17 Blood

Percent of blood volume that is RBCs 47% ± 5% for males Figure 17.1 1 Withdraw blood and place in tube. 2 Centrifuge the blood sample. Plasma • 55% of whole blood • Least dense component Buffy coat • Leukocytes and platelets • <1% of whole blood Erythrocytes • 45% of whole blood • Most dense component Formed elements 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 38C ~8% of body weight Average volume: 5–6 L for males, and 4–5 L for females

Functions of Blood 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 Regulation of Body temperature by absorbing and distributing heat Normal pH using buffers Adequate fluid volume in the circulatory system

Functions of Blood 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: a fluid connective tissue composed of 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

Platelets Erythrocytes Monocyte Neutrophils Lymphocyte Figure 17.2

RBCs or Erythrocytes

Erythrocytes Biconcave discs, anucleate, essentially no organelles Filled with hemoglobin (Hb) for gas transport

2.5 µm Side view (cut) 7.5 µm Top view Figure 17.3

Structural characteristics contribute to gas transport 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!

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

(a) Hemoglobin consists of globin (two alpha and two beta polypeptide b Globin chains Heme group a Globin chains (a) Hemoglobin consists of globin (two alpha and two beta polypeptide chains) and four heme groups. (b) Iron-containing heme pigment. Figure 17.4

O2 unloading in the tissues 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 (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.

Developmental pathway Stem cell Committed cell Developmental pathway Phase 1 Ribosome synthesis Phase 2 Hemoglobin accumulation Phase 3 Ejection of nucleus Proerythro- blast Early erythroblast Late erythroblast Reticulo- cyte Erythro- cyte Hemocytoblast Normoblast Figure 17.5

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

Hormonal Control of Erythropoiesis 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)

Hormonal Control of Erythropoiesis 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

1 5 4 2 3 IMBALANCE Homeostasis: Normal blood oxygen levels Stimulus: Hypoxia (low blood O2- carrying ability) due to • Decreased RBC count • Decreased amount of hemoglobin • Decreased availability of O2 5 O2- carrying ability of blood increases. IMBALANCE Enhanced erythropoiesis increases RBC count. 4 Kidney (and liver to a smaller extent) releases erythropoietin. 2 3 Erythropoietin stimulates red bone marrow. Figure 17.6, step 5

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 stimulate kidneys to produce erythropoietin. 1 Figure 17.7, step 1

Low O2 levels in blood stimulate kidneys to produce erythropoietin. 1 Erythropoietin levels rise in blood. 2 Figure 17.7, step 2

Low O2 levels in blood stimulate kidneys to produce erythropoietin. 1 Erythropoietin levels rise in blood. 2 Erythropoietin and necessary raw materials in blood promote erythropoiesis in red bone marrow. 3 Figure 17.7, step 3

Low O2 levels in blood stimulate kidneys to produce erythropoietin. 1 Erythropoietin levels rise in blood. 2 Erythropoietin and necessary raw materials in blood promote erythropoiesis in red bone marrow. 3 New erythrocytes enter bloodstream; function about 120 days. 4 Figure 17.7, step 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

blood cells are engulfed by macrophages of liver, spleen, and bone Aged and damaged red blood cells are engulfed by macrophages of liver, spleen, and bone marrow; the hemoglobin is broken down. 5 Hemoglobin Heme Globin Bilirubin Iron stored as ferritin, hemosiderin Amino acids Bilirubin is picked up from blood by liver, secreted into intestine in bile, metabolized to stercobilin by bacteria, and excreted in feces. Circulation Figure 17.7, step 5

blood cells are engulfed by macrophages of liver, spleen, and bone Aged and damaged red blood cells are engulfed by macrophages of liver, spleen, and bone marrow; the hemoglobin is broken down. 5 Hemoglobin Heme Globin Bilirubin Iron stored as ferritin, hemosiderin Amino acids Iron is bound to transferrin and released to blood from liver as needed for erythropoiesis. Bilirubin is picked up from blood by liver, secreted into intestine in bile, metabolized to stercobilin by bacteria, and excreted in feces. Circulation Food nutrients, including amino acids, Fe, B12, and folic acid, are absorbed from intestine and enter blood. Raw materials are made available in blood for erythrocyte synthesis. 6 Figure 17.7, step 6

