blood

vascular spasm

1. vascular spasm: when ❶❶ a blood vessel is injured and ❷❷ blood leaks into extracellular fluid, ​two immediate ​responses occur: ❸❸ vasoconstriction and increased tissue pressure. Both responses decrease the blood vessel diameter.

platete plug formation

2. plalete plug formation: When a vessel is injured, ❶❶ collagen fibers and chemicals in the vessel's tunica adventitia are exposed. The injured endothelial cells release a glycoprotein called von Willebrand factor (fahn VIL-uh-brant), or vWF, which ❷❷ binds to receptors on the surface of the platelets' plasma membranes. Together, the exposed collagen and vWF make the platelets sticky so they adhere to one another and the vessel wall. The binding of vWF and collagen to platelets triggers a series of events within platelets known collectively as platelet activation. Activated platelets release the contents of their granules—ATP, ADP, serotonin, calcium, clotting factors, and other chemicals—by exocytosis. ❸❸ Many of these factors attract and activate nearby platelets and cause them to clump together, or aggregate. Platelet aggregation forms the platelet plug. This plug seals the injured vessel temporarily, but the repair is short-lived without a molecular "glue" that can hold the platelets together.

Hemophilia

A hereditary disease where blood does not coagulate to stop bleeding. a medical condition in which the ability of the blood to clot is severely reduced, causing the sufferer to bleed severely from even a slight injury. The condition is typically caused by a hereditary lack of a coagulation factor, most often factor VIII.

List the specific formed elements and give a function for each. Also indicate the quantities of each.

Basophils (BAY-zoh-filz; "basic liking"), the least common leukocyte, make up less than 1% of total leukocytes in the blood. As implied by their name, basophils contain granules that take up the basic dye methylene blue, which stains them dark purple-blue. Note that the granules almost completely obscure the typically S-shaped nuclei in these cells. Basophils release chemicals from their granules that mediate inflammation. We discuss inflammation in the chapter on immunity

Luekemia

Blood cancer characterized by an increase in white blood cells

Explain the function of blood thinners and identify the conditions for which they are prescribed.

Blood thinners are medicines that help blood flow smoothly through your veins and arteries. They also keep blood clots from forming or getting bigger. They're used to treat some types of heart disease and heart defects, and other conditions that could raise your risk of getting dangerous clots.

DIC

Condition affecting the blood's ability to clot and stop bleeding. In disseminated intravascular coagulation, abnormal clumps of thickened blood (clots) form inside blood vessels. These abnormal clots use up the blood's clotting factors, which can lead to massive bleeding in other places. Causes include inflammation, infection, and cancer. Symptoms include blood clots and bleeding, possibly from many sites in the body. The goal is to treat the underlying cause and provide supportive care through intravenous fluids and blood transfusions.

Explain the consequences of being given an incorrect blood type during a transfusion.

During an ABO incompatibility reaction, the red blood cells inside your circulatory system break down. Blood clotting may occur throughout your body, shutting off the blood supply to vital organs or causing a stroke. Too much blood clotting can use up clotting factors and leave you at risk of excessive bleeding. Some of the products released from broken-down blood cells can cause kidney damage and possibly kidney failure. An ABO incompatibility reaction can be life-threatening unless your doctor successfully treats it right away. However, if you have a reaction and receive the correct treatment without delay, you should recover completely.

List the specific formed elements and give a function for each. Also indicate the quantities of each.

Neutrophils (noo-TROH-fills; "neutral liking") are the most common type of leukocyte, making up about 60% of total leukocytes in the blood. The neutrophils' granules take up both the acidic and basic dyes (hence the name neutrophil), staining their cytoplasm a light lilac color (see Figure 19.8). Their nuclei typically have three to five variably shaped lobes, which is the reason for their other name: polymorphonucleocytes (pah′- lee-mohr-foh-NOO-klee-oh-sytz; poly- = "many," morpho- = "shape"), sometimes shortened to PMNs or polys. Neutrophils are attracted to injured cells by chemicals released by the damaged cells, a process called chemotaxis (kee-moh-TAK-sis). This process occurs with any type of cellular injury, from trauma caused by stepping on a nail to infection by bacteria. When neutrophils reach the damaged tissue, they exit the blood and release the contents of their granules. These contents directly kill bacterial cells, enhance inflammation, and attract more neutrophils and leukocytes to the area. Neutrophils are also very active phagocytes that ingest and destroy bacterial cells.

