vessels, and immune system


QUESTIONS TO TEST WHAT YOU NOW KNOW!!!


Which of the following comprise a logical sequence of vessels as blood exits the heart?

A. Capillaries, arteries, veins

B. Veins, capillaries, arteries

C. Arteries, capillaries, veins

D. Arteries, veins, capillaries


After centrifuging, of the listed blood components, which contains the components of immune function?

A. Plasma

B. Buffy coat

C. Erythrocytes

D. Hematocrit


The major function of the most common plasma protein, albumin, is __________.

A. maintenance of plasma osmotic pressure

B. buffering changes in plasma pH

C. fighting foreign invaders

D. both a and b


Red blood cells are efficient oxygen transport cells. Of the following characteristics, which is the major contributor to the significant oxygen-carrying capacity of a red blood cell?

A. Red blood cells lack mitochondria.

B. Red blood cells don’t divide.

C. Red blood cells are biconcave discs.

D. Red blood cells contain myoglobin.


Each hemoglobin can transport ________ oxygen atoms.

A. 4

B. 40

C. 400

D. 4000


Oxygen binds to the _______ portion of hemoglobin.

A. globin

B. oxyhemoglobin

C. iron atom

D. amino acid


A patient with low iron levels would experience which of the following symptoms?

A. An increased white blood cell count

B. An increase in energy level

C. An increase in fatigue

D. A decreased white blood cell count


A hematopoietic stem cell will give rise to __________.

A. erythrocytes

B. leukocytes

C. platelets

D. all of the above


Predict the outcome of an overdose of the hormone erythropoietin.

A. The blood viscosity increases to levels that may induce heart attacks or strokes.

B. The oxygen-carrying capacity remains unchanged despite elevated red blood cell counts.

C. Red blood cell counts remain unchanged, but the number of reticulocytes increases.

D. Blood viscosity levels decrease while oxygen-carrying capacity increases.


What response would you expect after traveling to high altitude for two weeks?

A. Blood levels of oxygen would remain depressed for the duration.

B. A surge in iron release from the liver would occur.

C. The kidneys would secrete elevated amounts of erythropoietin.

D. There would be no change in blood composition.


If a patient has pernicious anemia, the inability of the body to absorb vitamin B12, the patient __________.

A. would have reduced blood iron levels

B. would have a decreased number of red blood cells

C. would have increased levels of hemoglobin

D. would not experience any effects on red blood cells


Which of the following statements is true regarding the mechanism controlling movement of white blood cells into damaged areas?A. White blood cells exit the capillary and move

through the tissue spaces with cytoplasmic extensions by following a trail of chemicals produced by other white blood cells.

B. Capillaries break open, flooding a damaged area with white blood cells.

C. The damaged tissues synthesize their own white blood cells.

D. None of the statements are true.


An elevated neutrophil count would be indicative of ________.

A. an allergic reaction

B. a cancer

C. an acute bacterial infection

D. a parasitic infection


Antihistamines counter the actions of which white blood cells?

A. Neutrophils

B. Lymphocytes

C. Basophils

D. Eosinophils


Leukemia is a general descriptor for which of the following disorders?

A. An abnormally low white blood cell count

B. Overproduction of abnormal leukocytes

C. Elevated counts of normal neutrophils

D. Overproduction of abnormal erythrocytes


A __________ is the progenitor of platelets.

A. thrombopoietin

B. thrombocyte

C. megakaryocyte

D. thrombocytoblast


Why don’t platelets form plugs in undamaged vessels?

A. Platelets aren’t formed until vessel damage occurs.

B. Only contact of platelets with exposed collagen fibers and von Willebrand factor causes them to be sticky and form plugs.

C. Plugs do form, but are removed by macrophages.

D. Platelets don’t form plugs, it is the megakaryocytes that form the plugs.


Activation of the extrinsic pathway of coagulation requires exposure of the blood to _________.

A. collagen

B. tissue factor III

C. prothrombin activator

D. serotonin


Why doesn’t a clot fill the entire vasculature system once it has started forming?

A. Rapid blood flow washes away and dilutes activated clotting factors.

B. Thrombin is inactivated by antithrombin III if it enters the general circulation.

C. Both a and b occur.

D. Neither a nor b occurs.


An oral heparin medication might be prescribed for a patient who:

A. is at risk for embolism (clots that spontaneously form and wedge in blood vessels).

B. has thrombocytopenia.

C. is a hemophiliac.

D. has a deficiency in a clotting factor.


Why is it possible for a person with type A negative blood to have a negative reaction when receiving a transfusion of whole type O negative blood?

A. Some type O cells possess B agglutinogens on their surface.

B. The Rh factor would cross-react.

C. Blood transfusions can only occur within the same blood group.

D. The type O blood may have high enough levels of anti-A antibodies that could cross-react with the recipient’s cells.

Documents

PowerPoint ® Lecture Slides prepared by Janice Meeking, Mount Royal College C H A P T E R Copyright © 2010 Pearson Education, Inc. 17 Blood