Figure 17.7 Low O2 levels in blood stimulate kidneys to produce erythropoietin. 1 Erythropoietin levels rise in blood. 2 Erythropoietin and necessary raw materials in blood promote erythropoiesis in red bone marrow. 3 New erythrocytes enter bloodstream; function about 120 days. 4 Aged and damaged red blood cells are engulfed by macrophages of liver, spleen, and bone marrow; the hemoglobin is broken down. 5 Hemoglobin Heme Globin Bilirubin Iron stored as ferritin, hemosiderin Amino acids Iron is bound to transferrin and released to blood from liver as needed for erythropoiesis. Bilirubin is picked up from blood by liver, secreted into intestine in bile, metabolized to stercobilin by bacteria, and excreted in feces. Circulation Food nutrients, including amino acids, Fe, B12, and folic acid, are absorbed from intestine and enter blood. Raw materials are made available in blood for erythrocyte synthesis. 6 Figure 17.7

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

Insufficient erythrocytes Causes of Anemia Insufficient erythrocytes Hemorrhagic anemia: acute or chronic loss of blood Hemolytic anemia: RBCs rupture prematurely Aplastic anemia: destruction or inhibition of red bone marrow

Low hemoglobin content Causes of Anemia 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 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

(a) Normal erythrocyte has normal hemoglobin amino acid sequence in the beta chain. 1 2 3 4 5 6 7 146 (b) Sickled erythrocyte results from a single amino acid change in the beta chain of hemoglobin. 1 2 3 4 5 6 7 146 Figure 17.8

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

Make up <1% of total blood volume 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

Differential WBC count (All total 4800 – 10,800/l) Formed elements Platelets Granulocytes Neutrophils (50 – 70%) Leukocytes Eosinophils (2 – 4%) Basophils (0.5 – 1%) Erythrocytes Agranulocytes Lymphocytes (25 – 45%) Monocytes (3 – 8%) Figure 17.9

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

Large, purplish-black (basophilic) granules contain histamine 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

(a) Neutrophil; multilobed nucleus (b) Eosinophil; bilobed nucleus, red cytoplasmic granules (c) Basophil; bilobed nucleus, purplish-black cytoplasmic granules Figure 17.10 (a-c)

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

Leave circulation, enter tissues, and differentiate into macrophages 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

(d) Small lymphocyte; large spherical nucleus (e) Monocyte; kidney-shaped nucleus Figure 17.10d, e

Table 17.2 (1 of 2)

Stimulated by chemical messengers from bone marrow and mature WBCs 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

Figure 17.11 Stem cells Hemocytoblast Myeloid stem cell Lymphoid stem cell Committed cells Myeloblast Myeloblast Myeloblast Monoblast Lymphoblast Developmental pathway Promyelocyte Promyelocyte Promyelocyte Promonocyte Prolymphocyte Eosinophilic myelocyte Basophilic myelocyte Neutrophilic myelocyte Eosinophilic band cells Basophilic band cells Neutrophilic band cells Eosinophils Basophils Neutrophils Monocytes Lymphocytes (a) (b) (c) (d) (e) Agranular leukocytes Some become Granular leukocytes Some become Figure 17.11

Leukocyte Disorders Leukopenia Leukemias 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

Developmental pathway Stem cell Developmental pathway Hemocyto- blast Promegakaryocyte Megakaryoblast Megakaryocyte Platelets Figure 17.12

Hemostasis

Fast series of reactions for stoppage of bleeding Hemostasis Fast series of reactions for stoppage of bleeding Vascular spasm Platelet plug formation Coagulation (blood clotting)