Emboli

a blood clot, air bubble, piece of fatty deposit, or other object that has been carried in the bloodstream to lodge in a vessel and cause an embolism.

Thrombi

blood clots

multiple myeloma

cancer of plasma cells. The plasma cells are a type of white blood cell in the bone marrow. With this condition, a group of plasma cells becomes cancerous and multiplies. The disease can damage the bones, immune system, kidneys, and red blood cell count. Symptoms may not be present or may be non-specific, such as loss of appetite, bone pain, and fever. Treatments include medications, chemotherapy, corticosteroids, radiation, or a stem-cell transplant.

Define and predict normal values for a hematocrit for both men and women and explain why there is a notable difference.

erythrocytes average about 44% of the total blood volume, a value known as the hematocrit. The hematocrit is generally higher in males (40-50%) than in females (36-44%) due to males' typically larger body size and greater muscle and bone mass.

List the specific formed elements and give a function for each. Also indicate the quantities of each.

erythrocytes average about 44% of the total blood volume, a value known as the hematocrit. The hematocrit is generally higher in males (40-50%) than in females (36-44%) due to males' typically larger body size and greater muscle and bone mass. The primary function of erythrocytes is oxygen and carbon dioxide transport, at which they are extremely effective. The structure of erythrocytes enables them to carry out their vital tasks of gas transport

Differentiate the granulocytes from the agranulocytes.

granulocytes: Neutrophils, eosinophils, basophils agranulocyte: lymphocytes, monocytes

Describe or draw hemoglobin and identify the function of and the forms of hemoglobin within the RBC. Where specifically are the O2 and CO2 binding sites?

hemoglobin is a large protein that consists of four polypeptide subunits: two alpha (α) chains and two beta (β) chains. Each polypeptide is bound to an iron-containing compound called a heme group. The heme binds to oxygen (O2) in parts of the body where the oxygen level is high (such as the lungs), forming a structure called oxyhemoglobin (HbO2). Where the oxygen level is low, as in the tissues surrounding systemic capillaries, hemoglobin releases oxygen to become deoxyhemoglobin.

Relate jaundice and bilirubin to hemolysis.

hemolytic jaundice is a result of the accelerated breakdown of red blood cells, leading to an increased production of bilirubin

Explain the general pattern of the steps in the process of hematopoiesis that create all the formed elements.(Fig. 19.11)

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Define the following dyscrasias including but not limited to: sepsis, malaria, hemophilia, leukemia (myeloid and lymphoid) , thalassemias, emboli, thrombi, polycythemia, anemia (specifically pernicious, folate deficiency, iron-deficiency and sickle-cell anemia) multiple myeloma, mononucleosis and DIC.

sepsis: Sepsis occurs when chemicals released in the bloodstream to fight an infection trigger inflammation throughout the body. This can cause a cascade of changes that damage multiple organ systems, leading them to fail, sometimes even resulting in death. Symptoms include fever, difficulty breathing, low blood pressure, fast heart rate, and mental confusion. Treatment includes antibiotics and intravenous fluids.

List the specific formed elements and give a function for each. Also indicate the quantities of each.

the granules of eosinophils (ee′-oh-SIN-oh-filz; "eosin liking") take up the dye eosin and so appear red. Eosinophils are relatively rare leukocytes that account for fewer than 3% of total leukocytes in the blood. Their nuclei are bilobed, resembling a barbell, with two circular lobes connected by a thin strand of nuclear material. Eosinophils are involved in the body's response to infection with parasitic worms and in allergic reactions. Their granules contain substances that assist in these functions, including enzymes and toxins that are specific to parasites, as well as chemicals that mediate (bring about) inflammation. In addition, eosinophils are phagocytes and ingest foreign compounds that have been bound by proteins of the immune system.

Explain the role of the liver and Vitamin K in coagulation.

vitamin K is needed for the liver to produce protien C. Active protein C catalyzes the reactions that degrade factors Va and VIIIa. To become active, protein C requires another protein, called protein S.

Coagulation

3. coagulation: The glue that binds platelets, endothelial cells, and other formed elements together is a sticky, threadlike protein called fibrin (FY-brin). Fibrin converts the soft, liquid platelet plug into a more solid mass by the process of coagulation (koh-aeh′- gyoo-LAY-shun; coag- = "bring together"). We normally find fibrin in plasma and in platelets in its inactive form, fibrinogen (fy-BRIN-oh-jen). Fibrinogen is converted into fibrin by the coagulation cascade, a series of reactions that occur at the surface of the platelets and/or damaged endothelial cells The coagulation cascade relies on clotting factors. Most clotting factors are enzymes produced by the liver that circulate in the blood in their inactive forms. The steps of the intrinsic/contact activation pathway proceed as follows (see Figure 19.14, left side): ❶❶ Exposed collagen fibers activate factor XII. The negative charges on the surface of the exposed collagen proteins attract and bind a clotting protein in the plasma called factor XII. Activated factor XII is known as factor XIIa ("a" stands for "activated"). ❷❷ Factors XI and IX become activated. Factor XIIa is an enzyme that activates another clotting protein in the plasma, factor XI. Factor XIa, in turn, enzymatically activates another clotting protein, factor IX. ❸❸ Factors IXa and VIIIa along with calcium ions form an enzyme complex that activates factor X. The intrinsic/contact activation pathway ends by forming a large enzyme complex that consists of factor IXa, another protein called factor VIIIa, and calcium ions. This enzyme complex activates factor X, which becomes factor Xa. Note that calcium ions are required for the factors to associate with platelets in the platelet plug. The extrinsic/tissue factor pathway proceeds as shown in Figure 19.14 (right side): ❶❶ Subendothelial cells display tissue factor. Beneath the endothelium is a layer of loose connective tissue called the subendothelium. When an injury to the blood vessel penetrates the endothelium, it damages the subendothelium beneath it. Damaged subendothelial cells, mostly fibroblasts, display tissue factor in their plasma membranes. ❷❷ Tissue factor activates factor VII. The clotting protein factor VII circulates in the blood in its inactive form. When it comes into contact with tissue factor, it changes in structure and becomes the active form, factor VIIa. ❸❸ Factor VIIa, tissue factor, and calcium ions form an enzyme complex that activates factor X. Factor VIIa forms a complex with tissue factor and calcium ions that enzymatically cleaves factor X into factor Xa. The calcium ions play the same role here as they did in the intrinsic/contact activation pathway: They are required for the interaction of factors with platelets in the platelet plug. In the common pathway, fibrin is produced (see Figure 19.14): ❹❹ Factors Xa and Va, along with calcium ions, form prothrombin activator, which converts prothrombin into thrombin. The common pathway begins with the formation of prothrombin activator, a large enzyme complex that consists of factor Xa, another protein called factor Va, and calcium ions. Prothrombin activator converts the inactive protein prothrombin to the active enzyme Thrombin. ❺❺ Thrombin turns fibrinogen into fibrin, which "glues" the platelet plug together. In the final step of the coagulation cascade, thrombin acts on the inactive protein fibrinogen, which is both present in plasma and released by platelets. Thrombin converts fibrinogen into fibrin, its active form. The fibrin threads form a mesh that glues together the platelet plug, other formed elements, and damaged endothelial cells, sealing the damaged blood vessel.