Vasoconstriction of damaged blood vessel Triggers Vascular Spasm Vasoconstriction of damaged blood vessel Triggers Direct injury Chemicals released by endothelial cells and platelets Pain reflexes

• Smooth muscle contracts, causing vasoconstriction. Step Vascular spasm 1 • Smooth muscle contracts, causing vasoconstriction. Step Platelet plug formation 2 • Injury to lining of vessel exposes collagen fibers; platelets adhere. Collagen fibers • Platelets release chemicals that make nearby platelets sticky; platelet plug forms. Platelets Step Coagulation 3 • Fibrin forms a mesh that traps red blood cells and platelets, forming the clot. Fibrin Figure 17.13

Coagulation A set of reactions in which blood is transformed from a liquid to a gel Reinforces the platelet plug with fibrin threads

Coagulation

Three phases of coagulation Prothrombin activator is formed (intrinsic and extrinsic pathways) Prothrombin is converted into thrombin Thrombin catalyzes the joining of fibrinogen to form a fibrin mesh

PF3 released by aggregated platelets Prothrombin activator Phase 1 Intrinsic pathway Extrinsic pathway Vessel endothelium ruptures, exposing underlying tissues (e.g., collagen) Tissue cell trauma exposes blood to Platelets cling and their surfaces provide sites for mobilization of factors Tissue factor (TF) XII Ca2+ XIIa XI VII XIa VIIa IX Ca2+ IXa PF3 released by aggregated platelets VIII VIIIa IXa/VIIIa complex TF/VIIa complex X Xa Ca2+ V PF3 Va Prothrombin activator Figure 17.14 (1 of 2)

Phase 2 Phase 3 Prothrombin activator Prothrombin (II) Thrombin (IIa) Fibrinogen (I) (soluble) Fibrin (insoluble polymer) Ca2+ XIII XIIIa Cross-linked fibrin mesh Figure 17.14 (2 of 2)

CLOTTING PATHWAYS Measured by PT/INR Intrinsic Pathway: Blood trauma (turbulence and viscosity) or collagen and blood contact. Drugs: Warfarin, ASA, Vitamin-E, EFA’s Extrinsic Pathway: Damage outside of blood vessels. Measured by: PTT Factors 2-7-9-10 Drugs: Heparin PROTHROMBIN ACTIVATOR made up of V&X: Started by X alone and V becomes active with + feedback

Figure 17.15

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

Thrombocytopenia: deficient number of circulating platelets 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

Impaired liver function 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

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

agglutinates with both sera) Blood being tested Figure 17.16 Serum Anti-A RBCs Anti-B Type AB (contains agglutinogens A and B; agglutinates with both sera) Blood being tested Type A (contains agglutinogen A; agglutinates with anti-A) Type B (contains agglutinogen B; agglutinates with anti-B) Type O (contains no agglutinogens; does not agglutinate with either serum)

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!!!

Capillaries, arteries, veins Veins, capillaries, arteries Which of the following comprise a logical sequence of vessels as blood exits the heart? Capillaries, arteries, veins Veins, capillaries, arteries Arteries, capillaries, veins Arteries, veins, capillaries Answer: c. Arteries, capillaries, veins

After centrifuging, of the listed blood components, which contains the components of immune function? Plasma Buffy coat Erythrocytes Hematocrit Answer: b. Buffy coat

maintenance of plasma osmotic pressure buffering changes in plasma pH The major function of the most common plasma protein, albumin, is __________. maintenance of plasma osmotic pressure buffering changes in plasma pH fighting foreign invaders both a and b Answer: d. both a and b

Red blood cells lack mitochondria. Red blood cells don’t divide. 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? Red blood cells lack mitochondria. Red blood cells don’t divide. Red blood cells are biconcave discs. Red blood cells contain myoglobin. Answer: c. Red blood cells are biconcave discs.