clot retraction

4. clot retraction: As the coagulation cascade completes, the actin and myosin fibers in platelets contract via a mechanism similar to that of the actin and myosin fibers in a skeletal muscle fiber. This action, known as clot retraction, brings the edges of the wounded vessel closer together, much as sutures (or "stitches") do with the edges of a skin wound (Figure 19.15). Clot retraction also squeezes serum (SEER-um)—a fluid consisting of plasma minus the clotting proteins—out of the clot. (Think of it as squeezing water out of a wet rag.)

thrombolysis

5. thrombolysis: After a wound has healed, the blood clot is no longer necessary and it dissolves in a process called Thrombolysis (thrahm-BAH-luh-sis; -lysis = "split"). Thrombolysis begins with Fibrinolysis (fy′-brih-nuh-LY-sis)—the breakdown of the fibrin glue that was produced in the coagulation cascade. Compared to the formation of fibrin, its dissolution is relatively straightforward (Figure 19.16): ❶❶ Endothelial cells release tissue plasminogen activator (tPA). Thrombolysis begins when healed endothelial cells produce and release the enzyme Tissue plasminogen activator (plaz-MIN-oh-jen) , or tPA. Thrombolysis can also be initiated by a similar enzyme called urokinase (yoo-roh-KY-nayz), which is produced by cells of the kidney and found in the plasma and interstitial fluid. ❷❷ tPA activates plasminogen. The inactive enzyme plasminogen, which is normally found in plasma, has a high affinity for fibrin proteins and binds them as they are incorporated into the blood clot. As a result, every blood clot contains a significant amount of plasminogen. When tPA contacts plasminogen, it catalyzes the reaction that converts it to the active enzyme Plasmin. ❸❸ Plasmin degrades fibrin, and the clot dissolves. Plasmin catalyzes the reaction that degrades both fibrin and fibrinogen. This causes the remaining components of the clot to dissociate from the endothelium

anemia

A condition in which the blood is deficient in red blood cells, in hemoglobin, or in total volume. The most common type of anemia is iron-deficiency anemia, which is due to inadequate dietary iron, reduced intestinal absorption of dietary iron, or slow blood loss (including menstruation). Without functional iron-containing heme groups, erythroblasts cannot make hemoglobin. Pernicious anemia results from vitamin B12 deficiency, which interferes with DNA synthesis of rapidly dividing cells, including hematopoietic cells in bone marrow. Erythrocyte destruction can lead to hemolytic anemia. Causes of hemolytic anemia include bacterial infections, diseases of the immune system or liver, and lead poisoning. Finally, the red bone marrow may stop producing erythrocytes, which results in aplastic anemia (-plasis = "formation"). Certain medications or exposure to ionizing radiation may induce aplastic anemia, but the cause in many cases is unknown.

Polycythemia

A disorder characterized by an abnormal increase in the number of red blood cells in the blood

Describe or draw the shape of RBC's. Be able to discuss the design of RBCs and relate it to functions of carrying and delivering respiratory gases, gas exchange and traveling through the blood vessels.

A typical Erythrocyte (eh-RITH-roh-syt; erythr- = "red"), or red blood cell (RBC), is a biconcave disc: a flattened, donut-shaped cell that is concave on both sides (Figure 19.2a and b). This shape gives erythrocytes a large surface-to-volume ratio, which is critical to their role in gas exchange. Erythrocytes are small cells, measuring only about 7.5 μm in diameter and 2.5 μm in width. At this size, you could fit about 70,000 erythrocytes on the head of a pin. Notice in the figure that mature erythrocytes are anucleate (have no nucleus) and also lack most other organelles. This means that mature erythrocytes are not capable of carrying out oxidative catabolism or protein synthesis. In fact, an erythrocyte consists of little more than a plasma membrane surrounding cytosol filled with enzymes and about one billion molecules of the oxygen-binding protein Hemoglobin, or Hb (HEE-muh-gloh-bin) (Figure 19.2c). The shape and composition of an erythrocyte facilitate its transport of oxygen through the blood, an example of the Structure-Function Core Principle (Module 1.5.5).

Discuss the life cycle of the RBC's ending with their destruction.

As erythrocytes age, their plasma membranes become less flexible, making their passage through tiny capillaries more difficult. This is particularly the case in the sinusoids of the Spleen, an organ located in the superior left abdominal cavity. Erythrocyte destruction proceeds by the following steps (Figure 19.6): ❶❶ Erythrocytes become trapped in the sinusoids of the spleen. Older erythrocytes are not flexible enough to exit the tortuous sinusoids. ❷❷ Spleen macrophages digest erythrocytes. In the sinusoids, erythrocytes encounter leukocytes called macrophages (discussed in ​Module 19.3​). Macrophages are phagocytes that ingest and destroy older erythrocytes and other cells. ❸❸ Hemoglobin is broken down into amino acids, iron ions, and bilirubin. The macrophages break down the hemoglobin of erythrocytes. The polypeptide chains of hemoglobin are broken down into amino acids, the iron ions are removed from the heme groups, and the remainder of the heme is converted first into the waste product biliverdin, a greenish pigment (verd = "green"). Generally, biliverdin is then converted into a second waste product, the yellowish pigment bilirubin (BIL-ih-roo-bin). Interestingly, biliverdin is responsible for the greenish color seen in bruises. As the biliverdin is converted to bilirubin, the bruise becomes yellow. 4a Iron ions and amino acids are recycled and used to make new hemoglobin in red bone marrow. Most of the iron ions and amino acids are transported to the red bone marrow to be incorporated into new hemoglobin, a form of molecular recycling. You can see in Figure 19.6 that the iron ions are transferred to a protein called transferrin (trans-FER-in) that carries them through the blood. 4b Bilirubin is sent to the liver for excretion. At the same time the events in 4a are occurring, bilirubin enters the blood and is transported to the liver, where it is modified and excreted in feces and urine.

List the general function of blood.

Exchanging gases. Oxygen is transported from the lungs to the tissues primarily by erythrocytes. Similarly, both erythrocytes and plasma transport carbon dioxide away from the tissues to the lungs. Distributing solutes. Plasma transports many solutes, including nutrients, hormones, and wastes. Additionally, blood transports ions and plays a role in regulating ion concentrations in the tissues. Performing immune functions. Both the cells (leukocytes) and proteins of the immune system use blood as a transport vehicle to reach almost any tissue in the body. Maintaining body temperature. Heat is a byproduct of many chemical reactions in the body, particularly metabolic reactions. Blood carries away the heat produced by an actively metabolizing tissue, which helps to maintain a constant temperature in that tissue. Sealing damaged vessels by forming blood clots. When a blood vessel is broken, platelets and certain proteins form a blood clot that seals the damaged vessel, preventing excessive blood loss. Preserving acid-base homeostasis. The pH of blood is generally maintained within the narrow range of 7.35-7.45. The pH remains fairly constant because blood composition controls many of the body's most important buffer systems. Also, many plasma proteins act as buffers. Stabilizing blood pressure. One of the primary factors that determine blood pressure is the volume of blood in the circulation (see Chapter 18). Blood volume is vital to maintaining blood pressure at a constant level.

Explain the cause of hemolytic disease of the newborn (erythroblastosis fetalis) and why the treatment of RhoGAM is given to Rh- mothers.

Hemolytic disease of the newborn (HDN) — also called erythroblastosis fetalis — is a blood disorder that occurs when the blood types of a mother and baby are incompatible. There are two causes, Rh incompatibility and ABO incompatibility. If a mother is Rh-negative and has not been sensitized, she is usually given a drug called Rh immunoglobulin, or RhoGAM. This specially developed blood product prevents an Rh-negative mother's antibodies from reacting to her baby's Rh-positive red blood cells.

Thalassemia

Inherited defect in the ability to produce hemoglobin, usually seen in persons of Mediterranean background.

List the specific plasma proteins, what their function is and where they are formed.