Each hemoglobin can transport ________ oxygen atoms. 4 40 400 4000 Answer: a. 4

Oxygen binds to the _______ portion of hemoglobin. oxyhemoglobin iron atom amino acid Answer: c. iron atom

An increased white blood cell count An increase in energy level A patient with low iron levels would experience which of the following symptoms? An increased white blood cell count An increase in energy level An increase in fatigue A decreased white blood cell count Answer: c. An increase in fatigue

A hematopoietic stem cell will give rise to __________. erythrocytes leukocytes platelets all of the above Answer: d. all of the above

Predict the outcome of an overdose of the hormone erythropoietin. The blood viscosity increases to levels that may induce heart attacks or strokes. The oxygen-carrying capacity remains unchanged despite elevated red blood cell counts. Red blood cell counts remain unchanged, but the number of reticulocytes increases. Blood viscosity levels decrease while oxygen-carrying capacity increases. Answer: a. The blood viscosity increases to levels that may induce heart attacks or strokes.

Blood levels of oxygen would remain depressed for the duration. What response would you expect after traveling to high altitude for two weeks? Blood levels of oxygen would remain depressed for the duration. A surge in iron release from the liver would occur. The kidneys would secrete elevated amounts of erythropoietin. There would be no change in blood composition. Answer: c. The kidneys would secrete elevated amounts of erythropoietin.

would have reduced blood iron levels If a patient has pernicious anemia, the inability of the body to absorb vitamin B12, the patient __________. would have reduced blood iron levels would have a decreased number of red blood cells would have increased levels of hemoglobin would not experience any effects on red blood cells Answer: b. would have a decreased number of red blood cells

Which of the following statements is true regarding the mechanism controlling movement of white blood cells into damaged areas? 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. Capillaries break open, flooding a damaged area with white blood cells. The damaged tissues synthesize their own white blood cells. None of the statements are true. Answer: 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.

An elevated neutrophil count would be indicative of ________. an allergic reaction a cancer an acute bacterial infection a parasitic infection Answer: c. an acute bacterial infection

Antihistamines counter the actions of which white blood cells? Neutrophils Lymphocytes Basophils Eosinophils Answer: c. Basophils

Leukemia is a general descriptor for which of the following disorders? An abnormally low white blood cell count Overproduction of abnormal leukocytes Elevated counts of normal neutrophils Overproduction of abnormal erythrocytes Answer: b. Overproduction of abnormal leukocytes

A __________ is the progenitor of platelets. thrombopoietin thrombocyte megakaryocyte thrombocytoblast Answer: c. megakaryocyte

Why don’t platelets form plugs in undamaged vessels? Platelets aren’t formed until vessel damage occurs. Only contact of platelets with exposed collagen fibers and von Willebrand factor causes them to be sticky and form plugs. Plugs do form, but are removed by macrophages. Platelets don’t form plugs, it is the megakaryocytes that form the plugs. Answer: b. Only contact of platelets with exposed collagen fibers and von Willebrand factor causes them to be sticky and form plugs.

prothrombin activator serotonin Activation of the extrinsic pathway of coagulation requires exposure of the blood to _________. collagen tissue factor III prothrombin activator serotonin Answer: b. tissue factor III

Rapid blood flow washes away and dilutes activated clotting factors. Why doesn’t a clot fill the entire vasculature system once it has started forming? Rapid blood flow washes away and dilutes activated clotting factors. Thrombin is inactivated by antithrombin III if it enters the general circulation. Both a and b occur. Neither a nor b occurs. Answer: c. Both a and b occur.

An oral heparin medication might be prescribed for a patient who: is at risk for embolism (clots that spontaneously form and wedge in blood vessels). has thrombocytopenia. is a hemophiliac. has a deficiency in a clotting factor. Answer: a. is at risk for embolism (clots that spontaneously form and wedge in blood vessels).

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? Some type O cells possess B agglutinogens on their surface. The Rh factor would cross-react. Blood transfusions can only occur within the same blood group. The type O blood may have high enough levels of anti-A antibodies that could cross-react with the recipient’s cells. Answer: d. The type O blood may have high enough levels of anti-A antibodies that could cross-react with the recipient’s cells.