Plasma proteins make up about 9% of plasma volume. These proteins—most made by the liver—are too large to fully dissolve in the water portion of plasma and so form a colloid. Important plasma proteins include: Albumin. As you read in​ Chapter 18​, Albumin (al-BYOO-min) is a relatively large protein produced by the liver that is responsible for blood's colloid osmotic pressure, or the pressure that draws water into the blood via osmosis, an example of the Gradients Core Principle (Module 1.5.5). To discover what happens when the liver cannot produce enough albumin, see A&P in the Real World: Cirrhosis. Immune proteins. The γ-globulins, also known as antibodies, are plasma proteins of the immune system. Unlike most plasma proteins, antibodies (see later in this chapter) are produced by leukocytes. The chapter on immunity will discuss antibodies in detail (see Chapter 20). Transport proteins. Recall that lipid-based compounds such as fats and steroids are hydrophobic (see Chapter 2). This feature makes their transport through blood problematic, because hydrophobic compounds tend to associate with one another and form clumps rather than associate with water molecules. These compounds may be transported safely through the blood by binding to transport proteins that are hydrophilic and can associate with water molecules. Examples of such transport proteins include globular proteins called α- and β-globulins and lipoproteins. Clotting proteins. A blood clot, which is a collection of platelets and clotting proteins, stops bleeding from an injured blood vessel​. Module 19.5 ​gives details on clotting proteins.

List the liquid and cellular (formed elements) components of the blood.

Plasma, the liquid extracellular matrix; and formed elements, the cells and cell fragments that are suspended in plasma. Blood contains three types of formed elements: (1) erythrocytes, or red blood cells (RBCs); (2) leukocytes, or white blood cells (WBCs); and (3) tiny cellular fragments called platelets.

Discuss or draw the homeostatic mechanism of erthyropoiesis.

Recall that hematopoiesis (heh′-mah-toh-poy-EE-sis; poiesis = "make, produce") is the process that produces the formed elements in blood (see Chapter 6). Hematopoiesis occurs in red bone marrow, which houses the cells from which all formed elements arise: the Hematopoietic stem cells, or HSCs. Erythropoiesis (ee-rith′-roh-poy-EE-sis), the formation of erythrocytes, is part of the larger process of hematopoiesis (Figure 19.4). Erythropoiesis begins when HSCs differentiate into progenitor cells called erythrocyte colony-forming units (CFUs). At this point they are committed, meaning they are able to become only a single cell type. Erythrocytes form at the incredible rate of about 250 billion cells per day. Erythrocyte CFUs next differentiate into proerythroblasts (-blast = "immature cell"), a process requiring the presence of the hormone erythropoietin (ee-rith′-roh-POY-eh-tin), or EPO, secreted by the kidneys. Proerythroblasts develop into erythroblasts, which rapidly synthesize hemoglobin and other proteins. Notice that as erythroblasts mature, their nuclei shrink and are eventually ejected from the cells, at which point they are called reticulocytes (reh-TIK-yoo-loh-sytz′). These cells retain some organelles, particularly ribosomes. When they eject these remaining organelles by exocytosis, they enter the bloodstream by squeezing through the large pores in the sinusoidal capillaries of the bone marrow and are considered erythrocytes. The entire process takes 5-7 days.

Perform a transfusion reaction (major cross match) to determine if a donor's blood type is compatible with a recipient's blood type. Interpret blood typing results.

Recipient Blood Type Matching Donor BloodType A+ A+, A-, O+, O -A -A-, O- B+ B+, B-, O+, O- B- B-,O- AB+ Compatible with all blood types AB- AB-, A-, B-, O- O+ O+, O- O- O-

Discuss the homeostatic mechanism of hemostasis. Identify the stages of the process, being sure to give a detailed explanation of how each stage works.

Significant blood loss threatens many homeostatic body functions, including blood pressure maintenance, tissue oxygenation, and electrolyte balance. Fortunately, the body has mechanisms that minimize the amount of blood lost from an injured blood vessel. These mechanisms are part of a process called hemostasis (hee-moh-STAY-sis; "blood stoppage"). Hemostasis involves a series of events that form a gelatinous blood clot to "plug" the broken vessel. We can summarize hemostasis in five steps: 1. vascular spasm 2. platelet plug formation 3. coagulation 4. clot retraction 5. thromboloysis

Malaria

This disease is commonly associated with poverty and is spread by mosquitos. A disease caused by a plasmodium parasite, transmitted by the bite of infected mosquitoes. The severity of malaria varies based on the species of plasmodium. Symptoms are chills, fever, and sweating, usually occurring a few weeks after being bitten. People traveling to areas where malaria is common typically take protective drugs before, during, and after their trip. Treatment includes antimalarial drugs.

Explain the agglutinogen and agglutinin differences between the major ABO and Rh blood types. Identify the universal donor and universal recipient blood types.

The ABO and Rh blood groups combine to give the eight common blood types. For example, the erythrocytes in a type AB− individual feature the A and B antigens, but no Rh antigen, whereas the erythrocytes in a type O+ individual feature only the Rh antigen, without A or B We can determine blood type in the laboratory, using antibodies that recognize and bind to individual antigens on erythrocytes. Antibodies are produced by cells derived from activated B lymphocytes, and they bind to foreign antigens. Each unique antibody has a unique antigen to which it binds. As you can see in Figure 19.18, antibodies cause bound antigens to clump together, or agglutinate. For this reason, antibodies are sometimes called agglutinins (uh-GLOO-tuh-ninz). Ultimately, agglutination promotes destruction of the erythrocytes, a reaction known as hemolysis (hee-MAW-luh-sis; lysis = "to separate or split"). To determine blood type, a blood sample is treated with three antibodies: Anti-A antibodies bind and agglutinate A antigens. Anti-B antibodies bind and agglutinate B antigens. Anti-Rh antibodies bind and agglutinate Rh antigens. As you can see in Figure 19.19, if agglutination occurs in response to an antibody, that antigen is present on the erythrocyte. If agglutination does not occur, that antigen is absent.

List the specific formed elements and give a function for each. Also indicate the quantities of each.

The largest leukocytes are the monocytes, which account for 4-8% of the total leukocyte population. Monocytes are easily distinguished from other leukocytes by their large U-shaped nuclei and light blue or purple cytoplasm that becomes visible when the cells are stained. Monocytes remain in the blood for only a few days before they exit the capillaries and enter the tissues, where some mature into very active phagocytes called​ macrophages​ (MAK-roh-fehj-uhz; "big eater"). Macrophages ingest dead and dying cells (such as old erythrocytes or those damaged from trauma), bacteria, antigens, and other cellular debris. In addition, they activate other parts of the immune system by displaying phagocytosed antigens to other leukocytes.

List the specific formed elements and give a function for each. Also indicate the quantities of each.

The second most numerous type of leukocyte, lymphocytes, make up about 30-34% of total leukocytes in the blood. They contain large, spherical nuclei and generally a thin rim of light blue cytoplasm that is visible when stained (see Figure 19.8). There are two basic types of lymphocytes: B lymphocytes (or B cells) and T lymphocytes (or T cells). Both B and T lymphocytes are activated by cellular markers called antigens (AN-tih-jenz). Antigens, which are generally glycoproteins, are present on all cells and most biological compounds. Although B and T lymphocytes are structurally similar, they differ in their functions. Activated B lymphocytes produce proteins called Antibodies that bind to antigens and remove them from tissues. Each population of B lymphocytes secretes antibodies with a specific structure that allows them to bind to only one unique antigen. Populations of T lymphocytes also show specificity for individual antigens. However, activated T lymphocytes do not produce antibodies. Instead, populations of T lymphocytes have specific receptors for individual antigens. When the receptors are bound, T lymphocytes activate other components of the immune system and directly destroy abnormal body cells, such as cancer cells and those that are virally infected. Antibodies and T lymphocyte receptors, then, are structured in such a way that they bind to only one unique antigen, an example of the Structure-Function Core Principle (